Stress and Obesity: The Biological Connection

Obesity causes many negative changes within our physiology. Obesity can cause systemic inflammation which causes an increase in production of reactive oxygen species (ROS) that cause oxidative stress.  Oxidative stress will contribute to mitochondrial dysfunction. Consuming excessive amounts of macronutrients and calories can overwhelm the Krebs cycle and the mitochondrial respiratory chain, resulting in mitochondrial dysfunction, and greater ROS formation. 

A quick review of the hormones, neuropeptides, and neurotransmitters that play a role in our metabolism will help you better understand how obesity can contribute to mitochondrial dysfunction.  Please read below for a quick recap. 

Cortisol. Researchers have also discovered that chronic stress can cause the body to release excess cortisol, a hormone critical in managing fat storage and energy use in the human body. Cortisol is known to increase appetite and may encourage cravings for sugary or fatty foods.

Neuropeptide Y. More recent studies also suggest that our bodies may process food differently when we're under stress. One study found that lab mice fed a diet high in fat and sugar gained significant amounts of body fat when placed under stressful conditions. Mice fed a normal diet, however, didn't gain as much weight despite stress. Researchers linked that phenomenon to a molecule called neuropeptide Y that is released from nerve cells during stress and encourages fat accumulation. A diet high in fat and sugar appears to further promote the release of neuropeptide Y.

Serotonin. When we reach for fattening comfort foods during stressful times, it may be an attempt to self-medicate. When you eat carbohydrates, it raises the body's serotonin level. Serotonin is the body's feel-good chemical. It makes you feel better. Not surprisingly, people under stress don't tend to make smart food choices. Very often the carbohydrates that people go for are laden with fat, like muffins, pastries, doughnuts, and cookies.

Hormonal Regulators of Appetite and Body Weight/Composition

Leptin and ghrelin are two hormones that have a major influence on energy balance. Leptin is a mediator of long-term regulation of energy balance, suppressing food intake and inducing weight loss. Ghrelin is a fast-acting hormone playing a role in meal initiation. Understanding the influence of various hormones and neurotransmitters will allow for successful nutritional therapies for helping the increasing obese population.

Insulin resistance was initially proposed as a concept in the 1930’s to describe the escalating insulin requirements seen in diabetic patients. Today, this metabolic abnormality is thought to have a major physiologic role not only in type 2 diabetes but also in conditions ranging from impaired glucose tolerance to coronary artery disease and polycystic ovarian syndrome. Insulin resistance is often defined as a decreased sensitivity of target tissues to the metabolic actions of insulin, including decreased insulin-mediated glucose disposal into skeletal muscle, impaired inhibition of hepatic gluconeogenesis, and a reduced ability of insulin to inhibit lipolysis in adipose tissue. One consequence of insulin resistance is that higher than normal blood insulin concentrations are required to produce normal physiologic responses to glucose. Initially this results in a long period of compensatory increases in insulin production by pancreatic beta-cells. As resistance progresses, it is often accompanied by a gradual decline in beta cell activity and decreasing beta cell mass, and when the pancreas can no longer sustain the overproduction of insulin, diabetes results.

Hyperglycemia is an important factor in the pathogenesis of microvascular complications of diabetes (e.g. neuropathy, retinopathy, and nephropathy). Oxygen-derived free radicals are believed to contribute to the development of atherosclerosis, cataracts, and some other complications of diabetes. Diabetics have been reported to have higher concentrations of lipid peroxidation products and significantly lower concentrations of antioxidants (Vitamin C, Vitamin E, and glutathione) when compared to healthy controls.

Hyperglycemia increases the rate of protein glycation and the formation of advanced glycation end products (AGE’s) which appear to contribute to the pathogenesis of atherosclerosis, renal damage, and other diabetic complications.

Another factor that contributes to the pathogenesis of diabetic complications is intracellular accumulation of sorbitol. When glucose levels are elevated, sorbitol is synthesized inside the cells faster than it can be metabolized. Since sorbitol cannot cross cell membranes, it builds up inside cells, leading to osmotic swelling, metabolic dysfunction, and cell death. Intracellular sorbitol accumulation may be a factor in the development of diabetic neuropathy, retinopathy, cataract, and other complications.

For years, many people have suspected that stress and obesity are linked — and now scientific research has found evidence to support this connection. Specific biochemical reactions appear to help explain this link.

Chronic stress combined with positive energy balance may be a contributor to the increased risk of obesity and cardiometabolic diseases.


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