Monday, December 30, 2013

Study confirms narcolepsy as an autoimmune disease

A new study that offers some of the most compelling evidence to date for the idea of "mimicry," where the immune system attacks a body protein because of its similarity to a pathogen protein, confirms that narcolepsy is an autoimmune disease.
Reporting in the latest online issue of Science Translational Medicine, researchers at Stanford University School of Medicine in California show how in genetically susceptible individuals, narcolepsy can be triggered because part of a wakefulness protein, called hypocretin, is very similar to part of a protein from the pandemic 2009 H1N1 "swine flu" virus.
Narcolepsy is a chronic disorder where the brain cannot control sleep-wake cycles, leading to sudden bouts of sleep, often accompanied by cataplexy, an abrupt loss of voluntary muscle tone that can cause collapse.
The National Institutes of Health estimates that narcolepsy affects around 1 in 3,000 Americans. Currently, there is no cure.

Immune system attacks brain cells that make the 'wakefulness' protein

In 2009, Emmanuel Mignot, professor of psychiatry and behavioral sciences at Stanford, who has been working on narcolepsy for over 20 years, led a study that gave the first genetic clue that narcolepsy is an autoimmune disorder where the body's immune system attacks brain cells that make the "wakefulness" protein hypocretin.
Prof. Mignot, who is co-senior author of the new paper, says:
"The relationship between H1N1 infection, vaccination and narcolepsy gave us some very interesting insight into possible causes of the condition. In particular, it strongly suggested to us that T cells of the immune system primed to attack H1N1 can occasionally also cross-react with hypocretin and somehow cause the destruction of hypocretin-producing neurons."
The latest work suggests new ways to interrupt the process before all the hypocretin-producing cells are lost and produce the dramatic symptoms of narcolepsy.
It also opens the prospect of a blood test to diagnose the disease, and it offers new insights into a link between a pandemic H1N1 vaccine used in Europe in 2009 and a spike in narcolepsy cases in Scandinavia the year after.
The team says their work will also give new ideas to researchers investigating other types of autoimmune disorders, particularly those involving the brain.
Co-senior author Elizabeth Mellins, an immunology researcher and professor of pediatrics at Stanford, adds: "By giving us a new way to think about how neurons in these patients die, it also suggests new therapeutic approaches that we would not have considered if we hadn't learned that this is an autoimmune disease."

Focus on T cells because of link to HLA signature

Previous studies have established that the vast majority of people with narcolepsy have a variant of the human leukocyte antigen (HLA) gene that is found in only a quarter of the general population.
For their work, Prof. Mignot and colleagues decided to focus on the T cells of the immune system because of their association with the HLA signature found in nearly all narcolepsy patients.
HLA is a molecule that sits on the surface of cells that present antigens and bits of proteins they gather from their environment. T cells come along and scan these proteins, and if any of these is "foreign," they start to divide and go around the body looking for it so as to destroy it.
However, if there is a case of mistaken identity on the part of the T cells, then things can go drastically awry. Prof. Mellins explains how they started to suspect this was the case in narcolepsy:
"When we saw that the portion of the hypocretin that seemed to be recognized by the immune system in narcolepsy patients was similar to a part of the pandemic 2009 H1N1 influenza hemagglutinin molecule, we were very hopeful that we were on the right track."
They found that a short, 13-amino-acid section of the H1N1 hemagglutinin protein was very similar to two equally short pieces of the hypocretin protein.
The resemblance was close enough so that the T cells of people who suffer from narcolepsy reacted strongly to the hypocretin protein segments.
The researchers tested this by presenting the small piece of the H1N1 protein to cultured T cells from narcolepsy patients, and saw how this increased the proportion of hypocretin-reactive cells.

Other pathogens may cause similar confusion in immune system

The team was also surprised to find hypocretin cross-reactive T cells in blood taken from narcolepsy patients before H1N1 began circulating in humans in 2009.
Prof. Mignot says this suggests other viruses or pathogens may sometimes cause a similar confusion in the immune system, adding that:
"Indeed, there is a growing appreciation that cross-reactivity of immune T cell recognition may not be as uncommon as once thought. Although this cross-reactivity may make the immune system more adaptable to new infections, it may also increase the chance of mistakes that could result in autoimmune diseases."
In another study published earlier this year, researchers at the UCLA Center for Sleep Research offer another clue to the cause of narcolepsy in humans. They suggest an excess of histamine brain cells may reduce hypocretin cells.
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HIV cure may lie in radioimmunotherapy

A new study suggests targeting HIV with radioimmunotherapy could eradicate HIV from infected cells. If given in conjunction with highly active antiretroviral therapy, it may form the basis of a cure.
Although highly active antiretroviral therapy (HAART) kills human immunodeficiency virus (HIV) in the bloodstream, it does not completely eliminate it from the body because the virus can linger in infected cells and replicate.
Researchers from the Albert Einstein College of Medicine of Yeshiva University in New York presented their findings at the 99th Scientific Assembly and Annual Meeting of the Radiological Society of North America (RSNA) in Chicago, IL, this week.
Study leader Ekaterina Dadachova, professor of radiology and of microbiology & immunology, says although there has been enormous progress in HIV treatments that slow progression to AIDS, the search for a permanent cure continues. She explains:
"To combat HIV, we need a method that will completely eliminate all HIV-infected cells without damaging non-infected cells."
In radioimmunotherapy (RIT), which has been used for a while to treat cancer, antibodies charged with radioactive isotopes target and destroy cancer cells.
The antibody selects the particular type of cancer cell and the attached radioisotope delivers a lethal dose of radiation that kills the target cell, while leaving untargeted (healthy) cells unharmed.

HIV infection reduced to undetectable levels

In previous work, Prof. Dadachova had already managed to use the approach in the lab to target and destroy human immune cells infected with HIV.
At the meeting, she and her colleagues presented the results of a study in which they used the approach to treat blood samples from people infected with HIV.
The blood samples came from 15 HIV patients receiving HAART treatment at the AIDS Center at Montefiore, the University Hospital for Einstein College and academic medical center.
The results showed that RIT targeted and killed HAART-treated lymphocytes - types of white blood cells - and in most samples, reduced HIV infection to undetectable levels.
The team then went on to see if RIT could reach HIV-infected cells in the brain and central nervous system.
This would be a big step because current antiretrovirals do not cross the blood-brain barrier very well, which is why so many HIV patients treated with HAART often have severe mental impairment.
For this test, they used a lab model of the blood-brain barrier made with human cells and discovered that the same radioisotope-charged antibodies used in earlier experiments could destroy HIV-infected cells in the brain without damaging the barrier.
Prof. Dadachova says:
"We found that radioimmunotherapy could kill HIV-infected cells both in blood samples that received antiretroviral treatment and within the central nervous system, demonstrating RIT offers real potential for being developed into an HIV cure."
In another study published recently in the Journal of Infectious Diseases, researchers from Lund University in Sweden describe how they found that an aggressive new HIV strain leads to AIDS more quickly than other current strains.
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Oxytocin activates 'social' brain regions in children with autism

Researchers from Yale University have found that while engaging with social information, children with autism spectrum disorders experienced enhanced brain activity after a single dose of the hormone oxytocin was administered through a nasal spray.
Results of their findings are published in the journal Proceedings of the National Academy of Sciences.
Oxytocin is a naturally occurring hormone in the human body that has been implicated in social bonding. In fact, other research recently found that oxytocin stimulates the reward center in the brain, increasing partner attractiveness and strengthening monogamy.
According to the researchers from Yale, theirs is the first study to analyze how oxytocin affects brain function in children with autism spectrum disorders (ASDs).
2 unbranded nasal sprays
Researchers delivered oxytocin to children and adolescents with ASDs via a nasal spray, which resulted in enhanced brain activity toward social cues.
Led by study author Ilanit Gordon, the team conducted a double-blind, placebo-controlled experiment involving 17 children and adolescents with ASDs who were between the ages of 8 and 16.5.
After the participants were given either the oxytocin spray or a placebo, the researchers measured brain activity via functional magnetic resonance imaging (MRI) while the children and adolescents judged both socially and non-socially meaningful pictures.
The "social" pictures were images of eyes, whereas the "non-social" pictures were images of vehicles.
Because autism is a result of a neurological disorder that affects normal brain function, individuals with ASD have difficulty with communication and social interaction skills.
How the brains of these individuals react to socially meaningful images is therefore helpful for treatments that "target the core social dysfunction in ASD," the researchers note.

