Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,483 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
Summary: Cycles of a fasting-mimicking diet (FMD)
can effectively reduce signs of immune system aging, insulin resistance,
and liver fat, thereby decreasing biological age in humans.
The
FMD is a five-day plan high in unsaturated fats but low in calories,
proteins, and carbohydrates, designed to emulate the effects of
water-only fasting while providing essential nutrients. This
intervention, which doesn’t require chronic lifestyle changes, has shown
in clinical trials to rejuvenate metabolic and immune functions,
lowering the risk factors for various age-related diseases and reducing
participants’ biological age by an average of 2.5 years.
The
findings bolster the case for the FMD as a manageable, periodic dietary
intervention to enhance health and longevity without drastic lifestyle
overhauls.
Key Facts:
FMD Benefits:
The fasting-mimicking diet has been linked to numerous health benefits,
including stem cell regeneration, reduced chemotherapy side effects,
decreased signs of dementia in mice, and lowered risk factors for
several chronic diseases in humans.
Clinical Trial Findings:
Participants in the FMD group of the study experienced significant
improvements in metabolic health, including reduced insulin resistance
and liver fat, alongside indications of a rejuvenated immune system.
Biological Age Reduction:
Through the FMD, participants were able to reduce their biological age
by an average of 2.5 years, showcasing the diet’s potential for
enhancing cellular and tissue function.
Source: USC
Cycles
of a diet that mimics fasting can reduce signs of immune system aging,
as well as insulin resistance and liver fat in humans, resulting in a
lower biological age, according to a new USC Leonard Davis School of
Gerontology-led study.
The study, which appears in Nature Communications on Feb. 20, adds to the body of evidence supporting the beneficial effects of the fasting-mimicking diet (FMD).
The FMD is a five-day diet high in unsaturated fats and low in
overall calories, protein, and carbohydrates and is designed to mimic
the effects of a water-only fast while still providing necessary
nutrients and making it much easier for people to complete the fast. The
diet was developed by the laboratory of USC Leonard Davis School
Professor Valter Longo, the senior author of the new study.
“This
study shows for the first time evidence for biological age reduction
from two different clinical trials, accompanied by evidence of
rejuvenation of metabolic and immune function,” Longo said. Credit:
Neuroscience News
“This is the first study to
show that a food-based intervention that does not require chronic
dietary or other lifestyle changes can make people biologically younger,
based on both changes in risk factors for aging and disease and on a
validated method developed by the Levine group to assess biological
age,” Longo said.
Previous research led by Longo has indicated
that brief, periodic FMD cycles are associated with a range of
beneficial effects. They can:
What has your doctor done with this senolytic research? ANYTHING AT ALL? Or are you allowing incompetence to continue to exist until it affects your children and grandchildren?
At 67 years old, Dr. Nir Barzilai
looks about the same as, if not younger than, he did 10 years ago. It’s
apparent in side-by-side photographs, and it’s what most people who
know him say. Barzilai lives a healthy lifestyle. He exercises every day, eats right, and practices intermittent fasting.
He’s
also been taking the diabetes drug metformin off label for 10 years. He
has never been diagnosed with diabetes or prediabetes—the conditions
for which the drug is approved and prescribed—but takes it for a
different off-label reason.
“We know that it targets aging,” said
Barzilai, who is a professor of medicine and genetics at Albert Einstein
College of Medicine and director of the American Federation for Aging
Research.
“People on metformin have 30% lower rates of almost every kind of cancer. It delays cognitive decline.
Even people with diabetes who are obese and have more disease to start
with but are on metformin have lower mortality rates than people without
diabetes who aren’t on the drug.”
What
he says is born out in numerous studies. Overall, this safe,
super-cheap, decades-old drug not only treats diabetes, but it also
seems to delay and compress the years of chronic illness associated with
the final stage of life and extend what geroscientists call the
“healthspan.”
Metformin is just one of many medications, including
other old ones and some brand new inventions, that academic researchers
and biotech startups are exploring to slow, stop, or perhaps even
reverse aging.
What is aging
All sorts of processes are
happening in our bodies as we age. Some of which make us more vulnerable
to the diseases most linked to old age: cancer, dementia, heart
disease, stroke, macular degeneration and so forth.
Doctors and
scientists in the longevity field are trying to determine which of those
processes is the strongest hallmark of overall aging and declining
health and how to target that process with a drug in the same way that
current drugs target specific diseases.
“We can target
aging,” Barzilai said. “We can delay it. And in several instances, we
can stop and reverse it. At one point we had hope. Then we moved to
promise. Now, we need to move to realize that promise. That’s where we
are.”
