Fungi in gut linked to higher Alzheimer's risk can be reduced through ketogenic diet

 What EXACTLY is your doctor doing to prevent Alzheimers? No excuses.

Fungi in gut linked to higher Alzheimer's risk can be reduced through ketogenic diet

Date:

August 31, 2020

Source:

Wake Forest Baptist Medical Center

Summary:

Specific fungi in the gut associated with a higher risk of Alzheimer's disease and found in people with mild cognitive impairment (MCI) can be altered in a beneficial manner by eating a modified Mediterranean diet, researchers have found.

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Specific fungi in the gut associated with a higher risk of Alzheimer's disease and found in people with mild cognitive impairment (MCI) can be altered in a beneficial manner by eating a modified Mediterranean diet, researchers at Wake Forest School of Medicine have found.

The small study is published in the current online edition of the journal EBioMedicine.

"Our study reveals that unique fungi co-living with bacteria in the gut of patients with MCI can be modulated through a Mediterranean ketogenic diet," said principal investigator Hariom Yadav, assistant professor of molecular medicine at Wake Forest School of Medicine, part of Wake Forest Baptist Health.

In the single-center, randomized, double-blind crossover pilot study, Yadav's team identified the organisms in the gut microbiome by sequencing the fungal rRNA ITS1 gene in 17 older adults (11 with diagnosed MCI and six with normal cognition) before and after a six-week intervention of a modified Mediterranean ketogenic diet or the American Heart Association Diet to determine its correlation with Alzheimer's markers in cerebrospinal fluid and gut bacteria.

"Although we do not fully understand how these fungi contribute to Alzheimer's disease, this is the first study of its kind to reveal their role in our mental health, which we hope will ignite thinking in the scientific community to develop better understanding of them in relation to Alzheimer's disease," Yadav said. "It also indicates that dietary habits such as eating a ketogenic diet can reduce harmful fungi in the gut which might help in reducing Alzheimer's disease processes in the brain."

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Story Source:

Materials provided by Wake Forest Baptist Medical Center. Note: Content may be edited for style and length.

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Journal Reference:

1. Ravinder Nagpal, Bryan J. Neth, Shaohua Wang, Sidharth P. Mishra, Suzanne Craft, Hariom Yadav. Gut mycobiome and its interaction with diet, gut bacteria and alzheimer's disease markers in subjects with mild cognitive impairment: A pilot study. EBioMedicine, 2020; 59: 102950 DOI: 10.1016/j.ebiom.2020.102950

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Wake Forest Baptist Medical Center. "Fungi in gut linked to higher Alzheimer's risk can be reduced through ketogenic diet." ScienceDaily. ScienceDaily, 31 August 2020. <www.sciencedaily.com/releases/2020/08/200831131633.htm>.

 

Disputed theory on Parkinson's origin strengthened

I wish we had some good news on stroke at least once a year.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=146158&CultureCode=en
Parkinson's disease may start in the gut
Parkinson's disease is strongly linked to the degeneration of the brain’s movement center. In the last decade, the question of where the disease begins has led researchers to a different part of the human anatomy. In 2003, the German neuropathologist Heiko Braak presented a theory suggesting that the disease begins in the gut and spreads to the brain. The idea has since, despite vocal critics, gained a lot of ground. Researchers at Lund University in Sweden now present the first direct evidence that the disease can actually migrate from the gut to the brain.
The so-called Braak’s hypothesis proposes that the disease process begins in the digestive tract and in the brain's center of smell. The theory is supported by the fact that symptoms associated with digestion and smell occur very early on in the disease.
Researchers at Lund University have previously mapped the spread of Parkinson’s in the brain. The disease progression is believed to be driven by a misfolded protein that clumps together and "infects" neighboring cells. Professor Jia-Yi Li's research team has now been able to track this process further, from the gut to the brain in rat models. The experiment shows how the toxic protein, alpha-synuclein, is transported from one cell to another before ultimately reaching the brain’s movement center, giving rise to the characteristic movement disorders in Parkinson’s disease.
“We have now been able to prove that the disease process actually can travel from the peripheral nervous system to the central nervous system, in this case from the wall of the gut to the brain. In the longer term, this may give us new therapeutic targets to try to slow or stop the disease at an earlier stage”, says Professor Jia-Yi Li, research group leader for Neural Plasticity and Repair at Lund University.
The research team will now carry out further studies in which the mechanisms behind the transport of the harmful protein will be examined in detail. The current study suggests that the protein is transferred during nerve cell communication. It is at this point of interaction that the researchers want to intervene in order to put a stop to the further spread of the disease.
http://link.springer.com/article/10.1007/s00401-014-1343-6

