Why the clitoris doesn’t get the attention it deserves – and why this matters

Jane Chalmers, Western Sydney University and Cat Jones, University of South Australia

Did you know the clitoris is a large and complex organ? If not, it’s probably not your fault: in anatomical textbooks, few words and diagrams are devoted to understanding the clitoris. Most label the very small portion of the organ visible on diagrams of the vulva, when in fact it’s almost entirely under the skin.

Studies of historical anatomical textbooks have shown that depictions of the clitoris were significantly limited and often omitted completely from the mid-19th into the 20th century.

During these times there were ideologies and subsequent theories relating to women’s bodies that likely encouraged and sustained censorship of the clitoris. For instance, there was Freud’s now defunct theory that clitoral stimulation was a sign of sexual immaturity and neurosis. Women were also taught not to enjoy sex; women had sex for reproductive purposes, while men had sex for pleasure.

These fallacies led to the neglect of the clitoris in research, literature and the public domain.

Although more recent research and feminist lobbying have improved the quality of information on the clitoris in current textbooks, most texts are still brief. These include minimal information, or information only on the external portion of the clitoris (the glans). This brevity has impacts on health care for women with clitoral and related pain.

This figure, published in 2014, depicts the clitoris as only the external clitoral glans and prepuce (hood).

What is the clitoris?

The clitoris lies at the junction of the labia minora (the inner lips of the vulva), just above the urethra. It is made up of four main parts: the glans, body, two crura and two bulbs. The glans is the only external part of the clitoris and is covered by a hood of skin.

The body, corpora, crura and bulbs of the clitoris are all made up of erectile tissue and converge below the glans. The body of the clitoris is generally 1-2cm wide and 2-4cm long.

Left: the clitoris from an anterior view. All four parts of the clitoris are visible in this view: the glans (external portion), the body, the bulbs and the crura. Right: the clitoris from a side view. Only one crus (plural: crura) and bulb are shown from this view. Note, the clitoris is a tri-planar organ, with each component lying in a different plane to one another.
Author provided

The crura extend laterally from the body of the clitoris and are on average around 5-9cm long. The bulbs of the clitoris are generally 3-7cm long and lie between the body, crura and the urethra.

The clitoris is highly innervated, with twice as many nerve endings as the penis, and receives a rich blood supply. This rich blood supply allows the erectile components to swell up, with the body and glans of the clitoris becoming up to three times larger during arousal – and you thought a penile erection was impressive!

The clitoris (left) and penis (right) emerge from the same cells in a zygote.
Screenshot/Huffington Post

Foetus genital and reproductive organs are differentiated at six weeks’ gestation. While the clitoris and penis arise from the same group of cells in a zygote, we now know they clearly have different forms and functions.

The penis has an obvious and well-researched role in the reproductive and urinary systems, while the function of the clitoris is usually stated as being purely for pleasure.

However, few studies have actually investigated the function of the clitoris. The close proximity of the clitoris to the urethra and vagina has led to suggestions that it plays a much larger role than sexual pleasure, such as assisting in maintaining immune health.

What we don’t know can hurt us

Censoring the clitoris in textbooks means doctors and other health-care professionals won’t be equipped to treat patients with clitoral concerns. Women are at risk of sexual dysfunction (such as lack of desire or arousal, decreased lubrication, inability to orgasm) from operations on their urinary and reproductive organs. This shows doctors need more in-depth knowledge, and we need further research into understanding the anatomy of the clitoris.

Don’t you forget about me.
Towe My/Flickr, CC BY

Because of its delicate yet complex make-up, the clitoris is prone to infections, inflammation and diseases. Some common examples are itching and soreness due to thrush infections, swelling due to bruising or inflammation, and pain of unknown origin (called clitorodynia).

Although it is not often spoken about, clitoral and vulvar pain are very common in women.

Educating patients about their condition can improve pain outcomes. Yet this may be difficult for doctors treating conditions such as clitorodynia, given they may not be receiving adequate information about the clitoris themselves.

On average, one-third of university-aged women are unable to find the clitoris on a diagram. We frequently use synonyms of females’ reproductive organs as derogatory terms (“pussy” to mean weak, “cunt” to mean an unpleasant person) and many women are often not comfortable using anatomically correct terms.

More than 65% of women say they feel uneasy using the terms vagina and vulva. Instead they use code names such as “lady parts”, even when discussing gynaecological issues with their doctors.

Given there is evidence to suggest our sense of body ownership can influence pain, perhaps this lack of body ownership over the clitoris helps to explain why conditions such as clitorodynia are common.

Jane Chalmers, Lecturer in Physiotherapy, Western Sydney University and Cat Jones, Artist in Residence, Body In Mind, Sansom Institute, University of South Australia

This article was originally published on The Conversation. Read the original article.

What happens during a heart attack and how is one diagnosed?

Explainer: what happens during a heart attack and how is one diagnosed?

Garry Jennings, Baker IDI Heart & Diabetes Institute

Most people usually link the phrase “heart attack” with “massive”; something you are indisputedly aware of.

Some are massive and, in these instances, it’s relatively easy to know if it is indeed a heart attack. Typically, there will have been crushing chest pain lasting more than a few minutes. One would hope this has led to an immediate call to 000 and a trip in an ambulance to hospital.

