Like many biological phenomenon, feeding behaviour is reliant on a negative feedback loop. This loop involves the detection of food in the gut and nutrients in the blood and a subsequent neuronal and hormonal response that corrects behaviour. A loop therefore exists between the nutrition of the individual and the feeding behaviour displayed. The most obvious and well studied of the interactions between nutrition and behaviour is the result of under nutrition. As the blood glucose levels, glycogen stores and fat reserves are diminished, hormonal and nervous signals are modified and behaviour is altered in order to allow an increase input of energy to correct the imbalance. Of course as well as under nutrition, overnutrition can cause opposite hormonal and neuronal signals that allow behavioural changes in order to decrease the amount of energy ingested. In this way the body through activity in the central nervous system is able to maintain body weight within narrow limits despite changes in available energy.
Based on this understanding it is difficult to comprehend why obesity should exist. There is an inherent mechanisms to maintain body weight and these mechanisms functions efficiently in healthy humans. So why do people become overweight and obese and why does the regulatory mechanisms not correct the imbalance? The answer to this question is complex, but recent advances in our understanding of the biochemistry of obesity have come from a wider understanding of the interaction between conditions that were previously considered separate. In fact if we review the common Western lifestyle diseases we see that most share a common aetiology characterised by systemic inflammation, oxidative stress, liver dysfunction and insulin resistance. This is no accident as Western lifestyle disease share a common causes and this cause is the poor quality diet that Westerners consume throughout their entire lives. This diet causes a series of slow to develop, chronic and subclinical metabolic changes that drive disease.
Termed the metabolic syndrome, this raft of metabolic aberrations are a driver of the main Western lifestyle diseases, with obesity at the centre of this mess. Poor quality food is the key that opens the door to these diseases, because it allows the development of aberrant metabolic changes which interfere with the normal nutritional loop that usually keeps the body weight and other biochemical parameters of the individual in check. High quality food is generally nutrient dense, and these nutrients within the food not only provide reserves of vitamins, minerals and other essential nutrients to the organisms, they also are often necessary for the correct digestion, absorption and assimilation of the energy from the food source. Modern processing methods often strips away these essential nutrients and the subsequent alterations to the metabolic regulation of the energy contained within goes awry, leading to the development of metabolic problems that ultimately cause the metabolic syndrome.
The hyperphagia and energy efficient state that often accompanies obesity is no accident. Based on a healthy feedback loop, as body weight increases feeding behaviour should be curtailed and energy utilisation increased in order to maintain a normal set point weight. However, the opposite happens and biochemistry is shifted to one of energy sequestration and conservation. This phenomenon although not widely reported has been understood at a behavioural levels for many decades, but only recently have the mechanisms by which this occurs been elucidated. The Western diet causes the development of insulin resistance, and secondary to this leptin resistance. Both leptin and insulin are signals that feedback to the hypothalamus of the brain, and in this way are pivotal in providing a correct response to the current nutritional state of the individual. With aberrations in the insulin and leptin signals, the hypothalamus is only able to interpret the signal as one of starvation, and proceeds to conserve energy and induce hunger.
Treating obesity is therefore not a case of further inciting the starvation signal in the hypothalamus by restricting energy and forcing energy expenditure. Such actions will inevitably lead to further determined efforts on the part of the body to sequester energy and to increase food intake. Instead, the insulin resistance and leptin resistance that are the cause of the misunderstanding must be corrected through adoption of a high quality diet. Such diets based on traditional eating patterns have been shown to reduce insulin resistance and return the normal homeostatic functions to the body, thus allowing a set point body weight to be maintained without the need to self regulate energy intake or energy expenditure. At the same time, such a diet reduces the risk of other Western diseases by reducing systemic oxidative stress and inflammation, and returning correct metabolic function to the liver. The failure to understand that obesity is a disease of starvation is the reason for the lack of success of most weight loss efforts.
Of course the hyperphagia associated with obesity can be explained further. As well as enacting behavioural changes in response to changes in energy intake, the brain may be able to modify feeding behaviour based on changes to the intakes of essential nutrients. Poor quality foods devoid of minerals may be able to encite changes in feeding behaviour in order to increase the chance of obtaining those nutrients. Pica is a behaviour associated with the seeking and eating of non-food items. It is not beyond the realms of logic that the hyperphagia associated with being overweight is in fact a response to a mineral deficient state. Eating more food, logically would increase the chance of obtaining the minerals required and allow correction of any imbalance. The protein leverage hypothesis too states that energy intakes are increased in response to consumption of food devoid of protein in order to supply a minimum requirement of amino acids. This explains to some extent the weight loss effects of mineral dense high protein diets.
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