Heart disease

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Researchers have discovered an imbalance in the amounts of fatty molecules called lipids inside the brain cells of people with Parkinson’s disease. A buildup of lipids in nerve cells may cause inflammation.

Parkinson’s disease is a movement disorder that gets progressively worse over time.

The death of dopamine-producing nerve cells in the substantia nigra region of the brain causes the illness. Dopamine is a neurotransmitter that plays several vital roles, including regulating motivation, reward, and movement.

However, the exact train of events leading to the death of dopamine-producing cells remains unclear.

Researchers have focused much of their attention on a misfolded form of a protein called alpha-synuclein as the trigger for Parkinson’s. Studies have found toxic clumps or aggregates of the misfolded protein in the brains of people with the disease.

However, an alternative theory proposes that lipid dysregulation and inflammation play a more important role, similar to the part played by fatty plaques and inflammation in the walls of arteries in cardiovascular disease.

Researchers at the Neuroregeneration Institute at McLean Hospital in Belmont, MA, have now discovered an accumulation of lipids in dopamine-producing neurons in the postmortem brains of people who had Parkinson’s.

The excess amounts of lipid in these nerve cells correlate with changes in lipid levels in neighboring cells called microglia and astrocytes. They also found evidence of inflammation.

When the researchers simulated a breakdown of lipid metabolism in an animal model of the disease, they saw remarkably similar changes.

“These results support our lipid-inflammation hypothesis in the causation of Parkinson’s disease initiation and progression,” says senior author Dr. Ole Isacson, who is the founding director of the Neuroregeneration Institute and a professor of neurology at Harvard Medical School in Boston, MA.

“[The results] may help us discover and develop new therapies by leaving behind conventional thinking about [Parkinson’s disease] pathology, which to some extent has been limited to neurons and protein aggregates,” he adds.

The study appears in the journal Proceedings of the National Academy of Sciences.

Postmortem tissue samples

The scientists compared postmortem brain tissue from 26 individuals with Parkinson’s with 23 age-matched controls without the disease.

They used fluorescent lipid-binding molecules to determine lipid levels in different brain cells in the substantia nigra.

In brain tissue from people with Parkinson’s, there was an accumulation of lipids inside dopamine nerve cells, which was matched by a deficiency of lipids within astrocytes in the same samples.

Astrocytes are star-shaped cells that support nerve cells, both structurally and through the exchange of nutrients and their byproducts.

In their paper, the researchers note that nerve cells have a limited capacity to use lipids for energy, with excess amounts being transported to neighboring astrocytes to avoid the buildup of toxic byproducts.

This did not seem to be happening correctly in the brains of individuals with Parkinson’s.

Compared with healthy brain tissue, the scientists also found excess amounts of lipid inside microglia, which are the brain’s immune cells.

They also discovered high levels of a signaling molecule called GPNMB. Scientists know that astrocytes produce this molecule in response to inflammation caused by the build up of lipids.

The scientists found that levels of this molecule correlated with the total amount of lipid in the brain tissue of individuals with Parkinson’s.

Mouse model of Parkinson’s

Finally, the scientists investigated whether they could reproduce these effects in mice by disrupting lipid metabolism in the animals’ brains.

One of the most significant genetic risk factors for Parkinson’s is a mutation in a gene for an enzyme that breaks down lipids.

When the researchers injected the mice with a chemical that inhibits this enzyme, they found the same pattern of changes in lipid distribution that they had seen in brain tissue from people with Parkinson’s.

Previous research has found telltale deposits of alpha-synuclein in mice injected with this enzyme inhibitor.

In their paper, the scientists conclude:

“Therapies and agents that reverse the pathological cell-type-specific lipid distribution in the [substantia nigra of people with Parkinson’s] could serve to prevent and reduce the progression of [Parkinson’s disease] and related neurodegenerative disorders.”

However, researchers need to carry out much more research to confirm the findings and translate them into effective and safe treatments.

In celebration of this year’s World Heart Day, Wella Health, a leading African health tech startup, is carrying out free blood pressure tests for over 100,000 Nigerians across its 600 partner pharmacies from Tuesday September 29 to October 29 this year.

World Heart Day is observed and celebrated every September 29. The global awareness day is intended to increase public understanding of cardiovascular diseases, prevention, early detection and treatment.

According to research, cardiovascular diseases commonly referred to as CVDs are the number one cause of death globally, killing 17.9 million people yearly and accounting for 31 per cent of all global deaths.

