Healthy Dieting

The discovery of leptin has prompted a gold rush of further hormone discovery around appetite. For instance, how does your body know when to stop eating because you are full up? An obvious mechanism is via nerves that run from the gut to the brain which are fired by physical distension of the gut — that too-stuffed-tomove feeling. The problem with this theory, although there are nerves that undoubtedly do this, is that a meal of boiled cabbage can still leave you feeling hungry, even though you feel completely bloated. Nor does putting 600 calories in through a line intravenously make you feel full the way that a 600-cal0rie Big Mac does.

Let me present ghrelin (usually pronounced `grellin’ but you may also hear `graylin’), the hormone of hunger, which is produced by the stomach — and its kissing cousin, PYY, the hormone of satiety (feeling full), produced by the intestine.

Hormone doctors and researchers are dazzled by ghrelin. At the recent World Congress of Endocrinology in Lisbon, every session on ghrelin was packed to the rafters. It’s a tiny chain of amino acids, produced by single cells in the stomach and a fantastically potent appetite-booster or as, scientists would say, an orexigen (which is a great Scrabble word). Inject ghrelin and suddenly you are not just peckish, but could eat a horse. Ghrelin levels fall when you have just had a meal and are at their highest during fasting.

Steve Bloom is head of the Division of Investigative Science at Imperial College; he and his team work at the Hammersmith Hospital. Researchers at the Hammersmith gave injections of either ghrelin or saline to volunteers and found that those who had had the horm0ne infusion ate 30 per cent more.

There seems to be a food pecking order with ghrelin. Levels fall most in response to carbohydrate, then protein, and finally fat, which is interesting because it could be one reason why we are seeing a rise in obesity with modern diets. During the Second World War, for instance, the diet was high in carbohydrates like potatoes and bread but low in fats, and hunger was fully sated by that diet. Today we get more of our calories from fats, which don’t provoke such a large fall in ghrelin, so you are still hungry despite a big meal.

Circulating ghrelin is increased in those people on low-calorie diets, those with cancer, anorexia and other wasting diseases. If you lose weight because you’ve dieted, ghrelin levels respond in a compensatory way, making you hungrier so you’ll put that lost weight back on again — a classic case of hormones working against you. Interestingly, however, weight loss following low-fat diets does not trigger a ghrelin adjustment, suggesting why these diets are more effective long-term ways to lose weight.

In June 2004, researchers from the University of California at Los Angeles (UCLA), led by Dr Julio Licinio, discovered that in lean men’s blood there is a giant burst of ghrelin between midnight and 6 a.m., which exceeds normal pre-mealtime surges. There was no such peak in obese men, suggesting that obesity itself down- regulates ghrelin. It defies the image of a fat man raiding the fridge at night, driven by insatiable hunger. Much of this new work redefines the popular notion of fat people’s behaviour.

The Hormone that Says ‘I’m Full Up’ — PYY

PYY (or PYY₃-₃₆ to be strictly accurate) is the exact opposite to ghrelin, in that it is low in fasting and rises after a meal. It inhibits appetite, and if you give this one to volunteers, they eat 30 per cent less food. What is particularly interesting is that they stay less hungry the next day too. The more calories you eat, the bigger the rise in PYY. This is why the huge calorie intake that is a Sunday roast with all the trimmings, plus pudding, results in you being not that hungry at breakfast on Monday. Slowly digested foods like high-fibre ones, give an even bigger rise, which is why you continue to feel full for longer if you choose to eat wholemeal pasta, for instance, rather than the normal variety. Again, comparing us to our grandparents, perhaps refined foods don’t cause such a big rise in PYY, so we go on eating. Neither of these hormones seems to have any other side effects.

The control of appetite is both hormonal and neural. These two hormones — ghrelin and PYY — both act on the hypothalamus, which has two responses — eat more and eat less — both mediated through neurotransmitters. The eat-less part works via the MC4R receptor that we mentioned earlier. The eat-more ones are called NPY (neuropeptide Y) and AgRP. Both are inhibited by leptin, but it is ghrelin that switches on the neurons that make you eat and switches off the ones that dampen your appetite. PYY does exactly the opposite.

I know I am a hormone enthusiast, and probably far too easily pleased, but as an example of hormones at their most elegant, this system takes some beating. So very clever when it works — but so awful when it doesn’t.

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