How vaccines change the way we think about disease

How vaccines change the way we think about disease

By Elena Conis, Emory University

The news on the current measles outbreak contains plenty of reminders that measles causes brain damage, pneumonia, hearing loss and death. A few lone voices have spoken up to say measles isn’t that serious, including an Arizona doctor who said it’s “really just a fever and a rash” – and soon found himself under investigation by his state’s medical board.

Back in the 1960s, it wasn’t controversial to call measles benign. Though the disease killed about 400-500 Americans a year, it was considered a normal part of childhood. It was so common, in fact, that to this day, people born in the pre-measles vaccine era are considered immune. But the introduction of the measles vaccine, and efforts to promote it, fundamentally changed things. In the five decades since we’ve been immunizing against it, measles has become increasingly known as a deadly killer.

This transformation in perception, from relatively benign to a serious disease, isn’t unique to measles. As I have discovered in my research, it’s a pattern that’s been repeated over and over again in the modern history of immunization. This is not to say that measles is now considered a mild infection, or to suggest that risk from the virus, or other vaccine-preventable diseases, is overestimated. The point I want to argue is that the introduction of a vaccine reframes our perception of the disease it prevents.

Vaccines change our perception of risk

How does this happen? New vaccines simultaneously drive down the number of people getting the disease and increase our awareness of the risks of the disease.

Vaccines shine a spotlight on their target infections and, in time, those infections — no matter how “common” or relatively unimportant they may have seemed before — become known for their rare and serious complications and defined by the urgency of their prevention.

A spotted vaccine delivery van labeled ‘Measles must go.’
CDC

This certainly happened to measles, whose first vaccine was uneventfully released in 1963.

At the time, many parents saw measles as a common and relatively harmless part of childhood – even though it infected three to four million people a year and caused roughly 48,000 hospitalizations annually. Many doctors felt as parents did, especially when comparing measles to such worrisome disease threats as smallpox and polio. Even the head of the Centers for Disease Control described measles as a disease “of only mild severity” which caused “infrequent complications.”

But the very development of the vaccine focused new scientific attention on the disease. Within a few years, scientists had compared measles to polio — the previous decade’s public health priority — and found it a much more serious threat to children’s health. Inspired by this finding, and frustrated by the public’s lack of enthusiasm for the vaccine, federal health officials launched a national campaign to publicize measles’ dangers.

The campaign officially spread the word, for the first time, that measles was “a serious disease that sometimes causes pneumonia, deafness, encephalitis and even death.” Public figures ranging from the Surgeon General to Ann Landers announced that measles could leave children blind, deaf and mentally impaired. And the campaign employed a poster child — disabled ten-year-old Kim Fisher — to illustrate the idea that measles immunization was necessary because “one death, one brain-damaged child, or even one child who needs hospitalization is one too many,” as one campaign supporter put it.

A new picture of measles emerges

As the campaign wore on, scientists continued to study the disease more closely than ever. Doctors began to report measles cases to health departments at unprecedented rates. And together, doctors and scientists began to pay more attention to the disease’s risks than even before. As a result, a new picture of the disease began to form: it appeared to cause more deaths than previously thought, brain damage in even mild cases, even harm to fetuses.

As the public continued to respond to the national campaign with “general apathy,” however, health officials redoubled their efforts to publicize measles’ “dramatic aspects,” and states began passing laws requiring the vaccine for schoolchildren. Within just over a decade, the country saw an all-time low of measles cases — and the disease had solidly acquired its new reputation as a deadly infection worthy of prevention at any cost.

A measles immunization campaign poster display at the Eradicate Measles Exhibit in 1972.
CDC/Don Lovell

We used to think mumps and chickenpox were ‘mild’ too

In the decades that followed the introduction of the measles vaccine, vaccine makers and health officials duplicated this approach with one new vaccine after another.

Mumps, often the butt of jokes in its pre-vaccine days, was no laughing matter within a decade of its vaccine’s introduction in 1967. Hepatitis B was considered an obscure infection of little import to most Americans when its vaccine first came out in 1981, but soon after it evolved into a “cousin” of AIDS known for lurking in nail salons, piercing parlors and playgrounds.

Since the development of the chickenpox vaccine in the 1990s, the virus has been transformed in the public imagination from an innocuous if uncomfortable rite of childhood to a highly contagious infection that can cause pneumonia, sepsis and sometimes death. And in just the last decade, human papillomavirus (HPV) has morphed from a little-known sexually transmitted infection to a widely known cause of multiple forms of cancer. Each of these transformations in perception was triggered by a new vaccine.

Each new vaccine invited deliberation on how it should be used. That, in turn, focused increased scientific attention on the disease. Often, as federal health officials and other scientists accumulated new information about the disease’s risks and complications, the vaccine maker did its part to market its vaccine. As talk of each disease and its more dramatic aspects spread, public and scientific perception of the disease gradually transformed.

In this country, high vaccination rates rest on a consensus about the diseases prevented by vaccines. When doctors, health officials and, in particular, parents view a disease as serious, they view its vaccine as one worth getting.

The recent increase in the number of philosophical objectors to measles vaccine shows that historical consensus about the disease itself has eroded in recent years. But history also shows that one surefire route to consensus about a disease is fear of that disease. And fear often spreads like wildfire during disease outbreaks, much like what is happening once again now with measles.

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When can you start having sex after a heart attack?

When can you start having sex after a heart attack?

By Jalees Rehman, University of Illinois at Chicago

Each year in the United States about 720,000 people have heart attacks and about 124,000 people in the UK and 55,000 people in Australia will have them as well. Since the 1980s, survival rates from heart attacks have improved – a lot of people get them, but more and more people are surviving. A recent study of patients in Denmark showed that in 1984-1988 31.4% of patients died within a month of having a heart attack. From 2004-2008 this was down to 14.8%.

