Vanadium for Type II Diabetes!? Beneficial Effect of Trace Element on Blood Glucose Management in Rat Model.

Some of you may remember that vanadium has once been hailed as nutrient repartitioner (it has been shown to increase glucose uptake into muscle tissue via GLUT4-receptors) in the fitness & bodybuilding community. After reports on possible toxicity issues, which were - at least in parts - based on reports of people who dosed according to the common "more helps more" mentality of our society, vanadium supplements, stand-alone or larger doses as part of micronutrient blends, have disappeared from the market. Science, on the other hand has not given up on this promising, yet non-benign "medication".

A recent study (Kurt. 2011) published in the journal Biometals underlines that the effects of vanadium, which was named after the Scandinavian goddess of beauty and fertility, Vanadis, do in fact border on those of a pharmaceutical drug. After treating rats with streptozotocin and thus inducing a metabolic profile that is generally considered an appropriate model for human type II diabetes, the researchers from the Department of Chemistry, at the University of Istanbul, supplemented the chow of their animals (control & STZ-induced type II diabetic rats) with 100mg vanadyl sulfate per kg of body weight. For an 80kg male human this would amount to a massive dose of 1.200mg vanadium sulfate per day, the consumption of which is not advisable until definitive human data on short- and especially long-term consequences are available.

Figure 1: Blood glucose levels (mg/dl) of rats at different time-points
(data adapted from Kurt. 2011)

Regardless of the results of future studies on the effects & safety of vanadium on humans, the study results (as shown in figure 1) clearly indicate that vanadium is able to counter, maybe even reverse, the negative effects streptozotocin has on blood glucose and insulin management in rats.

Its also noteworthy that, according to the scientists, the administration of vanadium also reversed the pro-oxidative effects of streptozotocin-induced diabetes. I am yet not sure if this conclusion Kurt et al. base on a reduction of anti-oxidant activity in the tissue of the diabetic rats is valid. After all, the latter could also be a direct consequence of potential toxic effects of the trace mineral. Until further human data will be available, I would thus strongly advice against taking high dose vanadium supplements, even if you have type II diabetes.

Save Our Children: No more "Obeldickses" - Lifestyle Intervention, Not Rigorous Dieting Key to Solving Childhood Obesity

What is good for adults cannot be bad for children!? Right so in the case of turning a sedentary life upside down: Changing the lifestyle, i.e. eating and exercise habits of overweight children (8 year olds) produced profound and above all persistent (>12 month) improvements in body weight, fat mass, waist circumference, and blood pressure!

In a recent report (Schaefer. 2011) on what the German scientists felicitously called the "Obeldicks" program (with reference to the obese Gaul from the famous comic book series),  Schaefer et. al. report the results of a large scale intervention program with 76 obese children and their parents. The program was based on three-pillar-strategy:

• physical activity training, 
• nutrition education, 
• and behavior counseling 

And the beneficial and more importantly lasting (>12 month follow up) effects it had on the participants should make it pretty clear that in a society, where pathological eating & movement patterns (driving to McDonalds, eating the SuperSizeMenue right in your car) become the norm, profound lifestyle changes are the only sustainable way to lose weight, improve or maintain health and promote long jeopardy.

So, if you want to die from diabetes, cancer or heart disease (you chose your favorite) in 10 years from now, that is your choice, BUT be fair and give your children the education and advice they need to get their acts together, they probably still have the chance.

Fat or Fire, What Comes First? Scientists Answer: Obesity Alone Triggers Inflammatory Signaling in Mice

The metabolic syndrome, i.e. the combination of obesity, inflammation and insulin resistance, is at the center of contemporary medical research. In my appearance on Carl Lenore's Super Human Radio, I already mentioned that from a logical perspective the mainstream belief, inflammation was the root of all evil, must be flawed. How should the reaction to a problem be the cause of the very problem itself? A recent study coming from a group of Korean scientists strengthens my conviction that out of the triad that not inflammation, but rather obesity or - one step further up in the genesis of the pathology - the combination of an unhealthy diet and a sedentary lifestyle is at the heart of the triad we now call the "metabolic syndrome".

