B vitamins and omega-3 fatty acids are essential nutrients involved in numerous metabolic processes that play a significant role in cognitive health. Due to the lack of new drugs to treat cognitive impairment, researchers are looking more and more at nutrients to delay or prevent cognitive decline. An interesting study just published January 6, 2016 in the Journal of Alzheimer’s Disease addressed this issue. Here, researchers investigated whether omega-3 fatty acid status had an effect on the use of B vitamins in mild cognitive impairment (MCI).
Previous studies have already established that B vitamins can slow cognitive decline in the elderly. In fact, last week I shared the importance of vitamin B12 in learning and memory later in life, and the relationship between age-related decreased B12 levels and their association with neurological disorders.
In this new study, we see that this effect of B vitamins on cognitive decline was most pronounced in those who had above average homocysteine levels, a biomarker related to B vitamin status that may be toxic to the brain. The research team found that there was a link between omega-3 levels, homocysteine, and brain atrophy rates. The connection may lie in the fact that homocysteine plays a role in regulating phospholipid metabolism and omega-3 distribution by the methionine cycle, and B vitamins are essential for the production of phospholipids.
Two hundred and sixty six participants with MCI over 70 year of age were randomized to B vitamins (folic acid, vitamins B6 and B12) or placebo for 2 years. Researchers measured baseline cognitive test performance, clinical dementia rating (CDR) scale, and plasma concentrations of homocysteine, DHA and EPA fatty acids. The final results for verbal delayed recall, global cognition, and CDR were better in the B vitamin-treated group according to increasing baseline concentrations of omega-3s. In contrast, the scores in the placebo group were similar across these concentrations. Among those with good omega-3 status, 33% of those on B vitamin treatment had global CDR scores >0 compared with 59% among those on placebo. Among all 3 outcome measures, higher concentrations of DHA alone significantly improved the cognitive effects of B vitamins, whereas EPA appeared to be less effective.
This study demonstrated that B vitamins have no effect on cognitive decline in MCI when omega-3 levels are low. However, when omega-3 levels are in an upper normal range, B vitamins can help slow down cognitive decline and brain atrophy. These findings suggest that a combination of fish oil supplements and B vitamins may help to improve cognition and reduce age-related memory decline.
Note: The ratio of EPA to DHA needs to be 2:1
My practice utilizes a wide array of Omega products. A wide array because what works for one patient may not necessarily work for another.
Call or write me for additional discussion on this all important connection between the Omega’s, Methylation, B Vitamins and Cognition
Walnuts are a delicious and healthy snack, and they make a great addition to sweet as well as savory dishes. But this nut’s benefits aren’t limited to culinary applications. Walnut-rich diets may be helpful in the fight against cancer through multiple mechanisms.
Like most other nuts, walnuts are low in carbohydrates and high in minerals and unsaturated fats. They’re a good source of manganese, copper, and magnesium, and, compared to most other nuts, walnuts contain a fair amount of omega-3 alpha-linolenic acid (about 2.5g/ounce). In fact, this is the highest amount of any tree nut. They are high in omega-6 linoleic acid as well (about 10.6g/ounce), but they stand out among other nuts in that most others contain very little omega-3 to balance that out.
Researchers have found that the omega-3s, phytosterols, and antioxidants in walnuts all may be especially beneficial for colon cancer. In a mouse model of colon cancer, mice fed the human equivalent of two servings of walnuts a day showed significantly reduced colorectal tumor growth, largely resulting from reduced angiogenesis. Researchers believe microribonucleic acids (miRNAs) may help explain the relationship between walnut consumption and disease risk. miRNAs are short, noncoding RNAs (21–25 nucleotides) that play a role in regulating posttranscriptional gene expression, affecting the stability and translation of messenger RNA. miRNAs may mediate cellular differentiation, development and apoptosis, and may act as an oncogene under certain conditions. Inhibition of some types of miRNA activity is associated with reductions in tumor growth, angiogenesis, metastasis, and enhanced tumor suppression in animal models of colorectal cancer.
Researchers determined that the walnut-rich diet led to higher incorporation of n-3 fats into the cell membrane of colorectal tumor cells, which decreased expression of inflammatory cytokines, leading to slower proliferation and increased apoptosis of cancerous cells. The colorectal tumors of walnut-fed mice contained significantly more total n-3 than the tumors of untreated mice, including ALA, but also EPA and DHA, suggesting that some of the ALA was elongated into the longer-chain fatty acids. This study showed a negative association between final tumor size and the total tissue concentration of omega-3 fatty acids, and an individual association with concentrations of DPA, EPA and DHA. These fatty acids may play a role in managing tumor size by affecting signaling involved in cellular proliferation and tissue vascularization.
The potential influence of walnuts on cancer isn’t solely due to its fatty acid composition. Researchers speculate that the phytosterol, β-sitosterol, in walnuts, may affect apoptosis and initiate arrest of cell proliferation. Walnuts also contain γ-tocopherol, which may result in tumor growth suppression by upregulating PPAR activity, and reducing angiogenesis. “Activated PPAR-γ signals antiproliferative, antiangiogenic, and prodifferentiation pathways in multiple tissue types.” β-Sitosterol has demonstrated pro-apoptotic effects, and an ability to arrest the first stage (G1) of cellular proliferation.
