Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,724 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.
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.
Showing posts with label eicosapentaenoic acid. Show all posts
Showing posts with label eicosapentaenoic acid. Show all posts
Fish oil has long been praised as brain-boosting, but new research suggests the story may be more complicated. Scientists found that in people with repeated mild head injuries, a key omega-3 fatty acid in fish oil—EPA—may actually interfere with the brain’s ability to repair itself. Instead of helping recovery, it appears to weaken blood vessel stability, disrupt healing signals, and even contribute to harmful protein buildup linked to cognitive decline.
A new study from the Medical University of South Carolina is raising fresh concerns about fish oil supplements, especially for people who experience repeated mild traumatic brain injuries. Writing in the journal Cell Reports, researchers report that these widely used supplements, often promoted as protective for the brain, could actually interfere with healing after injury.
The research was led by neuroscientist Onder Albayram, Ph.D., an associate professor at MUSC and a member of the National Trauma Society Committee. His team focused on the biological processes involved in repairing blood vessels in the brain after injury.
Rising Popularity of Omega-3 Supplements
Interest in omega-3 fatty acids, the key components of fish oil, has been growing rapidly. According to Fortune Business Insights, these supplements are now appearing not only in capsules but also in drinks, dairy alternatives, and snack products.
That surge in popularity does not surprise Albayram. "Fish oil supplements are everywhere, and people take them for a range of reasons, often without a clear understanding of their long-term effects," he said.
"But in terms of neuroscience, we still don't know whether the brain has resilience or resistance to this supplement. That's why ours is the first such study in the field."
Albayram collaborated with Eda Karakaya, Ph.D., Adviye Ergul, M.D., Ph.D., and several other researchers at MUSC and partner institutions. Among them was Semir Beyaz, Ph.D., at the Cold Spring Harbor Laboratory Cancer Center in New York.
EPA Identified as a Potential Weak Point in Brain Recovery
The team discovered what they describe as a context-dependent metabolic vulnerability. In simple terms, this means that changes in how cells use energy may reduce the brain's ability to recover under certain conditions. This vulnerability appears to be linked to the buildup of eicosapentaenoic acid, or EPA, one of the main omega-3 fatty acids found in fish oil.
In their experimental models, higher levels of EPA in the brain were associated with weaker repair after injury.
Albayram noted that not all omega-3s behave the same way. Docosahexaenoic acid, or DHA, is well known for its beneficial role in the brain and is a major part of neuronal membranes. EPA, however, follows a different pathway. It is less incorporated into brain structures, and its effects can vary depending on how long it is present and the surrounding biological conditions. Because of this, the long-term impact of omega-3 intake on brain recovery and blood vessel adaptation has remained unclear.
Experiments Link Diet, Brain Biology, and Recovery
To better understand these effects, the researchers used a series of models to connect diet, brain function, and healing. In mice, they examined how long-term fish oil use influenced the brain's response to repeated mild head impacts. Their focus was on signals related to blood vessel stability and repair.
They also studied human brain microvascular endothelial cells, which form part of the barrier between the brain and the bloodstream. In these cells, EPA, but not DHA, was linked to reduced repair capacity, aligning with the findings from the animal models.
To extend the findings to real-world disease, the team analyzed postmortem brain tissue from individuals diagnosed with chronic traumatic encephalopathy (CTE) who had a history of repeated brain injury.
The researchers described the results as having "implications for precision nutrition, therapeutic strategies and the design of dietary interventions targeting brain injury and neurodegeneration."
Key Findings From the Study
The study identified several major patterns, which are summarized below along with simplified explanations.
EPA-driven neurovascular instability triggers perivascular tauopathy and cognitive decline following TBI.
"In a sensitive brain state modeled in mice, long-term fish oil supplementation revealed a delayed vulnerability. The animals showed poorer neurological and spatial learning performance over time, together with clear evidence of vascular-associated tau accumulation in the cortex, linking impaired recovery to neurovascular dysfunction and perivascular tau pathology," Albayram said.
EPA reprograms cortical transcriptional responses and suppresses angiogenic signaling following traumatic brain injury.
"In the injured cortex, the team observed a coordinated shift in gene programs that normally support vascular stability and repair," Albayram said. "The pattern included reduced expression of genes tied to extracellular matrix organization and endothelial integrity, alongside broader changes consistent with altered lipid handling after injury."
