Damned Heretics

Condemned by the established, but very often right

I am Nicolaus Copernicus, and I approve of this blog

I am Richard Feynman and I approve of this blog

Qualified outsiders and maverick insiders are often right about the need to replace received wisdom in science and society, as the history of the Nobel prize shows. This blog exists to back the best of them in their uphill assault on the massively entrenched edifice of resistance to and prejudice against reviewing, let alone revising, ruling ideas. In support of such qualified dissenters and courageous heretics we search for scientific paradigms and other established beliefs which may be maintained only by the power and politics of the status quo, comparing them with academic research and the published experimental and investigative record.

We especially defend and support the funding of honest, accomplished, independent minded and often heroic scientists, inventors and other original thinkers and their right to free speech and publication against the censorship, mudslinging, false arguments, ad hominem propaganda, overwhelming crowd prejudice and internal science politics of the paradigm wars of cancer, AIDS, evolution, global warming, cosmology, particle physics, macroeconomics, health and medicine, diet and nutrition.

HONOR ROLL OF SCIENTIFIC TRUTHSEEKERS

Henry Bauer, Peter Breggin , Harvey Bialy, Giordano Bruno, Erwin Chargaff, Nicolaus Copernicus, Francis Crick, Paul Crutzen, Marie Curie, Rebecca Culshaw, Freeman Dyson, Peter Duesberg, Albert Einstein, Richard Feynman, John Fewster, Galileo Galilei, Alec Gordon, James Hansen, Edward Jenner, Benjamin Jesty, Michio Kaku, Adrian Kent, Ernst Krebs, Thomas Kuhn, Serge Lang, John Lauritsen, Mark Leggett, Richard Lindzen, Lynn Margulis, Barbara McClintock, George Miklos, Marco Mamone Capria, Peter Medawar, Kary Mullis, Linus Pauling, Eric Penrose, Max Planck, Rainer Plaga, David Rasnick, Sherwood Rowland, Carl Sagan, Otto Rossler, Fred Singer, Thomas Szasz, Alfred Wegener, Edward O. Wilson, James Watson.
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Many people would die rather than think – in fact, they do so. – Bertrand Russell.

Skepticism is dangerous. That’s exactly its function, in my view. It is the business of skepticism to be dangerous. And that’s why there is a great reluctance to teach it in schools. That’s why you don’t find a general fluency in skepticism in the media. On the other hand, how will we negotiate a very perilous future if we don’t have the elementary intellectual tools to ask searching questions of those nominally in charge, especially in a democracy? – Carl Sagan (The Burden of Skepticism, keynote address to CSICOP Annual Conference, Pasadena, April 3/4, 1982).

It is really important to underscore that everything we’re talking about tonight could be utter nonsense. – Brian Greene (NYU panel on Hidden Dimensions June 5 2010, World Science Festival)

I am Albert Einstein, and I heartily approve of this blog, insofar as it seems to believe both in science and the importance of intellectual imagination, uncompromised by out of date emotions such as the impulse toward conventional religious beliefs, national aggression as a part of patriotism, and so on.   As I once remarked, the further the spiritual evolution of mankind advances, the more certain it seems to me that the path to genuine religiosity does not lie through the fear of life, and the fear of death, and blind faith, but through striving after rational knowledge.   Certainly the application of the impulse toward blind faith in science whereby authority is treated as some kind of church is to be deplored.  As I have also said, the only thing ever interfered with my learning was my education. My name as you already perceive without a doubt is George Bernard Shaw, and I certainly approve of this blog, in that its guiding spirit appears to be blasphemous in regard to the High Church doctrines of science, and it flouts the censorship of the powers that be, and as I have famously remarked, all great truths begin as blasphemy, and the first duty of the truthteller is to fight censorship, and while I notice that its seriousness of purpose is often alleviated by a satirical irony which sometimes borders on the facetious, this is all to the good, for as I have also famously remarked, if you wish to be a dissenter, make certain that you frame your ideas in jest, otherwise they will seek to kill you.  My own method was always to take the utmost trouble to find the right thing to say, and then to say it with the utmost levity. (Photo by Alfred Eisenstaedt for Life magazine) One should as a rule respect public opinion in so far as is necessary to avoid starvation and to keep out of prison, but anything that goes beyond this is voluntary submission to an unnecessary tyranny, and is likely to interfere with happiness in all kinds of ways. – Bertrand Russell, Conquest of Happiness (1930) ch. 9

(Click for more Unusual Quotations on Science and Belief)

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Pew Survey measures the vast public ignorance that scientists can exploit

August 31st, 2005

Today (Wed Aug 31) the Times (page A9) has a predictable story by Laurie Goldstein retailing the results of a poll by the Pew Forum on Religion and Public Life and the Pew Center for the People and the Press, where the familiar and depressing result was to expose the grand level of public ignorance about one of the simplest and most easily appreciated scientific theories, the idea that life forms evolve naturally and without any help from supernatural intervention.

Fully 42 per cent held strict creationist views, believing that “living things have existed in their present form since the beginning of time.” Of the 48 per cent who have somehow cottoned on to the probability that humans evolved over time, one out of five (18 per cent) thought that this was helped along by some all-powerful entity pulling strings from behind the scenes – “guided by a supreme being.”

In line with this about two thirds – 64 per cent – thought along with the No Child Left Behind president that it would be fine to teach creationism alongside evolution in schools, while nearly two out of five Americans favored replacing the teaching of evolution with creationism.

(Here is Laurie Goodstein’s story in the Times:)

Teaching of Creationism Is Endorsed in New Survey

By LAURIE GOODSTEIN

In a finding that is likely to intensify the debate over what to teach students about the origins of life, a poll released yesterday found that nearly two-thirds of Americans say that creationism should be taught alongside evolution in public schools.

The poll found that 42 percent of respondents held strict creationist views, agreeing that “living things have existed in their present form since the beginning of time.”

In contrast, 48 percent said they believed that humans had evolved over time. But of those, 18 percent said that evolution was “guided by a supreme being,” and 26 percent said that evolution occurred through natural selection. In all, 64 percent said they were open to the idea of teaching creationism in addition to evolution, while 38 percent favored replacing evolution with creationism.

The poll was conducted July 7-17 by the Pew Forum on Religion and Public Life and the Pew Research Center for the People and the Press. The questions about evolution were asked of 2,000 people. The margin of error was 2.5 percentage points.

John C. Green, a senior fellow at the Pew Forum, said he was surprised to see that teaching both evolution and creationism was favored not only by conservative Christians, but also by majorities of secular respondents, liberal Democrats and those who accept the theory of natural selection. Mr. Green called it a reflection of “American pragmatism.”

“It’s like they’re saying, ‘Some people see it this way, some see it that way, so just teach it all and let the kids figure it out.’ It seems like a nice compromise, but it infuriates both the creationists and the scientists,” said Mr. Green, who is also a professor at the University of Akron in Ohio.

Eugenie C. Scott, the director of the National Center for Science Education and a prominent defender of evolution, said the findings were not surprising because “Americans react very positively to the fairness or equal time kind of argument.”

“In fact, it’s the strongest thing that creationists have got going for them because their science is dismal,” Ms. Scott said. “But they do have American culture on their side.”

This year, the National Center for Science Education has tracked 70 new controversies over evolution in 26 states, some in school districts, others in the state legislatures.

President Bush joined the debate on Aug. 2, telling reporters that both evolution and the theory of intelligent design should be taught in schools “so people can understand what the debate is about.”

Senator Bill Frist of Tennessee, the Republican leader, took the same position a few weeks later.

Intelligent design, a descendant of creationism, is the belief that life is so intricate that only a supreme being could have designed it.

The poll showed 41 percent of respondents wanted parents to have the primary say over how evolution is taught, compared with 28 percent who said teachers and scientists should decide and 21 percent who said school boards should. Asked whether they believed creationism should be taught instead of evolution, 38 percent were in favor, and 49 percent were opposed.

More of those who believe in creationism said they were “very certain” of their views (63 percent), compared with those who believe in evolution (32 percent).

The poll also asked about religion and politics, government financing of religious charities, and gay men and lesbians in the military. Most of these questions were asked of a smaller pool of 1,000 respondents, and the margin of error was 2.5 percentage points, Pew researchers said.

The public’s impression of the Democratic Party has changed in the last year, the survey found. Only 29 percent of respondents said they viewed Democrats as being “friendly toward religion,” down from 40 percent in August of 2004. Meanwhile, 55 percent said the Republican Party was friendly toward religion.

Luis E. Lugo, the director of the Pew Forum on Religion and Public Life, said: “I think this is a continuation of the Republican Party’s very successful use of the values issue in the 2004 election, and the Democrats not being able up until now to answer that successfully. Some of the more visible leaders, such as Howard Dean and others, have reinforced that image of a secular party. Of course, if you look at the Democratic Party, there’s a large religious constituency there.”

Survey respondents agreed in nearly equal numbers that nonreligious liberals had “too much control” over the Democratic Party (44 percent), and that religious conservatives had too much control over the Republican Party (45 percent).

On religion-based charities, two-thirds of respondents favored allowing churches and houses of worship to apply for government financing to provide social services. But support for such financing declined from 75 percent in early 2001, when Mr. Bush rolled out his religion-based initiative.

On gay men and lesbians in the military, 58 percent of those polled said they should be allowed to serve openly, a modest increase from 1994, when 52 percent agreed. Strong opposition has fallen in that time, to 15 percent from 26 percent in 1994.

That latter figure – 38 percent favored replacing evolution with creationism – is the mind boggling one.

Except, perhaps, if one watches the “Jay walking” sergment of Jay Leno’s nightly talk show on NBC, where the amiably reassuring host confronts passers by on the streets of Los Angeles with questions of childish simplicity, of the order of “Which country is to the North of the US?” or “Where is France?” As Leno shows time after time, the average youngish inhabitant of Los Angeles that he picks is completely stumped.

In principle this might be a classless democracy but it is sadly clear that those who expect the average American to know what scientists are talking about are unaware of how extraordinarily disadvantaged educationally two thirds of the population are.

Fooling all the people all the time

The chances of a public outcry when scientists in for example AIDS or cancer are exposed as pulling the wool over the public’s eyes for twenty years or more seem low to zero, for this basic level of ignorance is only the lower half of the pyramid of ignorance about science which stretches up to the top levels of power in Washington.

Small wonder that the scientists who perpetrate these unproductive paradigms on the basis of literature the most tested of which long ago showed that they were money wasting dead ends seem entirely unworried that they will ever be held to account for their actions.

It is not just the general public who are defenceless in the face of any scientists who want to engage them in the scientific equivalent of three card monte, it is the media editors and reporters, the senators and congressmen, and government officials who are in theory those who are meant to guard the public purse from any such scams.

They must depend on skilled advisors they trust, who must be able to comprehend such fields to the level where they can distinguish between viable and ill founded ideas in science, and have no political prejudice in making such assessments, even if their bosses do.

This is a tall order, as the present state of scientific policy under the hand of the Bush administration shows. There’s both left and right bias in the scientific claims that are made in the political realm, and the supply of impeccably objective and uncompromised advisors is very slim.

Yet this is a problem which must be surmounted if society is to be protected from being fooled into funding paradigms which are already exploded in the peer reviewed literature. In AIDS and cancer, in particular, it seems unlikely that the scientists who lead those fields and thus the public and governments round the world into funding the themes they sound will ever be held to account for their suppressing discussion of the difficulties that result, which according to the critiques that have survived the most hostile peer review to be published in the leading journals are inevitable because their theories do not make scientific sense.

For the only investigation which will make any difference at this stage would be either a sudden improvement in the alertness and objectivity of the coverage of these fields in the New York Times, and a long and comprehensive investigative report in that paper or just possibly a similar awakening in the pages of Harpers or the Atlantic; or a Congressional investigation with testimony from leading scientists of both stripes, that is to say, the human pillars of these two paradigms and their critical reviewers.

Perhaps this might be achieved by a pubic spirited patron willing to deliver copies to the major media, Senate and Congress of the book by Harvey Bialy, “Aneuploidy, Oncogenes and AIDS: The Life and Scientific Times of Peter H. Duesberg” (North Atlantic Books, 2004).

This invaluable survey, already a classic in the minds of many informed readers, is as we have noted earlier currently the definitive evisceration of the theory and practice of the purported sciences of AIDS and cancer as now perpetrated by the scientists who lead the field, and an account of how they managed to bamboozle even the editors of Nature and Science into helping them sideline the critiques of both paradigms by Berkeley’s Peter Duesberg, even though his rejecting reviews had been published in the very best journals after the most severe and hostile (and thus validating) peer reviewing in the recent history of either field.

The big problem here, however, is that Bialy’s book may be of great interest and satisfaction, even entertainment only to those intelligent readers with some acquaintance of the science involved in his classically precise and intellectually lively and often amusing work.

To the average reader, however, even the intelligent reader with some idea of what he is talking about, the book is a hard read, and not one which any editor, reporter, Senator, Congressman, or staff member will be able to fathom without devoting an unusual amount of time to studying its explanations of why Duesberg’s critique is irresistible even if the accumulated mass of theory and practice it takes apart has so far proved immovable.

On the other hand, the politics and behavior of the stars of science who play leading roles, and their essential corruption and evasion is dealing with Duesberg’s review of their stock-in-trade, is clear enough in Bialy’s book. It is the abundant, precise and rather technical science that he elegantly purveys throughout the book that stops most readers, unfortunately, even those who are already sympathtic to his theme.

Even for these sympathizers its difficult science – accurate and invaluable though it is to anybody seriously researching the issues it deals with, and utterly persuasive because of this precision – as a promoter of change in public policy and public opinion the book is likely to fail because it is simply not an easy enough read. With the science included at every relevant point without additional explanation for the layman it becomes at those points, as even one lay journalist actively supporting free speech and debate in these fields put it to us, “unreadable.”

For this reason we say that what the world is waiting for is a vivid journalistic expose of the politics and behavior of the scientists rather than yet another analysis of where they have gone wrong in science, a topic which has already seen fourteen very good books in AIDS which have gone nowhere, even though more than half of them do also expose very well the politics and behavior of the scientists involved.

A tipping point may be approaching

It is the focus on the politics and behavior without too much science which seems to be the crucial approach which might lead to the long awaited (by the AIDS heretics and the much smaller group of cancer theory skeptics) tipping point in these fields, such that a reexamination of the paradigms by a Congressional committee and/or the Times will be provoked.

Interestingly enough there is just such a piece in the works from a journalist of great talent who has achieved, according to the draft we read, the magical goal of reporting the politics and behavior of the scientists, drug companies, officials and activists in AIDS and their manipulation of the media, other scientists, and the data and the studies on which all depend in such clearly honest, accurate and readable terms that we expect almost all readers to smell a global-sized rat in the science of AIDS even though the discussion of the science of AIDS in the piece is minimal.

It will be interesting to see what the effect of this piece when published will be. We confidently expect its moral outrage to be shared by almost every impartial reader who encounters it, and thus that it will be influential in provoking the media and Wahsington at long last to look at the picture it draws with new eyes.

If that is so, it might be, after more than two decades of effectively complete suppression of free speech and alternative views in AIDS, a tipping point.

Cholera indexes how bad conditions can be in Africa

August 28th, 2005

Presumably cholera acts too quickly to be misdiagnosed as AIDS, but its outbreaks surely indicate how rough conditions are on the ground in many places. A little item in the Times from Reuters at the bottom of the second page on Sunday salutes this perennial threat.

The New York Times

August 28, 2005

Cholera Kills Hundreds in West Africa

By REUTERS

DAKAR, Senegal, Aug. 27 (Reuters) – Cholera outbreaks caused partly by heavy rains battering West Africa have killed hundreds of people in the last few months, prompting appeals for medicine to help thousands of sufferers, United Nations officials said this week.

(more)

The New York Times

August 28, 2005

Cholera Kills Hundreds in West Africa

By REUTERS

DAKAR, Senegal, Aug. 27 (Reuters) – Cholera outbreaks caused partly by heavy rains battering West Africa have killed hundreds of people in the last few months, prompting appeals for medicine to help thousands of sufferers, United Nations officials said this week.

The number of recorded cholera cases in West Africa this year is 24,621, with at least 401 deaths in Burkina Faso, Guinea, Guinea-Bissau, Liberia, Mali, Mauritania, Niger and Senegal, according to United Nations data.

In Guinea-Bissau, the hardest hit, cholera deaths have more than doubled since Aug. 9, rising to 188 from 84. An official in the Health Ministry in Bissau, the capital, which has borne the brunt of the epidemic, said more than 9,000 cases had been recorded and that the disease was spreading rapidly in the provinces.

In Congo, a cholera outbreak in a convoy of about 3,000 soldiers traveling with their families in the east killed at least 16 people and infected hundreds, aid officials said Friday. Relief workers said the convoy, had dropped off hundreds of infected people in villages along the way, spreading exposure to local residents.

Cholera can kill victims within 24 hours by inducing vomiting and diarrhea that cause severe dehydration, but it is treatable using a simple mixture of water and rehydration salts.

Often associated with heavy rains that flood latrines or contaminate wells, cholera usually kills people who are so poor they cannot afford basic health care.

Several countries have sent aid, including France, China and Portugal, but United Nations officials said more was needed.

Career advice to AIDS heretics from Kit

August 27th, 2005

“Try to keep an open mind and understand the viewpoints of others. Consider the minority opinion. But try to get along with the majority of opinion once it is accepted.”

(Martin Sheen as the trigger happy killer Kit in Terrence Malick’s Badlands, trying out the dictaphone in the rich man’s mansion).

Career advice for scientists from Kit

August 25th, 2005

“Try to keep an open mind and understand the viewpoints of others. Consider the minority opinion. But try to get along with the majority of opinion once it is accepted.”

(Martin Sheen as the trigger happy killer Kit in Terrence Malick’s Badlands, trying out the dictaphone in the rich man’s mansion).

The Times surveys the ID vs Darwin scene with equanimity

August 22nd, 2005

Perhaps inspired by George W’s suggestion for schools, the New York Times yesterday had on the front page for Hampton’s beach reading a nicely balanced, typically non-combative survey of the science, politics and funding of Intelligent Design and its bid to elbow aside evolution to share the center of the stage in the schools and in the media.

It is interesting to note the Harvard student roots of this phenomenon, and the fact that some of the original boosters have fallen by the way side, put off by the streaks of archconservatism and religious fundamentalism they found under the surface layer of open minded reason and speculation.

From our scientific perspective we can only ask both sides again why the gaps in evolutionary explanation need to be denied, and why God is needed to fill them.

See Politicized Scholars Put Evolution on the Defensive, by Jodi Wilgoren

The New York Times

August 21, 2005

Politicized Scholars Put Evolution on the Defensive

By JODI WILGOREN

SEATTLE – When President Bush plunged into the debate over the teaching of evolution this month, saying, “both sides ought to be properly taught,” he seemed to be reading from the playbook of the Discovery Institute, the conservative think tank here that is at the helm of this newly volatile frontier in the nation’s culture wars.

After toiling in obscurity for nearly a decade, the institute’s Center for Science and Culture has emerged in recent months as the ideological and strategic backbone behind the eruption of skirmishes over science in school districts and state capitals across the country. Pushing a “teach the controversy” approach to evolution, the institute has in many ways transformed the debate into an issue of academic freedom rather than a confrontation between biology and religion.

Mainstream scientists reject the notion that any controversy over evolution even exists. But Mr. Bush embraced the institute’s talking points by suggesting that alternative theories and criticism should be included in biology curriculums “so people can understand what the debate is about.”

Financed by some of the same Christian conservatives who helped Mr. Bush win the White House, the organization’s intellectual core is a scattered group of scholars who for nearly a decade have explored the unorthodox explanation of life’s origins known as intelligent design.

Together, they have mounted a politically savvy challenge to evolution as the bedrock of modern biology, propelling a fringe academic movement onto the front pages and putting Darwin’s defenders firmly on the defensive.

Like a well-tooled electoral campaign, the Discovery Institute has a carefully crafted, poll-tested message, lively Web logs – and millions of dollars from foundations run by prominent conservatives like Howard and Roberta Ahmanson, Philip F. Anschutz and Richard Mellon Scaife. The institute opened an office in Washington last fall and in January hired the same Beltway public relations firm that promoted the Contract With America in 1994.

“We are in the very initial stages of a scientific revolution,” said the center’s director, Stephen C. Meyer, 47, a historian and philosopher of science recruited by Discovery after he protested a professor’s being punished for criticizing Darwin in class. “We want to have an effect on the dominant view of our culture.”

For the institute’s president, Bruce K. Chapman, a Rockefeller Republican turned Reagan conservative, intelligent design appealed to his contrarian, futuristic sensibilities – and attracted wealthy, religious philanthropists like the Ahmansons at a time when his organization was surviving on a shoestring. More student of politics than science geek, Mr. Chapman embraced the evolution controversy as the institute’s signature issue precisely because of its unpopularity in the establishment.

“When someone says there’s one thing you can’t talk about, that’s what I want to talk about,” said Mr. Chapman, 64.

As much philosophical worldview as scientific hypothesis, intelligent design challenges Darwin’s theory of natural selection by arguing that some organisms are too complex to be explained by evolution alone, pointing to the possibility of supernatural influences. While mutual acceptance of evolution and the existence of God appeals instinctively to a faithful public, intelligent design is shunned as heresy in mainstream universities and science societies as untestable in laboratories.

Entering the Public Policy Sphere

From its nondescript office suites here, the institute has provided an institutional home for the dissident thinkers, pumping $3.6 million in fellowships of $5,000 to $60,000 per year to 50 researchers since the science center’s founding in 1996. Among the fruits are 50 books on intelligent design, many published by religious presses like InterVarsity or Crossway, and two documentaries that were broadcast briefly on public television. But even as the institute spearheads the intellectual development of intelligent design, it has staked out safer turf in the public policy sphere, urging states and school boards simply to include criticism in evolution lessons rather than actually teach intelligent design.

Since the presidential election last fall, the movement has made inroads and evolution has emerged as one of the country’s fiercest cultural battlefronts, with the National Center for Science Education tracking 78 clashes in 31 states, more than twice the typical number of incidents. Discovery leaders have been at the heart of the highest-profile developments: helping a Roman Catholic cardinal place an opinion article in The New York Times in which he sought to distance the church from evolution; showing its film promoting design and purpose in the universe at the Smithsonian; and lobbying the Kansas Board of Education in May to require criticism of evolution.

These successes follow a path laid in a 1999 Discovery manifesto known as the Wedge Document, which sought “nothing less than the overthrow of materialism and its cultural legacies” in favor of a “broadly theistic understanding of nature.”

President Bush’s signature education law, known as No Child Left Behind, also helped, as mandatory testing prompted states to rewrite curriculum standards. Ohio, New Mexico and Minnesota have embraced the institute’s “teach the controversy” approach; Kansas is expected to follow suit in the fall.

Detractors dismiss Discovery as a fundamentalist front and intelligent design as a clever rhetorical detour around the 1987 Supreme Court ruling banning creationism from curriculums. But the institute’s approach is more nuanced, scholarly and politically adept than its Bible-based predecessors in the century-long battle over biology.

A closer look shows a multidimensional organization, financed by missionary and mainstream groups – the Bill and Melinda Gates Foundation provides $1 million a year, including $50,000 of Mr. Chapman’s $141,000 annual salary – and asserting itself on questions on issues as varied as local transportation and foreign affairs.

Many of the research fellows, employees and board members are, indeed, devout and determinedly conservative; pictures of William J. Bennett, the moral crusader and former drug czar, are fixtures on office walls, and some leaders have ties to movement mainstays like Focus on the Family. All but a few in the organization are Republicans, though these include moderates drawn by the institute’s pragmatic, iconoclastic approach on nonideological topics like technology.

But even as intelligent design has helped raise Discovery’s profile, the institute is starting to suffer from its success. Lately, it has tried to distance itself from lawsuits and legislation that seek to force schools to add intelligent design to curriculums, placing it in the awkward spot of trying to promote intelligent design as a robust frontier for scientists but not yet ripe for students.

The group is also fending off attacks from the left, as critics liken it to Holocaust deniers or the Taliban. Concerned about the criticism, Discovery’s Cascadia project, which focuses on regional transportation and is the recipient of the large grant from the Gates Foundation, created its own Web site to ensure an individual identity.

“All ideas go through three stages – first they’re ignored, then they’re attacked, then they’re accepted,” said Jay W. Richards, a philosopher and the institute’s vice president. “We’re kind of beyond the ignored stage. We’re somewhere in the attack.”

Origins of an Institute

Founded in 1990 as a branch of the Hudson Institute, based in Indianapolis, the institute was named for the H.M.S. Discovery, which explored Puget Sound in 1792. Mr. Chapman, a co-author of a 1966 critique of Barry M. Goldwater’s anti-civil-rights campaign, “The Party That Lost Its Head,” had been a liberal Republican on the Seattle City Council and candidate for governor, but moved to the right in the Reagan administration, where he served as director of the Census Bureau and worked for Edwin Meese III.

In late 1993, Mr. Chapman clipped an essay in The Wall Street Journal by Dr. Meyer, who was teaching at a Christian college in Spokane, Wash., concerning a biologist yanked from a lecture hall for discussing intelligent design. About a year later, over dinner at the Sorrento Hotel here, Dr. Meyer and George Gilder, Mr. Chapman’s long-ago Harvard roommate and his writing partner, discovered parallel theories of mind over materialism in their separate studies of biology and economics.

“Bruce kind of perked up and said, ‘This is what makes a think tank,’ ” Dr. Meyer recalled. “There was kind of an ‘Aha!’ moment in the conversation, there was a common metaphysic in these two ideas.”

That summer of 1995, Mr. Chapman and Dr. Meyer had dinner with a representative of the Ahmansons, the banking billionaires from Orange County, Calif., who had previously given a small grant to the institute and underwritten an early conclave of intelligent design scholars. Dr. Meyer, who had grown friendly enough with the Ahmansons to tutor their young son in science, recalled being asked, “What could you do if you had some financial backing?”

So in 1996, with the promise of $750,000 over three years from the Ahmansons and a smaller grant from the MacLellan Foundation, which supports organizations “committed to furthering the Kingdom of Christ,” according to its Web site, the institute’s Center for Science and Culture was born.

“Bruce is a contrarian, and this was a contrarian idea,” said Edward J. Larson, the historian and author of a Pulitzer Prize-winning book on the Scopes Monkey Trial, who was an early fellow at the institute, but left in part because of its drift to the right. “The institute was living hand-to-mouth. Here was an academic, credible activity that involved funders. It interested conservatives. It brought in money.”

Support From Religious Groups

The institute would not provide details about its backers “because they get harassed,” Mr. Chapman said. But a review of tax documents on www.guidestar.org, a Web site that collects data on foundations, showed its grants and gifts jumped to $4.1 million in 2003 from $1.4 million in 1997, the most recent and oldest years available. The records show financial support from 22 foundations, at least two-thirds of them with explicitly religious missions.

There is the Henry P. and Susan C. Crowell Trust of Colorado Springs, whose Web site describes its mission as “the teaching and active extension of the doctrines of evangelical Christianity.” There is also the AMDG Foundation in Virginia, run by Mark Ryland, a Microsoft executive turned Discovery vice president: the initials stand for Ad Majorem Dei Glorium, Latin for “To the greater glory of God,” which Pope John Paul II etched in the corner of all his papers.

And the Stewardship Foundation, based in Tacoma, Wash., whose Web site says it was created “to contribute to the propagation of the Christian Gospel by evangelical and missionary work,” gave the group more than $1 million between 1999 and 2003.

By far the biggest backers of the intelligent design efforts are the Ahmansons, who have provided 35 percent of the science center’s $9.3 million since its inception and now underwrite a quarter of its $1.3 million annual operations. Mr. Ahmanson also sits on Discovery’s board.

The Ahmansons’ founding gift was joined by $450,000 from the MacLellan Foundation, based in Chattanooga, Tenn.

“We give for religious purposes,” said Thomas H. McCallie III, its executive director. “This is not about science, and Darwin wasn’t about science. Darwin was about a metaphysical view of the world.”

