Nicotine Weight Loss Vindicates the Alternative Hypothesis about What Makes Us Fat
Nicotine weight loss is a huge problem for defenders of the Caloric Balance Hypothesis, also known as the theory that "calories count."
As we've discussed elsewhere, the Caloric Balance Hypothesis tells us that fat can only be lost if we eat less and/or exercise more. A negative caloric balance drives us to burn off fat, and we get thinner. This is the conventional notion.
The alternative idea, the Lipophilia Hypothesis, tells us that a negative caloric balance is an effect rather than a cause of weight loss. For any permanent reduction in fat tissue to occur, the mobilization of energy from the fat tissue must exceed the deposition of calories into the tissue.
1. And this brings us around to the phenomenon of nicotine weight loss. As science writer Gary Taubes notes in his book, Good Calories Bad Calories, "nicotine... may be the most successful weight loss drug in history, despite its otherwise narcotic properties." He asserts that smokers weigh 6-10 pounds less than people who do not smoke. And when smokers quit, they gain those missing pounds back... and sometimes more. Around 10% of quitters gain 30+ pounds. This weight gain appears unavoidable.
Taubes then provides compelling evidence that these smokers are not necessarily eating more. And if anything, you would expect that someone who quit smoking might be exercising more -- not less. So there is a paradox here. He explains that ample evidence suggests that nicotine weight loss operates like this. Nicotine increases insulin resistance in fat cells and simultaneously decreases the activity of a key enzyme called lipoprotein-lipase (LPL) on these cells. Both of these actions drive mobilization of fat from fat cells.
2. This phenomenon of nicotine weight loss has lots of experimental evidence behind it. Consider this study from a 1976 article in The European Journal of Pharmacology: "Nicotine induced weight loss in rats without an effect on appetite."
In this study, the authors administered nicotine to rats:
"Their mean body weights were observed to be significantly lower than those of control groups administered 0.9% saline on a similar regimen. [The authors also noted that] the reduction in body weight after chronic nicotine administration proved highly replicable and it was produced in the absence of a significant decrease in food consumption."
Read that last sentence. Then go read it again. How do you square this observation with the Caloric Balance Hypothesis? The Caloric Balance Hypothesis tells us that eating less causes you to lose weight. But here we have an instance of experimental evidence in which eating behavior did not change at all and yet weight loss occurred in a "highly replicable" fashion.
Maybe that article was about rats, so it doesn't count. And this site is obviously in Gary Taubes' corner, so maybe you can't "trust" those quotes either.
3. But again, everywhere you look, evidence abounds to support the notion that nicotine weight loss contradicts what you'd expect if the Caloric Balance Hypothesis were valid. For instance: "Weight gain following smoking cessation."
In this article from the 1993 Journal of Consulting and Clinical Psychology, you can see the authors wrestle with the contradiction of nicotine weight loss even in their abstract. They note:
"Smoking generally suppresses body weight below "normal" and smoking cessation allows weight to return to normal. The weight gain following cessation appears to be due to a transient increase in eating coupled with the removal of acute metabolic affects of each cigarette, with no change in physical activity. Nevertheless, tobacco smoke (and specifically nicotine) does not appear to be simply either anorectic or thermogenic agent. Although there may be no easy explanation for the effects of smoking on energy balance, the most parsimonious explanation may be that smoking lowers body weight "set point" and cessation raises that point. The transient changes in eating are therefore secondary to the changes in body weight set point. This notion is supported by animal research on nicotine as well as with other drugs."
We're not here to debate the author's set point hypothesis -- Gary Taubes' explanation seems more parsimonious to this site's authors. But you can see how this phenomenon causes a huge problem to people who want to defend the Caloric Balance Hypothesis. If you're going to go on about a "set point," what's regulating that set point? Inevitably, you have to get drawn into discussions of what is going on biochemically at the level of the fat tissue, and thus all of a sudden you're in Lipophilia territory. Because you're not talking about thermogenic activity. You're not talking about appetite. You are not talking about "Calories In" or "Calories Out." You're talking about the metabolic regulation of the body's energy stores -- the LEFT side of our energy balance equation.