EPA utilization under permissive metabolic conditions impairs angiogenesis and endothelial integrity, recapitulating post-traumatic brain injury cerebrovascular dysfunction.
Albayram said that in human brain microvascular endothelial cells, EPA did not act as a universal toxin. "Instead, when cells were placed in conditions that encouraged fatty acid engagement, EPA was associated with weaker angiogenic network formation and reduced endothelial barrier integrity, matching key features of the neurovascular repair deficit seen in vivo."
CTE brain reveals neurovascular and fatty acid metabolic reprogramming consistent with EPA-linked vulnerability.
"In postmortem cortex from neuropathologically confirmed CTE cases with a history of repetitive brain injury, the researchers found evidence of disrupted fatty acid balance and broad transcriptional changes affecting vascular and metabolic pathways," Albayram said. "This human arm was used to provide translational context, asking whether chronic disease tissue shows convergent signatures of altered lipid handling and reduced vascular stability."
What the Findings Mean for Fish Oil Use
Albayram stressed that the study should not be interpreted as a blanket warning against fish oil. "I am not saying fish oil is good or bad in some universal way," he said. "What our data highlight is that biology is context-dependent. We need to understand how these supplements behave in the body over time, rather than assuming the same effect applies to everyone."
The researchers hope their work encourages a more careful look at omega-3 supplementation, both in clinical settings and among the general public. Their experiments focused on a specific scenario, repeated mild brain injury, and used CTE tissue to provide supporting observations rather than direct proof of cause and effect.
"As with any study, there are important boundaries," Albayram said. "In the human CTE tissue, we can observe patterns, but we cannot prove what drove them. We also cannot capture every variable that shapes omega-3 handling in real life, including overall diet, health status and lifestyle."
Next Steps in Understanding Omega-3 Effects
The team plans to continue investigating how EPA moves through the body, including how it is absorbed, transported, and distributed. They are especially interested in the mechanisms that control fatty acid movement.
"This paper is a starting point," Albayram said, "but it is an important one. It opens a new conversation about precision nutrition in neuroscience, and it gives the field a framework to ask better, more testable questions."
A new study from the Medical University of South Carolina is raising fresh concerns about fish oil supplements, especially for people who experience repeated mild traumatic brain injuries. Writing in the journal Cell Reports, researchers report that these widely used supplements, often promoted as protective for the brain, could actually interfere with healing after injury.
The research was led by neuroscientist Onder Albayram, Ph.D., an associate professor at MUSC and a member of the National Trauma Society Committee. His team focused on the biological processes involved in repairing blood vessels in the brain after injury.
Rising Popularity of Omega-3 Supplements
Interest in omega-3 fatty acids, the key components of fish oil, has been growing rapidly. According to Fortune Business Insights, these supplements are now appearing not only in capsules but also in drinks, dairy alternatives, and snack products.
That surge in popularity does not surprise Albayram. "Fish oil supplements are everywhere, and people take them for a range of reasons, often without a clear understanding of their long-term effects," he said.
"But in terms of neuroscience, we still don't know whether the brain has resilience or resistance to this supplement. That's why ours is the first such study in the field."
Albayram collaborated with Eda Karakaya, Ph.D., Adviye Ergul, M.D., Ph.D., and several other researchers at MUSC and partner institutions. Among them was Semir Beyaz, Ph.D., at the Cold Spring Harbor Laboratory Cancer Center in New York.
EPA Identified as a Potential Weak Point in Brain Recovery
The team discovered what they describe as a context-dependent metabolic vulnerability. In simple terms, this means that changes in how cells use energy may reduce the brain's ability to recover under certain conditions. This vulnerability appears to be linked to the buildup of eicosapentaenoic acid, or EPA, one of the main omega-3 fatty acids found in fish oil.
In their experimental models, higher levels of EPA in the brain were associated with weaker repair after injury.
Albayram noted that not all omega-3s behave the same way. Docosahexaenoic acid, or DHA, is well known for its beneficial role in the brain and is a major part of neuronal membranes. EPA, however, follows a different pathway. It is less incorporated into brain structures, and its effects can vary depending on how long it is present and the surrounding biological conditions. Because of this, the long-term impact of omega-3 intake on brain recovery and blood vessel adaptation has remained unclear.
Experiments Link Diet, Brain Biology, and Recovery
To better understand these effects, the researchers used a series of models to connect diet, brain function, and healing. In mice, they examined how long-term fish oil use influenced the brain's response to repeated mild head impacts. Their focus was on signals related to blood vessel stability and repair.
