Green tea beneficial for more than just obesity

Green Tea has once again been found as the Hail Mary for not just obesity but various other inflammatory biomarkers linked with poor health, finds a recent study.

The study was done on mice to find out what other benefits can green tea actually provide.

The researchers found that the mice were fed a diet of 2 % green tea extract fared better than those that are a diet without it, a finding that has prompted an upcoming study of green tea's potential benefits in people at high risk of diabetes and heart diseases.

The benefits were seen in the new study appear to stem from improved gut health, including more beneficial microbes in the intestines of the mice and less permeability in the intestinal wall which is commonly called as the leaky gut.

The results of studies looking at obesity management so far had been a real mixed bag.

Some seem to support green tea for weight loss, but a lot of other research had shown no effect, likely due to the complexity of the diet relative to a number of lifestyle factors. Our goal was to figure out how it revents weight gain, said the study's lead author.

The researchers devised an experiment that examined green tea's effects in male mice fed a normal diet and a high-fat diet designed to cause obesity. ( Female mice are resistant to diet-induced obesity and insulin resistance, a precursor to diabetes, so they weren't included).

For 8 weeks, half of the mice ate a high-fat diet designed to lead to obesity and half were fed a regular diet. In each of those groups, half ate green tea extract mixed in with their food.

After that, they measured body and fat tissue weight, insulin resistance, leaky gut syndrome and the inflammation of the fat tissue and intestines.

The mice fed a high-aft diet supplemented with green tea gained about 20% less weight and had lower insulin resistance than mice fed an otherwise identical diet without tea.

Those mice also had less inflammation within fat tissue and the intestine. Furthermore, the green tea appeared to protect against the movement of endotoxin, the toxic bacterial componenet, out of their guts and into the bloodstream.

Plus, the researchers found evidence of stronger-less " leaky" guts in these mice. Leaky gut is a problem in humans that contribute to widespread low-grade inflammation and has been implicated in a number of health problems.

The researchers also found that the green tea appeared to contribute to a healthier microbial community in the guts of the mice fed a high-fat diet. Mice fed the normal, or low-fat diet supplemented with green tea also had benefits including reduced weight gain and lower endotoxin levels and markers of leaky gut, but these were relatively  modest compared with the effects were seen in mice fed the high-fat diet.

10 cups a day is the amount of tea equivalent to what the mice were fed by the researchers.

The researchers are planning to experiment on human next and explore the effects of green tea on leaky gut in people with metabolic syndrome, a condition that pre-disposes people to type 2 diabetes and heart disease.

Green tea had a rich history in Asian countries and has been increasingly embraced in the West, in part for its potential health benefits. Catechins, anti-inflammatory polyphenols found in green tea, have been linked to anti-cancer activity and lower risk of heart and live disease.

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Researchers Find Gut Bacteria Can Trigger Brain Lesions That Lead to Strokes

In yet another study that has connected conditions in the gut to diseases of the brain, scientists have linked the cause of common blood vessel abnormalities in the brain to bacteria colonies in the stomach.

 These malformations can lead to strokes called cerebral cavernous malformations (CCMs), which don't leave patients with many options - if surgery can't be performed, there's little left but palliative care. But figuring out what causes these abnormalities could led to treatments that block them before they even occur.

 An international team led by researchers from the University of Pennsylvania studied genetically engineered mice that were prone to developing vascular lesions in their brains.

 Earlier research had shown that inherited forms of the condition could be caused by mutations knocking out certain genes. These genes would normally suppress key signals affecting the growth of brain cells that made up the walls of the blood vessels.

 While this discovery provides a way of identifying those at risk of developing a CCM, there are currently no drugs that replace the role of the missing genes, so not a lot can be done.

 But since CCM varies significantly in individuals with these mutations, there is probably more to the story than just a few broken genes.

 Enter the mouse studies

By studying the two populations of genetically engineered mice over a number of generations, the researchers discovered individuals that appeared to be resistant to developing the lesions, even though they still carried one of the CCM mutations.

 Within this population of mostly resistant mice, a few pups continued to develop malformations. But, somewhat tellingly, these young mice also had abscesses in their abdomens caused by injections they had received during the research, hinting at a potential cause.

 To test if these infections played a role in the development of CCM, 16 'resistant' mice were inoculated with a live species of gram negative bacterium called  Bacteroides fragilis , which is normally found in the gut.

Of those, nine went on to develop vascular lesions and inflamed and abscessed spleens, suggesting that the bacteria had spread from the site of their infection to affect the growth of cells lining the brain's blood vessels.

Usually, gram negative bacteria such as B. fragilis affect the responses of cells in mammals such as humans and mice through a type of molecule on their outer membrane called a lipopolysaccharide (LPS),  or endotoxin.

To see if it was this molecule specifically causing the malformation, the team injected the endotoxin from the bacteria into mice engineered with the mutated genes, as well as into normal, non-engineered mice.

As suspected, those with a broken gene that made them susceptible to CCM developed vascular lesions in their brain, while the mice with functional versions of the genes didn't.

The cells lining the blood vessels form what's called the blood brain barrier, which usually prevents toxic materials such as endotoxins and bacterial cells from getting into our central nervous system.

Just how the endotoxins are affecting these cells is something of a mystery.

"This still needs to be investigated," one of the team, Jaesung Peter Choi, from the University of Sydney in Australia, told ScienceAlert.

"However, we think CCM formation is driven by activation of immune receptors on the luminal, blood side of the blood-brain barrier."

When these immune receptors, called TLR4, are activated by an endotoxin, the cells of the blood brain barrier are encouraged to grow abnormally. The relevant genes would usually prevent this malformation, but in the mice with mutated versions, there's nothing to halt the process.

 Importantly, differences in the TLR4 immune receptor in people could also account for some of the variations in the condition seen in people with CCM mutations.
 
Change a home, change a gut

Comparing CCM-susceptible mice raised in germ-free conditions with those raised in less sterile conditions demonstrated the bacteria in our environment play a key role in turning a mere mutation into a deadly disease.

 While it's possible that therapies could be developed to target the TLR4 immune receptor, the researchers suggest focusing on the microbiome of the gut instead.

"Manipulation of gut microbiome-host interactions is a more exciting potential strategy to treat a life-long disease such as CCM," the team writes in the report.

To test if they could use antibiotics to influence the development of lesions in mutated mice, the researchers bred several generations of mice while administering antibiotics to their mother, testing each generation for lesions and the number of bacteria in their gut.

Just as they'd found with their germ-free mice, a 96 percent drop in bacteria coincided with a similar decline in lesions.
 
Blasting our immune systems with antibiotics might not be a straight-forward solution, of course, and we also have to keep in mind potential differences between mice and humans.

We are also still learning just how complex our microbiota are, and the multitude of health conditions which are linked with the diversity of microorganisms in our digestive system.

Yet for a condition that currently has few treatments, doorways to new ways to prevent lesions in those who are already susceptible is no doubt a giant step forward.

This research has been published in Nature.

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