Dementia Reversal

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• Reversal of cognitive decline: A novel therapeutic program •

Dementia Reversal?

Patient one: therapeutic program

As noted above, and following an extended discussion of the components of the therapeutic program, the patient began on some but not all of the system:

  1. she eliminated all simple carbohydrates, leading to a weight loss of 20 pounds;

  2. eliminated gluten and processed food from her diet, and increased vegetables, fruits, and non-farmed fish;

  3. in order to reduce stress, she began yoga, and ultimately became a yoga instructor;

  4. as a second measure to reduce the stress of her job, she began to meditate for 20 minutes twice per day;

  5. melatonin 0.5mg po qhs;

  6. increased her sleep from 4-5 hours per night to 7-8 hours per night;

  7. methylcobalamin 1mg each day;

  8. vitamin D3 2000IU each day;

  9. fish oil 2000mg each day;

  10. CoQ10 200mg each day;

  11. optimized her oral hygiene using an electric flosser and electric toothbrush;

  12. following discussion with her primary care provider, she reinstated HRT (hormone replacement therapy) that had been discontinued following the WHI report in 2002;

  13. fasted for a minimum of 12 hours between dinner and breakfast, and for a minimum of three hours between dinner and bedtime;

  14. exercised for a minimum of 30 minutes, 4-6 days per week.

The Full Report for all 10 patients

Of the first 10 patients who utilized this program, including patients with memory loss associated with Alzheimer's disease (AD), amnestic mild cognitive impairment (aMCI), or subjective cognitive impairment (SCI), nine showed subjective or objective improvement.

•One potentially important outcome is that all six of the patients whose cognitive decline had a major impact on job performance were able to return to work or continue working without difficulty.

Patient one: history

A 67-year-old woman presented with two years of progressive memory loss. She held a demanding job that involved preparing analytical reports and traveling widely, but found herself no longer able to analyze data or prepare the reports, and therefore was forced to consider quitting her job. She noted that when she would read, by the time she reached the bottom of a page she would have to start at the top once again, since she was unable to remember the material she had just read. She was no longer able to remember numbers, and had to write down even 4-digit numbers to remember them. She also began to have trouble navigating on the road: even on familiar roads, she would become lost trying to figure out where to enter or exit the road. She also noticed that she would mix up the names of her pets, and forget where the light switches were in her home of years.

Her mother had developed similar progressive cognitive decline beginning in her early 60s, had become severely demented, entered a nursing home, and died at approximately 80 years of age. When the patient consulted her physician about her problems, she was told that she had the same problem her mother had had, and that there was nothing he could do about it. He wrote “memory problems” in her chart, and therefore the patient was turned down in her application for long- term care.

After being informed that she had the same problem as her mother had had, she recalled the many years of her mother’s decline in a nursing home. Knowing that there was still no effective treatment and subsequently losing the ability to purchase long-term care, she decided to commit suicide. She called a friend to commiserate, who suggested that she get on a plane and visit, and then referred her for evaluation.

She began System 1.0 (Table 1), and was able to adhere to some but not all of the protocol components. Nonetheless, after three months she noted that all of her symptoms had abated: she was able to navigate without problems, remember telephone numbers without difficulty, prepare reports and do all of her work without difficulty, read and retain information, and, overall, she became asymptomatic. She noted that her memory was now better than it had been in many years. On one occasion, she developed an acute viral illness, discontinued the program, and noticed a decline, which reversed when she reinstated the program. Two and one-half years later, now age 70, she remains asymptomatic and continues to work full-time.

Patient two: therapeutic program

The patient began on the following parts of the overall therapeutic system:

  1. he fasted for a minimum of three hours between dinner and bedtime, and for a minimum of 12 hours between dinner and breakfast;

  2. eliminated simple carbohydrates and processed foods from his diet;

  3. increased consumption of vegetables and fruits, and limited consumption of fish to non-farmed, and meat to occasional grass-fed beef or organic chicken;

  4. probiotics;

  5. coconut oil i tsp bid;

  6. exercised strenuously, swimming 3-4 times per week, cycling twice per week, and running once per week;

  7. melatonin 0.5mg po qhs, and tried to sleep as close to 8 hours per night as his schedule would allow;

  8. herbs Bacopa monniera 250mg, Ashwagandha 500mg, and turmeric 400mg each day;

  9. methylcobalamin 1mg, methyltetrahydrofolate 0.8mg, and pyridoxine-5- phosphate 50mg each day;

  10. citicoline 500mg po bid;

  11. vitamin C 1g per day, vitamin D3 5000IU per day, vitamin E 400IU per day, CoQ10 200mg per day, Zn picolinate 50mg per day, and -lipoic acid 100mg per day;

  12. DHA (docosahexaenoic acid) 320mg and EPA (eicosapentaenoic acid) 180mg per day


Patient two: history

A 69-year-old entrepreneur and professional man presented with 11 years of slowly progressive memory loss, which had accelerated over the past one or two years. In 2002, at the age of 58, he had been unable to recall the combination of the lock on his locker, and he felt that this was out of the ordinary for him. In 2003, he had FDG-PET (fluoro-deoxyglucose positron emission tomography), which was read as showing a pattern typical for early Alzheimer’s disease, with reduced glucose utilization in the parietotemporal cortices bilaterally and left > right temporal lobes, but preserved utilization in the frontal lobes, occipital cortices, and basal ganglia. In 2003, 2007, and 2013, he had quantitative neuropsychological testing, which showed a reduction in CVLT (California Verbal Learning Test) from 84%ile to 1%ile, a Stroop color test at 16%ile, and auditory delayed memory at 13%ile. In 2013, he was found to be heterozygous for ApoE4 (3/4). He noted that he had progressive difficulty recognizing the faces at work (prosopagnosia), and had to have his assistants prompt him with the daily schedule. He also recalled an event during which he was several chapters into a book before he finally realized that it was a book he had read previously. In addition, he lost an ability he had had for most of his life: the ability to add columns of numbers rapidly in his head.

