'Fasting-mimicking diet' may promote health and longevity

A new study published in Cell Metabolism suggests following a calorie-restricted diet that mimics fasting for just 5 days a month for 3 months may promote longevity and reduce a number of risk factors for cancer, diabetes and cardiovascular disease.

Researchers found participants who followed a fasting-mimicking diet experienced a reduction in risk factors linked to aging, cardiovascular disease, diabetes and cancer.

Study co-author Valter D. Longo, of the FIRC Institute of Molecular Oncology in Italy and the University of Southern California, and colleagues say the research demonstrates the first anti-aging, healthspan-promoting intervention that doctors could feasibly recommend for patients.

Previous research from Longo in June last year suggested prolonged fasting - defined as consuming only water for 2-4 days - can "reboot" the human immune system. That is, fasting can help clear out damaged cells and regenerate new ones.

Another study published later that month also found periodic fasting may protect against diabetes among individuals at high risk for the condition.

However, Longo and colleagues note that humans find it psychologically challenging to engage in such extreme dieting, and it can also have adverse health effects - particularly for older individuals.

"These concerns point to the need for dietary interventions that induce prolonged fasting-like effects while minimizing the risk of adverse effects and the burden of complete food restriction," they note.

Fasting diet promoted cell regeneration, extending lifespan in mice

To address this need, the researchers developed a fasting-mimicking diet (FMD) - a low-protein, low-fat diet high in healthy fats. By activating markers associated with prolonged fasting, such as low glucose levels and high levels of ketone bodies, the diet was able to simulate the effects of fasting.

Firstly, the team tested the diet in middle-aged mice, feeding them the diet for 4 days, twice a month. Mice fed the FMD intervention were compared with mice fed a control diet.

The team found mice fed the FMD intervention had much higher numbers of stem cells, and they experienced regeneration of an array of other cell types, including bone, muscle, liver, brain and immune cells, compared with mice fed the control diet.

In addition, the FMD intervention appeared to extend the lifespan of mice and promote better overall health. They experienced better learning and memory, lower incidence of cancer and inflammatory diseases and fat loss without a reduction in lean body mass, compared with control mice.

Reduction in risk factors for aging, CVD, diabetes and cancer in humans

Next, the team tested a similar FMD intervention in a group of 19 generally healthy people aged 18-70. These participants were required to follow the diet for 5 days a month for 3 months. The diet provided them with between 34-54% of their normal caloric intake, as well as 11-14% proteins, 42-43% carbohydrates and 44-46% fat.

The 19 participants following the FMD intervention were compared with a group of 18 generally healthy aged-matched individuals who continued to follow their normal diet.

Compared with the participants who consumed their standard diet, those who followed the FMD intervention experienced a reduction in risk factors linked to aging, cardiovascular disease (CVD), diabetes and cancer, including lowered blood glucose, reduced markers of inflammation and weight loss.

The team notes that only 5% of FMD participants were disqualified from the study for failing to comply with the dietary regime.

Longo and colleagues say their findings indicate that following an FMD intervention periodically may promote longevity in humans and protect against risk factors for certain diseases. They add:

"Although the clinical results will require confirmation by a larger randomized trial, the effects of FMD cycles on biomarkers/risk factors for aging, cancer, diabetes, and CVD, coupled with the very high compliance to the diet and its safety, indicate that this periodic dietary strategy has high potential to be effective in promoting human healthspan."

The team says they are now putting the FMD intervention through a rigorous testing process in order to gain approval from the US Food and Drug Administration (FDA) for clinical use. This involves testing the efficacy of the diet in 60-70 participants, before moving to a clinical trial with 500-1,000 participants.

"This is arguably the first non-chronic preclinically and clinically tested anti-aging and healthspan-promoting intervention shown to work and to be very feasible as a doctor or dietitian-supervised intervention," says Longo.

The researchers stress that because the effects of the FMD intervention are potent, individuals should only follow such a diet under medical supervision.

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Will 'the female Viagra' really help women?

Later today, a committee of advisors to the Food and Drug Administration will vote on whether or not the agency should approve flibanserin - the much-hyped yet controversial "female Viagra." However, the drug has already been rejected twice previously by the organization, who cite safety concerns. In the wake of those decisions, battle lines have been drawn between those who feel the agency is discriminating against the sexual health of women and those who feel the language of sexual equality has been hijacked in an attempt to force an ineffective and unsafe drug on the market. We take a look at both sides of this dramatic debate.

Campaigners for flibanserin claim that 26 drugs have been FDA-approved for male sexual dysfunction and none for women.

