Swine Flu update: April 29, 2009

Part One of the Swine Flu epidemic here.

By the end of the day, panic over swine flu had reached pandemic proportions, with more than 117,607 news stories appearing on Google News. As media professor, Robert Thompson, at Syracuse University in New York, told Reuters this morning: “If as many people had swine flu as those [in media] that are covering swine flu, then it would be a pandemic to reckon with.”

He was more right than readers realize. As of tonight, the World Health Organization’s Swine Influenza Update reports 91 confirmed cases of the swine flu in the United States and one death; while Mexico has 26 confirmed cases, including seven deaths.

117 cases

117,607 news stories

That’s 1,005 news stories for each case of the flu.

It’s been heartbreaking to realize how many people have become truly frightened by the news stories. For consumers trying to find balanced information in the news, they’re encountering similarly overwhelming odds. But there have been tiny droplets of science and sense coming from experts that you can find — if you have time to wade through a thousand panic stories to find each one.

Death has come to the U.S.

The first U.S. death to swine flu instantly became all the proof needed to raise the panic bar about the threat of swine flu for our children and lead to schools being closed across the country.

What hasn’t been widely reported is that the 23-month old boy who became the first U.S. death to swine flu was from Mexico and had undisclosed “underlying medical problems.” He had been airlifted to Texas Children’s Hospital in Houston in critical condition. “While tragic and alarming, the case does not prove that the recently emergent virus has established a foothold in Southeast Texas,” health officials cautioned in the Houston Chronicle. “The boy was isolated in a hospital environment that made transmission of the virus unlikely, and no one in his family has exhibited symptoms.” As Dr. David Persse, Houston’s emergency medical services director said, this death doesn’t change the situation here.

Never before seen mutant virus

Media continues to describe the virus as an unexplained combination of swine, bird and human strains, lending to endless conspiracy theories and scares of mutant viruses. The core of beliefs that this strain of influenza could hold unique dangers to humans compared to ordinary seasonal influenzas originated from misinterpretations of CDC reports that the virus is a combination of bird, pig and human viruses, said Dr. Steven Salzberg, Ph.D., professor at the University of Maryland and Director of the Center for Bioinformatics and Computational Biology. The simplistic explanation reaching the public is incorrect. As we know, viruses naturally reshuffle their genetic material as they replicate. Dr. Salzberg explained that the current swine flu virus is actually a combination of two “already-circulating pig strains.”

The reason for the "triple reassortant" story is a bit complex, but (to simplify a bit): the history of one of the two parental swine flu strains indicates that part of that strain originated in birds — well over a decade ago. That strain is sometimes called "avian-like" as a result, but it's not an avian flu strain now. Second, the history of the other strain includes a small piece (one gene) that appears to have originated in humans — over 15 years ago. Again, it's a swine flu virus now, but there's a piece of it that might have come from humans. The event that created today's swine flu — the one we're worried about — is a combination (called a reassortment) between two pig strains, pure and simple.

There is no reason to suspect that this combination of flu viruses is any more deadly than any other recent swine influenza virus has been.

Pandemic around the corner

The most over-the-top rhetoric has come from the World Health Organization director general, Margaret Chan, when she raised the level of alert of an impending pandemic. “It is all of humanity that is under threat during a pandemic,” she said at a news conference in Geneva. “The biggest question right now is this: How severe will the pandemic be? All countries should immediately now activate their pandemic plans.”

The World Health Organization’s own data fails to support the scary proclamations of its director. WHO reports 91 confirmed human cases in the U.S., with one death, and Mexico has 26 confirmed cases, including seven deaths. Scattered cases have also been confirmed abroad, with no deaths. And, no different from earlier this week: “WHO advises no restriction of regular travel or closure of borders.”

The Department of Homeland Security instructed healthcare providers of the procedures they must follow should the government decide quarantines are necessary. Its notice said: “The Department of Justice has established legal federal authorities pertaining to the implementation of a quarantine and enforcement. Under approval from HHS, the Surgeon General has the authority to issue quarantines.” Under federal law, a quarantine order can be enforced by U.S. law enforcement agencies, including Federal Marshals, the FBI, U.S. Customs and Coast Guard Officers and the Bureau of Alcohol, Tobacco, Firearms and Explosives. Anyone violating a quarantine order can be punished by a $250,000 fine and one year prison term. As CBS News reports, a Defense Department planning document summarizing the military's contingency plan says the Pentagon is prepared to assist in “quarantining groups of people in order to minimize the spread of disease during an influenza pandemic” and aiding in “efforts to restore and maintain order.” Congress enacted the first federal quarantine law in 1796 during the yellow fever epidemic.

The CDC’s own influenza data fails to support any parallels of this swine flu outbreak as being as threatening as a yellow fever epidemic from two centuries ago or Spanish flu from nearly a century ago! The actual number of people sickened by any viral infection is naturally considered to be higher than confirmed cases, but today’s active surveillance by health departments enable reasoned estimates of disease prevalence. The actual numbers aren’t remotely close to tens of millions of deaths. But we don’t hear much about just how few cases there have really been — facts that offer a sense of perspective and balance.

While increasing number of cases of swine flu are being confirmed as testing increases, the number of cases and deaths continue to pale to those seen even with the typical seasonal influenza. As we’ve seen, government health statistics report 30,000 to 50,000 deaths each year in the U.S. attributed to typical seasonal influenzas, and the number of cases is considerably higher. Every week, the CDC reports the number of confirmed cases and this month, in just one week (April 12-18, 2009), for example, the CDC confirmed 25,925 cases of influenza in the United States and 55 child deaths.

Imagine what the media could do with those numbers to scare us. At the same rate of news coverage, that would be more than 25 million stories every week about the deadliness of the flu.

Mexico harboring a deadly form of the virus

Speculations abound as to why there have been more deaths in Mexico than here or any other developed country in the world. Scares are circulating that viruses from south of our border are somehow more deadly and dangerous and that we must keep “those people out.” As we’ve examined, the general health of people in poverty stricken countries such as Mexico is poorer, as is most people’s access to the quality and advanced medical care that we currently enjoy in our country — medical care that makes the difference for surviving the complications of viral infections. There’s a reason our healthcare is seen as the best in the world and our neighbors from Mexico come here for care.

But the “swine flu virus” (influenza A/H1N1) in Mexico is no different than here. Dr. Salzberg and colleagues and several other research groups around the country gained access to GISAID, where the genetic sequencing of flu viruses have been deposited. They found that the genetic sequencing of the virus from Mexico is virtually identical to those from the United States. “It would appear that any differences in virulence are due to differences in the people being infected, not to the virus itself,” he wrote. People living in situations of poverty are at higher risk of dying from all sorts of things that those in more developed countries no longer fear.

