Researchers connect brain blood vessel lesions to intestinal bacteria

bac 111.JPGNIH-funded pre-clinical study links gut microbes and the immune system to a genetic disorder that can cause stroke and seizures.

 A study in mice and humans suggests that bacteria in the gut can influence the structure of the brain’s blood vessels, and may be responsible for producing malformations that can lead to stroke or epilepsy.

The research, published in Nature, adds to an emerging picture that connects intestinal microbes and disorders of the nervous system. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health.

Cerebral cavernous malformations (CCMs) are clusters of dilated, thin-walled blood vessels that can lead to seizures or stroke when blood leaks into the surrounding brain tissue. A team of scientists at the University of Pennsylvania investigated the mechanisms that cause CCM lesions to form in genetically engineered mice and discovered an unexpected link to bacteria in the gut. When bacteria were eliminated the number of lesions was greatly diminished.

“This study is exciting because it shows that changes within the body can affect the progression of a disorder caused by a genetic mutation,” said Jim I. Koenig, Ph.D., program director at NINDS.

The researchers were studying a well-established mouse model that forms a significant number of CCMs following the injection of a drug to induce gene deletion. However, when the animals were relocated to a new facility, the frequency of lesion formation decreased to almost zero.

“It was a complete mystery. Suddenly, our normally reliable mouse model was no longer forming the lesions that we expected,” said Mark L. Kahn, M.D., professor of medicine at the University of Pennsylvania, and senior author of the study. “What’s interesting is that this variability in lesion formation is also seen in humans, where patients with the same genetic mutation often have dramatically different disease courses.”

While investigating the cause of this sudden variability, Alan Tang, a graduate student in Dr. Kahn’s lab, noticed that the few mice that continued to form lesions had developed bacterial abscesses in their abdomens — infections that most likely arose due to the abdominal drug injections.

The abscesses contained Gram-negative bacteria, and when similar bacterial infections were deliberately induced in the CCM model animals, about half of them developed significant CCMs.

“The mice that formed CCMs also had abscesses in their spleens, which meant that the bacteria had entered the bloodstream from the initial abscess site,” said Tang. “This suggested a connection between the spread of a specific type of bacteria through the bloodstream and the formation of these blood vascular lesions in the brain.”

The question remained as to how bacteria in the blood could influence blood vessel behavior in the brain. Gram-negative bacteria produce molecules called lipopolysaccharides (LPS) that are potent activators of innate immune signaling. When the mice received injections of LPS alone, they formed numerous large CCMs, similar to those produced by bacterial infection. Conversely, when the LPS receptor, TLR4, was genetically removed from these mice they no longer formed CCM lesions.  The researchers also found that, in humans, genetic mutations causing an increase in TLR4 expression were associated with a greater risk of forming CCMs.

“We knew that lesion formation could be driven by Gram-negative bacteria in the body through LPS signaling,” said Kahn.

“Our next question was whether we could prevent lesions by changing the bacteria in the body.”

The researchers explored changes to the body’s bacteria (microbiome) in two ways. First, newborn CCM mice were raised in either normal housing or under germ-free conditions. Second, these mice were given a course of antibiotics to “reset” their microbiome. In both the germ-free conditions and following the course of antibiotics, the number of lesions was significantly reduced, indicating that both the quantity and quality of the gut microbiome could affect CCM formation. Finally, a drug that specifically blocks TLR4 also produced a significant decrease in lesion formation. This drug has been tested in clinical trials for the treatment of sepsis, and these findings suggest a therapeutic potential for the drug in the treatment of CCMs, although considerable research remains to be done.

“These results are especially exciting because they show that we can take findings in the mouse and possibly apply them at the human patient population,” said Koenig. “The drug used to block TLR4 has already been tested in patients for other conditions, and it may show therapeutic potential in the treatment of CCMs, although considerable research still remains to be done.”

Kahn and his colleagues plan to continue to study the relationship between the microbiome and CCM formation, particularly as it relates to human disease. Although specific gene mutations have been identified in humans that can cause CCMs to form, the size and number varies widely among patients with the same mutations. The group next aims to test the hypothesis that differences in the patients’ microbiomes could explain this variability in lesion number.

This work was supported by the NINDS (NS092521, NS075168, NS100252, NS065705), the National Heart, Lung, and Blood Institute (HL094326, HL07439), NIDDK (DK007780), the DFG (German Research Foundation), Penn-CHOP, and the National Health and Medical Research Council, Australia.

The NINDS is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.

Part of the National Institutes of Health, the National Heart, Lung, and Blood Institute (NHLBI) plans, conducts, and supports research related to the causes, prevention, diagnosis, and treatment of heart, blood vessel, lung, and blood diseases; and sleep disorders. The Institute also administers national health education campaigns on women and heart disease, healthy weight for children, and other topics. NHLBI press releases and other materials are available online at https://www.nhlbi.nih.gov.

The NIDDK conducts and supports research on diabetes and other endocrine and metabolic diseases; digestive diseases, nutrition, and obesity; and kidney, urologic, and hematologic diseases. Spanning the full spectrum of medicine and afflicting people of all ages and ethnic groups, these diseases encompass some of the most common, severe, and disabling conditions affecting Americans. For more information about the NIDDK and its programs, visit www.niddk.nih.gov.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH…Turning Discovery Into Health®

Article

Tang et al. Endothelial TLR4 and the microbiome drive cerebral cavernous malformations. Nature. May 10, 2017.

Diet Soda Associated With Stroke, Dementia

But can’t determine causality; some associations diminished with adjustments

Higher consumption of artificially sweetened soft drinks was associated with an increased risk of both stroke and dementia in an analysis of more than 4,000 participants in the Framingham Heart Study Offspring cohort, researchers found.

In the observational study, those who drank at least one artificially-sweetened beverage a day were nearly three times more likely to develop ischemic stroke (HR 2.96, 95% CI 1.26–6.97) and 2.9 times more likely to develop Alzheimer’s disease (95% CI 1.18–7.07) over 10 years than those who abstained, Matthew Pase, PhD, of Boston University School of Medicine, and colleagues reported in the American Heart Association’s journal Stroke.

However, sugary beverages weren’t tied to an increased risk of stroke or dementia — a finding the authors called “intriguing,” and one that could have been due to survival bias.

“It is possible that individuals with high intakes of sugary beverages may have died earlier from other illnesses such as heart disease,” Pase told MedPage Today. “It is also worth noting that our sample consumed diet soda more frequently than sugar-sweetened soda and this may contribute to differences in findings between regular and diet soda.”

He cautioned that the association between artificially sweetened drinks and stroke and dementia seen in their study does not imply causation — a point emphasized by Marion Nestle, PhD, professor of nutrition, food studies, and public health at New York University, who wasn’t involved in the study.

“Association is not the same as causation, although the survival curves are impressive,” Nestle said. “I wish the authors had offered a plausible hypothesis for how artificial sweeteners could be causally related to stroke and dementia.”

Several other experts commented on the “controversial but inconclusive” nature of the association.

“The relationship with artificially sweetened beverages was not simple or straightforward,” said Keith Fargo, PhD, of the Alzheimer’s Association. “When the researchers controlled for other risk factors, particularly cardiovascular risk factors, it explained most of the association between artificially sweetened beverage intake and the development of dementia. This kind of data does not allow us to say that drinking [these] beverages causes dementia, or that cutting down on artificially sweetened beverages will reduce a person’s risk for dementia.”

Pase and colleagues analyzed data from the Framingham Heart Study Offspring cohort on people over age 45 years for the stroke arm (N=2,888) and people over age 60 years for the dementia arm (N=1,484). Both groups were primarily Caucasian and were just under 50% male.

