Written by Nicole Rakowski, Health Fitness Expert; PhD Health Policy and Management, DeGroote School of Business, McMaster University
Photo Africa Studio - stock.adobe.com
According to the World Health Organization (WHO), nearly two billion people worldwide are considered overweight, and 600 million are said to be obese—triple the number since 1971. Could doing away with weight watching in the name of body acceptance be harmful to our health? And if so, what can we do about it?
Once upon a time, women were consumed with weight watching—to suit swimwear, and a myriad unrealistic fashions and expectations. Thankfully, the movement towards body positivity has shifted us away from such narrow views, and strengthened us all with increased confidence, acceptance, and inclusivity. But, while we celebrate this much-needed progress, it’s important to also remember that for our own good, we can’t entirely do away with watching weight, because doing so could be detrimental to our overall health and well-being. We need to understand that the win is not in dismissing our weight altogether, but being mindful about it—not for looks, but for life.
Many people are aware of the fact that being overweight and struggling with obesity can take a hefty toll on our body and mind. What is perhaps less known is that our weight is connected to virtually every part of us—it sets the stage for our bone, brain, heart, and muscle health, and essentially every other aspect of our lives.
Obesity results from energy imbalances that occur when individuals consume more calories than their body burns, although it is not always that simple and some even argue this may be false. The environment, genetics, certain health conditions, medications, stress, emotional factors, and poor sleep can all contribute to obesity. While true, this topic is often nuanced and understanding the causes from a scientific standpoint is absolutely key in knowing what to do about it.
Do Genes Play a Role in Obesity?
Although obesity has reached epidemic proportions in certain environments around the world that promote physical inactivity and increased consumption of calorie-dense foods, not all individuals will respond the same way. The variation in how individuals respond to the same environment evidently suggests that genes can play a role in shaping obesity.
Genes essentially provide our bodies with a blueprint for responding to changes in our environment. According to the Centers for Disease Control and Prevention (CDC), studies of resemblances and differences among family members, adoptees, and twins offer scientific evidence (although some indirect) that a vast portion of the variation in weight among adults is attributable to genetic factors. Numerous studies have also compared non-obese and obese individuals for variation in genetics that could affect behaviors (such as a compulsion to overeat) or metabolic tendencies (such as decreased capacities to utilize dietary fats as fuels, or heightened tendencies to store additional fat). These studies highlight variants in several genes that have been known to cause polyphagia, otherwise known as extreme or insatiable hunger.
Obesity is far more likely to result from complex interactions amongst multiple genes, coupled with environmental influences (multifactorial obesity) as opposed to being caused by a specific variant of a single gene (monogenic obesity). Interestingly enough and first formulated by the American geneticist James V. Neel in 1962, the “thrifty genotype” hypothesis is worth drawing our attention to. This hypothesis states that the same genes that helped our ancestors survive famines or other food scarcities are now being challenged by environments where food is abundant throughout the year.
The “thrifty genotype” hypothesis states that the same genes that helped our ancestors survive famines or other food scarcities are now being challenged by environments where food is abundant throughout the year.
The “Real” Root Cause
Some scientists will argue that the root cause of the obesity epidemic is actually related to what we eat as opposed to how much we eat. The American Journal of Clinical Nutrition challenges the notion that weight gain occurs due to consuming more energy than is expended. Researchers such as Ludwig et al. state that conceptualizing this energy balance “restates” the principle of physics without considering the biological underpinnings and mechanisms of weight gain.
Some of us may have heard the term “carbohydrate-insulin model” which illustrates obesity as a metabolic disorder that is driven by what we consume, rather than simply how much. Public health messaging has been a large culprit in exhorting individuals to consume less and exercise more. But there is more to the story. Part of the obesity epidemic can be attributable to hormonal responses to changes in food quality; specifically, high-glycemic load foods, which fundamentally change our metabolism.
The Dangers of Obesity
Having excess weight negatively impacts almost every aspect of our health—from respiratory and reproductive function, to brain behavior such as memory and mood. Obesity heightens the risk of numerous debilitating and destructive diseases such as heart disease, certain cancers, and diabetes. Our bodies do not cope well with the mechanical stress of holding extra weight and, more often than not, have detrimental responses to the complex changes in hormones and metabolism. According to the Harvard School of Public Health, obesity diminishes the quality and length of life.
The condition most commonly influenced by excess body weight is type 2 diabetes. Fat cells (specifically those around the waist) secrete hormones and other substances that ignite inflammation. This can lead to decreased responsiveness to insulin and changes the way our body metabolizes fats and carbohydrates, which leads to heightened blood glucose levels and further complications. Another example is obesity’s relationship with cardiovascular disease, which can translate into coronary heart disease, stroke, and cardiovascular death. Even a 5-10 percent reduction in body weight can significantly lower blood pressure, LDL cholesterol and triglycerides, and improve cardiovascular risk factors.
The World Cancer Research Fund and the American Institute for Cancer Research concluded that there was convincing evidence of association between obesity and cancers of the esophagus, pancreas, colon and rectum, breast, endometrium, and kidney, along with an association between obesity and gallbladder cancer. Other studies have also confirmed direct associations between obesity and ovarian cancer.
If these dangers are not shocking enough, obesity can also influence various aspects of reproduction from sexual activity to conception and infertility (specifically ovulatory infertility). It also increases the risk of early and late miscarriage, gestational diabetes, preeclampsia, and complications during labor and delivery, and can also increase the chances of bearing a child with congenital anomalies.