Speaking on the campaign, CEO Wella Health, Dr Neto Ikpeme stated that cardiovascular diseases are often perceived as a problem strictly for older people. “Unfortunately, it is now more common in adolescents and young adults.”

According to the expert, for 25 to 34-year-old men and women, heart disease is the fourth leading cause of death while for 35 to 44-year-olds, heart disease is even deadlier and is the second biggest killer of men and third biggest killer of women.

“CVDs can affect anyone and at any age. The rise in obesity and diabetes at earlier ages also adds to the overall risk,” he added.

By offering free blood pressure tests to over 100,000 Nigerians in celebration of world heart day and later world stroke day coming up in October, Ikpeme said their goal is to join the global fight against cardiovascular diseases and minimise mortality, especially among young adult.

In his perspective, a blood pressure screening is important because high blood pressure usually has no symptoms and cannot be detected without being measured.

He noted, “High blood pressure is the number one risk factor for heart disease and often considered a silent killer.”

Experts have revealed that the primary causes of cardiovascular diseases are smoking, unhealthy diet, physical inactivity and the harmful use of alcohol which in turn show up in people as high blood pressure, high blood sugar and obesity.

His words, “Lifestyle changes including healthy eating, regular physical activity and quitting tobacco use are advised to improve heart health.”

Wellahealth is a health technology startup focused on providing affordable and accessible high-quality healthcare protection for all Africans.

A study in the United States demonstrates that mortality rates from heart failure are higher in counties where people face more poverty and social deprivation.

Heart failure, sometimes called congestive heart failure, is a chronic condition in which the heart is unable to pump enough blood around the body to meet its needs.

The condition is irreversible, although there are treatments that can help people live longer, more active lives.

About 5.7 million people in the U.S. have heart failure, according to the National Heart, Lung, and Blood Institute.

A new study suggests that the risk of dying from the condition is not spread evenly across the country, but that mortality rates are higher in poorer, more socially deprived areas.

Researchers at University Hospitals Cleveland Medical Center, OH, analyzed 1,254,991 deaths from heart failure across 3,048 counties between 1999 and 2018.

They used two standard indices of social deprivation: the Area Deprivation Index (ADI), which takes into account multiple local measures, including employment, poverty, and education, and the Social Deprivation Index (SDI), which is based on income and housing.

After adjusting for age, they found that the average death rate from heart failure per county was 25.5 deaths per 100,000 head of population.

However, counties with higher rates of socioeconomic deprivation had higher death rates from heart failure, and the association held up regardless of race or ethnicity, sex, and degree of urbanization.

The levels of deprivation that the ADI measures accounted for roughly 13% of the variability in heart failure mortality among counties. This scale of risk is similar to that of other recognized risk factors for heart failure, such as obesity and diabetes, say the scientists. Correlation with housing and income — the social factors that the SDI measures — accounted for 5% of this variability.

The study features in the latest issue of the Journal of Cardiac Failure.

Persistent inequality

The research revealed that the imbalance in survival rates between wealthy and deprived areas changed little between 1999 and 2018.

“Analysis of trends in heart failure mortality shows that these disparities have persisted throughout the last two decades,” says first author Dr. Graham Bevan, a resident physician at University Hospitals.

Bevan and his colleagues say that a range of factors may be responsible for the increased risk of dying from heart failure in poorer counties. These include reduced access to healthcare, substandard care, and poor health literacy.

They also note that the successful treatment of heart failure is dependent on patients adhering to a complex and often expensive drug regimen.

The authors write:

“Regardless of the contributing factors, the association between communities with high socioeconomic deprivation and [heart failure] mortality is strong and suggests that targeting social deprivation may be impactful in reducing [heart failure] mortality. Additionally, the yield of intensive [heart failure] preventive strategies may be higher in areas with high social deprivation.”

The American Heart Association (AHA) believe that aggressively tackling the major clinical risk factors for heart failure could significantly reduce the death toll. These clinical factors include hypertension, heart attacks, obesity, diabetes, and disorders of the heart valves.

“Living in a particular county should not mean you’re more likely to die from heart failure,” says co-author Dr. Sadeer G. Al-Kindi, a cardiologist at University Hospitals’ Harrington Heart and Vascular Institute.

“University Hospitals has a history of addressing healthcare disparities in underserved communities and, armed with the information from this study, we can thoughtfully create solutions to better serve these populations.”

One of the limitations of their study, the authors write, was that it relied on the information given on death certificates, which may not be accurate in every instance.

