How alcohol causes dementia

Alcohol use disorders are the most important preventable risk factors for the onset of all types of dementia, especially early-onset dementia. This according to a nationwide observational study of over one million adults diagnosed with dementia in France.

This study looked specifically at the effect of alcohol use disorders and included people who had been diagnosed with mental and behavioural disorders or chronic diseases that were attributable to chronic harmful use of alcohol. Of the 57,000 cases of early-onset dementia (before the age of 65), the majority (57%) were related to chronic heavy drinking.

The World Health Organization (WHO) defines chronic heavy drinking as consuming more than 60 grams pure alcohol on average per day for men and 40 grams per day for women. Heavy drinking and alcohol use disorders are the most important risk factors for dementia, and especially important for those types of dementia which start before age 65, and which lead to premature deaths," says study co-author and Director of the CAMH Institute for Mental Health Policy Research Dr. Jürgen Rehm.

Alcohol-induced brain damage and dementia are preventable, and known-effective preventive and policy measures can make a dent into premature dementia deaths. Alcohol use disorders shorten life expectancy by more than 20 years, and dementia is one of the leading causes of death. For early-onset dementia, there was a significant gender split.

Alcohol use disorders were also associated with all other independent risk factors for dementia onset, such as tobacco smoking, high blood pressure, diabetes, lower education, depression, and hearing loss, among modifiable risk factors. It suggests that alcohol use disorders may contribute in many ways to the risk of dementia.
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Molecule could prevent prediabetes

Levels of CoQ and the presence of insulin resistance were analysed in a range of experimental laboratory settings, mouse models and samples from humans, as part of an ambitious research collaboration conducted with the University of Sydney, Victor Chang Cardiac Research Institute, Duke University School of Medicine, Garvan Institute of Medical Research, Genentech Inc. and the University of New South Wales.

Concentrations of CoQ were found to be lower in insulin resistant body fat and muscle tissue. When the researchers replenished CoQ, insulin resistance or pre-diabetes was reversed. Co-author Dr Daniel Fazakerley from the University of Sydney's School of Life and Environmental Science and Charles Perkins Centre said CoQ provides a vital role in converting nutrients like fat and sugar into usable energy.

CoQ is found in mitochondria, the power plants in the cells of human body, where it is required for the flow of electricity to the cell's 'motor' which is responsible for energy production. Energy production can also generate reactive chemical species-often referred to as 'reactive oxygen species' or 'oxidants' as by-products, which can be damaging to cells. Previous studies have shown that these oxidants can cause insulin resistance. Our study has found that lower mitochondrial CoQ enhanced oxidant formation by mitochondria.

Replenishing CoQ in mitochondria, either in cells or in animals, we were able to restore 'normal' mitochondrial oxidants and reverse insulin resistance. Eating a high fat, high sugar diet has long been known to be a major risk factor for obesity and pre-diabetes. Replenishing CoQ could prove an invaluable preventive measure for insulin resistance- or pre-diabetes-linked diseases such as type 2 diabetes, cardiovascular disease, cancers and dementia.

However, oral CoQ supplements may not effectively restore mitochondrial CoQ due to its low absorption. The research has provided an impetus to find alternate means of increasing CoQ in mitochondria to treat insulin resistance and pre-diabetes. If not an external supplement, perhaps we can stimulate the body to form more of the coenzyme itself.
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MIND diet for cognitive decline

A diet created by researchers at Rush University Medical Center may help substantially slow cognitive decline in stroke survivors, according to preliminary research to the general population. The diet, known as the MIND diet, is short for Mediterranean-DASH Diet Intervention for Neurodegenerative Delay. The diet is a hybrid of the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets. Both have been found to reduce the risk of cardiovascular conditions such as hypertension, heart attack and stroke.

The foods that promote brain health, including vegetables, berries, fish and olive oil, are included in the MIND diet, the diet has slow cognitive decline in stroke survivors. MIND diet based on information from years of research about what foods and nutrients have good, and bad, effects on the functioning of the brain. The diet has been associated with reduced Alzheimer's risk in seniors who adhered to its recommendations. Even people who moderately adhered had reduced risk of Alzeimeir's disease D and cognitive decline.

