This Spice Stops Heart Attacks, Fights Cancer, and Restores Gut Bacteria

This Spice Stops Heart Attacks, Fights Cancer, and Restores Gut Bacteria

Study Reveals #1 Natural Bacteria Killer

Study Reveals #1 Natural Bacteria Killer

How to Remove Mucus, Bacteria, and Toxins From Your Lungs Using Himalayan Pink Salt

How to Remove Mucus, Bacteria, and Toxins From Your Lungs Using Himalayan Pink Salt

Mosquitos to be infected with bacteria in fight against Zika virus

Mosquitoes in two large areas of Brazil and Colombia are to be infected with bacteria that deprive them of the ability to transmit viruses, in an attempt to check the spread of Zika, which has been held responsible for brain damage in thousands of babies.

Funding the ambitious plan are two philanthropic foundations – the Wellcome Trust and the Bill and Melinda Gates Foundation – together with the Brazilian, UK and US governments. The scheme will cost $ 18m (£14.7m) and is supported by the World Health Organisation (WHO).

Wolbachia bacteria are carried by around 60% of the world’s insect species, but not by the Aedes aegypti mosquito, which transmits Zika, dengue, yellow fever and chikungunya viruses to humans.

Researchers at Australia’s Monash University have been working for the past decade to infect mosquitoes with Wolbachia in an effort specifically to eliminate dengue, but the Zika crisis in Latin America has focused attention and now major funding on their work.

Following successful trials in Australia, Indonesia and Vietnam, including small-scale projects last year in Latin America, Wolbachia-infected mosquitoes will be released across two large urban areas – in Rio de Janeiro in Brazil and in Antioquia in Colombia, starting next year. The infected mosquitoes breed with local mosquitoes and pass the Wolbachia bacteria on to their offspring, so the project is self-sustaining. In those areas where trials have been done so far, transmission of the viruses has stopped.

“Wolbachia could be a revolutionary form of protection against mosquito-borne disease. It’s affordable, sustainable, and appears to provide protection against Zika, dengue, and a host of other viruses. We’re eager to study its impact and how it can help countries,” said Dr Trevor Mundel, president of the global health division of the Bill and Melinda Gates Foundation.

The World Health Organisation earlier this year called for large-scale pilot studies of the Wolbachia mosquito-control method and the Pan-American Health Organisation offered technical support in countries affected by Zika.

The idea emerged from the Grand Challenges programme backed by the Gates Foundation, which each year calls for scientists to bid for funds with creative new ideas to solve some of the world’s most pressing health problems. Prof Scott O’Neill’s team from Monash University proposed Wolbachia infection of mosquitoes to stop dengue transmission in 2005.

Jeremy Farrar, director of the Wellcome Trust, told the Guardian it was vital for the scientists to ensure they had local support for what will still be a trial. “Community involvement is absolutely fundamental,” he said. A huge amount of work, over years, had gone on to explain the project to people living in areas where earlier trials had taken place. “Get that sort of community intervention wrong and you never recover from that,” he said.

There are great hopes for Wolbachia but it is too soon to suppose this is the answer to the Zika and dengue epidemics. Farrar said he would wait to see whether it worked. “I’m in equipoise. I really hope it will, but I’d like to see the evidence at scale.”

Sue Desmond-Hellman, chief executive of the Bill and Melinda Gates Foundation, in London with Farrar for the latest Grand Challenges meeting where new projects are presented and funding awarded, said she agreed.

“What I feel most confident about is that it is safe,” she said. “We know that Wolbachia is already found in 60% of the world’s insects. Everyone in this room has probably been bitten by something with Wolbachia.”

Aedes aegyti mosquitoes are found across large areas of the world, including the southern part of the United States, parts of Asia and Africa. Methods to control the populations or limit the damage they can do in transmitting viral infections are urgently needed. The director of the US Centers for Disease Control and Prevention said on Tuesday that there was not yet a way to contain the spread of infections.

“Zika and other diseases spread by [the Aedes aegypti mosquito] are really not controllable with current technologies,” said Thomas Frieden. “We will see this become endemic in the hemisphere.”