Also, the study was not designed to tease apart the effects of other recognized risk factors for heart failure mortality, some of which — such as lack of physical activity, obesity, diabetes, and high blood pressure — may also be associated with poverty. However, a recent study showed that these factors together failed to account for 57% of the geographical variation in deaths from heart failure among counties in the U.S.

This new study suggests that socioeconomic deprivation may help explain part of that variation.

A study links the consumption of ultra-processed foods with the shortening of the body’s telomeres.

Telomeres are structures located at the ends of our chromosomes. Although they contain no genetic information themselves, they preserve the integrity of chromosomes by keeping their ends from fraying, much as shoelace tips protect the laces.

Telomeres become shorter and less effective over time as chromosomes replicate. Scientists view them as markers of an individual’s biological age at a cellular level.

New research indicates that eating ultra-processed foods is linked to the accelerated shortening of telomeres and cell aging.

The researchers, from the University of Navarra in Pamplona, Spain, presented their findings at this year’s European and International Congress on Obesity (ECOICO 2020) in September.

The findings also feature in a study paper in The Americal Journal of Clinical Nutrition.

Lucia Alonso-Pedrero, who is a doctoral researcher at this university, led the study.

The rise of ultra-processed foods

The consumption of ultra-processed foods, or UPFs, is on the rise worldwide. UPFs are manufactured food products comprising the building blocks of naturally occurring foods: protein isolates, sugars, fats, and oils.

However, while their components are often extracted from natural sources, UPFs ultimately contain no, or very little, in the way of whole foods.

The companies that produce UPFs often add flavorings and emulsifiers for taste, as well as colorings and other cosmetic additives to achieve the desired appearance. UPFs are nutritionally poor and often unbalanced.

UPFs are highly profitable for their producers due to their inexpensive ingredients, cost effective manufacturing processes, and long shelf life in stores. What makes them so attractive to consumers is their convenience and their relative imperishability.

Previous research has not conclusively established a link between UPFs in general and telomere length (TL). However, researchers have noted associations between TL and alcoholsugar-sweetened beveragesprocessed meats, and foods high in saturated fat and sugar.

Other research indicates a UPF connection to several serious conditions, such as obesityhypertensiondepressionmetabolic syndrome, some types of cancer, and type 2 diabetes. However, these conditions also tend to be age-related and thus difficult to associate definitively with the consumption of UPFs.

UPFs and telomere length

The NOVA system classifies foods according to the degree of processing that their production involves, as opposed to their nutritional content. The goal of Alonso-Pedrero and her colleagues was to investigate the effect of UPF consumption in older adults using NOVA as a means of categorizing the foods that they consumed.

The researchers began their analysis with data from the SUN project, which the University of Navarra is conducting with other Spanish universities. The ongoing study began recruiting in 2000 and includes volunteers over the age of 20 years. Participants are required to fill out and return questionnaires every 2 years.

In 2008, all SUN participants over the age of 55 years took part in a genetic study that forms the foundation of the new research. A total of 886 individuals — 645 men and 241 women — provided saliva samples for DNA analysis and self-reported their daily food consumption. Their average age was 67.7 years.

The team sorted the participants into four groups of equal size, or quartiles, according to the number of UPF servings that they consumed daily:

  • low: under 2 servings
  • medium-low: 2–2.5 servings
  • medium-high: 2.5–3 servings
  • high: more than 3 servings

In terms of telomeres, Alonso-Pedrero and her colleagues detected a clear correspondence between TL and the consumption of UPFs.

The likelihood of shortened telomeres increased dramatically with the number of UPF servings, starting with the medium-low group. That group was 29% more likely to exhibit reduced TL, while the medium-high group was 40% more likely to do so. Those in the high group were 82% more likely to have shortened telomeres.

The study’s authors write:

“In this cross-sectional study of elderly Spanish subjects, we showed a robust strong association between UPF consumption and TL. Further research in larger longitudinal studies with baseline and repeated measures of TL is needed to confirm these observations.”

The researchers also made a number of general observations regarding those who consumed more than 3 servings of UPFs per day. People in this quartile:

  • were more likely to have diabetes, a family history of cardiovascular disease, and abnormal blood fats under their skin
  • were the participants most likely to snack between meals
  • consumed less protein, carbohydrate, fiber, fruit, vegetables, olive oil, and other micronutrients

Individuals who ate more UPFs were less likely to adhere to a healthful Mediterranean diet. In exchange, they consumed more fats, saturated fats, polyunsaturated fats, sodium, sugar-sweetened beverages, cholesterol, fast food, and processed meats.

The study authors also found that those who consumed higher amounts of UPFs were more likely to experience depression — especially when they were less active physically.