The MIND diet has 15 dietary components, including 10 "brain-healthy food groups" and five unhealthy groups-red meat, butter, cheese, pastries and sweets, and fried or fast food. To benefit from the MIND diet, a person would need to eat at least three servings of whole grains, a green leafy vegetable and one other vegetable every day along with a glass of wine, snack most days on nuts, have beans every other day or so, eat poultry and berries at least twice a week and fish at least once a week. The diet also specifies limiting intake of the designated unhealthy foods, limiting butter to less than half teaspoons a day and eating less than 5 servings a week of sweets and pastries, and less than one serving per week of whole fat cheese, and fried or fast food.

From 2004 to 2017, Cherian and colleagues studied 106 participants of the Rush Memory and Aging Project who had a history of stroke for cognitive decline, including decline in one's ability to think, reason and remember. They assessed people in the study every year until their deaths or the study's conclusion, for an average of 5.9 years, and monitored patients' eating habits using food journals.
The researchers grouped participants into those who were highly adherent to the MIND diet, moderately adherent and least adherent. They also looked at additional factors that are known to affect cognitive performance, including age, gender, education level, participation in cognitively stimulating activities, physical activity, smoking and genetics.

The study participants whose diets scored highest on the MIND diet score had substantially slower rate of cognitive decline than those who scored lowest. The estimated effect of the diet remained strong even after taking into account participants' level of education and participation in cognitive and physical activities. In contrast to the results of slower decline with higher MIND diet score, stroke survivors who scored high on the Mediterranean and DASH diets, did not have significant slowing in their cognitive abilities.

The Mediterranean and DASH diets have been shown to be protective against coronary artery disease and stroke, but it seems the nutrients emphasized in the MIND diet may be better suited to overall brain health and preserving cognition. According to Cherian, studies have found that folate, vitamin E, omega-3 fatty acids, carotenoids and flavonoids are associated with slower rates of cognitive decline, while substances such as saturated and hydrogenated fats have been associated with dementia.
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How to live longer

Many cells in human body, such as those which make up brain need to last a lifetime. To do this human cells have developed ways of protecting themselves. One way is through a process called autophagy, which literally means self-eating, where damaged components are collected together and removed from the cell.This is very important as accumulation of damage in cells has been linked to several diseases including dementia.

Lead author, Dr Viktor Korolchuk explains: "As we age, we accumulate damage in our cells and so it is thought that activating autophagy could help us treat older people suffering from dementia. In order to be able to do this we need to understand how we can induce this cell cleaning." In this study the authors were able to identify how a protein called p62 is activated to induce autophagy. They found that p62 can be activated by reactive oxygen species (ROS). ROS are by-products of our metabolism that can cause damage in the cell.

This ability of p62 to sense ROS allows the cell to remove the damage and to survive this stress. In lower organisms, such as fruit flies, p62 is not able to do this. The team identified the part of the human p62 protein which allows it to sense ROS and created genetically modified fruit flies with 'humanised' p62. These 'humanised' flies survived longer in conditions of stress. Abilities like sensing stress and activating protective processes like autophagy may have evolved to allow better stress resistance and a longer lifespan.

Specific mutations in human p62, which cause a neurodegenerative disease called amyotrophic lateral sclerosis (ALS), can prevent activation of p62 by ROS. These cells are then unable to induce protective autophagy, and the authors explain that this could underlie the premature death of neurons in patients with this devastating age-related disease. In contrast, 'humanised' p62 fruit flies did not live longer suggesting that other mechanisms may be required. The research demonstrates that a collection of small adaptations like that of human p62 could have accumulated over time and these adaptations could underlie our increased natural defences and longer lifespans. The discovery of these adaptations allows a better understanding of how to treat age-related diseases.
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Eating at the same time regularly may fight dementia

 Regular meals improve gene expression in the region of the brain associated with body control, which often degenerates in Huntington's disease (HD); a form of dementia. Such eating habits also boost sleep quality and heart health, which are related to HD, in mice with the condition. Researchers believe the findings will also apply to humans and may improve the quality of life for patients with such incurable diseases.

Study author Professor Christopher Colwell, from The University of California, LA, said: 'HD is a genetically caused disease with no known cure.'  Lifestyle changes does not only improve the quality of life but also delay disease progression for HD patients are greatly needed. One group of mice were given food during a six-hour period when they were most active, which is at night as the animals are nocturnal.

The remainder ate whenever they liked. The quantity of food was the same between both groups. Professor Colwell said: 'In humans, the time of food availability would be during the day when food is normally consumed while the fast would be extended past the normal night. 'Feeding schedules play a role in the treatment of Huntington's disease'. Results reveal regular meal plans improve gene expression in the region of the brain associated with body control, known as the striatum, which often degenerates in HD.