Kim et al. investigated the pro-inflammatory signaling cascade in either diet-induced (DIO) or leptin gene deficient (ob/ob) obese mice and found that obesity alone ...

[...] up-regulated the expression of TLR1–9 and TLR11–13 in murine adipose tissues, a phenomenon linked with downstream nuclear factor κB [inflammatory protein linked to linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection, and improper immune development], interferon regulatory factors, and STAT-1 activation, and up-regulated the expression of cytokines and chemokines via MyD88-dependent and MyD88-independent cascades [activate NF-κB].

Thus, obesity sets the scene for inflammation and inflammation in turn triggers a cascade of unfavorable metabolic and hormonal changes which in and out of themselves result in further weight gain...

Here, we have a self-enhancing pathologic circle, which - and this is probably an even more important result of the study - was especially "effective" in the group of diet-induced obese mice:

The magnitudes of the obesity-induced up-regulation of the TLR1, TLR4, TLR5, TLR8, TLR9 and TLR12 genes in the visceral adipose tissue were greater in the DIO mice than in the ob/ob mice. Similarly, the expression of the IFNα and IFNβ genes significantly increased in the adipose tissues of the DIO mice but did not change in the adipose tissues of the ob/ob mice.

So, its not in your genes, but in your hands, feet and mouth to ward off the plague of the 21st century: Exercise and eat healthy to get lean and/or stay lean and stave off inflammation and diabetes.

ALA + Vitamin E Make Up for Fructose Induced Cardiovascular and Metabolic Changes

Alpha Lipoic Acid (ALA) and vitamin E are among the most investigated and best-known natural antioxidants. And, despite the fact that scientists came to realize, that both, ALA as well as alpha-tocopherol, are far from being the saviors of the metabolically deranged, they were once hailed as, a recent study from the University of Queensland (Patel. 2011) demonstrates their therapeutic potential in an animal model that (unfortunately) is not far from the high fructose corn syrup fed morbidly obese man/woman in a western(-ized) society.

Patel et al. found that supplementation with vitamin E (either α-tocopherol or tocotrienol-rich fraction, 0.84 g/kg food) and α-lipoic acid (1.6 g/kg food) could prevent (high fructose diet + Vit E + ALA) and even reverse (Vit E + ALA after high fructose diet for 8 weeks; reversal protocol) "glucose intolerance, hypertension, and increased collagen deposition in the heart together with an increased ventricular stiffness" in rats fed a high fructose diet over a course of 16 (prevention) / 8 + 8 (reversal) weeks.

Figure 1: (a): Plasma glucose concentrations following oral gavage of glucose (2 g/kg) recorded after 16 weeks for rats fed with corn starch (⬤), fructose (⚪), or fructose with α-tocopherol and α-lipoic acid as either prevention (FTPP) (▲) or reversal (FTPR) (▾) protocols. (Patel. 2011)

As a faithful visitor of the SuppVersity, you probably won't be surprised to read that supplementation with a tocotrienol enriched vitamin E source produced even more favorable outcomes in terms of blood glucose (5.0 vs. 6.4mmol/L in the prevention groups) and the other markers of metabolic health. It should not astonish you, anyway. It's no coincidence that nature provides us with certain nutrients in certain ratios and isolated alpha-tocopherol is something you won't find in nature...

Gadgetry & Caffeine a Dynamic Duo for Sleep Deprivation and, Consequently, Obesity in School-Aged Children

Ever wondered what your children do, when you send them to bed in the evening? According to the results of a study from the Department of Family and Community Health at the University of Maryland School of Nursing, they probably drink Coke and watch TV or play video-games. Does not sound too bad? Well, Calamaro et al. found that children who

drank caffeinated beverages had 15 fewer minutes of sleep per night than did children who did not drink such beverages (b = –0.27, P = .002). Children with three technology items in their bedroom received 45 fewer minutes of sleep than did children without these items in their bedroom (b = –0.75, P = .010).