Finally, the findings linked the consumption of UPFs to excessive body weight, hypertension, and all-cause mortality.

Depending on the type of fats and oils, they can either be implicated in the development of a disease or one that can prevent diseases that may be caused by another kind of fat.

For instance, fats and oils have a very significant role to play concerning the health of the arteries, the heart, and the brain. This is occasioned by their involvement in the formation of arteriosclerosis. As we already are aware, this is the deposition of plaques on the arteries that eventually lead to the blockage of the vessels. The blockage of the vessels results in coronary artery disease, heart attack, and stroke.

The type of fats implicated in the formation of arteriosclerotic plaques is saturated fats, trans fats, cholesterol, and triglycerides.

As stated earlier, cholesterol is not appreciably water-soluble and to be transported in the bloodstream, which is predominantly water-based, it has to be bound to lipoproteins. Two major kinds of lipoproteins that we are interested in are the Low-Density Lipoprotein (LDL) and the High-Density Lipoprotein (HDL). When cholesterol is bound to LDL, we have what is known as LDL-Cholesterol. HDL bound to cholesterol is known as HDL-cholesterol. The LDL when bound to cholesterol is referred to as ‘bad’ LDL-cholesterol and if it is bound to HDL, it is known as ‘good’ HDL-cholesterol. Cholesterol is never bad or good but this description has been given because of the direction of transport of cholesterol when it is bound to the lipoproteins. The LDL, which transports cholesterol from the liver to the cells, increases the risk of plaque formation as cholesterol accumulates in the blood vessels. On the other hand, the HDL transports cholesterol from the cells to the liver where it is excreted in the bile. What this means, is that, if there is more HDL-cholesterol in circulation, the risk of arteriosclerosis and heart disease will be significantly reduced. When LDL-cholesterol becomes higher, therefore, the risk of arteriosclerosis and heart attack increases.

In considering what kind of fats and oils one should be eating, the effect of the diet on HDL or LDL must never be overlooked. For example, trans fats increase LDL-cholesterol and decrease HDL-cholesterol. Polyunsaturated and monounsaturated fatty acids represented by omega 3 and 6; increase HDL-cholesterol, while decreasing LDL-cholesterol. Saturated fats increase both the ‘bad’ LDL-cholesterol and the ‘good’ HDL-cholesterol.

We also need to remember that the consistency of the fats and oils differentiate between the animal fats and plant fats. Animal fats, mainly saturated fats are solid at room temperature, while the plant fats, more often referred to, as oils are liquid at room temperature. Trans fats, which are solid at room temperature, are partially hydrogenated fat and have been described as the worst kind of fat a human being can consume. Trans fats increase LDL-cholesterol and decrease HDL-cholesterol. Examples of common trans fats are margarine and shortening. These along with oils that are used for deep-frying of things such as potatoes and chicken should be avoided.

Saturated fats tend to increase the level of cholesterol in the blood and for this reason, nutritionists advise that this kind of fats, if not avoided completely should be eaten less frequently. To be sure, I have reproduced the sources of saturated fats as a guide for us: Fatty portions of red meat, pork, chicken, and turkey eaten with the skin, butter, dairy products such as whole milk, cheese, cream, and fried and baked foods. Some prepared foods, for example, sausage, pizza, and desserts are also high in saturated fats. There are certain oils from plants like palm oil, palm kernel oil, and coconut oil that are saturated fats but do not contain cholesterol.

The best kind of fatty acids are monounsaturated and polyunsaturated fatty acids. They both increase HDL-cholesterol and decrease LDL-cholesterol. They also reduce the risk of arteriosclerosis, coronary artery disease, heart attack, and stroke. Examples of these are omega 3 and 6 and they can be found in such plants as almonds, hazelnuts, macadamia nuts, peanuts, pecans, cashew nuts, avocados, and olives.

Polyunsaturated fats are predominantly found in flaxseed, walnuts (roasted), pumpkin seeds, sesame seeds, and sunflower seed. They are also found in freshwater fatty fish such as salmon, tuna, herring, sardines, mackerel, and trout.

As I bring this article to a close, the recommendation is: Eat more of the unsaturated fatty acids – omega 3 and 6, less of saturated fats, and none of the trans fats.

Scientists have found that eating a lot of rice increases the risk of dying from heart disease due to the naturally occurring arsenic in the crop.

Rice is the most widely consumed staple food source for a large part of the world’s population. It has now been confirmed that rice can contribute to prolonged low-level arsenic exposure leading to thousands of avoidable premature deaths per year.