Oxytocin 'assists social attunement'

The team found that, compared with the placebo group, the participants who received a single nasal dose of oxytocin experienced enhanced activity in the brain.
Ilanit Gordon explains further:
"We found that brain centers associated with reward and emotion recognition responded more during social tasks when children received oxytocin instead of the placebo. Oxytocin temporarily normalized brain regions responsible for the social deficits seen in children with autism."
She adds that the oxytocin assisted social attunement - a process whereby brain regions involved with social behavior and cognition are activated more for social stimuli and less for non-social stimuli.
The researchers say that the neural attunement they observed "might facilitate social learning, thus bringing about long-term change in neural systems and subsequent behavioral improvements."
"Our results are particularly important considering the urgent need for treatments to target social dysfunction in autism spectrum disorders," Gordon concludes.
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Low vitamin D levels may damage the brain

Vitamin D plays an important role in maintaining bone health, but a new study led by University of Kentucky researchers claims that deficiency of this vitamin may cause damage to the brain and other organs.
The results, published in Free Radical Biology and Medicine, showed that when middle-aged rats were fed a diet low in vitamin D for several months, they developed free radical damage to the brain. They also performed less well in cognitive functioning tests for learning and memory.
The researchers say that several brain proteins were found to have significantly higher levels and that this contributes to significant nitrosative stress in the brain, possibly leading to cognitive decline.
The researchers claim that vitamin D deficiency is increasing in the US and its effects on an aging brain should not be underestimated.
Prof. Allan Butterfield, lead author of the paper, explains:
"Given that vitamin D deficiency is especially widespread among the elderly, we investigated how, during aging from middle-age to old-age, low vitamin D affected the oxidative status of the brain.
Adequate vitamin D serum levels are necessary to prevent free radical damage in brain and subsequent deleterious consequences."

Catch some rays

Often called the "sunshine vitamin," dietary sources of vitamin D are limited, and the study notes that when times are hard, individual food intake is not always the most nutritious.
The result of this is low levels of the vitamin, particularly among the elderly population. Coupled with the widespread use of sunscreens and popularity of wearing of long-sleeved clothing in the sunshine, levels of vitamin D are declining.
Low levels of vitamin D have previously been linked to Alzheimer's disease, the development of certain cancers and heart disease.
Prof. Butterfield recommends that everyone should allow themselves at least 10-15 minutes' exposure to sunshine every day to ensure that vitamin D levels are adequate.
He also suggests that vulnerable people should contact their physicians to have their levels tested. If they are low, individuals should consider taking supplements and eating more foods containing the vitamin, including oily fish, eggs and fortified milk.
Medical News Today recently reported that dancers from Birmingham's Royal Ballet in the UK have benefitted from vitamin D supplements, citing a report that showed greater improvements in muscle strength and fewer injuries for dancers taking them.
However, researchers from Johns Hopkins caution that too much can do more harm than good. Levels over 21 nanograms per milliliter increased levels of c-reactive protein, which is associated with hardening of blood vessels and an increased risk of cardiovascular problems.
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Menstrual cramps relieved by erectile dysfunction drug

For many women, monthly menstrual cramps can stop them in their tracks, causing nausea, vomiting, diarrhea and dizziness. But according to researchers from Penn State College of Medicines, a common drug used to treat erectile dysfunction in men could provide some relief.
In a recent study published in the journal Human Reproduction, the researchers, led by Dr. Richard Legro, studied the effects of sildenafil citrate - commercially known as Viagra - on women with primary dysmenorrhea (PD).
According to the team, PD is the most common reason for pelvic pain in women. Although it is painful and disruptive, it is not due to other diseases.
Anti-inflammatory drugs - including ibuprofen - are the most widely used treatment for pain relief of menstrual cramps, but the researchers say it does not work for all women, and is associated with ulcers and kidney damage when used repeatedly.
Erectile dysfunction drugs have previously shown an improvement in pelvic pain when taken orally, the researchers note, but this can often result in headaches, which they say makes it largely unsuitable for chronic use.
As a result, the researchers from this latest study assessed the results of using sildenafil citrate vaginally, which they say had not yet been tried to alleviate PD.

Larger studies needed to confirm results

Little blue pill
Little blue pill: women who took a drug that is used to treat erectile dysfunction in men experienced relief from their menstrual pain.
To conduct their research, the investigators randomized 25 women between the ages of 18 and 35 to use either sildenafil or a placebo drug.
Working with researchers at Nova Gradiska General Hospital in Croatia, the team from Penn State collected data on how the participants rated their pain during a 4-hour period.
After 2 hours, the researchers observed that uterine artery pulsatility index was "significantly lower" in the group taking sildenafil citrate, compared with those in the placebo group.
More importantly, the patients in the sildenafil group experienced alleviated menstrual pain, and there were no reported side effects.
Although the researchers thought the drug would soothe pain by increasing blood flow, they observed that both sildenafil and the placebo increased uterine blood flow, so they say they do not yet understand why the drug alleviates pain.
Dr. Legro, who is also professor of obstetrics and gynecology and public health sciences at Penn State, says:
"If future studies confirm these findings, sildenafil may become a treatment option for patients with PD. Since PD is a condition that most women suffer from and seek treatment for at some points in their lives, the quest for new medication is justified."
The study was funded by the National Institutes of Health, but the authors note that they did not meet their sample size due to loss of funding.
As a result, they say larger, multi-center studies must be completed in order to confirm the findings of their study.
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Long-term antacid use linked to vitamin B12 deficiency

Antacids are commonly used to neutralize the acid in the stomach, helping many individuals who have acid reflux. But a new study suggests that using this medication consistently for 2 years or more is linked to a deficiency of vitamin B12, which can have adverse effects for the nervous system.
The research, published in JAMA, is among the first to show associations between long-term exposure to antacids and vitamin B12 deficiency in a large population-based study.
The investigators say that antacids, including proton pump inhibitors (PPIs) and histamine 2 receptor antagonists (H2RAs), are some of the most commonly used pharmaceuticals in the US.
However, because they suppress the creation of gastric acid, the team says antacids may lead to malabsorption of vitamin B12. This vitamin helps to keep the nervous system - consisting of the brain, nerves and spinal cord - healthy.
"Vitamin B12 deficiency is relatively common," say the researchers, "especially among older adults; it has potentially serious medical complications if undiagnosed."
They continue:
"Left untreated, vitamin B12 deficiency can lead to dementia, neurologic damage, anemia and other complications, which may be irreversible."
To conduct their study, the researchers, led by Jameson R. Lam of Kaiser Permanente in California, looked at the link between using antacids and vitamin B12 deficiency within the Northern California population of Kaiser Permanente patients.

Stronger association in women and younger age groups

tablet disolving
The study found a link between 2 years' use of antacids or more and a deficiency of vitamin B12.
With a study population consisting of 25,956 vitamin B12-deficient patients and 184,199 control patients without the deficiency, the researchers compared their use of acid inhibitors by using electronic pharmacy, laboratory and diagnostic databases.
They found that among the patients who were newly diagnosed with a vitamin B12 deficiency, 12% were given a 2-year or more supply of PPIs, compared with 7.2% of patients who were exposed to PPIs in the control group.
Similarly, 4.2% of the vitamin-deficient patients had a 2-year or more supply of H2RAs, versus 3.2% in the control group.
The researchers say that receiving a 2 or more years' supply of either of these medications was associated with a greater risk for becoming vitamin B12 deficient. They add that doses over 1.5 PPI pills per day were more strongly linked to the deficiency than doses under 0.75 pills per day.
Though they say cannot completely rule out confounding factors as they relate to their findings, they do note that using antacids "identifies a population at higher risk of B12 deficiency."
The magnitude of the association was stronger in women and younger age groups, they add, noting that the association decreased after patients stopped using the antacids.
The authors conclude:
"These findings do not recommend against acid suppression for persons with clear indications for treatment, but clinicians should exercise appropriate vigilance when prescribing these medications and use the lowest possible effective dose."
Vitamins have been a hot topic of late. A recent study cast doubts over vitamin D supplementation, while another suggested that low vitamin B9 in males' diets could cause birth defects in offspring.
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Multivitamins 'waste of money,' say medical experts

"Enough is enough: stop wasting money on vitamin and mineral supplements," say medical experts in an editorial of a leading journal that has just published three new studies examining whether routine use of vitamin and mineral supplements brings health benefits.
Writing in Annals of Internal Medicine, the editorial authors conclude that most supplements do not prevent chronic disease or death, some may even be harmful in well-nourished adults, and there is a large body of evidence to support this.
Their routine use is not justified and they should be avoided, they urge, noting that:
"This message is especially true for the general population with no clear evidence of micronutrient deficiencies, who represent most supplement users in the United States and in other countries." Editorial co-author Dr. Edgar Miller, professor of medicine and epidemiology at Johns Hopkins Bloomberg School of Public Health in Baltimore, MD, told CBS News that people would be better off spending money on healthy foods, such as "fruits, vegetables, nuts, beans, low-fat dairy," and getting exercise.