Beverage intake was quantified using the Harvard semiquantitative food-frequency questionnaire at three points: cohort examinations five (1991–1995), six (1995–1998), and seven (1998–2001). Participants were then followed for more than 10 years to determine development of stroke or dementia.

Notably, data collection did not distinguish between the types of artificial sweeteners used in the beverages.

Pase and colleagues found that higher recent and cumulative intake of artificially sweetened soft drinks was linked to an increased risk of ischemic stroke, all-cause dementia, and Alzheimer’s dementia — even after adjustment for total caloric intake, diet quality, physical activity, and smoking status.

However, the associations between recent and higher cumulative intake of artificially sweetened soft drinks and dementia were no longer significant after additional adjustment for vascular risk factors and diabetes mellitus.

“Because our study was observational, we are unable to determine whether artificially sweetened soft drink intake increased the risk of incident dementia through diabetes mellitus or whether people with diabetes mellitus were simply more likely to consume diet beverages,” Pase said.

Pase noted the findings complement their sister study, published in Alzheimer’s & Dementia, that found higher consumption of both sugary and diet beverages was associated with smaller brain volumes, a marker of accelerated brain aging.

Also using data from the Framingham Heart Study Offspring cohort, this study found that people who more frequently consumed sugary beverages, including sodas and fruit juices, were more likely to have poorer memory, smaller overall brain volumes, and smaller hippocampal volumes.

The researchers concluded that their studies highlight a need for more research into this area, especially given how often people drink artificially-sweetened beverages.

In an accompanying editorial in Stroke, Ralph Sacco, MD, of the University of Miami Miller School of Medicine, agreed, writing that the findings “encourage further discussion and more research into this question, for even small causal effects would have tremendous effects on public health due to the popularity of both artificially sweetened soft drinks and sugar sweetened soft drinks consumption. Both sugar-sweetened and artificially sweetened soft drinks may be hard on the brain.”

“This kind of research is critical for examining and uncovering public health relationships that may eventually lead to actionable recommendations,” added Fargo.

Rachel Johnson, PhD, MPH, RD, past chair of the American Heart Association’s Nutrition Committee and professor at the University of Vermont, suggested that people stick to water, low-fat milk, or other beverages without added sweeteners until more data are available: “We know that limiting added sugars is an important strategy to support good nutrition and healthy body weights, and until we know more, people should use artificially sweetened drinks cautiously,” she said in a statement.

The researchers acknowledged several study limitations, including the observational nature of the data, the absence of ethnic minorities, and the use of a self-reported questionnaire to obtain dietary intake data, which may be subject to recall bias.

“Even if someone is three times as likely to develop stroke or dementia,” Pase said, “it is by no means a certain fate.”

Pase reported funding from the National Health and Medical Research Council.

The Framingham Heart Study is supported by the National Heart, Lung, and Blood Institute and by grants from the National Institute on Aging and the National Institute of Neurological Disorders and Stroke.

Sacco received a National Institutes of Health grant for the Northern Manhattan Study. Gardener is also funded by the National Institutes of Health for her work on the Northern Manhattan Study.

Reviewed by F. Perry Wilson, MD, MSCE Assistant Professor, Section of Nephrology, Yale School of Medicine and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Primary Source: Pase M, et al “Sugar and artificially sweetened beverages and the risks of incident stroke and dementia a prospective cohort study” Stroke 2017; DOI: 10.1161/STROKEAHA.116.016027.

Secondary Source: Wersching H, et al “Sugar-sweetened and artificially sweetened beverages in relation to stroke and dementia are soft drinks hard on the brain?” Stroke 2017; DOI: 10.1161/STROKEAHA.117.017198.

Better health care in Canada than in America

I’m a Canadian, in Canada. Jack, my cousin in NC, asked me about health care in Canada and if a universal plan was do-able in the States. I said, “No”. I told him, 8 years ago, that the insurance companies would do EVERYTHING to stop it and they have. I told Jack that our system was far from ideal. Drugs, eye care and other services, like physio, were generally not included. However, the BIG health challenges, like cancer and heart disease, were covered well. It is a bit of patchwork quilt. However, there is no doubt that average folks were better cared for in Canada.

I have struggled to understand the American system. In 1983, my mother had a heart attack and required a triple bypass. At the reunion of her high school class in 1988, in Cleveland, she was sitting with an old friend. When mom told her about her health issues her friend said, “I have needed bypass surgery for the last 8 months, but my HMO won’t cover it.” These were both surgical nurses. My mom instantly realized that her old friend was telling her that she would likely be dead in six months. My mom’s reconstructed heart sank and I’m sure she was thankful that she was now living in Canada. My mom lived 14 more years.
Let’s be clear, there is little doubt that the wealthiest Americans have healthcare plans that put what I have to shame. However, what I have – the main provincial plan and a modest extended family plan through my wife’s work (for about $230/month) – would surpass what 80% of Americans have. I am now 61, retired and still well covered. My cousin, Jack is 75 and the last I heard he was still working.
The United States is the only first world country that does not have a comprehensive, universal health care plan. Yet, more is spent per capita on health care there than anywhere in the world. Clearly, something is amiss.


It is a sad indictment of America. My nephew, now 2, required 3 major heart surgeries in his first 5 months. His care, thank God, was covered by the Ontario health plan. If they were in the States his family would be scrambling and asking all of his aunts and uncles to mortgage their houses to help pay for his care – estimated at about $2 million. Maybe, YOU are in great health, but what would say to your sister IF she said, “Can you give me $30000 for your nephew’s care?” I am forever grateful for the public plan that saved my nephew’s life. If, as you contend, a shared cost system leads to more obesity and chronic ailments, then why do Canadians enjoy better health and live longer than Americans? Could it be that we have better preventative plans?


Every first world country with comprehensive health care plans have healthier and more fit communities. Childhood obesity rates in Canada are half of that in the States. That is because our public health programs know that the cost of addressing these issues with our youth are a fraction of the cost of dealing with them down the line. I agree, people need to be more responsible. However, it starts with education and ensuring that our children are raised to value good nutrition. Turn on the TV today and you will see nothing but a stream of ads promoting food products that are a one-way ticket to health issues. Children are bombarded with catchy ads for junk cereals and convenient, highly processed, snacks. And, the industries that produce this slow acting poisons, do so with the blessings of the government agencies. In some European countries the producers of junk cereal are not permitted to advertise on television. Some would call it a “nanny state”. However, if we are to educate children to make good food choices we need to ensure they have the best information required to make an informed choices. Overwhelming them with ads for junk cereals only serves to undermine the goals of a government healthcare system committed to lowering the shared costs.


Boy, you’re either naive or heartless. I had an emergency appendectomy when I was a healthy 35, as humanly possible, could run 10 miles, not over weight, etc. Cost: $10K with 80 percent picked up by my employer sponsored insurance. Twenty years later, a small spot of cancer appeared on my yearly mammogram. Again, I had employer sponsored insurance.

Today, I do not have employer sponsored health insurance, so I went to the ACA exchange. I’ve got a $3500 deductible with maximum out of pocket of $10,000, and I have those pesky pre-existing conditions.

Good choices and healthy living do a lot, but none of us, not even you, can control some aspects of ill health. To me, your attitude is part of the problem.


I bought private health care insurance for years pre-ACA. This will be a return to high premiums, high deductibles and very limited coverage. This will be access to health care only if you can afford it. It is all good and well for the Republican members of congress, because we, the tax payers, pay for their insurance. I bet they never lost sleep at night wondering how to pay out of pocket for simple things like getting your child treated for asthma, in addition to paying for your high monthly premium, because you hadn’t met the $10,000 family deductible yet, and forgoing the colonoscopy that you knew you should have, but couldn’t cover because you were paying out of pocket for your children’s health care.


