One pioneering Irish doctor called Dennis Burkitt had a major influence on our modern relationship with fibre. Burkitt was a legend, and probably the last of his breed of zealous explorer-scientists that the British Empire produced.
After his training in medicine and surgery he was sent during the Second World War to East Africa. Later, in his forties, he answered ‘God’s call’ to go and work as a missionary and doctor in central Africa. There he spent several years, and covered ten thousand miles travelling around the country visiting small hospitals and health centres performing operations and preaching.
To pass the time as he travelled, he drew maps on which he plotted the prevalent diseases. For instance, he discovered a lymphoma which affected children that only occurred in the malaria belt, and righty predicted that it was due to an infection, a virus, which could be treated. He also plotted the dietary and bowel habits of the natives, and in the 1970s came up with another theory.
I remember vividly a lecture he gave while I was a student at the London School of Hygiene, where he showed his travel snaps. These were mainly pictures of impressively large African turds taken in exotic locations. The Kalahari bushmen regularly produced specimens that weighed a massive two pounds on average, compared to the average ‘civilised’ European offering of 4 ounces. And on his maps he had linked the quantity of poo produced with the amount of fibre in the diet and the absence of Western diseases.
His notion was that the main benefit of fibre was as a bulking agent and stool softener that would speed up transit though your bowels so toxins couldn’t get back into your body and cause cancer. As a bonus, fibre also mopped up the fats that cause heart disease, and prevented haemorrhoids and varicose veins. His observations were astute and ahead of his time. He also criticised the modern trends of refining carbohydrates, denuding them of their high-fibre covering, and the eating of white flour.
He was convinced that the modern toilet position for defecating was bad for us and that a lack of fibre caused colon cancer. Subsequent studies failed to support this colon-cancer theory, and the latest studies have shown that, surprisingly, even constipation, which certainly causes other problems, is not a cancer risk factor, although high-fibre laxatives may be protective.1 Nevertheless, thanks to Burkitt’s missionary zeal, fibre had become trendy and part of our vocabulary.
‘Dietary fibre’ is the general term for the bits of food that can’t be digested. It used to be thought of as completely inert, with no real effect or interaction with the body except for its mechanical properties. But fibre comes in different forms and can be soluble like oats, beans and fruits, which are fermented in the colon, or insoluble like whole wheat, nuts, seeds, bran, fruit skins and many legumes and other vegetables such as green beans. However, even the insoluble type is not totally inert and can be fermented by bacteria to produce gases and other by-products. In general, fibre absorbs water and speeds up transit through our intestines. While most people accept that it is good for us, there is a lack of consensus about why. Prebiotics could be one reason.
Promoting the benefits of fibre in the diet was big business well before Burkitt’s work, and has an origin dating back to the time of the ancient Greeks.
All fibre is a form of carbohydrate, and so in theory provides four calories per gram in energy. But most is not absorbed, and food labels can be deceptive and confusing. In the 1980s at the height of the low-fat movement, the US population in particular were urged to eat lots of oat bran. Fibre has since 1993 been allowed as a health claim on US food labels, depending on how much fat is also in the food. These health claims haven’t helped change habits much: most Americans (and Britons) eat less than most other countries, consuming only half of the current recommendations (18 to 25 grams per day), and kids eat even less.
At the time the Food and Drug Administration approved a health claim for fibre, the observational data was in fact pretty shaky. A recent meta-analysis of these twenty-two reports on heart disease found quite big differences between studies (which is always a worrying indication of their quality). Nevertheless, it concluded that fibre was overall beneficial. The estimates were that you could reduce the risk of heart disease by 10 per cent for every extra 7 grams of fibre consumed.2 Nearly the same protective effects were found in reducing overall mortality, in seven studies of nearly a million people.3
In most studies whole-grain fibres were considered to be a major health factor, although benefits were primarily seen for other plant and vegetable sources. The data is weakest for fruit fibre. To increase your daily dietary fibre by 7 grams is not that onerous, requiring one extra portion (100 grams) of whole grains, one portion of legumes (beans or lentils), or one to two portions of green vegetables or four pieces of whole fruit (but only if you eat the skin).