Health scams abound

The Better Business Bureau is already warning consumers about scams capitalizing on swine flu fears. McAfee, a computer monitoring company, has been tracking swine flu scams and reports there’s been a huge jump of sites selling supposed swine flu treatments and products, offering everything from face masks to phony vaccines, many websites masquerading as offering medical information. Face masks sales are booming, even though the CDC is not recommending that people wear masks because of limited evidence that they effectively prevent the spread of the disease. As Peter Palese, a microbiologist and infectious-diseases expert at Mount Sinai Medical Center, told the Washington Post, face masks don’t do much good:

Face masks do one thing — they protect people in terms of preventing other people from getting close to them. So you get a sphere of privacy from wearing a mask, but it's largely psychological. The masks do help if someone sneezes right at you. However, the pore size of these masks lets viruses go through. Again it is not a clear-cut yes or no; there is some benefit, but there is not as much benefit as we would like.

Yet, nearly every news story about swine flu is accompanied by scary images of people wearing masks.

What’s really playing on our fears?

Frank Furedi, sociology professor at the University of Kent and author of Culture of Fear, explained that what we are seeing is a moral drama. His thought-provoking article in Spiked-online began:

Recent events show that, while society has the scientific know-how to cope with outbreaks of flu, it still sees disease as a harbinger of apocalypse. The explosion of global fear about the outbreak of a deathly flu virus in Mexico is more a response to the dramatisation of influenza than to the actual threat it poses. There is nothing unusual about the outbreak of flu. Every year, thousands of people die from the flu, and, in normal conditions, society has learned to cope with the flu threat. From time to time, an outbreak of flu turns into a global pandemic, leading to a catastrophic loss of life. However, there is no evidence that the so-called swine flu, which has so far claimed a relatively small number of lives, will turn into a pandemic. Rather, what we are faced with is a health crisis that has been transformed into a moral drama.

As he explains, actual health risks are being inflated today far beyond any real danger. The World Health Organization’s escalation of the pandemic threat of swine flu, he said, “is acting on a script that was cobbled together in the early years of the twenty-first century.”

Since the turn of the new millennium, the term ‘pandemic’ has become normalised and is increasingly used to frame global anxieties and fears. ‘Health alerts’ have been transformed into rituals, through which fear entrepreneurs remind us, in a quasi-religious fashion, that human extinction is a very real possibility. Terms like ‘epidemic’ and ‘pandemic’ appear with increasing frequency in newspapers, and are now used in everyday conversation, too. This tendency to inflate the dangers that we face leads to a situation where fearmongers now speculate about hundreds of thousands, millions or even billions of casualties occurring as a result of some crisis or disaster. Even highly prestigious journals and media outlets seem incapable of resisting the temptation to spread alarmist high-casualty scenarios.

Increasingly, public health officials sound as if they are rehearsing their roles for a disaster movie. They frequently argue that, since we had deathly flu pandemics in the past, it is inevitable that we will face another one very soon…The fatalistic view of an inevitable global flu catastrophe is made more ominous still by linking it with our anxieties about terrorism. Leading British scientist Hugh Pennington also made this link, when he stated in 2005 that avian flu ‘is the biggest threat to the human race’ and it ‘far outweighs bioterrorism; this is natural terrorism’. Inevitably, the dramatisation of the flu has spawned various apocalyptic stories about how viruses can be ‘weaponised’ and used to threaten human survival… In line with Hollywood fantasy plotlines, the report invited us to imagine the possibility of a terrorist purchasing ‘genes for use in the engineering of an existing and dangerous pathogen into a more virulent strain’. Alongside fears about the ‘weaponisation’ of viruses, the internet is awash with rumours about the conspiracy responsible for the current outbreak of swine flu…

As he concluded: “It seems the swine flu outbreak has infected our imaginations, giving shape and tangibility to our anxieties about everyday life. We should give the pigs a rest, and get on with living.”

Not everyone’s imaginations are running overtime, though. The internet has also been the source of some comical perspectives, none better than xkcd.com:

Click here for complete article (and single page version).

Flu Fears

The media loves a good scare and the word pandemic is a guaranteed headline grabber. By this evening, there were nearly 70,000 news stories about an influenza pandemic, many accentuated by pictures of crowds of people wearing blue surgical masks. But scaring you half to death with speculations of a new pandemic does little to help you. The known facts, offered in a balanced perspective, is really news you can use.

As is the case with virtually everything scary in the media, reputable scientists and health experts provide reassuring facts and information. The world is not coming to an end and there is surprisingly little cause for panic.

Words for shock value

Why have the words epidemic or pandemic been used in nearly every headline? The numbers of people who’ve tested positive for the flu are actually so low, these cases don’t come close to meeting either definition.

But the words strike fear into the hearts of people. Most consumers think pandemic means something like the Spanish flu pandemic of 1918-1919, which is said to have killed between 20 million to 100 million people. Something like that is unlikely to happen today, however. Nearly a century ago, the standards of living and medical care, for humans and animals, were vastly different. The country was recovering from World War I, with widespread poverty, hunger and unsanitary living conditions, coupled with no available antibiotics or flu medications or modern medical care.

In fact, most of us have lived through a flu pandemic and never even realized it. The Hong Kong flu pandemic in 1968-69, for example, killed an estimated 33,800 Americans. That sounds like a lot, but it’s about the same number of Americans who die from the flu in a typical year.

Swine flu has even been around us for years. It’s not new. Did you know that influenza as a disease of pigs was first recognized during that Spanish flu pandemic of 1918-1919? Swine flu was first isolated in laboratory tests from a human in 1974. Sporadic cases of swine influenza viral infections in humans have been reported in the United States, Canada, Europe and Asia for decades. “There are no unique clinical features that distinguish swine influenza in humans from typical influenza,” said Dr. Kendall P. Myers at the Center for Emerging Infectious Diseases at the University of Iowa, Iowa City, and colleagues.

Every few years, we are surrounded by dire warnings of an impending pandemic — such as the SARS, avian flu, and 1976 swine flu scares — pandemics that never materialized. As JFS covered during the avian flu scare (when we were being told that 81 million of us could die), these scary pandemic projections are based on computer models that assume the worse case scenarios: a world without medical care or medications, without veterinary medicine, and such social demise and unsanitary living conditions that people will die at the same rates they did a century ago during the Spanish flu pandemic. Most of all, they ignore the science.

Let’s look at some of that science. Because this story is evolving, the specifics will evolve, too, but the main point won’t. For a good scare, filled with sensationalized, exaggerated dangers, turn to mainstream media. For facts, go to the source.

