Why can’t I keep my weight under control?

That was the question I used to ask myself pretty regularly - from my teens right through to my early 50s - when I finally discovered the truth: it isn’t about will power, calories or following a short-term fix. It IS about addressing the root causes driving appetite and weight gain. 

The body’s “appestat”

Like a thermostat that keeps your house at a comfortable temperature, your body has an “appestat” which regulates your appetite. This appestat is located in your brain [1] and receives signals from different parts of the body which tells it about how much fuel is in storage (your fat stores), what sort of foods you have just eaten (hormones released from the gut), your blood sugar levels and how much energy you are using up. When this works properly it effectively balances your energy intake against your energy output keeping your fat reserves (and therefore your weight) at a steady level. But when you have problems with weight gain, this is because the appestat has stopped working properly.

Most weight loss approaches focus on manually regulating the calories in vs the calories out in an attempt to subvert the malfunctioning appestat. This is very inefficient. It’s as if your house boiler is stuck on and you are trying to control the temperature in the house by turning radiators on and off and opening and shutting windows. Your house temperature goes up and down and you mostly feel uncomfortable. It would be far better to fix the boiler and the thermostat than to try to regulate it all manually! 

What makes the appestat malfunction?

Why are you being driven to eat more than your body needs? There are many, many reasons! Some likely factors are:

1.    You’re eating foods that bypass the appestat.[2]

2.    You are not eating enough of an essential nutrient causing the body to drive you to eat more in an effort to obtain this nutrient (for many people the essential nutrient in question is protein).[3–5]

3.    Your body suspects there is famine ahead and needs to increase your fat stores just in case.[6–8]

4.    You have chronic low-grade inflammation.[9] Inflammation in the gut in particular is noted to be linked with obesity.[10,11]

5.    You are highly stressed, which may be due to mental stressors or physical stressors.[12,13]

6.    You’re not sleeping well or at the right times.[14,15]

7.    Your gut bacteria are not in balance.[11,16]

8.    Your digestive system is not sending the right signals to the appestat.[1,17]

9.    Genetic influences that affect the appestat function.[18,19]

Quite likely, if you’ve been struggling with your weight for a long time, more than one of these factors are in play. You’ll notice that willpower is not on this list! Of course, we can use willpower to prevent us from eating when we are still hungry but this is exhausting and can actually make things worse (see point 3 above). 

Resetting the appestat

Even without knowing the exact mechanisms that are causing your appestat to be out of kilter, there are several things you can do to help:

1.    Avoid foods that are high in both carbohydrates/sugar and fats: this combination has been shown to override the appestat so that once you start eating them you “just can’t stop”.[2]

2.    Focus on eating foods that are high in essential nutrients: protein, healthy fats, vitamins and minerals; get some sunshine (during the summer) to ensure your vitamin D levels are good.

3.    Rather than constantly trying to under-eat, alternate periods of fasting with periods of feasting: we evolved to go without food at times but to eat our fill when food was available. Nowadays, food is available all the time and instead of feasting and fasting, we graze. Those who practice intermittent fasting have found that, contrary to what you might expect, after a period of fasting their appetite is reduced not increased.

4.    Work to reduce inflammation in the body by avoiding sugars and eating a healthy diet. Identify if any particular foods or environmental factors may be increasing inflammation.

5.    Take steps to reduce stress or at least reduce the impact of stress: give yourself time to relax and unwind: don’t feel you need to be constantly achieving!

6.    Don’t ignore the importance of getting a good night’s sleep.

7.    Look after your gut bacteria: feed them the vegetable fibres they love such as leafy greens, broccoli, asparagus, leeks, onions, lentils and pulses.

8.    Eat in a relaxed state: eating on the go or in a rush adversely affects your gut and prevents the appropriate fullness signals to be sent to the appestat.

9.    You might think you can’t change your genetics but there is increasing evidence that you can influence how great an effect your genes have on your body. For example, one of the best-known genes that affect weight is the FTO gene. Studies have found that a higher protein diet and taking regular exercise can ameliorate some of its effects.[20]

Self-sabotage – maybe it’s your willpower after all?

Many dieters despair at the apparent ease with which they can self-sabotage their diets. What’s going on?

Our brains are always looking out to protect us from harm. This is one reason that constant under-eating tends to cause problems: your subconscious brain calculates that if you keep undereating you will eventually starve so steps must be taken to prevent that! Another way your brain may be protecting you is that if there is a good reason (to your subconscious brain that is) for you not to lose weight, then your appestat will continue to be set too high. An example of this is the link between adverse life experiences and subsequent obesity.[21] If you think that this may be a factor in your weight loss struggles, you should consider seeking counselling. 

What if you’ve tried all of that?

These guidelines are a good foundation of a healthy diet, but each person will have their unique biochemistry at play. This is where nutritional therapy can help you to drill down to discover what is going on and help you to work out what you need to do to address these underlying influences to reset your appetite, improve your health issues and say goodbye to yoyo dieting.

