Orthomolecular approach to Dementia and Alzheimer’s
Yes, dementia is a neurodegenerative brain disease that can often be helped with advanced orthomolecular nutritional therapy. Harold Foster provided an excellent book that reviews available research on Alzheimer’s and dementia and prognostic outcome is deemed promising with targeted clinical nutrient approaches (Foster HD: What Really Causes Alzheimer’s Disease? 2004).
The key to this treatment is having the flexibility of a targeted approach that addresses primary health syndromes common in mental health and neurodegenerative disease. Primary syndromes of import are heavy metal toxicity, hypothyroid metabolism, protein catabolism, and undermethylation metabolic mental health compromises.
Dementia cases not uncomonly have severe undermethylation and heavy metal deposition with low thyroid metabolism. Secondary metabolic issues common in neurodegeneration include pernicious anemia (B12 deficiency), iron deficiency and dysglycemia. The targeted approach will rule out all these syndromes and more and this is important because every case will have its own unique imbalance with associated varying severity.
The clinical nutrient (orthomolecular) approaches that addresses all of these nutrient biochemical aspects are otherwise not considered in conventional mainstream drug therapy. Another two seperate interventions in dementia and Alzheimers to note are targeted anti-oxidant therapy and advanced niacin therapy.
Anti-oxidant therapy is key in any neurodegenerative dominant disorder and targeted testing again can help focus therapy in this regard. Oxidation from metals (aluminum, etc.) and degenerative tissue processes needs to be addressed in an optimal approach to any dementia or neurodegenerative condition.
Niacin can be extremely helpful in dementia as is described below in the PubMed abstract by Morris et al. in 2004.
Morris, M.C., Evans, D.A., Bienias, J.L., Scherr, P.A., Tangney, C.C., Hebert, L.E., Bennett, D.A., Wilson, R.S., and Aggarwal, N. (2004). Dietary niacin and the risk of Alzheimer’s disease and cognitive decline. Journal of Neurology, Neurosurgery and Psychiatry, 75(8), 1093-1097.
Background: Dementia can be caused by severe niacin insufficiency, but it is unknown whether variation in intake of niacin in the usual diet is linked to neurodegenerative decline. We examined whether dietary intake of niacin was associated with incident Alzheimer’s disease (AD) and cognitive decline in a large, prospective study.
Methods: This study was conducted in 1993–2002 in a geographically defined Chicago community of 6158 residents aged 65 years and older. Nutrient intake was determined by food frequency questionnaire. Four cognitive tests were administered to all study participants at 3 year intervals in a 6 year follow up. A total of 3718 participants had dietary data and at least two cognitive assessments for analyses of cognitive change over a median 5.5 years. Clinical evaluations were performed on a stratified random sample of 815 participants initially unaffected by AD, and 131 participants were diagnosed with 4 year incident AD by standardised criteria.
Results: Energy adjusted niacin intake had a protective effect on development of AD and cognitive decline. In a logistic regression model, relative risks (95% confidence intervals) for incident AD from lowest to highest quintiles of total niacin intake were: 1.0 (referent) 0.3 (0.1 to 0.6), 0.3 (0.1 to 0.7), 0.6 (0.3 to 1.3), and 0.3 (0.1 to 0.7) adjusted for age, sex, race, education, and ApoE e4 status. Niacin intake from foods was also inversely associated with AD (p for linear trend = 0.002 in the adjusted model). In an adjusted random effects model, higher food intake of niacin was associated with a slower annual rate of cognitive decline, by 0.019 standardised units (SU) per natural log increase in intake (mg) (p = 0.05). Stronger associations were observed in analyses that excluded participants with a history of cardiovascular disease (ß = 0.028 SU/year; p = 0.008), those with low baseline cognitive scores (ß = 0.023 SU/year; p = 0.02), or those with fewer than 12 years’ education (ß = 0.035 SU/year; p = 0.002)
Conclusion: Dietary niacin may protect against AD and age related cognitive decline.