Often ambulance officers will have performed an electrocardiogram (ECG) and transmitted the results to the hospital, which will have selected and be ready with the appropriate treatment. In this case, the chest pain and the characteristic ECG changes are enough – those wiggly lines mean a lot to an experienced reader.

However, most heart attacks are not “massive”. In these instances, further tests are necessary and the diagnosis can become quite challenging. The pain may not be typical and the ECG may be normal or difficult to interpret.

Different types of heart attacks

“Heart attack” is not just one thing: there are five internationally recognised types.

The one we think of first is when a plaque in a large coronary artery – consisting of cholesterol, cells and cellular debris that has built up over the years – suddenly cracks or erodes. This exposes the inside of the plaque to the blood flowing down the artery. The blood clots at this point, causing a thrombosis that narrows or blocks the artery.

If the artery is completely blocked, this is likely to cause death of heart muscle cells downstream and myocardial infarction, colloquially called a heart attack.

Two different kinds of heart attack are distinguished by the ECG changes – STEMI (ST segment elevation myocardial infarction) and NSTEMI (non-STEMI) – which may require different treatments. STEMI generally means the artery has blocked completely. If the artery is only partly narrowed and the downstream muscle causes pain but survives the syndrome, it is known as unstable angina.

Cardiologists prefer the term acute coronary syndrome (ACS) to describe the spectrum of consequences of short-term lack of blood and oxygen to the heart muscle. As this is a spectrum, it is perhaps not surprising that it has been difficult to come up with a dichotomous separation of “heart attack” or “no heart attack”.

Heart attack or no heart attack

Medical advances over the decades have provided some clarity. But this has also caused a rethink among those trying to define the various levels of heart attack, both for management decisions and for practical purposes such as insurance.

For many years, diagnosis has depended on measurements of the changes in levels of enzymes released by dying heart muscle cells. These rise in the blood some hours after the initial event peaks and then gradually fall, with different enzymes following a different time course.

Until the 1990s, the enzymes that were used for this purpose included a panel of up to three. Each followed a vastly different time course. However, they are not specific to heart muscle cells and a rise could be due to many other conditions.

Testing was refined with the development of a muscle-specific enzyme test for creatinine kinase (CK). But the search was on for a test that would both identify loss of heart muscle by levels rising earlier and be more specific to the heart.

Measurement of troponin was the next big advance in the mid-1990s and revolutionised the classification of heart attacks. Troponin is released from muscle one to three hours after an artery is blocked and may stay high for up to 14 days. It is more specific to heart muscle than previous enzyme tests.

Over the past decade, the test has been refined to be more and more sensitive. But each test needs its own threshold level for an abnormal result, so an absolute result of a test in one laboratory may not be comparable to that of another.

Nevertheless, the availability and refinement of the troponin test used properly has introduced a level of certainty in the diagnosis of acute heart syndromes that was not previously available. Myocardial infarction can be ruled out earlier. Small infarcts can be identified that would previously have been missed.

The problem with measuring troponin

Troponin measurements introduced their own problems too. During the late 1990s, it seemed that a sizable proportion of people presenting to emergency departments had rising troponin levels but no other signs of heart attack. The tests were picking up smaller and smaller amounts of heart muscle damage.

So somebody presenting in the 1990s would get a different diagnosis to another person with the same problem presenting this decade in the high-sensitivity troponin era.

Clinicians are becoming aware of a number of situations where false positives can occur. This may result from damage to the heart from trauma, frequent defibrillator shocks, heart failure, disease of the aorta, pulmonary embolism, kidney failure, stroke, various drugs and critical illnesses such as burns and sepsis.

Troponin can also miss heart attacks if used alone, or the blood is taken outside the window when levels are elevated, or the laboratory uses an insensitive troponin test.

The Australian national guidelines for diagnosing myocardial infarction are due for release in the next few months by the National Heart Foundation and the Cardiac Society of Australia and New Zealand and will consider these problems. In the meantime, the third universal definition of myocardial infarction is the internationally recognised and accepted guideline.

Garry Jennings, Chief Executive Officer at National Heart Foundation of Australia; Senior Fellow, Baker IDI Heart & Diabetes Institute

This article was originally published on The Conversation. Read the original article.

Interactive body map: what really gives you cancer?

Emil Jeyaratnam, The Conversation and Sasha Petrova, The Conversation

There’s abundant advice out there on what you should or shouldn’t eat, drink, swallow, or stand next to, to avoid cancer. But it’s often lacking in evidence and the jumble of messages can be confusing.

This body map brings together the evidence on proven cancer causes. Using credible, scientific sources it answers questions about whether alcohol, red meat or sun exposure increase your cancer risk.

Cancer occurs when mutations in a cell’s DNA cause it to replicate without control, invading other tissues. Some cancer-causing mutations can be inherited; others induced, by infection with bacteria or viruses; or by environmental factors such as smoking, sun exposure and eating red meat.

This map’s focus is on induced factors. They are considered “modifiable” because avoiding them lessens your chance of cancer.

Choose your gender and click a risk factor to see which body area can be affected. Clicking the body region will show you how much engaging in risks such as drinking alcohol, taking the contraceptive pill, or eating pickled vegetables, will increase your chance of certain cancers.

When reading the map, keep in mind that every body and circumstance is unique; one risk factor cannot be considered in isolation when applied to a real life context.

