Nicotine and Metabolism: The Myths and Facts Behind this Controversial Compound

Although many of the social stereotypes that formerly surrounded nicotine use have diminished over the past decades, some of the potential myths behind this chemical still remain unclear to the public eye. There was a time when nicotine use through products such as snuff, cigarettes, or chewing tobacco was commonly associated with being part of the enlightened or social elite, and many of the cancer-causing properties of these products were yet to be unearthed. Although these sterotypes have become less prevalent, there is still a strong association between the use of nicotine-containing products and lowering one’s body weight. Whether through television ads, the modeling industry, or by simply observing friends who smoke, it is no mystery why many individuals tend to make this association. Although the harmful properties of nicotine containing compounds are well known, let’s take a closer look at one of the more common chemicals within these products, nicotine, and see if there is any biochemical evidence behind some of the speculation that ties nicotine use with lower body weight.

There are over 4000 chemicals present in cigarettes, and 50 of these are known to be carcinogenic. Surprisingly though, out of all 4000 chemicals, the majority of research associated with all of the compounds in tobacco zeros in on nicotine as the culprit for any effects it may play on metabolism within the human body. A recent study out of the University of New York in Syracuse showed that when nicotine was ingested by rats, an immediate drop in food intake was recorded. Although the effect diminished over time, the critical conclusion of this research was that even after the effects of nicotine seemed to normalize, the amount of food intake while nicotine was still being pumped into the rats was approximately 10% lower than before nicotine was ever administered. Moreover, when nicotine infusion was halted, a 20% increase in food intake occurred. So when rats were given a constant daily dose of nicotine and then suddenly stopped being given nicotine, they began eating even more than before nicotine was ever introduced into their bodies. This study not only explains why people who actively smoke tend to weight less, but it also explains why individuals who try to stop smoking often gain a substantial amount of weight in the process. So, there appears to be evidence that there is some correlation between nicotine use and weight control, but exactly how or what is doing this?

Two of the primary sources of energy production in the human body are fats and sugars. So let’s begin by focusing in on these two categories of chemicals in our attempt to see how nicotine my actually effect the body’s use and storage of energy. Recent studies from the Indiana University School of Medicine  suggest that the AMP-activated protein kinase (AMPK) plays a critical role in the regulation of fatty acid synthesis and oxidation. When nicotine is ingested, it leads to the production of reactive oxygen species. One of these oxygen species is peroxynitrite, which activates AMPK. This activated AMPK is then able to inhibit an enzyme within the body known as fatty acid synthetase (FAS). Fatty acid synthetase is responsible for the synthesis of fatty acids within the body from ingested food molecules. These synthesized fatty acids would traditionally be stored in adipose tissues and cause weight gain. However, since nicotine is able to inhibit fatty acid synthetase, it is able to prevent the buildup of adipose tissue within the body. Not only this, but since fatty acid synthetase is being inhibited, a buildup of another chemical within the body known as malonyl-CoA takes place. A buildup of malonyl CoA within the body sends signals that you are currently in a state of being ‘well-fed’, which prevents further food ingestion. So, nicotine is not only able to prevent the synthesis and storage of fats, but it also prevents further food ingestion through a build-up of malonyl-CoA

Now that we have examined a few of the ways that nicotine can effect fats within the body, let’s shift our focus to how nicotine effects sugars that we consume. The Lundberg Laboratory for Diabetes Research has shown that long-term use of nicotine has been associated with insulin resistance. Insulin is a hormone that is responsible for causing excess sugar in the bloodstream to be converted into glycogen, which is then stored within the liver or muscle tissues. In other words, insulin is responsible for lowering the level of blood sugar when it gets too high. Since nicotine use causes an inhibition of insulin, the body of a long-term nicotine user ends up have generally higher levels of blood sugar. Right after a person eats a meal, their blood sugar levels raise, and their body sends signals which tell the person to stop eating. So, higher levels of blood sugar act a signal for people to stop eating. By inhibiting insulin, nicotine is able to therefore create a false feeling of being ‘well-fed’, and ends up causing us to eat less as a result. Nicotine ingestion has also been linked to epinephrine and dopamine release within the body. Epinephrine is responsible for actually causing glycogen to break down within the body, which ends up releasing even more glucose into the blood! This further contributes to the inhibition of appetite. Although dopamine has been less clearly linked with appetite inhibition, it is known to be responsible for the addictive properties of nicotine. Dopamine release causes a feeling of well-being or euphoria. However, the use of nicotine also dulls the receptors in the body that are responsible for that dopamine release. As a response, your body ends up creating more receptors, which in turn become desensitized as they also get exposed to nicotine. In the end, a nicotine user ends up needing more and more nicotine to get the same feeling of euphoria. This is heavily attributed with why it is so difficult to quit smoking, since people become addicted to the dopamine release caused by cigarettes.

