Why We Eat (Too Much)

by Andrew Jenkinson

  Examples from nature may provide clues as to how our own omega messaging service evolved, and why these messages can alter our weight and immune system. Remember, omega-3 comes from leaves and omega-6 comes from seeds and nuts. In temperate climates, away from the tropics, the levels of omega-3 and omega-6 in the food available will vary as the seasons change. In the spring, as plants start to produce shoots, omega-3 becomes predominant in the diet. In the autumn, when the leaves start to fall, the seeds and nuts are more plentiful – therefore omega-6 will be in the ascendancy. Over a period of weeks and months the cell walls in an animal change in synchrony with their food environment. The omega-6 to omega-3 ratio is lower in the spring and summer and then increases in the autumn and winter.

  What effect do these seasonal cellular changes have on some animals? Their behaviour and biology change to prepare them for the approaching winter. As the strength of the sun starts to dissipate in the autumn, so the amount of food energy in the environment will also decrease. Animals have to start adapting to a decreasing supply of food energy in a cold winter environment that requires more heat energy to survive. Their metabolic balance becomes stressed as the environmental signals are predicting less energy in and more energy out. Birds have a logical way of dealing with this: if the energy equation doesn’t suit them, they fly south to countries where there is more abundant food energy from the sun. But what about animals stuck on land and unable to migrate long distances?

  We know the brown bear will develop a voracious appetite as winter approaches and will gain an extra 30 per cent of its body weight – all as fat – to be burned slowly during the long months of hibernation.12 It is hypothesized that the levels of omega-6 and omega-3 in the diet, and therefore in hibernating animals’ cell membranes, act as a trigger for hibernation, or torpor13 – more omega-6 leads to a rise in their weight set-point as they prepare for winter months without food. Whilst food energy is still available in the late summer and autumn, the brown bear will gorge until its ‘fuel tank’ is as full as the weight set-point has calculated is best for it to survive winter. When the cold sets in, the brown bear has another strategy for survival – it will reduce its temperature, and therefore its metabolic rate, by hibernating. Throughout the cold winter months, the brown bear will slowly burn through its energy reserves before temperature signals wake it in the spring.

  Another example of behaviour changing in response to environmental signals is that of the chipmunk.14 As autumn approaches, food availability changes (fewer berries and more nuts). The change in the omega ratio of the chipmunk’s cell walls is one of the signals thought to stimulate appetite and weight gain. In addition, it exhibits hoarding behaviour (you may recognize this), bringing nuts to store in its burrow to help it through the winter. The omega-6 to omega-3 ratio also signals when the animal should go into a torpor (a state of very low energy expenditure and metabolic rate, but the animal remains conscious).

  The yellow-bellied marmot, a type of ground squirrel that inhabits chilly Canada, spends eight months per year in hibernation. It eats mostly leafy plant foods, grasses, nuts, eggs and insects. If its omega-3 levels are artificially raised in the lab, then it just doesn’t get the signal to hibernate.15 This suggests that, in the wild, a change in the omega-3 to omega-6 ratio triggers the start of hibernation.

  Winter Food and Animal Biology

  These are examples of hibernating animals whose omega profiles have been studied. We know that there are other environmental triggers that start a hibernation response in wild animals, including changes in temperature, ambient light and vitamin D, but I think that there is a compelling case that changes in seasonal foods also lead to alterations in the behaviour and biology of animals, including humans. According to this theory, the changes we see in response to high omega-6 to omega-3 ratios are in fact primordial protective responses against a future harsh environment. It seems to make sense. As winter approaches, the omegas signal that we need a more accentuated appetite; that we need to seek food more urgently and to savour and enjoy that food more. We need less leaky and more metabolically stable cell membranes to prevent metabolic wastage. We develop stronger immune systems to help fight infection and heal tissues during the winter. Some scientists have speculated that the insulin resistance seen with an increased omega-6 to omega-3 ratio, which causes a higher blood glucose level, is a survival trait inherited from ancient organisms protecting themselves from freezing (the freezing point of water decreases as sugar is added to it). Certainly, some extreme hibernators, such as the yellow-tailed frog (which can actually cause some parts of its body to freeze) still use this strategy.16

