NFH ALA R+ SAP 90 Capsules :

Alpha-lipoic acid (ALA) R+ is the only antioxidant that is both fat- and water-soluble. This is important because alpha-lipoic acid can access all parts of living cells, giving it the ability to trap free radicals and protect against oxidation. One of the leading causes of cellular breakdown is free radical damage. ALA R+ is one of the few substances that can cross the blood-brain barrier. ALA supplementation increases glutathione levels, which helps the body metabolize toxins. ALA also increases the removal of glucose (sugar) from the bloodstream, which is very helpful for those with diabetes and the prevention of eye disease.

Supplementing with ALA R+ SAP provides a daily dose of the antioxidant lipoic acid which is both fat and water-soluble and is easily transported across cell membranes to optimize antioxidant levels throughout the day. Scientific research has shown that ALA offers protection against free radicals both inside and outside the cell wall while other antioxidants may provide only extracellular protection. ALA is able to regenerate other antioxidants like vitamin E, vitamin C and glutathione. In addition to antioxidant properties, ALA helps the body use glucose; hence its potential for helping people with diabetes.

NFH brand ALA R+ SAP is fully dispersible in water. The standard alpha-lipoic (SLA) acid is called racemic, consisting of two forms, the R+ and S– optical isomers in equal amounts. It is a synthetic product, attempting to mimic the body’s natural forms of alpha-lipoic acid. ALA R+ SAP is a natural form consisting only of the R+ isomers, making it much more bioavailable than the standard SLA form. ALA R+ SAP is reduced to the R–DHLA form (R+ form), that the body uses as a potent antioxidant, 28 times faster than SLA.

Alpha-lipoic acid promotes glutathione and other antioxidant regeneration. ALA R+ SAP is pharmaceutical grade and contains biotin. One study has shown that ALA may reduce the activity of biotin when taken at very high doses, therefore added 55% of the daily requirement is added to the formula.

Structure & Function of ALA:

Alpha-lipoic acid is reduced form of DHLA consist of an 8-carbon fatty acid chain (octanoic acid) containing two sulfur atoms, with a chiral centre at the C3carbon atom(1). ALA and DHLA naturally occur in the R configuration(3).

The high chemical reactivity of ALA and DHLA is primarily centered in its dithiolane ring and the position of the two sulfur atoms in the ring creates an exceptionally high electron density with a reduction potential of –0.32 V. As compared to the reduced glutathione/oxidized glutathione (GSH/GSSG) couple at –0.24 V, DHLA holds a higher cellular reducing potential offering more protection from oxidative damage than GSH, a recognized cellular protector(4).

Whereas most antioxidants are active only in lipid or aqueous phase, ALA is amphipathic and active in both lipid and aqueous phases(3).

Alpha-lipoic acid (ALA), also known as thioctic acid, is considered a powerful metabolic antioxidant. In the body, ALA is reduced to a dithiol form, dihydrolipoic acid (DHLA), by NADH or NAD(P)H(1).

ALA was first discovered in 1951 as a vital cofactor in the pyruvate dehydrogenase complex of the citric acid cycle, essential in the production of cellular energy and the breakdown of α-keto acids and amino acids(2). Initially, ALA was considered a vitamin, however R-ALA is naturally synthesized de novo by plants and animals, is both water- and fat-soluble and is widely found in cellular membranes and cytosol(1, 2).

Whereas endogenously synthesized ALA functions in a protein bound form, scientific and medical interest surrounds the therapeutic use of supplemental free LA for its ability to quench free radicals, interaction with other antioxidants, and function in chronic disease prevention.

Dietary ALA is concentrated in animal tissues with high metabolic activity such as the kidney, heart and liver(2, 4). Non-animal sources include spinach, broccoli, tomato, garden pea, Brussels sprouts and rice bran.

Being a low molecular weight antioxidant, dietary or oral ALA is readily absorbed and has the ability to cross the blood/ brain barrier, entering the brain and cerebrospinal fluid(1, 2, 4). Although ALA is synthesized de novo in the mitochondria via lipoic acid synthase, potentially therapeutic levels are only reached with supplementation of free ALA.

Pharmacokinetic studies have shown that about 20–40% of oral racemic ALA is absorbed(1). Furthermore, with plasma levels peaking 2 hours after supplementation, ALA is rapidly metabolized and excreted, returning to pre- supplementation levels in 4 hours. Supplementing oral ALA with food decreases maximal and total plasma ALA; however S-ALA uptake appears to be more adversely affected than the R-isomer.

Therapeutic doses in humans range from 200 to 1800 mg ALA/day(4), and it has been observed that an oral dose of 600 mg/day provides the optimum risk-to-benefit ratio(7).

ALA's sfety of use:

ALA supplementation has been found to be safe and associated with very few serious side effects(8). The no- observed-adverse-effect level (NOAEL) for ALA is considered to be 60 mg/kgbw/day. Safety analysis showed a dose- dependent increase in nausea, vomiting, and vertigo with oral supplementation over 600 mg/day(7).

Direct Free Radical Scavenger:

R-ALA and its reduced counterpart, dihydrolipoic acid (DHLA), are a potent antioxidant pair. Together they have the ability of quenching hydroxyl radicals, singlet oxygen, peroxide, hypochlorous acid, peroxynitrite, nitric oxide, and superoxide radicals.

