The idea of insulin resistance first emerged in a study conducted in 1936. Although it wasn't until nearly 40 years later that insulin resistance became a more common occurrence in diabetes care - this study cited a cause and effect of injected insulin in Type 2 diabetes.

Patients were tested on two different days. One day patients were given a drink containing glucose and their blood sugar was measured for the following 90 minutes. On the other day, patients were given a drink containing glucose at the same time they were given an injection of insulin. The subjects were clearly definable into two groups based on their reaction to the glucose drink with the insulin injection. Some patients had an immediate response to the insulin injection lowering their blood sugar and others had little or no response to the insulin injection.

The doctor conducting this study referred to this phenomenon as insulin sensitivity, rather than insulin resistance. He hypothesized that there was a sensitizing factor rather than something causing resistance to the cells absorbing the insulin. Over 70 years have passed and research now shows that arginine, the champion of amino acids can help improve insulin sensitivity, which is the same as diminishing insulin resistance.

Far from being inert and unchanging, a mere scaffolding to which the body's muscles and organs attach themselves, bones change constantly. Old bone cells die. New ones are born. But that's not all. According to an exciting new discovery, bones play a role in regulating blood sugar levels and fat deposits.

How is this possible? Bones act like a kind of endocrine organ, releasing osteocalcin, a hormone that influences bone formation. This hormone also increases both insulin production and the body's insulin sensitivity. It also reduces fat stores. Basically, osteocalcin levels in the bones are linked to blood sugar and body fat levels, and there is some sort of interaction back and forth.

It's a surprising finding for the uninitiated. However, some scientists are saying it makes sense when you think about it. Says Ronald Kahn, director of Harvard's Joslin Diabetes Center, "Obviously there does need to be some coordination between skeletal growth and body mass. If you carry around extra weight, your bones need to hold up under the extra pressure, so it's not surprising that your bones have a sense of body fat."

What makes for a long and healthy life? Why, you say, how about a healthy diet and liberal quantities of exercise? True! A healthy lifestyle keeps you in shape and is one factor that promotes longevity. But have you ever wondered exactly how this works on a physiological level? How does the brain understand you skipped the gym all summer and had French fries for lunch yesterday?

The answer, according to the results of a new study published in Science (July 2007), could relate to insulin levels in the brain. Researchers induced lab mice to overeat until they became obese and some exhibited symptoms of diabetes. Yet some of those same mice actually lived eighteen percent longer than their slender mice buddies. The researchers attributed that longevity to a gene that affects insulin. Put simply: the longevity gene (called Irs2) effectively "tricked" the brains of those mice into thinking they were slim and fit, when in fact the opposite was true.

For diabetics, the study raises an additional question: if raising insulin levels decreases the body's sensitivity to it, is it really desirable to treat type 2 diabetics with insulin over the long-term? Lead author of the study, Morris White of Children's Hospital in Boston, says it's highly preferable (when possible) to get type 2 diabetes under control through old-fashioned diet and exercise, rather than through insulin or other meds.

There has been some very exciting news lately about the benefits of a type of pumpkin. The pumpkin is shown to slow the destruction of beta cells and reduces the need for Type 1 diabetics to inject as much insulin.

The exciting thing is that this experiment found the benefits of the pumpkin were through oral consumption, not injection. The protective effect of pumpkin is thought to be due to both antioxidants and D-chiro-inositol, a molecule that mediates insulin activity. Boosting insulin levels has the effect of lowering blood sugar levels, which reduces levels of oxidative oxygen species that damage beta-cell membranes, preventing further damage and allowing for some regeneration. Beta cells levels in the diabetic rats are, however, unlikely ever to reach that of controls, because some of the cells will have been damaged beyond repair.

An ingredient expert pointed out to me that the pumpkin used in the study is not your canned pumpkin but a special variety of Asian pumpkin. You can check at you local Asian market if they have the Shark Fin pumpkin or if they can get it for you. He also surmised that it may be possible to parlay this breed of pumpkin into a whole new world of Health Foods.

Sleep disorders have been linked to exacerbating or even precipitating diabetes as well as depression. Poor sleep robs people of their health in general. But, for diabetics it can cause a worsening of their condition. A hypnotist can assist a person with diabetes by helping them to positively alter their behavior.

