Responses to Questions and Comments: August 2021

By Michael Jorrin, "Doc Gumshoe", August 24, 2021

I was hoping to keep COVID-19 out of this piece, but new things keep flooding in, and I can’t totally ignore them. However, I’ll save them to the end of the story. They are both “good news,” more or less, and I like to leave you with a bit of cheer, when possible.

Sleep and dementia/Alzheimer’s disease

The first comment that I’m addressing was in response to the recent piece about 
Alzheimer’s disease: “I’d like to know Doc Gumshoe’s thoughts about proper sleep and the link to AD.” Initially I thought that lack of “proper sleep,” whatever that might be, could be lumped in with Lancet’s “population attributable factors” such as hearing loss, hypertension, obesity, smoking, physical inactivity, and others. The Lancet authors thought that those factors were the cause of more than a third of all dementia cases. Not getting enough sleep, thought I, was just another aspect of an overall unhealthy lifestyle.

But then I did a bit of digging around and what I found was something of an eye-opener. It turns out that several careful studies have been conducted, and that not only has the connection between sleep and dementia been convincingly demonstrated, but that a specific mechanism has been identified and tracked.

Here’s what I found:

The underlying reality is that there is a well-recognized association between sleep and cognitive function. Fundamentally, sleep plays a vital role in learning and memory. Apparently, we take in a torrent of information while we’re awake and then sort it and file it during our sleeping hours. Then, when our little brain cells aren’t being flooded with new incoming perceptions that we take in through our senses, they have time to process it so that we can access it when we need it. When we don’t get enough of the right kind of sleep – deep, dreamless sleep in contrast with rapid eye movement (REM) sleep – our brains just don’t do a good job of processing the information they take in.

A study quantifying this effect was published in Nature Communications (Sabia S et al; 2012; 12, no. 2289). It was a very long-term study, in 7959 participants, followed for 25 years. Of these, 521 subjects developed dementia, The overall finding was that consistently sleeping less than 7 hours per night was associated with a 30% increased risk of dementia, independent of any other factors that might cause dementia. The increased risks varied with the ages of the subjects. Subjects in their 60s had the highest increased risk of dementia (37%), followed by those in their 70s (24%) and those in their 50s (22%). The results were judged to be statistically significant (P < 0.02).

When the study subjects were divided into thirds based on their hours of sleep duration , the increased risk for dementia in the subjects whose sleep duration was in the first tertile, (under 6 hours) was 63%. At the other end of the scale in the highest tertile, there was a very slight, statistically insignificant increased risk of dementia in subjects with sleep duration of up to 10 hours.

The lowest incidence of dementia was seen in subjects whose mean sleep duration was 7 hours.

But that’s by no means the whole story. As I poked around more, I came across several studies that seem to point to the reason that short sleep duration is linked with dementia. It appears that during deep sleep, the brain washes away the waste products that increase the risk for Alzheimer’s disease. A study led by Matthew Walker, a professor of neuroscience at U. C. Berkeley, found that poor sleep led to increased accumulations of amyloid beta (Aβ) and toxic tau, both of which are associated with Alzheimer’s disease. (Curr Biol 2020;30:21-4291-4298)

In the study, Walker’s team followed 32 subjects in their 70s who had taken part in a sleep study that looked for the slow electrical waves that signal deep sleep. The study used brain scans to monitor the levels of Aβ in each study subject over the six-year duration of the study. The study demonstrated a clear correlation between the amount of deep sleep and Aβ – the less sleep, the more Aβ accumulated.

A previous study, led by Laura Lewis at Boston University, demonstrated how during sleep waves of fluid wash through the brain. During the deep sleep period, the brain behaves like a dishwasher, and these waves of fluid get rid of the waste that builds up during the day – substances like Aβ and tau. These waves are preceded by a large, slow electrical wave. Lewis notes that these waves can be induced in mice, and may be able to be induced in human subjects.

