Arya M. Sharma, MD

Long-time readers will recall previous posts on the environmental impact of food production and how closely the societal root causes of the obesity epidemic may be linked to global warming (in more ways than one would think).

I now came across a most interesting and remarkably comprehensive and insightful analysis of the true environmental impact of our food environment.

This document, released by the Barilla Centre for Food and Nutrition (yes, the pasta folks are involved in this), answers important questions on just how different the carbon footprint of preparing pasta depends on how much water you use to cook 500 g of pasta (assuming a ± 20% pasta/water variable ratio and 10 min cooking time).

Such, ‘light-hearted’ trivia aside, the report actually provides some amazing insights into the ‘field-to-fork’ impact of food production and how it relates to everything from environmental impact to economies of scale.

The centre piece of the report is The Double Food-Environmental Pyramid, where one pyramid represents the traditional food recommendations and the other once (upside down) represents the environmental impact of those foods.

As it turns out (not surprisingly perhaps), in general, the more recommended foods tend to have a lower impact on the environment that the foods recommended for a lower consumption.

Thus, the double pyramid exemplifies how the food pyramid actually meets two important goals -maintains people’s health and protects the environment. In other words, eating ‘healthy’ is not just good for you but also for the planet (this is somehow reminiscent of ‘passive smoking’ because suddenly what YOU eat affects MY environment and, therefore, MY health).

Rather than fascinate you with an incredible amount of highly interesting trivia in this report, I suggest you download the original document here for a most interesting Holiday read.

Buon appetito!

AMS
Edmonton, Alberta

p.s. Hat tip to Annette Anderwald for pointing me to this publication!

Imagine that there were people with a genetic predisposition to asthma. Many different genes are involved - the more ‘asthma’ genes you have - the more severe your asthma.

Now imagine that people with a high genetic risk, a moderate genetic risk, a substantial genetic risk and a severe genetic risk for asthma were all living out in cottage country, where there is clean air with no air-borne dust or pollutants. Only those few individuals unfortunate enough to have ’severe’ genetic risk would have asthma - everyone else would be perfectly fine.

Researchers studying the relationship between asthma and genetics in cottage country would find that in most people genes have no effect on asthma symptoms and only in people with very severe asthma would there appear to be some genetic influence.

Now imagine that a busy highway is built straight through that community with lots of heavy car and truck traffic that significantly reduces air quality.

Now, even those with low genetic risk will start wheezing, those with moderate risk will start coughing, those with substantial risk will no longer be able to do heavy work outside, and those with the most severe risk will be confined to their beds under an oxygen tent.

Suddenly, researchers studying this community, will find that there is a close relationship between genetic risk and asthma symptoms - indeed, the difference between those who have no, some, moderate, substantial or severe asthma can almost entirely be explained by genetics. In fact, in those with any symptom of asthma - the entire ‘variance’ will be found to be almost completely attributable to their genetic risk - suddenly genes become the most important determinant of who has symptoms and who doesn’t!

Not surprisingly, exactly the same is true with obesity, according to a large twin study by Benjamin Rokholm and colleagues from the University of Copenhagen, published in the latest edition of PLoS One.

The researchers examined data on 15,017 monozygotic and dizygotic twin pairs born between 1931 through 1982.

Using classical twin-study methodologies, they found that the additive genetic variation was positively and significantly associated with obesity prevalence and the mean of the BMI distribution.

In other words, as the prevalence of obesity, prevalence of overweight and the BMI mean increased, so did the ‘genetic’ variation in BMI.

As in the theoretical asthma example, these findings are consistent with the notion that variations in genes related to body fatness are more important and lead to greater weight gain under the influence of an obesity-promoting environment.

While this study points to the idea that we need to get serious about tackling the environmental drivers of obesity, it also means that in the meantime, the existing environmental factors will disproportionately affect those with the greatest genetic risk.

So, while everyone is sedentary, get too little sleep, is stressed out and, therefore, eats too many calories - those with the greatest genetic load will gain the most weight, while those with no genetic risk will be just fine (we all know these people).

From a health services perspective this means that, while we wait for policy makers to pass new laws that will help reverse the many obesogenic factors in our current environment (which is likely to take as long as it will take them to reverse global warming), we need to provide appropriate help and care to those who are suffering the consequences from having chosen the wrong parents.

Genetics does not mean you cannot do anything about it - it just means that those with a greater genetic risk need to do much more (often with professional help) to manage their weight than those who happen to have lower genetic risk.

Of course it is also not helpful to tell those with the highest genetic risk to simply live like those with no genetic risk - because that is already exactly what they are doing - unfortunately, they have to do far more!

