Stroke patients have high levels of microplastics in the plaque clogging their arteries, researchers find

 What will your stroke medical 'professionals' do to alleviate this problem? NOTHING, LIKE USUAL!

Stroke patients have high levels of microplastics in the plaque clogging their arteries, researchers find

• Microplastics and nanoplastics might interact with the plaque that causes heart attacks and strokes.

• A new study found high levels of plastic in the arterial plaque of stroke and vision-loss patients.

• Cells in plastic-filled plaque also showed signs of altered gene activity, but it's unclear why.

Tiny, microscopic bits of plastic have been found almost everywhere researchers look — including throughout the human body.

Microplastics and their even tinier cousins, nanoplastics, are probably flowing through your blood and building up in your organs like the lungs and liver.

Now, a new study is connecting the dots on microplastics' mysterious correlation with heart attack and stroke risk.

"There is some microplastics in normal, healthy arteries," Dr. Ross Clark, a University of New Mexico medical researcher who led the study, told Business Insider before he presented his findings at the meeting of the American Heart Association in Baltimore on Tuesday.

"But the amount that's there when they become diseased — and become diseased with symptoms — is really, really different," Clark said.

Clark and his team measured microplastics and nanoplastics in the dangerous, fatty plaque that can build up in arteries, block blood flow, and cause strokes or heart attacks.

Compared to the walls of healthy plaque-free arteries, plaque buildup had 16 times more plastic — just in the people who didn't have symptoms. In people who had experienced stroke, mini-stroke, or vision loss, the plaque had 51 times more plastic.

"Wow and not good," Jaime Ross, a neuroscientist at the University of Rhode Island who was not involved in the study but has studied microplastics in mice, told BI after reading the results.

"It's very shocking to see 51 times higher," she said, adding that in her research, a signal that's just three times stronger is "very robust and striking."

What exactly the plastics are doing in there, if anything, remains a mystery. The new study offers some possible clues, though.

This research has not yet undergone the scrutiny of peer review, but Clark said he plans to submit it for publication in a peer-reviewed scientific journal later this year, after replicating some of their results.

Genetic activity looked different with plastic

Clark is a vascular surgeon, not a microplastics specialist. However, he got the idea for this study by talking with his colleague Matthew Campen, who recently discovered that human brains contain a spoon's worth of plastic.

Microplastics get way smaller than this.Getty Images

"We realized together that there really wasn't a lot of data on nanoplastics and microplastics in the vascular system, within blood vessels," Clark said.

Previous research had found that people with microplastics in their arterial plaque were more likely to have a heart attack or stroke or die.

To investigate why, Clark studied samples from 48 people's carotid arteries — the pair of superhighways in your neck that channel blood to your brain.

EDAS Surgery May Help Prevent Repeat Strokes from Brain Plaques

I have no clue if I have plaque in my brain arteries, I know I have some in a couple of coronary arteries and 1 carotid artery is completely closed up. You'll have to ask your doctor how to determine if you have brain plaque and are a candidate for this.

EDAS Surgery May Help Prevent Repeat Strokes from Brain Plaques

Early phase study showed potentially lower recurrence, death risk

• by Crystal Phend, Senior Associate Editor, MedPage Today October 18, 2018
• This article is a collaboration between MedPage Today® and:
  

For patients with a recent stroke or transient ischemic attack (TIA) attributed to intracranial atherosclerosis, a procedure to redirect scalp or dural arteries into the brain appeared to safely reduce risk of recurrent events in a phase IIa trial.
The procedure -- encephaloduroarteriosynangiosis (EDAS), a version of the procedure done for Moyamoya disease but with modifications to maintain cerebral perfusion -- was associated with a 9.6% composite 30-day rate of death or stroke of any cause or any ischemic stroke around the atherosclerotic artery by 1 year after surgery, as adjudicated by stroke neurologists.
By comparison, the rate had been 17.3% in a group with the same characteristics but treated with medicine alone in the SAMMPRIS trial.
That 7.7% absolute difference met criteria for non-futility, warranting a phase III trial for the surgery in this population that accounts for approximately 10% of ischemic strokes, Nestor Gonzalez, MD, of Cedars-Sinai Medical Center in Los Angeles, reported at the World Stroke Congress in Montreal.
A less conservative comparison using propensity-score matching for a larger group of medically-treated patients as controls suggested as much as a 12% absolute risk reduction in the primary endpoint, again within the bounds set for significance.
"The results are better than we expected," Gonzalez said. However, he cautioned, "as promising as the results are, they are not definitive results and they need to be tested in a phase III randomized clinical trial."
Seemant Chaturvedi, MD, of the University of Miami, agreed that such a trial will be needed but called for further testing first.
"Patients with intracranial stenosis who are refractory to best medical management are a high risk group. The 10% event rate at 1 year is not trivial," he told MedPage Today. "I would like to see an expanded multi-center trial with a diverse group of surgeons. We need to see if a low complication rate can be achieved in a broader setting. I think it is premature for a phase III trial."
But also commenting on the trial, Mark Alberts, MD, of the Ayer Neuroscience Institute at Hartford Healthcare in Connecticut, argued that "there are not a lot of other good options for these patients. It makes sense to me to really explore this in a larger study format.
"If the larger study is successful, it will certainly redefine the standard of care for these patients and provide these patients with a very valuable surgical option."
Two of the 52 patients (3.8%) in Gonzalez's ERSIAS trial had surgical wound dehiscence that required further surgery for debridement and closure. But other adverse events were generally mild, there were no cases of cerebral hemorrhage or cerebral edema, and the overall safety profile was "very good," he told MedPage Today.
The single-arm trial included patients with symptomatic 70% or greater atherosclerotic stenosis of the intracranial internal carotid artery or middle cerebral artery and poor to fair collaterals seen on catheter-based angiography. All patients got intensive vascular risk factor management by SAMMPRIS protocols and aspirin as antiplatelet therapy perioperatively.
Functional outcomes shifted toward less impairment by 1 year compared with baseline in the EDAS-treated cohort, as measured by modified Rankin scale scores. Cognitive assessments among those with no aphasia or neglect showed results on par with SAMMPRIS at 12 months and less than the expected decline after a stroke or TIA.
Among those with angiographic follow-up, more than 97% had Perren grade 2 or better neovascularization, and about 68% had good collaterals (ASITN grades 3-4).
A phase III trial is in the planning stages, Gonzalez said.