Still not impressed? What if I told you that these kids missed out on 15 to 60 minutes of what - to my mind - is the most healthiest, most anabolic and most lipolytic time of the day (sleep), and that the study provides evidence for the hypothesis that the immediate consequence of caffeine induced sleep deprivation is obesity? If you do now reconsider whether your 7 year old really needs his own TV-set and whether plain water ain't no viable alternative for Red Bull and Coca Cola, you've already taken the first step to make a change that could - in the years to come - save your children from turning from the "fat guy / girl" in elementary school into the fat and diabetic guy / girl at high school.

Review of Intervention Studies Shows: Weight Loss Success Independent of Meal Frequency

"Eat 3 large meals à day!", "Eat smaller meals every 2 hours!", "Eat a single meal and fast the rest of the day!" If you have been trying to find information on how to lose weight effectively, you probably heard all these "expert" advises. What if I told you that a recent review of 25 weight loss interventions shows that it simply does not matter!

In an extensive review of the literature, Palmer et al. (Palmer. 2011) conclude:

Manipulating the EF [eating frequency] of a client seeking weight management is unlikely to provide any additional benefits to weight, body composition or health. The theoretical benefits of manipulating EF may not be sustained in the real life clinical setting as a change to EF may be difficult to maintain over the longer term. Current evidence does not support many of the theories that encourage manipulating EF for weight management. Focus needs to be placed on dietary weight management strategies that are achievable and sustainable over the longer term.

Better body composition? Only inconclusive evidence. Better glucose tolerance in non-diabetics? Definitely not. Decreased risk of heart disease? Unlikely. Less hunger? At least not with three vs. six meals. Bottom line: Another myth debunked!

Licorice for Diabetes!? Licorice Extract Reverses (!) Diabetic Nephropathy in Rats

Diabetes is the big "D" in the metabolic synDrome and probably the most destructive of the various faces of the plague of the century. Now researchers from the United Arabian Emirates have found that licorice may ameliorate the destructive effects of high blood glucose levels on your kidneys.

In a rat experiment, Kataya et al. (Kataya. 2011) found that...

... oral ingestion (1 g/kg body weight) of licorice extract for 60 days after the onset of diabetes reversed the adverse effect of diabetes on rats. Licorice extract alleviated blood glucose levels, restored renal function, and attenuated body-weight loss. In addition, licorice extract modulated the adverse effect of diabetes on renal malondialdehyde, glutathione, superoxide dismutase, and catalase activity. Further, licorice extract restored the total antioxidant capacity of diabetic rat kidneys.

What I find most intriguing is that licorice ingestion at a dosage that would amount to roughly 12g for an average male human being could reverse, i.e. not only ameliorate, diabetic nephropathy. Yet, the sheer amount of extract you would have to consume raises the question if there would not be other complications / unwanted side effects of this protocol. According to Isbrucker & Burdock (Isbrucker. 2006), the "acceptable daily intake" of licorice is "0.015-0.229 mg glycyrrhizin/kg body weight/day" - depending on the concentration of the extract the scientists used, 12g may well exceed this critical limit (high cortisol, high BP, water retention could be the consequences).

L-Arginine Biscuits Exhibit Ameliorated Insulin Response. A Viable Alternative for People with Metabolic Syndrome!?

"L-Arginine ameliorates insulin resistance and has beneficial effects on blood pressure", "Fat people love cookies and tend to develop insulin resistance!" - if these two thoughts get together in the head of an Italian scientists, a new product is born: the L-Arginine Biscuit!

In a recent study Emanuela Setola (Setola. 2011) investigated the effect of a biscuit with 6.6g arginine on selected metabolic parameters of 7 healthy subjects. The results are encouraging:

A significant increase of nitric oxide (NOx) and cGMP levels were significantly increased with Biscuit +L-ARG 6.6 g and Powdered L-ARG as compared to Biscuit. AUC NOx and cGMP were significantly increased (p<0.04vs Biscuit). Percentage incremental increase of post-ischemic blood flow significantly increased with Biscuit +L-ARG 6.6 g and Powdered L-ARG, suggesting a functional effect of L-ARG added to the food preparation. Further, at 240 minute mean arterial blood pressure and peripheral vascular resistances slightly declined with Biscuit +L-ARG 6.6 g without reaching a statistical significance. At metabolic levels, the addition of L-ARG to a biscuit decreased insulin levels in the presence of similar glycemic levels, in particular a significant decrease of AUCinsulin during the test with Biscuit +L-ARG 6.6 g in comparison to Biscuit alone was found (p<0.05).