I feel sorry for Americans. The basic care I receive here in Ontario is better than most people get with insurance companies and once I get sick I still don’t have to worry about losing my plan. What Obama had the courage to do was to put forward a public health care plan that doesn’t even touch what I have. I knew, when he endeavored to do so 8 years ago the GOP and insurance companies would do EVERYTHING they could to vilify it and kill it. When you can afford $1000/month premiums for a comprehensive family plan you have nothing to worry. That is until you get sick. Then, the insurance company will shut you down. While the Canadian system is far from perfect over 95% of Canadians would not have a fear if they got cancer or needed bypass surgery. People rail about “entitlements” and how to pay for what the government has already committed to. We have the same concerns here in Canada. However, even the most conservative voices in Canada do not talk about scrapping our public health care system. We seem to have learned how to do more with less. Our health care costs are less per capita and we live longer and healthier lives. As or your challenges, I hope that the government understands that if people are worrying continuously about paying for health care they will be a more stressed out and unproductive workforce. There is a saying, “They know the cost of everything, but the value of nothing'” . That, sadly, is the GOP. My heart goes out to you, buddy.


It’s not just the poor. I’ve retired early with substantial savings. My wife, still working, has amassed a very healthy retirement nest egg, too. But that does us no good if insurers can go back to denying us coverage, or excluding wide swaths of care, because of our pre-existing conditions. Without medical insurance, all that we’ve worked for, throughout our decades of contributing to this economy and paying our taxes, could be wiped out, leaving us destitute and unable to afford the medical care we need to stay alive.

Prior to the ACA, when I tried to purchase health insurance privately, I was told by United Healthcare that the only way they would provide me a policy, with my pre-existing back problems, would be to exclude all care related to the spine. I asked (paraphrasing here, since it’s been quite a while) ‘so if I’m in an automobile accident in which I have a spinal injury that leaves me paralyzed, your company will pay nothing towards my medical expenses?’ The representative said, yes, that was true.


This is really frightening. Charge older people – many on fixed incomes, in the years of greatest medical costs – 3 times the insurance rate for younger ones? What sense does that make except to ensure older people suffer? Re continuous care younger people also are prone to risk having no insurance if financially strapped, so they may try to manage diabetes or heart issues on their own for a while. So then they can’t get anything? And no one knows when a catastrophic injury or illness may befall or a child born with some expensive medical problem. So (1) coverage has to be affordable and (2) there’s just no way around eliminating the pre-existing condition claus. That is, unless you’re either deeply cruel of heart or have the imagination of a gnat. So where does that lead? The ACA! It’s really disheartening reading these stories about people who opposed evil communist “Obamacare” until they got cancer or had a heart attack and suddenly faced huge bills they couldn’t possibly pay without it. Does it really take a personal crisis to open people’s eyes? Surely, as a nation and as humanity, we can do better than that!


Many people think that Trump will increase coverage and lower costs. He and Republicans will never support universal coverage and single payer which is the only way to achieve this. Wait until they discover that their coverage will cost more and won’t cover them when they are sick or will drop them quickly once they have a serious diagnosis. I had one of those policies years ago and they dropped us as soon as my daughter was diagnosed with asthma.


Healthy folks don’t need insurance, only ill folks do. Unfortunately, healthy folks turn into ill folks when they get older. Fact is, everyone sees the doctor, so we don’t need for-profit insurance which only works for relatively rare events like fire or theft. We just need a single payer system paid for by federal income taxes. No one need purchase health insurance ever again. No more profits paying for dividends, high executive salaries and stock options, or lobbyists. Our current system is definitely corrupt.


Cobra for us was 1800 a month for great coverage. Got charged $250 copay for a 450k liver transplant. Now who can save 450k in a hsa account, guess who trump and his cabinet. We need single payer with a tax everyone pays from cradle to grave. Anything else is stupid.


One of the reasons Medicare pays out a lot in benefits is that many people don’t see doctors for years before they reach age 65. When they become eligible for Medicare there are previously unaddressed conditions and other problems for which medical care is finally provided.

Decreased bone mineral density (BMD) leads to increased risk of cardiovascular (CV) disease

A study to optimise bone strength and reducing risk of fracture, while at the same time decreasing risk of cardiovascular disease was done by the following team:

1Saint Luke’s Mid America Heart Institute, Kansas City, Missouri, USA
2Cleveland Clinic Foundation, Center for Functional Medicine, Cleveland, Ohio, USA
3Center for Primary Health Care Research, Department of Clinical Sciences, Faculty of Medicine at Lund University, Malmö, Sweden
4Emeritus Professor of Nutritional Science, Colorado State University, Fort Collins, Colorado, USA
Correspondence to Dr James H O’Keefe; gro.sekul-tnias@efeekoj

The majority of Americans do not consume the current recommended dietary allowance for calcium, and the lifetime risk of osteoporosis is about 50%. However, traditional mononutrient calcium supplements may not be ideal. We comprehensively and systematically reviewed the scientific literature in order to determine the optimal dietary strategies and nutritional supplements for long-term skeletal health and cardiovascular health. To summarise, the following steps may be helpful for building strong bones while maintaining soft and supple arteries: (1) calcium is best obtained from dietary sources rather than supplements; (2) ensure that adequate animal protein intake is coupled with calcium intake of 1000 mg/day; (3) maintain vitamin D levels in the normal range; (4) increase intake of fruits and vegetables to alkalinise the system and promote bone health; (5) concomitantly increase potassium consumption while reducing sodium intake; (6) consider increasing the intake of foods rich in vitamins K1 and K2; (7) consider including bones in the diet; they are a rich source of calcium-hydroxyapatite and many other nutrients needed for building bone.

Keywords: QUALITY OF CARE AND OUTCOMES, CV RISK, CALCIUM, VITAMIN D

Key questions

What is already known about this subject?

  • The lifetime risk of osteoporosis is approximately 50%. Most people do not consume the Recommended Daily Allowance of calcium. Traditional mononutrient calcium supplements may not be ideal for promoting long-term cardiovascular and skeletal health.

What does this study add?

  • Calcium is ideally obtained from dietary sources. The form of calcium in bones and bone meal is calcium-hydroxyapatite, which may be particularly effective for building bone.

How might this impact on clinical practice?

  • Increased consumption of calcium-rich foods such as bones, fermented dairy products (e.g. yogurt, kefir, cheese), leafy greens, almonds, and chia seeds may be effective for improving both skeletal and cardiovascular health.

Introduction

Calcium: general physiology and epidemiology

Calcium is the most ubiquitous mineral in the human body. An average-sized adult body contains approximately 1000 to 1200 g of calcium, which is predominately incorporated into bones and teeth in the form of calcium-hydroxyapatite (Ca10(PO4)6(OH)2) crystals. The remainder circulates throughout the blood and soft tissues, and plays fundamental roles in cell conduction, muscle function, hormone regulation, vitamin (Vit) K-dependent pathways, and cardiac and blood vessel function.1

Some studies indicate only 30% of the US population consumes the Recommended Dietary Allowance of calcium, which is 1000–1200 mg daily.1 Furthermore, humans absorb only about 30% of calcium from foods depending on the specific source.1 The body will demineralise its own skeletal system to maintain serum calcium levels in situations where dietary calcium is insufficient and/or absorption is decreased, and/or excretion is increased.2

Osteopenia/osteoporosis: an epidemic

Starting at about age 50 years, postmenopausal women lose about 0.7–2% of their bone mass each year, while men over age 50 years lose 0.5–0.7% yearly. Between ages 45 and 75 years, women, on average, lose 30% of their bone mass, whereas men lose 15%.