The scientific information given to the media during the U.S. Centers for Disease Control and Prevention’s public briefings bears little resemblance to the versions that have made most of our nightly news and newspapers.

Seek and ye shall find

A point repeatedly emphasized to the media yesterday by Dr. Anne Schuchat, Director for the National Center for Immunization and Respiratory Diseases, was that they couldn’t credibly say the cases being identified in the laboratory are indicative of a new situation. Cases identified with increased surveillance is not the same thing as actual increased incidents.

As she said, we might never have even known about this a few years ago because health departments weren’t testing for unusual strains of influenza viruses. They only recently stepped up laboratory capabilities and in 2007 launched a new reporting system that now makes it mandatory for state health departments to report the detection of untypable influenza strains during their routine influenza season surveillance. “Ten years ago we were not doing that, so we may be seeing something and actively investigating something that has happened many times before,” said Dr. Schuchat. So, we really cannot say that this is anything new.

All of the cases have been detected through routine surveillance for seasonal flu after state labs found strains they couldn’t type and sent the samples to them. “We are doing more testing now and looking more aggressively for unusual influenza strains,” she said. “So we haven’t seen this strain before, but we haven’t been looking as intensively as we are these days.” Now, they’re in an active investigation mode, she explained. So, each case that tests positive for swine influenza A (H1N1) “prompts a contact tracing investigation that is much more aggressive than we would do with a routine season influenza patient.”

There’s been a lot of speculation in media that a new flu virus strain — with bits of avian, pig and human viruses and capable of spreading between people — is something ominous. But that’s just the nature of flu viruses: they replicate haphazardly, reshuffling their genetic material from multiple sources. “This natural reassortment will come up with a new flu virus,” said Dr. Christine Layton, Ph.D., MPH. “H1N1 swine flu is one of those, but we’ve certainly seen others in the past 30 years,” she explained to National Geographic News today.

That’s basically why a new influenza vaccine is developed every flu season. As the CDC explained, human infections of swine flu can and do happen.

When answering media questions about this year’s strain, Dr. Schuchat preferenced her answer by again emphasizing: “we’re looking a lot more intensively and so we may be finding more unusual things and we are really trying to have a balance of taking this very seriously. Actively investigating, sharing information as we have it, and trying to convey the idea that we really can’t differentiate whether this is truly new versus [or] that we have a better situational awareness now.”

Putting things in perspective

We’ve been hearing all sorts of numbers and speculations as to how many people have come down with the flu or are dying. We’re also being led to believe that the virus is actively spreading and sickening increasingly more people. “The number of cases has doubled,” television news reported tonight.

But, as Dr. Nancy Cox, Director of CDCs Influenza Division, explained to media yesterday, a total of seven cases of swine flu virus have been confirmed in California, but all of these patients had been sick weeks ago and all have recovered.

The number of confirmed cases nationwide now tallies about 40, but it’s not because the virus is spreading, said Dr. Richard Besser, acting director of the CDC. It’s because more tests are being completed. All of the patients have recovered. There have been no deaths. [That's not to say that there probably won't be, of course, because people do die from flus and respiratory infections.]

“So far this is not looking like very, very severe influenza,” said Dr. Schuchat.

The cases we’re seeing outside Mexico have been “no more serious than your average flu bug,” said Dr. Layton.

These numbers — 40 cases of this strain, that might have gone unrecognized from the regular seasonal influenza in past years, and no deaths — pale in comparison to the number of Americans who are estimated to die from the flu every year. According to government health statistics, about 30,000 to 50,000 people die every year from influenza in the United States. Princeton biologists estimated that from 1979 to 2001, annual deaths from influenza in the U.S. averaged 41,400. About a thousand times more people die every year from influenza than have from swine flu, yet there are no nightly death counts on the news during flu season each year.

Addendum: And how many cases of the flu are normally seen, for comparison? This week (April 12-18, 2009), the CDC confirmed 25,925 cases of influenza in the United States and 55 child deaths.

While estimates of annual influenza deaths vary depending on the methodology, each is consistent in showing that cases are not rising. For instance, MIT research found that there’s been a substantial decline in influenza deaths in the U.S. during the 20^th century. Not only that, but the influenza pandemics of 1967-8 and 1968-9 showed “substantial overlap in both degree of mortality and timing compared with nonpandemic seasons.” In other words: “The considerable similarity in mortality seen in pandemic and non-pandemic influenza seasons challenges common beliefs about the severity of pandemic influenza.” Don’t let the word pandemic play on your fears.

Deaths in Mexico

Media stories have been filled with ominous warnings about Mexico and suggesting that vast numbers of people are sick and dying, restricting their travel and near panic. But even the World Health Organization’s latest update reports only 26 confirmed cases and seven deaths in Mexico. (Canada has reported six cases with no deaths.) And, in contrast to the CDC:

“WHO advises no restriction of regular travel or closure of borders.”

The CDC’s MMWR Weekly report on the latest update of swine flu cases also emphasized that increased monitoring and testing for swine flu strains has been in effect the past couple of years along the border region. The CDC’s laboratory has only been able to identify the same strain of swine flu as seen in the U.S. in seven of the 14 samples sent to it from Mexico. They cautioned that not all of the reported flu cases from Mexico may actually be confirmed cases of swine flu. No clear data is available.

Most important, greater numbers of deaths in Mexico does not mean that a more virulent strain is present there. Mexico is a country with extreme poverty. Even in the 1990s, more than a third of households had no indoor plumbing and about 20% of homes had dirt floors. With poverty, hunger and lack of good medical care affecting large segments of the population, infections take a much higher toll. In 1990, one in five deaths were still due to infectious parasitic and respiratory illnesses and malaria claimed 31.1/100,000 people. Even the flu is more deadly for poor people.

Can you get swine flu from pork?

No. The U.S. Department of Agriculture reported this morning that there is no evidence that swine in our country are infected with this virus strain. Pigs in the United States are not contagious with this virus, nor can you get swine flu from touching pigs or eating pork. As the USDA explains, Federal veterinarians, state animal health officials and private practitioners regularly monitor U.S. swine for signs of disease and no cases have been found to be circulating anywhere in U.S. swine herds. Pork producers are on high alert and taking extra vigilance in animal safety practices.

You cannot get swine flu from eating cooked pork. Cooking pork to an internal temperature of 160°F kills all viruses.

What can you do to protect yourself and your loved ones?

