Sunday 16 October 2016

COCOA COMPOUND IMPROVES CARDIOVASCULAR BIOMARKER

To the tantalizing delight of cocoa lovers everywhere, a number of recent studies employing various methods have suggested that compounds in cocoa called flavanols could benefit cardiovascular health. Now a systematic review and meta-analysis of 19 randomized controlled trials (RCTs) of cocoa consumption reveals some further pieces of supporting evidence.
The meta-analysis in the Journal of Nutrition, an assessment of the combined evidence from all 19 RCTs, focused on whether consumption of flavanol-rich cocoa products was associated with improvements in specific circulating biomarkers of cardiometabolic health as compared to consuming placebos with negligible cocoa flavanol content. In all, 1,139 volunteers were involved in these trials.
The studies found that cocoa flavanol intake may reduce dyslipidemia (elevated triglycerides), insulin resistance and systemic inflammation, which are all major subclinical risk factors for cardiometabolic diseases.

The greatest effects were seen among trial volunteers who ate between 200 and 600 milligrams of flavanols a day (based on their cocoa consumption). They saw significant declines in blood glucose and insulin, as well as another indicator of insulin resistance called HOMA-IR. They also saw an increase in HDL, or "good," cholesterol. Those consuming higher doses saw some of the insulin resistance benefits and a drop in triglycerides, but not a significant increase in HDL. Those with lower doses of flavanols only saw a significant HDL benefit.
There were benefits evident for both women and men and didn't depend on what physical form the flavanol-rich cocoa product was consumed in -- dark chocolate vs. a beverage, for example.
Source: Science daily.


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HIGH CHOLESTEROL LINKED TO ARTHRITIS

High cholesterol might harm more than our cardiovascular systems. New research using animal models, published online in The FASEB Journal, suggests that high cholesterol levels trigger mitochondrial oxidative stress on cartilage cells, causing them to die, and ultimately leading to the development of osteoarthritis. This research tested the potential therapeutic role of mitochondria targeting antioxidants in high-cholesterol-induced osteoarthritis and provided proof-of-concept for the use of mitochondrial targeting antioxidants to treat osteoarthritis.

To make this discovery, Prasadam and colleagues used two different animal models to mimic human hypercholesterolemia. The first was a mouse model that had an altered gene called ApoE-/- that made the animals hypercholesteremic. The other was a rat model, and the animals were fed a high-cholesterol diet, causing diet-induced hypercholesterolemia. Both models were fed a high-cholesterol diet or control normal diet, after which they underwent a surgery that mimics knee injuries in people and was designed to bring on osteoarthritis.
Both the mice and the rats that were subjected to surgery and fed with high-cholesterol diets showed more severe osteoarthritis development than seen in the normal diet group. However, when both the mice and the rats are were exposed to the cholesterol-lowering drug atorvastatin and mitochondrion-targeted antioxidants, the development of osteoarthritis was markedly decreased in relation to the untreated groups.

Source: Science daily
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