He had a homocysteine of 18 mol/l, CRP <0.5mg/l, 25- OH cholecalciferol 28ng/ml, hemoglobin A1c 5.4%, serum zinc 78mcg/dl, serum copper 120mcg/dl, ceru- loplasmin 25mg/dl, pregnenolone 6ng/dl, testosterone 610ng/dl, albumin:globulin ratio of 1.3, cholesterol 165mg/dl (on Lipitor), HDL 92, LDL 64, triglyceride 47, AM cortisol 14mcg/dl, free T3 3.02pg/ml, free T4 1.27ng/l, TSH 0.58mIU/l, and BMI 24.9.

He began on the therapeutic program, and after six months, his wife, co-workers, and he all noted improvement. He lost 10 pounds. He was able to recognize faces at work unlike before, was able to remember his daily schedule, and was able to function at work without difficulty. He was also noted to be quicker with his responses. His life-long ability to add columns of numbers rapidly in his head, which he had lost during his progressive cognitive decline, returned. His wife pointed out that, although he had clearly shown improvement, the more striking effect was that he had been accelerating in his decline over the prior year or two, and this had been completely halted.

Patient three: therapeutic program

She began on the following parts of the therapeutic system:

  1. she fasted for a minimum of three hours between dinner and bedtime, and for a minimum of 12 hours between dinner and breakfast;

  2. eliminated simple carbohydrates and processed foods from her diet;

  3. increased consumption of vegetables and fruits, limited consumption of fish to non-farmed, and did not eat meat;

  4. exercised 4-5 times per week;

  5. melatonin 0.5mg po qhs, and tried to sleep as close to 8 hours per night as her schedule would allow;

  6. she tried to reduce stress in her life with meditation and relaxation;

  7. methylcobalamin 1mg 4x/wk and pyridoxine-5-phosphate 20mg each day;

  8. citicoline 200mg each day;

  9. vitamin D3 2000IU per day and CoQ10 200mg per day;

  10. DHA 700mg and EPA 500mg bid;

  11. her primary care provider prescribed bioidentical estradiol with estriol (BIEST), and progesterone;

  12. her primary care provider worked with her to reduce her bupropion from 150mg per day to 150mg 3x/wk.


Patient three: history

A 55-year-old attorney suffered progressively severe memory loss for four years. She accidentally left the stove on when she left her home on multiple occasions, and then returned, horrified to see that she had left it on once again. She would forget meetings, and agree to multiple meetings at the same time. Because of an inability to remember anything after a delay, she would record conversations, and she carried an iPad on which she took copious notes (but then forgot the password to unlock her iPad). She had been trying to learn Spanish as part of her job, but was unable to remember virtually anything new. She was unable to perform her job, and she sat her children down to explain to them that they could no longer take advantage of her poor memory, that instead they must understand that her memory loss was a serious problem. Her children noted that she frequently became lost in mid-sentence, that she was slow with responses, and that she frequently asked if they had followed up on something she thought she had asked them to do, when in fact she had never asked them to do the tasks to which she referred.

Her homocysteine was 9.8mol/l, CRP 0.16mg/l, 25- OH cholecalciferol 46ng/ml, hemoglobin A1c 5.3%, pregnenolone 84ng/dl, DHEA 169ng/dl, estradiol 275pg/ml, progesterone 0.4ng/ml, insulin 2.7IU/ml, AM cortisol 16.3mcg/dl, free T3 3.02pg/ml, free T4 1.32ng/l, and TSH 2.04mIU/l.

After five months on the therapeutic program, she noted that she no longer needed her iPad for notes, and no longer needed to record conversations. She was able to work once again, was able to learn Spanish, and began to learn a new legal specialty. Her children noted that she no longer became lost in mid-sentence, no longer thought she had asked them to do something that she had not asked, and answered their questions with normal rapidity and memory.

Patient me:

Cos I hate vegetables so much -- I buy :-
Bulk lettuce, spinach, asparagus, onion, mushroom, beetroot, broccoli.
Add tinned beans ( garbanzo, kidney, black, butter, refried, peas).
Add meat from a whole cooked chicken ($5 from COSTCO). No more processed meat.
--- Add a tinned soup ( tomato or chicken broth) and microwave it
--- Add microwaved beans + soup and put everything into a food mixer .

NO MORE:- potatoes, rice, pasta, soy, corn, processed meat, cheese and GRAINS( all bread, cereal, pancakes, cookies etc...)
Almost all my carbs come from beans and cashews.

My only source of sugar(fructose) is fresh fruit and what they sneak into tinned foods like tomato soup and sweet peas.

All pretty drastic but necessary. I call it the Caveman's Natural Lifestyle .
(Paleo Diet:- but includes fat-free milk, cashew nuts, lentils, beans, peas and all other legumes and excludes honey).



lost 45 lbs (from 230lbs to 185lbs)

Table 1. Therapeutic System 1.0



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 hrs each night, including 3 hrs prior to bedtime.

Reduce insulin levels, reduce A.

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.



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



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


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, -lipoic acid


Optimize Zn:fCu ratio

Depends on values obtained


Ensure nocturnal oxygenation

Exclude or treat sleep apnea


Optimize mitochondrial function

CoQ or ubiquinol, -lipoic acid, PQQ, NAC, ALCAR, Se,

Zn, resveratrol, ascorbate, thiamine


Increase focus

Pantothenic acid

Acetylcholine synthesis requirement

Increase SirT1 function



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

SOURCE Buck Institute  or    source on this site