Now Suzanne Higgs and Jason Thomas from the University of Birmingham, UK, in a paper published in Current Opinion in Behavioral Science review the role of social norms in eating behaviours and discuss how these norms could potentially be targeted to improve eating behaviours.
“We eat differently when we are with other people compared with when we eat alone. Our dietary choices also tend to converge with those of our close social connections. One reason for this is that conforming to the behaviour of others is adaptive and we find it rewarding. Norms of appropriate eating are set by the behaviour of other people, but also shared cultural expectations and environmental cues. We are more likely to follow an eating norm if it is perceived to be relevant based on social comparison. Relevant norms are set by similar others and those with whom we identify… Norm matching involves processes such as synchronisation of eating actions, consumption monitoring and altered food preferences.”
“Social norms may have had a role to play in recent rises in obesity by reinforcing new behaviour patterns associated with overeating and weight gain. For example, increases in average portion size may have created new consumption norms that are diffused through social networks. It might also be that the social context of eating has changed recently in ways that favour overconsumption. For example, more people eating away from home in fast food restaurants with others might be associated with social facilitation of eating.”
If, how and to what extent, eating culture can be changed at a population level through public health and policy interventions will certainly remain the subject of further study.
Yesterday, I posted about the interesting study by Madjd and colleagues suggesting that drinking water may be better for weight loss than drinking diet beverages.
But what exactly is the evidence that low-calorie sweeteners (of which there are many) may actually have non-caloric effects on energy intake or body weight?
The authors assessed both animal and human studies involving the consumption of low-calorie sweeteners in conjunction with an ad libitum diet.
In 62 of 90 animal studies exposure to low-calorie sweeteners did not affect or decreased body weight. Of 28 studies that did report increased body weight, 19 compared compared low-calorie sweeteners with glucose exposure using a specific ‘learning’ paradigm.
In humans, 12 prospective cohort studies found inconsistent associations between the use of low-energy sweeteners and body mass index, with overall minimal effects at best.
A meta-analysis of short-term randomized controlled trials (involving 129 comparisons) showed reduced total energy intake for low-calorie sweetener versus sugar-sweetened food or beverage consumption before an ad libitum meal (about −94 kcal per day), with no difference versus water (−2 kcal per day).
These findings were consistent with energy intake observations in sustained intervention randomized controlled trials (10 comparisons), a meta-analysis of which (with study durations ranging from 4 weeks to 40 months) showed that consumption of low-calorie sweeteners versus sugar led to relatively reduced body weight (nine comparisons), and a similar relative reduction in body weight compared to water (three comparisons).
Thus, contrary to what is often stated in popular media or even by some experts, there is little if any evidence either from animal or human studies that the use low-caloric sweeteners has any measurable impact on energy intake (other than reducing total caloric intake) or body weight.
Thus, the authors conclude that
“Overall, the balance of evidence indicates that use of low-energy sweeteners in place of sugar, in children and adults, leads to reduced energy intake and body weight, and possibly also when compared with water.”
Obviously, even this analysis is not going to silence the sceptics, who will continue to claim that somehow low-calorie sweeteners are still messing up your energy intake or metabolism.
However, it may be fair to conclude that if indeed such effects exist, their magnitude is likely marginally and of doubtful clinical significance.
I will continue recommending that my patients do their best to replace sugar with non-caloric sweeteners if giving up their liking for sweet foods or beverages is not an option.
Changes in caloric balance are long known to affect metabolic requirements – in general, overfeeding tends to increase metabolic rate, whereas underfeeding (or fasting) tends to lower metabolic rate. However, the magnitude of these changes tend to vary substantially between individuals.
Now a study by Martin Reinhardt and colleagues, published in the International Journal of Obesity, shows that this variation in response to overfeeding and fasting may predispose some individuals to obesity (thrifty phenotype).
Firstly, the researchers found that a greater %EE decrease with fasting correlated with a smaller %EE increase with overfeeding, or in other words, individuals who responded with a greater decrease in caloric expenditure in response to fasting also showed a lower increase in caloric expenditure with overfeeding.
The %EE decrease with fasting was associated with both fat mass and abdominal fat mass as well as a lower 24-hour core body temperature (even after accounting for a number of covariates). A 0.1°C lower core body temperature was associated with a 1.4% greater decrease in EE during fasting.
