UCLA professor Dale Bredesen does a study showing nearly complete resolution of dementia symptoms with a functional medicine approach: Optimize diet, increase and improve sleep, reduce stress, exercise regularly, stimulate brain function, analyze and replete nutrients including antioxidants and mitochondrial function, replace hormones including sex hormones and notably T3 in the elderly, remove heavy metals… The full article is long, but definitely check out the summary table link below.
Based on this initial research, Dr Bredesen has a book titled “The End of Alzheimers” and a formal treatment protocol called ReCODE has been developed which provides a comprehensive personalized program designed to improve cognition and reverse the cognitive decline.
Reversal of cognitive decline: A novel therapeutic program
Aging (Albany NY). 2014 Sep; 6(9): 707–717.
Published online 2014 Sep 27.
Author: Dale E Bredesen
This report describes a novel, comprehensive, and personalized therapeutic program that is based on the underlying pathogenesis of Alzheimer’s disease, and which involves multiple modalities designed to achieve metabolic enhancement for neurodegeneration (MEND).
The first 10 patients who have utilized this program include patients with memory loss associated with Alzheimer’s disease (AD), amnestic mild cognitive impairment (aMCI), or subjective cognitive impairment (SCI). Nine of the 10 displayed subjective or objective improvement in cognition beginning within 3-6 months, with the one failure being a patient with very late stage AD. Six of the patients had had to discontinue working or were struggling with their jobs at the time of presentation, and all were able to return to work or continue working with improved performance. Improvements have been sustained, and at this time the longest patient follow-up is two and one-half years from initial treatment, with sustained and marked improvement.
These results suggest that a larger, more extensive trial of this therapeutic program is warranted. The results also suggest that, at least early in the course, cognitive decline may be driven in large part by metabolic processes. Furthermore, given the failure of monotherapeutics in AD to date, the results raise the possibility that such a therapeutic system may be useful as a platform on which drugs that would fail as monotherapeutics may succeed as key components of a therapeutic system.
|Goal||Approach||Rationale and References|
|Optimize diet: minimize simple CHO, minimize inflammation.||Patients given choice of several low glycemic, low inflammatory, low grain diets.||Minimize inflammation, minimize insulin resistance.|
|Enhance autophagy, ketogenesis||Fast 12 hr each night, including 3 hr prior to bedtime.||Reduce insulin levels, reduce Aβ.|
|Reduce stress||Personalized—yoga or meditation or music, etc.||Reduction of cortisol, CRF, stress axis.|
|Optimize sleep||8 hr sleep per night; melatonin 0.5mg po qhs; Trp 500mg po 3x/wk if awakening. Exclude sleep apnea.|||
|Exercise||30-60′ per day, 4-6 days/wk||[37, 38]|
|Brain stimulation||Posit or related|||
|Homocysteine <7||Me-B12, MTHF, P5P; TMG if necessary|||
|Serum B12 >500||Me-B12|||
|CRP <1.0; A/G >1.5||Anti-inflammatory diet; curcumin; DHA/EPA; optimize hygiene||Critical role of inflammation in AD|
|Fasting insulin <7; HgbA1c <5.5||Diet as above||Type II diabetes-AD relationship|
|Hormone balance||Optimize fT3, fT4, E2, T, progesterone, pregnenolone, cortisol||[5, 42]|
|GI health||Repair if needed; prebiotics and probiotics||Avoid inflammation, autoimmunity|
|Reduction of A-beta||Curcumin, Ashwagandha||43–45|
|Cognitive enhancement||Bacopa monniera, MgT||[46, 47]|
|25OH-D3 = 50-100ng/ml||Vitamins D3, K2|||
|Increase NGF||H. erinaceus or ALCAR||[49, 50]|
|Provide synaptic structural components||Citicoline, DHA||.|
|Optimize antioxidants||Mixed tocopherols and tocotrienols, Se, blueberries, NAC, ascorbate, α-lipoic acid|||
|Optimize Zn:fCu ratio||Depends on values obtained|||
|Ensure nocturnal oxygenation||Exclude or treat sleep apnea|||
|Optimize mitochondrial function||CoQ or ubiquinol, α-lipoic acid, PQQ, NAC, ALCAR, Se, Zn, resveratrol, ascorbate, thiamine|||
|Increase focus||Pantothenic acid||Acetylcholine synthesis requirement|
|Increase SirT1 function||Resveratrol|||
|Exclude heavy metal toxicity||Evaluate Hg, Pb, Cd; chelate if indicated||CNS effects of heavy metals|
|MCT effects||Coconut oil or Axona|||
CHO, carbohydrates; Hg, mercury; Pb, lead; Cd, cadmium; MCT, medium chain triglycerides; PQQ, polyquinoline quinone; NAC, N-acetyl cysteine; CoQ, coenzyme Q; ALCAR, acetyl-L-carnitine; DHA, docosahexaenoic acid; MgT, magnesium threonate; fT3, free triiodothyronine; fT4, free thyroxine; E2, estradiol; T, testosterone; Me-B12, methylcobalamin; MTHF, methyltetrahydrofolate; P5P, pyridoxal-5-phosphate; TMG, trimethylglycine; Trp, tryptophan