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Dean Pomerleau

Does the Obesity Epidemic have a Mysterious Cause?

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All,

 

You may have seen the recent story in the popular press about the possibility of "mysterious" causes of the obesity epidemic with titles like:

 

and:
 
Here is the sensational way the reporter in the first story describes it:
 
According to research, a person with the same diet and exercise habits in the 80s would have a 2.3 point increase in their BMI in 2006 without changing anything at all — simply by existing 30 years in the future. That’s right — existing in our modern environment has contributed to a greater body mass among the population.
 
Wow - that sounds bizarre, scary, and oddly comforting at the same time. Maybe it's not our lifestyle choices that are making us fat, so maybe it's not our fault. I've got to read more! ...
 
They are reporting on a new study [1] that they (and the authors, to some degree) claim shows that over the last 30 years Americans have gotten fatter for reasons other than eating too much food and/or engaging in too little physical activity. The reporters speculate about a range of causes, including:
  • We are more stressed and sleep less.
  • We are exposed to more pesticides and industrial chemicals.
  • Because of our changing diet we have less healthy gut microbiomes.
  • We take more medications associated with weight gain than we used to, such as antidepressants.
  • We increasingly live in climate-controlled worlds that don't require us to burn calories to maintain our body temperature. 

So I decided to look at the actual study to see if it is sound, and what the authors actually said.

 

The paper [1] analyzed the NHANES data from 1971 to 2008, in which every few years researchers went to the homes of about 3000 Americans (men and women) to take measurements (e.g. height and weight) and ask them questions about their diet and lifestyle.  Here is the key table from the paper showing how the various measures changed over the years (note - they are interviewing different people every few years, this isn't a longitudinal study in which they follow the same people over time):

 

post-7043-0-92938200-1444932451_thumb.jpg

 

The first thing they observed is that BMI has gone up about 10% (3 units) in both men and women since the early '70s - the population has obviously gotten fatter. They also observed that self-reported calorie intake has gone up by 10-14% over that same period. So people are eating more, and getting (nearly proportionally) fatter - where is the discrepancy? The authors say that self-reported leisure time physical activity (PA) rose by 47% and 120% in men and women, respectively, over the latter part of the time period (physical activity wasn't recorded prior to 1980 in the NHANES protocol).

 

So, the authors conclude, if people say they are only eating 10-14% more, and are exercising a ton more, their weight shouldn't have gone up by 10%, so something else besides diet and exercise must explain their weight gain. No potential flaws in this logic, no siree ...  :)xyz

 

Seriously. The NHANES data was interviewing different people, using different questioning techniques and different questions over the years. 

 

In NHANES I (1971—1975) and NHANES
II (1976—1980), in-person interviews were used to
obtain self-reported dietary information via a 24-
h dietary recall questionnaire that assessed food
and beverage intake for weekdays only. In NHANES
III (1988—1994), dietary information was obtained
through a self-reported 24-h dietary recall using a
computer-assisted, automated, interactive method
for any day of the week. In NHANES 1999—2002, a
multiple-pass computer-assisted dietary interview
format was used to collect detailed self-reported
information about all foods and beverages that
were consumed the day prior to the in-person interview
(weekday or weekend). In NHANES 2003—2008,
24-h self-reported dietary recalls were performed
twice (3—10 days apart) using an automated multiple
pass method.
 
Right off the bat, people may have been more reluctant fudge the numbers on what / how much they ate during the face-to-face in-person interviews from 1971-1980, relative to the impersonal computer-based data collection used after 1980, which could easily have resulted in subjects underestimating calorie intake during the later years.
 
Plus, it's well known that self-reported diet recall is a crappy source of information about what people actually eat. More importantly, the heavier people are, the more likely they are to underreport how much they eat, and overreport how much physical activity they engage in. So as people got fatter over the years, the "mystery" of why they are gaining weight when not eating that much more, while exercising a lot more, may simply be that they lie more about their eating and exercise habits as they get fatter.
 
In fact, the authors suggest this effect as the first possible explanation for their findings:
 
Whether self-reported dietary intake accurately
reflects an individual’s true dietary intake has been
questioned [34]. Indeed, doubly-labelled water
studies typically show that individuals underreport
their energy intake, and that the magnitude of the
underreporting may be larger in people who are
obese [35].
 
<snip>
 
This finding is in line with those of several other studies
in which individuals with obesity reported consuming
similar or fewer daily calories than those who
are normal weight [7,11]. While this has frequently
been attributed to underreporting [19,20], several
additional possible explanations must be considered...

 

The authors then go on to speculate about a few of the 'mystery' causes of weight gain mentioned in the popular reports and listed above.

 

This seem to me to be a clear case of the authors of the study, and especially the reporters writing about the study, downplaying the most likely explanations (i.e. under/over reporting of diet and exercise by the obese, changes in protocol skewing results) in favor of speculative explanations that appeal to people's desire to avoid personal responsibility for their weight gain, e.g. "it isn't your fault - you've gained weight because of the mysterious obesity-promoting chemicals in our food or environment these days". 

 

To be fair, the second (CNN) article linked above does acknowledge at the end the possibility that the explanation could be a mundane combination of misremembering and/or intentional underreporting. But it nonetheless stresses the significance of mysterious causes, likely to gain more eyeballs for their story. Pretty sad...

