I am a bad blogger

Yes, it's true.  Mainly because I'm very slow and inconsistent in responding to comments.  So I want to kind of catch up on recent ones.

First, I get many very positive comments, both by postings on the blog and via email.  This is so gratifying to me.  After experiencing the amazing turnaround in my condition, my reason for getting up each day is to encourage others who are confronting, or may confront, the same monster.  Well, it's one of the reasons.  After selling over 11,000 copies of Beating the Dementia Monster, and unexpectedly encountering people who have stumbled on it and read it, I know my efforts have made a difference in some lives.

Anyway, what follows are my responses to comments over the past several months that seemed to anticipate that I would respond.  Note that the system doesn't always tell me who actually posted a comment, and it just identifies them as "Unknown."

Now Espresso fights Alzheimer’s disease? - August 15, 2023

Comment from “Unknown”: I reached out to the researcher - Question: "I currently drink coffee regularly, but espresso only on occasion. I'm trying to decide if I should make a change.  Did your research find that espresso is beneficial above regular coffee? Or is drinking coffee also a good move?" 

The researcher’s answer to Unknown: "We made a in-vitro research using only espresso.  We still don't know to what extent our findings are confirmed in vivo.  However, the molecules contained in the regular coffee are not so different in terms of type and amount, from that of espresso."

My response: I appreciate you investigating this further and sharing your findings!

Sushi for Brain Health? - January 15, 2024  

Comment from “Unknown”: I will be interested to hear how it goes. Also, I think I understand you as saying that the paste form of wasabi is ineffective.  Can you please clarify?  I'm not sure what other forms are available.  Thank you for your blog.  I find it both informative and inspiring.  Joan 

My response: Joan, sorry to be so slow replying to your comment!  I wasn't trying to say that the paste form is ineffective, rather that product sold as wasabi is often more horseradish than actual wasabi.  I suspect that the wasabi I've bought on Amazon was actually more horseradish.  There are web sites claiming to sell pure wasabi, but it can be pricey. 

Why the MIND diet excludes cheese, butter, and margarine -- now we may know. - May 28, 2024 

Comment from “Unknown”: I'm curious to know why stick margarine is specifically mentioned; does that mean other types of margarine (tub margarine, I suppose) are less likely to contribute to the kinds of detrimental effects found in the study?  And if so, what's different about them?  And thank you for this blog.  I follow it avidly. 

My response: Thanks so much for your kind words. In "Diet for the Mind," Dr. Morris said that stick (or block) margarine is more hydrogenated and contains more transfats.  She said that tub margarine is much better, but she preferred olive oil.  I stick with olive oil. 

Comment from Sui Generis: So where does this leave us with eggs? I've been eating two eggs every day for breakfast.  The sample meal planner at https://www.healthline.com/nutrition/mind-diet even includes them.  The articles you referenced don't mention eggs, but neither do they mention cheese. 

My response: Sui, from what I read, it seems that eggs have been completely let off the hook.  In "Diet for the Mind," Dr. Morris says they got a bad rap, and they're full of important nutrients.  The only reservations about them I've heard recently is that you shouldn't eat too many (more than two a day), because they haven't been studied enough.   I don't have any reservations about eating eggs, even more than two. 

Regarding cheese, Dr. Morris was very critical, notably regarding mozzarella, since Americans eat so much of it.  In the US, we put a lot more cheese on pizza than other countries, so pizza consumption seems to be implicated in Alzheimer's disease here.  It has a lot of saturated fat, which she believed is the culprit.  After seeing her own research findings, she cut her consumption of cheese way back. 

Genes that control dementia in the face of advancing Alzheimer's disease - June 14, 2024 

Comment from “Unknown”: Might therapies be developed to help more people "express" those protective genes? Do we all have the genes, even though they are only "expressed" in some people? That sounds like an intriguing possibility to me. 