According to the US Surgeon General’s Report, 1 in 2 Americans over age 50 years is expected to have or to be at risk of developing osteoporosis.3 Osteoporosis causes 8.9 million fractures annually, with an estimated cumulative cost of incident fractures predicted at US$474 billion over the next 20 years in the USA.3–6 Among adult women over age 45 years, osteoporosis accounts for more days spent in hospital than many other diseases such as diabetes, myocardial infarction (MI), chronic obstructive airway disease and breast cancer.3 Fragility fractures are the primary cause of hospitalisation and/or death for US adults ≥ age 65 years and older; and 44% of nursing home admissions are due to fractures.3

A Mayo Clinic study reported that compared to 30 years ago, forearm fractures have risen more than 32% in boys and 56% in girls. The authors concluded that dietary changes, including insufficient calcium and excess phosphate, were significantly associated with increased fractures.7 Public health approaches are crucial to prevent symptomatic bone disease, but widespread pharmacological prophylaxis is prohibitively expensive and carries potential serious adverse effects.

Cardiovascular disease and bone mineral disease: a calcium nexus

Strong epidemiological associations exist between decreased bone mineral density (BMD) and increased risk of both cardiovascular (CV) disease and CV death.8 For example, individuals with osteoporosis have a higher risk of coronary artery disease, and vice versa. This problem will be magnified if the therapies for osteoporosis (eg, calcium supplements) independently increase risk of MI.

Magnesium

Maintaining replete magnesium status may reduce risk for the metabolic syndrome, diabetes, hypertension and MI.30 Circumstantial and experimental evidence has also implicated magnesium deficiency in osteoporosis.31–34 Optimal dietary magnesium intake is about 7–10 mg/kg/day, preferably in the context of a net base-yielding diet, since a net acid-yielding diet increases excretion of both magnesium and calcium (table 2).

Table 2

Magnesium dietary sources

Potassium/sodium ratio affects calcium metabolism

A potassium/sodium ratio of 1.0 or higher is associated with a 50% lower risk of CVD and total mortality compared with a ratio under 1.0.35 Reducing excessive sodium intake is also associated with resultant decreased urinary calcium excretion, which may help to prevent against bone demineralisation.36 The average potassium content (about 2600 mg/day) of the typical US diet is substantially lower than its sodium content (about 3300 mg/day).35 Approximately 77% of dietary sodium chloride is consumed in the form of processed foods. By contrast, potassium is naturally abundant in many unprocessed foods, especially vegetables, fruits, tubers, nuts, legumes, fish and seafood. In fact, a high potassium/sodium ratio is a reliable marker for high intake of plant foods and lower intake of processed foods.35 High dietary sodium intake has been associated with endothelial damage, arterial stiffness, decreased nitric oxide production and increased levels of transforming growth factor β; whereas, high potassium dietary intake can counteract these effects.35 36

Evidence indicates that the lowest CV event rates occur in the moderate sodium excretion and high potassium excretion groups.37 Thus, it appears that a moderate sodium diet (2800–3300 mg/day) in conjunction with a high potassium intake (>3000 mg/day) might confer the optimal CV benefits for the general population.37

Vit K and bone health

Emerging evidence suggests that Vit K may confer protective effects for both the skeletal and CV systems. Vit K operates in the context of other fat-soluble vitamins, such as A and D, all of which are involved in maintenance of serum calcium concentration, along with the manipulation of materials leading to bone morphogenesis and maintenance of bone tissue.38 Specifically, the oxidation of Vit K results in activation/carboxylation of matrix Gla protein (MGP) which is partially responsible for mineralising bone.39

Also, Vit K is required for the activation (γ-carboxylation) of osteocalcin; the inactivated form, or per cent of undercaboxylated-osteocalcin (%ucOC), has been found to be a sensitive indicator of Vit K nutrition status.38 In cross-sectional and prospective analyses, elevated %ucOC, which occurs when Vit K status is low, is a marker of increased risk for hip fracture in the elderly.38

Several large observational studies appear to support the benefits of Vit K on bone health.38 A meta-analysis concluded that while supplementation with phytonadione (Vit K1) improved bone health, Vit K2 was even more effective in this regard.40 This large and statistically rigorous meta-analysis concluded that high Vit K2 levels were associated with reduced vertebral fractures by approximately 60% (95% CI 0.25% to 0.65%), hip fractures by 77% (95% CI 0.12% to 0.47%), and all non-vertebral fractures by approximately 81% (95% CI 0.11% to 0.35%). Moreover, the benefit of Vit K on bone may not be due to its ability to increase BMD, but rather to its effects at increasing bone strength.41

Vit K benefits in CV health

Mounting evidence suggests vascular calcification whether in the coronary or peripheral arteries is a powerful predictor of CV morbidity and all-cause mortality.42 Prevention of vascular calcification is therefore important as an early intervention to potentially improve long-term CV prognosis.

A major calcification inhibitory factor, is a Vit K-dependent protein synthesised by vascular smooth muscle cells.42 Increased Vit K2 intake has been associated with decreased arterial calcium deposition and the ability to reverse vascular calcification in animal models. Vit K2 prevents pathological calcification in soft tissues via the carboxylation of protective MGP. The undercarboxylated (inactive) species of MGP is formed during inadequate Vit K status, or as a result of Vit K antagonists.42 Low Vit K status is associated with increased vascular calcifications, and can be improved by effective Vit K supplementation (table 3).4344 In two different randomised, double-blind controlled trials, supplemental Vit K has been shown to significantly delay both the development of coronary artery calcification and the deterioration of arterial elasticity.45 46

Table 3

Vitamin K1 dietary sources

Dietary Vit K exists as two major forms: phylloquinone (K1) and menaquinones (MK-n). K1, the predominant dietary form of Vit K, is abundant in dark-green leafy vegetables and seeds. The main dietary sources for MK-n in Western populations are fermented foods, especially natto, cheese and curds (mainly MK-8 and MK-9).47

Calcium supplementation and bone health

A recent large meta-analysis of 26 randomised controlled trials reported that calcium supplements lowered the risk of any fracture by a modest but statistically significant 11% (n=58 573; RR 0.89, 95% CI 0.81 to 0.96).48

Importantly, a low dietary calcium intake with or without calcium supplementation is also associated with higher CV morbidity and mortality rates.51

Figure 3

Relationship of daily calcium intake to risk of CV mortality during follow-up. Data were fully adjusted for confounding variables. The calcium intake for optimising CV longevity is about 1000 mg/day, with higher and lower calcium intakes associated

Elevated serum calcium concentrations are associated with carotid artery plaque thickness, arterial and aortic calcification, and incidence of MI.57 58 Transient elevations in serum calcium levels have been noted following ingestion of 500–1000 mg of calcium supplements.63 64 By contrast, calcium from dietary sources or bone (calcium hydroxyapatite) ingestion results in much smaller changes in circulating calcium levels.

A plant-rich, grain-free diet alters the acid–base status so as to be slightly alkaline, which is conducive for bone health. However, plants are relatively poor sources of calcium compared to animal sources such as dairy products and animal bones. We suspect that milk, though an excellent source of bioavailable calcium, has potential adverse health effects for some individuals. Additionally, 65% of the world’s population show some decrease in lactase activity during adulthood. Importantly, fermented dairy has been linked to favourable outcomes for bone health and mortality risk.

