Philip Alcabes discusses myths of health, disease and risk.

Cholera: A Shame, Not a Whodunit

Titling Maggie Fox’s article on the source of the Haitian cholera outbreak “Whodunnit?,” Reuters makes distraction the main attraction.

Finger pointing about the “cause” of the outbreak — finger pointing at Nepalese peace keepers, the UN mission, relief workers, or Haitian health workers — is a way of avoiding the fundamental problem:  insufficient political will to create working infrastructure for poor countries.  Haiti being the leading example, the cholera outbreak being the case study.

Given how shaky the living arrangements have been for many Haitians since the January earthquake, given the pre-existing destitution and the anemia of efforts to fix that, it’s a tribute to the Haitian health system that cholera didn’t break out until October.  It might have been much sooner.

But now that cholera is spreading, it seems that more energy is going into using the outbreak to whip up political animus in, and about, Haiti than to figuring out how to make sure it doesn’t happen again.

This week, the politicization of the cholera outbreak seems to get worse by the day (Crawford Kilian’s cholera coverage at H5N1 continues to keep abreast of both the cholera outbreak and the political uses it’s being put to).   I talked to John Hockenberry and Celeste Headlee about this on The Takeaway yesterday, pointing out that the problem is social crisis, not Nepalese troops.  It’s poverty, lack of adequate sanitation, poor access to clean water — not foreigners.

Here’s the segment of The Takeaway:

In contrast to the misleading headline of Reuters’ piece, what Ms. Fox covers is not the (pseudo) mystery of “who brought cholera to Haiti?”  It’s the effort by CDC, the Haitian health ministry, and PAHO to determine whether the outbreak likely started from a single source or multiple ones.

The findings are reported in the Morbidity and Mortality Weekly Report this week:  Haitian cases all carried Vibrio cholerae of the O1 serogroup, serotype Ogawa (a very common strain), with DNA of a single pulse-field gel electrophoresis pattern.  Because of the propensity for mutation or recombination events in the reproduction of bacteria, it would be extremely unlikely for different people to be carrying bacteria with the identical PFGE pattern unless they had all been exposed to an identical strain.  [N.B.  Strictly speaking, cholera is not an infection:  the illness results from poisoning by V. cholera in the intestine, not from actual infection of tissue.  Therefore I write “exposed to” rather than “infected by.”]

Based on the findings so far, CDC and its partners concludes that the outbreak probably began with a single strain.

Did this strain arrive in cholera recently, or has it been around for some time and only recently came to attention as a cause of mass morbidity and mortality?  Did it arrive in a person and contaminate the environment via feces, or arrive in food or water?  Was there a single initiating exposure, or did cholera arrive inside multiple people or food items?  As Fox points out, the study can’t answer these questions.

It makes sense to seek information on how the outbreak got started in order to plan for better systems to prevent future outbreaks.  CDC is on the right track here.

But by calling this a whodunit, Reuters is pandering to people who want to inflame tempers, not spreading information about what can be done to make Haiti healthier.  Shame on you, Reuters.

Plague Did Not Begin in China. And Why Should Anyone Think It Did?

Nicholas Wade, the NY Times‘s science writer, jumps the gun with a story today asserting that plague began in China.  Maybe it’s understandable:  you don’t often get a front-page story if you’re a science reporter, so once in a while you take some shaky science and turn it into an international incident.

But to understand why the story is wrong means recognizing a weakness of science as it’s often practiced today.

Wade’s claim is based on two papers published this month.  A relatively well done study by Haensch et al. in PLoS Pathogens earlier in October tested human remains from well-identified plague pits — burial sites for medieval plague victims — in different parts of Europe.  Researchers amplified DNA sequences of the plague bacterium, Yersinia pestis, at specific genetic loci, and tested to see whether the DNA matched known sequences of contemporary Y. pestis genes.