As just noted, oat bran for breakfast was a big marketing sensation in the US in the 1980s and 90s, after early studies showed it reduced cholesterol levels dramatically. It was also promoted as miraculously reducing blood pressure and diabetes risk. The marketing gurus lost no time, and the New York Times reported in 1988 a frenzy over oat-bran muffins, as stores ran out and it became ‘the croissant of the 80s’. Conflicting studies followed which cast some doubt on the amazing health benefits claimed, until a more recent meta-analysis of sixty-six oat studies clarified the evidence. This showed no effect on diabetes or blood pressure but confirmed a consistent beneficial effect on blood cholesterol.4
Unfortunately, the benefit of oat bran turned out to be tiny, with only a modest 2 to 4 per cent reduction in cholesterol unless you had very high levels to start with. To achieve this meagre reduction you had to eat an enormous Daddy Bear-size bowlful (three packets) a day. The muffins were worse. Packed with extra calories and a high fat content, any modest health benefit of the bran was overwhelmed. Nevertheless, the scientists of the 1990s were confused about why bran would have such an effect at all. Thirty years later, microbes provide the answer.
Prebiotics and microbe fertilisers
Prebiotics are components of food that are closely involved with our healthy microbes. While not all fibre is prebiotic, all prebiotics are by definition non-digestible fibres. It is not surprising that when you measure levels of prebiotics (like the common prebiotic substance inulin), they mirror the fibre content of our diets. Data from my King’s College colleague Kevin Whelan shows a good correlation between inulin and fibre in the UK, indicating the two are closely linked. This connects the new science of prebiotics with the old-fashioned concept of fibre.
One important way in which our food and microbes interact is via prebiotics. Whereas probiotics are selected microbes that benefit the health of the host, prebiotics are the constituent parts of foods that act as fertilisers for the microbes in the colon. These largely non-digested fibres allow beneficial microbes to thrive, and they come in several forms. The first prebiotic we encounter in life comes handily packaged in breast milk and is called an oligosaccharide, which is a complex group of tightly bound sugars.5
Many prebiotics are referred to as resistant starches, as opposed to highly refined (that is, broken down) starches like rice or pasta that are easy to digest and release glucose. It has been crudely estimated that a healthy person needs about 6 grams of prebiotics a day to keep both their microbes and themselves healthy.
Several types of prebiotics are well established scientifically, and there are many others that have potential effects but lack real proof; and all forms are of course marketed equally on the internet. The well-known ones include the major player just mentioned, inulin (not to be confused with insulin), as well as oligofructose and galacto-oligosaccharide. You will come across them more and more, as they are being increasingly used by the food industry as additives; when combined with probiotics they are called synbiotics.
These prebiotic compounds come from natural ingredients such as chicory root, Jerusalem artichoke, dandelion greens, leeks, onions, garlic, asparagus, wheat bran, wheat flour, broccoli and bananas and some nuts.6 The percentages of the prebiotic inulin in each one vary enormously, from about 65 per cent in chicory root to only 1 per cent in a banana. Most increase their active amounts if dried, but lose half if cooked, so you’ll need to eat more if you don’t like your food al dente.
To achieve your prebiotic quota (6 grams) would mean eating each day half a kilo of bananas (ten), or alternatively only a teaspoon of diced chicory root or Jerusalem artichoke. Grains and bread too, surprisingly, contain about 1 per cent of inulins – rye bread slightly more than others – and even ‘plastic’ sliced white bread contains reasonable amounts.7 The decline in the consumption of fibrous vegetables has made bread the estimated main source of prebiotics and fibre in both the US8 (2.6 grams daily) and the UK (4 grams). Non Anglo-Saxon Europeans, particularly those on Mediterranean diets, have fibre intakes around three times higher.9
Garlic breath cures the common cold
Garlic, as well as being an excellent source of polyphenols and vitamins, is a first-class prebiotic that used to be a major discriminator between the cuisines and habits of northern and southern Europe, and has been used for millennia in Asia. Before the 1980s it was uncommon in the UK, and I remember in the early 1970s as a kid the novel sight of a Frenchman with an ostentatious moustache and dressed in a striped blue jersey and black beret cycling around the London suburbs festooned with strings of exotic and suitably expensive garlic and shallots. I also remember on school trips the overpowering smell of garlic breath on the early-morning Paris Metro – though I probably wouldn’t notice it as much now because the cosmopolitan experience of the London Underground is not so different.