In a small placebo-controlled randomised trial, women who took 1000 mg of calcium in the form of hydroxyapatite in conjunction with oral Vit D showed a significant increase in bone thickness, whereas those who took 1000 mg of a standard calcium carbonate supplement did not (figure 4).

In theory, consuming calcium-rich foods such as bones, fermented dairy (eg, unsweetened yogurt, kefir, cheese), leafy greens, almonds, and chia seeds may be an effective strategy for improving both calcium intake and long-term health.

Signs Of Stress In The Brain May Predict Arterial Inflammation, stroke

By Lecia Bushak

We’ve known for some time that chronic stress can lead to a slew of health problems, from an increased risk of developing depression to heart disease. But new research that will be presented at the American College of Cardiology’s 65th Annual Scientific Session has managed to gain deeper insight into how stress may cause inflammation and heart problems.

Researchers used medical imaging to examine biochemical activity in the brain and how it leads to arterial inflammation, which  can contribute to heart problems — including plaque buildup, heart attack, and stroke. They found that study participants who experienced high activity in areas of the brain associated with stress and fear were far more likely to have heart troubles later.

The study examined 293 patients who were on average 55 years old, and who had received a PET/CT scan between 2005 and 2008 for a cancer screening — though they had all been marked free of the disease. These same participants were also clear of heart disease at the time. The scans provided insight into brain activity, bone marrow, and arteries due to a method that made more active tissues glow brightly on the scan. The researchers divided the participants into groups based on the level of brain activity in their amygdala. High activity in the amygdala is associated with stress and fear responses.

Researchers found that brain activity in certain brain regions could possibly predict later heart problems.Pixabay, public domain

After following up on the cardiovascular health of the participants for five years, the researchers found that those who had been placed into the high-activity amygdala group had a 14-fold higher risk of heart problems for every unit increase in brain stress activity. In addition, 35 percent of those participants experienced a cardiovascular event within the five years, compared to only 5 percent of the low-stress group.

The results are “intriguing,” Dr. Ahmed Tawakol, co-director of the cardiac MR PET CT program at Massachusetts General Hospital and an author of the study, told Medical Daily. “Our study illuminates, for the first time, a relationship between activation of neural tissues — those associated with fear and stress — and subsequent heart disease events,” Tawakol said in the statement. “There is a need to develop greater knowledge in terms of the mechanism that translates stress into cardiovascular disease risk, given the prevalence and potency of stress as a risk factor.”

It wasn’t simply high activity in the amygdala that signaled cardiovascular trouble. The researchers also found that activation of the fear center in the brain went hand-in-hand with bone marrow activation and inflammation in the arteries. Bone marrow activation refers to bone marrow producing more cells, including white blood cells called monocytes, that may contribute to inflammation. The researchers were able to measure this by the increased production of monocytes and other bone marrow-derived cells.

It’s possible that stress activity in the brain, bone marrow activation, and arterial inflammation work together to create adverse cardiovascular effects, though the current study only highlights a correlation, and not necessarily a causation. In order for the researchers to move forward, Tawakol notes, they would have to establish that stress indeed causes heart problems. To do that, they’d have to set up a study that involves an intervention, one that would reduce the brain’s stress or emotional response and prove whether that lowered cardiovascular events as well. Only then can they begin discussing the notion of treating stress by targeting the stress response in the brain.

“If we find that treating stress in one way or another results in a reduction in heart disease, then we’re going to venture towards diagnosing and intervene,” Tawakol told Medical Daily. “Certainly we want to test the hypothesis that there are coping methods for stress that reduce stimulation of the [stress] system and reduce cardiovascular risk.”

Being prescribed medications or undergoing therapy may be one way of preventing future heart problems if the researchers do end up proving the causation. And reducing stress may be just as important as quitting smoking or monitoring your diabetes.

“Over the past several years, it’s become clear that stress is not only a result of adversity but may itself also be an important cause of disease,” Tawakol said in the press release. “The risks of heart disease linked to stress is on par with that for smoking, high blood pressure, high cholesterol and diabetes, yet relatively little is done to address this risk compared to other risk factors. We are hopeful studies like this bring us closer to understand how stress may lead to heart disease.”

Source: Ishai A, Tawakol A, et al. Greater Activity of the Brain’s Emotional Stress Center Associates With Arterial Inflammation and Predicts Subsequent CVD Events. American College of Cardiology , 2016.

Stroke and care after

Stroke

History of stroke:

Hippocrates, the father of medicine, first recognized stroke over 2,400 years ago. At this time stroke was called apoplexy, which means “struck down by violence” in Greek. This was due to the fact that a person developed sudden paralysis and change in well-being. Physicians had little knowledge of the anatomy and function of the brain, the cause of stroke, or how to treat it.

It was not until the mid-1600s that Jacob Wepfer found that patients who died with apoplexy had bleeding in the brain. He also discovered that a blockage in one of the brain’s blood vessels could cause apoplexy.

Medical science continued to study the cause, symptoms, and treatment of apoplexy and, finally, in 1928, apoplexy was divided into categories based on the cause of the blood vessel problem. This led to the terms stroke or “cerebral vascular accident (CVA).” Stroke is now often referred to as a “brain attack” to denote the fact that it is caused by a lack of blood supply to the brain, very much like a heart attack is caused by a lack of blood supply to the heart. The term brain attack also conveys a more urgent call for immediate action and emergency treatment by the general public.

Today, there is a wealth of information available on the cause, prevention, risk, and treatment of stroke. Although there is no cure, most stroke victims now have a good chance for survival and recovery. Immediate treatment, supportive care, and rehabilitation can all improve the quality of life for stroke victims.

What is stroke?

Stroke, also called brain attack, occurs when blood flow to the brain is disrupted. Disruption in blood flow is caused when either a blood clot or piece of plaque blocks one of the vital blood vessels in the brain (ischemic stroke), or when a blood vessel in the brain bursts, spilling blood into surrounding tissues (hemorrhagic stroke).

The brain needs a constant supply of oxygen and nutrients in order to function. Even a brief interruption in blood supply can cause problems. Brain cells begin to die after just a few minutes without blood or oxygen. The area of dead cells in tissues is called an infarct. Due to both the physical and chemical changes that occur in the brain with stroke, damage can continue to occur for several days. This is called a stroke-in-evolution.

A loss of brain function occurs with brain cell death. This may include impaired ability with movement, speech, thinking and memory, bowel and bladder, eating, emotional control, and other vital body functions. Recovery from stroke and the specific ability affected depends on the size and location of the stroke. A small stroke may result in problems such as weakness in an arm or leg. Larger strokes may cause paralysis (inability to move part of the body), loss of speech, or even death.

According to the National Stroke Association (NSA), it is important to learn the three Rs of stroke:

  • Reduce the risk.
  • Recognize the symptoms.
  • Respond by calling 911 (or your local ambulance service).

Stroke is an emergency and should be treated as such. The greatest chance for recovery from stroke occurs when emergency treatment is started immediately.

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What are the most common symptoms of stroke?

The following are the most common symptoms of stroke. However, each individual may experience symptoms differently. If any of these symptoms are present, call 911 (or your local ambulance service) immediately. Treatment is most effective when started immediately.

Symptoms may be sudden and include:

  • weakness or numbness of the face, arm, or leg, especially on one side of the body
  • confusion or difficulty speaking or understanding
  • problems with vision such as dimness or loss of vision in one or both eyes
  • dizziness or problems with balance or coordination
  • problems with movement or walking
  • severe headaches with no other known cause

All of the above warning signs may not occur with each stroke. Do not ignore any of the warning signs, even if they go away – take action immediately. The symptoms of stroke may resemble other medical conditions or problems. Always consult your physician for a diagnosis.