They also studied human brain microvascular endothelial cells, which form part of the barrier between the brain and the bloodstream. In these cells, EPA, but not DHA, was linked to reduced repair capacity, aligning with the findings from the animal models.
To extend the findings to real-world disease, the team analyzed postmortem brain tissue from individuals diagnosed with chronic traumatic encephalopathy (CTE) who had a history of repeated brain injury.
The researchers described the results as having "implications for precision nutrition, therapeutic strategies and the design of dietary interventions targeting brain injury and neurodegeneration."
Key Findings From the Study
The study identified several major patterns, which are summarized below along with simplified explanations.
EPA-driven neurovascular instability triggers perivascular tauopathy and cognitive decline following TBI.
"In a sensitive brain state modeled in mice, long-term fish oil supplementation revealed a delayed vulnerability. The animals showed poorer neurological and spatial learning performance over time, together with clear evidence of vascular-associated tau accumulation in the cortex, linking impaired recovery to neurovascular dysfunction and perivascular tau pathology," Albayram said.
EPA reprograms cortical transcriptional responses and suppresses angiogenic signaling following traumatic brain injury.
"In the injured cortex, the team observed a coordinated shift in gene programs that normally support vascular stability and repair," Albayram said. "The pattern included reduced expression of genes tied to extracellular matrix organization and endothelial integrity, alongside broader changes consistent with altered lipid handling after injury."
EPA utilization under permissive metabolic conditions impairs angiogenesis and endothelial integrity, recapitulating post-traumatic brain injury cerebrovascular dysfunction.
Albayram said that in human brain microvascular endothelial cells, EPA did not act as a universal toxin. "Instead, when cells were placed in conditions that encouraged fatty acid engagement, EPA was associated with weaker angiogenic network formation and reduced endothelial barrier integrity, matching key features of the neurovascular repair deficit seen in vivo."
CTE brain reveals neurovascular and fatty acid metabolic reprogramming consistent with EPA-linked vulnerability.
"In postmortem cortex from neuropathologically confirmed CTE cases with a history of repetitive brain injury, the researchers found evidence of disrupted fatty acid balance and broad transcriptional changes affecting vascular and metabolic pathways," Albayram said. "This human arm was used to provide translational context, asking whether chronic disease tissue shows convergent signatures of altered lipid handling and reduced vascular stability."
What the Findings Mean for Fish Oil Use
Albayram stressed that the study should not be interpreted as a blanket warning against fish oil. "I am not saying fish oil is good or bad in some universal way," he said. "What our data highlight is that biology is context-dependent. We need to understand how these supplements behave in the body over time, rather than assuming the same effect applies to everyone."
The researchers hope their work encourages a more careful look at omega-3 supplementation, both in clinical settings and among the general public. Their experiments focused on a specific scenario, repeated mild brain injury, and used CTE tissue to provide supporting observations rather than direct proof of cause and effect.
"As with any study, there are important boundaries," Albayram said. "In the human CTE tissue, we can observe patterns, but we cannot prove what drove them. We also cannot capture every variable that shapes omega-3 handling in real life, including overall diet, health status and lifestyle."
Next Steps in Understanding Omega-3 Effects
The team plans to continue investigating how EPA moves through the body, including how it is absorbed, transported, and distributed. They are especially interested in the mechanisms that control fatty acid movement.
"This paper is a starting point," Albayram said, "but it is an important one. It opens a new conversation about precision nutrition in neuroscience, and it gives the field a framework to ask better, more testable questions."
Materials provided by Medical University of South Carolina. Note: Content may be edited for style and length.
Journal Reference:
Eda Karakaya, Burak Berber, Onur Eskiocak, Jazlyn Edwards, Randy Bent Barker, Sarah Jamil, Weiguo Li, Yasir Abdul, Maria Ericsson, Thor Stein, Ann McKee, Adviye Ergul, Semir Beyaz, Onder Albayram. Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy. Cell Reports, 2026; 117135 DOI: 10.1016/j.celrep.2026.117135
Materials provided by Medical University of South Carolina. Note: Content may be edited for style and length.
The answer to that question is becoming clearer, thanks to new research.
Some 10% of American adults regularly take an omega-3 supplement,
despite uncertainty about whether these products truly live up to their
health claims. But two new studies published in November 2018 shed some
light on who might benefit from omega-3 supplements — and who probably
won't.
