RIP, Alan Greenspan: On Parkinson's Death Trends, U.S., 1999-2025
Also, links to prior posts on centenarians
22 Jun 2026, MSN: Alan Greenspan, Fed chair under 4 US presidents, dies at age 100
Alan Greenspan, an economist who served as chairman of the Federal Reserve under four U.S. presidents, died on Monday, his wife Andrea Mitchell said. He was 100.
Greenspan died at his home due to complications of Parkinson’s Disease, Mitchell said in a statement reported by NBC News, where she is the chief Washington and foreign affairs correspondent.
I’ll leave it to others to comment on Greenspan’s effects on monetary policy. I’m here to talk about mortality trends.
On Living to 100
I’ve written about trends of living to 100 (and beyond):
Jan 2024: What Are (and Were) the Chances of Living to 100?
What Are (and Were) the Chances of Living to 100?
Recently, we’ve had a spate of notable deaths in the U.S. at fairly advanced ages:
April 2022: Who Wants to Live Forever?
So you can read those, if you wish.
Of Greenspan’s cohort, born in 1926, using the Social Security Cohort Life Tables from the 2026 Trustees Report, about 0.56% of males made it to age 100.
Not too shabby.
He was the same generation as my grandparents.
Here’s a fun bit of Norm MacDonald at the White House Press Correspondents’ Dinner in 1997, where starting at 13:51 in the video, he has a bit where he’s roasting Alan Greenspan:
Probably didn’t expect Greenspan to outlive him, but there ya go.
Parkinson’s Mortality Trends, U.S., 1999-2025
As noted in the piece, Greenspan was considered to have died due to complications from Parkinson’s Disease.
Let’s see what has been happening with Parkinson’s Disease rates:
Oh. Hadn’t heard much about that, had you?
Well, look at this:
Parkinson Disease Mortality Among Adults Age 65 and Older: United States, 2024
Published: JUNE 2026
Key findings
Data from the National Vital Statistics System
In 2024, the age-adjusted Parkinson disease death rate for adults age 65 and older was 72.0 deaths per 100,000 standard population.
Parkinson disease death rates increased from 2014 (57.2) through 2021 (76.3), but the rate in 2024 was lower than in 2021.
In 2024, Parkinson disease death rates in adults age 65 and older were higher for men than for women in each age group (65–74, 75–84, and 85 and older).
Death rates from Parkinson disease were highest among White non-Hispanic adults age 65 and older compared with other race and Hispanic-origin groups.
Parkinson disease death rates varied by state of residence, ranging from 47.7 in New York to 102.1 in Utah.
Here is their graph: [focusing on 65+ ages]
By focusing on 2014-2024, you can’t tell that there is a long-term increase.
They also have split by race/ethnicity:
Longer-term trends, PD: Age 65+
Let’s look at the longer-term trends. I will stick to over age 65, as above, because those are the ages at which you see appreciable death rates:
From 1999 to 2025, the death rates due to PD almost doubled.
The increase from 2019 to 2025 was also appreciable.
Here is the breakout by sex:
Male, PD
Female, PD
Why the increase in PD?
This is the point at which I had a little “discussion” with Gemini, plus went down a path of reminiscences, as I had remembered a story about how the pathways of the discovery of how PD develops.