More than 50 countries have experienced an outbreak of Zika virus infections since 2015, according to WHO data, and there have been nearly 2,200 cases of microcephaly – babies with brain damage – associated with Zika, 28 of which have been reported in the US. The vast majority – 2,033 – were reported in Brazil.

Mosquitos to be infected with bacteria in fight against Zika virus

A Frequent Virus Is Consuming Your Gut Bacteria

The only time you are fully human is prior to you’re born. For the rest of your daily life, microbes from the setting colonize the ecosystems all around the physique, outnumbering your 37 trillion human cells by about 10 to one.

Above the past decade, scientists have been exploring how microbes residing on and inside the body influence our well being. Why do some make us sick whilst other folks defend against pathogens? Rather than making an attempt to increase each and every and every species in the lab then studying its sequence of DNA letters to make a single genome, researchers are utilizing an cost-effective approach: acquire samples from one particular spot (such as the gut), chop-up all the DNA, then read the short fragments. The outcome is a ‘metagenome’, the collected genetic materials from an entire microbial community.

Metagenomes make a large volume of information at fairly minimal value. For $ 170m, the 1st phase of the Human Microbiome Task catalogued the microbes at 5 sites – mouth, nose, skin, urogenital and gastrointestinal tracts – in 242 American adults. As properly as revealing the secrets of recognized species, info in the depths of metagenomes can also be mined to uncover microbes we never knew we had, such as a newly-discovered virus referred to as crAssphage.

A bacteriophage virus (CC BY-NC-SA 2. / original by origamiwolf: https://flic.kr/p/oDCK1)

A bacteriophage virus (CC BY-NC-SA two. / original by origamiwolf: https://flic.kr/p/oDCK1)

The crAssphage virus is a bacteriophage, or ‘eater of bacteria’. It infects species of Bacteroides, a group that helps make up the bulk of cells in the human gut and behaves as both great and poor bacteria. Most of the time our relationship is mutually beneficial: we give a residence, they support digest our meals. But they can also be hazardous, connected with well being problems such as weight problems, and one strain, enterotoxigenic Bacteroides fragilis, is linked to colorectal cancer. By preying on Bacteroides, crAssphage probably helps to preserve us healthful.

The virus was found by Dr Bas Dutilh, a bioinformatician at Radboud University Health care Centre in the Netherlands, who rebuilt its genome from DNA fragments in faeces. In programming, it’s normal to mix phrases and capitalize the first letter, and the personal computer instrument that Dutilh developed to assemble the viral genome is called crAss (for ‘cross Assembly’). He tells Forbes that the virus’s name wasn’t inspired by the place it was collected.

“Initially we did not give it any identify, it was just called ‘the new virus’,” says Dutilh, adding that one particular of the scientists reviewing his study paper advised providing the virus a name. “Then I was like, Oh okay, perhaps I can use this chance to market my computer tool. And fundamentally that’s how it received the name crAssphage.”

Reconstructing crAssphage’s genome was no indicate feat, as each metagenome contains DNA fragments from an complete community of microbes. Imagine a metagenome as a box total of pieces from hundreds of diverse puzzles. The genome of a identified organism can be assembled utilizing a associated species as a guide, like searching at the picture on the front of the box, but how do you locate something that you really don’t even know exists?

Dutilh’s laptop instrument pieces a genome collectively by detecting DNA fragments that are equally abundant within the exact same metagenome. Say you uncover puzzle pieces with the very same distinctive form in various boxes, except that box A includes 10 copies of each piece even though box B has 100 copies. Because the distinctive pieces are ‘co-abundant’ inside a box, they’re possibly components of the same puzzle.

Doing work with collaborators at San Diego State University, Dutilh utilized his crAss software to analyze faecal metagenomes from 12 folks. This unveiled a set of distinctive DNA fragments that could be assembled into a genome. DNA tests on a single of the 12 stool samples confirmed that crAssphage was there.

The researchers then searched public DNA databases and detected the virus in 73% of 466 faecal metagenomes from the US, Europe and South Korea. This broad distribution implies that crAssphage occurs in up to 3-quarters of individuals around the planet, and signifies trillions of viruses are possibly living in your gut correct now.