Also remember the percentages portrayed are “relative risks” which are different to “absolute risks”. The difference is explained in this accompanying piece, which will help you understand what relative risk really means for your chances of getting cancer.

Emil Jeyaratnam, Multimedia Editor, The Conversation and Sasha Petrova, Researcher, Health and Medicine, The Conversation

This article was originally published on The Conversation. Read the original article.

Kagame meets Rotarian doctors, commends their voluntary service

By: ATHAN TASHOBYA

President Paul Kagame, on Saturday evening, met with a team of 18 Indian surgeons who have been in Rwanda on a 12-day medical outreach programme which ran from February 25 to March 6.

The mission was organised by Rotary Club International in conjunction with the Ministry of Health.

The President met the medical team, to appreciate their contribution to Rwanda’s health sector, according to the Health Minister Agnes Binagwaho.

“The President extended his appreciation to the medical team, for their professional voluntary service, which has greatly benefited our medical sector, through offering hi-tech surgeries which we could not offer here in Rwanda,” Binagwaho said.

During their Medicare mission, the team offered free treatment to over 300 patients with different ailments at the University Teaching Hospital Kigali (CHUK) and Rwanda Military Hospital, as well as sharing their experience with the local physicians.

The medical outreach benefited patients suffering from varying physical deformations resulting from accidents, birth defects and the 1994 Genocide against the Tutsi.

A teaching session, involving specialists from the mission and military hospital specialists, was organised to benefit around 50 Rwandan doctors and paramedics from different hospitals.

Despite the fact that Rotary medicare missions are usually limited to only one per country, this year’s outreach was the fourth time that a rotary mission is being held in Rwanda.

This year’s medical mission also involved the president of Rotary International, K.R. Ravindran, who became the first Rotary international president to visit Rwanda in the organisation’s 111-year-old history.

Over the course of three years, the medical teams in the preceding Medical missions have been able to provide treatment and corrective surgeries to over 600 vulnerable Rwandan citizens that would otherwise have been beyond their reach.

Rajendra K Saboo, a former president of Rotary International, said that the physicians were delighted in meeting with the president

“His Excellency has been extremely gracious, kind and generous in giving the audience to our doctors,” said Saboo, adding that President Kagame offered to meet the doctors to appreciate their outreach service.

“On Thursday I asked President Kagame, if he had any message I would share with the doctors since they are the ones who do the work in the hospitals. He instead said that he would want to meet them and give the message personally; to express his gratitude to the doctors. I asked for a glass of water and he opened a fountain,” Saboo said.

He added that, this is not a one-off relationship, but rather, they would find ways through which the involved parties could enhance it further.

“We hope that in the future we will have a joint team including Rwandan doctors spreading to other parts of African, so that the continent’s future continues to evolve,” Saboo said.

Saboo said that the Medicare mission experience in Rwanda has been positive, in the sense that this year’s outreached saw the largest number of patients being operated on, compared to the previous missions, with the largest medical team than ever before.

“268 surgeries were made and over 310 medical procedures carried out; in the whole process there were many patients who have been operated on, screened and advised, and this will be a starter for the future which have shown us that we need to bring super specialties for the future mission,” Saboo added.

Rotary also offered to have 20 children from Rwanda going to India for open-heart surgery, and 10 doctors from here going to learn and also have the experience in an Indian hospital.

Rotary will we will take care of teaching and experience expenses for three months, according to Saboo.

http://kigalihe.com/

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Africa’s children need help coping with a myriad of stresses, not just HIV

Jennifer Beard, Boston University

HIV has exacted a terrible toll on many children in sub-Saharan Africa. Of more than 17.8 million children who have lost one or both parents to HIV globally, 15 million live in Africa. Another three million are infected with HIV. And each year very large numbers are made vulnerable when parents or family members become sick and are unable to work.

The global health community has made significant progress over the past 15 years to understand how to keep HIV-positive children alive and prevent infant infections. Between 2001 and 2013, paediatric infections decreased by 58%. And the number of children on antiretrovirals increased from 355,000 in 2009 to 740,000 in 2013.

Arguably, children – and their families – who are affected by HIV and receive donor assistance may be less vulnerable than their peers who have not had their lives touched by HIV, but still grow up in extreme poverty.

For this reason, the call to action to address childhood vulnerability in Africa must go far beyond the 17.8 million children infected and affected by HIV.

A global focus on HIV

The global community and the US in particular, through the President’s Emergency Plan for AIDS Relief, has invested billions of dollars in HIV programs. These investments are part of a global plan to ensure an AIDS-free generation by 2015.

The plan has largely centred on providing antiretroviral medication to HIV-positive people and preventing mother-to-child transmission. About one-third of HIV-positive adults and children access lifesaving treatment. And more than half of infected pregnant women access medicines that protect their babies from the virus.

But much still has to be done, as shown in our review in the Pediatric Clinics of North America journal.

Aside from providing lifesaving medication, donor efforts have also reduced the social and economic burden faced by HIV-affected families and children.

HIV-positive people not receiving treatment will inevitably become ill and will be unable to work. Their children will stop going to school to take care of them or their younger siblings. Many may not be able to afford school fees.

The social, emotional, and developmental health of children orphaned or otherwise affected by HIV is more difficult to measure and more difficult to address. Africa is home to 85% of AIDS orphans globally.