The story is retold in The Case of the Frozen Addicts:
In the summer of 1982, hospital emergency rooms in the San Francisco Bay Area were suddenly confronted with mysteriously “frozen” patients – young men and women who, though conscious, could neither move nor speak. Doctors were baffled, until neurologist J. William Langston, recognizing the symptoms of advanced Parkinson’s disease, administered L-dopa – the only known effective treatment – and “unfroze” his patient. Dr. Langston determined that this patient and five others had all used the same tainted batch of synthetic heroin, inadvertently laced with a toxin that had destroyed an area of their brains essential to normal movement. This same area, the substantia nigra, slowly deteriorates in Parkinson’s disease. As scientists raced to capitalize on this breakthrough, Dr. Langston struggled to salvage the lives of his frozen patients, for whom L-dopa provided only short-term relief. The solution he found lay in the most daring area of research: fetal-tissue transplants. The astonishing recovery of two of his patients garnered worldwide press coverage, helped overturn federal restrictions on fetal-tissue research, and offered hope to millions suffering from Parkinson’s, Alzheimer’s, and other degenerative brain disorders. This is the story behind the headline – a spellbinding account that brings to life the intellectual excitement, ethical dilemmas, and fierce competitiveness of medical research. This new updated edition of the classic neurological mystery tale, “The Case of the Frozen Addicts,” illuminates how the solution to a baffling mystery of the brain’s chemistry opened a new frontier in medicine and restored life to people without hope. “It begins with a series of quixotic discoveries, escalates to providing possible solutions for one of humanity’s most intractable medical problems, and then catapults the reader into the center of America’s hottest political arena – abortion and fetal sanctity. Bravo! A brilliant read.” – Laurie Garrett, author of The Coming Plague “[Langston and Palfreman] weave a highly readable and spellbinding medical detective tale… It is as absorbing as a good mystery, as entertaining as an exciting novel, and as enlightening as a good biography.” – Stanley Fahn, New England Journal of Medicine “I could not put it down… it is the lives of the ‘frozen addicts’ themselves – and the fullness with which this is presented – which makes the whole thing overwhelming.” – Oliver Sacks
I learned of this when I was studying neurology in grad school (I was going to model neurons), and as we all noted in class: it was a pity how much of what we knew about the brain was from pathology.
Before the 1982 case, medical researchers already knew that PD patients suffered from dopamine deficits. From Gemini:
Skipping over the bad batch of drugs episode, here were the conclusions:
So while there are genetic components to PD, to allow for a long-term increase in the disease, various environmental influences have been assumed:
Dorsey and Bloem (2024) argue that environmental toxicants such as pesticides, air pollution and trichloroethylene are linked to PD.[63] Certain pesticides and herbicides—such as paraquat, glyphosate, and rotenone—are the most established environmental toxicants for PD and are likely causal.[76][77] PD prevalence is associated with local pesticide use, and many pesticides are mitochondrial toxins.[78] Paraquat, for instance, structurally resembles metabolized MPTP,[76] which selectively kills dopaminergic neurons by inhibiting mitochondrial complex 1 and is widely used to model PD.[79][76] Pesticide exposure after diagnosis may also accelerate disease progression.[76]
This may be related to the following map from the earlier NCHS data brief:
The darkest color, which reflects the highest rates, are high agricultural states, and may be related to the use of particular pesticides and herbicides.
But what about Utah?
That might have to do with low use of substances that protect against PD:
Although no compounds or activities have been mechanistically established as neuroprotective for PD,[94][95] several factors have been found to be associated with a decreased risk.[94] Exercise[68] and diets rich in fruits, vegetables, whole grains, and fish are protective factors associated with lower risk of PD.[70] Consumption of caffeine as an ingredient of coffee or tea is strongly associated with neuroprotection.[96] Tobacco use and smoking are strongly associated with decreased risk, but it is unclear whether this results from a neuroprotective effect or reverse causation.[97][90][clarification needed] Various tobacco and smoke components have been hypothesized to be neuroprotective, including nicotine, carbon monoxide, and monoamine oxidase B inhibitors.[98][99]
Note that tobacco use (maybe it’s the nicotine?) is also associated… but is it because smokers die too young to get PD?
But also the caffeine use — and of course, the high concentration of LDS (and their eschewing of tea, coffee, etc.) may be related.
Going back to smoking/nicotine, one must keep in mind that lung cancer, emphysema, and similar causes of death have much higher rates than PD alone. So I wouldn’t advise taking up smoking just to prevent PD (especially since causal links aren’t very clear).
Similarly, if one looks at PD risk factors, other items aren’t so clear — it looks like the correlations may be of other risk factors (such as pesticide exposure… or just being white and/or old.)
One must be careful in trying to interpret these results. In the case of neurotoxins, there are some clear pathways, but in other cases, you’re just doubling down on the causes you already detected.
Greenspan: Interview
In the case of Greenspan, he may have had PD, but he lived a good long time even so.