US consumers spend over $28 billion a year on supplements

In the editorial, Dr. Miller and colleagues say despite "sobering evidence" of no health benefit and even of possible harm, US adults are spending more and more on multivitamins.
They note how use of multivitamins increased among US adults from 30% between 1988 and 1994 to 39% between 2003 and 2006, while overall use of dietary supplements grew from 42% to 53% over the same period.
There have been some dips - for instance, studies have linked certain supplements to negative outcomes - but overall the supplements industry has kept growing. In the US, it reached $28 billion a year in 2010. Trends in the UK and other European countries are similar, notes the editorial.
One point that stands out in the editorial is that consumers seem to react differently to evidence of negative results versus null results.
While overall use of supplements has gone up, use of certain individual supplements has gone down, for example beta-carotene and vitamin E. This decline followed reports of studies that showed these could be harmful.
On the other hand, evidence that daily supplements have null effects - that is, they make no difference to health - appear to have no effect on consumers and overall sales have kept growing.

Three studies suggest no benefit to supplements

In one of the studies published in the same issue as the editorial, Dr. Francine Grodstein, of Harvard School of Public Health, and colleagues examined data from the The Physicians' Health Study II, to look at the effect of long-term use of multivitamins on cognitive health.
The participants were nearly 6,000 male doctors aged 65 and over, who were randomized to take either a daily multivitamin pill or placebo pill for 12 years.
Tests of memory and cognitive function showed no difference between the two groups, and the researchers conclude:
"In male physicians aged 65 years or older, long-term use of a daily multivitamin did not provide cognitive benefits."
In another study, researchers reviewed evidence on the use of vitamin and mineral supplements to prevent heart disease and cancer, in order to update the guidelines for the US Preventive Services Task Force - an expert panel that advises the US government.
Their review found "limited evidence" to justify regular supplementation with vitamins and minerals for the prevention of cancer and cardiovascular disease (CVD).
They also note that beta-carotene appears to increase risk of lung cancer in smokers. And in the third study, researchers looked at the role of multivitamins and minerals in preventing a further heart attack, in more than 1,700 patients recruited at least 6 weeks after a heart attack (myocardial infarction).
Having a heart attack raises a person's risk of a further attack, stroke or death.
The patients were randomly assigned to receive either a daily high dose of multivitamins and minerals, or placebo pills for 5 years.
The study results showed no differences between the two groups in rates of chest pain, another attack, need for hospitalization, stroke or early death. However, the authors note that these results should be treated with caution since not all participants took the pills as they should.

Strong reaction from the supplement industry

The Council for Responsibile Nutrition (CRN), a group that represents the supplement industry, has voiced strong objections to the editorial.
They argue that while it is all very well to say instead of taking supplements people should concentrate on eating a healthy diet and exercising, this "fantasy" vision fails to recognize "real life."
Steve Mister, CRN's President and CEO, says:
"The editorial demonstrates a close-minded, one-sided approach that attempts to dismiss even the proven benefits of vitamins and minerals. It's a shame for consumers that the authors refuse to recognize the real-life need for vitamin and mineral supplementation, living in a fairy-tale world that makes the inaccurate assumption that we're all eating healthy diets and getting everything we need from food alone."
He says while not suggesting supplements are a panacea, he hopes the authors agree they have their place, especially as government studies show consumers are repeatedly failing to eat a healthy diet.
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What are the health benefits of green tea?

Green tea, native to China and India, has been consumed and hailed for its health benefits for centuries globally, but has only recently gained popularity in the US.
Tea is considered the most consumed beverage in the world behind water, however 78% of the tea consumed worldwide is black and only about 20% is green.1
All types of tea except herbal tea are brewed from the dried leaves of the Camellia sinensis bush. The level of oxidation of the leaves determines the type of tea.
Green tea is made from un-oxidized leaves and is the least processed type of tea and therefore contains the most antioxidants and beneficial polyphenols.
Green tea was used in traditional Chinese and Indian medicine to control bleeding and heal wounds, aid digestion, improve heart and mental health and regulate body temperature.4 Recent studies have shown green tea can potentially have positive effects on everything from weight loss to liver disorders to type 2 diabetes.
This Medical News Today information article on green tea provides a nutritional breakdown and an in-depth look at its possible health benefits, the different forms of green tea, and some precautions when consuming green tea.

Nutritional breakdown of green tea

Unsweetened brewed green tea is a zero calorie beverage. The caffeine contained in a cup of tea can vary according to length of infusing time and the amount of tea infused.
A cup of green tea
Green tea is becoming increasingly popular in the US
In general, green tea contains a relatively small amount of caffeine (approximately 20-45 milligrams per 8 oz cup), compared with black tea which contains about 50 milligrams and coffee with 95 milligrams per cup.2
Green tea is considered one of the world's healthiest drinks and contains the highest amount of antioxidants of any tea. The natural chemicals called polyphenols in tea are what are thought to provide its anti-inflammatory and anti-carcinogenic effects.
Epigallocatechin-3-gallate (EGCG) is the most studied and bioactive polyphenol in tea and has been shown to be the most effective at eliminating free radicals.1, 4
Green tea is approximately 20% to 45% polyphenols by weight, of which 60% to 80% are catechins such as EGCG.1

Possible health benefits of green tea

Below are the potential health benefits associated with green tea:
According to the National Cancer Institute, the polyphenols in tea have been shown to decrease tumor growth in laboratory and animal studies and may protect against damage caused by ultraviolet UVB radiation.
In countries where green tea consumption is high cancer rates tend to be lower, but it is impossible to know for sure whether it is the green tea that prevents cancer in these specific populations or other lifestyle factors.4
One large-scale clinical study compared green tea drinkers with non-drinkers and found that those who drank the most tea were less likely to develop pancreatic cancer, particularly women, who were 50% less likely to develop the disease.
Studies have also shown the positive impacts of green tea on breast, bladder, ovarian, colorectal, esophageal, lung, prostate, skin and stomach cancer.
Researchers believe that it is the high level of polyphenols in tea that help kill cancerous cells and stop them from growing, however the exact mechanisms by which tea interacts with cancerous cells is unknown.
Other studies have shown a lack of preventative effects of tea on cancer. The amount of tea required for cancer-preventive effects has also varied widely in studies - from 2- 10 cups per day.1
In 2005, the FDA stated that "there is no credible evidence to support qualified health claims for green tea consumption and a reduced risk of gastric, lung, colon/rectal, esophageal, pancreatic, ovarian, and combined cancers."1
Heart Disease:
A 2006 study published in the Journal of the American Medical Association concluded that green tea consumption is associated with reduced mortality due to all causes, including cardiovascular disease.
The study followed over 40,000 Japanese participants between the ages of 40 and 79 for 11 years, starting in 1994.
The participants who drank at least 5 cups of green tea per day had a significantly lower risk of dying (especially from cardiovascular disease) than those who drank less than one cup of tea per day.
Another study found that consuming 10 cups of green tea per day can lower total cholesterol, however, consuming 4 cups or less had no effect on cholesterol levels.1
Type 2 Diabetes:
Studies concerning the relationship between green tea and diabetes have been inconsistent. Some have shown a lower risk of developing type 2 diabetes for green tea drinkers than for those who consumed no tea, while other studies have found no association between tea consumption and diabetes at all.1
Weight Loss:
Green tea may promote a small, non-significant weight loss in overweight and obese adults; however, since the weight lost in the studies were so minimal, it is unlikely that green tea is clinically important for weight loss.
Other studies have found that green tea is helpful in preventing dental cavities, stress, chronic fatigue, treating skin conditions and improving arthritis by reducing inflammation.
Recent developments on the benefits of green tea from MNT news
Green tea or coffee may reduce stroke risk. Drinking green tea or coffee on a regular basis is associated with a reduced risk of stroke, according to a study published in the journal Stroke: Journal of the American Heart Association.5
Green tea may help fight prostate cancer. British researchers have scientifically proven that broccoli, turmeric, green tea and pomegranate help fight the most common cancer in men in the United States and the United Kingdom - prostate cancer.6

Forms of green tea

Green tea leaves
Green tea is available bottled and sweetened with sugar or an artificial sweetener, in single tea bags, loose-leaf, and in instant-powder. Green tea supplements are sold in capsule form or liquid extracts.
According to 2010 research presented at the American Chemical Society, bottled teas are not equivalent to brewed teas as some 16-oz bottled teas can contain fewer polyphenols than one cup of brewed tea.1
Green tea extract ointments have been approved by the FDA to topically treat genital warts.