  All these biological responses, which may be part of our ancient evolutionary baggage, if present, were designed to help our survival. In that case, then, a major cause of obesity is not a lack of willpower, or laziness, but the appropriately protective weight-gain response to a change in the environment. Unfortunately, the current changes in our food environment are extreme, not because of the seasons but because of our Western diet. No natural autumn season would produce such a big swing in the fatty acids towards omega-6 and away from omega-3, and no natural autumn would last indefinitely.

  This theory, although unproven, does make sense – it fits in with all that we have seen and heard about obesity. It explains all our previous mistakes and clarifies why some treatments work only partially and some don’t work at all. It fits in with our weight set-point theory and explains exactly why some of my patients are continually unsuccessful in trying to reduce their weight. But it also explains why – very occasionally – some have been successful. We can understand why some people’s weight set-point drifts up or down depending on which country they move to and the omega ratio of the food in their new environment.

  But this theory does not explain all cases of obesity. There are other factors in the environment that will alter our weight set-point upwards. These include our habit of snacking and the GI (sugar) index of our food, both of which will cause chronic insulin elevation and obesity. We will discuss this in the next chapter. We also learned, in chapter 3, that recurrent low-calorie dieting will also elevate our weight set-point as a protector against future food shortages. There is also the subgroup of patients, described in chapter 5, whose obesity has become extreme and uncontrollable: these people have developed leptin resistance, which will drive further weight gain even in the presence of positive environmental and dietary changes. We will bring together all these factors and discuss how we can optimize our weight set-point in Part Three of this book.

  As scientists and doctors, we sometimes fail to learn from our past mistakes. History should have taught us that in fifty, or a hundred or two hundred years from now our colleagues of the future will be amused by our current convictions and our misunderstanding of the biggest health crisis of a generation. Just as we saw with beriberi and scurvy – the answer is all around us. We just need to see it.

  Summary

  In this chapter we learned why the type of fat that we eat is so important to our health and our weight. We discovered that there are two particular fats – omega-3 and omega-6 – that cannot be made within our bodies and therefore, just like vitamins, are essential in our diet (that’s why they are called essential fatty acids). These two fats compete with each other for space on the walls of every cell in our bodies. The amount of each of the two omega fats that we eat reflects the amount seen on our cell walls. And the amount (or ratio) of the two fats on our cell walls has profound effects on our metabolism, our weight and the degree of inflammation within our bodies.

  From the 1980s onwards, scientists (and governments) recommended that we change our fat consumption away from natural saturated fats and towards polyunsaturated vegetable oils. Vegetable oils have extremely high levels of the omega-6 fat, which makes them stable and less prone to oxygenation (or ‘going off’), and therefore suitable for addition to foods that require a long shelf life. The consumption of seed oils (sunflower, rapeseed, soya) ha
s tripled within three decades. The resulting excessive amounts of omega-6 fats consumed in the Western diet translate directly into the make-up of the cell wall fats. The ratio of omega-6 to omega-3 fats in a population’s food supply is also mirrored in their cell walls. The change in the type and amount of fats consumed in the Western diet has resulted in an increase in the omega-6 to omega-3 ratio from a natural level of four omega-6s for every one omega-3 to the current level up to fifty omega-6s for every one omega-3.

  Increased cellular omega-6 levels cause an increase in inflammation (contributing to a range of Western diseases). Increased inflammation (via TNF-alpha) leads to poorer functioning of insulin and a dulling of the effect of leptin (the hormone produced by fat cells that keeps us thin). Poorer insulin function means that more insulin is required within the blood. Higher levels of insulin also result in a dulling of the leptin signal. All these effects result in a rise in the weight set-point and then, inevitably … weight gain.

