Stroke
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Dr. Rhonda Patrick discusses...
Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
In this clip, Dr. Roger Seheult and Dr. Rhonda Patrick describe long-haul COVID-19 and its ramifications for young people.
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Dr. Rhonda Patrick discusses...
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Dr. Rhonda Patrick answers audience questions on various health, nutrition, and science topics in this Q&A session.
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In this clip, Dr. Roger Seheult and Dr. Rhonda Patrick describe long-haul COVID-19 and its ramifications for young people.
Topic Pages
News & Publications
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A daily cup of coffee could reduce your risk of heart disease and diabetes by half. academic.oup.com
Drinking your daily cup of coffee or tea might do more than give you a boost—it could lower your risk of developing multiple serious cardiometabolic conditions simultaneously, like diabetes, heart disease, or stroke. A recent study found that moderate coffee or caffeine consumption may cut your risk of cardiometabolic multimorbidity by as much as 50%.
Researchers analyzed data from more than 172,000 participants enrolled in the UK Biobank who had no cardiometabolic diseases at the start. Participants reported their coffee, tea, and caffeine consumption; about half provided blood samples for metabolic marker analysis.
They found that people who drank about three cups of coffee daily (or consumed 200 to 300 milligrams of caffeine daily) were 40% to 50% less likely to develop multiple cardiometabolic diseases than those who drank little or no caffeine. They also discovered that specific blood markers, such as certain lipid components, were linked to coffee and caffeine consumption and a lower risk of cardiometabolic conditions.
These findings suggest that moderate coffee or caffeine intake reduces the risk of developing cardiometabolic diseases but also slows their progression if they occur. Other evidence points to the many health benefits associated with coffee and caffeine, but it’s crucial to remember their effects on sleep. Learn more in this Aliquot featuring Drs. Guido Kroemer, Satchin Panda, Elissa Epel, Matthew Walker, and Rhonda Patrick
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Chronic loneliness increases stroke risk by 56%, independent of depressive symptoms or social isolation. www.thelancet.com
Loneliness, a pervasive emotional state that adversely affects mental and physical health, increases the risk of many chronic health disorders, including cardiovascular diseases. A recent study found that loneliness increases the risk of stroke by as much as 56%.
Researchers analyzed data from the Health and Retirement Study, which included adults aged 50 years or older who were stroke-free at the start. Participants ranked their loneliness on a scale of three to nine, with scores above six considered “high.” Researchers tracked the incidence of stroke among the participants over 10 to 12 years.
They found that higher loneliness scores at baseline were associated with an increased risk of stroke, with a one-point increase in loneliness score corresponding to a 5% higher likelihood of stroke. Participants with high loneliness scores were 25% more likely to experience a stroke, even after accounting for social isolation without depressive symptoms. Notably, participants with consistently high loneliness over time were 56% more likely to experience stroke than those with consistently low loneliness.
These findings suggest that chronic loneliness is a major risk factor for stroke, independent of depressive symptoms or social isolation. Addressing loneliness may be crucial for stroke prevention, and regular assessments of loneliness in clinical settings could help identify people at higher risk.
Interestingly, sleep and loneliness are inherently linked, and poor sleep increases the risk of stroke. Not getting enough sleep triggers the onset of a “loneliness phenotype,” driving people who are sleep-deprived to avoid social interaction. Learn more about the effects of sleep on feelings of loneliness in this clip featuring Dr. Matt Walker.
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Taurine supplementation can help regulate blood glucose and lower blood pressure, reducing risk factors associated with metabolic syndrome. pubmed.ncbi.nlm.nih.govObesity Diabetes Cholesterol Triglycerides Blood Pressure Metabolic Syndrome Taurine Stroke Cardiovascular Supplements
Metabolic syndrome is a cluster of conditions that includes hypertension, high blood glucose, excess abdominal fat, and abnormal blood lipids. Having metabolic syndrome markedly increases a person’s risk of cardiovascular disease, type 2 diabetes, and stroke. A recent meta-analysis found that taurine supplementation improves conditions associated with metabolic syndrome.
Researchers analyzed the findings of 25 studies (with more than 1,000 participants) investigating links between taurine supplementation and metabolic syndrome. They also explored the effects of taurine dose and examined secondary outcomes of taurine supplementation, including body composition, lipid profile, and blood glucose control.