My response: I brought up “expressing” genes because the research article used the term, and I like to differentiate genes from the proteins that result from them.  Contrary to what a lot of people believe, genes don’t actually do anything.  They are simply the blueprints for the proteins that will do something. So, mRNA molecules read the genes and take the information to the the ribosomes.  The ribosome uses the information the mRNA read from the gene to assemble a chain of amino acids and, from the chain, form a protein molecule.  

You have the genes you were born with, and different people have different variations of many of them.  That’s why we look different from each other.  Identical twins have the same genes, and so they look the same as each other. 

But every gene exists in every cell of the body, even in cells where this gene or that gene will never be used.   So, genes are expressed selectively.   If a cell will be used to color your eyes, the genes governing eye color will be expressed as special proteins in that cell, but not in, say, a bone cell.  Expression of genes is controlled by “gene regulation networks.” 

This is a lot more than you asked for! 

Regarding your question, the point is that the important variable is which genes you drew in the lottery, rather than when genes will or won’t be expressed.   But … for people who drew the better genes, might there be therapies out there that would better exploit them by expressing them more or somehow differently?   That’s a good question.  But not one I’m qualified to answer. Nor have I seen anyone address it.

Genes that control dementia in the face of advancing Alzheimer's disease

We know from a variety of studies (and my experience!) that cognitive decline may be suppressed even when Alzheimer's disease advances.  The classic example is the Nun Study, in which a few women were found on autopsy to have evidence of advanced Alzheimer's disease but who did not display evidence of dementia before they died.  What was different about these people?  Inquiring minds want to know.

I came across an interesting study published in the journal Acta Neuropathologica Communications that found genetic makeup can play a role, especially with genes involved in immune response.  Researchers  from the Netherlands studied the brains of a sample of deceased people where it could be determined that they did or did not show evidence of dementia before they died.  Also, it could be determined whether they did or did not have Alzheimer's disease.  The presence of amyloid plaques, certain tau proteins, and atrophy gave evidence of Alzheimer's pathology.  They compared these parameters to the genetic makeup of these people.  The article was entitled, "Gene-expression profiling of individuals resilient to Alzheimer's disease reveals higher expression of genes related to metallothionein and mitochondrial processes and no changes in the unfolded protein response."  (I'm sure there's a longer title somewhere, but I haven't seen it yet.)

Long story short, there were people in the study with evidence of both Alzheimer's disease and dementia, a much smaller number of people without dementia but with evidence of Alzheimer's disease, and a number of people with evidence of neither Alzheimer's nor dementia.  There were certain special genes "expressed" in the population with Alzheimer's disease who did not have dementia that were not expressed in the other populations.  ("Expressed" means they were activated for use in producing specific proteins.)  These genes were largely associated with the immune response.  There was also correlation with the related proteins to how the brain reacts to metals entering the brain and in the processing of energy.

Note that, in Alzheimer's disease, it's metals in the brain that may oxidize and cause damage, which is why we eat blueberries.  Also, PET scans used to diagnose Alzheimer's disease are looking at how glucose is processed in the brain for energy.  There is a progressive breakdown in the metabolism of glucose in Alzheimer's disease.  So proteins from these genes, either directly or indirectly, appear to be suppressing the way in which Alzheimer's disease is promoting oxidation and interfering with metabolism of glucose.

I am certain that you do not want to read the research report.  However, if you're interested, here's an article from Science Direct that breaks it down for you in a way that's easier to understand.  But the article gets into something dearer to my heart that's not addressed directly in the research paper.  That is the population of people without these special genes and have Alzheimer's disease, but do not have dementia.  Since I was developing dementia, and my MRIs had the biomarkers for Alzheimer's disease, I surmise that I am one of these.  With regard to this population, the authors of the magazine article echo what we said in Beating the Dementia Monster -- lifestyle changes are the key to turning the disease around.