A study explained how people who do not get enough sleep on a regular basis tend to become less sensitive to insulin over time. The study found that healthy adults who averaged 5.2 hours of sleep a night secreted 50% more insulin than their more rested counterparts, who averaged 8 hours of sleep a night. As a result, "short sleepers" were 40% less sensitive to insulin.

Devin Hastings is a certified hypnotist who has been helping people change their lives for over 24 years. Devin has created a series of informative articles that will help diabetics transform their debilitating habits into healthier habits. See Devin's site for more details.

Studies found that cocoa butter might be better for diabetics than other fats. A manufacturer of cocoa and chocolate is exploring the health benefits of cocoa butter for diabetics.

The positive effect of cocoa butter on diabetes was discovered during a study to determine why men and women are affected differently by diabetes. The study tried to create insulin resistance in male and female rats by feeding them a diet rich in different kinds of fats. To everyone's surprise, the animals on a cocoa fat diet developed better insulin sensitivity than those fed with other kinds of fat. Other studies have looked at the flavanoids in dark chocolate for their blood pressure lowering and insulin sensitizing attributes, so this isn't the first time chocolate seemed to have sweet effects on diabetes.

Barry Callebaut is funding this research aimed at discovering the component in cocoa butter responsible for an improvement in insulin sensitivity, with the ultimate aim of developing chocolate products for diabetics. The company has not revealed the amount of funding it is providing for the trial, nor an anticipated timeline for resulting products to be available. The positive results for the first trail - which NutraIngredients.com has not seen in full - appear to have been a surprise for those involved.

Suffering succotash - do you believe the nerve of these scientists professing the antithesis of insulin-dependent diabetes!! Scientist have proven that supplementation of Gymnema sylvestre appears to enhance endogenous insulin production by regeneration of the residual beta cells in insulin-dependent diabetes. Wouldn't this study imply that insulin-dependent diabetes is curable??

GS4, a water-soluble extract of the leaves of Gymnema sylvestre, was given to 27 patients with insulin-dependent diabetes on insulin therapy. They received 400 mg per day. Their insulin requirements came down together, along with their fasting blood glucose, HbA1c and glycosylated plasma protein levels. Patients in the study receiving insulin therapy only (without Gymnema sylvestre supplementation) showed no significant reduction in serum lipids, HbA1c or glycosylated plasma proteins when followed up after 10-12 months.

There you have it, folks. A study published in the Journal of Ethnopharmacologyin October 1990 says - there are possible ways to regenerate beta cells in insulin-dependent diabetics, previously believed to be nonexistent and gone forever. Never say never, right Dr. Faustman?

Central obesity is associated with insulin resistance through factors that are not fully understood. Researchers studied the effects of three different diets on body fat distribution, insulin sensitivity and peripheral adiponectin gene expression.

Adiponectin is secreted from fat tissue into the blood. The presence of adiponectin can result in improved insulin sensitivity and glucose tolerance, and can assist in mobilizing sugar out of the blood The hormone plays a role in the suppression of the metabolic derangements that may result in type 2 diabetes, obesity, atherosclerosis and non-alcoholic fatty liver disease.

The study involved 11 volunteers who were the offspring of obese type 2 diabetic patients with noticeable abdominal fat deposits. The volunteers were considered insulin resistant and they maintained average hemoglobin A1c levels of greater than 6.5% without medication. All subjects underwent three dietary periods of 28 days each in a crossover design: a) diet enriched in saturated fat (SAT), b) diet rich in monounsaturated fat (MUFA; Mediterranean diet) and c) diet rich in carbohydrates (CHO). Weight, body composition and resting energy expenditure remained unchanged during the three dietary periods. However, when patients were fed a CHO-enriched diet their fat mass was redistributed towards their abdominal region and their periphery fat accumulation decreased compared with a diet MUFA-rich and high SAT diets. Changes in fat deposition were associated with decreased levels of adiponectin after meals and lower insulin sensitivity.

The results of this study conclude a diet rich in monounsaturated fat prevents central fat redistribution and a decrease in after meal adiponectin levels. These findings support the belief that a carbohydrate-rich diet in insulin-resistant subjects exacerbates the insulin resistance. The moral of the story is: to enhance insulin sensitivity - look for a diet rich in monounsaturated fats and less dense in carbohydrates. Chances are if you've tinkered around with your food pyramid - you already knew the results of this study.

