Why We Eat (Too Much) Page 13

  Malabsorptive Procedures

  What about malabsorptive procedures? We know that if you remove half of someone’s bowel they will initially lose weight, but after a while they will automatically adapt to their shorter intestines by eating more. Their weight will eventually settle back at its set-point. The gastric bypass was initially thought to work by producing malabsorption, but we now know that this is transient – the smaller bowel adapts by becoming more efficient.

  Sleeve Gastrectomy and the Gastric Bypass

  There are currently two main types of bariatric surgery that really do work, and they work by permanently changing the weight set-point: the sleeve gastrectomy and the gastric bypass.

  Both these procedures dramatically change the appetite and satiety hormones that we discussed in chapter 4. Ghrelin, the appetite accelerator, decreases considerably. This is the hormone that tells you to start looking for food when you have missed a meal – and the longer you go without food the stronger the signal gets. Eventually it will drive you to get any food with high calories – and it will make that food taste extra nice.

  Peptide-YY (PYY) and GLP-1fn1 are the two hormones that control satiety, i.e. the appetite off-switch. These hormones are elevated to very high levels after both the sleeve and bypass procedures. The combination of high satiety and low appetite signals means that after this type of surgery a patient’s behaviour will not be controlled by food any more – even if they have developed the leptin resistance that was described in chapter 5.

  Figure 6.1 The gastric bypass and the gastric sleeve

  Bariatric surgery has become much safer over the last few years, as technology has advanced. I would now equate the risk of this type of surgery with having an operation to remove gallstones. Most patients will only stay in the hospital for one night and will be back to their day-to-day activities within a week of surgery.

  If you are overweight or in the early stages of obesity I would not recommend this type of surgery. The guidance and suggestions in this book should be enough to help you reset your lifestyle, and sustained weight loss and a better quality of life should follow. However, if you are suffering with full-blown obesity and have developed leptin resistance or Type 2 diabetes, then this type of surgery may help you. Even if you follow all the weight set-point management strategies in this book, your body’s leptin resistance may block you from achieving a significant reduction in your weight. For those people I find bariatric surgery is a life-changing procedure.

  It is sad that we have come to a point in our human history where we need to develop more and more ways to treat man-made diseases. Bariatric surgery is one of these treatments. The surgeons who are trained to carry out these procedures are few and far between and yet the obesity problem is overwhelming. We are like a small group of firefighters rushing around putting out forest fires. But unless we help stop the cause of these fires, our efforts will be mostly futile.

  My Typical Patient’s Story

  I would like to finish Part One of the book by focusing on what happens to a typical patient of mine. This story is an amalgamation of the hundreds of interviews that I have had with patients in my clinic over the last decade. Most of the stories are quite similar, so it is easy to summarize their struggles with obesity over the years, and then explain everything in terms of metabology.

  My typical patient is female (80 per cent of patients undergoing bariatric surgery are female). She is in her forties and describes several members of her family who are also suffering with obesity (as we learned, 75 per cent of someone’s size is predetermined by genetics). She has been obese or overweight since her schooldays and says that the school nurse was the first person to put her on a low-calorie diet. The diet worked transiently and she lost some weight; however, after a few weeks her metabolism caught up with, and adapted to, her low-calorie intake. Eventually, despite complying with the diet, she found that she was not losing any more weight as her metabolism matched her calorie intake. She felt tired and hungry and irritable and could not concentrate at school. After no more weight loss she decided to stop the diet as it was not working any more. It is at this point that she started putting the weight back on rapidly, as her low metabolism and voracious appetite helped her body regain its desired weight set-point.

  She was worried that when she regained her weight it did not settle again at its previous level; on the contrary, she ended up with an even greater weight than before the diet. Her subconscious brain had calculated that she now lived in an environment where food was not predictable and therefore there could be another famine (or diet) around the corner. It is for this reason that her weight set-point now shifted upwards.

  As the years went by, our typical patient tried all the different types of diet on offer (she mentions Slimming World, LighterLife, the South Beach diet, the red and green diet, the cabbage soup diet, Rosemary Conley … the list goes on). The diets are all different, but for our patient the result was usually the same: transient limited weight loss, followed by metabolic adaptation to the diet and a decision to stop it; then weight regain, and after each of the diets a new higher weight set-point.

  Eventually our patient reaches a level of obesity where her fat cells cause an inflammatory reaction in her body. The inflammation stimulates insulin resistance, leading to an increased insulin level, and the higher insulin then causes the dreaded leptin resistance. A combination of the evolving leptin resistance and the legacy of previous dieting on her appetite (increased) and satiety (decreased) hormones means that the struggle with her weight gets more difficult the bigger she gets and the more she tries to diet.

  Figure 6.2 After dieting, a new weight set-point is established

  This is a typical recurring story of initially successful diets, then weight regain, followed by yo-yo weight fluctuation through the years and, despite the constant conscious battle to diet, an inexorable rise in weight until serious end-stage obesity is reached. It is only at this point, after years of effort and sacrifice, after years of receiving the wrong advice from doctors and dieticians, after years of being misled by the food industry into the health benefits of bad foods, that my typical patient will tearfully admit to failure and blame herself for it. Finally, she will give up on her fight with obesity: many battles have been fought, but the war has been lost. The subconscious brain has won.