Arsenic is well known acute poison, but it can also contribute to health problems, including cancers and cardiovascular diseases, if consumed at even relatively low concentrations over an extended period of time.

Compared to other staple foods, rice tends to concentrate inorganic arsenic. Across the globe, over three billion people consume rice as their major staple and the inorganic arsenic in that some to give rise to over 50,000 avoidable premature deaths per year has estimated rice.

Meanwhile, a study found Britons in the top 25 per cent of rice consumption are at six per cent increased risk of dying from cardiovascular disease than the bottom quarter.

The chemical gathers naturally in the crop and has repeatedly been linked to illness, dietary-related cancers and liver disease. In serious cases, it can result in death.

A collaborating group of cross-Manchester researchers from The University of Manchester and The University of Salford have published new research exploring the relationship, in England and Wales, between the consumption of rice and cardiovascular diseases caused by arsenic exposure.

Their findings, published in the journal Science of the Total Environment, showed that once corrected for the major factors known to contribute to cardiovascular disease (for example obesity, smoking, age, lack of income, lack of education) there is a significant association between elevated cardiovascular mortality, recorded at a local authority level, and the consumption of inorganic arsenic bearing rice.

Prof. David Polya from The University of Manchester said: “The type of study undertaken, an ecological study, has many limitations, but is a relatively inexpensive way of determining if there is plausible link between increased consumption of inorganic arsenic bearing rice and increased risk of cardiovascular disease.

“The modelled increased risk is around six per cent (with a confidence interval for this figure of two per cent to 11 per cent). The increased risk modelled might also reflect in part a combination of the susceptibility, behaviours and treatment of those communities in England and Wales with relatively high rice diets.”

While more robust types of study are required to confirm the result, given many of the beneficial effects otherwise of eating rice due to its high fibre content, the research team suggest that rather than avoid eating rice, people could consume rice varieties, such as basmati, and different types like polished rice (rather whole grain rice) which are known to typically have lower inorganic arsenic contents. Other positive behaviours would be to eat a balanced variety of staples, not just predominately rice.

Arsenic occurs naturally in the soil and is increased in locations that have used arsenic-based herbicides or water laced with the toxin for irrigation purposes.

Rice is grown under flooded conditions and this draws arsenic out of the soil and into the water, ahead of eventual absorption by the plants.

Rice is particularly vulnerable because arsenic mimics other chemicals the plant absorbed via its root system, allowing the toxin to bypass the plant’s defences.

Rising temperatures caused by global warming could cause the amount of arsenic in rice to triple by the end of the century, a new study warns.

Scientists at the University of Washington in the US grew rice and replicated various temperatures to mimic growing conditions under various global warming projections.

Trials were done at the current normal temperature of 77°F (25°C) as well as 82°F (28°C), 87°F (30.5°C), and 91°F (33°C) to mimic potential climates by 2100. Plants grown in warmer conditions were found to have higher levels of arsenic throughout the plant – including the grains.

MEANWHILE, rice is about the commonest, cheapest and easiest staple food prepared not only by Nigerian households but in most parts of the world as well.

Indeed, statistics from the United Nations Food and Agricultural Organisation (FAO) indicate that half the world’s population eats rice every day, making the staple a major source of nutrition for billions of people.

But recent studies have associated the much-loved staple with rise in chronic and degenerative diseases such as cancer, diabetes, gastrointestinal problems, depression, developmental problems in children, heart disease and nervous system damage.

Most worrisome are lung and bladder cancers.While researchers have found traces of arsenic from old industrial pesticides on rice grains sold globally, a study reported in the journal PLoS ONE, showed rice has 10 times more inorganic arsenic than other foods and the European Food Standards Authority has reported that people who eat a lot of it are exposed to troubling concentrations.

According to the study, the levels of arsenic in rice vary by type, country of production and growing conditions.Generally, brown rice has higher levels because the arsenic is found in the outer coating or bran, which is removed in the milling process to produce white rice.

The study noted that in the short term, the regular consumption of rice could cause gastrointestinal problems, muscle cramping and lesions on the hands and feet.

The researchers observed that the risk of arsenic poisoning is greatest for people who eat rice several times a day, and for infants, whose first solid meals are often rice-based baby food.

In July 2014, the World Health Organisation (WHO) set worldwide guidelines for what it considers to be safe levels of arsenic in rice, suggesting a maximum of 200 microgrammes per kilogramme for white rice and 400 μg kg−1 for brown rice.