 

Note: I'm not saying (definitively) that these other possible factors haven't contributed at all to the recent dramatic weight gain among the American population. All I'm saying is that this study provides extremely weak evidence to support such speculations, and that the mundane explanation of a positive energy balance due to eating too much and exercising too little is likely the cause of the vast majority of the observed weight gain.

 

--Dean

 

----------

[1] Obes Res Clin Pract. 2015 Sep 14. pii: S1871-403X(15)00121-0. doi:

10.1016/j.orcp.2015.08.007. [Epub ahead of print]

Secular differences in the association between caloric intake, macronutrient
intake, and physical activity with obesity.

Brown RE(1), Sharma AM(2), Ardern CI(1), Mirdamadi P(1), Mirdamadi P(1), Kuk
JL(3).

Full Text: http://www.obesityresearchclinicalpractice.com/article/S1871-403X(15)00121-0/pdf

BACKGROUND: To determine whether the relationship between caloric intake,
macronutrient intake, and physical activity with obesity has changed over time.
METHODS: Dietary data from 36,377 U.S. adults from the National Health and
Nutrition Survey (NHANES) between 1971 and 2008 was used. Physical activity
frequency data was only available in 14,419 adults between 1988 and 2006.
Generalised linear models were used to examine if the association between total
caloric intake, percent dietary macronutrient intake and physical activity with
body mass index (BMI) was different over time.
RESULTS: Between 1971 and 2008, BMI, total caloric intake and carbohydrate intake
increased 10-14%, and fat and protein intake decreased 5-9%. Between 1988 and
2006, frequency of leisure time physical activity increased 47-120%. However, for
a given amount of caloric intake, macronutrient intake or leisure time physical
activity, the predicted BMI was up to 2.3kg/m(2) higher in 2006 that in 1988 in
the mutually adjusted model (P<0.05).
CONCLUSIONS: Factors other than diet and physical activity may be contributing to
the increase in BMI over time. Further research is necessary to identify these
factors and to determine the mechanisms through which they affect body weight.

PMID: 26383959

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I agree, Dean. I am old enough to remember what we ate and how large the portions were. All the snack foods and prepared foods were just not available. People do exercise more now, but the calorie intake more than offsets that. Restaurant portions are huge now compared to then.  Those little children's hamburgers at McDonalds were the only hamburgers they sold when I was 10.  Sure, my Dad ate 2, but that is still tiny compared to the mega-burgers people eat now.  

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I agree, Dean. I am old enough to remember what we ate and how large the portions were. All the snack foods and prepared foods were just not available. People do exercise more now, but the calorie intake more than offsets that. Restaurant portions are huge now compared to then.  Those little children's hamburgers at McDonalds were the only hamburgers they sold when I was 10.  Sure, my Dad ate 2, but that is still tiny compared to the mega-burgers people eat now.  

 

Very good points Mary,

 

Relatively recent increases in portion size and the widespread availability of snack foods (e.g. via vending machines) are likely sources of increased calorie intake that could easily be overlooked / underestimated during dietary recall in the more recent years of NHANES data, thereby explaining a big part of the 'mystery'.

 

--Dean

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Also bear in mind that the contribution of exercise to weight control is tiny compared with the influence of added calories.  So tiny that in the vast majority of cases it can almost be ignored.

 

Obviously the effect of exercise varies with type, intensity, duration and the body weight being carried around doing it.  But the rule of thumb I have seen is that to burn off one pound of fat you need to walk at 4 mph for 50 or more miles.  Of course most obese people would have difficulty walking faster than 2.5 mph, and USUALLY* could not keep it up for more than ten minutes.  I admire anyone with the fortitude to willingly walk the 50 miles rather than go without 3500 calories. 

 

*  One exception is that when I was walking back up the Grand Canyon, two people, one of them with a BMI of ~35, passed me in the opposite direction jogging down, and much later passed me again, still jogging on the way up!  Astonishing. 

 

And regarding Mary's comment about portion sizes, someone made a study of dinner plates and found they have increased in size dramatically since the 1920s!  I can hardly imagine a better indicator.  How many people do not fill the entire plate, no matter the size of it?

 

Rodney.

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I think there is a lot of merit to those two articles you linked to, even if the actual mechanisms of some of those factors aren't made clear. Most of those things such as sleep, stress, food environment, processed food, etc. all play a role in appetite regulation. Sure, people get fatter because they eat more food, but the next logical question is 'why' they are eating more food.

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Good job, Dean. Even without looking at the abstract, I realized from the press reports that simply comparing two or more cohorts' self-reported energy and activity levels in such different cultural contexts over the span of four decades was going to be fraught; the fact (as you dig into it) that they're using separate cohorts from NHANES, and with different instruments for collecting the data, and your very reasonable hypothesis that since we know that overweight and obese people disproportionately underrreport energy intake, their data may be systematically distorted by greater underreporting on a population basis in later cohorts as the prevalence of overweight and obesity has risen.
 
I would add two things. First, along the lines that you've already suggested, I'll put forward the hypothesis that another secular trend may similarly have led to greater underreporting in later cohorts: the trend to increased snacking and between-meal eating. This is a well-documented sociological phenomenon, and studies show (PMIDs 7580640, 9578234, 12638596, and the full text of 21123466) that snack foods are disproportionately underreported, in part because they are less "socially approved" foods and in part because it's easier to forget a snack than a meal, even if your snack is a freakin' 775 Calorie Frappuchino. As the population has moved to consume more and more of their Calories between meals, more and more of their energy intake may have gone unreported.
 