They found that taurine doses ranged from 0.5 to 6 grams, with study durations ranging from five days to one year. On average, taurine supplementation reduced systolic blood pressure by 4 mmHg, diastolic blood pressure by 1.5 mmHg, fasting blood glucose by 6 milligrams per deciliter, and triglycerides by 18 milligrams per deciliter. The researchers did not observe an effect on high-density lipoprotein cholesterol. The reduction in diastolic blood pressure and fasting blood glucose was dose-dependent, with higher doses eliciting more robust effects.
These findings suggest that taurine supplementation improves factors associated with metabolic syndrome. Interestingly, other research shows that an acute bout of exercise increases blood taurine levels, providing a mechanistic link between exercise and better metabolic health.
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Daily cannabis use more than doubles the chance of stroke among non-tobacco users, suggesting cannabis use alone could contribute to cardiovascular disease risk. www.ahajournals.org
Cannabis, commonly known as marijuana, is a plant used for its psychoactive properties and influences on perception, mood, and consciousness. People consume cannabis for both recreational and medicinal purposes, seeking relief from pain, anxiety, and other conditions. A recent study found that regular cannabis use increases the risk of cardiovascular disease, particularly among those who don’t use tobacco.
Researchers analyzed data collected from more than 434,000 adult participants who provided information about their cannabis use. They looked at how often participants used cannabis in the past month and whether they reported having coronary artery disease, a heart attack, or a stroke. They conducted a separate analysis for participants who didn’t use tobacco.
They found that daily cannabis users were about 16 percent more likely to have coronary heart disease, 25 percent more likely to experience a heart attack, and 42 percent more likely to have a stroke. When they combined all three heart-related issues, they found that daily cannabis users were 28 percent more likely to face any of them than non-users.
However, when they focused on participants who had never smoked tobacco and only used cannabis, the findings were even more striking. Daily cannabis users who had never used tobacco were 49 percent more likely to experience a heart attack and 116 percent more likely to have a stroke. When the researchers combined all three heart-related issues, they found that daily cannabis users who had never used tobacco were 77 percent more likely to face any of the cardiovascular conditions.
These findings suggest that daily cannabis use increases the risk of cardiovascular disease, especially among non-tobacco users, indicating that cannabis use alone could contribute to cardiovascular risk. Compounds in cannabis have profound effects on the human body and can even pass into breast milk, affecting breastfed infants. Learn more in this episode featuring Dr. Rhonda Patrick.
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Roughly half of all adults living in the U.S. have hypertension, with men affected more than women (48 percent versus 43 percent, respectively). However, the sex differences in hypertension prevalence aren’t consistent throughout the lifespan: Women who are 65 and older are more likely to have hypertension than men, raising concerns that current blood pressure recommendations should consider sex. Now, findings from a new study suggest that having an average systolic blood pressure of 160 mm Hg or higher increases the risk of dying from cardiovascular disease (CVD) among women by 113 percent.
Researchers drew on data from more than 53,000 middle-aged adults enrolled in the NHANES studies. Over about ten years, they measured the participants' blood pressures three times and averaged the measures. They also tracked the participants' CVD-related death rates.
They found that links between blood pressure measures and CVD-related deaths differed by sex. Women experience a 61 percent increased risk of cardiovascular death when systolic blood pressure reaches between 130-139 mm Hg, and it soars to 113 percent when at 160 mm Hg or higher. In comparison, men see a 76 percent increased risk only when systolic measures are 160 mm Hg or higher.
When considering diastolic blood pressure, men had a higher risk of dying from CVD if measures were too low (below 70 mm Hg) or too high (80 mm Hg or more), compared to the risk associated with measures between 70 and 80 mm Hg. Again, for women, the risk was higher with diastolic measures that were too low (below 50 mm Hg) or too high (80 mm Hg or higher).
These findings suggest that having high blood pressure markedly increases the risk of death from CVD, and this risk begins at much lower measures among women than men.
Nearly two-thirds of adults in the United States have high blood pressure, defined as having a systolic pressure of 130 mmHg or higher or a diastolic pressure of 80 mmHg or higher. High blood pressure increases a person’s risk for heart disease and stroke and contributes to small vessel disease, a major risk factor for cardiovascular disease, dementia, and stroke. However, lifestyle factors, such as sauna use, help maintain healthy blood pressure. Learn more in this clip featuring Dr. Jari Laukkanen.
