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 commonly 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 that are important in dementia and Alzheimers are Anti-oxidant and Niacin Therapy.
Targeted 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.
Advanced niacin therapy (as used in the treatment of schizophrenia) can be extremely helpful in dementia as is described in the journal article by Morris et al. in 2004 titled Dietary niacin and the risk of Alzheimer’s disease and cognitive decline. This article considered that “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.” This prospective study with adults aged 65+ demonstrated that higher dietary intake of niacin slowed age-related cognitive decline and protected against the development of Alzheimer’s. Longitudinal follow-up for up to six years with cognitive assessment and clinical evaluation showed that those with the highest niacin consumption had substantially lower relative risks for incident Alzheimer’s. This protective effect was still pronounced after excluding individuals with CVD, low baseline cognition, and lower education histories.