Not a lot is acknowledged about crAssphage. It is also little to be seen under a light microscope, but will no doubt have the angular head, tail and ‘legs’ normal of bacteriophages. Its genome is 97,000 letters long and patterns in its DNA indicate the virus has 80 genes, only half of which are comparable to known genetic sequences. Some encode structural proteins and molecules that manipulate its host’s DNA-creating machinery, and a number of genes are predicted to encode proteins that attach to Bacteroides.

Bacteroides fragilis (source: http://phil.cdc.gov)

Bacteroides fragilis (supply: http://phil.cdc.gov)

Dutilh and his collaborators offered numerous lines of evidence that crAssphage infects Bacteroides. Parasites want hosts, so you would count on a relationship among numbers of bacteriophages and bacteria. Without a doubt, when the abundance of crAssphage DNA was in contrast against the bacterial strains in 151 metagenomes from the Human Microbiome Task, there was a clear correlation among the quantity of crAssphage and Bacteroides DNA. When the virus was utilised to search a database of 3000 bacterial genomes for CRISPR sequences – patterns in a bacterium’s immune method that record encounters with viral DNA (like antibodies matching antigens) – Bacteroides was the leading search outcome.

As properly as controlling gut bacteria in healthier people, crAssphage may a single day be utilised to fight disease. For instance, you could isolate a virus that specifically targets pathogenic strains of Bacteroides fragilis. A genetically-engineered crAssphage could also serve as a therapeutic vector for delivering medicines or vitamins.

So far, metagenome analysis has centered on bacteria. Viruses have been neglected, partly due to the fact it’s assumed their DNA evolves as well rapidly to detect. But as the discovery of crAssphage displays, they can be extremely abundant inside a microbial neighborhood.

“Our intestinal bacteria are 1 large ecosystem,” says Dutilh. “But to recognize that ecosystem, you need to have to understand the viruses as properly.”

A Frequent Virus Is Consuming Your Gut Bacteria

Lab-Modified Bacteria For Bodyweight Reduction In Mice -- Coming Quickly To A Gut Near You?

We currently know that the gut bacteria of obese people and slim men and women are diverse. So what if we were to import some bacteria specialized for bodyweight loss?

Nicely, we’ve presently carried out it to some mice. In the Journal of Clinical Investigation, researchers say that mice offered genetically-tweaked E. coli in their water gained less weight than controls when positioned on a higher-fat diet regime for eight weeks. They also had fewer markers of diabetes, like insulin resistance, and generally ate less than their compatriots acquiring absolutely nothing or handle bacteria. And for four weeks to 6 weeks following the researchers stopped dosing the water, the useful effects persisted.

The bacteria provided to the mice were genetically engineered to express predecessors of a family members of fats that prompt much less foods consumption. These fats are made in the small intestine, and tell an animal to stop consuming. Higher unwanted fat diet plans interfere with this method, so making use of modified bacteria may help dieters regulate their appetites.

Initial, the scientists picked a strain to target: a variety of E. coli. Then they altered the strain to add a gene identified in arabidopsis, the 1st plant to have its genome sequenced.

Arabidopsis thaliana – Acker-Schmalwand (Photo credit: Nuuuuuuuuuuul)

The gene prompts the bacteria to make precursors to the hormones launched in the tiny intestine when it processes body fat. These hormones, dubbed NAE, travel via the bloodstream to the brain to suppress appetite. The bacteria release these hormones in the gut of the mice who ingested them, without any apparent unwell-effects for their hosts. As for how they ate: they ate generally timed meals, just smaller sized ones than the control mice. They also appeared to move more, which includes in the course of the light phase of their day, when mice are usually asleep.

Much more than a third of grownups in the U.S. are obese, and the situation has been notoriously challenging to target with medication. Wyeth, which was subsequently purchased by Pfizer, had some successes with fenfluramine and dexflenfluramine just before the medication have been pulled from the market place in 1997, when they were linked to heart valve ailment in patients who took them with phentermine. Sanofi stopped building its obesity treatment Accomplia in the U.S. after Europeans removed it from the market for its back links to suicide and depression. Pfizer and Merck the two stopped development on obesity plans in 2008. Abbott Laboratories’ diet regime pill Meridia was similarly yanked from the market place in 2010 for its hyperlinks to heart attacks and strokes.