In 1976 Marks & Spencer nervously produced the UK’s first ready-meal and, controversially, it had garlic in it. Going by the exotic name of Chicken Kiev, it is now, not surprisingly, a dish whose origins are still being hotly disputed between Moscow and Kiev. It was a massive hit, and Brits have been steadily getting used to the taste ever since. McCain the potato company have even launched roasted garlic wedges as a snack, which would have been unthinkable in the UK just a few years ago.
Sometimes I come across southern Europeans who can’t stand garlic, which I find very strange, as I’ve always assumed all southern babies are fed it from birth and so get rapidly used to the strong taste. We conducted a study in over 3,000 of our twins to confirm if garlic eating in the UK population was mainly due to cultural exposure. Contrary to our expectations, the results showed a strong genetic component (49 per cent) in whether people ate garlic or not, with only a negligible influence coming from the family environment.10 This suggests that genes for taste receptors, particularly bitter flavours, are important, at least in the UK. These genes may be rarer in the southern Mediterranean where fewer people dislike garlic.
Garlic on its own has been hyped as having many health-giving properties, such as preventing and curing colds, cancer and arthritis. Although I have published some of these studies myself on arthritis, the results, though intriguing, have yet to be convincingly proven and could just be markers of a healthy diet or lifestyle.11 Garlic has a strong tradition in Mediterranean countries as a cold remedy. I once tried a Tuscan remedy for cold prevention. At the first symptoms you take three cloves of raw garlic and a full bottle of Chianti. The results were amazing. The next day I woke with garlic breath, a bad hangover and the predictable cold symptoms. I later was told that I should have taken it before getting the cold.
A recent independent Cochrane Review looked at the eight trials of garlic and colds. Sadly, they found only one worth assessing. The UK investigator randomised 146 people to Allium sativum (garlic) and the other group to a placebo. After twelve weeks, the garlic eaters had experienced three times fewer days of symptoms than the dummy group.12 The downside is that the dose was equivalent to over eight cloves of garlic a day, which could be a problem for some people. However, I can share this tip – that garlic breath can apparently be relieved more quickly by ingesting a mixture of parsley and yoghurt, which together provide an excellent microbial air freshener.
Garlic’s effect on lowering cholesterol and improving lipid profiles does seem more likely to be real, based on multiple replications of the results and a meta-analysis of several randomised studies.13 The benefits of garlic may, though, depend on what else you are eating, as well as which microbes are already in your colon.
Spring-cleaning your guts
I recently discovered the practical problems of eating natural prebiotics after ‘volunteering’ to have a colonoscopy at my own hospital. This has not yet become a widespread British hobby or bucket-list item, and I was doing it for several reasons. I had never had one, and my US colleagues, who seem to have them as often as they have haircuts, thought it very backward of me. Many countries now advise colonoscopy as a routine screening test for colon cancer for anyone over the age of fifty. Colon cancer is one of the most preventable cancers in men. I also try to practise what I preach. I am planning a colonoscopy study of twins, and I generally try out any invasive tests before asking our twin volunteers to do the same. At the same time I wanted to test my microbes, to see how they would react to being cleaned out, for them the equivalent of a giant tsunami invasion.
The days just before the test, when I had to cut down on fibre, were fine. Some people don’t eat enough to notice, but I held off the fruit and vegetables and whole grains. The fasting was fairly easy as I could still drink fluids. I was warned to carefully plan the next few hours after taking the sachet of strong laxatives. I shouldn’t be at work, definitely not on a crowded train, and if possible I should stay within ten yards of the toilet. I thought that was a bit excessive.
It took a while to work but, to spare you the details, I can say I was glad that for once I had heeded the advice. Twenty trips and a loo roll later I was finally cleansed and empty and ready. The actual procedure was for me painless and interesting, probably because I had one of the best endoscopists in London, Jeremy Sanderson, at the business end. He gave me a tiny dose of ‘happy juice’ as he called it, which is basically a short-acting Valium-type drug, and off we went.
I watched it all in colour on the large TV screen at the side of the bed as he worked his way around my slimy, gleaming intestines, taking eighteen tiny biopsies for our studies. I wanted to go back to work but was told to take the day off and relax, as the happy juice might have made me do odd things. In this laid-back state I started thinking about my billions of poor hard-working microbes that I had earlier flushed down the toilet.
