“Don’t people know that body size is genetic for some people! It’s not my fault. I diet and exercise. I think I have a healthier lifestyle than my friends. I don’t eat as much as they do, but I fail to lose an ounce.”
I’m tired of hearing this mantra. All I hear is excuses.
We’ve been told not to shame fat people for being lazy, sloppy, and other prejudicial terms. That weight bias is a real thing, a painful thing, and that shaming fat people does not lead them to lose weight. In fact, a fat person who has been shamed is more likely to remain fat. This has been clearly demonstrated.
Does that mean we should accept fat? Should we sit back and agree that it isn’t the fat person’s fault? That they are a victim of their genetics?
No. A thousand times no.
I listened to a discussion between Kelly Brownell, Phd., Director of the Yale Rudd Center for Food Policy & Obesity and Dr. Rudolph Leibel, professor of diabetes research, professor of pediatrics and medicine at Columbia University, who studies genetics of body weight regulation, adiposity, and cellular metabolism. In other words, he is an expert on genetic bases of obesity.
What did I learn/confirm?
The genetics of obesity, like the genetics of heart disease, is a complex genetic issue–meaning there is more than one gene implicated. Compare this to something like sickle cell anemia, which is a single gene. Complex genetic issues are more determined by the environment–hence, they require different techniques for analysis. The best way to study a complex genetic issue is through twin studies. Scientists look at how frequently the disease is correlated between twin pairs–both identical and fraternal twin types. When they compare how commonly obesity occurs in monozygous (identical) twins, it appears that 60% of the risk of obesity is heritable. Risk.
How can we interpret this? Does that mean that 60% of obese people are obese because of a genetic reason? No.
To state it another way, within a given environment–a given circumstance with regard to access to calories and physical activity–if you compare a person with genetic predisposition to obesity to a person without it, the risk of the former becoming obese vs. the latter is 40%. But the environment must be adequately permissive for the expression of obesity. If the environment is not permissive enough, than neither of them will become obese. If the environment is permissive enough, the there is a 40% likelihood that the high-risk (high genetic predisposition) person will become obese.
The environment is the responsible agent for the expression of obesity.
People tend to overstate the degree of genetic responsibility as some insoluble or insurmountable problem. But it is clear that if you change the environment, you can change the degree of obesity.
Scientists have identified 40 to 50 genes that are clearly implicated in weight regulation, but they do not yet understand the ways in which these genes interact with each other or with the environment to ultimately determine the risk of obesity clearly demonstrated by monozygous twin studies (that 60% figure mentioned earlier). They cannot look at any kind of genetic map and make an accurate prediction about who will become obese.
The absolute best predictor for obesity is to simply look at the family. If there are obese parents, or obese cousins, etc., the risk of obesity is far more clearly indicated than by genetic analysis.
Further research in genetics, it is hoped, will unveil which environmental factors have more of an impact on individuals. For example, scientists hope to gain insight on which individuals would respond better to dietary intervention, and others to exercise.
There are a lot of traits being passed genetically–such as hunger and satiety signals, energy expenditure issues, slower and faster metabolisms between individuals, etc. We know that in order for an individual to become obese, they must eat more than they spend, or spend less than they eat in terms of energy. Indeed, several genes that affect all aspects of these considerations–genes that affect satiety, energy expenditure, willingness to engage in physical activity, and more–have been identified. Perhaps scientists will identify more. But they still do not have enough understanding of these genes and how they interplay to make concrete determinations about individuals.
What we can say is that the difference in energy intake between a person who will become obese and a person who will not become obese is actually very small–lending support to frequent claims that obese people don’t really eat more than their peers. But these differences are expressed over long periods of time. Given the length of time, it becomes more difficult to accurately determine which aspect of lifestyle is really driving the obesity. It is impossible to accurately measure total caloric intake and total caloric expenditure, especially in regard to differing metabolic rates. We can make good approximations, but errors in nominal values, over time, can lead to an inaccurate result.
Given the margin for error, it seems much wiser for an individual to focus his attention more on energy intake, as opposed energy expenditure. It takes many hours of effort to burn energy; it takes only minutes to consume it. Hence, the energy intake side of the equation is more relevant, but whether its an issue of hunger or satiety that drives the excessive energy intake, we cannot know at this point. We lack the measurement tools.
So what are we going to conclude from all of this?
We conclude that a fat person with a genetic predisposition towards obesity must change their environment to change the degree of obesity expression. For people with a greater number of those 40-50 genes working against them, the challenge will be greater; a larger environmental change will be required. Some people are dealt an easy hand; some people have to work harder. This is life. It isn’t fair.
Genes can’t change. But the environment can change.
Generally speaking, each of us can control what goes into our mouths, and how much we move. It’s still a game of energy balance.
I need only to look at my own family to know that I have genetics stacked against me. It takes me more effort than my peers to maintain a desirable body shape–a lot more. Over time, I have learned that certain things are guaranteed to fatten me, like alcohol. I choose not to consume alcohol at times, and this has a profound impact on my social life. For most, abstaining from alcohol isn’t worth it. But you cannot have your cake and eat it too.
I can’t change my genes, but I can change my environment. So don’t tell me it isn’t fair. I know this. Don’t adopt the same environment as people with more favorable genes. Create a non-permissive environment for yourself. This is what lifestyle change implies.