The swine flu isn’t much different from any other flu or respiratory infection in how it’s spread, in its symptoms or in how you can protect yourself. As the CDC explains, just like seasonal flu is spread between people, the swine flu spreads mostly through respiratory droplets, such as infected people coughing or sneezing. You can also pick up flu viruses by touching something with viruses on it and then touching your mouth, eyes or nose. The symptoms of swine flu are the same as the typical flu: fever, cough, sore throat, body aches, headache, chills and fatigue, sometimes diarrhea and vomiting.

To help protect yourself:

1. Wash your hands with soap and water or hand sanitizer.

2. Don’t pick your nose.

3. Wash your hands.

4. Avoid close contact with people who are sick.

5. Wash your hands.

Forget about those blue surgical masks you see everyone wearing on television news. Viruses are tiny enough to go right through them or around the openings. They might help protect you from globs of mucus flying towards your face, but that’s about all. They’re mostly good for hyping the fear factor and looking scary.

For healthcare professionals caring for patients and engaged in aerosol-generating activities, such as respiratory treatments, the CDC recommends a fit-tested disposable N95 respirator. But even a respirator alone isn’t completely protective and offers limited protection from viruses. It can filter out particles down to 0.3 microns 95% of the time. You still have to: Wash your hands.

If you get sick

For heavens sake, stay home and don’t spread any respiratory virus with your friends, schoolmates, work buddies or fellow parishioners. And especially stay away from people who are more vulnerable to respiratory infections, such as babies, elderly, immunosuppressed patients and those with underlying medical conditions or chronic diseases. Just like the common sense advice your mother gave you when you had a cold: Cover your nose and mouth when you cough or sneeze. Throw your snotty tissue in the trash after you use it and don’t share your toothbrush or eating utensils. And wash your hands often with soap and water, especially after you cough or sneeze.

Medical care is available today for bad respiratory infections, including antibiotics for secondary bacterial infections. Laboratory testing has found the swine influenza A (H1N1) virus is susceptible to new prescription antiviral drugs, oseltamivir and zanamivir.

As the CDC cautions, if you or a loved one becomes sick and develops any of the following symptoms, seek emergency medical care.

In children, emergency warning signs that need urgent medical attention include:

· Fast breathing or trouble breathing

· Bluish skin color

· Not drinking enough fluids

· Not waking up or not interacting

· Being so irritable that the child does not want to be held

· Flu-like symptoms improve but then return with fever and worse cough

· Fever with a rash

In adults, emergency warning signs that need urgent medical attention include:

· Difficulty breathing or shortness of breath

· Pain or pressure in the chest or abdomen

· Sudden dizziness

· Confusion

· Severe or persistent vomiting

The bottom line is that there is no evidence we need to panic about another flu pandemic. The newspapers and television networks love a good scare, as do pharmaceutical companies. But scares do nothing to make us feel better. All influenza infections are worthy of prudent precautions, but panic can be far more virulent and more costly than the flu itself.

© 2009 Sandy Szwarc

For information on this evolving story, see the CDC Swine Flu “What’s New” page here.

Sadly, a lot of consumers don’t read, and pork producers are bracing for the worst. For readers who don’t submit to the media panic and who keep their common sense firmly intact: they may find some great deals on pork chops and ribs at the market this week.

Click here for complete article (and single page version).

Do our genes hold the secret to health and disease risk?

Genetic tests have received a lot of media attention. The public is being led to believe that genetic screening can identify people at risk for diseases, such as heart disease, cancer and diabetes, and that genes hold the promise of personalized medicine and nutrition. It all sounds so scientific.

It’s not.

While the marketing of genetic screening tests gets lots of buzz, the information from genetic research scientists, medical professionals, health departments, federal regulatory agencies and consumer protection groups rarely does. For years, they’ve been trying to warn the public about the lack of scientific validity and commercial interests behind genetic screenings, and the serious potentials for misuse of private genetic information. Meanwhile, just as health agencies across the country crack down on commercial genetic testing, the companies find another way to skirt regulatory censures.

Helen Wallace, Ph.D., Deputy Director of GeneWatch UK has equated tailoring your diet to your genetic make-up as being as scientific as tailoring your diet to your star sign. “With only a few exceptions, what the genomics companies are doing right now is recreational genomics,” said David B. Goldstein, Ph.D., director of the Center for Human Genome Variation, Institute for Genome Sciences and Policy at Duke University in Durham, NC. “The information has little or in many cases no clinical relevance.”

As Dr. Kenneth Offit, M.D., MPH, with the Department of Medicine at Memorial Sloan-Kettering Cancer Center in New York, has explained, personalized medicine is not scientifically supportable and genetic markers have not been shown to be valid in predicting disease, a caution also issued by the CDC, FTC and FDA.

Genetic markers are little more than a vast collection of hundreds of thousands of correlations gleaned from data dredges on vast populations, comparing genomes of patients and healthy people. They come from what are called genome-wide association studies, such as the Human Genome Project, that seek to identify inherited genetic variants associated with risks for diseases. Their significance, however, is far different from what the public is led to believe. The emerging consensus of the scientific community is that these correlations are not true disease markers but part of a blizzard of false positives that can be found anytime hundreds of thousands of markers are probed at the same time.

The scientific basis of genomic profiles for assessing health risks and personalize health interventions was recently reviewed by international genetic experts, led by A. Cecile J. W. Janssens from the Department of Public Health at Erasmus University Medical Center in Rotterdam, The Netherlands. Their review of the scientific evidence published from 2000, appeared in the American Journal of Human Genetics. Of the 260 studies in their analysis, examining genetic screening tests for 160 unique polymorphism disease associations, nearly two-thirds of the associations (62%) were found to not even be statistically significant. Of the significant ones, the odds ratios were modest, ranging from 0.54 to 0.88 for protective variants and 1.04-3.2 for risk variants.

As other experts have reported with other genetic links, for example, genes said to be associated with cardiovascular diseases were more frequently associated with noncardiovascular diseases than cardiovascular diseases! Dr. Janssens and colleagues concluded that there is no scientific evidence to support genomic profiles as assessing genetic risks for common diseases such as cancers or heart disease, or in developing personalized diet and lifestyle recommendations for disease prevention.

Concerns surrounding this issue go far beyond the recreational use of online genetic tests by consumers being sold ‘healthy’ diet and lifestyle products and interventions. In the UK, the Nuffield Council on Bioethics has just launched an investigation into personalized genomics and medical profiling, electronic medicine with its strong focus on screening and prevention, and genetic testing being claimed to predict a person’s risk of developing a range of diseases. As the NHS explains, these tests are different from proven DNA tests for single gene disorders, such as cystic fibrosis. Genetic screening tests are being criticized for delivering potentially misleading, unreliable and inconsistent results with no evidence for any real health benefits. There are numerous examples of investigations into different genetic screenings where healthy people are given vastly different reports of their risks for developing diseases.

