Mainstream propaganda claims that obesity is caused by laziness and greed. This propaganda originates from the food industry and their paid agents. It is important for the food industry to convince the population that the food they eat is safe. To do this they must claim that obesity is not caused by eating their poisonous processed foods, but instead by eating too much or any food. However, it is well evidenced in the nutritional literature that ad libitum intakes of high quality nutrition do not cause weight gain. However, it is known that eating Western foods high in sugar causes metabolic changes that leads to resistance of the hypothalamus to the hormone leptin. Because the hypothalamus receives a weak leptin signal due to this leptin resistances, it deduces that the adipose mass is not excessive. Forced calorie restriction and exercise under these conditions results in counterregulatory mechanisms to reduce energy expenditure, because it is perceived that energy stores are not adequate. These mechanisms include a shift to the catabolic state and changes to metabolism that resemble the starvation state.
Evidence that obesity is a perceived state of starvation is well reported in the nutritional literature. For example, in one study1 researchers used an in vitro technique to measure the ratio of free fatty acids and glycerol leaving adipocytes in tissue samples from lean and formerly obese subjects. It is known that in normal subjects the ratio of free fatty acids to glycerol leaving adipocytes is around 1.5 to 1. During periods of fasting this ratio can rise to around 3 to 1. This represents a reduction in the amount of free fatty acids being re-esterified as triglycerides following lipolysis in adipocytes, favouring a catabolic rather than anabolic state. This raises the circulating concentration of free fatty acids facilitating energy production. Interestingly, when the authors analysed the tissue of formerly obese subjects who were weight stable, they found a similar high ratio of free fatty acids to glycerol that would be expected in the fasting state. The formerly obese subjects therefore show metabolic characteristics of starvation or fasting in their adipocyte tissues.
These results suggests that obesity is a metabolic condition that at the cellular level shows characteristics of starvation. At the physiological levels this situation can be explained by the leptin resistance. Any attempt to decrease caloric intake or induce energy expenditure through exercise is met with strong resistance from the counterregulatory mechanisms that increase energy efficiency. At the same time catabolic processes are put in place to provide energy. Interestingly, obese individuals that do not restrict calories may not experience the same catabolic processes. Energy restriction in the face of leptin resistance may be required to trigger this catabolic state. This is evidenced in the same study cited above. When the authors investigated the free fatty acid ratio of weight table obese subject who had not lost weight previously they found the same free fatty acid to glycerol ratio as in lean subjects. Energy restriction may therefore be detrimental to obese individuals because it worsens the metabolic dysfunction that underlies their condition.
