Yet another study on the benefits of coffee was just published in the Journal of Agricultural and Food Chemistry. This ones demonstrates how this salubrious beverage improves insulin function and fatty liver by reducing inflammation. The authors observe:

“Epidemiological surveys have demonstrated that habitual coffee consumption reduces the risk of type 2 diabetes. The aim of this work was to study the antidiabetic effect of coffee and caffeine in spontaneously diabetic KK-Ay mice.”

The mice were not taken to Starbucks for mini espresso shots, but were…

“…given regular drinking water (controls) or 2-fold diluted coffee for 5 weeks.”

The results were pretty amazing:

“Coffee ingestion ameliorated the development of hyperglycemia and improved insulin sensitivity. White adipose tissue mRNA levels of inflammatory cytokines (MCP-1, IL-6, and TNFα), adipose tissue MCP-1 concentration, and serum IL-6 concentration in the coffee group were lower than the control group. Moreover, coffee ingestion improved the fatty liver.”

The authors summed up their findings by stating:

“…coffee exerts a suppressive effect on hyperglycemia by improving insulin sensitivity, partly due to reducing inflammatory cytokine expression and improving fatty liver. Moreover, caffeine may be one of the effective antidiabetic compounds in coffee.”

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This is why the ubiquitous high-fructose corn syrup is such a disaster for public health. The authors of this study published in The Journal of Clinical Investigation note that “Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance.” When they examined the effect in humans they found that all the following were increased markedly in the subjects on fructose but not glucose: visceral adiposity (fat around the organs), plasma triglycerides, fat in the liver, small dense LDL, oxidized LDL, fasting glucose and fasting insulin. At the same time insulin sensitivity decreased in the subjects consuming fructose but not glucose. The authors conclude: “These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.” [DNL = de novo lipogenesis which means making fat from scratch in the liver.] An accompanying commentary in the same journal states: “In the event that any readers harbor some remaining skepticism, an unprecedented thorough analysis in close to 900,000 participants from almost 60 prospective studies was very recently published, proving beyond any possible doubt that progressive excess mortality is caused by increased body adiposity…Stanhope and colleagues provide major scientific progress by demonstrating marked differences in the metabolic effects of these two major sugars with respect to their ability to promote intraabdominal lipid deposition and hepatic lipid production, while shifting cholesterol metabolism in an unfavorable manner and diminishing insulin sensitivity in humans.” Public health is groaning under a burden of overweight/obesity; how much disease could we prevent just by cutting out most of the sweet drinks (including most fruit juices) for children and adults?

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