Such eating habits also improve diseased mice's ability to run on a treadmill and balance on a beam, as well as assisting their heart rate, which is a sign of cardiovascular health. After three months of treatment, when mice reached the early disease stage, they showed improvements in their locomotor activity rhythm and sleep awakening time. The eating pattern  improved their heart rate variability, suggesting their nervous system dysfunction was improved.

Treated mice exhibited improved motor performance compared to untreated controls, this suggests feeding schedules could play a role in the treatment of HD and could lead to the development of new treatment options for neurodegenerative disorders. Regular meals boost gene expression in the brain region associated with body control. HD is a genetically caused disease with no known cure.

Lifestyle changes can improve the quality of life and delay disease progression for HD patients. Lifestyle interventions have been suggested to be preventative and therapeutic for diseases associated with ageing, such as type-2 diabetes, cardiovascular disease and neurodegenerative disorders.
Caloric restriction can prolong life span and protect against a variety of pathological conditions.
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Lack of sleep increases the levels of Alzheimer's protein

Chronic poor sleep has been linked to cognitive decline, and a new study from Washington University School of Medicine in St. Louis explains why: As a wakeful brain churns away through the night, it produces more of the Alzheimer's protein amyloid beta than its waste-disposal system can handle. Levels of the protein rise, potentially setting off a sequence of changes to the brain that can end with dementia.

This study is the clearest demonstration in humans that sleep disruption leads to an increased risk of Alzheimer's disease through an amyloid beta mechanism, the study showed that it was due to overproduction of amyloid beta during sleep deprivation. Sleeping poorly increases levels of brain proteins such as amyloid beta that are linked to Alzheimer's disease. But it wasn't clear why amyloid beta levels rise in a tired brain.

Neurologist studied eight people ages 30 to 60 with no sleep or cognitive problems. The participants were assigned randomly to one of three scenarios: having a normal night's sleep without any sleep aids ; staying up all night; or sleeping after treatment with sodium oxybate, a prescription medication for sleep disorders. Sodium oxybate increases slow-wave sleep-the deep, dreamless phase of sleep that people need to wake up feeling refreshed.

Each scenario occurred during 36 hours of monitoring, starting in the morning and continuing through the afternoon of the following day. The researchers took samples of the fluid that surrounds the brain and spinal cord every two hours to monitor how amyloid beta levels change with time of day and tiredness. All eight participants returned four to six months later to undertake a second scenario, and four people completed all three. Studying the same people under different conditions provides the statistical power to detect changes in amyloid beta levels.

Amyloid beta levels in sleep-deprived people were 25 to 30 percent higher than in those who had slept the night through. After a sleepless night, amyloid beta levels were on par with the levels seen in people genetically predisposed to develop Alzheimer's at a young age. brain changes. The brains of people with Alzheimer's disease are dotted with such plaques. Amyloid beta is a byproduct of normal brain activity.

The researchers found that when people stay awake, their brains continue to produce amyloid beta through the night. A sleeping brain produces much less. Asleep or awake, however, the brain clears the protein away at the same rate, so the increased production during sleep deprivation leads to higher levels of the damaging protein.
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Exercise improves memory and thinking

Mild cognitive impairment is an intermediate stage between the expected cognitive decline of normal aging and the more serious decline of dementia. Symptoms can involve problems with memory, language, thinking and judgment that are greater than normal age-related changes. Generally, these changes aren't severe enough to significantly interfere with day-to-day life and usual activities.

 A new guideline for medical practitioners says they should recommend twice-weekly exercise to people with mild cognitive impairment to improve memory and thinking. However, mild cognitive impairment may increase the risk of later progressing to dementia caused by Alzheimer's disease or other neurological conditions.

But some people with mild cognitive impairment never get worse, and a few eventually get better. Engaging in aerobic exercise like walking briskly, jogging, whatever you like for more than 100 minutes a week can improve memory. The level of exertion should be enough to work up a bit of a sweat but doesn't need to be so rigorous that you can't hold a conversation. Exercising might slow down the rate at which you would progress from mild cognitive impairment to dementia.
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Urea in the brain causes dementia

 The build-up of urea in the brain to toxic levels can cause brain damage - and eventually dementia. Metabolic linkages between Huntington's, other neurodegenerative diseases and type-2 diabetes. Huntington's Disease - one of seven major types of age-related dementia - is directly linked to brain urea levels and metabolic processes. Urea is similarly linked to Alzheimer's disease.