When those large, slow electrical waves are induced in mice, those lucky mice experience improvements in their cognitive abilities. Doc Gumshoe is somewhat skeptical that the cognition of mice can be accurately gauged, but let’s take that as a small bit of contributory data to the possibility that improvement in deep sleep could combat the progress of dementia and Alzheimer’s.

A study led by Dr Yo-El Ju at Washington University, St Louis found that treating patients with obstructive sleep apnea, besides giving these patients the gift of hours of deep sleep, also cleared Aβ from the brain. And the unexpected result is that these patients also began making less Aβ.

When I queried Pub Med for some of these studies, I was surprised to find that the numbers of studies that in some way linked sleep to dementia and Alzheimer’s run to the thousands. Conclusive proof that insufficient deep sleep is at least a cause – even if not the single cause – of Alzheimer’s would require studies of a scope and complexity that is hard to imagine. But the links are persuasive. Less deep sleep links to a higher incidence of dementia and more accumulation (or less clearing) of Aβ and tau protein. And dementia and Alzheimer’s are associated with both of those substances.

In that last sentence, the key words are “associated with.” The field of Alzheimer’s research accepts the association, but has not arrived at the conclusion that the true cause of AD is either one of those substances or a combination of the two. There is a bit of evidence that the presence of Aβ does not necessarily cause Alzheimer’s, specifically finding the presence of Aβ in the brains of persons with no sign of dementia of any kind. What that means is that some people can maintain their cognition despite the presence of Aβ. That may be due to one of those “population attributable factors,” namely cognitive reserve. Nonetheless, the overall association of that brain crud with Alzheimer’s is persuasive.

All in all, my sense is that advances are being made in the quest for effective treatment courses for Alzheimer’s disease.

The Bredesen Protocol

A reader commented “The Bredesen Protocol is said to produce a noticeable reversal of Alzheimer’s.” Doc Gumshoe actually discussed the Bredesen protocol in some detail in a piece on 21 February of this year, but here’s a short recap.

About Dr Bredesen and his protocol I would venture that he is not a total crackpot. In his book “The End of Alzheimer’s in our Time” he pointed to several factors, each of which may in some way contribute to the neurologic changes that cause the symptoms of AD. He has then formulated a complex protocol that purports to address each of these factors, and gone on to claim that adherence to this protocol will banish Alzheimer’s disease. In my opinion (and also the opinions of several experts) he has immensely exaggerated his claims, likely for the purpose of selling his protocol for about $1400 per shot – and that’s just for the protocol – supplements and actual treatment are extra.

Bredesen asserts that Alzheimer’s is a protective response to the three basic threats to the brain, these being inflammation, a shortage of essential hormones and nutrients, and toxins in the brain. Inflammation, according to Bredesen, is caused not only by a response to invading pathogens, but is also (and this appears to be a principal focus of his protocol) a response to foods containing trans-fats, gluten, and – in particular – sugar. With regard to toxins, his protocol includes “identification of the toxic exposure, removal of the source, and then such measures as detoxifying foods such as cruciferous vegetables, hydration with pure water, and sauna-based removal of a specific class of toxins.”

It has been pointed out that the “evidence” upon which Dr Bredesen bases his protocol is suspect. None of these studies included placebo-controlled trials. They were not designed to put Dr Bredesen’s hypothesis to a test, but merely to report that some patients treated by his protocol showed some improvement. They omit details about which elements of the protocol were followed, as well as information about the dose or treatment duration. They include no mention of participant inclusion and exclusion criteria, and no data on any non-responders.

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Dr Bredesen’s protocol doesn’t seem to include potentially harmful supplements or activities, so we might put it in the “might help – won’t hurt” basket. Overall, the protocol seems to line up with the healthy life-style principles that have been observed to contribute to a decreased incidence of AD. We should note that nearly all the components of Dr Bredesen’s protocol can be accessed without a fee. One should no