The findings published in PLoS suggest that the Black Death and perhaps subsequent waves of plague in Europe were indeed caused by Y. pestis — which would tend to debunk the theory proposed by some British researchers that the Black Death was some kind of viral hemorrhagic fever outbreak.  And they suggest that there were at least two widely different Y. pestis strains involved in different parts of Europe.  Here’s a bit of the abstract:

[O]n the basis of 17 single nucleotide polymorphisms plus the absence of a deletion in glpD gene, our aDNA results identified two previously unknown but related clades of Y. pestis associated with distinct medieval mass graves. These findings suggest that plague was imported to Europe on two or more occasions, each following a distinct route.

The main weakness here is that DNA could not be amplified from all of the plague pits the researchers studied, but after using alternative means to test the DNA debris against contemporary gene sequences the investigators concluded that the absence of genetic material reminiscent of one strain of Y. pestis was evidence that that strain was not in play in that part of Europe at the time.  Probably right, but stretching the available evidence.

It’s a common mistake, alas.  To paraphrase Karl Popper:  just because you see DNA from white swans and don’t see any DNA from black swans, doesn’t mean that black swans don’t exist.

Still, the PLoS paper is persuasive that more than one strain of the plague bacterium was circulating, and probably causing deaths, in the plague period in Europe.  Of course, it says nothing about China.

So where does the NYT reporter get his headline-grabbing story?  A paper to be published in Nature Genetics online (still embargoed at the time I’m writing, but a summary appears here) states that the sequences of plague DNA amplified from plague pit remains, as well as contemporary isolates, can be placed on a molecular clock because of the occurrence of unique mutations.  Winding the clock backward, the researchers conclude that the Ur plague organism, ancestor of all Y. pestis, came from the far east.

The molecular biology may be unimpeachable, but the inferences about history aren’t supportable by molecular evidence.  That might explain why they’re almost certainly wrong.

The problem (scientists, I hope you’re listening!) is that you may know very well what you know, but you can never know what you haven’t seen.  The hereditary tree has its roots in China.  Here is one proposed by some of the same authors in a 2004 PNAS paper:

In this set-up, isolates of Y. pestis from China seem closest to the primordial strains.

But of course, the molecular clock doesn’t take account of strains that are no longer extant.  And ones that haven’t been unearthed.  The contemporary researchers don’t see them (or don’t know how to look), so they don’t exist.

It’s a bad mistake, inferentially.  And historically.  It’s where the NYT writer goes wrong.  Almost certainly, plague did not begin in China.  It began as an enzootic infection of small mammals in the uplands of central Asia.  This is the story convincingly relayed by William H. McNeill in Plagues and Peoples a generation ago, and none of the many accounts I’ve read since then has debunked it.

Plague would have had to begin in an ecosystem in which it could circulate at moderate transmission rates with little pathogenicity among small mammals (the natural host of the bacterium).  Exactly where it started remains open to question, but it was probably in the area that is now Turkestan/Uzbekistan.  With the development of trade between that region and China, intermixing of local (central-Asian) animals with caravan-accompanying rats would have allowed Y. pestis to adapt to the latter.

Quite possibly China was the source of the first human outbreaks of plague — because the river valleys of China were settled and agricultural (therefore offering feeding opportunities for rats as well as multiple opportunities for rat-human interaction) long before Europe was.  That fact probably accounts for the biologists’ (mistaken) belief that their early samples show that Y. pestis started out in China.

But plague began as — and remains — a disease of animals.  To acknowledge that human outbreaks in China preceded the human outbreaks in Europe (the Justinian plague that began in the mid-sixth century, the Black Death that began in the 1340s, and subsequent visitations) is not the same as saying that plague originated in China.

Which it didn’t.  Plague is an animal disease from Central Asia.  Plague’s long history is the usual one:  ecosystem change, trade, animal-human interactions, alterations in climate and economic conditions, and occasional opportunities for mass human illness.   (One world, one health.)

Above all, remember that science is only capable of drawing conclusions about what scientists can observe.  Don’t be taken in by hair-raising stories.  Even in the NY Times.

A Blog Worth Following

If you haven’t already, put Crawford Kilian’s H5N1 blog on your regular reading list.  There, while you’ll still get updates on the H5N1 avian flu virus and occasional pieces on H1N1 flu (and you can see a multitude of archived posts from 2009  filled with international material on the progress of last year’s flu — and the reaction to it), you now get a much-expanded scope, including news and commentary on the spread of infectious diseases of different sorts.

