Archive for the ‘Insulin & Diabetes’ Category

Both are good for weight loss, which is better for high blood pressure: higher protein or higher fat?

Saturday, April 17th, 2010

European Journal of Clinical Nutrition 0310Most of you reading this are aware that a lower glycemic diet can promote weight and fat loss through its beneficial effect on insulin levels. But which is better for blood pressure control, a higher or lower protein to fat ratio? This study recently published in the European Journal of Clinical Nutrition was designed to answer that question.

“There is controversy over dietary protein’s effects on cardiovascular disease risk factors in diabetic subjects. It is unclear whether observed effects are due to increased protein or reduced carbohydrate content of the consumed diets. The aim of this study was to compare the effects of two diets differing in protein to fat ratios on cardiovascular disease risk factors.”

What did their data show? Interestingly,…

“Both diets were equally effective in promoting weight loss and fat loss and in improving fasting glycemic control, total cholesterol and low-density lipoprotein (LDL) cholesterol, but the…HP–LF [high protein-low fat] diet improved significantly both systolic and diastolic blood pressure when compared with the LP–HF [low protein-high fat] diet. No differences were observed in postprandial glucose and insulin responses.”

The authors conclude:

“A protein to fat ratio of 1.5 in diets significantly improves blood pressure and TG [triglyceride] concentrations in obese individuals with DM2 [type 2 diabetes].”

Insulin resistance and cancer

Wednesday, April 14th, 2010

Cancer ScienceInsulin resistance is the loss of sensitivity of the receptors on each cell that respond to insulin from to repeated over-stimulation by insulin due to high blood sugar levels. High levels of insulin “in the background” do many kinds of damage in the run-up to type 2 diabetes when the body’s capacity to produce ever higher compensatory levels of insulin finally fails and the blood sugar goes up. My patients will certainly recognize that insulin is, of course, a hormone—and that excessive levels are a tumor promoter (along with the related insulin-like growth factor (IFG1). This paper recently published in the journal Cancer Science looks at the epidemiological link between insulin resistance and cancer.

“Epidemiological evidence from our prospective study, the Japan Public Health Center-based Prospective (JPHC) study, and systematic literature reviews generally support the idea that factors related to diabetes or insulin resistance are associated with an increased risk of colon (mostly in men), liver, and pancreatic cancers… The suggested mechanism of these effects is that insulin resistance and the resulting chronic hyperinsulinemia and increase in bioavailable insulin-like growth factor 1 (IGF1) stimulate tumor growth.”

The data from the Japan Public Health Center-based Prospective (JPHC) study support this conclusion:

“…there is substantial evidence to show that cancers of the colon, liver, and pancreas are associated with insulin resistance, and that these cancers can be prevented by increasing physical activity, and possibly coffee consumption.”

That’s right, coffee consumption—see the numerous posts documenting the benefits of coffee. Past and forthcoming posts report on studies that describe the association of insulin resistance and other cancers. The ‘take home’ message is that it’s important to maintain insulin at a healthy level long before the onset of type 2 diabetes by lifestyle factors (good eating and exercise) and evidence-based supplementation appropriate to your genetic and circumstantial needs.

Limit insulin use as much as possible for type 2 diabetes

Saturday, April 3rd, 2010

Diabetes, Obesity and MetabolismMetabolic syndrome crosses the line to type 2 diabetes when insulin resistance worsens to the point that the pancreas can no longer increase insulin production to yet higher levels. By then the elevated insulin ‘in the background’ has already been doing damage throughout the body for years. If blood sugar can no longer be controlled with natural agents that re-sensitize insulin receptors and support blood sugar metabolism or other oral anti-diabetic agents, then exogenous (from the outside) insulin is used. But if higher levels of native insulin contribute to a variety of diseases, are higher therapeutic levels a concern? This study published in the journal Diabetes, Obesity and Metabolism investigates just that:

“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.

More aggressive blood pressure control for diabetes is not better

Friday, April 2nd, 2010

New England JournalHigh blood pressure is common with type 2 diabetes because the excessive levels of insulin that lead up to the breakdown in blood sugar control promote hypertension. This study recently published in The New England Journal of Medicine has practical importance for many people who require treatment for high blood pressure. The authors first note:

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.

Coffee protects against fatty liver disease

Sunday, March 28th, 2010

Digestive Diseases and SciencesThere seems to be one study after another about the benefits of coffee. This paper just published in the journal Digestive Diseases and Sciences verifies that coffee protects against Non-alcoholic Fatty Liver Disease (NAFLD), the most common cause of non-infectious hepatitis and a growing cause of liver failure. I very often see elevated liver enzymes on laboratory tests; no wonder, since this is commonly fueled by insulin resistance. The authors of this study began by observing…

“The benefits of coffee on abnormal liver biochemistry, cirrhosis and hepatocellular carcinoma have been reported…this study aims to investigate if coffee use has any relationship with bright liver, measured by ultrasound bright liver score (BLS), in patients with non-alcoholic fatty liver disease (NAFLD), and which relationship, if any, is present with BMI and insulin resistance.”

