Dr. Sharma's Obesity Notes

Gestational diabetes and excessive gestational weight gain have significant implications for the health of both mother and child.

Anne-Sophie Morisset and colleagues from Laval University, Quebec City, Canada, now examined the relationship between weight gain early in pregnancy and the risk for gestational diabetes, in a paper just published in the Journal of Womens Health.

The researchers examined data from medical records of women who delivered between January and December 2007 at the Laval University Medical Centre, which included 294 women (55 cases of gestational diabetes and 239 controls).

Weight gain in the first trimester was significantly higher in patients who developed gestational diabetes than in controls (3.4 vs. 1.9  kg), whereas whereas weight gain in the third trimester was significantly lower in diabetes patients compared to controls (4.1 vs. 6.3 kg).

Both prepregnancy BMI and first trimester weight gain were significant and independent predictors of diabetes suggesting that both preconception weight as well as weight gain during the first trimester may warrant greater clinical attention.

This is particularly important given the discussions and concerns about the fetal development theory of epigenetic program, which many today believe to be one of the key drivers of childhood obesity.

AMS
Edmonton, Alberta

Morisset AS, Tchernof A, Dubé MC, Veillette J, Weisnagel SJ, & Robitaille J (2011). Weight Gain Measures in Women with Gestational Diabetes Mellitus. Journal of women’s health (2002) PMID: 21332414

Almost exactly to this date 10 years ago, we published a paper in HYPERTENSION discussing the potential for weight gain associated with the use of beta (β) blockers (drugs that, at the time, were widely use for treating high blood pressure and presently continue to be routinely used for the management of coronary artery disease and heart failure).

As we discussed in our paper, sympathetic activation is an important metabolic adaptation limiting weight gain and, therefore chronic β-blocker therapy could increase the propensity for weight gain by reducing energy expenditure.

This question was now readdressed by Lee and colleagues from Sydney, Australia, in a paper just published in the International Journal of Obesity.

In the current study, the reseachers first performed a mechanistic study comparing energy expenditure, diet-induced thermogenesis, and habitual activity levels between volunteers (n=11) with uncomplicated hypertension treated with a β-blocker and anthropometrically matched controls (n=19) and found that β-blocker treatment reduced diet-induced thermogenesis by around 50%, fat oxidation rate by 32% and weekly habitual activity levels by 30%.

They then examined data from three cross-sectional studies consisting of around 200 patients with diabetes, 80 patients with hypertension and over 11,000 participants in a large multi-centre diabetes trial (ADVANCE).

In all three populations, β-blocker treated patients had higher body weights: about 9 kg higher in the diabetes patients, around 17 kg higher in the hypertension patients, and around 5 kg higher in the ADVANCE trial.

The authors conclude that total energy expenditure (both from reduction in post-prandial thermogenesis and reduced activity levels is reduced and therefore body weight may significantly increase under chronic β-blocker use.

These findings must be interpreted with some caution, as ß-blockers consist of a very heterogeneous group of compounds with varying propensity for weight gain (e.g. carvedilol and nebivolol may have far less impact on weight than propranolol or atenolol).

Furthermore, this side-effect of ß-blockade should not distract from the fact that this class of drugs has saved 100s of 1000s of lives in patients with coronary artery disease or heart failure and should definitely not simply be discontinued in patients who need them.

On the other hand, clinicians should be aware of this side effect and advise patients to carefully monitor their weight to decrease the risk for weight gain - as always, prevention of weight gain is easier than treatment.

Fortunately, we now have a variety of other drugs for the treatment of uncomplicated hypertension that are not only weight neutral but are also devoid of other unwanted metabolic effects of ß-blockade.

AMS
Freising, Germany

In my interactions with patients, I always ask them to tell me when their weight problems began and what they believe contributed to their weight gain.

Broadly speaking, there are two categories: people, who were big (or were considered big by others) as long as they can remember and those, who can often clearly pinpoint when their weight problem started. Individuals in the latter group can often recall a specific event or situation that led to their weight gain (e.g. when I miscarried, when I entered puberty, after my second child, when I moved to Canada, etc.).

After hearing hundreds of such stories, common themes emerge, which in the past have led me to make statements such as, “Many roads lead to obesity” or, “Obesity can happen to anyone - no one is immune”.