The last result, i.e. the decreased insulin release is probably the most interesting finding of this study and was further investigated by the researcher:

From the results of glucose and insulin, two indices were derived: a Modified Matsuda, (index of whole-body insulin sensitivity) and the Disposition Index (index of the product of insulin sensitivity and first phase insulin secretion). We were able to define that both indices were significantly increased with 6 Biscuits having 6.6 g of L-Arginine while intermediate values were found when 3 Biscuits (3.3 g) were eaten as compared to Biscuits without L-Arginine addition.

After all, I think it would be better to avoid cookies and biscuits completely, but if you just cannot resist, you may well add some arginine to the dough for this years Christmas baking.

Even Low "Normal" Plasma Testosterone Levels Associated with 2.5x Higher Risk of Insulin Resistance

"Your levels are in range!" Did you ever have your doctor say that to you? It appears as if next time you hear that sentence, you better ask him "Where 'in range' are my levels, exactly?" At least, the results of a recently published study by Menendez et al. (Menendez. 2011) suggests that it might be worth digging somewhat deeper into this issue. Studying a cohort of 282 men (aged 36 to 85 years) who had "normal concentrations of total testosterone", the scientists found:

Serum concentrations of testosterone and bioavailable testosterone were negatively correlated with age, body mass index, waist circumference, blood glucose, glycated hemoglobin levels and insulin. Serum concentrations of total testosterone, bioavailable testosterone and SHBG were lower in men with glucose intolerance or diabetes than in those with normal glucose tolerance. After multivariate analysis, age and total testosterone levels were independent predictors of the presence of diabetes or glucose intolerance. The risk of glucose intolerance or diabetes mellitus was over 2.5 times higher in men with total testosterone levels in the lowest quartile than in those with total testosterone in the top quartile.

While the results of this study are certainly interesting and significant, it is unfortunately impossible to tell, whether glucose intolerance and diabetes reduce the natural production of testosterone, OR low testosterone levels reduce glucose intolerance and lead to diabetes. In other words: What comes first, low testosterone or glucose intolerance? Further research will be needed to answer this question, but if you want my opinion, I suspect that they just go hand in hand, i.e. a bad diet lowers glucose tolerance, high sugar reduces testosterone production, low androgen levels impair glucose tolerance etc. - a viscous circle.

Zinc + Multimineral Supplement May Improve Glycemic Control & Lipid Levels in Adult Diabetics

Diabetes and Pre-Diabetes are omnipresent in today's food-abundance. Healthy, wholesome and nutrient dense foods, on the other hand are either rare or people are just too lazy to obtain them. Thus, it is no wonder that researchers found that mineral supplementation will benefit people with onset or full-blown diabetes.

Table 1: Nutrient composition of the preparation for the MVM/Z group (Gunasekara. 2011)

In their study, Gunasekara et al. (Gunasekara. 2011) investigated the effect of 4 months of either oral multivitamin/mineral plus zinc sulfate (22 mg/day) (MVM/Z, cf. Table 1) or multivitamin/mineral supplementation alone on blood glucose (fasting and postprandial) and glycosylated hemoglobin (Hb_A1C%) and serum levels of zinc, creatinine, and lipids.

The zinc+MVM group had a mean change of fasting blood sugar -0.33 mmol/L (standard error of the mean 0.21 mmol/L) and was significant (P = 0.05) when compared with the other two groups (mean change in the MVM group +0.19 (0.31) mmol/L and +0.43 (0.23) mmol/L in the control group, respectively). The Hb_A1C% level reduced significantly, irrespective of the baseline level, in zinc+MVM-supplemented individuals. In the other two groups, the change of Hb_A1C% level was not significant. Serum lipid levels reduced significantly in the zinc+MVM and MVM groups.

Overall, the addition of 22mg elemental zinc (as zinc sulfate) triggered profound changes to the effect of the multivitamin/mineral formula, on the basis of which the scientists conclude "zinc, either alone or in combination with other known antioxidant minerals and vitamins, may have supplementary benefits in the routine management of adult diabetes."

