Age related illnesses | May 23, 2014 | Author: The Super Pharmacist
Many foods, dietary supplements and herbal remedies are presented as alternative treatments having beneficial effects on memory and cognitive brain functions. They are thought to be helpful for patients with dementia and Alzheimer’s disease.
Some of the commonly cited supplements are:
Feeding problems: People with dementia and Alzheimer’s disease may have difficulty eating. This can be due to a number of reasons. They may simply forget to eat, they may no longer be capable of preparing their own meals, medications or chronic conditions may affect their appetite or they may actually find it difficult to chew and swallow food. This can lead to nutritional deficiencies which will only aggravate their condition. Caregivers should make sure that people with dementia and Alzheimer’s disease are not affected by feeding problems and are appropriately nourished and hydrated.
There is no specific diet recommended for dementia or Alzheimer’s disease. However the role of a healthy and balanced diet is as important as ever. Adequate hydration is equally essential. Some studies compare the existence of urinary tract infections (UTIs) and dementia, show a positive link. These studies suggest that dehydration is the common link between UTIs and dementia.
Components which cannot be good for any diet plan include excessive salt, refined sugar, saturated fats and cholesterol.
These dietary components should be moderated.
Lack of regulation and evidence for most supplements: Marketed dietary supplements are different from medications in two respects. Firstly, they are not regulated. Since they are considered “food” supplements, they are not subject to the same strict regulations for approval for use as drugs. Secondly, most supplements lack scientific research evidence to back their claims. Any decision to use supplements should be based on a proper knowledge of their pros and cons.
These are a type of polyunsaturated fatty acid found in seafood, canola oil and walnuts.
Link to brain biochemistry: One type of omega-3 fatty acid called docosahexaenoic acid (DHA) is a constituent of brain nerve cell membranes. It is thought the supplementation of this specific fatty acid could protect cells of the central nervous system, prevent inflammatory processes and subsequently slow the progression of dementia. Omega-3 fatty acids are welcome in the diet as they have a demonstrated beneficial role in preventing strokes and protecting the heart and blood vessels. Evidence of their role in reversing cognitive decline is inconclusive.
A type of water-soluble vitamin present mainly in animal-derived foods such as seafood, poultry, eggs and meat.
Link to brain biochemistry: Vitamin B12 is linked to myelin sheath synthesis for neurons of the brain which has a role in signal conduction. Vitamin B12 deficiency is a known cause of reversible dementia, where its provision can cure the patient. In patients with progressive causes of dementia such as Alzheimer’s disease with no underlying deficiency of this vitamin, there is no extra benefit of it as a dietary supplement. Blood test results can confirm the need for supplementation.
A type of water-soluble vitamin found in whole grain cereals, eggs and pork.
Link to brain biochemistry: Vitamin B1 is essential for numerous enzymatic reactions in the brain. Vitamin B1 deficiency is a cause of reversible dementia. It can develop under many circumstances; the classic example being chronic alcoholism. In all such cases its provision can cure the patient. In patients with progressive causes of dementia such as Alzheimer’s disease with no underlying deficiency of this vitamin, there is no extra benefit of it as a dietary supplement.
A type of fat-soluble vitamin common in plant such as nuts and seeds and oils - wheat germ, almone, olive and safflower oil.
Link to brain biochemistry: Vitamin E is well-known for its antioxidant properties. Oxygen free radicals can damage cells and tissues including nerve cells of the brain. Vitamin E gets rid of such radicals. Though some research suggests a beneficial role of vitamin E in dementia and Alzheimer’s disease, appropriate amounts should be used as too much of it can be harmful.
Extracts of the Ginkgo biloba plant are supposed to have antioxidant and anti-inflammatory properties.
Link to brain biochemistry: Oxygen free radicals can damage cells and tissues including nerve cells of the brain. It is thought that Ginkgo biloba gets rid of such radicals. Some studies suggest a beneficial role of Ginkgo for cognitive impairment.4 Other studies seem to find no difference from a placebo. The evidence is inconclusive.
This compound can be produced inside body cells. It acts as an antioxidant and is a component of the cellular respiratory chain.
Link to brain biochemistry: Oxygen free radicals can damage cells and tissues including nerve cells of the brain. It is thought that coenzyme Q10 gets rid of such radicals. Idebenone, a synthetic form of coenzyme Q10, has been used for Alzheimer’s disease, but no significant benefits have been recorded. Various forms of this supplement can be found in pharmacies. Recent studies show ubiquinol, the active form of coenzyme Q10, has superior absorption and higher bioavailability than other forms of coenzyme Q10 available on the market.
Freund-Levi Y, Eriksdotter-Jonhagen M, Cederholm T, Basun H, Faxen-Irving G, Garlind A, et al. Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study: a randomized double-blind trial. Arch Neurol. 2006;63:1402–8.
Lloret A, Badia MC, Mora NJ, Pallardo FV, Alonso MD, Vina J. Vitamin E paradox in Alzheimer’s disease: it does not prevent loss of cognition and may even be detrimental. Journal of Alzheimer’s disease : JAD.2009;17:143–149.
Morris M.C., Schneider J.A., Tangney C.C. Thoughts on B-vitamins and dementia. J. Alzheimer's Dis.2006;9:429–433.
Mazza M, Capuano A, Bria P, et al. Ginkgo biloba and donepezil: a comparison in the treatment of Alzheimer's dementia in a randomized placebo-controlled double-blind study. Eur J Neurol 2006;13:981–5.