30 Nov

Medical News Today: Alzheimer's: Are we on the right path to new drugs?

With the number of people living with Alzheimer’s disease expected to almost triple by 2050, the race is on to find a treatment that can prevent or slow the condition. But last week saw another crack emerge in the already rocky path toward an effective Alzheimer’s medication; pharmaceutical giant Eli Lilly announced the failure of what had previously been hailed a “breakthrough” in the treatment of the most common form of dementia.
[Alzheimer's disease description and drug]
Last week, Eli Lilly announced that the drug solanezumab had failed to slow cognitive decline in patients with mild Alzheimer’s.

In a statement released last Wednesday, Eli Lilly revealed that their drug solanezumab failed to slow cognitive decline in a phase III clinical trial of more than 2,000 patients with mild Alzheimer’s disease.

Solanezumab is a monoclonal antibody that aims to slow Alzheimer’s progression by targeting and breaking down beta-amyloid plaques in the brain, which are clumps of protein thought to play a significant role in the disease.

While there are a number of other drugs in development that work in a similar way, none had come as far as solanezumab; it is the first medication of its kind to reach the last stage of testing prior to being eligible for license application, and researchers were optimistic that the drug would yield success.

In 2012, early data from the trial suggested solanezumab could slow disease progression by around 34 percent for a subset of patients in the earliest stages of Alzheimer’s.

And last year, Medical News Today reported on further results from the trials that revealed the earlier solanezumab is given to patients with mild Alzheimer’s, the greater the chance of success.

The failure of solanezumab

Though these early results were met with caution, there were high hopes that solanezumab would become the first drug to slow Alzheimer’s disease. However, it seems these hopes have now been dashed.

Eli Lilly report that in the final stage of their trial – called EXPEDITION3 – patients with mild Alzheimer’s who were treated with solanezumab “did not experience a statistically significant slowing in cognitive decline compared to patients treated with placebo.”

“Lilly will not pursue regulatory submissions for solanezumab for the treatment of mild dementia due to Alzheimer’s disease,” the drug giant said in their statement.

Alzheimer’s organizations across the globe have spoken of their sadness following the trial results.

“After positive news last summer we had high hopes for this drug to become the first to slow down Alzheimer’s disease,” says Jeremy Hughes, chief executive of the Alzheimer’s Society in the United Kingdom. “It’s extremely disappointing to learn that it hasn’t delivered a meaningful change for people living with dementia, when the need is clearly so great.”

In a statement, the Alzheimer’s Association in the United States say they are “disappointed” with the results, but they add that there are other beta-amyloid targeting drugs in development that show promise.

However, many researchers claim the failure of solanezumab begs the question: is targeting beta-amyloid really a feasible way to treat Alzheimer’s disease?

Beta-amyloid and Alzheimer’s

Beta-amyloid is a “sticky” protein fragment produced by a molecule called amyloid precursor protein (APP). Beta-amyloid can accumulate between nerve cells – or neurons – in the brain, clumping together to form so-called plaques.

According to the National Institute on Aging, some individuals will develop these plaques as they age, but they are much more abundant in certain regions of the brain in people with Alzheimer’s disease, including the hippocampus – the region associated with learning and memory.

[Amyloid plaques between nerve cells]
Beta-amyloid plaques are believed by many to play a key role in Alzheimer’s disease.

As such, beta-amyloid is considered a hallmark of Alzheimer’s disease. However, precisely how it contributes to the condition is a topic of debate.

In fact, scientists remain unclear about whether beta-amyloid plays a role in the development of Alzheimer’s disease, or whether it is a byproduct of Alzheimer’s pathology. In other words, is beta-amyloid a cause or a symptom of Alzheimer’s?

The former is the more widespread theory. A study published in 2013 in the journal Science, for example, used mouse models to show how beta-amyloid destroys the connections between brain cells – called synapses – before forming plaques to cause nerve cell death.

However, other studies have suggested a protein called tau – which forms twisted strands known as “tangles” inside nerve cells – may be a primary cause of Alzheimer’s.

One such study – published earlier this year in the journal Science Translational Medicine – found that a greater abundance of tau in the brain’s temporal lobe was linked to poorer memory.

While Alzheimer’s researchers have increasingly looked to tau as a target for new drugs in recent years, the focus is still very much on beta-amyloid. But given the number of beta-amyloid-targeting drugs that have failed in testing, optimism for these types of medication is gradually dwindling.

Is the beta-amyloid theory dead?

Alzheimer’s disease has one of the highest drug failure rates. According to a 2014 study published in the journal Alzheimer’s Research & Therapy, of 244 compounds tested in Alzheimer’s clinical trials between 2000-2012, only one was approved by the Food and Drug Administration (FDA), representing a 99.6 percent failure rate.

Fast facts about Alzheimer’s

  • Alzheimer’s is the most common form of dementia, affecting more than 5.4 million Americans
  • In the U.S., someone develops Alzheimer’s every 66 seconds
  • This year, Alzheimer’s will cost the U.S. around $236 billion.

Learn more about Alzheimer’s

The vast majority of these clinical trials were for therapies that target beta-amyloid, accounting for 70 of 146 compounds tested. In comparison, only 13 of the compounds tested targeted the tau protein.

Looking at the overall statistics, it is hard not to question the feasibility of beta-amyloid-targeting drugs for the treatment of Alzheimer’s, and it seems the latest report of solanezumab’s failure has done nothing to quash this doubt.

Talking to BBC News, Prof. Peter Roberts, of the University of Bristol in the United Kingdom, said he was not surprised solanezumab failed to yield positive results for Alzheimer’s patients.