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Pericytes are pivotal in the formation and storage of long-term memories. www.sciencedaily.com
Tiny contractile cells surrounding the brain’s capillaries called pericytes regulate vascular blood flow and maintain blood-brain barrier integrity. Pericytes detach from the blood vessels in aging, driving the pathophysiology of neurological dysfunction, vascular dementia, and stroke. A recent study in rodents shows that pericytes also play roles in long-term memory formation.
Researchers measured the amount of insulin-like growth factor 2 (IGF2) produced by various cells in the hippocampus of rodents. IGF2, a peptide hormone produced in multiple tissues, regulates growth during fetal development and participates in the cell cycle throughout the lifespan. After determining that pericytes contributed the greatest amount of hippocampal IGF2, they assessed learning’s influence on IGF2.
They found that learning increased pericyte IGF2 production in the hippocampus, especially in the dentate gyrus, a highly vascularized area responsible for episodic memory – long-term memory that involves conscious recollection of previous experiences and their associated contexts, such as sounds and smells. Animals lacking the ability to produce IGF2 in their pericytes exhibited poor learning and memory.
The detachment and loss of pericytes play a crucial role in the progression of cerebral small vessel disease and neurodegenerative disorders that involve blood-brain barrier dysfunction. These specialized endothelial cells envelop a significant portion, up to 80 percent, of the brain capillary surface area in the cortex and hippocampus of the human brain. They also enwrap the tiniest vessels constituting the blood-brain barrier.
Exercise mitigates the proinflammatory state that drives pericyte loss in aging, possibly providing a mechanism for exercise’s memory-enhancing effects. Learn more about links between exercise, pericytes, and brain health in this episode featuring Dr. Axel Montagne.
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Connection identified between sleep disturbances and stroke risk. www.medscape.com
Sleep disturbances may increase a person’s risk of stroke, according to a new study. People who had trouble falling or staying asleep, snored, or had sleep apnea were more likely to have a stroke than those with normal sleep patterns.
Researchers gathered information about the sleep patterns of more than 4,500 adults. Roughly half of the participants had experienced a recent stroke.
They found that compared to participants who slept seven hours a night, those who slept fewer than five hours per night were more than three times as likely to have had a stroke, and those who slept more than nine hours were more than twice as likely to have had a stroke. Participants who had symptoms of apnea were roughly three times as likely to have had a stroke.
These findings suggest that disturbed sleep markedly increases a person’s risk of stroke. However, the researchers noted that it’s not clear whether sleep disturbances directly cause stroke, or if they are simply markers of other underlying health issues that increase the risk of stroke. Learn more about the health risks associated with poor sleep in this episode featuring Dr. Matthew Walker.
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Rising blood pressure in young adulthood damages brain blood vessels, reducing blood flow to the brain. journals.lww.com
Gradual increases in blood pressure from young adulthood to middle age increased the risk of poor brain health in older age, a 2022 study found. Having higher blood pressure over time damaged the brain’s delicate blood vessels, reducing blood flow to the brain.
The study involved 885 adults whose blood pressures were monitored regularly over a 30-year period. Using magnetic resonance imaging studies, researchers assessed the participants' brain health at the beginning and end of the study period.
The researchers found that participants who had either high blood pressure in young adulthood or moderate blood pressure that gradually increased over time showed marked signs of microvascular disease in the white matter of their brains. The two groups also showed reduced blood flow in the gray matter of their brains.
Microvascular disease, also called small vessel disease, is a condition characterized by blood vessel dysfunction. It commonly occurs with aging and contributes to the development of cardiovascular disease, dementia, and stroke. Small vessel disease in the brain contributes to approximately 50 percent of dementia cases worldwide.
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Quinol-based antioxidant cycle may maintain the "chemical shield" raised by estrogens that protects neurons from reactive oxygen species. (2003) www.sciencedaily.com
From the article:
“We now know how estrogen keeps brain cells alive even when exposed to an insult like stroke, Alzheimer’s disease or Parkinson’s disease.”
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“During a stroke, free radicals damage important cells in the body, most notably nerve cells,” said Laszlo Prokai, PhD, a chemist with UF’s College of Pharmacy.