Once a patient has made it through a heart attack and begins to recover, they get advice from their doctors on what to do to stay healthy and get back to normal. That includes a lot of things – when to go back to work, when they can start traveling again and what to eat. But there is an important item that a lot of doctors don’t talk about: sex.

There are no universal guidelines for getting back to ‘normal’

Providing advice about lifestyle can be more challenging than prescribing standardized medications or smoking cessation because “normal” life differs widely among patients and requires individualized counseling.

For instance, scientific evidence from large-scale clinical trials isn’t always available to help the cardiologist decide the ideal time for when an individual patient should return to work. A software engineer might get different advice than a butcher or construction worker who has to lift heavy objects all day long. Physicians have to carefully estimate the patient’s capacity for physical activity as well as the physical demands of the job and be pragmatic about how long a patient can take time off from work.

Sex also requires this kind individualized counseling. New research shows that patients want to talk about sexual activity with their doctors, but that all too often that conversation never takes place.

Time for a heart-to-heart with your doctor.
Heart via Syda Productions/Shutterstock

Let’s talk about sex

A recent study conducted in 127 hospitals in the United States and Spain suggests that doctors are not very good at broaching the topic of sexual activity after a heart attack.

Researchers studied 2,349 women and 1,152 men who had suffered from a myocardial infarction (the medical term for a heart attack). This study focused on younger heart attack patients (ages 18-55) and asked them whether they had discussed sexual activity with their doctors. With younger patients talking about life after a heart attack is especially important. The loss of sexual activity or function is a major quality of life issue, and can affect intimate relationships, reproduction and lead to depression.

In the month following the heart attack, only 12% of women and 19% of men had some discussion with a doctor about sex. In the US, most patients reported that they initiated the discussion, whereas in Spain, most discussions were initiated by the doctor. This means that more than 85% of patients received no advice from their doctors regarding if and when they could resume sexual activity.

The study found that the vast majority of patients were sexually active in the year before their heart attacks, and they valued sexuality as an important part of life. They also felt it was appropriate for physicians to initiate the discussion about having sex again.

It is interesting that in the US, patients were more likely to bring up sex and men were given more restrictive advice, while in Spain, physicians were more likely to bring up the topic and more restrictive recommendations were given to women.

The study did not specifically study the motivations of the physicians but these differences suggest that cultural differences and gender affect the counseling in regards to sexual activity. Future research could potentially also study the physicians and help uncover how culture and gender influence the counseling process.

This lack of communication between doctors and patients was not due to the patients’ unease: 84% of women and 91% of men said that they would feel comfortable talking to their doctors about sex. What is even more concerning is that the 15% or so of patients who received counseling often got inaccurate recommendations.

Sex is exercise. But doctors don’t talk about it that way

Two-thirds of those who talked about sex with their doctors were told that they could resume sexual activity with restrictions like limiting sex, taking a “passive role” or keeping their heart rate down during sex. But here’s the thing: sex is exercise. And after a heart attack doctors routinely ask patients whether they can tolerate mild to moderate physical activity such as mowing the lawn or climbing up two flights of stairs without chest pain or other major symptoms.

The Scientific Statement of the American Heart Association (AHA) on sexual activity states that it is reasonable to resume sexual activity as early as one week after an uncomplicated heart attack. If there are complications after the heart attack such as feeling out of breath or experiencing persistent chest pain then these problems need to be addressed first. And in the AHA guidelines there is no mention of “passive roles” or keeping heart rates down during sex. These restrictions are also quite impractical. How are patients supposed to monitor their heart rates and keep them down during sex?

The kind of restrictions recommended by doctors in the study – and presumably by medical practitioners who weren’t polled – are not backed up by science and place an unnecessary burden on a patient’s personal life. Hopefully, after reading the results of this study, doctors will take a more pro-active role and address the topic of sex with their heart attack patients with proper recommendations instead of leaving patients in a state of uncertainty. If a patient can handle moderate exercise, they can probably handle sex.

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Darling, I love you…from the bottom of my brain

Darling, I love you … from the bottom of my brain

By George Paxinos, Neuroscience Research Australia

In William Shakespeare’s comedy Merchant of Venice, the play’s heroine Portia sings:

Tell me where is fancy bred,
Or in the heart or in the head.

If you look at Valentine’s Day cards, it’s clear fancy is bred in the heart and not in the head; all the cards have red hearts on them. But they’re all wrong. Love does, in fact, live in the brain.

The irrelevance of the heart to love has been amply demonstrated by cardiac transplant surgeons. Heart transplant recipients do not fall in love with the lovers of the dead donors, Hollywood notwithstanding. Surely this proves that wherever else love may reside, in the heart it does not.

Further support for love’s actual home comes from neuroscience. This shows that love is a complex function, which includes appraisal, goal-directed motivation, reward, self-representation and body image – none of which can be found in the heart.

On the right track

Hippocrates’ view on the bodily origin of feelings could be taught in any neuroscience department today.
Eden, Janine and Jim/Flickr, CC BY

Historically, the erroneous attribution of love to the heart can be traced to the ancient Egyptians of the third millennium BC. They considered the heart to be the seat of thought, memory, will and emotion. Hearts, stomachs and intestines were considered important for afterlife, but not the brain. Before burial, the ancient Egyptians heedlessly discarded the brain, so for millennia pharaohs arrived brainless for their afterlife.

The problem with the brain is that, unlike the heart, it doesn’t flutter when lovers kiss.

The scientist credited with the discovery of the relationship between the mind and the brain was Alcmaeon (circa 520-450 BC; possibly a student of Pythagoras) who lived in the Greek-speaking colony of Kroton (Crotone of today’s southern Italy). It’s thought Alcmaeon was led to his astonishing conclusion by observing that all senses are connected to the brain through channel-like structures. Today, we call them nerves.

