More Detail on Dr. Ornish's Sudy of Lifestyle Interventioins for Alzheimer's Disease

We have written often about the distinction between longitudinal studies and randomized controlled trials.  To date, the majority of the research on lifestyle and Alzheimer's has been longitudinal studies.  You look at a population and take surveys on what people eat, what exercise they get, etc.  You assume that they are telling you (and themselves) the truth about what they do (and don't) eat, and how much real exercise they get.  Then you see how many of them develop dementia.  Many longitudinal studies produce disappointing results, but my view is that the quality of their data is very poor.

In a randomized controlled trial, you change peoples' lifestyles and measure the results.  Rather than rely on self-reporting in surveys, you either control the actual food they eat or measure the chemicals in their blood to see what they've been eating.  With respect to exercise, you supervise the exercise and measure it.  You measure the results with intense cognitive tests, MRIs, PET scans, and blood tests.  Oh, and then there's the control group - a set of test subjects who don't change their lifestyles, but are subject to the same results measurements.

Obviously, the randomized controlled trials are MUCH more reliable.  However, they are much more difficult -- and costly -- to actually perform. 

Back in July of 2024, we reported that Dr. Dean Ornish was completing a randomized control trial of lifestyle interventions for Alzheimer's disease.  We were heartened that he not only found improvements in memory and cognition tests, but he also found improvements in biomarker evidence, specifically Alzheimer's biomarkers in cerebrospinal fluid.  That's now one of the two gold standard tests for diagnosing Alzheimer's.  Dr. Ornish's study involved 51 patients between the ages of 45 and 90, all of whom had been diagnosed with MCI or early dementia due to Alzheimer's.  But only about half of these received the interventions.  For the intervention group, Dr. Ornish found positive results after 20 weeks.

The other day I came across another article referencing this research ... except the article called it "new."  Thinking it was newer than what we discussed before, I started to develop a new post on the research ... before realizing I'd already posted about it.  Nevertheless, I think it's worth revisiting, since the research is so compelling.  And it's so consistent with my own experience.

What I think is worth revisiting are specifics about the interventions used in the study.  So here they are:

Diet: 

Whole foods, minimally-processed plant-based (vegan) diet, high in complex carbohydrates (predominantly fruits, vegetables, whole grains, legumes, soy products, seeds and nuts) and especially low in harmful fats, sweeteners and refined carbohydrates.  It was approximately 14-18% of calories as total fat, 16-18% protein, and 63-68% mostly complex carbohydrates. Calories were unrestricted. Those with higher caloric needs were given extra portions.  Twenty-one meals/week and snacks plus the daily supplements listed below were provided throughout the 40 weeks of this intervention to each study participant and his or her spouse or study partner.  Twice/week, three meals plus two snacks per day that met the nutritional guidelines as well as the prescribed nutritional supplements were shipped overnight to participants and partners.  Participants were asked to consume only the food and nutritional supplements sent to them and no other foods.

This is similar to the MIND diet, except the MIND diet restricts cheese, stick margarine, and butter.  It also allows some poultry and fish. 

Group Support:

Each patient and their spouse or study partner met three times/week, four hours/session via Zoom: 

- One hour of supervised exercise (aerobic + strength training) 

- One hour of stress management practices (stretching, breathing, meditation, imagery) 

- One hour of a support group lecture on lifestyle 

- Additional optional exercise and stress management classes were provided. 

Supplements 

- Omega-3 fatty acids with Curcumin (1680 mg omega-3 & 800 mg Curcumin, Nordic Naturals ProOmega CRP, 4 capsules/day). 

- Multivitamin and Minerals (Solgar VM-75 without iron, 1 tablet/day).

- Coenzyme Q10 (200 mg, Nordic Naturals, 2 soft gels/day). 

- Vitamin C (1 gram, Solgar, 1 tablet/day).

- Vitamin B12 (500 mcg, Solgar, 1 tablet/day). 