Also, scientists have identified rice as one of the staple diets that are genetically modified (GMOs). Others include corn, soy, cotton, papaya (pawpaw), tomatoes, rapeseed, dairy products, potatoes, and peas.

GMOs are accused of causing cancer, destroying the environment and storing up devastating health risks for children. Controversies surround genetically modified organisms on several levels, including ethics, environmental impact, food safety, product labeling, and role in meeting world food requirements, intellectual property and role in industrial agriculture.

An online journal, China Daily, reported potential serious public health and environment problems with genetically modified rice considering its tendency to cause allergic reactions with the concurrent possibility of gene transfers.

Scientists including the American Academy of Environmental Medicine (AAEM) have warned that GMOs pose a serious threat to health, and it is no accident that there can be a correlation between it and adverse health effects.

In fact, the AAEM has advised doctors to tell their patients to avoid GMOs as the introduction of GMOs into the current food supply has correlated with an alarming rise in chronic diseases and food allergies.

It has been shown that eating a diet of white bread and rice could increase the risk of depression in older women, but whole grain foods, roughage and vegetables could reduce it.

According to a study published in The American Journal of Clinical Nutrition, refined foods cause blood sugar levels to spike rapidly – prompting the body to pump out the hormone insulin, which helps break down the sugar. But this process can cause symptoms of depression. The findings could pave the way for depression being treated and prevented using nutrition.

In a study that included data from more than 70,000 post-menopausal women, scientists found a link between refined carbohydrate consumption and depression.

Britain’s leading expert on rice and contamination, Andy Meharg, a professor of plant and soil sciences at Queens University in Belfast, prevented his own children from eating some rice products because of the arsenic levels.

Meharg said the current method for cooking rice, essentially boiling it in a pan until it soaks up all the liquid, binds into place any arsenic contained in the rice and the cooking water.

By contrast, cooking it in a coffee percolator allows the steaming hot water to drip through the rice, washing away contaminants. There was a 57per cent reduction in arsenic with a ratio of 12 parts of water to one of rice and in some cases as much as 85per cent.

Meharg said: “Rice both white and brown are of good nutritional value. Brown rice especially contains E and B vitamins and minerals such as iron, calcium, magnesium, phosphorus, potassium, sodium and zinc.

“White rice is not that good. More so the processed one that is genetically modified has higher levels of toxins.

“Firstly when you cook rice, rinse properly when it is warm before full boiling, and drain out the fluid. This will get rid of some of the toxins.”

Study author Dr. James Gangwisch, of Columbia University, United States, said: “This suggests that dietary interventions could serve as treatments and preventive measures for depression.

“Further study is needed to examine the potential of this novel option for treatment and prevention, and to see if similar results are found in the broader population.”

White refined foods, known as ‘bad carbs’, have also been said to contribute to obesity, low energy levels and insomnia. Different from their healthier counterparts, white carbs start with flour that has been ground and refined by stripping off the outer layer where fibre is found.

This missing fibre could do wonders for the body, helping reduce the risk of type 2 diabetes, lower blood cholesterol and help people feel fuller for longer. Generally, the more refined the grain-based food, the lower the fibre count. By purchasing organic rice, limiting one’s rice intake and eating a balanced diet, however, experts suggest that health issues associated with long-term arsenic consumption can be avoided.

People of African descent have up to three times the risk of dying from strokes as people of European descent, yet there has been little investigation of if and how genetic variants contribute to their elevated stroke risk.

A large international team of scientists has completed the largest analysis of stroke-risk genes ever undertaken in individuals of African descent. The new study examined the genomes of more than 22,000 people of African ancestry, identifying important genetic contributors to stroke risk. These findings will help doctors better understand stroke risk, identify those at high risk and prevent the debilitating condition.

“Given the undue burden that people of African ancestry endure from stroke and other cerebrovascular disease, the lack of investigation of risk factors in this group has been a substantial gap,” said researcher Bradford B. Worrall, MD, a neurologist at University of Virginia (UVA) Health System, United States of America (USA). “Our work is an important step toward filling that gap, albeit with much more work to be done. These findings will provide greater insight into ethnic-specific and global risk factors to reduce the second leading cause of death worldwide.”

Stroke is the leading cause of adult disability in the United States. But strokes strike African-Americans more often and at younger ages than people of European descent. In addition, African-Americans who survive strokes often face greater disability. Family history is a major risk factor for stroke, suggesting our genes play a significant role in our stroke risk. But most genetic stroke studies, until now, have primarily focused on people of European descent. And the results have not always held true in African-Americans.