Alcmaeon’s concept is thought to have passed on to the island of Kos, where Hippocrates (460-370 BC), the most significant physician of antiquity, worked. Hippocrates expressed an amazingly modern view:

Men ought to know that from the brain, and from the brain only, arise our pleasures, joys, laughter and jests, as well as our sorrows, pain, griefs and tears. Through it, in particular, we think, see, hear and distinguish the ugly from the beautiful, the bad from the good, the pleasant from the unpleasant…

Hippocrates’ view could be taught in any neuroscience department today.

A backwards step

Then things went downhill for the brain for a long while. Plato (429-347 BC) retained the primacy of the brain and attributed to it the seat of the rational, immortal soul. But, in his tripartite division of the soul, he confused matters and attributed to the heart the emotional soul.

While Plato retained the primacy of the brain for emotions, his student Aristotle placed the seat of the soul in the heart.
Image Editor/Flickr, CC BY

The worst blow to the brain came from Aristotle (384-322 BC), who was Plato’s student, the greatest classical biologist and first anatomist. Aristotle observed that humans have the largest brain for their body size, but strangely he attributed to the brain the pedestrian function of literally cooling the blood. He placed the seat of the soul in the heart.

Aristotle’s views were dismissed as absurd by Galen (130-201 AD), who was an admirer of Hippocrates and served as physician to the Roman emperor Marcus Aurelius. Galen proposed the psychic pneuma (mind) resided in the ventricles of the brain and, via the nerves, was in receipt of sensory information and controlled the muscles.

The cardiocentric (heart-centred, Aristotle) and encephalocentric (brain-centred, Galen) theories of the psyche/mind/emotions battled one another until the dawn of modern science.

Technology and the truth

Modern science has not only rejected the heart as the seat of love, but is making progress in identifying specific structures in the brain involved in the erotic, cognitive, emotional and behavioural components of love.

The first major work on the subject was published in 2000. Researchers studied the brain activity of people who were deeply in love via functional MRI while the subjects viewed pictures of their partners (compared to viewing friends of similar age and sex).

The cardiocentric and encephalocentric theories of the psyche/mind/emotions battled one another until the dawn of modern science.
Soffie Hicks/Flickr, CC BY

The caudate/putamen (brain area receiving dopamine and involved with reward), medial insula (a multi-sensory area involved in the allocation of attention and control of the heart rate) and the anterior cingulate (an area involved in autonomic regulation, emotion and obsessive-compulsive behaviour) were activated. The amygdala (an area involved in fear) was deactivated.

Researchers have since extended these observations by showing that sexual desire and love recruit some common brain structures that promote bodily sensations, reward expectation and social cognition.

The notion that love doesn’t reside in the heart but in the brain is now as well established as the theory of anthropogenic global warming. Clearly, it’s time the fallacious cardiocentric theory of love is abandoned and on Valentine’s Day lovers exchange images of the organ really responsible for their emotion, whose shape is every bit as beautiful as that of the heart.

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Fighting Malaria is going to take more than just Nets

Fighting malaria is going to take more than just nets

By Utibe Effiong, University of Michigan and Lauretta Ovadje, University of Michigan

In January, the New York Times highlighted how insecticide treated nets meant to protect people from mosquitoes and malaria are now being used to haul fish in Africa. Among those using these nets to catch fish, hunger today is a bigger risk than malaria tomorrow.

For those who have experienced life in countries like Nigeria, where malaria is endemic, the report does not come as a surprise. The nets are an important tool for preventing malaria, but without investing in infrastructure and engaging effectively with communities, it’s hardly surprising that these nets are not always used as intended.

How do insecticide treated nets work?

The use of bed nets as protection from mosquitoes dates back to antiquity. Cleopatra is reported to have used them. But insecticide treated nets (ITNs) only became available in the 1980s. Those nets needed to be re-impregnated with insecticide every six months. Recently, long-lasting insecticidal nets (LLINs), which last up to three years, have replaced ITNs in most countries.

The fabric of an ITN or LLIN protects those sleeping beneath it from physical contact with blood-sucking, parasite-transmitting insects. And the impregnated chemicals kill any mosquito that dares to get too close. These nets are so successful that they have been shown to reduce the death of children under five years of age from all causes by about 20% in several community-wide trials on the African continent.

Because LLINs have been associated with sharp decreases in malaria in countries where high usage has been achieved, the World Health Organization (WHO) now recommends that they are distributed to and used by all people (“universal coverage”) in malaria endemic areas including most of Africa, Central America, South America, the Middle East and South Asia. LLINs are most commonly distributed through mass campaigns approximately every three years and they are usually given out free of charge.

Map of malaria endemic countries in the Eastern hemisphere.
Centers for Disease Control and Prevention

How are nets being used in Nigeria?

Yet looking at Nigeria in particular – a country we are intimately familiar with – many researchers have found that levels of proper net usage are not very high. And fishing is only one of the many unapproved uses. ITNS and LLINs are also used as door blinds, window curtains, blankets, ceiling covers, tablecloths, and even as decorative dressing for weddings and burial ceremonies. Creative use of the nets is not confined to Nigeria – researchers have reported a similar pattern of mosquito net misuse in Ethiopia.

Nkechi Onyeneho, a Nigerian sociologist, says that the use of nets as window blinds or curtains in an attempt to protect everyone in a household may be a pragmatic approach if there are not enough nets for everyone to sleep under one. Onyeneho also found that low usage was associated with ignorance of instructions for use, a fear of the unfamiliar technology and with spousal disagreement. She even reports that, in some households, men monopolize the nets while the women and children sleep without them.

But this misuse might be somewhat effective. A systematic review from 2014 shows the potential for insecticide-treated screens and curtains to reduce vector borne diseases.

Family utilizes protective malaria bed nets in their home in Nigeria in 2008.
World Bank Photo Collection, CC BY-NC-ND

In another study, Best Ordinioha, a public health scientist, noted that even though most people hung their ITNs over their beds or sleeping mats, only 27.5% of those beds were occupied on the night before the survey. Reasons why included hot nighttime temperatures, low mosquito activity, forgetfulness, tiredness, and disruption of normal sleeping arrangements. Those who did not put up their nets at all had similar excuses. They also pointed to lack of a place to hang the nets, fear of chemical exposure, and the strong smell of the ITNs.