More inclusive approach needed

But our disease-centric focus for funding and interventions is far too limited. On a continent where millions of children are living in poverty, undernourished or struggling to stay in school and fulfil their potential, it is not enough to focus the bulk of donor funding on those affected by HIV.

An alternative and more inclusive approach would be to focus on adverse childhood experiences. From this broader perspective we can address the many variables influencing the health and well-being of the child.

Children in sub-Saharan Africa face myriad challenges which make them vulnerable. Losing a parent to HIV, being HIV positive and facing stigma and discrimination are also adverse childhood experiences. Another is growing up in extreme poverty.

I was working in rural, southern Kenya and I could not stop thinking about the widespread, extreme poverty unrelated to HIV. Some of the families in the largely Maasai community where I was staying may have been affected by HIV but the vast majority were not.

In Kenya, about 6% of the adult population has HIV. More may be at risk of becoming infected, but they are a minority. The biggest driver of vulnerability among children in this community is profound poverty exacerbated by too little food and scant water sources. Six of the 13 fastest-growing economies in the world are in Africa. Kenya is one of them. Yet 42% of Africans still live on less than US$1.25 per day.

Poverty affects children’s ability to attend school. Most African countries provide universal primary school education. But children can still be barred from school if they cannot pay fees for uniforms and books. Overall primary school completion for the continent is only 67%. More than 22 million children remain out of school.

In several countries hit hard by HIV, such as Cameroon, Rwanda, South Africa and Zambia, at least 90% of children are enrolled in primary school. This progress is the result of large investments by governments and foreign donors in universal primary education.

A study comparing school attendance and success between orphans and non-orphans in Lesotho, Malawi, Tanzania, Uganda and Zambia found that poverty was more strongly associated with school difficulties than orphan status. This was true for both primary and secondary students, and points to a conclusion that support targeting orphans is reducing their vulnerability, at least with regard to education.

It also suggests that we need to broaden our approach to childhood vulnerability in contexts with a high HIV burden where government and donor support has tended to focus on children affected by HIV.

Expanding our approach

The US Centres for Disease Control and Prevention have been funding research on adverse childhood experiences in the US for a number of years. The United Nations Children’s Emergency Fund has developed a methodology to assess the impact of multidimensional, overlapping deprivations on child vulnerability.

At the same time, public health researchers and child advocates have developed tools to measure and understand the sources of resilience that help some children to excel despite all odds. Sources of resilience include both internal factors such as hope for the future and self-esteem, and external factors such as access to education and financial resources.

We need to leverage the profound global empathy for children affected by HIV to address the needs of all vulnerable children on the continent.

Five months ago, the United Nations General Assembly ratified 17 new Sustainable Development Goals to replace the Millennium Development Goals. The breathtakingly ambitious goals include to “end poverty in all its forms everywhere” by 2030 and “ensure healthy lives and promote well-being for all at all ages”.

Some days, I am inspired by the audacity of these goals. But mostly I think about the children in Kimana, Kenya. Vulnerable? Yes. Affected by HIV? Mostly not. And I wonder what it will take to get them onto the global development agenda.

Jennifer Beard, Assitant Professor of Global Health, Boston University

This article was originally published on The Conversation. Read the original article.

What are panic attacks and what’s happening when we have them?

Explainer: what are panic attacks and what’s happening when we have them?

Lynne Harris, University of Sydney

What would you think was happening to you if out of nowhere your heart started to race, you were drenched in sweat, you found yourself trembling uncontrollably, short of breath, with chest pain and feeling nauseated, dizzy and lightheaded as though you might faint?

You might also be feeling very cold or very hot, with tingling sensations in your fingers and toes. You might feel removed from the world around you – as though it wasn’t real – and be worried that you might lose control or that you are going insane. You might try to work out what is happening and conclude you are having a heart attack or dying.

A panic attack is a sudden, intense feeling of fear or discomfort with at least four of the signs described above. For some people, a panic attack can come out of nowhere, like a sudden thunderstorm from a clear blue sky. For other people, panic attack may be more predictable, such as an abrupt escalation of a milder anxiety about giving a speech or speaking to someone in authority.

Just as a panic attack can follow an experience of relative calm or of mild anxiety, panic can resolve to a relatively calm state or to ongoing, less intense symptoms. But the symptoms of panic attack are severe and frightening. Many people experiencing a panic attack believe they are seriously ill and seek medical help.

What is happening to the body?

Often one of the first symptoms of a panic attack is hyperventilating (rapidly breathing in and out), which upsets the natural balance of oxygen and carbon dioxide in our system. One view says a low level of carbon dioxide in the blood directly triggers the symptoms of panic, such as feeling lightheaded and dizzy. When we breathe quickly we also build up oxygen in our blood. Paradoxically, too much oxygen is also associated with feeling short of breath.

Hyperventilation causes many of the other symptoms of a panic attack such as dizziness, blurred vision, tingling, muscle tension, chest pain, heart rate increases, nausea and temperature changes.

People who experience panic misinterpret the bodily signs of hyperventilation as indicating immediate physical danger and believe they have little control over the symptoms. When we then say things to ourselves such as “I might be having a heart attack” and “I can’t cope with this”, the anxiety gets worse.

In a 2013 study, researchers showed when people with no history of panic inhaled air with increased carbon dioxide they reported fear, discomfort and panic symptoms. People with a history of panic attack experience these symptoms at lower concentrations of carbon dioxide, suggesting they are hypersensitive to this internal signal for danger.

