Why We Eat (Too Much)

  Glucose is the End-Product of All Carbohydrates

  After we eat any food that contains carbohydrates, glucose starts to be dumped into the bloodstream. The pancreas senses this and starts to secrete insulin. Insulin’s job is to direct the blood glucose into our cells (mostly our fat cells). When insulin levels are high, the body switches to storage mode: insulin forces glucose from the blood and into fat cells, where it is converted to triglycerides.fn3 Once the blood glucose settles back down to our single teaspoonful level again, the insulin disappears – it is no longer needed.

  The amount of insulin that the pancreas secretes is proportional to the amount of glucose being dumped into the circulation. And the amount of glucose being dumped into our blood, and the speed at which it is being dumped, depend on what we have eaten. Therefore insulin levels are directly influenced by the type of food that we eat. Food or drink with a high sugar content (think Coca-Cola) will produce a surge in insulin. Foods containing complex carbohydrates (think of a stick of celery) that need time for the bowel to break them down will infuse their glucose much more slowly into the system and therefore produce a longer but less intense secretion of insulin – a trickle.

  As an example, a teaspoonful of sugar contains 4.2g of sugar – the same amount as in one eighth of a can of Coke, and the same amount contained in four sticks of celery. If we drank a mouthful of Coke, this would infuse sugar into our blood within minutes, causing a surge in our blood glucose (doubling the amount); therefore a large spike of insulin would be needed to deal with this. If we ate four sticks of celery, our intestines would need up to an hour, or two, to break down the complicated chains of carbohydrate contained within the celery into simple sugars. Therefore the blood-sugar level would rise extremely slowly. Insulin would also rise slowly to deal with the sugar. The total amount of insulin produced to deal with the Coke sugar would be exactly the same as the total amount of insulin required to deal with the celery. Remember, total insulin secretion over a long period of time is used as part of our set-point calculation: the more insulin, the higher the weight set-point. With carbohydrates, it is not the type of food that matters when calculating insulin and the set-point, it is the total amount of sugar.

  Highs and Lows on the Roller Coaster

  To expand on this a little, sugar is sugar whether it is in Coca-Cola or celery. However, if the food (or drink) that is taken in lets go of its sugar too fast, and if that food has a tremendous amount of sugar in it, then it will cause a violent spike in insulin secretion. The large surge in glucose entering the bloodstream is followed by a large surge in insulin. The insulin works to open up the fat cells to suck the sugar into them but … here is the catch: because of the insulin surge, too much glucose leaves the bloodstream, leading to the blood-sugar level falling. This sets off alarm bells in the brain which is dependent on glucose to function. The alarm gives us a feeling of anxiety and a very strong craving for any food containing sugar. The brain is stepping into critical survival mode – ‘Get sugar and get sugar fast!’ is the message. We cannot ignore these warning messages; we have to act on them, and therefore we seek sugar wherever it is. Fortunately, in the Western environment, sugar surrounds us. Unfortunately, sugar drenches most of our foodstuffs. What the brain wants is less than a spoonful of sugar, maybe half a spoonful; what it gets is more likely to be a low-fat blueberry muffin (containing nine spoonfuls of sugar). Sugar floods the bloodstream again and insulin is called into action once again – massive surges of it – and the cycle is repeated.

  This is the classic sugar roller coaster. Eat a highly refined sugary breakfast (cereal and/or toast + orange juice) and you will get a sugar spike soon afterwards. By mid-morning your blood sugar levels will have plummeted due to the large reactive spike in insulin forcing sugar away from your blood and into your fat cells. It is at this time – in the mid-morning – that you get that terrible craving for more sugar. The coffee shop is calling you – blueberry muffin time! Wow, up again, great feeling. Then, pre-lunch: scary, scary, the adrenaline is dropping; low sugar again. Let’s hit the supermarket and get a meal deal: sandwich, crisps (you need those endocannabinoids), a Coke. Yes! Up and down, up and down – all day …