Precautions and risks

There are little to no known side effects or contraindications to drinking green tea for adults. Those with severe caffeine sensitivities could experience insomnia, anxiety, irritability, nausea or upset stomach.3
Those taking anticoagulant drugs such as Coumadin/warfarin should drink green tea with caution due to its vitamin K content.3
If taken with stimulant drugs, green tea could possibly increase blood pressure and heart rate.3
Green tea supplements however, contain high levels of active substances that can trigger side effects and interact with other herbs, supplements, or medications.4 Green tea supplements are unregulated by the FDA and may also contain other substances unsafe for health or with unproven health benefits. Always check with a physician before starting any herb or supplement regimen.
In particular, pregnant or breastfeeding women, those with heart problems or high blood pressure, kidney or liver problems, stomach ulcers, or anxiety disorders should not take green tea supplements or extracts.4
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Friday, September 27, 2013

HIV spread may be prevented with discovery of new gene

Scientists have discovered a new gene that may have the ability to prevent human immunodeficiency virus (HIV) from spreading once it enters the body, according to a study published in the journal Nature.
Researchers from King's College London in the UK say the gene, called MX2, could lead to new effective and less toxic treatment against HIV - the virus that causes acquired immunodeficiency syndrome (AIDS).
For the study, the researchers conducted experiments on human cells, in which they introduced the HIV virus to two different cell lines. One cell line had the MX2 gene "switched on," while the other cell line had no MX2 expression.
On observing the effects, the researchers found that in the cells in which the MX2 gene was expressed, the HIV virus was unable to replicate, therefore stopping new viruses from being produced.
In the cell line in which the MX2 gene was switched off, the HIV virus replicated and spread.
Professor Mike Malim of the Department of Infectious Disease at King's College London, says:
"This is an extremely exciting finding which advances our understanding of how HIV virus interacts with the immune system and opens up opportunities to develop new therapies to treat the disease.
Until now, we knew very little about the MX2 gene, but now we recognize both its potent anti-viral function and a key point of vulnerability in the life cycle of HIV."
HIV virus
Researchers say a gene called MX2 may prevent the HIV virus (pictured) from spreading once in the body.
Photo credit: King's College London
According to the Mayo Clinic, HIV patients are currently recommended to take a minimum of three different anti-HIV drugs in order to avoid creating a form of drug resistance.
However, many of these drugs can cause serious side effects, including abnormal heartbeats, shortness of breath, skin rash, weakened bones and even bone death.
"Although people with HIV are living longer, healthier lives with the virus thanks to current effective treatments, they can often be toxic for the body, and drug resistance can become an issue with long-term use," says Prof. Malim.
He notes that it is important to continue finding new ways of mobilizing the body's natural defense system, and the MX2 gene appears to play an important role in initiating viral control in HIV sufferers.
"Developing drugs to stimulate the body's natural inhibitors is a very important approach because you are triggering a natural process and therefore won't have the problem of drug resistance," he adds.
"There are two possible routes - it may be possible to develop either a molecule that mimics the role of MX2 or a drug which activates the gene's natural capabilities."
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New rapid test could distinguish viral infections

A new blood test shows promise as a rapid way to help doctors determine whether a respiratory infection is viral or bacterial and thus reduce inappropriate use of antibiotics, which only work against bacteria.
The study is published in the journal Science Translational Medicine.
Study co-author Geoffrey Ginsburg, a professor at Duke University School of Medicine, says:
"Current tests require knowledge of the pathogen to confirm infection, because they are strain-specific. But our test could be used right away when a new, unknown pathogen emerges."
He explains the new test would be especially useful for spotting new viruses before they spread into outbreaks.
For example, in the case of pandemic flu or MERS, the new coronavirus that has erupted in the Middle East, it would be very important to diagnose new cases quickly, much faster than current diagnostic tests.
The new test uses a different approach to traditional diagnostics: instead of testing the pathogen, it tests the immune response in the infected person.
Image of a virus
The new rapid test was able to detect viral infections with 90% accuracy by determining how strongly genes in immune cells and other blood cells were switched on.
Using an approach called "reverse transcription polymerase chain reaction (RT-PCR)," the test evaluates how strongly certain genes in immune cells and other cells in the blood are switched on.
Previous studies have shown these genes are more active in people with respiratory infections caused by viruses. They are not switched on in healthy people or those whose infection is caused by bacteria.
In their study, the team describes how they evaluated the test in a group of over 100 people and found it was able to identify, with nearly 90% accuracy, the ones with viral infections.
The group comprised patients (some with viral infection, the rest with bacterial infection) and healthy controls. The patients had attended a hospital emergency department complaining of fever.
The test positively identified viral infection in 89% of cases, and it correctly ruled out viral infection in 94% of cases.
The team concludes:
"These results show that RT-PCR-based detection of a host gene expression signature can classify individuals with respiratory viral infection and sets the stage for prospective evaluation of this diagnostic approach in a clinical setting."
Christopher W. Woods, co-author and an associate professor of medicine, pathology and global health at Duke and the Durham VA Medical Center, says bacterial resistance, which is largely driven by overuse of antibiotics, is a big global public health problem, causing infections that are increasingly difficult to manage:
"A tool that enables us to accurately identify viral infections could curb the indiscriminate use of antibiotics and reduce the development of resistant pathogens."
The US Centers for Disease Control and Prevention (CDC) says taking antibiotics for viral infections can do more harm than good, citing for instance, that where children are concerned, antibiotics are the most common cause of emergency department visits for adverse drug events in the US.
The team is now working to reduce the time it takes for the test to report results.
It currently takes 12 hours to analyze 30 genes, so Prof. Ginsburg says there is scope to reduce both the time and the number of genes.
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Antidepressants linked to higher risk of type 2 diabetes

A new systematic review of published studies suggests when prescribing antidepressant medication, clinicians should be extra aware that they are linked to raised risk for type 2 diabetes, although the study does not suggest the drugs are the direct cause.
Reporting their findings in the latest issue of Diabetes Care, researchers from the University of Southampton say use of antidepressants has risen sharply over recent years, and there are concerns they may have an adverse effect on glucose metabolism.
They note 46.7 million prescriptions for antidepressants were issued in 2011 in the UK.
Antidepressant use has also soared in the US, where a 2011 study found they are now the third most widely prescribed group of drugs.
Several studies have shown that antidepressant use is linked to diabetes, but the results have been varied, depending on the methods and numbers involved and also on the types of drugs themselves.
For instance, one study that found a link between antidepressants and risk for type 2 diabetes discovered the risk almost doubled in patients using two types of drugs at the same time: tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs).

Antidepressant users more likely to have type 2 diabetes

Researchers found a link between people who take antidepressants and type 2 diabetes, although it does not mean there is a direct causal effect.
For their systematic review, Southampton health psychologist Dr. Katharine Barnard and colleagues assessed 22 studies and three previous reviews that looked at the link between antidepressant use and risk for type 2 diabetes.
They found that overall, people on antidepressants were more likely to have type 2 diabetes.
Within that, however, the picture is somewhat "confused, with some antidepressants linked to worsening glucose control, particularly with higher doses and longer duration, others linked with improved control, and yet more with mixed results."
They note that although study quality was variable, the more recent, larger studies suggest a modest effect.
The researchers also propose that different types of antidepressants may be linked to different amounts of risk and call for long-term randomized, controlled trials to examine the effects of individual drugs.

Several 'plausible' explanations

While their review was not designed to investigate causes, the team says there could be several plausible explanations for the link. For instance, some antidepressants cause patients to put on weight, which in itself increases risk for type 2 diabetes.
But they also point out that some of the studies they reviewed found the raised risk for type 2 diabetes persisted when they took out the effect of weight gain, suggesting other factors could be involved.
Dr. Barnard says:
"Our research shows that when you take away all the classic risk factors of type 2 diabetes; weight gain, lifestyle etc, there is something about antidepressants that appears to be an independent risk factor."
She says that in light of rising prescriptions, "this potential increased risk is worrying," and:
"Heightened alertness to the possibility of diabetes in people taking antidepressants is necessary until further research is conducted."
Co-author Richard Holt, professor in Diabetes and Endocrinology at Southampton, adds:
"While depression is an important clinical problem and antidepressants are effective treatments for this debilitating condition, clinicians need to be aware of the potential risk of diabetes, particularly when using antidepressants in higher doses or for longer duration."
He says doctors prescribing antidepressants should be aware of this raised risk for diabetes and ensure they monitor patients for the condition, as well as take steps to reduce the risk by encouraging changes to lifestyle.
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Vitamin B may reduce risk of stroke