A deep dive on brain health and dementia

I'm always on the lookout for new articles and, hopefully, new insights on brain health.  Recently, I came across an interview with Dr. Wendy Suzuki, Dean of the NYU College of Arts and Sciences.  Dr. Suzuki is a neuroscientist and the author of the book, Healthy Brain, Happy Life: A Personal Program to Activate Your Brain and Do Everything Better.  She has done important research on neuroplasticity; how the brain sort of "morphs" in response to various changes in living environment and other demands on the brain.  (This occurs as neurons constantly disconnect from one another and then reconnect with other neurons to form new pathways for information inside the brain.)  Since 2018, she has focused heavily on the role of physical exercise, especially aerobic exercise, on brain health.

So, while on the treadmill at the gym, I watched this hour-and-a-half interview with Dr. Suzuki on Steven Bartlett's popular YouTube podcast, The Diary of a CEO.  Now, except for the latter part when she discusses her faith life, there isn't much information that we didn't talk about in Beating the Dementia Monster.  She goes through most of what I've called "the dementia toolkit."  But she is quite expressive and entertaining, so it was worth the time I spent watching.  For example, she shocks Bartlett when she produces an actual human brain and has him hold it.

If you're looking for an enjoyable discussion of where neuroscience is today with respect to the lifestyle choices we make and our vulnerability to Alzheimer's disease and other brain diseases, you should take a look here.  Or maybe get her book.

Why the MIND diet excludes cheese, butter, and margarine -- now we may know

In the longitudinal studies the late Dr. Martha Clare Morris conducted that led to the development of the MIND diet, Dr. Morris found an association between consumption of red meat, butter, stick margarine, and cheese with the development of Alzheimer's disease.  So these are excluded from the MIND diet, even if they might be more tolerated in the Mediterranean diet.  When I speak to a group about diet, and I say that avoiding saturated fats helps insulate you from Alzheimer's disease, I hear groans.  Especially when I mention the cheese.

Longitudinal studies look at associations of behaviors and possible consequences over time, without necessarily explaining the reason for the associations.  So correlation isn't causation, and maybe there's some weird reason for the association that, if understood, would allow us to go back to cheese.  Unfortunately...

Saturated fats, cholesterol, and high-fat diets got a lot of bad press in the 1980s and 90s as being strongly correlated with heart disease.  But it turned out that the evidence for these associations was weak, and the government and health authorities backed off on strong recommendations that food high in saturated fats and cholesterol be avoided.  For example, it seemed like eggs were just poison, because they have so much cholesterol in the yolks.  But later research failed to find the strong link between egg consumption and the actual heart disease postulated by the cholesterol-heart disease hypothesis.  So they told us to go back to eating eggs.

So while the evidence of an association between a diet high in saturated fats and heart disease began to weaken, the association with Alzheimer's disease actually strengthened.  But what was the basis for the association?  I've been wondering this for a while.  And maybe we now know.

I came across this article on the science news web site, PsyPost.  It cites research from the journal, Nutrients, which claims to have found evidence that could explain the association between saturated dietary fats (cheese, butter, etc.) and Alzheimer's disease.  But it's kind of complicated, so you may just want to know that they think they're better able to explain the relationship between consumption of saturated fats and the development of obesity, type 2 diabetes, and Alzheimer's disease.  (Note that this particular study does not connect heart disease with a diet with saturated fats.)

Going a little deeper, the study examined the role of microRNAs (miRNA) in the "expression of genes."  Which means how proteins are generated when genes in DNA are read by messenger RNA (mRNA).  The miRNA (which have only been recently discovered) are supposed to regulate the production of proteins by exercising control over the mRNA that's making the proteins.  There are many different types of miRNA influencing the production of many different proteins.  Many of the miRNA live in parts of the brain like the hippocampus -- ground-zero for Alzheimer's disease.  Some can influence the development of insulin resistance in the brain.  As we explained in Beating the Dementia Monster, as insulin resistance advances we call it type 2 diabetes and it is strongly associated with Alzheimer's disease.