  There is some evidence that the foods that hibernating animals eat before winter sets in act as a trigger for rapid weight gain. The signal comes from the shift of food availability in the autumn/winter towards nuts and grains (omega-6) and away from shoots and leaves (omega-3) – affecting the animal’s cellular omega-6 to omega-3 ratio and triggering weight gain. Towards the end of this chapter we speculated whether humans have a similar evolutionary response to ‘autumn’ foods. In fact, the Western diet has a much stronger effect on our own omega-6 to omega-3 ratio than can be seen in a switch from spring to autumn foods. In addition, the Western diet remains much the same whatever the season. This could produce a permanent signal to gain weight – and be a strong contributor to the development of obesity in some people.

  Just like the deficiency diseases of the past – beriberi and scurvy – could a relative shortage of omega-3, compared to omega-6, be an important trigger for today’s health epidemic – obesity?

  TEN

  The Sugar Roller Coaster

  Glucose, Insulin and Our Weight Set-Point

  Have you ever wondered whether a particular sportsman uses drugs? Maybe they keep on getting better and stronger, despite getting older: they seem to be ahead of the pack and always look great – totally healthy, and their muscles just seem to defy fatigue. What could be their secret? Is it just good genes, eating well and training hard? Or could it be that they are very clever and take some kind of drug which is almost impossible to detect in the drug tests athletes have to undergo?

  Many bodybuilders, up to 10 per cent according to a recent report, now take such a drug.1 It is used to promote uptake of glucose from the blood into the muscles. This means that the muscles can store more energy and work for longer. It is also thought to protect against muscle breakdown. If you need more energy stored up in your muscles than your rivals, then this is the drug. Just one problem though: if you misuse it, it will kill you, within minutes.

  Only one major athlete has ever admitted to using this drug. But the testers never caught her – the drug we are talking about is eliminated from the body within minutes, leaving no trace. The athlete, Marion Jones, was the fastest woman in the world and a poster girl for American athletics. She admitted to using insulin – along with other drugs – to enhance her performance.

  Insulin causes blood sugar to be stored in cells to be used later. Normally it is produced by the pancreas gland in response to a high level of glucose in the blood.fn1 However, athletes can force the issue by taking in extra insulin plus extra sugar over a couple of hours (in a process called the hyper-insulinaemic clamp). This overfills their muscles with glucose – and gives them an endurance and performance edge over athletes who don’t use the technique. The downside is that if they do not understand that it is essential to take sugar when they take the insulin – if they don’t read the small print – then the insulin will consume all the available blood glucose, it will disappear into the cells, and none will be left over to feed the athlete’s brain. They can fall rapidly into a coma and die. Despite this risk, I suspect that there are high-profile athletes using this drug, under supervision, in the knowledge that they will never get caught and it will give them an advantage over their rivals.

  Insulin is a great drug for getting glucose into the muscle cells if you are an athlete. But if you are not constantly exercising, then it has a different effect. Instead of your muscles looking full and ripped, the insulin will force the glucose into your fat cells – and after a while your belly, and not your muscles, will look full, and possibly more ripe than ripped.

  I saw a patient recently who had been fighting diabetes and obesity for years. He was only twenty-five, but had suffered with diabetes since the age of ten. When he was put on to insulin therapy to treat the diabetes, he noticed that he put on a lot of weight. He hovered between 100kg (15 stone 10lb) on insulin, with good diabetic control, to 80kg (12 stone 8lb) off insulin, with poor diabetic control. When he felt that his obesity was getting too much, he would stop treating his diabetes, stop taking insulin, and his weight would fall. However, his weight-loss technique was not doing his body any good: he had already started to develop retinopathy (damage to the retina), a complication of poorly controlled diabetes that can eventually lead to blindness.

  Weight gain is a well-known side effect of insulin therapy for diabetes. Insulin forces the blood to surrender its energy reserves into fat cells. When insulin is in our bloodstream, the energy gate is only open one way – into fat cells, which will never let any energy out. The fat is locked in.

