It is quite clear that regardless of body control mechanisms, energy intake should correspond to the daily energy demand, otherwise energy surpluses will cause available energy to be stored as fat. This means that food intake has to be based on the daily energy demand. However, this demand fluctuates significantly, and is comprised of basal metabolic rate and energy demand resulting from physical activity. A worker (construction worker, forest worker, professional athlete, etc.) will metabolise about three times the energy an office employee would, for example.
To break down 1 kilogram fat per week, the energy supply would need to be reduced by approx. 7000 kcal. This would mean, for example, that an office employee would not be allowed to eat for three days. Based on our occupation, which usually goes hand in hand with a much lower caloric demand by physical activity, the basal metabolic rate becomes a very important factor. It is mainly influenced by muscle mass and body heat production (thermogenesis). Apart from the well-known calorimetric procedure, the basal metabolic rate can easily be determined by performing a bioelectric impedance analysis. The more muscles we have, the more calories we burn while at rest. Calories burned during physical activities are much less "significant" than those burned by "built" muscles when at rest.
In humans a very accurate (up to a couple of 1000kcal per year) regulation of the energy balance by food intake takes place, unless it is altered by artificial internal or external factors. This function is also called "Adipostat", which originates in the hypothalamus (central nervous system) and sets a defined preset weight for any individual. This weight is also called the "adiposity set-point". Up to now it is not fully understood how the brain is signalled that fat depots are filled, although more and more accurate approaches to describing control mechanisms are to be found nowadays. These control mechanisms function through several, at times overlapping, control circuits on the level of the vegetative nerve system (neurotransmitter) and the endocrine system (hormones), while fat tissue itself assumes the role of a hormone-creating organ. Dysfunction of any of these components may be responsible for the oversupply of energy and subsequent increased fat retention in the end, and thus development of adiposity. The following are just some of many possible examples outlined for illustration purposes.
Satiety or the sensation of hunger itself is regulated by a complex 3-path process: Fast reaction through hormones X, CKK, Amylin, and Insulin; intermediate reaction by filling the stomach (stretch receptors, hormone X, CKK, Amylin, VIP), and slow reaction by leptin, ß3-receptor, and neuropeptide Y. In mice the so-called ob-gene (obesity-gene) was detected. Its product, leptin, is produced increasingly in fat cells if the fat depot is filled, thus signalling the brain to stop food intake. Mutation of the ob-gene resulting in lack of leptin-production by fat cells caused unchecked weight gain in the animals examined. This regulation process coded by a single gene cannot be transferred to humans though. In adipose test subjects, increased leptin-levels are often found, causing diminished detection within the central nervous system (leptin receptor defect) with subsequently decreased hunger- or satiety sensation, which may be one cause for increased food intake. Thus, the thesis postulating hormonal activity in fat tissue itself is confirmed.
Another approach is that increased lipoprotein-lipase activity was recorded in adipose patients; a metabolic enzyme contributing considerably to fat retention within the body. Normal fat-tissue as present in the entire hypodermal area is not capable of producing body heat. In addition to padding, it serves mainly as an energy reservoir. However, brown fat-tissue is capable of thermogenesis (the metabolic activity where fat is reduced while creating body heat). In this process the ß3-receptor plays an important role. This receptor’s effect on fat cells may be defective (a gene defect) or dysfunctional, thus preventing sufficient thermogenesis with decreased caloric demand when in a state of rest.
On average adipose patients seem to have a lower body temperature than people of normal weight (- 0.2 to 0.3°C). Compared to slim people they can sleep without covers at night and still feel warm.
During evolution, fat retention probably played an important role for survival. Fat offered three nutritive-physiological advantages, which have nowadays become disadvantages due to our seated lifestyle and the high availability of food: High energy density (9.5 kcal/g), which is twice as much as carbohydrates and proteins have (fat hardly satiates) can therefore be eaten in large amounts – and fat is metabolised to depot fat (triglycerides) with almost no loss of energy. Fat burning is constant for each unique individual.
This means that at a given point in time the same amount of fat is always metabolised (depending on the test person’s fat consumption e.g. 40 – 120 grams per day) Thus, as the main calorie-supplier in food, fat will always be the first nutritional component to be reduced drastically to promote weight reduction. In a balanced diet fat should make up 30% of the total calorie intake. The required daily allowance of essential fatty acids (multiple unsaturated fatty acids) is contained in 1-2 tbs. of vegetable oil (sunflower oil, safflower oil). For someone with a desk job, the average daily demand is approx. 60-80 grams.
