What is Excess Body Fat?

In humans and animals, adipose or fatty tissue is the body’s way of storing metabolic energy over extended periods. Depending on current physiological conditions, fat cells or adipocytes either store fat that is derived from the diet or liver metabolism, or release stored fat as fatty acids in times of additional energy requirement. These metabolic activities are regulated by several hormones, of which insulin, glucagon and cortisol play the dominant role.

The location of the fatty tissue determines its metabolic profile.  ‘Visceral fat’ is located within the abdominal cavity, beneath the wall of the abdominal muscle, whereas ‘subcutaneous fat’ is located beneath the skin (and includes fat that is located in the abdominal area beneath the skin but above the abdominal muscle wall). Visceral fat was recently identified as being a significant producer of various hormonal-like messenger chemicals, among which several have directly been linked to inflammation and the inflammatory response.

Two major mechanisms contribute towards weight gain. Not only do existing fat cells slowly increase the amount of fat that they store, but new fat cells are continuously being formed by the body. Besides causing weight-gain, this mechanism also leads to the progressive enlargement and eventual distortion of fatty tissue, commonly referred to as cellulite. Once this has happened, a counterproductive phenomenon occurs. Instead of releasing more stored fat, the body biochemically starts to reduce the ability of fat cells to release their contents of stored fat, making it more difficult to lose weight.

Modern research seeking clues as to why this happens has discovered that the secret largely lies with certain biochemical messenger molecules released by the actual fat cell themselves. Called adipokines, these chemicals not only play a dominant role in triggering the formation of new fat cells, but also start causing another condition, referred to as insulin resistance.

How do you measure body fat?

The standard way to classify an individual’s body weight is to calculate their body mass index (BMI). This is done by using a formula that divides their weight (kg) by their height squared (m2).

Underweight:          BMI > 18.5 kg/m2
Normal weight:       BMI 18.5 to 24.9 kg/m2
Overweight:            BMI 25.0 to 29.9 kg/m2
Obese class I:         BMI 30.0 to 34.9 kg/m2
Obese class II:        BMI 35.0 to 39.9 kg/m2
Obese class III:       BMI ≥ 40 kg/m2

Since many other factors that may falsely influence an individual’s weight according to the BMI classification (e.g. increased muscle mass, for example) lead to an erroneous overweight or obese classification, other measurements are often used in conjunction with BMI to assess an individual’s weight classification more accurately. These measures include waist circumference and body fat percentage calculations.

It is interesting to note that a normal weight BMI classification does not exclude excess body fat.  This may sound counter-intuitive, but recent medical research has shown that many individuals with BMIs below 25 actually have excess body fat that would only be detected by assessing body fat percentage, or by more sophisticated methods such as computer-aided tomography (CAT scans).  These individuals are now classified as ‘metabolically obese, normal weight’ (MONW).

Why is the distribution of excess body fat significant?

While overweight and obesity, in general, are associated with an increased risk of several diseases and premature death, research is showing that excess adipose tissue in the abdominal cavity (central or abdominal obesity) has a much greater influence on chronic inflammation. This is due to the fact that central adipose tissue has a significant hormonal effect on inflammatory cytokines, chemical substances released by cells, especially fat cells.

The resulting inflammation has been identified as a key role-player in a multitude of diseases including atherosclerosis, insulin resistance, diabetes, hypertension and many more.  In fact, it is now thought that chronic inflammation is the leading cause of all the components of the metabolic syndrome and could be the factor that forms the link between all its components.

The latest National Cholesterol Education Programme Adult Treatment Panel III (NCEP ATP III) defines central obesity as a waist circumference of ≥102cm in men and ≥88cm in women. In individuals with insulin resistance, the NCEP ATP III recognises that an increased risk of cardiovascular disease and diabetes exists at waist circumferences of ≥94cm in men and ≥80cm in women, which are the cut-off points used by the International Diabetes Federation (IDF).

How common is excess body fat?

The current global pandemic of obesity and excess weight is clearly illustrated by the 1.6 billion overweight adults worldwide, of which at least 400 million are obese. These numbers are expected to escalate in both developed and developing countries.

In the Western world, and specifically the USA, the prevalence of obesity has increased by 50% in each of the past two decades, with two-thirds of the US population being overweight, half of whom are obese. The majority of the increase is occurring in children, adolescents and men.

In 2008 the World Health Organisation estimated that 65% of South Africans were overweight (58.5% of men and 71.8% of women) and the figure is anticipated to rise, both locally and globally.

How are excess body weight and insulin resistance linked?

Adipose tissue (fat cells) has historically been accredited with only two main functions, namely that of storing energy for later use and preserving body temperature via improved insulation.