“The problem, to my mind, is completely fundamental. There is still no convincing evidence that shows a clear relationship between amyloid deposition and deficits in cognition in humans,” he said. “All we really know is that evidence of amyloid deposition begins up to maybe 20 years before the onset of Alzheimer’s disease.”

Some researchers believe solanezumab’s failure is further confirmation that beta-amyloid is simply the wrong target for an Alzheimer’s treatment.

“The amyloid hypothesis is dead,” George Perry, a neuroscientist at the University of Texas at San Antonio, told Nature News. “It’s a very simplistic hypothesis that was reasonable to propose 25 years ago. It is not a reasonable hypothesis any longer.”

“We’re flogging a dead horse,” added Peter Davies, an Alzheimer’s researcher at the Feinstein Institute for Medical Research in Manhasset, New York. “There’s no sign of anybody getting better, even for a short period, and that suggests to me that you have the wrong mechanism.”

A different approach to beta-amyloid may be needed

Many scientists, however, remain optimistic that beta-amyloid is the right target for Alzheimer’s drug development, but some suggest the way the protein is targeted may need to be reassessed.

In the case of solanezumab, the drug binds to beta-amyloid plaques in the brain and breaks them down. However, Prof. Roxana O’Carare, a professor of clinical neuroanatomy at the University of Southampton in the U.K., speculates that the protein may need to be removed from the brain completely.

“The brain is not equipped with lymph vessels as other organs have. Instead fluid and waste are eliminated from the brain along very narrow pathways that are embedded within the walls of blood vessels,” she explained to BBC News.

“These pathways change in composition and fail in their function with increasing age and with the risk factors for Alzheimer’s disease, resulting in the buildup of amyloid in the walls of blood vessels.”

“When a vaccine such as solanezumab is administered,” Prof. O’Carare added, “the sticky plaques of amyloid from the brain break down, but the excess waste and fluid is unable to drain along the already compromised drainage pathways.”

There might still be hope for solanezumab

While Eli Lilly say they will no longer seek regulatory approval for solanezumab, the drug continues to be tested in a number of clinical trials.

The Anti-Amyloid Treatment in Asymptomatic Alzheimer’s Disease study, or the A4 study, is one such trial. Initiated in 2014, the phase III trial is testing the safety and efficacy of solanezumab in 1,150 patients at risk of Alzheimer’s due to beta-amyloid buildup.

Although solanezumab fell at the last hurdle in Eli Lilly’s trial, some Alzheimer’s researchers and organizations believe it is not necessarily the end of the road for the drug.

“We sincerely hope that the ongoing Alzheimer’s prevention trials (A4 study, Alzheimer’s Prevention Initiative, DIAN-TU) that are testing solanezumab and other anti-amyloid agents will continue,” say the Alzheimer’s Association in a statement.

“These other programs have different ways of acting on the amyloid pathway and some are also addressing the disease at a much earlier stage when these drugs may still prove to be effective.”

‘Dementia can and will be beaten’

Researchers are keen to point out that there are a number of other drug compounds being tested that have shown promise against Alzheimer’s in early trials.

The Alzheimer’s Association note that one therapeutic strategy being investigated is alleviating inflammation of the brain, or neuroinflammation, which some researchers have suggested may play a role in Alzheimer’s disease.

Earlier this year, the Alzheimer’s Association announced that four new phase I and phase II trials will each be receiving $1 million in funding to further investigate the link between neuroinflammation and Alzheimer’s.

“Increasing evidence suggests neuroinflammation plays an important role in the brain changes that occur in Alzheimer’s and other neurodegenerative diseases,” says Maria Carrillo, Ph.D., chief science officer of the Alzheimer’s Association.

“By further understanding the role and the timing of neuroinflammation and immune responses, we will be able to further accelerate novel candidate Alzheimer’s therapies,” she adds.

So it seems that in the wake of the disappointing news about solanezumab, it is certainly not time to give up on the prospects of new treatments that can prevent, slow, or halt Alzheimer’s disease.

“Dementia is society’s biggest health challenge – and we’ve seen time and again that developing effective treatments is incredibly difficult. This is only one drug of several in the pipeline and they aim to tackle dementia in different ways, so we should not lose hope. Dementia can and will be beaten.”

Jeremy Hughes, chief executive of the Alzheimer’s Society

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30 Nov

Medical News Today: Huntington's disease affects muscle as well as brain

New research on mice finds Huntington’s disease – a hereditary, progressive disorder involving death of nerve cells in the brain – may also concern defects in skeletal muscle tissue. The finding could lead to better treatments for improving motor function, and it may also offer biomarkers for monitoring the disease without having to examine the brain.
man in wheelchair
In a study of mice, researchers find evidence to suggest disruption in muscle maturation could also be a feature of Huntington’s disease.

The study – by researchers from Wright State University in Dayton, OH, and California State Polytechnic University in Pomona – is published in The Journal of General Physiology.

People with Huntington’s disease increasingly experience uncontrolled movements, poor coordination, muscle rigidity, emotional problems, and loss of cognition or ability to think. The most common form usually appears in a person’s 30s or 40s.

The disorder arises from a faulty gene that disrupts the DNA translation and subsequent production of the huntingtin protein, which in turn causes cell malfunction.

Scientists believe the thinking, mood, and behavioral features of Huntington’s disease arise from death of nerve cells in the striatum and cerebral cortex regions of the brain.

However, there is speculation that some of the features that affect motor function – such as involuntary movements and muscle rigidity – could be a result of mutant huntingtin in skeletal muscle.

In previous work, the team behind the new study had found mice with an early-onset form of Huntington’s disease had defects in their skeletal muscles in the late stages of the disease. They noticed a reduction in function of a protein called ClC-1 that ferries chloride ions into cells.