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“In layman’s terms, a spill occurs when the blood starts flowing into the blocked territory, and the overflow hydroxyl radical is the spill,” Prokai said. “The estrogen is the mop, soaking up the hydroxyl radicals before they do damage. But when the mop is saturated, you have to squeeze it to continue mopping. This mechanism has never been fully understood before.”
When the estrogen and hydroxyl radicals combine, an unusual molecule called a quinol is produced. In this form, the hydroxyl radicals are harmless, but the estrogen is no longer useful as an antioxidant. Prokai investigated and discovered chemicals in the body transform the quinol back to estrogen, effectively wringing out the mop and making it useful again.
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In terms of therapies, scientists believe administering the quinol — the saturated mop — will deliver the protective benefits of estrogen, because the body will naturally wring it out and convert it to estrogen, while side effects associated with direct estrogen therapy, such as feminization in men, may remain in check.
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Neuron-derived estrogen may be critical for astrocyte activation and neuroprotection of the ischemic brain, mouse study suggests. (2020) www.sciencedaily.com
From the article:
In the face of low brain oxygen that can occur with stroke or other brain injury, these astrocytes, star-shaped brain cells that help give the brain its shape and regularly provide fuel and other support to neurons, should become “highly reactive,” increasing cell signaling, releasing neuroprotective factors and clearing neurotoxins, scientists report in The Journal of Neuroscience.
[…]
To try to understand how astrocytes take on this enhanced role, they knocked out the enzyme aromatase, which is critical to estrogen production, in neurons in the forebrain, the largest region of the human brain, in their animal model.
They found that one way estrogen made by neurons is protective in ischemia is by suppressing signaling of the fibroblast growth factor, FGF2, which is also made by neurons and known to suppress astrocyte activation, Brann and his colleagues write. Normally neurons use this FGF2 brake to help keep astrocyte response from getting out of control.
[…]
In this scenario, when they used a neutralizing antibody to block FGF2, astrocytes became more active and neuron damage was decreased. “The astrocyte activation came back and we saw the protective growth factors that they make,” Brann says. Giving more estrogen produced similar benefits, including improving cognition after ischemia.
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They also saw less of known neuroprotective growth factors, like brain derived neurotrophic factor and insulin-like growth factor 1, which astrocytes normally release at an increased rate in response to a stressor like ischemia, and more suppressive substances like the brake FGF2 [when the estrogen producing enzyme aromatase was knocked out].
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Activated astrocytes also help clear glutamate, the brain’s most abundant excitatory neurotransmitter that normally helps neurons communicate. But without estrogen from the neurons, the glutamate transporter, GLT-1, which removes about 90% of the glutamate, is significantly decreased and the chemical can accumulate at toxic levels in the brain and become a major cause of neuron destruction. “Glutamate is essential for brain function, but if it’s overproduced, it’s brain toxic,” Brann says.
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From the publication
The purpose of this paper is to analyze the guidelines for TTh [testosterone therapy] from international organizations and compare their recommendations.
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All agree that TD [testosterone deficiency] is a clinical syndrome that requires a low testosterone level as well as signs and/or symptoms for a diagnosis to be made. The exact cut -off varies or is not provided, but the organizations suggest a cut -off level between 300 -350 ng/dl. All societies recommend routine laboratory monitoring within the first year and annually after. The guideline committees acknowledge limited data on cardiovascular disease and testosterone. The consensus is to withhold TTh within 3 -6 months of an MI or stroke or in patients with severe heart failure.(2, 4) Prostate cancer is another gray area. Although the consensus is that there is no data to suggest TTh causes prostate cancer.
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After 8 years of studying 656 men, none of testosterone-treated men died from cardiovascular events vs 19 without therapy. (2017) www.sciencedaily.com
From the article:
The researchers followed a group of men for eight years who had been on TTh [testosterone therapy] and compared them with another group of men who remained untreated for the same time period. They found there were only two deaths in the TTh group and neither was related to CV events. In the non-treated control group, there were 21 deaths, 19 of which were related to CV events. Furthermore, there were 26 non-fatal myocardial infarctions and 30 non-fatal strokes in the control group but none in the T-treated group.
