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Posted

The virus may be correlated with a variety of things in Chickens that result in a lower BMR, but noting that a viral infection alters a chicken's activity level, which results in entirely predictable changes in body composition, is quite a bit less earth-shattering a claim than "Virus Causes Obesity!"

Good point

 

Though I think the main value of the chicken trial is that, it being a prospective controlled trial, it provides evidence against reverse causality (i.e. fat increases likelihood of having/getting virus).

 

re: PIMA's: Yes, I agree exercise and diet almost assuredly play large roles in obesity. The PIMA's, though, are not the best of your examples to illustrate this point. If they are geographically separated communities, they could easily be disporportionately affected by a communicable virus.

 

 

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Posted
- the sample size in this study seems ridiculously small

 

p < .001 baby!

 

I don't think large sample sizes are as necessary in a controlled laboratory experiment as they are in a (phase III) human trial. Plus I don't think you should really be concerning yourself too much about generalizability when your experiments are on chickens! grin.gif

 

Looking at the paper again, I did find this possibly worrying bit of info:

"DISCLOSURES

Dr. Atkinson owns all shares of Obetech, LLC, a company that markets assays to detect infection with human adenovirus-36 and owns patent rights for these assays."

 

 

-- Your momma's so fat, when I tell her to haul ass, she's gotta make two trips.

Posted

Not a terribly impressive paper IMO. As I suspected, there was no difference in the bodyweight of the infected vs. non-infected chickens. The law of conservation of energy still stands. Amazing. "A reduction in metabolic rate might explain the increased fat deposition, but the small changes over time would be impossible to detect with current technology. The greater body fat deposition, despite similar body weight, suggests a shift from lean body mass deposition to fat deposition during the growing period of Ad-37-infected chickens. Further research will be necessary to understand the mechanisms of these changes."

 

What also stood out was that:

-The results in the chickens were not consistent with the results that they obtained in the cells infected with the same viruses. "This is a disappointing finding because it suggests that the in vitro assay will not be a good screening test to predict response to human adenoviruses in whole animals. Both of the human adenoviruses that produce obesity in vivo increased preadipocyte differentiation, but Ad-31 had a dichotomous effect in vivo vs. in vitro. It seems possible that an in vitro effect on preadipocytes may be a tool to detect candidate viruses for an adiposity-promoting effect, but in vivo studies will be necessary to determine which of the remaining human adenoviruses are capable of increasing adipose tissue in animals."

 

 

-The prime candidate for the "fat virus" actually reduced serum triglyceride levels in the chickens. Normally an increase in serum triglycerides is associated with obesity. This is also at odds with the other viruses associated with obesity in animals, and in these cases brain damage caused by the viral infection, rather than direct changes in lipid metabolism, is thought to be responsible for the changes in body composition.

A reduction in metabolic rate might explain the increased fat deposition, but the small changes over time would be impossible to detect with current technology. The greater body fat deposition, despite similar body weight, suggests a shift from lean body mass deposition to fat deposition during the growing period of Ad-37-infected chickens. Further research will be necessary to understand the mechanisms of these changes."

 

-The highly incestuous thicket-o-references at the back of the paper was also quite impressive.

 

So they can't rule out simple changes in BMR as a result of viral infection, the "fat-virus" that's responsible for the flabby chickens behaved no differently than the "non-fat" viruses in cell culture, the serum LDL profile in the chicken infected with the "fat-virus" was the opposite of the profile that's normally associated with obesity, and inconsistent with the LDL profile observed in other viral infections associated with obesity, where the changes are thought to be associated with brain-damage, the sample size is microscopic, they suggest nothing in the way of a mechanism, the research hasn't been repeated in an independent facility *and* the guy behind the paper is the sole-owner of a company established to sell a test for these "fat-viruses."

 

What I love best about this little episode is the dichotomy between the evidence in the paper, what gets reported in the press, and what people ultimately believe on the basis of those press reports. "Obesity Caused by Virus!!!!!!!!!!"

 

Interesting hypothesis, might possibly end-up as a footnote in a review of obesity at some point, but the evidence-to-claim and evidence-to-hype ratios are way, way out of line at this point.

 

 

Posted

It's also funny that you are reverting to the "you get all of your knowlegde about science from Rush Limbaugh" business, when I have a BS in Biochem and work in basic research, in virology, and your expertise is in statistics.

 

Reminds me of the economists and statisticians who try to refute reams and reams of actual scientific data on pollution and global warming....

  • 10 months later...
Posted

I thought of Chuck when I heard the bit about this research on the radio today.

 

Somehow I suspect that prolonged starvation will thwart the waistline-inflating ravages of these bacteria.

 

We'll probably discover a gazillion endogenous and exogenous factors - ghrelin, leptin, etc, etc, etc, etc, etc, etc, etc, etc, that cause time-limited micro-permutations in weight and obesity, but the ratio of caloric input to expenditure is always going to be the overwhelming determinant of one's body-composition.

Posted

It sounds like this new thought fits right in there. That these bacteria increase the caloric input for the same amount of food, right?

 

Bottom line though, is that it's not their fault. We all owe obese people lots of sympathy and should help them out with free medical treatment paid for with our insurance premiums and tax dollars.

 

Posted

This paper is actually being published in Nature, so most of the questions that are popping into my head must have been addressed by reviewers. I'll have to read the original at some point, but I'd be amazed if this actually holds up over time as anything more than an exceedingly minor factor relative to energy balance, or has any clinical relevance whatsoever.

 

What's most interesting about this story is not the science, but rapidity with which the population will grasp at any finding which in any way exculpates them from any responsibility whatsoever for their body's composition. Billions of years of evolution and somehow every other organism on the planet with a digestive tract has managed to avoid the cruel scourge of the obesity bacteria. Ditto for all of recorded history except the one period where we've had a sustained agricultural surplus and removed physical toil from the average western person's working life. Ditto for any society where food is still scare of any kind of physical exertion is required to secure sufficient calories to survive.

 

 

 

 

Posted
It sounds like this new thought fits right in there. That these bacteria increase the caloric input for the same amount of food, right?

 

Bottom line though, is that it's not their fault. We all owe obese people lots of sympathy and should help them out with free medical treatment paid for with our insurance premiums and tax dollars.

 

I know this last bit is tongue-in-cheek, but we're already there. The transmogrification of character flaws like addiction, gluttony, and sloth into medical disorders that the population has no more responsibility for or control over than cancer played a significant role in bringing us to this sorry juncture.

 

 

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