Obesity is characterised by metabolic dysfunction. In particular the main physiological change that drives obesity is insulin resistance. Insulin resistance develops in response to a low quality diet high in refined and processed carbohydrate foods, particularly refined crystalline fructose. Secondary to insulin resistance other metabolic abnormalities develop including changes to substrate oxidation, cholesterol and lipid metabolism irregularities, dysfunction to the normal appetite regulatory systems and leptin resistance. These secondary metabolic dysfunctions are likely driven by the insulin resistance, which ultimately causes raised levels of fasting insulin and disturbance to the normal insulin glucagon cycle that occurs postprandially. As insulin control deteriorates, its inhibitory effects of catabolic pathways predominates and this shift metabolic regulation away from normal physiological ranges. The extent of the metabolic dysfunction that develops in obesity is still not fully clear.
It has recently been shown that the obese may have an altered ability to detect the presence of long chain fatty acids in foods. The reason for this altered taste sensation is not known, but has been studied. In one study1, researchers assessed the ability of obese and lean subjects to detect the presence of the long chain omega-6 fatty acid linoleic acid (LA, C18:2 (n-6)) through exposure of the mouth to increasing concentrations of emulsified LA solution followed by spitting the containing solution. The results of the study showed that there were large variations between the thresholds for detection of the LA in the test solution. The variation would be expected in a test of a biological parameter such as taste perception. However, the mean detection threshold was 0.053 % and 0.071 % for the lean and obese subjects, respectively. Therefore the lean subjects were able to detect the LA at lower concentrations compared to the obese subjects, although the reason for this is not understood.
There was no association between the taste threshold and the body mass indices (BMI) of the subjects. However, five of the subjects were unable to differentiate between the highest concentration of LA (5 %) and these subjects were all obese. Analysis of the 24 hour food diaries of the subjects showed that these obese subjects consumed more dietary lipids and more energy when compared to the other subjects. Subjects given a 1 % emulsified solution of LA to taste and then spit experienced significant increases in plasma levels of triglycerides, which the authors suggested were hepatic in origin. However, this effect was seen only in the lean subjects, and no increase in plasma triglycerides was observed when obese subject tasted the same 1 % emulsified LA solution. This data hints at a disturbance in the oral to brain to hepatic loop that is involved in the cephalic phase of digestion. Animal studies suggest that obesity is the cause, not the effect of this change to orosensory perception for long chain fatty acids.
Dr Robert Barrington’s Nutritional Recommendation: The obese are very often criticised as being lazy and greedy. ‘If only they would eat less and exercise more, they would lose weight’. This viewpoint is common amongst laypersons and medical experts alike, but the nutritional literature does not support this contention. Obesity is driven by low quality foods, particularly refined carbohydrates including refined crystalline sugars. These low quality foods drive insulin resistance and this leads to a raft of metabolic changes that negatively affect appetite, taste perception, physical activity output and general well being. These changes create a ‘deflationary spiral’ of metabolic abnormalities that make it improbable that weight loss can occur without reversal of the underlying insulin resistant state. Altered taste perception is just one facet of this multifactorial dysfunction that develops in the obese. Successful weight loss can only be achieved through improvements in diet quality that reverse the insulin resistant state.
RdB
