Studies show this BRAIN FOOD builds cognitive reserve and brain plasticity, enhancing cognitive function and protecting against dementia and stroke.

What’s even more surprising is that you don’t need a pharmaceutical supplier, but you can produce this amazing chemical right in your own natural bioreactor, known as your colon or large intestine.

(“Butyrate, neuroepigenetics and the gut microbiome: Can a high fiber diet improve brain health?” Neuroscience Letters 2016; vol 625: 56-63).

As scientific interest in the microorganisms that live in our gut and known as our microbiome, has grown in recent years, attention has become focused on the impact of our diet on chronic disease and longevity including its effect on our brain.

Convincing evidence based on published university studies now demonstrates that butyrate, a short chain fatty acid (SCFA) produced by bacterial metabolism (fermentation) of certain fibre in the colon, can enhance cognitive function and prevent neurodegeneration and promote brain plasticity. Similarly, butyrate is able to reduce the infarct size in models of ischemic stroke, limiting damage to the brain and improving behavioural outcomes.

The prospect of accomplishing this goal of fully-functional, disease-free longevity with a single, naturally occurring small molecule, as shown in the following diagram, is exciting.

The epigenetic effects of butyrate: potential therapeutic implications for clinical practice

Roberto Berni Canani1,2*, Margherita Di Costanzo1 and Ludovica Leone1

Source: Bernini Canani et al Clinical Epigenetics 2012; Vol 4:4

Abstract

Butyrate is a short chain fatty acid derived from the microbial fermentation of dietary fibers in the colon. In the last decade, multiple beneficial effects of butyrate at intestinal and extra intestinal level have been demonstrated. Thmechanisms of action of butyrate are different and many of these involve an epigenetic regulation of gene expression through the inhibition of histone deacetylase. There is a growing interest in butyrate because its impact on epigenetic mechanisms will lead to more specific and efficacious therapeutic strategies for the prevention and treatment of different diseases ranging from genetic/metabolic conditions to neurological degenerative disorders. This review is focused on recent data regarding the epigenetic effects of butyrate with potential clinical implications in human medicine

Brain BDNF Expression May Explain Cognitive Reserve

Pauline Anderson Medscape January 27,2016

High expression of brain-derived neurotrophic factor (BDNF) may help to explain why some patients with Alzheimer’s disease (AD) pathology (ie. Senile plaques and neurofibrillary tangles) don’t exhibit cognitive decline.

A new study showed not only that high levels of brain BDNF expression were independently associated with slower rates of cognitive decline but also that the relationship was strongest among patients with the most AD pathology.

The results suggest that boosting BDNF expression may be a therapeutic strategy to preserve cognition.

“This is a major big deal”, said lead author Aron S. Buchman , MD, Professor Neurological Sciences, Rush University Medical Center and Rush Alzheimer’s Disease Center, Chicago Illinois.

Having a protein “to go after” is much better than telling patients to pursue higher education or have a purpose in life – two factors linked to slower cognitive decline, said Dr Buchman. “I don’t know what the construct is for ‘purpose in life’, and I wouldn’t know how to translate that into clinical treatment, but this is something that investigators can get a hold of and look at”.

The study was published online January 27 in Neurology.

BDNF, which is encoded by the BDNF gene, is a member of the neurotrophic family of growth factors. It is expressed in areas of the brain, including the hippocampus, cortex and basal forebrain (areas of brain learning and memory), and in periphery tissues such as kidneys, prostate, blood, and saliva.

The study included 535 persons from two clinical autopsy studies – the Religious Order Study and the Rush Memory and Aging Project – whose mean age at death was 88.5 years. They had been examined annually for an average of 6.3 years, but some for up to 20 years, and agreed to a brain autopsy upon death.

This lengthy follow-up period before death makes the study “unique”, commented Dr Buchman.

During the annual clinical examinations researchers assessed global cognition and five cognitive components: episodic memory, semantic memory, working memory, visual spatial skills, and perceptual speed.

From the autopsies, investigators measured BDNF expression in tissue taken from the gray matter of the dorsal prefrontal cortex.