The defect appeared to be faulty translation of the DNA code for making the ClC-1 protein. This could give rise to hyperexcitability of the muscles and offers a possible explanation for some of the physical movement symptoms of the disease.

Disruption in muscle maturation could be a feature

However, what was not clear from the previous work was whether the defect in protein code processing was just a result of the death of nerve cells controlling the skeletal muscle or whether it arose during onset and progression of the disease.

Fast facts about Huntington’s

  • A less common form of Huntington’s disease – the juvenile form – begins in childhood or adolescence
  • The disease affects 3-7 per 100,000 people of European ancestry
  • It appears to be less common in other groups, such as people of Japanese, Chinese, and African descent.

Learn more about Huntington’s

For their new study, the team looked at what happened in the translation of the DNA code for making the ClC-1 protein during onset and progression of Huntington’s disease in mice engineered to develop it. They compared the results with what happens in healthy, wild-type mice (the controls).

The genetic information held in DNA is carried by molecules called messenger RNA to the machinery for making proteins that make cells work. The researchers were interested in what happens to the messenger RNA that carries the code for ClC-1 protein.

They found a defect in the encoding of messenger RNA for ClC-1 protein in both Huntington’s and control mice when the animals were young. However, as they aged, the defect corrected itself to produce functional ClC-1 only in the healthy mice.

The finding suggests disruption in muscle maturation could be a feature of Huntington’s disease – in mice at least.

On further examination, the team found the Huntington’s mice expressed a form of myosin – a motor protein that is normally only found in the muscle of newborn mice. They also found evidence of this in mice with adult-onset Huntington’s disease.

“Our results support the idea that HD [Huntington’s disease] is a myopathy as well as a neurodegenerative disease and may provide a new opportunity to improve patient care by targeting skeletal muscle tissue.”

Senior author Dr. Andrew A. Voss, Wright State University

The researchers also believe the findings offer a way to use biomarkers of skeletal muscle defects to track progress of the disease without having to examine brain tissue in patients.

Learn how Huntington’s risk genes are more common than previously thought.

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30 Nov

Medical News Today: Depression vs. Sadness: How to Tell the Difference

Millions of people around the world experience depression at one point or another in their lives.

The Anxiety and Depression Association of America (ADAA) note that depression is one of the most common mental health illnesses in the United States.

Sadness is an integral part of depression, but it is not the same thing. It is important to know and understand the differences because confusing them can lead to inappropriate treatment.

What is sadness?

unhappy woman with shopping bags
Sadness may be linked to a specific trigger.

Sadness is a normal human emotion that everyone experiences at some time. A number of events can leave people feeling sad or unhappy, such as the loss or absence of a loved one, divorce, loss of job or income, financial trouble, issues at home, or social anxiety.

Failing an exam, not getting a job, or other disappointing events can also trigger sadness.

However, a person who is sad can usually find some relief from crying, venting, or talking out frustrations. This is because sadness is more likely to be linked to a specific trigger.

Sadness usually passes with time. If it does not pass, or if the person becomes unable to function normally, this could be a sign of depression. If symptoms worsen or last longer than 2 weeks, the person should talk to their doctor.

What is depression?

Depression is a mental disorder that affects every part of a person’s feelings and perception. It affects behaviors and attitudes and can affect people of any gender or age.

In 2015, around 16.1 million people aged 18 years or above in the U.S. had experienced at least one major depressive episode in the last year. This represented 6.7 percent of all American adults.

Symptoms include feelings of discouragement, sadness, hopelessness, a lack of motivation, and a loss of interest in activities that are normally enjoyable. In severe cases, the person may think about or attempt suicide.

The person may no longer feel like spending time with family or friends. They may stop pursuing their hobbies and feel unable to go to work or school.

Daily habits may change unexpectedly and without reason. A person with depression may find it difficult to continue doing the things they normally enjoy.

If these feelings of doubt last more than 2 weeks, a healthcare professional may diagnose the person with major depressive disorder (MDD).

Signs and symptoms of MDD include:

  • Daily depressed mood with noticeable signs of hopelessness, sadness, and loss of interest
  • Daily loss of interest in normal activities for an extended amount of time
  • Significant weight loss or gain without trying – there may be a 5 percent change in body weight
  • Insomnia, sleeplessness, or increased amounts of sleep that affect normal schedules
  • Tiredness and low energy
  • Feelings of worthlessness, excessiveness, or guilt on a daily basis
  • Inability to concentrate or make decisions
  • Recurrent thoughts of death, suicidal thoughts, or suicide attempts or plans

A person who experiences any five of these symptoms for more than 2 weeks is considered to have a more serious problem than sadness.

For a diagnosis of MDD, the doctor should link the symptoms only to depression and not to another medical diagnosis, such as substance abuse or disability.

Unlike sadness, depression can leave a person struggling to express their feelings. If the person tries to release the stress, the overpowering feelings and negative thoughts can prevent them from building themselves up again.

Treatment for depression

a therapist takes notes with a patient
Depression may be treated with medication or psychotherapy.

If a person has symptoms of depression for longer than 2 weeks, they should seek professional help. A physician can help to determine the level of help needed by the individual.

Following diagnosis, possible treatments include medication, counseling, and cognitive behavioral therapy (CBT).

Medications

Medications include a type of antidepressant known as selective serotonin reuptake inhibitors (SSRIs). These work by increasing levels of serotonin in the brain. Serotonin is a chemical messenger that helps to affect mood and social behavior. Examples of SSRIs include citalopram, escitalopram, fluoxetine, and sertraline.

According to the Mayo Clinic, these drugs can ease the symptoms of depression, although they do carry a risk of adverse side effects.

For example, when people first use antidepressants, there is a risk that their symptoms will worsen before getting better. Family members should monitor the patient closely and seek medical attention if they are concerned.