What I value about H5N1 is the tracking of the mosquito-borne viral diseases, like dengue and chikungunya as well as H1N1, that reveal the effects of the elision of ecosystem boundaries; the close attention to outbreaks that stem from changes in human-animal interactions — like the recent outbreak of plague in Tibet and, of course, H5N1; and the watch it keeps on the vaccine trade, as in yesterday’s post picking up a report in The Nation on the purchase of flu vaccine from France and one last week on a US tech company’s trials of a new flu vaccine (which won’t help the public but is, apparently, already helping the company to get richer).

The kind of close attention to the details of complex interactions amongst humans, animals, and both the natural environment and the economic one that H5N1 shows is indispensable.   It should spur more interest in wresting public health away from the simple-minded mass-vaccination schemes of medical officials in the U.S. and other wealthy countries — the point of which is usually to transfer public monies into the hands of pharmaceutical companies.  And move us to toward a more complex and inclusive view of the nature of health.

Public Health Priorities: Follow the Money

Thanks to Crof at H5N1 for bringing to our attention a strong editorial in yesterday’s Bangkok Post.   The editorialists note that H1N1 preparedness efforts were not always successful and that WHO, fresh from announcing that the H1N1 pandemic is over, is now promoting fears of renewed outbreaks of H5N1 (avian) flu.  The editorial continues:

While it would be foolish to dismiss such warnings as this latest one on bird flu, it is important we keep a sense of proportion and not let them distract us from countering the unfashionable but widespread potential killers such as tuberculosis, HIV/Aids, diabetes, cancer, dengue and malaria. These are the diseases already causing widespread illness and economic harm….

Rather than competing for cash, the threat from newer diseases should serve as a catalyst to combat existing epidemics.

Competing for cash is key.

Funding for TB languishes, dengue incidence expands, more people with the AIDS virus are getting treated but new infections continue to occur, water scarcity (and displacement because of wars and natural disasters) makes diarrheal illness a persistent problem, and malaria transmission continues to threaten billions of people who live in tropical and subtropical regions — but flu preparedness dominates the public health scene.   Why?

Here’s the infernal logic of WHO and the public health officers of wealthy countries (U.S., U.K., etc.):  (a) At the start of the H1N1 outbreak in 2009, a sensible worst-cast forecast was about a million deaths worldwide; the more likely scenario was well under 500,000 deaths.  (b) TB + malaria + diarrhea + AIDS together kill 6 or 7 million people a year.   (c) Immunization against flu is notoriously variable in its effectiveness and mass immunization is almost never effective (except if instituted in an isolated population well before the flu virus makes inroads into the population).

Sounds like it would be worth it to pump lots of resources into reducing the incidence of malaria, TB, AIDS, and diarrhea.  But that’s hard.  It takes political will.  Whereas immunizing against flu is easy: it just takes money.  And national health officials were eager (it turned out) to transfer billions of dollars, pounds, and euros into the hands of vaccine manufacturers in order to be able to immunize their populations against H1N1 flu.

To an official whose job is to watch out for the needs of the economic machine, immunization pays.

One flu vaccine manufacturer estimates that in the U.S., employers lose $2.1 billion each year in productivity because of flu-related absences from work.  Let’s be skeptical about this estimate, coming as it does from one of the beneficiaries of federal largesse in response to flu fears.  But the point is clear enough:  it was a great boon to the private sector to have the federal government spend $1.6 billion of taxpayer money on flu vaccine in 2009 even though the outbreak was mild and vaccine did virtually nothing to stop it.  Because with the feds footing the bill, the burden on corporations was slight, whereas the private sector would have lost a lot of money if many Americans had fallen ill with flu.

It’s not just the vaccine manufacturers and pharmaceutical companies who stand to capitalize on the absurd calculus of protecting American businesses instead of poor people’s lives:  scientists do, too.

