The latest facts about health, fitness and nutrition based on science
5/14/2017 0 Comments
by Dr. Matthew Chircop
It is true to say that people who have been both eating healthily and moderately active throughout most of their life tend to be resistant to weight gain and obesity. It is also true to say that short term increases in activity level and reduction in calorie intake can induce transient weight loss. However, the vast majority of people who have gained a significant amount of weight over a long period of time will spend years “yo-yo-ing” - periods of increased activity and reduced calorie intake with associated weight loss, followed by the exact opposite. Some are quick to point to some character flaw or moral weakness. Alternatively, re-emergence of unhealthy eating and activity habits related to disordered psychological reward systems and deficient coping mechanisms. However, we can’t blame the individual’s psychology alone, because it appears as though another villain is at least partly to blame – leptin.
Leptin is a hormone produced by fat tissue, with two daily peaks in production (occurring in the early morning and in the evening). The most important determinants of leptin levels are how much body fat you have (the more body fat you have, the more leptin you produce) and the levels of macronutrients within the blood (all three types of macronutrients stimulate leptin release but to different extents).
Leptin normally functions to signal satiety (i.e. the opposite of hunger) by acting on the brain), and appears to be central to controlling whole body energy metabolism overall. Starvation induces a significant reduction in leptin levels before any significant loss of body fat tissue. This reduction in leptin not only increases appetite, but also (acting via the different hormone systems): causes infertility; slows the basal metabolic rate; slows or ceases growth and development; and mobilises energy stores. Crucially, whilst leptin levels increase beyond normal in an overfed state, this does not appear to generate a signal that results in a subsequent reduction in food intake or body fat storage.
Disordered states of leptin function cause insulin resistance and obesity in humans and animal models. Specifically, there are two main disordered states. The first, and less common in humans, is those who, due to a genetic abnormality, lack leptin. In those individuals, the administration of normal physiological amounts of leptin reverses the obesity and insulin resistance. The second, and most common in humans, is due to a chronic state of energy excess, which causes a chronically elevated leptin level, and is associated with resistance to the effects of leptin. This is often followed by insulin resistance and obesity. In those individuals, administering leptin at even higher levels (far above normal) does not reverse the disorder.
However, increasing leptin levels might have a role in weight loss maintenance. That is, if leptin levels could be kept high whilst the person reduces their calorie intake and increases their activity levels (and reducing total body fat mass) then this might reduce the frequency and severity of weight regain. Some experts have indicated that falling leptin levels due to weight loss activate various mechanisms which drive subjects to regain weight, such as increasing hunger, cravings for calorie-rich foods, and decreasing energy expenditure (through changes in thyroid hormone levels , and possibly behaviourally as well). In this way, leptin could also be seen to be the hero in the fight for long term weight and hunger control.
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