by Dr. Matthew Chircop
The exact reasons underlying these troublesome statistics are unknown. Several mechanisms have been proposed.
On the one hand, a combination of psychological and social factors are thought to contribute to recidivism (repeating an undesirable behaviour). These include lapsing into counter-productive behaviours (eating more, moving less), ongoing unhealthy relationships with food and physical activity, and persistent stress combined with inadequate or inappropriate coping mechanisms.
On the other hand, a biological basis underlying weight regain is currently thought to be just as important as, if not more important than, the aforementioned psychological and social factors.
Appetite and energy balance regulation involves complicated relationships between several “hunger/satiety hormones”, the reward (or pleasure) system in the brain, and the mood/emotional system in the brain. One hormone, in particular, has been implicated in the maintenance (and possibly the genesis) of obesity – leptin. For more information about leptin and its role in obesity, I suggest you read the first article in this series.
Of particular interest is the fact that leptin levels are higher in obese than normal weight subjects, and higher in normal weight subjects who have not previously been obese than in normal weight subjects who have previously been obese. In fact, it is thought that obesity involves the development of resistance to the effects of leptin, such that higher and higher leptin levels are required to signal satiety (which is the absence of hunger). It is also known, from studies in rodents, that this leptin resistance can be reversed in subjects who subsequently return to a normal weight.
Production of CRP, which binds leptin, is just one of the many mechanisms underlying the development of leptin-resistance in the chronically over-fed state.
It is possible that a return to normal leptin sensitivity also occurs in previously obese (now normal weight) human subjects, but I would anticipate that this probably takes months in humans. During that time, the leptin levels would have fallen significantly - even more than would account for both the reduction in fat mass (which produces leptin) and macronutrient intake (which normally stimulates leptin release). And, therefore, hunger levels are bound to be much higher in normal weight previously obese human subjects than in normal weight never obese human subjects. To make matters worse, leptin levels also have an effect on thyroid hormone levels, such that lower levels of leptin are correlated with reductions in the levels of thyroid hormone. Thyroid hormone tends to increase whole body metabolism, and a reduction in thyroid hormone levels (due to a fall in leptin production) could result in a significant reduction in the total daily energy expenditure - effectively meaning that people in that situation would be "over-eating", even though they are eating much less than what an average, never-obese person eats (factoring in age, build and activity levels).
This is the possible biological basis for the many previously overweight individuals who have successfully lost weight, only to “fall off the wagon” and eventually regain the weight within 5 years. Eventually, many people in that situation would tend to develop prolonged, significantly higher than normal levels of hunger, and reduced total daily energy expenditure. It is no wonder they eventually “crack” under the pressure and start eating more and moving less.
But what if there was a way you could get some relief from this unrelenting hunger, and metabolic slowing, for days to weeks at a time?
Contact us if you would like to learn more about our meal plans to help your lose those pesky last few kilos.
We design personalised meal plans that contain recipes with food that you tell us you like - you don't have to deny yourself of the tasty food you love (help to reduce your STRESS).
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