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Reversing Alzheimer’s: What Could it Mean for Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia?

Reprinted with the kind permission
of Cort Johnson and 
Health Rising [1].

Alzheimer’s, ME/CFS and FM share at least two things; both inflammation and cognition are involved. Alzheimer’s also costs the U.S. economy over 200 billion a year, is incurable and is for the most part unstoppable – even when using the drugs approved for it.

What to say then about an unusual UCLA study which produced significant remissions in its Alzheimer’s patients using a multi-pronged approach? An approach that included some treatments FM and ME/CFS patients will recognize.

Alzheimer’s is the elephant in the room facing the medical systems of United States and other developed countries. Alzheimer’s is a devastating disease to have, to watch and ultimately to die from. Already the third to sixth leading cause of death in the U.S. (depending on who you ask), it’s expected that millions more people now living will eventually be diagnosed with Alzheimer’s.

It’s also incredibly expensive. Treating Alzheimer’s and other forms of dementia are believed to cost the U.S. economy over $200 billion a year. Several drugs may be able to slow the progression of the disease but the benefits are usually small, and none have been able to reverse it.

Alzheimer’s is a disease affecting the hippocampus and other areas of the brain that ultimately results in death as patients lose control of their bodily functions. The cognitive problems in chronic fatigue syndrome (ME/CFS) and fibromyalgia (FM) are much milder, but some are similar to those found in early Alzheimer’s. They include getting lost, losing things, forgetting dates and appointments, difficulty finding the words to express oneself, slowed information processing, difficulty multitasking and difficulty planning. All three diseases are believed to have a neuro-inflammatory component.

Recently an unusual study attempted to treat Alzheimer’s in a new way. The authors – most of whom work at UCLA – believe that Alzheimer’s results from an environment in the brain which promotes synaptic death and nervous system reorganization. Their goal was to create an environment in the brain conducive to synaptic growth.

This study included ten patients with “mild” Alzheimer’s. Mild in Alzheimer’s, it turns out, is mild only in reference to severe Alzheimer’s. The cognitive problems faced by the people in this study made it difficult for many to continue working. Problems recognizing faces, adding numbers, getting lost close to home, etc., etc., were common. One person had begun shutting down his business, was considering committing suicide. Another had lost the ability to speak in different languages. Others had lost jobs. One couldn’t play guitar anymore. The long term prognosis for each was bleak.


The UCLA doctors put them on a personalized treatment protocol called called metabolic enhancement for neurodegeneration [2] (MEND). The protocol contained some drugs but relied heavily on alternative health modalities, including supplements, diet, exercise, brain stimulation, stress reduction and sleep practices.

Doctors typically treat patients based on whether their test results indicate a pathological situation is present. This group, however, tried to optimize their patients’ results even when they fell into the normal range. They also attempted to treat systems not parts of systems; i.e., they endeavored to enhance the workings of entire central nervous system network implicated in Alzheimer’s in an attempt to return to homeostasis.

A look at this large protocol will find alternative treatments that many in the ME/CFS and FM community are familiar with: ketogenic, low grain and low inflammation diets, melatonin, testosterone, tryptophan, L- carnitine, curcumin, CoQ10, Ashwagandha, antioxidants, probiotics, resveratrol were just some of the possible supplements suggested. Some drugs (T3, progesterone, pregnenolone), stress reduction (meditation, yoga) and sleep practices rounded the protocol.

Tests for insulin resistance, sleep apnea, homocysteine, serum B-12, CRP, heavy metals, cortisol, estradiol, progesterone, thyroid and others were done.


It was pretty audacious to propose that a program focused mostly on supplements, a few drugs, diet, exercise, sleep and stress reduction could achieve remission in a disease like Alzheimer’s. Alzheimer’s, after all, gets almost $1 billion a year in NIH funding and is considered a death sentence. Could a protocol that uses mostly alternative health treatments be the best answer right now for it?

The study size was small; the authors think so. They called the magnitude of the improvements they saw “unprecedented” and asserted that their results “have far-reaching implications for the treatment of Alzheimer’s disease, MCI, and SCI” (i.e. dementia) and for the development of “personalized programs that may enhance pharmaceutical efficacy.”

