Obesity as a Hormonal Disorder
This blog is intended to be viewed through a clinical lens, as an alternative explanation to be explored in pathological, not subjective obesity. When it comes to obesity, it should always be taken into consideration that each individual has a different ideal weight. Determining obesity based on the number on the scale or BMI is outdated and contributes to skewed societal norms and fat phobic culture.
We see in the medical, nutrition and personal training spheres, the calories in/out method is still widely being taught and executed. This is based on the theory that obesity is caused by insufficient movement paired with an over consumption of calories. As we dive into the hormonal implications of obesity and weight gain, we can see how this school of thought is incomplete and by implementing it in a clinical setting can have detrimental effects. Obesity is a field that is still not fully understood, but here we propose the idea of obesity as a complex hormonal disorder.
Obesity is a worldwide epidemic, placing an increasing strain on global health systems. Excess adipose tissue (body fat) negatively impacts all body systems and is therefore associated with insulin resistance, hyperglycemia, type II diabetes, arterial hypertension, dyslipidemia (high triglycerides, low HDL, high small dense LDL), many types of cancer and more.
Unfortunately, despite extensive research on causal and mediating mechanisms, the conventional treatments using calorie-restricted diets still lack long-term efficacy.
Meta-analyses of calorie restricted diets and lifestyle interventions show that roughly 2/3rds of obese dieters regain more weight than originally lost.
The Importance of Understanding Obesity as a Holistic Practitioner:
Excess weight, obesity and related health concerns are common issues seen in those who seek out nutritional practitioners. Given the lack of long-term efficacy in conventional dietary and lifestyle interventions, it is of paramount importance to understand the complex interplay of factors that underlie obesity in order to effectively and appropriately guide clients.
The Conventional Model of Obesity - Calories in and calories out
Obesity is defined as being the result of an imbalance in energy consumption and energy expenditure which leads to increased adiposity over time. The problem with this approach is that it is a symptom based treatment that doesn’t address the underlying systemic issues that may cause, exacerbate or maintain the obese state. Presently we don’t really understand the underlying cause, but emerging research is starting to shed light on what might be the key to understanding this worldwide health issue: and that answer might lie in our hormones.
Bodyweight is controlled by a complex interplay between the central nervous system, peripheral signals of energy balance from fat tissue and the GI tract as well as the endocrine system. Consistently, obesity is associated with significant changes to endocrine function and hormones. While it is thought that many of these changes may be secondary to obesity, research is beginning to show that some of these hormones may play a role in its pathogenesis.
Let’s Meet Our Hormonal Players
One of the most well-known changes that occurs in obesity is insulin secretion and insulin resistance. Research continually shows that obese individuals have increased insulin concentrations.
It is one of the main hormones that controls blood sugar and when blood glucose levels increase after a meal, insulin is released to shuttle glucose into cells for energy. It also promotes fat storage. Overtime, excess insulin production can lead to the state of insulin resistance whereby cells stop listening to this hormone and glucose is therefore not effectively brought into body cells for energy. As insulin is anabolic, the result is a chronic metabolic state that promotes fat storage.
Adipocytes secrete leptin in direct proportion to body weight and nutritional status. This secretion is greater from subcutaneous compared to visceral fat mass. So why is that important? Leptin’s main role is to signal energy sufficiency therefore playing a key role in satiety and energy balance. Since leptin is secreted by fat cells, in obese individuals, studies consistently find higher circulating leptin levels than in non-obese participants.
So how does this contribute to obesity? - Leptin resistance. While the mechanism of leptin resistance is currently unknown, it may be the result of defects in the leptin signal or transport through the blood brain barrier to higher order brain centers. Obese individuals appear to be resistant or insensitive to leptin because despite high circulating levels, appetite and body fat do not reduce.
Complicating the picture even further, these high leptin levels rapidly decrease with calorie-restriction and weight loss resulting in the classic adaptation to hunger: appetite increases and metabolic rate decreases. This may be one of the reasons that calorie-restricted diets tend to have a low long-term success rate.
Another hormone that is secreted by adipose tissue is adiponectin. This hormone has been shown to enhance cell responsiveness to insulin (increased insulin sensitivity). Interestingly, there is a strong negative correlation between plasma adiponectin levels and fat mass and studies show that levels are decreased in obesity compared with normal weight individuals.
Stress and weight gain. This is a subject that has been long investigated. While results in studies are mixed, we do know that glucocorticoids (cortisol) increase appetite and the preference for energy dense food.
Glucocorticoids can also cause redistribution of white adipose tissue to the abdominal region and suppresses the activity of brown adipose tissue, resulting in abdominal obesity and decreased mitochondrial function. Abdominal obesity is more metabolically active than other fat and can lead to a negative metabolic-hormonal cascade.
With respect to cortisol, what has been consistently demonstrated is that urniary free cortisol levels are significantly increased in obese women with excess abdominal fat than compared to normal weight individuals. In those with increased abdominal fat we also see exaggerated responses to cortisol and increased free and total cortisol rates. This fundamentally suggests that excess cortisol production may contribute to the development of obesity.