6 Weeks of 400mcg Chromium per Day Improve Insulin Sensitivity and Lean Body Mass in Obese Children over Lifestyle Intervention Alone

Chromium, once hyped as a next generation anti-diabetes and lean mass agent, has disappeared from the best-selling lists of supplement vendors. Too few studies were able to confirm the encouraging results from rodent experiments. Possible toxicity issues put the icing on the cake and people just stopped buying it.

A very recent study published in the Journal of Nutritional Biochemistry (Kim .2010) took another look at whether chromium, which irrefutably is a vital co-factor in insulin production and secretion, may not yet be beneficial for patients with pre-diabetes. The scientists supplemented a group of 25 obese children (age 9-12y) who participated in a 6-week diet and lifestyle intervention with 400mcg chromium chlorid a day and monitored changes in body mass index (BMI; kg/m²), BMI Z-score, waist circumference, body composition and fasting plasma glucose. The results were positive- body composition and insulin sensitivity improved:

[...] children who received chromium chloride demonstrated more positive changes versus the placebo group in HOMA (−1.84±1.07 vs. 0.05±0.42, P=.05), QUICKI (0.02±0.01 vs. −0.002±0.01, P=.05), lean body mass (2.43±0.68kg vs. 1.36±1.61kg, P=.02) and percentage body fat (−3.32±1.29% vs. 0.65±1.05%, P=.04)

Once again, chromium did not prove to be the panacea of the age of obesity, but supplemental chromium can be a beneficial co-factor in the treatment of metabolic disorders in general and diabetic complications in particular. Without appropriate life-style interventions it will however prove similarly useless as many other supplements which have been "proven in clinical studies to do XYZ"...

Exercise at the Anaerobic Threshold Increases GH Release and Burns Fat in Obese Patients with Type 2 Diabetes

Scientists still argue about the most important contributing factor to the ever increasing obesity epidemic in the Western World: Is it bad dietary habits or our sedentary lifestyle - honestly, I don't care... you got to work on both if you want to stay healthy.

The results of a recent study published by scientists from the Toho University Sakura Medical Center (Yamaguchi. 2010) do yet underline the importance of exercise (and I mean exercise, as in sweating and panting, not just walking to your car!) in the "health equation", i.e. "diet + exercise = health". The scientists had their 19 obese type 2 diabetics either keep their sedentary lifestyle or performed 2× 30-min bouts of exercise (treadmill walking) everyday in the morning and evening during the 4-week study period. What is of particular importance is that the exercise intensity was determined by pretesting the exercise capacity of each participant, so that all patients exercised at their individual anaerobic threshold. The results of this regimen (cf. table 1) were quite remarkable:

Table 1: Baseline characteristics and changes in clinical and biochemical variables.BMI: body mass index, VFA: visceral fat area, SFA: subcutaneous fat area, BP: blood pressure, FPG: fasting plasma glucose, HbA_1C: hemoglobin A_1C, HOMA-IR: homeostasis model assessment of insulin resistance, TC: total cholesterol, TG: triglyceride, HDL-C: HDL-cholesterol, LDL-C: LDL-cholesterol, IGF-1: insulin-like growth factor-1, LPL mass: LPL mass in preheparin serum.

In view of recent research findings about the relation of visceral fat (VFA) and metabolic derangements, the remarkable reduction of VFA by -21.7% vs. -5.5% in the control group is of paramount importance for the subjects' health. The researchers attribute this success mainly increases in growth hormone which were elicited by the exercise intervention. In that, it is important to note that we are talking about a 100% increase in growth hormone after a 30-min bout of exercise.

Although this is just speculation on my part, I think it is questionable whether walking for more than 30 minutes, but at a lower intensity would have provided similar results. Or in other words: If the key is to trigger metabolic changes (via natural hormonal pathways) intensity (not overexerting oneself, though) is key.

BAT: Brown Adipose Tissue in Humans - An Update

In the latest edition of Current Opinion in Lipidology we find a mini-summary (COL. 2010) on current findings on the existence and metabolic purpose of brown adipose tissue (BAT) in human beings. These days the previously accepted position that adults have little to no BAT is put into question by the results of PET, where brown fat becomes especially visible upon cold exposure, when its metabolic activity is increased as a result of thermogenesis.

