Again, I am writing on an information stumbled on recently. The thing is, once you start to look into a certain area, you realise as you go along, there are several interconnections.

As related last week, I have been looking at non alcoholic fatty liver disease (NAFLD). I saw a piece on the subject in the Medscape of November 11, 2014 by Nancy A. Melville titled “ Cognitive Deficits Linked to Non alcoholic Liver Disease”. Patients with non alcoholic fatty liver disease (NAFLD) show deficits in cognitive function even in the absence of cardiovascular disease risk factors. In a study of 5662 adults with moderate to severe hepatic steatosis (liver injury/inflammation occasioned by deposition of fat) showed that, in addition to its association with the cardiovascular risk factors that have been linked with cognitive impairment, NAFLD is also independently associated with the deficits. The results were presented at the American Neurological Association (ANA) 2014 Annual Meeting.

The patients evaluated were enrolled in the Third National Health and Nutritional Examination Survey (NHANES III). All patients were administered three cognitive function tests. These were the Simple Reaction Time Test (SRTT), the Symbol Digit Substitution Test (SDST), and the Serial Digit Learning Test (SDLT). The Simple Reaction Time Test (SRTT) measures the minimal time needed to respond to a stimulus. It is a basic measure of processing speed. The Symbol Digit Substitution Test (SDST) is sensitive to brain damage. It is a neuropsychological test sensitive to brain damage, dementia, age and depression. The test is not sensitive to the location of brain damage (except for damage comprising part of the visual field). The Serial Digit Learning is a supraspan learning task that involves repeated presentation of a sequence of either eight or nine digits.

After adjusting for factors including age, sex, race, body mass index, waist circumference, hypertension, diabetes, hypercholesterolemia, acute myocardial infarction, and stroke, the researchers found NAFLD to be associated with worse cognitive performance on the SRTT test, the SDST, and the SDLT. These adjustments were necessary because the listed conditions themselves in the main constitute risk factors for the development of NAFLD.

Additionally, patients with NAFLD showed associations between cognitive test results on the SDLD and liver enzymes, including alanine aminotransferase and aspartate aminotransferase. No association was seen between liver enzymes and cognitive function among patients without NAFLD. Considering the high prevalence of fatty liver disease, the implications of poorer cognitive function is significant. Over the past three decades, non alcoholic fatty liver disease (NAFLD) has gone from an obscure liver disorder to the most prominent chronic liver disease worldwide.1 2 NAFLD is a growing cause of end-stage liver disease and has been recognized as an aetiology of hepatocellular cancer (HCC), even in the absence of underlying cirrhosis.3 NAFLD is highly prevalent across nearly all continents and is geographically heterogeneous in its prevalence from country to country. In line with the worldwide increases in obesity and type 2 diabetes,5 6 in recent years, NAFLD has shown novel epidemics in both developed and developing countries. Understanding temporal trends in NAFLD prevalence is vital to better understanding its disease burden and preventing additional cases of NAFLD. Approximately 0.9 billion people suffered from NAFLD in 2017. What sets NAFLD apart from other common liver diseases is the sheer number of patients worldwide. Unfortunately, we also observed increasing trends in NAFLD prevalence globally. Consequently, the complications and sequelae of NAFLD might also be on the rise.

One potential pathway for the link between NAFLD and cognitive decline is with the pivotal role of the liver for the metabolism of many substances — and the subclinical inflammation that may therefore be present in the body.

The pathogenesis of NAFLD and NASH is a quite complex process involving multiple pathways and risk factors, first of all being diet imbalances. The progressive lipid deposition in the liver leads to the alteration of lipid metabolism/lipid peroxidation, insulin resistance, oxidative stress, and inflammatory damage. This promotes a state of peripheral insulin resistance and low-grade systemic inflammation. For this reason, an increasing amount of evidence suggests that NAFLD and NASH not only affect liver function, but also induce multiple extrahepatic manifestations that also involve the central nervous system, e.g., depression, cognitive impairment, Alzheimers disease (AD), and dementia. There is also a link between upset in gut microbes as a result of NAFLD and cognitive dysfunctions. The detrimental stimuli that lead to NAFLD and NASH in the liver could induce cognitive impairment or

AD-type neurodegeneration in the brain. Many signaling pathways are demonstrated to be altered in both NAFLD/NASH and CNS dysfunction (depression, cognitive impairment, dementia, and AD), suggesting that these diseases share similar pathogenetic mechanisms.

There is increasing search for treatment options for the management of NAFLD/NASH. Notwithstanding these efforts, diet, weight loss and increased

physical activity are time tested options. The take home message is that what you eat (and your lifestyle) not only impacts the liver. It has consequences on your gut flora and among others even how your brain functions.

Until then, daily/regularly consume polyphenol-rich cocoa. It is beneficial in NAFLD.





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