According to the researchers, long-term TTh [testosterone therapy] in men with hypogonadism appears to be an effective approach to achieve sustained improvements in cardiometabolic function and reduces the risk of CV events. “The low CV events observed in the T-group compared to the untreated (control) group strongly suggest that TTh is protective. We believe that the protective effect of T on the CV system provides clinicians with the opportunity to utilize this approach for secondary prevention for hypogonadal men with a history of CV events,” explained corresponding author Abdulmaged M. Traish, PhD, professor of biochemistry and urology at BUSM.
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After 3 years of testosterone therapy in 755 high-risk men, 22 with high doses suffered cardiovascular events vs. 125 without therapy. (2016) www.sciencedaily.com
From the article:
“The study shows that using testosterone replacement therapy to increase testosterone to normal levels in androgen-deficient men doesn’t increase their risk of a serious heart attack or stroke,” said cardiologist Brent Muhlestein, MD, co-director of cardiovascular research at the Intermountain Medical Center Heart Institute. “That was the case even in the highest-risk men – those with known pre-existing heart disease.”
[…]
The research team studied 755 male patients at Intermountain Healthcare hospitals. The men were between the ages of 58 and 78, and all had severe coronary artery disease. They were split into three different groups, which received varied doses of testosterone administered either by injection or gel.
The conclusions:
– After one year, 64 patients who weren’t taking testosterone supplements suffered major adverse cardiovascular events, while only 12 who were taking medium doses of testosterone and nine who were taking high doses did.
– After three years, 125 non-testosterone-therapy patients suffered major adverse cardiovascular events, while only 38 medium-dose and 22 high-dose patients did. “Although this study indicates that hypo-androgenic men with coronary artery disease might actually be protected by testosterone replacement, this is an observational study that doesn’t provide enough evidence to justify changing treatment recommendations,” Dr. Muhlestein said.
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Testosterone may increase risk of heart attack and stroke by promoting vascular calcification. (2016) www.sciencedaily.com
From the article:
Scientists at the University of Edinburgh examined the effects of testosterone on blood vessel tissue from mice. They found that the hormone triggers cells from the blood vessels to produce bone-like deposits – a process called calcification. When the mouse cells were modified, by removing the testosterone receptor, so they could no longer respond to testosterone, they produced far less of the calcium deposits.
The team also looked at blood vessel and valve tissue from people with heart disease who had undergone surgery for their condition. They found that cells from these tissues contained bone-like deposits and also carried the testosterone receptor on their surface. This suggests that testosterone may trigger calcification in people.
Calcification causes blood vessels to harden and thicken, which means the heart has to work harder to pump blood around the body. It is strongly linked to increased risk of heart attack and stroke. Calcification can also affect the heart’s valves, meaning that the valves cannot open and shut properly and may need to be replaced.
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Testosterone replacement therapy can increase men's risk of stroke and heart attack by 21% during the first two years of use. (2019) www.sciencedaily.com
From the article:
The study analyzed a large database of electronic medical records of patients enrolled in primary care practices in the United Kingdom and formed a cohort of 15,401 men, aged 45 years or older, with low testosterone levels (hypogonadism). Users of TRT [testosterone replacement therapy] had a 21 percent greater risk of cardiovascular events compared with nonusers, corresponding to an additional 128 events. The increased risk appears to be transient, declining after two years of TRT use, which the investigators attribute to a phenomenon called “depletion of susceptibles.”
“Our findings show that the use of TRT was associated with an increased risk of stroke, TIAs [transient ischaemic attack], or cardiac arrest during the first two years of use,” noted Christel Renoux
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Interleukin-6 (IL-6) may play a causal role in the increased ischemic damage after stroke associated with social isolation in mice. (2009) www.sciencedaily.com
From the article:
Researchers at Ohio State University found that all the male mice that lived with a female partner survived seven days after a stroke, but only 40 percent of socially isolated animals lived that long.
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The amount of tissue damage in the brain was about four times larger in the mice housed alone compared to those housed with another mouse.
“The number of neurons dying is significantly decreased in the pair-housed mice,” DeVries said.
In addition, socially housed mice had significantly less edema, or excess water in the brain, when compared to the isolated animals.
“In clinical stroke, edema is a major concern because it can lead to additional neuronal damage, so it is significant that pair housing reduced edema,” Karelina said.