Another study found that as many as a third of respondents admitted to using their ITNs as fishing nets. Even though most participants were aware that the nets were meant for malaria control, only a third slept under them. The problem? Cost as well as inconvenience. Although the nets can be obtained for free, sometimes people must purchase them.

Women from a rural Ethiopian village receive free bed nets as part of the largest distribution campaign in African history, led by UNICEF. (Golo Sodoma, Ethiopia, 2005)
Gates Foundation, CC BY-NC-ND

Making nets free is only part of the solution

Even when the nets are provided free of charge, the fact remains that, for many poor people, the fear of hunger trumps the fear of disease. Mr. Ndefi, the Zambian fisherman quoted in the New York Times, summed it up well: “I know it’s not right but without these nets, we wouldn’t eat.” This is the reality for millions in Nigeria who live on less than a dollar each day.

The solution to the global malaria scourge goes beyond the use of ITNs, LLINs, and other well-meaning public health measures. It begins with lifting people out of poverty. It’s only when people can meet their basic needs that health and safety become important. Public health programs continue to fail in countries like Nigeria because of poverty in the midst of plenty.

Here, infrastructure development is critical. Electricity, potable water, usable roads, primary health care, universal basic education and broadband internet connectivity are the tools for poverty eradication. Most fishermen who can afford a regular fishing net do not misuse their ITNs. But some still do, and this is where grassroots participation in public health policy becomes essential.

Grassroots strategies work best

When people are participants in the decision-making process, they are more likely to comply with policy. If the decision to distribute ITNs was made after consultation with primary communities, and collective resolve was made to use the nets appropriately, there would be far fewer cases of misuse.

Community engagement also creates room to address fears and correct misconceptions about public health programs. But certain concerns such as those related to the toxicity of the chemicals used on the ITNs are not easily dispelled. Here, there is a real need for community based participatory research that lets affected groups become part of the solution. And of course, there remains a need for further research for insecticides that are more human and environment friendly.

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What is Polycystic Ovary Syndrome?

Explainer: what is polycystic ovary syndrome?

By Roger Hart, University of Western Australia

Polycystic ovary syndrome (PCOS) is a hormonal condition that disrupts ovulation and the menstrual cycle. It’s the most common female hormonal condition, affecting roughly one in 12 Australian women.

Women with PCOS often have enlarged ovaries that contain small fluid-filled follicles, or cysts. These cysts are where the condition gets its name: polycystic = many cysts.

But although up to a third of women may have polycystic ovaries seen on an ultrasound, not all have the hormonal problems and physical symptoms that define PCOS.

For women with PCOS, the hormonal imbalances cause a number of symptoms such as irregular or absent periods, weight gain, acne, excessive body hair, mood changes, dark patches of skin and thinning head hair.

Because women with PCOS may not ovulate regularly or may not ovulate at all, some women may have difficulties getting pregnant.

While the cause for the hormonal imbalance is not yet known, it is believed to have some genetic basis.

Symptoms and related illnesses

PCOS is often first diagnosed in the late teen years, when young women notice the greasy skin of adolescence refusing to go away, as well as irregular and unpredictable periods.

To diagnose PCOS, GPs assess the patient’s symptoms and may take some blood test to check her hormone levels. The GP may also order an ultrasound of the uterus, ovaries and pelvis.

Women with PCOS are often more likely to put weight on around their waists. This form of body fat distribution is associated with the development of diabetes and heart disease later in life, so GPs may do further testing for these conditions.

Women with PCOS are also at increased risk of cancer of the womb, as the irregular periods and absent ovulation can lead to uncontrolled thickening of the lining of the womb.

But while some women with PCOS can present with a range of conditions, others may have no symptoms at all. These women may never develop any significant symptoms, or only experience symptoms when they are above a healthy weight.

Treatment

To decrease the risk of cancer, heart disease and diabetes, women with PCOS need to take particular care with their health from an early age. Doctors will provide advice to women with PCOS about diet and exercise, and some women may find their symptoms resolve as they lose weight.

To alleviate symptoms of PCOS, doctors may prescribe the contraceptive pill. The pill regulates hormones and is an excellent way to control greasy skin and irregular periods, as well as providing contraceptive protection.

Woman with early signs of diabetes may be prescribed metformin, which addresses the cause of diabetes and helps with the symptoms of PCOS. It can also lead to regular ovulation for woman trying to get pregnant. Interestingly, if taken during pregnancy it may reduce the risk of miscarriage.

The downsides to metformin treatment is it can make women feel sick, bloated or cause diarrhoea.

For symptoms related to high male hormones such as increased body hair, thinning head hair or acne, doctors may prescribe anti-androgen medications to reduce these hormone levels. These medications are often combined with birth control pills and should not be taken when trying to get pregnant.

Fertility

Women with PCOS who are trying to get pregnant can often conceive naturally by achieving and maintaining a healthy weight.

Some women may need gentle stimulation of the ovary, by tablets or injections, to stimulate ovulation (this also allows women to time sex around ovulation). Expert fertility doctors must oversee this process to ensure patients are not at risk of a multiple pregnancy.

Unless a woman has problems with her fallopian tubes or her partner’s sperm count, it’s rare that she will require IVF to get pregnant.

If, for other reasons, a woman with PCOS does need IVF treatment, she has a increased risk of an exaggerated response to the drugs: a condition known as “hyperstimulation”, where the ovaries become swollen and painful. However, under the care of a fertility doctor, the risk of hyperstimulation is very low.

If you’re concerned about PCOS, talk to your GP to get your symptoms under control and help reduce the risk of complications such as diabetes, heart disease and fertility problems.

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What is Insomnia and what can you do about it?

Explainer: what is insomnia and what can you do about it?

