This is my fifth and presumably last article on the Human Energy Metabolism. I would like to dedicate this article to the discusson of some bacics as well as advanced principles of nutritional biochemistry and also some interesting statistics related to the topic of obesity.

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Obesity - an epidemic Problem

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Illustration of adipocytes of the adipose tissue - Image Source

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First of all we have to answer one basic question:

How you do define or measure obesity?

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The assessment of the body weight related to the square of the body height is a well established methodology and is generally known as the Body Mass Index, or short the BMI.

From this definition, a nice overview of the different body mass conditions depending on the BMI can be derived:

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As you can see, there are different degrees of adipositas. The classification of obesity into three different degrees of severity makes sense from a medical point of view. On the one hand, because the risk of secondary diseases varies according to the severity of obesity and on the other hand, because also the therapy may vary.

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Obesity is a health risk

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In the following graphs the relative risk for cardiovascular disease (A) and cancer (B) are plotted against the BMI. In this study as many as 115.195 nurses participated in a 16 year-trial. All of which were non-smokers. The relative risk of those with a BMI under 19.0 was set at unity. The results show that death due to cardiovascular disease was four times higher in obese women, when compared to the rate for the leanest women.

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There seemed to be some association of obesity with cancer, though this association was clearly less dramatic than for cardiovascular disease (risk was "only" 2-fold higher). Furtermore obesity is a strong risk factor in developing Type II Diabetes.

In some cases, obesity itself is not a disease of its own, but a symptom caused by another disease. Examples for this case would be Hypothyroidism or the Cushing syndrome, second of which is caused by an overproduction of the hormone cortisone.

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Causes for Obesity

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A) Chronic imbalance between caloric uptake and the real physical need
Protein and glycogen stores are regulated within very narrow limits. Fat reserves, however, can grow enormously, resulting in the build-up of adipose tissue. The formation of adipocytes is largely a result of a diet rich in fatty acids, i. e. percentage of body fat roughly correspond to dietary fat content.

B) Behavioral factors
Eating habits as well as the amount of physical activity very much influence above mentioned imbalance. 30 min daily physical exercise are recommended.

C) Educational & social factors
The replacement of traditional local diets by global Western diet, as well as the lack of knowledge concerning healthy food are two major factors. Furthermore there is a non-surprising connection between the income of families and their caloric uptake. Since fat and sugars are overwhelminlgy sold rather cheap, low income families tend to consume high caloric diets.

D) Inborn disturbances
Mutations in genes linked to fat or energy metabolism may also be the causes for obesity. At this point, leptin or the associated leptin receptor may be mentioned as suitable examples.

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The Role of Leptin

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Leptin (Greek: leptos = thin) is a 16 kDa polypeptide produced by adipocytes. Leptin was first discovered in homozygous mice carrying a defect in the OB (obese) gene. Humans do indeed have a homologous protein (ca. 84 % identical). As a result these mice tend to overeat and have twice the body weight as normal mice.

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Leptin acts as a satiety signal resulting in reduced food uptake. This was shown by leptin-treated OB homozygous mice, which lost 50 % more body weight than untreated mice on the same calory restricting diet. This suggests that leptin also controls energy expenditure (probably in skeletal muscles!).

Leptin binds to the leptin receptor OB-R, a transmembrane protein, predominantly expressed in a brain region called Hypothalamus. The hypothalamus produces Neuropeptide Y (36 amino acids long) what is known to act as an eating signal. Upon binding of leptin to OB-R, the production of this specific peptide is inhibited.
OB-R appears in at least six variants resulting from tissue-specific splicing.

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The Formation of Energy Stores

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The processes of our body - a sophisticated biochemical machinery - have an efficiency unequal to 100 %. This means that the build-up of energy storages is associated with some kind of inefficiency, hence energetic loss. However, this strongly depends on the particular biochemical pathway and thus on the macronutrients consumed. This fact is shown in more detail in the next representation.

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Conclusions:

• Dietary fats are stored directly and with high energy yield.
• Carbohydrates are stored in the glycogen stores. These are limited and excess of carbohydrates is converted to fatty acids, which in turn are stored in adipocytes.
• Therefore growth of adipose tissue is mainly a result of too much fat intake!
• However, excessive uptake of carbohydrates (and protein) can also lead to growth of adipose tissue!

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Overview of the Epidemic

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Global Prevalence for Obesity - click to enlarge
Image Source

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Although this data is taken from the year 2008 it is still quite representative. For very much detailed and more recent information, also within single countries, have a look at the interactive WHO Database.

Between 1985 and 2008, there was a study called Behavioral Risk Factor Surveillance System (short BRFSS) in America, which looked at the incidence of obesity. These studies provided impressive and clear results proving an unfortunate trend. Take a look at them:

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This concludes my series on the Human Energy Metabolism. I hope I was able to provide some interesting insights. Follow and support my work for more chemical, biochemical, physiological or general scientific articles.

Previous articles of this series can be found here:

• Part #1 - Organ-specific Requirements
• Part #2 - The Respiratory Quotient
• Part #3 - Diabetes mellitus
• Part #4 - Fasting and Starvation

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Best,
mountain.phil28

References:

1. Fit & Leicht articles: 1, 2, 3
2. WHO Global Health Observatory (GHO) Data
3. BRFSS, Behavioral Risk Factor Surveillance System, Prevalence of Obesity Among Adults, 2007, MMWR 2008, 57(36), 765-8
4. Further information and non-direct cited images are taken from "Biochemistry I" lectures at the TU Graz.