‘The relationship between the mind and the body is more complex than has previously been presumed . . . the body too might be influencing the mind to a greater degree than has previously been recognized.’
Iris Hung & Aparna Labroo1
THE 81-YEAR-OLD woman was sick and dying. Dr Max Nieuwdorp was, he admits, ‘young and naïve’.2 But he was also determined to save the elderly patient’s life.
She had been admitted to Amsterdam’s Academic Medical Centre with complications following a urinary tract infection. After the antibiotics used to treat her infection had annihilated her colon’s natural microbial population, Clostridium difficile, a far less beneficial bacterium, took up residence in her guts. When Dr Nieuwdorp first met his patient she was unable to eat, running a high fever, had bedsores, an inflamed bowel and chronic diarrhoea. Repeated doses of the antibiotic vancomycin, the treatment of choice for C. difficile, had proved ineffective. As increasingly happens, the notorious pathogen – which kills 300 patients a day in the US alone – had developed a resistance to what is generally an effective treatment.3 With the most powerful weapon in their pharmaceutical armoury useless, there was little her physicians could do other than make their patient’s last few hours as comfortable as possible.
But Max, recently appointed to a residency in internal medicine at the hospital, refused to give up. The treatment he had in mind, however, was so unorthodox that his supervisor, Joep Bartelsman, first thought the young doctor had to be joking.
Before we describe what that treatment involved, let’s take a step back to review a relationship which has intrigued philosophers and scientists for centuries: the interactions between what are generally referred to as the mind and the body, but which we prefer to describe as the brain and the body.fn1
Despite the seemingly obvious link between a person’s psychological wellbeing and their physiological health, the medical community has generally shunned this holistic approach. Today, however, we are starting to see a resurgence of interest in the role this relationship plays in both health and weight gain. We can look to physiologists and neuroendocrinologists to provide insights into what is known as the brain–gut axis; to uncover the lines of communication that occur between these two organs in order to help us understand how each affects, and is affected by, the actions of the other. Many believe that advances here will shed light on the current obesity pandemic.
This brings us back to our young doctor and his proposed treatment for the dying 81-year-old.
‘I want,’ Max Nieuwdorp told a surprised Joep Bartelsman, ‘to administer a faecal transplant.’ In non-medical terms he was proposing to pump the stool of a healthy person – her son – into the lady’s guts!4
In fact this wasn’t a new idea; ancient Chinese healers had been known to employ a mixture they termed ‘yellow soup’, hot water mixed with faeces, to carry out a similar procedure. Even in more modern times faecal matter transplant had been employed with some success – Ben Eiseman and his Colorado-based team of surgeons used the technique to treat a select group of patients suffering from colitis. Most were cured within two weeks.5
Yet, it has been Drs Bartelsman and Nieuwdorp who have re-established this technique within academic circles, and pushing for its inclusion as a treatment in a broader, more accessible context. While recognising that a lot of people, including many doctors, would regard this as a bizarre and perhaps a disgusting treatment, Dr Bartelsman gave his approval – after all, there was nothing to lose. Both doctors knew that however distasteful it might seem, it was the old lady’s last and only chance of survival. Using a blender, the medics mixed her son’s stool with a saline solution and then infused the resultant liquid into their patient by means of an enema. That done, all they could do was cross their fingers and wait to see whether the highly unorthodox procedure would succeed.
It did. And beyond their best expectations. Three days later the lady walked unaided out of the hospital. Her life saved by something, which, under normal circumstances, would have been flushed away down the lavatory.
To understand what this has to do with obesity, we need to go back over half a century and review the pioneering work of Ben Eiseman, Chief of Surgery at Denver General Hospital.