It may have been the drug, but I became quite emotional. I felt sorry for those faithful microbes that I had being trying to carefully cultivate for the last year. I knew from studies of antibiotic-treated patients and others who’d had colonoscopies that over 99 per cent are wiped out. Gritty survivors hang on in unusual places, and if, like me, you still have one, they can hide in the haven of the appendix – could this be its long-lost purpose, perhaps? They can also collect in the caecum, a corner of the colon that always contains some fluid, a smelly oasis in the desert. Microbes can lie low, too, in the tiny crevices of the intestinal wall, clinging on by forming biofilms with each other – although no one quite knows how they resist so well the tidal waves rushing through the bowel.
The three-day prebiotic diet
There are only a few reports following colonoscopy in humans, and the largest comprised fifteen patients. After a month, most recovered their previous microbial flora. However, three of them developed major changes for unknown reasons.14 Anecdotally, when I ask my Gastro colleagues they say that every now and again some patients with mild colitis or IBS do report a miraculous cure after the clear-out. This is likely to be due to major changes in their gut microbes. Anyway, I wanted to give the survivors in my bowel a reward for their persistence and decided to go on an intensive three-day prebiotic diet.
First, I needed supplies. No one had any Jerusalem artichokes as they were out of season, so I had to substitute globe artichokes. Despite the similar name, Jerusalem artichokes are sunflower roots that look like potatoes and are called ‘sunchokes’ in the US. They are affectionately known as ‘fartichokes’ by the Brits, some of whom appear to suffer special – possibly genetic – side effects. I found chicory (a.k.a. endive, the unopened bitter leaves popular in northern France and Belgium), but not the high-inulin-content chicory root itself, which would have been ideal. Dandelion leaves were never going to be easy as I don’t live on a farm, and dandelion wine didn’t count.
The rest was not a problem – garlic, onions, leeks, asparagus, broccoli, etc. I also added flax seeds (linseed), pistachios and a variety of other nuts. I made a giant salad, finely chopping the ingredients and adding a few bits of lettuce and tomato and parsley for seasoning, plus of course extra virgin olive oil and balsamic dressing and some whole-grain rye bread. It tasted good to me, though having this raw food three times a day produced a few side effects like a bit of wind at both ends, and no one wanted to kiss me. Just after the purging and colonoscopy I had felt great, which is a common report after many purges or fasts, and something that we don’t fully understand.
But was this effort worth it for my microbes?
The British Gut Project lab had tested the results and found that the microbes just after the wash-out, although diminished, were pretty much the same mix of species as before the laxative maelstrom. However, one week after my rebirthing diet, thanks possibly to the prebiotics and the impressive survival and reproductive skills of my microbes, I had more bifidos and a richer variety overall than I had before, including some new species that had grown enough to be counted. The prebiotics had apparently done some theoretical good, in me at least, but a study of one is far from proof.
Do prebiotics really work, in properly conducted trials, versus a placebo? Most scientific prebiotic studies use doses of the actual chemicals rather than chopping up and eating the foods that contain them, as they are easier to measure and quantify. Between 5 and 20 grams of inulin per day is most commonly used in trials, and some trials use oligosaccharides while others use a combination. To qualify as a proper prebiotic, there has to be as a minimum standard a significant increase in bifidobacteria. There are many prebiotics that haven’t been formally tested in humans, though this doesn’t stop them being marketed and sold.
A recent meta-analysis summarised the results of twenty-six trials exploring prebiotics’ effect on weight, which involved a total of 831 people. The overall quality of the trials was poor. As well as being small-scale, they were also of short duration, lasting a few days to a maximum of three months.15 While most studies showed an increase in beneficial microbes, the effects on weight loss were not obvious or consistent. Only five studies actually tested obese volunteers.16 Despite these problems, there was a remarkably consistent 40 per cent increase in self-reported feelings of fullness after meals, as well as a reduction in blood insulin and glucose levels.
The likely explanation behind these consistent findings is that prebiotics provide the fertiliser to increase the numbers of our healthy microbes (like bifidos) and to effect subtle changes in other mysterious microbes that we haven’t yet quantified. These microbes then produce short-chain fatty acids that have a range of important effects on the body.17 The most important of these is butyrate, which plays a part in releasing hormones in the gut to help suppress hunger and reduce the rise of glucose and insulin that otherwise put fat into storage mode. It is unlikely to be a coincidence that butyrate is also most successful in toning down the immune response and creating a state of calm tolerance.
