The Problem with “Peer Review”

I just came across this article mentioned in the comments on this post at Sociological Images. I think it’s really interesting, and is of definite value in the determination of what is real, and what is not real, regarding the science of body size.

In Search of an Optimal Peer Review System, by Richard Smith, an editor of the BMJ for 30 years.

Namely, it highlights the pitfalls of the peer review system as we know it today. I think this article is a really valuable resource for anyone who currently reads, edits, and writes articles for science journals, and for those people who who rely on those who can wade through such articles for summaries and so on.

The moral of the story is, there are a lot of biases, luck, and basically non-science that goes into publishing science. This article shows how that state of affairs is more the norm than otherwise.

My advice is to always check out the affiliations of the authors, the other articles they’ve written, and their funding. Usually one can get a sense for agenda and possible confirmation bias this way. And trust your logic when reading articles. Look out for sketchy things like small or over-corrected sample studies, data dredges, and heavy use of  odds ratios when reporting results.

The business of science is, these days, far from infallible. That’s why just quoting one, two, or five studies isn’t going to prove your case. You have to use your own sense of reason to wade through things and really get down to the nitty gritty, or rely on those who make it a point not to take any study at face value.

Obesity virus – it’s old news.

There has been a humongous press release today calling obesity contagious. A human adenovirus, similar to the common cold, has been implicated in causing potentially 30% of all known obesity.

What wasn’t released was that this is old news.

Yup, they’ve been doing these animal studies for a while, trying very hard to find a correlation between human obesity and increased body weights in animal injected with various viruses, including the human adenovirus.

Read for yourself.

Infectobesity: Obesity of Infectious Origin — Dhurandhar (2001)

(Journal of Nutrition. 2001;131:2794S-2797S.)

The Department of Nutrition and Food Science and the Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 48202

Abstract: In the U.S., the prevalence of obesity increased by 30% from 1980 to 1990, and this increase appears to be continuing. Although obesity has multiple etiologies, an overlooked possibility is obesity of an infectious origin. Six pathogens are reported to cause obesity in animals. Canine distemper virus was the first virus reported to cause obesity in mice, followed by Rous-associated virus-7, an avian retrovirus, which has been shown to cause stunting, obesity and hyperlipidemia in chickens. Next, the obesity-promoting effect of Borna disease virus was demonstrated in rats. Scrapie agents were reported to induce obesity in mice and hamsters. The final two reports were of SMAM-1, an avian adenovirus, and Ad-36, a human adenovirus that caused obesity in animals. Additionally, an association with human obesity is the unique feature of SMAM-1 and Ad-36. Although the exact mechanism of pathogen-induced obesity is unclear, infection attributable to certain organisms should be included in the long list of potential etiological factors for obesity. In addition, the involvement of some pathogens in etiology of obesity suggests the possibility of a similar role for additional pathogens.

Human adenovirus-36 is associated with increased body weight and paradoxical reduction of serum lipids — R L Atkinson1, N V Dhurandhar2, D B Allison3, R L Bowen4, B A Israel5, J B Albu3 and A S Augustus6

International Journal of Obesity (2005) 29, 281–286. doi:10.1038/sj.ijo.0802830

  1. 1Obetech Obesity Research Center, Richmond, VA, USA
  2. 2Department of Nutrition and Food Science; Wayne State University, Detroit, MI, USA
  3. 3Obesity Research Center, St Luke’s-Roosevelt Hospital, Columbia University, College of Physicians and Surgeons, NY, USA
  4. 4Bowen Center, Naples, FL, USA
  5. 5Department of Pathobiological Sciences, University of Wisconsin, Madison, USA
  6. 6Departments of Medicine and Nutritional Sciences; University of Wisconsin, Madison, USA

Abstract:

BACKGROUND: Human adenovirus-36 (Ad-36) increases adiposity and paradoxically lowers serum cholesterol and triglycerides in chickens, mice, and non-human primates. The role of Ad-36 in human obesity is unknown.

OBJECTIVES: To determine the prevalence of Ad-36 antibodies in obese and nonobese humans. To evaluate the association of Ad-36 antibodies with body mass index (BMI) and serum lipids.

DESIGN: Cohort study. Volunteers from obesity treatment programs, communities, and a research study.

SUBJECTS: Obese and nonobese volunteers at the University of Wisconsin, Madison, WI, and the Bowen Center, Naples, Florida. Obese and thin volunteer research subjects and 89 twin pairs at Columbia University, New York.