The U.S. Food and Drug Administration (FDA) have expressed concern that some SSRIs can cause serious side effects in younger people and birth defects if taken during pregnancy. As a result of this, the drugs carry a black box warning, which is an important notice on the leaflet outlining the possible dangers of the drugs.

When prescribing such drugs, physicians must carefully balance the pros and cons of use.

Psychotherapy and counseling

Psychotherapy involves talking to a trained professional. This can help to uncover the issues underlying the condition.

It may be used on its own or along with antidepressants. A therapist can help to identify problem areas, teach coping mechanisms, and educate a patient about their condition.

A person with severe depression may be admitted to the hospital if they are in immediate danger or if they are unable to take care of themselves.

Outpatient facilities can help with long-term care.

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30 Nov

Medical News Today: Heart attack risk over eight times higher for younger smokers

As printed on almost every cigarette pack, smoking increases the risk of heart disease. While this is a known fact, the actual numbers often remain ignored. A new study looks at the risk of developing heart attack in younger smokers.
[A woman breaking a cigarette in half]
New research finds younger smokers are at much greater risk of heart attack.

According to the Centers for Disease Control and Prevention (CDC), over 16 million Americans live with a disease caused by smoking.

Cancer, heart disease, and stroke are only a few of the conditions caused by smoking. Tobacco use also causes lung diseases, diabetes, and chronic obstructive pulmonary disease (COPD).

The CDC report that 1 in 3 deaths from cardiovascular disease (CVD) are caused by tobacco.

CVD includes several types of heart conditions. The most common form of CVD in the United States is coronary heart disease, which ultimately leads to heart attacks.

New research examines the link between smokers’ age and the risk of developing a specific type of heart attack.

Studying the risk of STEMI heart attack in younger smokers

Researchers from the South Yorkshire cardiothoracic center in the United Kingdom examined 1,727 adults who were undergoing treatment for a type of heart attack known as STEMI.

STEMI stands for ST-segment elevation myocardial infarction, and it refers to the electrocardiogram pattern that can be seen when a large portion of the heart muscle is dying. STEMI is a very serious type of heart attack where one of the heart’s major arteries is suddenly and completely blocked.

The researchers used data from the Office for National Statistics Integrated Household Survey in South Yorkshire.

Almost half of the 1,727 patients – or 48.5 percent – were current smokers. Just over 27 percent were former smokers, and a quarter were nonsmokers.

The results were published in the journal Heart.

Smokers under 50 more than eight times likelier to have a STEMI

Overall, the study revealed that current smokers had a likelihood of developing STEMI three times higher than ex- and nonsmokers combined.

Current smokers were also three times likelier to have peripheral vascular disease than nonsmokers. In vascular disease, fatty deposits build up in the arteries and stop the blood supply to the legs.

Along with ex-smokers, current smokers were twice as likely to have also had coronary artery disease.

Current smokers were likely to be 10-11 years younger than former or nonsmokers when they had their STEMI.

The highest risk was found among smokers under 50 years of age, who were almost 8.5 times more likely to have a STEMI heart attack than nonsmokers and ex-smokers combined.

The risk was inversely associated with age, meaning that it decreased as the age increased. For instance, among adults aged 50-65, the risk fell to five times higher, while in smokers over the age of 65 the risk was only three times higher.

The smoking prevalence rate among STEMI patients under the age of 50 was 75 percent.

Strengths and limitations of the study

This is the first study that uses population data combined with case data to demonstrate that the risk of acute STEMI heart attack is much higher in younger smokers than older ones.

The study could help guide health policies to target segments of the population where a higher prevalence of smoking was noticed, and where there is a higher risk.

Additionally, the authors note their study could also improve current social perceptions on smoking, age, and associated health risks:

“This study may also help to tackle the misconception by young smokers that acute STEMI is a disease of the elderly, by showing that this group is very vulnerable and has the highest risk from their smoking.”

However, given that this is an observational study, it cannot explain the reasons why the risk is so much higher in younger adults. Since younger smokers do not have many of the other risk factors for heart attack, such as high cholesterol, increased blood pressure, or diabetes, the results are all the more difficult to explain.

Authors speculate, however, that smoking may be the most important risk factor, as other cited research shows cigarette smokers are more vulnerable to arterial plaque rupture.

The study is also limited in the sense that it is based on just one regional specialist cardiothoracic center in the U.K., and it did not include patients who died before admission.

Additionally, the study did not account for those considered unsuitable for percutaneous coronary intervention (PCI) treatment at the center.

Study highlights the need for prevention among younger patients

“All current smokers must be encouraged into smoking cessation therapy to reduce their risk of acute STEMI, with a focus on the youngest smokers whose increased risk is often unrecognized,” the authors note.

In a linked editorial, cardiologist Dr. Yaron Arbel, of the Tel-Aviv Medical Center in Israel, further insists on the need for prevention campaigns aimed at the younger age groups.

“Most smokers know that smoking is bad. However, exact numbers have a tendency to hit home more often. Therefore studies like the present one are especially important.”

He adds that since most young patients lack conventional risk factors, common treatment practices are less beneficial for them. Therefore, efforts should concentrate on prevention, not treatment.

“Our goal should be to provide them with the tools to achieve abstinence,” Arbel notes. “In difficult cases, even reducing the number of cigarettes smoked daily might make a difference.”

Learn how e-cigarettes may be just as harmful as tobacco for oral health.

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30 Nov

Medical News Today: Exercise extends life, but which exercise is best?

The health benefits of exercise are known to all; it reduces the risk of heart disease and extends lifespan. New research sets out to understand, in the world of sports, which ones are best for staving off illness.
[Two people indulging in sports]
All sports are healthful, but which sport is the most healthful?