In 1958 Eiseman published a report in the journal Surgery on four patients suffering from ‘pseudomembranous colitis’, a painful, highly debilitating and potentially fatal inflammation of the colon associated with C. difficile. After all other treatments had proved ineffective, Eiseman decided to try an approach which had actually first been carried out in fourth-century China. Using the method that Max Nieuwdorp would duplicate years later, he obtained faecal matter from donors, blended it with saline and transplanted it into his patients. All made rapid recoveries.6
Despite Eiseman’s success, it was not until the mid 1980s that Australian gastroenterologist, Professor Thomas Borody, of The Centre for Digestive Diseases in Sydney, Australia, brought the idea back into mainstream medicine. Polish-born Borody, who had immigrated to Australia with his parents as a child, was in a quandary about how best to treat a female patient with ulcerative colitis. This is a painful and distressing inflammation of the colon, resulting in abdominal pain, diarrhoea and weight loss. Some doctors believe it to be an autoimmune condition, that is, one in which the immune system, mistaking harmless bacteria as a threat, attacks the colon causing it to become inflamed. There is, at present, no known cure and all doctors can do is try to relieve the symptoms.
Having tried the recommended drugs, which included steroids, without success, Dr Borody was uncertain what to do next. Thumbing through the medical literature in search of guidance, he chanced upon Eiseman’s paper and decided to try it: ‘I looked at the method and I kind of made up the rest of it,’ he recalled. Once again, this unorthodox treatment produced an almost instant cure.
Although faecal transplants were clearly effective, most doctors at that time dismissed them as both repulsive and dangerous.7
‘I was initially ostracized,’ Thomas Borody recalled in 2011: ‘A professor of medicine named me on television as being a charlatan for doing faecal transplants and he had no idea of the science behind it . . . even now my colleagues would avoid talking about this or meeting me at conferences, although this is changing.’8
Despite the treatment’s acknowledged success, even some of the physicians who practise it admit to revulsion: ‘Part of me has not overcome that feeling of disgust with human waste. I think it’s universal,’ admits Alex Khoruts, Belarussian-born gastroenterologist and immunologist at the University of Minnesota. ‘We’re supposed to avoid the stuff . . . it’s essentially like the elephant in the room for the gastroenterologist. We talk about all the other parts of the digestive tract, but we’re so ignorant about this component . . . so our level of knowledge hardly exceeds that of a fifth-grader who just says, exactly as you said, “Eeewww.”’9
Even as late as 2006, when Max Nieuwdorp and Josep Bartelsman decided to treat another six C. difficile patients using the same procedure, their embarrassment at doing so was such that they waited until the other doctors had gone to lunch before carrying it out. Today, Nieuwdorp and Bartelsman have taken the lead in publishing articles and empirical reviews on the procedure. The success rate for faecal bacteriotherapy, to give the procedure its medical name, has been remarkable. Nine out of ten C. difficile patients are reported to be free from their infection after only one transplant. Faecal transplants have also been reported to lead to improvements in sufferers of Parkinson’s disease, multiple sclerosis, Crohn’s disease, ulcerative colitis, acne, Type II diabetes, muscular dystrophy and perhaps even obesity.10
So what is it that brings about such astonishing outcomes? How can there be any benefit in transplanting into one person the discarded waste of another?
To answer these questions we need to go deep inside the human body and examine the actions of the multitude of bacteria living inside our guts. It is on the health of this unseen and unsung army of microscopic helpers that our own health, sometimes our lives, depends.
In the late seventeenth century, a Dutchman named Antony van Leeuwenhoek acquired an interest in microscopy. Although he came from a relatively humble background, van Leeuwenhoek taught himself to grind lenses and build microscopes. During a long life (he died aged 91), van Leeuwenhoek constructed around 500 of these simple devices. While they were really no more than powerful magnifying glasses, they afforded a glimpse into a previously invisible and unexplored world.
Using one of his microscopes to examine plaque scraped from his teeth, van Leeuwenhoek discovered: ‘Little living animalcules, very prettily a-moving.’11
More than a century later, Ferdinand Cohn, a German botanist, named these ‘animalcules’ ‘bacteria’, from the Greek bakterion, meaning a ‘short rod’, since that is what some he observed under his microscope resembled. By 1853, Cohn had gone on to identify three types of these microorganisms: bacteria, with their short, rod-like structures, bacilli (longer rods) and spirilla (spiral forms).
