Obesity is a Disease.
I am very interested in the pathophysiology of obesity — I believe it is a socioeconomic problem; a multifactorial disease that is highly nuanced, and consequently, highly disputed. I wrote this argumentative paper for my Anatomy and Physiology class, but I thought I’d upload it here too.
One more thing — I am very interested in your opinion. Have a question, comment, or contention? Let me know! My beliefs, although scientifically supported, are malleable, and I always want to learn and grow.
Worldwide, in 2021, the prevalence of children and adults with obesity was 5 and 13%, respectively. This equates to 107.7 million children and 603.7 million adults. Moreover, it was estimated that obesity accounted for approximately 4 million deaths worldwide in 2021 (Ritchie and Roser, 2017). The general rhetoric around weight loss goes, “just eat less and exercise more! Be in a calorie deficit! Walk 10,000 steps a day, and do HIIT once a week! Eat only protein, don’t eat too much fat, and, for the love of God, do not eat too many carbs!”
You’ve probably heard this advice hundreds of times over — from your doctor, your mom, your trainer, health “experts’’ on the internet, or your well-intentioned best friend. To an extent, they’re right. For the average, metabolically healthy, genetically typical person, eating in a calorie deficit and improving the macronutrient makeup of their diet will result in weight loss. But what about the 18% of the world that are not metabolically healthy, nor genetically lucky? And what if they’ve grown up around unhealthy eating behaviours? What if they have little access to nutritious food? Suddenly, it’s a whole lot harder to lose weight. A person who can check off any one of these boxes is predisposed to obesity, and keeping weight off as an obese individual has proven to be incredibly difficult. The rhetoric that obesity is a result of one’s own flawed moral compass, that it is a “choice” and that it can be solved with a commitment to a diet is belittling and naive at best. We learn more and more about obesity every day, and what we know for sure is that it’s a complex chronic disease caused by a combination of environmental factors, including socioeconomic status, chemical and toxic load, and food quality. These “obesogenic” elements induce the hypothalamus to increase the body’s baseline weight. Because of the complex nature of obesity, most medical institutions and organizations now consider obesity a chronic disease, and we should too: to decrease the rampant stigma towards those struggling with it.
Chronic diseases are not congenital, but are triggered by external stimuli, like stressful events, poor nutrition, and smoking. Obesity, as a chronic disease, is much the same. Babies are not born obese. They become obese, not by chance or lack of discipline; to the contrary — they live in obesogenic environments. Hippocrates was the first to assert that environmental influences had an impact on health and emphasized the importance of achieving harmony between the individual, social, and natural environments. In the modern era, the phrase “obesogenic environment” has been used to describe the effects that the environment, opportunities, or conditions of living have on encouraging obesity in both individuals and populations. Paired with genetics that predispose the body towards excess adiposity, it is unsurprising that so many people suffer from the disease of obesity. Our genes have not changed appreciably over the past several decades implying that environmental changes must have caused the current obesity epidemic. One of my favourite analogies, “genetics load the gun, but your environment pulls the trigger”, models this paradigm perfectly — and in today’s modern world, there’s a whole lot of trigger-pulling going on. I have chosen to highlight three environmental factors that contribute to obesity: socioeconomic status, chemical and toxic load, and food quality. However, obesity is likely caused by a combination of these and the many factors I have not listed here.
Socioeconomic status (or SES) is a way of categorizing people based on their income, job, and level of education. Low socioeconomic status is an environmental factor that heavily influences the health outcomes of those who hold it. For example, dozens of studies have shown that lower socioeconomic status is robustly associated with obesity. Several mechanisms have been identified; like having little access to nutritious food, little access to outdoor spaces (and by accord exercise), and living in a stressful environment. In one study, participants who were experimentally induced to feel poor consumed significantly more calories from snack foods compared with participants who were induced to feel wealthy (Bratanova et al, 2016).
Chemical and toxic load is another example of an environmental factor strongly correlated with obesity. Never before have humans been exposed to so many synthetic substances, most of which have not been tested for safety over the long term. Most obesogens are endocrine disruptors, chemicals that interfere with the body’s hormones and metabolism. BPA is the textbook example of an obesogenic chemical. Most people know of Bisphenol-A as toxic to the reproductive system, but its estrogen-mimicking properties induce insulin resistance, inflammation, oxidative stress, and promote the formation of fat cells. Similarly, phthalates, a group of chemicals used in plastic, have been shown to modulate androgenic and cell signaling hormones and are directly correlated to the development of obesity and Type 2 Diabetes. Triclosan, an ingredient found in most personal care products like soap and skincare, is linked to numerous human health problems, including obesity (Yueh and Tukey, 2016). Other endocrine-disrupting chemicals are frequently found in drinking water all over the world, particularly in populations of lower SES (Liu, 2016).
