To anyone following the “biological” literature on obesity, it should be pretty evident by now that environmental factors can epigenetically modify genes in ways that allow “information” on environmental exposures in parents to be directly transmitted to their offspring.
Now a paper by Peter Huypens and colleagues from the Helmholtz Zentrum München, Germany, published in Nature Genetics, shows that both maternal and paternal exposure to weight gain induced by a high-fat diet in mice can substantially increase the risk for obesity in their offspring.
The key novelty in this study was the fact that the researchers isolated egg and sperm from both male and female mice that had been exposed to high-fat diets (or not) and used these germ cells in various combinations using in-vitro fertilization to create the offspring that were then implanted into surrogate female mice.
In all cases, risk for obesity as well as signs of insulin resistant tracked with both the male and female exposures, pretty much confirming that diets eaten by mothers and fathers can directly influence “genetic” risk for obesity in the next generation.
If transferable to humans (and there is little reason to doubt that this is the case), these findings suggest that a large proportion of the “heritability” of obesity is due to epigenetic modification that transfers risk from one generation to the next.
This means that efforts to prevent childhood obesity need to focus on the parents rather than the kids – kids born to mothers and fathers who have obesity are already born with a substantial higher risk than those born to lean mothers and fathers.
Perhaps our best chances of tackling obesity in the next generation of kids is to focus efforts on younger adults of child-bearing age.
One of the most pervasive problems with quitting cigarettes, is the accompanying weight gain – in fact, post-cessation weight gain is reportedly the number one reason why smokers, especially women, fail to stop smoking or relapse after stopping.
But what exactly happens when you stop smoking?
This is the topic of a comprehensive review article by Kindred Harris and colleagues published in Nature Reviews Endocrinology.
The paper begins by examining the magnitude of weight gain generally experienced after smoking cessation – an amount that can vary considerably between individuals.
As for mechanisms, the authors note that,
“Several theories have been proposed to explain increased food intake after smoking cessation. One theory is that the ability of nicotine to suppress appetite is reversed. Substitution reinforcement, which replaces the rewards of food with the rewards of cigarettes could occur. Nicotine absence increases the rewarding value of food. Reward circuitries in the brain, similar to those activated by smoking, are activated by increased intake of food high in sugar and fat. Furthermore, nicotine withdrawal leads to an elevated reward threshold, which might cause individuals to eat more snacks that are high in carbohydrates and sugars.”
There are also known effects of smoking on impulsive overeating and individuals with binge eating disorder are at risk of even greater weight gain with cessation.
Smoking cessation also has metabolic effects including a drop in metabolic rate that may promote weight gain and new evidence shows that smoking cessation can even change your gut microbiota.
The authors provide evidence that behavioural interventions can prevent much of the cessation weight gain and argue that such programs should be offered with cessation programs.
Finally, it is important to always remember that the health benefits of smoking cessation by far outweigh any health risks from weight gain, which is why fear of weight gain should never stop anyone from quitting.
Thus, a study by Claire Chevalier and colleagues from Geneva, Switzerland, published in CELL, not only shows that cold exposure (of mice) changes their gut microbes but also that, when transplanted into sterile mice, these “cold” microbes stimulate the formation of thermogenic brown fat.
All of this makes evolutionary sense, as the increase in heat-generating (and calorie-burning) brown fat with cold exposure would protect the organism against cold exposure – however, that gut bacteria would be involved in this process is indeed rather surprising.
Unfortunately, at least for those thinking that “cold bacteria” may be the panacea for stimulating brown fat and thus weight loss are likely to be disappointed.
The researchers also show that with prolonged exposure to cold, these “cold bacteria” induce changes to the structure and function of the gut that enable more glucose to be absorbed.
While in the short-term, this extra fuel can be used by the brown fat to generate heat, in the long-term, some of these extra calories probably go towards building more white fat and thus weight gain.
Again, this makes evolutionary sense. After all, it is ecologically a far better strategy to insulate the house than to waste extra calories heating it.
This is why, the naive notion that simply lowering ambient temperature as a means to generate more brown fat and thus, burn more calories, may not be all that effective.
Indeed, these experiments suggest rather that chronic cold exposure would ultimately stimulate extra insulation, i.e. more subcutaneous fat and weight gain.
Funnily enough, these findings turn the hypothesis that reducing room temperature would promote weight loss into exactly the opposite. Perhaps it is the excessive use of air-conditioning to generate freezing indoor temperatures (as any European visitor to the US will readily attest to), is part of the problem.
Fascinating stuff for sure.
Now, an analysis from a large randomised controlled trial of smoking cessation by Charles Courtemanche and colleagues published for the National Bureau of Economic Research, that this weight gain may be more that most people think.
The researchers look at data from well over 5,000 participants in the Lung Health Study.
Using various statistical models, they conclude that the average weight gain is about 12 pounds, with the effect being greatest in the young, women and those starting out with a ‘normal’ weight.
They also calculate that the reduction in smoking over the past decades accounts for about 15% of the obesity epidemic.
From the longitudinal analysis they also conclude that the weight gain is not temporary nor likely reversible. If anything, the impact of smoking cessation on weight becomes greater as time passes.
Thus, while the authors remind us that the benefits of smoking cessation on health still by far outweigh any health detriments from a 12 lb weight gain.
Nevertheless, the data should remind us that smoking cessations efforts should always go hand in hand with efforts to prevent excessive weight gain.
Thus, The Lancet should no doubt be commended on partnering with the World Obesity Federation to constitute an international panel of 22 experts under the leadership of Boyd Swinburn (New Zealand) and William Dietz (USA) to
“…stimulate action on obesity and strengthen accountability systems for the implementation of agreed recommendations to reduce obesity and its related inequalities and to develop new understandings of the underlying systems that are driving obesity in order to develop innovative approaches towards making those systems less obesogenic.“
While (perhaps to my surprise) I have previously heard of only one of the panelists (Shiriki Kumanyika, Emeritus Professor of Biostatistics and Epidemiology, University of Pennsylvania), I am sure that all of the panelists bring a wide range of expertise to the table.
The overall mandate of the Commission is rather ambitious, with the following declared goals:
First, the Commission will stimulate action and strengthen accountability systems for the implementation of agreed recommendations to reduce obesity and its related inequalities at global and national levels.
Second, it will develop new understandings of the underlying systems that are driving obesity and also devise innovative approaches to reorient those systems in a sustainable and scalable way to encourage healthy weight.
Third, it will also establish mechanisms for regular, independent reporting on progress towards national and global obesity targets, implementation of recommended policies and actions, and specific systems analyses of obesity drivers and solutions.
Clearly, the Commission has its work cut out for it, as their goal is to address all underlying systems that are driving obesity, including nutrition, physical activity, urban planning, food systems, agriculture, climate change, economics, governance and politics, law, business, marketing and communication, trade and investment, human rights, equity, systems science, consumer advocacy, monitoring and evaluation, Indigenous health, epidemiology, medicine, and health care.
The Commission will have its inaugural meeting in February, 2016, in Washington DC, USA, to determine its work plans.
I guess we should stay tuned to see exactly what that plan will look like.