Men Have Faster-Shrinking Brains, But Women Get an Alzheimer's Diagnosis About Twice as Often as Men

 In the October 13, 2025 online edition of the journal Nature, we have an article with a headline of "Men's brains shrink faster than women's; what that means for Alzheimer's."  Alzheimer's is a disease involving a decline in mental function, and for older people the term is basically equivalent to dementia. 

Now, under the hypothesis that the brain makes the mind and that brains store memories, if men's brains shrink faster than women's as people age, there should be a higher rate of Alzheimer's disease in men. But the article tells us that the opposite is true. The article says, "Nearly twice as many women are diagnosed with Alzheimer’s disease as men." 

The article tells us that the conclusion that men's brains shrink faster than women's is based on a large study involving 12,500 MRI scans from 4,726 people who had at least two scans per person, taken an average of three years apart. We are given an example of the shrinkage rate: the claim that the postcentral cortex in men shrinks by 2% per year for men, versus 1.2% per year for women. 

The article's findings are contrary to claims that dementia or Alzheimer's disease is proportional to brain tissue loss. It is therefore very misleading for the article to include a visual like the visual it has. The visual shows a normal brain and a shrunken brain, with a caption of "A healthy brain and a brain affected by Alzheimer's disease." This is an old propaganda technique long used by those trying to suggest that brains are the source of minds and that brains are the storage place of memories. The technique involves showing photos of a normal brain and a shrunken brain, with a caption saying that the shrunken brain is the brain of the person with Alzheimer's. 

Contrary to the impression created by such a photo pair, a book on dementia says on page 35 that "there are many reports of people carefully diagnosed...as clearly having the clinical symptoms of dementia and yet showing no evidence of brain pathology."  On the same page the book gives this quote from a neuroscientist named Robert Terry:

"Over the years, investigators have sought assiduously for lesions or tissue alterations in the Alzheimer's brain which...might at least correlate with clinical determinants of the disease severity....Despite 30 years of such efforts, clinico-pathologic correlations have been so weak or entirely lacking that determination of the proximate, let alone the ultimate, cause of Alzheimer's disease (AD) has not been possible."

I may note that studies on the relation between dementia and brain volume are often guilty of various flaws. One flaw sometimes occurring is when the brains of people diagnosed with dementia or Alzheimer's are compared to the brains of healthy controls. If such a diagnosis was made after brains scans of subjects were done, the state of the brain may have influenced what type of diagnosis a person got, making the diagnosis a poor way of independently comparing brain states and mental states. A better technique is to judge dementia or Alzheimer's purely on the basis of performance on mental tests such as the MMSE, and to compare performance on such tests with brain states. The MMSE is the Mini-Mental State Examination, and is the most common test for cognitive impairment. 

The paper here shows graphs comparing MMSE scores and gray matter volumes, and shows no strong correlation between the two. We have in Figure 2 a scatter plot showing dots, each of which represents a correlation between gray matter in some region of the brain, and the corresponding MMSE scores. None of the correlations are strong, with none being higher than .5. Almost all of the correlations are weak, being well under .5; and the average correlation is only about .25.  A strong correlation is one such as .8 or .9. 

We do not have in the paper a graph showing negative correlations between regions of the brain and the corresponding MMSE scores. If such a graph had been given, we would probably have seen just as many or almost as many negative correlations (between brain volumes in different regions and MMSE scores) as positive correlations. Using the phrase "gray matter atrophy" to refer to brain shrinkage, the paper states, "The associations between gray matter atrophy, hypoperfusion, and cognitive impairment in AD [Alzheimer's disease] are still unknown, especially the causal pathways between them." The Nature article discussed in this post makes it all the more clear that there is no clear causal relation between brain shrinkage and dementia or Alzheimer's disease.

Below is interesting data from Table 1 of the paper here. We have data on six elderly female subjects called "super-agers." The MMSE number is the score on the Mini-Mental State Examination, a test of cognitive ability including short-term recall and also long-term semantic memory.  The maximum score on the test is 30. Notice the lack of correlation between brain weight and IQ, and the lack of correlation between brain weight and the MMSE score. The  MMSE scores for the 1st and 2nd subjects are identical, with the 2nd subject being very slightly smarter, even though the second subject has a brain weight 25% smaller. That same 2nd subject has an IQ of 135 -- in the 99th percentile for humans -- despite her  brain being very far below the average female brain size of about 1200 grams. The 4th subject has a brain much smaller than the fifth subject, but has the same perfect MMSE score, and an IQ score 10% higher. These results are consistent with the idea that your brain is not the source of your mind, and not the explanation of your memory powers. 