If eating lots of prebiotics isn’t your thing, you can skip the vegetables; and you can easily buy synthetic butyrate supplements in the US and online, with full FDA blessing. But this comes with several caveats. First, it won’t have been properly tested in humans;18 second, it wrongly assumes that butyrate on its own has the same effect as when surrounded by all the other natural chemicals; and finally, you should know that the natural butyrate substance is what you smell when butter goes rancid and what gives human vomit its distinctive aroma. Greenpeace have even used it as a stink bomb to throw at whalers.
Deadly grains and Franken-wheat
We have talked about the key role of whole grains in the context of Mediterranean-style diets, and as a source of prebiotics as well as of fibre. There is a growing movement that, by contrast, believes that whole grains are inherently unhealthy. Others go further, asserting that all grains are poisoning us and are to blame for obesity and all Western illness. Responsibility for this phenomenon lies largely with some bestselling books that have appeared in the US such as that by Dr William Davis, a US cardiologist whose website proclaims: ‘Wheat Belly was the original book that turned the nutritional world topsy-turvy and exposed healthy whole grains as the genetically altered Frankenwheat imposed on the public by agricultural geneticists and agribusiness.’19 According to this doctrine, we are all to some extent intolerant of, or allergic to, this innovation of ten thousand years ago, and we have never been able to adapt. We should give up all foodstuffs containing grains, or risk the dire consequences.
Now it is certainly true that some people are intolerant of a protein component of wheat and of most other grains known as gluten, which sticks the molecules together (gluten means ‘glue’ in Latin) and gives bread its elastic properties. It is this protein that causes the auto-immune condition coeliac disease, which triggers a shrinking of the finger-like projections (villi) of the intestines’ lining as well as serious digestive problems and malabsorption. Contrary to popular perception the disease is pretty rare, proven cases occurring only in 1 in 300 people, while the potential for getting it (along with blood antibodies) is only about 1 in 100.
In the UK and the USA, ten times more people think they have the disease than actually do, based on blood or gut changes; and, ironically, only about one in ten with the real disease gets properly diagnosed. The upsurge in interest in gluten has led to a big increase in fast-food chains and restaurants offering gluten-free products. This is a market worth $9 billion in sales in the US alone, and showing 20 per cent annual increases. It is big business, and the trend is spreading to Europe. Even small corner shops are stocking gluten-free cakes and breads now, while saying goodbye to soy and quorn.
In his book Davis claims as a justification of his diet plan that most coeliac sufferers lose weight when they go on a gluten-free (GF) diet. In fact, the opposite is true, and as a doctor I have only ever seen skinny coeliac sufferers who can’t absorb food properly. In the study that Davis quoted, more than three times as many patients gain weight than lose it on a GF diet (95 as against 25), even those already overweight.20
Anyway, despite the lack of scientific evidence, the diet, the book and the recipes hit a chord with the American public, already suspicious of the food companies, and they have been a great success, with book sales of over a billion dollars in the US. Some people undoubtedly lose weight, but in most this may have nothing to do with the gluten. As we have seen many times before with specific restrictive diet regimes, they are excluding many food groups and dramatically reducing snacking opportunities.
Cutting out wheat, barley and rye from your diet could be OK if you replaced them with other healthy vegetables, but this often doesn’t happen. For many people their diet becomes restricted to odd items like gluten-free cheese pizza and gluten-free beer. Consequently, they may lose out on valuable sources of B vitamins, fibre and prebiotics and see a big deterioration in the variety of their microbes.
Real coeliac sufferers are highly motivated to stick to the diet, as they become profoundly ill after ingesting even a small amount of gluten. But for most normal overweight people, without symptoms, to cut out all grains for life is obviously much harder. Small amounts of gluten are hard to avoid because they are routinely added to most processed foods and sauces to bind them and improve the texture. Avoiding processed foods may be the only real benefit of GF diets.
Saliva mutations and vegetable evolution
The concept of the benefits of grain-free diets derives from the assumption, already mentioned, that up until nine thousand years ago our ancestors had never eaten them. So we haven’t had the time to evolve the genes and the mechanisms to digest grains properly, causing a toxic allergic reaction that inflames our intestines and causes obesity and other problems. What is more, the high calorie count of all those grains we ingest can’t be a good thing. We have already discussed how human genes mutated around seven thousand years ago to enable many of us to drink raw milk, and just a few years ago a similar notion concerning the supposed toxicity of dairy foods was very popular.