Dr. Nir Barzilai has been taking the diabetes drug metformin off label to treat aging.
Targeting undead cells
Dozens
of biotechs want to be the first to realize that promise through drugs
called senolytics. In certain diseases, these pharmaceuticals can clear
out toxic, old, dysfunctional cells and leave only young, healthy, well
functioning ones behind. Senolytic Dasatinib (Sprycel) is FDA-approved
for certain types of chronic myelogenous leukemia.
Here’s why researchers think senolytics could do more than treat one specific disease.
Your
cells constantly reproduce and divide throughout their lifespan to
create new, healthy cells. When they stop doing this, they die. But with
some cells, even though they’ve stopped reproducing, they don’t die off
like they should. These undead cells, called senescent cells, stick
around and give off toxic substances that can harm the healthy cells
around them—like the one bad apple that spoils the whole bunch.
As
you get older, your aging body becomes less efficient at clearing out
senescent cells, so they accumulate, especially around the sites where
chronic diseases develop, like macular degeneration.
Unity Biotechnology has a senolytic, dubbed UBX1325,
in phase 2 clinical trials for diabetic macular edema (DME) and
age-related macular degeneration (AMD). In both conditions, damage to
the retina can lead to vision loss.
Preliminary findings in DME
patients in the trial suggest that the drug clears out problem-causing
senescent cells in the eye and allows the remaining healthy cells to
repair and regenerate the retina and bring lost vision back.
“It
takes about 8 weeks to kick in, and at 24 weeks, you can see that the
tissue has dramatically remodeled,” said Anirvan Ghosh, PhD, Unity CEO.
“We had patients who had big gains in vision and big improvements in
retinal structure.”
As incredible as these results are, vision
restoration isn’t the endgame for Unity or most any company invested in
senolytics development. The idea is to develop another drug that will
have this same effect on another progressive disease and another and
another until, ideally, researchers can figure out how to make a drug
that would clear out all senescent cells, not just the one type behind a
certain disease.
“In different tissues, it’s not always the same
cell type that becomes senescent. I think next we will have
tissue-specific senolytics for a specific disease or if you’re high-risk
for that disease.” But to target aging, rather than just individual
diseases, he says, “We’d have to have something that clears these cells
from multiple tissue types.” That’s the long-term goal. And it may still
be a long road to get there.
Understanding biological age
While
zombie cells build up in the aging body, wreaking havoc as their
numbers grow, critical changes are taking place on the surface of DNA,
too. That is, in the epigenome, a landscape of proteins and chemicals that sits atop your genetic material.
These
changes over time are the result of your environment, behaviors and
exposures throughout your lifetime. Think: pollution, trauma, diet,
exercise, and secondhand smoke. They don’t change your DNA, but they
change the way your DNA acts. Genes that once functioned perfectly may
at some point in life slow down, speed up, shut off, or just go
generally haywire. Any dysregulation can cause disease or the signs and
symptoms of old age.
Epigenetic changes are like scratches on a record: You can still hear the music, but it’s not what it used to be.
Led by Harvard Medical School professor and molecular geneticist David Sinclair, PhD, Tally Health
is already bringing epigenetic approaches to aging directly to
consumers. The company offers a cheek swab test that estimates
customers’ biological age—how old they seem based on their epigenetics
rather than their birth year.
“Biological age
is a much better representation of health status than birthday
candles,” Sinclair says. “Birthday candles don’t tell you how well
you’ve been living and they certainly don’t tell you how many years
you’ve got left.”
Tally Health creates personalized
recommendations based on customers’ biological age for how they might
reduce that age because, as Sinclair points out, “Your biological clock
is not unidirectional.”
For now, the means to turn back the clock
are mostly lifestyle changes. But Sinclair, who has founded several
biotechs, and others are researching and developing drugs that might
slow or restart the clock so genes will act like they are young again.
Sinclair and his collaborators have shown that this is possible
in the eyes of blind mice. In newborn mice, if the optic nerve – the
nerve that carries messages from the retina to the brain—is damaged, it
will recover. But in old mice, it can no longer heal.
In
Sinclair’s lab, they crushed the optic nerves of mice to blind them. The
serious injury to the eye caused epigenetic changes that resemble those
that happen in old age. They then injected the nerves with genes that
contained factors they expected would reprogram the genes to behave like
they were young again.
The treatment reversed the age-related
epigenetic changes in the eyes, rescued retinal cells, and led to
regeneration of neurons. Since then,
Sinclair and his colleagues have corrected similar age-related
epigenetic changes in muscle and kidney tissue. Other researchers have
successfully used the technique to extend the overall lifespan of mice.