‘Bright liver’ refers to the appearance of a fatty liver on ultrasound imaging, and a higher BLS measurement means more fat deposits in the liver. What did they find?

Less fatty liver involvement is present in coffee vs. non-coffee drinkers. Odds ratios show that obesity, higher insulin resistance, lower HDL cholesterol, older age and arterial hypertension are associated with a greater risk of more severe BLS; to the contrary, coffee drinking is associated with less severe BLS…Coffee use is inversely associated with the degree of bright liver, along with insulin resistance and obesity…”

Their conclusion is similar to numerous other studies:

“A possible opposite, if not antagonistic, role of coffee with regard to overweightness and insulin resistance, similar to that reported in hepatocarcinoma and cirrhosis, is envisaged in the natural history of NAFLD.”

Low testosterone is associated with insulin resistance

Wednesday, March 24th, 2010

European Journal of EndocrinologyA study published recently in the European Journal of Endocrinology links to the previous post on erectile dysfunction as a predictor of death with cardiovascular disease. The authors mention the well-known fact that:

Insulin resistance is associated with metabolic syndrome and type 2 diabetes, representing a risk factor for cardiovascular disease.”

They set out to investigate a link between insulin resistance and low testosterone, even in the absence of overweight. What did their data show?

“In older men, lower total testosterone is associated with insulin resistance independently of measures of central obesity. This association is seen with testosterone levels in the low to normal range.”

Do you see the connections between erectile dysfunction, cardiovascular disease, insulin resistance and low testosterone that are emerging here?

Another warning about metformin for diabetes and Vitamin B12

Tuesday, March 16th, 2010

Diabetes Care 0210Judging from the tone of this paper just published in the journal Diabetes Care, there are still too few professionals and lay people alike who are not aware that Vitamin B12 must be attended to when taking the type 2 diabetes drug metformin. The authors focus on the varying severity of diabetic neuropathy and observe:

“Long-term use of metformin is associated with malabsorption of vitamin B12 (cobalamin [Cbl]) and elevated homocysteine (Hcy) and methylmalonic acid (MMA) levels, which may have deleterious effects on peripheral nerves.”

It won’t surprise any readers of these posts that their data showed…

“Metformin-treated patients had depressed Cbl levels and elevated fasting MMA and Hcy levels. Clinical and electrophysiological measures identified more severe peripheral neuropathy in these patients; the cumulative metformin dose correlated strongly with these clinical and paraclinical group differences.”

Their conclusion:

“Metformin exposure may be an iatrogenic cause for exacerbation of peripheral neuropathy in patients with type 2 diabetes. Interval screening for Cbl deficiency and systemic Cbl therapy should be considered upon initiation of, as well as during, metformin therapy to detect potential secondary causes of worsening peripheral neuropathy.”

Remember, when taking metformin you need to check your B12 levels, not by measuring it in the serum (blood) which is unreliable, but with methylmalonic acid in the blood or urine (not perfect but better) and keeping an eye on homocysteine.

RDW is an inexpensive but powerful indicator often overlooked on your routine blood test

Sunday, March 7th, 2010

Archives of Internal Medicine 0210RDW stands for Red (Blood Cell) Distribution Width, an index for the degree of variability in the size and shape of your red blood cells. Recent studies are showing it to be a powerful indicator of overall health and the risk of death from multiple causes. RDW is always included in the standard Complete Blood Count (CBC), one of the most routine lab tests in modern medicine, but there’s evidence that the usual lab reference range is too broad and it’s value is not widely appreciated. It has been established for some time that RDW predicts mortality form cardiovascular disease, but this study recently published in the Archives of Internal Medicine is particularly interesting because it shows that RDW predicts mortality in the general population independent of cardiovascular disease. The authors state:

“Higher RDW values were strongly associated with an increased risk of death…Even when analyses were restricted to nonanemic participants or to those in the reference range of RDW (11%-15%) without iron, folate, or vitamin B12 deficiency, RDW remained strongly associated with mortality. The prognostic effect of RDW was observed in both middle-aged and older adults for multiple causes of death.”

Two weeks later the another paper was published in the same journal on the same topic that begins with this observation:

“Red blood cell distribution width (RDW), an automated measure of red blood cell size heterogeneity (eg, anisocytosis) that is largely overlooked, is a newly recognized risk marker in patients with established cardiovascular disease (CVD).”