Not like these drugs, which need to be taken day-to-day, today’s outcomes suggest bacteria can be dosed as infrequently as after every single 4 weeks, whilst retaining their beneficial effects, the researchers wrote. And the effect of the hormonal precursors is both constrained and certain: there weren’t any significant elevations of NAE in the blood of the mice — just in the liver and the brain.

One benefit of utilizing laboratory-modified bacteria rather than the wild-variety probiotics is that most useful bacteria really don’t colonize the gut well. Utilizing bacteria that are greater-adapted to the gut signifies they’re far more most likely to consider hold. What’s far more, genetically modified bacteria can be manufactured responsive to particular cues, like food consumption — that means, they’d behave considerably much more like our gut currently does, which may make the bacteria’s chemical cues much more efficient in the entire body.

Far more work requirements to be carried out: mice aren’t humans, following all. But possibly bacteria will prevail the place capsules have failed.

Lab-Modified Bacteria For Bodyweight Reduction In Mice -- Coming Quickly To A Gut Near You?

Deadly Bacteria Can Dwell For A Week On Planes, Study Displays

Do not touch that armrest! That was the poor news for airplane vacationers right now as researchers released benefits showing that some of the deadliest germs can live for up to a week on airplane seats, tray tables, armrests, and other surfaces.

In reality, think of the germiest surface you can picture – a toilet flush deal with, maybe? Your airplane armrest is way worse, say Auburn University researchers James Barbaree and Kiril Vaglenov, who presented some stomach-churning analysis nowadays at the annual meeting of the American Society for Microbiology (ASM).

With aid from engineers, Auburn’s staff of microbiologists carried out a rather easy experiment. They asked Delta Airlines for samples of six different supplies commonly employed on planes, such as a plastic tray table, a metal toilet flush, the cloth utilized in seat pockets, a plastic window shade, a rubber armrest, and seat leather used in upgraded seats.

Then they applied two varieties of bacteria, E. coli and Staphylococcus aureus (MRSA) to the 6 surfaces, mimicked the situations existing within an airline cabin (twenty percent humidity, 75-degree temperature), and watched.

Germs can linger on your tray table, armrest, even your window shade, researchers say. (image: wiki media)

The benefits:

MRSA survived for up to 7 days on the the surfaces that surround your plane seat, compared to just 4 days on the toilet flusher. The much more porous the surface, the longer the bacteria lived. .To break it down further, MRSA lasted for 7 days on cloth (seat pocket) 6 days on rubber (armrest) 5 days on plastic (tray table and window shade) and 4 on metal.

E. coli bacteria had been a tiny less persistent, surviving for 4 days on the armrest, 3 days on the tray table and window shade, and two days on the toilet flusher.

But here’s the kicker: even though the plastic surfaces have been a small much less welcoming to the bacteria, they presented a more effective mode of transportation. In other phrases, even though MRSA could last just five days on your armrest, it jumps happily from there to your hands.

And these are not bugs to be taken lightly E. coli is one particular of the five deadliest food-borne illnesses and people have died in recent outbreaks. Meanwhile MRSA is becoming resistant to antibiotics, foremost to incurable fatal infections.

What to do? Follow this 15-stage strategy for protecting oneself from germs whilst flying. Top on the listing, the researchers said, was wiping all surfaces with antibacterial wipes and using hand sanitizer following touching armrests, tray tables and other plane surfaces. And, of program, wash your hands as usually as attainable.

The investigation was performed in Auburn University‘s department of Biological Sciences with funding offered by the Federal Aviation Administration (FAA)’s Airliner Cabin Environmental Study Center (ACER).

Up coming up for Vaglenov, Barbaree, and colleagues is tuberculosis they’re currently studying airline transmissibility of these bacteria and numerous other critical pathogens. Regular fliers, keep tuned.

For more overall health news, adhere to me right here on Forbes.com, on Twitter, @MelanieHaiken, and subscribe to my posts on Facebook.

Deadly Bacteria Can Dwell For A Week On Planes, Study Displays

I had the bacteria in my gut analysed. And this may be the long term of medicine

We are all familiar with “gut feelings”, “gut reactions” and “gut instincts”, but how much do we really know or care about our guts? As we become increasingly more aware of what we put in our stomachs, it’s striking how ignorant we remain of what takes place in our intestines. And it turns out there is an awful lot going on down there.