The institute also has support from secular groups like the Verizon Foundation and the Gates Foundation, which gave $1 million in 2000 and pledged $9.35 million over 10 years in 2003. Greg Shaw, a grant maker at the Gates Foundation, said the money was “exclusive to the Cascadia project” on regional transportation.

But the evolution controversy has cost it the support of the Bullitt Foundation, based here, which gave $10,000 in 2001 for transportation, as well as the John Templeton Foundation in Pennsylvania, whose Web site defines it as devoted to pursuing “new insights between theology and science.”

Denis Hayes, director of the Bullitt Foundation, described Discovery in an e-mail message as “the institutional love child of Ayn Rand and Jerry Falwell,” saying, “I can think of no circumstances in which the Bullitt Foundation would fund anything at Discovery today.”

Charles L. Harper Jr., the senior vice president of the Templeton Foundation, said he had rejected the institute’s entreaties since providing $75,000 in 1999 for a conference in which intelligent design proponents confronted critics. “They’re political – that for us is problematic,” Mr. Harper said. While Discovery has “always claimed to be focused on the science,” he added, “what I see is much more focused on public policy, on public persuasion, on educational advocacy and so forth.”

For three years after completing graduate school in 1996, William A. Dembski could not find a university job, but he nonetheless received what he called “a standard academic salary” of $40,000 a year.

“I was one of the early beneficiaries of Discovery largess,” said Dr. Dembski, whose degrees include a doctorate in mathematics from the University of Chicago, one in philosophy from the University of Illinois and a master’s of divinity from Princeton Theological Seminary.

Money for Teachers and Students

Since its founding in 1996, the science center has spent 39 percent of its $9.3 million on research, Dr. Meyer said, underwriting books or papers, or often just paying universities to release professors from some teaching responsibilities so that they can ponder intelligent design. Over those nine years, $792,585 financed laboratory or field research in biology, paleontology or biophysics, while $93,828 helped graduate students in paleontology, linguistics, history and philosophy.

The 40 fellows affiliated with the science center are an eclectic group, including David Berlinski, an expatriate mathematician living in Paris who described his only religion to be “having a good time all the time,” and Jonathan Wells, a member of the Unification Church, led by the Rev. Sun Myung Moon, who once wrote in an essay, “My prayers convinced me that I should devote my life to destroying Darwinism.”

Their credentials – advanced degrees from Stanford, Columbia, Yale, the University of Texas, the University of California – are impressive, but their ideas are often ridiculed in the academic world.

“They’re interested in the same things I’m interested in – no one else is,” Guillermo Gonzalez, 41, an astronomer at the University of Iowa, said of his colleagues at Discovery. “What I’m doing, frankly, is frowned upon by most of my colleagues. It’s not something a ‘scientist’ is supposed to do.” Other than Dr. Berlinski, most fellows, like their financiers, are fundamentalist Christians, though they insist their work is serious science, not closet creationism.

“I believe that God created the universe,” Dr. Gonzalez said. “What I don’t know is whether that evidence can be tested objectively. I ask myself the tough questions.”

Discovery sees the focus on its fellows and financial backers as a diversionary tactic by its opponents. “We’re talking about evidence, and they want to talk about us,” Dr. Meyer said.

But Philip Gold, a former fellow who left in 2002, said the institute had grown increasingly religious. “It evolved from a policy institute that had a religious focus to an organization whose primary mission is Christian conservatism,” he said.

That was certainly how many people read the Wedge Document, a five-page outline of a five-year plan for the science center that originated as a fund-raising pitch but was soon posted on the Internet by critics.

“Design theory promises to reverse the stifling dominance of the materialist worldview, and to replace it with a science consonant with Christian and theistic convictions,” the document says. Among its promises are seminars “to encourage and equip believers with new scientific evidence that support the faith, as well as to ‘popularize’ our ideas in the broader culture.”

One sign of any political movement’s advancement is when adherents begin to act on their own, often without the awareness of the leadership. That, according to institute officials, is what happened in 1999, when a new conservative majority on the Kansas Board of Education shocked the nation – and their potential allies here at the institute – by dropping all references to evolution from the state’s science standards.

“When there are all these legitimate scientific controversies, this was silly, outlandish, counterproductive,” said John G. West, associate director of the science center, who said he and his colleagues learned of that 1999 move in Kansas from newspaper accounts. “We began to think, ‘Look, we’re going to be stigmatized with what everyone does if we don’t make our position clear.’ “

Out of this developed Discovery’s “teach the controversy” approach, which endorses evolution as a staple of any biology curriculum – so long as criticism of Darwin is also in the lesson plan. This satisfied Christian conservatives but also appealed to Republican moderates and, under the First Amendment banner, much of the public (71 percent in a Discovery-commissioned Zogby poll in 2001 whose results were mirrored in newspaper polls).

“They have packaged their message much more cleverly than the creation science people have,” said Eugenie C. Scott, director of the National Center for Science Education, the leading defender of evolution. “They present themselves as being more mainstream. I prefer to think of that as creationism light.”

A watershed moment came with the adoption in 2001 of the No Child Left Behind Act, whose legislative history includes a passage that comes straight from the institute’s talking points. “Where biological evolution is taught, the curriculum should help students to understand why this subject generates so much continuing controversy,” was language that Senator Rick Santorum, Republican of Pennsylvania, tried to include.

Pointing to that principle, institute fellows in 2002 played important roles in pushing the Ohio Board of Education to adopt a “teach the controversy” approach and helped devise a curriculum to support it. The following year, they successfully urged changes to textbooks in Texas to weaken the argument for evolution, and they have been consulted in numerous other cases as school districts or states consider changing their approach to biology.

But this spring, at the hearings in Kansas, Mr. Chapman grew visibly frustrated as his supposed allies began talking more and more about intelligent design.

John Calvert, the managing director of the Intelligent Design Network, based in Kansas, said the institute had the intellectual and financial resources to “lead the movement” but was “more cautious” than he would like. “They want to avoid the discussion of religion because that detracts from the focus on the science,” he said.

Dr. West, who leads the science center’s public policy efforts, said it did not support mandating the teaching of intelligent design because the theory was not yet developed enough and there was no appropriate curriculum. So the institute has opposed legislation in Pennsylvania and Utah that pushes intelligent design, instead urging lawmakers to follow Ohio’s lead.

“A lot of people are trying to hijack the issue on both the left and the right,” Dr. West said.

Dr. Chapman, for his part, sees even these rough spots as signs of success.

“All ideas that achieve a sort of uniform acceptance ultimately fall apart whether it’s in the sciences or philosophy or politics after a few people keep knocking away at it,” he said. “It’s wise for society not to punish those people.”

Jack Begg, David Bernstein and Alain Delaquérière contributed reporting for this article.

Now this morning we have another informative Times piece by Kenneth Chang, a science reporter with a wide perspective and a mathematical objecticity, on exactly what evidence in evolution the ID promoters are saying has to be explained by divine intervention. In Explaining Life’s Complexity, Darwinists and Doubters Clash, by Kenneth Chang

The New York Times

August 22, 2005

In Explaining Life’s Complexity, Darwinists and Doubters Clash

By KENNETH CHANG

At the heart of the debate over intelligent design is this question: Can a scientific explanation of the history of life include the actions of an unseen higher being?

The proponents of intelligent design, a school of thought that some have argued should be taught alongside evolution in the nation’s schools, say that the complexity and diversity of life go beyond what evolution can explain.

Biological marvels like the optical precision of an eye, the little spinning motors that propel bacteria and the cascade of proteins that cause blood to clot, they say, point to the hand of a higher being at work in the world.

In one often-cited argument, Michael J. Behe, a professor of biochemistry at Lehigh University and a leading design theorist, compares complex biological phenomena like blood clotting to a mousetrap: Take away any one piece – the spring, the baseboard, the metal piece that snags the mouse – and the mousetrap stops being able to catch mice.

Similarly, Dr. Behe argues, if any one of the more than 20 proteins involved in blood clotting is missing or deficient, as happens in hemophilia, for instance, clots will not form properly.

Such all-or-none systems, Dr. Behe and other design proponents say, could not have arisen through the incremental changes that evolution says allowed life to progress to the big brains and the sophisticated abilities of humans from primitive bacteria.

These complex systems are “always associated with design,” Dr. Behe, the author of the 1996 book “Darwin’s Black Box,” said in an interview. “We find such systems in biology, and since we know of no other way that these things can be produced, Darwinian claims notwithstanding, then we are rational to conclude they were indeed designed.”

It is an argument that appeals to many Americans of faith.

But mainstream scientists say that the claims of intelligent design run counter to a century of research supporting the explanatory and predictive power of Darwinian evolution, and that the design approach suffers from fundamental problems that place it outside the realm of science. For one thing, these scientists say, invoking a higher being as an explanation is unscientific.

“One of the rules of science is, no miracles allowed,” said Douglas H. Erwin, a paleobiologist at the Smithsonian Institution. “That’s a fundamental presumption of what we do.”

That does not mean that scientists do not believe in God. Many do. But they see science as an effort to find out how the material world works, with nothing to say about why we are here or how we should live.

And in that quest, they say, there is no need to resort to otherworldly explanations. So much evidence has been provided by evolutionary studies that biologists are able to explain even the most complex natural phenomena and to fill in whatever blanks remain with solid theories.

This is possible, in large part, because evolution leaves tracks like the fossil remains of early animals or the chemical footprints in DNA that have been revealed by genetic research.

For example, while Dr. Behe and other leading design proponents see the blood clotting system as a product of design, mainstream scientists see it as a result of a coherent sequence of evolutionary events.

Early vertebrates like jawless fish had a simple clotting system, scientists believe, involving a few proteins that made blood stick together, said Russell F. Doolittle, a professor of molecular biology at the University of California, San Diego.

Scientists hypothesize that at some point, a mistake during the copying of DNA resulted in the duplication of a gene, increasing the amount of protein produced by cells.

Most often, such a change would be useless. But in this case the extra protein helped blood clot, and animals with the extra protein were more likely to survive and reproduce. Over time, as higher-order species evolved, other proteins joined the clotting system. For instance, several proteins involved in the clotting of blood appear to have started as digestive enzymes.

By studying the evolutionary tree and the genetics and biochemistry of living organisms, Dr. Doolittle said, scientists have largely been able to determine the order in which different proteins became involved in helping blood clot, eventually producing the sophisticated clotting mechanisms of humans and other higher animals. The sequencing of animal genomes has provided evidence to support this view.

For example, scientists had predicted that more primitive animals such as fish would be missing certain blood-clotting proteins. In fact, the recent sequencing of the fish genome has shown just this.

“The evidence is rock solid,” Dr. Doolittle said.

Intelligent design proponents have advanced their views in books for popular audiences and in a few scientific articles. Some have developed mathematical formulas intended to tell whether something was designed or formed by natural processes.

Mainstream scientists say that intelligent design represents a more sophisticated – and thus more seductive – attack on evolution. Unlike creationists, design proponents accept many of the conclusions of modern science. They agree with cosmologists that the age of the universe is 13.6 billion years, not fewer than 10,000 years, as a literal reading of the Bible would suggest. They accept that mutation and natural selection, the central mechanisms of evolution, have acted on the natural world in small ways, for example, leading to the decay of eyes in certain salamanders that live underground.

Some intelligent design advocates even accept common descent, the notion that all species came from a common ancestor, a central tenet of evolution.

Although a vast majority of scientists accept evolution, the Discovery Institute, a research group in Seattle that has emerged as a clearinghouse for the intelligent design movement, says that 404 scientists, including 70 biologists, have signed a petition saying they are skeptical of Darwinism.

Nonetheless, many scientists regard intelligent design as little more than creationism dressed up in pseudoscientific clothing. Despite its use of scientific language and the fact that some design advocates are scientists, they say, the design approach has so far offered only philosophical objections to evolution, not any positive evidence for the intervention of a designer.

‘Truncated View of Reality’

If Dr. Behe’s mousetrap is one of the most familiar arguments for design, another is the idea that intelligence is obvious in what it creates. Read a novel by Hemingway, gaze at the pyramids, and a designer’s hand is manifest, design proponents say.

But mainstream scientists, design proponents say, are unwilling to look beyond the material world when it comes to explaining things like the construction of an eye or the spinning motors that propel bacteria. What is wrong, they ask, with entertaining the idea that what looks like it was designed was actually designed?

“If we’ve defined science such that it cannot get to the true answer, we’ve got a pretty lame definition of science,” said Douglas D. Axe, a molecular biologist and the director of research at the Biologic Institute, a new research center in Seattle that looks at the organization of biological systems, including intelligent design issues. Dr. Axe said he had received “significant” financing from the Discovery Institute, but he declined to give any other details about the institute or its financing.

Stephen C. Meyer, director of the Center for Science and Culture at the Discovery Institute, compares the design approach to the work of archaeologists investigating an ancient civilization.

“Imagine you’re an archaeologist and you’re looking at an inscription, and you say, ‘Well, sorry, that looks like it’s intelligent but we can’t invoke an intelligent cause because, as a matter of method, we have to limit ourselves to materialistic processes,’ ” Dr. Meyer said. “That would be nuts.”

He added, “Call it miracle, call it some other pejorative term, but the fact remains that the materialistic view is a truncated view of reality.”

William Paley, an Anglican priest, made a similar argument in the early 19th century. Someone who finds a rock can easily imagine how wind and rain shaped it, he reasoned. But someone who finds a pocket watch lying on the ground instantly knows that it was not formed by natural processes.

With living organisms so much more complicated than watches, he wrote, “The marks of design are too strong to be got over.”

Mainstream scientists say that the scientific method is indeed restricted to the material world, because it is trying to find out how it works. Simply saying, “it must have been designed,” they say, is simply a way of not tackling the hardest problems.

They say they have no disagreement with studying phenomena for which there are, as yet, no explanations.

It is the presumption of a designer that mainstream scientists dispute, because there are no artifacts or biological signs – no scientific evidence, in other words – to suggest a designer’s presence.

Darwin’s theory, in contrast, has over the last century yielded so many solid findings that no mainstream biologist today doubts its basic tenets, though they may argue about particulars.

The theory has unlocked many of the mysteries of the natural world. For example, by studying the skeletons of whales, evolutionary scientists have been able to trace the history of their descent from small-hoofed land mammals. They made predictions about what the earliest water-dwelling whales might look like. And, in 1994, paleontologists reported discovering two such species, with many of the anatomical features that scientists had predicted.

Darwin’s Finches

Nowhere has evolution been more powerful than in its prediction that there must be a means to pass on information from one generation to another. Darwin did not know the biological mechanism of inheritance, but the theory of evolution required one.

The discovery of DNA, the sequencing of the human genome, the pinpointing of genetic diseases and the discovery that a continuum of life from a single cell to a human brain can be detected in DNA are all a result of evolutionary theory.

Darwin may have been the classic scientific observer. He observed that individuals in a given species varied considerably, variations now known to be caused by mutations in their genetic code. He also realized that constraints of food and habitat sharply limited population growth; not every individual could survive and reproduce.

This competition, he hypothesized, meant that those individuals with helpful traits multiplied, passing on those traits to their numerous offspring. Negative or useless traits did not help individuals reproduce, and those traits faded away, a process that Darwin called natural selection.

The finches that Darwin observed in the Galápagos Islands provide the most famous example of this process. The species of finch that originally found its way to the Galápagos from South America had a beak shaped in a way that was ideal for eating seeds. But once arrived on the islands, that finch eventually diversified into 13 species. The various Galápagos finches have differently shaped beaks, each fine-tuned to take advantage of a particular food, like fruit, grubs, buds or seeds.

Such small adaptations can arise within a few generations. Darwin surmised that over millions of years, these small changes would accumulate, giving rise to the myriad of species seen today.

The number of organisms that, in those long periods, ended up being preserved as fossils is infinitesimal. As a result, the evolutionary record – the fossils of long-extinct organisms found preserved in rock – is necessarily incomplete, and some species appear to burst out of nowhere.

Some supporters of intelligent design have argued that such gaps undermine the evidence for evolution.

For instance, during the Cambrian explosion a half a billion years ago, life diversified to shapes with limbs and shells from jellyfish-like blobs, over a geologically brief span of 30 million years.

Dr. Meyer sees design at work in these large leaps, which signified the appearance of most modern forms of life. He argues that genetic mutations do not have the power to create new shapes of animals.

But molecular biologists have found genes that control the function of other genes, switching them on and off. Small mutations in these controller genes could produce new species. In addition, new fossils are being found and scientists now know that many changes occurred in the era before the Cambrian – a period that may have lasted 100 million years – providing more time for change.

The Cambrian explosion, said David J. Bottjer, a professor of earth sciences at the University of Southern California and president of the Paleontological Society, is “a wonderful mystery in that we don’t know everything yet.”

“I think it will be just a matter of time before smart people will be able to figure a lot more of this out,” Dr. Bottjer said. “Like any good scientific problem.”

Purposeful Patterns

Intelligent design proponents have been stung by claims that, in contrast to mainstream scientists, they do not form their own theories or conduct original research. They say they are doing the mathematical work and biological experiments needed to put their ideas on firm scientific ground.

For example, William A. Dembski, a mathematician who drew attention when he headed a short-lived intelligent design institute at Baylor University, has worked on mathematical algorithms that purport to tell the difference between objects that were designed and those that occurred naturally.

Dr. Dembski says designed objects, like Mount Rushmore, show complex, purposeful patterns that evince the existence of intelligence. Mathematical calculations like those he has developed, he argues, could detect those patterns, for example, distinguishing Mount Rushmore from Mount St. Helens.

But other mathematicians have said that Dr. Dembski’s calculations do not work and cannot be applied in the real world.

Other studies that intelligent design theorists cite in support of their views have been done by Dr. Axe of the Biologic Institute.

In one such study, Dr. Axe looked at a protein, called penicillinase, that gives bacteria the ability to survive treatment with the antibiotic penicillin. Dr. Meyer, of the Discovery Institute, has referred to Dr. Axe’s work in arguing that working proteins are so rare that evolution cannot by chance discover them.

What was the probability, Dr. Axe asked in his study, of a protein with this ability existing in the universe of all possible proteins?

Penicillinase is made up of a strand of chemicals called amino acids folded into a shape that binds to penicillin and thus disables it. Whether the protein folds up in the right way determines whether it works or not.

Dr. Axe calculated that of the plausible amino acid sequences, only one in 100,000 trillion trillion trillion trillion trillion trillion – a number written as 1 followed by 77 zeroes – would provide resistance to penicillin.

In other words, the probability was essentially zero.

Dr. Axe’s research appeared last year in The Journal of Molecular Biology, a peer-reviewed scientific publication.

Dr. Kenneth R. Miller, a professor of biology at Brown University and a frequent sparring partner of design proponents, said that in his study, Dr. Axe did not look at penicillinase “the way evolution looks at the protein.”

Natural selection, he said, is not random. A small number of mutations, sometimes just one, can change the function of a protein, allowing it to diverge along new evolutionary paths and eventually form a new shape or fold.

One Shot or a Continual Act

Intelligent design proponents are careful to say that they cannot identify the designer at work in the world, although most readily concede that God is the most likely possibility. And they offer varied opinions on when and how often a designer intervened.

Dr. Behe, for example, said he could imagine that, like an elaborate billiards shot, the design was set up when the Big Bang occurred 13.6 billion years ago. “It could have all been programmed into the universe as far as I’m concerned,” he said.

But it was also possible, Dr. Behe added, that a designer acted continually throughout the history of life.

Mainstream scientists say this fuzziness about when and how design supposedly occurred makes the claims impossible to disprove. It is unreasonable, they say, for design advocates to demand that every detail of evolution be filled in.

Dr. Behe, however, said he might find it compelling if scientists were to observe evolutionary leaps in the laboratory. He pointed to an experiment by Richard E. Lenski, a professor of microbial ecology at Michigan State University, who has been observing the evolution of E. coli bacteria for more than 15 years. “If anything cool came out of that,” Dr. Behe said, “that would be one way to convince me.”

Dr. Behe said that if he was correct, then the E. coli in Dr. Lenski’s lab would evolve in small ways but never change in such a way that the bacteria would develop entirely new abilities.

In fact, such an ability seems to have developed. Dr. Lenski said his experiment was not intended to explore this aspect of evolution, but nonetheless, “We have recently discovered a pretty dramatic exception, one where a new and surprising function has evolved,” he said.

Dr. Lenski declined to give any details until the research is published. But, he said, “If anyone is resting his or her faith in God on the outcome that our experiment will not produce some major biological innovation, then I humbly suggest they should rethink the distinction between science and religion.”

Dr. Behe said, “I’ll wait and see.”

While there are certainly baffling mysteries in the all-or-none leaps that evolution seems to have achieved in a number of instances, why is it that “God” is a better explanation than “we don’t know”?

If anything it seems to us that there is a paradox here, in that such seekers of truth lack the humility that all religions teach, and in saying that human understanding having not yet found an explanation of the mechanics of such leaps, therefore the explanation is supernatural, are close to the kind of hubris which has always made humanity ridiculous, especially in the early days of Darwinism when many were outraged at the idea that man could share the same ancestors as apes.

Now we have the likes of William Dembski arguing that what is not explained is therefore a sign of an unseen guiding hand. Well, maybe it is, but we would bet it isn’t a supernatural one.

Oscar Wilde advises AIDS heretics

August 20th, 2005

“One should never take sides in anything—taking sides is the beginning of sincerity, and earnestness follows shortly after, and the human being becomes a bore.”

16 mainstream papers say that the AIDS ‘pandemic’ does not exist

August 16th, 2005

Here as promised are the mainstream papers which say HIV is effectively non infectious, heterosexually, and thus any idea of HIV/AIDS being an infectious global pandemic is null and void.

That is to say, the global pandemic to which the much prized Laurie Garrett just devoted two years of her hard working career recording, analyzing and writing up in a splendidly glossy report for the Council of Foreign Relations is, as we have noted, an entirely dead parrot of an idea–quite impossible according to the very mainstream AIDS literature that it claims supports it, and which it appears the inimitable Garrett failed adequately to consult.

In short, in writing the report she has in effect constructed a gilded cage for a bird which is already dead.

But we are getting ahead of ourselves. The first paper is a kind of meta-study, looking at all the studies available by 2001.

Let’s look at it and see what it can tell us about the nature of the Great Global AIDS/HIV pandemic. First we notice….

Great Heavens! How can this be?! The authors have come up with the following stunning finding: all the studies it reviews together produce the conclusion that the chance of transmitting HIV-1 from man to woman during one bout of lovemaking is…

one in a thousand!!

Analysis of data from North American and European studies of heterosexual couples provide estimates of per-sex-act HIV-1 transmission of approximately 1 in 1000

This of course immediately raises the question, how on earth can a raging global AIDS/HIV pandemic arise from an agent that is transmitted at the rate of once every thousand copulations?! Even the group of clearly pious, mainstream-ideology authors of the paper are evidently taken aback. Seeing the problem, they are reduced to saying rather feebly, in the next sentence, “the magnitude of the HIV-1 epidemic would argue that these estimates might be unreasonably low.”

Low indeed. Impossibly low, in fact. In itself, it disproves the existence of any heterosexual AIDS pandemic in the world.

That is why it is worth parsing in detail. Contemplate what would have to take place for an epidemic to emerge from a rate of transference of one in a thousand bouts. A man with HIV would have to fornicate with his woman or women one thousand times, on average, to transmit the virus once. Even if he had sex once every night, three years wouldn’t be enough to ensure a single transmission.

For any kind of epidemic to transpire, enough sex for transmission has to take place in a relatively short time, far shorter than the average time heterosexual men take to provoke and consummate one thousand sexual engagements. Cohabiting couples are generally assumed to engage in sex twice a week. One thousand bouts would take them ten years.

No infection is going to spread if it takes ten years for the agent to jump ship to ship. This rate rules out any pandemic. Even love making once a day wouldn’t be enough to support a spreading infection, let alone an epidemic. A pandemic? Fugeddabahtit!!

In fact, if there really is the sexually driven glohal pandemic everyone led by the UNAID, WHO and Laurie Garrett and the Council of Foreign Relations credits as gospel the supermen of the AIDS pandemic must get a lot busier than that. Even ten copulations a day wouldn’t do it. That would “only” be 100 days of Olympic ten-times-a-day sex per transfer.

A virus that took 100 days to infect another body is too slow. That is just too long a delay to get any kind of epidemic under way. It would have to be five times that rate, or 50 copulations a day to do it in twenty days. This is the rough minimum, we would guess, to support any kind of epidemic spread.

To repeat, if the couples went at it at the rate of 50 bouts of sex a day it would take on average twenty days for the virus to hop from gent to lady. Maybe that would sustain an epidemic. But how many men do you know–or women for that matter–who are interested in let alone capable of fifty bouts of sex a day?

But that is what the finding of this mainstream paper–which collates the findings of 15 other orthodox research papers on the topic–implies.

Perhaps the African and Asian males who have engendered the AIDS pandemic, the one that the Council of Foreign Relations report has recently warned us may plunge the world into wars, famine and devastation, are a Godlike breed, who have Olympian sexual powers far beyond the norm or even the imagination of their counterparts in the USA.

More likely, however, is that quite simply, the global AIDS pandemic is a fantasy and a chimera, an impossible narrative construct of such a gargantuan level of absurdity that science and politics have not to date ever seen the like.

This, at least, is what the papers on the (non) infectiousness of HIV tell us, as summarized so helpfully by this paper. They may be found any time on your computer at Pub Med. Here they are for the record, the meta-paper and a list of the papers it summarizes:

The meta-paper

1. Viral burden in genital secretions determines male-to-female sexual transmission of HIV-1: a probabilistic empiric model

by Hrishikesh Chakraborty et al AIDS 2001 15:621-627 From the Department of Biostatistics, Rollin School of Public Health, Emory University, Atlanta, Georgia etc. Reprint requests to Myron Cohen, Department of Medicine, 3003 Old Clinic Building CB7005, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7005.

On page 2, this paper says that

“The probability of per-partner sexual transmission has been examined in 11 different studies (6) whereas the per-sex-act probability of transmission has been reported in 13 studies (7-19). The probability of transmission of HIV-1 from male to female during an episode of intercourse has been examined in seven of these studies (7,14-19). Analysis of data from North American and European studies of heterosexual couples provide estimates of per-sex-act HIV-1 transmission of approximately 1 in 1000 (0.0001, ranging from 0.0008 to 0.0002) (6), although the magnitude of the HIV-1 epidemic would argue that these estimates might be unreasonably low.” .

The references in the footnotes for this statement are

.

6. Mastro TD, Kitayaporn (sic) D. HIV-1 Type 1 transmission probabilities, estimates from epidemiological studies. AIDS Research Human Retroviruses 1998 14:223-227

7. Peterman TA, Stonebumer RL, Allen JR, Jaffe HW, Curran JW. Risk of human immunodeficiency virus transmission from heterosexual adults with transfusion-associated infections. JAMA 1988 259.55-58.

8.Fuschl MA et al Evaluation of heterosexual partners, children, and household contacts of adults with AIDS. JAMA 1987, 257:640-644.

9. Longini IM Jr et al The stages of HIV-1 infection, waiting times and infection transmission probabilities. In Lecture Notes in Biomathematics, Vol. 83 Mathematical and Statistical Approaches to AIDS Epidemiology. Edited by Castillo-Chavez, C. Berlin: Springer-Verlag; 1989: 111-136.

10. Cameron DW et al. Female to male transmission of human immunodeficiency virus type 1: risk factors for seroconversion in men. Lancet 1989, 2: 403-407.

