I’M TAKING DAILY IBUPROFEN AND HOPING.
I’m
85 and if I make it to 90 I’ll have a 50/50 chance of developing Alzheimer’s. For those who don’t know (or remember), Alzheimer’s
is a condition where neurons die, the brain shrinks, and people can’t form new
memories, or think and function normally.
Labeled a “degenerative disease”, it starts in the hippocampus of the
brain up to 15 years before a person has memory changes, and it spreads like an
infection. At a microscopic level pathologist
see amyloid “plaques” outside of nerve cells and Tau tangles inside them. Smart
scientists have theories as to what’s happening and why, but we still don’t
know how to cure or slow the problem.
And
that brings me to ibuprofen and a study that was published in the New England
Journal of Medicine in 2001. Back then a
group of researchers studied the pharmacy records of “6989 people who were living
in a suburb of Rotterdam, Netherlands.
All were 55 years of age or older and they were free of dementia.” During those years people who took NSAIDs like
ibuprofen needed a prescription, so there was a record of who took what and
when they took it. The researchers
followed the 7000 for about 6.8 years and tallied their findings.
During the almost 7
years some people died, 293 developed Alzheimer's, 56 suffered from vascular dementia,
and 45 had other types of dementia.
A relative risk of 1.0
means no difference between people who didn’t
take NSAIDS and people who did take
NSAIDS.
A relative risk
greater than one means more of the people taking NSAIDS developed Alzheimer’s.
A relative risk of
less than one means fewer people taking NSAIDS developed Alzheimer’s.
In this study:
“The relative risk of a person who occasionally took ibuprofen like medications was 0.95; the occasional use of ibuprofen had no effect.
When people took
NSAIDS often, their risk was 0.83. (maybe a very slight effect??) –
And in people who regularly
took NSAIDS the incidence of Alzheimer’s was 0.20. It was much lower. In this study regular ingestion of ibuprofen
made a major difference.
The risk did not vary
according to age nor did the medicine decrease the risk of vascular dementia.”
In an editorial in the New England Journal, John C.S. Breitner, a
Canadian Psychiatrist, and Peter P. Zandi, a Johns Hopkins psychiatric epidemiologist, mentioned two studies where
researchers in Rochester and the Mayo clinic “found no association between Alzheimer’s
and the use of NSAIDs during the two years preceding the onset of dementia.” They also talked about “a prospective study
conducted as part of the Baltimore Longitudinal Study of Aging. In that study regular users of NSAIDs were half
as likely develop Alzheimer’s as compared with nonusers.”
The authors suggested that in studies where NSAIDS seemed to
prevent Alzheimer’s, the medicine “only benefited people who had taken the
drugs for “at least two years before the onset of dementia.” Once a person has symptoms ibuprofen didn’t
make a difference. It didn’t help
The Netherlands study was published 21 years ago and over the
years experts who are smarter than me poked holes in the idea that ibuprofen prevents
dementia. Most modern experts don’t
believe doctors should recommend the regular prophylactic use of NSAIDs.
Many people I talked with are leery of ibuprofen and its side
effects. So what is ibuprofen?. Where did it come from and what good and harm
does it do?.
The story starts in 400 B.C. when the Greek healer Hippocrates treated
pain and fever with extracts from the leaves and bark of the willow tree. In the 1800s we learned the chemicals he and
other healers were using were salicin and salicylic acid. In
the late 1800s a chemist named Charles Frédéric Gerhardt and later a German chemist working for
the Bayer Company, modified salicylic acid and created acetylsalicylic acid—the drug we call aspirin.
In the 1950s chemists working for the Boots herbal Medicine Company of Nottingham England tried to create a more effective form of the drug or a new medicine that would help people who had rheumatoid arthritis. They constructed and tested hundreds of small chemical modifications of acetylsalicylic acid and were unable to come up with a new medicine. Then they started modifying and testing a number of other chemicals. One of the substances they altered was propionic acid (carboxylic acid). It’s a “naturally occurring liquid and it smells like body odor. “ It was initially “isolated from the degradation products of sugar in 1844 by Johann Gottlieb.
By 1961 the Boots chemists had endured years of research,
endless testing of compounds and many disappointments. Then one of them, Stewart Adams, created a substance
that controlled pain,
lowered fever, and lessened inflammation.
( 2-(4-isobutylphenyl)
propionic acid—ibuprofen. ) Boots pharmaceutical patented and marketed the drug
and it was a best seller. It’s been around for decades and we know a lot about
its side effects and risks.
In high doses ibuprofen can cause stomach and duodenal ulcers,
and people with kidney problems should probably avoid it. “Young healthy subjects will rarely experience adverse renal
effects with the use of NSAIDs, but elderly patients and those with
co-morbidities (e.g., congestive heart failure, liver cirrhosis or chronic
kidney disease) and those taking certain drugs may develop acute renal failure. Ibuprofen can modify inflammation and there’s some
evidence that it affects wound healing.
