Losing weight and keeping it off are two very different things. Regaining weight is the norm rather than the exception, and up to two thirds of dieters regain more weight following a diet, than they lost in the first place (11).
Our bodies have powerful mechanisms in place to maintain the status quo. To function optimally many variables need to be kept within narrow ranges. The pH of your blood for example, body temperature and body water percentage are all tightly controlled to keep them within set limits to avoid disease or even death. This is called homeostasis.
One of the variables that is kept constant is our body weight (10). If we overeat our body compensates to some extent by burning off the excess through increased production of body heat and metabolic rate (6). We also feel less hungry, we feel full more quickly, and for longer periods of time and we are more active (2, 13). It also works the other way, if we under-eat, for example on a kcal restricted diet, our metabolism slows down, and we feel more hungry and tired. We are also more inclined to obsess about food and meal times and meals feel less satiating (4).
Leptin regulates our weight in the long run
Leptin is a hormone secreted by fat cells, the heart and the stomach, and the amount of leptin is directly related to the amount of fat we have. Leptin tells the brain, more precisely the hypothalamus, how much energy there is in storage if food were to become scarce. Leptin is also what ramps up our metabolism and body heat production and reduces feeding behaviour.
On a kcal restricted diet, leptin production drops dramatically, as it would during a period of starvation. Our brain does not distinguish between the two (1). Some of it can be expected as your fat mass reduces, but not all of it. The body anticipates food shortage and starts to preserve energy.
In obese people the effect of leptin is blunted. Even though they have very high levels of leptin, they don’t seem to eat less or have a higher metabolism than lean people. The brain does not react to leptin anymore. This phenomena has been named leptin resistance and works in much the same way as insulin resistance in diabetes type 2 (9): overfeeding leads to an accumulation of body fat, as fat mass increases, leptin production increases and overexposure to leptin seems to damage the brain as it becomes insensitive to it (12). This results in more overfeeding, more weight gain, more leptin production etc. A vicious circle which is hard to break. How exactly the brain becomes insensitive or where the tipping point is, still isn’t clear. What is clear, is that leptin is not our friend when you’re trying to lose weight.
Ghrelin, CCK, GLP-1 and PYY regulate eating behaviour
CCK, GLP-1 and PYY are hormones secreted in our intestines in response to food intake. They work together to ensure proper digestion and in turn stimulate production of each other and digestive enzymes. They make us feel full and reduce our appetite. These satiety hormones are all suppressed by ghrelin (3). Ghrelin is produced in the stomach, makes us feel hungry and is mainly regulated by food intake. Levels will be high during periods of fasting and drop almost immediately after we start eating. Whilst Leptin is more involved in the long term regulation of bodyweight, ghrelin tells your brain when it’s time to eat and CCK, GLP-1 and PYY tell you when you’ve had enough.
People on a diet have increased levels of ghrelin in their blood, which in turn reduces satiety hormones, which explains why you feel hungrier, and meals feel less satiating.
Does that mean every attempt to lose fat is doomed to fail?
No, the laws of thermodynamics still hold true. If you consistently maintain an energy deficit you will lose fat. It just becomes harder over time because our bodies are resistant to change.
The trick is to find ways of maintaining an energy deficit which is as sustainable as possible:
- Load up on whole foods, fiber and vegetables
- Prioritise your sleep
- Take your time. Sustainable fat loss requires time and consistency.
References
- Babaei, S., Sáez, A., Caballero-Solares, A., Fernández, F., Baanante, I.V. and Metón, I., 2017. Effect of dietary macronutrients on the expression of cholecystokinin, leptin, ghrelin and neuropeptide Y in gilthead sea bream (Sparus aurata). General and comparative endocrinology, 240, pp.121-128.
- Benton, D. and Young, H.A., 2017. Reducing calorie intake may not help you lose body weight. Perspectives on Psychological Science.
- Blanco, A.M., Bertucci, J.I., Valenciano, A.I., Delgado, M.J. and Unniappan, S., 2017. Ghrelin suppresses cholecystokinin (CCK), peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) in the intestine, and attenuates the anorectic effects of CCK, PYY and GLP-1 in goldfish (Carassius auratus). Hormones and behavior, 93, pp.62-71.
- Cameron, J.D., Goldfield, G.S., Cyr, M.J. and Doucet, É., 2008. The effects of prolonged caloric restriction leading to weight-loss on food hedonics and reinforcement. Physiology & behavior, 94(3), pp.474-480.
- Cummings, D.E., Frayo, R.S., Marmonier, C., Aubert, R. and Chapelot, D. (2004). Plasma ghrelin levels and hunger scores in humans initiating meals voluntarily without time- and food-related cues. American Journal of Endocrinology and Metabolism. 287: E297-E304.
- Dulloo, A.G. and Jacquet, J., 1998. Adaptive reduction in basal metabolic rate in response to food deprivation in humans: a role for feedback signals from fat stores. The American journal of clinical nutrition, 68(3), pp.599-606.
- Figueiro, M.G., Plitnick, B. and Rea, M.S. (2012). Light modulates leptin and ghrelin in sleep-restricted adults. International Journal of Endocrinology.
Holt, G.M., Owen, L.J., Till, S., Cheng, Y., Grant, V.A., Harden, C.J. and Corfe, B.M., 2017. Systematic literature review shows that appetite rating does not predict energy intake. Critical reviews in food science and nutrition, 57(16), pp.3577-3582.
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