So why are we thought by some not to be flexible enough to safely adapt to eating grains or other starches in the space of nine thousand years? There is now evidence that we can adapt. The enzyme amylase is the one to concentrate on here. As with many other mammals, amylase is in our saliva to break down carbohydrates and in the pancreas for releasing into the small intestine.
A group of American geneticists had the bright idea of looking into how many copies of the gene there were in different populations around the world following very different starch diets.
Starch is part of all plants, and is virtually the only carbohydrate in potatoes, pasta and rice, as well as being found in wheat and root vegetables. Starch can be relatively easy to break down, as in cooked potatoes, or difficult (resistant) as in raw vegetables. After mastering cooking all those millennia ago, we began to eat these tough root vegetables that previously, when raw, were either not worth the nutritional effort or potentially toxic. We then started to cultivate them in large quantities in different parts of the world.
The American researchers compared the genes of rainforest Africans and Arctic Siberians with those of grain-eating Europeans and Africans and rice-eating Japanese. Sure enough, they found large differences in the number of copies of the gene.21 Tribes on the traditional diet carried many fewer copies than those now on a starch diet. The more copies of the gene you had, the more amylase enzyme you produced and the better able you were to break the starch down.
We share over 99 per cent of our genes with monkeys. However, monkeys who mainly eat fruit and occasionally meat have no copies of the amylase gene. As with milk drinking, we in the West have adapted rapidly to our high-starch environment, probably because this gave us a major evolutionary advantage. The current theory is that having extra copies of the gene may have protected children from dying from diarrhoeal diseases as they could still get energy from starch.
With colleagues from Imperial College London we took this story further, using our twins. We worked out how many copies of the amylase gene each twin had and compared the numbers of copies with their body weight. This gave us a clear result – but not in the direction I had expected.
Those with the most gene copies and therefore the most amylase enzyme – meaning they could in theory digest the starch more easily – were the leanest; and those poorly adapted and with fewer copies (and poor digestion) were the fattest.22 I had expected that better digestion would signal that they were extracting more calories from carbs and so weight gain would be the result, not the reverse.
This was a puzzle I was determined to crack and I thought that microbes could give us the answer, as what happens to food early on in the digestion process dramatically alters the structure of the food that enters the colon, where the interactions with our microbes occur. As is often the case, studying twins could point us in the right direction.
Carbohydrate-eating gene differences
Linda and Frances are sixty-eight-year-old twins taking part in our research. They don’t often get mistaken for twins as Linda is 12 stone and Frances 8½ stone and being non-identical, like ordinary sisters, they only share half their genes. Linda was only 6 ounces heavier at birth but had always been the bigger of the two as long as they could remember. At the age of sixteen, seeing her sister attracting boyfriends, she went on the first of several diets – initially a semi-starvation diet that briefly got her close to her sister’s weight, but she soon slipped back. They lived together till their mid-twenties. They had similar tastes and always consumed the same foods and drinks and had the same portion sizes. Linda, despite doing more exercise and sport, just kept on gaining weight while Frances didn’t.
‘We always knew that we had different metabolisms,’ explained Frances. ‘I often felt guilty as it wasn’t fair for her and I could always eat what I liked.’ Linda commented: ‘I wasn’t bitter or angry but did keep trying to lose weight by dieting and exercise, as I could see that she was getting all the boyfriends.’
Over the years Linda has tried many diets. The most sustained was the Atkins Diet, for six months, which worked well until she got bored with the repetition and stopped. She also tried the cabbage soup diet, ‘which also worked for a few months but had other side effects, as you can imagine. I’ve realised that for me diets are pretty pointless so I’ve stopped controlling my food too much, but I still go to the gym and play golf and tennis and have an allotment to stay healthy and have fresh vegetables.’
As part of the amylase research project we had extracted their DNA from their blood, along with a thousand other pairs of twins. We then measured the numbers of copies of the gene they both had – which, incidentally, is still a very tricky procedure, and as each test is rather imprecise we did it six times, then averaged the results. In their case the results were clear-cut. Linda had only four copies of the amylase gene and Frances had nine. For each copy of the amylase gene you are short of, your risk of obesity increases by 19 per cent. So for Linda, despite much the same diet, her risk was approximately double that of her sister.
