The Health October 2022 | Page 24

What we eat , or rather what we don ’ t , is key to remaining healthy

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THE HEALTH | OCTOBER , 2022

| Column |

BRAIN BITES
BY DR WAEL MY MOHAMED

RESEARCHERS have identified a route that begins in the stomach and terminates in the brain with a pro-inflammatory protein that seems to contribute to the formation and progression of Alzheimer ’ s disease .

The Neuroscience Centre and the Departments of Cell Biology and Anatomy , Neurology , and Ophthalmology at LSU Health New Orleans , overseen by Dr Yuhai Zhao and Dr Walter J . Lukiw , present for the first time a route that starts in the stomach and ends with a strong pro-inflammatory toxin in brain cells , which contributes to the onset of Alzheimer ’ s disease ( AD ). They also provide a simple solution for avoiding it . The results were reported in Frontiers in Neurology .
The researchers revealed evidence that BF-LPS is formed by a molecule containing an extremely strong neurotoxin ( lipopolysaccharide or LPS ) synthesised by Gram-negative bacteria bacteroides fragilis in the human gastrointestinal ( GI ) tract . LPSs are the most powerful pro-inflammatory neurotoxic glycolipids known to be generated by microorganisms .
In this work , the researchers describe the BF-LPS route from the stomach to the brain and its subsequent mechanisms of action . BF-LPS seeps via the gastrointestinal tract , circulatory system , and brain compartments .
Intake of dietary fibre
Then it produces inflammation in brain cells and inhibits the cell integrity-promoting protein neurofilament light ( NF-L ). In Alzheimer ’ s disease neurons , a deficiency of this protein leads to progressive neuronal cell shrinkage and , finally , cell death . They also believe that sufficient fibre consumption might arrest the process .
This newly identified pathogenic circuit has three distinct characteristics . Because the AD-stimulating pathway originates inside us — in the microbiota of our GI tract — it is “ locally sourced ” and active throughout our lives . BF-LPS is a natural result of microbial metabolism in the gastrointestinal system .
Intake of dietary fibre may alter the microbiome abundance of bacteroides fragilis , the source of the neurotoxic BF-LPS . In other words , dietary-based approaches to microorganism balance in the microbiome may be an attractive method for altering the abundance , speciation , and complexity of enterotoxigenic forms of AD-relevant microbes and their

Eating your way to good health

What we eat , or rather what we don ’ t , is key to remaining healthy

potential for pathological discharge of highly neurotoxic microbial-derived secretions , such as BF-LPS and other LPS .
According to the researchers , a better understanding of the interaction between the GI tractcentral nervous system axis and the GI-tract microbiome and Alzheimer ’ s disease could lead to new diagnostic and therapeutic approaches for the clinical management of Alzheimer ’ s disease and other fatal , progressive , and age-related neurodegenerative disorders .
It is estimated that the average American eats between 10 and 15 grams of fibre each day . The USDA recommends that women under 50 consume 25 grams of fibre daily , while men should get 38 grams .
Those women and men above 50 should consume 21 grams and 30 grams of fibre per day , respectively . According to the National Institutes of Health , Alzheimer ’ s is the most prevalent diagnosis for dementia patients and the sixth highest cause of mortality in the United States . The frequency of Alzheimer ’ s disease is projected to climb to 13.8 million by 2050 , from an estimated 5.8 million Americans aged 65 and older .
Faecal implants : Futile or future ? Alzheimer ’ s mouse models exhibited
Dr Wael MY Mohamed is with the Department of Basic Medical Science , Kulliyyah of Medicine , International Islamic University Malaysia ( IIUM ). behavioural and cognitive changes after faecal implant manipulation of the gut flora . According to the researchers , the findings might contribute to developing anti-dementia medications using probiotics and faecal transplants .
In a mouse model of Alzheimer ’ s disease , new research reveals a causal relationship between changes in the gut microbiota and behavioural and cognitive deficits for the first time . The study , published in the journal Frontiers in Behavioural Neuroscience , shows new avenues for employing probiotics to treat and prevent dementia symptoms associated with neurodegenerative diseases like Alzheimer ’ s .
In the most recent work , researchers modified the digestive systems of mice using faecal implants . They found behavioural and cognitive differences between three genotypes and men and women .
Two implicated genotypes were associated with an elevated risk of Alzheimer ’ s disease in adulthood . Alterations in the gut microbiota were revealed to have a demonstrated effect on behavioural and cognitive changes in mice .
Both probiotics and faecal transplants , which have previously been used to change the gut microbiome in people , may be effective in preventing dementia via targeted administration . Since the relationship between these effects and the gut microbiota is affected by genotype and sex , much more research is required to establish the mechanism of these behavioural and cognitive consequences .
Probiotics are available overthe-counter , but each patient must receive the correct and beneficial treatment . The microbiota of the gut is a complex ecology . Choose a probiotic that enhances brain health and function for each patient while minimising unpleasant side effects .
Finally , are we really what we eat ?... Because real people deserve real food . – The Health