In the presence of excess body fat, however, adipose tissue also assumes a hormonal function and manufactures various chemical substances called ‘inflammatory cytokines’. For various reasons, some of these inflammatory cytokines disrupt insulin’s role on a cellular level and render it less effective. The medical term for this condition is ‘insulin resistance’. To get the same task done as before, the body compensates by producing, even more, insulin, causing levels to rise above the norm.

Because of insulin’s obesity-promoting effects, the subsequent elevation of insulin levels makes the individual more prone to gaining weight. In addition, higher insulin levels also make it more difficult to lose weight. Once this condition sets in, a vicious cycle begins, explaining why many overweight individuals find that their metabolism has effectively slowed down.

How are excess body fat and the metabolic syndrome linked?

The prevalence of the metabolic syndrome increases dramatically as BMI increases. Compared to normal and under-weight individuals, research has shown that overweight individuals are six times more likely to meet the criteria for the syndrome. This risk rises even further in obesity, where females are 17 more likely and males are 32 times more likely to meet the criteria of the metabolic syndrome.

As described, excess body fat induces a generalised, chronic, low-grade inflammatory state. This is now considered to be the leading cause of all the components of the metabolic syndrome and the syndrome in its entirety.

How are excess body weight and stress linked?

Cortisol, a glucocorticoid (steroid hormone), is produced from cholesterol in the two adrenal glands located above each kidney. It is normally released in response to events and circumstances such as waking up in the morning, exercising and acute stress. Cortisol’s far-reaching, systemic effects play many roles in the body’s effort to carry out its processes and maintain homeostasis.

Cortisol also plays an important role in human nutrition. It regulates energy by selecting the right type and amount of substrate (carbohydrate, fat, or protein) the body needs to meet the physiological demands placed on it. When chronically elevated, cortisol can have negative effects on weight, immune function, and chronic disease risk.

One of the ways that elevated cortisol can lead to weight gain is via visceral fat storage. Cortisol can mobilise triglycerides from storage and relocate them to visceral fat cells (those under the muscle, deep in the abdomen). Cortisol also aids adipocytes’ development into mature fat cells. The biochemical process at the cellular level has to do with enzyme control (11-hydroxysteroid dehydrogenase), which converts cortisone to cortisol in adipose tissue. More of these enzymes in the visceral fat cells may mean greater amounts of cortisol produced at the tissue level, adding insult to injury (since the adrenals are already pumping out cortisol). Also, visceral fat cells have more cortisol receptors than subcutaneous fat.

A second way in which cortisol may be involved in weight gain goes back to the blood sugar-insulin problem. Consistently high blood glucose levels, along with insulin suppression, lead to cells that are starved of glucose. But those cells are crying out for energy and one way to regulate energy is to send hunger signals to the brain, which can lead to overeating. And, of course, unused glucose is eventually stored as body fat.

Another connection is cortisol’s effect on appetite and cravings for high-calorie foods. Studies have demonstrated a direct association between cortisol levels and calorie intake in populations of women. Cortisol may directly influence appetite and cravings by binding to hypothalamus receptors in the brain. Cortisol also indirectly influences appetite by modulating other hormones and stress responsive factors known to stimulate appetite.

What are the complications of excess body fat?

Excess body fat is directly linked to a wide variety of diseases, including insulin resistance, diabetes, chronic inflammation, cardiovascular disease, the metabolic syndrome and certain types of cancers. It is estimated that every 0.45kg gained between the ages of 30 and 42 years increases the risk of disease by 1%. This doubles to 2% between the ages of 50 and 60.

Excess body fat also contributes significantly to premature death, with studies suggesting that the risk increases by 20- 40% in non-smoking overweight individuals and by at least 2- 3 times among obese individuals.

How can lifestyle interventions affect excess body fat?

Generally speaking, the start of weight gain is an excess of calories: too many calories consumed and too few calories utilised. However, once excess body fat induces inflammation and insulin resistance, the weight gain process becomes more complicated due to the obesity-inducing effect of insulin.

Lifestyle interventions, including weight loss, increased physical activity and stress management have repeatedly been shown to improve chronic inflammation and insulin sensitivity, which in turn improve all the components of the metabolic syndrome.

While the thought of losing a tremendous amount of weight can be demoralising, it is important to realise that even small losses have a significant impact. The loss of every 0.45kg reduces an individual’s disease risk by 1%. This can be a very good motivator for overweight and obese individuals and the starting point to a healthier lifestyle.

References

  • Karelis AD, David H, et al. “Metabolic and Body Composition Factors in Subgroups of Obesity: What Do We Know?” The Journal of Clinical Endocrinology and Metabolism Volume 89 Issue 6 June 1, 2004.
  • Kassi E, Pervanidou P, Kaltsas G, et al. Metabolic syndrome: definitions and controversies. BMC Medicine 2011,9:48
  • The National Health and Nutrition Examination Survey (NHANES) 2003-2004