One of the most obvious changes seen in obesity with regards to hormone dysregulation is that of growth hormone. Regardless of age, the higher the BMI, the lower the secretion of growth hormone. It has been theorized that the reason for this impared secretion in obesity might be due to a disturbance in peripheral hormone signals that impact the hypothalamus. These peripheral hormone signals are gut hormones.
Peripheral Gut Hormones:
Ghrelin is a peptide hormone produced predominantly in the stomach and it stimulates growth hormone secretion, appetite, positive energy balance, controls gastric motility, acid secretion and influences behaviour and sleep. Its levels are inversely related to body mass, body fat mass, plasma leptin levels as well as glucose and insulin levels.
Most interesting to the topic of obesity is that ghrelin appears to play a role in the metabolic and neuroendocrine response to food consumption. While it may seem counterintuitive, circulating levels of ghrelin are decreased in obesity. Studies suggest that ghrelin may play a critical role in feeding, weight control and long-term regulation of body weight and energy balance.
Peptide-YY is a peptide hormone released by enteroendocrine L-cells in the GI tract. Secretion and circulating levels of PYY directly increase in response to nutrient intake, caloric load, food consistency and nutrient composition. The function here is to reduce food intake. It therefore plays a key role in post meal satiety signalling the body to feel full and increase energy expenditure. In studies of obese subjects, results seem to indicate that obese individuals possess lower post-meal PYY concentrations as well as divergent differences between fasting PYY concentrations when compared to lean individuals.
Glucagon-Like-Peptide-1 is a peptide released from the ileum and colon in response to the ingestion of macronutrients: fat, carbohydrates and proteins. It’s role lies in decreasing the rate of gastric emptying to the duodenum, hinders the secretion of gastric acid and stimulates gastric distension to limit acute excessive intake of food, enhance satiety and positively contribute to energy homeostasis. Like the other peripheral hormones, dysregulation of GLP-1 is noted in the obese, compared to healthy weight individuals.
Obese individuals show slightly increased levels of TSH compared to normal weight subjects, without the presence of autoimmune thyrdoitits or related disorders. One theory suggests that increased TSH levels may be due to hormone resistance in obese subjects. Furthermore, fasting and weight loss are correlated with a decrease in thyroid hormone production. This suggests that, like decreased leptin levels, thyroid hormones may contribute to the difficulties in maintaining weight loss.
So why is this happening in the first place?
There is no real consensus as to why hormonal imbalances are presesnt in obese individuals. On the one hand, excessive weight gain and increased adiposity could lead to body-wide metabolic disturbances which dysregulate hormones. On the other hand, dietary, lifestyle and environmental factors could lead to dysregulation of metabolic and hormonal pathways that cause hormonal dysregulation and therefore fat accumulation.
One interesting theory involves the impact of the environment via toxic chemical exposure. There are a class of environmental toxins termed obesogens that have shown to disrupt hormonal and metabolic pathways resulting in dysregulation and fat accumulation.
These common chemicals interfere with the production, release, transport, metabolism, binding, action and elimination of hormones that are responsible for human metabolism. They are even able to reprogram different signalling pathways. Some can even directly impact obesity by increasing the size of fat cells. These common chemicals may be key players in the rise in obesity worldwide.
polycyclic Aromatic hydrocarbons (byproducts of fuel burning)
bisphenol A (plastics)
flame retardants (found on furniture)
phthalates (found in fragrances and cosmetics)
alykylphenols in a variety of cleaning products
parabens that are used as antimicrobial agents to preserve a number of common household products and in personal care products
The Chicken or the Egg: Why it doesn’t matter what comes first?
It is clear that science has yet to understand the underlying etiology of obesity beyond the simplistic model of calories in and calories out. However, what is becoming clear is the role of hormones.
Whether obesity causes a hormonal dysregulation or obesity is the symptom of hormonal dysregulation doesn’t really matter here. What is important is that the obese state means hormonal imbalance. To ignore this fact is to ask a client to fight an uphill battle. Therefore, in order to effectively work with clients struggling with excess weight and obesity, these imbalances need to be addressed to yield consistent, positive results. The calorie in and out method might produce temporary results but it disregards the irregular physiology seen in induviduals with excess adipose tissue and therefore promotes chronic disease down the line.
Katie Hogg is a soon to be graduate from the Institute of Holistic Nutrition (IHN), Toronto. She holds a Bachelor of Arts from the University of Western Ontario with a major in Psychology. Her own personal struggle with chronic, undiagnosed health issues lead her to pursue her education in Holistic Nutrition after experiencing first hand the profound benefits that changes in diet, lifestyle and supplementation had on her health. This experience led her to develop a profound passion for learning, researching and sharing up-to-date information to nutrition and health based questions. Aside from her passion for all things food, health and nutrition, Katie spends her time painting, reading and hiking with her dog.