Bacteria have existed on earth almost since the dawn of time. The oldest known fossils, almost 3.5 billion years old, are those of bacteria-like organisms. There are around 40 million bacterial cells in a teaspoon full of soil, and a million in half an egg-cup of fresh water. The 5×1030 (that’s 10 followed by thirty zeros, an almost inconceivably large number) bacteria on Earth form a biomass greater than that of all the plants and animals combined. Bacteria give yogurt its tang. They make sourdough bread sour and beer alcoholic. They break down dead organic matter and contribute to diseases, ranging from allergies and asthma to cancer and heart disease. Crucially, bacteria also produce molecules that kill other bacteria. It is in this ability of ‘good’ (i.e. health-giving) bacteria to kill and replace ‘bad’ bacteria in the human gut that the efficacy of faecal transplants lie. Seventy per cent of our immune activity takes place within the gut. Unfortunately, antibiotics cannot tell the difference between ‘good’ and ‘bad’ bacteria; when successful they just kill them all indiscriminately, leading to potentially serious consequences for health.
‘We are,’ says Thomas Borody ‘10 percent human, 90 percent poo.’12 Distasteful as this may seem, the point he is making is in regard to microorganisms; our body plays host to a vast and diverse community of microorganisms that live on us and in us. On our hands, feet, face, chest, abdomen, feet and genitals, in the mucosal linings of our mouth, in stomach and intestines. Known collectively as the ‘microbiome’, it is estimated to consist of more than 1,000 different species and over 7,000 different strains.13
The microbiome is becoming such an important priority in health research that the American National Institute of Health has recently spent over $173 million in order to describe and characterise the role of the human microbiome and microbiota.14
While microbiome refers to the total number of organisms and their genetic material, the term ‘microbiota’ is used to describe the population present in specific bodily systems, such as the intestines. Our intestinal microbiota, which weighs approximately a kilogram, or a little over 2 lb, contains some 100 trillion microorganisms at densities of around 1012 cells per millilitre. Ninety-nine per cent of these microorganisms are bacteria; between 500 and 1,000 bacterial species are estimated to reside within the colon, the final loop of intestine. What is sometimes referred to as our ‘gut flora’ also includes fungi, protozoa and archaea. The latter, single-celled prokaryotes (meaning they have no nucleus) are very similar to bacteria, for which they were once mistaken, but are now known to be a different type of organism. That said, little else has been established about their functions inside our bodies.
Once regarded as mere tenants, microscopic stowaways hitching a ride on their hosts, recent research has shown a far more intimate connection exists between us and these intestinal microorganisms.15 They help us digest fibrous materials and harvest calories; as much as 15% of the energy used by the average adult could not be obtained without their assistance. Around 95% of a body’s serotonin, a neurotransmitter linked, among other things, to mood and depression, is manufactured in the intestinal microbiota. They also protect their hosts from marauding and harmful bacteria. Laboratory animals that have been engineered to have a complete absence of intestinal microbiota have no functioning immune system. As a result, their white blood cells remain dormant, their intestines fail to develop correctly, their hearts are shrunken and they suffer other health difficulties. So many, so varied and so important are the activities of these bacteria that the intestinal microbiota can justifiably be described as our body’s forgotten organ.16
In return for their assistance, the microbes gain from us a warm, moist home that provides protection and nourishment. To get some idea of the extent of the presence of microorganisms in our gut, consider this: two thirds of faecal matter’s dry mass consists of microorganisms.
