This is the first in a three-part series on obesity – read more in the series here.
Camilla, a Melbourne-based businesswoman, attests to the daily personal toll of obesity. She chooses aisle seats on planes so her bulk only encroaches on one other passenger. When meeting clients in restaurants, she arrives early to scan for chairs without constricting arms.
She copes graciously with the daily disapproval – tacit admonishments for a certain moral failing or lack of executive control: “I’ve always felt that it was my own responsibility. But it’s not a choice to be overweight. Because if I could choose, this is not how I would want to be.”
Are people like Camilla weak-willed, or are they wired to eat? Research suggests food purveyors have nailed irresistible combinations of fat, sugar and salt (think the honey-roasted almond) and that our genes and physiology are conspiring to make us give in. And if willpower is to be more than just an impotent bystander we must heed new findings in that field too.
The body is generally good at homoeostasis, keeping variations in things such as temperature to a minimum. A set point for weight makes evolutionary sense; too thin and we risk starvation, too fat and our sluggish bulk runs the gauntlet of predation. Yet adult obesity rates have nearly tripled in developed countries, from 25% in 1980 to over 68% in 2012. So what might be loosening the firm grip of energy homoeostasis?
The “satiety hormone” leptin is made in fat tissue and regulates weight by keeping the brain updated on the state of fat stores. If victuals are scarce and fat reserves dwindle, leptin drops – a change sensed by the brain’s all-purpose thermostat, the hypothalamus.
The upshot is you feel hungry and move around less in a two-pronged strategy to conserve energy. In times of plenty when fat stores rise, so too does leptin, which makes you feel full and stops overeating. But, somewhat mysteriously, leptin can work very quickly, way before any changes in fat mass.
Michael Schwartz, director of the Diabetes and Obesity Centre of Excellence at the University of Washington, explains that leptin production alters according to the metabolic state of the fat cell. Just skipping lunch can shift fat cells into catabolic mode, leptin secretion plummets, and you get hungry.
No longer just a static energy depot, fat has, over the past couple of decades, shaped up as a dynamic endocrine organ to rival the pancreas or the thyroid gland.
But the outward march of girths suggests leptin isn’t quite the failsafe fat controller. When obesity takes hold leptin goes up, stays up, and there is a gradual resistance to its effects. So what might be messing up the “I’m full” signal that leptin is usually so good at delivering?
The evidence is mounting that the cardinal ingredients of the Western world’s favourite diet are actually making us hungrier.
Schwartz says one of the prime suspects in leptin resistance is dietary fat. Within days of gorging on lard, beef tallow and coconut oil, rats mobilise inflammatory cells in the hypothalamus, damaging the neurons that are supposed to protect against weight gain.
But fat has an accomplice. Fructose, ubiquitous in the flavour enhancer high fructose corn syrup, causes leptin resistance in rats. And so the evidence is mounting that the cardinal ingredients of the Western world’s favourite diet are actually making us hungrier.
If you have any doubts that leptin holds titanic sway over the urge to eat consider what happens when you can’t make any at all. This is the miserable lot of children with a single mutation affecting the ob gene. They become morbidly obese, something that is almost miraculously reversed with leptin replacement.
Indeed, variants in genes coding for leptin and a host of other proteins involved in energy homoeostasis are major contributors to obesity worldwide, accounting for up to 70% of the variation in body mass index.
On the flipside of the hormonal coin is ghrelin. This “hunger hormone” is produced by the gut when the stomach is empty and signals to the hypothalamus to get us eating again. As with leptin, our dietary predilections may be shifting the ghrelin balance and steering us inexorably towards obesity.
A study last year found baby mice that were overfed produced less ghrelin, were more resistant to it, became obese and stayed that way to adulthood. Sebastien Bouret, a developmental neuroscientist at the University of Southern California and a co-author on the study, says those ghrelin changes cause overeating later in life, possibly by making animals hypersensitive to ghrelin.
“This paper suggests that overnutrition in kids might also be associated with the same hormonal and metabolic disturbances,” says Bouret.
But another study published last year tangles the web still further. It found blocking ghrelin in young rats promoted nerve growth in the hypothalamus and that giving ghrelin stunted nerve growth in the same area. But those opposing effects yielded identical results: the rats got fat.
The sobering upshot is that both over- and under-eating in pregnant women, and the lower/higher ghrelin levels that go with them, put their babies at risk of obesity, diabetes and cardiovascular disease in later life.
At first glance, this might seem an open and shut case that, in a world of limitless calories, our fate is inextricably determined by our genes and hormones. So, is willpower really just a comforting myth?
Next in the series: Free will, food and obesity: do we really have a choice?
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