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In addition, findings revealed that mice that lived with others had significantly higher levels of a cytokine in their brain called interleukin-6 (IL-6) that has an anti-inflammatory response in the brain, helping to limit damage caused by the stroke.
The finding about IL-6 is especially interesting, Karelina said, because IL-6 appears to have opposite effects in the brain than it does in the rest of the body.
“IL-6 reduces inflammation in the brain, so it is protective in a stroke, but it is a pro-inflammatory in the periphery of the body,” Karelina said.
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TNF-alpha blocker administration clinically improved patients with chronic neurological dysfunction following stroke and traumatic brain injury (2012) www.sciencedaily.com
From the article:
The observational study¹ of 629 patients, conducted over the course of nearly two years, documents a diverse range of positive effects, including statistically significant rapid clinical improvement in motor impairment, spasticity, cognition, etc. in the stroke group, with a similar pattern of improvement seen in the traumatic brain injury (TBI) group. The study involved 617 patients treated an average of 42 months after stroke and 12 patients treated an average of 115 months after TBI, long after further spontaneous meaningful recovery would be expected.
The study was conducted at the Institute of Neurological Recovery (INR) in the USA.
The drug utilized was etanercept [a TNF blocker], a therapeutic that selectively binds and neutralizes an inflammatory immune molecule that may remain elevated for years following stroke. Etanercept was administered utilizing a novel delivery method, invented by Edward Tobinick M.D., lead author of the study.
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Drinking coffee may reduce risk of subarachnoid hemorrhage in women. (2011) www.sciencedaily.com
Drinking coffee may reduce the risk of stroke in women.
A stroke occurs when blood flow to the brain is interrupted, killing brain cells. It is the second leading cause of disability and death worldwide, affecting the lives of roughly 102 million people. Evidence suggests that inflammation plays an important role in the pathogenesis of strokes. Findings from a 2011 study suggest that coffee reduces the risk of stroke in women.
Coffee is one of the most consumed beverages worldwide. It is rich in polyphenolic compounds, including quercetin, chlorogenic acid, and others, that exert beneficial health effects in humans. Evidence suggests that coffee reduces inflammation.
The study involved nearly 35,000 women enrolled in the Swedish Mammography Cohort. The women, who had no history of cardiovascular disease or cancer at the time of their enrollment, completed questionnaires about their coffee consumption and other lifestyle habits. Using hospital medical records, the investigators gathered information about whether the women experienced a stroke during a 10-year follow-up period.
They found that drinking coffee was associated with a reduced risk of strokes, even after taking other risk factors into consideration, such as smoking, body mass index, diabetes, hypertension, or alcohol consumption. On average, drinking 1 to 2 cups daily reduced risk by 22 percent; 3 to 4 cups reduced risk by 25 percent; 5 or more cups reduced risk by 23 percent.
These findings suggest that moderate coffee consumption reduces the risk of stroke in women. Other lifestyle behaviors may reduce stroke risk, too, such as sauna use, which may reduce risk by as much as half. Learn more in this presentation by Dr. Rhonda Patrick.
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Alcohol consumption increases the risk of cardiovascular diseases such as aortic aneurysms and reduces life expectancy. (2018) www.eurekalert.org
From the article:
The upper safe limit of drinking was about 5 drinks per week (100g of pure alcohol, 12.5 units or just over five pints of 4% ABV2 beer or five 175ml glasses of 13% ABV wine).
However, drinking above this limit was linked with lower life expectancy. For example, having 10 or more drinks per week was linked with 1-2 years shorter life expectancy1. Having 18 drinks or more per week was linked with 4-5 years shorter life expectancy.
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The researchers also looked at the association between alcohol consumption and different types of cardiovascular disease. Alcohol consumption was associated with a higher risk of stroke, heart failure, fatal aortic aneurysms, fatal hypertensive disease and heart failure and there were no clear thresholds where drinking less did not have a benefit.
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Hypertensive smoking women have up to 20-fold higher risk of brain aneurysm ruptures. (2013) www.sciencedaily.com
From the article:
- If smoking women with high systolic blood pressure values have 20 times higher rate of these brain bleeds than never-smoking men with low blood pressure values, it may very well be that these women diagnosed with unruptured intracranial aneurysms should be treated. On the other hand, never-smoking men with low blood pressure values and intracranial aneurysms may not need to be treated at all.