Microbiologists have made some startling advances in revealing our innermost secrets. It turns out that there is a complex ecosystem deep within us that is home to a fantastic diversity of life – of which very little belongs to our species.

For most of us, suspicious of foreign bodies, it’s a struggle to comprehend that at our very core we are less than – or rather much more than – human. But, the fact is, there are about 100 trillion organisms living in the gut. If you put them all together they would be about the size of a football. In terms of cells, the microbial kind outnumber their human counterparts by about three to one. And in terms of genes, the microbial advantage is more like 300 to one.

That means there is a tremendous amount of us that is not, so to speak, us. This raises a whole range of interesting philosophical and anatomical questions, of which the most urgent might be: should we be worried?

Well, I wasn’t much concerned about bacteria before I got the contents of my gut tested. I took a fairly relaxed view that as long as the lavatory was regularly bleached, I brushed my teeth and kept the kitchen surfaces reasonably clean then I didn’t have to think too much about what goes on at the microbial level. But there’s nothing like spooning your own faecal matter into a Perspex container to make you stop and contemplate just what it is that we’re full of. That unpleasant task is precisely what I found myself doing last October, as I gathered a stool sample to send off, cold-packed to the BioSciences Institute at University College Cork in Ireland.

The institute is one of Europe’s leading centres for the study of what is now referred to as the microbiome – that is all the bacteria, viruses, fungi, archaea and eukaryotes that inhabit the human body, inside and out. The simplistic view of these guests has traditionally centred on their parasitic or pathogenic aspects. Either they were fairly harmlessly hitching a free ride or were a direct threat to their host.

But the latest thinking presents this vast army of microbes as a vital component in furnishing and maintaining human health. Such is the microbiome’s importance that it is now viewed by scientists as a separate organ with its own dynamic metabolic activity. But what precisely is that activity and is it all going to plan with me?

Paul O’Toole is a professor at the School of Microbiology and Alimentary Pharmabiotic Centre, which is part of the BioSciences Institute at Cork. A keen marathon runner, he looks like he knows a thing or two about intestinal fortitude. He co-ordinated a government-funded study – fortuitously launched just before the Irish economy collapsed – entitled Eldermet, which was aimed at helping the Irish food industry develop food products for old people. To do that, they needed a knowledge base of the gut microbiota. So O’Toole began examining how diet affects the microbiota of Ireland’s elderly population.

There is an element of poacher-turned-gamekeeper to his career because he started out as something of a bacterial enemy. “I spent about 15 years working on pathogens where you’re trying to kill them,” he tells me in his office. “I did my PhD in staphylococcus. One organism, one gene. I worked on a condition called skull-to-skin syndrome where staphylococci infect the umbilical stump and if they produce a toxin all the baby’s skin peels off.”

From combatting staphylococci, he moved into probiotics – the organisms that are supposed to be good for us – which in commercial form have been decanted into capsules and yoghurts and advertised to the public as “friendly bacteria”. But he discovered that he couldn’t effectively study probiotics in isolation because their benefits were often indirect.

“I realised I needed to study the whole canvas,” he says. And that was how he came to find himself involved with the microbiome, just when it was starting to become the subject of intensive biomedical research.

There are two labs, O’Toole explains, that processed my sample. The first was the wet lab, where, through various molecular assaults, DNA was extracted, 95% of which was bacterial. This was then sent to an external company to be sequenced – there were over 30,000 sequences – and then a huge file of data was crunched by what O’Toole called “a bunch of computer nerds who sit around all day generating stats” in the institute’s data lab.

Just a year ago, that process cost upwards of £400. Now it can done for as little as £15. What you get are a couple of pie charts that list the microbiota found in the gut at different phylogenetic levels and a narrative explanation as to what their significance is. Phylogentic levels in this instance simply refer to different levels of resolution.

At the broadest level, the phylum level, my microbiota, in common with everyone else’s, was dominated by two types: firmicutes and bacteroidetes. The western diet, by which we tend to mean the North American diet, is high in fat and protein. In this diet bacteroidetes usually make up more than 55% of the gut microbiota, and sometimes, in North America itself, as much as 80%. In Europe, the average numbers vary from country to country. In my case I had 34%.