‘The human body can be viewed as an ecosystem,’ Elizabeth Costello of Stafford University School of Medicine asserts, ‘and human health can be construed as a product of ecosystem services delivered in part by the microbiota.’17
An unborn baby is the only truly ‘human’ human on earth. Up to the moment of birth, we are all 100 per cent human. From that point on, 90% of the cells in our body are microbes, as we have over 100 trillion microbes all over the body. We become, in a sense, 10% human and 90% microorganism. Our microbiome contains around 150 times more genes than our human genome. The microbe cells are much smaller than our own, meaning the microbiome only weighs in at around 200 grams, but its effect on our body and behaviour is profound.18
‘Think of it as a hulking instruction manual compared to a single page to-do list,’ suggests Moises Velasquez-Manoff, author of An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases.19
Except in rare cases where microbes invade the amniotic cavity, the foetus remains in a completely sterile environment and free from any of the microorganisms among which life outside the womb will be spent. The moment the membranes of the amniotic sac rupture and the mother’s waters break, all this changes abruptly and dramatically. Even as they travel down and out of the birth canal, vaginally delivered infants receive a strong input of vaginal and possibly urogenital and faecal microbiota.20
Apart from their route of entry into the world (a vaginal or Caesarean birth), a person’s microbiome will be influenced by such factors as whether they are breast or bottle fed;21 their diet, hygiene, social and sexual behaviours; genetics; interaction with other children, parents, pets, the home environment; and whether or not they receive antibiotics. In short by virtually anything and everything with which they come into contact.
Within a few years, a bustling community of between 500 and 1,000 species will have been formed, with some having been passed down from one generation to the next – like family heirlooms. By their first birthday, an infant will be the possessor of a unique and idiosyncratic gut microbiota that sets the stage for health later in life.22
‘Blood, urine, saliva, and spinal fluid, these are the human bodily fluids most explored by scientists over the decades’, points out science writer Trisha Gura. ‘Yet any woman who has ever nursed a newborn will cite a major omission: breast milk.’23
It is only in the past few years that what microbial ecologist David Mills of the University of California has described as ‘a genius fluid that was outrageously understudied’ has really started to be appreciated.24
Previously the majority of doctors regarded breast milk as simply a source of food for the rapidly growing infant. Doubtless many parents only ever think of it as such, even now. But while human milk certainly contains a rich mixture of fats, proteins and sugars, in many ways more vital than the nourishment it provides is the protection it affords. Breast milk is replete with immune cells, stem cells for regeneration, and thousands of bioactive molecules. These protect the infant against infection, prevent inflammation, strengthen the immune system, promote organ development and help form the microbiome.
The key here is a bacterium with the tongue-twisting name of Bifido-bacterium longum biovar infantis which dominates the microbiome during the first months of life, making up as much as 90% of its bacterial content. After weaning, that proportion has fallen to just 3% of the adult microbiome. How this bacteria gets into the baby’s gut initially is not yet known – it may be as a result of swallowing amniotic fluid while passing through the birth canal, or even through the milk itself.
Fascinatingly, contained within human milk are substances known as human milk oligosaccharides (HMOs) – some 200 have been identified – whose purpose is to feed not the baby but the bacterium. ‘Mother is recruiting another life form to babysit her baby,’ comments food chemist Bruce German.25
This ‘babysitting’ role consists of protecting the neonate against a host of potentially deadly infections. One way it does this is by consuming the available food and so starving harmful microbes, such as salmonella, listeria and campylobacter. Another of its functions is to provide food, in the form of short-chain fatty acids (SCFAs), for other beneficial bacteria.
These continue to change and develop for the next fifteen or sixteen years, achieving maximum diversity and stability at adolescence and remaining stable until the later stages of life.26 It is only as we age that our microbiota starts to decline, becoming less diverse and stable, predisposing the elderly to infections such as C. difficile. The number and variety of bacteria increase exponentially the further one travels along the digestive tract, with the final section – the five-foot-long, greyish-purple colon – harbouring the majority of intestinal microbiota. The bacteria here are largely what are termed ‘obligate anaerobes’, meaning they will perish if exposed to oxygen. They maintain a high population density by deriving nutrients from food in the gut and from the intestinal epithelial lining. The processes through which bacteria derive food for themselves produce by-products that in turn affect our body chemistry, which may lead to enhanced satiety. For example butyric acid – found in milk, butter and Parmesan cheese – is produced by bacterial fermentation of dietary fibres, and may serve as an energy source and lead to feelings of fullness.27
While each individual microbiome is completely unique, we do all share a broadly similar profile, 90% of which comprises bacteroidetes, firmicutes and proteobacteria. Thus it has been suggested there is a ‘core’ microbiome. Bacteroidetes are rod-shaped bacteria that, in addition to living in our mouth, guts and skin, are also found in such environments as the soil, sea water and on the skin of other animals.