Caffeine intake makes insulin more resistant to changes in blood sugar levels, Canadian researchers report.

The researchers evaluated sugar metabolism in 23 men before and after a three-month exercise program. Before and during the exercise program, the men were given caffeine or a placebo. The subjects included 8 sedentary lean men, 7 obese men with type 2 diabetes, and 8 obese men without diabetes. Before the exercise program, caffeine reduced insulin sensitivity by 33% in the lean and obese men and 37% in the obese men with diabetes compared to placebo. After the exercise program, insulin sensitivity fell 23% after caffeine intake in the lean men, 26% in the obese men, and 36% in the obese diabetic men. Comparison of the two study phases showed that exercise did not improve insulin resistance related to caffeine intake. It seems that caffeine weakens or offsets any of the beneficial effects of exercise or weight loss on insulin resistance. While the clinical implications remain unclear, the findings are a "red flag" for doctors and are particularly important for obese patients and those with diabetes.

Don't go throwing-away your Starbucks gift card - although the effects of caffeine on insulin were duly noted, the fact remains that coffee may cut the risk of diabetes. Although the findings seem to contradict recent reports that coffee intake may cut the risk of diabetes, coffee contains several other substances that may affect sugar metabolism, such as antioxidants, potassium and magnesium. Caffeine without all of the other substances that are found in coffee produces a different result. Like peanut butter and chocolate - peanut butter by itself is a high-fat protein. When you combine it with chocolate you have a melodic mix disdainfully referred to as candy but happily celebrated in the form of a REESE'S Peanut Butter Cups. It's all in the delivery, folks.

Until recently, little evidence existed regarding the effects of soy consumption on the metabolic syndrome in humans. Researchers evaluated the effects of soy consumption on metabolic symdrome and found it improved glycemic control and lipid profiles in postmenopausal women.

The study evaluated the plasma lipids, lipoproteins, insulin resistance, and glycemic control in 42 postmenopausal women with the metabolic syndrome. Participants were randomly assigned to consume a control diet (Dietary Approaches to Stop Hypertension, DASH), a soy-protein diet, or a soy-nut diet, each for 8 weeks. Red meat in the DASH period was replaced by soy-protein in the soy-protein period and by soy-nut in the soy-nut period.

The soy-nut regimen decreased the insulin resistance score significantly compared with the soy-protein or control diets. Consumption of soy-nut also reduced fasting blood sugar significantly than did the soy-protein or control diet. The soy-nut regimen decreased LDL cholesterol more than did the soy-protein period and the control diet. Soy-nut consumption significantly reduced serum C-peptide concentrations compared with control diet but consumption of soy-protein did not.

Consumption of the soy-nut leg of the experiment significantly reduced C-peptide concentrations because it was evident that the diabetic women were not creating as much insulin to counter the sugar rise in their blood. C-peptide is ONLY present when your body is producing insulin. So can one logically deduce that naturally occurring insulin causes insulin resistance? Uh oh. Sounds like we've got a pickle of a situation happening here.

Knocking out the gene for a peptide associated with insulin was shown to protect mice against the harmful effects of a high-fat diet. Urocortin 3 plays a role in the increased production of insulin in response to high caloric intake in animals.

Scientists found that by removing the urocortin 3 gene from mice, they did not develop the age-related insulin resistance and high blood sugar observed in the normal control mice. The metabolisms of normal mice were compared to the metabolisms of those without the urocortin 3 gene. When placed on a high caloric diet for three months, the mice without the urocortin 3 gene packed on the same amount of weight but had lower insulin levels. But these mice also had lower blood sugar, improved glucose tolerance curves and they did not develop the fatty livers the control mice experienced.

Scientists hypothesize that by curtailing the abnormally high insulin levels, they were able to manipulate insulin sensitivity and avoid some of the untoward consequences of the high food intake and weight gain. Like many of us diabetics already know too well - while insulin is effective at lowering blood sugar it also promotes fat storage. This is a natural protective response to prepare for times when food may not be available. When insulin is produced at too high a level for too long, the body becomes insulin resistant and blood sugar and certain blood lipids gradually creep up, which can cause progressive damage to multiple organs.

Urocortin 2 and urocortin 3 are part of the system that governs the body's response to insulin. Scientists already know that mice on a high-fat diet do better if either urocortin 2 or urocortin 3 is removed. Now they want to know if the mice will respond even better if both are missing. Such results may instruct us how best to develop therapeutic means to exploit these powerful effects.