With that background, the researchers studied the diets of mice (again...) along with changes in their memories and other abilities.  The researchers also examined the mouse brains in autopsy.  They controlled the mouse diets so that the mice consumed known amounts of saturated fats.  The researchers found that a diet high in saturated fat seemed to disrupt the miRNA in its task of allowing proper generation of proteins and the work of insulin in signaling cells to consume glucose.  An important part of both type 2 diabetes and Alzheimer's disease is the failure of cells to properly take up and metabolize glucose.  And so they call Alzheimer's disease type 3 diabetes.  (We discussed all of this in Beating the Dementia Monster.)

It appears to me that this is a very different pathway to type 2 diabetes than the one we discussed in Beating the Dementia Monster.  The better known pathway is excessive consumption of carbohydrates generates a steady output of insulin that overwhelms the cells.  The insulin is supposed to signal the cells to take up glucose, but it hits a point where the overwhelmed cells stop taking up glucose.  Then glucose levels in the blood get excessively high and begin damaging organs.

This was all fascinating to me, but I'm not sure how many of you are still here.  The bottom line?  Staying away from red meat, butter, stick margarine, and cheese remains part of a diet for those of us avoiding or fighting Alzheimer's disease.

It's not just me, folks!

When I tell my story, I'm often met with skepticism.  And why shouldn't people doubt me?  The concept in popular culture about Alzheimer's disease is that it is genetic, with a steady, inevitable progress to the grave.  Most people have known someone, likely in their own family, who developed the disease and followed that seemingly inevitable path of memory and cognitive degeneration.  I don't mind telling you that I sometimes wonder myself ... until I recall how my life was in 2015 and 2016.  So, is my story credible?  Am I somehow unique?   

I recently came across this article in the New York Post about two people who claimed to have "reversed" their biomarkers for Alzheimer's disease through changes in diet and exercise.  Sound familiar?  The article references a documentary series on CNN about Alzheimer's disease, which, in turn, highlights research by the well-known diet doctor, Dr. Dean Ornish.  The series is narrated by Dr. Sanjay Gupta.  Ornish has been conducting research in how lifestyle changes can influence the advance of Alzheimer's disease, and he is now publishing his results.  

The key to understanding the evidence (and the skepticism about our experience) is to recognize that the role of lifestyle is only obvious following significant and often difficult changes in lifestyle.  Some people are already living well and/or do not have any predisposing characteristics.  Others have genetic markers and/or have poor habits regarding exercise and diet.  But it's rare to see someone change their lifestyle and record how it affects memory and cognition.

Ornish uses the phrase "for the first time" regarding his research on reversing Alzheimer's disease, without giving due to the FINGER study, which we hope will be confirmed by the US POINTER study.  Of course, as we pointed out in Beating the Dementia Monster, Dr. Dale Bredesen also claims credit for reversing Alzheimer's disease "for the first time."  I won't claim to be "for the first time;" I'll say instead that I have company.  

I'd like to say I have a lot of company, but I don't have enough.  My mission at this point in my life is to encourage as many people as possible to change how they live, hoping they will be happier and more productive.

In Gupta's series, one thing he did was travel to Okinawa where the longest lived people in the world live.  He hoped to find out what in their diet causes their longevity.  He may be wasting his time.  Many people in Hawaii who identify as Japanese are of Okinawan heritage.  After living in American culture for generations, they are consuming as much pizza and McDonald's as anyone.  My wife is of Okinawan ancestry, the youngest of eight.  We visited Hawaii a couple of months ago and spent some time with her oldest brother.  At 91, he still plays golf twice a week.  It seems to me that (if Alzheimer's doesn't interfere) it's genetic makeup causing Okinawans to live long lives.

Exercise and Dementia - A much more complex picture

In Beating the Dementia Monster, we tried to provide a reasonably straightforward understanding of how it was that exercise, especially sustained aerobic exercise, might have such a powerful effect in countering Alzheimer's and some other diseases associated with metabolic syndrome.  The simple narrative was that during exercise, the body generates the brain-derived neurotrophic factor (BDNF) protein that repairs damaged neurons and prompts stem cells in the hippocampus to form new neurons.  While that all appears to be true, it turns out that there's a much more complicated story.  According to some new research, exercise, one way or another, does something in just about every tissue in the body.  And many of these effects make additional contributions to brain health.

