This article was originally distributed via PRWeb. PRWeb, WorldNow and this Site make no warranties or representations in connection therewith.
SOURCE: Nutri-Med Logic Corp
A newly published study Investigating associations between 10 nutrients and cognition, more specifically nutrients with either anti-inflammatory, pro-inflammatory, anti-oxidant or methyl donor properties, found only higher dietary intake of one nutrient, Omega-3, had the strongest association with lower levels of the proteins Abeta 40-42, two proteins with key roles in Alzheimer’s and cognitive decline. Agreeing with this study, Nutri-Med Logic Corp adds, while many studies have suggested a protective role for anti-inflammatory, anti-oxidant and methyl donor nutrients but it is the inherent neuro-protective nature of the DHA Omega-3 Fatty Acids that makes it an effective dietary intervention.
Miami, Florida (PRWEB) May 09, 2012
A newly published study investigating the dietary association of nutrients and cognitive decline or Alzheimer’s, more specifically nutrients such as saturated fat, monounsaturated fatty acid (Omega-9, found in olive oil), polyunsaturated fatty acids of Omega-3 and Omega-6, vitamin E, vitamin C, Beta-carotene, vitamin B-12, folate (B-9) and vitamin D, suggests that Omega-3 resulted in better protection against elevated levels of Abeta 40-42, proteins associated with development and progression of Alzheimer’s.
This recent study incorporated a group of nutrients, all of which are thought to confer protection against Alzheimer’s.
Beta Carotene (precursor to vitamin A), vitamin E and vitamin C are all known for their anti-oxidant properties and countering oxidative stress. Compelling evidence has associated oxidative process to neuro-degeneration and the development of diseases such as Alzheimer’s. Anti-oxid Redox Signal. 2012 Jan 18.
Oxidative stress denotes lack of adequate anti-oxidant defense (redox imbalance). Anti-oxidants generally help in neutralizing free radicals, molecules that damage the cells. Abeta 42, a major cause of early-onset familial Alzheimer’s has been associated with oxidative stress both in vitro and in vivo, in addition to which, it has been suggested that oxidative stress increases the precursor to Abeta 40-42. (1)
While lack of vitamin D has been more associated with the development of osteoporosis but a recent study has suggested that vitamin D3 helps in Alzheimer’s by activating cell signaling networks that could clear away plaques, formed by Abeta 40-42. Journal of Alzheimer’s. Vol. 29, No. 1, March 2012.
Vitamins B-9 (folate) and B-12 are both methyl donors. Methyl is a nutrient found in vitamins B-6, B-9 and B-12, as well as Choline. Methyl reduces the levels of another damaging protein (Homocysteine), which is considered to be an independent risk factor in Alzheimer’s and dementia but correlated with Abeta levels. Studies have shown that an increment in the blood homocysteine level (5 µmol per liter) increases the risk of Alzheimer's disease by 40 percent. (2)
While Omega-6 is a pro-inflammatory nutrient, found in red meat, and its excess consumption has been associated with degenerative conditions, Alzheimer included, but a recent study has proposed that a mixture of Omega-6 and Omega-9 alters the production of Abeta 40-42, the two key proteins blamed for Alzheimer’s. J Neurosci Res. 2011 Nov;89(11).
Saturated fat (high fat diet) has been suggested to decrease memory and learning through reducing brain-derived neurotrophic factor (BDNF), proteins that support survival of brain cells.(3)
While "practically" all of the nutrients, selected in this study, have been previously suggested by other recent or landmark studies to confer protective properties against Alzheimer’s, but when compared to Omega-3 none seems to be more effective or even as effective in protection against the formation of plaques, a key and specific cause of Alzheimer's. Plaques from Abeta 40-42 result in ultimate death of brain cells responsible for memory.
Of the important Omega-3 Fatty Acids, DHA fatty acids is precursor to Neuro-Protectin D-1 (NPD-1). Studies have shown that NPD-1 (a DHA-derived 10,17S-docosatriene) promotes brain cell survival via the induction of neuroprotective gene-expression programs that suppress Abeta42-induced neurotoxicity as well as opposing pre-mature death of brain cells. (4)
DHA Omega Fatty Acids is referred to as brain’s essential fatty acids.
DHA is also a precursor to Resolvin D, molecules that resolve inflammation in the brain. Numerous studies have suggested that chronic inflammation enhances the production of Abeta 40-42, suggesting a link between excessive pro-inflammatory agents and Alzheimer's disease. Omega-3 Fatty Acids of EPA and DHA are anti-inflammatory nutrients, not only beneficial in resolution of the inflammation in the brain but also in resolving systemic inflammation.
In conclusion, Nutri-Med Logic Corp agreeing with this study adds that adequate dietary supplementation of Omega-3 not only lowers the Abeta 40-42, proteins that damage brain cells, but also it resolves the inflammation in the brain, protects the brain cells from oxidative stress-induced cell injury and premature death.
Nutri-Med Logic Corp is also a producer of dietary supplements such as a Pharmaceutical Grade R-Alpha Lipoic Acid (the natural type of Lipoic Acid), a universal anti-oxidant and the dietary supplement of choice for the Diabetics, in Germany for decades;
Producer of PolyEnylPhosphatidylCholine (PPC 425mg), an extract of soy, a pure and effective dietary source of choline and the recommended dietary supplement for those with Fatty Liver and Alcoholic Liver Disease, in Europe for decades.
Nutri-Med Logic's products are Formulated Based on Nutritional Logic, made from the highest quality raw materials that are manufactured in pharmaceutical facilities, encapsulated in pharmaceutical facilities and packaged in pharmaceutical facilities.
It must be noted that the studies, statements or sources above and below have not been evaluated by The FDA and, thus, one should not relate the cause of any diseases, stated herein, to lack of the dietary supplements, stated herein, nor equate their supplementation to prevention, treatment or cure.
1. J. Biol. Chem;Apirl, 1996, 271, 10169-10174
2. New Engl J Med; 2002 346: 476-83
3. Neuroscience. 2002;112(4):803-14
4. J. Clin Invest. 2005 Oct;115(10):2774-83.
For the original version on PRWeb visit: http://www.prweb.com/releases/prweb2012/5/prweb9489437.htm
1115 Mt. Auburn Road
Closed Captioning Contact: