Is Biden Too Old or Have Other Presidents Been Too Young?

There is a column in today’s New York Times by Jennifer Senior that makes the case that President-elect Biden’s age could really be an advantage.  She points out the positive things that can happen as we age.  Like experience and expertise.  Many people have pointed out that Joe Biden knows how Washington works and can draw on that experience to get things done.  Of course, some critics have suggested that his knowledge of Washington is obsolete, that the Republican Party and its soulless leader in the Senate will not cooperate or compromise to pass important legislation.  But is there a better idea than trying to reach across the aisle to make things happen, or a better person than Mr. Biden to try to make that work?  

 

Senior notes another quality that Biden brings to the Presidency--wisdom.  We often say that older people are wise, but then we don't treat them as wise.  Of course, not all older people are wise, and age alone does not lead to wisdom.

 

What actually constitutes wisdom was a long-standing issue in Gerontology, but a program of research conducted by Paul Baltes and his colleagues has provided a compelling framework for understanding wisdom.  One aspect of wisdom is drawn from experience—factual and procedural knowledge.  That is, a wise person has access to a lot of facts in a domain as well as knowledge about how things work and how problems get solved in that domain.  One implication is that wisdom is not a general characteristic.  Rather, people can act wisely in domains where they have expertise, but may not give “wise” counsel in other domains.

 

Expertise, however, is not enough.  Another aspect of wisdom is what Baltes and colleagues called “excellence in mind and virtue.”  Here, they mean that the wise person strives toward excellence and the common good.  The wise person is not focused on themselves.  They are not saying, “I did it this way, and so that’s what you should do.”  They are instead applying knowledge about a specific situation that takes into account both the situation and the people involved.  Another way to say this is the wise person has empathy, which is another finding in the research conducted by Baltes and colleagues.  

You can see in this definition of wisdom a major difference between the 74 year old outgoing President and the 78 year old President-elect. Or as Senior wrote, the voters “decided to replace a savage clown and chaos-sowing novice with a man defined by decency and nearly half a century of public service.”

 

Aging, of course, has its perils.  The older we get, the more likely something bad will happen.  But Biden’s knowledge and temperament and his concern about other people, all of which have been honed over the course of his life, indicate he is up to the tasks ahead.  

 

 

Link to “Stop Worrying About Biden’s Age” by Jennifer Senior

https://www.nytimes.com/2020/11/12/opinion/biden-age-president.html?referringSource=articleShare

 

To read more about wisdom:  Baltes, P. B., & Smith, J. (2008).  The fascination of wisdom:  Its nature, ontogeny and function,  Perspectives on Psychological Science. 3, 56-64.  doi: 10.1111/j.1745-6916.2008.00062.x

Photo:  Elephant on a stairway in Lisbon.

 

The Silly Science Around Alzheimer’s Continues

A week hardly goes by without a new claim about causes of Alzheimer’s disease or cognitive impairment.  The New York Times Health Correspondent, Jane Brody, has never missed an opportunity to hype a potential cause or cure, no matter how suspect the evidence is.  This past week she wrote about vision and hearing loss as possible causes.

This is an idea that has been around for awhile.  And while some scientists make a plausible argument that reduced sensory input might lead to lower cognitive abilities, that is a far step from causing plaques, tangles, strokes, or other dementia-related pathologies.  We have yet to hear a plausible explanation for the biological mechanism the connects hearing loss, which occurs within the ear, or vision loss, which occurs in the eye, to dementia, which occurs in the brain.  Hearing loss and vision loss definitely limit and distort the quality of information a person is able to take in, but they do not cause brain cells to progressively deteriorate the way we know they do in dementia. 

The most plausible explanation is that the findings are an artifact. Think about how cognitive functioning is assessed.  We show someone visual images and/or present verbal information that they are to repeat or remember.  If you can’t see or hear well, you are more prone to make mistakes on tests.  That is a fundamental premise of neuropsychological testing.  Whenever Judy saw someone for testing who had hearing loss her first priority was to be sure that conditions were optimal for hearing (quiet room, speaking in a low register and projecting her voice directly to the person), and when that wasn’t sufficient, using written materials to supplement verbal instructions.