In this largest SAH risk factor study ever, the study group also identified three new risk factors for SAH: previous myocardial infarction, history of stroke in mother, and elevated cholesterol levels in men. The results revise the understanding of the epidemiology of SAH and indicate that the risk factors for SAH appear to be similar to those for other cardiovascular diseases.
- We have previously shown that lifestyle risk factors affect significantly the life expectancy of SAH survivors, and now we have shown that the same risk factors also affect dramatically the risk of SAH itself.
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Lifting weights for less than an hour a week may reduce your risk for a heart attack or stroke by 40 to 70 percent, according to a new study www.sciencedaily.com
Current public health guidelines recommend that adults engage in muscle-strengthening activities such as resistance training at least twice a week. Research indicates that resistance exercise provides a wide range of health benefits, including increased muscle mass and strength, greater bone density, and improved mood. Findings from a 2019 study also suggest that resistance exercise reduces the risk of the number one killer worldwide: cardiovascular-related disease and death.
The study involved more than 12,000 adults (average age 47 years) who were enrolled in the Aerobics Center Longitudinal Study - an ongoing prospective investigation of links between exercise and cardiovascular health. Participants underwent a comprehensive examination that included collection of a detailed medical history, assessment of cardiovascular and metabolic health parameters, and information-gathering about the participants’ resistance exercise habits.
They found that participants who engaged in resistance exercise one to three times (or a total of up to 59 minutes) per week were 40 to 70 percent less likely to experience a cardiovascular disease-related event than those who never engaged in resistance exercise. Engaging in resistance exercise more than four times (or more than an hour) per week did not confer any additional protection. The authors' analysis indicated that the decreased risk was due in part to resistance exercise’s effects on lowering body mass index, a known risk factor for cardiovascular disease.
These findings suggest that resistance exercise promotes cardiovascular health. Aerobic exercise is also important for cardiovascular health. Learn about the cardiovascular benefits of aerobic exercise in our overview article.
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Hypertension in mid-life reduces brain volume and increases risk of dementia. neurosciencenews.com
Many people develop hypertension (high blood pressure) with age, putting them at risk of cardiovascular disease, chronic kidney disease, retinal damage, and stroke. Hypertension is also a risk factor for Alzheimer’s disease and dementia, due to damage caused by years of vessel injury, microbleeds, and lesions. Authors of a recent study report that hypertension diagnosed in early or midlife, but not late life, is a predictor of dementia.
Because hypertension damages the delicate small blood vessels of the heart, kidneys, eyes, brain, and other organs, it is a risk factor for a wide range of chronic diseases. Previous research has shown that hypertension, by restricting blood flow, reduces brain volume in key areas associated with dementia, such as the prefrontal cortex and hippocampus. As the number of young adults with hypertension increases to an estimated 1.6 billion globally by 2025, research on the risks of hypertension in earlier life are needed.
The authors collected data from more than 135,000 participants with hypertension and 135,000 matched control participants without hypertension from the United Kingdom Biobank, a long-term study of United Kingdom citizens. The researchers categorized participants into four categories: younger than 35 years; 35 to 44 years; 45 to 54 years; and 55 to 64 years. They used magnetic resonance imaging data to measure brain volume, and hospital records, death records, and self-reports to assess dementia status. Participants in the study provided data at a baseline appointment between 2006 and 2010 and at a follow-up appointment between 2014 and 2021.
Participants diagnosed with hypertension at any age had smaller brain volume than their matched control participant without hypertension. Participants diagnosed earlier in life had the greatest reductions, with participants diagnosed between ages 35 and 44 exhibiting a 0.8 percent loss in volume and participants before age 35 exhibiting a 1.2 percent loss. Specifically, hypertension was associated with loss of peripheral cortical gray matter, brain tissue necessary for higher brain functions such as learning, memory, and attention. Participants diagnosed with hypertension between ages 35 and 44 were at a 61 percent higher risk of dementia than the matched control participants without hypertension.
The authors concluded that hypertension diagnosed in early mid life, but not late life, is associated with decreased brain volume and increased risk of dementia. Lifestyle strategies that reduce blood pressure, such as exercise, sauna use, dietary modification, and stress management, may reduce dementia risk.