The opposite to a North American diet is what O’Toole calls a “natural diet”. “Our antecedents on the plains of Africa weren’t chewing on burgers,” he explains. “They were running around eating plant foods and leaves and occasionally eating a squirrel if they were lucky.”

On a plant-based diet, the microbiota is tipped in favour of the other major phylum, firmicutes. Some of the complex carbohydrates in plants cannot be digested by our bodies alone. They have to be broken down by the gut microbiota, which produce enzymes to chop up the long chains and ferment them into short-chain fatty acids such as butyrate – which is made exclusively by bacteria – acetate and propionate.

These fatty acids are beneficial to the body. Butyrate, for example, provides an energy source that the cells lining our intestines can directly access. It also controls the proliferation of cells in the intestine and is thought to possess anti-carcinogenic properties. All of which meant that my score of 51% firmicutes was a healthy sign.

Zooming into the genus level, which offers a more detailed look at my microbial composition, the good news continued. I had three times as much of the butyrate-producing roseburia than the healthy cohort used in O’Toole’s study. Many more lachnospira than normal but many fewer bacteroides (not to be confused with bacteroidetes) and alistipes – as O’Toole put it, in more scientific terms, “bugger all”.

Again these were positive results. Lachnospira degrade pectins and ferment dietary fibres and I have three times more than typical. And bacteroides are often associated with meat-based, high-protein, high-fat diets, just as alistipes tend to be more present in people who eat less plant-based food. In sum that meant my gut – the lack of six-pack notwithstanding – was probably in good shape. Of course, it’s not the sort of thing you can boast about at dinner parties. “I’ve got significantly higher than average amounts of lachnospira,” is unlikely to be a conversational gambit that will impress non-microbiologists, even if you do manage to pronounce the word correctly. But just as we now know that high cholesterol is something to be avoided, so too might we soon begin to become aware of the sorts of bacteria counts that are markers for good health, especially as the price of testing comes down.

There were, however, one or two results that O’Toole struggled to make sense of. In particular my high levels of natranaerobius, a genus of bacteria that thrive in high-salt, highly alkaline environments. Did I eat a lot of sushi? No, while I love fish, I tend to prefer it cooked. Did I prepare a lot of fish? No more than once a week.

Although he found nothing sinister in the natranaerobius, it perturbed him that he couldn’t quite put his finger on the cause of its abundance in my gut. But by then he had managed to make a blind prediction of my diet that was uncannily accurate. He saw very little evidence of meat-eating – I haven’t eaten meat for 30 years. But there was plenty of evidence of high fibre, which is good because bacteria feed on fibre. If we don’t feed bacteria, they feed off us – specifically the mucus lining in our large intestine. There was also evidence of lots of fish and a large range of vegetables. All of which exactly represents my diet.

I suggest that it must be satisfying to get his prediction so right.

“It’s a bit spooky all right,” he agrees. “But it made me think about the utility of it. I mean, it’s not particularly useful to tell people what they eat.”

O’Toole is interested in the diagnostic potential of the microbiome. “We could probably guess what your inflammatory parameters are,” he says, fixing me with one of those expressions in which GP’s specialise when looking up from studying your medical notes: neutral, unyielding, and anxiety-inducing. Not only do I not know what my inflammatory parameters are, I don’t know what inflammatory parameters means.

O’Toole explains that significant links have been established between gut microbiota and inflammation, sarcopenia and cognitive function.

“Inflammation,” he says, “is not a swollen thumb. Inflammation means how activated your immune system is. I would guess that your inflammatory markers are baseline. Flat. In old people they’re not. In old people, the immune system is typically turned on and that’s not good, because if it’s turned on, when they get a winter flu all their energies are expended chasing ghosts. So you want to turn down the inflammation.”

Sarcopenia means loss of muscle mass. It happens as we get older because the body becomes less efficient at turning protein into muscle, which is why older people need to have more protein. “We think that the narrowing of gut bacteria in old people is making the intestine less efficient at absorbing proteins,” says O’Toole.

Cognitive function is partly related to what’s known as the brain-gut access. As all those phrases like “gut wrenching” and “gut feeling” suggest, there is indeed an intimate link between the brain and the gut. Our intestines are acutely responsive to shifts in our emotions and mental states. But it’s a two-way street: studies suggest that our brains and emotions are also sensitive to what’s going on in our guts.