Imagine dear old Uncle Bill, who is hard of hearing, being asked a standard dementia screening question:  “What’s today’s date?”  And Bill answers, “I haven’t been on a date in years.”  How might that answer be interpreted?  Before jumping to the conclusion that he has dementia, it’s important to consider he didn’t hear the question correctly.  Or maybe he’s just a wiseass.  Either way, it may not be dementia.

Many of the studies that have reported correlations between hearing loss and cognitive function have been conducted over the phone.  It’s hardly an optimal way to assess someone with hearing loss.  But even clinical studies may confound hearing loss and cognitive problems, if the person conducting the tests is not well-trained.  The studies are also largely correlational, and don’t show decline in cognition over time.  Brody cites two large studies, one with 3,000 people, and one with 30,000 people, that present correlations of cognition and hearing loss, but a large sample is not necessarily better.  It’s easier to find statistical significance with a large sample, but what is called “effect size,” that is, the size of the association, may be quite small. 

We would all like to know that there is something that we could do that might prevent dementia.  And if we have hearing loss that affects daily life, it would be a good idea to get evaluated for hearing aids or other hearing devices, because that could make things easier at least in some situations.  But that’s a far cry from advising someone to get hearing aids in order to prevent the development of dementia.

How Are You Doing?

 

How are you doing?  We are getting along well.  We are not seeing our grandkids as much as we’d like or traveling or doing other things we enjoy.  But we are doing all right.

 

It’s the country we are worried about.  This is the most important election in our lives.  We have had presidents in the past who lied (Nixon about Watergate, Johnson about Vietnam), but we have never had a president who lies constantly and threatens to destroy our democracy.

 

We urge you to vote, if you have not done so already.  And get your friends and relatives to vote, too.  

 

If you are still undecided, or know someone who is undecided, take a look at the excellent column by Nicholas Kristof (link is below).

 

At the beginning of the primaries, we wrote a blog suggesting that Biden (and Trump, too) were too old to be president.  Joe has shown us to be wrong during the campaign.  Instead of trying to match Trump in vitriol, he has presented a vision of what this country could become by bringing people together.  He speaks powerfully from his experiences.  He knows that more anger and bitterness will not get us anywhere.  Our country has lots of problems.  Joe promises to get to work on them, with our support.  That’s wisdom that comes with age.

 

We hope to tune back in next week to celebrate the end of this long nightmare.

 

 

Link to Nicholas Kristof’s column:

 

https://www.nytimes.com/2020/10/30/opinion/donald-trump-polarization.html?campaign_id=45&emc=edit_nk_20201030&instance_id=23642&nl=nicholas-kristof&regi_id=60761850&segment_id=42887&te=1&user_id=98f3fcf260219e79a11053d8948e41ec

 

Photo:  Fall colors. Frick Park, Pittsburgh

The Vote is in!

                                                                    

Not that vote.  But an important vote in our family.  As a diversion from the corona virus, election and other upsetting stories in the daily news, we have been finding wonderful food that can be ordered on-line.  A few weeks ago we ordered babkas from Zabar’s in New York for ourselves and our kids.  They were wonderful.  Even our grandkids were thrilled.  We had tasted Zabar’s babka in the past, but it has been awhile, and we had forgotten how good they could be.

 

But then the question came up—is the chocolate babka better than the cinnamon babka?  You may remember the Seinfeld episode about babkas.  Jerry and Elaine were standing in line, waiting to buy a chocolate babka as hostess gift for the dinner party they were going to.  But the couple a head of them buy the last chocolate babka.  The baker offers to sell them a cinnamon babka, which Elaine calls “the lesser babka.”

 

We thought a taste test of our own was appropriate.  Jerry and Elaine went to Royale Bakery for a babka, but it has closed.  A New York friend of ours said the place to go when you are bringing a babka as a gift is Green’s Bakery in Brooklyn.  So we placed our order.

 

The vote is in.  The winner is (drum roll)  -- the cinnamon babka from Zabar’s.  The consensus was that Green’s chocolate babka was better than Zabar’s, but Zabar’s cinnamon babka was the best overall.  Not the lesser babka at all.

 

FYI.  The Seinfeld episode, “The Dinner Party,” is Season 5, Episode 13, and is available on Prime Video.

  

What’s in a Name? Could COVID-19 Be too Mild a Name to Gain Compliance with Preventive Approaches?