INTERVENTIONS: Study 1: 502 subjects; serum neutralization assay for antibodies to Ad-2, Ad-31, Ad-36, and Ad-37; serum cholesterol and triglycerides assays. Study 2: BMI and %body fat in 28 twin pairs discordant for Ad-36 antibodies.

MAIN OUTCOME MEASURES: Presence of antibodies to adenoviruses, BMI, serum cholesterol and triglycerides levels.

RESULTS: Significant (P<0.001) association of obesity and positive Ad-36 antibody status, independent of age, sex, and collection site. Ad-36 antibodies in 30% of obese, 11% of nonobese. Lower serum cholesterol and triglycerides (P<0.003) in Ad-36 antibody-positive vs -negative subjects. Twin pairs: antibody-positive twins had higher BMIs (24.5plusminus5.2 vs 23.1plusminus4.5 kg/m2, P<0.03) and %body fat (29.6plusminus9.5% vs 27.5plusminus9.9%, P<0.04). No association of Ad-2, Ad-31, or Ad-37 antibodies with BMI or serum lipids.

CONCLUSIONS: Ad-36 is associated with increased body weight and lower serum lipids in humans. Prospective studies are indicated to determine if Ad-36 plays a role in the etiology of human obesity.

I’m not Sandy at Junkfood Science, but I’m a reasonable researcher and I’d like to know this: if this adenovirus causes 30% of fat people to be that way, why did 11% of thin people in the study group carry the virus?

Also: “Twin pairs: antibody-positive twins had higher BMIs (24.5plusminus5.2 vs 23.1plusminus4.5 kg/m2, P<0.03) and %body fat (29.6plusminus9.5% vs 27.5plusminus9.9%, P<0.04).” So there’s a 1.4 kg/m^2 +- ~5 kg/m^2. If I remember correctly from my error analysis class, the margin of error being greater than the actual difference means you can not say there exists an association. This also covers the 2.1% body fat difference, since the margin of error is ~10%.
So this was a null study.
So why the new press release? Was there a new study? Turns out that the person interviewed about the possibility of a “contagious” obesity was the person who had preemptively coined the term “infectobesity” in his 2001 animal study: Dr Dhurandhar himself:

For the past ten years, Dr Nikhil Dhurandhar from Louisiana has been carrying out animal and human studies on the virus, Adenovirus-36.

He believes it could be one of the mechanisms causing some people to put on weight more quickly.

As far as I can tell, there has been no new study. However, there was this interesting (dare I say, fear-mongering?) article in the Journal of Pediatric Obesity, by one of Dhurandhar’s 2005 study, Dr. Richard Atkinson:

Could viruses contribute to the worldwide epidemic of obesity?

Author: Richard L. Atkinson a
Affiliation: a Obetech Obesity Research Center, Richmond, VA

Published in: journal International Journal of Pediatric Obesity, Volume 3, Issue S1 2008 , pages 37 – 43

The prevalence of obesity in children increased rapidly starting about 1980 in both developed and developing countries. Studies of changes in diet and physical activity, television watching, and food advertisements on television suggest that these are not sufficient to explain the epidemic. The pattern of rapid spread is suggestive of an infectious origin. The concept of virus-induced obesity is not new. Eight viruses have been shown to cause obesity in animals and there is evidence for virus-induced obesity in humans. Recent evidence on animal and human adenoviruses suggests that these adenoviruses may infect adipocytes to alter enzymes and transcription factors resulting in accumulation of triglycerides and differentiation of preadipocytes into mature adipocytes. The E4orf1 gene of Ad-36 has been shown to be responsible for the adipogenic effect. It appears that a portion of the worldwide epidemic of obesity since 1980 could be due to infections with human adenoviruses.

The abstract and title are filled with fear-words like “epidemic,” “rapid,” “rapidly” – though any statistician will tell you that child weights and heights have not increased rapidly at all, though the definition of obesity has itself been revised downwards twice since 1980.

The question to ask when there has been a press release of this magnitude – old news being picked up by nearly EVERY news outlet in the span of a few hours – who are they trying to scare, and why?

This is old news. Its release could only be the sign of one thing: someone is trying to make you even more disgusted and afraid of fat people than society has told you to be thus far. Someone stands to benefit from your fear. Fear leads to desperation, which leads to people signing onto things they would normally not sign onto.

My guess is that they’re trying to push a new childhood immunization, which would line the pockets of whomever would develop it. Or they’re trying to further cordon off fat children (because all the suggestions in these abstracts is that it is “caught” during childhood).

Either way, it’s old news, and it’s clearly a press-release to make people afraid. Who stands to profit from this fear remains to be seen.