The author points out that adipocytes (fat cells) and myocytes (muscle cells) do not only share the same origin, the metabolically active BAT exhibits other similarities to muscle cells, as well - it is a metabollically active tissue and of particular importance in the context of insulin sensitivity and glucose disposal:

BAT glucose uptake rate is 10-15-fold higher in cold than in normal room temperature. Other factors that may increase the activity of sympathetic nervous system and uncoupling protein 1 are several including the complex network of hormonal and neuronal signals. Preliminary results suggest that BAT resembles skeletal muscle not only by origin but also by the effect of insulin on the tissue.

Doubtlessly, more research has to be done on the issue of BAT vs. WAT (white adipose tissue) and their relation to obesity, diabetes and the metabolic syndrome. In spite of that, even what we know today suggests that a better understanding of this hitherto overlooked remainder from the days when our ancestors ran around naked could help to find a solution for some of the "fat" health problems of the western societies.

B-Vitamins & Diabetes: Protective or Causative?

In a very interesting study, scientists from China and Japan (Zhou. 2010) found that "long-term exposure to high level of the B vitamins may be involved in the increased prevalence of obesity and diabetes in the US in the past 50 years". At first this appears to be counterintuitive, since we have been told over and over that B-Vitamins are not only good for our health, but that we could not even "overdose" them. While the latter has been questioned for years and certainly is not the case for e.g. B6 and niacin, even the former seems questionable, if you read the results from the above mentioned study:

The prevalences of diabetes and adult obesity were highly correlated with per capita consumption of niacin, thiamin and riboflavin with a 26- and 10-year lag, respectively (R2 = 0.952, 0.917 and 0.83 for diabetes, respectively, and R2  = 0.964, 0.975 and 0.935 for obesity, respectively). [...] The relationships between the diabetes or obesity prevalence and per capita niacin consumption were´similar both in different age groups and in male and female populations. The prevalence of adult obesity and diabetes was highly correlated with the grain contribution to niacin (R2 = 0.925 and  0.901, respectively), with a 10- and 26-year lag, respectively.

These results (especially those referring to the detrimental effect of niacin) confirm test-tube studies conducted by a group of scientists from South Korea earlier this year (Choi. 2010), who found that

NA [nicotinic acid] alters gene expression in insulin-sensitive tissues by various mechanisms. Some of the NA-induced changes in gene expression are discussed as potential mechanisms underlying wanted and unwanted effects of NA treatment.

Just anecdotal: My personal perspective on B-vitamins has changed since my overall energy and well being, as well as my physique have largely improved after stopping to take those B-vitamin (over-)loaden mulit-vitamin preparations like Now ADAM, CL Orange Triad, Animal Pak, ON Opti-Men etc. But remember: it is mere speculation that this could in fact be related to their high B-vitamin contents - could be any other constituent, as well.

Chromium Ain't Dead Yet: Positive Effects of Chromium Glycinate on Glucose Metabolism and Memory Acquisition in Rats Fed High-Fat Diet

"Chromium"? Sounds familiar, eh? Not too long ago, everybody was all over supplementing with chromium picolloniate to improve insulin sensitivity, to lose fat and to gain muscle. Most human studies, however, failed to reproduce the encouraging results from rodent studies. From todays perspective fat loss and muscle gain, if they occurred would probably have to be considered an indirect effect due to improvements in insulin management, the latter, on the other hand appear to be very real and may even benefit your cognitive performance.