The study showed that high BDNF expression was associated with a slower rate of cognitive decline. The rate was reduced by almost half (48.3%) in persons with the highest level (90th percentile) of BDNF expression compared with the lowest (10th percentile). Levels of BDNF expression showed an independent association with cognitive decline after adjustment for age, sex, education, and neuropathologies.

“This means that there’s another pathway linking BDNF with cognitive decline that doesn’t have to do with the pathology”, said Dr Buchman.

The study also showed that those with the most AD pathology who had high BDNF expression levels, had rates of cognitive decline that were about 40% slower than those with the same degree of AD pathology but had low levels of BDNF expression.

Cognitive Reserve

Researchers have long wondered why some patients with AD pathology had normal cognition until they died. If amyloid or tau tangles cause cognitive decline, there must be something that’s preventing these people from becoming demented.

“This led the field to hypothesize that there are factors that provide neural reserve or cognitive reserve or resilience factors that protect against the deleterious effects of the pathology” said Dr Buchman. Over the years, researchers have learned that acquiring higher education, having a purpose in life, and being physically and socially active are among these protective factors.

But these aren’t that easy to translate into clinical recommendations, especially for a 75 – or 80-year-old. Zeroing in on BDNF may offer another more practical way to get this protection. These new results could take the focus off traditional approaches of developing strategies or drugs to stop the production of amyloid plaques or tangles, or to remove these pathologies once they develop. “What this study is saying is that we have now identified a protein (BDNF) that suggests an alternative’, said Dr Buchman.

In an accompanying editorial, Michael Schnaider Been MD, Department of Psychiatry, The Icahn School of Medicine at Mount Sinai, New York and Joshua Sonnen MD Department of Pathology, University of Utah, Salt Lake City, said the study results promote the idea that increasing BDNF gene expression ”might be a reasonable therapeutic strategy for AD in humans”.

Increasing BDNF Levels Safely and Naturally – The NEUROLEX Epigenetic Diet

The two evidence-based avenues available which are known to increase levels of BDNF are; (i) regular exercise, and (ii) diet, and it’s here we turn again to the diagram illustrated in page 2 above,

You will notice that those fibres which escape digestion in the upper GI tract, passing directly to the large intestine are metabolised by health-promoting resident gut bacteria producing butyrate as a principal metabolite, and it’s this colon-produced chemical, which then converts to sodium butyrate, that as a histone deacetylation inhibitor (HDACi) and BDNF promoter is responsible for these key wide-ranging epigenetic gene-regulating chemo-protective and therapeutic effects in almost all chronic age-related diseases and conditions..

The two ways which are known to increase the body’s production of BDNF are (i) regular moderate exercise, and (ii) sodium butyrate. (“Exercise and Sodium Butyrate transform a Subthreshold Learning Event into Long-Term Memory via a Brain-Derived Neurotrophic Factor (BDNF) – Dependent Mechanism” Neuropsychpharmacology 2013; vol 38: 2027-2034).

Published research demonstrates that increasing serum levels of BDNF Reduces significantly the stroke risk (“Serum Brain-Derived Neurotrophic Factor and Vascular Endothelial Growth Factor Levels Are Associated With Risk of Stroke and Vascular Brain Injury. Framingham Study” Stroke 2013; vol 44: 2768-2775).

Over a decade of intensive research by the Australian medical research Neurolex company has led to development of a 100% natural, safe, drug-free soluble vegetable fibre modified for enhanced butyrate yield, protected by current patent applications. The gene-regulating disease chemopreventive and therapeutic, BDNF – enhancing evidence-based mechanisms of this fibre, although extremely complex and multifactorial are supported by a robust body of many thousands of published animal a

nd human studies. Our Research Director Dr Maxell Strong PhD, himself a long-term fully-recovered stroke survivor, is happy to share this science with Medical Practitioners, Specialists, Researchers and others interested, and[VS1] can be contacted at any time (Email: maxwellstrongresearch@gmail.com or Mob 0418 413657)

www.neurolex.com.au

BRAIN FOOD builds cognitive reserve

NEUROLEX PTY LTD

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