Obesity and smoking are the two largest causes of premature death in the United States []. Obesity causes over 160,000 preventable deaths per year, while cigarette smoking causes over 440,000 []. The list of diseases caused by obesity and smoking are myriad. To name a few, obesity increases the risk of type II diabetes, heart disease, and stroke, while smoking leads to respiratory problems, heart ailments, and lung cancer.

Unfortunately, the rate of obesity is on the rise and has become a national epidemic.

What an irony, then, that smoking decreases appetite and weight, a fact that has been long known by scientists and smokers alike []. With recent headlines like “Nicotine treatment ‘could control obesity’” [], does this mean that smokers should not quit, or that obese individuals should take up smoking? Absolutely not!

Apart from all of the well-known detrimental effects of smoking upon one’s health and lifespan, quitting smoking only causes an average weight gain of less than 10 pounds []. Even so, some smokers cite fear of weight gain as one of the reasons why they will not quit.

A recent study is shedding light on how smoking operates to decrease weight. A team of scientists from Yale University, Baylor College of Medicine, and the University of Hawaii have discovered how nicotine tricks the brain into decreasing appetite []. One interesting discovery they made is that the appetite-reducing pathway is unrelated to nicotine’s addictive properties. Thus, targeting this pathway may allow scientists to develop a drug that can treat obesity without conferring an addiction to nicotine, or perhaps help smokers quit without gaining weight.

What controls appetite in our brain?

Our brains are each made up of many distinct regions, each with numerous functions. The hypothalamus is a region deep inside the brain that controls homeostasis, a term scientists use to refer to the process of maintaining basic functions required for life at levels that are neither too high nor too low [].

Figure 1. The hypothalamus is located deep inside the brain. Among its many functions, it controls appetite []. (Click to enlarge.)

The hypothalamus can be further divided into smaller regions. One such region, the arcuate nucleus, is the key center for the regulation of appetite []. The arcuate nucleus contains a special class of brain cells called pro-opiomelanocortin (POMC) neurons. Neurons transmit information via electrical pulses and by releasing molecules that are recognized by other nearby cells. POMC neurons are a subtype of neurons named after the molecule they release pro-opiomelanocortin, which is a precursor to many other hormones. Activation of POMC neurons results in decreased appetite, less eating, and more energy use. In fact, children who do not have a functional POMC gene suffer from early-onset obesity, because they effectively lose those signals for reduced appetite usually transmitted by POMC neurons.

How does nicotine decrease appetite?

Now that we know which regions of the brain control appetite, can a drug such as nicotine alter these regions so that our appetite decreases? This is the question researchers set out to answer in a paper published early this month in Science [].

These scientists conducted their studies in mice, a commonly used animal for modeling human diseases. They fed the mice nicotine and a similar drug called cytisine, and measured their body weight, body fat, and food intake. What happened? Well, the more nicotine or cytisine the mice ate, the less weight they gained, the less fat they stored, and the less food they ate!

What caused this effect? The researchers narrowed this effect down to the workings of the POMC neurons in the arcuate nucleus within the hypothalamus. After treating mice with nicotine and cytisine, they found that POMC neurons were activated and even had faster electrical pulses. Thus, they concluded that these drugs cause POMC neurons to pulse more, leading to decreased appetite.

A magic pill for obesity?

Can this new discovery be used to develop a magic pill for helping smokers quit without weight gain, or even for treating obesity? That is the hope, especially since the way that nicotine decreases appetite is different from the way it causes addiction []. While nicotine reduces appetite by activating the ARC in the hypothalamus, it simultaneously causes addiction by activating the region of the brain that regulates pleasure. Thus, there is promise that a drug targeting the nicotine receptors in POMC neurons may decrease appetite but not be addictive. Yet much more research remains to be done. Because these studies were done in mice, researchers must verify that nicotine interacts the same way with humans’ POMC neurons. Furthermore, we still need to find a safe way to activate these POMC neurons and ensure that this activation will not cause harmful side-effects.

In addition, obesity is more complex than just the workings of POMC neurons. Other aspects of our brain physiology also impact our weight, in ways ranging from affecting our desire to eat to our body’s ability to absorb nutrients from food. To give one example, it turns out that the brain is also responsible for food cravings []. The regions of the brain responsible for memory and pleasure seem to be the culprit. Guess what foods people tend to crave? Those high in fat and sugar, the very source of weight gain! It is as though our brain is programmed to fuel the obesity crisis. This is why losing weight often feels like a losing battle. A true “magic pill” would need to hit all the different ways our bodies monitor and affect appetite – a tall order that scientists are continually working toward.

In the meantime, there are existing, safe methods for losing weight. Although we may have heard it all before, the most effective way to shed pounds is by changing one’s behavior for the long run, not by adopting fad diets or quick-fix gimmicks []. Eat a balanced diet with less fat and sugar, and exercise regularly. Losing weight may be hard given the brain’s own programming against it and today’s environment, but adopting a healthy lifestyle may be a better solution than anything a pill could offer in the future.

Vicky Zhou is a Ph.D. candidate at Harvard Medical School.

References:

[] David H. Freedman, “How to fix the obesity crisis,” Scientific American, February 2011, <http://www.nature.com/scientificamerican/journal/v304/n2/pdf/scientificamerican0211-40.pdf>

[] “Nicotine Triggered Appetite Suppression Site Identified in Brain,” ScienceDaily, June 9 2011, <http://www.sciencedaily.com/releases/2011/06/110609151535.htm>

[] “Nicotine treatment ‘could control obesity’,” BBC News, June 10 2011, <http://www.bbc.co.uk/news/health-13711975>

[] Yann S. Mineur, et al, “Nicotine Decreases Food Intake Through Activation of POMC Neurons,” Science, June 10 2011, Vol 332, pgs 1330-1332

[] “The Role of the Hypothalamus,” Barrow Neurological Institute, <http://www.thebarrow.org/Neurological_Services/Hypothalamic_Hamartoma_Center/203771>

[] Elaine Magee, “The Facts About Food Cravings,” WebMD, <http://www.webmd.com/diet/features/the-facts-about-food-cravings>

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