Scientific Evidence Links High Carbohydrate Intake to the Development of Alzheimer's and Other Neurological Diseases

"Fats are bad, carbs are healthy!" I hope nobody out there still believes this late 20th Century slogan. If you do, chances are you will soon forget about it due to the neuronal damage you are inflicting to your brain by eating a high carb diet.

In a very recent review, a group of international scientists (Seneff. 2011) summarize the current state of research as follows:

[...] an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease. A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. 

They also compiled a comprehensive list of take-home-massages, some of which may have far reaching consequences:

• Researchers have identified mitochondrial dysfunction and brain insulin resistance as early indicators of Alzheimer's disease.

• ApoE-4 is a risk factor for Alzheimer's disease, and ApoE is involved in the transport of cholesterol and fats, which are essential for signal transduction and protection from oxidative damage.

• The cerebrospinal fluid of Alzheimer's brains is deficient in fats and cholesterol.

• Advanced glycation end-products (AGEs) are present in significant amounts in Alzheimer's brains.

• Fructose, an increasingly pervasive sweetening agent, is ten times as reactive as glucose in inducing AGEs.

• Astrocytes play an important role in providing fat and cholesterol to neurons. [...]

• Glycation damage interferes with the LDL-mediated delivery of fats and cholesterol to astrocytes, and therefore, indirectly, to neurons. [...]

• Synthesis of the neurotransmitter, glutamate, is increased when cholesterol is deficient, and glutamate is a potent oxidizing agent.

• Over time, neurons become severely damaged due to chronic exposure to glucose and oxidizing agents, and are programmed for apoptosis due to highly impaired function. [...]

• Simple dietary modification, towards fewer highly-processed carbohydrates and relatively more fats and cholesterol, is likely a protective measure against Alzheimer's disease.

So, if you have not already forgotten what you just read, make sure to cut back your carbohydrate consumption, limit fructose intake and stop being afraid of fats and cholesterol before you cannot remember anymore.

Go for Gold: Golden Kiwifruit Outperforms her Green Sister in Terms of Antioxidant Potential

Groundbreaking research ;-) at the Faculty of Pharmaceutical Sciences at the Teikyo University in Tokyo, Japan, did now reveal that Kiwis, especially the golden variate outperforms other highly acclaimed health foods in terms of their antioxidant potential.

Comparison of the anti-oxidant effects in vitro demonstrated that kiwi fruit had stronger anti-oxidant effects than orange and grapefruit, which are rich in vitamin C; gold kiwi had the strongest anti-oxidant effects. Kiwi fruit inhibited oxidation of biological substances in the human body. In particular, kiwi fruit may inhibit early lipid oxidation.

While it is common knowledge that Kiwis contain a lot of vitamin C, the scientists underline that most of its beneficial effects come from the various forms of polyphenols in the fruits.

Fig. 1: Inhibition of Lipid Oxidant by Fruit Juices (Iwasawa. 2011)

So, next time you see some of these hairy little Chinese gooseberries at your local grocery store, grab some golden ones and bump up your antioxidant defenses.



On a side note: According to Dr. Smith from the Life Extension Foundation, Kiwi is also the common food with the highest amount of PQQ ("the new CoQ10" LEF is promoting) you can possibly find - unfortunately, you would probably have to eat truckloads to get the desired effect ;-)

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.

Pot Belly and High Triglycerides Indicative of Low LDL & HDL Particle Size

A recent study by scientists from the Mayo Clinic in Minnesota (Irving. 2011) found that the most reliable indicators of LDL & HDL particle size in 84 healthy non-diabetic men and women were a huge amount of trunk fat and high triglyceride levels.

[...] the accumulation of atherogenic lipoprotein particles (e.g. small, dense, low-density lipoprotein particles and small, high-density lipoprotein particles) was associated with low levels of insulin sensitivity, cardiorespiratory fitness, and higher levels of adiposity. However, multivariate forward-stepwise regression revealed that triglycerides, followed by truncal fat mass, were the strongest predictors of the lipoprotein particle size and concentration data.

These results are of particular interest to those who cannot afford having a comprehensive lipid panel done. Since the standard tests often do not provide any information about the size of the cholesterol particles, looking and triglycerides and truncal fat may be a useful indicator of whether or not it will be necessary to check cholesterol particle sizes, as well.

On a side note: Other than it has long been thought, current research suggests that neither the amount of total cholesterol, nor the amount of LDL cholesterol, but rather the size of the cholesterol lipo-proteins is the main determinant of how likely one is to develop arteriosclerosis: Large particle size = benign; small particle size = dangerous.

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."

1.5g of Vitamin C do not Alter Neutrophil Function in Athletes: ROS & SOA Elevations Remain Unchanged

The verdict is still out there on whether antioxidant supplementation before or around exercise is a good or a bad thing for professional athletes. A recent study by Yamai et al. (Yamai. 2011) which investigated the effect of 1.5g of vitamin C /day on the neutrophil function of judoists found no evidence for either of the propositions - neutrophil counts were not statistically different between the two groups of the 22 male judoists after a 7-day intensified training camp for:

[...]although the typical changes seen following a single bout of normal exercise, namely an increase in SOA [serum opsonic activity] and ROS [reactive oxygen species], and a decrease in PA [neutrophil phagocytic activity], were recorded following the pre- and post-camp ULEs in both groups, significant difference in change rates were not seen between both groups.

These results go hand in hand with many other more recent investigations into the beneficial effects of vitamin C and combinations of antioxidants (a factor the scientists raise in their discussion of the results) on exercise performance in (elite) athletes. So, even if vitamin C won't hurt you, it probably won't help either.

The (Re-)Discovery of 17{beta}-hydroxyestra-4,9,11-trien-3-one: Low Dose Trenbolone Safely Promotes Myotrophic Actions in Skeletal Muscle and Provides Partial Protection Against Bone Loss and Visceral Fat Accumulation

Sometimes it is interesting to see how agents that have been around all along reappear back on the medical scene, all of a sudden. A recent study conducted by a group of scientists from Florida (Yarrow. 2011) that compared the effect of different doses of 17{beta}-hydroxyestra-4,9,11-trien-3-one aka Trenbolone on muscle hypertrophy and prostate health of testosterone seems to have the potential to trigger such a "revival":

In both intact and orchiectomized animals, all TREN doses and supraphysiologic testosterone-enanthate augmented androgen-sensitive levator ani/bulbocavernosus muscle mass by 35-40% above Shams (p≤0.001), and produced a dose-dependent partial protection against orchiectomy-induced total and trabecular bone mineral density losses (<0.05) and visceral fat accumulation (<0.05). The lowest doses of TREN successfully maintained prostate mass and hemoglobin concentrations at Sham levels in both intact and orchiectomized animals; whereas supraphysiologic testosterone-enanthate and high-dose TREN elevated prostate mass by 84% and 68%, respectively (<0.01). 

Whether this indicates that "trenbolone therapy" in men would actually be an alternative to the traditional androgen therapy to counter muscle wasting and other medical conditions remains to be elucidated. This is especially valid in view of the fact that the variables controlled in this study did not encompass any of the side-effects steroid (ab-)users tend to report on injectable trenbolone. In other words: Just because it does not enlarge your prostate, this does not mean that it is safe.