Second, however, and along lines suggested by James, those same decades have seen some changes in Americans' environments and lifestyles other than our collective energy intake and our conscious, volitional energy expenditure that there is good reason to think may also have contributed to the obesity epidemic, by reducing non-volitional, unconscious energy expenditure and shifting fuel partitioning into fat storage. As summarized in this press release, for example:

  • Less sleep can cause increased body weight;
     
  • Endocrine disruptors, including DDT and PCBs can increase body fat;
     
  • Keeping ones home or office at one temperature year around promotes body fat;
     
  • Smoking cessation increases weight because nicotine has both thermogenic and appetite suppressant effects;
     
  • Certain pharmaceuticals, including antipsychotics, antidepressants, contraceptives and antihistamines increase weight;
     
  • Some age and ethnic groups that have a higher prevalence of obesity than others have increased as a proportion of the population;
     
  • Greater maternal age may increases risk of offspring obesity;
     
  • Obesity may perpetuate its own increase through a fetally-driven positive feedback loop;
     
  • Obesity has a genetic component and individuals with genetic predisposition toward obesity may be reproducing at a higher rate; and
     
  • The probability that two individuals will mate is related to how similar their body types in adiposity and this can increase the number of offspring with high levels of adiposity.

... and we know that all of these things have increased over the last several decades in the United States and other countries that are now struggling with the obesity epidemic.
 
The above points are taken from (1) below, which is very provocative reading; the same authors subsequently followed up with (2), which covers and updates the evidence base on those same "mysterious causes," while adding another possible contributor (certain persistent viral infections — seriously!), and is available free in full text.
 
References
1: McAllister EJ, Dhurandhar NV, Keith SW, Aronne LJ, Barger J, Baskin M, Benca RM, Biggio J, Boggiano MM, Eisenmann JC, Elobeid M, Fontaine KR, Gluckman P, Hanlon EC, Katzmarzyk P, Pietrobelli A, Redden DT, Ruden DM, Wang C, Waterland RA, Wright SM, Allison DB. Ten Putative Contributors to the Obesity Epidemic.  Crit Rev Food Sci Nutr. 2009 Nov;49(10):868-913. doi: 10.1080/10408390903372599. Review. PubMed PMID: 19960394; PubMed Central PMCID: PMC2932668.

http://www.tandfonline.com/doi/full/10.1080/10408390903372599

(System won't let me post a "live" link to this perfectly respectable academic publishing website: copy-paste into your browser).
 
2: Keith SW, Redden DT, Katzmarzyk PT, Boggiano MM, Hanlon EC, Benca RM, Ruden D, Pietrobelli A, Barger JL, Fontaine KR, Wang C, Aronne LJ, Wright SM, Baskin M, Dhurandhar NV, Lijoi MC, Grilo CM, DeLuca M, Westfall AO, Allison DB. Putative contributors to the secular increase in obesity: exploring the roads less traveled. Int J Obes (Lond). 2006 Nov;30(11):1585-94. Epub 2006 Jun 27. Review. PubMed PMID: 16801930.

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The Carb-Sane Asylum recently made a blog post titled "The Problem with NHANES Dietary Data" with an interesting table showing NHANES overweight/obesity and dietary data:

http://carbsanity.blogspot.com.au/2015/10/the-problem-with-nhanes-dietary-data.html

 

 

Also, a poster at Carb-Sane Asylum pointed out this:

 

1. PLoS One. 2013 Oct 9;8(10):e76632. doi: 10.1371/journal.pone.0076632. eCollection

2013.

 

Validity of U.S. nutritional surveillance:National Health and Nutrition

Examination Survey caloric energy intake data, 1971-2010.

 

Archer E(1), Hand GA, Blair SN.

 

Author information:

(1)Department of Exercise Science, Arnold School of Public Health, University of

South Carolina, Columbia, South Carolina, United States of America.

 

Comment in

Adv Nutr. 2015 Mar;6(2):230-3.

Adv Nutr. 2015 Mar;6(2):229-30.

 

IMPORTANCE: Methodological limitations compromise the validity of U.S.

nutritional surveillance data and the empirical foundation for formulating

dietary guidelines and public health policies.

 

OBJECTIVES: Evaluate the validity of the National Health and Nutrition

Examination Survey (NHANES) caloric intake data throughout its history, and

examine trends in the validity of caloric intake estimates as the NHANES dietary

measurement protocols evolved.

 

DESIGN: Validity of data from 28,993 men and 34,369 women, aged 20 to 74 years

from NHANES I (1971-1974) through NHANES 2009-2010 was assessed by: calculating

physiologically credible energy intake values as the ratio of reported energy

intake (rEI) to estimated basal metabolic rate (BMR), and subtracting estimated

total energy expenditure (TEE) from NHANES rEI to create 'disparity values'.

 

MAIN OUTCOME MEASURES: 1) Physiologically credible values expressed as the ratio

rEI/BMR and 2) disparity values (rEI-TEE).

RESULTS: The historical rEI/BMR values for men and women were 1.31 and 1.19, (95%

CI: 1.30-1.32 and 1.18-1.20), respectively. The historical disparity values for

men and women were -281 and -365 kilocalorie-per-day, (95% CI: -299, -264 and

-378, -351), respectively. These results are indicative of significant

under-reporting. The greatest mean disparity values were -716 kcal/day and -856

kcal/day for obese (i.e., ≥30 kg/m2) men and women, respectively.