However, the food industry swamps consumers with ready-to-eat products usually with a substantial fat content. Going to fast-food restaurants or take-aways which serve primarily high-fat products, is often more convenient than opting for a balanced selection of foods and the time consuming preparation they entail. On top of this we often do not even know the fat content of our foods.
As opposed to fats, burning carbohydrates can be "trained". As carbohydrate intake is increased the metabolic rate also increases, while energy output is raised. The more carbohydrates are taken in, the larger the percentage of the daily energy demand that will be covered by carbohydrates. This has nutritional and physiological implications for controlling weight and means carbohydrates should be reduced as a second step only after reducing fats.
Ethyl alcohol as found in wine, beer and any spirits shows rather "exquisite" metabolic characteristics. An intake of approx. 15 grams per day of alcohol above the basal metabolic rate, is sufficient to cause a weight gain of 3 kg in one year. This is equivalent to a remarkable 30 kg within 10 years.
These aspects are covered in cardiovascular risks.
Several secondary diseases, (see also Secondary diseases and Complications) suggest hormonal dysfunctions in adipose patients. Adipocytes produce hormones themselves, along with being receptors for several messengers. There is an interrelation between altered hormone balances and the android fat type. Insulin resistance, for example, means reduced cellular receptiveness for insulin, thus more of the hormone is released. Several dysfunctions have been detected, including dysfunctional cortisone production (overproduction of the adrenal cortical hormone), increased unbound testosterone (male hormone) with decreased male-hormone binding globulin in females, decreased testosterone levels in males (with development of secondary female gender-specific characteristics like pilosity, development of lactiferous glands, voice pitch), lowered progesterone levels in females, as well as lowered growth hormone concentration.
A correlation between ovarian dysfunction and adiposity can also be found for polycystic ovary syndrome (PCO, cystic change of the ovaries), which is considered the most common endocrine cause of infertility. In patients who at least "subjectively" reported infertility, it is not uncommon that pregnancies occur again after massive excess weight reduction, and are successfully carried to the full term, as our postoperative records also confirm.
For even small amounts of excess weight the composition of bile from the liver changes. The amount of cholesterol in bile will increase rapidly in adipose patients, thus heightening the risk of cholesterol calculus development, gallbladder infections, cholesteatosis and last but not least gallbladder carcinoma. Very rapid weight reduction may also promote development of bile-stones.
In extremely obese patients a transformation of the liver tissue can be observed, causing deviant liver values, which will generally normalise during the course of weight reduction.
As excess weight increases there will also be a rising number of complaints in the locomotor system. The extent depends on (apart from weight) several different factors like daily strain by physical activity, pre-existing conditions, injury amongst many others. The most common form of deterioration is the accelerated abrasion of the large joints and the spine that may well lead to complete invalidity. Almost all morbid adipose patients are severely restricted in their range of movement.
In adipose males and females the risk of contracting malignant tumours is increased by the factor 1.55 or 1.33 (Schapira et al. 1994, American Cancer Society, study conducted on 750000 adipose patients older than 12 years. The android fat type is especially at risk. Hormonal influences may affect contraction of endometrial, ovarian, mamma, cervix, and prostate carcinoma. Apart from this, there are also increased occurrences of gastrointestinal carcinoma like gallbladder- and rectum- and bowel cancer, and also malignant tumours of the pancreas, the liver and the kidney. To date, causes are unclear.
The Yo-Yo effect is a common phenomenon. After coming off a diet, and thus returning to the old nutritional habits, the original weight will be regained or even exceeded by kilograms within a few weeks. With successful weight reduction the daily calorie demand will also decrease. This demand may decrease even super-proportionally during radical diets or fasting as often performed in clinical environments, as well as due to protein deficiency with reduction of muscle mass (muscle being the single largest protein depot) caused by unbalanced nutrition. Thus, the basal caloric rate, which is indirectly related to muscle mass may also be reduced drastically. At such a drastically reduced daily calorie demand, the patient will also fill his fat depots at a related rate. Aside from this, humoral (hormonal) factors affected by the diet will signal hunger to the brain more often, thus an increased sensation of hunger after coming off the diet will influence eating habits.
Mentally the continued gain of weight after diets will cause frustration and desperation, and the frequently peaking weight progress curve cause a multiple increase in the risk of diseases and mortality, compared to obese patients with constant weight (Balssiger 1997).