Bloomfield Free Press promo

Is obesity really a disease?

Obesity is unquestionably a major risk factor for disease and an increasingly serious societal problem, but is it actually a disease? I would argue that obesity, defined purely by a BMI of >30, is really just a number – an objective finding. In the long-honored tradition of medical science, an objective finding is not a disease, unless it is tied to a pathogenesis. For example, anemia is just a number, and clinicians search for a specific pathogenesis in each patient to determine the proper treatment.

Regarding the pathogenesis of obesity, the textbook “Endocrine and Reproductive Physiology 5th edition” (Elsevier) plainly states: “The amount of energy stored by an individual is determined by calorie intake and calories expended as energy/day.” We can dig deeper and ask why the calorie intake/expenditure imbalance occurs – is it voluntary, for example? But to claim that obesity is not a choice is to say that putting food in one’s mouth is not a choice. If we go that far, we must accept the pathogenesis of obesity as a food addiction or dependence issue, which is an unpopular assessment and considered “fat shaming” by many.

In any case, it is helpful to remember that the human body has elaborate mechanisms of homeostasis. If we accumulate too much sodium, potassium, calcium, water, acid, etc., a normally functioning human body will get rid of the excess. However, we do not have a mechanism for excreting excess caloric intake, meaning that the human body must store all excess energy that is absorbed. Thus, the process of storing energy is not a disease; it is simply normal metabolism.

To state it another way, a disease results from abnormal cellular or physiological functions over which we have no control. I can’t give myself lupus or lung cancer or a stroke. On the contrary, nutritional deficiencies or excesses are something we can both cause and prevent. For example, I could choose to restrict my vitamin D intake and “give myself” vitamin D deficiency. I could choose to drink water until I developed hyponatremia. Neither of these represents a pathological physiology but instead represents a normal response to inappropriate intake. From this perspective, obesity is simply a nutritional excess, not a disease. Claiming otherwise offends the scientific standards of medical science and our understanding of cellular metabolism.

In some circles, experts seem to claim that the “calorie in–calorie out” equation is a myth. However, biochemically, it is simply not possible to do cellular work without metabolic energy. Whether your metabolic rate is high or low, all of your cells still use energy. Even apologists of the obesity epidemic don’t directly deny that weight loss can be achieved by decreasing caloric intake; they only seem to claim that it “shouldn’t be so hard.”

Any fan of the popular reality show “Alone” has witnessed the rapid weight loss of the survivalists who are dumped in the wilderness and left to find food and shelter on their own, some of them losing 60-80 pounds or more in the short course of the competition. The cause of their weight loss is clear – lack of food. Unsurprisingly, there is no randomized controlled trial in which a group of obese individuals is given a calorie-restricted diet and an exercise regimen and fails to lose weight. Let’s admit that if a medical researcher discovered such a clear, inexpensive, and unfailing treatment for any actual disease, we would be awarding her a Nobel prize. Instead, we celebrate a new blockbuster weight loss drug estimated to bring in $60 billion of drug company revenue – a drug that must be taken for life and be accessible to everyone at the taxpayer’s expense. Does anyone else feel suspicious?

Admittedly, there is a rapidly growing understanding of the regulation of hunger and satiety, as well as genome-wide association studies highlighting genes that predispose to obesity. Perhaps we will ultimately find that each individual has a predetermined “BMI setpoint” that determines their equilibrium body mass. If so, we still need to define obesity as more than a number; that is, call it by its pathogenesis: Appetite Threshold Disorder (ATD), BMI setpoint disorder (BMI-SPD), Food Dependence, or Food Use Disorder. In that case, obesity is a potential but not obligatory consequence of the disease. That is, an individual with ATD could either be thin or obese, entirely based on their energy intake, and an individual without ATD could also be either thin or obese.

Recall that Pavlov’s classic experiments on conditioning focused on appetite, and I would argue that our greatest barrier, as a society, to a healthy weight is the cultural conditioning that bombards us daily across the full spectrum of life, and the conscious or subconscious suggestion that hunger pangs must be satisfied at every moment of the day.

Look around you. The ten shelves of candy at the grocery store checkout, the fridge full of sugary drinks next to the gas station pump, the piles of junk mail coupons for fast food and all-you-can-eat buffets, the bowls of bite-size chocolates on office desks, the obligatory “coffee and donuts” at meetings, etc. Even my own call room is packed with shelves of tempting snacks. Consider also that expert flavorists are working on making animal feeds more tasty so that livestock eat more and grow fast – and of course, they’ve done the same thing for human food for decades – to get us to buy and eat more. Luckily, our prefrontal cortex is more developed than livestock, making us more capable of resisting impulses to eat.

In 2013, the American Medical Association officially recognized obesity as a chronic disease, citing a number of favorable impacts that would result from such a label (less stigma, more research, better reimbursement, etc.). Ten years later, we are more obese than ever – and it is no longer our fault – but true to the modern health care playbook, we have tapped into a very lucrative, growing, and secure revenue stream.

Additionally, I find it very ironic that the primary side effect of the breakthrough GLP-1 and GLP-1/GIP receptor agonists is nausea. From a practical standpoint, it seems that all we really need is a medication that causes nausea – and I think we already have plenty of those. But they wouldn’t make any money.

Personally, I love food and constantly struggle to limit my caloric intake. My BMI is not ideal. Maybe I have ATD or BMI-SPD, but the burden is on me. I have a humble respect for the damage my mouth can do, but I realize that I have no obligation to respond to hunger pangs by eating.

Finally, I admit that the obesity epidemic is a very complex and serious societal issue, and I cannot address here all of the psychosocial, biological, genetic, economic, educational, and cultural factors implicated in the growing prevalence of obesity. Above all, I am not “fat-shaming.” I am simply stating that obesity, by the current definition, is not a disease. If I am shaming anyone, it is the medical community for not being bold enough to give obesity “the disease” a proper pathophysiological name and for not being honest enough to attack food-related cultural conditioning as the primary cause of the obesity epidemic.

David M. Mitchell is a hospitalist.

Source link

About The Author

Scroll to Top