 

CONCLUSIONS: Across the 39-year history of the NHANES, EI data on the majority of

respondents (67.3% of women and 58.7% of men) were not physiologically plausible.

Improvements in measurement protocols after NHANES II led to small decreases in

underreporting, artifactual increases in rEI, but only trivial increases in

validity in subsequent surveys. The confluence of these results and other

methodological limitations suggest that the ability to estimate population trends

in caloric intake and generate empirically supported public policy relevant to

diet-health relationships from U.S. nutritional surveillance is extremely

limited.

 

PMCID: PMC3793920

PMID: 24130784 [PubMed - indexed for MEDLINE]

 

http://www.ncbi.nlm.nih.gov/pubmed/24130784

Edited by Brett Black

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There are two other factors that seem obvious but I did not see mentioned:

 

One is that food costs as a percentage of income have fallen in the US from 18% to 10% in the past 50 years. http://www.ers.usda.gov/data-products/ag-and-food-statistics-charting-the-essentials/food-prices-and-spending.aspxas income per person has been rising.   So it has been getting easier and easier to be able to afford to buy more food.   People who previously had simply been unable to afford to buy plenty of food now can.   And do.

 

Second, there have been considerable advances in food tastiness 'science' making it tempting to eat more, and more often, than previously.  And in addition there has been a profusion of enticing, tasty - and usually unhealthy - foods available in grocery stores.

 

Intuitively, I suspect these two causes may account for the majority of the increase in per capita caloric intake.

 

Rodney.

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And here is yet another cause:  I have no doubt that the recognition by restaurants of the implications for their businesses of the economic principle economists call "marginal profitability" has had substantial effects on the amount of food people eat at restaurants.  Here is how it works.

 

All businesses have some costs that are fixed no matter how many customers they have (rent in the case of a restaurant, for example.)  while other costs are variable in direct proportion to the number of customers served (of which the amount of raw food the restaurant has to purchase is the most obvious example).  Other costs are part fixed and part variable (labor being by far the largest)..

 

This means that having just a few extra customers will make a substantial difference to profits because it causes the restaurateur to incur only the additional variable costs.  So attracting just a few extra customers each day will result in a substantial improvement in profits.

 

It has another effect.  Let's say fixed costs are 20% of total costs and that the cost of additional raw food purchased is 20% of total costs.  Now suppose the restaurateur decides to DOUBLE (for sake of example) the size of the portions and raise his prices by 20% to cover the entire costs of the extra raw food he has to buy.  What would happen to his total costs and his number of customers?  The answer is:

 

His costs on the meal are increased by the cost of the additional food he must purchase, which is only a rather small percentage of his total costs, so he will have to raise his prices only a little.  BUT THIS STRATEGY IMPRESSES THE HELL OUT OF HIS CUSTOMERS who see, compared with the competition, hugely generous portions at only a somewhat increased price.  When the customer sees twice as much food at a price only 20% higher, AEE of course, he will frequent this restaurant in preference to others who serve the smaller portions.

 

Then, with the larger number of customers he can take advantage of 'economies of scale'.  The restaurant is full every night and, as mentioned earlier above, he can spread his fixed costs over a much larger number of meals.  His profits are thereby greatly improved and his competition, serving smaller portion sizes, eventually has so few customers they cannot make a profit.  Survivial of the fittest in a situation like this means survival of the restaurants serving larger portions, and the disappearance of the others in a form of natural selection, in this case with the customers being the selectors.

 

[Of course, while I take the example of *doubling* portions, that is merely illustrative.  A serious restaurateur might experiment with diffferent degrees of 'generosity' to find what amount most impresses his customers without weighing them down with ridiculously large amounts of food.] 

 

The point is that there is a huge incentive for restaurants to serve larger portions than their competitors.   Serving demonstrably larger portions at only a comparatively small increase in price (which can easily be done because the additional cost of food is rather small) will attract customers away from competitors and either put them out of business or force them to follow suit.

 

I rather doubt it is necessary to enlist the support of any of the ten factors listed in Michale R's post of Yesterday 12:46 pm, to account for the increasing rate of obesity.  The three I have highlighted in this post and my previous post above, might very easily account for the entire effect, imo.

 

Rodney.

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There are, of course, hundreds or thousands of factors that could be cited as contributors to the recent obesity epidemic, depending on what kind of cause you look at (mechanistic, policy, economic, sociologic, etc) and at what level you look at them. The question posed in this thread — and suggested by the prima facie reading of the abstract of PMID: 26383959, which triggered the thread — is "Does the Obesity Epidemic have a Mysterious Cause?" — that is, a cause other than those affecting food intake or volitional energy expenditure. We had popular press stories saying that "A study published recently in the journal Obesity Research & Clinical Practice found that it’s harder for adults today to maintain the same weight as those 20 to 30 years ago did, even at the same levels of food intake and exercise [emphasis mine]".
 
Explanations like the falling relative cost of food, the food industry making processed and restaurant foods tastier, and economic and other incentives driving a rise in portion sizes has doubtless had a significant role in driving the obesity epidemic, but they all go through a non-mysterious cause, operating as they do through leading people to eat more food. The issue, again, was that PMID: 26383959 claimed to find that people have not been eating more during that time period — a conclusion that, as Dean has shown, rests on very shaky premises (as does the also-reported huge increase in exercise: indeed, others have reported huge decreases in exercise (self-selected and especially occupational) over that same period).
 
