Life in the Fat Lane: Do my genes force me to eat doughnuts?

I'm large; I'm greedy. So am I just one big character defect?

My mother was a great lover of opera, but she flatly refused to go to Pavarotti’s last performance on the grounds that he was ‘so revoltingly fat’.  In her book, being fat was the most reprehensible, unforgivable of sins, and entirely due to character defect.

My mother was also a great lover of Labradors, unconcerned by either their immense greed or propensity to put on weight.  Even when they teamed up with the family poodle to dislodge the remains of the Sunday roast off the top of a very tall fridge, she smiled fondly: she should have locked it in the larder; Labradors will do anything to get at food – everyone knows that – and it was her job to stop them.

There was a reason why Pavarotti was vast:  he ate ravenously – cramming vast amounts of food into his mouth as fast as he could lift his spoon, sometimes with his wife clinging onto his spoon-hand to slow it down.

I am not in the same league as Pavarotti, but the other day, after a 10.5k walk, I could have murdered a large piece of cake… or two… or – well I am not going to get into full disclosure on my exact capability cake-wise.    And besides, it didn’t happen.  There was no cake – I don’t keep it in the house – so I had to put up with my body protesting loudly for the rest of the evening. Had there been, my willpower wouldn’t have stood a chance.    

So what drives this ravening hunger?  And why is willpower not enough to control it?  Pavarotti did not get to be a world-class tenor without a massive helping of self-discipline.

One factor is cortisol, the stress hormone. It’s meant to help you run faster when you are being chased by a sabre-toothed tiger – a short, sharp affair, lasting just long enough to see whether you or the tiger get to eat dinner. There’s still plenty of stress around, but mostly of the sort that’s not helped by running away fast.   And if, instead of a quick do-or-die affair, it’s a long-term thing, the cortisol can become a lot less helpful and have all kinds of unpleasant effects on the body; one of these is massive hunger.

Being a world-class tenor is as good a way as any to create perma-stress: when your star-status and huge fees rely on your top notes being fabulous in front of adoring fans who’ve paid large sums for their tickets, life is not relaxing.

But cortisol can’t be the whole answer – not all singers have massive appetites, and it’s stressful singing in public whether you’re doing it at the Royal Opera House or the village hall.   And not all people who eat huge amounts get fat.  Annoyingly.

According to Giles Yeo,* a major factor is evolution and our genes.

It sounds like the perfect cop-out for greed, but thousands of years ago, when the food supply was sporadic and difficult to catch, we needed copious fat reserves to fuel chasing after four-legged edibles and survive long periods without food.  However, accumulating fat was no piece of cake in the days before you could deep-fry a Mars Bar, so the body had to devise clever ways to make the most of what it could get.

One of these was the hunger hormone, ghrelin.   It lives in the upper gastrointestinal tract, and its job was to make you seriously hungry before mealtimes so you could eat up your antelope before it went off – and wouldn’t turn your nose up if it didn’t taste that good.  This was helpful in the days when nothing tasted that good.

Another hormone that kept our ancestors alive was the anti-starvation leptin: it lived in the fat cells and kept the brain up to date about fat stored.  If there was enough to cope with nothing to eat for a week or two, the brain knew it was safe to stop eating and spend some of the stored energy. If stocks were too low, it made the person hungry. If they were seriously low, it made them ravenously hungry so they would eat absolutely anything: picky eaters did not thrive.  I will pause here to give 21^st century parents a moment to deal with their conflicted feelings.  And it also slowed the metabolic rate to induce lethargy so the person wouldn’t waste remaining energy stores by running around.

Biochemically-engendered gluttony and sloth.

And on top of clever hormones, there were genetic mutations and variations that gave people get-fatter advantages: bigger appetites, persistent hunger, or a liking for – and ability to detect – high calorie food: in the pre-Krispy-Kreme Era (the rarely-used, original name for the Stone Age), the ability to spot a doughnut at a hundred paces and hunt it down would give a person a distinct survival advantage over someone who would settle for the nearest carrot.