A raft of studies over the last few decades has unequivocally shown that physical activity benefits health.

Sports participation has been shown to decrease mortality in middle-aged and older individuals.

In particular, vigorous sporting activity is considered to hold the most benefits. However, to date, exactly which activities are best for longevity has not been thoroughly investigated.

Previous studies addressing the question have lacked strength.

Research, published this week in the British Journal of Sports Medicine, set out to examine the relationship between sports and mortality (including cardiovascular-based mortality).

They designed their study to investigate which types of sporting activity provided the strongest beneficial effect.

Taking data from 11 annual health surveys for England and Scotland between 1994-2008, the team used data from 80,306 adults with an average age of 52. Each participant was asked which activities they had carried out in the previous 4 weeks, and whether the activity had been intense enough to make them sweaty and breathless.

The types of activities that were collected included chores, such as DIY and gardening. They also collated information about the types of sports they had been involved in. The six most popular were cycling; swimming; aerobics/keep fit/gymnastics/dance; running/jogging; football/rugby; and racquet sports – badminton/tennis/squash.

Overall, just 44 percent of respondents met the recommended levels of physical activity.

On average, each individual was tracked for 9 years. During that time, 8,790 died, and 1,909 of them died from heart disease or stroke.

Breaking the data down by sports type

Once the analysis had accounted for potentially influential factors, differences could be measured between the various sporting activities. Compared with participants who had done no exercise, risk of death was:

  • 47 percent lower in those who played racquet sports
  • 28 percent lower in swimmers
  • 27 percent lower in aerobics
  • 15 percent lower in cyclists.

Perhaps surprisingly, cycling, running/jogging, and football/rugby were not associated with any kind of protection from cardiovascular disease. When joggers and runners were compared with those who did not run or jog, there was a 43 percent decrease in risk of death from all causes and a 45 percent reduction in cardiovascular risk; however, when confounding variables were adjusted for, this effect disappeared.

Few of the respondents said that they played football or rugby frequently, this may account for its lack of apparent influence on health outcomes. Additionally, because these sports tend to be seasonal, even an avid football or rugby player might have long periods where they do not play a match.

The effects of intensity

When the intensity of the exercise was investigated, for some sports, the higher the intensity, the greater the positive influence on longevity. But, for other activities, there was a U-shaped curve – lesser intensity was more beneficial than higher intensity or no activity at all.

Although the intensity findings are intriguing, the authors warn that this part of the analysis included only a small number of deaths, making the findings tentative; further investigation is necessary to firm them up.

Also, the findings are based on an observational study, meaning that cause and effect can not be concluded. Regardless of this, the findings add further weight to the already weighty hypothesis that exercise reduces mortality and that any sport is better than no sport.

Learn how exercise might safeguard against memory loss.

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30 Nov

Medical News Today: Psoriasis on the Eyelids: Symptoms and Treatment

Psoriasis is an autoimmune disease that causes a skin condition, in which skin cells build up quickly on the surface of the skin. It can occur on any area of the body, including the eyelids.

While there isn’t a cure for psoriasis, there are several prescription and non-prescription treatments available. In addition, there are home remedies that can reduce symptoms and offer relief.

What is psoriasis?

Psoriasis is a lifelong skin disease. The symptoms may be better at some times and worse at others. The exact prevalence of psoriasis isn’t exactly known, but about 1 to 2 people out of every 100 have the condition.

Scalp psoriasis on the back of the head.
Plaque psoriasis is the most common form of psoriasis.

There are several different types of psoriasis. Plaque psoriasis, which is the type causing patches on the scalp and skin, is the most common. The plaques are extra skin cells that create thick and silvery scales and red patches on the skin. These patches are often itchy and can be painful.

Psoriasis usually occurs on the scalp, joints, hands and feet. However, psoriasis can appear almost anywhere on the body, including the face and eyelids. About 10 percent of people with psoriasis have eyelid involvement.

The condition cannot be spread from person-to-person. However, psoriasis can spread on a person’s body. Dry skin is more prone to develop psoriasis plaques. Trauma to the skin such as a cut or scrape makes that area more likely to get psoriasis as well.

Symptoms

Psoriasis symptoms vary, but the most common symptoms include:

  • Skin with red patches covered with silvery, dandruff-like scales
  • Dry skin that may crack and bleed
  • Itchy, burning, or sore skin
  • Nails that become thicker, pitted, or have ridges
  • Stiff, achy, or swollen joints

Psoriasis ranges in severity from a handful of spots to patches on large areas of the skin. The condition tends to get better and worse at times and can even go into remission.

Causes

Psoriasis is related to the immune system, and the body is incorrectly reacting to the body’s skin cells. The immune reaction is what causes the rapid growth and turnover of skin cells.

Certain things can trigger the first signs of psoriasis or recurrences:

  • Infections
  • Stress
  • Dry weather
  • Some medications

Psoriasis and the eyelids

Psoriasis on or around the eyelids is very difficult to live with because the skin in this area is very sensitive. The swelling may even cause the eyelashes to rub against the eyeball. The itchiness will also make psoriasis of the eyelid uncomfortable and painful at times.

Psoriasis around the eye.
Psoriasis on or around the eyelids can be a difficult condition to manage.

In addition, since the eyeball is nearby, any topical medications such as a steroid can lead to more severe problems such as glaucoma.

Symptoms of psoriasis of the eyelid

As the scales of skin flake off the eyelids, they may stick to the eyelashes.

The rims of eyes may become red and crusty.

If inflammation continues for some time, the edges of the eyelids may turn up or down. If they become inverted, lashes can rub against the eyeball. Irritation and other complications can result.