Why has it been so hard to get people to comply with simple protective approaches that reduce the spread of the COVID-19 virus?  It is a simple matter to wear a mask outdoors and in shops.  It is simple to maintain a safe distance.  Yet go almost anywhere and you see someone with the mask below the nose or hanging below the chin.  Or someone who gets far too close to you.  People complain bitterly that these restrictions are trampling on their freedom. Freedom to infect others?

 

Part of the problem, of course, is due to the politicians, starting at the top, who have minimized risks from the beginning and encouraged people not to take any precautions.  But maybe the problem is partly due to the name, COVID-19 Pandemic.  The word “COVID” does not sound threatening.  It doesn’t carry any meaning.  Would a different name be more motivating for people to take precautions?

 

Looking back in history, plagues had more evocative names.  The Great Plague, also called the Black Death or Bubonic Plague, swept across Europe and Asia several times.  In the 14^th century, the Great Plague wiped out between two thirds and three quarters of the population in parts of Europe.  Those names carry some heft to them.  Likewise, other illnesses that led to widespread infection and death had names that conveyed threat:  Small pox, typhus, typhoid, cholera, malaria.  Or more recent names—Ebola and Zika.  And of course, Human Immunodeficiency Virus (HIV/AIDS).  They sound ominous.  Even “Spanish flu” sounds more serious than just ordinary influenza or H1N1 flu.  

 

And why call it a pandemic?  Plague is more dramatic.  It’s something people react to.  The term “plague” calls to mind all those apocalyptic paintings of victims from the 14^th century and later plague outbreaks.  New York Times columnist Roger Cohen recently quoted Camus, who wrote that the plague “never goes away. It is waiting to exploit stupidity.”  That fits our response. 

 

What, then, should we call it that would better get attention?  President Trump started calling it the China Virus, which everyone saw as just another attempt to divert attention from his incompetence in letting the virus spread in the US, even as much of the world was implementing shutdowns and other efforts to control the virus. Such as wearing masks.

 

But it is not just that COVID-19 originated in China.  Viruses have regularly been making the jump from animals to humans in China.  The source is believed largely to be markets where wild animals are sold for food.  For years, the US and other countries have been talking with China about closing these markets, and there is some indication that they may be willing to do so. That would be an important step that could reduce the annual flu epidemic and prevent other novel viruses such as COVID-19.

 

To further that goal, we thought that COVID-19 should be re-named for one of its animal hosts, bats.  Bats are ugly.  We use their images for decorations for Halloween.  But Bat Virus is not strong enough.  Bats play an important role in eating mosquitoes in this country, and, after all, they are not responsible for the virus.  So we propose instead that COVID-19 be renamed the Bat Shit Plague.  There’s nothing nice or comfortable about that.  The bat isn’t being blamed directly.  And the name conveys how terrible the virus has been.  Maybe people unwilling to take precautions for COVID-19 will take steps to avoid the Bat Shit Plague. It’s a thought.

 

 

  

  

In the Midst of the Covid19 Crisis, Ageism Raises Its Ugly Head

Ageism been there all along during the COVID pandemic.  There was the quote a few months ago from Dan Patrick, the Lieutenant Governor of Texas, “Lots of grandparents would rather die than see health measures damage the US economy.”  It was only a matter of time before a national politician would raise that argument.  And there it was last week.  President Trump passed along a tweet claiming that only 6% of all deaths attributed to COVID 19 were actually due to the virus, and “the other 94% had 2-3 other serious illnesses & the overwhelming majority were of very advanced age.”  So they don’t matter.  The figures are, not surprisingly, also wrong.  But the truth is that many people are willing to write off the deaths of older people.

 

This is particularly the case of older people from disadvantaged groups.  Scholars who study age prejudice often talk about “double jeopardy,” that ageist beliefs and behaviors have an even greater impact on minorities.  Infections and death rates are higher among African Americans.  That’s not surprising, given long-standing disparities in income and access to health care.  African Americans are also more likely to hold jobs that could expose them to COVID 19 and less likely to be able to work remotely.