480 was not a viable angina treatment, Pfizer took an interest instead in its unintended effects. As a treatment for erectile dysfunction, UK-92480 was much more effective than a placebo. In 1998, the drug was approved for this use by the Food and Drug Administration (FDA), and it was rechristened Viagra.

In the 17 years since, drugs acting as variations on Viagra's mechanism have also made it to market as erectile dysfunction treatments. What has been conspicuous in its absence, however, has been "a Viagra for women."

Following the FDA's second decision not to approve flibanserin, in fall 2014, two well-funded media campaigns - Even The Score and Women Deserve - set about engaging women's groups, starting up petitions and lobbying policymakers on the issue. A mantra of these campaigns is the figure "26-0."

What 26-0 relates to is a claim made by Cindy Whitehead, the CEO of Sprout Pharmaceuticals (who now own flibanserin) - and reportedly the creative mind behind Even The Score and Women Deserve - that 26 drugs have been FDA-approved for male sexual dysfunction and none for women.

Watch Women Deserve's Viagra parody video below:

"Women have waited long enough," write Even The Score, of their pro-flibanserin petition, which is reported to have attracted more than 40,000 signatures. "In 2015, gender equality should be the standard when it comes to access to treatments for sexual dysfunction."

Accusations of data manipulation

However, critics have claimed that Even The Score's campaign is built on misinformation. The 26 products for male sexual dysfunction are actually different regional brands of the four main erectile dysfunction treatments, which themselves adhere to a similar mechanism.

Do 43% of American women really have a sexual dysfunction?

Another statistic wielded by the campaigns - the claim that 43% of American women have a sexual dysfunction - has also come under fire. The figure is drawn from a contentious 1994 survey that gave its female respondents the option of answering yes or no to whether they had any sort of sexual problem, but the survey did not collect any data on what the nature of the problem was - even the senior author of that study has reportedly claimed the statistic is misused.

A claim published on womendeserve.org that "a biological lack of desire to have sex negatively impacts 1 in 10 American women" was questioned in a high-profile LA Times piece by Kinsey Institute research fellow and sexologist Prof. Ellen Laan, and Leonore Tiefer, professor of psychiatry at NYU School of Medicine and founder of the New View Campaign.

"No diagnostic test has identified any biological cause - brain, hormone, genital blood flow - for most women's sexual problems," the pair wrote. Rather, they claim that low sexual desire in women more likely reflects a difference in desire between the two partners.

"It is unethical and unscientific to attribute a couple's discrepancy in desire to the woman's biological deficit," they continue, pointing out that studies have shown women's response to both test medications and placebo drugs is high. "These repeated findings do not support the 'unmet medical need' theory."

What Laan and Tiefer's article and the New View Campaign emphasize is that Viagra and flibanserin are false equivalents. Viagra treats erectile dysfunction, while Sprout claim that flibanserin is an antidote for low sexual desire in women. Viagra does not increase male libido; rather it acts on the mechanism that allows an erection to happen.

What flibanserin is concerned with - boosting sexual desire - is more amorphous and complex. New View even argue that male and female sexual dysfunctions are also not equivalents, so a female Viagra would therefore not be appropriate for women.

'Hypoactive sexual desire disorder' and the DSM

The New View Campaign take issue with the current sexual dysfunction classification implemented by the American Psychiatric Association (APA) in its 1980 edition of the Diagnostic and Statistical Manual of Disorders (DSM), which envisions male and sexual "dysfunction" as equivalents across four categories: sexual desire disorders, sexual arousal disorders, orgasmic disorders and sexual pain disorders.

The illness that flibanserin is purported to treat - hypoactive sexual desire disorder - was removed from the DSM in 2013.

They consider that this has led to a reductive, mechanistic perception of how female sexuality works in relation to male sexuality. They argue that women's sexual problems are less physiological and genital-focused than men's, that "women generally do not separate 'desire' from 'arousal,' women care less about physical than subjective arousal, and women's sexual complaints frequently focus on 'difficulties' that are absent from the DSM."

"The DSM takes an exclusively individual approach to sex, and assumes that if the sexual parts work, there is no problem; and if the parts don't work, there is a problem," summarize the campaigners.

Instead, the campaigners say, it has fostered a commercial drive to produce "a female Viagra" - a pharma sensation that will repeat the massive success of that drug for a new audience, regardless of whether pharmacology is the correct intervention, or to what extent there is a problem that requires treatment.

In fact, the specific illness that Sprout argue flibanserin treats - hypoactive sexual desire disorder (HSDD) - was removed from the DSM in 2013.