 

References

1.       Dodds W. Central Nervous System Regulation of Appetite in Humans and Pet Animals. Ann Clin Exp Metab. 2017;2(1):1013.

2.       DiFeliceantonio AG, Coppin G, Rigoux L, et al. Supra-Additive Effects of Combining Fat and Carbohydrate on Food Reward. Cell Metab. 2018;28(1):33-44.e3. doi:10.1016/j.cmet.2018.05.018

3.       Gosby AK, Conigrave AD, Lau NS, et al. Testing Protein Leverage in Lean Humans: A Randomised Controlled Experimental Study. Morrison C, ed. PLoS One. 2011;6(10):e25929. doi:10.1371/journal.pone.0025929

4.       Martens EAP, Westerterp-Plantenga MS. Protein diets, body weight loss and weight maintenance. Curr Opin Clin Nutr Metab Care. 2013;17(1):1. doi:10.1097/MCO.0000000000000006

5.       Tremblay A, Bellisle F. Nutrients, satiety, and control of energy intake. Appl Physiol Nutr Metab. 2015;40(10):971-979. doi:10.1139/apnm-2014-0549

6.       Sainsbury A, Wood RE, Seimon R V., et al. Rationale for novel intermittent dieting strategies to attenuate adaptive responses to energy restriction. Obes Rev. 2018;19:47-60. doi:10.1111/obr.12787

7.       Fothergill E, Guo J, Howard L, et al. Persistent metabolic adaptation 6 years after “The Biggest Loser” competition. Obesity. 2016;24(8):1612-1619. doi:10.1002/oby.21538

8.       Müller MJ, Enderle J, Pourhassan M, et al. Metabolic adaptation to caloric restriction and subsequent refeeding: the Minnesota Starvation Experiment revisited. Am J Clin Nutr. 2015;102(4):807-819. doi:10.3945/ajcn.115.109173

9.       Keane KN, Calton EK, Carlessi R, Hart PH, Newsholme P. The bioenergetics of inflammation: insights into obesity and type 2 diabetes. Eur J Clin Nutr 2017 717. 2017;71(7):904. doi:10.1038/ejcn.2017.45

10.     Spreadbury I. Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Diabetes, Metab Syndr Obes Targets Ther. 2012;5:175. doi:10.2147/DMSO.S33473

11.     Saad MJA, Santos A, Prada PO. Linking Gut Microbiota and Inflammation to Obesity and Insulin Resistance. Physiology. 2016;31(4):283-293. doi:10.1152/physiol.00041.2015

12.     Hirotsu C, Tufik S, Andersen ML. Interactions between sleep, stress, and metabolism: From physiological to pathological conditions. Sleep Sci. 2015;8(3):143-152. doi:10.1016/j.slsci.2015.09.002

13.     Tomiyama AJ. Stress and Obesity. Annu Rev Psychol. 2019;70(1):703-718. doi:10.1146/annurev-psych-010418-102936

14.     Deng H-B, Tam T, Zee BC-Y, et al. Short Sleep Duration Increases Metabolic Impact in Healthy Adults: A Population-Based Cohort Study. Sleep. 2017;40(10). doi:10.1093/sleep/zsx130

15.     Knutson KL. Does inadequate sleep play a role in vulnerability to obesity? Am J Hum Biol. 2012;24(3):361-371. doi:10.1002/ajhb.22219

16.     Torres-Fuentes C, Schellekens H, Dinan TG, Cryan JF. The microbiota–gut–brain axis in obesity. Lancet Gastroenterol Hepatol. 2017;2(10):747-756. doi:10.1016/S2468-1253(17)30147-4

17.     Miquel-Kergoat S, Azais-Braesco V, Burton-Freeman B, Hetherington MM. Effects of chewing on appetite, food intake and gut hormones: A systematic review and meta-analysis. Physiol Behav. 2015;151:88-96. doi:10.1016/j.physbeh.2015.07.017

18.     Rohde K, Keller M, la Cour Poulsen L, Blüher M, Kovacs P, Böttcher Y. Genetics and epigenetics in obesity. Metabolism. 2019;92:37-50. doi:10.1016/j.metabol.2018.10.007

19.     Kleinendorst L, van Haelst MM, van den Akker ELT. Genetics of Obesity. In: Experientia Supplementum (2012). Vol 111. ; 2019:419-441. doi:10.1007/978-3-030-25905-1_19

20.     Merritt DC, Jamnik J, El-Sohemy A. FTO genotype, dietary protein intake, and body weight in a multiethnic population of young adults: a cross-sectional study. Genes Nutr. 2018;13:4. doi:10.1186/s12263-018-0593-7

21.     Palmisano GL, Innamorati M, Vanderlinden J. Life adverse experiences in relation with obesity and binge eating disorder: A systematic review. J Behav Addict. 2016;5(1):11-31. doi:10.1556/2006.5.2016.018