Researchers have uncovered evidence that suggests vitamin B supplements could help to reduce the risk of stroke, according to a study published in the journal Neurology.
Vitamin B supplements are said to be beneficial for many health issues, including stress, anxiety, depression, dementia, Alzheimer's disease and heart disease.
However, according to Xu Yuming of Zhengzhou University in Zhengzhou, China, previous studies have conflicting findings regarding the use of vitamin B supplements and stroke or heart attack.
"Some studies have even suggested that the supplements may increase the risk of these events," he adds.
In order to determine the role of vitamin B supplements in the risk of stroke, Prof. Yuming and colleagues analyzed 14 randomized clinical trials involving a total of 54,913 participants.
All studies compared use of vitamin B supplements with a placebo, or a very low dosage of the vitamin. All participants were then followed for a period of 6 months.
During this time, there were 2,471 reported strokes over all of the studies.
Results of the analysis revealed that the participants taking the vitamin B supplements had a 7% reduced risk of stroke, compared with those taking the placebo supplements or a low dosage of vitamin B.
However, the findings showed that taking vitamin B supplements did not reduce the severity of strokes or the risk of death.
The researchers found that a supplemental form of folate (vitamin B9) - a vitamin frequently found in fortified cereals - actually reduced the effect of vitamin B on the risk of stroke.
Additionally, the study showed that vitamin B12 did not have any effect on the risk of stroke.
The study authors explain that their "meta-analysis demonstrated that homocysteine-lowering therapy with B vitamin supplementation significantly reduced stroke events."
They continue:
We did not find significant benefit for reduction of stroke events in subgroup analyses according to intervention dose, reduction of homocysteine level, or baseline blood vitamin B12 concentration. Further analyses of B12 limited to folate-replete participants (with background of cereal folic acid fortification) also revealed no benefit."
However, the researchers note that the effect of vitamin B on stroke risk is dependent on many underlying aspects:
"Factors including the background of folate fortification of cereal products, follow-up time, status of absorption and response to B vitamin supplementation, the existence of chronic kidney disease (CKD) or high blood pressure (HBP), and baseline participant medication use can influence the effects of B vitamins supplementation."
According to the Centers for Disease Control and Prevention (CDC), stroke is the leading cause of death in the US, killing nearly 130,000 Americans every year.
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Universal flu vaccine closer after natural immunity study

UK scientists believe they have taken a significant step closer to a universal flu vaccine that would protect against all strains of seasonal flu and curb future pandemics.
The team, led by researchers at Imperial College London, reports the achievement in Nature Medicine.
Lead investigator Professor Ajit Lalvani, from the National Heart and Lung Institute at Imperial, says:
"New strains of flu are continuously emerging, some of which are deadly, and so the Holy Grail is to create a universal vaccine that would be effective against all strains of flu."

Flu virus always changing surface proteins

Current flu vaccines spur the immune system to make antibodies that recognize proteins on the surface of the virus. When these are spotted in an immunized person, the immune system mounts an attack against the virus.
The difficulty with this approach is that the flu virus is always changing its surface proteins, so different vaccines have to be developed every year as new strains emerge, leaving vaccine developers inevitably one step behind.
But the core of the flu virus is more stable and changes little as strains evolve, and researchers conducting lab experiments have suggested some immune cells may already protect against flu because they recognize unchanging proteins in the virus.
For instance, a group of US scientists recently took a step toward a universal flu vaccine with animal tests that suggested their vaccine caused the animals' immune system to make antibodies to those parts of the flu virus that do not change from strain to strain.

'Natural experiment'

However, this latest study is the first to use a "natural experiment" in a real human pandemic, the 2009 swine flu pandemic.
Prof. Lalvani describes it as a unique opportunity to find out whether the immune system could recognize and protect us against new strains for which we lack antibodies.
He and his colleagues asked 342 volunteers to donate blood samples and undergo nasal swabs just as the pandemic got under way. They then tracked the volunteers by sending them email questionnaires about their health and any symptoms over the next two flu seasons. If any volunteers had flu symptoms, they took a nasal swab and sent it to the lab.
The team found the volunteers who caught the flu but had either no symptoms or only mild symptoms were those whose blood samples at the start of the 2009 swine flu pandemic had more CD8 T cells, a type of immune cell that kills viruses. Those who fell severely ill had fewer of these cells.

'Blueprint' for vaccine - make more CD8 T cells

The researchers believe a vaccine that spurs the immune system to make more CD8 T cells could protect against serious disease from all flu viruses, including those that cross into human populations from birds and pigs.
Prof. Lalvani says the findings provide a "blueprint" for developing a universal flu vaccine:
"The immune system produces these CD8 T cells in response to usual seasonal flu. Unlike antibodies, they target the core of the virus, which doesn't change, even in new pandemic strains."
"We already know how to stimulate the immune system to make CD8 T cells by vaccination. Now that we know these T cells may protect, we can design a vaccine to prevent people getting symptoms and transmitting infection to others."
Such a vaccine could significantly limit seasonal flu and protect people against future pandemics, he adds.
It would be a different approach to conventional vaccines, which stimulate the immune system to develop antibodies in response to exposure to parts of a virus.
Researchers writing in PLOS Pathogens earlier this year, suggested a more effective route to a universal flu vaccine would be to combine T cell vaccines and antibody vaccines.
According to the World Health Organization (WHO), annual flu epidemics result in about three to five million cases of severe illness, and between one quarter and half a million deaths worldwide.
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Gene that triggers 'memory extinction' discovered

Many of us are the bearers of "bad" memories that, to this day, continue to affect our lives. Now, scientists say they have discovered a gene essential for "memory extinction," the process by which our brain replaces older memories with new experiences.
Researchers from the Massachusetts Institute of Technology (MIT) say the discovery could help people suffering from post-traumatic stress disorder (PTSD) by replacing "fearful" memories with more positive associations.
The gene, Tet1, has been found to play a critical role in memory extinction by controlling a small group of other genes that are necessary for the process.
For the study, published in the journal Neuron, the research team experimented on mice who had the Tet1 gene "knocked out," as well as on mice who had normal levels of the gene.
In order to measure the mice's ability to abolish memories, the mice were "conditioned" to fear a certain cage in which they received a small electric shock. Once the memory of the "cage shock" was formed, the mice were placed into the cage, but the researchers did not give them the shock.

Tet1 triggers 'memory extinction'

The researchers found that after a period of time, mice with normal Tet1 levels appeared to lose their fear of the cage, indicating that new memories replaced the old ones.
Li-Huei Tsai, director of MIT's Picower Institute for Learning and Memory, explains:
"What happens during memory extinction is not erasure of the original memory. The old trace of memory is telling the mice that this place is dangerous. But the new memory informs the mice that this place is actually safe. There are two choices of memory that are competing with each other."
However, the researchers add that the mice without the Tet1 gene remain fearful and are unable to extinguish the memory.
The team carried out another set of experiments that tested the mice's spatial memory.
These experiments showed that the mice without the Tet1 gene had the ability to learn to navigate a water maze, but they were unable to extinguish the memory of how to navigate the maze, further supporting the findings of the previous experiment.

Tet1 removes DNA methylation

The researchers explain that the Tet1 and other Tet proteins help to regulate the modifications of DNA that determine whether a certain gene will be expressed or not.
Tet1 alters the levels of DNA methylation - a modification that controls access to genes. High methylation levels prevent genes from being expressed, while low methylation levels allow them to be "switched on."
Tet1 and Tet proteins were found to remove DNA methylation, after the mice without Tet1 showed significantly lower levels of hydroxymethylation - the process leading to the removal of methylation - in both the hippocampus and cortex of the brain. These areas are key for learning and memory.

Demethylation higher in early memory genes

The researchers found that demethylation was most significant in a group of 200 genes, particularly a small subset referred to as "immediate early genes" - critical for memory formation.
In the mice without the Tet1 gene, it was found that immediate early genes were highly methylated, meaning it would be difficult for these genes to be expressed.
Previous research from MIT showed that an immediate early gene called Npas4 regulates other immediate early genes. In this study, the researchers found that in the promoter region of the Npas4 gene, methylation levels in mice without the Tet1 gene was almost 60%, compared with 8% in mice who had the Tet1 gene.
"It's a huge increase in methylation, and we think that is most likely to explain why Npas4 is so drastically downregulated in the Tet1 knockout mice," notes Prof. Tsai.
Matthew Lattai, associate professor of behavioral neuroscience at Oregon Health and Science University, who was not a part of the study, says the findings could pave the way for treatments for PTSD:
"By demonstrating some of the ways that regulatory genes are methylated in response to Tet1 knockout and behavioral experience, the authors have taken an important step in identifying potential pharmacological treatment targets for disorders such as PTSD and addiction."
Furthermore, the research team also discovered why mice without the Tet1 gene still have the ability to learn new tasks.
They found that during fear conditioning, the methylation of the Npas4 gene reduced to 20% - a level low enough for Npas4 to be expressed, therefore creating new memories.
The team hypothesize that the mice's fear is so strong that it may trigger other demethylation proteins, such as Tet2 or Tet3.
Overall, the researchers say that their findings suggest there is a threshold level needed in order for methylation to take place, and that Tet1 is responsible for maintaining low methylation to make sure that the genes needed for memory formation are ready to be "turned on" when needed.
Further research from the team will involve searching for ways to artificially increase Tet1 levels and seeing whether this could "boost" memory extinction. Additionally, they plan to determine the effects of erasing all Tet genes.
Meelad Dawlaty of MIT's Whitehead Institute, adds:
"This will not only help us further delineate epigenetic regulation of memory formation and extinction, but will also unravel other potential functions of Tets and methylation in the brain beyond memory extinction."
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Breast health linked to eating peanut butter and nuts

