A number of avenues have been taken to study the treatment of age-related cognitive decline/impairment (think diseases like Alzheimer's Disease). Nutrition has gotten a lot of focus, with studies looking at Omega 3 fatty acid intake and fruit and vegetable consumption (even in the form of juices) potentially lowering the risk of Alzheimer's Disease (AD) and protecting against cognitive decline (1,2,3).
Another major area for nutrition in the prevention of cognitive decline (and seemingly most age-related diseases) has looked into mitigating oxidative stress - a major factor in the pathogenesis of Alzheimer's Disease is the oxidative up-regulation of beta and gamma secretase, required for the generation of beta-amyloid plaques (4). There are other components of the disease including the ApoE4 genotype (6), as well as advanced glycated end products and blood brain barrier permeability but I won't discuss that at the moment - though it's good to know that the latter is a major component and is why some call Alzheimer's type 3 Diabetes.
If oxidative stress is an issue, it stands to reason that antioxidants may have some therapeutic effect. Unfortunately, past research looking at vitamin E wasn't overly promising (5). However, a couple new studies came out recently with more promising results - one in JAMA (7) that showed 2000 IU/day (500IU above the set Upper Limit - practically unattainable consuming foods) supplementation of alpha-tocopherol slowed cognitive function's decline; the other in Experimental Gerontology (EG) (8) that looked at serum markers of both tocopherols and tocotrienols, markers of oxidative damage and cognitive impairment, showed that those older adults with elevated serum levels of tocopherols and tocotrienols at baseline were protected against cognitive impairment 8 years later (while they did their best to control statistically for confounding variables, they still can't say that individuals continued to have elevated serum Vitamin E levels beyond baseline measurements).
From these studies, there's 3 things I'd like to point out:
1. Vitamin E is not one chemical - I've said this before. Though the JAMA article saw positive effects to alpha tocopherol, the medical community has largely only paid attention to form of Vitamin E, ignoring the other 7 components in the vitamin E complex. The authors in (8) note that other Vitamin E metabolites likely have protective effects and need more consideration - their study built on another cohort Swedish cohort that also looked at all 8 forms of vitamin E and found similar results regarding the importance the whole vitamin E complex (9).
2. Treatment vs Habitual Consumption - these studies are a good examples of the difference between treatment and preventative medicine. The JAMA study looked at those with mild to moderate AD and began treatment with high doses of vitamin E. The EG study followed individuals who began with no known cognitive impairments and followed up with individuals 8 years later. The JAMA study employed a large vitamin E supplement as treatment, whereas the EG study measured the effectiveness of maintaining regular higher serum levels of Vitamin E (assuming baseline values were reflective of habitual intakes) in reducing cognitive decline. Both warrant further research and show some promise for Vitamin E's role as both a preventative measure and treatment for age-related cognitive decline.
3. Where's the E in our Diet ??- after the 'i' and before the 't' is the only good answer there. Or at least, if you look at MyPlate, it would appear so. My biggest beef with MyPlate is that there's no place for nuts and seeds - the best and most health-promoting way to get your vitamin E (yes, there are other sources, but nowhere near as potent as nuts/seeds). You'll be hard pressed to find any evidence that suggests regular nut and seed consumption of 1-2 servings a day is detrimental. Yet the plate is missing a category that they fit into well - some will argue protein, but every time i've seen the table presented, it always states lean protein; and a serving in the old pyramid was 1 tbsp of nut butter as a protein food (about 3.5g of protein ??). The plate needs some reworking.
For now, it seems that high doses of vitamin E might play a beneficial role in delaying cognitive impairment for those with mild to moderate, and moderately severe Alzheimer's Disease - however, for clinicians, benefits need to be weighed against symptoms of hypervitaminosis E (increased hemorrhaging-already a potential worry for the older population) , and associations between Vitamin E supplementation and all-cause mortality (10). It also appears that regularly consuming dietary sources of both tocopherols and tocotrienols has an appreciable effect on delaying the onset of Alzheimer's symptoms. More research needs to be undertaken, looking at more time points, and in an age range less close to the onset of Alzheimer's.
Let's get more nuts and seeds back into the diet! They're not only great for vitamin E, but for slowing down digestion of carbohydrates, potentially protecting against insulin resistance/diabetes, another major risk factor for AD (11).