  This is the thrill of the sugar roller coaster. But this is a new ride. Before the US government’s dietary guidelines in 1977 (the McGovern Report), many people would have consumed a hearty breakfast of fried eggs and bacon or sausage – the full English. This would usually carry people through the morning until a small lunch was contemplated – there was no thrilling high-sugar rush and no subsequently scary low-sugar dive. But we were then told that the saturated fat in the full English breakfast was going to kill us, so we had to stop eating it. Instead we ate low-fat (high refined carbohydrate) breakfasts and took our early-morning seats on the sugar roller coaster.

  Figure 10.1 The blood-sugar roller coaster Source: J. Brand-Miller et al. (2009). Glycaemic index, postprandial glycaemia, and the shape of the curve in healthy subjects: analysis of a database of more than 1,000 foods. Am J Clin Nutr, 89 (1), January, 97–105.

  ‘The Snack You Can Eat Between Meals Without Ruining Your Appetite’

  The food industry had a new opportunity after the publication of the 1977 dietary guidelines. People were consuming new ‘healthy’, low-fat, high-sugar breakfasts and did not feel so well mid-morning. They craved a mid-morning snack, but it was not normal eating behaviour to snack between meals. Our benevolent food industry came to the rescue.

  Sensing the new need for people to top up their sugar mid-morning and mid-afternoon, and also sensing a money-making opportunity, the food industry set about changing our eating habits. It had already started to change the food we ate – but this new type of food itself required that we change our eating habits as well. Eating three square meals per day, and embracing a normal hunger (working up a healthy appetite) between meals, would need to change to accommodate the new type of high-sugar food we were consuming.

  Slowly the advertisers started to suggest that it would be a good idea to treat children to a snack between meals, that it would be good for their concentration at school, that it would not ruin their appetite. New light and fluffy-looking chocolate snacks were developed, and we were assured that this was ‘a snack that you can eat between meals without ruining your appetite’. Slowly, over the years, our eating behaviour changed inexorably until it was not at all unusual to see people enjoying a snack between meals – something that would have been seen as odd prior to the 1970s. Eventually snacking became normal – even snacking in public was considered normal behaviour. Our behaviour had been changed, and a multi-billion-pound snack industry had been spawned.

  The cumulative effect of the sugar roller coaster is that we consume much more glucose, much more sugar, than we would normally crave from a healthy balanced diet. By eating so much highly processed food, and with the new culture of satisfying ourselves during the day on snacks, we are increasing the total amount of insulin that is required to cope with these waves of glucose. As we know, the total amount of insulin that we use is reflected in our weight set-point. Higher than average insulin levels over several weeks will increase your set-point, and weight gain will follow. Whereas lower than average insulin levels over several weeks will lower your set-point and effortless weight loss will follow.

  So it is not about the total number of calories that we are consuming with our constant snacking – if these calories counted as part of an energy in/out equation we would quickly balloon to 200kg, and remember that the massive increase in the number of calories that we are consuming in our sugary snacks is burned off by ratcheting up our metabolic afterburners. This is our normal metabolic adaptation to over-eating (as discussed in chapters 1 and 3). The crucial point – which contributes to people gaining weight – is the effect of insulin on the weight set-point. Insulin dulls the leptin signal and the body gets the message to store extra energy. As the insulin level increases, so leptin resistance appears. If our master weight c
ontroller, leptin, is not heard, our set-point will rise and our weight will follow it.

  Once we decrease our average insulin level, our weight set-point, and then our weight, will fall. In Part Three we will look at ways that we can do this by adjusting the way we eat. We will also learn, with the help of my expert eating psychologist, ways to wean ourselves off that addiction we may have to sugar.

  How Does Alcohol Affect Our Weight Set-Point?