Medical News Today spoke to Thea Cacchioni, an assistant professor of women's studies at the University of Victoria in British Columbia, who testified against flibanserin the first time it was unsuccessfully submitted for FDA approval in 2010. She asserted bluntly of flibanserin's position in the modern pharmaceutical landscape: "there is no recognized illness it treats."

"There are many problems with the HSDD disorder, as I mentioned in the hearing," Cacchioni told us, "how could we ever come up with a baseline level of normal desire? Norms of desire vary from era to era and culture to culture. Also, research shows that most desire problems are caused by external factors - interpersonal, relationship issues, social judgements and pressures related to especially women's sexuality, feelings of inadequacy, work stress, etc."

As fascinating as the cases for and against the idea of a pharmaceutical intervention for female sexual dysfunction are, the issues that Cacchioni and others expressed the greatest concern about when testifying in 2010 were much less philosophical and more to do with hard data.

Does flibanserin work and is it safe?

Firstly, does flibanserin work? The evidence presented to the FDA was perceived as being somewhat subjective - clinical trial found that it produced an additional 0.7 "sexually satisfying events" per month.

Secondly, is flibanserin safe? The drug's clinical trials saw a 14% drop-out rate due to adverse effects. The full data were not reported on what these adverse effects were, but what is known is that women taking flibanserin had 10 times the risk of dizziness and four times the risk of sleepiness compared with a control group.

"These may sound minor," explained Cacchioni, "but since this drug was tested on a highly select group of women, there is concern over what would happen if a wide population of women take this drug on a daily basis? What drug interactions will we see? Is there a risk of impaired driving?"

Whether or not Sprout will be "third-time lucky" in today's quest for FDA approval hinges on new evidence the agency has requested the pharma company submit regarding the possibility of impaired driving.

Cacchioni, who has also written a book on the issue - "Big Pharma, Women, and the Labour of Love," out in August - is not convinced the new data will be enough to swing an FDA approval, despite the intense media attention and public interest the case has received.

"Clearly, Sprout is hiding something," she told us, "since they have followed up on this important request by submitting evidence from only 25 volunteer participants, 23 of whom are men! They claim they could not find any more women who were moderate drinkers."

She adds:

"I have faith that the FDA will stand its ground and not approve flibanserin. If they do, they are sending a very dangerous message - that drug companies and their marketing machines can pressure them into approving drugs that are unsafe and ineffective."

In a recent blog for Science 2.0, Josh Bloom - director of chemical and pharmaceutical sciences at The American Council on Science and Health in New York City, NY - says that while the statistical significance of improvement in sexual arousal was excellent in flibanserin's trial, a "statistically significant improvement in a study is not the same as a significant clinical improvement." He elaborates that, in terms of evidence of improvement, "there are no 10-fold differences as was the case with adverse effects. The differences in efficacy are roughly in the 1.5-fold range."

"Which brings up the exact same question that the FDA is faced with every time it decides whether a drug gets approved or not," Bloom writes. "Do the benefits outweigh the risks? The FDA has already said no three times. This should have been over with long ago."

So why are Sprout persisting with flibanserin? The company was founded in 2011 by Cindy and Robert Whitehead, who raised $50 million to save the drug from the scrapheap, after it was first declined by the FDA.

The drug's creators, the German pharma company Boehringer Ingelheim, gave up on flibanserin. Like Viagra, the drug was not developed to be a treatment for sexual dysfunction - it was a prospective antidepressant. Antidepressants that increase serotonin have a side effect of dampening sexual response. However, flibanserin seemed to improve it - possibly by raising the levels of the neurotransmitters dopamine and norepinephrine while decreasing serotonin.

Flibanserin as sexual equality battlefield

Sprout, via the Even The Score and Women Deserve campaigns - coordinated with the largely big pharma-funded International Society for the Study of Women's Sexual Health - have painted the battle to get flibanserin to market as an ideological struggle against a patriarchal and discriminatory regulatory system that is not fit for meeting the health needs of women.

Despite support from the National Council of Women's Organizations, the Black Women's Health Imperative, Jewish Women International and the Association of Reproductive Health Professionals, the emotive pro-flibanserin campaign has not washed with everyone. Ellen Laan and Leonore Tiefer were scathing in their dismissal of its rhetoric:

"As professional sexologists and advocates of women's sexual rights, we were horrified by the campaigns' use and abuse of the language of equality to pressure the FDA to approve a potential billion-dollar blockbuster 'pink Viagra.' The only two drugs for women's sexual dysfunctions that have come to the FDA in the 16 years since Viagra was approved were rejected. [...] The drugs for women didn't work and were unsafe. Not approving them isn't sexism, it's proper regulation."