11. DeGruttola V et al Infectiousness of HIV-1 between male homosexual partners J. Clin Epidemiology 1989 42:849-856

12. Mastro TD et al Probability of female-male transmission of HIV-1 in Thailand. Lancet 1994 343:204-207

13. Sateen GA et val Modelling the female-to-male per-act HIV-1 transmission probability in an emerging epidemic in Asia. Stat Med 1994 13:2097-2106

14. Padian N et al Male-to-female transmission of human immunodeficiency virus. JAMA 1987 258:788-790.

15. Wiley JA et al Heterogeneity in the probability of HIV-1 transmission per sexual contact: the case of male-to-female transmission in penile-vaginal intercourse Stat Med 1989 8:93-102

16. Duerr A et al Probability of male-female HIV-1 transmission among married couples in Chiang Mai, Thailand Tenth International Conference on AIDS, Yokohama, August 1994 (Abstract 105C). 17. Downs MA et al Probability of heterosexial transmission of HIV-1:relationship to the number of unprotected sexual contacts. J. Acquired Immune Defic Sindr Hyum Retrovirol 1996 11: 388-395.

18. Leynaert B. Et al Heterosexual transmission of Human immunodeficiency virus: variability of infectivity throughout the course of infection. Am J Epidemiol 1998 148:88-96

19. Shiboski SC et al Epidemiological evidence for time variation in HIV-1 infectivity J Acquir Immun Defic Syndr Hu Retrovirol 1998 19: 527-535.

These are not all, by the way. There have been quite a few other papers since, saying the same thing. Here’s one from 2002, a year later:

Stephane Hugonnet et al Incidence of HIV Infection in Stable Sexual Partnerships: A Retrospective Cohort Study of 1802 Couples in Mwanza Region, Tanzania. JAIDS Journal of nAcquired Immunodeficiency Syndrome 30: 73-80 2002

This paper concludes in its abstract:

“HIV negative individuals in discordant partnerships are at high risk of infection, and preventive interventions targeted at such individuals are urgently needed……Individuals living in discordant couples (that means one HIV positive one negative) were at greatly increased risk of infection compared with individuals in concordant-negative couples.”

In its introduction it states that

“the majority of infections worldwide are attributable to heterosexual transmission. In sub-Saharan Africa, the worst afflicted region, heterosexual transmission accounts for at least 90 per cent of adult infections.”

All in all, what sounds like a dangerous state of affairs illuminated by the sterling work of these researchers on data from 1802 couples in Mwanza. For after all, if “HIV negative individuals in discordant partnerships are at high risk of infection”, then indeed heterosexual transmission could account for 90 per cent of adult infections.

But when we look closer, we discover the same problem, this time also being neatly brushed under the carpet. There is in fact little or no danger, as indicated by the authors’ very own result. The “high risk” of a heterosexual coupling changing a discordant couple into a concordant couple—these musical sounding technical terms refer to whether couples share the same HIV status or not—turns out to be exactly the same as in the collection of papers before 2000: 1 in 1000.

Buried in the pile of comforting statistical jargon, which is mostly less than meets the eye (py means person-year, RR means rate ratio, etc), is this simple statement: Seroincidence rates in discordant couples were 10 per 100 person-years (py) and 5 per 100 py for women and men respectively (rate ratio RR = 2.0 CI (confidence interval = 0.28-22.1.)

What does this mean in plain English? That in any of these Mwanza couples with the man HIV+ and woman HIV-, the chances of the woman being converted to HIV+ are so low that on average it takes ten years to happen. For the man to be infected the other direction would take twice as long, twenty years.

The standard assumption in such work is that couples make love twice a week, so that is 100 times a year. So ten years is 1000 times. The chances of a woman converting in a single bout are therefore 1 in 1000, with the chances of the man converting from a HIV+ woman partner 1 in 2000.

Exactly the chances which are found in every other paper on this topic. The figure is marvelously consistent: 1 in a thousand.

The Mwanza study researchers thus find themselves in a great difficulty and as a result have to contradict themselves as they state what is certainly a paradigm buster of a finding.

At such a low rate of conversion, not only is it NOT true that “HIV negative individuals in discordant partnerships are at high risk of infection” (unless you call a 1 in 10 chance over a year of 100 bouts ‘high risk’), but it is also not true that “preventive interventions targeted at such individuals are urgently needed”.

Far from it. For their very own finding proves that any AIDS epidemic through mainstream sex is quite impossible. The rate of transfer of HIV is just too low, far too low. According to these mainstream, orthodox researchers HIV is realistically not an infectious virus at all, at least between heteroexuals in Africa. It simply could not support any epidemic.

In fact, the paper indicates a simple conclusion, which the authors for whatever reason are either blind to or do not wish to speak out loud. That finding is that there is no HIV/AIDS epidemic in Mwanza or anywhere else.

Clearly the infectivity of HIV is far too low to spread through heterosexual sex in the US and Europe, and that is why such an epidemic has never been seen here or there in the two decades the AIDS alarm has been noised so loudly in headlines and homilies from the press to the pulpit. By the same logic it is also too low to support any heterosexual AIDS epidemic anywhere in the rest of the world.

In other words, as we have said before, the AIDS pandemic is a non starter, a nag that expires even before it is even able to take its position at the starting gate. It is utterly non-viable, at least in the real, external world of health and science.

How far this kite may fly on the wings of obtuse venality, incompetence, officiousness, powerseeking, self-importance, conformity, credulity and billion dollar funding in the fantasy world of political, social and medical culture is of course another matter entirely.

Apparently, it can stay up without a drop of real fuel for twenty one years simply on the cross currents and updrafts of hot air generated by the major writers and players of the ongoing drama “World AIDS Pandemic” and is capable of flying high for many more years unless and until it is shot down by anti-paradigm guns more powerful than those of simple logic and common sense, not to mention its own research.

By the way, there are more papers to list, papers from the orthodox mainstream research factory, and we will append them here later today.

But the main point is already established. HIV is effectively not infectious between man and woman, and the AIDS heterosexual global pandemic cannot and therefore does not exist.

This is the conclusion of the orthodoxy itself, reached in its own papers. Verily the right hand knoweth not what the left hand doeth.

Harvard brings sanity to the evolution debate

August 14th, 2005

An AP report in the New York Times today (Sun Aug 14) tells us that Harvard is jumping into the evolution debate with a $1 million a year project of research into the origin of life.

What’s interesting is that, at least according to the AP, it begins with the admission that some mysteries of life’s origin remain to be illuminated.

Not that this will provide much comfort to the intelligent design faithful, who believe that such theoretical gaps should be filled with the Creator (while never telling us how the Creator appeared). For a Harvard scientist, David Liu, is quickly quoted as saying he believes it will all be explained without involving divine intervention.

Quite why the fact that as yet we cannot fathom how something complex arose from simpler origins in evolution should provoke scientists to jump ship for the Church is beyond us. Do those who are infatuated with the possibility of God taking a hand really think that science won’t explain all the gaps in evolution in the end, however long it takes?

The real problem in the evolution debate is that most scientists in the field will not admit there are gaps in the theory that have to be explained. This is why the intelligent design crowd is able to make headway by pointing them out.

Maybe Harvard will set a good example now and admit freely that there remain some leaps in evolution that have to be explained, and that science is a continual process of filling in such gaps in our understanding and knowledge.

Perhaps the basic premise of intelligent design, that any such gap if big enough must indicate the presence of God, can then be dispensed with.

See below, Harvard Jumps Into Evolution Debate:

The New York Times

August 14, 2005

Harvard Jumps Into Evolution Debate

By THE ASSOCIATED PRESS

Filed at 9:33 p.m. ET

CAMBRIDGE, Mass. (AP) — Harvard University is joining the long-running debate over the theory of evolution by launching a research project to study how life began.

The team of researchers will receive $1 million in funding annually from Harvard over the next few years. The project begins with an admission that some mysteries about life’s origins cannot be explained.

”My expectation is that we will be able to reduce this to a very simple series of logical events that could have taken place with no divine intervention,” said David R. Liu, a professor of chemistry and chemical biology at Harvard.

The ”Origins of Life in the Universe Initiative” is still in its early stages, scientists told the Boston Sunday Globe. Harvard has told the research team to make plans for adding faculty members and a collection of multimillion-dollar facilities.

Evolution is a fundamental scientific theory that species evolved over millions of years. It has been standard in most public school science texts for decades but recently re-emerged in the spotlight as communities and some states debated whether school children should also be taught about creationism or intelligent design.

The theory of intelligent design says life on earth is too complex to have developed through evolution, implying that a higher power must have had a hand in creation.

Harvard has not been seen as a leader in origins of life research, but the university’s vast resources could change that perception.

”It is quite gratifying to see Harvard is going for a solution to a problem that will be remembered 100 years from now,” said Steven Benner, a University of Florida scientist who is one of the world’s top chemists in origins-of-life research.

Errors in warming skeptics’ troposphere data—it did warm after all

August 12th, 2005

Today (Fri 12 Aug) Andrew Revkin fires a bombshell across the bows of the global warming skeptics by citing two Science articles which show that a key fact they depend on is an error—the lowest layer in the atmosphere, the troposphere, did not stay stable over the last two decades and cool in the tropics.

A laborious reassessment of the weather satellite data has shown that the troposphere did warm in line with other records and climate change model predictions, according to Science.

That settles that—or does it? Fred Singer’s weekly comment hasn’t come yet, but only recently he was saying in regard to another paper “this is not the first time Science has published an incorrect paper.” Can one have confidence in Singer? That is up to you to decide. But his tone and substance induce maximum confidence in us, however unpalatable his assessments might be to the environmentally concerned.

The depressing thing is that if he is right, environment anxiety has led to all kinds of negative results which all those who care about the invironment would actually deplore. One remarkable observation Singer makes is that the shuttle disasters were due to environment political correctness of a kind.

“Green orthodoxy may be responsible for both the Challenger and Columbia space shuttle disasters”.

He quotes from a business periodical:

But the root cause for both the disintegration of the shuttle Columbia due to thermal tiles damaged by chunks of insulating foam falling off the large external fuel tank, the earlier loss of Challenger, and the repetition of the foam problem with Discovery, may be the decision imposed on NASA to use parts and materials that were more environmentally friendly.

In 1997, during the 87th space shuttle mission, similar tile damage occurred during launch. NASA’s Greg Katnik stated in his December 1997 review of the problems of STS-87: “During the STS-87 mission, there was a change made on the external tank. Because of NASA’s goal to use environmentally friendly products, a new method of ‘foaming’ the external tank had been used for this mission and the STS-86 mission.”

That’s from a piece, “Green For Launch”, in Investor’s Business Daily Issues & Insights Friday, August 5, 2005.

Nothing wrong with what NASA did, of course, unless safety was sacrificed in the environmental cause. Then you might wish they had looked after their crew members as assiduously as they cared for the environment.

Here is today’s piece by Revkin, Errors Cited in Assessing Climate Data:

August 12, 2005

Errors Cited in Assessing Climate Data

By ANDREW C. REVKIN

Some scientists who question whether human-caused global warming poses a threat have long pointed to records that showed the atmosphere’s lowest layer, the troposphere, had not warmed over the last two decades and had cooled in the tropics.

Now two independent studies have found errors in the complicated calculations used to generate the old temperature records, which involved stitching together data from thousands of weather balloons lofted around the world and a series of short-lived weather satellites.

A third study shows that when the errors are taken into account, the troposphere actually got warmer. Moreover, that warming trend largely agrees with the warmer surface temperatures that have been recorded and conforms to predictions in recent computer models.

The three papers were published yesterday in the online edition of the journal Science.

The scientists who developed the original troposphere temperature records from satellite data, John R. Christy and Roy W. Spencer of the University of Alabama in Huntsville, conceded yesterday that they had made a mistake but said that their revised calculations still produced a warming rate too small to be a concern.

“Our view hasn’t changed,” Dr. Christy said. “We still have this modest warming.”

Other climate experts, however, said that the new studies were very significant, effectively resolving a puzzle that had been used by opponents of curbs on heat-trapping greenhouse gases.

“These papers should lay to rest once and for all the claims by John Christy and other global warming skeptics that a disagreement between tropospheric and surface temperature trends means that there are problems with surface temperature records or with climate models,” said Alan Robock, a meteorologist at Rutgers University.

The findings will be featured in a report on temperature trends in the lower atmosphere that is the first product to emerge from the Bush administration’s 10-year program intended to resolve uncertainties in climate science.

Several scientists involved in the new studies said that the government climate program, by forcing everyone involved to meet five times, had helped generate the new findings.

“It felt like a boxing ring on occasion,” said Peter W. Thorne, an expert on the weather balloon data at the Hadley Center for Climate Prediction and Research in Britain and an author of one of the studies.

Temperatures at thousands of places across the surface of the earth have been measured for generations. But far fewer measurements have been made of temperatures in the air from the surface through the troposphere, which extends up about five miles.

Until recently Dr. Christy and Dr. Spencer were the only scientists who had plowed through vast volumes of data from weather satellites to see if they could indirectly deduce the temperature of several layers within the troposphere.

They and other scientists have also tried to analyze temperature readings gathered by some 700 weather balloons lofted twice a day around the world.

But each of those efforts has been fraught with complexities and uncertainties.

The satellites’ orbits shift and sink over time, their instruments are affected by sunlight and darkness, and data from a succession of satellites has to be calibrated to account for eccentricities of sensitive instruments.

Starting around 2001, the satellite data and methods of Dr. Christy and Dr. Spencer were re-examined by Carl A. Mears and Frank J. Wentz, scientists at Remote Sensing Systems, a company in Santa Rosa, Calif., that does satellite data analysis for NASA.

They and several other teams have since found more significant warming trends than the original estimate.

But the new paper, by Dr. Mears and Dr. Wentz, identifies a fresh error in the original calculations that, more firmly than ever, showed warming in the troposphere, particularly in the tropics.

The error, in a calculation used to adjust for the drift of the satellites, was disclosed to the University of Alabama scientists at one of the government-run meetings this year, Dr. Christy said.

The new analysis of data from weather balloons examined just one possible source of error, the direct heating of the instruments by the sun.

It found that when data were examined in a way that accounted for that effect, the temperature record produced a warming, particularly in the tropics, again putting the data in line with theory.

“Things being debated now are details about the models,” said Steven Sherwood, the lead author of the paper on the balloon data and an atmospheric physicist at Yale. “Nobody is debating any more that significant climate changes are coming.”

Autism epidemic may be an illusion

August 11th, 2005

One point that went unmentioned in the Meet the Press segment on autism and vaccines on Sunday (see previous post but one) was the possibility that this vaguely defined and measured syndrome may not be expanding in an epidemic after all.

This is according to the New Scientist, the lively and fairly responsible British weekly which leaves most US science coverage in the popular press in its dust. However, since the paper has run with the herd on AIDS and its anomalies ever since the HIV paradigm was reviewed and rejected in the top scientific literature, its analysis as always must be taken with a little pinch of salt.

Nonetheless, the piece is convincing to us, especially as the one and only relevant study so far backs up the conclusion that we have an epidemic of diagnosing autism rather than the ailment itself, though that in itself is real enough when it occurs.

And those familiar with AIDS as the all time pandemic of (mis)diagnosis will recognize the signs of a fantasy epidemic.

(NB: As an example perhaps of just how easy it is to expand the “epidemic”, if you read the definition of autism in the accompanying box, Epidemic or illusion? by Clare Wilson,

“In psychological terms, people with autism seem to lack “theory of mind” – the recognition that other individuals may hold a different perspective on things than themselves”

you may also recognize the symptom, as we do, in the one you live with :-))

This is the whole article, The autism epidemic that never was 13 August 2005 New Scientist Print Edition by Graham Lawton

NewScientist.com

Epidemic or illusion?

The autism epidemic that never was

* 13 August 2005

* From New Scientist Print Edition. Subscribe and get 4 free issues.

* Graham Lawton

RICHARD Miles will never forget the winter of 1989. The 34-year-old company director and his family spent that Christmas on the island of Jersey in the English Channel, where he had grown up. It was also then that he first noticed something was badly wrong with his 14-month-old son Robert. The bright, sociable child, who had already started talking, became drowsy and unsteady on his feet. Then he started bumping into furniture. Within weeks his language had dried up and he would no longer make eye contact. “It was as if the lights went out,” says Miles. His son was eventually diagnosed with autism.

Miles, who now campaigns for more research into autism, is convinced that his son is part of an autism epidemic. Ten years ago, he points out, Jersey had just three autistic children in special-needs education. It now has 69. Robert was one of a cluster of nine children on the island diagnosed around the same time.

Similar rises have been reported across the world, from Australia to the US, and from Denmark to China. Back in the 1970s, specialists would typically see four or five cases of autism in a population of 10,000. Today they routinely find 40, 50 or even 60 cases. Perhaps the starkest illustration of autism’s relentless rise comes from California. In 2003, the state authorities stunned the world when they announced that over the previous 16 years, the number of people receiving health or education services for autism had risen more than sixfold. The world’s media went into overdrive.

What could be causing so many children to lose their footing on a normal developmental trajectory and crash-land into the nightmare world of autism? The change has occurred too suddenly to be genetic in origin, which points to some environmental factor. But what? There is no shortage of suspects. In the UK, blame is often laid at the door of the combined measles, mumps and rubella (MMR) vaccine. In the US, mercury added to a range of childhood shots has been accused. Food allergies, viral infections, antibiotics and other prescription drugs have all been fingered, often by campaign groups run by mystified and angry parents. The problem is that none of these suggested causes has any solid scientific evidence to support it (see “The usual suspects”).

Perhaps there’s a simple explanation for this: there is no autism epidemic. On the face of it that sounds ridiculous – just look at the figures. But talk to almost any autism researcher and they will point to other explanations for the rise in numbers. Some say it’s still an open question, but others are adamant that the autism epidemic is a complete myth. And if the most recent research is anything to go by, they could be right. Studies designed to track the supposedly increasing prevalence of autism are coming to the conclusion that, in actual fact, there is no increase at all. “There is no epidemic,” says Brent Taylor, professor of community child health at University College London.

Autism is a developmental disorder sometimes noticeable from a few months of age but not usually diagnosed until a child is 3 or 4 years old. It is characterised by communication problems, difficulty in socialising and a lack of imagination (see “What is autism”). It is not a single disorder, but comes in many forms, which merge into other disorders and eventually into “normality”. There is no biochemical or genetic test, so diagnosis has to be made by observing behaviour. Autistic children also often have other medical conditions, such as hyperactivity, Tourette’s syndrome, anxiety and depression. The upshot is that “one person’s autism is not another person’s autism,” says epidemiologist Jim Gurney of the University of Minnesota in Minneapolis.

In recognition of this ambiguity, autism is considered part of a continuum within a broader class of so-called “pervasive developmental disorders” (PDDs) – basically any serious abnormality in a child’s development. Autism itself is divided into three categories: autistic disorder, Asperger’s syndrome (sometimes called “high-functioning autism”), and pervasive developmental disorder-not otherwise specified (PDD-NOS), sometimes called mild or atypical autism. Together these three make up the autistic spectrum disorders.

“Californian authorities stunned the world when they announced a sixfold rise in autism over the past 16 years”

Confused? You’re not the only one. The difficulty of placing children with developmental problems on this spectrum has led to several major shifts in the way autism is diagnosed in the past 30 years. In the late 1970s, the autism label was kept for those with severe problems such as “gross language deficits” and “pervasive lack of responsiveness”. But since 1980 the diagnostic criteria have been revised five times, including the addition of PDD-NOS in 1987 and Asperger’s in 1994.

This massive broadening of the definition of autism, particularly at the milder end of the spectrum, is one of the main factors responsible for the rise in cases, says Eric Fombonne of McGill University in Montreal, Canada, a long-standing sceptic of the epidemic hypothesis. Tellingly, around three-quarters of all diagnoses of autism today are for Asperger’s and PDD-NOS, both of which are much less severe than the autism of old. “There is no litmus test for who is autistic and who is not,” says Tony Charman of the Institute of Child Health at University College London.

Changes in diagnostic criteria apart, there are other reasons to believe that autism is simply being diagnosed more often now than in the past. One is the “Rain Man effect” – the huge increase in the public awareness of autism following the 1988 film starring Dustin Hoffman. Awareness has also increased massively among healthcare workers. “Twenty years ago there were maybe 10 autism specialists in the country. Now there are over 2000,” says Taylor.

Another factor is that one of the stigmas of autism has largely disappeared. Until about 10 years ago a prominent idea was that autism was caused by an unloving “refrigerator mother”. Now it is a no-blame disease. “Parents are more willing to accept the label,” says Taylor. One expert New Scientist spoke to went as far as to describe autism as “trendy”.

Finally, while some parents still have to fight for help for their autistic children, far more services are now available. This has encouraged doctors to label borderline or ambiguous cases as autism – they know this is often the best way to get the child some help. It also makes autism an attractive diagnosis for parents. “I hear stories of parents who are anxious to get a particular diagnosis if that is what is required to obtain the services their child needs,” says Sydney Pettygrove, a paediatrician at the Arizona Health Sciences Center in Tucson. In the UK, says Simon Baron-Cohen of the Autism Research Centre at the University of Cambridge, “in every town there are trained clinicians who can make a diagnosis.”

It is hard to quantify these trends, but many epidemiologists now believe that they can account for the apparent rise in autism the general public and media take for granted. Proving it, however, is difficult – if not impossible. The main problem is that an epidemiological study carried out in the 1980s simply cannot be compared with one done last week. There will be so many differences in diagnostic procedures and in the willingness of doctors and parents to label a child autistic that comparisons are meaningless. “You can’t control for everything,” says Charman.

And so attention has shifted to what epidemiologists sniffily refer to as “service provider data”, such as the California figures. Ever since 1973, the authorities there have been keeping records of the number of people receiving some kind of state help in connection with autism. In 2003, California’s Department of Developmental Services (DDS) announced a chilling figure that captured the world’s attention. In the 16 years to 2002, cases rose from 2778 to 20,377 (see Graph). Among autism campaigners these figures are often cited as incontrovertible and final proof of the existence of the autism epidemic.

But there are serious problems with this interpretation. First, the figures are raw numbers from public services, not a proper epidemiological study. Critics point out they are not corrected for changes in diagnostic criteria or for the growing awareness of autism.

“Prisons and institutions could be full of autistic adults labouring under wrong diagnoses such as schizophrenia”

There is evidence, for example, that as the California autism numbers have risen, diagnoses of mental retardation have fallen. Researchers at Boston University School of Medicine in Massachusetts have found a similar pattern in the UK. This effect, dubbed “diagnostic substitution”, cannot explain all the increase but is one example of how diagnostic fashions can skew the data.

Another potential flaw is that the California figures don’t take into account the fact that the state’s population is growing rapidly. Between 1987 and 1999, the total population rose by nearly 20 per cent, and the age group 0 to 14 rose even more steeply, by 26 per cent.

As a result of these doubts and unknowns in the California figures, most epidemiologists refuse to draw firm conclusions from them. “The report doesn’t change anything,” says Charman. “It’s not a systematic study.” In fact, the preface of the most recent California report contains a health warning not to read too much into the numbers. “The information should not be used to draw scientifically valid conclusions,” it says.

Some researchers, notably Robert Byrd of the MIND Institute at the University of California, Davis, have attempted to correct for all the unknowns. In an analysis published on the state DDS website nearly three years ago, Byrd concluded that the rise is real. “Autism rates are increasing,” he told New Scientist. Some scientists accept that Byrd’s analysis lays to rest the idea that population growth could have significantly swelled the figures. But his methods for investigating the other potential sources of bias have been heavily criticised, and tellingly, Byrd has not yet succeeded in getting his study published in a peer-reviewed journal. Until he does, it is hard to know how much weight to give his conclusions.

Perhaps the strongest case against the “better diagnosis” theory is that, if true, there should be a “hidden hoard” of autistic adults who were never properly diagnosed in childhood. To parent Richard Miles, this is compelling. “My doctor cannot believe that he could have missed so many cases in the past,” he says. But Taylor disagrees. As a former general practitioner, he says there are many children today diagnosed with autism who would not have been labelled as such in the past.

This view is difficult to substantiate, but in 2001 a team led by Helen Heussler of Nottingham University, UK, had a crack. They re-examined the data from a 1970 survey of 13,135 British children. The original survey found just five autistic children, but using modern diagnostic criteria Heussler’s team found a hidden hoard of 56. That’s over a tenfold rise in numbers, which puts the California figures in perspective. Heussler and her colleagues concluded that “estimates from the early 1970s may have seriously underestimated the prevalence”.

Lorna Wing, a veteran autism researcher at the Institute of Psychiatry in London, agrees. In the 1970s she spent a lot of time working with special-needs children in the London district of Camberwell. Wing reckons that at the time, fewer than 10 per cent of autistic children were correctly diagnosed. She also thinks that prisons and institutions are full of autistic adults labouring under wrong diagnoses such as treatment-resistant schizophrenia or ADHD.

Ultimately, however, it may be impossible to tell whether there has been a genuine rise in the incidence of autism over the past 30 years. “There is no clear evidence that there has been an increase, but there’s no proof that there hasn’t,” says Charman. Even the arch-sceptic Fombonne accepts this. “We must entertain the possibility,” he says. “But we don’t have the evidence.”

But researchers can answer another question: is the incidence of autism continuing to rise? There is a tried and tested method of tackling this sort of question. You carry out a large prevalence study among a particular age group, and then repeat it a few years later with a new set of individuals, in the same place and using exactly the same methods. Several such studies into autism are ongoing, notably one funded by the US Centers for Disease Control and Prevention in Atlanta, which will look at changes in incidence across 11 states.

One team, however, is ahead of the game. Back in July 1998, Fombonne and Suniti Chakrabarti of the Child Development Centre in Stafford, UK, started screening every child born in a four-year window (1992 to 1995) who lived in a defined area of Staffordshire, 15,500 children in total. As a result, they established baseline figures for autistic spectrum disorders – about 62 per 10,000. Then they did it again, in exactly the same place and exactly the same way, this time with all the children born between 1996 and 1998. In June this year, they reported that the prevalence of autism was unchanged (American Journal of Psychiatry, vol 162, page 1133). “This study suggests that epidemic concerns are unfounded,” concludes Fombonne.

Similar surveys need to be done in other parts of the world to rule out the possibility that there is something unusual about Staffordshire. And the Staffordshire result has failed to convince campaigners and parents, including Miles. But what is clear is that after the first direct test of whether autism is rising, it’s 1-0 to the sceptics.

That doesn’t mean we should stop searching for the causes of autism. The disorder itself is real, and if researchers knew what was behind it much suffering could be averted. But the Staffordshire surveys do suggest that there is no environmental problem that is triggering autism in ever-greater numbers and which must be identified as a matter of urgency. That will not be much comfort to families with autistic children. But it should make everyone else feel a bit more secure.

From issue 2512 of New Scientist magazine, 13 August 2005, page 37

What is autism?

The developmental disorder that is now called autism was first described by doctors in 1943. Psychiatrists say there are three key features: lack of imagination, communication difficulties, and problems interacting with others. In practice, those affected have a bewildering range of strange behaviours. These can include fear of physical contact, hearing and visual problems, bizarre obsessions and a touching inability to lie.

Apart from the fact that about three-quarters of those affected are male, it is hard to make generalisations because the condition varies widely between patients. Contrary to popular belief, freakish talents for maths or music, say, are uncommon. In fact, about three-quarters of people with autism have learning difficulties, but those who do not may manage to hold down a job.

Parents usually realise something is wrong because children fail to develop normally. But up to one third of cases are “regressive” – children seem to go backwards when they are about two, losing their language and social skills.

In psychological terms, people with autism seem to lack “theory of mind” – the recognition that other individuals may hold a different perspective on things than themselves. This leaves them in a bewildering world where people seem to act according to incomprehensible rules and behave in meaningless ways. They also have impaired “executive function”, the ability to plan future actions. And patients have weak “central coherence”, the ability to extract meaning from experiences without getting bogged down in details. In other words, they can’t see the wood for the trees.

Clare Wilson

The usual suspects

Both genes and environmental factors play a role in the development of autism. But if there has indeed been a sudden rise in cases, the only possible cause is an environmental change because our genes can’t be altering that fast. Numerous candidates have been proposed.

“LEAKY GUT”

Thanks partly to anecdotal reports linking autism with bowel problems, some researchers believe that the condition could be caused by various dietary components leaking through the gut wall into the bloodstream, allowing them to reach the brain. One possible cause could be increased use of antibiotics disturbing the natural balance of gut bacteria.