By Imogen Rehm, Swinburne University of Technology; Hailey Meaklim, Swinburne University of Technology, and Jo Abbott, Swinburne University of Technology

We all have a poor night’s sleep from time to time: those nights when you lie awake for hours trying desperately to go to sleep but can’t stop worrying about tomorrow. Or when you repeatedly wake up throughout the night, or can’t get back to sleep in the early hours of the morning.

One-third of the world’s population experience short-term sleeping difficulties. These usually last only a few weeks. But for an unlucky 3% of Australians, these sleep disturbances may last a lot longer and lead to a diagnosis of insomnia.

A person with insomnia is unable to fall asleep, stay asleep, and/or wakes up too early at least three times a week for at least three months. This can lead to considerable distress.

Sufferers experience persistent tiredness, low energy and difficulties with concentration, attention and memory. They may feel down, stressed or anxious, not only about getting a good night’s sleep but about their ability to do their daily activities.

What causes insomnia?

Biological, social and psychological factors interact to trigger and maintain sleeping difficulties.

Biological factors include changes to the body’s natural 24-hour body clock, or circadian rhythms, which control the timing of when we feel sleepy and awake throughout the day. Circadian rhythms are sensitive to body temperature, light and physical alertness. When there is too much or too little of a combination of these factors, the body doesn’t release enough sleep-inducing hormones such as melatonin to feel sleepy.

Social factors, such as shift work or frequent international travel, can contribute by causing our body clock to become out of sync with the environment it’s in. Our bodies adjust slowly to these changes and depend on our being able to get sunlight exposure and exercise.

Psychological factors, including unhelpful thoughts (“I’m never going to get to sleep tonight”) and behaviours (watching the clock during the night), can reduce the amount and quality of sleep a person gets.

These factors interact in complex ways. Sleep sensitivity, or a family history of sleep disturbance, for example, make some individuals vulnerable to developing insomnia because they’re more likely to have their sleep disturbed by stressful events, such as a relationship breakdown.

Being unable to fall asleep often leads to bedtime worrying, which makes it even harder to fall asleep. To try to make up for a lack of sleep, you might then start going to bed earlier, sleep in or take daytime naps. Over time, these unhelpful thoughts and behaviours can create a cycle that makes the insomnia worse.

How do you treat insomnia?

Successful treatment of insomnia requires getting help to change as many of the interacting factors as possible, rather than trying one or two things in isolation. This is what cognitive-behavioural therapy, or CBT, tries to do.

CBT re-trains people to view the bedroom as a place of sleeping instead of a place where they lie awake tossing and turning and worrying about not sleeping. CBT also helps people change their lifestyle and sleeping environment, learn relaxation skills and challenge the unhelpful worries and beliefs that contribute to insomnia.

CBT has been found to reduce sleeping difficulties by 50% on average, and reduces insomnia symptoms to a level where they are no longer considered clinically severe.

When people visit their GP for insomnia treatment, they’re often encouraged to use many of the techniques CBT uses. But these skills are difficult to teach in a short consultation, so many patients don’t use them.

Sleeping medications may then be prescribed to help a person fall asleep and stay asleep when correctly used for a short period. But sleeping medications only provide short-term relief and can be harmful or addictive if used longer term.

If your symptoms persist, your GP may refer you to a specialist doctor or psychologist for CBT.

Another credible alternative is web-based treatment. Research from Japan to America shows that, for some people, online insomnia treatment modules may be as effective as visiting a health professional in person.

We’re piloting a seven-week, interactive CBT program to help Australians with insomnia, called Sleep-e. So far, the data looks promising, suggesting it can reduce the severity of insomnia in people waiting for treatment at a public hospital-based insomnia clinic.

To get a good night’s sleep, try to establish a relaxing bedtime routine. Limit the use of computer tablets and mobile devices before bed. If you can’t sleep, get up and do a relaxing activity, such as reading a book, and return to bed only when you feel sleepy again.

Online programs can help you to practise good sleep hygiene habits, change unhelpful sleeping patterns and reduce the worry that can contribute to insomnia, helping you to get a better night’s sleep.

For further information about Sleep-e see Mental Health Online or email the research team. Other online programs are available for a fee, including SHUTi and Sleepio.

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What exactly is Coronavirus?

Explainer: what exactly is coronavirus?

By Arinjay Banerjee, University of Saskatchewan and Grant Hill-Cawthorne, University of Sydney

The conflicts in Syria and Iraq are straining public health systems and public health efforts meant to prevent and detect the spread of infectious diseases. This is generating a “perfect storm” of conditions for outbreaks. Among the infections raising concern is Middle East Respiratory Syndrome, caused by a type of coronavirus, which emerged in 2012.

Infection with the MERS virus can cause fever, cough and shortness of breath, and is particularly dangerous in older people or people with weakened immune systems or other illnesses. In severe cases it can cause respiratory failure and occasionally lead to kidney failure. As of January 27 the MERS virus has infected 956 individuals and killed 351. Cases have been reported throughout the Middle East, but also in Asia, Africa, Europe and North America.

The MERS virus belongs to the coronavirus family. Even if you haven’t heard of coronaviruses until now, you have probably heard of some of the illnesses different types of coronaviruses can cause, like Severe Acute Respiratory Syndrome (SARS). And if you’ve been coughing and sneezing thanks to a cold, then you could have had a bout of infection with a coronavirus. They aren’t new, or even that rare, but we still don’t know very much about them.

The MERS coronavirus up close.
National Institute for Allergy and Infectious Diseases/Reuters

Why are some coronaviruses more lethal than others?

Coronaviruses infect humans on a regular basis and are one of a number of viral groups that lead to symptoms that we clump together and call the common cold: coughing, sore throat, runny nose, sneezing and fever. While this may leave you feeling unwell for a few days, they are rarely lethal. The common cold-causing coronaviruses have been with humans for some time and therefore we have natural immunity to them, reducing the risk of lethal infections.

