This cartoon video explains the gut microbiome. Here is another informative video on the gut microbiome.
Diet rapidly and reproducibly alters the human gut microbiome. Increases in the abundance and activity of Bilophila wadsworthia on the animal-based diet support a link between dietary fat, bile acids and the outgrowth of microorganisms capable of triggering inflammatory bowel disease6
Gut microbiome dysbiosis arises due to elevated levels of pathogenic or pro-inflammatory bacterial organisms that produce neurotoxins, accompanied by a reduction in protective or anti-inflammatory bacterial organisms that produce neurological compounds, including norepinephrine and tryptophan.
Major bacterial species of the GI tract, such as the abundant Gram-negative bacilli Bacteroides fragilis (B. fragilis) and Escherichia coli (E. coli), secrete a remarkably complex array of pro-inflammatory neurotoxins which, when released from the confines of the healthy GI tract, are pathogenic and highly detrimental to the homeostatic function of neurons in the central nervous system (CNS). Bacterial lipopolysaccharide (LPS) in brain lysates have been found in the hippocampus and superior temporal lobe neocortex of Alzheimer’s disease (AD) brains. Mean LPS levels varied from two-fold increases in the neocortex to three-fold increases in the hippocampus, AD over age-matched controls, however some samples from advanced AD hippocampal cases exhibited up to a 26-fold increase in LPS over age-matched controls.
Collinsella, common in those who eat a low-fiber diet, is associated with Alzheimer’s as well as Lewy Body Dementia, as discussed below. Collinsella, isn’t only associated with Alzheimer’s and the APOE variant but rheumatoid arthritis, atherosclerosis, and Type-2 diabetes as well.
A tally of 6 good gut bugs and 4 bad gut bugs suggest a whole-food, unprocessed, plant-based diet is neuroprotective.
A diverse, rich, gut microbiota may prevent diverticular disease.
This microbial imbalance can result in cognitive impairments, elevated levels of enterotoxins, lipopolysaccharides, trimethylamine N-oxide (TMAO), pro-inflammatory chemokines and cytokines, increased amyloid fiber deposition, as well as reduced anti-inflammatory chemokine and cytokine levels and short-chain fatty acid (SCFAs).
Intestinal inflammation for extended periods leads to disruption of blood-brain barrier (BBB) and the subsequent transfer of intestine-derived molecules to brain tissues through the vagus nerve.
Among the lifestyle factors that are associated with the metabolic syndrome, disruption of the circadian system, known as circadian dysrhythmia, is increasingly common. Disruption of the circadian system can alter microbiome communities and can perturb host metabolism, energy homeostasis and inflammatory pathways, which leads to the metabolic syndrome. This blog post may be applicable.
The gut microbiome may be key to avoiding Lewy Body Dementia (DLB)
There are three bacteria involved in DLB: Collinsella, Ruminococcus, and reduced levels of Bifidobacterium. Collinsella is increased by a low-fiber diet. Bifidobacterium is increased by a high-fiber diet. Some species of Ruminococcus are associated with Crohn’s disease and with inflammatory bowel disease. The researchers also found similarities between the gut bacteria involved in Parkinson’s disease and DLB. In both diseases, the bacteria. On the other hand, the bacteria that produce short-chain fatty acids (SCFA) in the gut decreased. Bifidobacterium increases brain-derived neurotrophic factor, a key protein that supports the growth, development and maintenance of neurons in the central and peripheral nervous systems.
The bacteria that produce short-chain fatty acids (SCFA) in the gut was decreased in DLB patients. “Decreases in SCFA-producing bacteria have been repeatedly reported in Parkinson’s disease, Alzheimer’s disease, and ALS,” explains Ohno. “This suggests that it is a common feature of neurodegenerative diseases.” SCFA are important because they produce regulatory T cells. These types of cells play a critical role in regulating the immune system by suppressing neuroinflammation.”
Proinflammatory gut microbiota might promote AD development through interaction with APOE. Collinsella (due to a low-fiber diet) has also been linked to Alzheimer’s.
Compared with young adults, the gut microbiota of centenarians exhibits higher microbial diversity, xenobiotics biodegradation and metabolism, oxidoreductases, and multiple species (the potential probiotics Lactobacillus, Akkermansia, the methanogenic Methanobrevibacter, gut butyrate-producing members Roseburia, and SCFA-producing species including Clostridiales, uncl Ruminococcaceae) known to be beneficial to host metabolism.