There have been some reports of people with autism doing better on diets that exclude dairy foods and gluten, a protein found in wheat and barley. And a few small studies have found that some patients seem to improve after injections of the gut hormone secretin, which could possibly be related. But neither of these approaches have been borne out by larger placebo-controlled trials.

MMR JAB

The combined measles, mumps and rubella (MMR) vaccine was fingered by gastroenterologist Andrew Wakefield, formerly of the Royal Free Hospital in London. He suggested that giving children three vaccines simultaneously could damage their gut. Along with vociferous campaigning by parents, this led to a fall in uptake in the UK of this important childhood vaccine.

However, numerous large-scale studies showed no link between receiving the vaccine and developing autism. A recent study from Japan may prove the final nail in the coffin for the MMR theory. It found that diagnosed cases in that country continued to rise even after the triple jab was withdrawn (Journal of Child Psychology and Psychiatry, vol 46, p 572).

MERCURY IN VACCINES

In the US, mercury is public enemy number one. The mercury-containing preservative thimerosal – which has been used in a range of childhood vaccines although it is now being phased out – is claimed to cause autism by damaging the developing brain directly. But a review last year by the US Institutes of Medicine rejected a causal link between autism and either mercury or the MMR jab.

Clare Wilson

Malaria and TB are the twin scourges of the world, not AIDS

August 9th, 2005

If “AIDS” is a fantasy breeding misdiagnosis across the globe, as the skeptics conclude and the best scientific literature indicates, what is the reality? What are the millions who suffer from “AIDS” actually suffering from, which is being statistically rewritten as “AIDS”? If, as Rian Molan found out about South Africa, the overall totals of illness and death are not changing to any significant extent, where does the supposed three million or so global death total in “AIDS” come from?

Two major candidates are, of course, malaria and tuberculosis. These are world wide scourges of very ancient origin which continue to kill many more millions than are claimed as “AIDS” and labeled as “AIDS” deaths. They offer a reservoir from which to pull as many “AIDS” illnesses and deaths as are required by the diagnosticians of “AIDS” and their helpmates, the fundraisers, political opportunists, do-gooders, ex-presidents, current presidents, Columbia economists, UNAIDS statisticians, UN officials, socially smart scientist charity presidents, Hollywood celebrities, ACTUP founders, health agency bureaucrats, and the rest of the million strong cast of the $10 billion annual theatrical production that is justified by this simple script rewrite.

For some reason America forgot about malaria for a long time, perhaps because it was eradicated from many countries a while back by DDT. When DDT was banned, however, malaria came back with a vengeance, and this year as many as 500 million people will contract malaria, and more than one million will die, most of them children—but not all. In fact, pace Rachel Carson and her “Silent Spring”, there is some question whether banning DDT is worth it. Eagle eggshells have been saved, but in the less developed countries there have been an estimated fifty million lives lost from malaria.

Only this week, this was literally brought home to us when a beautiful young black Staten island journalist, Akilah Amapindi, 23, returned from Namibia for the National Association of Black Journalists convention in Atlanta, where she was scheduled to speak on a panel. Instead, she was taken ill and died in a matter of five days from what was diagnosed as a “particularly severe form of malaria.”

Here is the story from a fellow young journalist writing a shocked commentary in the Oregon Daily Emerald, and also a Newsday story which suggests that one cause of death might have been trusting whoever answers the phone at the “US Embassy in Manhattan”, whatever that might be:

“Before heading to Africa, Amapindi had telephoned the U.S. Embassy in Manhattan about inoculations required for the region and was told travelers to Windhoek didn’t require anti-malarial drugs, Harper said.”

This story was printed from Oregon Daily Emerald.

Site URL: http://www.dailyemerald.com.

We must advocate for better health services

Guest Commentary

August 11, 2005

During the beginning of August, myself and other members of the National Association of Black Journalists (Oregon chapter) had the privilege of attending the NABJ national convention in Atlanta, Ga. A week of attending workshops, keynote speeches, career fairs and networking came to an unsettling close with the deaths of two outstanding journalists. Peter Jennings, former ABC news anchor died Sunday night from lung cancer that he was diagnosed with only this year.

Jennings played a key role in developing what broadcast news has become today, and will be dearly missed worldwide. But what was even more shocking was the death of 23-year old journalist, Akilah Amapindi. Amapindi was, like myself, a student member of NABJ. She arrived in Atlanta on Sunday to begin a student project at the convention, and was hospitalized early Tuesday and diagnosed with malaria. On the following Sunday at the gospel brunch, we received word of her passing.

However, it wasn’t until later that day, after two plane flights and a three-hour layover, that her death really hit me. Amapindi, was only the one-third the age of Peter Jennings. She represented a new era — a generation of journalists that represent the face of the world (she was born in Jamaica and lived in Staten Island, N.Y.), a generation of journalists using new and old media (Amapindi worked in print, broadcast and interactive Web), and a generation of journalists and people who are committed to social justice and human rights (Amapindi founded a service sorority at Kenyon College, Ohio).

Amapindi had most likely been infected with malaria during her internship at Namibian Broadcasting Corporation in southern Africa, which she had just completed in July. Her work and aspirations are an inspiration, and although I never met her, I feel close to Amapindi because we both represent that new generation.

It is the responsibility of our generation to concern ourselves with world-shaping news regarding politics, culture, economics, science and health. Because malaria is a parasite infection, it will be much more difficult to create a vaccine for it. And although the impact of malaria is not recognized in the Western world because of the lack of deaths here, the deaths accumulating in the developing world should be enough indication that there is a need for increased research and funding.

Malaria causes or contributes to 3 million deaths per year, the majority of them children. Children are dying at a rate of four per minute, 5,000 a day and 35,000 a week. The number of malaria-related deaths in Africa is close to that of HIV/AIDS, but the amount of funding for research and treatment is in no way comparable.

The deaths of Peter Jennings and Akilah Amapindi on August 7, 2005, send two important messages to the world, especially the developed world:

1. We need to take care of our own health; risk of lung cancer and HIV/AIDS can be eradicated or significantly reduced by the choices we make.

2. We need to voice the concerns of health and other issues to our government representatives, advocating for more funding for health services, sciences, and training. By making the changes in our lifestyle to reduce the risks, we can allow more funding to go towards health epidemics that are less preventable.

There is more information on malaria at www.malaria.org. Also, Amapindi did not have health insurance, and her family does not have finances to ship her body to Jamaica, or for memorial services. Donations can be sent to: Akilah Amapindi Memorial Fund: c/o NABJ, 8701-A Adelphi Road, Adelphi, MD 20783-1716.

Jordan Thierry is a student at the University.

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© 2005 Oregon Daily Emerald

Newsday.com

Staten Island journalist dies of malaria

Woman, 23, went to Africa to work and get to know her dad, but fell ill upon her return

BY KATTI GRAY

STAFF CORRESPONDENT; Staff writer Zachary Dowdy contributed to this story.

August 8, 2005

ATLANTA – To feed her wanderlust and launch a reporting career, Akilah Amapindi signed on in July 2004 as a Namibian Broadcasting Corp. intern, a stint that would let her get acquainted with her father in his homeland.

The 2004 graduate of Ohio’s Kenyon College wound up anchoring the network’s 5 p.m. news bulletin several times, a rare achievement for a fledgling journalist. When the African internship ended seven months later, the Staten Islander, 23, enlisted as a photographer’s assistant for a film on Samuel Nujoma.

Retracing the exile of the first Namibian president through the Mozambican bush, an unvaccinated Amapindi, it is suspected, contracted mosquito-born malaria, according to her mother.

She died early yesterday at a hospital in Atlanta, where she was attending the National Association of Black Journalists’ annual convention.

“She told us that they slept under those big nets, but, in the morning, they would wake up and there would be four or five big fat mosquitoes inside. They knew they had been bitten,” said her mother, Unnah Harper, who settled in Staten Island more than 13 years ago from Jamaica with her only child.

“Knowing that she is gone forever, oh, the pain of it,” Harper said.

Yesterday, in an Atlanta hotel room, Harper tended to the details of burying Amapindi. Harper said the salary she makes as a nurse’s assistant isn’t enough to pay the costs of flying her daughter’s remains back north. She didn’t want her child cremated.

Amapindi also had no health insurance, losing her mother’s coverage after graduation.

The recent graduate was eager to travel to Namibia so she could get to know her father, John Amapindi, whom she first met four years ago.

Before heading to Africa, Amapindi had telephoned the U.S. Embassy in Manhattan about inoculations required for the region and was told travelers to Windhoek didn’t require anti-malarial drugs, Harper said.

Her daughter probably didn’t consider she would risk illness in the countryside, she added.

Amapindi suffered a severe bout of diarrhea before leaving Africa. Chills and aching muscles almost kept her from going to the Georgia convention, but over-the-counter medicine brought her temporary relief, her mother said.

Her health deteriorated in Atlanta. She was admitted to Emory Crawford Long Hospital for blood tests on July 31 and discharged at 3:30 a.m. the next day without a diagnosis.

Tuesday, she again sought medical care, at Grady Hospital, where doctors concluded she had malaria. Amapindi died after five days of treatment.

“She had tears in her eyes every time they wanted to do another medical procedure,” said Bob Butler, an Infinity Broadcasting Corp. executive and student convention project volunteer. “I could see a calculator going off in her head.”

Her mother had been at her bedside since Tuesday.”I kept telling her, ‘I love you. You’re going to get better,’ but she was not responsive,” Harper said.

“We were hoping for something miraculous,” said Harper’s sister, Sybrena “Jackie” Kennedy, who flew in from Kingston.

Staff writer Zachary Dowdy contributed to this story.

Copyright 2005 Newsday Inc.

Of course, death from malaria is infrequent and in just five days seems remarkably fast, so perhaps one can be permitted to wonder (with a correspondent, medical research consultant Robert Houston) to what extent this Fierce Malaria was actually ordinary malaria helped along by whatever crash application of drugs was applied by the local hospital.

Today, however, the New York Times has a nicely reassuring, science-as-progress-in-discovery piece in the Science Section on how some intrepid researchers in Kenya found out about the ability of the malaria parasite to bend mosquitoes to its will, and make them drink more human blood from more humans when the parasite is ready to transfer by making those with malaria temporarily more attractive to mosquitoes. It is only slightly marred by the photo editor having attached a picture of a wasp and wasp pupae on top of a caterpillar, and labeling it “mosquitoe pupae and a newly emerged adult using a caterpillar as a host.”

One interesting aspect of the article relates how the scientists found out about the parasite’s ability to direct mosquitoe behavior, by setting up tents in Kenya and with the permission of the parents, experimenting on Kenyan children in the early stages of malaria as they slept in the tents and mosquitoes feasted upon their blood.

The mosquito plasmodium carried by a mosquito travels from the mosquito into the liver, where it takes time to develop offspring in the blood in the the form of gametocytes which mosquitoes can then take up again. What the study discovered was that the children with gametocytes attracted twice as many mosquitoes as the children who were uninfected or infected but not to the stage of producing gametocytes.

In case you are worried about the children, we are assured that they were all treated with anti-malarial drugs, which took two weeks to clear them of the parasites. Of course, then they were subjected to more mosquitoes feasting off their blood, but their parents were OK with this presumably in a good cause and also to ensure they were medicated.

The infected children did not show symptoms like fever, a common situation in Africa. Nevertheless, the researchers treated them with anti-malaria drugs on the day of their study. Two weeks later, after the medicine had cleared the parasites, the scientists repeated the experiments with the same three children. They found that the cured children were no more attractive to the mosquitoes than the others.

The Times Science section article, Manipulative Malaria Parasite Makes You More Attractive (to Mosquitoes) is by Carl Zimmer:

The New York Times

August 9, 2005

Manipulative Malaria Parasite Makes You More Attractive (to Mosquitoes)

By CARL ZIMMER

Malaria is a staggeringly devastating disease, striking an estimated 300 million to 500 million people a year and killing more than a million of them. Scientists have long wondered how the parasite that causes malaria – a single-cell creature, plasmodium, carried by mosquitoes – manages to be so successful.

New research has shown an unexpected source of its success. The parasite makes infected humans smell more attractive to mosquitoes.

The research, published on Monday in the journal Public Library of Science Biology, was carried out by a team of French and Kenyan scientists led by Jacob Koella, an evolutionary biologist at Pierre and Marie Curie University in Paris. Dr. Koella is a leading expert on the ways in which parasites manipulate their hosts.

Beginning in the 1970’s, scientists discovered that a number of parasites can alter the behavior and physiology of their hosts for their own advantage, sometimes drastically.

Some parasitic wasps, for example, force their caterpillar hosts to eat different foods. When one species of wasp crawls out of its host, the fatally wounded caterpillar will act as the parasite’s bodyguard, defending it from predators.

Many parasites that need to live inside two different hosts during their life cycles also manipulate their hosts. A single-celled parasite called toxoplasma lives inside cats and then inside their prey, like rats. Research shows that infection with toxoplasma makes rats lose their fear of the odor of cats. Tapeworms that live in fish can turn them white and make them jump around near the surface of the water, where the fish are more likely to be eaten by birds, which the tapeworms make their new host. “It’s amazing how much manipulation is going on in parasites,” Dr. Koella said. “It would be hard to find a case where there wasn’t some manipulation.”

Scientists consider most of these examples as products of natural selection. A parasite’s reproductive success depends on its ability to be transmitted toa new host. “And manipulation appears to be an obvious way to do it,” Dr. Koella said.

In the late 90’s, Dr. Koella documented how plasmodium, the cause of malaria, manipulated its mosquito host. When the mosquitoes first take up plasmodium in a drink of human blood, they become more cautious about finding another victim. Their reluctance makes them less likely to be killed.

Dr. Koella points out that at this stage in the life cycle the parasite needs time to develop in the mosquito before it can be transmitted. “Before the parasite is transmitted to a human, its only goal is to survive, and to help the mosquito to survive,” he said.

The mosquito’s behavior changes when the parasite is ready to move on to a human. Dr. Koella found that mosquitoes carrying infective plasmodium become twice as likely as other mosquitoes to bite more than one person in a night. On top of that, they spend more time on each host drinking blood.

Dr. Koella argues that this shift in behavior raises the parasite’s odds of entering a human host.

Given its ability to control mosquitoes, scientists have wondered whether the plasmodium may also be able to manipulate humans. After it enters the human body, it needs time to develop in the liver. Those parasites then produce offspring that can invade blood cells, and eventually a few of these give rise to offspring, known as gametocytes, that can be taken up by a mosquito and survive.

Scientists have investigated whether infected hosts are more attractive to mosquitoes than uninfected ones. The results have been ambiguous.

“I think the main problem with the previous studies is that they couldn’t really tease apart the effect of infection and the intrinsic differences in attractiveness among people,” Dr. Koella said.

Mosquitoes find their victims by sniffing carbon dioxide and body odors. Some people apparently smell “better” to mosquitoes than others.

To rule out such factors, Dr. Koella and his colleagues used a new experimental plan. He and a student, Renaud Lacroix, teamed with Wolfgang Mukabana of the University of Nairobi and Louis Goagna of the International Center of Insect Physiology and Ecology in Kenya.

They set up three tents, each large enough for a person to sleep in. A fan pumped air from the tents into a central chamber swarming with about 100 mosquitoes. Mosquitoes that were attracted to one of the tents would fly toward it, only to become stuck in a trap.

The researchers asked parents in western Kenya to allow them to test their children for malaria. For each round of the experiment, they chose one uninfected child in an early stage of infection and a child who was carrying gametocytes. The children slept for a few hours in the tents, and the scientists checked the traps to measure how many mosquitoes had been attracted to each child.

After studying 12 sets of children, the scientists discovered a striking pattern. “Gametocyte-infected children attracted about twice as many mosquitoes as either uninfected ones or ones infected with nontransmissible stages,” Dr. Koella said. “The results really jump out.”

The infected children did not show symptoms like fever, a common situation in Africa. Nevertheless, the researchers treated them with anti-malaria drugs on the day of their study. Two weeks later, after the medicine had cleared the parasites, the scientists repeated the experiments with the same three children. They found that the cured children were no more attractive to the mosquitoes than the others.

“It’s a beautiful piece of science, and it’s a tremendously exciting finding,” said Andrew F. Read of the University of Edinburgh, an expert on malaria who was not involved in the research. Dr. Read cautioned that the researchers drew their conclusions from a relatively small number of trials.

“Obviously,” he said, “you’d be really pleased if another group went out and found the same thing. But it’s a logistical nightmare to do that stuff. So I’m very impressed with what they have managed.”

At this point, Dr. Koella can only speculate about how the parasite is altering its human host. Because the children carrying gametocytes in his study did not have fevers, plasmodium probably could not attract mosquitoes by making people hotter.

He suspects that the gametocytes are releasing chemicals that somehow alter the odor of human hosts, “but which aspects of the odor are changed is difficult to say.”

If future research supports his findings, that could go a long way to explain why malaria is so widespread.

“Scientists used to see the mosquito as a syringe that moves the parasite from one human to the other,” Dr. Koella said. “The fact that the parasite manipulates the mosquito to this extent can help to explain the incredibly intense transmission of malaria.”

“If it really is increasing attractiveness, whatever is causing that is going to be hugely interesting,” Dr. Read said.

Plasmodium’s manipulation may point to new strategies to fight the disease. “The obvious spin-off if you found the mechanism is that you could interfere with it,” Dr. Read said. “It might suggest certain kind of repellents to deactivate things coming off of people. Or whatever these parasites are doing could be used to distract mosquitoes away from people and trap them. It would suggest a lot of possibilities.”

Correction: Aug. 10, 2005, Wednesday:

A picture caption in Science Times on Tuesday with an article about ways that parasites control their hosts misidentified insects that were using a caterpillar. They were wasp pupae and a newly emerged adult wasp – not mosquito pupae and an adult mosquito.

An excellent piece of research, and the scientists that managed to pull it off deserve praise. Now we know even more about why the malarial mosquito is something to be avoided at all costs. But isn’t it another example of how the New York Times fails to cover sufficiently the important topic, which is how lives might be saved from malaria by reintroducing DDT?

If future research supports his findings, that could go a long way to explain why malaria is so widespread.

We would venture to guess that what best explains why malaria is so widespread is the absence of DDT.

At the very least, those who have read the best scientific literature and know that it has established without effective contradiction in the same peer-reviewed journals that AIDS is a global charade must hope that at least some of the funds now to be devoted to shoveling useless and dangerous HAART drugs at thousands of ignorant Africans and Asians—just as they have been administered to thousands of ignorant Americans—might be diverted to distributing anti-malarial drugs throughout the world, if not reviving the use of DDT to help wipe out this scourge of humanity.

But to argue that DDT should be used to save lives it seems we have to turn to the right wing press. In the New York Sun today (August 12 Fri) there is a zinger of a column by Alicia Colon presenting the case for bringing back DDT in malaria ridden countries.

Millions have died without DDT

Among the facts Colon mentions are that Rachel Carson’s “Silent Spring” led to the 1972 ban on DDT in the US and also internationally by virtue of the US warning countries they would not get foreign aid if they used it. This was the result: malaria deaths, reduced by DDT to 50,000 deaths a year, climbed back into the millions. In Sri Lanka, cases of malaria plummeted from 3 million in 1946 to just 29 in 1964. Five years after the DDT ban, the death rate climbed back to more than half a million a year.

“Silent Spring” was a most unscientific book, says Colon, quoting one critic, J. Gordon Edwards, a professor of entomology at San Jose State University who testified in defense of DDT at hearings before the ban. He wrote an editorial for 21st Century Science and technology magazine which was called “The Lies of Rachel Carson”. He pointed out that Carson quoted Albert Schweizer in the dedication of the book as saying “Man has lost the capacity to foresee and forestall. He will end by destroying the Earth.” But Schweiser was speaking of nuclear war, not insecticides, it turns out. In his autobiography, he wrote of “how much labor and waste of time these wicked insects do cause us… but a ray of hope, in the use of DDT, is now held out to us.”

Surely we can somehow save millions of lives as well as eagles’ eggs if, as Colon writes, DDT is not a carcinogen, and does not harm humans, even if you ingest it. Its inventor, Paul Miller, was given the Nobel for it in 1948. Meanwhile, Africa and Asia are being crippled by malaria and tuberculosis, particularly Africa, as Jared Diamond’s “Guns, Germs and Steel” book and now TV series pointed out.

Colon ends by recommending “Intellectual Morons—How Ideology Makes Smart People Fall for Stupid Ideas” by Daniel Flynn. It certainly sounds relevant.

Here is her column, Junk Science’s Cataclysmic Path:

August 12, 2005 Edition > Section: New York > Printer-Friendly Version

Junk Science’s Cataclysmic Path

BY ALICIA COLON

August 12, 2005

URL: http://www.nysun.com/article/18521

Psuedo-science can be fatal. It’s estimated that since the ban of the insecticide DDT, more than 50 million people have died of malaria. A young aspiring journalist from the Bulls Head section of Staten Island is one of the latest victims. Akilah Amapindi, 23, contracted the disease while working as a radio intern in southern Africa.

A few years ago, I learned that the boyfriend of a neighbor of mine had died of malaria while abroad. I am ashamed to admit that when I heard the sad news, my first instinct was to doubt the cause of death, subconsciously suspecting that drugs were the real culprit.

At the Martin Luther King Jr. dinner the Congress of Racial Equality held earlier this year, I heard CORE’s chairman, Roy Innis, speak of the senseless devastation wreaked on Africa due to the lack of modern technology in agriculture. CORE then held a conference at the United Nations to discuss the efficacy and realistic necessity of using DDT to control and minimize the damage done by malarial mosquitoes in developing countries.

The more one reads about the havoc wrought by agenda-driven environmentalists, the more one is astounded by how easily Americans can be frightened by speciously researched enviro-babble. Is global warming real? Sure. It’s been warming and cooling off for millions of years, and guess what? We humans have very little to do with it and it’s sheer arrogance to think that we can cure it.

In the 1960s, Rachel Carson’s “Silent Spring” generated worldwide interest in the environment and raised an alarm about the damage caused by chemical pesticides. Her book and the subsequent demonizing of the insecticide led to the 1972 ban on DDT in the United States. DDT was not banned internationally, but countries were warned that they would not get foreign aid if they used it. According to statistics from the United Nations, malaria before the ban had become a relatively minor disease, with about 50,000 deaths a year worldwide. A few years later, that figure had climbed into the millions.

DDT was not a carcinogen. It did not harm humans. Indeed, it could be ingested. It was one of the most effective killers of disease-bearing mosquitoes.

Dr. Paul Muller, its inventor, was honored with the Nobel Prize in 1948. When it was introduced in Sri Lanka, cases of malaria dropped from 3 million in 1946 to just 29 in 1964. Five years after the DDT ban, the death rate had climbed back to more than a half-million a year.

I was still a teenager when “Silent Spring” was published, and all I knew at the time was that it was about bugs, so my interest level was nonexistent. But Rachel Carson has been lauded over the years as the matriarch of today’s militant environment movement. What is interesting to note is that many legitimate scientists have always condemned her book as a tissue of cleverly told lies designed to exclude any argument that challenged Carson’s conclusions.

J. Gordon Edwards was a professor of entomology at San Jose State University who testified in defense of DDT at hearings before the ban. He wrote an editorial in 1992 for 21st Century Science and Technology Magazine that was called “The Lies of Rachel Carson.” In it he pinpointed all of Carson’s deliberate obfuscations and faulty research, from the very beginning of “Silent Spring” to its end.

For example, Carson quotes the famed Albert Schweitzer in the dedication of the book this way: “Man has lost the capacity to foresee and to forestall. He will end by destroying the Earth.” But Schweitzer was speaking of nuclear warfare, not insecticides. In reality, he wrote in his autobiography, “How much labor and waste of time these wicked insects do cause us … but a ray of hope, in the use of DDT, is now held out to us.” Funny how Carson left that out.

Perhaps the best explanation for why junk scientists have so much success in promoting their hokum theories is that there are so many “intellectual morons” in the world of academia. An author, Daniel Flynn, in his latest nonfiction work, “Intellectual Morons – How Ideology Makes Smart People Fall for Stupid Ideas,” coined that term.

The tragic death of a young woman in our city due to a disease that would have been eradicated had not hysterical, bone-headed lemmings fallen for flawed data should be our wake-up call. Before blindly accepting scientific hypotheses as fact, we should be cognizant of where that research is coming from and what group is financing it. Science and a personal political agenda are a very bad mix.

August 12, 2005 Edition > Section: New York > Printer-Friendly Version


The tragic death of a young woman in our city due to a disease that would have been eradicated had not hysterical, bone-headed lemmings fallen for flawed data should be our wake-up call. Before blindly accepting scientific hypotheses as fact, we should be cognizant of where that research is coming from and what group is financing it. Science and a personal political agenda are a very bad mix.

Very true, it would help if officials make sure that their science is accurate before formulating policy, especially if millions of lives are at stake. Why is it that the right wing seem to nail the liberal-progressive-left wing so often on this point?

Perhaps Daniel Flynn has the answer. Unfortunate his Intellectual Morons—How Ideology Makes Smart People Fall for Stupid Ideas is not out till the end of September.

Autism, vaccines and public trust in live debate on Meet The Press

August 7th, 2005

Autism in children and whether it has been caused by the mercury laden preservative in vaccines since the 1930s, thimerosal, remains a hot enough media topic to appear this morning (Sunday Aug 7) on television’s Sunday front page, Tim Russert’s Meet The Press on NBC. The program did a splendid job covering all the points as Russert hosted a science establishment field general and a skeptical independent science writer.

Russert faced these two well chosen guests who are in fact currently the two key people in the vaccine-autism debate and asked all the tough questions. The exchange provided a case study in how authoritative science can come into conflict with anecdotal evidence from people who are sure the science is wrong.

If that proves to be the case, and science’s exculpation of vaccines in autism doesn’t hold up—and in a few years we will see the result of withdrawing thimerosal completely from vaccines— big epidemiological studies in human health will come under closer scrutiny than ever.

If not, it will show how misleading anecdotal and even lab evidence can be in finding the threads of cause and effect in the vast tapestry that is human health.

The skeptic featured was David Kirby, a friend of questioners in this field. He wrote the bible for the vaccine-skeptical among the parents of autistic children, Evidence of Harm: Mercury in Vaccines and the Autism Epidemic, a sober analysis of the issue which raised questions as yet unanswered. He feels that the correspondence between mercury in vaccines (in the form of the preservative thimerosal) and the remarkable rise in autism needs to be explained. Nobody has yet answered the questions raised, he said. The doses received by children were far in excess of the federal safety guidelines.

The president of the Institute of Medicine, Dr. Harvey Fineberg, replied that we are not even sure that there has been such a huge rise in autism, because its vague definition and recognition has been expanding too. Asked to define it he came up with “basically, an inability to relate to others.”

All the evidence together at first did produce some suggestive data, he acknowledged, but by May 2004 (when the IOM report was issued) there were additional epidemiological studies covering hundreds of thousands of children compared systematically and uniformly, and the best of those studies (US, British, Danish and Swedish) all show no association between receiving vaccines with thimerosal and autism. That settled the issue as far as he was concerned.

(Special note: A recent study in Japan also found the diagnosis of autism continued to rise after the MMR triple vaccine was withdrawn (Journal of Child Psychology and Psychiatry, vol 46, p 572)).

Kirby responded by disparaging the epidemiology as inadequate. He said that the studies were flawed, some seriously, and that anyway epidemiology was not enough to inform us adequately. Indeed, he pointed out, it had been rejected as inadequate to prove a cause by the court system. The committee leaned entirely too much (2 to 1) on epidemiological studies, he said, rather than lab toxicology and anecdotal testimony. You need to look at the individual kids and the toxicology of cells in the lab and so forth. There were only seven toxicological reports and no toxicologists on the committee.

In line with this Russert noted that among the many emails the program had received since announcing the topic were some from the National Autism Associations saying that biological and clinical data had been ignored by the IOM and the studies the IOM relied upon were all tainted by association with the CDC or equivalent bodies in the other countries.

