Hot New Topics > Stress and Weight Loss

What is stress? From a biochemical point of view it is any event that activates our stress response system. This system is composed of two components, the Sympathetic Nervous System (SNS) and the Hypothalamic- Pituitary- Adrenal (HPA) axis .

Perceived stress results in the activation of the sympathetic nervous system with subsequent production of stress hormones, previously called adrenalin and noradrenalin.
These stress hormones are responsible for most of the acute symptoms of perceived stress. They produce increases in energy, heart rate, blood pressure, muscle tension, sweat production, anorexia and nervousness.

These reactions are designed to allow you to quickly escape or defend yourself during times of stress, known as the fight or flight response to stress. Unfortunately, our time urgent, complex modern lifestyles result in chronic activation of this system which accounts for many of the modern day stress related disorders not found in traditional societies.

The Price You Pay When Using Stimulant Drugs for Fat Loss

Various stimulant drugs (caffeine, nicotine, amphetamines, etc) and reactive foods can stimulate the release of these stress hormones to give people a sense of enhanced energy and stimulation. This typically results in short term suppression of appetite. Thus many people lose weight using these stimulants due to reduction of caloric intake.

This is why smokers trying to quit will often put on weight rather quickly with many taking it up again to help control their weight or looks. Unfortunately, most people don’t understand that these same stress hormones are a major cause of atherosclerosis, heart disease, immune dysfunction and cancer. So the use of stimulants to lose weight should be considered a very dangerous strategy.

The Stress Response

The HPA system results in the production of cortisol and androgens by the adrenal gland, which mobilizes glucose for increased energy demands whilst providing anti-inflammatory protection to organs. Under normal conditions, cortisol has a strong negative feedback effect on the brain which shuts down the stress response, thereby protecting the individual from excessive stress reactions.

Unfortunately, this safety mechanism begins to fail under the influence of chronic stress and inflammation so the brain doesn’t receive the turn off message. These people typically have elevated cortisol levels due to an increased central (brain) drive from down regulation of cortisol receptors with subsequent lack of proper negative feedback.

Chronic Stress Response and Loss of Appetite Control

A raised level of cortisol due to chronic stress has a number of negative consequences.
Firstly, it impairs the delicate satiety feedback system that controls our appetite. Normally as fat cells receive excess calories as fat or glucose, they send out a hormone called Leptin, which turns off our appetite centers and stimulates the burning of fat. Unfortunately, raised levels of cortisol, cause down regulation of leptin receptors, therefore the brain, thyroid and muscles can’t receive the leptin message. Therefore the person seems to have an insatiable appetite and consumes much higher levels of calories with subsequent development of obesity. This phenomenon is known as leptin resistance and is a common occurrence in obese individuals.

Prolactin Reduces Leptin Production

Prolactin is another Pituitary hormone released during stress. It is well known for its effect of enhancing the growth of milk ducts in the breast for lactation (breast feeding). However it plays many other roles in both men and women. One major role involves the inhibition of the production of Leptin by the fat cells. Therefore, a temporary deficiency of Leptin results along with a lack of its appetite suppressing effects. Just another way stress can cause disturbances in the normal feedback control of appetite with subsequent development of obesity.

Different Types of Fat Cells

Secondly and probably most importantly is the role that chronically raised levels of cortisol plays in stimulating the proliferation of visceral adipose (fat) cells. Visceral fat is the fat that accumulates in the abdominal cavity particularly around the liver. The fat we typically see around our legs, buttocks and waist is called subcutaneous fat, in that it is deposited just under the skin.

These different fat locations are extremely important to understand because of the major metabolic difference they produce. Visceral fat being the most dangerous type due to its ability to release high amounts of poisonous free fatty acids and inflammatory cytokines (hormones) directly into the liver and muscles. These compounds cause dysfunction of insulin activity and impaired clearance of glucose and fat, a state known as insulin resistance.

Cortisol Responses in Obesity Subtype 2

Different Obesity Subtypes have different cortisol responses to any given stress. Obesity Subtype 2 has higher than normal early morning cortisol peaks indicating a lack of negative feedback during the night. This represents a prolonged or intermittent acute stress response due to a stress response system (HPA) that has been previously sensitized by various lifestyle and environmental stressors. (Smoking, alcohol, caffeine, low socioeconomic status, etc).

Cortisol Response in Obesity Subtype 3

Obesity Subtype 3 is associated with chronically elevated levels of cortisol levels due to a greater deterioration in negative feedback inhibition on the HPA axis. These people have reduced morning cortisol peaks that steadily rise during the day. This causes an overall greater adrenal output of cortisol over the day. These people are at risk to developing increased visceral fat deposits as a result of chronically elevated cortisol. This can occur even in individuals that are not overweight. This silent type of obesity is called Sarcopenic Obesity.

Sarcopenic Obesity and Accelerated Aging

Sarcopenic obesity refers to the progressive loss of lean muscle mass and builds up of visceral fat. As mentioned above, this can also occur in people that are not overweight due to the redistribution of muscle and fat without increases in overall weight. This process typically occurs as we age and particularly accelerates from age 60 onwards.
The major concern with sarcopenic obesity is it stills is highly linked to increased risk to cardiovascular disease, diabetes and cancer.

Recent alarming studies have determined that as high as 35% of adults aged between 25 and 45 have significant sarcopenic obesity placing them at high risk for early onset of age related disease (accelerated aging). The major problem being, that most of these people would not be considered overweight and therefore are completely unaware of their increased risk to early onset disease.

Cortisol and Obesity Subtype 4

Obesity subtype 4 refers to people that are extremely hypometabolic or known to have a slow metabolism (low ability to burn fat). They typically present with a flat cortisol stress response curve indicating the presence of adrenal exhaustion and low cortisol output.
So unlike obesity subtypes 2 and 3 who have raised levels of cortisol levels and visceral fat, type 4 does not have cortisol induced visceral fat deposits. They have other hormonal abnormalities and tend to have much higher levels of subcutaneous fat. Subcutaneous fat is still associated with a high risk to degenerative disease but much less than visceral fat due to its reduced impact on the development of insulin resistance compared to visceral fat.