Centenarians’ microbiota differs functionally from that of young-old adults; for example, they produce more short-chain fatty acids. A higher relative abundance of Cristensenellaceae in centenarians than in young people has been observed in Italy, China and Korea This abundance is associated with human longevity in general and a normal body mass index and low risk of cardiometabolic disease. Furthermore, a high prevalence of Bifidobacterium longum and Eubacterium coprostanoligenes in the oldest-old group may lower the risk of this pathology.
The beneficial effects of butyrate on cancer, non-alcoholic fatty liver disease and inflammation are mediated through autophagy and apoptosis.
FOXO transcription factors are at the interface of crucial cellular processes, which regulate apoptosis, DNA repair, metabolism, oxidative stress resistance and longevity. Experimental drugs that activate FOXO can restore the functionality of geriatric stem cells, enabling an old muscle to activate regenerative processes that are typical of a young muscle.
Mediterranean diet ingredients such as olive oil, which are high in polyphenols, activate AMPK pathways. This partially stimulates autophagy by blocking the mTOR complex, which has age-protective benefits. A diet high in polyphenols causes the interaction of AMPK and sirtuins, which leads in the deacylation and inactivation of nuclear factor kappa B (NF-kB), which is probably crucial for the control of immune response and inflammation.
A dietary model rich in polyphenols or integration with polyphenol supplements can help to counteract the dysbiosis of the gut microbiota linked to age but, primarily, to modulate oxidative stress to improve intestinal permeability, which is closely associated with chronic activation of the inflammatory response .
The microbiome’s biochemical signals also regulate the growth and function of energy-producing mitochondria across many cell types, including those in fat, muscles, heart and the brain. When these cues are missing in ultraprocessed diets, mitochondria function less well, and their dysregulation has been linked to obesity, diabetes, Alzheimer’s disease, mood disorders and cancer.
Our bodies are designed to be in the fasted state 12-14 hours per day. Fasting does not begin for 5 hours after eating. Gut lining repair takes place in the fasted state.
Intermittent fasting can alter the composition of the human gut microbiome by increasing taxonomic diversity and promoting microbial remodeling. During fasting, a particular family of anaerobic bacteria called Lachnospiraceae is responsible for a process called butryogenesis in the gut, which has beneficial metabolic and anti-aging effects.
Intermittent fasting vs. irritable bowel syndrome.
A robust, diverse, gut microbiome may help one keep one’s marbles despite aging
The human microbiome has important roles in maintaining homeostasis, and disruption of microbial colonization of an infant has systemic effects that may influence health later in life, potentially promoting the development of autoimmunity, allergies, metabolic diseases, and even cancer.
Mucosal-associated invariant T cells (MAITs) protect the blood-brain barrier. Without those T cells, mice lost their marbles. MAIT cell production is connected to the bacteria in your gut microbiome. People who grew up in relatively sterile environments or took antibiotics frequently make fewer of them than people who grew up in more rural areas, where there is more exposure to beneficial bacteria. But everyone may improve their microbiota by changing their diet or living environment. This is just one more reason to pursue a natural and healthy lifestyle.
Akkermansia muciniphila is a key microbiome component to encourage. This highly referenced video shows how.
This study has discovered that plant protein keeps our gut bacteria happy, helping researchers better understand how to manage good gut health.
A healthy gut biome can be messed up with antibiotics. Antibiotics strong enough to kill off gut bacteria can also stop the growth of new brain cells in the hippocampus. The gut microbiome can be healed over a few weeks by consuming a fiber-rich diet. Taking probiotic pills at this time may do more harm than good.
In this cross-sectional study, β-diversity, a measure of gut microbial community composition, was statistically significantly associated with all measures of cognitive function. Alterations in the composition of the gut microbiome have been shown to independently cause an increase in risk of dementia, along with other traditional risk factors. The presence of microbiome-associated metabolites and bacterial products in the systemic circulation may increase, especially with the inflammatory process that can lead to dementia.
A healthy gut biome is essential to avoid brain fog.
Studies in two different animals show that proteins made by bacteria harbored in the gut may be an initiating factor in the disease process of Alzheimer’s disease, Parkinson’s disease and ALS.
Several studies have shown associations between gut microbial measures and neurological outcomes, including cognitive function and dementia. Mechanisms have not been fully established, but there is growing support for a role in microbiota-generated short-chain fatty acids.
Furthermore, they possess anti-inflammatory properties and prevent leaky gut and positively modulate host microbial ecosystems, and the presence of Ω-3 FAs, primarily DHAs, in brain lipids is thought to be important for maintaining brain structure and function as well as cognitive health.