Since 2016, the Molecular Transducers of Physical Activity in Humans Consortium (MoTrPAC), has been conducting a 10-year project funded by the NIH Common Fund to further investigate these phenomena.  The results are pretty remarkable.  (But you may want to take a Dramamine before you visit their web site.)

So far, MoTrPAC has produced three peer-reviewed studies.  One paper published in the journal Nature maps molecular responses to endurance training across 18 organs, including the brain and the cardiovascular system.  Another, in Nature Communications, reports that endurance training influences the expression of disease-associated genes.  A third, published in Nature Metabolism, identified sex differences in how fat tissue responds to training.  (It turns out that males burn more fat than females.) 

The most important of these studies was "Temporal dynamics of the multi-omic response to endurance exercise training," published in Nature.  But, well, the study was based primarily on work with rats.  They compared rats who worked out hard on the cage wheel with rats denied access to any way of exercising.  However, the researchers meshed what they learned about rats with other research with humans to draw conclusions about exercise by humans.

What did they find?  Exercise provoked an incredible array of molecular changes across the entire body. Some were shared across tissues, suggesting common responses, while others only happened in one or a few organs.  Some of these molecular responses rose or fell as endurance training progressed.  While all tissues showed changes in response to exercise, some showed more change than others.  Blood, brown and white fat, adrenal gland, and colon cells changed dramatically, while there were only small changes in the hypothalamus, cortex, testes, and vena cava.  For proteins, the calf muscle, heart, and liver experienced the biggest effects.  And, of course, they confirmed what we said about BDNF in Beating the Dementia Monster. 

The ALZFORUM concludes, "Researchers have long puzzled over whether the benefits of physical activity on cognition and memory might be due to a direct effect on the brain, and/or to improvements in other tissues, such as the cardiovascular and immune systems.  [MoTrPAC] could help them tease apart these effects, and point to the most optimal exercise interventions."

So ... more research is necessary.

That online test and ... chocolate!

Last time I wrote, I talked about the online cognitive test from LANGaware.  The first time I took it on April 23, I came up as cognitively impaired.  I took the test two more times since then and came up normal.  However, my "normal" had some deficits.  In my post of April 23, I shared the map of my cognition, showing those of my strengths and deficits that had been measured.  I took one more test after that showing a wider range of strengths, but still substantial deficits.  Still within normal.

The obvious question is "the practice effect."  Did I do better simply because I had practiced their test?  All I can say is that, with each test, they based their results on largely differing measures.  I presume that helps with the practice effect, since I studied the results for each test to understand where I'd been short before taking the next test.  So ... who knows?

But I also came across a very reassuring video reinforcing my joy in eating dark chocolate!  Now I've sworn off milk chocolate since its sugar content surely causes more problems than it helps.  But dark chocolate contains flavanols, polyphenols, and catechins that are powerful antioxidants.  Maybe even more than blueberries.  These are great for both heart health and brain health.  (The neurologists always say, "What's good for the heart is good for the brain!")

In the video, the neurologist describes the benefits of eating dark chocolate, noting that chocolate with too much sugar won't help you.  (So no milk chocolate.)  If fact, you should verify that it is 70% or more cacao

I noticed that brands like Lindt and Ghirharde can be a bit pricey.  However, Sam's Club at Walmart, 72% cacao, is reasonably priced.  For a while, we could get Jojo's Dark Chocolate Bars at Costco, but they have been discontinued.  That was my favorite.

I love chocolate, so the warnings that come with this dietary recommendation from the experts can be discouraging.  Only one or two pieces a day.  Otherwise, they say, you negate the positive effects with the amount of sugar you will be consuming.