Firmicutes (from the Latin firmus (strong) and cutis (skin)) are a phylum that includes some notable pathogens, or disease-causing bacteria, and have a unique relationship with obesity. Organisms with higher concentrations of firmicutes are often heavier and have greater fat mass. They are either round (cocci) or rod-like structures (bacilli). Because they produce endospores, which are resistant to desiccation, firmicutes are able to survive in extreme environmental conditions, and thus can inhabit the gut with relative ease.28
Proteobacteria were named after the Greek sea god Proteus because, like him, they are able to assume a great number of shapes. This major phylum includes various pathogens such as salmon ella and vibrio (which can cause gastroenteritis, septicaemia and cholera). It also includes Helicobacter pylori; this lives in the stomach, where it helps regulate levels of the hydrochloric acid used to break down food, though it can also cause peptic ulcers, chronic gastritis and even stomach cancer.29 We will be revisiting Helicobacter pylori a little later in this chapter when we talk about the role of antibiotics in disrupting and deregulating the microbiota.
‘We depend on our microbial partners for essential services,’ says Ruth Ley from the Department of Microbiology at Cornell University, ‘such as energy harvest from food, its detoxification, a supply of vitamins, and protection against harmful invaders.’30
Gut flora defends us against pathogens by strengthening the wall of the colon to help prevent bad bacteria from entering and by producing antimicrobial substances such as the antibody immuno globulin A (Iga). As mentioned above in connection with breast milk, by competing for food these beneficial bacteria also starve unwelcome invaders out of existence. There is also strong evidence to indicate that they play a pivotal role in determining whether or not someone becomes obese, a theory to which we will return later in the chapter.
And crucially our gut flora help keep us nourished by unlocking energy from the fermentation of undigested carbohydrates and the absorption of short-chain fatty acids. They play a role in synthesising vitamins B and K as well as metabolising such essential substances as bile and sterols. The gut microbiota produce a dizzying array of enzymes that enhance digestion. Without them we would not otherwise be capable of processing difficult-to-digest foods such as complex carbohydrates, fat and protein; we would not be able to absorb them properly and they would therefore end up being stored in the body, contributing to the development of excess fat.
Several factors, such as infection, disease and diet can adversely affect the microbiome.31 Researchers have found, for example, that switching from a low-fat diet to one high in fats and sugars can alter the structure of the microbiota within a single day. So too does our increasing use of antibiotics. Given the integral role of these bacteria in our digestive processes, it’s hardly surprising that this can have significant effects.
Abnormal patterns of microbiota are consistently seen in those who suffer from obesity, and its associated illnesses.32 One way in which microbiota contribute to gut health and hunger pangs may be through the modulation of the hormone ‘ghrelin’. The stomach produces two hormones responsible for controlling hunger. One is leptin, which we described in the previous chapter; the other is ghrelin (from the Indo-European root ghre meaning ‘to grow’).
Ghrelin switches our appetite on while, as we have explained, leptin turns it off again. Mounting evidence suggests that ghrelin interacts with a particular bacterium found in the gut called Helicobacter pylori; eradicating these bacteria from the gut causes metabolic disturbances.
‘When you wake up in the morning and you’re hungry it’s because your ghrelin levels are high,’ Martin Blaser, Professor of Internal Medicine and Microbiology at New York University explained in a paper in 2005. ‘The hormone is telling you to eat. After you eat breakfast, ghrelin goes down.’33 Problems arise when antibiotics are taken to treat an infection. These destroy not only the harmful but also the helpful bacteria in the gut, including H. pylori.