Most of the potential contributors to the obesity epidemic explored in PMID: 19960394 are of the latter sort; Rodney, and others, let's please restrict this thread to those and other "mysterious" causes.

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A new study [1] out this week, discussed in the popular press here, lends support to a "mysterious" cause of obesity that hasn't been explicitly mentioned (as far as I've seen) in covering this story - overprescription of antibiotics, which can (among other things), mess up the gut microbiome (which has been mentioned) and lead to obesity - via alteration in nutrient absorption and perhaps even changes in hunger and food preferences.

 

Kids who had received seven or more courses of antibiotics during childhood were on average about 3 lbs heavier by age 15.

 

"While the magnitude of the weight increase attributable to antibiotics may be modest by the end of childhood, our finding that the effects are cumulative raises the possibility that these effects continue and are compounded into adulthood," [lead researcher Brian] Schwartz said in the release.

 

In a weird serendipity - two minutes after I posted this message, I got an email pointer to a free pdf ebook from the folks at uBiome entitled 7 Science Secrets About Bacteria and Weight Loss (shared with permission).

 

Here are the sections from the ebook (note the relevance of section 3 to the subject of this post):

 

0. Why bacteria and weight loss? 3
1. Overweight people have less bacterial variety 4
2. Eat beans to get bacteria like a skinny person 5
3. Meat that contains antibiotics can lead to weight gain 6
4. Cut your risk of Type 2 diabetes by boosting bacterial diversity 7
5. Fool your brain into believing you’re not hungry 8
6. Taking fiber supplements can work as well as fiber from food 9
7. Stop your bacteria from eating into your gut lining 10
8. Pulling it all together 11

 

Here is one of the most interesting passages from section 3, related to the topic of this post:

 

In a study at the New York University School of Medicine, researchers injected mice with a “subtherapeutic antibiotic treatment” (antibiotics at a level low enough to have no health benefits) containing the same low dose of antibiotics that humans often unknowingly consume in animal meat [NB - this includes farm-raised fish, esp. salmon - DP]. Over time the result was that these mice became fat, despite eating the same amount of calories as mice in a control group.

 

As the last sentence makes clear, antibiotics would definitely qualify as a "mysterious" cause of obesity by Michael Rae's definition. I believe [2] is the mice study the researchers are referring to.

 

The ebook looks like worthwhile reading!

 

--Dean

 

-----------

[1] International Journal of Obesity accepted article preview 21 October 2015; doi: 10.1038/ijo.2015.218

 

Antibiotic use and childhood body mass index trajectory

 
B S Schwartz1,2,3,4, J Pollak1, L Bailey-Davis4, A G Hirsch4, S E Cosgrove3, C Nau5, A M Kress2, T A Glass2 and K Bandeen-Roche6
 
Abstract
 
Background/Objectives: Antibiotics are commonly prescribed for children. Use of antibiotics early in life has been linked to weight gain but there are no large-scale, population-based, longitudinal studies of the full age range among mainly healthy children.
 
Subjects/Methods: We used electronic health record data on 163 820 children aged 3–18 years and mixed effects linear regression to model associations of antibiotic orders with growth curve trajectories of annual body mass index (BMI) controlling for confounders. Models evaluated three kinds of antibiotic associations – reversible (time-varying indicator for an order in year before each BMI), persistent (time-varying cumulative orders up to BMIj), and progressive (cumulative orders up to prior BMI [bMIj-1])—and whether these varied by age.
 
Results:  Among 142 824 children under care in the prior year, a reversible association was observed and this short-term BMI gain was modified by age (P<0.001); effect size peaked in mid-teen years. A persistent association was observed and this association was stronger with increasing age (P<0.001). The addition of the progressive association among children with at least three BMIs (n=79 752) revealed that higher cumulative orders were associated with progressive weight gain; this did not vary by age. Among children with an antibiotic order in the prior year and at least seven lifetime orders, antibiotics (all classes combined) were associated with an average weight gain of approximately 1.4 kg at age 15 years. When antibiotic classes were evaluated separately, the largest weight gain at 15 years was associated with macrolide use.
 
Conclusions: We found evidence of reversible, persistent, and progressive effects of antibiotic use on BMI trajectories, with different effects by age, among mainly healthy children. The results suggest that antibiotic use may influence weight gain throughout childhood and not just during the earliest years as has been the primary focus of most prior studies.
 
------------
[2] Nature. 2012 Aug 30;488(7413):621-6. doi: 10.1038/nature11400.

Antibiotics in early life alter the murine colonic microbiome and adiposity.

Cho I(1), Yamanishi S, Cox L, Methé BA, Zavadil J, Li K, Gao Z, Mahana D, Raju K,
Teitler I, Li H, Alekseyenko AV, Blaser MJ.

Author information:
(1)Department of Medicine, New York University School of Medicine, New York, New
York 10016, USA.

Comment in
Nat Rev Gastroenterol Hepatol. 2012 Nov;9(11):615.
Cell Metab. 2012 Oct 3;16(4):408-10.
Nat Rev Endocrinol. 2012 Nov;8(11):623.
Nature. 2012 Aug 30;488(7413):601-2.