Genomics: association studies

The current issue of the New England Journal of Medicine features articles discussing genomics from a variety of genetic researchers. The overriding take-home message is that genome-wide association studies are the world’s largest data dredges and challenge us to remember that: health risk factors are correlations, correlations do not make causation, relative risks are different from absolute risks, and statistical significance is not the same as being tenable or biologically relevant.

While the more than one hundred genome-wide association studies have mined the genome for countless associations, in reality, they have little real meaning, Dr. Goldstein said. “Most common gene variants that are implicated by such studies are responsible for only a small fraction of the genetic variation that we know exists,” he wrote. Among the facts universally known about human variation, said Richard C. Lewontin, Alexander Agassiz Professor Emeritus of Zoology at Harvard University, is that “any two unrelated human beings differ by about 3 million distinct DNA variants.”

Genome-wide association studies identify common genomic markers, single-nucleotide polymorphisms (SNPs), and although the strongest among these common variants have been identified, scientists are finding that they’re packing much less of a punch than had been anticipated, said Dr. Goldstein.

An unreasonably large number of such variants appear to account for the genetic component in risks for common diseases, such as diabetes and cancers, as well as for inherited traits, such as height. The estimated number of SNPs required to explain 80% of the population variation in height (the most common estimate of height's heritability), for example, is 93,000 SNPs. If it takes “a large chunk of the genome to explain the genetic component of a disorder,” he said, genetics provide relatively little guidance about the biology of these conditions because most genes are “height genes” or “type 2 diabetes” genes.

“In pointing at everything, genetics would point at nothing,” he said.

Genetic screening tests, which focus on just a few variants, are unlikely to credibly identify people at highest risk for common diseases, and instead, are more likely to overestimate the significance of genetic results to the public and, especially, to be misused.

“Most variants that have been identified to date are markers, not causal variants,” he wrote, “and are generally assumed to reflect the effects of some other, as-yet-unidentified common variant.” Or, some of these associations may also be multiple rare variants that occur, by chance, more frequently in association with one allele at a common SNP than with the other.

“It seems much more likely,” he said, “that most genetic control is due to rarer variants, either single-site or structural.” These aren’t going to be found in genome-wide association studies, he said. “It’s hard to have any enthusiasm for conducting genome scans with the use of ever larger cohorts.”

As epidemiologists Peter Kraft and David Hunter of Harvard School of Public Health in Boston explained, the vast majority of these risk-marker alleles identified in genome-wide association studies also confer very small relative risks. Most range from 1.1 to 1.5, they said, far below the relative risk of 3.0 that researchers would consider tenable — above random chance for such data dredges, for instance — even though they meet mathematical criteria of statistical significance. Even when combining these alleles, these genetic markers have a poor ability to identify or predict those people who are susceptible to disease, they said.

A striking fact about genome association studies, they wrote, is that even collectively, genetic markers explain only a tiny fraction of the genetic role for most diseases. For example, the approximate number of risk alleles that would be needed to statistically increase a sibling’s risk for getting diseases such as diabetes, heart disease and many cancers go far beyond a single marker. It would take 550 to 1,374 alleles, each associated with a 10% relative risk of a disease, combined to reach a tenable relative risk of 3.0.

But this still fails to show that these correlations are clinically meaningful or have a causal role. “The clinical value of a genetic test also depends on its sensitivity, specificity, and positive and negative predictive values; the costs and benefits of interventions; and the availability of data linking specific variants to improved clinical outcomes,” wrote Drs. Kraft and Hunter. The fact is that even when we can detect subtle differences in risk as more allele are identified, most people will fall around the medium level of risk. For less common diseases, the predictive value of a genetic test “will almost always be low,” they said.

So, while genetic tests claim to identify someone with genetic markers for a disease, wrote Drs. Kraft and Hunter, “the identified variants do not contribute more than a small fraction of the inherited predisposition.”

Genomics is not only considerably more complicated than most consumers hear, it appears to be little more than a fad — one with tremendous potential for financial and political misuse.

As neurology professors John Hardy and Andrew Singleton wrote in this NEJM issue, genome-wide association studies have identified large numbers of associations and made it routine to identify common, low-risk variants. But “the initial contention surrounding the viability of genome-wide association studies has largely subsided” with what many now see as diminishing returns. “Genome-wide association studies identify loci and not genes per se and cannot easily identify loci at which there are many rare risk alleles in any given population.” This approach had been created to fit the “common disease–common variant hypothesis of human disease,” they wrote.

However, the realization “that has taken many observers by surprise is that most loci that have been discovered through genome-wide association analysis do not map to amino acid changes in proteins. Indeed, many of the loci do not even map to recognizable protein open reading frames.” In other words, they might affect gene expression, but such effects are extremely varied and complex and can occur at numerous stages (transcription, messenger RNA stability, and splicing or translation efficiency). Ever sorting it all out is an extremely unlikely probability.

Then, there’s the widespread belief in the role of environmental and behavioral influences on disease. “To state that most complex diseases are caused by an interaction between genome and environment is a cliché,” they wrote. “Such interactions, while likely, have for the most part not been demonstrated, and we should be cautious about universally subscribing to this belief without evidence.” Yet, they pointed out, “this is one of the goals of the recently announced Genes, Environment, and Health Initiative of the National Institutes of Health.”

The most disturbing re-emerging trend is the use of genetic markers to “identify” biological weaknesses and disease risks associated with race and ethnicity. Genomics is stimulating a new field of race-based public health, government-funded research and health policy, euphemistically couched as addressing “health disparities.” If you missed the coverage of the science of genomics, race and genetics, and health disparities, please read and think about the Council for Responsible Genetics’ review, “History of Race and Science,” and the Social Science Research Council’s “Is Race Real?” series, and follow it to its historical, logical and troubling conclusions.

The great and terrible war which has now ended was a war made possible by the denial of the democratic principles of the dignity, equality and mutual respect of men, and by the propagation, in their place, through ignorance and prejudice, of the doctrine of the inequality of men and races…Biological studies lend support to the ethic of universal brotherhood… For every man is a piece of the continent, a part of the main, because he is involved in mankind. — United Nations Educational, Scientific and Cultural Organization, The Race Question, Paris, 1950.

The risky gene

In light of the growing popularity of genomics in public health, an article in Patterns of Prejudice offered another thought-provoking perspective. “The risky gene: epidemiology and the evolution of race,” was written by epidemiologist Philip Alcabes, Ph.D., associate professor of Urban Public Health at Hunter College and the City University of New York.

