The other responses were, “Yeah, that’s pretty bad, OK, so now what?” These issues of diet, obesity, and processed foods causing health problems are hugely complex. To get to the answers, let’s do what we pilots naturally do and pull back on the stick, gain some altitude, and look at the big picture. This month I’ll talk about genetic and metabolic factors that lead to obesity and next month we’ll tackle how it can be managed, in addition to the dietary changes I’ve already stressed.
There’s ample data that supports the principles detailed last month that a significant proportion of the country’s obesity problem is related to choices with diets and lifestyle. Since human genetics haven’t changed and the rate of obesity in America has nearly tripled since the 1960s (70% of our population is now overweight), a lot of this has to be related to environmental factors and life choices. Still, it’s way too simplistic to just write off obesity like a math equation, “take in more calories than you burn and you store all the extra as fat.” To get an idea of just how complex this subject is, click on the National Library of Medicine site, affectionately known as “PubMed“ in the medical world, and type “obesity” in the search bar. You’ll get 48,879 links to recent peer-reviewed medical publications on the topic.
Last month I quoted the medical definition of “obesity” as a body mass index (kg/m2) BMI > 25; all that means is you’re carrying around too much weight for your height. It’s easy to find out if you qualify; just click on this link or any BMI calculator app. In medical speak, obesity is “a response to environmental stimuli, genetic predispositions and abnormalities, that has a characteristic set of signs, symptoms, and diseases consistent with anatomical alterations in weight.” That’s quite a mouthful—pun intended—but what’s it all mean? The key to this definition is that obesity is both genetic and environmental. Due to this dual threat, just modifying your environment (like changing dietary choices and lifestyle) to control your weight is only part of the solution. It’s this genetic predisposition to obesity that makes it really hard for some people to lose weight and maintain the weight loss. That’s part of the answer to my reader’s question, “So, what’s up with that?”
Most genetic explanations center on a “set point theory“ that assumes strong genetic and hormonal control of body weight run by feedback systems that keep you around a fairly constant set point, called the “body-inherent” weight. The control systems adjust food intake in proportion to the difference between the current and genetically predetermined set point weight. Recent research has mainly focused on the biology of the feedback loop between adipose tissue (fat) and the different parts of the brain. Two chemicals, insulin and another one called leptin, primarily manage the feedback loops. Leptin is an amino acid hormone (actually 146 amino acids strung together) manufactured and released from adipose (fat) tissue and the stomach. Its production is driven by one of those genes; appropriately called the “obese gene,” abbreviated as the “Ob” gene, and located on the 7th chromosome. Leptin regulates your appetite and is the “satiety signal,” meaning leptin tells your brain that you’ve eaten enough and, as long as you heed that little voice in the back of your head, it’s time to put the food and dishes away. There are two genetic factors that go into determining your weight. The first is how much you need to eat to reach your satiety set point and the other is how much leptin it takes to shut off your appetite at your “satiety” weight point since your brain’s sensitivity to leptin is also genetically predetermined. Leptin is secreted from fat cells, so the amount of leptin you have is proportional to the amount of fat you carry around, or fat mass (FM). The more fat you have, the more leptin you secrete, and the more it takes to reach your “satiety point.”
The other chemical in this chain reaction is insulin. One of the many adverse health side effects of increased weight is that increasing levels of leptin increases insulin levels at the same time. Your body secretes insulin in response to dietary intake in order to store those extra calories. As we all know, the storage site for excess calories is fat cells. Too much leptin leads to making too much insulin (hyperinsulinemia), and with that your body develops resistance to insulin and rising blood glucose levels (hyperglycemia). That’s what drives the very common association of adult-onset obesity and adult-onset diabetes (Type II diabetes) with all of its medical and health consequences. The vicious cycle of increasing leptin and insulin continues to spin and leads to even more fat deposition, more insulin and leptin secretion, and more insulin resistance, more weight gain and worsening diabetes. Artificially made forms of leptin are under investigation in the treatment of obesity, but replacement in typically obese patients has shown no real clinical value. Hyperinsulinemia (diabetes) is treated with insulin or an oral insulin substitute.
Compared with the set point idea, an alternative model to explain changes in body weight is out there that postulates there are multiple “body weight steady states.” The feedback loops are the same but this model says that during weight gain or weight loss, the differences between caloric intake and energy use diminish more and more owing to increases or decreases in fat mass. Your body weight fluctuates and leads to a new steady state at a lower or higher body weight. This new steady state in body weight is called the “settling point.” In this situation, the body’s “set point” (i.e., a constant “body-inherent” weight regulated by a proportional feedback control system) is replaced by various “settling points” that are influenced by energy and nutrient intake in order for the body to balance energy use with caloric consumption. The catch here is that adjusting your body’s steady state weight is really difficult in our world of overabundance and junk food. As the article cautions, “A prudent lifestyle and thus cognitive control are preconditions to achieve effective biological control and a stable body weight.” This is a key reason patients have trouble losing weight and maintaining lower total body fat content.
With all that as background, it brings us to the second question you had after reading those dire statistics: “OK, so what now?” Stay tuned; next month I’ll cover that topic. Until then, eat right, get off the couch, and as always, fly safe!