Sinclair expects to release results of his study which tests this
concept in primates in a few months.
The holy grail, of course, is to erase the scratches that time puts on our own epigenetic records. Sinclair says that’s coming.
“Resetting
the whole human body in this way is a different matter,” he says. “Are
we one day going to be able to turn ourselves back 20 years? I don’t see
any reason why that won’t be possible. It’s just a question of when.”
Drugs that treat aging
But
some drugs that could lower risk for multiple age-related diseases at
once and, perhaps, treat aging as a whole, might already be on the
shelves of the pharmacy.
Rapamycin, an mTOR inhibitor, got FDA
approval in 1991 as an immune suppressor that prevents organ recipients
from rejecting a new organ. By shutting off the mTOR protein, it
prevents immune system cells from proliferating to attack the donated
organ.
“But in every species that’s been studied to date – yeast,
worms, flies, mice – when they are given rapamycin, healthspan and
lifespan are extended. No other therapeutic has that degree of
validation,” says Joan Mannick, MD, CEO of Tornado Therapeutics.
Mannick
and other mTOR researchers believe that, among the other deleterious
processes of aging, mTOR proteins might start to malfunction, too. In a
healthy, young person, mTOR, which supports cell growth, is active when
we eat. That’s critical for growth, development and reproduction. When
we fast, like during the night, mTOR is inactive, which allows for cell
repair.
This, by the way, is probably one of the reasons
intermittent fasting has so many health benefits, Mannick says, because
it blocks mTOR and allows for more cell repair.
As we get older,
mTOR may stay active all the time—opening the door to out-of-control
cell growth that can lead to cancer and closing the door on cell repair.
In older adults, low doses of rapamycin, an mTOR inhibitor, seem to set
mTOR activity back to its youthful state: on when you need it, off when
you don’t.
“When they get rapamycin, their immune systems, which
have already been damaged by old age, start to function better,” Mannick
says. “There’s research to suggest that when you rejuvenate the immune
system, you make a lot of other organ systems function better. But we
need well-powered, placebo-controlled clinical trials to find out the
dose, what conditions it improves, and who responds best.”
To carry out that research, Tornado Therapeutics has acquired a portfolio of rapamycin derivatives, or “rapalogs,” from Novartis,
which they are studying as treatments for aging. If it can increase the
lifespan of every plant and animal that’s been exposed to it, Mannick
and the company’s investors, such as Cambrian Bio, bet it might increase
the human lifespan, too.
“I think in the next 5 to 10 years, FDA
will have approved the first drug to target aging biology,” Mannick
says. “It very well could be a new rapalog that is going to have
benefits for an aging-related condition as our first step to a much
broader aging medicine advance.”
Type 2 diabetes is an age-related
condition. Numerous studies show that metformin, a drug that’s
FDA-approved to treat it, may also lower risk for cancer, heart disease,
stroke, dementia, or death for any other reason, including COVID-19.
The
benefits, researchers suspect, are a result of metformin’s ability to
control blood sugar, blunt the effects of a lifetime of oxidative stress
on the body, and protect cardiovascular function. That is, it may meet a
host of needs that grow greater as we age.
Of course, the
overwhelming majority of data on metformin’s benefits comes from people
with diabetes. Numerous clinical trials currently underway are looking
at its effects on specific diseases in people who don’t have diabetes.
But longevity researchers, like Barzilai, want to prove to the FDA that
it doesn’t have to be taken for a specific disease. Older adults should
simply take it for aging.
Barzilai’s TAME (Targeting Aging with Metformin)
trial, which will last six years, aims to prove that anyone between the
ages of 65 and 79 can extend their healthspan with metformin.
“We’re using metformin as a tool,” he says, “to show the FDA that aging itself can be targeted.”
Targeting the healthspan
No
matter which approach becomes the first prescription drug for aging,
researchers in the area tend to agree it’s coming soon. It would be
expected to improve and extend life not only for average older adults,
but also for those who currently tend to get chronic diseases and die
sooner: childhood cancer survivors, people living with HIV, people
living in poverty.
Researchers predict the implications will be
huge when the healthy years of life last longer for everyone. Economist
Andrew Scott calculated that
a slowdown in aging that increases life expectancy by just one year
would be worth $38 trillion. A ten-year increase would be worth $367
trillion.
“That’s because with this kind of increase in life
expectancy, we are not spending that time in the hospital, we are not
sick,” Barzilai says. “We’re shopping, we’re traveling, we are
participating in society. We are living life. And that’s what we want.”