Food quality is a determinant of health, and accordingly, body size. Some scientists hypothesize that suboptimal macronutrient composition of the diet is a cause of obesity, but the truth is that it is more convoluted than that. Isolating macronutrients like fats and carbohydrates is not only inconclusive in evidence, but also places blame on obese individuals; if they only tried a Ketogenic diet and ate low calorie, they wouldn’t be obese! Further, evidence has shown that it is not macronutrient makeup that drives obesity, but rather food quality and how it affects subsequent energy consumption. Economic and policy pressures to increase agricultural production of inexpensive crops (such as corn and soy) makes for an industrialized food system that produces and intensively markets cheap, convenient, highly-processed “added value” foods. The comparatively high salt, sugar, fat, and flavouring contents of these foods, together with their artificially enhanced supernormal appetizing qualities, lead to higher consumption. Research done on teenagers whose diet consisted mainly of ultra-processed food found that they were 45% more likely to have obesity. Another study showed that adults who ate a highly processed diet ate 500 calories more per day than a non-processed food-consuming control group (Neri, 2022). But why do the ingredients in processed food lead to increased consumption? Common additives like artificial colours and flavours, partially hydrogenated oils, high fructose corn syrup, preservatives, and accidentally-added pesticides, plastics, and pollutants have all been directly or indirectly correlated to obesity. Polysorbate 80, an emulsifier found in frozen desserts, shortenings, baking mixes and icings, and canned vegetables, was found to alter the gut microbiome negatively, provoking inflammation and correlating with obesity (Singh and Ishikawa, 2016). BHT, a preservative found in cereals and prepared snacks disrupts endocrine and immune function (Lanigan, 2002). Glyphosate, a pesticide commonly used on crops like oats, corn, wheat, and fruit is known to cause obesity, cancer, and kidney disease. Moreover, these effects were shown to be multi-generational, meaning the effects of glyphosate lasted up to four generations.
I want to ask one more question, a question that requires a little bit of thought. WHO eats processed food? If you answered “most everyone in the world,” you’re right. However, the reality is that those who eat the most processed food are those with low socioeconomic status. Highly processed food grown with pesticides and packaged with preservatives is much cheaper than its organic, fresh counterpart. It is also more accessible for individuals living in food deserts; areas where there is little access to whole food, and accordingly little education about healthy eating. A feedback loop of unhealthy behaviours is passed down generationally, and the root societal problem is never fixed. Chemical and toxic load are directly correlated to obesity, and are difficult to control: the purity of drinking water, the materials that make up everyday objects, and the ingredients in things like skin care products are the responsibility of the institutions that supply them. Food quality is in the hands of the producers and the politicians who have power over the producers. Ultimately, obesity is so much more than an individual fault, and rather the outcome of life in an obesogenic environment.
I want to pose a question: can you control everything your brain does? Do you have autonomy over your heartbeat? Your lungs? The answer is no. In the way that your heart and lungs are autonomous functions controlled by the brain, the same may be said for adiposity.
The hypothalamus, a structure deep within the brain, controls most of the mechanisms relating to energy expenditure and hunger. Neurons involved in the regulation of feeding are located in this structure, and manage hormonal processes that relate to fat burning, satiety, fat storage, and fullness. Regulation of body fat by the hypothalamus is automatic, so it can be compared to an automatic thermostat, or adipostat, that likes to maintain homeostasis: balance. However, in obese individuals, the adipostat may shift unfavourably, recalibrating the body’s homeostasis, or “set point” higher than those of normal body weight (Hernandez, 2016). A set point in an obese individual is not just a consequence of laziness and overeating; to the contrary, it is a dysfunction of the hypothalamus worsened by a spiderweb of factors like hormones, socioeconomic status, metabolic health, energy balance, and toxins. In short, the hypothalamus wants to maintain a healthy body, but in the case of obesity, it recalibrates higher than optimal, causing a set point that is notably higher than in non-obese individuals. It is important to note that because the hypothalamus so tightly regulates the set point, it is incredibly hard to shift. Many dieters find that they regain weight lost in the long run, despite their best efforts to keep it off. In an infamous study, the Minnesota Starvation Experiment, 36 men were induced to lose 25% of their body weight by restriction of more than half their daily caloric need. During the rehabilitation period — even though participants were warned against it — some engaged in extreme overeating. Additionally, by the end of the semi-starvation period, the participant’s Basal Metabolic Rate (the number of calories burned at rest) had decreased by 40% from their baselines (Keys et al, 1950). In extrapolating these findings to the subject of obesity, we can conclude that caloric restriction induces the body to replace calories lost, as well as try to compensate for starvation by lowering the number of calories needed at baseline. That’s because losing weight triggers biological mechanisms that make it harder to keep the weight off. Metabolism acts like a spring: The more effort you put into losing weight, the more you can stretch that spring out — that is, lose weight. But if you let up the tension on the spring — by stopping whatever eating and exercise routine (i.e. calorie restriction) that helped you lose weight — your metabolism will spring back and you’ll regain the weight you lost.