Weinberg responded that the committee had fairly evaluated all the evidence and all the studies for their strengths and weaknesses. They simply had found no association in the population. Yes, some studies more valid than others, and the committee had assessed them accordingly. You can read the entire report for yourself, he pointed out, by downloading it from their http://www.IOM.edu web site. In sum, they have a growing body of evidence which is imperfect but all taken together is convincing that there is no association between receipt of vaccines containing thimerosal and the development of autism.

So if it was harmless, Russert asked, why was it removed from vaccines? Well, there was no question that mercury is a neurotoxin and that it was prudent to remove it, and that had been done. But that was not because the studies were suspect, Fineberg insisted. That was simply an added measure of precaution that was sensible and correct. Any parent watching can now be confident that their child this year will receive vaccines without thimerosal, though some vaccines still had it prior to 2003 It is still in some flu vaccines, but there are flu vaccines for children available without it.

Russert then asks Fineberg the tough question, which is, So then should parents whose children were vaccinated before 2003 have some concerns? This is how he answers:

DR. FINEBERG: Prior to 2003, there were some that still had thimerosal, but the concern is not reaching the level of evidence related to the development of autism. The concern is a more general concern about mercury as a potential neurotoxin.

This little double think on the part of Dr. Fineberg was a little worrying. He seemed to be trying to have his cake and eat it ie reassure us that the danger had been removed, but at the same time deny the danger.

1) Vaccines have had thimerosal removed as a precautionary measure and parents can be reassured by that, and

2) the concern of parents whose children received thimerosal before that was done need not worry either, since the studies are showing no need to worry.

In other words, no one need worry. This was Dr. Fineberg’s reassuring message to the thousands of hysterical, paranoid and disenchanted parents out there watching this exchange.

Kirby for one was not going to stop worrying. He said that the report was issued 14 months ago and things have been moving rapidly since, with increasing evidence that some children have a genetic inability to process mercury very well. In the nineties, levels of exposure of two year olds reached 125 times the EPA limit. He talked of primate studies which show the ethyl mercury in vaccines converts to inorganic mercury in the brain very, very quickly and gets trapped, and in infant brains there is evidence you get hyper inflammation and the rapid nerve growth you see in autism.

All this biology is new since the IOM report so now he wondered if the IOM committee will meet again to consider the new evidence.

So will you meet again? Fineberg was asked by Tim Russert. Apparently not in the near future. Fineberg feels that the new evidence isn’t very important. David Kirby’s reading of the new evidence exceeded the facts, he said.

Russert said that many parents had written in and said that chelation treatment to remove the mercury had produced vast improvement in their autism-afflicted children. How about that?

Tim, said Dr Fineberg, autism is a complicated illness and many children show improvements over time. Keep in mind that the history of medicine is strewn with discarded treatments that people believed in at one time. The only way to decide if they work or not is to do systematic clinical trials.

Kirby was then asked by Russert if he credits parents’ complaints there is a government conspiracy between the CDC, the IOM and the FDA to withhold information from them and the public? He replied that he never uses such loaded words but he does think there has been a lack of transparency. Fineberg said he didn’t know what was meant by lack of transparency, exactly. Russert told him that parents want the information on children that HMOs have and won’t release for privacy reasons, and the CDC should get it for them and release it.

Fineberg didn’t agree that any problem of that kind if it exists had had any effect on the conclusions he and the others drew up. He said the IOM did urge the CDC to share the data with qualified researchers, and no one could complain that the IOM is not transparent since anyone can read the evidence it collected and the reasoning applied to it on the IOM site. .

Russert asked Kirby what he wanted to be done, since he has acknowledged that there is a possibility the cause could be something else entirely than thimerosal. We need clinical trials for treatments say Kirby, for example, chelation is being studied at University of Arizona, and the government should fund that kind of study. And we need to listen to the parents who are being dimissed by the scientists.

For example, parents said their children were born normal and then regressed, and they were scorned by scientists who said it was impossible. Yet now a video study at the University of Washington has proved them correct. We also need to release the data base the HMOs are hanging on to and make the system more transparent. The IOM’s own report acknowledges that there is a lack of trust and lack of transparency in the system.

“The lack of transparency of some of the processes also affects the trust relationship between the NIP, the National Immunization Program, and the general public.”

It is this lack of trust and transparency which is threatening the vaccine program, Kirby said, not the talk about mercury. Later in the exchange he mentioned leaked reports of pressure being put upon the IOM by the CDC, saying he had transcripts of internal private meetings which are not available through the Freedom of Information Act, but which the CDC should release.

But Fineberg emphatically denied there was any such pressure.

In fact, the whole reason why the Institute of Medicine, the National Academy of Sciences, the National Research Council exists is to be an independent voice outside of government to work on behalf of the needs of the American people. That’s what we do. Agencies do not always hear from us what they want to hear.

As he pointed out, the topics of stem cells, climate change and ways of fixing the Hubble Telescope have all yielded advice from these independent sources which government officials have found unwelcome.

Russert then asked Fineberg about the one page memo of instructions the CDC gave the IOM on how to conduct its thimerasol study, which is not being released, but didn’t get a straight answer as to why it could not be released. Instead, Fineberg simply emphasized that the experts convened by the IOM are not paid for their work and they assess the evidence on behalf of the American public whose taxes pay for the study.

Tim Russert then wound up the discussion by saying that surely we will know in a few years if there is a link between thimerosal and autism because thimerosal is now taken out of vaccines. Both his interviewees agreed with him, Kirby saying that even though the biology should be looked at more closely, any drop in case rates that shows up in the epidemiology will be “hugely significant.”

Fineberg having insisted that the work of the IOM is independent and not attuned to agency requirements, Russert asked him straight out if he is absolutely certain there is no link between thimerosal and autism? The best evidence indicates no association, Fineberg replied. These studies can never be absolutely certain in their findings but it is clear that other avenues are much more promising ways to spend our precious research dollars.

Kirby, on the other hand, said he believed “absolutely” that there is an association and that one day thimerosal will be shown to have caused cases of autism.

Conclusion: politics muddies science again

All in all, an excellent discussion which boiled down to this: plenty of charges and denials arising from the withholding of data from suspicious parents and others who believe often from their own experience there is a link, but in the final analysis, Dr Fineberg of the Institute of Medicine insisted his experts did an independent job and assessed the evidence thoroughly, and the impressively wide epidemiology just doesn’t yield up any visible link between thimerosal and autism.

Meanwhile, the well researched David Kirby continues to side with the parents in emphasizing that the biology of toxicity studied in the lab and in the children is recently even more suggestive than before that there is cause and effect, and that therefore it is possible that the field studies have not been done or reported properly.

Both agree that the epidemiology may soon be decisive. Since the possible culprit has been removed from vaccines given children since 2003, the link or lack of it should emerge fairly clearly in a few years.

If the link shows up, then it will be a powerful indictment of the design and quality of the very large epidemiological studies carried out so far in four countries on this question. If the link doesn’t show up, then it will confirm how misleading anecdotal and even lab evidence can be in determining cause and effect in human health.

Meanwhile parents are left uncertain whether to trust the estanlishment and its science because that science is partly curtained off by the arrogance and self-serving secrecy of the bureaucracy, and its spokesmen who insist on “reassuring the public” in such a blatantly one-sided way that the public is not reassured at all, especially a public consisting of parents frantic to protect their children in a state of mind confused and undermined by the withholding of information.

Here is the transcript from Meet The Press:

TRANSCRIPT SUN 7 AUG 2005

TIM RUSSERT: 500,000 American children have autism. The diagnosis rate has gone from one in 10,000 births in the ’80s to one in 166 births in 2003. Why the increase? What’s the cause? Why is there such controversy, with charges of a government conspiracy? With us: the president of the Institute of Medicine, Dr. Harvey Fineberg, and the author of “Evidence of Harm: Mercury in Vaccines and the Autism Epidemic,” David Kirby.

Coming next, autism: what we know and what we don’t know. Dr. Harvey Fineberg of the Institute of Medicine and David Kirby, author of “Evidence of Harm: Mercury in Vaccines and the Autism Epidemic,” a medical controversy, next, right here on MEET THE PRESS.

(Announcements)

MR. RUSSERT: The controversy over childhood vaccines and autism, after this brief station break.

(Announcements)

MR. RUSSERT: And we are back.

Dr. Fineberg, Mr. Kirby, welcome both.

In your book, Mr. Kirby, you raise early on two questions. “Why did the Centers for Disease Control and Prevention (CDC) and the Food and Drug Administration (FDA) allow mercury exposures from childhood vaccines to more than double between 1988 and 1992 without bothering to calculate cumulative totals and their potential risks? Why … was there a corresponding spike in reported cases of autism spectrum disorders? Why did autism grow from a relatively rare incidence of 1 in every 10,000 births in the 1980s to 1 in 500 in the late 1990s? Why did it continue to increase 1 in 250 in 2000 and then 1 in 166 today?” Have you answered those questions?

MR. DAVID KIRBY: No, nobody’s answered those questions. And we have to answer those questions as soon as possible. We need to solve this mystery. We need to get this controversy behind us so we can go on to find ways to help these kids. Mercury is toxic. It’s a known neurotoxin. If it gets into the brain, it could stay there virtually forever. Children born in the ’90s received mercury far in excess of federal safety limits. That’s indisputable. And yet we’re looking at a neurotoxin. And yet most of the evidence developed by the public health sector has been looking at the epidemiology. And we really need to look at what this mercury is doing inside the bodies and brains of these children if we’re going to solve this mystery one way or the other.

MR. RUSSERT: Dr. Fineberg, in your 2004 report from the Institute of Medicine, you said this: “While some information suggests that autism rates may be rising, it is not clear whether the observed increase is real or due to factors such as heightened awareness of the disorder or the use of a broader diagnostic definition. …”

Do you think there’s an epidemic of autism or do you think it’s simply a change in defining it?

DR. HARVEY FINEBERG: There’s definitely a huge number of cases diagnosed with autism, Tim. What is clear is that number recognized has increased dramatically. It’s also clear that the definition was broadened markedly in the 1980s and 1990s, and there were increased incentives to recognize children from increased awareness and availability of services. No one knows with certainty what part of the increase is genuine, a genuine increase in numbers, and what part is from increased recognition of people who were already there but not previously recognized. Remember we’re talking about a spectrum of diagnoses here, autism spectrum diseases, which range in severity from relatively mild to relatively severe.

MR. RUSSERT: For a layman, in a few words, how would you explain autism?

DR. FINEBERG: Autism is a severe neurodevelopmental disorder that is characterized by social withdrawal, by repetitive behaviors and by some kind of focal attention in its classic form. Basically, it’s an inability to relate to others.

MR. RUSSERT: Let me go back and review two of the studies that the Institute of Medicine did because this has helped feed much of this controversy and discussion. Back in 2001, the headline on your press release was “Link Between Neurodevelopment Disorders And Thimerosal Remains Unclear. Current scientific evidence neither proves nor disproves a link between the mercury-containing preservative thimerosal and neurodevelopmental disorders in children, says a new report from the Institute of Medicine… While very few vaccines given to children in the United States today still contain thimerosal, prudence dictates that precautionary measures be taken to decrease thimerosal exposure even further. … It is medically plausible that some children’s risk of a neurodevelopmental disorder could rise in part through increased mercury exposure from thimerosal-containing vaccines.”

Thimerosal being a preservative that is put into the vaccine. Then about three years later in May of 2004, the Institute of Medicine issued this headline: “MMR Vaccine And Thimerosal-Containing Vaccines Are Not Associated With Autism, IOM Report Says. Based on a thorough review of clinical and epidemiological studies”–I always destroy that word–“neither the mercury-based vaccine preservative thimerosal nor the measles-mumps-rubella (MMR) vaccine are associated with autism, says a new report from the Institute of Medicine…”

What changed in those three years?

DR. FINEBERG: When you’re dealing with a problem as complex as autism, Tim, you have to look at it from many different points of view and assemble evidence from many different vantage points. Biological evidence in humans and in animals, toxicologic evidence, how does the body deal with toxins, and evidence looking at the actual experience in populations. When the 2001 report was written, there was a lot of suggestive information about the toxic properties of mercury and the problem of autism incompletely understood. By 2004, the main change was that there were completed additional studies that were actually looking in the population at the relationship of receipt of vaccines containing thimerosal and the development of autism.

These studies were carried out in the United States, in Great Britain, in Denmark and Sweden. These studies covered hundreds of thousands of individuals, children, in these populations. They compared systematically in different ways whether you received vaccine with no thimerosal, with some thimerosal, with more thimerosal, and they looked at the relationship of those experiences with the development of autism. Uniformly, the best of those studies all show no association between receiving vaccine of different amounts with thimerosal or without and the development of autism. It was the absence of that association which was the main reason for reaching the conclusion that the evidence points to no association between vaccines and autism.

MR. RUSSERT: Mr. Kirby?

MR. KIRBY: Well, I think those flawed epidemiological studies range from severely flawed to seriously questionable. And I also think that you cannot rely solely on epidemiology to prove or disproof causation. In fact, I have right here–this is from the federal court system, but they ruled that epidemiology is not acceptable to prove there is no causal link between an adverse event and a pharmaceutical.

MR. RUSSERT: Explain that in layman’s language.

MR. KIRBY: Well, it means that you really, like the doctor said, you can look at the kids as well as look at the large population studies. You need to look at the biology, the toxicology; you need to look at the cellular level. You need to look at immunology, and I would say that what the IOM did last year–I was at that meeting on February 9. Virtually half of the evidence that was presented against the theory was epidemiological–I have the same problem as you. The other half supporting the theory was largely biological. And yet the committee gave a preponderance of evidence or emphasis to the epidemiological evidence and rather, I would say, gave short shrift to the biological evidence.

Dr. Fineberg has mentioned that there are 215 references in the report. I counted them up. By my count, it’s roughly a 2:1 ratio, about 115 references for epidemiology, 60 references for biology, and of those, only seven were toxicological reports. Now, we’re talking about a known neurotoxin, and there were no toxicologists on the committee, either. So I think even Dr. McCormick, the chairwoman of the committee, told me that there was definitely an emphasis on the epidemiology over the biological evidence.

MR. RUSSERT: When we announced this program, as you might expect, we heard from both sides who are very emotional and passionate about this topic. The National Autism Associations, Dr. Fineberg, wrote a letter to us including this: “The five studies the Institute of Medicine based its conclusion upon are fatally flawed, have never been replicated and have ties to the CDC”–Center for Disease Control– “(or foreign equivalent mandating vaccines in other countries) and/or the pharmaceutical industry. However, the Institute of Medicine chose to completely ignore the biological and clinical data supporting the link between thimerosal exposure and injuries to children conducted by independent, appropriately- credentialed researchers.”

DR. FINEBERG: Tim, the Institute of Medicine panel that came together represented a spectrum of experts who were asked to look at all of the evidence, and they did. They assessed the evidence that bears on the question. Some of it is biological, as I mentioned; some of it has to depend on what you actually find when you go out and look in the population. Is there or is there not an association? Keep in mind that there are many neurotoxins in the world. Dozens of natural and industrial substances have neurotoxic properties. When you’re trying to assess a specific association, there are biological studies that are relevant, and there are epidemiological studies that are relevant. All of these studies are not equally valid. Some have more deficiencies and limitations than others.

The committee went through very carefully and assessed each of those studies representing its strengths and weaknesses. All of this is laid out in its report, which is available for download to anyone who wants it from the IOM Web site, www.iom.edu. And anyone can read for themselves how the committee evaluated critically and carefully all of this evidence.

When the letter you read states that these five studies were not replicated, I can’t help but think that each one of them has been replicated four times. We have now a growing body of evidence, while imperfect, altogether convincing and all reaching the same conclusion, even though they vary in their methods and in their approaches. And that conclusion was no association between the receipt of vaccines containing thimerosal and the development of autism.

MR. RUSSERT: Why was thimerosal then taken out of the vaccination?

DR. FINEBERG: There’s no question that mercury is a neurotoxin. And if there were ways, which there are, to protect vaccines without using mercury-containing substances, it was prudent to remove it, not because there was evidence that it caused autism or even definitive evidence that the amounts in those vaccines caused any neuro problems, but because it was an added measure of precaution that was sensible and correct. And I might add that the latest vaccines that contained any thimerosal as a preservative, with the exception of some flu vaccines, were completed in 2001 and outdated in 2003. So anyone watching this program, any parent can be confident that when they take their child to the pediatrician to be immunized this year, they will receive vaccines without thimerosal as a preservative.

MR. RUSSERT: But prior to this year, there may be some concern?

DR. FINEBERG: Prior to 2003, there were some that still had thimerosal, but the concern is not reaching the level of evidence related to the development of autism. The concern is a more general concern about mercury as a potential neurotoxin.

MR. RUSSERT: Mr. Kirby?

MR. KIRBY: Well, if I could get back to the IOM report, that meeting was held 14–or the report was actually issued 14 months ago. This story is moving very, very fast. In those last 14 months, there has been an equally growing body of evidence, again on the biological side, that would suggest that, in a small subset of children with a certain genetic predisposition, they are unable to properly process the mercury that they were exposed to. And, by the way, the rates of exposure were quite high in the 1990s. At two months of age, children got three shots for a total of 62.5 micrograms of mercury. For their body weight, that’s 125 times over the EPA level. For me to reach that level, that would be about 1,125 micrograms.

We know that certain children with autism, again, seem to have higher levels of mercury accumulating in their body. We know that when we give mercury to infant primates, the–there’s two types of organic mercury: ethyl mercury in vaccines, methyl mercury in fish. What they found was that the ethyl mercury, once it got into the brain, it converted to inorganic mercury very, very quickly. Inorganic mercury basically gets trapped in the brain, and there’s evidence to suggest that, in an infant brain, in the first six months to a year when the brain is still growing, when inorganic mercury gets trapped in that brain, you’re going to have this hyper neuro inflammation, or the rapid brain growth that we see in autistic children.

These are the types of things that I think need to be researched further. Yes, we need to look at the epidemiology. There’s a whole lot of new biology. This has all been published. None of the biology was published at the time of the IOM hearing. It has since been published, and I actually wonder if the IOM would consider reconvening a new committee or a new hearing to consider the evidence that’s come out in the year and a half since the last report.

MR. RUSSERT: Would you?

DR. FINEBERG: Tim, Mr. Kirby’s description about the certitude of this evidence, I think, exceeds the actual balance of evidence that is produced when you look at the totality. It’s true that mercury is handled differently in the body when it’s in the form of so-called ethyl mercury, which is in vaccines, and methyl mercury, which was actually the form which was–on which the standards of exposure were based. That’s the type found in fish, as has been mentioned. But when you look back at the studies of actual poisonings of children with large amounts of methyl mercury and ethyl mercury, most toxicologists believe that the ethyl form of the mercury is less toxic than the methyl form–less toxic to the nervous system. And that’s based on many experiences with poisoning by these different forms of mercury.

MR. RUSSERT: Many parents have written us over the last couple of days saying that they have put their child in the process of collation, which removes the mercury poisoning from the system, and they say they’ve seen vast improvement. Wouldn’t that suggest that there may be some relationship between the mercury from thimerosal and the removal from the child?

DR. FINEBERG: Tim, autism is a complicated illness, and children with a variety of treatments and non-treatments show improvement over time, which is all to the good. But when you have a single story and a repeated story of an experience that a parent has with a treatment like chelation, you have to keep in mind that the history of medicine is strewn with discarded treatments that people at one time believed in very, very strongly. When you have one case after another, it’s one anecdote after another, and the plural of anecdote in scientific terms is not evidence. The only way to know whether a treatment works or does not work compared to other things is to do the clinical trial, comparing those who are given the treatment in a systematic and balanced way with those who are not.

MR. RUSSERT: Mr. Kirby, in your book, you talk about a conference on June 7 to 8 in 2000 in Simpsonwood, Georgia. We’ve gotten many e-mails and letters about a government conspiracy, that the CDC and the FDA and the Institute of Medicine and everyone has gotten together and really tried to deny information to the parents of children with autism. Do you believe that?

MR. KIRBY: Well, I think the word “conspiracy” and “cover-up,” those are very loaded words and I never use them. I do think there has been a lack of transparency and I would think Dr. Fineberg would probably agree with that statement. In this entire process…

MR. RUSSERT: Do you agree with that?

DR. FINEBERG: I don’t agree that the lack of transparency had had any bearing on conclusions, and I’m not sure what we mean by a lack of transparency.

MR. RUSSERT: Right now many parents are seeking information from studies from the CDC through the Freedom of Information Act, and they’re being told that the HMOs now have that information and they cannot share it because of privacy. And the parents are saying that’s outrageous. It could easily be obtained by the CDC and disburse that science, that data so people can look at it and make their own judgments. Should the CDC at least do that?

DR. FINEBERG: In fact, Tim, the Institute of Medicine looked separately in a different study at this system that was in place and did urge the CDC to make these records more available to qualified researchers. But that is not the same as a lack of transparency in the studies or in the reports. All anyone has to do in the case of the Institute of Medicine report is to read the report. All of the logic is laid out, all of the weighing of considerations. Not everyone may agree with each assessment, but they have all the relevant evidence right before them.

MR. RUSSERT: Mr. Kirby, you have said, “I am totally willing to accept there are other factors at play. It may turn out not to be thimerosal at all.” What do you think should be done?

MR. KIRBY: Well, I think, first of all, we need clinical trials for treatments. We need to try to help these children as best we can. There is a clinical trial of chelation therapy under way right now at University of Arizona. Dr. Fineberg said we need these trials. I wish the government was funding them. We need to listen to these parents as well. And I think that they’ve gotten a lot of dismissal from the scientific community. Parents were telling scientists that their children were born normally and then regressed. A lot of people dismissed that and said that couldn’t be the case. We now know from a brand- new study from the University of Washington using videotapes of one-year birthday and two-year birthday that is indeed the case. If the parents were right about regression, maybe they’re right about chelation.

Just getting back to transparency for one second if I could and this whole safety data base that we’re trying to get access to from the report that Dr. Fineberg cited, it says right here, “The lack of transparency of some of the processes also affects the trust relationship between the NIP, the National Immunization Program, and the general public.” The lack of trust and the lack of transparency is what’s threatening the vaccine program, not talk about mercury. So the doctor’s own committee said that there was a lack of transparency again inside this process of analyzing this data that was presented at that conference in Georgia.

MR. RUSSERT: Many of the National Autism Association and other groups, Doctor, point to Task Order 74.

DR. FINEBERG: Yes.

MR. RUSSERT: This is the arrangement between the CDC and the Institute of Medicine, a one-page memo which helps define the study and why it won’t be released. Is there a reason?

DR. FINEBERG: I don’t know what exactly that’s referring to, Tim, but when the Centers for Disease Control contracts with the Institute of Medicine to undertake a study, they do pay the actual costs of the study. But keep in mind that the panel of experts that are assembled by the Institute of Medicine receive no compensation whatsoever for their volunteer service. And when a government agency conveys money to the Institute of Medicine, it’s not the agency’s money. It’s the American people’s money. And our obligation is to do the best we can to assess the evidence on behalf of the American public.

MR. RUSSERT: Since thimerosal is now out of the vaccine, latest as of 2003, we will know in a few years whether or not there is a connection…

MR. KIRBY: That’s correct.

MR. RUSSERT: …definitively by the number of cases?

MR. KIRBY: I think so, but again I think we need to look at the biology, but the epidemiology is very important. If the case rates start to drop in the next couple years, I think that will be hugely significant. If I could also just get back to this commission by the CDC of the report, I’d like to do that as well.

MR. RUSSERT: Real fast.

MR. KIRBY: Well, there’s evidence that there was pressure put on the committee by the CDC, and we have internal transcripts. I think that’s what you were referring to. There are transcripts of private meetings. Some of them were leaked. They’re not obtainable through the Freedom of Information Act. Many people are trying to get copies of the other transcripts, and I do hope that the IOM will make those available in the name of transparency in this.

MR. RUSSERT: Was there pressure?

DR. FINEBERG: Absolutely not, Tim. In fact, the whole reason why the Institute of Medicine, the National Academy of Sciences, the National Research Council exists is to be an independent voice outside of government to work on behalf of the needs of the American people. That’s what we do. Agencies do not always hear from us what they want to hear. Sometimes the evidence does not point in a direction that is welcome. Stem cell guidelines or information about climate change or, for example, the ways to fix the Hubble Telescope which came out of the national academies–all of these are studies undertaken on behalf of the American public and the same was true for our assessment of vaccine safety.

MR. RUSSERT: You’re absolutely convinced there’s no connection between thimerosal and autism?

DR. FINEBERG: I’m convinced that the best evidence all points to the lack of an association. These studies can never prove to the point of absolute certainty an absence of an association. But I would say this, other avenues of research looking at other possible causes today are much more promising ways to spend our precious resources.

MR. RUSSERT: And our viewers should know that there is no thimerosal now in vaccinations, other than flu vaccinations, and so it’s safe for your children to do–have that done.

DR. FINEBERG: And even some flu vaccines for children are now available without thimerosal, as well.

MR. RUSSERT: You believe there is a possibility of a connection?

MR. KIRBY: Absolutely. And I think one day we’ll find out that there might have been–this has contributed to some of the cases in autism in this country.

MR. RUSSERT: Thank you for a very civil discussion. To be continued. We’ll be right back.

Duesberg smashes through on the Western front

August 5th, 2005

One of the most remarkable comebacks in science is happening as you read this blog. Peter Duesberg is winning on his Western front—cancer—the world war he had all but lost in the East—AIDS.

Stymied for twenty years in trying to overturn the Soviet-style dictatorship of the promoters of HIV/AIDS, Duesberg has also been blockaded for even longer in trying to overturn the richly funded and currently still fashionable theory of mutation in “oncogenes” as the cause of cancer.

Thirty years ago, having been responsible himself for kickstarting the paradigm by discovering the first and only proven example of an oncogene in a chicken virus, Duesberg then demonstrated his utter political impracticality (ie integrity, public spiritedness and vocational idealism) by soon renouncing the whole idea of oncogenes in humans—that individual human genes are linked to specific cancers eg prostate or breast. In fact, the first article he wrote which eviscerated the theory of HIV causing AIDS (in Cancer Research in 1987) only did it as an afterthought. The paper was in fact largely aimed at the other hollow paradigm, which also proved too entrenched to dislocate. Nobel prizes which would have gone to Duesberg were awarded to inferior scientists who toed the line.

Now, however, Duesberg is finally proving victorious on this Western front, where he can be said to be overrunning Europe and soon the world, since his new (though once mainstream) theory of where to look for the cause of cancer—in aneuploidy, the phenomenon common to cancer cells before they are cancerous, where they prove to have abnormal numbers of chromosomes, up to twice as many as a normal cell, in fact. Duesberg is attracting followers galore among the best of his opponents, who are already trying to steal his thunder and play down his contribution. They are also trying to keep their cake while it is being eaten up, of course, by suggesting that both oncogenes and aneuploidy are involved in cancer, Like cancer, oncogene theory is not going to die easily.

Upcoming reviews of Bialy book

All this is explained with hyperlucidity in Harvey Bialy’s powerful sleeper of a book, Oncogenes, Aneuploidy and AIDS: The Life and Scientific Times of Peter H. Duesberg, which we have mentioned previously as the equivalent of a Stealth Bomber attack on the HIV and oncogene paradigms. Published last summer, it is being read by the scientific cognoscenti in ever widening circles but as yet has not reached the tipping point, it appears. But two powerfully supportive reviews are about to appear, adding to the review in Nature/Biotechnology last year in which the Australian independent-minded scientist and consultant George Miklos endorsed it as fully describing why both the HIV/AIDS and the oncogene paradigms have proved sterile as scientific explanations.

The two reviews, both of them scientifically well informed, will appear in the Journal of Scientific Exploration online, one of the more cogent and scientifically informed platforms for political dissent in science on the Web. They make the situation very clear, by quoting key points from the Bialy book, and we will give them a post to themselves following this one.