Panic attacks can occur with a range of diagnosed mental illnesses, including anxiety disorders, depressive disorders and substance use disorders, as well as physical illnesses, especially illnesses that affect heart function, breathing, balance and digestion. It is very important to understand and deal with panic attacks so they don’t lead to a more serious condition known as panic disorder.

People with panic disorder have a history of panic attacks and worry they will have further panic attacks. They change the way they live to ensure they do not have another panic attack. They avoid activities like exercise that cause feelings similar to panic attack (shortness of breath, sweating) and avoid situations where they fear another panic attack may occur. This avoidance brings many additional problems, as social, family and occupational worlds shrink due to fear of panic.

What should you do if you have a panic attack?

Panic attacks are common, with almost 23% of a people from a large US study of the general population reporting at least one panic attack during their lives. Panic attacks are more common in females than males. They are also more common in family members of people with panic disorder.

Panic attacks are more common among people who believe symptoms of anxiety are dangerous and harmful, rather than annoying and uncomfortable. They are also more likely if you are under emotional pressure, have been ill, are tired, are hungover or smoke.

As many of the symptoms of panic attack are physical and can be caused by a number of physical conditions, the first thing to do if you have symptoms like the ones described here is to see your doctor to check whether there is a medical reason for the symptoms.

If the symptoms are due to panic, then there are effective psychological approaches for controlling panic attacks. These focus on:

monitoring and slowing breathing, as overbreathing causes many panic sensations
correcting the interpretations about what the symptoms mean by looking at the things we say to ourselves before, during and after a panic attack. It is very important to remember the symptoms are “just anxiety” and are not life-threatening.

There is useful information about panic attack and how to cope with it available through Lifeline.

Lynne Harris, Professor of Psychological Sciences, School of Psychological Sciences, Australian College of Applied Psychology and Honorary Assoc Prof with the Faculty of Health Sciences, University of Sydney

This article was originally published on The Conversation. Read the original article.

Does cannabis cause mental illness?

Peter Gates, UNSW Australia

Cannabis is the most commonly used illicit drug in Australia, with one in three adults using it at some point in their life. It’s legal in some places around the world, and offered medicinally in others. But what does smoking pot do to your mental health?

The potential harms associated with using cannabis depend on two things above all others.

The first is the age at which you first begin to use cannabis, particularly if it’s before 18. Using cannabis during key stages of brain development can impact on synaptic pruning (when old neural connections are deleted) and the development of white matter (which transmits signals in the brain).

The second is the patterns of use: the frequency, dose and duration, particularly if you’re using at least weekly. The bigger or more potent the dose, the more tetrahydrocannabinol (THC) you are ingesting. THC is the main psychoactive component of cannabis and appears to act on areas of our brain involved in the regulation of our emotional experiences.

Depression and anxiety

Many studies of the relationship between cannabis use and mental illnesses such as depression and anxiety have suffered from methodological issues by not controlling for related factors.

The few longitudinal studies that have been conducted have mixed findings.

A 2014 review of the existing research concluded that using cannabis placed an individual at moderate risk of developing depression.

Unfortunately it was not within the scope of the research to determine if cannabis use was causing depression or if the relationship instead reflects the association between cannabis use and social problems. Cannabis use is associated with other factors that increase risk of depression such as school dropout and unemployment.

The relationship between cannabis use and anxiety is also complex. Many people use cannabis for its euphoric and relaxing effects. But some people also experience feelings of anxiety or paranoia when intoxicated. As such, cannabis could be used to relieve anxiety or stress for some while causing others to feel anxious.

A 2014 review of the available research concluded that using cannabis placed an individual at a small risk of developing anxiety. But the authors noted that while the weight of evidence supported the coexistence of cannabis use and anxiety, there was relatively little evidence to suggest that cannabis caused anxiety.

Not included in these previous reviews of depression and anxiety disorders were two recent investigations of cannabis use in the United States using data from 2001-2002 and 2004-2005. These included a host of variables such as demographic status and family environment.

Each found a significant association between cannabis use and the onset of depression and anxiety disorders. But this association was no longer significant when considering the impact of the included variables.

Clearly, the relationship between cannabis use and depression and anxiety disorders is complex and involves the individual’s reasons for cannabis use and external situations. That is, cannabis may be used to help cope with social problems that were not necessarily caused by cannabis use.

Schizophrenia

In contrast, the relationship between cannabis use and risk of developing symptoms of psychosis has been well established in many different review articles.

This research has found that early and frequent cannabis use is a component cause of psychosis, which interacts with other risk factors such as family history of psychosis, history of childhood abuse and expression of the COMT and AKT1 genes. These interactions make it difficult to determine the exact role of cannabis use in causing psychosis that may not have otherwise occurred.

Regardless, the connection between cannabis use and psychosis is not surprising. There is a strong resemblance between the acute and transient effects of cannabis use and symptoms of psychosis, including impaired memory, cognition and processing of external stimuli. This combines to make it hard for a person to learn and remember new things but can also extend to the experience of deluded thinking and hallucinations.

We also know that cannabis use by people with established psychotic disorder can exacerbate symptoms.

Overall, the evidence suggests cannabis use will bring forward diagnosis of psychosis by an average of 2.7 years.