In terms of respiratory complications, obesity has been directly linked to asthma, obstructive sleep apnea, and can significantly impair our overall respiratory function via mechanical and metabolic pathways. The accumulation of fat around the abdomen for instance can limit the descent of the diaphragm and visceral fat can reduce the flexibility of the chest wall, which can narrow the airways in our lungs. Furthermore, the risk of developing Alzheimer’s disease, dementia, gallstones, and eventual mortality are all directly linked to obesity.
All in all, obesity has the potential to harm virtually every aspect of our health. It isn’t necessarily a permanent condition, and prevention at the early stages is key to ensuring a good quality of life.
Our bodies do not cope well with the mechanical stress of holding extra weight and often have detrimental responses to the complex changes in hormones and metabolism.
What Can You Do About It?
Changing our focus and attention to what we eat rather than only looking at how much we eat is a far more effective strategy for weight management. We also need to be aware when making purchasing decisions—whether at the grocery store, a restaurant, or otherwise. In today’s society, we are surrounded by heavily marketed, cheap processed foods with a high glycemic load that make it easy for individuals to consume unhealthy choices, which can be further exacerbated by today’s sedentary lifestyles.
Overeating isn’t always the main culprit of obesity. Our society is largely to blame for advertising foods that cause hormonal responses that essentially change our metabolism, drive fat storage, and lead to weight gain. Rather than urging the population to eat less, a strategy that has been proven time and time again is not always sustainable, we need to urge individuals to change their paradigm to think about what we consume. Reducing our consumption of rapidly digestible carbohydrates that flood and overwhelm our food supply is one option.
Other factors such as not having access to parks and affordable gyms makes it hard for individuals to be physically active. Certain conditions such as underactive thyroid, Cushing syndrome, or polycystic ovary syndrome can also contribute to weight gain. Certain medications such as corticosteroids, antidepressants, or seizure medications can all have an influence. Our bodies also release hormones during sleep that help control our appetite and the body’s use of energy—a lack of sleep can contribute to obesity or being overweight.
It is important to understand that the environment, genetics, certain health conditions, medications, stress, emotional factors, and poor sleep can all contribute to obesity. This considered, we must remember to be kind and patient with ourselves and each other, realizing that the world we live in continues to influence our ability to maintain a healthy weight. And in the process, embrace conversations about weight with compassion rather than dismiss them, so we can continue celebrating the really big things in life—health, opportunity, and longevity.
The environment, genetics, health conditions, medications, stress, emotional factors, and poor sleep can all contribute to obesity.
References:
Castillo, J. J., Orlando, R. A., & Garver, W. S. (2017). Gene-nutrient interactions and susceptibility to human obesity. Genes & nutrition, 12, 1-9.
Centre for Disease Control and Prevention (CDC). (2023). Obesity. Genomics & Precision Health Home. Retrieved from: https://www.cdc.gov/genomics/resources/diseases/obesity/index.htm#:~:text=Genes%20give%20the%20body%20instructions,is%20due%20to%20genetic%20factors.
de las Fuentes, L., Waggoner, A. D., Mohammed, B. S., Stein, R. I., Miller, B. V., Foster, G. D., ... & Davila-Roman, V. G. (2009). Effect of moderate diet-induced weight loss and weight regain on cardiovascular structure and function. Journal of the American College of Cardiology, 54(25), 2376-2381.
Dengo, A. L., Dennis, E. A., Orr, J. S., Marinik, E. L., Ehrlich, E., Davy, B. M., & Davy, K. P. (2010). Arterial destiffening with weight loss in overweight and obese middle-aged and older adults. Hypertension, 55(4), 855-861.
Huda, S. S., Brodie, L. E., & Sattar, N. (2010, April). Obesity in pregnancy: prevalence and metabolic consequences. In Seminars in Fetal and Neonatal Medicine (Vol. 15, No. 2, pp. 70-76). WB Saunders.
Look AHEAD Research Group. (2010). Long-term effects of a lifestyle intervention on weight and cardiovascular risk factors in individuals with type 2 diabetes mellitus: four-year results of the Look AHEAD trial. Archives of internal medicine, 170(17), 1566-1575.
Ludwig, D. S., Aronne, L. J., Astrup, A., de Cabo, R., Cantley, L. C., Friedman, M. I., ... & Ebbeling, C. B. (2021). The carbohydrate-insulin model: a physiological perspective on the obesity pandemic. The American journal of clinical nutrition, 114(6), 1873-1885.
McClean, K. M., Kee, F., Young, I. S., & Elborn, J. S. (2008). Obesity and the lung: 1· Epidemiology. Thorax, 63(7), 649-654.
Qasim, A., Turcotte, M., De Souza, R. J., Samaan, M. C., Champredon, D., Dushoff, J., & Meyre, D. (2018). On the origin of obesity: identifying the biological, environmental and cultural drivers of genetic risk among human populations. Obesity reviews, 19(2), 121-149.
Stothard, K. J., Tennant, P. W., Bell, R., & Rankin, J. (2009). Maternal overweight and obesity and the risk of congenital anomalies: a systematic review and meta-analysis. Jama, 301(6), 636-650.
Sun, X., Li, P., Yang, X., Li, W., Qiu, X., & Zhu, S. (2017). From genetics and epigenetics to the future of precision treatment for obesity. Gastroenterology report, 5(4), 266-270.
Van Andel Research Institute. (2022). Scientists redefine obesity with discovery of two major subtypes. Science News. Retrieved from: https://www.sciencedaily.com/releases/2022/09/220912132339.htm
WCRF, A. (2007). Food, nutrition, physical activity, and the prevention of cancer: a global perspective. AICR, Washington DC.
WHO (2023). Obesity and overweight. Retrieved from: https://www.who.int/news-room/fact-sheets/detail/obesity-and-overweight