Tom Bethell tells non-scientists why aneuploidy is the new path to cancer’s mysteries, and oncogenes are not

Such reviews which boil down and clarify in stark outline the problems in AIDS, cancer and science in general that Bialy’s book exposes are what is needed. For the one problem with Bialy’s brilliant book is its paradoxical virtue, namely that it is too precisely and concisely expressed in scientific terms to be easily understood by the lay public, even though it is also full of telling scientific and social anecdote. Now, however, a very accessible account of what is involved on the oncogene side has been written by the essayist Tom Bethell in the Spectator.

If you come from outside science this will tell you all you need to know about what “aneuploidy” is, and why after years in the wilderness Duesberg is showing every sign of being given a seat anew at the High Table in science.

THE AMERICAN SPECTATOR JULY/AUGUST 2005

Challenging Conventional Wisdom

Is cancer caused by gene mutations?

Tom Bethell

THE AMERICAN SPECTATOR JULY/AUGUST 2005

Challenging Conventional Wisdom

Is cancer caused by gene mutations?

Tom Bethell

SCIENTISTS THESE DAYS TEND TO BELIEVE that almost any trait can be attributed to a gene. The gene obsession, showing up in science journals and on the front page of the New York Times, culminated in the Human Genome Project. The human genome was sequenced, then that of the fruit fly, the mouse, the chimpanzee, the roundworm, yeast, and rice. Computers cranked out their mindless data. It has been a bonanza for techies and the computer industry but the medical benefits have remained elusive.

Now they are talking about a Cancer Genome Project. It would determine the DNA sequence in 12,500 tumor samples and is supposed to reveal cancer causing mutations by comparing the order of the letters of the genetic code in tumor cells with sequences in healthy tissue. But there is no single cancer genome, and the project will not improve our understanding of cancer.

Cancer has proved resistant to every “breakthrough” and treatment hype, and the new approach will only sustain the error that has dominated cancer research for 30 years. Since the mid-1970s, leading researchers have doggedly pursued the fixed idea that cancer is caused by gene mutations. I believe it will prove to have been one of the great medical errors of the 20th century.

WHERE TO BEGIN? One place is a story in the Washington Post, a few months back, headlined “Genetic Test Is Predictor of Breast Cancer Relapse.” The test “marks one of the first tangible benefits of the massive effort to harness genetics to fight cancer,” Rob Stein wrote. No real benefits yet? I think that is correct. Two well-publicized genes supposedly predispose women for breast cancer, but in over 90 percent of cases these genes have shown no defect.

Genes that (allegedly) cause cancer when they are mutated are called oncogenes. They were reported in 1976 by J. Michael Bishop and Harold Varmus, who were rewarded with the Nobel Prize. Varmus became director of the National Institutes of Health (NIH) under President Clinton; Bishop, chancellor of the University of California in San Francisco, one of the largest medical-research institutions in the country. The two scientists had “discovered a collection of normal genes that can cause cancer when they go awry, Gina Kolata later reported in the New York Times. About 40 such genes had been discovered. Normally harmless, “they would spring into action and cause cancer if they were twitched by carcinogens.” When mutated, in other words. This was “a new era in research.”

The following week, on October 20, 1989, Science magazine also reported the award. The article claimed: “…the work of the Bishop-Varmus group has had a major impact on efforts to understand the genetic basis of cancer. Since their 1976 discovery, researchers have identified nearly 50 cellular genes with the potential of becoming oncogenes.” Their work was “already paying off clinically.”

And so it went. Researchers began to find more and more of these oncogenes; then “tumor suppressor genes” were added. Now, in the Washington Post article, we read that “researchers sifted through 250 genes that had been identified as playing a role in breast cancer.”

So, up to 250 genes are “playing a role.” The Sanger Institute, which was also involved in the human genome project, claimed recently that “currently more than one percent of all human genes are cancer genes.” The latest figure is 25,000 genes in total for humans, so that is surely where the 250 “cancer genes” came from.

At the beginning, the oncogene theory posited that a single gene, when mutated, turned a normal cell into a cancer cell. We have gone from 1 to 250, the latter “playing a role.” This “multiplication of entities” — genes — is the hallmark of a theory that is not working. It’s what philosophers call a “deteriorating paradigm.” The theory gets more and more complex to account for its lack of success. The number of oncogenes keeps going up, even as the total number of genes goes down. Six years ago some thought humans had 150,000 genes in all. Now it’s one-sixth that number. How long before they find that all the genes “play a role” in cancer?

IT ALWAYS WAS UNLIKELY that a single mutated gene would turn a cell into a cancer cell. Mutations occur at a predictable rate in the body. As the cells of the body number perhaps trillions we would all have cancer if a single hit was sufficient. Then came the “multiple hit” theory. Three or four, maybe six or seven genes would all have to mutate in the same cell during its lifetime. Then, bingo, your unlucky number had come up. That cell became a cancer cell. When it divided it just kept on and on dividing.

Meanwhile, the underlying theory never changed. The research establishment remains in thrall to the idea that cancer is caused by gene mutations. It was and is unable to lay its hands on the genes responsible, but it believes they are in there somewhere.

There are several problems with the theory, but the most basic is this. Researchers have never been able to show that a mutated gene, taken from a cancer cell, will transform normal cells in the petri dish. They are unable to show that the allegedly guilty party is capable of committing the crime. They can transport these mutated genes into test cells. And the supposed deadly genes are integrated into the cell’s DNA. But those cells do not turn into cancer cells, and if injected into experimental animals, they don’t cause tumors. That’s when the experts said, well, there must be four or five genes all acting at once in the cell. But they have never been able to say which ones, nor show that in any combination they do the foul deed.

There is even a genetically engineered strain of mice called OncoMouse. They have some of these oncogenes in every cell of their small bodies. You would have thought they would die of cancer immediately. But they leave the womb, gobble up food, and live long enough to reproduce and pass on their deadly genes to the next generation.

I have a suggestion for Gina Kolata, who still works on these issues for the New York Times. Why not try asking Varmus or Bishop exactly which genes, either individually or in combination, cause cancer in humans or anything else? I tried calling Bishop at UCSF a few months back but couldn’t get through. He will respond to the New York Times, surely. But maybe not with a straight answer.

The desire to start over with a “cancer genome project” tells you they know they are not even at first base. Dr. Harold Varmus, now president of the Memorial Sloan-Kettering Cancer Center in New York, told the Times in March that the new project could completely change how we approach cancer.

Completely change? Maybe we do need a complete change. What about his decades-old Nobel work? Was that a waste? In a way I think it was worse than that, because when an erroneous theory is rewarded with the top prize in science, abandoning that theory is difficult. The backtracking required is an embarrassment to all.

JOURNALISM PLAYS A CRUCIAL ROLE. Especially in the field of medical science, there is a big problem. It exists at all major newspapers and I don’t mean to single out the New York Times. Science journalists don’t see themselves as qualified to challenge the experts. If a reporter were to do so, quoting nonapproved scientists, top-echelon NIH officials would surely complain to editors, and the reporter would be reassigned. The nation’s health would be said to be endangered.

All this contrasts with the far greater freedom that journalists enjoy in the political arena, including defense and foreign policy. About 35 years ago, leading newspaper editors decided to chart their own course and form their own judgments. The context was the Vietnam War, more specifically the Pentagon Papers. A big report critical of U.S. policy was leaked to the press, and the Nixon administration went to great pains to suppress it. National security was invoked, judicial restraining orders were issued, but eventually the “public’s right to know” trumped “national security.” The material was published.

That was the background from which Woodward and Bernstein and the Watergate investigation emerged a year later. And we were the better off for it. The real danger, then and now, was that of unchecked government power. And we are seeing that exercised in the realm of medical science, where we do not have a press that dares to think independently.

HOW DID THE IDEA TAKE ROOT that gene mutations cause cancer? Well, in the 1920s researchers bombarded fruit flies with X-rays and mutant flies resulted. Humans exposed to large X-ray doses a hundred years ago proved to be at high risk for skin cancer and leukemia. It was convincingly shown that X-rays produced both mutations and cancers.

Working at the NIH in the 1960s, the biochemist Bruce Ames used bacteria to detect the mutagenic properties of various substances. Some carcinogens proved to be mutagenic, hence the gene-mutation theory of cancer. Robert A. Weinberg, who directs a cancer research lab at MIT, says that by the 1970s he and others had come to believe that “Ames was preaching a great and simple lesson” about carcinogens: “Carcinogens are mutagens.”

Some are, but some of the best known are not. Neither asbestos nor coal tar, found in cigarettes, are mutagenic. They are carcinogens but they don’t affect the DNA — the genes. But there was one more crucial discovery still to be made. Or rather, rediscovery.

Robert Weinberg later claimed that a mutation in a single gene indeed had transformed a cell in vitro. But it turned out that the cell-line, one that had been provided by the NIH, was already “immortal,” or cancerous. It did not have the right number of chromosomes.

Normal cells have 46 chromosomes — 23 each from mother and father. Such cells are “diploid,” because their complement of chromosomes is doubled.

In case you never took biology, genes are segments of DNA strung along the chromosomes. The largest chromosomes, such as Chromosome 1 or 2, include several thousand genes each. Sometimes babies are born with one extra copy of the smallest chromosome, and because it is in the germ line this defect is in every cell of the body. Such babies have Down syndrome. Having an extra chromosome is serious business.

Here is the key point: cancer cells do not have the correct complement of chromosomes. Their “ploidy” is not good, so they are said to be aneuploid. Cancer cells are aneuploid. This defect arises not in the germ line, but in the grown body. Cells divide in the course of life, by a process called mitosis, and sometimes there is an error in the division. The chromosomes do not “segregate” properly (do not end up equally in the two daughter cells) and an extra chromosome may be hauled off into one of the new cells. Such over-burdened cells will usually die, but sometimes the error repeats and magnifies and increases. The cell just keeps on dividing, its control mechanisms overridden by the abundance of extra DNA in the cell. A tumor forms in that part of the body, and that is cancer. Some cancer cells may have as many as 80 chromosomes instead of 46. They may actually have double the right number of genes.

The aneuploid character of cancer cells is the first thing that Theodor Boveri and others noticed when they began to look at cancer under the microscope, 100 years ago. Leaving unresolved the question of what causes aneuploidy, early researchers thought that this was surely the genetic cause of cancer. Mutation didn’t enter into it. But gradually the early research was buried. In the last generation, textbooks on the cell and even textbooks on cancer have failed to mention aneuploidy or its bizarre chromosomal combinations. Weinberg wrote two books on cancer without mentioning aneuploidy. Overlooking what was plainly visible in the microscope, researchers worked for years with those defective, immortalized cell lines, assuming that their extra chromosomes were unimportant.

An analogy suggests the magnitude of the error. Cells today are compared to factories, so let’s think of an automobile plant. A cancer cell is the equivalent of a monster car with (let’s say) five wheels, two engines, and no brakes. Start it running and you can’t stop the damned thing. It’s hazardous to the community. The CEO wants to know what’s gone wrong so he sends underlings into the factory. There they find that instead of the anticipated 46 assembly lines, there are as many as 80. At the end of the process this weird machine gets bolted together and ploughs its way out the factory door.

But today’s gene mutation theorist is someone who says: “That’s not it. The extra assembly lines are irrelevant. What is happening is that three or four of the tens of thousands of workers along the assembly lines are not working right!” In the analogy, genes along the chromosomes correspond to workers along the assembly lines.

Any CEO would fire the lunatic who thought a few errant workers, and not the bizarre factory layout, had caused the mayhem. But in the realm of cancer research, those who do say that are rewarded with fat grants, top posts, and awards. That’s a measure of what has happened to cancer research.

I HAVE LEFT THE MOST DRAMATIC PART to the end. The man who rediscovered the old work on chromosomes and cancer and has drawn attention to it ever since, supported by investigations of his own, is none other than Peter Duesberg of U.C. Berkeley. He was already in the dog house at NIH for saying that AIDS is not an infectious disease and that HIV is harmless. All his grants were cut off in retribution. But as a member of the National Academy of Sciences he could still publish in respectable journals. So for the last seven years he has been drawing attention to the cancer matter. The NIH is pursuing the wrong theory, he says. Talk about persona non grata! No more grants for him! (And he has not received any.)

A researcher at the University of Washington who became controversial at NIH in an unrelated field warned Duesberg that “in the present system of NIH grants, there is no way to succeed.” No matter how much they prate in public about thinking outside the box and rewarding “high-risk” proposals, “the reviewers are the same and their self-interest is the same.” In the cancer field, grant proposals are reviewed by, and won by, proponents of the gene mutation theory.

Wayt Gibbs published a good article about Duesberg’s cancer findings in the Scientific American (July 2003). And this response is beginning to emerge in journals like Science: Er, well, there’s nothing new here … We have always known that aneuploidy is important in cancer. (Yes, but it was forgotten and then buried beneath the paper mountains of new research.) There is a quiet search for a “political” compromise: Can’t we say that both gene mutation and aneuploidy “play a role” in the genetics of cancer?

A leading cancer researcher, Bert Vogelstein of Johns Hopkins, told me some time back that “at least 90 percent of human cancers are aneuploid.” More recently, his lab reported that aneuploidy “is consistently shown in virtually all cancers.” A few years ago, Varmus from Sloan-Kettering did answer my e-mail query, writing: “Aneuploidy, and other manifestations of chromosomal instability are major manifestations of many cancers and many labs have been working on them.” But, he added: “Any role they play will not diminish the crucial roles of mutant protooncogenes and tumor suppressor genes.”

But why not? Maybe aneuploidy is sufficient.

At the end of May, Duesberg was invited to speak at NIH. His topic: “Aneuploidy and Cancer: From Correlation to Causation.” About 100 people showed up at Building 10. The Genetics branch of the National Cancer Institute (NCI) is interested in aneuploidy, and well aware of the political sensitivities. But I am told that the director of the NCI Andrew von Eschenbach, a political appointee, is not particularly interested in aneuploidy. He should be, though, because he is a cancer survivor himself and in speeches calls for “eliminating the suffering and death from cancer by 2015.”

Duesberg challenged the audience to prove him wrong. He is looking for diploid cancer: a solid tumor with the correct complement of chromosomes. He is not much interested in the compromise solutions — “a bit of both theories.” Prove me wrong, he says. A woman in the audience did suggest cases of tumors that looked diploid, but Duesberg knew the literature here and immediately referred her to a more recent study showing that these tumors, on closer microscopic inspection, proved to be aneuploid.

Maybe in the end he will show that in order to achieve a real breakthrough, it’s important not to be funded by the NIH. If so, we will all have learned a very expensive lesson.

Tom Bethell is a senior editor of The American Spectator.

JULY/AUGUST 2005 THE AMERICAN SPECTATOR

Who can be blamed?

If all this Duesbergian science proves out, and in both AIDS and cancer it is enshrined in the highest peer reviewed scientific literature, those responsible for misleading the world for so long on AIDS will not only have the shattered lives and eventual deaths of millions on their hands, deaths which include hundreds among the flower of art and culture in the US as well as millions of trusting innocents in the rest of the world, but also the responsibility of stalling the work on cancer of a scientist who is among the very best in the world.

In other words, to put it bluntly, the Bob Club and their fellow travelers among scientists, journalists, politicians and bureaucrats may well have blocked the discovery of a preventive for cancer in the last eighteen years. They not only crippled the work of Duesberg by vetoing his access to public funds (an interference which continues to date, and which was alleviated only by the intervention of private patrons such as Robert Leppo of San Francisco) but they diverted vast amounts of attention, personnel and public money to a scientific chimera.

Did they do this knowingly? This is the $64,000 question in science. There are many arguments to suggest that such self-interested opposition to enlightenment is unconscious, because it is self-deceptive and driven by all kinds of supportive emotions—envy, greed, fear and loathing—which are unseen devils in the subconscious of us all.

What makes it hard to accept that the right hand did not know what the left hand was up to is the degree of intelligence of most of the Club members. None of them have the fleet lightfootedness of Duesberg’s penetrating wit, which grasps the finer points so rapidly that while waiting for his lumbering opponents to catch up in debate, part of the brain is left idling and unfortunately liable to concoct a wickedly amusing phrase at their expense.

But Robert Gallo, Anthony Fauci and David Baltimore are no dummies, as their highly successful career moves show. At some point in the last twenty years, even these Ptolemaic apologists must have finally appreciated the mountainous size of the anomalies in the HIV/AIDS paradigm they have tried to explain away, and the complete absence of explanation or preventive that their theory has led to.

Or cure. Do they really think that the HAART regime counts as a cure, and renders the criticism null and void? According to Duesberg’s 2003 Journal of Biosciences wrap up, the scientific literature states that whatever temporary improvement may be felt or imagined by patients, it does not prevent eventual death, which it hastens fourfold.

But of course, in science as in life those committed to a viewpoint rarely read opposing arguments without prejudice, if they read them at all.

How Rian Malan sniffed out the rat in South African AIDS

August 4th, 2005

Rian Molan’s Nov 2001 Rolling Stone article on the South African AIDS mirage exposed the fiction in the ‘facts’

Appropos of the global AIDS (non) pandemic issue, it seems worth asking this question. Which would you rather believe on AIDS, the New York Times or the Rolling Stone?

The AIDS reporters at the Times are headed by Lawrence Altman, who has consistently hewed to the party line with rare exceptions where he actually notes some of the smaller anomalies of mainstream AIDS thinking.

Perhaps this is because he was trained at the CDC, and is therefore unlikely to contradict that institution too often, despite its atrocious performance on AIDS and AIDS statistics, which mathematician Serge Lang of Yale has trashed so thoroughly in his book Challenges (Springer-Verlag New York 1998) and in Lang Files, mailed around the country to key journalists including Altman.

Rolling Stone on the other hand achieved the following remarkable report in 2001, which states that AIDS in South Africa (then said by UNAIDS to be running at 17 million Africans dead of AIDS and 25 million more with HIV, with one in four South African adults infected) was a no show. Couldn’t be found. Didn’t seem to exist. No AIDS epidemic.

What? Yes, Rian Molan, a South African novelist of some repute, was asked by Jan Wenner of Rolling Stone to do a nice report on AIDS in South Africa in all its gory glory, and apparently was promised enough ready money and expenses to set out with great confidence and enthusiasm to do same. But almost immediately he ran into a problem: where were all the AIDS patients? According to everybody’s belief and the news media reports domestic and international. there should have been so many of them the sick should have been littering the sidewalks of Capetown and the Soweto shantytowns and kraals of that fair country (the climate is roughly equivalent to European countries of the same latitude).

But nada. Ryan couldn’t find the epidemic. Yes, there were plenty of patients sick and dying but no more than there had ever been, as far as he could find. Even the coffin makers were complaining. Where was all the booming business they had been led to expect?

Molan emailed Wenner to this effect and was told not to worry, the AIDS epidemic was surely there, just keep going. So he did. To no avail. Finally, he had the bright idea of going to check the death statistics of South Africa. Well, what d’ya know? They hadn’t budged by any significant amount that didn’t reflect the burgeoning population growth that South Africa in common with the rest of the sub-Sahara has enjoyed for the past quarter century.

In other words, no bulge. So, no discernible AIDS epidemic. And no payment to Molan, it looked like. But Wenner said, Well, write the story anyway. and he did. And this is it below, if you care to read it. But don’t tell anyone you read it, at least not before finding out whether they are a fully paid up member of the AIDS orthodoxy. For in general, such corrective heresy does not go down too well with HIV supporters.

As indeed Rian Molan’s wife clearly appreciated. As Molan later told it, she stood behind him with a rolling pin as he typed threatening to whack him over the noggin if he continued to write such subversive thoughts.

Here are a few sample paragraphs to whet the appetite of those readers who find reading more than a hundred words at a time on the Web daunting. Let us say one thing, though: Rian’s article is the best quick survey of the problems with the “global AIDS pandemic” available anywhere. You’ll see exactly why, among other things, HIV testing in Africa is a farce.

A statistical non-epidemic

Geneva’s computer models suggested that AIDS deaths here had tripled in three years, surging from 80,000-odd in 1996 to 250,000 in 1999. But no such rise was discernable in total registered deaths, which went from 294,703 to 343,535 within roughly the same period. The discrepancy was so large that I wrote to make absolutely sure I had understood these numbers correctly. Both parties confirmed that I had, and at that exact moment, my story was in trouble. Geneva’s figures reflected catastrophe. Pretoria’s figures did not.

How scientists really behave

There was a time when I imagined medical research as an idealized

endeavor, carried out by scientists interested only in truth. Up close, it turns out to be much like any other human enterprise, riven with envy, ambition and the standard jockeying for position. Labs and universities depend on grants, and grant making is fickle, subject to the vagaries of politics and intellectual fashion, and prone to favor scientists whose work grips the popular imagination. Every disease has champions who gather the data and proclaim the threat it poses. The cancer fighters will tell you that their crisis is deepening, and more research money is urgently needed. Those doing battle with malaria make similar pronouncements, as do those working on TB, and so on, and so on. If all their claims are added together, you wind up with a theoretical global death toll that “exceeds the number of humans who die annually by two- to threefold,” said Christopher Murray, a World Health Organization director.

No one for the coffins

One newspaper account I found told of a company called Affordable Coffins, purveyor of cheap cardboard caskets, which had more orders than it could fill. But the firm was barely two months old when the story ran, and two rival entrepreneurs who launched similar products a few years back had gone under. “People weren’t interested,” said a dejected Mr. Rob Whyte. “They wanted coffins made of real wood.” So I called the real-wood firms, three industrialists who manufactured coffins on an assembly line for the national market. “It’s quiet,” said Kurt Lammerding of GNG Pine Products. His competitors concurred – business was dead, so to speak. “It’s a fact,” said Mr. A. B. Schwegman of B&A Coffins. “If you go on what you read in the papers, we should be overwhelmed, but there’s nothing. So what’s going on? You tell me.”

How the WHO cook up the stats

.. the WHO devised an alternative, by which Africa’s AIDS statistics are now primarily based. It works like this: On any given morning anywhere in sub-Saharan Africa, you’ll find crowds of expectant mothers ling up outside government prenatal clinics, waiting for a routine checkup that includes the drawing of a blood sample to test for syphilis.

According UNAIDS, “anonymous blood specimens left over from these tests are tested for antibodies to HIV,” a ritual that usually takes place once a year. The results are fed into a computer model that uses “simple back-calculation procedures” and knowledge of “the well-known natural course of HIV infection” to produce statistics for the continent In other words, AIDS researchers descend on selected clinics, remove the leftover blood samples and screen them for traces of HIV The results are forwarded to Geneva and fed into a computer program called Epi-model: If a given number of pregnant women are HIV-positive, the formula says, then a certain percentage of all adults and children are presumed to be infected, too. And if that many people are infected, it follows that a percentage of them must have died. Hence, when UNAIDS announces 14 million Africans have succumbed to AIDS, it does not mean 14 million infected bodies have been counted. It means that 14 million people have theoretically died, some of them unseen in Africa’s swamps, shantytowns and vast swaths of terra incognita.

It’s malaria, stupid

It seemed something was confounding the tests, and the prime suspect was plasmodium falciparum, one of the parasites that causes malaria: Of the twenty-one subjects who tested positive, sixteen had had recent malaria infections and huge levels of antibody in their veins. The researchers tried an experiment: They formulated a preparation that absorbed the malaria antibodies, treated the blood samples with it, then retested them. Eighty percent of the suspected HIV infections vanished. The researchers themselves admitted that these findings were inconclusive. Still, considering that Africa is home to an estimated ninety percent of the world’s malaria cases, the implications of the report seemed intriguing.

And TB

Back in 1994, Max Essex, head of the Harvard AIDS Institute, and some colleagues of his observed a “very high” (sixty-three percent) rate of ELISA false positives among lepers in central Africa. Mystified, they probed deeper and pinpointed the cause: two cross-reacting antigens, one of which, lipoarabinomannan, or LAM, also occurs in the organism that causes TB. This prompted Essex and his collaborators to warn that ELISA results should be “interpreted with caution” in areas where HIV and TB were co-endemic. Indeed, they speculated that existing antibody tests “may not be sufficient for HIV diagnosis” in settings where TB and related diseases are commonplace.

Bumping up the numbers to no avail

A year later, I decided to return to my point of departure to see if the discrepancy persisted. I wrote to the country’s Department of Home Affairs, which manages the death register, and asked for the latest numbers. In response came a set of figures somewhat different from those initially provided – the consequence, I am told of people who died without any identity documents. Here is the final analysis:

Deaths registered in 1996 – 363,238.

Deaths registered in 2000 – 457,335.

As you see, registered deaths have indeed risen – not to the extent prophesied by the United Nations, perhaps, but there is definite movement in an ominous direction. Deaths are up across the board, but concentrated in certain critical age groups: females in their twenties, and males age thirty to thirty-nine.A team of experts commissioned by the Medical Research Council has studied this changing death pattern and found it to be “largely consistent with the pattern predicted by [ours] and other models of

the AIDS epidemic.” Their conclusion: AIDS has become the “biggest cause” of mortality in South Africa, responsible for forty percent of adult deaths. And yet, and yet, and yet, even this is not the end of our tale, because another governmental body, Stats SA, has challenged these findings. The Washington Post reported that the South African census bureau called the MRC study “badly flawed,” saying “the samples were

not representative, and assumptions about the probability of the transmission of the virus that causes AIDS were not necessarily accurate.”

The shockingly inadequate method

The UNAIDS computer model of Africa’s epidemic is in fact completely dependable, Dr. Schwartlander says because it relies on a “very

simple formula. You take the pregnancy-clinic numbers. You take the

median survival time – around nine years in Africa. You say this is roughly the distribution curve. Calculation of deaths is completely plausible if – and this is important – you have a good idea of the prevalence of HIV and how it spreads over time.” Why then, I asked, do we have so many different estimates of AIDS deaths in South Africa? “I’m not shocked,” he said. “The models may completely disagree at a particular point in time, but in the end the curves look incredibly similar. They’re goddamn consistent.”

If that’s true, I said, then why would we have 457,000 registered deaths here last year when the UN says 400,000 of them died of AIDS? One of those numbers must be wrong.

Note that Molan, even though he implies Thabo Mbeki may be on the right track in his suspicions, never quite gets to the stage of accepting or even imagining that HIV might not cause anything at all, and the whole puzzle easily resolved by simply throwing out this problematical paradigm, and instead of what may be a vast process of reinterpreting all these other sources of human sickness and death such as malaria and TB, and calling them AIDS, simply recognize them for what they are: Not AIDS but TB, Not AIDS but malaria, etc.

In other words, you don’t have to be an “HIV denialist” to see that the whole African pandemic is a crock. But you do lack an answer as to what the heck is going on.

Here is the whole classic tale, which essentially went nowhere in terms of rocking the HIV=AIDS boat, possibly because Jan Wenner runs into Mathilde Krim too often on the dinner party circuit in Manhattan.:

eprinted from RollingStone Magazine, November 22, 2001

AIDS in Africa: In Search of the Truth

By Rian Malan

“The frightening numbers were all that mattered. Once they were shown

to be accurate, further debate would be rendered obscene. So I set

out to confirm the death toll. I thought it would be easy—my first

mistake…”

===

1. MY FIRST MISTAKE

Africa’s era of mega death dawned in the fall of 1983, when the chief

of internal medicine of a hospital in what was then Zaire sent a

communiqué to American health officials, informing them that a

mysterious disease seemed to have broken out among his patients. At

the time, the United States was being convulsed by its own weird

health crisis. Large numbers of gay men were coming down with an

unknown disease of extraordinary virulence, something never seen in

the West before. Scientists called it GRID, an acronym for

Gay-Related Immune Deficiency. Political conservatives and holy men

called it God’s vengeance on sinners. American researchers were thus

intrigued that a similar syndrome had been observed in heterosexuals

in Africa. A posse of seasoned disease cowboys was convened and sent

forth to investigate.