Sure, the best way to get our severe asthma patient out of the oxygen tent would be to shut down the highway (or mandate cleaner cars) - in the meantime, however, let’s make sure there’s enough oxygen flowing into the tent for those who need it.

AMS
Edmonton, Alberta

Rokholm B, Silventoinen K, Angquist L, Skytthe A, Kyvik KO, & Sørensen TI (2011). Increased Genetic Variance of BMI with a Higher Prevalence of Obesity. PloS one, 6 (6) PMID: 21738588

Stress, anxiety, sleep deprivation, and other common sequelae of modernisation have been shown to disrupt ingestive behaviour often promoting hyperphagia and affecting metabolism in ways that would promote accumulation of excess fat.

In a paper just published in Obesity Reviews by Lysa Huneault and colleagues from Laval University, Quebec City, Canada, the authors argue that modernisation and globalisation may account for the substantial increase in people with obesities around the world.

Following a brief discussion of the role of stress hormones in weight gain, and the little known fact that removal of the adrenal gland (a major source of stress hormones) protects animals from becoming obese, the authors argue that

“globalization and modernization which favour a labour context imposing additional stress and changes in life habits promoting a positive energy balance.”

According to their hypothesis, the increase in knowledge-based work (rather than traditional physical exertion in manual labour), and the decrease of quality and duration of sleep both induce an increase in stress hormones like cortisol, which can lead to an increase in food intake, a reduction in energy expenditure and body fat gain.

The authors argue that:

“from a socioeconomic perspective, globalization leads every nation of the world in conflict with itself and may consequently represent a real problem. On one hand, there are preoccupations related to productivity and money making. On the other hand, people have to adopt a daily lifestyle leading to hyperphagia and decreased energy expenditure in order to maintain their economic competitiveness.”

While this is certainly a most entertaining and stimulating discussion, the article of course cannot belie the fact that obesities were around well before globalisation, often affecting those that were well-off and comfortable rather than those who would have experienced the daily stress of simply making ends meet.

Of course, one may also argue that the latter would have readily gained weight had they had access to cheap, everpresent, highly palatable, calorie-dense foods as in our current environment (which undeniably is indeed a consequence of modernisation and globalisation).

Certainly, this article puts into perspective the rather complex ecological and macroeconomical factors that can interact with human biology to overwhelm hemeostatic functions that evolved to ensure survival under very different circumstances - concept that was nicely summarized in the Foresight Map.

Recognition of these factors certainly pose important challenges for public health endeavours that focus on attempting to change individual behaviours, which represent but natural and normal responses to an unnatural and obesogenic environment.

As Angelo Temblay, the senior author of this paper once said:

“Managing obesity is so challenging because it requires adopting unnatural behaviours to counteract an unnatural environment.”

AMS
Edmonton, Alberta

Huneault L, Mathieu ME, & Tremblay A (2011). Globalization and modernization: an obesogenic combination. Obesity reviews : an official journal of the International Association for the Study of Obesity PMID: 21366834

One of the common misconceptions around the obesity epidemic is that obese kids have lifestyles that are so much worse than those of their non-obese peers.

This assumption, as noted in a recent post, was not really borne out by the findings in the Canadian Health Measures Survey, which did not find marked differences in physical activity between overweight and lean kids (at least not when corrected for the increased effort it takes to move larger bodies).

Indeed, the survey showed that virtually ALL Canadians (young and old, lean and overweight, male and female) do not get even the rather modest amounts of recommended physical activity a day.

So if overweight kids are not moving less (nor, as I suspect, are eating more), then why are some kids overweight and others are not?

If the environmental effects are pretty much the same for everyone, why do we even have lean and obese kids?

This question was addressed by Andreas Beyerlein and colleagues from the Ludwig-Maximilians University of Munich, Germany, in a study just publshed in PLoS One.

The researchers analysed data on over 7,000 3-10 year-old and almost 6,000 11-17 year-old children from a representative cross-sectional German health survey conducted between 2003 and 2006 to look at the impact of maternal BMI, maternal smoking in pregnancy, low parental socioeconomic status, exclusive formula-feeding, and high TV viewing time on BMI.

It turns out that in both age groups, the estimated effects of all risk factors (except formula-feeding) on BMI were greatest for children with the highest BMI. Thus, for example, increased time spent watching TV was associated with a much greater impact on BMI in the overweight and obese kids than in the normal weight kids.

Or as the researchers point out:

“…risk factors for childhood overweight are associated with greater shifts in the upper parts of the children’s BMI distribution than in the middle and lower parts.”

In other words, it is not that lean kids don’t also watch a lot of TV or have mothers who smoked during pregnancy - it is just that kids at the higher end of the BMI distribution appear far more sensitive to these factors than their leaner counterparts.