The risk of developing schizophrenia increases with the duration and dose of cannabis use. Regular cannabis users have double the risk of non-users. Those who have used cannabis at some point in their life have a 40% increased risk compared with non-users.

That said, it is important to view this increased risk in context. The proportions of individuals with psychosis among the population and among cannabis users are low. Current estimates suggest that if frequent long-term cannabis use was known to cause psychosis, the rates of incidence would increase from seven in 1,000 in non-users to 14 in 1,000 cannabis users.

If you or a family member or friend have problems or concerns about cannabis, visit www.ncpic.org.au or access the free national Cannabis Information and Helpline on 1800 30 40 50.

Peter Gates, Senior Research Officer, National Drug & Alcohol Research Centre, UNSW Australia

This article was originally published on The Conversation. Read the original article.

Do Wi-Fi and mobile phones really cause cancer? Experts respond

Simon Chapman, University of Sydney; Darren Saunders, UNSW Australia; Rodney Croft, University of Wollongong, and Sarah Loughran, University of Wollongong

On 16th February, Catalyst aired an episode on the ABC titled “Wi-Fried”, hosted by Dr Maryanne Demasi, claiming that radiation from mobile phones and Wi-Fi may constitute a brain cancer risk.

We invited experts who have conducted research into this area to respond to the claims made in the programme.

Rodney Croft, University of Wollongong

Instead of science journalism, Catalyst aired a misleading program, which followed the views of a few individuals in arguing that radiofrequency emissions from wireless devices were harmful.

Although the program failed to disclose this, such views are not supported by science and should be taken merely as the personal views of some fringe scientists.

In fact, the scientific consensus is strong, and is that there is no substantiated evidence that the low levels of radiofrequency emissions encountered by mobile telecommunications can cause any harm.

For more details about the international scientific consensus on this issue you may find the website of the International Commission on Non-Ionising Radiation Protection (ICNIRP) of interest, or closer to home, that of the Australian Centre for Electromagnetic Bioeffects Research.

Professor Rodney Croft is Director of the National Health & Medical Research Council of Australia’s Centre for Research Excellence in Electromagnetic Energy, he is a current ICNIRP Commissioner, and Professor of Health Psychology at University of Wollongong.

Darren Saunders, University of NSW

It’s really disappointing to see the bastion of TV science in Australia approach a story in this way.

Scaremongering and pseudoscience have plenty of other outlets on TV, and there are so many amazing science stories to be told locally and internationally. There was very selective reporting of existing data and sensationalist headlines.

Catalyst has missed an opportunity to use this topic as a way to demonstrate scientific or critical thinking.

With so many scientists questioning the content and angle of stories like this, then it’s probably time for Catalyst to reflect on its approach.

The really frustrating aspect is that rebuttals and factchecks won’t undo the damage. There are very real public health effects of scaremongering like this, creating anxiety and fear.

The two main flaws in the argument that stand out scientifically are:

The lack of any demonstrable increase in brain cancer incidence over time. We have been exposed to the same kind of non-ionising electromagnetic radiation long before mobile phones and Wi-Fi became commonplace, and
The absence of a plausible biological mechanism for how this kind of radiation can cause cancer. There were very poor analogies made with microwave ovens and smoking, which are purely emotive and not based on actual science. Comparing a microwave to a mobile phone is like comparing a Saturn V rocket to your lawnmower.

Dr Darren Saunders is a cancer biologist at the University of NSW and visiting fellow at the Kinghorn Cancer Centre, Garvan Institute.

Sarah Loughran, University of Wollongong

The ABC’s Catalyst programme “Wi-Fried” asked the question of whether Wi-Fi and radiation from wireless devices could be affecting our health.

Unfortunately a very disappointing and inaccurate story was presented, with the underlying suggestion throughout the episode that exposure to the radiofrequency fields emitted by these devices is not safe.

Many claims were made without providing any substantiated science to support what was essentially individual and selective opinions that were used to paint an incorrect picture of the current state of knowledge.

Indeed there is currently no scientific evidence that exposure to low level radiofrequency, such as emitted by mobile phones and Wi-Fi, has an impact on health.

By not providing a balanced view of the science, Catalyst has left viewers with misleading messages related to the use of such devices, which may serve to perpetuate fear related to a health risk that currently does not exist.

Dr Sarah Loughran is a researcher at the National Health & Medical Research Council of Australia’s Centre for Research Excellence in Electromagnetic Energy. She is currently a member of the World Health Organisation (WHO) Environmental Health Criterion Evaluation Committee on Radiofrequency Fields, the scientific expert group of ICNIRP, and is on the board of directors for the Bioelectromagnetics Society.

Simon Chapman, University of Sydney

Dr Devra Davis, who was featured extensively in the Catalyst programme, asserted that it was too early to see any rise in brain cancer caused by mobile phones or Wi-Fi, and argued that brain cancers after the Japanese atomic bombs did not appear for 40 years. This is simply incorrect.

There is no evidence of any increase in the rate per 100,000 population of brain cancer in any age group in Australia from 1982 to the present, other than for the very oldest age group where the increase started well before mobile phones were introduced in Australia and so cannot be explained by mobile phones. All cancer in Australia is notifiable, and over 85% of brain cancer is histologically verified: it is not just a doctor’s opinion.

This paper also reports on central nervous system cancers (including brain cancers) in those exposed to atomic bomb radiation in Japan. This table from the paper shows those diagnosed before 1985 (i.e. before 40 years). You can see that there were 110/187 cases diagnosed in the first 40 years, i.e. 58.8%.

