Why We Eat (Too Much)

by Andrew Jenkinson

  The scientific battle over sugar and fat culminated in Dietary Goals for the United States, in 1977, the first ever government advice to a population on what to eat and what not to eat. As a result, a decrease in the amount of saturated fat, an increase in the amount of sugar and an explosion in the amount of vegetable oils consumed occurred from the 1980s onwards, leading to the sudden rise in the incidence of obesity in Western populations.

  Figure 8.6 The history of humans’ relationship with food

  This, then, is how we constructed our obesogenic environment. In the next chapters, we will see how this environment affects our health, and how best to create a new, safer food environment.

  NINE

  The Omega Code

  Is Obesity a Deficiency Disease?

  Ninety per cent of the diseases known to man are caused by cheap foodstuffs. You are what you eat.

  Victor Lindlahr, nutritionist and author of You are What You Eat

  One dark winter morning in London, just as I had reached the hospital, I was called urgently by my team to see a new patient on the ward whom they described as ‘sick’. ‘Sick’ tends to be informal medical jargon for ‘extremely unwell’, so I headed quickly through the clutter of equipment blocking the hospital corridors, dodging stray wires from scanners and swerving around breakfast trolleys.

  When I arrived at the bedside I was greeted by my team of efficient junior doctors, with their medical students in tow. A crowd had gathered around our new patient. I introduced myself to her and sat down on her bed, so she could tell me what the problem was. Sonia, our patient, did not look well at all. She was an Indian woman in her thirties. Her large body seemed to have been thrown on to the hospital bed from a height. One leg swung over the side of the bed, the other was bent; her arms were outstretched and the bed sheets were twisted around her as if she had been unable to make herself comfortable. She was not in a hospital gown and it looked as if the nurses had given up removing her normal attire halfway through the job. Sonia looked very tired. When I tried to talk to her, she was too weak to reply: only a whisper came out and I could not decipher it.

  I looked around the bed for clues. A wheelchair indicated that her condition had been better when she had arrived the previous night, but now it didn’t look as if she could even sit up in a chair at all. Her health was deteriorating rapidly. A ‘Get Well Soon’ balloon hung behind the bed, signalling that she had concerned relatives. Several vomit bowls were scattered around, none of them containing much apart from mouthfuls of saliva and bile. I checked her vital signs. No temperature, her pulse was steady and her blood pressure was OK, indicating that she probably had no infection or internal bleeding. Her breathing was normal and when I pressed on her abdomen it was not tender – there was no sign of bowel perforation or obstruction.

  Sonia weighed 130kg, the senior of my team informed me. She had undergone gastric bypass surgery one month before and everything had seemed OK when she was discharged from hospital. Her husband had informed the team that she had started to vomit within a week of surgery and this had continued for three weeks. She had started to become weaker over the preceding forty-eight hours. It was a mystery: all the routine blood tests we run on patients came back normal, apart from signs of dehydration. The juniors had given her lots of intravenous fluids since her admission and this should have improved her condition if it had been purely down to fluid loss. But she was still too weak to move or talk. She just stared into space.

  Sonia’s mood seemed abnormally low; she did not want to communicate and just stared at us. It was as if she had become severely depressed following surgery. One of the medical students thought that maybe she had become acutely catatonic – frozen with depression. There was a suggestion that we should call in the resident psychiatrist, as there weren’t any other clues as to why she was behaving in this way.

  I ordered some further blood tests and asked that the team prescribe an infusion of nutrients that we would normally give to alcoholics admitted after a prolonged binge.

  The next morning, I met the team again at Sonia’s bed. We had a diagnosis. She was also feeling better – slightly confused by all the fuss, but sitting in the chair by the bed, reading her magazine. She had developed a disease that has remained quiescent in the world for hundreds of years. Back then, it had affected poor rice-eaters in the tropics; then it lay dormant, waiting for the right conditions to return. It was so rare nowadays that it appeared in small print in the medical students’ handbooks: Sonia had beriberi.

  Thiamine (vitamin B1) deficiency can catch up with you quite fast. We only have eighteen days’ supply of this vitamin in our system. It tends to affect refugees, hunger-strikers and famine-sufferers. But now, with the advent of this new type of surgery to help people lose weight, it has had a minor resurgence. Remember, after bariatric surgery the hormonal urge to eat is taken away (as seen in chapter 6) and so if a patient vomits there is no instinctive urge to replenish the system. Once the deficiency takes hold, it causes numbness, paralysis and psychiatric symptoms – a scary combination. If left undiagnosed it can eventually lead to death. Fortunately, in Sonia’s case, the cocktail of vitamins we gave her included thiamine and it immediately reversed her condition. She made a quick and full recovery. Her husband and young sons were pleased to have her back.

  Lessons from History – Beriberi

  The resurrection of an ancient disease in our modern world, and our difficulty in dealing with it, interested me. Beriberi had not been recognized as a deficiency for many centuries – over that time millions of people lost their lives to the condition. Before the real cause of beriberi was known, the treatments given were ineffective. It was not until thiamine was isolated as an essential vitamin that it was conquered.