Antibiotics administered in low doses have been widely used as growth promoters
in the agricultural industry since the 1950s, yet the mechanisms for this effect
are unclear. Because antimicrobial agents of different classes and varying
activity are effective across several vertebrate species, we proposed that such
subtherapeutic administration alters the population structure of the gut
microbiome as well as its metabolic capabilities. We generated a model of
adiposity by giving subtherapeutic antibiotic therapy to young mice and evaluated
changes in the composition and capabilities of the gut microbiome. Administration
of subtherapeutic antibiotic therapy increased adiposity in young mice and
increased hormone levels related to metabolism. We observed substantial taxonomic
changes in the microbiome, changes in copies of key genes involved in the
metabolism of carbohydrates to short-chain fatty acids, increases in colonic
short-chain fatty acid levels, and alterations in the regulation of hepatic
metabolism of lipids and cholesterol. In this model, we demonstrate the
alteration of early-life murine metabolic homeostasis through antibiotic
manipulation.

PMCID: PMC3553221
PMID: 22914093

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In a study at the New York University School of Medicine, researchers injected mice with a “subtherapeutic antibiotic treatment” (antibiotics at a level low enough to have no health benefits) containing the same low dose of antibiotics that humans often unknowingly consume in animal meat [NB - this includes farm-raised fish, esp. salmon - DP]. Over time the result was that these mice became fat, despite eating the same amount of calories as mice in a control group.

 

--Dean

 

-----------

[

PMID: 22914093

 

Hi Dean!

 

thanks for the interesting post!

 

I think I must note, however, that not all farm raised salmon are equal:  E.g., my local supermarket (the flagship Wegman's) claims otherwise for their farm raised salmon (which comes from Canada, Scotland and Norway).

 

That said, I much prefer wild sockeye salmon in my sashimi.

 

:)xyz

 

  -- Saul

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I'm sure you all know not to consume farmed salmon from the northeast Atlantic because of the dioxin and related pollutants, right?

 

PCBS IN FARMED SALMON

Test results show high levels of contamination

 

Much more here:

 

https://www.google.com/webhp?q=farmed+salmon+dioxin

 

"Faroe Islands even?? But they're so far north, 'n pure, 'n Scandinavian and hip 'n stuff!!" Nope.

 

Zeta

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I'm sure you all know not to consume farmed salmon from the northeast Atlantic because of the dioxin and related pollutants, right?

 

Agreed Zeta.

 

Saul may be confident his salmon is pristine, but personally I'd be a bit more cautious if I were a fish-eater. Here is another reason to be nervous about salmon - it appears not so easy to avoid farm-raised northeast Atlantic salmon due to mislabeling, according to a new study (pdf) by Oceana.org, reported on here.

 

Here are highlights:

 

Overall, 43 percent of the salmon tested were mislabeled. The most common form of mislabeling occurred when farmed Atlantic salmon was sold as “wild” salmon [69% of salmon labelled 'wild' was actually Atlantic farmed salmon! See graph below - DP]. One fish labeled as wild salmon was actually rainbow trout.
 
The problem was the worst in restaurants, where “diners were three times more likely to be misled than shoppers in grocery stores,” said Oceana. Sixty-seven percent of restaurant samples were mislabeled, compared to 20 percent of grocery store samples.
 
Here is a handy graph of salmon substitutions:
 
post-7043-0-91046500-1446586446_thumb.jpg
 
As you can see, the most common 'bait and switch' was the mislabeling of farm-raised Atlantic salmon "wild" or some other types of salmon.
 
--Dean

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[Note: This is a cross post from the Air pollution avoidance thread, since it seems at least as relevant to the topic here as there. -Dean]

 

In the midst of the worst bout of smog on record in Bejing, comes this article on what could be another "mysterious" source of obesity - air pollution. It discusses out some the evidence supporting a link between air pollution and obesity & type II diabetes. To quote from the article:

 

[Researchers] examined the medical records of 62,000 people in Ontario, Canada over a 14-year period. He found that the risk of developing diabetes rose by about 11% for every 10 micrograms of fine particles in a cubic metre of air – a troubling statistic, considering that the pollution in some Asian cities can reach at least 500 micrograms per cubic metre of air. 

 

...

 

Controlling for other factors (such as wealth and diet), the children born in the most polluted areas were 2.3 times more likely to be considered obese, compared to those living in cleaner neighbourhoods.

 

The researchers suggest that air pollution may cause and inflammatory response beginning the lungs, but spreading to become systemic, which in turn impairs insulin sensitivity and causes fat to accumulate in fat cells:

 

Not only does that [inflammation] interfere with the tissue’s ability to respond to insulin; the subsequent inflammation may also interfere with the hormones and the brain processing that govern our appetite, says Michael Jerrett at the University of California, Berkeley.
 
All of which knocks the body’s energy balance off-kilter, leading to a constellation of metabolic disorders, including diabetes and obesity, and cardiovascular problems such as hypertension.

 

I'm fortunate to live in a quite rural area, but for those who are exposed to high levels of particulate matter in the air, it might be worth doing something about it - wearing a mask, getting an air filter, or moving! See this thread on avoiding air pollution for discussion.

 

--Dean

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Hi Zeta:

 

Regarding your:

 

I'm sure you all know not to consume farmed salmon from the northeast Atlantic because of the dioxin and related pollutants, right?

 

PCBS IN FARMED SALMON

Test results show high levels of contamination

 

Much more here:

 

https://www.google.com/webhp?q=farmed+salmon+dioxin

 

"Faroe Islands even?? But they're so far north, 'n pure, 'n Scandinavian and hip 'n stuff!!" Nope.

