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.
This is once again demonstrated in a fascinating series of experiments by Stefano Guidotti and colleagues from the University of Groningen, The Netherlands, in a paper published in Physiology and Behaviour.
The researchers performed their experiments in mice that were selectively bred over 50 generations to voluntarily spend hours in running wheels. Interestingly, the female “runner” mice remain resistant to becoming obese as adults when exposed to a high-fat diet even when they don’t have access to a running wheel.
Thus, these mice are resistant to developing obesity whether they run or just sit around.
What the researchers now show is that this “resistance” to gaining excess weight (bred over generations) can be fully cancelled out simply by exposing the mice to a high-fat diet for a couple of days shortly after birth.
With this exposure, these mice (and even their offspring) are suddenly no longer resistant to weight gain later in life and in fact gain as much weight on high-calories diets as normal mice.
Even more interestingly, the short term perinatal exposure to the high-energy diet does not cancel out their love for running. When given a wheel, they continue running just as much as before but even this no longer prevents them from gaining weight.
Thus it appears that exposure to a high-energy diet during the perinatal period can have profound effects on the risk of developing adult obesity even in animals bred to be obesity resistant – and, the love for running, does not appear to protect against weight gain.
Or, as the authors put it,
“..resistance to high-energy diet-induce obesity in adult female mice from lines selectively bred over ~ 50 generations for increased wheel running behavior was blocked by additional perinatal high-energy diet exposure in only one cycle of breeding. An explanation for this effect is that potential allelic variants underlying the trait of diet-induced obesity proneness were not eliminated but rather silenced by the selection protocol, and switched on again by perinatal high-energy diet exposure by epigenetic mechanisms”
Moreover, this effect of perinatal high-energy diet exposure and its “reversal effect” on obesity resistance can be passed on to the next generation.
Reason enough to wonder just how much the rather dramatic changes in perinatal feeding of infants over the last few decades may be contributing to the obesity epidemic.
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.
As readers are well aware, the crux of the obesity problem is that the body tends to defend it’s highest body weight. This is why anytime you try to lose weight, the complex neuroendocrine kick in to try to “sabotage” your efforts and seemingly won’t rest till the weight is regained.
So why does bariatric surgery work? Why do people who undergo bariatric surgery not simply eat back the extra calories required regain all of the weight they lost in the first year after surgery?
One of the notions is that the surgery itself makes it hard to overeat (restriction) or works by interfering with digestion (malabsorption) – but there is now increasing evidence that neither of these mechanisms appear to be the real reason surgery is so successful.
Now, a study by Zheng Hao and colleagues from Baton Rouge, LA, published in OBESITY, provides evidence to support the idea that gastric bypass surgery may produce favourable long-term outcomes by reprogramming the way that they body regulates its weight.
The studies (performed in mice), show that after Roux-en-Y gastric bypass surgery, the animals begin to regulate body weight at a level that is lower than before surgery.
What was most surprising in these experiments, was that mice which were starved down to a rather low weight before surgery, actually regained weight after surgery (albeit to a weight that is still well below where they would have been before the experiment) and that this weight gain was mainly due to an increase in lean-body mass.
This response is very different from animals (or humans) regaining weight after dietary caloric restriction, where most of the weight gain is due to an increase in fat mass.
Thus, it seems that the neuroendocrine alterations that happen with surgery, trigger mechanisms that appear to defend against a higher level of body fat, while remaining sensitive to the defense of lean mass.
How exactly this works remains unclear but the hope is that by better understanding the molecular and physiological mechanisms underlying this reprogramming we may be able to develop medications that will mimic the effects of surgery.