By eating more peanut butter during their high school years, girls could be improving their breast health in adulthood, according to a US study published recently in the journal Breast Cancer Research and Treatment.
Dr. Graham Colditz, of Washington University School of Medicine in St. Louis, and colleagues found that girls aged 9 to 15 who ate peanut butter and nuts twice a week were 39% less likely to develop benign breast disease by the age of 30 than girls who did not.
Benign breast disease includes lumps or tender spots that turn out to be fibrous tissue and/or cysts, as well as other conditions like hyperplasia, an overgrowth of the cells that line the ducts in the glandular breast tissue.
Although benign breast disease is not cancerous, it can raise the risk of developing breast cancer later in life.
Dr. Colditz, associate director for cancer prevention and control at the Alvin J. Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine, says:
"These findings suggest that peanut butter could help reduce the risk of breast cancer in women."
For their study, he and his colleagues looked at health data on over 9,000 American schoolgirls recruited to The Growing Up Today Study between 1996 and 2001. This included detailed information about food consumption as captured in food frequency questionnaires that the girls filled in on enrollment.
The data also included reports from the girls between 2005 and 2010, when they were 18 to 30 years old, that indicated whether they had ever been diagnosed with biopsy-confirmed benign breast disease.
When they compared the two sets of data, the researchers found that participants who had eaten peanut butter or nuts twice a week were 39% less likely than peers who never ate those foods to receive a diagnosis for benign breast disease.
The data suggest pulse foods - soy and other beans and lentils - and corn may also be linked to reduced risk of benign breast disease, but because they did not feature as much in the diets of these girls, the evidence was not so strong.
The researchers also note that:
"Girls with a family history of breast cancer had significantly lower risk if they consumed these foods or vegetable fat."
And they concluded that "consumption of vegetable protein, fat, peanut butter, or nuts by older girls may help reduce their risk of BBD [benign breast disease] as young women."
This is not the first study to tie diets rich in vegetable fats - such as those present in peanut butter, nuts and pulse foods - to a lower risk for benign breast disease. But it is the first to find the evidence by comparing data captured during adolescence with followed-up cases of diagnosed disease, as opposed to asking young women to recall what they ate when they were in high school.
Dr. Colditz says girls would do well to eat more peanut butter and nuts and consume less junk foods and sugary drinks, especially in view of the rise in obesity.
Funds from the Breast Cancer Research Foundation and the National Institutes of Health (NIH) helped finance the study.
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Saturday, July 27, 2013

NICE gives green light to treatment for wet AMD in final guidance

The National Institute for Health and Care Excellence (NICE) has published final guidance recommending aflibercept solution for injection as an option for treating wet age-related macular degeneration (AMD).
Wet AMD is an eye condition that affects the macula (a tiny part of the retina at the back of the eye). AMD causes problems with central vision - for example, straight lines may appear wavy and blind spots may develop in the field of vision.
Macular degeneration is diagnosed as either dry (non-neovascular) or wet (neovascular). Neovascular refers to growth of new blood vessels in an area, such as the macula, where they are not supposed to be.
There are an estimated 26,000 new cases of wet AMD in the UK each year. Risk factors include increasing age, cigarette smoking (smokers having a 3.6 times greater risk of developing age-related macular degeneration compared with people who have never smoked), and exposure to high levels of UV light. It is also more common in women than men [i].
Aflibercept is recommended as an option for treating wet age related macular degeneration only if: it is used in accordance with the recommendations for ranibizumab in NICE technology appraisal guidance 155 [ii] (re-issued in May 2012), and the manufacturer provides aflibercept solution for injection to the NHS under the terms agreed with the Department of Health as part of a patient access scheme.
Professor Carole Longson, Health Technology Evaluation Centre Director at NICE said: "Wet AMD can have a significant impact on vision, independence and quality of life. Today's guidance, which comes soon after aflibercept received its licence, provides healthcare professionals with clear advice on where and when this treatment can add value as another treatment option for those affected by this distressing condition. "
This is NICE's final guidance on this technology and now replaces local recommendations across the country.

About the guidance

  • The guidance is available on the NICE website.
  • People currently receiving aflibercept solution for injection whose disease does not meet the criteria detailed above should be able to continue treatment until they and their clinician consider it appropriate to stop.
  • Aflibercept solution for injection (Eylea, Bayer Pharma) is a soluble vascular endothelial growth factor (VEGF) receptor fusion protein which binds to all forms of VEGF-A, VEGF-B, and the placental growth factor. Aflibercept solution for injection prevents these factors from stimulating the growth of the fragile and permeable new blood vessels associated with wet age-related macular degeneration. Aflibercept solution for injection has a UK marketing authorisation 'for adults for the treatment of neovascular (wet) age-related macular degeneration (AMD)'.
  • The summary of product characteristics states that the recommended dose for aflibercept is 2 mg and that treatment should be given monthly for 3 consecutive 2 mg doses, followed by 1 injection every 2 months. Each 100 microlitre vial contains 4 mg of aflibercept. Aflibercept solution for injection must only be administered by a qualified doctor experienced in administering intravitreal injections. The summary of product characteristics also states that there is no need for monitoring between injections. After the first 12 months of treatment, the treatment interval may be extended based on visual and anatomic outcomes. In this case, the schedule for monitoring should be determined by the treating doctor.
  • The list price of aflibercept 40 mg/ml solution for injection is £816 per 100-microlitre vial (excluding VAT; 'British national formulary' [BNF] edition 52).
  • The Committee noted that its preferred analyses incorporated the confidential discount to the list price of aflibercept and a range of discounts (from 0 to 50%) to the list price of ranibizumab. It also noted that, when discounts to the list price of ranibizumab ranged from 0 to 45%, aflibercept had lower costs and quality-adjusted life years (QALYs) than ranibizumab, which resulted in ICERs for aflibercept compared with ranibizumab ranging from £1,692,500 to £16,700 saved per QALY lost and that, when a 50% discount was applied to the list price of ranibizumab, aflibercept was dominated by ranibizumab in both the worse-seeing eye and better-seeing eye model. However, the Committee was aware that, in both the manufacturer's and the ERG's analyses, the differences in total costs and QALYs were very small. The Committee therefore concluded that aflibercept could be recommended as a cost effective use of NHS resources if ranibizumab would otherwise be the treatment used.
  • The independent Appraisal Committee decided that an appraisal consultation document (ACD) was not needed for this appraisal, so the recommendations went straight to a final appraisal determination (FAD). This happens when the Committee recommends a treatment in line with its licensed indication.
  • The manufacturer of aflibercept has agreed a patient access scheme with the Department of Health. This involves a confidential discount applied to the list price of aflibercept solution for injection. The level of the discount is commercial-in-confidence.
  • NICE technology appraisals apply across the NHS in England and Wales.
  • Section 7(6) of the National Institute for Health and Care Excellence (Constitution and Functions) and the Health and Social Care Information Centre (Functions) Regulations 2013 requires clinical commissioning groups, NHS England and, with respect to their public health functions, local authorities to comply with the recommendations in this appraisal within 3 months of its date of publication.
  • Further details on NICE technology appraisals.

Statement from RNIB

Steve Winyard, RNIB's Head of Campaigns, said: "We welcome the news NICE has approved the use of a further drug to treat the biggest cause of sight loss in the UK.
"Not only does it mean patients now have the choice of two different drugs to treat their condition, it also means if they choose the newly approved drug it could mean less visits to the hospital.
"Some people with wet AMD do not respond to the current NICE approved treatment and another option could mean the difference between saving and losing their sight.
"We've recently launched a national campaign encouraging over 50s to spot the signs of wet AMD, which affects about 40,000 people each year and can destroy a person's sight in as little as three months.
"Losing your central vision can have profound consequences with many people unable to carry out basic tasks such as driving, chopping vegetables, or writing a shopping list. However, it doesn't have to be this way and people should not be losing their sight unnecessarily when there's treatment available."
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New links between diet and acne

A review carried out by the University of Hull has shed new light on the relationship between acne and diet.
Published in Dermatological Nursing, the comprehensive review assesses the latest evidence and findings about the effects of food and nutrition on acne and suggest that high glycemic index foods such as milk could exacerbate the skin condition.
The review was carried out by HONEI (Humber Obesity Nutrition Education and Innovation) a centre for food research, based at the University of Hull.
Acne is one of the most common skin conditions and is often associated with adolescents but its prevalence among adults is increasing.
Facial acne can be stigmatising and deeply upsetting. Research has shown that the adverse social, psychological and emotional effects of acne can be comparable to those of more serious chronic conditions such as; epilepsy, diabetes arthritis or psoriasis.
Extensive studies have been carried out to assess the impact diet has on acne and research has so far suggested some diets, such as those containing high glycemic index foods e.g. milk can exacerbate acne.
HONEI is a world-leading centre of food related research and has previously conducted studies into the effect of dark chocolate on cholesterol levels as well as studies on soy to determine whether it could help combat certain health problems associated with osteoporosis and type 2 diabetes. HONEI is also currently undertaking extensive research into the benefits of polyphenols on cardiovascular health.
Dr Katerina Steventon, Research Fellow with HONEI and the University of Hull's Faculty of Health and Social Care, said: "There is growing evidence of the link between diet and acne which is becoming stronger as new evidence comes to light, although nothing has been fully proven yet, it is only a matter of time.
"The research review suggests a low glycemic index diet but also a healthy diet, rich in fruit and vegetables, can have a protective effect on acne. Further research is needed to fully understand the role diet plays in acne in specific populations."
HONEI will be carrying out its own primary research examining the effects of certain foods on acne later this year.
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Full moon affects not only werewolves but human sleep too