In my case –so far at least-- my kidneys and stomach are working
well and I’m getting older every day. I
also ache some and ibuprofen helps that.
If daily ibuprofen might significantly lower my risk of Alzheimer’s, I’m
taking it.
1. https://www.nejm.org/doi/full/10.1056/nejmoa010178
Nonsteroidal Antiinflammatory Drugs and the Risk of Alzheimer's Disease
November 22, 2001 N Engl J Med 2001; 345:1515-1521 DOI: 10.1056/NEJMoa010178
2. https://www.nejm.org/doi/full/10.1056/nejmra0909142
Alzheimer's Disease
3. Do Nonsteroidal Antiinflammatory
Drugs Reduce the Risk of Alzheimer's Disease?
List of authors.
·
John C.S. Breitner,
M.D., M.P.H.,
·
and Peter P. Zandi,
Ph.D., M.H.S.
N Engl J Med 2001; 345:1567-1568
DOI: 10.1056/NEJM200111223452110
Addendum: In her 2017 TED talk Lisa Genova mused that one
in three of the 85 year olds in her audience already has Alzheimer’s
disease. (Lisa is a neuroscientist and
the author of the book Still Alice.)
Lisa pointed out that “despite decades of research we don’t know how to cure
or modify the disease.”
She said
scientists tend to explain the disease as follows: the brain is made of trillions of nerve
fibers that communicate with one another. Nerves don’t touch. They correspond by sending chemical messages
across gaps, intersections or synapses. We
call these chemicals “neurotransmitters.” Nerves also dump a metabolic waste protein
called amyloid into the synapses. Janitor
cells called microglia metabolize and remove it. Problem is those glias don’t remove all the
amyloid. Over the years the debris builds
up. Scientists think it takes 15 to 20 years
before a worrisome amount of amyloid accumulates. In the synapses the amyloid proteins bind to
one another, form sticky plaques, and grow in size. Eventually many people reach a tipping point.
Something triggers “a molecular cascade.”
One explanation: The microglia become activated and release
chemicals that cause inflammation and cellular damage. A crucial neuro-transport protein called tau
becomes hyper-phosphorylated (activated).
Then it twists itself into tangles and chokes off neurotransmitters from
the inside. Once the match is lit –once the
inflammatory process starts—it spreads and damages and destroys more and more
of the brain.
Some companies
tried to cure or modify Alzheimer’s by removing the amyloid. In some cases it helps a little, but once the
process has started the approach usually doesn’t work well. What about a drug that helps prevent or delay the
inflammation from starting? What about
ibuprofen??
https://www.ted.com/talks/lisa_genova_what_you_can_do_to_prevent_alzheimer_s?language=en
inflammation as a central mechanism in Alzheimer's disease
ReplyDeleteJefferson W Kinney a,∗, Shane M Bemiller b, Andrew S Murtishaw a, Amanda M Leisgang a, Arnold M Salazar a, Bruce T Lamb b
PMCID: PMC6214864 PMID: 30406177
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by cognitive decline and the presence of two core pathologies, amyloid β plaques and neurofibrillary tangles. Over the last decade, the presence of a sustained immune response in the brain has emerged as a third core pathology in AD. The sustained activation of the brain's resident macrophages (microglia) and other immune cells has been demonstrated to exacerbate both amyloid and tau pathology and may serve as a link in the pathogenesis of the disorder.
Over the last 10 years, a third core feature of AD has emerged that may provide insight into AD pathogenesis, as well as provide a link between the other two core pathologies.
A number of investigations initially demonstrated that in addition to Aβ plaques and NFT, the brains of patients with AD exhibited evidence of a sustained inflammatory response. The inflammatory response has now been observed in multiple studies of postmortem tissues of AD patient samples and is routinely observed in preclinical model systems of AD.
As the microglia are involved in clearance of Aβ, they release a number of proinflammatory cytokines that recruit additional microglia to plaques [125], [126], [127], resulting in a characteristic halo of activated microglia surrounding plaques [112], [128]. More recent data indicate that as microglia become less able to clear Aβ, peripheral macrophages may be recruited to Aβ plaque deposition in an effort to clear Aβ [129]. The recruitment of peripheral macrophages into the brain likely exacerbates the effects of sustained inflammation and thus AD pathology.
there are animal studies that suggest the herb tumeric decreases microglial inflammation in the brain and there is anecdotal evidence that populations that ingest a large amt of tumeric has a lower incidence of Alzheimer's. according to wikipedia Turmeric is a flowering plant in the ginger family that is native to the Indian subcontinent and Southeast Asia that requires temperatures between 20 and 30 °C (68 and 86 °F) and high annual rainfall to thrive. Plants are gathered each year for their rhizomes. The rhizomes can be used fresh, but they are often boiled in water and dried, after which they are ground into a deep orange-yellow shelf-stable spice.
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