The Huntington's study also showed that the high urea levels occurred before dementia sets in, which could help doctors to one day diagnose and even treat dementia, well in advance of its onset. Urea and ammonia in the brain are metabolic breakdown products of protein. Urea is more commonly known as a compound which is excreted from the body in urine. If urea and ammonia build up in the body because the kidneys are unable to eliminate them, for example, serious symptoms can result.

Alzheimer's and Huntington's are at opposite ends of the dementia spectrum. Dementia results in a progressive and irreversible loss of nerve cells and brain functioning, causing loss of memory and cognitive impairments affecting the ability to learn. Currently, there is no cure.

The team used human brains, donated by families for medical research, using cutting-edge gas chromatography mass spectrometry to measure brain urea levels. For levels to be toxic urea must rise 4-fold or higher than in the normal brain. Treating this metabolic state in the brain may help in the regeneration of tissue that can reverse dementia.
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Education reduces the risk of Alzheimer's disease

The theory that education protects against Alzheimer's disease has been given further weight by new research. Alzheimer's disease is the leading cause of dementia. Building of 'plaques' and 'tangles' of misshapen proteins lead to the gradual death of brain cells. People affected by Alzheimer's experience memory and communication problems, disorientation, changes in behavior and progressive loss of independence.

The causes of Alzheimer's are largely unknown, and attempts to develop drug treatments to stop or reverse its effects have been disappointing. This has led to increasing interest in whether it is possible to reduce the number of cases of Alzheimer's disease by tackling common risk factors that can be modified.

Many studies have shown that the more years spent in full time education, the lower the risk of Alzheimer's. But it is difficult to unravel whether this is an effect of education improving brain function, or whether it's the case that people who are more educated tend to come from more wealthy backgrounds and therefore have a reduction in other risk factors that cause Alzheimer's disease.

Researchers examined looking DNA and compared genes associated with environmental risk factors – for example, genes linked to educational attainment or to smoking – and seeing which of these genes are also associated with Alzheimer's disease. If a gene is associated with both, then it provides strong evidence that this risk factor really does cause the disease. Researchers studied genetic variants that increase the risk of a variety of different environmental risk factors to see if these were more common in patients with Alzheimer's disease. They found the strongest association with genetic variants that predict higher educational attainment.

This provides further strong evidence that education is associated with a reduced risk of Alzheimer's disease, improving education could have a significant effect on reducing the number of people who suffer from this devastating disease. Exactly how education might reduce the risk of Alzheimer's is uncertain.

Previous studies have shown that the same amount of damage in the brain is associated with less severe and less frequent Alzheimer's in people who have received more education. One possible explanation is the idea of 'cognitive reserve' – the ability to recruit alternative brain networks or to use brain structures or networks not normally used to compensate for brain ageing. Evidence suggests that education helps improve brain wiring and networks and hence could increase this reserve.
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Intense workout can improve memory

The latest study showed that six weeks of 20-minute bouts of interval training led to significant improvements in high-interference memory. Researchers discovered that these workouts led to increases in a protein involved in the growth, function and survival of brain cells.

Intense workout could reduce the rates of Alzheimer's disease and other types of dementia, improvements in this type of memory from exercise might help to explain the previously established link between aerobic exercise and better academic performance. Intense workout prevents memory impairment brought on by conditions such as dementia.
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HIV treatment prevents cognitive decline

HIV-positive patients have the same risk of dementia as any other person if they take viral-suppressing medication and live a healthy lifestyle. One of the most debilitating effects of HIV is the neurocognitive decline, which can range from memory and language issues to dementia. Until now, research suggested that even those who take anti-retroviral therapy, the viral suppressing drug, had a higher risk of brain disorders than the general population.

Those who successfully suppress their viral load and live healthily have the same lifetime risk of dementia and other brain disorders as any other person. Older patients' brains may already have been ravaged by the disease, and medication couldn't reverse the damage, which would typically trigger symptoms within three or four years.

Researchers examined adults with HIV treated with cART with good viral suppression as well as those who did not have HIV for comparison. Both groups were about half women, with an average age of around 48 for the HIV-positive adults and 51 for the HIV-negative adults. Over the course of two years, the researchers assessed their brain changes using MRI scans.