What are some other symptoms of stroke?

Other, less common, symptoms of stroke may include the following:

  • sudden nausea, vomiting, or fever not caused by a viral illness
  • brief loss or change of consciousness such as fainting, confusion, seizures, or coma
  • transient ischemic attack (TIA), or “mini-stroke”

A TIA can cause many of the same symptoms as a stroke, but TIA symptoms are transient and last for a few minutes to up to 24 hours. Call for medical help immediately if you suspect a person is having a TIA, as it may be a warning sign that a stroke is about to occur. Not all strokes, however, are preceded by TIAs.

Risk Factors for Stroke

Evaluating the risk for stroke is based on heredity, natural processes, and lifestyle. Many risk factors for stroke can be changed or managed, while others that relate to hereditary or natural processes cannot be changed.

Risk factors for stroke that can be changed, treated, or medically managed:

  • High blood pressure – The most important controllable risk factor for stroke (brain attack) is controlling high blood pressure (140/90 or higher). High blood pressure can damage blood vessels called arteries that supply blood to the brain. According to the Centers for Disease Control and Prevention (CDC), reducing the systolic (or top number) blood pressure by 12 to 13 points can decrease the risk for a stroke by 37 percent.
  • Diabetes mellitus – Diabetes is treatable, but having it increases the risk for stroke. People with diabetes have two to four times the risk of having a stroke than someone without diabetes. Talk with your healthcare provider on specific ways to manage your overall health and diabetes care.
  • Heart disease – Heart disease is the second most important risk factor for stroke, and the major cause of death among survivors of stroke. Heart disease and stroke have many of the same risk factors.
  • Cigarette smoking – Apart from other risk factors, smoking almost doubles the risk for ischemic stroke (blockage of a blood vessel supplying blood to the brain). The use of oral contraceptives, especially when combined with cigarette smoking, greatly increases stroke risk.
  • History of transient ischemic attacks (TIAs) – A person who has had one (or more) TIA is almost 10 times more likely to have a stroke than someone of the same age and sex who has not had a TIA.
  • High red blood cell count – A moderate increase in the number of red blood cells thickens the blood and makes clots more likely, thus increasing the risk for stroke.
  • High blood cholesterol and lipids – High blood cholesterol and lipids increase the risk for stroke. High cholesterol levels can contribute to atherosclerosis (thickening or hardening of the arteries) caused by a build-up of plaque (deposits of fatty substances, cholesterol, calcium). Plaque build-up on the inside of the walls of arteries can decrease the amount of blood flow to the brain. A stroke occurs if the blood supply is cut off to the brain. Atherosclerosis is a slow, progressive disease that may start as early as childhood.
  • Lack of exercise, physical inactivity – Lack of exercise and physical inactivity increases the risk for stroke.
  • Obesity – Excess weight increases the risk for stroke.
  • Excessive alcohol use – More than two drinks per day raises blood pressure, and binge drinking can lead to stroke.
  • Drug abuse (certain kinds) – Intravenous drug abuse carries a high risk of stroke from cerebral embolisms (blood clots). Cocaine use has been closely related to strokes, heart attacks, and a variety of other cardiovascular complications. Some of them, even among first-time cocaine users, have been fatal.
  • Abnormal heart rhythm – Various heart diseases have been shown to increase the risk of stroke. Atrial fibrillation (an irregular heartbeat) is the most powerful and treatable heart risk factor of stroke. About 15 percent of strokes occur in people with atrial fibrillation.
  • Cardiac structural abnormalities – New evidence shows that heart structure abnormalities including patent foramen ovale and atrial septal defect increase risk for embolic stroke.

Risk factors for stroke that cannot be changed:

  • Age – For each decade of life after age 55, the chance of having a stroke more than doubles.
  • Race – African-Americans have a much higher risk of death and disability from a stroke than Caucasians, in part because the African-American population has a greater incidence of high blood pressure and diabetes.
  • Gender – Stroke occurs more frequently in men, but more women than men die from stroke.
  • History of prior stroke – The risk of stroke for someone who has already had one is many times that of a person who has not had a stroke.
  • Heredity/genetics – The chance of stroke is greater in people who have a family history of stroke.

Other risk factors of stroke to consider:

  • Where a person lives – Strokes are more common among people living in the southeastern United States than in other areas. This may be due to regional differences in lifestyle, race, cigarette smoking, and diet.
  • Temperature, season, and climate – Stroke deaths occur more often during periods of extreme temperatures.
  • Socioeconomic factors – There is some evidence that strokes are more common among low-income people than among more affluent people.

Statistics of Stroke

More about stroke/brain attack:

Consider the following statistics regarding strokes:

  • Stroke is the third largest cause of death, ranking behind diseases of the heart and all forms of cancer.
  • Almost every 40 seconds in the United States, a person experiences a stroke.
  • Over 4 million US adults live today with the effects of a stroke.
  • The American Stroke Association, a division of the American Heart Association, estimates strokes cost the US $68.9 billion in 2009.
  • Women account for about 6 in 10 stroke deaths.
  • Black males have almost twice the risk of a first-ever stroke compared with white males.
  • Hispanics have an increased risk of stroke compared with non-Hispanic whites.
  • Each year about 795,000 people suffer a new or recurrent stroke in the US.
  • Stroke accounts for about 1 out of every 17 deaths in the US.

What are the different types of stroke?

Strokes can be classified into two main categories:

  • 87 percent are ischemic strokes – strokes caused by blockage of an artery.
  • 13 percent are hemorrhagic strokes – strokes caused by bleeding.

What is an ischemic stroke?

An ischemic stroke occurs when a blood vessel that supplies the brain becomes blocked or “clogged” and impairs blood flow to part of the brain. The brain cells and tissues begin to die within minutes from lack of oxygen and nutrients. The area of tissue death is called an infarct. About 87 percent of strokes fall into this category. Ischemic strokes are further divided into two groups, including the following:

  • thrombotic strokes – caused by a blood clot that develops in the blood vessels inside the brain.
  • embolic strokes – caused by a blood clot or plaque debris that develops elsewhere in the body and then travels to one of the blood vessels in the brain via the bloodstream.

What is a thrombotic stroke?

Thrombotic strokes are strokes caused by a thrombus (blood clot) that develops in the arteries supplying blood to the brain. This type of stroke is usually seen in older persons, especially those with high-cholesterol levels and atherosclerosis (a build-up of fat and lipids inside the walls of blood vessels).

Sometimes, symptoms of a thrombotic stroke can occur suddenly and often during sleep or in the early morning. At other times, it may occur gradually over a period of hours or even days. This is called a stroke-in-evolution.

Thrombotic strokes may be preceded by one or more “mini-strokes,” called transient ischemic attacks, or TIAs. TIAs may last for a few minutes or up to 24 hours, and are often a warning sign that a stroke may occur. Although usually mild and transient, the symptoms caused by a TIA are similar to those caused by a stroke.

Another type of stroke that occurs in the small blood vessels in the brain is called a lacunar infarct. The word lacunar comes from the Latin word meaning “hole” or “cavity.” Lacunar infarctions are often found in people who have diabetes or hypertension (high blood pressure).

What is an embolic stroke?

Embolic strokes are usually caused by an embolus (a blood clot that forms elsewhere in the body and travels through the bloodstream to the brain). Embolic strokes often result from heart disease or heart surgery and occur rapidly and without any warning signs. About 15 percent of embolic strokes occur in people with atrial fibrillation, a type of abnormal heart rhythm in which the upper chambers of the heart do not beat effectively.

What is a hemorrhagic stroke?