- Magnesium L-Threonate (Mg) (144 mg, Magtein, 2 tablets/day). 

- Hericium erinaceus (Lion’s Mane, Stamets Host Defense, 2 grams/day). 

- Super Bifido Plus Probiotic (Flora, 1 tablet/day).

Some Crazy Stuff about Shingles and Dementia

We've discussed before, both in this blog and in Beating the Dementia Monster, that there seems to be a correlation between people getting their shingle shot and a reduced incidence of developing Alzheimer's disease.  The case for this continues to strengthen, as illustrated in some recent studies in Wales and Australia.  I believe it's likely that my disease stems from my history of three episodes of shingles.

In our book, we noted that some researchers believe that the amyloid plaques we're trying to get rid of are actually part of the body's defense against a variety of microbial pathogens.  The plaques may be trying to encapsulate the pathogens and stop their propagation in the brain.  In our discussion of pathogenic causes of Alzheimer's, we noted researchers have also correlated another pathogen, the bacteria causing gum disease (p. gingivalis), with the advent of Alzheimer's symptoms.  At autopsy, evidence of the presence of the herpes virus and p. gingivalis are usually found in the brains of Alzheimer's victims.

So here's a question.  How does the role of pathogens in the brain correlate with the positive effects of applying The Dementia Toolkit, notably with respect to exercise and diet?  Well, according to one paper, perhaps "environmental factors like stress, diet, sleep, and exercise may influence Alzheimer's risk in part by modulating the innate and adaptive immune responses to [pathogens]."  In other words, the time you spend on the treadmill is regulating the ability of the pathogen to cause damage in your brain.  The paper appeared in the journal, Molecular Psychiatry.  It was entitled, "The viral hypothesis: how herpesviruses may contribute to Alzheimer’s disease."

What's prompting me on this topic is a new study in Australia about a relatively small but consistent correlation between the shingles shot and the advent of dementia.  The study replicated the results of a similar study in Wales.  The Australian study was published in the JAMA Network.  It's a little complicated, but by studying the medical records of more than 101,000 patients with a mean age of about 62 years, there was a 1.8% decrease in the probability of receiving a dementia diagnosis during a 7.4-year period.  That's not a lot, but hopefully most of us will have several more 7.4 year periods after we turn 62.  And the rate of development of the disease increases with age.  So what would that mean for a 7.4-year period beginning at the age of 75?  It might be a lot more than 1.8%

But what may be more important here is the insight this research gives us on the causes and mechanisms of the disease.  As time as gone on, most researchers have migrated away from a simplistic understanding that the disease is fundamentally about the development of amyloid plaques and microtubule tangles.  As a minimum, the amyloid hypothesis has been maturing, and some have abandoned it.

I apologize for being a bit of a slug about posting here.  My wife and I took a trip to a resort area in the Cascades for a few days, and then I was in Seattle for an overnight stay in the hospital while they wired me up to study my sleeping brain.  I'm hoping this will yield a positive outcome for my chronic insomnia.  And, I'll admit it, I have a harder time these days finding the energy to research and write on these topics.  And the YouTube channel is a lot of work.  So I do what I can.

The Lancet Adds Two New Risk Factors for Alzheimer's

The Lancet is one of the premier scientific journals in medicine.  We wrote back in 2022 of the results of the work of the Lancet commission on dementia.  With the unlikelihood that an outright cure for Alzheimer's disease would appear anytime soon, the commission's report highlighted a list of the modifiable lifestyle and other factors that influence the development of the disease.  They will be familiar to anyone who has read Beating the Dementia Monster or who follows this blog.  They were:

- physical inactivity,
- excess alcohol consumption,
- obesity,
- smoking,
- hypertension,
- diabetes,
- depression,
- traumatic brain injury,
- hearing loss,
- few years of education,
- social isolation, and
- air pollution.

The 2022 report included this graphic which showed how the different risk factors map out over someone's lifetime.  Note their conclusion that 60% of the total factors are simply unknown.  Nevertheless, 40% are potentially modifiable - things you can do to affect your susceptibility to the disease.