  At each point in the history of beriberi, many years before the true cause was discovered, doctors would be convinced that their current treatment was the correct one, even when it was clearly ineffective. I wondered whether, in the future, we might look back on our current understanding of obesity and see a similar pattern to the misunderstanding and mistreatment of beriberi sufferers before vitamin B1 was discovered. Certainly, our current advice and treatment does not seem to be working to affect the obesity crisis, but doctors are still convinced that the current treatments are the correct ones.

  Like obesity, beriberi did not make an appearance as a rampant disease until food started to be processed.1 And then it only affected those populations that consumed polished rice, rice that had the outer husk (and inner germ) removed to make it easier to store and transport. Poorer villagers in South East Asia who did not have access to rice mills were protected against the disease. They consumed wild rice prepared in the traditional way by pounding it within a bowl and then sieving the fractured husk away. This rice was perfect if consumed within twenty-four hours, but it could not be stored or transported. The oil in the remaining germ of the rice would rapidly become rancid and attract mould and insect infestation. It was therefore of no use for trading, and of no use to supply large numbers of people in remote locations, such as armies on the move. Polished rice could be stored for many months and could therefore be shipped and traded. In addition to its storage advantage over wild rice, polished rice had one other desirable quality – it tasted better. But, unbeknown to those consuming the polished rice, the husk and germ layers that had been removed contained an element essential to their health – vitamin B1. If polished rice made up the bulk of their dietary intake, which was the case for many populations, then they would be vulnerable to developing beriberi.

  Beriberi was first described in ancient Chinese manuscripts dating back to 2000 BC. The name originates from a Sinhalese translation of ‘weak-weak’. Roman legionaries noted that when an outbreak occurred, it could kill 30 per cent of an army and represented a greater danger than any enemy. It seemed to affect groups of people living closely together, particularly soldiers, sailors and prisoners. Early observers of the condition noted that it struck the rice-e
ating towns and cities in the south of China, but seemed to spare the wheat-eating peoples who inhabited the north. A dietary deficiency was therefore suspected.

  However, this information was not available to British colonial doctors and scientists who were sent to analyse the condition that was killing large numbers of the King’s subjects in the Far East. They concluded, at various stages in history, that the condition could be due to:

  A miasma, or foul-smelling cloud of gas

  An infectious agent

  An anti-toxin contained within rice.

  Misunderstanding and Confusion

  The colonial scientists and researchers initially thought that beriberi was caused by a miasma, a cloud of foul-smelling air emanating from unsanitary conditions and rotting food. Even our beloved Florence Nightingale espoused this theory and was responsible for improving the air quality in the military hospitals that she ran. The side effect of cleaning up the hospitals, so that they smelled better, was that communicable diseases were better controlled and fewer people died – reinforcing the belief in miasma as a cause of many diseases.

  Outbreaks of the disease affected isolated towns and villages and therefore some scientists concluded that it might be caused by an infectious agent, or a toxin. Others noted that it affected rice-eating areas only and so thought it might be caused by some sort of anti-vitamin contained in the rice. As with many conditions prevalent at this time, poor scientific communication between countries and cultures led to incorrect theories being propagated for many years by the doctors.

  Even within countries there was a lack of consensus and understanding which cost many people’s lives. In 1895, Kanehiro Takaki, a doctor commissioned in the Japanese navy, thought that protein deficiency was the cause of beriberi. He introduced extra protein rations (which happened to contain enough vitamin B1) to all sailors on long voyages and observed the complete eradication of the condition. Unfortunately, his medical counterparts in the Japanese army did not believe his theory and continued to think that beriberi outbreaks were due to an infectious disease. They continued with the same rations of plentiful polished white rice, and not much else, and tightened up on sanitation. The result? Ten years after beriberi had been completely eradicated in the Japanese navy, 80,000 of their army developed the condition, 8,000 of them losing their lives to it in the 1904–5 war with Russia.2

  In hindsight, there was ample evidence that beriberi was caused by some sort of a nutritional deficiency. The problem was that no scientist ever had all the evidence together in one place at the same time: it was historical, disparate and scattered. The breakthrough as to the real cause, when it did finally come, was down to our old scientific friend and companion – luck.

  The Breakthrough

  In the 1890s Dutch scientists in the East Indies (now Indonesia) had been given the task of finding an infectious cause for beriberi. They took blood from caged hens that had developed it and injected the serum into unaffected caged hens. The hens that had been injected with the serum promptly developed symptoms of the condition – confirming their theory that beriberi was due to an infection. However, the scientists, being sensible, wanted to double-check their findings. They repeated the experiment, but this time the hens which had been injected with ‘infected’ beriberi blood remained healthy. Now they were confused. Why would the same experiment yield two opposing outcomes? They scratched their heads to analyse if there was any difference between the two experiments. The only disparity they could find was that the warden who looked after the hen coops had changed. When they questioned him, they found that the old warden had fed his chickens with polished rice whereas the new keeper fed them wild rice! They had finally proved that beriberi was caused by something lacking in polished rice. Within a few years, research teams had isolated vitamin B1 in the husk of the wild rice and purified it for treatment. Beriberi, after causing millions of deaths, had finally been understood and cured.