Hemorrhagic strokes occur when a blood vessel that supplies the brain ruptures and bleeds. When an artery bleeds into the brain, brain cells and tissues do not receive oxygen and nutrients. In addition, pressure builds up in surrounding tissues and irritation and swelling occur. About 13 percent of strokes are caused by hemorrhage (10 percent are intracerebral hemorrhage and 3 percent are subarachnoid hemorrhage strokes). Hemorrhagic strokes are divided into two main categories, including the following:

  • intracerebral hemorrhage – bleeding from the blood vessels within the brain.
  • subarachnoid hemorrhage – bleeding in the subarachnoid space (the space between the brain and the membranes that cover the brain).

What is an intracerebral hemorrhage?

Intracerebral hemorrhage is usually caused by hypertension (high blood pressure), and bleeding occurs suddenly and rapidly. There are usually no warning signs and bleeding can be severe enough to cause coma or death.

What is a subarachnoid hemorrhage?

Subarachnoid hemorrhage results when bleeding occurs between the brain and the meninges (the membrane that covers the brain) in the subarachnoid space. This type of hemorrhage is often due to an aneurysm or an arteriovenous malformation (AVM).

  • An aneurysm is a weakened, ballooned area on an artery wall and has a risk for rupturing. Aneurysms may be congenital (present at birth), or may develop later in life due to such factors as hypertension or atherosclerosis
  • An AVM is a congenital disorder that consists of a disorderly tangled web of arteries and veins. The cause of AVM is unknown.

What are recurrent strokes?

Recurrent strokes occur in about 25 percent of stroke victims within five years after a first stroke. The risk is greatest right after a stroke and decreases over time. The likelihood of severe disability and death increases with each recurrent stroke. About 3 percent of stroke patients have a second stroke within 30 days of their first stroke, and about one-third have a second stroke within two years.

What are the effects of stroke?

The effects of stroke vary from person to person based on the type, severity, and location of the stroke. The brain is extremely complex and each area of the brain is responsible for a special function or ability. When an area of the brain is damaged, which typically occurs with a stroke, an impairment may result. An impairment is the loss of normal function of part of the body. Sometimes, an impairment may result in a disability, or inability to perform an activity in a normal way.

The brain is divided into three main areas, including the following:

  • cerebrum (consisting of the right and left sides or hemispheres)
  • cerebellum
  • brain stem

Depending on which of these regions of the brain the stroke occurs, the effects may be very different.

What effects can be seen with a stroke in the cerebrum?

The cerebrum is the part of the brain that occupies the top and front portions of the skull. It is responsible for control of such abilities as movement and sensation, speech, thinking, reasoning, memory, sexual function, and regulation of emotions. The cerebrum is divided into the right and left sides, or hemispheres.

Depending on the area and side of the cerebrum affected by the stroke, any, or all, of the following body functions may be impaired:

  • movement and sensation
  • speech and language
  • eating and swallowing
  • vision
  • cognitive (thinking, reasoning, judgment and memory) ability
  • perception and orientation to surroundings
  • self-care ability
  • bowel and bladder control
  • emotional control
  • sexual ability

In addition to these general effects, some specific impairments may occur when a particular area of the cerebrum is damaged.

Effects of a right hemisphere stroke:

The effects of a right hemisphere stroke may include the following:

  • left-sided weakness (left hemiparesis) or paralysis (left hemiplegia) and sensory impairment
  • denial of paralysis or impairment and reduced insight into the problems created by the stroke (this concept is called “left neglect”)
  • visual problems, including an inability to see the left visual field of each eye (homonymous hemianopsia)
  • spatial problems with depth perception or directions such as up/down and front/back
  • inability to localize or recognize body parts
  • inability to understand maps and find objects such as clothing or toiletry items
  • memory problems
  • behavioral changes such as lack of concern about situations, impulsivity, inappropriateness, and depression

Effects of a left hemisphere stroke:

The effects of a left hemisphere stroke may include the following:

  • right-sided weakness (right hemiparesis) or paralysis (right hemiplegia) and sensory impairment
  • problems with speech and understanding language (aphasia)
  • visual problems, including the inability to see the right visual field of each eye (homonymous hemianopsia)
  • impaired ability to do math or to organize, reason, and analyze items
  • behavioral changes such as depression, cautiousness, and hesitancy
  • impaired ability to read, write, and learn new information
  • memory problems

What effects can be seen with a stroke in the cerebellum?

The cerebellum is located beneath and behind the cerebrum towards the back of the skull. It receives sensory information from the body via the spinal cord and helps to coordinate muscle action and control, fine movement, coordination, and balance.

Although strokes are less common in the cerebellum area, the effects can be severe. Four common effects of strokes in the cerebellum include the following:

  • inability to walk and problems with coordination and balance (ataxia)
  • dizziness
  • headache
  • nausea
  • vomiting

What effects can be seen with a stroke in the brain stem?

The brain stem is located at the very base of the brain right above the spinal cord. Many of the body’s vital “life-support” functions such as heartbeat, blood pressure, and breathing are controlled by the brain stem. It also helps to control the main nerves involved with eye movement, hearing, speech, chewing, and swallowing. Some common effects of a stroke in the brain stem include problems with the following:

  • breathing and heart functions
  • body temperature control
  • balance and coordination
  • weakness or paralysis in all four limbs
  • chewing, swallowing, and speaking
  • vision
  • coma

Unfortunately, death is common with brain stem strokes.

http://surgery.med.miami.edu/vascular-and-endovascular/patient-care-services/stroke


Connie’s suggestion for the after stroke care for her sister in the Philippines:

After her mini brain surgery, my sister (over 50 yrs of age)  is now having panic attacks and gets headache, nausea and dizziness easy. So I suggested the following to her: add lemon/kalamansi in her water, take potassium tabs in the morning, and her multi-vitamins 2x a day, extra Omega 3 rich in DHA tabs and other essential minerals and vitamins. Eat avocado, soft boiled eggs, cooked peanuts (with skin), guava, pineapple, fish and veggies (green, yellow and all the colors, heart of banana, bamboo shoots, green jackfruit, squash,saluyot,okra,bitter melons leaves and veggie,) and to avoid stress. In the Philippines, there is smog/air pollution and second hand smokes that she has to avoid if possible. The weather is not relaxing in the city with less fresh air and extremely hot environment.

A hug will give her calmness. More to come….

Gender bias in treating or preventing blood clots in women

Animation of the formation of an occlusive thrombus in a vein. A few platelets attach themselves to the valve lips, constricting the opening and causing more platelets and red blood cells to aggregate and coagulate. Coagulation of unmoving blood on both sides of the blockage may propagate a clot in both directions.

A thrombus occurs when the hemostatic process, which normally occurs in response to injury, becomes activated in an uninjured or slightly injured vessel. A thrombus in a large blood vessel will decrease blood flow through that vessel (termed a mural thrombus). In a small blood vessel, blood flow may be completely cut off (termed an occlusive thrombus), resulting in death of tissue supplied by that vessel. If a thrombus dislodges and becomes free-floating, it is considered an embolus.

Some of the conditions which elevate risk of blood clots developing include atrial fibrillation (a form of cardiac arrhythmia), heart valve replacement, a recent heart attack (also known as a myocardial infarction), extended periods of inactivity (see deep venous thrombosis), and genetic or disease-related deficiencies in the blood’s clotting abilities.

Formation

Platelet activation can occur through different mechanisms such as a vessel wall breach that exposes collagen, or tissue factor encryption.[clarification needed] The platelet activation causes a cascade of further platelet activation, eventually causing the formation of the thrombus.[2]This process is regulated through thromboregulation.