The coronavirus is an RNA virus, and can mutate and recombine, producing strains that are different from those that the immune system “remembers.” This is called antigenic drift and is the reason we get colds every year – the virus changes a bit every season.

Drifting creates a virus which differs from its predecessor but some similarities remain, so the body might still be able to recognize it and mount a “memory” response, which would lead to no or milder symptoms.

The reason that the MERS coronavirus can be lethal is because the human immune system has never seen this virus before, and has no “memory” from previous exposure. This is what makes an infection with the MERS virus more severe than the cold-causing coronaviruses.

Bats are thought to be reservoirs of coronavirus.
Ethan Daniels/Shutterstock

Where do coronaviruses come from?

Within eight months in 2003, the SARS virus spread to 29 countries, infected 8,098 people and killed 774 of them. And now, a decade after the SARS epidemic, we are facing the ongoing outbreak of another potentially deadly coronavirus – MERS.

The SARS coronavirus led to a new found interest in human coronaviruses. Researchers started looking for coronavirus reservoirs, places where the virus can be maintained in the wild by transmitting between, but not killing, its hosts. Because coronaviruses can mutate and recombine, they can sometimes jump species.

Both SARS and MERS coronaviruses are very closely related to bat coronaviruses, suggesting that both these viruses could have emerged from bats. The SARS virus is believed to have spilled over from bats to civet cats to humans. The MERS virus is believed to have spilled over from Egyptian cave bats to humans, with camels acting as the intermediate host species.

It is the cross-species – called zoonotic – transmission of these viruses that makes them have more severe consequences. Our immune system does not have any remembered immunity to these viruses, and therefore infection is likely to become more widespread before it is controlled. This is a particular problem for older people or those with other health problems – in fact it is these kinds of patients who have experienced the brunt of MERS coronavirus infections.

How do we control the spillover of coronaviruses?

Controlling spillovers is not as easy as it sounds. As humans exploit the virgin forests and come into contact with exotic species of animals, one cannot predict the various different viruses that humans would encounter, some of which have never been seen before. The scientific community has only recently started looking at bats and the viruses that they harbor. They are also trying to explore how bats survive infection by these viruses and extrapolate that knowledge to humans.

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Is the Ebola Virus mutating?

Explainer: is the Ebola virus mutating?

By Connor Bamford, University of Glasgow

The world has been keeping a very close eye on the Ebola virus for nearly a year now following the extraordinarily large outbreak seen in Western Africa, which has so far killed more than 8,000 people. One of the things that scientists and public health officials look at is how the genetics of the virus changes. This is because Ebola virus gene sequences have in the past allowed scientists to work out patterns of spread during an outbreak and when and where it likely originated.

While we would like to predict how the virus behaves directly from its gene sequences, we do not yet have the ability to do this. So when the BBC reported that “scientists tracking the Ebola outbreak in Guinea say the virus has mutated,” what did it really mean? Is the virus now more contagious and therefore better able to spread and even more of a worry for those fighting to stop it?

The answer is probably no. Of course the virus is mutating – mutation is a fundamental living process and all viruses do it. The news article contained no new surprising information but it did highlight a lack of understanding – or appreciation – of mutation in viruses and other organisms.

The truism

Mutation refers to the process of genetic change. Naturally, genetic information is encoded in a genome, which is made of either DNA or, in some organisms, a similar molecule called RNA. Genomes are important because they control almost every function of an organism: whether a human has blue or brown eyes; whether a fly has two or four wings, or whether a virus is sensitive to a drug or is resistant.

Genetic information is specified by strings of letters: A, T (U in RNA), C and G. If one sequence has ATCG and then changes to AGCG then we say it has mutated. This is one example of mutation and is referred to as a “single nucleotide change”. It is one of the most simple and common occurrences, especially in viruses such as Ebola.

Mutation is one of the most important processes in living things and is a central feature of things with genomes; without mutation there would be no life on this planet. This is because mutation supplies genetic diversity that can be acted on by evolutionary processes, such as natural selection, to change a particular function of an organism. This only happens when there is a selective advantage to the mutation and its change in function.

For example: a bacteria has a mutation that makes it resistant to an antibiotic that is used commonly – but under conditions without that antibiotic present, it will be no more adapted than its non-resistant cousin. But when you add the antibiotic into the mix then the resistant one will grow more than its sensitive cousin. Therefore it is said that mutation fuels evolution.

The importance of mutation

Some organisms mutate and can evolve at a much greater rate than other organisms. Viruses with genomes composed of RNA, like the Ebola virus, have especially high mutation rates. As it turns out, some other of these RNA viruses also pose a great threat to human health, including the influenza viruses, human immunodeficiency virus (HIV), Hepatitis C virus (HCV) and the measles virus.

One of the more pressing consequences of mutation is in a health setting. There are lots of known examples of mutations affecting human health, including the appearance of antiviral resistance in the influenza A virus, HIV, and HCV; the evasion of vaccine immunity of the influenza A virus between flu seasons, and the emergence of novel pathogens, namely in the origins of influenza pandemics, such as that of the H1N1 virus in 2009-10.

One of the other ways that mutation could do harm is by altering our capacity to diagnose an infection. Viral diagnostics is now commonly based on sequence-specific approaches, such as the polymerase chain reaction (PCR) and sequencing. If a mutation made a virus unable to be picked up by our lab diagnostics then it would be invisible to us.

Mutation and Ebola

During this outbreak, the Ebola virus has infected more than 20,000 people and led to the deaths of around 40% of those people. Recently the strategy to tackle Ebola has been three-fold: diagnose cases and isolate them; treat those confirmed cases, in isolation, using standard care and targeted antiviral drugs; and work to develop preventative strategies, such as a safe and effective vaccine. These strategies appear to have been effective at controlling the outbreak.

Gearing up.
Remko de Waal/EPA

But no Ebola antiviral drug has so far completed phase III clinical trials, nor have any of the vaccines, although trials are due to begin in the affected countries.

