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Gut-Alcohol-and-liver-diseaseScientists have discovered that some individuals harbour a #bacterium in their #gut that produces enough #alcohol to damage their #liver even without having drunk any alcohol. The link between the gut and non-alcoholic fatty liver disease (#NAFLD) was established when Drs were treating a patient who presented with severe non-alcoholic steatohepatitis (#NASH) and auto-brewery syndrome (#ABS), where an individual can become #drunk after eating sugary foods. This was despite consuming an alcohol-free diet. The individual had an ultra-high blood alcohol concentration (#BAC) which was found to have happened as a result of bacteria. The patient did recover after dietary changes and antibiotic treatment.

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Hidden in the stately steppes of gentle rice paddies, nestled in shiny clusters of red and purple palm fruit, lurking in tiny annatto seeds from the achiote tree… lies a quartet of potent anti-inflammatory, highly protective molecules called tocotrienols. They are cousins to the four tocopherols. Together, all eight comprise the Vitamin E family, a lipid-loving arsenal of molecules essential to health. Each has its own healing profile. According to molecular biochemist Chandan Sen, of Ohio State University, “Current studies of the biological functions of vitamin E continue to indicate that each member of the vitamin E family possesses unique biological functions often not shared by other family members.”[1]

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Hidden in the stately steppes of gentle rice paddies, lurking in shiny clusters of red and purple palm fruit, nestled in tiny annatto seeds from the achiote tree…lies a quartet of potent anti-inflammatory, highly protective molecules called tocotrienols. They are cousins to the four tocopherols. Together, all eight comprise the Vitamin E family, a lipid-loving arsenal of molecules essential to health. Each has its own healing profile. According to molecular biochemist Chandan Sen, of Ohio State University, “Current studies of the biological functions of vitamin E continue to indicate that each member of the vitamin E family possesses unique biological functions often not shared by other family members.”[1] 

By Michael Ash, BSc, DO, ND, F.DipIOn

One of my primary areas of research and expertise is the gut microbiota and its diverse impact on our health. Your liver receives nearly 70% of its blood supply from the intestine, and represents a first line of defence against gut-derived antigens. Intestinal bacteria—and the antigens they produce—play a key role in the maintenance of gut-liver axis health. Modulation of the gut microbiota to achieve and maintain symbiosis represents a new way to treat or prevent non-alcoholic fatty liver disease (NAFLD). Along with the concomitant use of tocotrienols and glycophospholipids, we may be starting to see the emergence of a truly profound intervention for a complex metabolic disease, using safe,natural compounds.

Dr Todd Born ND explores the increasingly common problem of NAFLD.

Nonalcoholic fatty liver disease (NAFLD) refers to the presence of hepatic steatosis when no other causes for secondary hepatic fat accumulation (eg, heavy alcohol consumption) are present.  NAFLD may progress to cirrhosis and is likely an important cause of cryptogenic cirrhosis.[1],[2]  NALFD is now the most common cause of abnormal liver biochemistry in North America and likely in the UK and is also known to be associated with some drugs, genetic defects, obesity, insulin resistance and type 2 diabetes.[3]

At first sight one may wonder why a paper published in the British Journal of Clinical Pharmacology is being highlighted on this web site.[1] Yet Dr Guiney and his colleagues have evolved a very elegant approach to complex metabolically relevant data collection using a simple, non-invasive test that should be celebrated as an example a combination of science, economics and human/animal care, sometimes assumed not to exist in large research establishments. This paper expanded on a previous study published in 2010.[2]

Neonatal Jaundice Linked to Autism

Wednesday, 20 October 2010 by

Many parents and clinicians are looking for clues often of a wild and speculative format to explain why their child may have developed autism, for whilst there appear to be a number of genes involved in autism, the genetic cause has yet to be convincingly supported, suggesting that there remains an environmental factor that influences an epigentic change that allows for relevant genes to be expressed.

A paper published in the journal Pediatrics[1] suggests a possible relationship between a clinically recognised early life condition and the development of ASD suggesting that this sensitive window – if exposed to the described neurological insult can act as an epigenetic activator with long term consequences.  In addition to the local neurological interaction, this study also pulled a large amount of data from Danish birth records and found two risk mitigators:

If the mother was primiparous (a woman who has given birth only once) and the birth dates were in between April and September – the risk of autism declined dramatically.

So what did they find: The researchers uncovered a complex interplay between endogenous liver function, frequency of pregnancy and time of conception/birth.

This paper looked at Jaundiced newborns  (caused by hyperbilirubinemia – increased levels of bilirubin in the blood) and found they had a remarkably close to 90% higher likelihood of subsequently having any psychological developmental disorder compared with comparable neonates without jaundice (HR 1.87, 95% CI 1.58 to 2.21, P=0.001)

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coverimageCompared with our ancestors, Western societies today lead a lifestyle that is much more sedentary, probably as a result of cultural changes stemming from modern socio-economic morays. Taking into account differences in body size, our energy expenditure per kilogram of body weight has been estimated to be <40% of that of our prehistoric ancestors.[1] Current estimates suggest that 7 out of 10 adults are inactive or lack adequate conditioning,[2] and this lack of adequate exercise, combined with dietary indiscretion, has contributed to the worldwide epidemic of obesity and non-alcoholic fatty liver disease (NAFLD). NAFLD, is now considered to be around 20–30% prevalence in Western countries.

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