 

It’s not only despicable politicians and social media trolls who are saying ageist things.  Ageism has been part of the response to COVID 19 in the mainstream media, as documented in a recent article by Bronwen Lichtenstein in The Gerontologist.  Examining the media in the US, United Kingdom and Australia, she found that the vulnerability of older adults was frequently described with name-calling, blame, and “so-be-it” reactions.  There was also considerable debate in the articles she reviewed herd immunity.  Like the Lieutenant Governor of Texas, proponents argued that the herd immunity approach was the best way to support the economy, even though it would likely increase mortality substantially among older people.

 

The country that went full speed ahead to try to reach herd immunity was Sweden.  Their approach of minimizing restrictions had the expected effect of higher rates of illness and mortality, with older people paying a disproportionate price.  Drawing on recent data in the Washington Post, Sweden has a death rate of 575 deaths per million people in the population.  That compares to 610 deaths per million in the UK (which also took a herd immunity approach initially but has since pulled back on it), 545 deaths per million in the US, 111 deaths per million in Germany, and 9 deaths per million in Japan.  Likewise, Sweden is at the high end of countries for deaths in care homes.  Forty-seven percent of all deaths in Sweden occurred in care homes, compared to 45% in the US, 39% in Germany and 14% in Japan.  

 

But despite the expectation that the economy would not suffer if businesses and social interactions continued as usual during the pandemic, Sweden’s economy is not doing particularly well, and certainly not better than its Nordic neighbors, which have much lower rates of infections and mortality.  For example, Denmark has 623 total deaths (107 deaths per million), Norway has 264 deaths (48 deaths per million), and Finland has 335 deaths (60 deaths per million).  

 

The throw away attitude toward older people is most apparent in the death rates in care homes.  Basic procedures for containing infection were woefully inadequate in some facilities in the US and in other countries.  And then there is Japan, which stands out for its very low rate of deaths in care facilities.  It’s not because of a smaller proportion of the population in care facilities. Japan has a universal long-term care insurance program and the number of people in care facilities has grown steadily, and is now about equal to the US, according to the Washington Post article.  The article went on to speculate on what led to the low rates of deaths in care facilities.  One factor was that rates remained low in the population as a whole.  Beyond that, three other factors played a role:  implementation of stronger measures to prevent infections, higher standards of hygiene, and perhaps not surprisingly, the traditional importance of elders in Japanese culture.  

 

Photo:  We found the graffiti message on this old viaduct to be intriguing.  Is it a comment on our times?

 

Source of Statistics for the Nordic countries:  Statista:  https://www.statista.com/statistics/1113834/cumulative-coronavirus-deaths-in-the-nordics/

 

Washington Post, Japan Has the World’s Oldest Population. Yet It Dodged a Coronavirus Crisis at Elder Care Facilities.  https://www.washingtonpost.com/world/asia_pacific/japan-coronavirus-elderly-death-rate/2020/08/29/f30f3ca8-e2da-11ea-82d8-5e55d47e90ca_story.html

https://www.boomlive.in/world/donald-trump-endorses-false-claim-that-cdc-cut-covid-19-death-toll-9580

 

 

A New Diagnostic Tool for Alzheimer’s Disease: What Does It Tell Us?

You may have read recently about a new, more accurate test for identifying people with Alzheimer’s disease (AD).  Finding a reliable marker of the disease has long been a goal of researchers.  The ability to confirm diagnosis would help improve research of all kinds, but especially drug trials, because there would be more certainty that participants in the trials had Alzheimer’s and not another form of dementia.  An early marker of AD would also be enormously helpful for designing prevention studies.  We know, however, that many stories about Alzheimer’s disease in the media exaggerate or misinterpret the findings of studies. So we decided to take a look at the article about the new diagnostic tool, which has been published on-line in JAMA.

 

The paper reports on findings from three studies of people with and without Alzheimer’s.  The goal of the three studies was to test how well a marker found in blood samples, P-tau217, distinguished between people with a confirmed diagnosis of Alzheimer’s disease and people without the disease. Tau, as you may know, is a protein normally found in nerve cells that can become twisted, forming one of the primary markers of Alzheimer’s disease, neurofibrillary tangles.  P-tau217 is a marker of those abnormal cells.  

 

Study 1 consisted of people with and without dementia who had volunteered to be followed over time until their death.  Plasma samples of P-tau217 were obtained prior to death and compared with postmortem findings in the brain as well as with prior diagnosis.  