If the Ebola virus were to mutate would this inhibit this current positive response? Or even one in the future? This is an important and valid point because it could impact our ability to control this epidemic and a similar one in the future, which is critical to save human lives.

Studies that have looked at genome mutations of the virus have shown changes in the genes that are also the targets for antiviral treatments, including those for vaccination. They build a strong case that we should be keeping an eye on these sequences now and into the future. But this is as far as our predictive capacity goes. Without testing how these mutations function in the virus under controlled experimental conditions we will not able to say for certain. However, studies of this sort have not yet been published.

Is Ebola becoming more contagious?

One big concern is whether or not the Ebola virus might evolve to become more contagious in the human population. Two ways this might be achieved is through the virus causing a less incapacitating disease that allows it to be shed more; or spreading via the airborne route rather than via bodily fluids.

Anavaj Sakuntabhai, a geneticist at the Institut Pasteur in France, which put out the warning about Ebola mutating, said they had now seen several cases where people didn’t have any symptoms at all – asymptomatic cases. “These people may be the people who can spread the virus better, but we still don’t know that yet,” he said. “A virus can change itself to less deadly, but more contagious and that’s something we are afraid of.”

But as yet, and this is something which Sakuntabhai admits, we have no evidence that the first is happening and that the virus is evolving to make people less sick. Increased detection of cases with less pronounced disease may be a function of our greater ability to diagnose Ebola in general. And it has been suggested that asymptomatic cases of Ebola virus infection may be more common than once thought.

It is still very unlikely that the Ebola virus is evolving to become airborne, despite the headlines. There is no precedent for a virus changing its mode of transmission and considering how many chances the Ebola virus has had to make such a change during this outbreak and previous ones, without doing so, suggests that evolution of this property might be one step too far.

Putting an end to the outbreak

Recently, the number of cases of Ebola has begun to drop across the three affected nations. This suggests that our interventions have begun to work. This positive response is thus most likely due to the excellent job that front line clinicians and lab staff have done in diagnosing, isolating and treating those patients with the standard care available. If this response continues then we may see the last case in this outbreak appear by the end of 2015.

So despite all of the worries around mutation, this outbreak is being controlled successfully and without targeted antiviral treatments in place. Our focus should be to finish the job in hand and put a stop to this epidemic using what we know works.

Read more about how the outbreak in West Africa began here.

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Will the Millenium Development Goals hit their Targets?

Will the Millennium Development Goals hit their targets?

By Anna Childs, The Open University

At the dawn of the 21st century, 189 UN member states adopted the Millennium Declaration as the first common framework for promoting global development, committing to eight goals (six covering health and education) with time-bound targets and indicators. Much of the commentary from that period draws on UN secretary-general Ban Ki-Moon’s reference to the goals as “ambitious but feasible”. In 2015, as the Millennium Development Goals (MDGs) come of age, the qualifier has dropped to simply ambitious. And nothing short of a miracle will see all goals comprehensively realised by the year’s end.

In Bill and Melinda Gates’ seventh annual letter on global development, they suggest that “the lives of people in poor countries will improve faster in the next 15 years than at any other time in history”. This is thanks to major breakthroughs driven by technological innovations, such as new vaccines, cheaper smart-phones and hardier crops: “[People in poor countries] will be living longer and in better health. They will have unprecedented opportunities to get an education, eat nutritious food, and benefit from mobile banking.”

But looking back over the past 15 years, what have been the achievements of one of the world’s most ambitious projects and what didn’t work so well, despite the grand aspiration? It is easy enough to check the summary progress for the MDGs on health and education – MDGs one to six – through official UN data. For each goal there are statements of achievement, tempered by one or more statements of what is yet to achieve.

1: Eradicate extreme poverty and hunger

The very first is the biggie: halve, between 1990 and 2015, the proportion of people whose income is less than US$1.25 a day. This target was met five years early, although it should be noted that this was largely due to acceleration due to economic growth in China and to some extent India initiated before the goals came into being, an argument often raised in critical discourse around the MDGs.

Additional targets in this goal included the achievement of full and productive employment and decent work for all, and to halve the proportion of people who suffer from hunger. UN data indicates that the hunger target should be met in time, but impedance in global economic growth generally between 2008 and 2013, along with significant outstanding gender gaps, mean that the employment target is way off course.

2: Achieve universal primary education

The second goal aims to ensure that by 2015 children everywhere, boys and girls alike, will be able to complete a full course of primary schooling.

More in primary school but millions still aren’t.
Feed my starving children., CC BY

The UN says: “Enrolment in primary education in developing regions reached 90% in 2010, up from 82% in 1999, which means more kids than ever are attending primary school.”

It then goes on to say that in 2012, 58m children of primary school age were out of school. If this figure represented a nation it would be the 24th most populous on the planet, just above South Africa in a list of 248.

3: Promote gender equality and empower women

The third goal is to eliminate gender disparity, focusing first on primary and secondary education (2005) and then all levels (2015). The UN said: “The world has achieved equality in primary education between girls and boys, but few countries have achieved that target at all levels of education.”

The reality is that the significant majority of those 58m children out of school are girls and the UN admits that: “in many countries, gender inequality persists.”

4 & 5: Reduce child mortality and improve maternal health

Goals four and five are to reduce child mortality by two-thirds and improve maternal health. Notwithstanding population growth, the global figure for child mortality has reduced by about half, from 12.7m deaths (of children under five) in 1990 to 6.3m in 2013 and the UN translates this as “about 17,000 fewer children dying each day” – which is to be celebrated. However it also notes that “an increasing proportion of child deaths are in sub-Saharan Africa and southern Asia. Four out of every five deaths of children under age five occur in these regions.”