Complications

One complication of psoriasis is the risk of developing uveitis, an inflammation within the eye. It is rare, but it can cause inflammation, dryness, and discomfort. It can have a drastic effect on the eyesight, if not treated

Topical antibiotics may be used to treat infection, and patients are usually prescribed oral corticosteroids, such as prednisone, to reduce inflammation.

Using topical steroids on the eyelid can cause serious side effects. The steroid can enter the eye and cause problems such as cataracts and glaucoma. It’s important to follow a doctor’s recommendation exactly in using topical or oral steroids.

A common complication of psoriasis is joint inflammation, which happens to up to 40 percent of people with psoriasis. This inflammation causes symptoms of arthritis and is referred to as psoriatic arthritis. A doctor will make an evaluation as to whether the joint pain is psoriatic arthritis or if there is another cause.

Treatments and home remedies

Anyone with symptoms of psoriasis, especially on the eyelids, should see a doctor. Often, patients see their family practitioner and may be referred to a skin specialist, or dermatologist.

People already diagnosed with psoriasis should see a doctor if their condition worsens or they have worrisome medication side effects.

While there isn’t a cure, psoriasis treatments and home care measures can offer some relief. Cortisone creams and exposing the skin to small amounts of natural sunlight can provide significant help.

Prescription medications

A woman is applying eye lotion.
Special steroid medication made for use around the eyes can help treat psoriasis in this area.

In some cases, a special steroid medication made for use around the eyes may be used to treat scaling. A doctor must carefully supervise the treatment because eyelid skin can be easily damaged.

If topical steroids are overused in and around the eyes, glaucoma or cataracts may develop. This is the reason the doctor may suggest having pressure within the eye checked regularly by an ophthalmologist.

Protopic ointment or Elidel cream is the preferred method of treatment for psoriasis around the eyes. These medications are not steroids but have an effect on the immune system.

Protopic ointment or Elidel cream won’t cause glaucoma and is effective on eyelids, but can sting the first few days of use. Using these medications for eyelid psoriasis can help someone with psoriasis avoid the potential side effects of topical steroids.

Home remedies and self-care

  • Keep skin well-moisturized: This is the first step in controlling itchiness because it reduces redness and itching and helps the skin heal. Dermatologists recommend heavy creams and ointments, which keep water in the skin. Heavy moisturizers can be found over-the-counter.
  • Gently washing the eyelids with cool water and a sensitive skin or baby shampoo may relieve irritation.
  • There are over-the-counter products that remove excess skin and lessen cracking. Salicylic acid and coal tar are two common remedies.
  • Cool baths or showers can soothe skin, but hot showers or bath can dry the skin and worsen psoriasis.
  • Apple cider vinegar is a gentle disinfectant and can soothe psoriasis during flare ups. Vinegar can be added to bath water or applied directly to the skin. Do not use vinegar on skin that is cracked or bleeding.
  • Cover scales with lotion and bandage if there are open lesions that can become infected. This method doesn’t work for the eyes or face but can help if there are scales elsewhere.

Treatments to avoid

Topical steroids applied to the eyelid can get in the eye and cause serious side effects. Topical steroids can cause glaucoma and cataracts. A person with psoriasis of the eyelid should consult with their doctor about treatment options.

Living with psoriasis of the eyelid

Makeup

Makeup can reduce the appearance of redness and scales. Makeup designed for sensitive skin is a good choice.

However, makeup can interfere with topical medications and can further irritate the eyelid. People with psoriasis should speak to a doctor about the best ways to use makeup and manage eyelid psoriasis.

Eyebrow piercings

For people with psoriasis, getting an eyebrow piercing poses the risk of getting psoriasis in the eyebrow. Psoriasis can be caused by trauma to the skin such as a cut, bruise, and piercings or tattoos as well.

A person with psoriasis may want to speak to a doctor about getting a piercing or tattoo.

People with eyebrow piercings and psoriasis may get psoriasis in that area and eyebrow hair may fall out. They should consult with a doctor about prevention and treatment options.

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Source: medicalnewstoday

30 Nov

Mouthguard a Key Defense Against Sports-Related Injuries

News Picture: Mouthguard a Key Defense Against Sports-Related Injuries

Latest Prevention & Wellness News

MONDAY, Nov. 28, 2016 (HealthDay News) — Safety gear for athletes playing contact sports should include mouthguards, say dental experts at the University of Alabama at Birmingham.

Sports-related dental injuries send more than 600,000 people to the emergency room every year, the U.S. Centers for Disease Control and Prevention reports.

Most of these injuries involve the front teeth, but the tongue and cheeks can also be hurt while playing sports, the UAB team said.

The best way to protect the mouth and teeth during sports is to wear a mouthguard, says Dr. Ken Tilashalski, associate dean for academic affairs at the UAB School of Dentistry. Mouthguards have been shown to reduce the risk of sports-related dental injury by 60 times, he said.

“Wearing a mouthguard reduces the chances of tooth fractures, tooth dislocations and soft tissue cuts,” Tilashalski said in a university news release. “The guards also protect against jaw fractures and concussions by absorbing the energy of a traumatic blow to the chin.”

The three types of mouthguards include:

  • Stock: These are preformed and ready to wear, but they may not fit well inside the mouth.
  • Boil and bite: These may be customized and molded to the mouth by softening in boiling water before biting down.
  • Custom-made: A dentist tailor-makes these mouthguards to fit an individual’s mouth. These mouthguards provide the best fit and the highest level of protection.

“For my kids, I have chosen to use custom mouthguards as they fit and feel better, do not interfere with speech, and are essentially invisible,” Tilashalski said. “Mouthguards need to be replaced as they wear down, and athletes in the tooth-forming years will have to have these replaced more often as the mouth grows and the teeth change.”