It appears there is some truth in the saying that it is harder to get a good night's sleep when the moon is full. Tests on Swiss volunteers as they spent nights in a sleep lab showed a link between moon phases and sleep patterns: sleep was more disturbed when there was a full moon.
Led by a team from the University of Basel, the researchers report in the July 25th online issue of Current Biology how they found a full moon disrupts sleep quality.
Lead author Professor Christian Cajochen, who is based at the Centre for Chronobiology at the Psychiatric Hospital of the University of Basel, and colleagues analyzed data taken from over 30 healthy volunteers of various ages as they slept in a sleep lab.
As the participants slept, their brain activity, eye movements, and hormone levels in different phases of sleep were measured.
Neither the lab researchers who took the sleep measurements nor the participants were aware that the authors were later going to do an analysis of the sleep data against moon cycles.
It was only after the lab results were produced that it was decided to compare them to moon phases.
Also, the participants could not see the moon from their beds in the sleep lab.
The analysis showed that the participants did not sleep so well when there was a full moon. This was reflected in both subjective measures (where the participants themselves said whether their night's sleep had been good or not) and the objective measures.
On nights with a full moon:
  • Brain activity associated with deep sleep (during non-rapid eye movement) fell by nearly a third,
  • On average it took the volunteers 5 minutes longer to fall asleep, and their sleep was 20 minutes shorter, and
  • There was a drop in levels of melatonin, a protein that helps regulate sleep and wake cycles.
The authors write:
"This is the first reliable evidence that a lunar rhythm can modulate sleep structure in humans when measured under the highly controlled conditions of a circadian laboratory study protocol without time cues."
Cajochen suggests the response to moon phase that they observed, which they call the "circalunar rhythm," could be a relic of ancient times when human behavior was more heavily influenced by the moon.
It would seem that even for some of today's humans, paying attention to phases of the moon can be a lifesaver. A study published in 2011 suggests you are less likely to end up as a lion's dinner if you pay close attention to the moon; in southeastern Tanzania, that is.
There is evidence that many organisms, especially those that live in the sea, are influenced by moonlight.
However, this study finds that even without being able to see the moonlight, the body is somehow still responding to the fact it is a full moon.
It remains for other studies now to uncover the biology that explains this influence.
A large study from the Netherlands published earlier this month suggests that a good night's sleep boosts the benefits of a healthy lifestyle on the heart.
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'Marijuana in adolescence can cause permanent brain damage'

New research may give backing to parents telling teens to "just say no." A study in mice from the University of Maryland School of Medicine reveals that regular use of marijuana during adolescence could damage brain function, potentially increasing the risk for schizophrenia and other psychiatric problems.
The study, which was recently published in Neuropsychopharmacology, had scientists examining cortical oscillations - patterns of the brain's neuron activity - in mice. These oscillations become abnormal when schizophrenia or other psychiatric disorders are present.
Researchers exposed young mice to low doses of tetrahydrocannabinol (THC), which is the active ingredient present in marijuana, for 20 days. Then the mice were returned to their family to continue developing.
When the mice became adults, the scientists discovered that their cortical oscillations were severely modified, and the mice showed signs of impaired cognitive functions.
Sylvina Mullins Raver from the University of Maryland says: "The striking finding is that, even though the mice were exposed to very low drug doses, and only for a brief period during adolescence, their brain abnormalities persisted into adulthood."

Effects of marijuana (or not) on adult brains

Interestingly, the researchers originally set out to test a hypothesis that marijuana use effects cortical oscillations in adults. But when they repeated the experiment on adult mice who had never been exposed to the drug previously, they found that both the oscillations and cognitive behavior stayed normal.
So, it appears that adolescence is the period of development when marijuana use can take its biggest toll. Senior author Dr. Asaf Keller adds:
"We looked at the different regions of the brain. The back of the brain develops first, and the frontal parts of the brain develop during adolescence.
We found that the frontal cortex is much more affected by the drugs during adolescence. This is the area of the brain that controls executive functions, such as planning and impulse control. It is also the area most affected in schizophrenia."

Implications for marijuana legalization

Now that marijuana has been legalized in 19 US states and the District of Columbia, the study's results about long-term effects of marijuana use are particularly relevant. The authors point to controversy spanning back to 20 years ago about whether or not marijuana use can cause permanent damage and contribute to psychiatric disorders.
Dr. Keller adds: "There is likely a genetic susceptibility, and then you add marijuana during adolescence and it becomes the trigger."
The research team will continue to study the changes in cortical oscillations with a view to potentially reverse the effects some day.
"We are hoping we will learn more about schizophrenia and other psychiatric disorders, which are complicated conditions,"
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Visit gym or take a pill? Drug mimics exercise

Science gets a lethargic cheer from lazy people around the world this week, as a study published in Nature magazine reveals that we may one day be able to take a compound that produces similar effects in the body as exercise.
The study comes from researchers at the Scripps Institute in Jupiter, FL, who injected overweight mice with a compound they created. As reported in the New York Times, the results show that the researchers' compound increased activation of Rev-erb, a protein involved in controlling circadian rhythms and biological clocks. As such, the mice lost weight and improved their cholesterol, even while continuing to eat a high-fat diet.
What's more, the mice used more oxygen during the day and 5% more energy than the control group. The interesting thing to note here is that the treated mice did not exercise any more than the untreated mice. In some cases, the Times report says, the treated mice were lazier and more inactive than they were before the injections.

How the compound works

People exercising in gym
Though researchers from Scripps Institute created a compound that mimics exercise, they still say many benefits of exercising cannot be recreated in a drug.
In muscles, regular exercise increases the amount and power of mitochondria, which are the powerhouses that generate most of the cell's energy.
When the researchers injected their compound into various muscle cells in the mice, those cells then released an increased amount of Rev-erb. As a result, those cells created new mitochondria and strengthened the existing ones.
Thomas Burris, co-author of the study, said that the drug "certainly seems to act as an exercise mimic," and reportedly said that the drug might be able to allow people who are disabled or incapacitated to attain benefits of exercise without actually physically doing it.

But is taking a pill for exercise really recommended?

The results of the study will prompt several discussions about the ethical, as well as the physical, implications of using a pill to achieve exercise results. For example, would it become a banned doping drug used by professional athletes?
Thomas Burris says that he has been warned by other scientists "to expect some weird phone calls." But he says his main goal is to help people who are unable to exercise rather than those who choose not to.
Burris also notes that there are many benefits to exercising that cannot all be recreated in a drug.
Recent studies have shown that exercise can have an effect at the DNA level against fat cells, as well as help the brain become more resilient.
In short, if you are able to exercise, you probably should.
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Common blood pressure drugs may slow dementia decline

A class of drug used to lower blood pressure could potentially slow the rate of cognitive decline in dementia and even boost brain power, according to a study published by BMJ Open.
Researchers from Ireland analyzed the cognitive decline and brain power of 361 patients with an average age of 77. All had been diagnosed with either Alzheimer's disease, vascular dementia, or a mixture of both.
Of these patients, 85 were already using the blood pressure-lowering (antihypertensive) drugs known as ACE inhibitors (angiotensin-converting enzyme inhibitors). This is a commonly used class of antihypertensive drug. Thirty of the patients who were newly prescribed ACE inhibitors during the first six months of treatment were also analyzed for their brain power activity.
Between the years 1999 and 2010, the researchers used the Standardized Mini Mental State Examination (SMMSE) or the Quick Mild Cognitive Impairment (Qmci) to test the cognitive decline of each patient. This was done on two separate occasions, six months apart.
The patients who were taking ACE inhibitors had slower rates of cognitive decline in the study compared with patients who were not taking the drugs.
The study also revealed that in patients who had been newly prescribed the ACE inhibitors over the six-month period, their brain power improved in comparison with both those already taking them and those not taking them at all.
However, the study authors add that this could be due to the newly prescribed patients having better control over their medication regimen, or due to better blood pressure control or improved blood flow to the brain.
The researchers say:
"This [study] supports the growing body of evidence for the use of ACE inhibitors and other [blood pressure-lowering] agents in the management of dementia.
Although the differences were small and of uncertain clinical significance, if sustained over years, the compounding effects may well have significant clinical benefits."
The researchers warn, however, that previous research has indicated that ACE inhibitors may be harmful in some cases, so if future benefit of the drugs in dementia is proven, it may be limited to certain groups of patient.
The study authors call for further research and a controlled trial to confirm their findings. They say:
"If these data can be reproduced in a randomized trial of sufficient length, incorporating appropriate outcome measures, such as an amyloid positron emission tomography (PET), then these agents are likely to have significant benefits in delaying or even preventing dementia."
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Virus discovery: 'blast' mechanism used to infect host