Cacchioni concurs, suggesting that perhaps the reason why no drugs have been shown to be safe or effective "is that most sexual problems are related to interpersonal, psychological, and social factors, including the social construction of sexual norms."

"Perhaps," she concludes, "we are putting too much pressure on ourselves to realize a level of desire that is not realistic for everyone across the life course."

With several FDA rejections and $50 million of investment already behind them, it will be interesting to see how Sprout and Even The Score will continue to frame the debate for "a female Viagra" if approval today is not forthcoming.

If it does succeed in winning approval, however, the Whiteheads could have a blockbuster drug on their hands with a market value of billions.

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Study links PTSD to premature aging

Individuals with post-traumatic stress disorder may be at greater risk for premature aging. This is according to a new study published in the American Journal of Geriatric Psychiatry.

Researchers found people with PTSD were more likely to have shorter telomere length - an indicator of premature aging.

Around 7-8% of the US population will experience post-traumatic stress disorder (PTSD) at some point in their lives.

The condition can occur after exposure to a traumatic event. A person with PTSD may experience nightmares, have flashbacks of the event, avoid places or situations that remind them of the event and suffer hyperarousal symptoms - such as nervousness and tension.

PTSD has been associated with increased risk of numerous other health problems, including insomnia, severe depression, eating disorders and substance abuse.

This latest study, conducted by researchers from the University of California-San Diego School of Medicine and the Veterans Affairs San Diego Health System, is the first of its kind to associate PTSD with a biological process like premature aging.

To reach their findings, the team conducted a comprehensive review of studies connected to early aging among individuals with PTSD dating back to 2000.

Since there is no standard definition for premature or accelerated aging, the researchers say, they looked at nonpsychiatric disorders that incorporate early aging, such as progeria syndrome and Down's syndrome, as a guide.

The team identified 64 studies that they deemed appropriate for investigation into the link between PTSD and aging. They were able to use these studies to assess how PTSD affects biomarkers of accelerated aging - such as telomere length - and how it affects onset and prevalence of age-related medical conditions and overall mortality.

PTSD linked to shorter telomere length, earlier mortality

The researchers found that, compared with individuals without PTSD, people with the condition had reduced telomere length.

Telomeres are caps on the end of each DNA strand that protect the chromosomes. Telomere length reduces with each cell replication and this is considered to be a marker of aging.

The team also found that people with PTSD were more likely to have increased levels of pro-inflammatory markers, such as C-reactive protein (CRP) and tumor necrosis factor alpha (TNFα), which are said to be markers of aging.

There was also a high incidence of PTSD alongside age-related conditions, the team notes, such as cardiovascular disease, type 2 diabetes and dementia.

What is more, some of the studies reviewed suggested a mild-to-moderate link between PTSD and earlier mortality, which the team says is consistent with premature or accelerated aging among people with the condition.

Though the researchers say their study does not show whether PTSD is a specific cause of premature aging, they believe it highlights the need to class PTSD as more than just a mental illness.

First study author Dr. James B. Lohr, professor of psychiatry at UC-San Diego, adds:

"Early senescence, increased medical morbidity and premature mortality in PTSD have implications in health care beyond simply treating PTSD symptoms. Our findings warrant a deeper look at this phenomenon and a more integrated medical-psychiatric approach to their care."

The team stresses that further studies are needed to confirm their findings and determine the mechanisms behind the association between PTSD and premature aging.

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Gut microbes important for serotonin production

Serotonin is probably best known as a brain chemical that affects emotions and behavior, an imbalance of which is thought to contribute to depression. Less well-known is that scientists estimate 90% of serotonin is made in the gut, and imbalances in this peripheral serotonin have been linked to diseases ranging from irritable bowel syndrome and cardiovascular disease, to osteoporosis.

90% of serotonin is made in the gut.
Image credit: E. Hsiao/Caltech

Now, researchers from the California Institute of Technology (Caltech) in Pasadena report a study in the journal Cell that shows certain bacteria in the gut play an important role in the production of peripheral serotonin.

Senior author Elaine Hsiao, research assistant professor of biology and biological engineering at Caltech, says studies of mice and other lab animals are increasingly showing that changes in gut microbes affect behavior.

She explains that she and her colleagues were interested in finding out more about how gut microbes and the nervous system talk to each other, and:

"To start, we explored the idea that normal gut microbes could influence levels of neurotransmitters in their hosts."

In the gut, there are three types of cell we know of that produce serotonin: immune cells, nerve cells or neurons, and enterochromaffin (EC) cells.