From these findings the authors conclude that,
“body temperature may be a further defining feature of the human thrifty phenotype and offer insight into contributors to the inter-individual variation observed in energy expenditure responses to caloric restriction or excess.”
They also suggest that perhaps careful measurements of body core temperature could be harnessed to direct weight loss or weight maintenance efforts during life style interventions.
If nothing else, the study nicely documents that we are not all equal when it comes to how our bodies respond to over or underfeeding.
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Do Variations in Breast Milk Composition Account for the Conflicting Evidence Regarding Its Protective Effects On Excess Weight Gain?
As father of three nursing mothers, I am all for breast feeding. Indeed, in several previous posts, I have cited the epidemiological data to suggest that breast feeding may be protective against childhood obesity.
However, this data is far from clear. There are in fact many conflicting studies on this issue, as a result of which breast feeding as protection for weight gain was presented as one of the “obesity myths” in a recent paper in the New England Journal of Medicine.
Now, a study by Tanya Alderete and colleagues from the university of Southern California, Los Angeles, published in the American Journal of Clinical Nutrition, suggests that the variable reports on the role of breast feeding in protecting against excess weight may be related to variations in its composition.
The researchers studied the composition of human milk oligosaccharides (HMOs) in 25 mothers and correlated these to with infant growth and body composition at 1 and 6 mo of age.
As the authors discuss, diversity and HMO composition of breast milk appeared to have disparate effects on body composition and body weight.
Thus, for example, each 1-μg/mL increase in levels of lacto-N-fucopentaose (LNFP) I was associated with an approximately 1 lb lower infant weight at 1 month and a 1.11-kg lower weight with am 0.85-g lower lean mass and a 0.79-g lower fat mass at 6 months.
In contrast, disialyl-lacto-N-tetraose and LNFPII were associated with small but significant increases in body fat mass.
Overall, these effects are not trivial,
“When examined collectively, LNFPI, DSLNT, and FDSLNH explained 33% more of the variance in infant fat mass than did sex, prepregnancy BMI, weight gain during pregnancy, and 6-mo infant age alone.”
As one potential mechanism, the authors suggest that different HMO’s may have differential effects on gut bacteria in these infants.
“HMOs are thought to aid in the growth and metabolic efficacy of the developing infant micro biome…Although we did not collect stool samples, preliminary findings observed in the current study may be partially attributed to the prebiotic effects of HMOs. In support of this, a recent study found a distinct fecal microbiota composition in breastfed compared with formula-fed infants, in which the fecal microbiota in breastfed infants correlated with the HMOs consumed (particularly LNFPI and DSLNT).”
Whatever the mechanism, as the authors note,
“These findings support the hypothesis that differences in HMO composition in mother’s milk are associated with infant growth and body composition.”
Obviously, these kind of studies cannot prove causality nor do they provide definite mechanistic insights.
However, they may open an avenue to better understanding why the literature is so conflicted when it comes to the relationship between breastfeeding and excess weight gain.
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This is largely, because to win a debate you need to take a biased and one-sided view of the topic and speak with conviction – at least if the intention is to sway the audience.
The problem is that presenting a radical stand-point convincingly may lead the audience to believe that this is your actual position on the matter (rather than simply a role assigned to you by the organizer).
To not fall into that trap, these debates often end up with the debaters agreeing more than disagreeing.
Case in point a debate at Obesity Week, on whether or not people with obesity who are metabolically healthy should be advised to lose weight.
The pro side was represented by Mark Hamer, who essentially made the argument that truly metabolically healthy obesity (MHO) is a rather rare phenotype and will in most cases (sooner or later) progress to unhealthy obesity (UHO), so that differentiating between the two both in clinical practice and in public health recommendations to lose weight is neither practical nor necessary.
On the con side, Sam Klein argued that on the one hand, MHO individuals appear far more resistant to developing metabolic risk factors (even with weight gain) and that weight-loss always comes with a cost and that interventions should therefore be focussed on people who stand to benefit the most, i.e. people who already have metabolic problems.
Klein also pointed out that we not be tempted to treat “hyperBMIemia” – but take the actual health of the patient into account.
In the end, as expected, the debaters came to agree on the fact that everyone could stand to benefit from improving their “lifestyles”, particularly their activity levels (which really wan’t the question that was being debated).
If nothing else, the debate revealed the ongoing conflict between population messages (every one should strive for a “healthy” weight – whatever that is) and clinical decision making, where recommendations need to be personalized to the actual risk of the individual.