Prevention and treatment

Blood clot prevention and treatment reduces the risk of stroke, heart attack and pulmonary embolism. Heparin and warfarin are often used to inhibit the formation and growth of existing thrombi; the former binds to and activates the enzyme inhibitor antithrombin III, while the latter inhibits vitamin K epoxide reductase, an enzyme needed to synthesize mature clotting factors.

Some treatments have been derived from bacteria. One drug is streptokinase, which is an enzyme secreted by several streptococcal bacteria. This drug is administered intravenously and can be used to dissolve blood clots in coronary vessels. However, streptokinase is nonspecific and can digest almost any protein, which can lead to many secondary problems. Another clot-dissolving enzyme that works faster and is more specific is called tissue plasminogen activator (tPA). This drug is made by transgenic bacteria and it converts plasminogen into the clot-dissolving enzyme plasmin.[3] There are also some anticoagulants that come from animals that work by dissolving fibrin. For example, Haementeria ghilianii, an Amazon leech, produces an enzyme called hementin from its salivary glands.[4] As of 2012, this enzyme has now been successfully produced by genetically engineered bacteria and administered to cardiac patients.

Prognosis

Thrombus formation can have one of four outcomes: propagation, embolization, dissolution, and organization and recanalization.[5]

  1. Propagation of a thrombus occurs towards the direction of the heart. This means that it is anterograde in veins or retrograde in arteries.
  2. Embolization occurs when the thrombus breaks free from the vascular wall and becomes mobile. A venous embolus (mostly from deep vein thrombosis in the lower limbs) will travel through the systemic circulation, reach the right side of the heart, and travel through the pulmonary artery resulting in a pulmonary embolism. Arterial thrombosis resulting from hypertension or atherosclerosis can become mobile and the resulting emboli can occlude any artery or arteriole downstream of the thrombus formation. This means that cerebral stroke, myocardial infarction, or any other organ can be affected.
  3. Dissolution occurs when the fibrinolytic mechanisms break up the thrombus and blood flow is restored to the vessel. This may be aided by drugs (for example after occlusion of a coronary artery). The best response to fibrinolytic drugs is within a couple of hours, before the fibrin meshwork of the thrombus has been fully developed.
  4. Organization and recanalization involves the ingrowth of smooth muscle cells, fibroblasts and endothelium into the fibrin-rich thrombus. If recanalization proceeds it provides capillary-sized channels through the thrombus for continuity of blood flow through the entire thrombus but may not restore sufficient blood flow for the metabolic needs of the downstream tissue.[citation needed]

Stroke in women

A number of factors are likely behind the surprising rise in strokes in women, including:

  • Increasing rates of obesity (women’s waists have grown by nearly two inches in the last 10 years)
  • Vitamin D3 deficiency due to lack of sun exposure. Sun avoidance also increases your risk of vitamin D sulfate deficiency, which may be an underlying cause of arterial plaque buildup (a risk factor for stroke)
  • Rising prevalence of high blood sugar levels
  • eating unprocessed, preferably organic, foods, exercising and maintaining a healthy weight will help to reduce your risk of stroke. Two additional risk factors that can have a direct impact on your stroke risk are:
    • Psychological distress. According to a 2008 study published in the journal Neurology, the more stressed you are, the greater your risk. The researchers actually found that for every notch lower a person scored on their well-being scale, their risk of stroke increased by 11 percent. Not surprisingly, the relationship between psychological distress and stroke was most pronounced when the stroke was fatal.
    • Hormone replacement therapy (HRT) and birth control pills. If you’re on one of the hormonal birth control methods (whether it’s the pill, patch, vaginal ring or implant), it is important to understand that you are taking synthetic progesterone and synthetic estrogen — something that is clearly not advantageous if you want to maintain optimal health. These contraceptives contain the same synthetic hormones as those used in hormone replacement therapy (HRT), which has well-documented risks, including an increased risk of blood clots, stroke, heart attack, and breast cancer.

Diet Soda May Dramatically Increase Your Stroke Risk

Earlier this year, research presented at the American Stroke Association’s International Stroke Conference showed that people who drink just one diet soda a day may increase their risk of stroke by 48 percent!

According to the authors:

“This study suggests that diet soda is not an optimal substitute for sugar-sweetened beverages, and may be associated with a greater risk of stroke, myocardial infarction, or vascular death than regular soda.”

While more research will likely be needed to confirm this potential link, there’s plenty of evidence showing that artificial sweeteners such as aspartame and sucralose (Splenda) can be dangerous to your health. I believe aspartame is, by far, the most dangerous artificial sweetener on the market. Reports of adverse reactions to the US FDA also support this, as aspartame accounts for over 75 percent of the adverse reactions to food additives reported to the FDA.

Embolism

An embolism is the lodging of an embolus, a blockage-causing piece of material, inside a blood vessel.[1] The embolus may be a blood clot (thrombus), a fat globule, a bubble of air or other gas (gas embolism), or foreign material. An embolism can cause partial or total blockage of blood flow in the affected vessel.[2] Such a blockage (a vascular occlusion) may affect a part of the body distant from where the embolus originated. An embolism in which the embolus is a piece of thrombus is called a thromboembolism. Thrombosis, the process of thrombus formation, often leads to thromboembolism.

An embolism is usually a pathologic event (that is, part of illness or injury). Sometimes it is created intentionally for a therapeutic reason, such as to stop bleeding or to kill a cancerous tumor by stopping its blood supply. Such therapy is called embolization.


Gender bias in treating or preventing blood clots in women

In health care, gender disparities are especially pernicious. If you are a woman, studies have shown, you are not only less likely to receive blood clot prophylaxis, but you may also receive less intensive treatment for a heart attack. If you are a woman older than 50 who is critically ill, you are at particular risk of failing to receive lifesaving interventions. If you have knee pain, you are less likely to be referred for a knee replacement than a man, and if you have heart failure, it may take longer to get EKGs.

When Dr. Elliott Haut and his team at Johns Hopkins Hospital in Baltimore designed their blood clot prevention protocol back in 2006, they didn’t expect to discover systemic gender bias. But the data were clear and the implications were alarming: Women who were trauma patients at Johns Hopkins Hospital were in considerably greater danger of dying of preventable blood clots than men.

Why? Because doctors were less likely to provide them with the appropriate blood clot prevention treatment. At Hopkins, as at many hospitals, both men and women were receiving treatment at less than perfect rates, but while 31 percent of male trauma patients were failing to get proper clot prevention, for women, the rate was 45 percent. That means women were nearly 50 percent more likely to miss out on blood clot prevention.

Blood clots, gelatinous tangles that can travel through the body and block blood flow, kill more people every year than breast cancer, AIDS and car crashes combined. But many of these clots can be avoided — if doctors prescribe the right preventive measures.

Such implicit bias, as researchers now understand, happens when we unintentionally use stereotypes or associations to make judgments. “Perhaps we take women’s symptoms less seriously, or we interpret them as having an emotional cause as opposed to a physical cause,” said Dr. Christine Kolehmainen, the associate director for women’s health at the Middleton Memorial Veterans Hospital in Madison, Wis. Studies bear this out: in one study of patients with irritable bowel syndrome, doctors were more likely to suggest that male patients receive X-rays and more likely to offer female patients tranquilizers and lifestyle advice.

In the case of blood clot prevention, doctors’ assumptions about women’s risk factors could lead to disparities in treatment. “There might be stereotypes about women’s biology or environment or occupation that could all play into medical decision-making,” Kolehmainen said.

Whether unintentional, unconscious or simply based on erroneous assumptions, treatment differentials clearly exist. Interventions like the Hopkins checklist can help correct them.


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