1. http://www.ncbi.nlm.nih.gov/pubmed/16216930
2. http://www.ncbi.nlm.nih.gov/pubmed/12873849
3. http://www.ncbi.nlm.nih.gov/pubmed/16945610
4. http://www.ncbi.nlm.nih.gov/pubmed/21901428
5. http://www.ncbi.nlm.nih.gov/pubmed/18469254
6. http://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-genetics-fact-sheet
7. http://jama.jamanetwork.com/article.aspx?articleid=1810379
8. http://www.ncbi.nlm.nih.gov/pubmed/24113154
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738400/
9. http://www.ncbi.nlm.nih.gov/pubmed/20413888
10. http://www.ncbi.nlm.nih.gov/pubmed/21235492
11. http://www.ncbi.nlm.nih.gov/pubmed/21787319
Another major area for nutrition in the prevention of cognitive decline (and seemingly most age-related diseases) has looked into mitigating oxidative stress - a major factor in the pathogenesis of Alzheimer's Disease is the oxidative up-regulation of beta and gamma secretase, required for the generation of beta-amyloid plaques (4). There are other components of the disease including the ApoE4 genotype (6), as well as advanced glycated end products and blood brain barrier permeability but I won't discuss that at the moment - though it's good to know that the latter is a major component and is why some call Alzheimer's type 3 Diabetes.
If oxidative stress is an issue, it stands to reason that antioxidants may have some therapeutic effect. Unfortunately, past research looking at vitamin E wasn't overly promising (5). However, a couple new studies came out recently with more promising results - one in JAMA (7) that showed 2000 IU/day (500IU above the set Upper Limit - practically unattainable consuming foods) supplementation of alpha-tocopherol slowed cognitive function's decline; the other in Experimental Gerontology (EG) (8) that looked at serum markers of both tocopherols and tocotrienols, markers of oxidative damage and cognitive impairment, showed that those older adults with elevated serum levels of tocopherols and tocotrienols at baseline were protected against cognitive impairment 8 years later (while they did their best to control statistically for confounding variables, they still can't say that individuals continued to have elevated serum Vitamin E levels beyond baseline measurements).
From these studies, there's 3 things I'd like to point out:
1. Vitamin E is not one chemical - I've said this before. Though the JAMA article saw positive effects to alpha tocopherol, the medical community has largely only paid attention to form of Vitamin E, ignoring the other 7 components in the vitamin E complex. The authors in (8) note that other Vitamin E metabolites likely have protective effects and need more consideration - their study built on another cohort Swedish cohort that also looked at all 8 forms of vitamin E and found similar results regarding the importance the whole vitamin E complex (9).
2. Treatment vs Habitual Consumption - these studies are a good examples of the difference between treatment and preventative medicine. The JAMA study looked at those with mild to moderate AD and began treatment with high doses of vitamin E. The EG study followed individuals who began with no known cognitive impairments and followed up with individuals 8 years later. The JAMA study employed a large vitamin E supplement as treatment, whereas the EG study measured the effectiveness of maintaining regular higher serum levels of Vitamin E (assuming baseline values were reflective of habitual intakes) in reducing cognitive decline. Both warrant further research and show some promise for Vitamin E's role as both a preventative measure and treatment for age-related cognitive decline.
3. Where's the E in our Diet ??- after the 'i' and before the 't' is the only good answer there. Or at least, if you look at MyPlate, it would appear so. My biggest beef with MyPlate is that there's no place for nuts and seeds - the best and most health-promoting way to get your vitamin E (yes, there are other sources, but nowhere near as potent as nuts/seeds). You'll be hard pressed to find any evidence that suggests regular nut and seed consumption of 1-2 servings a day is detrimental. Yet the plate is missing a category that they fit into well - some will argue protein, but every time i've seen the table presented, it always states lean protein; and a serving in the old pyramid was 1 tbsp of nut butter as a protein food (about 3.5g of protein ??). The plate needs some reworking.
For now, it seems that high doses of vitamin E might play a beneficial role in delaying cognitive impairment for those with mild to moderate, and moderately severe Alzheimer's Disease - however, for clinicians, benefits need to be weighed against symptoms of hypervitaminosis E (increased hemorrhaging-already a potential worry for the older population) , and associations between Vitamin E supplementation and all-cause mortality (10). It also appears that regularly consuming dietary sources of both tocopherols and tocotrienols has an appreciable effect on delaying the onset of Alzheimer's symptoms. More research needs to be undertaken, looking at more time points, and in an age range less close to the onset of Alzheimer's.
Let's get more nuts and seeds back into the diet! They're not only great for vitamin E, but for slowing down digestion of carbohydrates, potentially protecting against insulin resistance/diabetes, another major risk factor for AD (11).
1. http://www.ncbi.nlm.nih.gov/pubmed/16216930
2. http://www.ncbi.nlm.nih.gov/pubmed/12873849
3. http://www.ncbi.nlm.nih.gov/pubmed/16945610
4. http://www.ncbi.nlm.nih.gov/pubmed/21901428
5. http://www.ncbi.nlm.nih.gov/pubmed/18469254
6. http://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-genetics-fact-sheet
7. http://jama.jamanetwork.com/article.aspx?articleid=1810379
8. http://www.ncbi.nlm.nih.gov/pubmed/24113154
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738400/
9. http://www.ncbi.nlm.nih.gov/pubmed/20413888
10. http://www.ncbi.nlm.nih.gov/pubmed/21235492
11. http://www.ncbi.nlm.nih.gov/pubmed/21787319
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