I’m conscious of my need to get back into the swing of blogging so I’m taking the easy route and using exerts from my ‘yet to be published book’. This week, given the lead up to Christmas indulgence it’s all about food…..
In November 2014, 2.1 billion people were classed as overweight or obese, which is a staggering 30% of the global population and the numbers are continually increasing. Research commissioned strategic experts McKinsey estimates that ‘obesity is only set to rise, with an increase to 50% of the global population by 2030.’
But why, after all no one wants to be overweight? WHO (the World Health Organisation) states that ‘the fundamental cause of obesity and being overweight is an energy imbalance between calories consumed and calories expended’. So this should be a simple problem to solve: eat less (fewer calories consumed) and exercise more (more calories expended). Simple!
Unfortunately our brain and body are far more complex than the simple equation of energy in, energy out. A big part of the problem is we don’t factor in the way our ancient brain works, but research is increasingly pointing to how obesity is less to do with ‘will power’ and more to do with a mismatch between our brains and the modern world.
Our ancient ancestors main driver was to survive in a harsh environment. Salty, fatty and sugary food was scarce but all were critical to stay alive . Hence their brains evolved to reward us when they found food that was:
- Fatty, fat stores enabled our ancestors to survive periods of famine
- Salty, salt is lost through sweat and our ancestors were very active. Salt is essential to nerve functioning
- Sweet, sugar gave our ancestors the quick energy injection that enabled them to escape danger.
Eating fatty foods, but even more so the scarcely found salty and sugary food (there wasn’t an abundance of salted caramel in the 5th Century BC), activated neurons in the brain such as the dopamine pathways that made them feel good, to encourage them to eat more of that rare food while it was available.
We have the same brain today but unfortunately the foods that contain fat, salt and sugar are abundant and when we eat these foods our brain rewards us. This feels good, particularly when we’re a bit low or stressed. So we do it again – and we are rewarded again and again and again, building stronger and stronger pathways in the brain, teaching us at a subconscious level, that when we eat ‘bad’ food it feels good and therefore is good.
If we’re hungry or perceive ourselves to be deprived (like when we’re on a diet or just ‘being healthy’) our brain experiences this as pain. As our brain evolved to avoid pain and seek reward, we come upon a new equation ‘the fundamental cause of obesity/being overweight is a reward / pain imbalance between eating fatty, salty sugary food and feeling deprived.’
The cruel twist of fate is that once someone is overweight, his or her sensitivity to dopamine dramatically reduces. This means that if you are overweight you have to eat much more of the foods that once made you feel good, in order to get that feel good factor again. So the ‘unhelpful’ pathways in the brain get strengthened even more which makes kicking the habit harder still. Meaning the harsh reality is that an overweight person will find it harder to eat less or stop eating unhealthy food than someone who is not overweight (Yi Zhang et al, 2013).
There are other significant physiological mechanisms, which influence weight loss and gain (which if people are interested, I can write more about another time) but for now, I don’t want to leave you with a fear of eating over Christmas. There are factors that help undo these mechanisms, the easiest and most obvious being exercise. Not because it has the black and white effect that WHO would have us believe, but because it impacts the reward/pain equation.
Exercise not only counters our body storing fat, it also increases the levels of endorphins circulating in our brains improving mood, quality of sleep and reducing stress. Reducing stress, and reducing levels of cortisol specifically, prevents the build-up of fat around our abdomen. Decreasing stress also makes it less likely that we feel the need to relieve anxiety with food and as a result the primitive driver to derive pleasure and comfort from food is partially countered.
A study carried in Denmark (Andreasen et al., 2008) showed that exercise (although not in everyone) also causes changes in appetite regulating hormones, which suppresses hunger and it even impacts the expression of the obesity genes. The study involving a whoping 17,058 people showed that it didn’t matter if people had a genetic predisposition to being obese, if they were physically active, their weight was no higher or lower than people who did have the obesity gene.
If you find the pain of exercise and the pain of withdrawing from your favourite indulgences too much – try reading ‘The Happiness Trap’ . Such ‘Acceptance Based Behavioural Treatments’ have been found to significantly help, which makes sense given that they work with the way our brain is made up.
But although our brain and the environment are set up against us we are gradually improving our knowledge (science and techniques to deal with it) and adapting the environment (e.g. Jamie Oliver’s Sugar Rush campaign), so if like me you cannot resist all the temptations of Christmas, don’t lose hope.
Happy Christmas Everyone!
References and Links
The Happiness Trap by Russ Harris
Jamie Oliver’s strategy to combat childhood obesity
Evan M. Forman, Meghan L. Butryn, Stephanie M. Manasse, Ross D. Crosby, Stephanie P. Goldstein, Emily P. Wyckoff, J. Graham Thomas. Acceptance-based versus standard behavioral treatment for obesity: Results from the mind your health randomized controlled trial. Obesity, 2016; 24 (10): 2050
Andreasen, C.H., Stender-Petersen, K. L., Mogensen, M. S., et al. Low physical activity accentuates the effect of the FTO rs9939609 polymorphism on body fat accumulation. Diabetes 2008;57 (1) 95- 101
Zhang Y., Kent Jr. J.W., Olivier M., Ali O., Broeckel U., Abdou R.M., Dyer T., Comuzzie A., Curran J.E., Carless M.A., Rainwater D.L., Göring H.H.H., Blangero J. and Kissebah A.H. (2013) QTL-based association analyses reveal novel genes influencing pleiotropy of Metabolic Syndrome (MetS). Obesity 21(10): 2099-111