Gut microbes appear to influence serotonin production by EC cells

For their study, Prof. Hsiao and colleagues wanted to find out which cells the gut microbes might be influencing to have an effect on serotonin levels.

In the first part of the study, they compared peripheral serotonin levels produced from these cells in two groups of mice: one with normal gut microbes and another group of germ-free mice without gut bacteria.

The team found that in the germ-free mice, their EC cells produced around 60% less serotonin than the mice with normal gut bacteria.

And when they restored bacteria colonies in the gut of the germ-free mice, their EC cells began producing normal levels of serotonin - showing the effect on the EC cells can be reversed.

In the next part of the study the team set out to find which bacteria in particular were interacting with the EC cells to make serotonin.

They introduced single species and groups of gut microbes one by one into the germ-free mice, and found that serotonin levels went up when there was a certain mix of about 20 species of spore-forming bacteria.

Introducing this particular bacterial mix into the germ-free mice increased the movement of food through their digestive tract. It also changed activity in their blood platelets, which use serotonin to boost clotting.

Bacteria control gut microbiota metabolites to influence serotonin production

Further exploration in cell cultures revealed some of the molecular mechanisms underpinning the findings. The team found several metabolic byproducts of gut bacteria are controlled by the mix of spore-forming bacteria and act on EC cells to alter serotonin production.

When the researchers increased these metabolic byproducts in germ-free mice, it increased their levels of peripheral serotonin.

Other investigations have shown bacteria can make serotonin on their own. The researchers say their study suggests a lot of the serotonin in the body relies on the interaction between bacteria and host cells.

Prof. Hsiao says a lot more research needs to be done before findings like theirs are ready for clinical use, and offers a word of caution:

"We identified a group of bacteria that, aside from increasing serotonin, likely has other effects yet to be explored. Also, there are conditions where an excess of peripheral serotonin appears to be detrimental."

She and her team now plan to find out how their findings may apply to the human brain.

Researchers are also discovering other surprising things about serotonin in the body. For example, Medical News Today recently learned how a previously unknown source of serotonin could affect antidepressant activity.

One of the main drawbacks of SSRIs (selective serotonin reuptake inhibitors - a class of antidepressants that prevent reuptake of serotonin by increasing levels of it outside cells) is that they take a while to kick in. A study led by the University of Florence found that the source of this extracellular serotonin is not what experts have assumed, and finding out more about it should help improve drugs that target serotonin.

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Drop in abuse and overdose after opioids were made crush-resistant

After 2010, when oxycodone - a high-dose opioid painkiller sold as OxyContin - was switched by its manufacturer to a new abuse-deterrent formulation, overdose rates fell substantially, researchers have found.

In addition to potential misuse by people receiving the original prescription, opioid painkillers may be diverted to illicit users.

The formulation change also saw a drop in the levels of dispensing, and the lower opioid overdose and prescribing levels also correlated with the withdrawal from the market of another narcotic drug in the same year, propoxyphene.

OxyContin is an extended-release formulation to deliver its higher painkilling dose in a more controlled way, but misuse of this opioid for a quicker "high" had been possible by crushing or dissolving the medication to bypass this design. The new formulation, however, is resistant to this abuse strategy.

Propoxyphene (Darvon) was withdrawn from the US market in 2010 because of data about its cardiac side-effects. First approved for sale as an analgesic in 1957, it soon became prone to misuse - and the authors cite that, by 1977, propoxyphene was the "second-leading agent in prescription drug-induced deaths."

The authors of the study in JAMA Internal Medicine describe the reduction in dispensing following these two pharmaceutical industry changes in 2010:

"The introduction of abuse-deterrent OxyContin and withdrawal of propoxyphene at the end of 2010 were associated with sudden, substantial and sustained decreases in prescription opioid dispensing.

The estimated decrease in opioid dispensing at 2 years would be enough to supply 5 mg of oxycodone each day of the fourth quarter of 2012 to 5% of the population."

Fall in level of morphine-equivalent amounts dispensed

The researchers analyzed the prescribing of opioids to commercial health plan members across the US to reach the estimated average level of morphine-equivalent dose (MED).

For all opioids combined, between 2003 and the third quarter of 2010, the dispensing rate rose from 95 mg to 163 mg MED per plan beneficiary.

Immediately following the interventions, the dispensing rate dropped by 14.8 mg MED per member, and a downward trend then continued to buck predictions, leading to the rate in the last quarter of 2012 being estimated at 139 mg MED per member, down from the 163 mg peak.

Against the predicted trend of opioid prescriptions, this represented a 19% decrease following the 2010 changes. Further, the estimated rate of overdose also dropped - by 20%.