VITAL
The first study was the Vitamin D and Omega-3 Trial (VITAL), a large
multiyear study with 25,871 healthy adults with no history of
cardiovascular (heart or blood vessel–related) disease and at "usual
risk" for it. The group was racially diverse and chosen to be
representative of the general population, says the study's lead author
Dr. JoAnn E. Manson, professor of medicine and the Michael and Lee Bell
Professor of Women's Health at Harvard Medical School.
Researchers tested, among other things, whether a moderate dosage (1
gram a day) of an omega-3 supplement could help prevent major
cardiovascular events, compared with a placebo. Cardiovascular events
included not only heart attacks, but stroke, and angioplasty procedures
to clear blocked arteries.(Oh god, completely out-of-date.
"The findings are somewhat complex and nuanced. It's not a simple
yes, or no, or one-size-fits-all answer. Some groups tended to benefit,
while other groups didn't," says Dr. Manson.
Although a daily 1-gram omega-3 supplement did not significantly
reduce major cardiovascular events over all, there was a 28% reduction
in heart attacks and promising signals for other heart-related
endpoints, she says. While the supplement didn't seem to protect most
healthy people against future heart problems, certain groups did appear
to benefit, particularly people who ate less than 1.5 servings of fish a
week or didn't eat fish at all. "For these people, there was a
significant 19% reduction in the primary endpoint of major
cardiovascular events, with a 40% reduction in heart attacks," says Dr.
Manson.
The supplements also appeared to benefit African American
participants, who saw a 77% reduction in heart attack for those
receiving the omega-3 supplement, compared with those taking the
placebo, says Dr. Manson. It's unclear why this group benefited more,
and additional studies are needed to confirm the finding.
REDUCE-IT
The second study, called the Reduction of Cardiovascular Events with
EPA–Intervention Trial (REDUCE-IT), included more than 8,000 middle-aged
and older adults who had elevated triglyceride levels and who had
already experienced a cardiovascular event or had other significant risk
factors for one. It aimed to find out if a daily high-dose, 4-gram
prescription omega-3 medication could protect participants against
future cardiovascular events, compared with a placebo. This trial, led
by Dr. Deepak Bhatt, a cardiologist and professor of medicine at Harvard
Medical School, found a substantial 25% reduction in the risk of dying
from heart disease or suffering a cardiovascular event among people who
took the medication, compared with those who had the placebo.
High doses of omega-3 supplements, like the high-dose omega-3 product
used in this trial, aren't appropriate for everyone because they pose
risks, such as bleeding or an increase in a type of abnormal heart
rhythm known as atrial fibrillation, says Dr. Manson. "However, while
high doses are associated with some risk, overall benefits of the
high-dose omega-3 product used in the trial appeared to outweigh the
risks for people with high triglyceride levels and a history of, or at
high risk of, cardiovascular disease," says Dr. Manson.
Choosing the right supplement
Looking for an over-the-counter omega-3 supplement? Here's what to look for:
A 1-gram dose, unless your doctor recommends more.
A combination of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Each of these fatty acids provides different health benefits.
A quality supplement. Good quality indicators are seals from U.S. Pharmacopeia, NSF International, or ConsumerLab.com.
If your triglyceride levels are abnormally high and you have an
elevated risk for cardiovascular disease, talk to your doctor about
whether a high-dose omega-3 prescription might be an option.
Putting the findings into practice
So, what do these findings mean for you? People in good health. If you're healthy and at low
or average risk for heart disease, chances are you don't need an omega-3
supplement, provided you eat fish often, says Dr. Manson. You should eat at least two servings a week of fatty fish,
such as salmon, tuna, or herring. Aim for fish that are high in two
different omega-3 fatty acids, eicosapentaenoic acid (EPA) and
docosahexaenoic acid (DHA), each of which provides unique health
benefits.
Getting your omega-3 fatty acids from food is always preferable to a
supplement. Not only do you get the marine omega-3 fatty acids from the
fish, but you also potentially replace less healthful foods in your
diet, such as red meat, processed foods, or refined grains, says Dr.
Manson. "It's a good lifestyle change to make and has been a
recommendation for a while. Nothing in these studies supersedes the
recommendation for moderate fish intake," she says. Non–fish eaters and African Americans. However, if
you can't eat fish or don't like fish, an omega-3 supplement is
something to consider. (Algae-based supplements are an option if you are
a vegetarian or allergic to fish.) African Americans might also
consider a supplement because of the unique benefits revealed in this
trial.