All of the participants in the trial met the criteria for Alzheimer’s before the trial. None of them met the criteria for it or dementia afterwards. Neuropsychological testing indicated that all had normal cognitive functioning results afterwards.

Individual Results

Some of the improvements were astonishing. One man’s CVLT-IIB (cognitive test) score increased from 3rd percentile to 84th percentile (3 standard deviations), another from the first 1st percentile to 50th percentile, another from the 13th percentile to 79th percentile, and another from 24th percentile to 74th percentile. This person went from considerably below average to considerably above average in many of his cognitive tests.

Another person who had been an excellent student bumped up her test results from the 35th percentile to the 98th percentile.

A professional writer and editor with a master’s degree in English often misplaced or used the wrong words and had problems with spelling. Her overall cognitive assessment (neurocognitive index) increased from the 16th percentile to 73rd percentile, her composite memory from the 1st percentile to 61st percentile, her verbal memory from the 3rd percentile to 93rd percentile, her executive function from the 14th percentile to 58th percentile, and her processing speed from 37th percentile to 81st percentile.

A 49-year old who had lost the ability to speak in two languages was able to do that again. The guitarist was able to play his guitar again. Some patients had more modest gains, but the fact that all posted gains in cognitive functioning was, according to the study, highly unusual for Alzheimer’s.

Except for one patient who went off the protocol and subsequently declined, the patients in this study – some of whom have been followed for four years – have maintained their progress. (When the one patient went back on the protocol, he improved again.)

Multi-varied Approach Necessary (?)

“It is possible that it will be necessary to target multiple pathways simultaneously in order to effect an improvement in symptoms and pathophysiology.” The authors

This small study suggests that the standard approach to clinical trials – provide a drug and determine if there’s a response – may be insufficient for many chronic diseases. Because by their nature most chronic diseases are complex entities that affect several systems, it makes sense that a diverse protocol might be the most effective. Unless a core pathway is discovered, a multi-varied approach is probably best. This study suggests that many clinical trials may fail not because the treatment in question doesn’t work but because it hasn’t been tested with other treatments.

The cancer community figured this out long ago. Six factors that are present in every cancer have been identified. Because hitting one factor isn’t always enough, a variety of drugs that target several are often used. (The FDA, however, still requires each cancer drug to be tested in isolation – an approach that Dr. DeVita, a former National Cancer Institute Director, harshly criticized in his recent book The Death of the Cancer.)

The authors used an analogy similar to the leaky boat analogy often used in ME/CFS and FM:

“Imagine having a roof with 36 holes in it, and your drug patched one hole very well—the drug may have worked, a single ‘hole’ may have been fixed, but you still have 35 other leaks, and so the underlying process may not be affected much…The point of the program then is to make sure that all holes are plugged so that the roof becomes whole again, so to speak.” Bredesen [3]

The patients didn’t need to do the dozens of interventions possible; in fact, none of the patients did all the recommended treatments – they just needed to do enough of them to have an effect – to reach what these researchers believe is a threshold for change. That sounds very similar to Dr. Myhill’s statement (paraphrased) that her job is getting her ME/CFS patients to 51%; after that, the body does the rest.

Diabetes of the Brain?

Some researchers believe Alzheimer’s is primarily a metabolic disease and call it “diabetes 3” or “diabetes of the brain.” That idea rests on the finding of impaired glucose uptake in the hippocampus. It turns out that the same factor in the brain that clears out amyloid deposits in the brain also clears out insulin. That factor’s preference for insulin over amyloid proteins means that people with high insulin levels may have trouble clearing out amyloid deposits.

In “A Nutritional Approach to Healing and Preventing Alzheimer’s and Metabolic Syndrome [4],” Amy Berger, MS NTP, proposes that Alzheimer’s Disease (AD) is the result of high insulin levels, insulin resistance and difficulties metabolizing glucose – not in the body as with Type II diabetes, but in the brain. She believes that the brain cells in Alzheimer’s are essentially starving in the midst of plenty because they’ve lost the ability to produce energy efficiently from glucose.

Berger proposes that a low carbohydrate, low glycemic diet (a Paleolithic-like diet) will shift the basis from energy production in the brain from glucose – which is being poorly metabolized – to by-products of fat metabolism called ketones. Several studies suggest these diets may be helpful in Alzheimer’s.