Although there appears to be significant evidence suggesting that nicotine use does indeed lead to lower body weight and a higher metabolic rate, the negative side effects of nicotine-containing products, along with the addictive nature of nicotine itself in no way make it a viable means of weight loss. If anything, I feel this information should serve as a further red flag to the intentionality behind companies that produce nicotine products. The fact that they would incorporate such an addictive compound into their product that has been obviously attributed to causing various types of cancer within the body should help prevent anyone from voluntarily using these substances.

Additional information can be found at the following resources concerning both nicotine use, and the studies cited in this blog.

Bouchard, Claude. “Inhibition of Food Intake by Inhibitors of Fatty Acid Synthase” The New    England Journal of Medicine. Volume 343: Pgs.1888-1889. December 2001.

Eliasson, Bjorn. Taskinen, Marja-Riitta. Smith, Ulf. “Long-term Use of Nicotine Gum Is Associated With Hyperinsulinemia and Insulin Resistance.” Circulation. 1996;94:878-    881. Lundberg Laboratory for Diabetes Research, Department of Internal Medicine, Sahlgrenska University Hospital, Goteborg, Sweden, and the Department of Medicine, University of Helsinki (M.-R.T.), Finland. 2008.

Talmage, David. Role, Lorna. “Nicotinic Receptor-Mediated Effects on Appetite and Food       Intake.” Journal of Neurobiology: 53(4): 618-632. Department of Anatomy and Cell  Biologiy. Columbia University. New York, NY. 2002.

Indiana University School of Medicine. “AMPK: Master Metabolic Regulator.” The Medical     Biochemistry Page. 2008


~ by bradleyriley2010 on November 21, 2009.

2 Responses to “Nicotine and Metabolism: The Myths and Facts Behind this Controversial Compound”

  1. This is really interesting and I have a funny (personal) story! I told my fiances mother that if she didn’t stop smoking I wouldn’t allow our future children (her grandchildren) to the house. Kinda drastic, but it really is unhealthy and I really am against second hand smoke. And it think it’s okay if you want those chemicals in your body, but by your actions impacting the health of others is not cool. Anyways, she actually quit! Which was great! But she gained weight for sure. And now every-time she starts talking about her weight she blames it on me.

    Anyway, I believe you said (or I heard it from some class presentation) that once you have nicotine and then stop, your weight is actually greater than when you started. So not only do you lose weight when you start smoking and then gain weight back to normal when you quit, but you gain extra. This seems very frustrating for people who are trying to quit smoking but know they are going to gain weight. It seems like maybe someone should come up with a “quit smoking” plan that also involves weight loss and maintenance help. So I searched for something…and found this recent article! –“Interventions for preventing weight gain after people quit smoking”

    Even though this article talks about some treatments that help you quit smoking and minimize weight gain, they said that weight maintenance only lasted for no more than one year.

  2. Brad,

    I found this post really interesting. I have some musings that I would like to share. I learned in Health Psychology about “chippers,” a term for smokers who smoke infrequently and irregularly. These chippers may binge smoke when they do smoke, but then go days, weeks, or even months before smoking again. While there is a lot of research done on what mechanisms prevent these smokers from feeling a nicotine craving, and why they don’t get addicted like the average smoker, I’ve not seen anything on the metabolic effects of “chipping.” I wonder what your take is on how chipping would affect metabolism? I know a few “chippers” and some of them are overweight, but one is very thin. Could their metabolic differences be related to their “chipping” habits? Would infrequent chipping actually benefit the metabolism?

    Another interesting potential nicotine effect (outside of its influence on metabolism) is its inverse correlation with Parkinson’s disease, indicating that nicotine use may have some protective effect on cells that are involved in the disease. People who smoke are significantly less likely to develop Parkinson’s disease. As a result of this study (we learned about it in Molecular Neurobiology), my lab group and I decided to test the effects of acetylcholine and nicotine on dopamine-expressing cells in culture. When treating with acetylcholine in low concentration, this stimulation actually improved cell survival after an assault with chemicals producing free radicals (chemicals known to be correlated with the development of Parkinson’s disease). We were unable to test low concentrations of nicotine due to time, but I still wonder if nicotine may have some protective effects for the brain due to the stimulation of nicotinic acetylcholine receptors.

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