By: Jonah Stavsky  | 

In Defense of Obesity

We’ve all been there — sitting around the dinner table with family and friends — and, when the dessert plate finally arrives, the conversation begins. Uncle Peter is convinced the carbs are to blame. Cousin Sarah begs to differ, as she understood fats to be the culprit — if you eat fat, you get fat. Brother Andrew asserts the importance of protein for proper nutrition. Mom, after having recently read an article about the probiotics in fermented foods such as kombucha, claims it's all about the bacteria. Dad, skeptical as always, proposes the supremacy of exercise in losing weight.

Calories in, calories out — that’s what we’ve all been taught. As a personal fitness trainer, I, too, emphasize this idea to my clients. However, according to current research, this view is proving far more complicated than initially thought — more on this later. Then there’s the willpower argument. If we could just put the fork down, the pounds would melt away. Again, it's not that simple.

The etiology, or cause of obesity is complicated — considerably beyond what people realize. The obese population are often stigmatized as lazy or simply lacking this so called willpower. In this article, I’d like to describe just a few of the many etiological theories surrounding the obesity epidemic — some of which may surprise you. In doing so, I’d like you to re-evaluate your assumptions regarding obese individuals, and the conscious, or subconscious biases, termed “fat biases”, you may have towards them. Moreover, I intend to provide general advice for those who may be struggling with their weight. Therefore, If you are among the more than two-thirds of Americans who are either overweight or obese, I urge you read closely; and if you are among the one-third who are not, you should read even closer.

When presented with a disease or a condition, doctors and scientists tend to look to our genes — and for good reason. After all, the three billion letter sequence inscribed in our cells, to a large extent, codes for the type of individual we will become. Ideally, a “diseased” gene would be located and repaired. Unfortunately, more often than not, a multitude of genes are implicated in a condition; it is therefore a matter of solving the genetic puzzle to obtain the cure — a task which is easier said than done. Regardless, progress has been made in this area of research.

The most commonly implicated gene in obesity is the MC4R gene, which codes for the melanocortin 4 receptor — a deficiency of which has been highly associated with overeating. Nevertheless, this cannot account for the steep statistics on obesity. More likely, several genes acting in synchrony contribute to the phenotype, or visible characteristics, of an obese individual. Furthermore, even if the specific genes connected to obesity were discovered, how would that help? Aren’t we stuck with our genes? This previously held notion has become obsolete due to advances in the exciting field of biotechnology, in which gene-editing is a real possibility — take out the broken, put in the fixed. However, our genes cannot take all the credit for the obesity epidemic.

Neuroscientists, particularly neurophysiologists, have brought their fascinating discipline to bear on the issue of obesity and overeating. Why do people overeat? It seems like a simple enough question. Alas — the answer is multifaceted, to say the least. In accordance with darwinian evolution, humans have evolved, through natural selection, to live and eat in a certain way. In theory, our current health may depend on the development of a lifestyle resembling that of our ancestors. While the implications of this theory have yet to be concluded among experts, we can still do our best to extrapolate.

In the hunter-gatherer era, food was scarce. Our bodies, therefore, developed adaptations that allowed us to get the most out of a potential encounter with food. Let us say, for example, that one of our ancestors came into contact with a delicious looking blueberry bush, which would inevitably result in overindulgence. In order to take full advantage of the fruit, the signals that make us hungry, which work through a hormone called ghrelin, are extremely powerful. If we don’t eat, ghrelin runs rampant, and has us soon scavenging for food, whether it be miles away on a berry bush, or next-door in the fridge. On the other hand, the hormone leptin, along with others, signals to our brains that we are full. When we eat a big meal, leptin skyrockets, and we feel satiated. Here’s the kicker: the signals to stop us from eating are much weaker than those forcing us to eat. Who knows when the next food encounter would be? Through this mechanism, our ancestor at the blueberry bush is able to stock up on plenty of energy, overindulging for a kind of hibernation, so to speak — similar to a grizzly bear consuming salmon before winter.

Furthermore, our brains have developed in a way that reinforces the act of eating. When we eat, the brain releases dopamine — the famous “feel good” neurotransmitter — similar to a heroin injection, albeit to a significantly smaller extent. And people wonder why food is addictive! Parallel with our ancestor at the blueberry bush, this dopaminergic response allowed our ancestors to continue eating and not die out — survival of the fittest at its best. In modern times, however, when food is so readily available (i.e fast food), these mechanisms have backfired. In essence, what was once a live-saving adaptation, is now killing us.