They focused on the cortical thickness and subcortical volumes. They also assessed their cognitive performance using neuropsychological assessments. Those with HIV had poorer cognition and reduced brain thickness and volume than adults without HIV. However, by the end of the study, there were barely any differences between the two groups.
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Air pollution increases the risk of untimely death

Air pollution could cause brittle bone disease, according to new research. The study linked pollution exposure to low levels of parathyroid hormone, which regulates calcium production, leading to weaker bones and more hospitalizations for fractures. Smog-filled towns and cities have been linked to an increased risk of stroke, heart disease, lung cancer, acute respiratory diseases such as asthma and dementia.

The pollutant particle was linked to higher levels of parathyroid hormone, a small rise in PM2.5 concentrations would lead to an increase in bone fractures in older adults. Those living in areas high in PM2.5 and black carbon from heavy traffic had lower levels of parathyroid hormone, which is key to building calcium, and less bone mineral density than others exposed to less of the pollutants.

Osteoporosis, the most common reason for a broken bone among the elderly, is a disease in which bones become brittle and weak as the body loses more bone mass than it can rebuild. Particulate matter, including PM2.5, is known to cause systemic oxidative damage and inflammation, which they suggest, could accelerate bone loss and increase risk of bone fractures in older individuals. Smoking which contains several particulate matter components has been consistently associated with bone damage.

Within a year of a bone fracture, death risks for older individuals increase by up to 20 percent, with only 40 percent regaining full independence. Vitamin B can reduce pollution fueled cardiovascular disease, and damage to DNA. The best way to prevent air-pollution-related diseases is through policies to improve air quality. Air pollution is considered the most important risk factor for mortality at the population level, it is also a risk factor for osteoporosis.
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Stress can shrink the brain

Stress management is a critical and often misunderstood aspect of a brain-healthy lifestyle. Regardless of your degree of risk of developing dementia, stress reduction is crucial to overall health and happiness. Some forms of stress are good for brain -these are purposeful actions that bolster brain reserves, making the brain stronger and more resilient. Unrelenting and uncontrolled stress can destroy the brain and it can start at any age.

Neglect and emotional abuse sustained at a young age have been associated with memory deficits in adulthood. A process called ‘myelination’ by which the neuron’s connections are coated with a protective fatty membrane called myelin to ensure effective communication starts before the age of five and continues into early twenties.

Stress has been shown to significantly affect growth in developing brains, and lower cognitive resilience in childhood-myelination was inefficient or incomplete, which could increase the risk of developing dementia. Stress puts the body in overdrive and subsequently increases the level of stress hormones- cortisol.

These affect blood sugar levels and cause damaging long-term problems such as anxiety, depression, disrupted sleep and depressed immune function, which then makes us more vulnerable to infections and increases the risk of Alzheimer’s disease.

Stress affects each of us differently, but our brains are vulnerable. Studies show chronic stress decreases levels of the crucial protein responsible for the production of new brain cells. It puts the brain in a state of high inflammation, causing structural damage and impairing its ability to clear harmful waste products.

Uncontrolled stress initiates a hormonal cascade that taxes the brain on many levels. It even changes the structure of the brain, destroying cells and effectively shrinking it. Creating a personalised plan of eat a brain-boosting diet, being active, good night rest, avoiding stress, and challenge your brain can be of good help. Stress damages the entire body, but the brain is more susceptible to the damage even more than the heart.
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Dangers of taking excess caffeine

Caffeine is a natural stimulant found in tea, coffee and cacao plants, it stimulates the brain and central nervous system. Regular intake of caffeine lowers the risk of developing Alzheimer’s disease and dementia.

Taking excess caffeine increases the amount of acid in the stomach and may cause heartburn or upset the stomach. Excess caffeine consumption may raise blood pressure.

An overdose of caffeine may cause rapid or irregular heartbeat and breathing trouble. In rare cases, caffeine overdose can result in death due to convulsions or irregular heartbeat.

Drinking caffeine in large amounts may interfere with absorption and metabolism of calcium, this can cause osteoporosis. Too much caffeine can also cause slowed fetal growth and increased risk of miscarriage.
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Social activities can prevent dementia

Brain cells may die as we get older, mental and social activities promote new connections between cells. Keeping the brain active increases connections between brain cells and builds up cognitive reserve.

Regular mental activities can keep the brain healthy, learn something new everyday. Challenging yourself with mentally stimulating activities can prevent dementia.