The effects of these genes have been measured by people who go in for that sort of thing.  With some of them, the effect is dramatic: people with the MC4R gene – which affects hunger – were on average, two-and-a-half-stone heavier by the time they were eighteen than their contemporaries without it.  With others, it is the accumulation of many tiny variations: in a study of a particular set of genetic mutations to do with hunger, the more of them a person had, the higher their BMI.

In short, people who were genetically hungrier were consistently fatter.

With another gene mutation, in an experiment offering food of low, medium, and high fat – all carefully disguised to taste identical – people with the gene unerringly went for the high fat option; people without the mutation invariably went for either the low or medium fat option.

And the mutations do not only occur in humans: 25% of Labradors carry a particular gene mutation that makes them massively food-obsessed and always hungry.

I suspect I may be 25% Labrador.

And a mutant lard-eater.

And as for those hunger genes: I remember being in France once with my skinny younger sister. We were wondering around the historic centre of Dijon  at lunchtime, and there were lots of stalls selling delicious things to eat.  I was looking forward to eating all of them.

‘I don’t think I’ll bother with lunch, I am not very hungry,’ announced my sister. ‘Perhaps we could have something to share,’ she said.

Share? Lunch?  Not be hungry enough to bother with it …   I had never considered having lunch and decided not to bother because I wasn’t very hungry.  For clarification purposes, there have been occasions when I have not had any lunch, but it has never, ever been because I wasn’t hungry.

So for millennia, we have been evolving, tiny mutation by tiny mutation, to be highly efficient at getting fat and staying fat.   There was no call for us to evolve ways of getting rid of excess fat because no one got the chance to get fat.

And it was all marvellous until we did discover how to deep-fry a Mars Bar, and the Krispy Kreme Era finally dawned.    Our fabulously fattening genes failed to slink away when it was quite obvious they were no longer wanted*, and ghrelin still works full-tilt to give us an appetite to eat up our antelope – or super-sized fat-burger as it’s called these days.

*Until the next famine.

And as a bonus, if we lose the weight that our mammoth-eating appetite has helped us gain, our ghrelin levels increase, making us even hungrier than we already were on the diet.

So why doesn’t leptin get its act together?  Its job is to stop us eating when we are fat enough, so if it were doing it properly there would be millions of diet-book authors starving in garrets.

One answer is something called leptin-resistance: the leptin sends a message to the brain that the fat stores are full, but the brain takes no notice and does its usual number of inducing greed and indolence – which are supremely difficult to resist: if the brain thinks you are starving, it does not want its efforts to keep you alive ruined by willpower.   And in people whose leptin is working as it should, if they lose weight – and therefore fat stores – the leptin sends a message to the brain that catastrophe is imminent. The brain leaps into action and  – well, you know the rest.

So leptin doing its job and not doing its job is very good at thwarting weight loss.

Evolution has made doing something about being fat very, very difficult:  it’s not a question of resisting a bit of mild peckishness for a month or two, but daily mortal combat with a biology that’s fighting tooth and nail to get fat and stay that way.

And the fight is all in our brain: one part of it can read about the dangers of obesity, and look into the mirror and not like what it sees, and see certain types of food and know they shouldn’t be eaten because, heart and soul, it doesn’t want us to be fat.    And if we are fat, it gives us clear instructions in its sternest voice to do something about it, because it knows that if we don’t, we will die.

But round the corner is another bit of the brain making sure we will do no such thing, because it knows that if we do, we will die.

There are many contributors to obesity:  living in a hyper-fattening food environment – dominated by a food industry making heroic efforts to deliver obesity-on-a-plate 24-hours a day – is a major driver, but with a  supporting cast of stress, inactive lifestyles, poverty, and mental health issues.   But without evolution and disordered biochemistry, all those factors would get nowhere.

So, no, my genes don’t force me to eat doughnuts, but they do everything in their power to make sure I do.

* Principal Research Associate at the Metabolic Diseases Unit at Cambridge University, and author of Gene Eating

‍