After each use, rinse your mouthguard and store it in a hard container to prevent the buildup of germs, Tilashalski added. Players should also avoid chewing on their mouthguard to extend its life.

Mouthguards are most often associated with organized sports, but young people participating in other risky activities should also protect their teeth and mouth from serious and costly injuries, Tilashalski cautioned.

“Many cases of facial trauma are actually seen in unorganized or pickup sports activities. Biking, skating and skateboarding are the recreational sports that have the highest chances of injury,” he said.

“I have four soccer players at home. Having a mouthguard in place seems a small price to pay to prevent a lifetime of dental treatment as a consequence of a knocked-out tooth,” he added.

— Mary Elizabeth Dallas

MedicalNews
Copyright © 2016 HealthDay. All rights reserved.

SOURCE: University of Alabama at Birmingham, news release, Oct. 25, 2016

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Source: MediciNet

30 Nov

Alzheimer's Protein Plaques May Also Harm the Heart

News Picture: Alzheimer's Protein Plaques May Also Harm the HeartBy Dennis Thompson
HealthDay Reporter

Latest Alzheimers News

MONDAY, Nov. 28, 2016 (HealthDay News) — Protein fragments that form plaques in the brains of Alzheimer’s patients might also stiffen their heart muscle and increase their risk of heart failure, a new study reports.

The protein fragments are called amyloid beta. Tests of heart tissue samples revealed that the hearts of Alzheimer’s patients had increased levels of amyloid beta, the study showed.

Sticky amyloid beta chunks create plaques between neurons that are a hallmark of Alzheimer’s disease. Similar deposits can be found in the heart, said senior researcher Dr. Federica del Monte. She’s an associate professor with Harvard Medical School and Beth Israel Deaconess Medical Center’s Cardiovascular Institute, both in Boston.

“We found that some forms of heart failure are basically an Alzheimer’s disease in the heart,” del Monte said. “They basically have the same biological defect. In one case, it affects the brain. In one case it affects the heart.”

The study included 22 people with Alzheimer’s who were an average age of 79. They were compared to 35 healthy people in a control group whose average age was 78, the study said.

Testing revealed that people with Alzheimer’s disease tended to have increased thickness in the wall of their left ventricle, one of the lower chambers of the heart. The ventricles had a reduced ability to expand and take in blood before it’s pumped out of the heart, the researchers said.

These risk factors are directly related to a condition called heart failure with preserved ejection fraction. This is a type of heart failure where the ventricles become too stiff over time to effectively draw blood into the heart, said Dr. Alfred Bove. He’s a cardiologist and professor emeritus with Temple University’s Lewis Katz School of Medicine in Philadelphia.

And, amyloid beta deposits could contribute to this condition, added Bove, who’s also past president of the American College of Cardiology.

“If the heart muscle has deposits of something in it, it will get stiffer,” he said. “If it doesn’t relax appropriately, it can produce heart failure even though the squeezing capacity of the heart muscle is still pretty intact.”

Based on these findings, doctors of Alzheimer’s patients should be alert to possible heart problems and other potential organ failures, del Monte said.

“Patients with Alzheimer’s disease, now they have new drugs that prolong their life,” del Monte said. “It is likely they will also have cardiac problems, and maybe other organ problems. It is not a brain issue only. It is a systemic disease.”

Elevated amyloid beta levels have been found in other tissues of Alzheimer’s patients, including the gut, the kidneys and the muscles, both del Monte and Bove said.

“It’s not surprising one would find the beta amyloid in the heart as well, because it looks like it’s not isolated to the brain,” Bove said. “It deposits in lots of tissues, and where it deposits, it has an effect.”

That negative effect could be due to the way amyloid beta affects the body’s use of calcium, a nutrient that’s important both to neuron transmission and contraction of the heart muscle, del Monte said.

This study will need to be replicated in a larger number of people to gather a better understanding of amyloid beta deposits in the heart, both del Monte and Bove said.

Unfortunately, at this time there’s little that can be done for Alzheimer’s patients with heart problems related to their disorder, Bove said.

“We don’t really know how to treat this form of heart failure,” he said. “We try things, but there are not a lot of definitive therapies.”

The new study appears Nov. 28 online in the Journal of the American College of Cardiology.

MedicalNews
Copyright © 2016 HealthDay. All rights reserved.

SOURCES: Federica del Monte, M.D., Ph.D., associate professor, Harvard Medical School and Beth Israel Deaconess Medical Center’s Cardiovascular Institute, Boston; Alfred Bove, Ph.D., M.D., professor emeritus, Temple University’s Lewis Katz School of Medicine, Philadelphia, and past president, American College of Cardiology; Nov. 28, 2016, Journal of the American College of Cardiology

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Source: MediciNet

30 Nov

3 Keys to Cutting Your Risk of Heart Failure

News Picture: 3 Keys to Cutting Your Risk of Heart FailureBy Alan Mozes
HealthDay Reporter

Latest Heart News

MONDAY, Nov. 28, 2016 (HealthDay News) — Middle-aged adults who’ve avoided obesity, high blood pressure and diabetes are far less likely than others to experience heart failure in their later years, new research reports.

Investigators found that a 45-year-old without those three key risk factors has as much as an 86 percent lower risk for heart failure compared with someone with poor control of weight, blood pressure and blood sugar.

“This paper provides more evidence to demonstrate the importance of a heart-healthy lifestyle,” said study co-author Dr. John Wilkins. He’s a cardiologist and assistant professor of medicine and preventive medicine at the Northwestern University Feinberg School of Medicine in Chicago.

Good lifestyle habits can help prevent obesity, high blood pressure and diabetes in many people, “which will substantially reduce their chances of developing cardiovascular disease later in life,” Wilkins said.