On October 18th, 1993, they walked into Kinshasa’s Mama Yemo

Hospital, led by Peter Piot, 34, a Belgian microbiologist who had

been to the institution years earlier, investigating the first

outbreak of Ebola fever. A change was immediately apparent. “In 1976,

there were hardly any young adults in orthopedic wards,” Piot told a

reporter. “Suddenly – boom – I walked in and saw all these young men

and women, emaciated, dying.” Tests confirmed his worst

apprehensions: The mysterious new disease was present in Africa, and

its victims were heterosexual. When researchers started looking for

the newly identified human immunodeficiency virus, it turned up

almost everywhere – in eighty percent of Nairobi prostitutes,

thirty-two percent of Ugandan truck drivers, forty-five percent of

hospitalized Rwandan children. Worse, it seemed to be spreading very

rapidly. Epidemiologists plotted figures on graphs, drew lines

linking the data points and gaped in horror. The epidemic curve

peaked in the stratosphere. Scores of millions – maybe more – would

die unless something was done.

These prophecies transformed the destiny of AIDS. In 1983, it was a

fairly rare disease, confined largely to the gay and heroin-using

subcultures of the West. A few years later, it was a threat to all of

humanity itself. “We stand nakedly before a pandemic as mortal as any

there has ever been,” World Health Organization chief Halfdan Mahler

told a press conference in 1986. Western governments heeded his

anguished appeal for action. Billions were invested in education and

prevention campaigns. According to the Washington Post, impoverished

AIDS researchers suddenly had budgets that outstripped their spending

capacity. Nongovernmental AIDS organizations sprang up all across

Africa – 570 of them in Zimbabwe, 300 in South Africa, 1,300 in

Uganda. By 2000, global spending on AIDS had risen to many billions

of dollars a year, and activists were urging the commitment of many

billions more, largely to counter the apocalypse in Africa, where 22

million were said to carry the virus and 14 million to have died of

it.

And this is about where I entered the picture – July 2000, three

months after South African President Thabo Mbeki announced that he

intended to convene a panel of scientists and professors to

re-examine the relationship between the human immunodeficiency virus

and AIDS. Mbeki never exactly said AIDS doesn’t exist, but his action

begged the question, and the implications were mind-bending. South

Africa was said to have more HIV infections (4.2 million) than any

other country on the planet. One in five adults were already

infected, and the toll was rising daily. As his words sank in,

disbelief turned to derision.

“Ludicrous,” said the Washington Post.

“Off his rocker,” said the Spectator.

“A little open-mindedness is fine,” said Newsday. “But a person can

be so open-minded, his brains can fall out.”

The whole world laughed, and I rubbed my hands with glee: South

Africa was back on the world’s front pages for the first time since

the fall of apartheid; fortune awaited the man of action. I went to

see a friend who happens also to be an AIDS epidemiologist. He was so

enraged by what he called the “genocidal stupidity” of Mbeki’s

initiative that he’d left work and gone home, where I found him

slumped in depression. “Hey,” I said, snap out of it. Let’s make a

deal.” And so we did: He’d talk, I’d type, and together we’d tell the

inside story of Thabo Mbeki’s AIDS fiasco. All that remained was to

consider to consider the evidence that had led our leader astray.

According to newspaper reports, Mbeki had gleaned much of what he

knew from the Web, so I revved up the laptop and followed him into

the virtual underworld of AIDS heresy, where renegade scientists

maintain Web sites dedicated to the notion that AIDS is a hoax,

dreamed up by a diabolical alliance of pharmaceutical companies and

“fascist” academics whose only interest is enriching themselves. I

visited several such sites, noted what they had to say, and then

turned to Web sites maintained by universities and governments, which

offered crushing rebuttals. Can’t say I understood everything,

because the science was deep and dense, but here’s the gist:

Look at AIDS from an African point of view. Imagine yourself in a mud

hut, or maybe a tin shack on the outskirts of some sprawling city.

There’s sewage in the streets, and refuse removal is nonexistent.

Flies and mosquitoes abound, and your drinking water is probably

contaminated with feces. You and your children are sickly,

undernourished and stalked by diseases for which you’re unlikely to

receive proper treatment. Worse yet, these diseases are mutating,

becoming more virulent and drug-resistant. Minor scourge such as

diarrhea and pneumonia respond sluggishly to antibiotics. Malaria now

shrugs off treatment with chloroquine, which is often the only drug

for it available to poor Africans. Some strains of tuberculosis –

Africa’s other great killer – have become virtually incurable. Now

atop all this is AIDS.

According to what you hear on the radio, AIDS is caused by a tiny

virus that lurks unseen in the blood for many years, only to emerge

in deep disguise: a disease whose symptoms are other diseases, like

TB, for instance. Or pneumonia. Running stomach, say, or bloody

diarrhea in babies. These diseases are not new, which is why some

Africans have always been skeptical, maintaining that AIDS actually

stands for “American Idea for Discouraging Sex.” Others say nonsense,

the scientists are right; we’re all going to die unless we use

condoms. But condoms cost money and you have none, so you just sigh

and hope for the best.

Then one day you get a cough that won’t go away, and you start

shedding weight at an alarming rate. You know these symptoms. In the

past, you could take some pills and they would usually go away. But

the medicines don’t work anymore. You get sicker and sicker. You wind

up in the AIDS ward.

The orthodox scientists, if they could see you lying there, would say

your immune system has been destroyed by HIV, allowing the

tuberculosis (or whatever) to run riot. The dissidents would say no

way – the virus is a harmless creature that just happens to accompany

immune-system breakdown caused by other factors, in this case a

lifetime of hunger and exposure to tropical pathogens.

Incensed by this, the orthodoxy whistles up a truckload of studies

from all over Africa showing that HIV-positive hospital patients die

at astronomical rates relative to their HIV-negative counterparts.

The dissidents claim to be unimpressed. This proves nothing, they say

except that dying hospital patients carry the virus.

The orthodoxy grits its teeth. There’s only one way to crush these

rebels, and that’s to show that AIDS is a new disease that has caused

a massive increase in African mortality, which is of course the truth

as we know it: 22 million Africans infected, with 14 million more

already dead from it.

These frightening numbers were all that mattered, it seemed to me.

Once they were shown to be accurate, further debate would be rendered

obscene, and Thabo Mbeki would be guilty as charged, a fool who’d

allowed himself to be swayed by a tiny band of heretics universally

dismissed as wackos, fringe lunatics and scientific psychopaths. So I

set out to confirm the death toll. Just that. I thought it would be

easy – a call or two, maybe a brief interview. I picked up the phone.

It was my first mistake.

2. A Forbidden Thought

There was a time when I imagined medical research as an idealized

endeavor, carried out by scientists interested only in truth. Up

close, it turns out to be much like any other human enterprise, riven

with envy, ambition and the standard jockeying for position. Labs and

universities depend on grants, and grant making is fickle, subject to

the vagaries of politics and intellectual fashion, and prone to favor

scientists whose work grips the popular imagination. Every disease

has champions who gather the data and proclaim the threat it poses.

The cancer fighters will tell you that their crisis is deepening, and

more research money is urgently needed. Those doing battle with

malaria make similar pronouncements, as do those working on TB, and

so on, and so on. If all their claims are added together, you wind up

with a theoretical global death toll that “exceeds the number of

humans who die annually by two- to threefold,” said Christopher

Murray, a World Health Organization director.

Malaria kills around 2 million humans a year, roughly the same number

as AIDS, but malaria research currently gets only a fraction of the

resources devoted to AIDS. Tuberculosis (1.7 million victims a year)

is similarly sidelined, to the extent that there were no new TB drugs

in development at all as of 1998. AIDS, on the other hand, is

replete, employing an estimated 100,000 scientists, sociologists,

caregivers, counselors, peer educators and stagers of condom

jamborees. Until the attacks of September 11th diverted the world’s

anxieties (and charity dollars), the level of funding for AIDS grew

daily as foundations, governments and philanthropists such as Bill

Gates entered the field, unnerved by the bad news, which usually

arrived in the form of articles describing AIDS as a “merciless

plague” of “biblical virulence,” causing “terrible depredation” (as

Time recently put it) among the world’s poorest people.

These stories all originate in Africa, but the statistics that

support them emanate from the suburbs of Geneva, where the World

Health Organization has its headquarters. Technically employed by the

United Nations, WHO officials are the world’s disease police,

dedicated to eradicating illness. They crusade against old scourges,

raise the alarm against new ones, fight epidemics, and dispense

grants and expertise to poor countries. In conjunction with UNAIDS

(the joint United Nations Program on HIV/AIDS, based at the same

Geneva campus), the WHO also collects and disseminates information

about the AIDS pandemic.

In the West, the collection of such data is a fairly simple matter:

Almost every new AIDS case is scientifically verified and reported to

government health authorities, who inform the disease police in

Geneva. But AIDS mostly occurs in Africa, where hospitals are thinly

spread, understaffed and often bereft of the laboratory equipment

necessary to confirm HIV infections. How do you track an epidemic

under these conditions? In 1985, the WHO asked experts to hammer out

a simple description of AIDS, something that would enable bush

doctors to recognize the symptoms and start counting cases, but the

outcome was a fiasco – partly because doctors struggled to diagnose

the disease with the naked eye, but mostly because African

governments were too disorganized to collect the numbers and send

them in. Once it become clear that the case-reporting system wasn’t

working, the WHO devised an alternative, by which Africa’s AIDS

statistics are now primarily based.

It works like this: On any given morning anywhere in sub-Saharan

Africa, you’ll find crowds of expectant mothers ling up outside

government prenatal clinics, waiting for a routine checkup that

includes the drawing of a blood sample to test for syphilis.

According UNAIDS, “anonymous blood specimens left over from these

tests are tested for antibodies to HIV,” a ritual that usually takes

place once a year. The results are fed into a computer model that

uses “simple back-calculation procedures” and knowledge of “the

well-known natural course of HIV infection” to produce statistics for

the continent In other words, AIDS researchers descend on selected

clinics, remove the leftover blood samples and screen them for traces

of HIV The results are forwarded to Geneva and fed into a computer

program called Epi-model: If a given number of pregnant women are

HIV-positive, the formula says, then a certain percentage of all

adults and children are presumed to be infected, too. And if that

many people are infected, it follows that a percentage of them must

have died. Hence, when UNAIDS announces 14 million Africans have

succumbed to AIDS, it does not mean 14 million infected bodies have

been counted. It means that 14 million people have theoretically

died, some of them unseen in Africa’s swamps, shantytowns and vast

swaths of terra incognita.

You can theorize at will about the rest of Africa and nobody will

ever be the wiser, but my homeland is different – we are a

semi-industrialized nation with a respectable statistical service.

“South Africa,” says Ian Timaeus, London School of Hygiene and

Tropical Medicine professor and UNAIDS consultant “is the only

country in sub-Saharan Africa where sufficient deaths are routinely

registered to attempt to produce national estimates of mortality from

this source.” He adds that, “coverage is far from complete,” but

there’s enough of it to be useful – around eight of ten deaths are

routinely registered in South Africa, according to Timaeus, compared

to about 1 in 100 elsewhere below the Sahara.

It therefore seemed to me that checking the number of registered

deaths in South Africa was the surest way of assessing the statistics

from Geneva, so I dug out the figures. Geneva’s computer models

suggested that AIDS deaths here had tripled in three years, surging

from 80,000-odd in 1996 to 250,000 in 1999. But no such rise was

discernable in total registered deaths, which went from 294,703 to

343,535 within roughly the same period. The discrepancy was so large

that I wrote to make absolutely sure I had understood these numbers

correctly. Both parties confirmed that I had, and at that exact

moment, my story was in trouble. Geneva’s figures reflected

catastrophe. Pretoria’s figures did not. Between these extremes lay a

gray area populated by local experts such as Stephen Kramer, manager

of insurance giant Metropolitan’s AIDS Research Unit, whose own

computer model shows AIDS deaths at about one-third Geneva’s

estimates. But so what? South African actuaries don’t get a say in

this debate. The figures you see in your newspapers come from Geneva.

The WHO takes pains to label these numbers estimates only, not

rock-solid certainties, but still, these are estimates we all accept

as the truth.

But you don’t want to hear this, do you? Nor did I. It spoiled the

plot, so I tried to ignore it. Since it was indeed true that the very

large numbers of South Africans were dying, then the nation’s coffin

makers had to be laboring hard to keep pace with growing demand. One

newspaper account I found told of a company called Affordable

Coffins, purveyor of cheap cardboard caskets, which had more orders

than it could fill. But the firm was barely two months old when the

story ran, and two rival entrepreneurs who launched similar products

a few years back had gone under. “People weren’t interested,” said a

dejected Mr. Rob Whyte. “They wanted coffins made of real wood.”

So I called the real-wood firms, three industrialists who

manufactured coffins on an assembly line for the national market.

“It’s quiet,” said Kurt Lammerding of GNG Pine Products. His

competitors concurred – business was dead, so to speak.

“It’s a fact,” said Mr. A. B. Schwegman of B&A Coffins. “If you go on

what you read in the papers, we should be overwhelmed, but there’s

nothing. So what’s going on? You tell me.”

I couldn’t, although I suspected it might have something to do with

race. Since the downfall of apartheid, in 1994, illegal backyard

funeral parlors have mushroomed in the black townships, and my

sources couldn’t discount the possibility that these outfits were

scoring their coffins from the underground economy. So, I called a

black-owned firm, Mmabatho Coffins, but it had gone out of business,

along with some others I tried calling. This was getting seriously

weird. The death rate had almost doubled in the past decade,

according to a recent story in South Africa’s largest newspaper.

“These aren’t projections,” said the Sunday Times. “These are the

facts.” And if the facts were correct, I thought, someone somewhere

had to be prospering in the coffin trade.

Further inquiries led me to Johannesburg’s derelict downtown, where a

giant multistory parking garage has recently been transformed into a

vast warren of carpentry workshops, each housing a black carpenter,

set up in business with government seed money. I wandered around

searching for coffin makers, but there were only two. Eric Borman

said business was good, but he was a master craftsman who made one or

two deluxe caskets a week and seemed to resent the suggestion his

customers were the sort of people who died of AIDS. For that, I’d

have to talk to Penny. Borman pointed, and off I went, deeper and

deeper into the maze. Penny’s place was locked up and deserted.

Inside, I saw unsold coffins stacked ceiling-high, and a forlorn

CLOSED sign hung on a wire.

At that moment, a forbidden thought entered my brain. This may sound

crazy to you, thousands of miles away, but put yourself in my shoes.

You live in Africa – OK, in the post-colonial twilight of

Johannesburg’s once-white suburbs, but still, close enough to the

AIDS front line. For years, experts tell you that the plague is

marching down the continent, coming ever closer. At first nothing

happens, but there dawns a day when the HIV estimates start rising

around you, and by 2000 the newspapers are telling you that one in

five adults on your street is walking dead.

This has to be true, because it’s coming from experts, so you start

looking for evidence. Laston, the gardener at Number 10, is

suspiciously thin, and has a hacking cough that won’t go away. On the

far side of the golf course, Mrs. Smith has just buried her beloved

servant. Mr. Beresford’s maid has just died, too. Your cousin Lenny

knows someone who owns a factory where all the workers are dying.

Your newspapers are regularly predicting that the economy will surely

be crippled, and schooling may soon collapse because so many teachers

have died.

But then you find yourself staring into Penny’s failed coffin

workshop and you think, Jesus, maybe something is wrong here…

Is this likely? Look, I believe that AIDS exists and it’s killing

Africans. But as many as all the experts tell us? Hard to say. In my

suburb, I can assure you, people’s brains are so addled by death

propaganda that we automatically assume almost everyone who falls

seriously ill or dies has AIDS, especially if they’re poor and black.

But we don’t really know for sure, and nor do the sufferers

themselves, because hardly anyone has been tested. “What’s the

point?” asks Laston, the ailing gardener. He knows there’s no cure

for AIDS, and no hope of obtaining life-extending anti-retrovirals.

Last winter, he came down with a bad cough, and everyone said it was

AIDS, but it wasn’t – come summer, Laston got better. Then Stanley

the bricklayer became our street’s most likely case. Stan maintained

he had a heart condition, but behind his back, everyone was

whispering, “Oh, my God, it’s AIDS.” But was it? We had no idea. We

were playing a game, driven by hysteria.

No one wanted to hear this. Worried friends slipped newspaper

clippings into my mailbox: CEMETERY OVERFLOWS…. HOSPITALS

OVERWHELMED…. PRISON DEATHS UP 535 PERCENT. I checked out all the

evidence, but often there was some other possible explanation, like

cut-price burial plots or a TB epidemic in the overcrowded jails or a

funding crisis in government hospitals. After months of this, even my

mother lost patience. “Shut up!” she snapped. “They’ll put you in a

straitjacket.” Mother knows best, but I just couldn’t get those

numbers out of my head: 294,703 registered deaths in 1996, 343,535

four years later. I called my friend the AIDS epidemiologist and

said, “Listen, I am beset by demons and heresies, can you not save

me?” So we had lunch, and I aired my doubts, whereupon he pointed in

the direction where truth lay, and I set out to find it.

3. A Bell is Rung

And here we are on a hilltop on the equator, overlooking the

landscape where Africa’s first recorded outbreak of AIDS took place.

It’s a village called Kashenye, which lies on the border between

Uganda and Tanzania, close to where the Kagera River flows into Lake

Victoria. In 1979 or thereabouts, according to local legend, a trader

crossed the river in a canoe to sell his wares in Kashenye. Business

done, he bought some beers and relaxed in the company of a village

girl. Some time later, she fell victim to a wasting disease that

refused to respond to any known medication, Western or tribal.

Not long after, according to Edward Hooper in his book Slim, a

similar drama unfolded in Kasensero, a fishing village over on the

Uganda side of the river. There the first victim was also a local

girl, and the agent of infection was said to have been a visitor from

Kashenye. In due course, several more citizens of Kashenye contracted

the wasting disease. Their neighbors cried foul, accusing Kashenye of

putting a hex on them. Kashenye responded with similar allegations.

Soon, villagers on both banks of the river were discarding objects

brought from the other side, believing them to be bewitched. But

nothing helped. By 1983, the contagion was in all the cities on the

Western shore of Lake Victoria. Within a few years the region became

known as the epicenter of Africa’s AIDS epidemic, and Ugandan

president Yoweri Museveni was predicting that “apocalypse” was

imminent.

His prophecy was based largely on testing done among small groups of

high-risk subjects. Many factors were unknown, however, including the

true extent of infection in the general populace, the rate at which

it was spreading, the speed at which it killed. To formulate an

effective battle plan, AIDS researchers desperately needed more data

in these areas.

They cast around for a place to study, and lit on the Masaka district

in Uganda, a ramshackle area just west of Lake Victoria and probably

100 miles north of Ground Zero. The rate of infection there among

adults was not particularly high – just more than eight percent – but

there were other considerations making it a good place to study: The

district was politically stable, and there was an international

airport three hours away. In 1989, a Dutch epidemiologist named Daan

Mulder began to lay the groundwork for what would ultimately become

the longest and most important study of its kind in Africa.

Assisted by an army of field workers, Mulder drew a circle around

fifteen villages outside Masaka and proceeded to count every

resident. Then he took blood from all those who were willing – 8,833

out of 9,777 inhabitants – screened it for HIV infections and sat

back to see what happened. Every household was visited at least once

a year, and every death was noted and entered into Mulder’s database,

along with the deceased’s HIV status.

The first results were published in 1994, and they were devastating.

The HIV-infected villagers of Masaka were dying at a rate fifteen

times higher than their uninfected neighbors. Young adults with the

virus in their bloodstream were sixty times more likely to perish.

Overall, HIV-related disease accounted for a staggering forty-two

percent of all deaths. The AIDS dissidents were crushed, HIV theory

was vindicated. “If there are any left who will not even accept

[this],” commented the U.S. Centers for Disease Control upon the

release of the results, “their explanation of how HIV-seropositivity

leads to early death must be very curious indeed.”

Clearly, only a fool would second-guess such powerful evidence, so I

just visited the villages where Mulder’s work was done, verified what

he’d found and headed back toward the airport, my story about Mbeki’s

stupidity back on track. But on my way I spent an hour or two in

Uganda’s Statistics Office, and what I learned there changed things

yet again.

In 1948, Uganda’s British rulers attempted a rough census in the

Masaka area and concluded that the annual death rate was “a minimum

of twenty-five to thirty per thousand.” A second census, in 1959, put

the figure at twenty-one deaths per thousand. By 1991, it had fallen

to sixteen per thousand. Enter Daan Mulder with his blood tests,

massive funding and armies of field workers. He counted every death

over two years, and then five, and here is his conclusion: The crude

annual death rate in Masaka, in the midst of a horrifying AIDS

plague, was 14.6 per thousand – the lowest ever measured.

I was relieved to discover that there was another possible

interpretation of these statistics. Daan Mulder’s work began at a

time when Uganda was emerging from two decades of terror and chaos.

Doctors had fled the country, hospitals had collapsed and nobody kept

track of mortality trends in the dark years of the Seventies and

Eighties. According to British statistician Andrew Nunn, one of

Mulder’s collaborators, disease-related rates must have fallen to

all-time low levels in the Seventies, when no one was counting, and

then surged massively with the advent of AIDS around 1980.

“In fact,” says Nunn, “evidence suggests it’s epidemic.” (Mulder

himself cannot be asked to explain his findings – he has since died

of cancer.)

Nunn’s explanation may be so, but the same can’t apply to neighboring

Tanzania, which embarked in 1992 on an even larger mortality study.

Like Mulder’s, it was funded by the British government and supported

by scientists from the British universities. The Adult Morbidity and

Mortality Project recruited 307,912 participants, each of whom was

visited at least once a year in the next three years and questioned

about recent deaths or disease. The final results were rather like

Masaka’s: AIDS was the leading reported cause of adult mortality, but

the average death rate in the communities studied was 13.6 per

thousand – ten percent lower than the death rate measured in the

census of 1988, which was rated “close to 100 percent” complete by

Dr. Timaeus, the UNAIDS consultant. Timaeus is a leading authority on

African mortality in the AIDS era, and it was to him that my

difficult question ultimately fell.

Professor Timaeus,” I said in his London office, “this study appears

to show that there was no increase in the death rate between 1988 and

1995, in the heart of Tanzania’s AIDS epidemic.”

He shrugged. “This survey covered only part of the country,” he said.

“True,” I said, “but a fairly large part, with hundreds of thousands

of participants.”

“But were they representative?” he countered.

I had no idea. Timaeus smiled and said, “I think this is the more

critical evidence.”

Whereupon he produced a sheath of graphs and papers and laid them on

the table. There was, he said, a “regrettable” lack of knowledge

about mortality trends in Africa, attributable to “inertia,”

indifference and a crippling lack of up-to-date data. These factors

bedeviled the demographer, but Timaeus said he knew of several ways

around them, most dramatic of which is the so-called sibling-history

technique of mortality estimation. It works like this:

Since 1984, researchers financed by the U.S. Agency for International

Development have conducted detailed health interviews with several

thousand mothers in developing countries worldwide. Among the

questions put to them are these: How many children did your mother

have? How many are still alive? When did the others die? Timaeus

realized that close analysis of the answers might reveal trends that

were failing to show up elsewhere. He set to work, and published the

results in the journal AIDS in 1998. “In just six years (1989-1995)

in Uganda,” he wrote, “men’s death rates more than doubled.” Similar

trends were revealed in Tanzania, he reported, where “men’s deaths

apparently rose eighty percent” in the same period.

Again, this seemed to settle the matter, but again, there were

puzzling complications. For a start, Timaeus’ study coincided with

Daan Mulder’s epic mortality study, which ran for seven years without

detecting any significant change in the death rate. The same is true

of Tanzania’s giant adult-mortality survey, which fell in the heart

of the period when Timaeus says male mortality was surging upward but

which failed to document any such thing.

Could there have been some problem with Timaeus’ data? Kenneth Hill

is the Johns Hopkins university demographer who helped conceive the

sibling-history technique. Recently, he and his team embarked on a

worldwide evaluation of its performance in the field, to check on its

accuracy. Last year, an article co-authored by Hill reported that the

method was prone to something called, “downward bias” – meaning that

people remember recent deaths pretty clearly, but those from years

back tend to fade. According to the article, which appeared in

Studies in Family Planning, this usually leads to a false impression

of rising mortality rates as you near the present. This has happened

even in counties where there was little or no AIDS. In Namibia, for

instance, the sibling method detected a 156 percent rise in the

fourteen years prior to 1992, when the country’s HIV infection rate

ranged from zero to one percent. “This lack of precision,” Hill and

his associate wrote, “precludes the use of these data for trend

analysis.”

“I disagree,” said Timaeus, who believes they got their math wrong.

Neither Hill nor any members of his team wanted to respond on the

record, but I drew one of them into a conversation on another subject.

“Do you accept the high levels of HIV infection being reported by

Geneva?” I asked.

“I don’t have much faith,” he said. “It’s essentially a modeling

exercise, and the exercise has always seemed to have a political

dimension.”

That rung a bell. I was living in Los Angeles in 1981, when the very

first cases of GRID were detected. I knew men who were stricken, and

I sympathized entirely with their desperation. They wanted government

action and knew there would be little as long as the disease was seen

as a scourge of queers, junkies and Haitians. So they forged an

alliance with powerful figures in science and the media and set forth

to change perceptions, armed inter alia with potent slogans such as

“AIDS is an equal-opportunity killer” and “AIDS threatens everyone.”

Madonna, Liz Taylor and other stars were recruited to drive home the

message to the straight masses: AIDS is coming after you, too.

These warnings were backed up by estimates such as the one issued by

the CDC in 1985, stating that 1.5 million Americans were already

HIV-infected, and the disease was spreading rapidly. Dr Anthony

Fauci, now head of the National Institute of Allergic and Infectious

diseases, prophesied that “2 to 3 million Americans” would be

HIV-positive within a decade. Newsweek’s figures in a 1986 article

were at least twice as high. That same year, Oprah Winfrey told the

nation that “by 1990 one in five” heterosexuals would be dead of

AIDS. As the hysteria intensified, challenging such certainties came

to be dangerous. In 1988 New York City Health Commissioner Stephen C.

Joseph reviewed the city’s estimate of HIV infections, concluded that

the number was inaccurate and halved it, from 400,000 to 200,000. His

office was invaded by protesters, his life threatened. Demonstrators

tailed him to meetings, chanting, “Resign, resign!”

In hindsight, Dr. Joseph’s reduced figure of 200,000 might itself be

an exaggeration, given that New York City has recorded a total of

around 120,000 AIDS cases since the start of the epidemic two decades

ago. In 1997, a federal health official told the Washington Post that

by his calculation, the true number of HIV infections in the United

States back in the mid-Eighties must have been around 450,000 – less

than one-third of the figure put forth at the time by the CDC.

If the numbers could be gotten so wrong in America, what are we to

make of the infinitely more dire death spells cast upon the

developing world? In 1993, Laurie Garrett wrote in her book The

Coming Plague that Thailand’s AIDS epidemic was “moving at

super-sonic speed.” It has stalled at just below two percent,

according to UNAIDS. In 1991 All India Institute of Medical Sciences

official Vulmiri Ramalingaswami said AIDS in India “was sitting on

top of a volcano,” but infection levels there have yet to crest one

percent. The only place where the AIDS apocalypse has materialized in

its full and ghastly glory is in Geneva’s computer models of the

African pandemic, which show millions dead and far worse coming.

Why Africa, and Africa only? I now know a possible reason. Read on.

4. “Crap!” An Expert Declares

In many ways, the story of AIDS in Africa is a story of the gulf

between rich and poor, the privileged and the wretched. Here is one

way of calibrating the abyss.

Let’s say you live in America, and you committed an indiscretion with

drugs and needles or unprotected sex a few years back, and now find

yourself plagued by ominous maladies that won’t go away. Your doctor

frowns and says you should have an AIDS test. She draws a blood

sample and sends it to a laboratory, where it is subjected to an

exploratory ELISA (enzyme-linked immunosorbent assay) test. The ELISA

cannot detect the virus itself, only the antibodies that mark its

presence. If your blood contains such antibodies, the test will

“light up,” or change color, whereupon the lab tech will repeat the

experiment. If the second ELISA lights up, too, he’ll do a

confirmatory test using the more sophisticated and expensive Western

Blot method. And if that confirms the infection, the Centers for

Disease Control recommends that the entire procedure be repeated

using a new blood sample, to put the outcome beyond all doubt.

