This is how dieting can make you fat.
In principle weight loss is easy: if you consistently burn more calories than you ingest, you will lose weight...
In practice, though, losing weight is very difficult and not many people succeed. Actually, let me re-phrase this a little – people can initially lose weight by restricting their food intake, but this weight is promptly re-gained, sometimes leading people to become heavier than they were at the start of their weight-loss journey (Swanson & Dinello, 1970). This is dubbed "yo-yo dieting", and to understand why diets fail, and why this may fuel the obesity epidemic our society is currently battling, we have to take a step back to examine what causes obesity in the first place.
Some people think that the obesity crisis is caused by our obesogenic environment, a world where food is ever-present and we are continuously encouraged and stimulated to eat more low quality and energy-dense products. Our preference for fat and sugar over fruits and vegetables is rooted in our genes, which gave our ancestors an evolutionary advantage in a world where food was scarce. Nevertheless, simply having access to potentially unlimited amounts of food does not fully explain the obesity crisis. If this was the only reason for our society getting heavier, we would expect obesity rates to be about the same in economically-similar countries, and this is clearly not the case. Despite the populations of the US and Japan having similar ease of access to energy-dense food, the obesity rates in the two countries are 33% and 3.3%, respectively (Nettle, Andrews, & Bateson, 2016). So other factors are clearly contributing to the extra weight we carry.
And even though our brains are encouraging us to eat high calorie foods to ‘aid’ our survival, from an evolutionary perspective, it doesn’t make sense for our genes to be geared towards accumulating as much fat as possible. Carrying excessive weight can be beneficial for humans and animals, in terms of providing a buffer against starvation, but it also increases energy requirements and restricts movement, meaning the organism risks falling prey to its predators. Therefore, eating excessively (and storing extra fat) is only advantageous in certain instances, for example when food resources are scarce and the risk of starvation is greater than the risk of a predator attacking. So, it makes sense that animals (including humans) are particularly sensitive to food uncertainty and respond to this perceived hardship by storing fat. Storing more fat in response to limited food accessibility has been termed the ‘insurance hypothesis’.
Over the years, the insurance hypothesis has gained support from many viewpoints. Birds given food intermittently and at unpredictable times of the day, significantly increased their weight compared to birds which were given exactly the same amount of food in a predictable setting (Ekman and Hake, 1990). The birds responded to an unpredictable food supply by storing more fat and ensuring they would have enough in case their food access would be restricted in the future. A similar association between food insecurity and body weight has been observed in humans, especially in high-income countries (Nettle et al., 2016). Individuals who are facing a perceived economic hardship (e.g. they do not have enough money to buy food for the entire month) consume more calories when they do have access to food, potentially to ‘save’ up for when the anticipated food shortage comes. And the word ‘anticipated’ is very important here, as the economic hardship does not necessarily have to be a realistic threat. When people were asked to imagine themselves interacting with a person with a much higher economic status (i.e. they were made aware of their lower status, and reminded about the things they do not have) they subsequently ate more calories (Cheon & Hong, 2017). The researchers showed that the manipulation had no negative impact on participants’ affect and self-concept, suggesting they were not just eating because they were sad or because they felt bad about themselves – there was something inherent about feeling that the participant was in a worse position than the imagined high-status person, which fuelled their intake.
But why are we even considering the insurance hypothesis when talking about diet-induced weigh gain? It’s because researchers speculate that being on a diet i.e. restricting food intake for prolonged periods of time, and the associated weight-loss, act as ‘economic hardship’ triggers for the brain. You don’t have much food throughout the day, you start to lose weight and your brain goes haywire. Our brains are unable to tell the difference between intentional weight-loss and weight-loss resulting from a real lack of resources. For our bodies, weight-loss is a traumatic process, a desperate cry of ‘if this carries on you’ll die of starvation!’. Equipped with the knowledge from the beginning of this article you can see what happens next: the brain spots a threat to its food supply, it gears up our need to ingest high-calorie foods, we are surrounded by these temptations and we eventually give in, doing exactly what our brain is encouraging us to do – regain the weight we lost.
The biology behind this phenomenon is slightly complex. Firstly, our brains have something called a ‘weight set-point’, i.e. the weight our brain perceives as ideal for us. This is why you don’t see big fluctuations in your weight on a day-to-day basis – one salad won’t make you skinny and one burger won’t make you fat – our brains always try to return us to our weight set-point. People who are overweight or obese have a shifted or abnormal weight set-point – at some point all the extra calories they ingested led to weight gain, which stuck around long enough for the brain to accept it as the new weight set-point. When you lose weight, there is a mismatch between your actual weight and the weight desired by your brain – so your brain deploys a secret weapon against you: hormones. The key hormones involved in eating are leptin and ghrelin – leptin helps you feel full and ghrelin is responsible for feelings of hunger. When you lose weight, less leptin is produced and ghrelin production is upped (Sumithran et al., 2011). So, the food you eat is not making you feel as satiated as before the dieting began and you are feeling hungry all the time. Also, your body now burns far fewer calories than it would, compared to if you have never lost weight (adaptive thermogenesis), to help you not lose weight (thanks body). Your body is doing everything it can to stop your weight-loss and to get you back to your starting weight (or higher). What’s scary is that these biological changes persist for a really long time. Even if you are just trying to maintain your new lower weight, research suggests these changes last for a year (Rosenbaum, Hirsch, Gallagher, & Leibel, 2008; Sumithran et al., 2011), or even as long as six years (Fothergill et al., 2016).
Counterintuitive as it may sound, diets are one of the worst tools to lose weight. When we restrict our food intake our bodies think we are going through a food shortage and gear us towards eating more, which leads to any lost weight being promptly regained, and, sometimes, to a rebound to a higher weight than before the diet began. For a considerable period post-diet, our metabolism slows down to conserve energy, and our hormones make us less full after eating so we feel generally hungrier. But there are people out there who, despite all these hurdles, manage to lose weight and to keep it off, so not all hope is lost. My next article will discuss how we can fight diet-induced weight gain and maximise the likelihood we’ll stay trim in the dietary aftermath...