  If insulin levels in our bloodstream are high, then we can expect that our weight set-point will be raised. This is what happens in diabetic patients. If insulin is withdrawn – as in my patient who was fighting obesity – weight loss follows. There are many scientific studies that confirm that altering insulin levels will lead to changes in body weight. Increase insulin and you will increase weight; decrease insulin and you will lose weight. Insulin changes the set-point – up or down – and then the weight will follow.

  High insulin = higher weight set-point

  Lower insulin = lower weight set-point

  An interesting study from San Diego, California, confirmed that insulin works on the set-point.2 The weight of fourteen diabetics was measured as their insulin therapy was slowly increased over a six-month period, until their blood glucose had been controlled. It confirmed that the subjects gained over 8kg (1 stone 4lb). However, when they analysed just how much the subjects were eating while on insulin therapy, they were very surprised: despite the weight gain the subjects seemed to be eating 300kcal less per day than they had prior to insulin treatment. As we learned in chapter 3, insulin causes the master controller of our weight – leptin, the hormone produced from our fat – to malfunction. This leads to leptin resistance and a high weight set-point. The metabolic effects of leptin resistance (in this case caused by high insulin levels) are the same as if leptin levels had been reduced by weight loss from an illness or a famine (or a diet): low metabolic rate. Despite the subjects eating less, their metabolism had slowed down, resulting in weight gain – a perfect example of how insulin drives the set-point upwards and the metabolism downwards. So, as well as acting directly on cells to encourage energy storage and weight gain, insulin also acts indirectly to promote weight gain – by causing leptin resistance.

  Insulin ➞ leptin resistance ➞ lower metabolism ➞ higher weight set-point

  What happens when we give a patient a drug to lower insulin levels? Will this have a beneficial effect on their weight? Robert Lustig’s research group from Tennessee looked at the effect of reducing insulin levels in obese volunteers.3 They were given a series of injections of octreotide that reduced insulin secretion from the pancreas. After the course of treatment the group had lost weight (on average 3.5kg or 7.7lb). In addition, their insulin sensitivity (how effective the insulin was) improved. The group reported that their appetite had been reduced by the treatment.

  Decreasing insulin level ➞ decreased
weight

  The Omega Foods That Influence Insulin Levels

  We saw in chapter 9 that certain factors influence whether insulin works well or poorly. One of these is the omega-3 to omega-6 ratio. If there is too much unfriendly omega-6 in the cell membrane (because of excessive vegetable oil and grains in the diet), then insulin won’t signal properly. You will need to produce more of it to get the same effect. Omega-6 also triggers inflammation and the production of TNF-alpha. We saw in chapter 5 that this also acts independently to reduce the effectiveness of insulin on the cell membrane (as well as causing leptin resistance). So, the fatty acids in the Western diets – the ones used in oils and shortenings, including the supposed heart-healthy vegetable oils – cause us to need more insulin and therefore our weight set-point rises. High omega-6 fats in the diet, and the TNF-alpha inflammation that they cause, act indirectly to make the cells less receptive to insulin (they cannot sense it as well) – meaning that more insulin is required.

  Western diet ➞ high omega-6 to omega-3 ratio ➞ insulin resistance ➞ more insulin ➞ higher weight set-point

  High omega-6 to omega-3 ratio ➞ inflammation ➞ insulin resistance ➞ higher weight set-point

  A Teaspoon of Sugar …

  Our brain needs sugar – it needs the glucose in our bloodstream to function.fn2 We need to maintain an optimum blood level of this precious brain fuel: too little and we will fall into a coma, too much and the glucose causes inflammatory havoc. But the actual amount of sugar carried in our blood is surprisingly small.

  Most people have 5 litres of blood pumping around their bodies. How much sugar does it contain? Imagine filling a bucket with 5 litres of water. How much sugar should we add to our bucket of water to make it the same sweetness as our blood? The answer may amaze you – we need to mix in just one teaspoonful of sugar to reach our optimal blood level of 80mg/dl. We have large reserves of sugar stored in our muscles and our liver, but only one teaspoonful is present in the whole 5 litres of our blood. Our glucose-transporting hormones, particularly insulin, are essential in maintaining this level of glucose in our blood to keep us alive and healthy.