  We have seen that you can’t fight against your weight set-point by dieting – the only way to beat it is to understand it. We now know how the set-point works to keep your weight at a desired predetermined level, even if you are over-eating or under-eating. And we are now aware, from chapter 2, of the genetic and epigenetic factors involved in set-point calculation. But obesity, even in those people who are genetically primed for it, is not triggered until you are exposed to an obesogenic environment. In Part Two, we will learn how humans came to construct an environment so unsuited to them.

  Part Two

  * * *

  LESSONS IN OBESOGENICS

  How Our Environment Determines Our Weight

  SEVEN

  The Master Chef

  Why Cooking Matters

  When I get home in the evenings I often find my teenage daughters watching TV programmes like MasterChef, The Great British Bake Off and Ramsay’s Kitchen Nightmares. I don’t understand their fascination with watching cooking and baking programmes, especially, I joke, when I never see food like this coming out of our kitchen. But I’m in the minority. Why do most people, just like my daughters, show an interest in these programmes? Why, in supermarkets, do you see crowds forming around the demonstration of a new gadget to make courgettes into spaghetti or to cut a cucumber into spiral shapes? Why are we reassured by watching someone chopping vegetables and cooking a meal in front of us – whether it be at home or in a new trendy teppanyaki restaurant? Why is the media full of recipes, and restaurant reviews, and articles on the latest new ‘superfood’?

  Why are humans just crazy about all things food? Once you know the answer to this
question you will possess an important piece of the puzzle of obesity. I will demonstrate in this chapter why food selection, preparation and cooking define us as humans – and why, without fire and cooking, we could never have evolved into the intelligent beings we are today. This little-known secret explains where we came from and where we are heading in the future. It also explains the food-orientated, obesogenic world we have built around ourselves today.fn1 It’s all about getting enough energy to evolve, from the beginnings of life to the present day. Let me explain.

  The Replicants

  In order to understand who we are now, at this moment, we must take a journey back in time to the origins of life on Earth. Think of a dark, stormy, tropical sea 4 billion years ago, before there was any oxygen in the atmosphere. Simple carbon-based chains of chemicals drifting around this primordial sea found, by chance, a formula to make new copies of themselves. These long chains would attract other chemicals that were floating in the sea until a double chain had been formed. The double chain then separated into two single chains which then continued the process of duplication. These were the first ‘replicants’, the chain of chemicals consisting of a primitive form of DNA. These ancient replicant chains turned out to be quite successful. They were able to coordinate the construction of more and more complex structures around themselves, eventually becoming one-celled organisms (think bacteria). Within the protective wall of these cells lived the replicant DNA code – the master controller – always coaxing and guiding the cell to further its spread. The survival of the code of life was all that mattered. Richard Dawkins, in his book The Selfish Gene, eloquently describes these organisms, constructed around themselves by the DNA, as survival machines: expendable biological vessels whose function was simple – grow, survive, reproduce.1

  The Making of ATP Batteries

  Our one-celled ancestors had a slight problem, though: they didn’t have enough energy to grow bigger. They had developed fantastically efficient little micro-batteries – millions within each cell – that carried energy from food at the cell surface and dumped it into whichever part of the cell that needed to grow or move. These ‘machines’ (called ATP (adenosine triphosphate) in medical language) worked by charging up on food energy, then moving to discharge this energy within the cell, thus converting food energy into the type of energy currency that cells can understand and use. But the amount of energy the cells could produce was limited because they could not process oxygen, stunting their development into more complex organisms. Our one-celled ancestors were stuck in this evolutionary jam, remaining single celled for 2.5 to 3 billion years … Finally a solution came along – a development that would super-power our ancient cells and still, to this day, powers our metabolism.

  New Tenants

  A new type of bacterium was using oxygen to help it produce energy (oxygen started to appear in the atmosphere 3 billion years ago). This tiny bacterium had a unique internal corrugated membrane (basically a turbo engine) that enabled many more micro-batteries to charge at the same time. To our slow primitive one-celled ancestor these bacteria were like power stations – taking in and converting massive amounts of energy. How could they compete with them? Well, they didn’t – they worked with them.

  The new super-charging bacteria were either ingested (but not digested) by our one-celled relatives or the bacteria smuggled themselves inside our cells as parasites. Either way they survived and thrived inside our energy-deficient cell. It was a mutually beneficial relationship: our cell protected them and they produced lots of energy for us. They became endosymbionts, or a cell living inside the cell of another organism.