The result of losing H. pylori as collateral damage in this way is often an increase in weight – without H. pylori to modulate ghrelin concentrations in both the stomach and blood plasma, appetite can run out of control. In one study, ninety-two US veterans treated with antibiotics gained significant amounts of weight compared to their counterparts who did not use antibiotics.34
Given the frequency with which we now use antibiotics in medicine, H. pylori is actually being eradicated from our bodies at a shocking rate. Two or three generations ago, 80% of Americans had H. pylori present in their guts. Today it can be found in fewer than 6% of American children, so while not essential to human survival, it is important within the context of obesity.
‘We now are more than 60 years into the antibiotic era and, in developed countries, children regularly receive multiple courses of antibiotics for various ailments, especially otitis media (ear infection),’ said Blaser in 2005. ‘If each course of antibiotics eradicated H. pylori in 5 to 20% of cases, the cumulative effect of childhood antibiotic regimens would remove a substantial proportion of colonisations.’35
So one of the key factors in the obesity pandemic may be changes, partly due to antibiotic use, in intestinal bacteria. One of the reasons people overeat may be because their depleted microbiota have difficulty in regulating their appetites or absorbing sufficient energy from food.36
In light of its relationship with ghrelin, H. pylori has become another target in the quest to understand the exponential rise of obesity. But how can something happening in our guts influence the sensation of hunger experienced in our brain?
Long before scientists had any notion that microorganisms resident in the guts played an essential role in the brain’s development and function, they knew that there is, inside our guts, what amounts to a second brain. Known as the Enteric Nervous System (ENS), it contains around a hundred million neurons, about the same number as in the brain of a cat.37 The Enteric Nervous System forms part of the Autonomic Nervous System or ANS, whose important role in stress and anxiety will be described in Chapter 9.
Our two brains, the one in the head and the other in the guts, are in constant two-way communication. Together they regulate digestion to precisely meet the body’s varying energy demands. As a result anything that affects our ‘gut’ brain also influences our ‘head’ brain, and vice versa.
The major neural communications route is along the tenth cranial nerve, also known as the vagus or, less often, the pneumogastric nerve. Vagus, from the Latin for ‘wandering’, is well chosen – it is the longest of the twelve cranial nerves; after emerging from the base of the skull, it meanders down to the major internal organs such as the heart, kidneys, uterus (also known as the viscera) and also branches to the heart, lungs, larynx, stomach and ears. To the brain it carries information about the digestive system; from the brain it sends signals that regulate viscera’s motility, local blood flow and the secretion of enzymes.
When communications break down (and they are vulnerable to attack from a wide variety of sources) the system becomes ‘deregulated’, potentially resulting in, among other conditions, inflammation, chronic abdominal pains, eating disorders and obesity.38 While the importance of the brain–gut axis has been recognised for decades, researchers have only recently realised that the microbiome is also an active and highly-influential contributor to this two-way communication network.39 The messages it sends to and receives from the brain play a pivotal role in whether or not someone becomes obese.
In the early years of the twenty-first century, Dr Ruth Ley and her colleagues at Washington University were working with the same strain of obese Jackson mice we met in the previous chapter. These animals lack the hormone leptin, which, as we explained, controls the body’s ‘fat thermostat’. Without it, the mice cannot monitor the amount of fat in their body and quickly become massively obese through overeating.
The team noticed that these mice had 50% fewer bacteroidetes and 50% more firmicutes than their leaner counterparts. When they examined human gut flora, they found the same imbalance in obese people as in the obese mice. The relative proportion of bacteroidetes increased in obese people as they lost weight by eating a low-fat or low-carbohydrate diet, while the firmicutes decreased.40
Other researchers reported the same effect in patients following bariatric surgery. As with the mice, the ratio of firmicutes to bacteroidetes decreased. These differences suggest that variations in weight between overweight and undernourished individuals, and how much each eats, may be dictated to a large extent not by their brain but by their microbiota.41
The link between microbiota and obesity became even clearer when Ruth Ley and her team studied a special strain of mice, bred to have no microbiota of their own. These intestinal tabula rasa mice could eat as much of various fattening foods as they liked without ever putting on significant extra weight. After eight weeks on a diet that was 40% fat, they had put on less than half as much weight as their ‘normal’ peers, despite eating the same amount of food. When the researchers transplanted the microbiota from fat and lean mice into the germ-free strains, those colonised by bacteria from fat donors packed on far more weight than those paired with lean donors.