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Sulforaphane protects the brain during stroke via hormetic preconditioning. www.sciencedirect.com
Stroke is one of the leading causes of death and disability worldwide, claiming the lives of roughly 5 million people and leaving another 5 million permanently disabled every year. A 2013 study demonstrated that sulforaphane protects the brain during ischemic stroke via hormetic preconditioning.
Ischemic stroke occurs when blood flow to the brain is reduced or interrupted, starving neurons of oxygen and nutrients. Neuronal death occurs in the immediate area of a stroke within the first few hours of the incident, but nearby cells can be rescued with appropriate therapies. Heme oxygenase-1 (HO-1), an antioxidant enzyme, attenuates neuronal injury. Nrf2, a protein that regulates the expression of antioxidant and stress response proteins, induces HO-1 expression.
The authors of the study gave mice sulforaphane (5 milligrams per kilogram of body weight) or corn oil with saline via injection. After the mice experienced a stroke, the authors measured the animals' Nrf2 and HO-1 gene expression and assessed behavioral changes, blood-brain barrier integrity, and neurological deficits.
The mice that received sulforaphane treatment showed increased HO-1 expression, reduced blood-brain barrier damage, and fewer neurological deficits than mice that received the corn oil/saline. Levels of peroxynitrite, a short-lived reactive oxygen species associated with cell death, increased in the mice, suggesting that hormetic preconditioning mediated the protection sulforaphane provided against stroke.
These findings suggest that dietary or supplemental interventions (such as sulforaphane) that precondition the brain against injury offer promise as strategies to reduce complications associated with stroke.
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BDNF mimetic 7,8-dihydroxyflavone protects neurons against cell death. www.sciencedaily.com
BDNF’s neuroprotective capacity suggests that it could be useful in preventing or treating neurodegenerative diseases. Circumventing problems with BDNF’s delivery, half-life, and other limitations has proven challenging. A 2010 study found that 7,8-dihydroxyflavone, a BDNF mimetic, exerted neuroprotective qualities similar to those of BDNF.
7,8-dihydroxyflavone is a type of flavonoid compound present in a variety of plants. Flavonoids exert antioxidant and anti-inflammatory effects, among others. Some evidence indicates that 7,8-dihydroxyflavone might be useful in reversing the damage associated with lead poisoning in children.
The authors of the study screened 2,000 bioactive compounds to gauge their ability to protect rodent and human neurons from apoptosis and identified five compounds, including 7,8-dihydroxyflavone, that showed potential in protecting the cells. Then they treated the cells with BDNF and the various compounds and deprived the cells of oxygen and glucose.
They found that none of the compounds was as effective as 7,8-dihydroxyflavone in protecting the cells from apoptosis. In fact, 7,8-dihydroxyflavone was even more protective than BDNF. They also found that 7,8-dihydroxyflavone exerted its protective qualities by activating a receptor called TrkB, to which BDNF binds. They replicated their findings in an in vivo study of mice, indicating that 7,8-dihydroxyflavone enhances neuronal survival.
These findings demonstrate that flavonoid compounds that mimic the effects of BDNF show potential as therapeutics against neurodegenerative diseases.
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Neonatal brain damage decreased by ~50% when a triglyceride lipid emulsion containing omega-3 DHA was injected within two hours of ischemic stroke www.sciencedaily.com
Animal research.
From the article:
The study compared the effectiveness of emulsions with two omega-3 fatty acids – DHA and eicosapentaenoic acid (EPA) – as well as optimal doses and therapeutic window. The researchers found that DHA provided protection while EPA did not. The therapeutic window ranged from 90 minutes prior to several hours after with the optimal window for treatment 0 – 2 hours.
Prior work:
Dr. Bazan’s group at the LSU Health Sciences Center New Orleans Neuroscience Center of Excellence has increasingly shown that DHA is a potentially powerful treatment for stroke for nearly ten years. His study published in 2011 found DHA triggered production of Neuroprotectin D1 (NPD1), a naturally occurring neuroprotective molecule in the brain derived from DHA and discovered by Dr. Bazan. Not only did DHA treatment salvage stroke-damaged brain tissue that would have died, its repair mechanisms rendered some areas indistinguishable from normal tissue by 7 days.