Cigarette Smoking "Another Factor in the Obesity Epidemic"
Obesity rates in the US have more than doubled in the last 30 years, and rates of childhood obesity and extreme adult obesity have tripled. One third of US adults are considered obese, and another third overweight. This is the "obesity epidemic".
The obesity epidemic has coincided with significant changes in the US diet, which are clearly involved. However, there's another probable contributor that's often overlooked: declining smoking rates.
Here's a graph of cigarette consumption over the last century in the US (1):
The obesity epidemic has coincided with significant changes in the US diet, which are clearly involved. However, there's another probable contributor that's often overlooked: declining smoking rates.
Here's a graph of cigarette consumption over the last century in the US (1):
You can see that cigarette smoking has declined quite a bit since its peak in 1963-- a decrease of 63 percent to be exact. It didn't start declining in earnest until 1976 however-- just before the obesity epidemic began.
How Does is Work?
The main active ingredient in cigarettes is nicotine. Nicotine acts by binding to a specific type of receptor on neurons (nerve cells) called the nicotinic acetylcholine receptor. Acetylcholine is one of the main signaling molecules (neurotransmitters) that neurons use to communicate with one another. Nicotine suppresses food intake, increases energy expenditure, and lowers body fatness. Smokers tend to be leaner than non-smokers, even though they usually have a cluster of unhealthy lifestyle habits (2, 3), and they rapidly gain weight when they quit (4, 5). Administering nicotine to rodents under controlled conditions also reduces food intake and body weight substantially (6).
Since the brain (and particularly the hypothalamus) is the organ in charge of regulating food intake and body fatness, one might guess that nicotine acts there either directly or indirectly. As predicted, nicotine infused directly into the hypothalamus reduces food intake (7), and a recent high-impact paper demonstrated in mice that nicotine exerts its effects on food intake primarily via POMC cells, a type of neuron in the hypothalamus that is important for the regulation of food intake and body fatness (8).
Have Declining Smoking Rates Contributed to the Obesity Epidemic?
Public health authorities have been waging a war on cigarette smoking since it was firmly established as a risk factor for a number of serious conditions (e.g., cancer and heart attacks)*. There's no doubt that regularly smoking cigarettes is bad for your health-- in fact it's probably one of the most unhealthy habits there is. However, smoking kept us leaner than we should have been in the 1950s, 1960s, and 1970s, likely preventing the gradual changes in the US diet and lifestyle from exerting their full effect on our waistline. As the appetite suppressive effects of cigarettes went away, and our diet became increasingly commercialized, per capita daily calorie intake increased by about 20 percent, and the adult obesity rate doubled.
Here's a graph that I find striking (based on CDC and NHANES data):
How Does is Work?
The main active ingredient in cigarettes is nicotine. Nicotine acts by binding to a specific type of receptor on neurons (nerve cells) called the nicotinic acetylcholine receptor. Acetylcholine is one of the main signaling molecules (neurotransmitters) that neurons use to communicate with one another. Nicotine suppresses food intake, increases energy expenditure, and lowers body fatness. Smokers tend to be leaner than non-smokers, even though they usually have a cluster of unhealthy lifestyle habits (2, 3), and they rapidly gain weight when they quit (4, 5). Administering nicotine to rodents under controlled conditions also reduces food intake and body weight substantially (6).
Since the brain (and particularly the hypothalamus) is the organ in charge of regulating food intake and body fatness, one might guess that nicotine acts there either directly or indirectly. As predicted, nicotine infused directly into the hypothalamus reduces food intake (7), and a recent high-impact paper demonstrated in mice that nicotine exerts its effects on food intake primarily via POMC cells, a type of neuron in the hypothalamus that is important for the regulation of food intake and body fatness (8).
Have Declining Smoking Rates Contributed to the Obesity Epidemic?
Public health authorities have been waging a war on cigarette smoking since it was firmly established as a risk factor for a number of serious conditions (e.g., cancer and heart attacks)*. There's no doubt that regularly smoking cigarettes is bad for your health-- in fact it's probably one of the most unhealthy habits there is. However, smoking kept us leaner than we should have been in the 1950s, 1960s, and 1970s, likely preventing the gradual changes in the US diet and lifestyle from exerting their full effect on our waistline. As the appetite suppressive effects of cigarettes went away, and our diet became increasingly commercialized, per capita daily calorie intake increased by about 20 percent, and the adult obesity rate doubled.
Here's a graph that I find striking (based on CDC and NHANES data):
Notice that the plateaus (1960 to late 70s) and the steepest slopes (late 70s to 2006) line up almost perfectly.
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