NAME	AGE	MMSE (MAX=30)	IQ	BRAIN WEIGHT (GRAMS)
SA1	87	29	133	1240
SA2	90	29	135	990
SA3	99	25	112	1020
SA4	87	30	119	1090
SA5	81	30	107	1269
SA6	90	29	111	1100

A similar table with data for 50 subjects can be found in the year 2021 paper "Is there a correlation between the number of brain cells and IQ?" We read this summary of the results:

"In our sample of 50 male brains, IQ scores did not correlate significantly with the total number of neurons (Fig. 1A), oligodendrocytes (Fig. 1B), astrocytes (Fig. 1C) or microglia (Fig. 1D) in the neocortex, nor with the cortical volume (Fig. 2A), surface area (Fig. 2B) and thickness (Fig. 2C). This also applied to estimates of the four separate lobes (frontal-, temporal-, parietal-, and occipital cortices; see Supplementary Material). Neither did IQ score correlate significantly with the volumes of white matter (Fig. 2D), central gray matter (Fig. 2E) or lateral ventricles (Fig. 2F), nor with the brain weight (Fig. 3A), or body height (Fig. 3B). All of these correlation coefficients were less than 0.2." 

Can we imagine a more complete research failure of the "brains make minds" hypothesis?

Appendix: In the scientific paper entitled, “A guide to appropriate use of Correlation coefficient in medical research,” we read the following: “A correlation coefficient of 0.2 is considered to be negligible correlation while a correlation coefficient of 0.3 is considered as low positive correlation.” Below is Table 1 from that paper, which has the heading of "Rule of Thumb for Interpreting the Size of a Correlation Coefficient."

Size of Correlation	Interpretation
.90 to 1.00 (−.90 to −1.00)	Very high positive (negative) correlation
.70 to .90 (−.70 to −.90)	High positive (negative) correlation
.50 to .70 (−.50 to −.70)	Moderate positive (negative) correlation
.30 to .50 (−.30 to −.50)	Low positive (negative) correlation
.00 to .30 (.00 to −.30)	negligible correlation

If you do a Google image search for "correlation coefficient interpretation," you will find several tables or guidelines that list all correlation coefficients of 0.2 or less as either "negligible," "very poor," or "very weak," and some of them (like the table above) actually list all correlation coefficients of .3 or less as "negligible.

The Lesson of the Telomere Myth

When I was a teenager, I had not yet discovered reasons for believing that we are all souls that will survive death. I did not study psychic phenomena before about the age of twenty. In my teenage years I knew nothing about the many physical shortfalls of the brain (discussed in the posts of this blog) that provide reasons for thinking that the brain cannot be the source of the human mind, and for thinking that the brain cannot be an explanation for the storage or instant recall of human memories. But I had what I thought was a reason for thinking that I might live way past the age of 100: the fact that science books kept telling me that extending human life was a pretty simple matter. In countless science books and articles I was told a hundred times that vastly extending the human lifespan was a mere matter of lengthening telomeres. 

Telomeres are little cap-like structures at the end of chromosomes, structures in the nucleus of each cell. Year after year between 1970 and 2020, we were told that the shorter the telomeres were in a person's chromosomes, the more signs of aging the person would show. The claim was that young people had chromosomes with longer telomeres, and that the older people got, the shorter their telomeres got. It was often said that  each time a cell reproduced, the telomeres in its chromosomes got a little shorter. We were told countless times during these years by innumerable authorities that there was probably an easy way to greatly extend human lifespan: simply lengthen a person's telomeres.  We were told innumerable times during these years that scientists were working on this task, and that before long they would figure out how to lengthen a person's telomeres. The result, we were told, would be a greatly lengthened human lifespan. 

I remember reading one of these authorities depicting how it would be around the year 2000 or 2010 (I don't remember exactly which year was imagined). According to the authority, there would be some liquid called telomerase that a person could receive by injection. The authority gave us a depiction of something like a 100-year-old person playing tennis every day, and having the vigor of a 30-year-old, all because she had got regular shots of this wonderful fluid that would lengthen her telomeres. 

A 2011 book called The Immortality Edge was written by two doctors and someone else. It told us that aging would be "cured" by about the year 2015. On one page we read this:

"If we reset telomere lengths in cells or in tissues, we can reverse aging in these cells and tissues. Currently, we are just about able to reset telomere lengths in your body. We have several compounds that promise exactly that, and we are rapidly finding more and more effective compounds. If we could go forward a century, and ask an average person when people first 'cured' human aging, the date will be somewhere in the current decade ; not fifty years from now, but now." 