 

Zeta

 

I am afraid the people who call themselves "The Environmental Working Group" are near the top of my list of 'Non-profits' largely organized to lobby, misinform and generate publicity in order to raise funds they can then pay to themselves to earn a nice living.  I mentioned this 'non-profit' issue a few days ago in a different thread.

 

At the time that report you linked was published (quite a few years ago now) I wrote to them pointing out that (you will note they were careful to avoid mentioning any hard numbers in their releases) the levels of contaminants in the case they were talking about was not just parts per million, it was not even parts per billion, but several PARTS PER TRILLION.

 

I then asked them whether, given all toxicologists agree that "the dose makes the poison", they would please provide serious references giving reason to believe that such nanoscopically minute levels might reasonably be expected to cause harm. 

 

Of course, they never replied:  A typical non-response from people knowing they had been caught with their pants down.  And I posted about it at another health website at the time.

 

I would not trust ANYTHING coming out of the mouths of these people.

 

I do eat salmon from time to time and farmed salmon occasionally.  No one has yet given me any reason I could take seriously that it would be better avoided.

 

.......  but as usual, we each make our own decisions.

 

Rodney.

 

==============

 

"The unverified conventional wisdom is almost invariably mistaken."  (And yes, I believe the PCB contamination issue in salmon is a very classic case of this.)

Edited by nicholson

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Rodney,

 

I do eat salmon from time to time and farmed salmon occasionally.  No one has yet given me any reason I could take seriously that it would be better avoided.

 

Did the evidence and studies presented in these two videos from Dr. Greger about the association of pollution in farm raised salmon and diabetes not give you pause?

 

I am afraid the people who call themselves "The Environmental Working Group" are near the top of my list of 'Non-profits' largely organized to lobby, misinform and generate publicity in order to raise funds they can then pay to themselves to earn a nice living.

 

It may be confirmation bias, but I too am kinda skeptical of the EWG's "Dirty Dozen" and "Clean Fifteen" ranking of the most and least polluted fruits & vegetables. This Lifehacker article does a pretty good job debunking the EWG's lists, and their advocacy of organic over conventional due to the issue of pesticides. The article cites this study [1], which found that only one of 120 samples of the 12 foods on the "dirty dozen" list (sampled 10 times each from different sources), contained greater than 1% of the established "Chronic Reference Dose" (RfD) for pesticides, which is level below which the EPA considers the exposure not to be harmful. Less than 6% of the samples exceeded 0.1% of the RfD.

 

Three quarters of the pesticide/commodity combinations demonstrated exposure
estimates below 0.01% of the RfD (corresponding to exposures one million times
below chronic No Observable Adverse Effect Levels from animal toxicology
studies), and 40.8% had exposure estimates below 0.001% of the RfD.

 

The article also points out the organic produce is not pesticide free. In fact, organic farmers sometimes use large amounts of (organic) pesticides that aren't necessarily any less harmful to human health than synthetic pesticides, and which are not nearly as carefully regulated.

 

Lifehacker's advice? Eat more fruits and veggies from whatever source. If you're concerned about pesticides, buy from local farmers whose pesticide practices you can inquire directly about, or better yet, grow your own produce.

 

--------------

[1] J Toxicol. 2011;2011:589674. doi: 10.1155/2011/589674. Epub 2011 May 15.


Dietary exposure to pesticide residues from commodities alleged to contain the
highest contamination levels.

Winter CK(1), Katz JM.

Author information:
(1)Department of Food Science and Technology, University of California, One
Shields Avenue, Davis, CA 95616, USA.

Probabilistic techniques were used to characterize dietary exposure of consumers
to pesticides found in twelve commodities implicated as having the greatest
potential for pesticide residue contamination by a United States-based
environmental advocacy group. Estimates of exposures were derived for the ten
most frequently detected pesticide residues on each of the twelve commodities
based upon residue findings from the United States Department of Agriculture's
Pesticide Data Program. All pesticide exposure estimates were well below
established chronic reference doses (RfDs). Only one of the 120 exposure
estimates exceeded 1% of the RfD (methamidophos on bell peppers at 2% of the
RfD), and only seven exposure estimates (5.8 percent) exceeded 0.1% of the RfD.
Three quarters of the pesticide/commodity combinations demonstrated exposure
estimates below 0.01% of the RfD (corresponding to exposures one million times
below chronic No Observable Adverse Effect Levels from animal toxicology
studies), and 40.8% had exposure estimates below 0.001% of the RfD. It is
concluded that (1) exposures to the most commonly detected pesticides on the
twelve commodities pose negligible risks to consumers, (2) substitution of
organic forms of the twelve commodities for conventional forms does not result in
any appreciable reduction of consumer risks, and (3) the methodology used by the
environmental advocacy group to rank commodities with respect to pesticide risks
lacks scientific credibility.

PMCID: PMC3135239
PMID: 21776262 [PubMed]

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Smoking and Obesity

 

Smoking was mentioned in the list Michael quoted in this post above as one of the possible "mysterious" causes of the obesity epidemic, but smoking cessation probably hasn't received enough attention, either in this thread, or in society in general, as a possible cause of why people are getting fatter.

 

Here is a good popular press article on the topic. On average smoking is down ~66% from it's peak in the 1960s, when nearly half the population lit up regularly. Overall that has been a tremendous boon to our health, preventing literally millions of cases of lung cancer and cardiovascular disease in the past 45 years. But nicotine is both thermogenic and an appetite suppressant - so quitting, or simply never starting, is associated with weight gain. Plus the craving for a cigarette is often satisfied with food when someone is trying to quit smoking, exacerbating the problem of weight gain. 