  Scurvy, Another Deficiency Disease

  Let’s look at another example of a disease caused by a deficiency – one that was also misunderstood for centuries and caused suffering and countless deaths. This condition was thought to be due to:

  Poor morals and filth

  Homesickness

  Too little exercise

  A miasma of foul-smelling putrid air (again).

  This condition could cause personality changes, extreme tiredness and cravings for foods (not unlike the symptoms experienced by dieters). Swollen and rotting gums and skin rashes would develop and wounds wouldn’t heal. Eventually victims would succumb to blindness, psychosis and internal bleeding, with terrifying bouts of vomiting and the passing of foul-smelling blood.

  Scurvy, caused by a lack of vitamin C, was a well-known condition even before the era of long-distance seafaring.3 ‘Land scurvy’ was a common affliction of the Crusaders on their treks through the deserts of the Middle East. Napoleon’s armies were similarly affected on their long campaigns, and it was noted by Napoleon’s own physician that eating horse meat seemed to protect his men from the condition. The meat was fresh and contained adequate amounts of vitamin C to prevent scurvy developing. The Napoleonic soldiers developed a taste for healthy horse meat and continued to eat it even after they left the army, starting a French tradition that has been passed through the generations and continues to this day.

  The British navy had noted that scurvy killed more sailors than any enemy could. Of the 184,000 British sailors to have taken part in the Seven Years War against France and Spain in 1756, over 133,000 were reported missing or died from disease, and by far the most common disease was scurvy. William Clowes, naval surgeon, wrote that ‘their gums were rotten even to the very roots of their teeth, and their cheeks hard and swollen … they were full of aches and pains, with many blemishes and reddish stains or spots’.

  The Cure – Elixir of Vitriol?

  The cause of scurvy – a lack of fresh fruit and vegetables (containing vitamin C) – had been known to seafarers for centuries, but the medical establishment had never accepted this. Instead, they treated the condition with fizzy drinks designed to activate the digestive system. These drinks consisted of an ‘elixir of vitriol’ – sulphuric acid mixed with barley water, with spices added to disguise the foul taste. Stores of these drinks were aboard every ship in the British navy for countless years, despite having no effect as a cure for scurvy.

  The real cure had been found and then lost many times over the centuries. All sailors knew instinctively that consuming fresh fruit and vegetables protected against the condition. In the sixteenth century the Portuguese had planted orange and lemon groves next to their ports so that sick sailors could quickly regain their health.

  James Lind, a young Scottish naval surgeon, had gained experience of scurvy at first hand whilst on voyages to the Caribbean. His observations gave him a wider perspective and understanding of the condition than many in the medical establishment. He also had a healthy disregard for authority and a disdain for the corruption of medical knowledge. Convinced of the true cause of scurvy, he was frustrated that this was not being understood by the self-proclaimed experts.

  James Lind’s Trials

  In 1747, Lind conducted the first ever controlled clinical trials to assess the treatment of scurvy. Twelve sailors who had developed symptoms of scurvy were split randomly into pairs and each pair was given a different treatment. The treatments on offer were:

  Elixir of vitriol (the standard treatment of the time)

  A quart of cider a day

  Vinegar – two spoonfuls, three times a day

  A paste of garlic, horseradish, balsam and mustard seeds

  Sea water! – half a pint a day

  Two oranges and one lemon a day.

  Within days the two sailors receiving the citrus fruits had recovered and were able to return to their duties. In 1753, Lind published his Treatise of the Scurvy outlining his experiment.4 In the same publication, he wrote on the state of medical knowledge, ‘theories
were invented … according to the whim of each author, and the philosophy then in fashion … The learned ignorance of the age lay concealed under a veil of unmeaning, unintelligible jargon.’ He was proved correct … it took another forty years before his theories were put into practice by the Admiralty.

  The British Navy, although slow to implement Lind’s theories, remained ahead of all their rivals in other countries and gained a significant military advantage. In fact, the 1804 blockade of Napoleonic ships within French ports, an exercise requiring sailors to stay for months on board their ships, would not have been possible without the Royal Navy’s purchase of 50,000 gallons of lemon juice for its sailors. The blockade prevented Napoleon’s grand plan of a sea invasion of Britain and changed the course of history.

  In 1867 all naval vessels were ordered by Parliament to carry a supply of limes and lime juice. The association of British sailors with limes spawned the nickname ‘limeys’ – still in use today to describe British expats living abroad – and is a reminder of a long-forgotten disease.

  Could a Dietary Deficiency Lead to Obesity?

  To return to the modern day, could a dietary deficiency be a signal to our body to move our weight set-point upwards? Could a nutritional defect in our Western diet be misinterpreted by our bodies as a sign of an impending famine or a long hard winter – the signal to gain some extra fat as insurance? If this is the case, if obesity could have been triggered by a deficiency in some people, it would make it similar to the historical diseases beriberi and scurvy – those deficiency diseases that were misunderstood by doctors and scientists for so long.