Did you know that the United States is the only industrialized nation in the world that does not collect health data according to economic class? “Instead,” he began, “we report almost every morbidity and mortality statistic by race.”

Today is the heyday of behavioural epidemiology. Eat too much and you can become obese. Smoke and you raise your chances of dying of cancer. Have sex without a condom and you might die of AIDS. Life seems thick with risk, some of it still waiting to be detected by a passing epidemiologist. What did you eat for breakfast? Do you buckle up?

Epidemiology has departed from systematically, scientifically generating knowledge for the purpose of better understanding the social inequities that result in health problems among disadvantaged. “Now, the people who generate such knowledge are the activists and advocates, spokespersons for one or another identity group,” he said.

Is American epidemiology turning away from its original raison d’eˆtre in order to join in the pursuit of a new American order in which those inequities, like poverty and housing discrimination, that are easily seen to be causes of health problems, are to be ignored? …

No epidemiologist can tell you what your risk of disease is based on your behaviour… Which is exactly why you hear so many conflicting stories about whether or not you are supposed to be eating broccoli and Grape Nuts. Still, the thrust of epidemiology lately goes towards calculating the risk allegedly associated with particular activities.

Research articles on behavioral disease risk published in professional journals now far outnumber epidemiological studies examining the greatest health risk, socioeconomic status. “What my colleagues do not realize is that their work also supports the delivery of health-risk-avoidance messages to the public in terms that are heavily moralistic,” he said.

Their work contributes, albeit indirectly, to a new set of pariahs in our society: smokers, women who drink coffee while pregnant, unhelmeted motorcyclists, people who have ‘unprotected’ sex… I must emphasize that epidemiology has very little to say about whether you will be better off if you engage in ‘safe’ behaviors…

“Epidemics” have especially been used at other times in history to justify discrimination against certain group, and explained with genetics. For example, he wrote:

The leading killer throughout the nineteenth century was tuberculosis (TB). Here, too, the effects of social structure were displaced on to behaviour, and behaviour was used to define, and then indict, a race. TB is transmitted by the only unavoidable and unmodifiable activity of life, breathing. It is the classic example of a disease whose distribution is determined purely by social conditions… Unsurprisingly, it was the leading killer among tenement dwellers in the industrial revolution era, and it remains dangerous to the poor in densely populated places everywhere today. In the United States before the Civil War, TB was responsible for 20 percent or more of all deaths, and was more pernicious in the industrial cities of the North than in the still agrarian South… Proponents of slavery seized on the North/South difference in TB…in particular, cited the lower rate among slaves compared to Northern Blacks as evidence that black people were a race apart: the predisposition of the African American towards TB could be contained only through the benign paternalism of slavery….

In our own time, higher rates of both AIDS and heart disease among black Americans have been attributed to habits… Heart disease is supposedly a function of diet, or an eating ‘culture’ that disdains low-fat foods, or hip-hop advertising campaigns by McDonalds. Here, too, culpability is fixed by holding African Americans responsible for mythic behaviour: sexual abandon, sexual deviance, primitive eating and dancing rituals… If only they could control themselves…

In each of these cases, the victims of disease were seen as having brought it on themselves, through some activity rumored to be characteristic of their group, he said, much like the “obese.”

Aspersions cast on behaviour are magnified by linking the behaviour to a fearsome disease. And the disease thereby helps to identify people as members of the reprobate group.

Identifying behavioural causes of disease produces more investment in yet more campaigns to get people to alter their behaviour and live the healthy life. And that allows us, as a society, to continue to ignore the social problems, economic policies and other forms of social stratification that underlie differences in disease susceptibility... The distance between ‘us’ and ‘them’ is highlighted by their supposed indiscretions. It makes them a group apart, a race. And while it incriminates them, it exonerates us.

I believe that implicating people in the harming of society, through the allegation that their behaviour causes widespread disease, and imagining that people’s behaviour expresses their place in a purported hierarchy of races are two harmful forces in public health… In the United States, ‘race’ is often the name we give to such discontinuities when they really come from class. In general, the race allegation refers to deficits in wealth or access to power. But it also, nowadays, resonates with assumptions about fitness. You are part of a race if you are identifiable as a member of the lesser classes, not just of the lower strata economically, but of the groups whose disease rates are higher.

We can say that the differences we observe in disease rates arise from genetics, or we can say that the differences arise from engaging in improper behaviour. But in either case what we mean is that “those people” — the ones who are ‘at higher risk’, the ones who are ‘hereditarily’ susceptible — are the loci of disease. They carry risk in their genes. They are socially suspect. They are implicated. And since we are innocent, we do not have to solve, or necessarily even examine, the vexing problems of modern society that truly make some people sick while others are well.

Government research funding

These observations from the scientific community — on the science of genomics and its role in the pursuit to identify those at risk of disease and find treatments — take on added relevance when we compare them to the research and health policies our government is supporting.

Tomorrow is the deadline to cash in on the $200 million allocated to the NIH for comparative effectiveness research as part of the American Recovery & Reinvestment Act of 2009 (Stimulus Bill). What isn’t often publicized is that federal research grants only go to projects that specifically support the issues and agendas outlined by the government.

Here is a sampling of research topics the NIH has designated for its new initiative called the Challenge Grants in Health and Science Research:

● The role of health behaviors in cancer prevention (behavioral change studies are encouraged, including diet, physical activity and adherence to cancer screening)

● Role of nutrition in cancer (“application of multiscale modeling to linking effects of nutrition from the molecular to cellular to organism to population studies”)

● New genomic technologies (“physician utilization and/or patient acceptability”)

● Unified informed consent for biobanking and subsequent analysis of human biospecimens (informed consent “remains a challenge that impedes efforts related to biobanking” and the later use of genetic material for research)

● Health disparities and participation in research (identify barriers to minority participation in biomedical and clinical research)

● Development of an electronic health information infrastructure and the sharing of health information

● Translating genetics (“genetics and genomics have great promise for the development of personalized medicine…examples of studies include those related to board sharing and use of new genetic information and technologies”)

● Fingerprints (genetic markers) for the early detection and treatment of cancer

● Projects to “support a large scale bioinformatics effort to identify biomarkers…”

● Biomarker discovery and validation among racial and ethnic minority populations

● Policy for Challenge Grants (“incorporation of analysis of race/ethnicity differences into Challenge Grants”)

● Oversampling minority populations in clinical research (“financial incentives/supplements to NCI-supported clinical trials where oversampling for minority populations is feasible”)