This table shows the incidence of a variety of cancers of those exposed to atomic bomb radiation over the years.
Cancer/DOI 10.1002/cncr.20543

And this quote from the methods shows that there were another 27 who died before 1958 from central nervous system cancers, i.e. within 13 years of the bombs.

We excluded 73 tumors in individuals who were not in Hiroshima or Nagasaki at the time of the bombings, 35 individuals who did not have available organ dose estimates, and 27 individuals who died or were diagnosed before January 1, 1958.

We have had mobiles in Australia since 1988. Some 90% of the population use them today and many of these have used them for a lot longer than 13 years, but we are seeing no rise in the incidence against the background rate.

Davis is arguing that we would see a sudden rise 40 years later. That is not what we see with cancer; we see gradual rises moving toward peak incidence, which can be as late as 30-40 years (as with lung cancer and smoking for example).

New cases of brain cancer in Australia, 1982 to 2011 (age-adjusted)
Australian Institute of Health and Welfare, CC BY

Simon Chapman is Emeritus Professor in Public Health at the University of Sydney

Simon Chapman, Emeritus Professor in Public Health, University of Sydney; Darren Saunders, Senior Lecturer in Medicine, UNSW Australia; Rodney Croft, Professor of Health Physiology, University of Wollongong, and Sarah Loughran, Research Fellow, University of Wollongong

This article was originally published on The Conversation. Read the original article.

Zika via sex and blood: how worried should we be?

Beverley Paterson, University of Newcastle

For a fairly non-descript virus, Zika continues to surprise us. Zika has hit the headlines yet again with the news that there’s been transmission in Brazil of two cases by blood transfusion.

This is on top of the recent news about sexual transmission of the virus in the United States. Zika is a “vector-borne” virus – that is, it is transmitted by a vector, in this case a mosquito. In general, you need to get bitten by an infected mosquito before you can be infected by Zika. At least that’s what we thought.

With the news that this mosquito-borne virus has likely been transmitted by blood transfusion and sex, Zika is now set to become a widely researched and much-pondered phenomenon.

Blood transmission

The potential for Zika transmission via blood transfusion has been speculated for some time. The two cases in Campinas, Brazil, are the first known Zika infections acquired through this transmission method.

Britain, the US, Hong Kong, Canada and Australia are all now deferring blood donations from donors who have recently been to Zika-affected countries. These deferrals makes transmission by transfusion a low risk. Blood donations are routinely screened for a variety of diseases.

Sexual transmission

Previously we had heard reports of a scientist who had been infected with Zika while working in Africa. After returning home, his wife, who hadn’t travelled to Africa, was also infected – but not their children. The most obvious explanation was that sexual transmission was the reason his wife was infected.

As a vector-borne virus we thought Zika could only be transmitted via mosquito. But we thought wrong.
Esteban Biba/AAP, CC BY

At the time this seemed unusual. There had never been another vector-borne virus that had been transmitted in this way. Most scientists would have been somewhat sceptical.

Later, in the French Polynesian outbreak, it was reported that a man had virus in his semen ten weeks after first having Zika-like symptoms. These results were filed away as one of those unusual but unimportant findings. Zika, after all, was not a big issue.

No condom, no sex

Some countries are approaching the idea of sexual transmission cautiously. The United Kingdom has advised men who are returning from places with current Zika outbreaks with a female partner who is at risk of getting pregnant or is already pregnant to use condoms for 28 days – even if they haven’t had any symptoms.

For those who have had symptoms, the advice is to use a condom for six months.

While this might seem like an over-reaction – after all, there have only been two cases of known sexual transmission of the virus and millions of Zika cases – it is the uncertainty that makes public health officials cautious.

Should we be worried?

We don’t know whether other Zika cases have been infected through sex. We don’t know whether it’s possible for someone who has been infected through sexual transmission to then infect someone else through sex. We don’t know how long the virus might remain in semen.

We know the virus has been found in semen but not whether a woman can transmit the virus sexually. We know that it can be transmitted from the mother to the fetus. We know the virus can be found in urine but hasn’t been reported in breastmilk. We don’t know quite a lot.

From an evolutionary perspective it’s more important to know what will kill you than what will help you grow a better crop next year. When we hear about pandemic influenza, Ebola and now Zika, we do worry.

Infectious diseases, particularly new diseases, are scary because they are unknown. Throughout history, plagues have decimated human populations. With every new disease, particularly those that hit the headlines, there is the fear that this is the one that will impact you and your loved ones. Zika is unlikely to be that one, as it doesn’t have a high fatality rate like some past influenza pandemics and Ebola.

The good news is that you can do something about Zika if you’re in an affected area. Don’t get bitten by mosquitoes and do practice safe sex.

Beverley Paterson, Epidemiologist, Senior Lecturer, University of Newcastle

This article was originally published on The Conversation. Read the original article.

Here’s why we don’t have a vaccine for Zika (and other mosquito-borne viruses)

Suresh Mahalingam, Griffith University and Michael Rolph, Griffith University

As Zika fear rises, especially in the wake of the World Health Organization last night declaring a state of public health emergency, people are inevitably asking why we don’t have a vaccine to protect against the mosquito-borne virus.