It is the sub-Saharan Africa region that remains the heart of global crisis, with extensive under-performance across the MDGs, particularly in maternal health where – with the highest adolescent birth rate and greatest unmet need for family planning – it is a strong contributor to the gap between the target reduction of 75% and the actual fall of 45%. Asia has made the fastest progress, but started the furthest back in the race.

Asia has made fastest progress but sub-Saharan Africa has the biggest problem.
UK Department for International Development, CC BY-SA

In the target for universal access to reproductive health, more women are receiving antenatal care – but access to contraception, family planning and reproductive health care remains low in developing regions and continues to be a cause for concern.

6: Combat HIV/AIDS, Malaria and other diseases

The goal to combat HIV/AIDS, malaria and other diseases is the hardest to summarise, as even the targets (to halt a disease and reverse its spread) are difficult to quantify at scale. Generally, new infections are declining and deaths are down but the formal statements that have been made on achievements here are mostly unrelated to pre-MDG figures, providing snapshots of progress within the period rather than against a baseline.

The pros and cons of universal objectives

One of the biggest criticisms of the MDGs is that the universal targets set the same objectives for everyone. Countries which were way behind to start with have had much further to go, meaning goals that were feasible for some have been impossibly ambitious for others.

Even within countries, the data for rural areas is often significantly different than data for the cities, leading to a mean indicator that is grossly divergent from the reality for most people both at national and international level. We can talk in simple terms about meeting or not meeting the global outcomes of the MDGs, but the massive amounts of (often shaky, albeit improving) data that sit behind official UN statistics show myriad complexities across countries and regions. While advocating a need for equity in development, we have not seen equity in development goals.

It is then, in itself, massively ambitious to make statements of global parity from which local actions can be devolved. At their best, the MDGs have brought together diffuse public, private, and non-profit organisations across global north-south divides and amid tremendous complexities to co-operate over a common enterprise with some outstanding results.

The MDGs kick-started unprecedented progress and improved the lives of hundreds of millions of people, mobilising development efforts through and towards an emphasis on outcomes. They have contributed to the empowerment of whole populations by providing standards to which governments can be held accountable. And finally let’s not forget that they have provided learning – something that the Gates Foundation and others can build on – and maybe that is their greatest legacy in informing what comes next.

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Why mosquitoes seem to bite some people more

Health Check: why mosquitoes seem to bite some people more

By Cameron Webb, University of Sydney

There’s always one in a crowd, a sort of harbinger of the oncoming mosquito onslaught: a person mosquitoes seem to target more than others. What is it about these unlucky chosen few that makes them mosquito magnets?

There are hundreds of mosquito species and they all have slightly different preferences when it comes to what or who they bite. But only females bite; they need a nutritional hit to develop eggs.

Finding someone to bite

Mosquitoes are stimulated by a number of factors when seeking out a blood meal. Initially, they’re attracted by the carbon dioxide we exhale. Body heat is probably important too, but once the mosquito gets closer, she will respond to the smell of a potential blood source’s skin.

Studies have suggested blood type (particularly type O), pregnancy and beer drinking all make you marginally more attractive to mosquitoes. But most of this research uses only one mosquito species. Switch to another species and the results are likely to be different.

There are up to 400 chemical compounds on human skin that could play a role in attracting (and perhaps repulsing) mosquitoes. This smelly mix, produced by bacteria living on our skin and exuded in sweat, varies from person to person and is likely to explain why there is substantial variation in how many mozzies we attract. Genetics probably plays the biggest role in this, but a little of it may be down to diet or physiology.

One of the best studied substances contained in sweat is lactic acid. Research shows it’s a key mosquito attractant, particularly for human-biting species such as Aedes aegypti. This should act as fair warning against exercising close to wetlands; a hot and sweaty body is probably the “pick of the bunch” for a hungry mosquito!

Probably the most famous study about their biting habits demonstrated that the mosquitoes that spread malaria (Anopheles gambiae) are attracted to Limburger cheese. The bacteria that gives this cheese its distinctive aroma is closely related to germs living between our toes. That explains why these mosquitoes are attracted to smelly feet.

But when another mosquito (such as Aedes aegypti) is exposed to the same cheese, the phenomenon is not repeated. This difference between mosquitoes highlights the difficulty of studying their biting behaviours. Even pathogens such as malaria may make us more attractive to mosquitoes once we’re infected.

Only females bite because they need a nutritional hit to develop eggs.
Sean McCann/Flickr, CC BY-NC-SA

Researchers are trying to unscramble the irresistible smelly cocktails on the skins of “mosquito magnets”. But the bad news is that if you’re one of these people, there isn’t much you can do about it other than wearing insect repellents.

The good news is that you may one day help isolate a substance, or mixes of substances, that will help them find the perfect lure to use in mosquito traps. We could all then possibly say goodbye to topical insect repellents altogether.

Attraction or reaction?

Sometimes, it’s not the bite as much as the reaction that raises concerns. Think of the last time the mosquito magnets in your circle of friends started complaining about being bitten after the event where the purported mosquito feast took place. At least, they appear to have attracted more than the “bite free” people who were also at the picnic, or concert or whatever.

But just because some people didn’t react to mosquito bites, doesn’t mean they weren’t bitten. Just as we do with a range of environmental, chemical or food allergens, we all differ in our reaction to the saliva mosquitoes spit while feeding.

People who don’t react badly to mosquito bites may think they haven’t been bitten when they’ve actually been bitten as much as their itchy friends. In fact, while some people attract more mosquito bites than others, there’s unlikely to be anyone who never, ever, gets bitten.

The problem is that people who don’t react to mosquito bites may all too easily become complacent. If you’re one of them, remember that it only takes one bite to contract a mosquito-borne disease.

Finally, there is no evidence from anywhere in the world that there is something you can eat or drink that will stop you being bitten by mosquitoes. No, not even eating garlic, or swallowing vitamin B supplements.

Perhaps if we spent as much time thinking about how to choose and use mosquito repellents as we do about why mosquitoes bite our friends and family less than us, there’d be fewer bites all around.

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