The study was funded by the NINDS and Ruth and Raymond Stotter Endowment.
Gonzalez disclosed no relevant relationships with industry.

last updated 10.25.2018

• Primary Source

  World Stroke Congress

  Source Reference: Gonzalez NR, et al "EDAS Revascularization for Symptomatic Intracranial Atherosclerotic Steno-occlusive disease. Phase IIa Study" WSC 2018.

"Beet" Alzheimer's with Betanin

First step, so don't do this on your own.  I'm already daily eating pickled beets for these reasons;

Dietary Nitrate Lowers Blood Pressure: Epidemiological, Pre-clinical Experimental and Clinical Trial Evidence

BEETS TO BEAT HEART DISEASE - 2010

Beet Juice Beats Hypertension

 Beet Juice Lowers Blood Pressure

 The latest here; Not to be followed until your doctor prescribes it.

"Beet" Alzheimer's with Betanin

Beets get red from betanin. Betanin slows the accumulation of brain plaque, Alzheimer's #1 culprit. Learn how. See NutritionFacts.org's Dr. Greger on the way fresh beets fight dementia, and how much to eat or drink.

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"Our data suggest that betanin, a compound in beet extract, shows some promise as an inhibitor of certain chemical reactions in the brain that are involved in the progression of Alzheimer's disease," says Li-June Ming, Ph.D. "This is just a first step, but we hope that our findings will encourage other scientists to look for structures similar to betanin that could be used to synthesize drugs that could make life a bit easier for those who suffer from this disease."

Article continued below the video...
NutritionFacts.org Video: See how beets dramatically improve blood flow and blood pressure throughout the body, followed by a look at the best studies on how beets help the brain fight dementia. (The video focuses on dementia 3-minute-28-seconds into the video.) At the end of the article below, see the second "Beets" video, discussing the best amount to eat or drink.

Superagers with amazing memories have Alzheimer’s brain plaques

How is your doctor making sure you get to be a super ager? Any protocols at all?

Sounds like confirmation of Bernadette from the nun study.

Superagers with amazing memories have Alzheimer’s brain plaques

By Jessica Hamzelou in San Diego

Having an agile mind in your 90s might sound like wishful thinking, but some people manage to retain youthful memories until their dying days. Now post mortems have revealed that these “superagers” manage to do this even when their brains have the hallmarks of Alzheimer’s diseases.
Superagers have the memory and cognition of the average person almost half their age, and manage to avoid Alzheimer’s symptoms. Aras Rezvanian at Northwestern University in Chicago, Illinois, and his colleagues have been looking at brain samples donated by such people to try to understand what their secret might be.
The group looked at eight brains, all from people who had lived into their 90s, and had memory and cognition scores of the average 50-year-old until their final days. Specifically, the team studied two brain regions – the hippocampus, which is involved in memory, and the prefrontal cortex, which is key for cognition.

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They found that the brain samples of the superagers had plaques and tangles in them to varying degrees. These are sticky clumps and twisted fibres of protein that seem to be linked to the death of neurons, and are usually found in the brains of people with Alzheimer’s disease after they die. Of the eight superager samples, two had such a high density and distribution of these proteins that they resembled the most severe cases of Alzheimer’s.

Plaque protection

When the team counted the neurons in the brain samples, they found that they had many more neurons than samples from people who had died with Alzheimer’s. This is surprising, as it is thought that plaques are toxic and lead to the loss of neurons during Alzheimer’s disease.
“The oldest old with superior memory can display the full range of Alzheimer’s pathology,” says Rezvanian, who presented his findings at the Society for Neuroscience annual meeting on Monday. “It points to some unknown factors that protect some elderly from the plaques and tangles of Alzheimer’s,” he says.
Perhaps superagers just had more neurons to begin with, says Changiz Geula, who led the study. “They may actually be losing cognition and neurons, but start at high levels,” he says.
The findings support growing evidence that plaques and tangles might not be a direct cause of Alzheimer’s, says Cheasequah Blevins at University of Texas at Austin. “A lot of money was spent on getting rid of plaques, but it didn’t help – it actually made the patients quite sick,” she says. The next step is figuring out what the protective factor might be, she says.
Read more: Superagers with amazing memories have shrink-resistant brains; Drug that stops brain plaques may show if they cause Alzheimer’s