 

Study 2 was part of a large Swedish study that was following people with Alzheimer’s Disease and other neuropathological disorders and well as persons without dementia.  Amounts of P-tau217 were compared to other markers of the disease as well as to diagnosis.

 

Study 3 used a sample from an ongoing study in communities in Colombia, where many people have an autosomal dominant gene for Alzheimer’s disease that leads to the disease at early ages, typically when carriers of the gene are in their 40s.  Blood samples were obtained from people with and without the gene who were part of the study.

 

What did they find?

 

Across the three studies, P-tau217 from blood and plasma differentiated between cases of Alzheimer’s disease and non-disease subjects better than or as well as other markers, including findings from PET and MRI scans and samples of P-tau217 from cerebral spinal fluid.  P-tau217 was highly correlated with the amount of tau (tau density) found in the brain at autopsy in Study 1 and with estimates of tau in the brain from PET scans in the other two samples.  In Study 3, people with the dominant gene for Alzheimer’s disease began showing increased P-tau217 in their mid-20s, or about 20 years before symptoms typically occur.

 

What are the implications?

 

            The main take away from the study is that P-tau217 is a reliable marker of Alzheimer’s disease and of one of the main pathologies in AD, neurofibrillary tangles.  The blood test for P-tau217 is easier to administer and less painful than tests using cerebral spinal fluid, and more readily available and less expensive than PET scans, but just as accurate for determining diagnosis as either of the other methods.

 

            But does P-tau217 predict Alzheimer’s among people who are not symptomatic?  Here the media loudly proclaimed that P-tau217 could detect AD up to 20 years prior to symptoms.  This was based on the finding that people in their 20s in the Colombia sample who carried to dominant gene for AD and could expect to become symptomatic in their 40s had elevated levels of P-tau217.  It remains to be determined higher levels of P-tau217 are found years before onset of symptoms only in certain genetic variants of the disease, or if they can be detected early across most or all cases of AD.  That’s a big “if.”

 

Is P-tau217 ready for widespread use for diagnosis?

 

            No.  There are two hurdles that are by no means easy to overcome.  First, there needs to be a reliable cut-off score, that is, how much P-tau217 indicates a disease process.  The cut-off used in this research worked well in differentiating people already characterized as having AD from controls without the disease, but whether that score would work as well in community samples where people may have early symptoms remains to be seen.  Every effort to push diagnosis earlier in the disease process runs the risk of increasing false positive diagnoses.    

 

            The second hurdle is how far ahead can P-tau217 reliably predict AD.  P-tau217 may predict in a sample with a strong genetic determinant, where we know that people holding the gene will develop the disease, but may not do as well as a predictor for other forms of the disease.  Studies to determine how far ahead a P-tau217 score might predict symptoms would take considerable time to conduct—doing the test today and waiting a few years or more to find out who gets the disease and who does not.

 

Do you want to know your risk for Alzheimer’s?

 

            This is, of course, the key question.  Would you want to know?  One reason to consider the test is if one of the rare, dominant gene forms of AD runs in your family.  In that case, getting a genetic test would be more definitive than the P-tau217.  For cases that occur in later life,  60+,  the APO E4 allele has been linked to AD.  The APO E4 is not a dominant gene so having one copy of it does not mean you will get AD, and even having two copies may not result in AD.  Genetic tests can identify if you have one or two copies of the APO E4 allele. 

 

            The other reason to consider the P-tau217 test is if you think you are having symptoms.  Having occasional memory lapses is not reliably a symptom of AD.  Everyone forgets.  But if memory and other cognitive abilities seem to worsen, then the P-tau217 test could help clarify what is behind the cognitive problems. 

 

            But the question still remains – would you want to know?  If you tested positive for a gene associated with AD or for P-tau217, what would you do differently?   What changes would you make in your life?

 

            Growing older has been described by our friend Bo Malmberg as “sooner or later.”  Sooner or later, something bad will happen.  The implication is to live a full life now.  

 

            

 

Reference:  Palmqvist, S., et al. (2020).  Discriminative Accuracy of Plasma Phospho-tau217 for Alzheimer Disease vs Other Neurodegenerative Disorders.  JAMA, doi:10.1001/jama.2020.12134 (published on-line with free access).