Zika is generally a mild illness, causing fever, rash and joint pain, which usually resolves within seven to ten days. It was originally restricted to small outbreaks in the Pacific islands, Southeast Asia and Africa.

Due to the previously low impact of the virus and the estimated US$160-500 million it costs to develop a vaccine, Zika vaccine has not been on the radar. Other severe and potentially fatal mosquito-borne diseases such as malaria, dengue, and West Nile virus affect millions of people each year and have been a higher priority.

That has all changed with the recent “explosive” spread of Zika in the Americas and the potential link with microcephaly (reduced head size and brain damage) in babies of pregnant women who were infected.

Now we’re playing catch up on the research needed to develop vaccines. We know very little about how Zika replicates, how it causes disease, or how the immune system protects against infection.

So what is the status of Zika vaccine development? And how does this compare with the other mosquito-borne viruses that continue to have such a devastating impact on the world’s health?

Vaccine development

The ideal vaccine induces a strong response from the immune system, gives long-term protection with few doses, and causes no side effects. Though quickly developing such a vaccine is rarely this simple.

Zika

It’s early days, but scientists from the Public Health Agency of Canada, the Butantan Institute in Brazil, and the US National Institutes of Health have started work on Zika vaccines. These research teams may have vaccine candidates ready for initial clinical trials towards the end of the year.

Although full regulatory approval of a successful vaccine would take many years, it could potentially be used in public health emergencies within a year.

Yellow fever

The yellow fever vaccine, developed in 1938, has been highly successful at protecting against the virus, which can cause bleeding, jaundice, kidney and liver failure and, ultimately, death. Of the 44 countries at risk of yellow fever in Africa and the Americas, 35 have incorporated Yellow Fever vaccines into infant immunisation programs.

It is a live vaccine, in which a “weakened” virus induces a protective immune response against subsequent infection.

The Yellow Fever vaccine successfully protects against the virus, but is .
UNAMID/Flickr, CC BY-NC-ND

Live vaccines generally give strong protection, but safety is a significant issue, particularly in people with a weakened immune system.

Dengue

Dengue fever is a widespread tropical disease caused by dengue virus, which is transmitted by mosquitoes. Late-stage clinical trials of dengue vaccines are underway, and a vaccine has recently been licensed for use, but so far only in Mexico.

The field is littered with promising but failed vaccines that could not provide protection against the major strains of dengue virus. Nonetheless, there is hope that one will be available more widely in the coming years.

Chikungunya

Chikungunya virus has recently emerged as a serious human pathogen, causing fever and excruciating pain in the joints that can last months.

As with Zika, chikungunya was long considered unimportant because of its limited geographic distribution. Its dramatic expansion over the past decade, particularly in Southeast Asia and the Americas, has led to mobilisation of the vast medical research capabilities of the United States in response to the threat of it becoming established there.

Chikungunya vaccine development is proceeding rapidly, with a number of vaccines entering clinical trials. Researchers have reported early successes, but we are at least several years away from getting an approved vaccine.

Malaria

The big one is malaria, which kills more than 400,000 people a year. Scientists have been working on malaria vaccines for decades.

The RTS,S vaccine, developed by Glaxo Smith Kline, was successful in clinical trials and may soon be routinely used.

However, it only worked for some patient groups and provided only partial protection. Given its partial efficacy, there is debate in the medical community about the vaccine’s value.

The search continues for better vaccines.

Why is it so difficult to develop vaccines?

There is no recipe for the perfect vaccine. Despite the ever-increasing sophistication of vaccine technology, vaccine development often comes down to “suck it and see”. Many vaccines look promising in pre-clinical testing, only to fall over during the slow and expensive clinical trial process.

For many infectious diseases, we still don’t know what type of immune response is the most effective in providing protection. Since vaccines induce a protective immune response against infection, this can make vaccine design very difficult.

Vaccine safety is a major issue. “Live” or “attenuated” vaccines that involve a related or weakened version of the pathogen are often the most effective. But there is still the potential for these vaccines to cause disease, especially in recipients with weakened immune systems.

Vaccines go through a long process of clinical trials and assessment by regulators before they are approved for routine human use. This is a necessary process, but it sets a very high bar for approval. One of the most successful vaccines ever produced – the smallpox vaccine – is a live vaccine and would probably not have been approved by today’s regulators due to safety concerns.

Smallpox was eradicated in 1980.
Pan American Health Organization/Flickr, CC BY-ND

For dengue, there is an additional complication. People previously infected with dengue are at risk of developing much more severe disease when infected with a second, related dengue strain. Similarly, dengue vaccination could also lead to enhanced disease, rather than protection, when a person subsequently encounters the virus. This additional safety concern has markedly complicated and slowed dengue vaccine development.

Urgent priority

Zika causes mild fever in humans that on its own does not make a strong argument for a vaccine. But the possible link to microcephaly in unborn children, even though not yet definitely confirmed, makes vaccine development – and necessary funding – an urgent priority.

It’s also important to fund basic research to provide a necessary springboard for current and future vaccine development programs.

In the meantime, people in affected areas, including travellers, should take care to avoid mosquito bites by wearing long clothing and using repellents, bed nets and window screens.

Suresh Mahalingam, Principal Research Leader, Institute for Glycomics, Griffith University and Michael Rolph, Senior research fellow, Griffith University

This article was originally published on The Conversation. Read the original article.