  These primordial super-charging bacteria did well out of this alliance. They are still part of us and of all animal cells today. Our bodies are powered by them. They have become a vital part of us, helping to convert complicated food energy into cellular energy (or heat). These cellular power stations are called mitochondria, originating from those primordial bacteria and assimilated within us.fn2

  With our energy-generating capacity super-powered by our helpful bacterial tenants, more and more complex organisms developed and evolved until the present day: we now have an estimated 10 million species on Earth. But for all the diversity between these life forms – fungi, plants, fish and animals – they all have one thing in common: their DNA originates from that single replicant template in the primordial sea. Ninety-nine per cent of all the species that ever lived on Earth became extinct, but those of us that are left are the modern dynamic survival machines – controlled by our DNA bosses, powered by mitochondrial endosymbionts and directed to survive, grow and reproduce.

  Since that first chemical replication of a simple protein in the primordial sea, there has never been a dropped generation. In those 4 billion years there is a 100 per cent success rate in terms of growing and surviving long enough for each generation to reproduce and pass the master DNA code on to their offspring. Generation after generation evolved and adapted to the changing landscapes and environments of the Earth. With our complex family tree we have accumulated 4 billion years of ancestral heritage, or baggage, in our genes, and this has moulded who we are now and how we survive.

  In the same way that an artist adds successive layers of paint to the canvas to finish their masterpiece, so we, as humans, contain deep layers of evolutionary history that cannot be changed: this work of art took 4 billion years to complete, with each evolutionary change adding a fresh layer, a new look.

  The Energy Budget

  Every living organism today is related to our common one-celled ancient ancestor, and that means every organism uses the same system of energy to survive and thrive. Bacteria, plants, algae, fungus and all animals from snakes to birds to humans – we all have those ATP batteries converting food energy into usable energy for cells. Even viruses use ATP batteries (but not their own – they borrow the ATP from whichever cell they have invaded).

  Our primordial energy rules provide every animal with a maximum amount of energy that it can use per day. This is called the energy budget. The bigger the animal, the larger the energy budget. But unfortunately, a budget is exactly what it means – a limit to resources. Evolution has to budget enough energy to keep all the organs happy in each species: enough of a balance to keep the animal (or survival machine) alive, the heart pumping, the lungs breathing, the muscles working, the stomach digesting. But one organ needs more power to run than the others. This shining beacon of energy extravagance is the organ that differentiates humanity from all other species – the brain. How could we, confined to a limited energy budget, afford to make our developmental leap with a big, energy-hungry brain? The answer to this evolutionary puzzle explains why we humans love certain types of food.

  Chimps Don’t Get Fat

  Fifteen million years ago our close cousins the chimpanzees developed from gibbons. Chimps are obviously still around today, so we know that they stay in the rainforest mostly and forage for fruits, nuts, insects and occasionally meat. As an aside, in many rainforests where chimpanzees live there is a total abundance of foods all year round. Chimps can gorge on this type of food for as long as they like, and yet, even with plentiful food, wild chimp populations never develop weight problems.

  About 1.9 million years ago some chimpanzees started behaving differently. They started walking on their hind legs for longer and longer periods of time. Because of their new upright stance their distance vision improved and they were eventually able to leave the rainforests on two feet and roam the savannahs, hunting and exploring and inhabiting new areas of the world. As time passed they grew in height and developed into extremely efficient runners with more stamina and endurance than other animals – until they were able to run exhausted prey down. This meant more success in hunting and therefore more meat and protein. This species was called Homo erectus.

  Then came the biggest shift of all, the shift from the smaller-brained Homo erectus to the large-brained humans that we are. This occurred about 150,000 years ago when
the first anatomically modern Homo sapiens evolved. The process of evolving a large brain in a new species is called cephalization (from the Greek word enkefalos for brain). It might be worth reminding ourselves that our large brain made us not only clever, but vicious – so when we did eventually branch off from our brother Homo erectus, we killed them, all of them, along with our slightly dimmer but stronger Neanderthal cousins (whom we still share a part of our DNA with).

  The Expensive-Tissue Hypothesis

  How could humans have afforded to develop a brain four times larger than our ancestors – an organ that used up so much energy? We could not break the energy rules embedded within us; we would have to start from scratch and go back 4 billion years. One of our other organs would have to be sacrificed in order to free up this energy within our confined budget.

  Evolutionary scientists had been debating this question for years with no agreement on how it could be done until a research paper entitled ‘The Expensive-Tissue Hypothesis’ by the anthropologists Dr P. Wheeler and Dr L. C. Aiello gave us an explanation.2 The paper began by calculating the energy budget of animals according to their size. The amount of energy that an animal can use up over time is called its metabolic rate. This is the same as the amount of power that it needs to function.fn3

  Think about power, and the amount of power different animals require in order to function. Imagine that food energy did not exist and animals needed to be plugged in, like electrical appliances, for them to work. In mammals the amount of energy or power needed to live is dependent on their weight. A dog will need much less power to function than a 65kg human – unless the dog happens to be a 65kg Irish Wolfhound, in which case it will have the same energy requirements as the human! It is all about the total number of mitochondria that each animal has in its cells – these are our biological engines and determine how much cellular energy our micro-batteries can produce per second.