T ypically, cognitive function is only slowly diminished as we get older, but in some cases it can quickly accelerate.

“There are physiological reasons like Alzheimer’s and senile dementia that explain rapid cognitive impairment,” O’Toole says. “But the rate of loss could also be affected by compounds made by bacteria, and that’s what we’re targeting. Bacteria produce chemicals which are analogues – in other words they look identical to normal human transmitters. What we hope is that we can improve the ability of old people to process data.”

Common to all these issues, particularly among the aged, is the narrowing of the gut microbiota which, in turn, is usually the result of a narrowing of diet. This is a point that O’Toole repeatedly emphasises.

“Diversity is the key. What we see with people on narrow diversity diets is that the microbiota collapses. A good analogy would be an ecosystem like a rainforest, where you’ve got loads of plants and animals interacting. It’s evolved over tens of thousands of years, then one of the key species, a tree, gets cut down and you get ecological collapse.

“And if you had a gentleman whose wife died and she had done all the cooking, and then he’s suddenly eating toast and marmalade, the diversity of gut microbiota will collapse – because diversity of diet correlates with diversity of microbiota – and you will get a range of health problems associated with that.”

He goes on to tell me that my microbial diversity is impressively wide and that, by way of summary, he would suggest that my diet is “pretty bloody good”. Forget the 5-2 diet, I suddenly feel like writing a bestselling diet book entitled Guts: The Microbial Guide to Healthy Eating. In one sense, of course, it’s no great achievement. Studies show that it only takes a short time of a changed diet to dramatically change the microbiota, although it changes back just as quickly as soon as the diet is dropped.

But this apparently superficial relationship between food and microbes is in reality rather profound because first it speaks of a co-evolution with the human body over tens of thousands of years. Like all organisms and species, humans have evolved to have a particular relationship with a particular set of microbes.

There are hundreds of thousands of kinds of microbes on Earth but only about a thousand enjoy an association with humans. Thus, secondly it suggests that we need to stop thinking of ourselves as separate entities from the microbes that have colonised our bodies.

“We came through the period of medicine in which we developed antibiotics,” says O’Toole. “Until the second world war we were dying from stupid things like pneumonia and galloping septicemia from a small wound. So antibiotics were a major success. Then we’ve had the backlash where we’ve prescribed them too much and can’t control the pathogens. But now we have a more intelligent understanding of humans as chimeras.”

A germ-free existence would be an unhappy one. Tests have shown that a mouse raised in a lab devoid of bacteria fails to develop a proper immune system or an effective digestive system. It has to consume a lot more food to extract calories. Humans are first colonised by microbes during birth. Then through breast milk, which contains both probiotics (beneficial microbes) and prebiotics (compounds that foster the growth of probiotics).

“There is strengthening evidence,” says O’Toole, “that the explosion of auto-immune diseases and immune disregulation diseases in western society may be due to suppression of gut bacteria from infancy onwards.

“The immune system in babies is probably taught to distinguish between self and non-self in the context of bacteria. There are two recent papers in the publication Nature showing that butyrate is important in enlisting regulatory T-cells, a branch of immune cells that control the processes involved in inflammatory bowel disease and irritable bowel syndrome.”

It takes about two years from birth through a process of selection for a child to attain a mature microbiome. There are several phenomena that may contribute to childhood microbial diminishment. One is the increase in caesarian sections.

“Babies who were previously colonised in the birth canal with their mother’s microbiota now have a gut microbiota that is more like the walls of the hospital than it is mum’s vaginal microbiota.”

Another is lack of breast milk, and a third is the increased use of antibiotics. O’Toole says that one study suggests that repeated use of antibiotics tips the microbiota towards one that promotes obesity. In fact there are many studies around the globe that are still in their infancy but which point up connections between the microbiota and diseases and complaints as diverse as irritable bowel syndrome, inflammatory bowel disease, type-two diabetes, Parkinson’s, Alzheimer’s, autism, depression, cardiovascular disease and colon cancer.

But so far none of it is conclusive and much is highly speculative. After the initial claims about the potential health benefits of microbiome research – the kind that tend to help funding – there has been a bit of a sceptical backlash.