The new meta-analysis comes from the Consortium of Minority Population genome-wide Association Studies of Stroke (COMPASS). The researchers revisited previous studies to identify genetic risk factors specific to people of African descent. In total, they examined the genomes of 3,734 people who had suffered strokes and more than 18,000 who had not.

The researchers discovered that a common variation near the HNF1A gene was strongly associated with increased stroke risk in those of African ancestry. The gene previously has been associated to both stroke and cardiovascular disease.

While that variant had the strongest link to stroke risk, the researchers identified 29 other variants that also appear likely to influence stroke risk.

The variants occur at 24 different locations on human chromosomes. Sixteen of the “loci,” as the locations are known, appeared also to influence stroke risk in other populations, the researchers report.

“Studies of this nature are critical given the paucity of genetic studies focused on people of African descent and other minority populations and the substantial health disparities related to stroke in these groups,” said Keith Keene, PhD, a former UVA researcher and frequent collaborator of Worrall’s who now leads the Center for Health Disparities at East Carolina University’s Brody School of Medicine.
“Furthermore, we increasingly recognize the power of looking at genetic risk factors across different race ethnic groups, known as trans-ethnic analyses, for unlocking the underlying biology of diseases like stroke. If we understand the biology, we can develop new treatment and prevention strategies.”

In a paper outlining their findings, the researchers note the importance of such studies in understanding stroke risk among minorities. These studies have “huge potential to provide insight into the mechanisms underlying stroke disparities,” the researchers write. “Our study identified novel associations for stroke that might not otherwise be detected in primarily European cohort studies. Collectively, this highlights the critical nature and importance of genetic studies in a more diverse population with a high stroke burden.”

Leptospirosis is a bacterial disease that affects humans and animals. Bacteria of the genus Leptospira cause it. In humans, it can cause a wide range of symptoms, some of which may be mistaken for other diseases. Some infected persons, however, may have no symptoms at all.

Without treatment, Leptospirosis can lead to kidney damage, meningitis (inflammation of the membrane around the brain and spinal cord), liver failure, respiratory distress, and even death.
Infection

The bacteria that cause leptospirosis are spread through the urine of infected animals, which can get into water or soil and can survive there for weeks to months. Many different kinds of wild and domestic animals carry the bacterium.

These can include, but are not limited to: cattle, pigs, horses, dogs, rodents, and wild animals. When these animals are infected, they may have no symptoms of the disease.

Infected animals may continue to excrete the bacteria into the environment continuously or every once in a while for a few months up to several years. Humans can become infected through: contact with urine (or other body fluids, except saliva) from infected animals and contact with water, soil, or food contaminated with the urine of infected animals.

The bacteria can enter the body through skin or mucous membranes (eyes, nose, or mouth), especially if the skin is broken from a cut or scratch. Drinking contaminated water can also cause infection. Outbreaks of leptospirosis are usually caused by exposure to contaminated water, such as floodwaters. Person to person transmission is rare.
Sign and symptoms

In humans, Leptospirosis can cause a wide range of symptoms, including: high fever, headache, chills, muscle aches, vomiting, jaundice (yellow skin and eyes), red eyes, abdominal pain, diarrhea, and rash.

Many of these symptoms can be mistaken for other diseases. In addition, some infected persons may have no symptoms at all.The time between a person’s exposure to a contaminated source and becoming sick is two days to four weeks. Illness usually begins abruptly with fever and other symptoms. Leptospirosis may occur in two phases: after the first phase (with fever, chills, headache, muscle aches, vomiting, or diarrhea) the patient may recover for a time but become ill again; and if a second phase occurs, it is more severe; the person may have kidney or liver failure or meningitis.

The illness lasts from a few days to three weeks or longer. Without treatment, recovery may take several months.
Prevention

The risk of acquiring leptospirosis can be greatly reduced by not swimming or wading in water that might be contaminated with animal urine, or eliminating contact with potentially infected animals. Protective clothing or footwear should be worn by those exposed to contaminated water or soil because of their job or recreational activities.
Prevention

Leptospirosis is treated with antibiotics, such as doxycycline or penicillin, which should be given early in the course of the disease. Intravenous antibiotics may be required for persons with more severe symptoms. Persons with symptoms suggestive of leptospirosis should contact a health care provider.

New research has identified a possible mechanism for blood clotting issues in some COVID-19 patients.

A new study suggests a possible mechanism for the elevated presence of blood clots in COVID-19 patients.

The research, published in the journal Circulation, may help clinicians develop more effective treatments for COVID-19.

