“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.”

“Prevalence of chronic kidney disease (CKD) in people with diagnosed diabetes is known to be high, but little is known about the prevalence of CKD in those with undiagnosed diabetes or prediabetes. We aimed to estimate and compare the community prevalence of CKD among people with diagnosed diabetes, undiagnosed diabetes, prediabetes, or no diabetes.”

Their data paints a worrisome picture:

“Fully 39.6% of people with diagnosed and 41.7% with undiagnosed diabetes had CKD…Among those with CKD, 39.1% had undiagnosed or prediabetes.”

Remember dear reader that chronic kidney disease means that there has been an irretrievable loss of kidney tissue; this is beyond normal age-related changes. This is yet another important reason to confirm that your strategy for maintaining healthy insulin function is suiting your needs. This is not difficult to determine with the right test assessment. The authors conclude:

“CKD prevalence is high among people with undiagnosed diabetes and prediabetes. These individuals might benefit from interventions aimed at preventing development and/or progression of both CKD and diabetes.”

“Aim: To compare population-based rates of all-cause and cardiovascular (CV) mortality in newly treated patients with type 2 diabetes according to levels of insulin exposure.”

The authors collected data for 12,272 individuals on cumulative insulin exposure and its correlation with death from cardiovascular diseases and death from any disease. What did the data show?

“The highest mortality rates were in the high exposure group…we observed a graded risk of mortality associated with increasing exposure to insulin… Analyses restricted to CV-related and non-vascular mortality showed virtually identical results.”

Here’s how they summed up their findings:

“We observed a significant and graded association between mortality risk and insulin exposure level in an inception cohort of patients with type 2 diabetes that persisted despite multivariable adjustment.”

Wouldn’t you think this is one reason why other studies have shown that too aggressive pharmaceutical blood sugar control results in worse outcomes? There are a number of evidence-based natural agents that support insulin receptor sensitivity and other functional aspects of type 2 diabetes. The more these can be used to minimize the dependence on increasing insulin the better.

“There is no evidence from randomized trials to support a strategy of lowering systolic blood pressure below 135 to 140 mm Hg in persons with type 2 diabetes mellitus. We investigated whether therapy targeting normal systolic pressure (i.e., <120 mm Hg) reduces major cardiovascular events in participants with type 2 diabetes at high risk for cardiovascular events.”

They constructed their study to discriminate outcomes between reducing blood pressure to less than 140 mm Hg and less than 120 mm Hg:

“A total of 4733 participants with type 2 diabetes were randomly assigned to intensive therapy, targeting a systolic pressure of less than 120 mm Hg, or standard therapy, targeting a systolic pressure of less than 140 mm Hg. The primary composite outcome was nonfatal myocardial infarction, nonfatal stroke, or death from cardiovascular causes. The mean follow-up was 4.7 years.”

I have told patients for years that it is not desirable to aggressively medicate blood pressure much below a systolic reading of 135-140 mm Hg because the increased pressure is a compensatory effort by the body to deliver oxygen to the tissues against increased resistance. There has to be a happy medium. What did the data from this investigation show?

“Serious adverse events attributed to antihypertensive treatment occurred in 77 of the 2362 participants in the intensive-therapy group (3.3%) and 30 of the 2371 participants in the standard-therapy group (1.3%).”

This compelled them to conclude that:

“In patients with type 2 diabetes at high risk for cardiovascular events, targeting a systolic blood pressure of less than 120 mm Hg, as compared with less than 140 mm Hg, did not reduce the rate of a composite outcome of fatal and nonfatal major cardiovascular events.

“the relationship between habitual sleep disturbances and the incidence of type 2 diabetes.”

The authors analyzed 10 studies that included 107,756 male and female participants. Their clear-cut conclusion:

“Quantity and quality of sleep consistently and significantly predict the risk of the development of type 2 diabetes. The mechanisms underlying this relation may differ between short and long sleepers.”

The mechanisms include hormone dysregulation, low-grade chronic inflammation, and gastroesophageal reflux disease (GERD; see earlier post on how medication can worsen this association). For help with sleep disorders there are sound functional medicine resources that address the biological component, cognitive behavioral methods (see recent post about internet-based CBT for insomnia), and neurotherapies including neurofeedback and brain wave entrainment tools.

Considering the importance of inflammation in chronic disease, the second paper is especially interesting in that it documents reductions in subclinical inflammation and oxidative stress as mechanisms by which coffee lowers the risk of type 2 diabetes. Noting that “Coffee consumption is associated with a decreased risk of type 2 diabetes,” the authors state that their “aim was to investigate the effects of daily coffee consumption on biomarkers of coffee intake, subclinical inflammation, oxidative stress, glucose, and lipid metabolism.” They observed a number of interesting effects, including beneficial lowering of the LDL/HDL ratio and IL-18, and an increase in adiponectin. Meanwhile, no adverse changes were seen on the oral glucose tolerance test. They conclude: “Coffee consumption appears to have beneficial effects on subclinical inflammation and HDL cholesterol, whereas no [adverse] changes in glucose metabolism were found in our study.”