The prescribing data, drawn from over 31 million insured members, were analyzed by Dr. Marc Larochelle, of the Harvard Medical School and Boston University School of Medicine, and coauthors. They conclude:

"Our results have significant implications for policymakers and health care professionals grappling with the epidemic of opioid abuse and overdose. Changes imposed through regulatory mandates or voluntary company actions may be a viable approach to stemming prescription abuse."

A note of caution is made with this call, however, to reduce opioid supply without harming access to the therapeutic benefit of painkilling treatments.

The authors also warn that interventions at the supply end do not cure the present demand problem, even though it "might decrease new-onset addiction in the future."

Alongside the opioid findings, the authors found that heroin overdose, conversely, increased by 23% in the study period. The authors note:

"Regardless of the mediating mechanism, a transition from prescription opioid to heroin abuse has been well documented and further efforts are needed to improve identification and treatment of these individuals."

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Scientists 'incredibly excited' by asthma treatment breakthrough

A breakthrough study has uncovered a potential root cause of asthma and a drug that reversed symptoms in lab tests. The finding brings hope to the 300 million asthma sufferers worldwide who are plagued by debilitating bouts of coughing, wheezing, shortness of breath and tightness in the chest.

While the breakthrough will be welcomed by all asthma sufferers, it will particularly excite the 1 in 12 patients who do not respond to current treatments.

The study - led by Cardiff University in the UK - reveals for the first time that the calcium-sensing receptor (CaSR) plays a key role in causing the airway disease.

The team used human airway tissue from asthmatic and nonasthmatic people and lab mice with asthma to reach their findings.

In the journal Science Translational Medicine, they describe how manipulating CaSR with an existing class of drugs known as calcilytics reversed all symptoms.

Calcilytics block the calcium-sensing receptor and were originally developed for the treatment of osteoporosis - a condition that makes bones more likely to break - also referred to as "brittle bone disease."

One of the crucial study results is that the symptoms the drug reversed include airway narrowing, airway twitchiness and inflammation - all of which make breathing more difficult.

Daniela Riccardi, principal investigator and a professor in Cardiff's School of Biosciences, describes their findings as "incredibly exciting," because for the first time they have linked airway inflammation - which can be triggered for example by cigarette smoke and car fumes - with airway twitchiness. She adds:

"Our paper shows how these triggers release chemicals that activate CaSR in airway tissue and drive asthma symptoms like airway twitchiness, inflammation, and narrowing. Using calcilytics, nebulized directly into the lungs, we show that it is possible to deactivate CaSR and prevent all of these symptoms."

While the finding is likely to be welcomed by all asthma sufferers, it will particularly excite the 1 in 12 patients who do not respond to current treatments and who account for around 90% of health care costs associated with the disease.

Could be treating asthma patients in 5 years - huge implications for other airway diseases

Calcilytics were first developed about 15 years ago for the treatment of osteoporosis, but while they proved safe and well tolerated in trials, results have been disappointing in patients with osteoporosis.

However, the fact they have already been developed and tested gives researchers the unique opportunity to repurpose them and hugely reduce the time it usually takes to bring a new drug to market.

Once funding is secured, the team hopes to be testing the drugs on humans within the next 2 years. Prof. Riccardi concludes:

"If we can prove that calcilytics are safe when administered directly to the lung in people, then in 5 years we could be in a position to treat patients and potentially stop asthma from happening in the first place."

The researchers believe their findings about the role of CaSR in airway tissue could have important implications for other respiratory conditions such as chronic obstructive pulmonary disease (COPD), chronic bronchitis. There are currently no cure for these diseases, which predictions suggest will be the third biggest killers worldwide by 2020.

In the following video, Prof. Riccardi and colleagues talk about their findings and a patient with asthma describes her excitement about the potential implications.

Asthma UK, the Cardiff Partnership Fund and the Biotechnology and Biological Sciences Research Council (BBSRC) helped finance the study.

Last month, Medical News Today learned of another important study that uncovered new clues about overproduction of mucus in asthma and COPD in the behavior of ion channels - membrane-sited proteins that help regulate the flow of charged particles in and out of cells.

The researchers, from Washington University School of Medicine in St. Louis, believe their findings will lead to treatments for a range of diseases including asthma, COPD, cystic fibrosis and even certain cancers.

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How worried should we be about ticks?

 For many people, spring has well and truly arrived. The time is now right to enjoy the outdoors and to roam freely in the woods and the long grass. But be wary! It is not just humans that like to get out and about at this time of year...

Wooded and bushy areas with high grass and leaf litter are favored habitats of ticks.