Then, just last year, the commission released a new study which updated their conclusions.  They noted that, as people live longer, the number of people who live with dementia continues to rise.  But they also noted that, as the age-specific incidence decreases in high-income countries, there is a need to identify and implement prevention approaches.  So much of the report's recommendations focus on changes in governmental policy.

The main takeaways from the new report (after acknowledging the original report) is the addition of two new risk factors: vision loss and high LDL cholesterol (i.e., "bad cholesterol").  But they also said, "The potential for prevention is high and, overall, nearly half of dementias could theoretically be prevented by eliminating these 14 risk factors. These findings provide hope."  They also said, "Although change is difficult and some associations might be only partly causal, our new evidence synthesis shows how individuals can reduce their dementia risk."

I am still waiting for the Alzheimer's Association Facts and Figures Report for 2025.  In the past, this has been a rich resource, even richer than the Lancet's dementia commission reports.  But they still haven't published it.  You can, however, add it to your "wish list" -- which I did.  I presume this means they're still working on it, and we'll see it soon.  In the past, it's been available during the first week in March.  Oh, and, here's a first: I'll need to pay for it now.  Not free anymore.  But I can afford the $7.95.

Good New from the ADRC

So yesterday, I got a call from the University of Washington's Alzheimer's Disease Research Center (ADRC).  They wanted to give me feedback from my testing on March 17 that we discussed in this post.  My results had been reviewed by a neuropsycholgist, and they could share some insights.  The insight?  "You did just fine."  Which I already knew, since I've taken so many of these tests now.  

Because it was for research, they couldn't give me any details beyond that.  However, the principal investigator for the research is also my neurologist, and I'm to see her this summer ... I think.  Because this test was so comprehensive, I'm thinking they may not need to test me again, just do the other parts of a periodic evaluation.

So, it's now been a full 10 years since my initial diagnosis from my local neurologist, and it will be 10 years in July from my diagnosis in Seattle.  I feel well (for the most part), and my memory and cognition continue to be intact.  I can only attribute this to staying faithfully with the Dementia Toolkit.

When I said "for the most part," I was thinking about my continuing issues with cerebellar dysfunction ataxia.  That doesn't seem to be improving, at least not perceptibly.  Nevertheless, life is good.

Audiobook of Beating the Dementia Monster Is Now Out!

We have now published the audiobook edition of Beating the Dementia Monster.  It is available on Audible (Amazon), Apple Books, Spotify, and many other platforms.  My thanks go to our publisher, Echo Point Books.

Covid, vaccines, and Alzheimer's disease ... complicated interconnections

In our last post, we posited a simplistic view of how a covid infection could promote Alzheimer's disease, specifically in severe cases from the strains circulating in 2020.  We said that a covid infection causes a "cytokine storm" that leads to inflammation in the brain severe enough to perhaps initiate Alzheimer's disease.  Recall that the genes most closely associated with Alzheimer's disease appear to do so by creating an inflammatory environment in the brain.  But, according to an editorial in the June 2023 issue of the journal Infectious Disorders (Bentham Science), the process is really quite complex, and the spike protein vaccines may do the same thing.  The editorial was entitled "COVID-19 and Alzheimer's Disease: The Link Finally Established."  (This link might be easier to read.)  The authors have been involved in research on the relationship between Alzheimer's and covid.

What's even more disturbing is that covid (and perhaps the vaccines) actually accelerate the development of Alzheimer's.  We noted in other posts (and in Beating the Dementia Monster) that the disease may actually begin 15 or 20 years before the first symptoms, but symptoms may begin appearing only four years or so after a covid infection. 

A fuller explanation of how covid and the spike proteins might cause Alzheimer's involves the Renin-angiotensin system, or RAS.  RAS involves every cell in the body, but most specifically the kidneys, the liver, blood vessels, the lungs, the adrenal glands, the pituitary gland, and the hypothalamus.  (The pituitary gland and the hypothalamus are in the brain.)  The most notable thing about the RAS is that it regulates blood pressure through a very complex process. 