Researchers have discovered the first "pressure-driven infection mechanism" in a human virus, which blasts infectious DNA into cells with pressure eight times higher than that of a typical car tire.
The study, published in the Journal of the American Chemical Society, suggests that this discovery could open the door to new treatments for viral infections.
Researchers from the US and Sweden analyzed the pressure inside the herpes simplex virus 1 (HSV-1), the infection that causes cold sores.
It was found that the HSV-1 virus enters human cells, settles on the nucleus and then blasts its way into DNA using high pressure built up from a "nanometer-scale protein shell" called the capsid, researchers explain. The capsid is the shell that contains the viral genome.
The researchers say that the viruses responsible for infections such as influenza and HIV are quickly becoming resistant to drugs that target viral proteins. The proteins can quickly disguise themselves and become resistant to ant-viral drugs as a result of genetic mutation.
For example, previous research published in PLoS Computational Biology has suggested that drug resistance to HIV, the virus that causes AIDS, can be caused by pre-existing mutations, which can actually progress even more once treatment is initiated.
Findings such as this one have led to a search for weaknesses in viruses that do not involve viral proteins, the researchers add, a reason why this study was conducted.
Previous research has also shown many viruses that infect bacteria, called bacteriophages, use the same pressure-driven mechanism in order to blast their DNA into bacteria nuclei.
They add that the same mechanism also exists in eight related viruses, including chickenpox in children, shingles in adults, and the virus responsible for mononucleosis.
The researchers believe that evolution has meant that this technique is now apparent in viral infection, paving the way for the development of treatments that can defeat particular viruses, such as HSV-1, in the same way.
They say:
"Despite billions of years of evolution separating eukaryotic viruses and bacteriophages, pressure-driven DNA ejection has been conserved. This suggests it is a key mechanism for viral infection and thus presents a new target for antiviral therapies."
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"More harm than good" from red grape antioxidant

A natural antioxidant found in red grapes, resveratrol, may not be as beneficial as previously thought. New research in older men suggests that it may counteract the benefits of cardiovascular exercise.
The study comes from researchers at the University of Copenhagen, who suggest that eating an antioxidant-rich diet may hinder the health benefits of exercise, such as lower blood pressure and cholesterol.
The researchers note that since aging is associated with impaired vascular functions due to oxidative strain, resveratrol - which has been shown to decrease vascular disease and improve cardiovascular health - was initially expected to improve cardiovascular health in older men. After all, it has been proven in animal studies to be of benefit in that department.
But in a surprise twist, the researchers found that unlike in our animal counterparts, resveratrol actually impairs the cardiovascular benefits of exercise in older men.
For 8 weeks, the researchers followed 27 men who were around 65 years of age and in good health. During that time, the men all took part in high-intensity exercise, but half of the men received 250 mg of resveratrol each day, while the other half received a placebo pill.
Lasse Gliemann, a researcher who worked on the study, explains the results and design of the experiment:
"The study design was double-blinded, thus neither the subjects nor the investigators knew which participant received either resveratrol or placebo."
"We found that exercise training was highly effective in improving cardiovascular health parameters, but resveratrol supplementation attenuated the positive effects of training on several parameters, including blood pressure, plasma lipid concentrations and maximal oxygen uptake."
So even though the men were gaining health benefits from exercising, the ones who took a daily dose of resveratrol saw many of these benefits effectively wiped out.
There have been several studies lately both lauding and denouncing the health benefits of resveratrol. A 2012 study, for example, shows resveratrol's potential as a therapy for diabetes, Alzheimer's disease and heart disease. Yet, another study from the same year reveals that the antioxidant may not benefit healthy women.
Though there are arguments for and against the compound found in red wine, this particular study from the University of Copenhagen suggests that "reactive oxygen species, generally thought of as causing aging and disease, may be a necessary signal that causes healthy adaptions in response to stresses like exercise."
In short, ingesting too many antioxidants may not be a good thing, but the researchers do say that the amount of resveratrol given to the men in the study exceeds what would normally be ingested through food alone.
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Hope that nerve damage in MS could be repaired

By shedding light on how cells regenerate the myelin sheath surrounding nerve fibres in the brain, a new study published in Nature Neuroscience opens the door to treatments that could repair nerve damage and restore lost function in patients with multiple sclerosis (MS).
MS is a disease in which the immune system attacks and destroys myelin, the protein that insulates the nerves in the spinal cord, brain and optic nerve and stops the electrical signals from leaking out.
As the myelin is gradually destroyed, patients experience symptoms ranging from mild numbness in the limbs to paralysis or blindness.
The disease progresses not just because the immune system gradually destroys the myelin, but also because a natural repair process fails. Cells called oligodendrocytes are able to repair the myelin damage themselves - "remyelination" - but in MS this fails after a while.
There are over 400,000 living with MS in the European Union. There are currently no approved therapies that tackle the disease by promoting regeneration of the myelin.

Two immune cell findings may be important for future therapy

In this latest study, led by the Universities of Edinburgh and Cambridge in the UK, researchers describe how they studied immune cells called macrophages, known to be involved in remyelination, and found two important features that could lead to new therapies that promote myelin regeneration:
  1. For remyelination to proceed, macrophages have to become anti-inflammatory
  2. Macrophages release a protein called activin-A that actively encourages remyelination.
First author Dr Veronique Miron, of the Medical Council Centre for Regenerative Medicine at the University of Edinburgh, says in a statement:
"Approved therapies for multiple sclerosis work by reducing the initial myelin injury - they do not promote myelin regeneration.
This study could help find new drug targets to enhance myelin regeneration and help to restore lost function in patients with multiple sclerosis."
For their study, Miron and colleagues examined myelin regeneration in human tissue samples and in mice.
They wanted to understand what stimulates remyelination and which biological molecules, cells, or other factors may be involved that could serve as targets for regenerative treatments that restore lost vision, movement and other functions in people with MS.
Previous studies have shown that macrophages - immune cells that gobble up disease pathogens, debris and other undesirable materials, among other things - are also involved in regeneration.
For example, there is a group of macrophages called M2 that is essential for regenerating skin and muscle.

Hunt for potential drug targets

So what Miron and the team wanted to find out was whether M2 macrophages were also involved in myelin regeneration, and if so, were there particular molecules involved in stimulating remyelination that could serve as useful drug targets?
On examining a mouse model of human myelin damage and regeneration, the team found that M2 macrophages were present and increased in number when remyelination started. This suggests, they say, that M2 macrophages may control remyelination.
Previous research had already established that oligodendrocytes are the cells that normally produce the myelin found in the brain and spinal cord, so Miron and colleagues set about trying to discover if M2 macrophages were able to trigger the oligodendrocytes on their own, or whether they needed to work with another group of cells or processes.
To find out they put some oligodendrocytes in a test tube and exposed them to proteins released by M2 macrophages.
The result was a success. Exposure to M2 macrophage proteins spurred the oligodendrocytes to make more myelin.
The researchers also found that when they took M2 macrophages out of the equation, remyelination dramatically reduced, showing they were necessary for myelin to regenerate.
This was confirmed in further examinations of mouse models of remyelination, and brain tissue from people with MS. The researchers found in both cases that high numbers of M2 macrophages are present when remyelination is efficient, and the numbers are vastly reduced when it is not.
The team also found that a protein produced by macrophages, activin-A, contributes to the regenerative effects of M2 macrophages.
They found high levels of activin-A in M2 macrophages when remyelination was starting and also when they added the protein to oligodendrocytes in test tubes they started to make myelin.
To confirm the role of activin-A, the researchers blocked its effect on oligodendrocytes after myelin damage, and discovered the M2 macrophages were not as able to stimulate them to make more myelin.
They conclude that their findings point to a key step in myelin regenration, namely that when M2 macrophages release activin-A, they spur oligodendrocytes to make myelin.

Potential for synergistic drugs

The study suggests it may be possible to partner drugs that reduce the initial myelin damage, with ones that regenerate it in the central nervous system and thus restore lost functions in MS patients.
The researchers now plan to look in more detail at how activin-A works and whether its effects can be enhanced.
The study was funded by the MS Society, the Wellcome Trust and the Multiple Sclerosis Society of Canada.
In another study published earlier this year, researchers described how a new treatment for MS that resets the patient's immune system was found to be safe and well tolerated in a small trial.
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