Popular singer Avril Lavigne found this out to her cost last year. Her 30th birthday was disrupted by the onset of Lyme disease, an illness that left her bedridden for 5 months.

"I felt like I couldn't breathe, I couldn't talk and I couldn't move," she said in an interview with People. "I thought I was dying." But what was it that caused the bacterial infection? Lavigne believes that she was bitten by a tick at some point in the spring.

It seems strange that something as seemingly innocuous as a tick, often close in size to a pinhead, could damage someone's health to the extent that they are fearful for their life, but Lavigne's situation is shared by many. In 2013, the Centers for Disease Control and Prevention (CDC) report that there was a total of 27,203 cases of Lyme disease confirmed in the US.

This figure does not tell the whole story when it comes to ticks, however. Although closely associated with Lyme disease, these small arthropods are capable of carrying a wide variety of other pathogens that can cause human disease.

How worried should we be? In this Spotlight feature, we place the diminutive tick under the microscope and find out how much of a danger to health these little bugs can be, as well as what steps should be taken if you are unfortunate enough to be bitten by one.

What are ticks?

Although they look similar to both insects and spiders, a tick is neither of these two creatures. Ticks are arthropods - invertebrates with jointed legs - that belong to the same class of arachnids as mites. They are small external parasites that feed purely on the blood of other creatures.

There are two main kinds of tick: hard ticks (ixodidae) and soft ticks (argasidae). The difference between the two is that hard ticks are protected by a hard protective plate on their backs that restricts the rate at which they can feed. Soft ticks are more leathery and are unrestricted by a protective plate, enabling them to feast more quickly.

Some ticks will only feed on a particular type of animal, while some are far less selective and will happily feed on other creatures if their regular host animal is unavailable. As well as between different species, the feeding habits of ticks can vary across the four stages of their life cycle: egg, larva, nymph and adult.

Ticks are typically very small and can be quite difficult to spot if they are not actively searched for, particularly in places such as the armpits and in the hair.

Ticks locate potential hosts by detecting breath, odors, body heat, moisture, vibrations and even shadows in some cases. As ticks are unable to fly or jump, they wait for hosts on the tips of grasses and shrubs in a position known as "questing." When questing, ticks hold onto the grass or shrub with their back pairs of legs while their first pair of legs is outstretched, ready to climb onto a host when they brush past.

When feeding, ticks do not burrow into the skin. Rather, a tick will grasp the surface of the skin and insert its feeding tube. Some tick species will secure themselves further with barbs on their feeding tubes, or by secreting a cement-like substance.

Ticks can be very difficult to notice if you are not actively looking for them. In addition to being quite small, ticks can also secrete saliva with anesthetic properties, numbing the area where the tick is feeding and preventing the host from feeling that the tick has attached itself.

Once attached, a tick will begin to feed. The amount of time taken to feed varies between species, but hard ticks can take as long as several days to feed fully. When most ticks finish feeding, they drop off of their host and prepare for the next stage of their life cycle.

While tick bites can provide a small amount of discomfort, the real danger with ticks comes from the pathogens that some ticks carry. If feeding on a host animal with a bloodborne infection, ticks can ingest the pathogens along with the blood. These pathogens can then be transmitted to other hosts the next time a tick attaches itself to feed.

Ticks and Lyme disease

Ticks are almost synonymous with Lyme disease, a bacterial infection characterized by fatigue, fever, headaches and a skin rash (these symptoms are common to many tickborne diseases). Untreated, Lyme disease can spread through the body, affecting the heart, joints and nervous system.

As a bacterial infection, Lyme disease is frequently treated with antibiotic medication such as doxycycline or amoxicillin. If the disease is allowed to develop over a course of several weeks, patients may require the administration of intravenous antibiotics, depending on the severity of the disease's progression.

However, being on the receiving end of a tick bite is by no means a guarantee that Lyme disease has been contracted. The chances of catching Lyme disease depend on a number of factors, including the type of tick that has been encountered and the length of time for which it was feeding.

Specifically, Lyme disease bacteria are only transmitted in the US by blacklegged ticks, also known as deer ticks. Ticks are not born carrying Lyme disease pathogens and will only acquire the infection after feeding on an infected animal - typically a mouse. For this reason, larval deer ticks will not transmit these pathogens.

Blacklegged ticks are only located in specific areas of the country. The CDC report that most Lyme disease infections are found in these endemic locations:

• North-central states, mainly Wisconsin and Minnesota
• Northeast and mid-Atlantic areas, from northeastern Virginia to Maine
• The West Coast, particularly northern California.