If the RAS is disrupted, it causes problems with:

- blood vessel constriction (raising blood pressure)

- toxic storms of pro-inflammatory cytokines

- the production of reactive oxygen particles that kill cells

- the formation of clots that obstruct blood vessels

- the growth of blood vessels and tumors

- the desaturation of blood in oxygen

- a deficit of oxygen supply to various cells, tissues, and organs

- organ fibrosis

- increases in organ volume

- nitric oxide levels, affecting inflammatory, immune, and memory phenomena

Is that enough?  There are certainly well established relationships between Alzheimer's and high blood pressure, inflammation, and oxidation from reactive oxygen.

While the authors stated that the vaccine spike proteins are capable of causing the same mischief as the virus itself, it appeared to me that they floated this as an hypothesis.  They didn't cite any research that found an unambiguous link between vaccinations and the development of Alzheimer's.

From everything I've seen, these concerns are most relevant to the original strain and the delta strain that appeared in the first two years of the pandemic.  But we're still waiting to see what becomes of people who were over 65 when they had a covid infection severe enough to hospitalize them.

Covid Promotes Alzheimer's ... Apparently

The evidence that viruses attacking the nervous system promote Alzheimer's disease is pretty well established.  Think herpes, the virus causing cold sores and shingles.  We've discussed this here before and also in Beating the Dementia Monster.  But what about viruses that don't directly attack the nervous system ... like covid?  There's interesting and troubling news on this front.

In research recently published in Nature Medicine, "Plasma proteomic evidence for increased β-amyloid pathology after SARS-CoV-2 infection," researchers examined a cohort of 1,252 people who had been infected with covid-19.  This was in the UK, and the researchers had access to previous blood test results for Alzheimer's biomarkers for these individuals.  So, for these people, and a for similar cohort of people who had not been infected (a control group), they compared biomarker evidence for Alzheimer's.  Test participants ranged in age from 46 to 80 years of age.  Many of those infected had mild cases, but some had infections serious enough to have been hospitalized.

What did they find?

People who had serious infections, especially serious enough to be hospitalized, showed increased biomarker evidence of Alzheimer's pathology.  They also did less well on cognitive and memory tests.  The specific biomarker they measured was the ratio of two forms of beta amyloid peptide that signal the disease.  The researchers estimated that a serious covid infection was the equivalent of a four-year advance of the disease.

The age of the participants was a factor -- the older, the more vulnerable -- but the presence of high blood pressure was also a factor.

In Beating the Dementia Monster, we discussed the production of a form of beta amyloid that is water soluble and of one that is not.  Both are produced in everyone.  The one that is soluble dissolves innocuously, but the one that is not soluble clumps on to nerve cells and apparently kills them.  Measuring the ratio of these two forms in fluid from a spinal tap or from a blood sample provides strong indication as to whether or not the Alzheimer's pathology is progressing.  So this is what the researchers measured.

Covid-19 is not known to attack nerve cells directly, but it does precipitate "cytokine storms" -- inflammation.  (We discussed this back in 2020.)  Inflammation and oxidation are two fundamental environmental factors in promotion of the disease.  The genetic promoters, notably the APOE4 gene, seem to work by creating an inflammatory environment in the brain.  No one seems to be claiming this with certainty, but it seems likely that any infection that causes inflammation in the brain can promote Alzheimer's.  While it's not yet well understood, there are ways in which inflammation outside the brain can sometimes cross the blood-brain barrier and cause inflammation inside the brain.  So a covid infection in the lungs may precipitate a cytokine storm and cause inflammation in the brain.

The good news is that the varieties of covid now in circulation are not causing the severe disease that covid was causing a few years ago.  Nevertheless, many of us recovered from serious infections a few years ago and may now be more vulnerable to developing Alzheimer's disease.