ME/CFS and FM: Diabetes-like Illnesses?

Ron Davis has resisted the pull to have the neurological institute NINDS take over ME/CFS because he believes it’s too early to know what ME/CFS is. His preliminary metabolomics results suggest ME/CFS may be a metabolic disorder that better belongs in the National Institute of Diabetes and Digestive and Kidney Diseases [5](NIDDK).

Some time ago, Marco noted some of the similarities between ME/CFS and FM and diabetes in a blog. First, there’s the energy problem:

“What is often missed is the fact that untreated diabetes is a state of energy deficiency. After all, if insulin does not move glucose into the cells, the cells lack the energy they need to function properly.”

Anecdotally we do seem to have problems with blood sugar regulation [6], share some early symptoms of diabetes (dry eyes and mouth, frequent urination); plus physical and mental fatigue and exercise problems in ME/CFS and FM suggest some (unidentified) problem with energy metabolism. One theory [7] suggests that an altered metabolic stress response in ME/CFS patients results in the ‘selfish brain’ starving the peripheral organs and muscles of glucose.

Marco pointed out that fatigue, exercise intolerance, early muscle pain and difficulty recovering from exercise are all found in Type II diabetes. [8] Perhaps because of blood vessel damage, oxygen uptake to the muscles is delayed in diabetes. Autonomic nervous system dysfunction is also present in the form of low heart rate variability and slowed heart rate recovery after exercise.

Small fiber neuropathy – found in about 40% of FM patients – is common in diabetes. Leptin resistance – a real possibility in ME/CFS given the normal leptin levels found thus far – is also common. The cognitive problems – slowed mental speed and processing – found in diabetes are similar as well.

Unfortunately, insulin and cerebral glucose intake are not well studied in either ME/CFS or FM, but a trend towards metabolic problems may be present. A finding of increased insulin resistance [9] in FM patients with memory issues and FM patients overall [10] in another has been found. Another study found significantly higher insulin levels [11] in ME/CFS patients.

A couple of studies suggest that the risk for metabolic syndrome may be increased in either fibromyalgia [12] or chronic fatigue syndrome (ME/CFS [13]). In metabolic syndrome, carbohydrate intake results in high levels of glucose or insulin, elevated triglycerides, LDL and reduced HDL.

Brain glucose uptake studies have had mixed results in ME/CFS and FM. Reduced glucose uptake in different brain regions in different people [14] were found in a significant number of ME/CFS patients in one study, but another very small study found little evidence of it. [15]Cerebral glucose uptake was also normal in a small FM study [16].


This was a very small study (10 people), but the objective evidence and the findings – that all the participants improved – was startling in a disease like Alzheimer’s. The study, which is being expanded, suggested that a multidimensional approach that relies mostly on alternative treatments may be successful even in horrific diseases like Alzheimer’s if they are caught early enough. The fact that the improvement has lasted up to four years is encouraging as well. The study also suggested that treatments need each other to work properly and that more treatment protocols should be tested in clinical trials.

Dr. Teitelbaum’s chronic fatigue syndrome (ME/CFS) study of some years took a similar approach. Teitelbaum’s use of personalized treatment protocols made it impossible to provide a set protocol, but the study did move the needle on ME/CFS for many.

ME/CFS and FM, of course, provide some unique difficulties that Alzheimer’s patients do not have. We don’t know the locus for either, both are probably filled with subsets, and because so much less is known about each, much more guesswork is needed.

Cognitive problems are common, and inflammation is believed to be a key factor, and metabolic problems may be present as well in all three diseases. Many of the recommendations make sense for people with ME/CFS and FM. The UCLA researchers’ attempt to improve brain health in Alzheimer’s might very well have resonance for ME/CFS and FM.


About the Author: ProHealth is pleased to share information from Cort Johnson.  Cort has had myalgic encephalomyelitis /chronic fatigue syndrome for over 30 years. The founder of Phoenix Rising and Health Rising, he has contributed hundreds of blogs on chronic fatigue syndrome, fibromyalgia and their allied disorders over the past 10 years. Find more of Cort’s and other bloggers’ work at Health Rising [17].