 

So it's likely that the trend towards people quitting smoking, and never starting, is responsible for at least some fraction of the tremendous increase in overweight/obesity we've seen in the US over the last 40 years. I was actually a bit surprised how low the estimated impact of smoking cessation was on obesity in the US. According to the researcher interviewed:

 

"The decline in the prevalence of cigarette smoking didn't have a large effect, comparatively speaking, but it had an effect,” said Baum. “It can explain about as much as 4 percent of the increase in obesity, according to our estimates.”

 

The fact that many fewer people are smoking today than in the 1970s, and concomitantly suffering from less cancer and cardiovascular disease, could explain, at least in part, the paradoxical dramatic increase in the healthiest BMI that has apparently occurred in the last 40 years - from an optimal BMI of 18 in the mid-70s to an optimal BMI of nearly 26 in the most recent cohort, as discussed here. Basically the idea is that without the ill effects of smoking on cancer and cardiovascular health, and with better medicine for treating these main killers (i.e. statins, metformin, stents, etc.) people can get away with being chubbier today while still avoiding cancer and lung disease. In other words, it doesn't pay as many dividends as it once did to be healthy-thin1

 

--Dean

 

1as opposed to unhealthy-thin due to smoking, poor diet and/or latent cancer - which isn't good for you and never will be!

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All,

 

In this post above, Michael mentions in passing the possibility that infections with certain viruses could be another possible mysterious cause of obesity, citing [1] but not going into any details himself. I presume Michael is referring to this statement from the free full text of [1]:

 

Other factors potentially involved in the [obesity] epidemic with varying degrees of evidential support include an epidemic of adenovirus-36 [2]...

 

It looks like great minds think alike, but in this case, Dr. Greger beat Michael to it ☺. Today Dr. Greger had a blog post highlighting his 2014 video (embedded below), titled Infectobesity: Adenovirus 36 and Childhood Obesity. In it he discusses the paradoxical association between chicken consumption and obesity. Long thought to be healthier than beef or "the other white meat" (pork), chicken turns out to be the meat most associated with weight gain and obesity - 40% more obesogenic than beef. Some blame it on the ever-increasing level of fat in the muscle tissue of chickens grown from an egg to the slaughterhouse in only 42 days. But researchers have long thought this couldn't be the whole explanation.

 

They now suspect it may have to do with infection with adenovirus-36 (Ad-36), which is common in chickens and which 1 out of 5 obese people is infected with as well. Other suggestive evidence comes from the fact that obese kids have an Ad-36 infection rate of 28%, while only 10% of non-obese kids are infected. While there haven't been (and won't be) randomized intervention trials in people to prove causality, longitudinal studies show that adults infected with Ad-36 gain more weight over a 10-year period than people who aren't infected. And in a petri dish, fat cells infected with Ad-36 absorb more fat and grow larger. 

 

So while there is no smoking gun that Ad-36 causes weight gain in humans, nor as far as I can tell is there direct evidence that you can get it by eating infected chicken (or how thoroughly you have to cook chicken to be sure you've killed the virus), the evidence is suggestive that chicken may not be the healthy white meat it was once thought to be. This seems like yet another example of a flip-flop in nutritional science that people complain (and satirize) so much about. But in my book, you can't go wrong eating a diet consisting of the core healthy foods that Sthira outlined today in this post - all of them vegan...

 

--Dean

 

 

-----------

[1] Int J Obes (Lond). 2006 Nov;30(11):1585-94. Epub 2006 Jun 27.

 
Putative contributors to the secular increase in obesity: exploring the roads
less traveled.
 
Keith SW(1), Redden DT, Katzmarzyk PT, Boggiano MM, Hanlon EC, Benca RM, Ruden D,
Pietrobelli A, Barger JL, Fontaine KR, Wang C, Aronne LJ, Wright SM, Baskin M,
Dhurandhar NV, Lijoi MC, Grilo CM, DeLuca M, Westfall AO, Allison DB.
 
Author information: 
(1)Section on Statistical Genetics, University of Alabama at Birmingham,
Birmingham, AL 35294-0022, USA.
 
 
OBJECTIVE: To investigate plausible contributors to the obesity epidemic beyond
the two most commonly suggested factors, reduced physical activity and food
marketing practices.
DESIGN: A narrative review of data and published materials that provide evidence 
of the role of additional putative factors in contributing to the increasing
prevalence of obesity.
DATA: Information was drawn from ecological and epidemiological studies of
humans, animal studies and studies addressing physiological mechanisms, when
available.
RESULTS: For at least 10 putative additional explanations for the increased
prevalence of obesity over the recent decades, we found supportive (although not 
conclusive) evidence that in many cases is as compelling as the evidence for more
commonly discussed putative explanations.
CONCLUSION: Undue attention has been devoted to reduced physical activity and
food marketing practices as postulated causes for increases in the prevalence of 
obesity, leading to neglect of other plausible mechanisms and well-intentioned,
but potentially ill-founded proposals for reducing obesity rates.
 
PMID: 16801930
 
------------
[2] Atkinson RL, Dhurandhar NV, Allison DB, Bowen RL, Israel BA, Albu JB et al. Humanadenovirus-36 is associated with increased body weight and paradoxical reduction of serum lipids. Int J Obes 2005; 29: 281–286.

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