Category Archives: Health

What happens to biopsy tissue after it’s tested? Your cells could be helping important cancer research

If you’ve ever had a tumour removed or biopsy taken, you may have contributed to life-saving research. Though you probably won’t have been told exactly what research your cells would be used for, tissue samples like these are vital for helping us understand and improve diagnosis and treatment of a whole range of illnesses and diseases. But once they’re removed, how are these tissue samples used exactly? How do they go from patient to project?

When tissue is removed from a person’s body, most often it is immediately put into a chemical preservative. It is then taken to a lab and embedded in a wax block. Protecting the tissue like this retains its structure and stops it from decomposing so it can be stored at room temperature for long periods of time.

This process also means that biochemical molecules like protein and DNA are preserved, which can provide vital clues about what processes are occurring in the tissue at that stage in the person’s illness. If we were looking at, for example, whether molecule A occurs in one particular tumour type but not in others (which would make it helpful for diagnosis) we would want a large number of each type to test. But there may not be enough patients of each type currently in treatment, so it is useful to have a library of samples to draw from.

Read more:
More people can donate tissue than organs – so why do we know so little about it?

Or we might want to test if patients with tumours containing molecule B are less likely to survive for five years than those without this molecule. This sort of question requires samples with a follow-up time of at least five years. But the answer may help doctors decide whether they need to treat their current patients with B more aggressively or with a different kind of treatment.

To analyse tissues, lab scientists cut very thin slices from the wax blocks and view them under a microscope. The slides are stained with dyes that show the overall tissue structure, and may also be stained with antibodies to show the presence of specific molecules.

Studies often need large numbers of samples from different patients to adequately answer a research question, which can take some time to collect. Take my work for example. My team is interested in finding more about a protein called brachyury, and how it relates to bowel cancer. But to do this we need to compare lots of samples, so we are using tissue from 823 bowel cancer patients and 50 non-cancer patients in our research.

When not in use, the tissue blocks are – with patient consent – placed in a store that researchers can access. The UK has several of these stores, known as biobanks or biorepositories, holding all kinds of tissues. Some cancer biobanks also store different kinds of tumours and blood samples.

Read more:
How biobanks can help improve the integrity of scientific research

While there are no reliable figures available on how many samples are held in all biobanks, or how often they are used, we do know these numbers are significant. The Children’s Cancer and Leukaemia Biobank alone has banked 19,000 samples since 1998. The Northern Ireland Biobank reports that 2,062 patients consented for their tissues to be used in research between 2017-2018, and 4,086 samples were accessed by researchers in that period.

Identifying biomarkers

Projects that use biobanks are often trying to identify biomarkers. These are any biological characteristics that give useful information about a disease or condition. Our team is looking at whether the protein brachyury is a useful biomarker to improve bowel cancer diagnosis.

Brachyury is essential for early embryonic development, but it is switched off in most cells by the time you are born. However, several studies imply that finding brachyury in a tumour indicates a poorer outcome for the patient. But to work out if this link is correct, we need to look at biobank samples. Doing this will help us work out more accurately which patients are at higher risk of cancer recurrence or metastasis. This is important when doctors are deciding on the best course of treatment.

In our research, we also need clinical details, such as what happened to the patient and all the information available at the time of diagnosis. Then we can assess whether testing for brachyury would have added useful information to the diagnosis. Information that accompanies each block is anonymised, which means the researcher analysing the data won’t know the patient’s name or be able to identify them from the sample. But they can see any relevant clinical details such as tumour stage, age, sex and survival.

Biobank samples have had already improved treatment of childhood acute lymphocytic leukaemia. Samples from the Cancer and Leukaemia Biobank were used to demonstrate that children with an abnormality in chromosome 21 had poorer outcomes that those without it. This led to treatment being modified for these children so they are no longer at a disadvantage.

People are often applauded for raising money for research by undertaking gruelling or inventive challenges. Patients who decide their tissue can be used in research should be similarly applauded. Without their unique and valuable gift, we wouldn’t be able to further our understanding, diagnosis and treatment of all kinds of illnesses and diseases.

Helena Robinson receives funding from Cancer Research Wales.

Source: The Conversation: Health

http://theconversation.com/what-happens-to-biopsy-tissue-after-its-tested-your-cells-could-be-helping-important-cancer-research-121057

AMPK: new research into cancer’s ‘good cop/bad cop’ protein could help develop more effective drugs

The basic unit of all living things is the cell – and the human body contains tens of trillions of them. Cancer can be triggered by the abnormal growth and division of just one of these, which goes on to form a lump or tumour.

Research over the past 30 years has shown that cancer is caused by mutations in the DNA of single cells. Many of these mutations are harmless, but if they affect DNA that provides instructions for making proteins controlling cell growth and division, they can trigger cancer.

The conventional view is that these changes cause cancer if they either switch off “good cop” proteins that normally restrain cell growth and division (tumour suppressors), or switch on “bad cop” proteins that promote cell growth and division (tumour promoters). But our latest research suggests that this simple classification into tumour suppressors and promoters falls down in the case of a protein that I first defined at the University of Dundee in the 1980s, called AMPK.

If AMPK can act as a good cop or a bad cop, then turning on its ability to suppress tumours could help us prevent cancer, and turning off its ability to promote tumours could help us treat the disease once it’s developed.

AMPK and its role in cancer

AMPK (short for adenosine monophosphate-activated protein kinase) is a protein that modifies other proteins, switching them on or off. It is itself switched on by falling cellular energy levels, such as when the supply of nutrients or oxygen are low due to a poor blood supply.