So how exactly do people with obesity tend to explain their excess weight and do men and women differ in their explanations?

This fascinating topic was now explored by Louise Smith and Lotte Holm from the University of Copenhagen, in a paper just published in the Scandinavian Journal of Public Health.

The researchers conducted extensive in-depth interviews of 20 Danish middle-aged men and women who had experienced obesity, randomly selected from a representative nationwide dietary survey.

While some of the participants had lost weight, others were weight stable. Some reported being overweight from childhood, others reported steady or sudden weight gain later in life.

Most interestingly, there were clear gender differences in the explanations offered for weight gain between men and women.

In men, the following central themes emerged: Firstly (and most commonly), men reported life-course transitions (usually from youth to adulthood), whereby they perceived education or work-related obstacles that prevented or reduced physical activity levels as most relevant. Men also frequently referred to injuries that reduced their physical activity.

Some men reported eating for comfort or due to personal problems, most often related to work, unemployment, or financial concerns - rarely to social or relationship problems.

Some men also mentioned work environments that promoted overeating (e.g. when I began work as a cook).

The stories that women told were strikingly different. Although women also presented “life-course” explanations, these were less frequently related to shifting living conditions or social obligations, but rather to transitions in the female biological cycle such as puberty, pregnancy, and menopause.

The second theme in women was related to changes in social relationships (e.g. when I met my husband, when we moved in together, etc.).

The third theme in women was overeating related to personal problems, in all cases related to intimate social relationships (e.g. I did not receive adequate love in my childhood, I was brought up in a family with an alcoholic father, etc.).

The fourth theme in women was related to the use of psychopharmaca (e.g. for depression, when I began having lithium, etc.).

As the authors point out, it is perhaps not all that surprising that women are more likely to relate the beginning of their weight problems to their biology (which is clearly far more striking and eventful in women than in men) and to problems in their intimate and personal relationships.

In contrast, men look at both life-transitions and emotional stressors more in the context of work (e.g. new job, retirement, unemployment, financial trouble) or blame injury or other circumstance for reduced activity levels.

Thus, as previous research has shown, when it comes to overeating, women typically invoke family obligations, whereas men allude to obligations outside the family.

The fact that the use of psychopharmaca came up as a distinct theme in women but not in men, may be related to the fact (as the authors suggest) that these drugs are far more commonly used in women than in men.

These gender differences are not only striking but may also have important implications for addressing obesity both in populations and in individuals.

Firstly, nowhere in this discourse of life stories, did “lack of knowledge” come up as a driver of weight gain. Thus, it is perhaps not at all surprising, that the public health strategies focussing on “educating” the public on healthy eating and activity, have thus far had virtually no impact on obesity rates.

Rather, based on their findings, the authors suggest that obesity prevention strategies need to target men and women differently and must take into account their very different life histories:

In women, obesity prevention strategies are perhaps best focussed at key times during their biological lifecycles (e.g. at puberty, around pregnancies and menopause) and emotional eating may be best dealt with by addressing and improving coping skills in personal relationships (i.e. at home, within families, etc.).

In men, obesity prevention efforts are perhaps best targeted at periods of educational or professional transition. Emotional eating in men may be best dealt with by addressing social stressors related to work and livelihood and are probably best offered in the workplace.

Certainly a lot for the public health folks to chew on.

In light of these findings I cannot but help emphasize just how important it is to engage and listen to the people who actually have the problem, which we as researchers and health professionals are trying to help solve.

This is exactly the intention of the Canadian Obesity Awareness and Control initiative for Health (COACH), which I blogged about earlier this week.

If you have not yet taken the COACH survey but would like support this initiative, please take three minutes to complete this survey now.

Click here to take survey

As always, I would love to hear from my readers as to whether or not they can relate to these findings - Copenhagen may not be as far away as we think.

AMS
Edmonton, Alberta

Hat tip to Nathalie for bringing the study to my attention.

Smith LH, & Holm L (2011). Obesity in a life-course perspective: An exploration of lay explanations of weight gain. Scandinavian journal of public health PMID: 21270139

Eric Ravussin

This morning, at the XI International Congress of Obesity, I attended a review session on the issue of whether or not it is possible to predict weight gain.