Remember that movie with Billy Crystal and Robert De Niro, Analyze This? Well we all don't have super-risky mobster lifestyles to induce depression like Paul Vitti's, but according to a new study of depressed type 2 diabetics -- depression has a negative impact on blood sugar control.

Researchers treated 93 patients with type 2 diabetes and depression with the antidepressant bupropion (Wellbutrin). They chose the drug because it is capable of reducing depression and weight simultaneously. The hypothesis behind the treatment was mood enhancement and weight reduction would, in fact, improve blood sugar control. (Always a gold star day in my book!) The results were documented in the March issue of Diabetes Care, and showed that antidepressant treatment produced benefits beyond just mood improvement. Patients also lost weight, improved self-management of their diabetes, and improved their A1c levels.

In the 6 months following the conclusion of the study, depression improvement predicted maintenance of improved blood sugar control. This confirms the research hypothesis that depression improvement can produce better blood sugar control, independent of weight loss and overall diabetes management. The importance of weight-independent physiological factors like insulin sensitivity and inflammation improve during depression relief and contribute to better long-term control of diabetes.

The moral of this story? You tell me. I spotlight the research - I like it when you guys give me answers.

According to research conducted by Ohio State University, conjugated linoleic acid (CLA) may help reduce body fat, but it also increases your risk for nonalcoholic fatty liver disease.

In 2003, a study showed that a 2 month supplementation of CLA lowered body mass and blood sugars in diabetics. The recent studies conducted on mice fed a CLA supplemented diet lost weight very fast, but also accumulated excessive amounts of fat in their livers - a side effect of rapid weight loss. In addition, excessive accumulation of fat in the liver is associated with insulin resistance, a factor exacerbating type 2 diabetes.

Although the recent findings were conducted on mice, CLA may or may not have a similar effect on humans. CLA has been a hot selling item in supplement stores for years. I wonder what the results would be if people who have taken CLA (the t10c12 variety) for years were to discontinue use for 4 weeks. I would be curious to see the baseline and follow-up tests for body mass, insulin sensitivity and fat accumulation in the liver. Any med students out there interested in setting-up a lab profiling hepatic function in CLA poppers?

Chromium picolinate is one of the most widely debated supplements in diabetes health. A study has shown that it improves glycemic control in patients with type 2 diabetes not adequately controlled while taking sulfonylurea, a drug that increases insulin release from the beta cells in the pancreas.

A 40-week study was designed to examine the effect of adding daily chromium picolinate supplementation to an antidiabetic medication, sulfonylurea. A commonly prescribed treatment for type 2 diabetes was given to 29 subjects for 24 weeks, in conjunction with either chromium picolinate or a placebo. Blood sugar levels of study participants taking chromium picolinate dropped significantly compared to the placebo group. In addition, insulin sensitivity for participants taking the chromium picolinate was increased when compared to those in the placebo group. Study participants taking chromium picolinate also experienced significantly lower abdominal body fat accumulation than the placebo group, and experienced less overall weight gain.

This study demonstrates that chromium picolinate supplementation for type 2 diabetes who are taking sulfonylurea agents significantly improves insulin sensitivity and glucose control. In addition, chromium picolinate was shown to reduce weight gain and fat accumulation compared with the placebo group. The results of this study were first published in August 2006 - but knowing about chromium picolinate today leaves you with ample time to adjust for greater insulin sensitivity and less fattening days to come!

A study conduced by the Howard Hughs Medical Institute found that people with insulin resistance have higher levels of fat inside their muscle cells.

A mitochondrial impairment inside muscle cells result in a buildup of fats that can cause insulin resistance, contributing to the development of diabetes. Intramuscular fat interferes with the ability of insulin to effectively enter the cell. It was found that the rate of ATP production in the muscles of those who are insulin-resistant was decreased by 30% compared to normal subjects without signs of insulin-resistance.

A little, yellow flower has shown promise in overcoming the obstacle of insulin resistance. Studies show that berberine activates an enzyme in the muscle and liver tissues that improve insulin sensitivity.. It lowers blood sugar by inhibiting absorption of sugars from the intestine and enhancing production of insulin. If that wasn't enough - berberine has been shown to reduce body weight, too. This pretty little flower may be worth a look-see after all.