Cognitive stimulating activities like reading, playing games and dancing can improve brain functions and prevent dementia. Regular mental activities can keep the brain healthy.

Socialising reduces risk of depression that can result from isolation. Social interaction is also good for the brain because it stimulates connections between brain cells. Combining physical and mental activity are very effective in preventing dementia.
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Walnut increases good gut bacteria

Eating handful of walnuts a day can reduce risk of heart disease, cancer and dementia. Walnut improves digestive health by nourishing and increasing good bacteria in the gut.

Walnuts are rich in fatty acid, alpha-linoleic acid, fiber and they contain one of the highest concentrations of antioxidants in omega-3 fatty acids, phytochemicals and antioxidants.

Daily handful consumption of walnuts has been associated with reduced risk of heart disease and cancer. It promotes the growth of good bacteria which have anti-inflammatory properties.

The health of the gut is related to overall health. We need prebiotics every day and regular diet for healthy bifido bacteria to become active. Eating foods containing prebiotics or taking prebiotic supplements is very important to remain healthy.

Walnuts act as a prebiotic, it promotes the growth of good bacteria that keeps the digestive system healthy. This will stimulate the good bacteria in the gut, maintain it and boost immune system.

High bacterial diversity is associated with sound health while low diversity has been linked to obesity and inflammatory bowel disease.
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Regular physical exercise prevents dementia

Regular physical exercise prevents cognitive impairment, boosts brain metabolism and dementia in old age. Physical exercise enhances general body fitness and also has a positive impact on brain metabolism and memory.

Researchers examined older people that engaged in regular physical activities with magnetic resonance tomography MRT and magnetic resonance spectroscopy MRS.

They discovered that physical activity had improved their brain metabolism by preventing an increase in choline, it enhanced stable cerebral choline concentrations.

Regular physical exercise prevents an increase in choline- a macronutrient that is important for liver function, normal brain development, nerve function, muscle movement, supporting energy levels and maintaining a healthy metabolism.

High concentration of this metabolite often rises as a result of the increased loss of nerve cells, which typically occurs in the case of Alzheimer’s disease.
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Dementia risk factors

Dementia is caused when the brain is damaged by diseases like Alzheimer’s disease or a series of strokes. Healthy lifestyle can reduce the risk of developing dementia.

Older people suffering from Alzheimer's disease are prone to dementia disease because of irregular blood supply to the brain.

Drinking of alcohol regularly increases the risk of dementia. Alcohol can damage the brain directly as a neurotoxin and by reducing nutrients that get to the brain.

The accumulation of fats and cholesterol in the lining of arteries can prevents blood flow to the brain.

Poor management of diabetes can leads to too much sugar in the blood which can damage brain and different organs in the body.

Genetics- Having more than one family member that have the disease increases the risk of developing it.

High blood pressure affects the white matter regions of the brain, and this can leads to dementia.

Depression has been associated with mild mental impairment and cognitive function decline.

Smoking exposes brain to toxins and hinders blood flow, smokers are prone to diseases that reduce blood flow to the brain.
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Working for long hours causes irregular heartbeat

According to the latest research, working more than 55 hours a week increases the risk of developing serious heart problems.

Long hours of work increases the risk of irregular heartbeat by 40 per cent than those that work for normal hours or less while long shifts increase the risk of stroke.

Atrial fibrillation is the most common heart rhythm problem, it is affecting many people and can lead to stroke, heart failure and dementia. Researchers discovered that long working hours are associated with an increased risk of atrial fibrillation.

Common cause of cardiovascular disease are older age, male sex, diabetes, high blood pressure, high cholesterol, overweight, smoking and sedentary lifestyle.
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Heartburn drugs increases untimely death

Proton pump inhibitors (PPIs), a heartburn drug is linked to different health problems like kidney damage, bone fractures and dementia.

Researchers examined medical records of users of PPIs and people who took another class of drugs for treatment of stomach acid. They discovered that there is an increased risk of death among PPI users.

Researchers compared patients taking H2 blockers with those taking PPIs for one to two years and discovered that patients taking  PPIs had a 50 percent increased risk of dying over the next five years.

PPIs and H2 blockers are used for treating serious medical conditions like upper gastrointestinal tract bleeding, gastroesophageal reflux disease, heartburn and esophageal cancer.
Long-term use of PPIs increased risk of death.
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