But even with modern food availability, wouldn’t we still be able to regulate our appetites? Sure — so long as we are eating the right foods. The human stomach was designed to signal satiety to our brains in specific, although complicated, ways. One of the simplest manners in which this is done is through stretch receptors. When we eat, the stomach expands, and stretch receptors tell our brain that we’re full. Note that the effectiveness of this system is dependent on food volume. Fruits and vegetables are high volume, low calorie foods; that is to say, you get more nutrition and satiety for your caloric buck. Sociologically, however, many societies, especially those of Americans, have decided to compress foods, increasing their density — effectively decreasing your caloric buck per unit of satiety.

An example I like to give to my clients: in front of you lies a single donut or a table lined to the brim with broccoli — each contains the exact same amount of calories. Which is going to make you more full? The correct answer, of course, is the broccoli. However, if you thought to yourself, “but I want the donut!” you were looking for the immediate dopaminergic response that accompanies a densely packed container of fat, sugar, and salt — stripped of vitamins, minerals, and fiber — thereby falling right into the food industry’s trap. Accordingly, my advice to someone who complains of chronic hunger (all other variables being equal), is to take a look at the density of their foods. Yes — orange juice is healthy — but whole oranges are even healthier.

While exercise and proper nutrition are currently the most powerful tools available as a means for fat loss, certain individuals may benefit from alternative perspectives on the issue. With that, I’d like to turn to more recent theories which attempt to reconcile our environment with our genes — the so called nature versus nurture debate.

On the forefront of this reconciliation is the field of epigenetics. Essentially, we previously believed that gene transcription was set in stone. However, research has uncovered the ability of our genes to turn on and off, like a light switch, in order to regulate certain bodily processes. While the topic of epigenetics requires a separate article in and of itself (or perhaps a book, of which there are several published), the basics can be applied to obesity. Have you ever heard that sitting is the new smoking? This is in accordance with epigenetic research, in which sitting has been found to turn off “fat loss genes”, while standing and walking turned them back on. Incredibly, some of these changes could be permanent — a person may be able to assign an “on tag” to their genes which could be passed on to their children. Your current lifestyle could affect your future offspring on a genetic level, predisposing them to start their journey off on the right, or perhaps wrong foot. Furthermore, what we eat may also be able to turn and tag genes off and on — a truly exciting concept for the field of nutritional science.

Additionally, the study of the human microbiome has taken hold of the public. While estimates vary, it seems as though we have more bacterial cells than human cells inside of us — in a way, we are more bacteria than we are human. Besides being an interesting fact, why should we care? While research into the human microbiome is vast and ongoing, its implications for obesity are already apparent.

In several studies, scientists have given the same diet to regular mice and germ free mice (mice born without any bacteria inside of them), and watched as the germ free mice became exponentially fatter than the regular mice — their caloric intake remaining constant. Moreover, when the microbes of a fat mouse were transferred to the colon of a skinny mouse, the skinny mouse began to gain weight; again, this was done with a consistent diet. How does this work? Science simply isn't sure yet, although progress is being made everyday. The fact of the matter is, that fields such as epigenetics and the human microbiome (and several others not mentioned) highlight the vast complexity of obesity. The cause of the issue clearly extends far beyond what we currently know; calories in, calories out may not be the whole story.

The obesity statistics, as previously highlighted, are startling. Simply being even 20% overweight exponentially increases a person's odds of receiving a diagnosis of heart disease, stroke, cancer, high blood pressure, and diabetes, to name a few. Yet, as we have seen, the cause of obesity is complex. Accordingly, it is vital to account for these variables when deciding how one should perceive obese or overweight individuals. Moreover, how exactly do we place, or even define fault? Are we to blame an obese child for the way she was raised by her parents? What about her genetics? Epigenetics? What if she is still obese into adulthood? Can we blame her then? Her brain is now wired to crave fat, sugar, and salt, from a point in her life in which free will was limited. These philosophical questions regarding the place of fault, or blame, if you will, demonstrate further nuances into the stigmatization of obese individuals.

It is possible to perceive that the only difference between medical conditions such as obesity and heart disease is the external expression of the former, in that obesity is plain to see. You might never know about the hidden medical conditions of your friends, family, and colleagues. Obesity, however, is out for everyone to see — perhaps a duly unjust circumstance. Therefore, the selective stigma attached to obese individuals can be irrational and may even perpetuate comorbidities such as anxiety and depression. Instead, we should seek to evaluate obesity in a more understanding, yet scientific manner — to question our assumptions when assigning blame to any medical condition. Ultimately, by acting in this way, we can create an atmosphere conducive to prevention and healing.

A Note on the Author: Jonah Stavsky is a pre-medical student at YU completing a major in biology and a double minor in psychology and public health. Jonah is an American Council on Exercise (ACE) Certified Personal Trainer with dual speciality certifications in behavior change psychology and fitness nutrition.