Several articles have pointed out that there has been plenty of hyperbole but not enough substance. And as yet the medical profession isn’t rushing to produce microbiome specialists.

“Medicine is notoriously slow to adopt new ideas,” says O’Toole. He cites the case of Barry Marshall, an Australian doctor whose claim to have established a bacterial cause of peptic ulcers and gastric cancer was comprehensively ridiculed by the medical establishment in the 1980s. “About 20 years later he got the Nobel prize.”

The problem, he says, is that microbiologists have been very good at discovering gut bacteria and identifying what roles they might play, but they have been slow to develop mechanisms to establish firm causal links and practical applications.

“I personally hope it doesn’t become the solution for everything because it’s not going to be credible, it’s simply not true. There’s plenty of evidence that most human major diseases have a physiological or lifestyle basis, but it’s probable in some of those that the gut microbiota is a modulating factor that contributes to the overall risk.”

Right now, O’Toole would like to like to reduce the lower diversity microbiota in the elderly by means of dietary supplements. “But we worry that, as the World Wildlife Fund says, extinction may be forever. That if a particularly good bacterium is missing from an elderly person, we may not be able to get it back by diet alone.”

The solution in that case might be fecal microbiota transplantation, which O’Toole helpfully clarifies, “is the idea of transplanting someone else’s poo into a recipient”. Which neatly brings us back to where I started. If collecting your own excrement is counter-intuitive, then injecting it into someone else runs against every decent human instinct.

But it’s already happening in North America and O’Toole suggests that such transplants may help prevent ulceration of the colon – a condition that nearly killed my father some years back.In the end, it’s all comes back to what you put in and take out. And in that tireless cycle of life, we shouldn’t be appalled if not even our waste need go to waste.

It was commonly believed that too much stress was the primary cause of chronic gastritis and peptic ulcers. Then, in 1984, Australian physician Barry Marshall drank a petri dish of Helicobacter pylori taken from a patient with gastritis, and eight days later developed massive inflammation of the gut – he later shared a Nobel prize for his trouble.

Found in the stomach of an estimated 50% of people, most of the time H. pylori is commensal, living on us without any negative side effects. The remedy, however, is not as straightforward as simply eradicating the bacterium, as some experiments have revealed a link between low levels of H. pylori in children and an increased risk of asthma.

An early coloniser of teeth, Streptococcus mutans is one of 25 species of oral streptococci to live in the oral cavity.

Normally they cause few problems, turning sucrose into a “glue” to cohere to teeth, helping to form dental plaques. However, if S. mutans is given other types of sugar – glucose, fructose or lactose, for example – in addition to the plaques, it also starts producing lactic acid.

While dental plaques comprise hundreds of species of bacteria, it is this combination of lactic acid and plaque caused by S. mutans that is a primary cause of tooth decay.

It is already known that type 2 diabetes can be caused by a number of genetic and environmental components, but recent research has shed some light on a possible microbial element. It was found that patients with type 2 diabetes had lower rates of butyrate-producing bacteria, an important food for cells lining the colon.

It was also found that there was a clear relationship between people with type 2 diabetes and the specific species of bacteria found in their gut. This association is so great that the analysis of gut microbiomes can be used as a diagnostic test for type 2 diabetes.

Gut bacteria produce hundreds of neurotransmitters, which are used by the body to regulate learning, memory and mood. In addition, gut bacteria are also known to produce up to 95% of the body’s supply of serotonin, which is a contributor to feelings of wellbeing and happiness. The evidence suggests that an increased understanding of gut microbiota may produce novel treatments for anxiety and depression.

While chronic infection of H. pylori has been known to increase the risk of stomach cancer by four to six times, it is now becoming clearer that other bacteria may have a role to play in increasing or decreasing a person’s susceptibility to other forms of cancer. A study of 70,000 individuals showed that patients with periodontitis – inflamed and bleeding gums due to poor oral hygiene – had double the risk of cancers of the oral cavity and digestive tract. The risk of cancer rose with increasing severity of periodontitis and was specifically associated with the oral bacterium Porphyromonas gingivalis.

I had the bacteria in my gut analysed. And this may be the long term of medicine