● “Designing clinical research studies based on unique health characteristics of a minority community cohort with regard to co-morbidities” (including the development of clinical guidelines, upgrading surveillance and tracking systems in these communities)

● Health informatics (integrated electronic medical records) to increase cancer prevention compliance among primary care physicians

● Cancer Intervention and Surveillance Modeling Network (consortium focused on use of modeling to determine best strategies for prevention, screening and treatment strategies among the population)

● Enhancing electronic tools to assess patient-reported symptoms, functioning or health-related quality of life and/or health behaviors such as physical activity

● Implementing FDA regulation of tobacco products

● Quantum biology in cancer (an “emerging interdisciplinary field… biological interactions are modeled using mathematical computation and physical measurements in light of quantum mechanics effects”)

● “Augmenting Genome-Wide Association Studies” (high priority)

● “Role of gene-environment interactions in cancer health disparities research” (“Minority and underserved communities usually depict higher incidence and mortality rates for a number of different cancers”)

● Genomic analysis and development of a bioinformatic pipeline for rapid genomic analysis

● Molecular and population epidemiology and health disparities (“including the novel identification and validation of functional or ancestral biomarkers for risk susceptibility”)

● Genome-wide association studies in cancer prevention (“as well as the influence of environmental factors”)

● “Enhance genomic studies with social determinants of disparities”

● “Genomics research targeting minority populations”

● Genetic and environmental associations in cancer incidence

● Health disparities cancer research (“The role of biological factors in cancer health disparities is now a reality with studies that show that genetic risks to cancer varies by racial/ethnic groups.”)

Science or something else? Do enough Americans understand science and remember recent history to see?

© 2009 Sandy Szwarc

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Rejection of science squared

Or: Computer modeling is not science

Fat people are now being blamed for contributing to climate change by breathing. Actually, it’s worse than that. Headlines are saying: “Fatties cause global warming.”

Hundreds of news stories this week are based on the latest carbon dioxide paper just published in the online version of the International Journal of Epidemiology. Its authors were Phil Edwards, senior lecturer and lead organizer of the module “Statistics for Epidemiology and Population Health,” and Ian Roberts, both in the Department of Epidemiology and Population Health at London School of Hygiene & Tropical Medicine. [There’s that new field of population health again.]

As JFS readers will remember, professor Roberts had written the article in New Scientist, published in 2007 also around Earth Day, titled: “How the obesity epidemic is aggravating global warming.” It had accused fat people of killing polar bears and had begun by stating: “WE KNOW the world is warming and we know humans are causing it...”

While being called a study by epidemiologists and the media, reading the actual text of their new paper reveals the methodology:

“The upward shift in the population distribution of BMI could also have important environmental consequences… we assume… since it can be assumed… the equations used were… to estimate, we assumed… estimates were applied… these broad assumptions which affect predicted energy expenditure… since it can be assumed… on the basis of these assumptions, we estimate that… might therefore be responsible… we would expect the overweight population to have higher transportation fuel energy use… to estimate, we assumed that… we assumed… our model estimates that… expresses the idea that… would not be surprising…might reasonably expect…to estimate, we have assumed… if we assume… our estimates… it is likely… might therefore be considered… if we assume… if… it is likely that… We used a normal (Gaussian) distribution to model... and a log-normal distribution to model the skewed distribution reflecting a higher prevalence of obesity and morbid obesity in the ‘overweight’ population. These are theoretical statistical probability distributions, which may not be expected to describe perfectly the shapes of the population distributions of BMI observed in high-income countries… In our model, we have assumed... If...then we would have over-estimated average energy expenditure in the overweight population.… When we assume plausible…

We have estimated the additional green house gas emissions due to increases in population adiposity. In doing so, we have made a number of assumptions all of which can be questioned.”

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Does it really matter how your numbers measure up? Or can you ditch the tape measure?

Why was one of the most important studies from the U.S. Centers for Disease Control and Prevention buried?

Can we tell by a physical feature or measurement what our risks are for dying prematurely? As increased body weight and now BMI (body mass index) have proven to be poor predictors of mortality risk, the explanation sometimes suggested is that BMI doesn’t differentiate fat (“bad”) from muscle (“good”).* Increasingly trendy ways to identify “unhealthy obesity” include measures such as body fat, the shape of bodies (“apple” or “pear” figures), waist circumference and waist-to-hip ratio (“belly fat”). Do any of these measures really matter or are they just different ways to make us self-conscious about our bodies and provide marketing tools for healthy diets, lifestyles and anti-obesity programs?

The best way to answer these questions and determine if there’s even a credible link between a body measurement and mortality is to look at the most reliable and objective data available: actual measurements on a large representative sample of the population and actual mortality data. Senior scientists at the National Center for Health Statistics at the CDC and the National Cancer Institute did just that. Their results were published in this month’s American Journal of Clinical Nutrition.

The Third National Health and Nutrition Examination Survey (NHANES III, 1988–1994) conducted the most precise measurements of body size and composition available on a large representative sample of the U.S. population. These measurements included:

● BMI [weight (kg)/height (m)²]

● percentage of body fat measured by bioelectrical impedance

● skinfold thicknesses

● circumference of waist, hip, and arm

● waist-hip ratio

● waist-height ratio

National death certificate data in the national Death Index linked mortality data through 2000 to these detailed measurements in NHANES III. CDC authors, Katherine Flegal, Ph.D., and Barry Graubard, Ph.D., calculated the number of excess deaths associated with the anthropometric and body composition measures for each age and gender, comparing low, medium and high risk levels of each measurement to their reference ranges. (The reference ranges are the recommended “normal” numbers considered measures of good health, such as BMIs of 18.5 – <25. It's that zero line on the graph below.)

They found:

● The fractions of all-cause mortality associated at low levels of all the variables were similar and small, ranging from 0.3% to 2.5%.

● For intermediate levels of each body measure compared with the reference measurements, the associations with all causes of mortality were negative (-1.8% to -9%) — meaning, having higher than ideal numbers were associated with lower mortality — and the association with percentage body fat was only 0.1%.

● Finally, for the highest measurements — regardless of the anthropometric or body composition variable — there were no tenable correlations to excess mortality — they were all statistically weak, ranging from -1.7% to 1.5% compared to “ideal” numbers.

● Even comparing the different body measurements to each other “showed no significant differences between estimates of excess deaths for any pair of variables at any level.

In other words, having a higher number for any measure of body shape or size, or body composition, is not predictive of higher risks of dying from all causes compared to people with “healthy” numbers and picture-perfect bodies. In fact, like the preponderance of evidence supports, thinner isn't better and the healthiest numbers appear to be those larger than current recommendations. Threatening the largest, fattest among us with early graves simply is not supportable by objective measures.