For these two groups, a daily 1-gram supplement could provide a good
balance between safety and efficacy. "Talk to your health care provider
about whether you're a candidate for a supplement," says Dr. Manson. Already taking omega-3s? If you're already taking an
over-the-counter omega-3 supplement, you don't necessarily need to stop
taking it if you don't fall into one of the categories above, unless
your doctor tells you to. But if you're not taking an omega-3
supplement, whether you should start really depends on your individual
risk factors, says Dr. Manson.
Regardless of whether you opt for an omega-3 supplement, you should
always strive to maintain a healthy diet and lifestyle. "No dietary
supplement is a substitute. We already know that, and I think this is an
important point to reinforce," says Dr. Manson. "Healthy lifestyle
practices, including regular physical activity, healthy diet, and not
smoking, will reduce heart disease risk by close to 80%, and that's
really the main recommendation for heart health," she says. Cardiovascular risk factors. If you have an elevated
triglyceride level and a history of cardiovascular disease or have
major risk factors for it, a high-dose omega-3 medication may be
advisable. This is true even if you're already taking a statin
medication. The omega-3 drug does not replace the statin.
Fast facts about the two trials
The Vitamin D and Omega-3 trial (VITAL)
This study was published online Nov. 10, 2018, by The New England Journal of Medicine. Funding source: The U.S. National Institutes of Health. Who: 25,871 healthy, racially diverse individuals, including 12,786 men ages 50 and older and 13,085 women ages 55 and older. What: A daily 1-gram omega-3 prescription supplement
that included a combination of two omega-3 fatty acids,
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). A 1-gram
dose was chosen because it is a moderate amount that is unlikely to
produce side effects. A control group took a placebo. Key takeaways:
Omega-3 supplements likely won't benefit people who eat at least 1.5 servings of fish per week.
Omega-3 supplements may benefit people with low fish consumption or those with African American heritage.
The Reduction of Cardiovascular Events with EPA–Intervention Trial (REDUCE-IT)
This study was published online Nov. 10, 2018, by The New England Journal of Medicine. Funding source: Amarin, Inc., the company that makes the prescription-strength medication used in the study. Who: 8,179 middle-aged men and women who had high
triglyceride levels and risk factors for heart disease or had already
experienced a heart attack, stroke, or cardiovascular event. Risk
factors included conditions such as high blood pressure and diabetes.
Everyone in the trial was taking a statin to reduce high cholesterol. What: A daily high-dose, 4-gram prescription omega-3
medication or a placebo. Unlike over-the-counter omega-3s, the
medication included EPA only. Key takeaways: This medication may help to protect
high-risk individuals from cardiovascular events. Those taking it were
25% less likely to die from heart disease or to have a heart attack,
stroke, or a type of chest pain called angina. They were also less
likely to need a procedure to open a blocked heart artery. If you have a
high triglyceride level and have had a heart attack or stroke or have
risk factors for cardiovascular disease, you might benefit from taking
the high-dose omega-3 product.
You don't want another stroke so have your doctor create a diet protocol for this. You need to know EXACT amounts per body weight and sex. No guessing allowed.
In this investigation, researchers
tested the premise that total marine n-3 polyunsaturated fatty acids
(PUFA), especially eicosapentaenoic acid (EPA) and docosahexaenoic acid
(DHA) in diet and adipose tissue (biomarkers of long-term intake and
endogenous exposure), are inversely linked to ischemic stroke risk and
its subtypes. Study participants included 57,053 enrollees of the Diet,
Cancer and Health cohort (aged 50-65 years). A full 1,879 participants
had an ischemic stroke during 13.5 years of follow-up. Apart from
cardioembolism, EPA was associated with lower risks of most types of
ischemic stroke, whereas inconsistent findings were observed for total
marine n-3 PUFA and DHA. The EPA content in adipose tissue was inversely
linked to small-vessel occlusion.
Useless without giving us protocol amounts per weight and sex. And we have to figure out what EPA and DHA are. Why the fuck was this research done if not to accomplish helping those at risk for stroke? Damn it all, not your job?
We
hypothesized that total marine n-3 polyunsaturated fatty acids (PUFA),
in particular eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)
in the diet and in adipose tissue (biomarkers of long-term intake and
endogenous exposure) were inversely associated with the risk of ischemic
stroke and its subtypes.