According to another heart specialist, Dr. Gregg Fonarow, “This means doing everything necessary to maintain a healthy body weight — including eating a heart-healthy diet and remaining physically active, and having regular monitoring to ensure healthy blood pressure and blood sugar levels.”

The new report indicates that “while there are therapies available once heart failure develops, the most effective strategy is to prevent heart failure in the first place,” said Fonarow. He is a professor of cardiology at the University of California, Los Angeles.

Heart failure affects an estimated 5.7 million adults in the United States. The disabling condition occurs when the heart can no longer pump enough blood and oxygen throughout the body.

The U.S. Centers for Disease Control and Prevention says that about half of those who develop heart failure will die within five years.

For this study, Wilkins and his associates analyzed data from four heart studies launched across the United States between 1948 and 1987.

Through 2007-2008, the researchers tracked outcomes for over 19,000 men and women whose heart health was assessed at age 45. The investigators followed another 24,000 whose heart status was determined at age 55.

Heart failure developed in nearly 1,700 participants tested at 45, and in almost 3,000 of those examined at 55, the findings showed.

But men who were free of high blood pressure, diabetes and obesity at 45 went on to live free of heart failure almost 11 years longer than men who had all three conditions. For women, the advantage was about 15 years, the study found.

On average, men and women without any of those three heart risks lived 35 years and 38 years longer, respectively, without developing heart failure.

Similar trends were seen among those assessed at 55, the researchers said.

Of the three heart-failure risk factors cited, diabetes appeared to have the greatest effect. Those without diabetes at 45 lived about nine to 11 years longer without heart failure, compared with those who did have the blood-sugar disease.

According to Fonarow, “this study quantifies the degree to which preventing the onset of high blood pressure, obesity, and diabetes can pay huge dividends in terms of lifelong health free from heart failure, cardiovascular disability, large health care expenditures, and premature cardiovascular death.”

Lona Sandon, an assistant professor of clinical nutrition at the University of Texas Southwestern Medical Center at Dallas, noted that to enjoy these benefits, many Americans may first need to adjust their behavior.

“We need to make some pretty intense changes to our eating habits and physical activity,” she said.

“The majority of us still come up short on key foods known to support health: fruits, vegetables, whole grains,” Sandon said. “Few come anywhere near the recommended amount.”

Physical activity is no different, Sandon added. “Many of us spend way too much time in sedentary environments. The 30 to 60 minutes you might squeeze in at the gym a few times a week barely scratches the surface to help support a healthy weight, blood pressure and reduce diabetes risk,” she said.

The findings were published online Nov. 28 in JACC: Heart Failure.

MedicalNews
Copyright © 2016 HealthDay. All rights reserved.

SOURCES: John T. Wilkins, M.D., M.S., cardiologist, and assistant professor of medicine, department of preventive medicine, Northwestern University Feinberg School of Medicine, Chicago; Gregg Fonarow, M.D., professor, cardiology, University of California, Los Angeles; Lona Sandon, Ph.D., RDN, LD, assistant professor, department of clinical nutrition, school of health professions, University of Texas Southwestern Medical Center at Dallas; Nov. 12, 2016, JACC: Heart Failure

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Source: MediciNet

30 Nov

Mouthguard a Key Defense Against Sports-Related Injuries

News Picture: Mouthguard a Key Defense Against Sports-Related Injuries

Latest Prevention & Wellness News

MONDAY, Nov. 28, 2016 (HealthDay News) — Safety gear for athletes playing contact sports should include mouthguards, say dental experts at the University of Alabama at Birmingham.

Sports-related dental injuries send more than 600,000 people to the emergency room every year, the U.S. Centers for Disease Control and Prevention reports.

Most of these injuries involve the front teeth, but the tongue and cheeks can also be hurt while playing sports, the UAB team said.

The best way to protect the mouth and teeth during sports is to wear a mouthguard, says Dr. Ken Tilashalski, associate dean for academic affairs at the UAB School of Dentistry. Mouthguards have been shown to reduce the risk of sports-related dental injury by 60 times, he said.

“Wearing a mouthguard reduces the chances of tooth fractures, tooth dislocations and soft tissue cuts,” Tilashalski said in a university news release. “The guards also protect against jaw fractures and concussions by absorbing the energy of a traumatic blow to the chin.”

The three types of mouthguards include:

  • Stock: These are preformed and ready to wear, but they may not fit well inside the mouth.
  • Boil and bite: These may be customized and molded to the mouth by softening in boiling water before biting down.
  • Custom-made: A dentist tailor-makes these mouthguards to fit an individual’s mouth. These mouthguards provide the best fit and the highest level of protection.

“For my kids, I have chosen to use custom mouthguards as they fit and feel better, do not interfere with speech, and are essentially invisible,” Tilashalski said. “Mouthguards need to be replaced as they wear down, and athletes in the tooth-forming years will have to have these replaced more often as the mouth grows and the teeth change.”

After each use, rinse your mouthguard and store it in a hard container to prevent the buildup of germs, Tilashalski added. Players should also avoid chewing on their mouthguard to extend its life.

Mouthguards are most often associated with organized sports, but young people participating in other risky activities should also protect their teeth and mouth from serious and costly injuries, Tilashalski cautioned.

“Many cases of facial trauma are actually seen in unorganized or pickup sports activities. Biking, skating and skateboarding are the recreational sports that have the highest chances of injury,” he said.

“I have four soccer players at home. Having a mouthguard in place seems a small price to pay to prevent a lifetime of dental treatment as a consequence of a knocked-out tooth,” he added.

— Mary Elizabeth Dallas

MedicalNews
Copyright © 2016 HealthDay. All rights reserved.

SOURCE: University of Alabama at Birmingham, news release, Oct. 25, 2016

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Source: MediciNet