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Finally, Kuk and the other study authors think that the microbiomes of Americans might have somehow changed between the 1980s and now. It’s well known that some types of gut bacteria make a person more prone to weight gain and obesity. Americans are eating more meat than they were a few decades ago, and many animal products are treated with hormones and antibiotics in order to promote growth. All that meat might be changing gut bacteria in ways that are subtle, at first, but add up over time. Kuk believes the proliferation of artificial sweeteners could also be playing a role.
My son was off to a worrisome start. Why, I wondered, didn’t doctors work harder to prevent this collateral damage, not with store-bought probiotics, but with “microbial restoration”? Why didn’t we reinfuse patients with their own microbes after antibiotics?
The scientific term for this is “autologous fecal transplant.” In theory, it could work like a system reboot disk works for your computer. You’d freeze your feces, which are roughly half microbes, and when your microbiome became corrupted or was depleted with antimicrobials, you could “reinstall” it from a backup copy.
The tantalizing links between gut microbes and the brain
Neuroscientists are probing the idea that intestinal microbiota might influence brain development and behaviour.
Peter Andrey Smith
14 October 2015
Gut bacteria has been found before to be different in those with celiac disease, which is caused by the immune system reacting to gluten and damaging the inner lining of the small bowel, reducing the ability to absorb nutrients.
But it was never known whether the disease caused the changes in gut bacteria or the other way around.
"It's one of the first studies to show what is the chicken and what is the egg," said Butzner, who is also chair of the professional advisory council of the Canadian Celiac Association. "It certainly gives us a much stronger impression that (by) altering the microbiota of the small intestine, you may be able to increase or decrease risk of getting celiac disease."
The study published Oct. 8 in the American Journal of Pathology compared immune responses and pathology in three groups of mice with different gut bacteria. All had the human DQ8 gene making them susceptible to celiac disease.
They found the inflammatory response to gluten was affected by the microbiota.
Today, these two trendy fields are colliding head-on. Working independently, two teams of scientists have shown that gut microbes—at least in mice—can dramatically affect the immune system's ability to deal with cancer. These microbes affect an individual's natural immunity to cancer, and how well they respond to immunotherapy drugs. And certain species of bacteria are especially potent at driving anti-tumor immunity, suggesting new ways of making new cancer drugs that much more potent.
ate:
November 19, 2015
Source:
Weizmann Institute of Science
Summary:
Scientists have released new results underscoring the importance of a personalized diet, prepared based on complex factors such as your gut microbes and lifestyle. Surprisingly, the foods that raise blood sugar levels differ dramatically from person to person.
Which is more likely to raise blood sugar levels: sushi or ice cream? According to a Weizmann Institute of Science study reported in the November 19 issue of the journal Cell, the answer varies from one person to another. The study, which continuously monitored blood sugar levels in 800 people for a week, revealed that the bodily response to all foods was highly individual.[/color]
[color=#0000FF]The study was unique in its scale and in the inclusion of the analysis of gut microbes, collectively known as the microbiome, which had recently been shown to play an important role in human health and disease. Study participants were outfitted with small monitors that continuously measured their blood sugar levels and were asked to record everything they ate, as well as such lifestyle factors as sleep and physical activity. Overall, the researchers assessed the responses of different people to more than 46,000 meals.
The scientists were able to show that lifestyle also mattered: The same food affected blood sugar levels differently in the same person, depending, for example, on whether its consumption had been preceded by exercise or sleep.
For example, a large number of the participants' blood sugar levels rose sharply after they consumed a standardized glucose meal, but in many others, blood glucose levels rose sharply after they ate white bread, but not after glucose. "
The GI theory goes that there are many different types of carbs and they can be graded into how rapidly the body converts them into glucose. The faster the burn rate, the higher the index and the more rapid the rise in blood sugar. This surge in blood sugar also triggers a rise in insulin and the combination of these events if sustained over time is believed to lead to unhealthy metabolic changes leading eventually to obesity and diabetes.
This nutritional dogma has been the backbone of the advice to avoid eating high GI foods such as pasta, rice and potatoes and replace them with low GI alternatives such as beans or lentils. In many cases people give up carbs completely or avoid refined carbs and instead go for approaches like the Atkins Diet. This cutting down on “bad” carbs also sounds like common sense and most doctors, health professionals and members of the public, including myself when I started writing my book The Diet Myth, assume that proper scientific and clinical trials have been carried out that back up these ideas. But what if none of it were true and we had been misled?
We all have around 100 trillion bacteria mainly living in our colons (outnumbering our cells by ten to one) and unlike our genetic code, which is 99.9% similar across individuals, we probably only share less than 20% of our microbes on average.
Our gut microbes live off the fibre in foods that make it to the lower part of the intestines. The researchers found that the highly variable microbial profile in the guts of the volunteers determined how quickly the food was broken down and the rate at which glucose appeared in the blood. This was a much stronger effect than the type of carb being eaten. Some people could eat potatoes without any surge in blood sugar and others with the wrong set of microbes just had to look at one and their blood levels peaked.
Unlike our genes, our microbes are to some extent changeable. The team went on to successfully modify the diets of the subjects with the worst looking profiles.
color=#FF00BF]The cheaper forms of olive oil (those labelled regular or virgin) didn’t show any benefit – it had to be extra virgin. The difference between the grades of oil lies not just in the lower acidity, freshness and richer taste but in the number of chemicals released called polyphenols. High grade extra virgin oil, especially if cold extracted, has around 30 polyphenols that act as antioxidants, which reduce inflammation and also help reduce the effects of aging particularly on the heart and brain.