Regeneration of Endogenous Antioxidants:

Studies show that ALA has the ability to regenerate vitamin C, coenzyme Q10, glutathione, and vitamin E. Unlike ascorbic acid, DHLA can be recycled from ALA, and therefore is not destroyed by quenching free radicals. Furthermore, ALA administration has been shown to increase reduced glutathione (GSH) synthesis by up-regulating enzyme of γ-glutamylcysteine ligase (GCL)(11).

Heavy Metal Chelation:

R-ALA has been shown to bind iron, copper, mercury and cadmium, which can stimulate free radical damage by generating highly toxic hydroxyl radicals. ALA and DHLA exhibit the ability to chelate the redox-active transition metals leading to increased excretion, thereby enhancing detoxification. ALA may therefore mitigate oxidation reactions that are accelerated by metals such as copper and iron. Copper has been implicated in lipid peroxidation: studies have shown that DHLA chelates copper and may slow this peroxidation process(1). ALA has also been found to decrease iron uptake from transferritin, and increases iron deposition to ferritin, thereby increasing levels of ferritin(11).

Protein Repair and Protection:

ALA is capable of repairing methionine, essential in proteins with a low turnover rate. Tissue damage can be cause by protein oxidation and by glycosylation of hemoglobin. Upon examination of the effects of R-ALA, 20% less protein oxidation was exhibited, and 25% less protein carbonyl was found in the liver(1). Recent studies confirm the known applicability of R-ALA in the mitigation of complications of diabetes mellitus such as cataracts, polyneuropathy, and nephropathology(1).

R-ALA in Oxidative Stress:

ALA is a cofactor of a variety of enzymatic processes. Results suggest that the strong protective effects of R-ALA (a cofactor in mitochondria) have a place in age-related diseases associated with a decline in mitochondrial function and oxidative stress(11).

ALA's anti-inflammatory effescts:

R-ALA has been shown to have 10× the anti-inflammatory effects compared to the combined R-ALA and S-ALA(12). When comparing R-ALA to vitamin C and glutathione, studies show R-ALA to be the most demonstrate improved glucose oxidation and glycogen synthesis, and ultimately resulted in decreased glucose regulating hormone levels and free fatty acids.

Higher resistance to the function of the glucose regulating hormones may further be complicated by the accumulation of triglyceride in skeletal muscle. Triglyceride accumulation is affected by ALA by activating AMP-activated protein kinase (AMPK)(17). AMPK decreases accumulation of triglycerides, enhances cellular metabolism and improves glucose regulating sensitivity.

Another complication of diabetes is microangiopathy. A step in the progression of microangiopathy is accelerated apoptosis of endothelial cells. This process impairs the endothelial barrier function and induces a higher turnover of cells in order to keep it intact. R-ALA has been shown to improve both micro- and macroangiopathy(14).

ALA and vision health:

Another area of complication in diabetes mellitus is ocular health. Research shows R-ALA to have a positive impact on retinoblastoma protein, a tumor-suppressive protein(14). Using cultured human fetal retinal pigment epithelial cells (hfRPE), it was found that R-ALA reduced levels of ROS caused by tert-butyl hydroperoxide (tBOOH) (0.2 mM of R-ALA decreased levels by 23%, and 0.5 mM of R-ALA reduced ROS by 49%)(11). R-ALA (0.5 mM) also increased viability of oxidant treated hfPRE cells from 38% to 90% of control cells(11). These results are attributed to an up-regulation of enzyme GCL and reduced glutathione(11). In rodent models, only R-ALA, but not S-ALA, demonstrated this effect(11).

Oxidant-induced mitochondrial dysfunction and apoptosis of retinal pigment epithelial cells (RPE) is thought contribute to age-related macular degeneration(11). ALA may exert a protective mechanism via direct antioxidation, mitochondrial protection and by increasing intracellular glutathione. These protective effects are also seen in studies of oxidative stress in RPE produced by acrolein (a mitochondrial toxicant found in cigarette smoke)(18). ALA also aids in the prevention of iron accumulation in epithelial cells of the lens(5).

AlA and Parkinson's disease:

Parkinson’s disease (PD) is a neurodegenerative disorder associated with loss of dopaminergic neurons. There has been a proven link between the inflammatory response, increased cytokine formation, and neurodegeneration. Oxidative stress is central in the pathogenesis of this disease. Furthermore, dopaminergic neurons are also prone to autooxidation, accelerated by iron and copper. Patients diagnosed with PD exhibit decreased glutathione levels, and increased ROS levels in the substantia nigra. ALA has been implicated as beneficial in medical treatment of Parkinson’s as ALA can cross the blood brain barrier and accumulate in cells where it can improve levels of GSH, bind metals such as iron, and combat ROS(19).

ALA and dementia:

Dementia is caused by neurodegeneration, and vascular changes and Alzheimer’s disease. ALA has been suggested as a treatment in the early stages as it activates choline acetyltransferase which increases the levels of acetylcholine (ACh), and by increasing glucose uptake(6, 20). ALA also increases glutathione, commonly deficient in those suffering from Alzheimer’s disease. ALA has the ability to chelate transition metals that can contribute to ROS production(20). Clinically, studies have shown that R-ALA may positively impact the progression and development of Alzheimer’s disease and related dementias(21).

Ingredients:

Purity Contains no preservative, artificial flavor or color, sugar, dairy, wheat, gluten, corn or yeast.

Suggested Dose:  1 to 2 capsules daily with meals or as directed by your health care practitioner.