With BMI shown to not be a credible measure to predict greater risk of dying from all causes, what the authors did next may have seemed overkill, but necessary to address the continued stigma associated with obesity.

These senior scientists at the National Center for Health Statistics had previously found that among U.S. adults, there is “little or no association of excess all-cancer mortality with any of the BMI categories. None of the estimates of excess deaths was statistically significantly different [from null].” In this study, they proceeded to look specifically at deaths just from causes popularly believed to be associated with obesity. Was adiposity really associated with higher deaths from these conditions? They examined deaths from 21 different “obesity-related” diseases, including: cardiovascular disease, cancers (colon cancer, breast cancer, esophageal cancer, uterine cancer, ovarian cancer, kidney cancer, or pancreatic cancer) and diabetes or kidney disease. For the low risk level of measurements, the associations with deaths “were all quite small and close to zero,” they wrote. There were no statistical associations for the intermediate levels. Finally, “for the obese level, none of the 21 differences would have been significant even at a P value of 0.05,” they reported. Without even a credible association, being fat cannot be pointed to as a credible cause.

How have we been misled?

As the CDC authors explained in reviewing the body of evidence, the very same flaws that have plagued the methodology of studies behind the denunciation of obesity based on BMI, now afflict claims based on these alternative measures. When we disregard the principles of fair test — quality of the data (subjective versus actual measurements), objectivity and selectivity (randomized and representative of population), control for bias and confounding factors, interpretations of findings, etc. — it’s easy to be persuaded of something that isn’t scientifically sound. The most notable problem is failing to understand what “risk factor” means and that “correlation is not causation.” The literature often reports weak associations in terms of relative risks, rather than absolute risks, they said. “Relative risks compare the risks at lower and higher levels of a variable, but do not provide estimates of the overall contribution of these levels to mortality.” It is often assumed that any associations between BMI and mortality are due to adipose tissue, but actual mechanisms for blaming fat tissue have yet to be explained, they pointed out. Meanwhile, significant confounding factors affecting health outcomes, such as social and economic factors or even age are often not considered in correlations, and ignore that larger body size and fat can offer survival advantages.

Even the literature on cardiovascular disease incident and mortality associated with BMI or waist-hip ratio are not convincing.** “In our analysis,” the authors concluded, “use of the waist-hip ratio did not result in any systematic differences from BMI or other individual variables.”

As they wrote in their discussion section:

BMI is an imperfect measure of adiposity and its use in epidemiologic studies has been criticized. It is sometimes suggested that weak or negative associations between BMI and mortality are due to the lack of the ability of BMI to discriminate between lean and fat mass and that associations would be strengthened if different measures were used. In NHANES III, associations between mortality and elevated BMI were weak… However, the associations of the corresponding levels of other anthropometric variables—including waist, hip, and arm circumferences; percentage body fat estimated from bioelectrical impedance; waist-hip ratio; the sum of four skinfold thicknesses, and the waist-stature ratio — also tended to be weak and in general were quite similar to the association of BMI with mortality…

These findings do not suggest that the weak adiposity- mortality associations would be stronger if measures of adiposity other than BMI were used.

Everywhere we turn, tape measures are being unfurled and our waists and hips measured, our bodies are weighed and pinched — all purportedly to measure our health and risks for an early grave. But they don’t. Foremost, they are measures of the natural, hereditary diversity of human body shapes, types and sizes, and reflections of aging.

But convincing us that fixating on our appearance and how our body measures up is more than superficiality, but about “being healthy” — and convincing us that judging others by their bodies and how they measure up is more than prejudice, but concern “for their health” — sells much more than tape measures and health risk assessments. Whether it’s someone telling us what to do if our BMI and waist measurements don’t meet government guidelines, how to get rid of belly fat, or what to do if our waist-to-hip ratios and body shapes aren’t ideal — the advice is the same: diet, exercise and lose weight. Obesity, healthy eating and lifestyles are big business and big government.

This latest study from scientists at the CDC used the government’s soundest and most objective data evaluating the risks of death associated with people larger than government recommendations. Why was this major study buried? Where were the press releases and thousands of headlines?

© 2009 Sandy Szwarc. All rights reserved.

* This explanation seems to be most popular with men, who naturally have considerably less body fat and more muscle mass than women. They carefully ignore the fact that even the most ‘morbidly obese’ women live longer than ‘normal’ weight men. It’s not about fat or body type.

** How many people read reports closely to see what they’re really saying and what the evidence really shows? A recent consensus statement on waist circumference issued by government and private obesity and diabetes stakeholders was published concurrently in the journals Obesity and Diabetes Care and offers a good test in reading comprehension. This consensus statement illustrates just what Drs. Flegal and Graubard at the CDC were saying.

This consensus statement — from Shaping America’s Health: Association for Weight Management and Obesity Prevention; NAASO, The Obesity Society; the American Society for Nutrition; and the American Diabetes Association — begins by saying that obesity, BMI, body fat and now waist circumference, are “risk factors” for a range of chronic diseases and have been shown in epidemiological studies to correlate with heart disease and premature death. This counts on readers incorrectly believing a risk factor is the same as a health risk. But in reviewing the medical literature, they wrote:

…It is not known whether the storage of an absolute or relative excess amount of triacylglycerols in abdominal fat depots is directly responsible for increased disease risk, whether such deposition is simply associated with other processes that cause risk, or both… The mechanism(s) responsible for the relation between excess abdominal fat distribution and cardiometabolic disease is not known, but several hypotheses have been proposed…

Specific relative risks between waist circumference and these outcomes vary, depending on the population sampled and the outcome measured… Data from most clinical weight-loss and exercise training trials have shown that reductions in waist circumference occur concomitantly with reductions in obesity-related cardiometabolic risk factors and disease. However, these results do not prove that the reduction in waist circumference was responsible for the beneficial effect on health outcome…

Based on NHANES III data, 99.9% of men and 98.49% of women would have received the same treatment recommendations proposed by the NHLBI Expert Panel by evaluating BMI and other cardiovascular risk factors, without an assessment of waist circumference. However, it is likely that different waist circumference cutpoint values could provide more useful clinical information… for identifying “metabolically obese, lean” patients who might benefit from lifestyle therapy but would not have been considered for treatment because of a normal BMI.

In other words, it provides a means to include more people in need of lifestyle interventions to get them to eat and live a certain way. However, while the metabo syndrome is used to promote a plethora of preventive health interventions and pills, as we’ve seen, none of the risk factors in the metabolic syndrome has been shown to credibly predict cardiovascular disease or premature death.

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