Original of this article was published on ZRT Laboratory Blog. Last reviewed: May 2026.
“Man. Because he sacrifices his health in order to make money. Then he sacrifices money to recuperate his health. And then he is so anxious about the future that he does not enjoy the present; the result being that he does not live in the present or the future; he lives as if he is never going to die, and then dies having never really lived.”
This famous quote strikes me as particularly appropriate for a conversation about stress — especially when we think about the rapidly increasing obesity rates in today’s world.
Today’s Biggest Health Problem?
Most medical experts cite obesity as our most urgent health problem. More than 65% of Americans are overweight to obese, and the numbers are still on the rise — in spite of billions of dollars spent on clinical research aimed at solving problems like diabetes, heart disease, high blood pressure, cancer, and sleep apnoea, all of which are associated with obesity.
Obesity increases free fatty acids, which leads to dyslipidaemia, hypertension, and insulin resistance. This condition, collectively called metabolic syndrome, can progress to type 2 diabetes and/or cardiovascular disease. Obesity also causes mechanical stress to the body, resulting in sleep apnoea, osteoarthritis, low back pain, and shortness of breath. Finally, all the hormones in the body become imbalanced as a result of excessive weight, contributing to further weight gain.
The Bad News Is Getting Worse
In 1970, 45% of Americans were obese. Current projections suggest that figure could reach 74% by 2020. What happened? The answer probably lies in a combination of changed lifestyles, increased sugar and processed food consumption, reduced physical activity, and greater lifestyle stress — as people pay less and less attention to how their habits contribute to their health.
Weight loss may not be too difficult for a motivated person willing to change their eating and exercise habits, but long-term weight management is a different challenge entirely — particularly when hormones are working against you.
How Stress Impacts Weight Gain
For proper weight management, it is extremely important to understand the role of the Hypothalamic-Pituitary-Adrenal (HPA) axis. Any type of stress can lead to HPA dysfunction and related disorders like Cushing’s syndrome, chronic stress, panic disorders, hypothyroidism, adrenal insufficiency, chronic fatigue syndrome, and fibromyalgia. Dysregulation of the HPA axis is a leading cause of metabolic problems that contribute to body fat accumulation.
During a stress response, CRH (Corticotropin-releasing hormone) and AVP (Arginine vasopressin) are secreted. AVP activates the noradrenergic neurons of the Locus Caeruleus/norepinephrine (LC/NE) system and CRH activates adrenocorticotrophic hormone (ACTH) release by the pituitary. The LC/NE system is responsible for the immediate “fight or flight” response, whereas ACTH drives the production of cortisol from the adrenal cortex.
The glucocorticoid hormone cortisol is a major player in the stress response. Cortisol’s main job is to increase gluconeogenesis, decrease insulin sensitivity, reduce growth hormone production, lower thyroid hormones, and inhibit the immune response, while increasing fat and protein mobilisation for energy needs. When cortisol levels are elevated chronically, these short-term survival functions are prolonged, leading to increased visceral adiposity (belly fat) and the conditions known as metabolic syndrome.
To assess whether chronic stress is disrupting your cortisol rhythm and contributing to weight gain, our All Day Cortisol Test (LCMS) measures cortisol across four time points throughout the day — revealing whether your HPA axis is in a state of chronic activation or adrenal depletion.
The Bottom Line on Stress & Weight
Acute stress causes a short-term increase in glucocorticoid release, which induces fatty acid mobilisation and decreased food intake. Chronic stress, by contrast, is associated with sustained cortisol secretion, redistribution of subcutaneous fat to visceral adipose tissue, central obesity, and multiple metabolic and endocrine abnormalities.
When cortisol levels increase under stress conditions, DHEA production also begins to decrease through “the pregnenolone steal” — meaning that under chronic stress, increased cortisol production depletes other hormones sharing a common precursor, including DHEA, progesterone, aldosterone, testosterone, and oestrogens. If the stressor becomes chronic, a phase of stress adaptation begins, characterised by decreased cortisol production, sometimes known as “adrenal fatigue.”
Food consumption also increases during this time as a result of interactions between neuropeptide Y (NPY) and melanocortins, as well as leptin and insulin. Excess cortisol enhances NPY content and induces leptin resistance, thereby inhibiting leptin-induced reduction of food intake — meaning increased cortisol actively induces overeating, worsening obesity despite elevated leptin levels.
Oestrogens influence energy intake and expenditure via hypothalamic signalling and play an important role in body weight, fat distribution, and metabolism. Obesity is also frequently associated with low testosterone levels, involving complex changes in body fat mass, adipokine release, and inflammatory pathways.
For women, our Female Weight Management Profile Test measures the key hormones involved in weight regulation — including cortisol, DHEA-S, oestradiol, progesterone and testosterone — helping to identify the specific hormonal drivers behind weight gain and metabolic dysfunction.
In conclusion, the adipose tissue is actively involved in the metabolism of cortisol, and chronic stress contributes to obesity through a complete imbalance of several hormones impacted by cortisol production. For a broader view of how stress hormones interact with metabolic and cardiovascular markers, our Hormone & CardioMetabolic Test Kit combines hormone testing with key cardiometabolic markers — ideal for anyone concerned about the long-term metabolic consequences of chronic stress.
Original of this article was published on ZRT Laboratory Blog.