The sudden emergence and rapid global spread of the new coronavirus have meant clinical responses have focused on supporting those with severe infections, supplemented with emergency societal interventions, such as widespread social distancing, to reduce infection rates.

Because SARS-CoV-2 is a new virus, previous treatments developed for similar strains will not necessarily work. Instead, possible therapies need to be identified in theory, tested and, once safe, implemented in the real world. However, this all takes time.

SARS-CoV-2 is mainly a danger because for some patients — particularly those with certain underlying health conditions, compromised immune systems, or who are later in life — a type of severe acute respiratory syndrome can develop, similar to pneumonia.

COVID-19, the disease caused by the virus, makes a person’s lungs inflamed.

COVID-19 and coagulation

According to an interview in The Guardian with Prof. John Wilson, president-elect of the Royal Australasian College of Physicians, if this inflammation is severe, inflammatory material can collect in the bottom of a person’s lungs. This can make it difficult for them to gain enough oxygen into their blood, cause organs to shut down, and potentially lead to death.

However, in addition to this pneumonia-like reaction, clinicians have also noticed that patients with COVID-19 can develop organ damage in a way not directly linked to a lack of oxygen in the blood. This is particularly common in the kidneys and heart.

There is some evidence that a problem with blood coagulation causes this organ damage. Coagulation is the process where a person’s blood thickens. It is crucial in stopping a person from bleeding if they get a cut.

However, if a person’s blood coagulates too much or too little, they can have serious issues: too little, and they can develop internal or external bleeding, as seen in hemophilia. Too much and they could develop blood clots that can cause a stroke or heart attack.

The authors of the recent study note that COVID-19 may increase coagulation in some people’s blood, which consequently causes organ damage as blood vessels become blocked. However, it is not yet clear how or why this occurs, which impedes the development of effective treatments.

Neutrophils and platelets

In the study, the researchers studied 62 patients, including autopsies on five of whom had died. Of these individuals, 38 had confirmed COVID-19.

After conducting multidimensional flow cytometry — a way of measuring the presence of particular cells in a fluid — and comparing these results to the control groups, the researchers identified a significant number of neutrophils and platelets in the subjects.

Neutrophils are a type of immune cell that combat pathogens entering the body, such as the SARS-CoV-2 virus, while platelets are a type of blood cell necessary for coagulation.

The researchers found that these two cells seemed to react to and activate one another, resulting in excessive coagulation, blockage of blood vessels, and serious damage to nearby tissue.

Furthermore, when activated, the neutrophils exude web-like structures designed to help them trap bacteria, but experts believe they exacerbate the blocking of blood vessels.

According to Dr. Konstantin Stark, of the University Hospital Ludwig-Maximilian-University Munich, Germany, and a co-author of the paper:

“These findings contribute to a better understanding of the pathophysiology that underlie disease progression in COVID-19. The study also identifies immunothrombosis as a promising target for the prevention and treatment of lung failure and thrombotic complications that arise in cases of COVID 19.”

Thanks to advanced medical treatments, women diagnosed with breast cancer today will likely survive the disease. However, some treatment options put these women at greater risk for a number of other health problems.

A new study out of Brazil shows that postmenopausal women with breast cancer are at greater risk for developing heart disease. Results are published online in Menopause, the journal of The North American Menopause Society (NAMS).

Cardiovascular disease remains the main cause of death in postmenopausal women, and women treated for breast cancer are at greater risk of developing heart disease than those not diagnosed with breast cancer. These cardiovascular effects may occur more than five years after radiation exposure, with the risk persisting for up to 30 years.

The goal of the new study was to compare and evaluate risk factors for cardiovascular disease in postmenopausal women who are survivors of breast cancer and women without breast cancer. The researchers found that postmenopausal women who are survivors of breast cancer showed a markedly stronger association with metabolic syndrome, diabetes, atherosclerosis, hypertriglyceridemia, and abdominal obesity, which are major risk factors for cardiovascular disease. The risk of cardiovascular mortality similarly increased to match death rates from the cancer itself.

Findings were published in the article “High risk for cardiovascular disease in postmenopausal breast cancer survivors.”

“Heart disease appears more commonly in women treated for breast cancer because of the toxicities of chemotherapy, radiation therapy, and use of aromatase inhibitors, which lower estrogen. Heart-healthy lifestyle modifications will decrease both the risk of recurrent breast cancer and the risk of developing heart disease,” says Dr. JoAnn Pinkerton, NAMS executive director. “Women should schedule a cardiology consultation when breast cancer is diagnosed and continue with ongoing follow-up after cancer treatments are completed.”