In 2013, 95% of confirmed Lyme disease cases in the US were reported in just 14 states: Connecticut, Delaware, Maine, Maryland, Massachusetts, Minnesota, New Hampshire, New Jersey, New York, Pennsylvania, Rhode Island, Vermont, Virginia and Wisconsin.

Being bitten by a blacklegged tick in one of these states still does not guarantee the transmission of Lyme disease. In most cases a tick carrying the Lyme disease pathogens needs to be attached for at least 36-48 hours before the bacteria are transmitted. Removing a tick promptly after being bitten greatly reduces the risk of acquiring the disease.

The disease was first recognized in the Lyme area of Connecticut in 1975 and takes its name from here. However, although Lyme disease is the most common tickborne illness in North America and Europe, it is not the only one. Recently, news reports have suggested that one such disease is beginning to emerge in this northeastern state.

Other ticks, other diseases

Although it shares many symptoms with Lyme disease, the Powassan virus differs in that there is no treatment currently available for it. According to Dr. Theodore Andreadis, of the Connecticut Agricultural Experiment Station, the virus can be fatal in some cases.

Ticks should be removed promptly upon discovery. Although specialized removal equipment is available, a regular pair of tweezers should suffice.

Powassan virus can also be transmitted much quicker than Lyme disease. "These ticks will transmit this virus when they feed within a matter of hours, whereas with Lyme disease, for example, ticks generally have to feed up to 2 days before they're capable of transmitting it," Dr. Andreadis told CBS New York.

Dr. Andreadis also stated that there have yet to be any reported human cases of the virus in this region, but people should be more careful than ever when venturing into woodland environments that could be home to ticks carrying these pathogens.

Lyme disease and Powassan virus are not the only conditions that can be spread by the blacklegged tick. Other diseases transmitted by this species include anaplasmosis and babesiosis.

Of course, blacklegged ticks are not the only species of tick known to spread disease to humans. Across the US, for instance, a number of different species can be found that carry a variety of different pathogens potentially dangerous to humans.

The lonestar tick is a repeat offender when it comes to spreading disease. Found in southcentral and eastern states in the US, this hard tick can carry pathogens that cause diseases such as ehrlichiosis, southern tick-associated rash illness (STARI) and tularemia. Recent studies suggest that they may also transmit heartland virus.

Another tick to look out for is the Rocky Mountain wood tick, found in the Rocky Mountain states at elevations of 4,000 to 10,500 feet. These creatures can carry pathogens that cause Colorado tick fever, Rocky Mountain spotted fever (RMSF) and tularemia.

It is not just the slow-feeding hard ticks that can carry harmful pathogens either. Tick-borne relapsing fever (TBRF) is transmitted by swifter soft ticks and cases have been reported in 15 states so far: Arizona, California, Colorado, Idaho, Kansas, Montana, Nevada, New Mexico, Ohio, Oklahoma, Oregon, Texas, Utah, Washington and Wyoming.

These examples illustrate the fact that although Lyme disease typically occurs in very specific areas of the US, there are other tickborne diseases that can be found in other areas, so long as the environment is suited to the ticks.

Preventing and treating tick bites

There are a number of precautions that can be taken in order reduce the chances of a tick attaching, feeding and potentially transmitting an infection. When questing, ticks are most likely to be found in wooded and bushy areas, with high grass and leaf litter, so either avoid or be cautious in these types of environment.

Clothing can provide some protection from ticks. Wearing long-sleeved tops can protect the arms, and tucking pant legs into socks and boots can prevent ticks from having easy access to legs. Repellents are also available that can be applied to both skin and clothing. Those containing 20-30% DEET (N, N-diethyl-m-toluamide) offer several hours of protection.

After being out in an environment that could be home to ticks, it is recommended that you conduct a full-body tick check, especially as it is hard to notice them without actively searching.

As stated before, prompt removal of ticks is crucial to reducing the risk of infection. Although specialized tick removal devices are available, a regular pair of fine-tipped tweezers is more than adequate.

Using the tweezers, grasp the tick as close to the surface of the skin as possible. With steady, even pressure, pull upwards. Twisting and jerking the tick can cause some of its mouth-parts to remain embedded in the skin. If this occurs, carefully attempt to remove the remaining parts with the tweezers.

Once removed, clean the affected area and your hands, and dispose of the tick by submersing it in alcohol, placing it in a sealed container or disposing of it down the toilet. Do not crush a tick with your fingers.

Ticks are most active in the warmer months, between April and September, so now is the time to be particularly wary of these questing bugs. Although ticks are capable of spreading harmful diseases, with proper caution, these little beasties should not prevent you from being able to enjoy the great outdoors.

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