Many people used the idea of telomere lengthening to help them make money. Biologists wrote books claiming to tell you how to live longer by lengthening your telomeres. Companies sold many millions of bottles of supplements that promised to help you live longer by lengthening your telomeres. Speaking what now sounds like nonsense, one leading neuroscientist stated this in 2017:

"Telomeres are listening to you. They absorb the instructions you give them...So if you want to keep your brain sharp, you have to know about your telomeres and stay in touch with them." 

The quote is from a book on telomeres, one with a chapter entitled "Your Cells Are Listening to Your Thoughts." 

But alas a recent New York Times story has this headline: "Link Between Long Telomeres and Long Life Is a Tall Tale, Study Finds."  We read this: "The longer a person’s telomeres, researchers found, the greater the risk of cancer and other disorders, challenging a popular hypothesis about the chromosomal roots of vitality." We also read, "Far from extending life, long telomeres appear to cause cancer and a blood disorder known as CHIP, a condition that increases the risk of blood cancers and heart disease." 

This should not have come as too big a surprise, because there always were good reasons for doubting the idea that lifespan is proportional to telomere length. The New York Times story cites one such reason that was well-known for very long:

" 'Some organisms have crazy long telomeres, like mice,' said Dr. Benjamin Ebert, chairman of medical oncology at the Dana-Farber Cancer Institute. 'And mice don’t live that long.' ”

Another good reason for doubting the idea that lifespan is proportional to telomere length is that metabolism and biochemistry are fantastically complex, with a vast number of interlocking dependencies.  It therefore never made any sense to think that you could make people live much longer just by doing one simple little thing.  The organization and functional complexity of a human body is vastly greater than that of a car. The idea that you could do one little thing to make people live 50% longer was always kind of like the idea that some mechanic could make your car run well for 300,000 miles, just by adjusting one little thing in the engine. 

A 2019 paper had found "there is no strong correlation between the life span of a species and initial telomere length." The same paper had claimed "we find a strong correlation between the telomere shortening rate and the life span of a species," but its data does not convincingly back up such a claim. For example, Figure 2G is an example of very dubious curve fitting. It shows 7 species with average lifespans from 20 to 80 years all having a slow telomere shortening rate of less than 500 base pairs per year, and only one other species depicted on the graph (the mouse, with a telomere shortening rate of about 7000 base pairs per year). Such data does not convincingly tell a tale of aging being proportional to telomere shortening. Figure 2A shows that mice (with lifespans of only a few years) start out with telomeres that have twice as many base pairs as the number of telomere base pairs that humans start out with. 

What is the lesson of this telomere affair? We might put it this way.

(1) Biologists love simple claims they can make with little soundbites such as "man arose because of lucky random mutations," "you can stay young by keeping your telomeres long," and "your mind is like some vapor arising from the bubbling soup of your neural activity." 

(2) Biologists may long keep making such claims (despite a lack of robust evidence for them) when there is some large group of people that wants to hear such claims, such as all the atheists and agnostics who want to hear a claim that we have an understanding of human origins or that we have a neural explanation for human minds, or the millions eager to hear they may live to be 150 once biologists figure out how to lengthen telomeres. 

(3) Biologists may keep making such claims while ignoring plain-as-the-nose-on-their-face evidence against such claims, like biologists ignoring the fact (mentioned above) that mice with "crazy long" telomeres have very short lives, biologists ignoring the implications of more than 20,000 different types of protein molecules in the human body (most having way too many well-arranged parts to be explained as the products of random mutations), and biologists ignoring all the physical shortfalls of the brain (such as lack of indexing and addressing, heavy signal noise, unreliable synaptic transmission, and very short synapse protein lifetimes) which help discredit claims the mind comes from the brain, particularly when you consider things such as the instant accurate recall of obscure facts learned five decades ago, the instant formation of complex human memories, and how some savants can perfectly do in their minds very complex math calculations at blazing speeds.  

Contrary to the predictions of telomere enthusiasts, there has been little change in US life expectancy during the past thirty years. The 2019 paper "Inconvenient Truths About Human Longevity" notes how much hot air has come from people talking about radical lifespan extension. The paper argues that average human life expectancy will not advance beyond about 85 years. To a materialist, such an idea may seem horrid. But to people who have studied the countless reasons (discussed at this site) for thinking that the brain is not the source of the human mind, such an idea need not be a sad one. Earth is a place of great trouble and sorrows, and it may well be that by wise design 98% of us are prevented from living here for more than about 85 years. Souls presumably have no maximum lifespan.