Robert Webster is an eminent virologist who has become dean of those American scientists who purport to be able to foresee a future flu catastrophe.  Perhaps he’s right, but of course nobody knows.  So when Webster says

We may think we can relax and influenza is no longer a problem. I want to assure you that that is not the case,

as he just did in a meeting in Hong Kong, it’s a good sign that the preparedness crusaders are worried about their funding.  They should be.

The preparedness crusaders have been unmasked as shameless shills for the private sector,  even if the vaccine and antiviral manufacturers aren’t paying them directly.  And the ones who are scientists have been revealed as self-important promoters of their own research — so fiercely protective of their own turf that they might use their prestige and the imprimatur of science to hoodwink officials into ignoring the more serious, and more certain, problems of the developing world.

Let’s hope that more opinion makers take the stand that the editors in Bangkok just did.

Putting Obesity in Perspective

Michael Pollan’s essay in this week’s NY Review of Books offers a framework for looking at modern food and eating.  If public health advocates took Pollan’s perspective, the vitriol of their anti-obesity crusade could turn into a force for real social reform.

Reviewing five books on what he calls the “food movements,” Pollan notes the widespread discontent with contemporary industrialized food production (I’ll call this “American eating,” although its dominance is increasing around the world).  And he suggests that its common theme is cultural discomfort. The food movement, Pollan argues, has “set out to foster new forms of civil society”:

It makes sense that food and farming should become a locus of attention for Americans disenchanted with consumer capitalism.  Food is the place in daily life where corporatization can be most vividly felt…  The corporatization of something as basic and intimate as eating is, for many of us today, a good place to draw the line.

This is a refreshing insight.  It’s thankfully broad, taking  the focus away from health, and therefore from the anti-obesity crusade and the “toxic food environment” view promoted by health advocates.

But Pollan’s perspective is especially refreshing because it renews the conversation about our private lives — particularly the extent to which we’ve ceded our innermost values to the demands of corporate profit and government policies.  And those demands, as Marion Nestle often points out (recently here), are generally linked.

Pollan reminds us that our innermost values are literally innermost:  they have to do with what goes into our stomachs.

I’ve already stated my argument that the anti-obesity crusade is really about control, not health (see here and here).   The crusaders do cite “public health” as a rationale for the war against obesity.  But when they describe what’s wrong, they do so in terms that are sometimes medical (diabetes, hypertension), sometimes technical (serving sizes, calorie counts, the infamous toxic food environment), and sometimes medieval (gluttony, laziness).  Their inability to articulate the source of the problem is a signal that they’re sure something is out of control but unsure exactly what.

The public health approach to obesity is a failure.  It doesn’t let us talk about what needs to be reformed.  And it’s often allied with efforts to make sure the poor stay poor — even though wealth inequality is surely part of the problem in the first place.  The public health industry’s demands for additional regressive taxation in the form of increased “fat” taxes on sugary beverages or high-calorie foods reveal its preference for the status quo.  Make the poor pay more for their soda and fast food; that will make them think twice about supporting industries that are making us fat.

Even well-meaning public health professionals who advocate government intervention against low-price-but-low-nutrition food  as a way of curtailing obesity ignore the central role of food and eating to liberty and happiness — they’re interested primarily in how many additional years of life (however unhappy) could be purchased by trading in the fries in favor of broccoli.  Or, worse, they’re interested only in the dollar costs to taxpayers — in terms of hypertension and heart disease — of tolerating obesity.

Pollan, today’s most thoughtful and insightful philosopher on the subject of food and eating, offers a more satisfying view.  Sure, you may want to change American eating because you think obesity is bad for people’s health.   But you might want to change eating simply because the food scene is distressing, because it crystallizes and exemplifies the many ways that we give over our private (innermost!) moral decisions to the influences of corporate/consumerist thinking.  You might want to change it because, as Pollan reminds us (in regard to a new book by Janet Flammang), the dominance of American statecraft by corporations allows the preparation of food to be relegated to the least valued, least powerful, and lowest paid workers.  You might want food to taste better — valuing pleasure over longevity.

With Pollan’s broad view, you  don’t have to join the anti-obesity crusade.  You don’t have to speak the technical language of risk.  The common language of freedom, desire, and pleasure will do.