When we apply this to obesity, it is clear that obese individuals who try to lose weight may find it difficult to do so, and if they succeed, may find it even more challenging to keep weight off, whilst their hypothalamus is fighting against them to restore homeostasis (Hall et al, 2016). This is why, like many chronic diseases, obesity tends to recur and can worsen over time.
Because of the complex web of factors that contribute to the development of obesity, many reputable organizations including Obesity Canada, the Canadian Medical Association, the American Medical Association and the World Health Organization now consider obesity to be a chronic disease. Britannica calls a disease “any harmful deviation from the normal structural or functional state of an organism,” and Merriam Webster names it “a condition of the living animal or plant body or of one of its parts that impairs normal functioning and is typically manifested by distinguishing signs and symptoms.” It is easy to conclude that at textbook value, obesity is as much a disease as myocarditis and sickle cell, and recognizing obesity as a disease, not an individual lifestyle choice, helps us shift the deeply held societal belief that people with obesity simply lack willpower and just need to eat less and exercise more.
Many wrongly consider the obese to be lazy and indulgent. Classifying obesity as a disease may help undermine these negative stereotypes by reminding the public that obesity is a chronic disease caused by many factors, including but not limited to the brain and the environment. Labeling it as a disease is expected to improve attitudes and financial support for obesity treatment. This would include more resources for health promotion, research into the behavioral, environmental, and genetic causes, as well as prevention and treatment. It would improve insurance coverage and reimbursement for screening, health promotion, prevention, and treatment. The economic and emotional costs of obesity will keep rising in the absence of comprehensive, evidence-based, and person-centered treatments. Ultimately, because of the nature of obesity as a multifactorial, societal, and environmental problem, it is a disservice not to classify obesity as a disease, not only for the 18% percent of the population that suffers from it; but for the health of generations to come.
Works cited:
Amato, A. A. (2021, February 1). Obesity and endocrine-disrupting chemicals. EC. Retrieved October 11, 2022, from https://ec.bioscientifica.com/view/journals/ec/10/2/EC-20-0578.xml
Bentham Science Publishers. (n.d.). The Hypothalamus and Obesity: Ingenta Connect. Retrieved October 11, 2022, from https://www.ingentaconnect.com/content/ben/cdt/2005/00000006/00000002/art00009
Brain Regulation of Appetite and Satiety. (2008, December). Science Direct. Retrieved October 11, 2022, from https://www.sciencedirect.com/science/article/abs/pii/S088985290800056X?via%3Dihub
Childhood obesity is a complex health issue. (2022, March 21). Centers for Disease Control and Prevention. Retrieved October 11, 2022, from https://www.cdc.gov/obesity/basics/causes.html
Egger, G. (1997, August 23). An “ecological” approach to the obesity pandemic. The BMJ. Retrieved October 11, 2022, from https://www.bmj.com/content/315/7106/477
Elmquist, J. K. (1999, February 1). From Lesions to Leptin. Neuron. Retrieved October 11, 2022, from https://www.cell.com/neuron/fulltext/S0896-6273(00)81084-3?_returnURL=https://linkinghub.elsevier.com/retrieve/pii/S0896627300810843?showall=true
Heshka, S. (2001, October 23). Is obesity a disease? Nature. Retrieved October 11, 2022, from https://www.nature.com/articles/0801790?error=cookies_not_supported&code=f582688a-956d-41a0-a982-7513269913f5
Hobbs, M. (2020, March 18). Obesogenic environments and obesity: a comment on ‘Are environmental area characteristics at birth associated with overweight and obesity in school-aged children? Findings from the SLOPE (Studying Lifecourse Obesity PrEdictors) population-based cohort in the south of England’ — BMC Medicine. BioMed Central. Retrieved October 11, 2022, from https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-020-01538-5