‘These results, now you have explained them to us, do make sense. I can see why my sister and I are different and do indeed have different metabolisms in how we react to food. It may be too late for us, but can we test our children?’
The results were so surprising that we spent a year checking them, and as with most diet stories ours made a big media splash. To put it into context, we had found a gene effect that was around ten times larger than anything found before, including the obesity gene, which was the first to be easily discovered (called FTO) but now looks much less important and is a useless predictor in individuals. The downside is that this gene effect is currently very difficult to measure accurately without incurring large costs.
A potato is not the same for all of us
The other major paradigm shift is that until now the vast majority of the genes discovered for obesity have been thought to act on the brain. This has led to the continued perception that it is just a question of greedy signals from the brain causing the weak-willed obese person to overeat. What we found is that metabolic effects (that is, those affecting energy) are ten times greater. Our signals of gene copies were very much harder to pick up, and there may be many more like the amylase gene for other food types that we’ll discover in the future. Although the field is likely to change again, the latest work shows us that in contrast to our earlier beliefs, obesity genes (like FTO) may work on fat cells and metabolism rather than purely on the brain.
We also looked at the microbial and metabolic patterns of those of our twins who had the highest and lowest copies of the amylase gene and found major differences in some of the Firmicutes family (clostridiales), which have been associated with obesity. We don’t have the full story yet, but so far it looks like the altered digestion of the starches in maladapted people triggers a change in microbial composition and the production of different fatty acids. This in turn could lead to more rapid increases in insulin on eating starch, which ultimately leads to predisposed people storing more fat. This indicates that some people eating exactly the same bowl of potatoes or pasta will have a greater amount deposited as fat because of the effect of their genes on their microbes. So a potato is not a potato to everyone – to some people that potato, energy-wise, is like a double portion.
Finding more of these gene copies could help us in the future to divide people into different groups of food eaters. People like Linda who find themselves in a high-grain-eating environment but lack the right genes may be better off reducing the high-carb starches and eating fats instead, which their bodies and microbes may be better designed for.
The good news for the rest of us is that we can adapt to new foods and environments faster than we think. As well as the extra gene copies to produce more starch-digesting enzymes in areas with high-starch diets, we also mutated our genes to be able to consume cow’s milk, and there are no doubt many other similar gene mutations we haven’t discovered yet. We also know that exposure to different diets can actually change our genes (epigenetically). The human body is much more flexible than we ever believed. We are not mass-produced like robots – we are much more plastic, with the ability to adapt to our surroundings. This has been the secret of our survival and success on the planet and has enabled us to exploit all the diverse diets and environments available. This works well for the population as a whole, but individuals like Linda may not be able to adapt their genes or their metabolism and may need to alter their diet or their microbes.
FODMAP diets and bloated bellies
Most people with irritable bowel symptom (IBS) have heard of the FODMAP diet (which means free of joined up bits of fructose called fructans). This cuts out many foods that contain short-chain carbohydrates which are poorly absorbed but includes grains and beans that may be responsible for gas and bloating. The diet can have dramatic effects on some sufferers. Most of these are beneficial, but the diet can increase symptoms that are hard to predict. The downside, long term, is that fibre intake is reduced as well as many good sources of polyphenols like onion and garlic being lost; and there may be adverse effects in many people on the health and diversity of their microbiome.23 Once symptoms have been alleviated the trick is to slowly reintroduce a few fibre-rich foods to see if they are tolerated. The wide variation in the microbes of sufferers can make this unpredictable too.
The health benefits of the Mediterranean diet I mentioned earlier are probably not just to do with olive oil, red wine, nuts and dairy. The range and fibre content of other foods used weekly is large. We have mentioned tomatoes, onions and garlic as part of the basic sauce that goes on top of most of the grains, which usually take the form of bread, rice or pasta. But let’s not forget the other legumes (including beans), chick peas and so on or the cruciferous vegetables that are commonly eaten. As well as containing polyphenols that have important effects on the microbiota, a lot more fibre needs to be consumed. We currently eat much less than we should and we cannot afford to permanently cut out these major and varied sources of fibre and nutrients on the back of the latest restrictive health craze.