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...

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.