Obesity, Smoking and Addiction

Morbid obesity and cigarette smoking represent the two most substantial causes of preventable death in the Western world. According to recent estimates, about 1/3 of all adult Americans are morbidly obese (meaning that their excess of body weight is large enough that it causes illness or disability), and these numbers are increasing; approximately 15% of the American public smokes – though the proportion smoking  in many parts of  the developing world is much higher. The rates metabolic complications that correlate with obesity, including diabetes, are also on the rise. Because both obesity and smoking influence risk for cardiovascular disease, stroke and cancer (the three leading causes of death in the United States), smoking and obesity account for substantial disease burden, health care dollar expenditures and deaths. They cut many human lives short and exert a substantial impact our national economy.

So, why do so many people engage in over-eating and smoking, when it’s obvious that these behaviors are harmful? In the case of smoking, the nicotine content in a cigarette – coupled with its other ingredients – produces feelings of reward and relaxation that people find desirable. The high sugar and fat content of many of the food items readily available today do the same because they taste so good. Because they are such powerful rewards, these stimuli are sought out and consumed by people, though there are significant differences between individuals, but what is now causing great concern is the degree to which these behaviors are leading to a generation of health problems – inherited by those who haven’t even made these choices themselves. These inherited factors are not just genetic.

Exceptional new work from Oregon Health & Science University (OHSU) has now shown that monkey mothers who consume a diet rich in sugar and fat during pregnancy give birth to offspring that are themselves prone to acquiring excessive body fat, exhibit heightened anxiety responses and carry a host of changes in gene expression and brain chemistry that underlie these susceptibilities. In essence, mothers who eat an unhealthy diet influence the physiology of their offspring in ways that make them obesity prone. Kevin Grove, the OHSU researcher leading these studies, indicated that an unhealthydiet during pregnancy:

“is programming the [fetal] brain to also seek that high fat diet and those highly palatable diets later in life, which are going to make them at higher risk for obesity and diabetes…”

Similar results have been found for smoking; for example, studies in rats show that when a fetus is exposed to nicotine during gestation (as they are when pregnant women smoke), the resulting offspring is at higher risk of seeking out nicotine and developing a pattern of routine intake. In other words, in both cases, mothers – by engaging in excessive eating and/or smoking during pregnancy, affect the life-long pattern of behaviors in their children.

Once some (but not all!) individuals begin smoking or eating high sugar/fat foods, they experience progressive loss of control and an associated spiral into food and cigarette addiction. The hallmarks of this dependence include 1) unsuccessful attempts to quit or control the behavior, 2) continued engagement in the behavior despite knowledge of a problem caused by it and 3) giving up life activities previously enjoyed because of the behavior. Put differently, what makes an addiction what it is is the fact that individuals cannot voluntarily stop, reduce or control their food/cigarette consumption. Once again, research reveals that it is genetic factors that differentiate those that descend into addiction from those that are resistant to it.

Today, research in humans and animals is focused on the biological factors that cause the compulsive nature of addiction. Studies in rats have revealed that changes in the activity of a neurotransmitter called dopamine contribute to the emergence of food and drug addiction. Studies in monkeys are beginning to reveal how obesity and food addiction take hold. For example, the news program Nightline ran a profile of research going on at the Oregon National Primate Research Center at OHSU that addresses the biological origins and consequences of obesity caused by intake of high sugar and fat diets, coupled with relatively low activity levels. These studies are showing what genes, proteins and biological pathways contribute to obesity and help to explain why it is so difficult to escape. As stated in the program:

“The animals [at OHSU] may hold the answer to curing a health problem tied to many of the leading causes of death in the United States…”

Across this nation, there is scarcely a family that is not affected by the sickness and death caused by smoking and/or obesity. This includes scientists who study animals in order to find cures for these problems. A researcher at UCLA, Professor Edythe London, who has been ruthlessly targeted by opponents of animal research, described her commitment to solving the riddle of cigarette dependence in a 2007 OpEd entitled “Why I use animals in my research”.

“My personal connection to addiction is rooted in the untimely death of my father, who died of complications of nicotine dependence. My work on the neurobiology of addiction has spanned three decades of my life…. To me, nothing could be more important than solving the mysteries of addiction and learning how we can restore a person’s control over his or her own life. Addiction robs young people of their futures, destroys families and places a tremendous burden on society.”

For many who have a personal insight into the devastating effects of addictions like compulsive smoking and/or over-eating, the humane and regulated use of a small number of animals in order to prevent suffering in the future is justified. Though their loved ones have suffered and/or died, there is hope for others, and scientific progress aimed at accomplishing this will not stop, no matter how much the nature of addiction or the animal research aimed at ending it are misunderstand and misportrayed.


David Jentsch