Medications for Mental Illness: a Risk Factor for Obesity?

Overeating may be related to drugs changing hunger hormone signals

/ Author:  / Reviewed by: Robert Carlson, M.D

What is the connection between mental illness, medication and being overweight? Science is uncovering evidence that managing a psychiatric condition with drugs may be a risk factor for obesity.

Researchers are pushing the boundaries of what is known, tentatively exploring how the feeling of not being satisfied after eating is related to metabolism, bioenergetics, signaling molecules, diet and general wellness.

A balancing act is required when patients complain that the medications they are taking make them want to eat too much. Given that so many other disorders are associated with obesity, clinicians are certainly concerned about the costs of a medication potentially being greater than the benefits.

Patients can have a mixture of different disorders, and doctors have learned that the presence of one tends to predict certain others. A person who drinks heavily, for instance, is more likely to be depressed, compared to the norm.

The term clinicians and public health workers use to describe how diseases tend to be associated is "co-morbidity", an area of great concern for doctors. Developing one disease can increase the risk for developing another.

Researchers are probing the limits of our knowledge about cells, physiology and genetics to understand why altered biochemistry can affect one's wanting to eat more. Meanwhile, there is evidence accumulating that psychiatric disorders are risk factors for weight gain.

Why this should be is not clear, but it has something to do with the complex relationship between cravings, food-seeking behavior, body chemistry, metabolism and mental health.

Why would obesity be a side effect of taking psychiatric medications?

In some respects, human appetite, bioenergetics, and metabolism remain one of the great mysterious areas of science.

There is still basic disagreement on whether an eaten calorie in, say, bacon has the same bioenergetic load as a calorie from almonds or soda. "Calories in, calories out" is a traditional way of understanding the relationship between energy taken in and energy used.

Yet there is increasing interest in an alternative way of thinking that emphasizes that there are different metabolic responses to calories in different sorts of food. It may very be that it is the types of food people with different genes and body chemistries seek out in different situations, and not just the number of calories, that may have negative effects on their weight.

There is really a great deal to be learned about the basics of how cells process energy, how medical drugs produce side effects and how signaling molecules make us feel hungry or full.

Why should one of the side effects of taking medication be increased appetite? Science has clues but does not yet have a definitive understanding, and may never. The complexity of the roughly 20,000 genes in each of the estimated 10 trillion cells in the human body pushes science to the limits of knowledge.

Medications are made to target signaling systems in the body. They interact with the intended chemical or physiological target, such as a gene on DNA or the surface of a bacterium. However, drug molecules dissolve in the blood stream and float around and often attach to, interfere with or otherwise interact in unintended ways with other structures and various systems.

When the bloodstream has drug molecules floating around, other chemical messengers or physiological pathways can get altered. Most of the time this is not a huge problem. Drugs are designed to bind to or interact with particular chemicals or molecules first and foremost, and if there is some additional physiological interactions, digestive processes will tend to work to metabolize it.

However, the sheer mind-blowing intricacy of the communications and signaling systems in cells vastly outstrips what scientists can know or control. Tinkering with a protein or hormone or gene in one place can produce unwanted interactions elsewhere, creating side effects. Such effects may not be a big problem, but the history of medicine does also feature high-profile unintended adverse effects of medication, which has occasionally resulted in tragedy.

A more common situation is that people experience adverse events after taking a drug that are serious enough to require monitoring and management. Sometimes these side effects include nausea, sleeplessness, listlessness, palpitations or any of a whole host of unpleasant symptoms. Doctors prescribe drugs for people with psychological and emotional disorders, and hope the benefits outweigh any adverse effects.

Do bodily hunger signals change when people take psychiatric drugs?

Our sense of hunger and being satisfied from eating is evidently controlled by a series of hormones such as leptin and ghrelin, working in conjunction with a number of regulatory genes that get switched on and off. It seems that the delicate metabolic checks-and-balances operations of these chemicals can get thrown out of whack all too easily.