  Alcohol is made from sugar. Those of us who drink regularly are reminded by the media just how many calories are contained in our evening glass of wine. We are told that alcohol contains 7kcal per gram – much more than the energy in a gram of carbohydrate or protein (4kcal), and almost as much as a gram of fat (9kcal). A large glass of wine or a pint of beer contains over 200kcal, the same as a large slice of pizza. Have a couple of glasses and you are reaching 20 per cent of your recommended daily calorie intake. If you are celebrating in a nice restaurant and have an aperitif, followed by a couple of glasses of wine, then the calorie content from your alcohol (600kcal) can be more than from the food.

  We know that alcohol can cause many serious illnesses, from cirrhosis of the liver to heart disease and cancer, but how much does our alcohol consumption contribute to our obesity crisis? When we count the calories, it looks bleak. For adults, the average weekly alcoholic calorific intake in the UK is over 1,800kcal – enough to make you think about quitting. But this book is all about not counting calories and instead questioning how different factors affect us metabolically. So, for now, let’s push away those guilty thoughts about how many calories we consume in alcohol and think about how it influences our weight set-point.

  The Drinking Man’s Diet

  In the 1960s an interesting diet briefly became popular. The Drinking Man’s Diet, a book by Robert Cameron, self-published in 1962, suggested that if you substituted the calories consumed from sugar and starches and replaced them with alcohol you would shed some excess weight. The diet was based on the observation that many alcoholics fail to gain weight despite consuming massive amounts of calories from alcohol. How do heavy drinkers metabolize or burn off these excess calories? The question has baffled nutritionists for years.

  In 1991, researchers from Mount Sinai in New York answered the puzzle.4 They studied a group of alcoholic men whose weight was stable on 2,500 calories of food daily. When they added 2,000 calories of alcohol to the 2,500 calories of food, they found no weight gain. The alcoholics were somehow able to burn off the excess calories contained in the alcohol and maintain their weight. When the researchers replaced the alcohol with 2,000 calories of chocolate, the subjects gained weight. They found that in heavy drinkers a cellular mechanism occurring in the liver seemed to be able to literally burn alcohol calories, creating increased thermal energy (in a similar way to the thermogenesis described in chapter 3).fn4 Subsequent research showed that as well as turning alcohol calories into heat, heavy drinkers could also increase their metabolic rate by stimulating their sympathetic nervous system (just as in our over-eating experiments in chapter 1), resulting in a faster heart rate and higher blood pressure – all helping to dissipate energy.5

  Most doctors will notice that when they examine a patient who has recently been bingeing on large amounts of alcohol their skin feels hot. No fever, or temperature – just hot. These studies explain this phenomenon. In heavy drinkers, alcohol is broken down and converted, not to chemical energy to be used or stored in the body, but to heat energy which is radiated through the skin. This is the reason a heavy drinker, during an alcohol binge, will not feel the cold, even in sub-zero conditions.

  If, as it appears, much of the calorie energy in alcohol is burned off as heat, and not stored in alcoholics, what about more moderate drinkers or occasional drinkers? How is alcohol energy processed in most of us? Alcohol energy itself cannot be stored in the body in the same way that fat or carbohydrates can be. The body treats it like a poison, breaking it down first into a chemical called acetaldehyde (which causes your hangover) and then into acetate (vinegar’s essential component), before finally being converted to carbon dioxide and water. During the breaking down of alcohol, small particles of nicotinamide adenine dinucleotide (NADH) are released. These particles contain the energy to charge up those ATP micro-batteries (discussed in chapter 7) in our liver cells. So some energy is produced during alcohol breakdown, but none is directly stored and must be used immediately. The liver cells suddenly have lots of cellular ATP batteries charged, lots of energy on board. During the period that alcohol is being degraded (averaging 2 units per hour), the liver uses this free supply of energy. This means that it does not have to use its normal source of energy: fat. Therefore fat starts to accumulate in the liver cells, resulting in a condition called fatty liver.