Other studies support a protective role for walnuts as a whole food, as opposed to isolated omega-3 fats, lending more evidence to synergistic effects of multiple compounds in walnuts beyond the known effects of n-3s. “Mouse studies in which walnuts were added to the diet have shown the following compared with the control diet: 1) the walnut-containing diet inhibited the growth rate of human breast cancers implanted in nude mice by ∼80%; 2) the walnut-containing diet reduced the number of mammary gland tumors by ∼60% in a transgenic mouse model; 3) the reduction in mammary gland tumors was greater with whole walnuts than with a diet containing the same amount of n–3 fatty acids, supporting the idea that multiple components in walnuts additively or synergistically contribute to cancer suppression.”
The combined effects of multiple compounds in walnuts support a role for this whole food in the fight against cancer—one that might not be achievable through administering isolated individual substances. Nutritional and nutraceutical supplements have their place in maintaining optimal health, and sometimes nature can also package nutrients together just right.
Vitamin E & the Brain
Among fat-soluble vitamins, vitamin E often gets sidelined in favor of compounds with better-known functions. People automatically associate vitamin A with vision and eye health, vitamin D with calcium homeostasis and bone health, and vitamin K with proper blood clotting. When vitamin E makes a rare appearance in discussions about health and nutrition, it’s often in the context of infertility, since deficiency of this nutrient is associated with reproductive difficulties in animals and humans. But with advances in technology, scientists continue to uncover previously unknown and under-appreciated roles for vitamins and minerals. In the case of vitamin E, this nutrient might have a significant role to play in brain health and neurological function.
Results of a recent animal study support a requirement for sufficient vitamin E in order to deliver and maintain adequate levels of DHA and DHA-dependent phospholipids in the brain. Neuronal cell membranes are rich in cholesterol and polyunsaturated fats, which are highly susceptible to oxidation. With vitamin E having an antioxidant function, a deficiency can have dangerous consequences for brain health. In fact, severe vitamin E deficiency can manifest as cerebellar ataxia, demonstrating the importance of this nutrient for proper functioning of the central nervous system. Vitamin E deficiency also results in reduced myelination of spinal cord fibers, and leads to neuropathic and myopathic lesions all of which may have disastrous consequences for cognition and neuromuscular coordination.
A small, double-blind, placebo-controlled crossover study demonstrated that vitamin E supplementation led to improved scores on the Abnormal Involuntary Movement Scale (AIMS) in tardive dyskinesia patients who had had the condition for less than five years. The vitamin intervention was less effective in subjects with more longstanding disease.
The cerebrospinal fluid (CSF) of Alzheimer’s disease patients has been shown to be low in Vitamin E.While this specific finding may play a direct role in disease pathology, it might also simply be a reflection of overall poor nutrient status resulting, in part, from the modern diet, which is high in refined carbohydrates and low in micronutrients. However, considering the important role of vitamin E in the central nervous system, a lower level of this nutrient in CSF may expose neurons to profound free radical damage, leading to memory loss and declining cognitive function. Compared to placebo, patients with moderately advanced Alzheimer’s given 2000 IU of vitamin E per day experienced delayed deterioration of cognitive function. . Other studies indicate vitamin E is more effective in combination with another important antioxidant, vitamin C.
Reviews and meta-analyses of studies involving the use of supplemental vitamin E show mixed results, leading researchers to stress using caution regarding high doses of vitamin E. Some study authors suggest emphasizing food sources of vitamin E, or a multivitamin with around 30 IU of alpha-tocopherol, rather than isolated vitamin E supplements that deliver a higher dose. As is true for the use of any nutritional compound in a healthcare setting, caution should, of course, be practiced when dosing vitamin E. However, the mixed outcomes of studies employing vitamin E may be the result of confounding from the makeup of the supplements themselves. For example, a high alpha-tocopherol preparation may result in different effects than one with a higher fraction of gamma-tocopherol.
While frank vitamin E deficiency is rare, it is not unheard of. Vitamin E Deficiency can result from inborn errors of tocopherol transfer proteins, as well as disorders of lipid absorption, transport, and assimilation. Conditions that affect digestive efficiency, such as celiac disease and Crohn’s disease, may interfere with proper absorption of fat-soluble nutrients. Biliary insufficiency resulting from compromised liver or gallbladder function may also contribute. An additional cause of vitamin E deficiency (as well as deficiency of many other nutrients) is bariatric surgery. While this can be a lifesaving procedure for many people, altering the anatomy of the digestive tract can have severe consequences for nutrient absorption, and extra care should be given to ensuring sufficient nutrient uptake in the body.
The foods richest in vitamin E are nuts and seeds, whole grains, and vegetable oils, such as corn, soybean, and safflower oils. However, overly large intake of these oils is not recommended, due to the potential for skewing the dietary omega-6/omega-3 fatty acid ratio toward the generally pro-inflammatory omega-6 pathways.
NOTE: GCEL (Glutathione) is 5000 times stronger than Vitamins C & E,
- Vitamin C has 5 extra electrons to donate
- Vitamin E has 3 extra electrons to donate
- GSH has 1 million extra electrons to donate