Extrinsic and intrinsic factors including dietary habits can regulate the composition of the microbiota. Microbes release metabolites and microbiota-derived molecules to further trigger host-derived cytokines and inflammation in the central nervous system, which contribute greatly to the pathogenesis of host brain disorders such as pain, depression, anxiety, autism, Alzheimer’s diseases, Parkinson’s disease, and stroke.
Food patterns and dietary habits result in a change of brain physiology which can be explained by food-derived metabolites. Metabolites derived from food play important roles in the pathogenesis of brain-related diseases. Recent findings showed the food-derived metabolites include not only SCFAs but also phosphatidylcholine, trimethylamine oxide (TMAO), L-carnitine, glutamate, bile acids, lipids, and vitamins. The food derivatives and microbe-fermented small molecular metabolites are released by gut microbiota into the blood which interacts with the host and further contributes to a variety of disorders, including brain diseases.
A low to moderate protein intake is associated with a lower production of trimethylamine N-oxide (TMAO) and L. ruminococcus abundance. TMAO could induce brain aging and age-related cognitive dysfunction and aggravate the cerebral aging process.
Shown by a cohort of 89 people between 65 and 85 years of age: certain bacterial products of the intestinal microbiota are correlated with the quantity of amyloid plaques in the brain.
Gut health vs. lipopolysaccharides
Endotoxin is a lipopolysaccharide (LPS), constituting much of the outer membrane of gram-negative bacteria, present at high concentrations in gut, gums and skin and in other tissue during bacterial infection. Blood plasma levels of endotoxin are normally low, but are elevated during infections, gut inflammation, gum disease and neurodegenerative disease. Adding endotoxin at such levels to blood of healthy humans induces systemic inflammation and brain microglial activation.
High blood levels of lipopolysaccharides and certain short-chain fatty acids (acetate and valerate) were associated with both large amyloid deposits in the brain. Lipopolysaccharides, a protein located on the membrane of bacteria with pro-inflammatory properties, have been found in amyloid plaques and around vessels in the brains of people with Alzheimer’s disease. Conversely, high levels of another short-chain fatty acid, butyrate, were associated with less amyloid pathology.
Ω-3 fatty acids have been linked to improvements in the composition and diversity of the gut microbiome in middle-aged and elderly women, and the concurrent administration of Ω-3 fatty acids and probiotic strains provides amplified health benefits. Ω-3 fatty acids increase levels of lipopolysaccharide-suppressing bacteria (i.e., Bifidobacteria) while decreasing levels of lipopolysaccharide-producing bacteria (i.e., Enterobacteria); furthermore, they interact with the Firmicutes/Bacteroidetes ratio, increasing Lachnospiraceae taxa, and thus promoting the production of the SCFA butyrate. EPA and DHA have also been shown to positively influence the gut microbiota composition by supporting a lean phenotype.
The excessive intake of saturated fat and refined carbohydrates is typical of western diet, which also has a negative impact on cognitive functioning since high fat and sugar change intestine bacteria colonies and increase intestinal permeability and lower blood brain barrier. This develops a vulnerability to the influx of lipopolysaccharides from circulation to the brain, which results in cognitive dysfunction.
Bacteroides fragilis (gram negative) gut bacteria ➝ blood vessel lesions.
Bacteroides fragilis is also inflammatory (bad news).
Butyrate, a short-chain fatty acid, is increased by a diet rich in high-fiber plant-based foods such as wholegrains, vegetables, fruits, nuts/seeds and legumes. Soluble fiber is prebiotic. It prevents all-cause mortality.
The good gut bacteria such as bacteroides are in a battle with bad gut bacteria such as firmicutes. Soluble and insoluble fiber will give the good bacteria nutrients to win the war. Fiber also prevents leaky gut syndrome. Fiber will cause the good bacteria to produce spermidine.
Probiotics and prebiotics are best eaten, not taken as a pill. Probiotics will be of no benefit unless prebiotics are consumed as well. This means eating a whole-food, unprocessed, plant-based diet.
Spices such as turmeric, oregano, cumin, ginger, and cinnamon feature polyphenols that will benefit gut health.
Adding a daily ounce of peanuts or about a teaspoon of herbs and spices to your diet may affect the composition of gut bacteria, an indicator of overall health. Cocoa is also rich in polyphenols.
Healthy ageing correlates with microbiome diversity. There is some indication that curcumin is able to modulate gut microbial composition (i.e., biodiversity), reducing some negative consequences of aging.
I would like to thank you for the efforts youve put in writing this blog. I really hope to see the same high-grade blog posts from you in the future as well. In fact, your creative writing abilities has encouraged me to get my own website now 😉
Comments are closed.