  So we now know a side effect of metabolizing alcohol can be the risk of developing a fatty liver, but what about our weight and our waistline? Large studies on the effect of alcohol on weight seem inconclusive.6 Some show that it can cause weight gain, others that it has no effect on body weight at all. One study showed weight loss in women if they began to drink alcohol.7

  If alcohol causes significant weight gain, then we would expect that the countries with the highest per capita consumption of alcohol would also be prominent in our obesity league tables. The Baltic nations, Russia and Eastern European countries make up the top 10 in our alcohol league table; France and South Korea appear further down. Whereas the obesity league tables are dominated by the Pacific Islands, and the non-drinking Middle Eastern States – Kuwait, UAE, Qatar, Bahrain and Saudi Arabia. None of the nations in the top 20 alcohol league table appears at the top of the obesity league tables, and the obesity league table is dominated by non-drinking countries. On that basis, there does not seem to be a compelling link between alcohol and weight.

  Beer Belly

  This finding doesn’t fit in with our common, day-to-day observation that people (particularly men) who spend a lot of their lives in the pub develop a ‘beer belly’ – an excess accumulation of fat around the waist. One explanation for this could be the effect that alcohol has on the steroid hormone cortisol. We now know that alcohol causes higher levels of cortisol to be produced.8 Cortisol is normally produced in response to chronic stress. Patients who have a condition called Cushing’s syndrome, where excess cortisol is constantly produced, or patients who take long-term steroid tablets for arthritis or other inflammatory diseases, will develop changes in the distribution of fat around their body. These include increased abdominal fat (described in textbooks on Cushing’s as a ‘pot belly’), a round face (moon face) and skinnier arms and legs. As regular heavy drinkers increase their cortisol levels, they too will eventually develop a similar appearance to patients with Cushing’s syndrome – a large ‘beer belly’.

  Alcohol, Insulin and Appetite

  Interestingly, alcohol can improve insulin’s function, making it more efficient. But the side effect of this is that when we drink alcohol it can lead to lower levels of blood sugar. The brain senses this and tells us to go and eat – producing the late-night craving for an after-drink kebab, or the early-morning need for a fry-up.

  Alcohol, because of its effect on blood-sugar levels (and cortisol), can make us eat more. The calories in the alcohol itself are used by our bodies very inefficiently, but alcohol heightens our appetite, telling us to eat high-calorie foods. If the extra food that we take in is high in sugar, wheat or vegetable oils (i.e. Western food), then those foods, if consumed regularly, will raise the set-point.

  Alcohol and Our Weight

  If alcohol leads us to eat more, then why don’t the countries with the highest alcohol consumption appear in the obesity league tables? The answer comes from the quality and type of foods available to those populations. The people of the Baltics, Eastern Europe, Russia, France and South Korea have not yet fully embraced highly processed Western foods, so despite their high alcohol consumption, even when they do over-eat it is with foods that do not
raise the weight set-point. Therefore weight does not become an issue.

  If the calories in alcohol are not stored, then how do we explain the common observation that people lose weight when they stop drinking? They tend to be people who drank quite heavily before quitting. When they stop drinking alcohol, their appetite returns to normal, and their eating behaviour improves. This, combined with a drop in their cortisol levels, leads to a decrease in their weight set-point and subsequent weight loss.

  Is Quitting Alcohol Good for Weight Loss?

  We now know that the calories in our glass of wine or vodka and tonic are used by the body very inefficiently. Alcohol, despite containing 7kcal/gram, contributes much less energy than carbohydrate’s 4kcal/gram – hence the Drinking Man’s Diet and its brief popularity. The energy in alcohol is released because our body is trying to degrade this poisonous substance. Even in moderate drinkers some of this energy is lost to thermogenesis and heat dissipation. The rest of the energy produced while alcohol is being broken down can power the liver. This creates a moderate energy saving and the laying down of the fat that would normally have been used.