Disappearing Bacterium May Protect Against Stroke

Do you really think your doctor subscribes to the journal, Gut? What did they learn from this knowledge? Any way to reduce stroke risk?
http://www.sciencedaily.com/releases/2013/01/130109080825.htm
A new study by NYU School of Medicine researchers reveals that an especially virulent strain of the gut bacterium Helicobacter pylori (H. pylori) isn't implicated in the overall death rate of the U.S. population, and may even protect against stroke and some cancers. The findings, based a nationwide health survey of nearly 10,000 individuals over a period of some 12 years, are published online, January 9, in the journal Gut.

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Those individuals carrying the most virulent strain of H. pylori, the study found, had a 55 percent reduced risk of deaths from stroke compared with their counterparts who were not infected with H. pylori. Participants with the most virulent strain also had a 45 percent reduced risk of death from lung cancer.
These surprising findings emerged from an analysis by Yu Chen, PhD, MPH, associate professor of population health and environmental medicine, and Martin J. Blaser, MD, professor of internal medicine and professor of microbiology, of individuals who participated in a national survey designed to assess the health and nutritional status of adults and children in the United States. Previous studies by Dr. Blaser have confirmed the bacterium's link to gastric diseases ranging from gastritis to stomach cancer. He and Dr. Chen have more recently shown that H. pylori may protect against childhood asthma. The most virulent H. pylori strains have a gene called cagA.
"The significance of this study is that this is a prospective cohort of participants representative of the U.S. population with a long follow-up," says Dr. Chen. "We studied both the overall H. pylori as well as cagA strain of H. pylori, which is more interactive with the human body. We found that H. pylori is not related to the risk of death from all causes, despite it being related to increased risk of death from gastric cancer."
"This finding confirms earlier work, however, that gastric cancers are now uncommon in the United States," says Dr. Chen. "We also found that H. pylori was related to a reduced risk of stroke and lung cancer, and these effects were stronger for the cagA strain, suggesting its mixed role in human health," she says.
H. pylori, an ancient bacterium, lives in the mucous layer lining the stomach where, until recently, it survived for decades. More than half of the world's population harbor H. pylori in their upper gastrointestinal tract. Mainly transmitted in families, the bacterium is usually acquired before age 10. In developing countries H. pylori is still prevalent, but is vanishing in the developed world thanks to better sanitation and widespread use of antibiotics.
To better understand the relationship between H. pylori and the overall death rate, or all-cause mortality, the researchers analyzed data from 9,895 participants in the National Health and Nutrition Surveys (NHANES III), enrolled from 1988 to 1994. Test results for H. pylori and cagA were available on 7,384 subjects at the time of enrollment, and participants were followed until 2000.
There was no association of either H. pylori-positivity or cagA-positivity with all-cause mortality in the population, the researchers found. Participants with and without H. pylori experienced a similar risk of death from all causes. Consistent with past reports, a strong association was observed between H. pylori and gastric cancer mortality, according to the study. Individuals who were H. pylori positive were 40 times more likely to die from gastric cancer. The study also found that participants with cagA-positivity had a 55 percent reduced risk of deaths from stroke compared with their counterparts who were H. pylori negative/ cagA-negative. Participants with cagA-positivity also had a 45 percent reduced risk of deaths from lung cancer.
"The most interesting finding was that there is a strong inverse association with stroke which could be protective," says Dr. Blaser. "There is some precedent for this and it is possible that the same cells (T reg cells) that H. pylori induces that protect against childhood asthma could be the protective agents, however, the findings need to be confirmed."