Methods—
The
Diet, Cancer and Health cohort consisted of 57 053 participants aged 50
to 65 years at enrolment. All participants filled in a food frequency
questionnaire and had an adipose tissue biopsy taken at baseline.
Information on ischemic stroke during follow-up was obtained from The
Danish National Patient Register, and all cases were validated. Cases
and a random sample of 3203 subjects from the whole cohort had their
fatty acid composition of adipose tissue determined by gas
chromatography.
Results—
During
13.5 years of follow-up 1879 participants developed an ischemic stroke.
Adipose tissue content of EPA was inversely associated with total
ischemic stroke (hazard ratio [HR], 0.74; 95% CI, 0.62–0.88) when
comparing the highest with the lowest quartile. Also, lower rates of
large artery atherosclerosis were seen with higher intakes of total
marine n-3 PUFA (HR, 0.69; 95% CI, 0.50–0.95), EPA (HR, 0.66; 95% CI,
0.48–0.91) and DHA (HR, 0.72; 95% CI, 0.53–0.99), and higher adipose
tissue content of EPA (HR, 0.52; 95% CI, 0.36–0.76). Higher rates of
cardioembolism were seen with higher intakes of total marine n-3 PUFA
(HR, 2.50; 95% CI, 1.38–4.53) and DHA (HR, 2.12; 95% CI, 1.21–3.69) as
well as with higher adipose tissue content of total marine n-3 PUFA (HR,
2.63; 95% CI, 1.33–5.19) and DHA (HR, 2.00; 95% CI, 1.04–3.84). The EPA
content in adipose tissue was inversely associated with small-vessel
occlusion (HR, 0.69; 95% CI, 0.55–0.88).
Conclusions—
EPA
was associated with lower risks of most types of ischemic stroke, apart
from cardioembolism, while inconsistent findings were observed for
total marine n-3 PUFA and DHA.
Correspondence
to Stine Krogh Venø, MD, Department of Cardiology, Aalborg University
Hospital, Søndre Skovvej 15, 9000 Aalborg, Denmark. Email s.venoe@rn.dk
I really hate these literature searches and meta-analysis, they always seem to need more followup to be useful rather than doing it right in the first place and doing some real research. Regardless, I bet your doctor does nothing with this information. I assume higher CHD risk pretty much correlates to higher stroke risk, to be confirmed with your doctor. A. Because s/he never read it. B. Because s/he could not be bothered to understand how to implement it in a protocol. C. It is not my job. I am waiting for SOMEONE ELSE TO SOLVE THE PROBLEM.
Mayo Clinic Proceedings, 01/17/2017 Alexander DD, et al.
The
target of this study was to assess the impact of eicosapentaenoic and
docosahexaenoic acid (EPA+DHA) on coronary heart disease (CHD), and to
lead meta–analyses of prospective cohort studies to estimate the
association between EPA+DHA consumption and CHD risk. Outcomes show that
EPA+DHA might be connected with lessening CHD risk, with a greater
benefit found among higher–risk populations in RCTs.
Methods
For this study they design a systematic literature search. From
January 1, 1947, to November 2, 2015 they search Ovid/Medline, PubMed,
Embase, and the Cochrane Library, 18 RCTs and 16 prospective cohort
studies examining EPA+DHA from foods or supplements and CHD, including
myocardial infarction, sudden cardiac death, coronary death, and angina,
were recognized.
Random–effects meta–analysis models were utilized to generate summary relative risk estimates (SRREs) and 95% CIs.
Heterogeneity was analyzed in subgroup and sensitivity examinations and by meta–regression.
Dose–response was assessed in stratified dose or consumption investigations.
Publication bias evaluations were performed.
Results
Among RCTs, there was a nonstatistically significant decrease in
CHD risk with EPA+DHA provision (SRRE=0.94; 95% CI, 0.85–1.05).
Subgroup examinations of information from RCTs demonstrated a
statistically significant CHD risk decrease with EPA+DHA provision among
higher–risk populations, including participants with elevated
triglyceride levels (SRRE=0.84; 95% CI, 0.72–0.98) and elevated
low–density lipoprotein cholesterol (SRRE=0.86; 95% CI, 0.76–0.98).
Meta–analysis of information from prospective cohort studies
resulted in a statistically significant SRRE of 0.82 (95% CI, 0.74–0.92)
for higher consumptions of EPA+DHA and risk of any CHD event.