Until recently it was thought these antioxidant polyphenols acted directly on genes and blood vessels. But it turns out that they also work via our gut microbes that make up our microbiome. This is the community of trillions of diverse bacteria which live in our large intestine. They feed off the different polyphenols and produce other small chemicals (short chain fatty acids) that dampen down inflammation and help our immune system.
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The more bugs the better
Complex high fat foods such as extra virgin olive oil, when eaten with a wide variety of other healthy polyphenol-dense foods, provide the basis for a rich and diverse community of gut microbes. This diversity is increasingly being shown to be important for our health. The original PREDIMED study didn’t measure gut microbes directly (although subsequent research is doing so) but the striking benefits of the Mediterranean diet and particularly extra virgin olive oil are that they are superb gut microbe fertilisers and improve gut health.
IT is now well established that our health depends on the interaction between gut bacteria and the immune system. It has been suggested that the rich diversity of bacteria in our gut is the result of the two systems co-evolving and working on each other. Now, a new study provides evidence for one side of the theory - that the immune system influences the evolution of gut bacteria.
The study, from the Instituto Gulbenkian de Ciência (IGC) in Portugal, is published in the journal Nature Communications.
From experiments with lab mice, the IGC researchers discovered that when the immune system is defective, the mix of gut bacteria changes, as does the pace and the manner in which they adapt - however, it is not easy to predict what these ways are.
The team suggests their findings support the idea that treatments for immune-related intestinal disorders - such as inflammatory bowel disease (IBD) - should not be based on generalized but on personalized medicine, because this takes into account the unique composition of the individual's gut bacteria.
The gut is a complex, ever-changing environment that gut bacteria are highly responsive to. They need to adapt and evolve quickly, for example, just to cope with changes in the food we eat every day.
Mice exposed to the cold, they discovered, became 50% more efficient over the course of the study at absorbing nutrients from their food. Those held at room temperature, by contrast, showed no change in their digestive efficiency. The cold-dwelling mice also became 40% more sensitive to insulin, while those in the room-temperature enclosures did not. That suggested the mice in the chiller cabinets were not only extracting more value from their food, they were also becoming better at burning it, and thus generating heat.
Given its role in obesity, Dr Trajkovski suspected the gut microbiome might be playing a part is these unpredicted results. The team thus reran the experiments and sampled the animals’ gut floras. They also looked at the rodents’ intestinal walls, to see if the anatomy of these had changed in ways that would make it easier for them to absorb food.
The gut floras of the two groups were radically different. In particular, and intriguingly, the chilled mice lacked a species called Akkermansia muciniphila that is often absent from the guts of obese people—an absence that may be involved in their putting on extra weight.
The cold-dwelling mice also had different intestinal anatomy. Their villi, the tiny projections from the intestinal wall that absorb food into the body, were more than 50% longer than those of mice living at room temperature.
]Lewis and his colleagues collected stool samples from 38 adults, along with information about their age, sex, weight, and health status. Study participants, including members of the Cheyenne and Arapaho tribe and non-native people included for comparison, also completed a three-day food journal. The researchers characterized the microbial community using DNA sequencing and also evaluated the samples for 500 metabolites.
The findings showed that the American Indian participants shared microbiome features common to industrialized populations. However, the Cheyenne and Arapaho showed a reduced abundance of a bacterial genus, Faecalibacterium, a group known for its anti-inflammatory effects. The American Indians also showed a fecal metabolite profile similar to one described in people with metabolic disorders.
"This [metabolite] profile had similar features to those observed in clinical cases of inflammatory bowel disease," Lewis says. "At first, this may seem unsurprising because obesity and inflammatory disorders are known to be among the major health disparities observed within some American Indians groups. Yet, our study was not designed to target people with inflammatory disorders. Seeing this metabolite pattern in a non-clinically oriented research design was eye opening."
Lewis says that those differences will probably "come down to social practices and the built environment, rather than specific connections to a person's genetic ancestry." In other words, he thinks that the differences are more likely to be explained by environment and lifestyle factors than by ancestry and genetics.
The types of fatty acids in the diet may affect the severity and duration of flare-ups that people with multiple sclerosis and other autoimmune diseases experience.
This was the conclusion a team of neurology researchers reached after finding that the length of fatty acids they fed to a type of mouse bred for the study of multiple sclerosis (MS) changed the function of T-helper immune cells in the gut so as to either intensify or alleviate the symptoms of the autoimmune disease.
The researchers - from the Friedrich-Alexander-University Erlangen-Nuremberg and the Ruhr University Bochum, both in Germany - report their findings in the journal Immunity.
They compared the effect of long-chain fatty acids, most prevalent in the western diet, with that of short-chain fatty acids, which are typically found in fiber-rich diets and are only metabolized by gut bacteria.
The team found that medium- and long-chain fatty acids, such as lauric acid, triggered the growth and spread of proinflammation T cells from the intestinal wall to other parts of the body, including the brain, and led to worse symptoms in the MS mice.
In contrast, short-chain fatty acids - primarily in the form of propionic acid or its salt propionate - spurred the growth and release of regulatory T cells from the intestinal wall and reduced symptoms in the mice. These cells keep the immune system in check by regulating excessive inflammation responses and autoreactive immune cells.
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