Weight gain and Metabolic disease.
November 7, 2016 Admin 0
Previously we have examined the effects of the Western diet, fructose intake and other factors which can lead to obesity and more specifically ; metabolic syndrome. Weight gain and obesity are traditionally characterised by an increase in adipose (fat) tissue. However, this adipose tissue is not the primary cause of the harmful effects of being overweight, This is evidenced by the fact that obese people who have high levels of subcutaneous fat are often not at increased risk of typical Western lifestyle diseases, but those with high levels of abdominal fat are at increased risk.
Therefore it can be inferred that it is the presence of the underlying metabolic condition that characterises the fat distribution pattern, and not the fat per se that is the cause of the disease. Therefore in order to reverse the obese state and regain health the primary goal should be to reverse the underlying metabolic dysfunction, and not to simply remove body fat. The body fat is just a reflection of the underlying metabolic regulation, and can therefore be considered a symptom of it. Treating obesity and weight gain, if it is of the abdominal type, should therefore involve treating the metabolic dysfunction.
Paradoxically, researchers continue to target adiposity as the goal in treating the overweight in studies and this raises a number of questions. The first question is whether the often short duration of studies are an accurate representation of long term health changes? For example, studies of around 12 weeks are commonly used to assess weight loss. Secondly, does a loss of total body weight give enough information as to the beneficial effects of the treatment administered? A loss of body mass indicates that weight has been lost, but does not give any information on which body compartment the weight has been lost from. Based on the ease and lost low cost with which body compositional changes can be calculated, it would seems that this is perhaps done on purpose for reason to hide the large amount of muscle tissue that is often lost in energy restriction studies. This ability for energy restriction to cause ‘weight loss’ without taking into account treatment of the underlying metabolic condition is the elephant in the room.
Energy restriction is not an effective long term strategy to facilitate body composition improvements. Focus instead should be on the consumption of high quality foods and their avoidance of metabolic poisons such as fructose and refined starches. This strategy will allow the reversal of the underlying metabolic disorder that is the cause of these diseases. This will then subsequently facilitate fat loss and body composition improvements.
Healthy weight loss should centre on eating high quality foods. It is a poor quality diet containing low quality foods that is the cause of weight gain. These foods contain metabolic poisons, most notably, fructose and refined starches. These foods can induce insulin resistance and this insulin resistant state then causes metabolic changes that result in the accumulation of body fat. Insulin resistance disrupts many hormonal signals and neuronal feedback systems and this can lead to appetite stimulation and disruption to normal homeostatic mechanisms that maintain a correct metabolic response to food ingestion. The result is that body fat accumulation is favoured and this leads to weight gain. Starving the individuals to remove this excess weight will not be a successful long term strategy because it does not address the underlying metabolic problem. However it does cause ‘weight loss’ in the short term. Measuring this ‘weight loss’ in the short term allows it to appear as through energy restriction is a solution to obesity.
Madjd, A., Taylor, M. A., Mousavi, N., Delavari, A., Malekzadeh, R., Macdonald, I. A. and Farshchi, H. R. 2016. Comparison of the effect of daily consumption of probiotic compared with low-fat conventional yogurt on weight loss in healthy obese women following an energy-restricted diet: a randomized controlled trial. American Journal of Clinical Nutrition. 103: 323-329
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