By way of explanation, the authors suggest:

“…genetic variants with a possibly increased susceptibility of carriers to certain risk factors might offer an explanation for differences in the effect magnitude of risk factors by BMI percentiles”.

Thus, kids who are genetically predisposed to obesity are far more likely to pack on the pounds when spending hours in front of the TV than kids who are genetically less obesity prone. The same could probably be said for overeating or any of the other environmental drivers of obesity, which have much greater effects in terms of promoting weight gain in some kids than in others.

From a prevention and treatment perspective, this means that overweight and obese kids will have to work much harder at changing their lifestyles or avoiding obesogenic stimuli than thin kids, who can “luckily” get away with their similarly “lazy and gluttonous” lifestyles.

Readers will see how this relates back to the whole topic of weight-bias and discrimination, where we so easily fall into the mode of blaming obesity largely on unhealthy lifestyles and will power, when thin people may just turn out to be genetically more fortunate.

What this means for obesity prone kids is that they may not be able to eat as much ice cream or spend as much time in front of their TVs and computers as their skinny friends - but then again, who said life had to be fair?

This should of course not be used as an excuse to do nothing but rather seen as a good reason to fully appreciate and empathize with kids who carry extra weight - some will need to work very hard at controlling their weight - others seem to have simply drawn the “get out of jail free” card.

AMS
Toronto, Ontario

Beyerlein A, Toschke AM, Schaffrath Rosario A, & von Kries R (2011). Risk factors for obesity: further evidence for stronger effects on overweight children and adolescents compared to normal-weight subjects. PloS one, 6 (1) PMID: 21283747

As in most countries, the population levels of obesity in Canada vary considerably from province to province (as they do within provinces). Although there are many “theories” on why this may be the case there has been little work done on trying to unravel the “explained” and “unexplained” regional variation based on a comparison of factors known to affect obesity levels such as socio-economic status, urban-rural distribution, and other variables.

This issue was now addressed by Daniel Dutton and Lindsay McLaren from the University of Calgary, Alberta, in a paper just published in OBESITY.

Using data from the nationally representative Canadian Community Health Survey (CCHS) (2004), the researchers attempted to decompose the difference in mean BMI between regions, into differences explained by different levels of the covariates between regions and a share explained by those covariates having different effects on BMI in the different regions.

Canada was split into five regions for this analysis: British Columbia, the Prairies (Alberta, Saskatchewan, and Manitoba), Ontario, Quebec, and the Atlantic provinces (Nova Scotia, New Brunswick, Prince Edward Island, and Newfoundland). The Atlantic provinces, which currently have the highest obesity rates in Canada, were used as the reference group.

While some differences between provinces (e.g., average BMI for males in Quebec compared to the Atlantic provinces) are mostly explained by the different levels of socio-demographic and behavioral covariates, others (e.g., average BMI for females in Quebec compared to the Atlantic provinces) are mostly explained by the different effects of the covariates on BMI.

One example of a surprising difference between regions is that the impact of increased fruit and vegetable consumption on BMI is substantially stronger in Ontario and Quebec women than in Atlantic women.

The authors have the following explanation to offer regarding this finding:

“One possibility is that the quality of fruits and vegetables consumed differs by region. For example, fruit servings in the Atlantic provinces may consist of more canned fruits (due to a climate less conducive to growing a variety of fruits or geographical distance affecting the efficiency of transporting perishables to the region), which are often packed in syrup, adding to the calorie count, compared to fresh fruits. Another plausible explanation is that consumption of other foods varies regionally, and differentially offsets the impact of fruit and vegetable consumption. For example, if high levels of consumption of fruits and vegetables in the Atlantic region are associated with higher consumption of food overall (including less healthy foods), perhaps reflecting dietary social norms, then we would observe different returns to the consumption of fruits and vegetables.”

Thus, even if covariates (e.g. promoting the consumption of fruit and vegetables) were made to be identical in the different regions, the difference in average BMI between regions would still persist.

As the authors note:

“Thus, targeting covariates in different regions through plans like physical activity or nutrition policy, income equalization, or education subsidies will have ambiguous effects for addressing disparate obesity levels, being plausible policy options in some regions but less so in others.”

Therefore, while some drivers of obesity may best be addressed by federal policies, each region may have to adopt their own strategies to fully address the obesity problem - what works well in one province may have little to no effect in others.

It appears that what applies in clinical practice, also applies for efforts at the regional level: one size does not fit all.

AMS
Edmonton, Alberta

Dutton DJ, & McLaren L (2011). Explained and Unexplained Regional Variation in Canadian Obesity Prevalence. Obesity (Silver Spring, Md.) PMID: 21253004