To try to discover why shifting the bacterial balances affected body weight, the Washington University researchers next compared the microbiota of fat and lean mice at a genetic level. Samples from fat mice showed much stronger activation of genes that code for carbohydrate-destroying enzymes in the various bacteria, which break down otherwise indigestible starches and sugars. As a result, these mice were able to extract more energy from their food than were lean ones. The bacteria were also manipulating the animals’ own genes, triggering biochemical pathways that store fats in the liver and muscles, rather than metabolising them. While these effects are relatively small, the researchers believe that, over the course of months or years, they can result in very large weight fluctuations.42
Certain microbial populations secrete enzymes, not encoded in the human genome, that enable calories to be extracted from otherwise indigestible polysaccharides (sugars) in our diet. This results in an increase in bacterial fermentation products, the short-chain fatty acids, which influence various aspects of our metabolism, resulting in the storage of fat in the host. The microbiota has also been shown to influence bile acid production, insulin resistance and inflammation, all of which contribute to metabolic disease.43
The fact that – as mentioned above – the composition of the gut microbiota varies between individuals has led some researchers to make the controversial suggestion that there is a ‘core gut microbiome’ which greatly increases the risk of a person becoming obese. Equally, there may be a specific combination of bacteria that impart optimal health benefits.
A recent study examined the effects of infusing intestinal microbiota from nine lean men into another nine males suffering from both metabolic syndrome and obesity. Six weeks afterwards, those with metabolic syndrome showed significantly improved bacteria profiles (more varied bacteria in the gut) and improved insulin sensitivity profiles. In fact, the dramatic improvement of insulin sensitivity has led researchers to speculate whether more traditional forms of enhancing gut bacteria (i.e. via oral supplements) may have an important role in the future of obesity control medicine.44
Success in this area has prompted a surge in research that should lead to greater understanding of our gut health, and indeed our health in general. Metagenomics, the name given to this new and rapidly expanding field of research, uses sophisticated screening techniques to characterise the microbial community at a genome level in health and disease. Over the past few years, huge strides have been made in understanding the composition, diversity and functions of the human microbiome. If researchers are able to identify what constitutes obesity-promoting or obesity-resistant gut flora, such knowledge will open up new doors of opportunity for preventive, diagnostic and therapeutic approaches in disorders of microbiota–brain–gut axis.45
Research success in understanding the interactions between genetics, diet and human gut microbiota could lead to ways of reducing or even eliminating obesity through modifying intestinal microbiota by means of diet, prebiotics, or advanced probiotics. While this field of study is still in its infancy, evidence is emerging which strongly suggests intestinal microbiota also play a key role in the development of various aspects of brain function, including anxiety, emotions, cognition and – even more fascinating – sociability. Well-designed and well-conducted randomised trials are now needed to further assess the clinical potential for treating neurodevelopmental and mood disorders.
There is still a great deal that we don’t know about our life-long passengers – the exact ways they sense and respond to their host’s condition, the details of how they are passed on or how they are affected by our diet. By answering these questions, scientists could then assess whether actively shifting our bacterial balances could help to stem the worldwide increase in obesity levels.
Of course, gut microbiota are not the whole story behind the current obesity epidemic. We need to understand how they interact with other factors that affect our risk of becoming obese, such as lifestyle choices, marketing and advertising techniques, the availability of HED foods and our genetic make-up.
In the next chapter we will be exploring the relationship between the gut and the brain in greater depth to explain how what goes on in the head can profoundly affect what goes on around the waist.
fn1 The reason we make this distinction is a simple one. No one knows what the ‘mind’ is. Even its existence as something somehow distinct from the body has come to be doubted by many neuroscientists, ourselves included.