Science is investigating the specific mechanisms of why a drug to combat schizoaffective disorder or depression would modify leptin and ghrelin signals so as to make one want to keep eating and eating. Probably the medication modifies the dynamic ebb and flow of serotonin, a chemical in the brain and body which seems to be involved in many, if not most of our emotions and feelings and moods.

The truth is probably amazingly complicated. The signaling chemicals serotonin, blood sugar, leptin, ghrelin, the pleasure chemical dopamine and a series of genes being activated and deactivated all work together to produce the sensation in the brain and mind that "I want more food".

Science has yet to specify the particular mechanisms that explain the desire to keep eating because of changes in hormonal signals and cell physiology. Yet there is evidence that taking drugs to manage a psychiatric condition increases risk for obesity. Evidently the psychiatric problem interacts with the drugs to change molecular signals in the brain and body. The result is overeating for too many people already struggling to manage mental illness.

The danger for obesity among users of psychotropic medications

Paula Caplan, PhD, wrote in the January 2012 issue of Fat Studies that "...many psychiatric drugs cause weight gain in significant percentages of the people who take them". She specifically notes that "...antidepressants, mood stabilizers, and antipsychotics can cause extreme weight gain".

A similar assessment comes from a systematic review of data about the effects of taking psychiatric drugs on weight gain. Writing in the June 2012 issue of the journal PLOS One, Dr. Robert Dent and colleagues report that "...weight gain is associated with psychotropic medication use" and that "...psychotropic-associated weight gain carries significant risk".

Does the use of these medications cause obesity in all who take them? No. It would be more accurate to state that while for some people taking psychiatric drugs along with other factors causes weight gain, for others this is not so clear. For other people, use of antidepressants, mood stabilizers, and antipsychotic drugs can be thought of as a "risk factor" for obesity.

The idea of a "risk factor" does not of course mean that any individual who is being treated for these conditions with medications is going to gain weight. Rather, this applies to group averages and probabilities: the chances for obesity go up, on average, if you take certain medications. As the saying goes: your mileage may vary.

People who inherit genes that predispose them to a medical risk may never develop that condition, and people who inherit genes that make them less likely to develop a condition may still become afflicted. Developing a condition tends to be a multifaceted affair, with potential contributions from behavior, upbringing, diet, lifestyle, stress, and much else.

There are genes that increase the risk of developing a mental disorder as well as for being overweight. There may turn out to be genes that increase the risk of developing side effects of medication. At this point, knowing whether one has inherited a version of a gene may modify the calculations doctors use for risk for disease, but most therapies or behavioral interventions to treat the condition would be the same regardless. Genetic data is currently more useful for diagnosis than for treatment, though that will likely change in coming decades.

The critical issue for patients managing a psychiatric condition is to get informed about risks, and work with doctors to monitor mood, appetite, feelings of energy levels, any weight gained, levels of blood triglyceride and "good" and "bad" cholesterol and possibly insulin levels as well. Obesity can result from many sources, but psychiatric meds seem to be a factor.

Conclusion

Much remains to be learned about the relationships between obesity, mental health and medication effects. The interdisciplinary research that investigates the way these affect each other is still relatively new.

There is evidence that mental health conditions are risk factors for weight problems. Science has yet to definitively explain why, but it likely involves relationships between psychological well-being, brain chemistry and metabolic processes involving hunger hormones.

There is evidence of an association between obesity and use of antidepressants, mood stabilizers and antipsychotics, Researchers believe taking medication to manage mental disorders may very well be a risk factor or cause for weight gain. This does not mean that any particular person who takes drugs for a psychiatric disorder will gain weight, but they should monitor their situation and keep their doctor informed about changes with weight, hunger, and mood.

Doctors try to carefully monitor possible side effects of medications such as weight gain. For persons with a psychiatric disorder who are taking medication, the possibility that they are at greater risk is a source of concern. Yet, knowledge is power, and being more informed about these risks is what empowered patients need to do.

Review Date: 
July 5, 2012