Member, S. (n.d.-a). Obesity in Canada. Obesity Canada. Retrieved October 11, 2022, from https://obesitycanada.ca/obesity-in-canada/
Member, S. (n.d.-b). What Causes Obesity? Obesity Canada. Retrieved October 11, 2022, from https://obesitycanada.ca/understanding-obesity/
Model of the home food environment pertaining to childhood obesity. (2008, March 1). Oxford Academic Nutrition Reviews. Retrieved October 11, 2022, from https://academic.oup.com/nutritionreviews/article/66/3/123/1858048
Neri, D. (2022, August 1). Associations Between Ultra-processed Foods Consumption and Indicators of Adiposity in US Adolescents: Cross-Sectional Analysis of the 2011–2016 National Health and Nutrition Examination Survey. Journal of the Academy of Nutrition and Dietetics. Retrieved October 11, 2022, from https://www.jandonline.org/article/S2212-2672(22)00033-8/fulltext
Obesity — Symptoms and causes. (2021, September 2). Mayo Clinic. Retrieved October 11, 2022, from https://www.mayoclinic.org/diseases-conditions/obesity/symptoms-causes/syc-20375742
Obesity as chronic disease | British Columbia Medical Journal. (n.d.). Retrieved October 11, 2022, from https://bcmj.org/cohp/obesity-chronic-disease
Poverty, inequality, and increased consumption of high calorie food: Experimental evidence for a causal link. (2016, May 1). Science Direct. Retrieved October 11, 2022, from https://www.sciencedirect.com/science/article/abs/pii/S0195666316300277?via%3Dihub
Rajamani, U. (2017, August 9). RETRACTED ARTICLE:Endocrine disruptors induce perturbations in endoplasmic reticulum and mitochondria of human pluripotent stem cell derivatives. Nature. Retrieved October 11, 2022, from https://www.nature.com/articles/s41467-017-00254-8
Sherman, T. (2015, December 10). How Do We Gain Weight? 03: Hypothalamic Obesity | Georgetown Food Studies. Retrieved October 11, 2022, from https://blogs.commons.georgetown.edu/gufoodstudies/2015/12/10/how-do-we-gain-weight-03-hypothalamic-obesity/
Simmons, A. L. (2014, February 23). What Are We Putting in Our Food That Is Making Us Fat? Food Additives, Contaminants, and Other Putative Contributors to Obesity. SpringerLink. Retrieved October 11, 2022, from https://link.springer.com/article/10.1007/s13679-014-0094-y?error=cookies_not_supported&code=77873ca1-c5a1-4a4b-a3a6-116025892cca
Wilding, J. (2012, September 11). Are the causes of obesity primarily environmental? Yes. The BMJ. Retrieved October 11, 2022, from https://www.bmj.com/content/345/bmj.e5843.full
Zani, S. (2021, March 22). Obesity: A chronic disease, not a choice. Faculty of Medicine & Dentistry. Retrieved October 11, 2022, from https://www.ualberta.ca/medicine/news/2021/03/obesity-a-chronic-disease,-not-a-choice.html
Ritchie, H. (2017, August 11). Obesity. Our World in Data. Retrieved October 11, 2022, from https://ourworldindata.org/obesity
Persistent metabolic adaptation 6 years after “The Biggest Loser” competition. (2016, May 2). Wiley Online Library. Retrieved October 11, 2022, from https://doi.org/10.1002/oby.21538
Liu, G. (2018, February 13). Perfluoroalkyl substances and changes in body weight and resting metabolic rate in response to weight-loss diets: A prospective study. PLOS Medicine. Retrieved October 12, 2022, from https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002502
Triclosan: A Widespread Environmental Toxicant with Many Biological Effects. (2016, January). Annual Review of Pharmacology and Toxicology. Retrieved October 12, 2022, from https://www.annualreviews.org/doi/10.1146/annurev-pharmtox-010715-103417?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed
Final Report on the Safety Assessment of BHT. (2002). Sage Journals. Retrieved October 12, 2022, from https://journals.sagepub.com/doi/10.1080/10915810290096513
Gómez-Hernández, A. (2016, September 27). Differential Role of Adipose Tissues in Obesity and Related Metabolic and Vascular Complications. Retrieved October 12, 2022, from https://www.hindawi.com/journals/ije/2016/1216783/
The Starvation Experiment | Duke Center for Eating Disorders. (n.d.). Retrieved October 15, 2022, from https://eatingdisorders.dukehealth.org/education/resources/starvation-experiment