In other words, we’re talking six tests in all, doubly confirmed.

Such a protocol is probably foolproof, but as you draw away from the

First World, health-care standards decline and people grow poorer,

meaning that confirmatory tests become prohibitively expensive. In

Johannesburg, for instance, a doctor in private practice will

typically want three consecutive positive ELISAs before deciding that

you are HIV-positive. But his counterpart in a government-sponsored

testing center has to settle for two ELISA tests.

In the annual pregnancy-clinic surveys on which South Africa’s

terrifying AIDS statistics are based, the protocol is one ELISA only,

unconfirmed by anything. In America one ELISA means almost nothing.

“Persons are positive only when they are repeatedly reactive by ELISA

and confirmed by Western Blot,” says the CDC. The companies that

manufacture ELISAs agree: The tests must be confirmed by other means.

“Repeatedly reactive specimens may contain antibodies” to HIV, one

firm’s literature says, “Therefore additional, more specific tests

must be run to verify a positive result.”

In parts of Africa, however, at least for the purpose of data

gathering, such precautions are deemed unnecessary. That’s partly

because the World Health Organization itself actually evaluates

commercial HIV tests as they come on the market. In these trials, new

tests are measured against a panel of several hundred blood samples

from all over the world. Some of the samples are HIV-positive, some

are not. The ELISAs are tested to make sure they can tell which are

which. Among the scores of brands evaluated throughout the years, a

handful have proved to be useless. But those manufactured by

established biotechnology corporations usually pass with flying

colors, typically scoring accuracy rates close to perfect.

In South Africa, such outcomes were often cited in furious attacks on

President Mbeki. “HIV tests such as the latest-generation ELISA are

now more than ninety-nine percent accurate.” reported the Weekly Mail

and Guardian. The tests have confidence levels of 99.9 percent, said

professor Malegapuru Makoba, head of the Medical Research Council.

Science had spoken, and science was unanimous: The tests were fine,

and Mbeki was a fool, according to the Weekly Mail, “trying to be a

Boy’s Own basement lab hero of AIDS science.”

It was a good line. I laughed, too, but there came a moment when it

ceased to be funny.

My education in the complexities of the ELISA test started when I

came across an article in a scientific journal published last year.

It told a story that began in 1994, when researchers ran HIV tests on

184 high-risk subjects in a South African mining camp. Twenty-one of

the subjects came up positive or borderline positive on at least one

ELISA. But the results were confusing: A locally manufactured test

indicated seven, but different people in almost every case. A French

test declared fourteen were infected.

It seemed something was confounding the tests, and the prime suspect

was plasmodium falciparum, one of the parasites that causes malaria:

Of the twenty-one subjects who tested positive, sixteen had had

recent malaria infections and huge levels of antibody in their veins.

The researchers tried an experiment: They formulated a preparation

that absorbed the malaria antibodies, treated the blood samples with

it, then retested them. Eighty percent of the suspected HIV

infections vanished.

The researchers themselves admitted that these findings were

inconclusive. Still, considering that Africa is home to an estimated

ninety percent of the world’s malaria cases, the implications of the

report seemed intriguing. I asked Dr. Luc Noel, the WHO’s

blood-transfusion-safety chief, for his opinion. He insisted there

was no cause for concern. Then he handed me a booklet detailing the

outcome of the WHO’s evaluation of commercial ELISA assays. In it, I

found two of the three tests that had been used in South America –

the very ones that supposedly went haywire, kits manufactured in

Britain and France, respectively. One was rated By WHO as

ninety-seven percent accurate, the other, ninety-eight percent.

On the other hand, I couldn’t help noticing that according to the

literature Noel had given me, the disease police apply at least five

confirmatory tests to every blood sample before such high accuracy

rates are achieved. What happens if you use just two, or one? And if

your subjects are Africans whose immune systems are often, as UNAIDS

head Peter Piot once phrased it, “in a chronically activated state

associated with chronic viral and parasitic exposure.” There may be

an answer of sorts.

The Uganda Virus Research Institute is possibly Africa’s greatest

citadel of HIV studies. Seated on a hilltop overlooking Lake Victoria

and generously funded by the British government, the UVRI employs

around 200 scientists and support personnel, runs an array of

advanced AIDS studies, tests experimental drugs, labors to produce an

AIDS vaccine and has generated scores of scientific papers during the

past decade.

In 1999, the Institute screened thousands of blood samples using

ELISA tests that have achieved excellent results in a WHO evaluation.

Test-driven in a lab in Antwerp, Belgium, one test scored 99.1

percent accuracy, while the other achieved a perfect 100. But in the

field, in Africa, it was another story entirely. There, exactly 3,369

samples came up positive on one ELISA, but only 2,237 of those (66

percent) remained positive after confirmatory testing. In other

words: a third of Ugandans who tested positive on at least one of

these supposedly near-perfect ELISAs were not carrying the virus.

What does this say about countries where AIDS statistics are based on

a single ELISA? A high-ranking source at UVRI – one who insisted on

anonymity – said that the WHO estimates for AIDS in such countries

“could be as much as one-third higher than they actually are.”

I took this up with Dr. Neff Walker, a senior adviser at UNAIDS, who

at first seemed puzzled. “The standard WHO/UNAIDS protocol calls for

two tests in countries with a higher prevalence,” he said.

But according to a WHO report, “Confirmation by a second test is

necessary only in settings where estimated HIV prevalence is known to

be less than ten percent.” This means that in countries like mine,

estimates are based on one unconfirmed test.

Dr. Walker conceded that, but said it wasn’t particularly important

given that most African counties have what he called “quality

assurance” programs in place.

“I feel,” he said, “that if a government found any evidence of too

many false positives in their testing, they would report it.

Governments would like to find evidence of a lower prevalence, as

would we all, and since they have the data to easily check your

hypothesis, they would do so and report it.”

But would they? High AIDS numbers are not entirely undesirable in

poverty-stricken African countries. High numbers mean deepening

crisis, and crisis typically generates cash. The results are now

manifest: plane loads of safari scientists flying in to oversee

research projects or cutting-edge interventions, and bringing with

them huge inflows of foreign currency – about $1 billion a year in

AIDS-related funding, and most of it destined for the countries with

the highest numbers of infected citizens.

On the ground, these dollars translate into patronage for politicians

and good jobs for their struggling constituents. In Uganda, an AIDS

counselor earns twenty times more than a schoolteacher. In Tanzania,

AIDS doctors can increase their income just by saving the

hard-currency per diems they earn while attending international

conferences. Here in South Africa, entrepreneurs are piling into the

AIDS business at an astonishing rate, setting up consultancies,

selling herbal immune boosters and vitamin supplements, devising new

insurance products, distributing condoms, staging benefits, forming

theater troupes that take the AIDS prevention message into schools. A

friend of mine is co-producing a slew of TV documentaries about AIDS,

all for foreign markets. Another friend has got his fingers crossed,

since his agency is on the shortlist to land a $6 million safe-sex ad

campaign.

Sometimes it seemed I was the only one in South Africa who found this

odd. Dr. Ed Rybicki, a University of Cape Town microbiologist, caught

sight of part of this article while it was being prepared and found

it alarming. “Vast inflation of HIV figures by bad tests?” he wrote

in an email. “Naaaaah. The test manufacturers have done a hell of a

lot of research, which is not published because it is part of quality

control, rather than part of a global cartel conspiracy to make

Africans HIV-positive!” He allowed that there was “probably some

truth” in stories about “various factors confusing the HIV test” but

accused me of stringing them together in an irresponsible way.

“Crap!” he ultimately declared. “Utter garbage.”

I defer to Dr. Rybicki in matters of science, but his denunciation

rested on the flawed assumption that, as he wrote to me, “In South

Africa, tests are repeated, and repeat positives are confirmed by

another method, meaning there is a threefold redundancy.” Maybe

that’s how it works in universities or research labs. But when it

comes to UNAIDS statistics, one test is evidently enough.

5. Can You Wait Ten Years?

And so we return to where we started, standing over a coffin under a

bleak Soweto sky, making a clumsy speech about a sad and premature

death. Adelaide Ntsele died of AIDS, but the word didn’t appear on

her death certificate. Here in Africa, those little letters

stigmatize, so doctors usually put down something gentler to spare

the family further pain. In Adelaide’s case, they wrote TB. But her

sister Elizabeth had no such need of such false consolation. She

donned a red-ribbon baseball cap and appeared on national TV, telling

the truth: “My sister had HIV/AIDS.” As a nurse, Elizabeth had no

qualms with the doctors’ diagnosis, and she concurred with their

decision to forgo surgery and let Adelaide die. “It was God’s will,”

she says, and she was at peace with it. I was the one beset by all

the doubts.

Did Adelaide really die of AIDS? It certainly looked that way, but

she also had TB, the second-most-frightening disease in the world

today, on the rise everywhere, even in rich countries, sometimes in a

virulent drug-resistant form that kills half its victims, according

to the CIA’s recent report on infectious disease. Eight years ago,

the WHO declared resurgent TB a “global emergency,” but the contagion

continues to spread, particularly in the cluster of southern African

countries simultaneously stricken by the worst TB and HIV epidemics

on the planet. It takes a blood test to establish the underlying

presence of an HIV infection in people with TB, and at least one

scientist who knows about these things has imputed that the tests

might not be entirely reliable.

Back in 1994, Max Essex, head of the Harvard AIDS Institute, and some

colleagues of his observed a “very high” (sixty-three percent) rate

of ELISA false positives among lepers in central Africa. Mystified,

they probed deeper and pinpointed the cause: two cross-reacting

antigens, one of which, lipoarabinomannan, or LAM, also occurs in the

organism that causes TB. This prompted Essex and his collaborators to

warn that ELISA results should be “interpreted with caution” in areas

where HIV and TB were co-endemic. Indeed, they speculated that

existing antibody tests “may not be sufficient for HIV diagnosis” in

settings where TB and related diseases are commonplace.

Essex was not alone in warning us that antibody tests can be confused

by diseases and conditions having nothing to do with HIV and AIDS. An

article in the Journal of the American Medical Association in 1996

said that “false-positive results can be caused by nonspecific

reactions in persons with immunologic disturbances (e.g., systemic

lupus erythematosus or rheumatoid arthritis), multiple transfusions

or recent influenza or rabies vaccination…. To prevent the serious

consequences of a false-positive diagnosis of HIV infection,

confirmation of positive ELISA results is necessary…. In practice,

false-positive diagnoses can result form contaminated or mislabeled

specimens, cross-reacting antibodies, failure to perform confirmatory

tests…. or misunderstanding of reported results by clinicians or

patients.” These are not the only factors that can cause false

positives. How about pregnancy? The U.S. National Institutes of

Health states that multiple pregnancies can confuse HIV tests. In the

past few years, similar claims have been made for measles, dengue

fever, Ebola, Marburg and malaria (again).

But let’s put all that science aside, for a moment. Lots of people

thought it was wrong for me even to pose questions such as these,

especially at a moment when rich countries, rich corporations and

rich men were considering billion-dollar contributions to a Global

AIDS Superfund. They were brought to this point by a ceaseless

barrage of stories and images of unbearable suffering in Africa, all

buttressed by Geneva’s death projections. Casting doubt on those

estimates was tantamount to murder, or so said Dr, Rybicki, the Cape

Town microbiologist.

“AIDS is real, and is killing Africans in very large numbers,” he

wrote. “Presenting arguments that purport to show otherwise in the

popular press is simply going to compound the damage already done by

Mbeki. And a lot more people may die who may not have otherwise.”

Rybicki was right. But what are the facts? After a year of looking, I

still can’t say for sure.

When I embarked on this story, you may recall, no massive rise in

registered deaths was discernable in South Africa. A year later, I

decided to return to my point of departure to see if the discrepancy

persisted. I wrote to the country’s Department of Home Affairs, which

manages the death register, and asked for the latest numbers. In

response came a set of figures somewhat different from those

initially provided – the consequence, I am told of people who died

without any identity documents. Here is the final analysis:

Deaths registered in 1996 – 363,238.

Deaths registered in 2000 – 457,335.

As you see, registered deaths have indeed risen – not to the extent

prophesied by the United Nations, perhaps, but there is definite

movement in an ominous direction. Deaths are up across the board, but

concentrated in certain critical age groups: females in their

twenties, and males age thirty to thirty-nine.

A team of experts commissioned by the Medical Research Council has

studied this changing death pattern and found it to be “largely

consistent with the pattern predicted by [ours] and other models of

the AIDS epidemic.” Their conclusion: AIDS has become the “biggest

cause” of mortality in South Africa, responsible for forty percent of

adult deaths.

And yet, and yet, and yet, even this is not the end of our tale,

because another governmental body, Stats SA, has challenged these

findings. The Washington Post reported that the South African census

bureau called the MRC study “badly flawed,” saying “the samples were

not representative, and assumptions about the probability of the

transmission of the virus that causes AIDS were not necessarily

accurate.”

And that’s my story: enigma upon enigma, riddle leading to riddle,

and no reprieve from doubt. Local actuarial models say 352,000 South

Africans have died from AIDS since the epidemic began. The MRC says

517,000. The figure from a group I haven’t even mentioned yet, the

United Nations Population Division, is double that – 1.06 million –

and the unofficial WHO/UNAIDS projections are even higher. I have

wasted a year of my time and thousands of Rolling Stone’s

editorial-budget dollars, and all I can really tell you is that my

faith in science has been dented. These guys can’t agree on anything.

Ordinary Africans everywhere see that the scourge is moving among

them. The guide who showed me around Uganda had lost two siblings.

Our driver had lost three. On the banks of the Kagera River, where

the plague began, we met a sad old man who said all five of his

children had died of it.

But ask these people about access to health care, and they laugh

ruefully. “The coffee price is collapsing,” they say. No one has

money. We can’t even afford transport to hospital, let alone

medicine.” All across rural east Africa, doctors confirmed the

charge: no money, no medicine. Even mission hospitals now ask

patients for money.

“What can we do?” asks Father Boniface Kaayabula, who works at a

Catholic mission in rural Uganda. “We have no money, too. We must ask

people to pay, and only a very few can.”

So what do poor Africans do if they fall sick? They go to roadside

shacks called “drug stores” and buy snake oil. Chloroquine for

malaria, on a continent where that former miracle drug has lost most

of its curative power; nameless black-market antibiotics for lung

diseases, in a setting where up to sixty percent of pneumonia is

drug-resistant; penicillin for gonorrhea, administered by an amateur

“injectionist” who might be unaware that the quantity needed to knock

out the infection has risen a hundredfold in the past decade. For the

poorest of the poor, even such dubious nostrums are beyond reach.

They try to cure themselves with herbs, they fail, and they die.

What’s to be done? Dr. Joseph Sonnabend is a South Africa-born

physician who was running a venereal-disease clinic in New York back

in the early Eighties, when GRID first appeared. He became known

throughout the world as a pioneer in AIDS treatment. When President

Mbeki launched his controversial inquiry into the disease last year,

Sonnabend came home to participate, an experience he likens to

“entering hell.”

As founder of the AIDS Medical Foundation, which became the American

AIDS Research Foundation, or AmFAR, Sonnabend has no patience with

those dissidents who dispute the syndrome’s existence or HIV’s power

to cause it. But he also believes there are “opportunists” and

“phonies” whose chief skill is “manipulation of fear for advancement

in terms of money and power.” In fact, he quit AmFAR, his own group,

because he felt it was exaggerating the threat of a heterosexual

epidemic. A decade later, he’s still fighting the lonely battle for

wise policies, especially in Africa.

In Pretoria, he says, one faction argued for the bulk of available

funds to be committed to the purchase of AIDS drugs. But merely

dumping AIDS drugs into resource-poor countries is pointless,

Sonnabend argued, although he does believe there are limited

situations where they could be safely and effectively used. The

prevention of mother-to-child transmission is one; another is in

people with advanced disease where facilities to adequately monitor

the use of drugs are in place. Unfortunately, the cost of

establishing an infrastructure to do this on a large scale would be

enormous, and without this hardly anyone would benefit, save drug

manufacturers.

The answer, he feels, is to eliminate conditions that render Africans

vulnerable to HIV in the first place. A year down the line, Sonnabend

is still trying to organize an international conference to discuss

the disposition of the money lodged in the Global AIDS Superfund. The

way he sees it, $1 billion a year would be enough to transform the

lives of ordinary Africans and curb the AIDS epidemic, but only if

it’s not squandered on unsustainable “drugs into people” programs.

“There’s a place for AIDS drugs and prevention campaigns,” he says,

“but it’s not the only answer. We need to roll out clean water and

proper sanitation. Do something about nutrition. Put in some basic

health infrastructure. Develop effective drugs for malaria and TB and

get them to everyone who needs them.”

On the other hand, we have researchers like the ones from Harvard

University who insist that biomedical intervention is morally

inescapable. “We can raise people from their deathbeds,” said

professor Bruce Walker. They calculated that it should be possible to

provide Africans with AIDS drugs for as little as $1,100 a year.

Granted, says Sonnabend, but this makes little sense if that one

lucky person’s neighbors are dying for lack of medicines that cost a

few cents.

So who’s right? Depends on the numbers, I guess. In the end, I

attempted to bring all my unanswered questions on that topic to the

man who was there when the epidemic first hit this continent, Dr.

Peter Piot, who has today risen to the role of chief of UNAIDS.

But my call to him was directed instead to UNAIDS’ chief

epidemiologist, a physician named Dr. Bernhard Schwartlander.

The UNAIDS computer model of Africa’s epidemic is in fact completely

dependable, Dr. Schwartlander says because it relies on a “very

simple formula. You take the pregnancy-clinic numbers. You take the

median survival time – around nine years in Africa. You say this is

roughly the distribution curve. Calculation of deaths is completely

plausible if – and this is important – you have a good idea of the

prevalence of HIV and how it spreads over time.”

Why then, I asked, do we have so many different estimates of AIDS

deaths in South Africa?

“I’m not shocked,” he said. “The models may completely disagree at a

particular point in time, but in the end the curves look incredibly

similar. They’re goddamn consistent.”

If that’s true, I said, then why would we have 457,000 registered

deaths here last year when the UN says 400,000 of them died of AIDS?

One of those numbers must be wrong.

“You say there are 457,000 registered deaths in South Africa?”

Schwartlander said, momentarily nonplussed. “This is an estimate

based on projections.”

No, said I, it’s the actual number of registered deaths last year.

“We don’t really know,” he replied. “Things are moving very fast.

What is the total number of people who actually die? For all we know,

it could be much higher. HIV has never existed in mankind before, and

there’s no anchor point set in stone.” The UNAIDS numbers are, after

all, only estimates. We are not saying this is the number. We are

saying this is our best estimate. Ten years from now, we won’t have

these problems. Ten years from now, we’ll know everything.”

Ten years! Had I known, I could have saved myself a lot of grief. For

even as I tried to track down the old numbers, bigger new ones were

supplanting them – 17 million Africans dead of AIDS and 25 million

more with HIV, UNAIDS now estimates; not one in five South African

adults infected but one in four. Are these numbers right? Who knows?

Rian Malan is the author of “My Traitor’s Heart: A South African

Exile Returns to Face His Country, His Tribe and His Conscience.”

Is New York tap water really as good as bottled?

August 1st, 2005

This morning (Aug 1 Mon) the science editor of the Economist, Tom Standage, holds forth on the Op-Ed page on the common theme that a blindfold test by a group of the author’s friends proves that a more expensive, supposedly better tasting product in fact is no more appealing than the lower cost variety.

In this case it is bottled water that is reckoned to taste no better than tap water, but the same kind of semi-scientific experiments have been used from time to time to torture wine dealers and connoisseurs with supposed proof that the finest and more expensive wines from France, say, do no better than Californian or Australian in similar blindfold taste tests.

One would think that the scientific editor of the Economist would be more intelligent and less naive than to take such things at face value. The whole point of science is to get away from subjective measurement, and to check human perception as much and as often as possible with physical and mechanical instrumentation.

Of course, there is nothing more subjective than the taste of a liquid, and any scientific measurement can merely tell us the constituents and chemistry involved, and not all of that. But still, most people will go along with Mr Standage in crediting the results of blindfold tests.

After all, the ultimate arbiter of the taste of good wine wine or bottled water is the well heeled connoisseur or consumer, and here they are being proved to be foolishly imaginative and inconsistent in their perceptions. What idiots they are proved to be! They cannot actually tell the taste very well at all, for once they are blindfolded, they lose track.

What this overlooks is the obvious, a fairly well known phenomenon. The human perception of taste and smell or even what is seen depends on the mental framework in which the sensation is placed. the perception of any sense input or data into the mind is entirely dependent on what is there already.

One of the rather dramatic ways this in shown is when those who have always been blind somehow have their sight restored. Such patients find that they are completely disoriented and have no idea how to make sense of the world of sight. It takes considerable time before they are able to achieve any competence.

Evidently, what happens in blindfold testing is that some of the mental framework is removed and thus the perception of taste is partially crippled. The connoisseur is reduced to a primitive, because the relational structure against which the taste is compared and evaluated is removed. In the case of the bottled water, that would be the label, the bottle, and the store where it was bought, and so on. (Ever noticed how much better things can seem in the well appointed store or gourmet emporium than when they are taken home?)

This phenomenon has also often been seen in the audiophile world, where the engineering types laugh at the Absolute Sound reviewers who claim that $5000 speaker cables sound different from Radio Shack wire at $3 a yard. The physical characteristics that might account for any audible superiority cannot be detected by an engineering analysis, according to the critics on both sides. And blindfold tests reliably make fools out of the reviewers who praise the more expensive product.

Here of course it is impossible to tell who is right. For the imagination that must play a part is clearly going to be strongly influenced by a hefty difference in price. Perhaps the audiophile believers do hear a difference, just for that reason. From what we know scientifically, the users of Radio Shack wire are getting the better bargain, but it is always possible that the well heeled audiophiles are getting the money’ worth also.

20/20’s John Stossel also ran an item recently of the same kind demonstrating that yuppies who are willing to pay $30 a bottle for Grey Goose vodka or other premium vodkas, which are making a huge splash in trendy bars these days, failed to pick it out in a blind taste test evcen when it was served neat. In fact, they often rejected it as unsatisfactory or one of the worst tested. Smirnoff’s vodka, on the other hand, which costs nearly two thirds less at $13 a bottle, was often picked as the best tasting.

Not to know that peceptions are inevitably altered in this functional manner by blindfold tests is to ignore the brain research of the last twenty years, and we are surprised that the Economist science editor hasn’t read it. He should start with the books of Anthony Damasio.

Of course, this doesn’t affect Tom Standage’s overall theme that much. Even if bottled water does taste better, its constituents are very often no better or even less desirable than tap water’s in New York City. And so yes, we agree with Tom that the money paid for bottled water might be more decently spent on helping the human race in the rest of the world enjoy clean tap water too.

The New York Times

August 1, 2005

Bad to the Last Drop

By TOM STANDAGE

London

IT’S summertime, and odds are that at some point during your day you’ll reach for a nice cold bottle of water. But before you do, you might want to consider the results of an experiment I conducted with some friends one summer evening last year. On the table were 10 bottles of water, several rows of glasses and some paper for recording our impressions. We were to evaluate samples from each bottle for appearance, odor, flavor, mouth, feel and aftertaste – and our aim was to identify the interloper among the famous names. One of our bottles had been filled from the tap. Would we spot it?

We worked our way through the samples, writing scores for each one. None of us could detect any odor, even when swilling water around in large wine glasses, but other differences between the waters were instantly apparent. Between sips, we cleansed our palates with wine. (It seemed only fair, since water serves the same function at a wine tasting.)

The variation between waters was wide, yet the water from the tap did not stand out: only one of us correctly identified it. This simple experiment seemed to confirm that most people cannot tell the difference between tap water and bottled water. Yet they buy it anyway – and in enormous quantities.

In 2004, Americans, on average, drank 24 gallons of bottled water, making it second only to carbonated soft drinks in popularity. Furthermore, consumption of bottled water is growing more quickly than that of soft drinks and has more than doubled in the past decade. This year, Americans will spend around $9.8 billion on bottled water, according to the Beverage Marketing Corporation.

Ounce for ounce, it costs more than gasoline, even at today’s high gasoline prices; depending on the brand, it costs 250 to 10,000 times more than tap water. Globally, bottled water is now a $46 billion industry. Why has it become so popular?

It cannot be the taste, since most people cannot tell the difference in a blind tasting. Much bottled water is, in any case, derived from municipal water supplies, though it is sometimes filtered, or has additional minerals added to it.

Nor is there any health or nutritional benefit to drinking bottled water over tap water. In one study, published in The Archives of Family Medicine, researchers compared bottled water with tap water from Cleveland, and found that nearly a quarter of the samples of bottled water had significantly higher levels of bacteria. The scientists concluded that “use of bottled water on the assumption of purity can be misguided.” Another study carried out at the University of Geneva found that bottled water was no better from a nutritional point of view than ordinary tap water.

Admittedly, both kinds of water suffer from occasional contamination problems, but tap water is more stringently monitored and tightly regulated than bottled water. New York City tap water, for example, was tested 430,600 times during 2004 alone.

What of the idea that drinking bottled water allows you to avoid the chemicals that are sometimes added to tap water? Alas, some bottled waters contain the same chemicals anyway – and they are, in any case, unavoidable.

Researchers at the University of Texas found that showers and dishwashers liberate trace amounts of chemicals from municipal water supplies into the air. Squirting hot water through a nozzle, to produce a fine spray, increases the surface area of water in contact with the air, liberating dissolved substances in a process known as “stripping.” So if you want to avoid those chemicals for some reason, drinking bottled water is not enough. You will also have to wear a gas mask in the shower, and when unloading the dishwasher.

Bottled water is undeniably more fashionable and portable than tap water. The practice of carrying a small bottle, pioneered by supermodels, has become commonplace. But despite its association with purity and cleanliness, bottled water is bad for the environment. It is shipped at vast expense from one part of the world to another, is then kept refrigerated before sale, and causes huge numbers of plastic bottles to go into landfills.

Of course, tap water is not so abundant in the developing world. And that is ultimately why I find the illogical enthusiasm for bottled water not simply peculiar, but distasteful. For those of us in the developed world, safe water is now so abundant that we can afford to shun the tap water under our noses, and drink bottled water instead: our choice of water has become a lifestyle option. For many people in the developing world, however, access to water remains a matter of life or death.

More than 2.6 billion people, or more than 40 percent of the world’s population, lack basic sanitation, and more than one billion people lack reliable access to safe drinking water. The World Health Organization estimates that 80 percent of all illness in the world is due to water-borne diseases, and that at any given time, around half of the people in the developing world are suffering from diseases associated with inadequate water or sanitation, which kill around five million people a year.

Widespread illness also makes countries less productive, more dependent on outside aid, and less able to lift themselves out of poverty. One of the main reasons girls do not go to school in many parts of the developing world is that they have to spend so much time fetching water from distant wells.

Clean water could be provided to everyone on earth for an outlay of $1.7 billion a year beyond current spending on water projects, according to the International Water Management Institute. Improving sanitation, which is just as important, would cost a further $9.3 billion per year. This is less than a quarter of global annual spending on bottled water.

I have no objections to people drinking bottled water in the developing world; it is often the only safe supply. But it would surely be better if they had access to safe tap water instead. The logical response, for those of us in the developed world, is to stop spending money on bottled water and to give the money to water charities.

If you don’t believe me about the taste, then set up a tasting, and see if you really can tell the difference. A water tasting is fun, and you may be surprised by the results. There is no danger of a hangover. But you may well conclude, as I have, that bottled water has an unacceptably bitter taste.

Tom Standage, author of “A History of the World in Six Glasses,” is the technology editor of The Economist.

* Copyright 2005 The New York Times Company

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