When an international team of scientists supplemented male Wistar rats (n = 60; weighing 200–220 g) on a high-fat (40%, high-fat diet (HFD)) diet with either chromium-glycinate (CrGly) or chromium-acetate (CrAc) at doses of 0, 40, or 80 μg/kg body weight (BW) for 12 weeks, chromium supplementation ameliorated the detrimental effects of HFD on GLUTs, and Memory (32% reduction in expressions of glucose transporters 1 and 3 (GLUTs) in brain tissue and a 27% reduction in mean percentage time spent in the target quadrant and a 38% increase in spatial memory acquisition phase (SMAP)):

Compared with supplemental Cr as CrAc, CrGly was more effective to ameliorate response variables (i.e., restoration of tissue Cr concentration, enhancement of cerebral GLUTs expressions, and reduction of the glucose/insulin ratio and SMAP) in a dose–response manner, especially in rats fed HFD. Supplemental Cr as CrGly may have therapeutic potential to enhance insulin action and alleviate memory acquisition in a dose-dependent manner, through restoring tissue Cr reserve and enhancing cerebral GLUTs expressions.

So, after all chromium certainly ain't no magic bullet, it is likely, however, that patients who suffer from obesity and diabetes, as well as athletes who have been found to be at risk of chromium deficiency, may in fact benefit from your occasional dose of supplemental chromium.

Vitamin D & Insulin: A Question of Race?

Could it be that vitamin D intake is more important for people with an African American (AA) background than for their European American (EA) neighbors? This is exactly, what a study that was recently published in Nutrition&Metabolism (Alvarez. 2010) seems to suggest.

In 115 African American (AA) and 137 European American (EA) healthy, premenopausal women the scientists  determined with 4-day food records and assessed the individual insulin sensitivity indexes (SI), as well as the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) values. The results are quite unequivocal:

Vitamin D intake was positively associated with SI (standardized β = 0.18, P = 0.05) and inversely associated with HOMA-IR (standardized β = -0.26, P = 0.007) in AA, and the relationships were independent of age, total body fat, energy intake, and % kcal from fat. Vitamin D intake was not significantly associated with indices of insulin sensitivity/resistance in EA (standardized β = 0.03, P = 0.74 and standardized β = 0.02, P = 0.85 for SI
and HOMA-IR, respectively). Similar to vitamin D, dietary calcium was associated with SI
and HOMA-IR among AA but not EA.

While the scientists refrain from premature speculation about the underlying reasons of the observed discrepancy, they highlight the importance of both, adequate vitamin D, as well as dietary calcium consumption for premenopausal women of African American descent. What I consider noteworthy is the fact that the mean vitamin D intake of both groups was way beyond even the currently suggested 400IU (most experts already suggest 1.000-2.000 IU per day). With a mean vitamin D intake of 111.5IU and 133.7IU per day. All subjects carry the risk of being "vitamin D deficient" and this is where increased intake may produce significant positive effects on various health marker (cf. More on Vitamin D).

Mitochondrial Density in Muscle is Key Determinant of Metabolic Flexibility

If you happened to have listened to Carl Lenore's interview with Mike T Nelson's on SuperHumanRadio, last week, you will be familiar with the concept of metabolic flexibility and how important it is for your body to be able to adapt quickly to varying energy demands and sources. A recent study by scientists from the Pittsburgh School of Medicine (Chomentowski. 2010) had a similar background. Along with several markers of metabolic flexibility the group measured intermyofibrillar and subsarcolemmal (SS) mitochondrial content in a sample of forty sedentary adults with a wide spectrum of insulin sensitivity (insulin-sensitive lean subjects, insulin-resistant nondiabetic subjects, and subjects with type 2 diabetes mellitus).

Intermyofibrillar mitochondrial content was lower in the insulin-resistant nondiabetic subjects and type 2 diabetes mellitus groups, significantly correlating with glucose disposal in both men (R = 0.72, P < 0.01) and women (R = 0.53, P < 0.01). In contrast, SS mitochondrial content was similar among groups. Lower intermyofibrillar mitochondrial content was not explained by mitochondrial size, altered fiber-type distribution, or differences in maximum aerobic capacity. Intermyofibrillar mitochondrial content was significantly correlated with fasting respiratory quotient (R = -0.46, P = 0.003) and metabolic flexibility (R = 0.38, P = 0.02).

The correlation between low intermyofibriallar mitochondrial content and insulin-resistance the researchers found seems to substantiate the longstanding recommendation to exercise and build muscle or make existing muscle work more effectively to prevent and treat diabetes and the metabolic syndrome. However, dietary factors and genetics may as well be important factors influencing mitochondrial density.