They set out to investigate

“the association of RDW with all-cause mortality and with CVD, cancer, and chronic lower respiratory tract disease mortality in 15,852 adult participants.”

Their conclusion:

“Higher RDW is associated with increased mortality risk in this large, community-based sample, an association not specific to CVD.”

Journals of GerontologyAnother paper just published in The Journals of Gerontology confirms these findings with an analysis of seven community-based studies of older adults. Their conclusion:

“RDW is a routinely reported test that is a powerful predictor of mortality in community-dwelling older adults with and without age-associated diseases.”

Diabetes Care 0210.2This paper just published in the journal Diabetes Care reports on the link between RDW, metabolic syndrome and cardiovascular disease: “A possible explanation for the observed association between RDW and MetS is that high RDW reflects an underlying inflammatory state that leads to impaired erythrocyte (red blood cell) maturation and anisocytosis (size variation), as suggested previously (1–3). In fact, MetS exacerbates oxidative and inflammatory stress in obese adults, which is a potential mechanism for the increased cardiovascular risk in this condition.”

European Journal of Heart FailureAnd as you would expect, the European Journal of Heart Failure recently published a study on heart failure that compares RDW with N-terminal brain natriuretic peptide (NT-proBNP) in which the authors conclude:

“Red cell distribution width is a readily available test in the HF-population with similar independent prognostic power to NT-proBNP across the first to third quartiles. Prognostic models in HF (heart failure) should include RDW.”

Digestive Diseases and SciencesAnd the ‘plot thickens’. In this paper published in the journal Digestive Diseases and Sciences the investigators observe:

“Impaired iron absorption or increased loss of iron was found to correlate with disease activity and markers of inflammation in inflammatory bowel disease (IBD). Red cell distribution width (RDW) could be a reliable index of anisocytosis with the highest sensitivity to iron deficiency.”

Their compelling conclusion:

“Among the laboratory tests investigated, including fibrinogen, CRP, ESR, and platelet counts…analysis indicated RDW to be the most significant indicator of active UC [ulcerative colitis]. For CD [Crohn's disease], CRP was an important marker of active disease.”

Archives of Pathology & Laboratory MedicineLastly, you’ll appreciate the broadest statement yet about the value of this inexpensive and readily available marker. In a recent paper published in the Archives of Pathology & Laboratory Medicine. The authors begin by chiming in with the neighborhood chorus:

“A strong independent association has been recently observed between elevated red blood cell distribution width (RDW) and increased incidence of cardiovascular events;”

but they aim to

“assess whether RDW is associated with plasma markers of inflammation.”

Their conclusion:

“To our knowledge, our study demonstrates for the first time a strong, graded association of RDW with hsCRP and ESR independent of numerous confounding factors.”

In other words, RDW is inexpensive, easily obtained, and a powerful marker for inflammation in general, the common denominator of most chronic disease.

Here’s the ‘take home’ message (if you’ve gotten this far): If you have almost any blood work done at all it’s likely to include RDW automatically. Make good use of it, keeping in mind that laboratory reference ranges do not reflect the latest research and your doctor may not be aware of this. Functional medicine doctors want RDW to be no more than 13%.

A possible explanation for the observed association between RDW and MetS is that high RDW reflects an underlying inflammatory state that leads to impaired erythrocyte maturation and anisocytosis, as suggested previously (13). In fact, MetS exacerbates oxidative and inflammatory stress in obese adults, which is a potential mechanism for the increased cardiovascular risk in this condition

Another reason to get enough sleep: diabetes

Thursday, March 4th, 2010

Diabetes Care 0210.2Getting short-changed on sleep causes multiple harms. Here’s a paper just published in the journal Diabetes Care that assessed

“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.

Two new studies again show benefits of coffee

Saturday, February 27th, 2010

American Journal of Clinical NutritionCoffee is in the science news again, with two interesting papers that document its benefits. Both were recently published in the American Journal of Clinical Nutrition. The first paper adds more evidence that drinking coffee reduces the risk of type 2 diabetes. The study involved 69,532 French women who were observed over an 11 year period. The authors report an “inverse association [diabetes]…for both regular and decaffeinated coffee and for filtered and black coffee, with no effect of sweetening. Total caffeine intake was also associated with a statistically significantly lower risk of diabetes. Neither tea nor chicory consumption was associated with diabetes risk.” Interestingly, the authors also noted that the observed benefit was particularly pronounced with coffee consumed at lunch. Their conclusion: “Our data support an inverse association between coffee consumption and diabetes and suggest that the time of drinking coffee plays a distinct role in glucose metabolism.”

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.”