In his introductory comments, Johannes Hebebrand from Essen, Germany, emphasized that even in carriers of mutations that are associated with obesity (for e.g. mutations in the MC4 receptor), excess weight is not necessarily seen in all or even the majority of carriers of such mutations. These findings suggest that current genetic markers are not sufficient to clinically predict an individual’s risk of weight gain.

Eric Ravussin (picture), from the Pennington Research Centre in Baton Rouge, Louisiana, the winner of the 2010 Willendorf Award for Clinical Research, pointed out that one of the strongest predictors of future weight gain may well be lower energy requirements, which in turn is closely related to fat-free mass.

This makes intuitive sense, as it would obviously be easier for someone with lesser energy requirements to move into positive energy balance than someone who has higher energy needs. Although energy needs are in part determined by the level of physical activity, the data supporting the notion that less physical activity is indeed a causal factor (rather than a mere association) in the obesity epidemic are far from conclusive.

He discussed the concept of the “energy flux gap”, which implies that in order to gain weight over time, one would need a substantial sustained surplus of calories to gain and maintain a higher body weight. According to his studies using double-labeled water to measure energy expenditure, he estimated that it would take a sustained 10% excess caloric intake to induce a 7% weight gain. His calculations clearly imply (and are consistent with the observational evidence from population studies) that the obesity epidemic is primarily driven by increased food intake and not by decreased physical activity.

Indeed, it appears that both in animal models and humans, there is an inverse relationship between metabolic rate and caloric intake, which means that paradoxically, individuals with lower metabolic needs tend to also have a stronger drive to eat more.

Other important determinants of obesity risk include fat oxidation rates, where individuals who are better at using fat as a fuel, are less prone to weight gain that people with low fat oxidation rates. Twin studies show that this differential substrate use is very much determined by genetic factors.

Overall his data suggests that perhaps the best (and only) way to determine obesity risk at a metabolic level is to actually challenge the system by doing short-term caloric restriction or feeding studies. These studies can not only show weight gain or weight loss, but also help determine metabolic flexibility or peoples’ ability to switch from fat storage to fat burning with increased fat intake.

Perhaps clinicians need to pay more attention to actually measuring metabolic rates and responses in metabolic rates and substrate utilisation to determine obesity risk and response to treatment.

AMS
Stockholm, Sweden

Yesterday, I blogged about the finding that increased body fat appears to precede lower activity levels and not the other way round (which is probably why attempts to increase physical activity in kids has so far not done much in terms of obesity prevention).

Almost on cue, the latest issue of the Canadian Medical Association Journal (CMAJ) publishes a study by McMaster University’s John Cairney and colleagues, suggesting that kids with developmental coordination problem (perhaps unfairly described as “clumsiness”) may be particularly prone to weight gain.

The study builds on previous reports that kids with developmental coordination disorder were found to be less likely to participate in physical activities.

The researchers studied 2278 (95.8%) of 2378 fourth grade kids (ages 9 to 10) from 75 schools in southwestern Ontario, Canada. Children were followed up over two years, from the spring of 2005 to the spring of 2007.

Not only did the 111 children (46 boys and 65 girls) who had possible developmental coordination disorder have a higher mean BMI and waist circumference at baseline than the other kids, but these differences persisted or increased slightly over time.

In fact, kids with with possible developmental coordination disorder were four times more likely to become obese over the course of the study.

While this study is of course strongly suggestive of less physical activity being a risk factor for childhood obesity, it should be noted that the researchers did not directly measure activity levels. There was also no report of their energy intake or their mental health status (e.g. cognitive ability, depression, attention deficit disorder, etc.), which may significantly affect ingestive behaviours.

There was also no mention of low birth weight, which may be associated both with developmental coordination disorder and excess post-partum weight gain.

Finally, as the authors themselves are careful to note, obese kids have been noted to be less coordinated - so again, it is not clear if the sequence here is “clumsiness -> inactivity -> obesity” or “obesity -> inactivity -> clumsiness” or even “obesity -> clumsiness -> inactivity”.

As always, solving ‘chicken or egg’ questions from cross-sectional or even longitudinal data remains challenging. This is exactly why we need more intervention studies.

AMS
Edmonton, Alberta

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