Once activated, AMPK kick starts activities in the cell that restore energy, while restraining cell growth and division. This growth-restraining element suggests that AMPK would act as a tumour suppressor. Indeed, experiments in mice show that a lack of AMPK in developing B or T cells (white blood cells) accelerates the development of cancers of those cells – B cell or T cell lymphomas – seemingly confirming its suppressor role.

But other studies in mice have shown that if T cell lymphoma is allowed to develop, and then the AMPK gene is deleted, the ensuing disease is less severe, suggesting that AMPK is a tumour promoter. How can this be reconciled with the previous results?

It appears that AMPK normally acts as a tumour suppressor but if, despite its best efforts, a tumour does arise, then it switches to being a tumour promoter instead. This may occur because AMPK protects the tumour cells against the stresses that occur from their rapid cell growth and division and poor blood supply. This helps these abnormal cells to survive rather than die.

Implications for humans

Although these studies were done in animals, human cancers can be studied by comparing the sequences of DNA from tumours and surrounding normal tissue. This approach shows that some genes encoding AMPK components have undergone mutations in cancers that would damage their function (suggesting, if anything, a tumour suppressor role). Yet others have been amplified (meaning the number of copies increased), suggesting a tumour promoter role instead. So AMPK appears to play both “good cop” and “bad cop” roles in human cancer, too.

Our research has important implications. To exploit the good cop (tumour suppressor) function of AMPK, humans at high risk of developing cancer might be treated with drugs that switch it on. Intriguingly, such a drug (metformin) already exists and is used to treat type 2 diabetes.

Unfortunately, we found that metformin was not effective in protecting T cell lymphoma in mice because it could not enter the developing T cells. But an older diabetes drug, phenformin, could enter the cells and protect against lymphoma.

Although phenformin is no longer used to treat diabetes because of side effects, these risks might be more acceptable in preventing cancer than they are in treating diabetes.

Conversely, to exploit the bad cop (tumour promoter) functions of AMPK, drugs that inhibit it (switch it off) might be given to enhance the effectiveness of treatments such as chemotherapy and radiotherapy. Surprisingly, given that cancer is caused by mutations in DNA, chemotherapy and radiotherapy also work by causing DNA damage. They are effective because rapidly dividing cells, such as cancer cells, are more likely to be killed by DNA damage than normal, non-dividing cells.

Our research shows that AMPK is switched on by drugs used in chemotherapy, and that this helps cancer cells to survive these treatments. The obvious implication is that drugs that inhibit AMPK might increase the effectiveness of existing chemotherapy or radiotherapy treatments. Although these drugs don’t exist yet, the findings of this research mean they could now be developed.

Grahame Hardie received funding from Cancer Research UK for this research.

Source: The Conversation: Health

http://theconversation.com/ampk-new-research-into-cancers-good-cop-bad-cop-protein-could-help-develop-more-effective-drugs-120929

UK drug deaths continue to rise – time for action

Every year since 2013, the UK’s Office for National Statistics has reported an increase in drug-related deaths in England. Last year, we reported that drugs had overtaken traffic accidents as a leading cause of death. This year, they have outstripped suicides among men aged 35-49. As these deaths continue to rise ever higher, the government continues to cut funding for drug treatment and actively blocks services that would save people’s lives.

Just this week, prime minister Boris Johnson promised to spend billions of pounds on ineffective criminal justice policies, including £2.5 billion a year to expand the prison population by another 10,000 people. It is highly doubtful whether these pledges will be any more real than previous unfulfilled promises, but they stand in stark contrast to sharp cuts in investment in preventing people from dying from drugs.

Government figures show a 27% reduction in spending on drug treatment services for adults since 2015-16. In some places with very high rates of drug-related deaths – such as Blackpool, Hartlepool, Liverpool and North Tyneside – the budget for drug treatment has been cut by more than half.

Drug-related deaths are not spread equally among British communities. The greatest burden is among those living in the most deprived areas. Until recently, the media has largely ignored communities which lose middle-aged opiate users on a daily basis. More attention has been paid to young people dying as a result of party drugs, such as ecstasy.

As the deaths mount, this is beginning to change. Heartbreaking stories of deaths, such as Kevin Lane, are getting more coverage. Lane had struggled with drug dependency for several years. He also had mental health problems – an all too common combination for people who have problems with drugs. His life ended prematurely when he was found in a shop toilet having overdosed on heroin aged just 32.

The shocking practice of “cuckooing” – where drug dealers take over the homes of vulnerable people – also shows that people who use drugs deserve protection, not just blame.

Ignoring the evidence

In Scotland, record levels of drug deaths have been recognised as a symptom of entreneched poverty. Deaths both north and south of the Scottish border are a public health crisis triggering calls for a different approach by bereaved families, advocacy groups and many others. But Westminster has failed to implement evidence-based measures, recommended by the Advisory Council on the Misuse of Drugs, for reducing deaths.

Instead of investing in effective opioid-substitution treatment, it has slashed the available funding. It has left it to cash-strapped local authorities to provide heroin-assisted treatment. And it has refused to support drug consumption facilities. These facilities save lives, but they need political support and funding – not easy when the public perceive these as facilitating drug use rather than a means to reducing drug-related harm.

All drug-related deaths are avoidable. We know how to reverse this dreadful trend in mortality, but this knowledge needs to be acted on by politicians. Unless this happens, we fear that next year yet another record in drug-related deaths will be reported.

Alex Stevens is a member of the Advisory Council on the Misuse of Drugs, but does not speak for it here.

Ian Hamilton does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Source: The Conversation: Health

http://theconversation.com/uk-drug-deaths-continue-to-rise-time-for-action-120449

There is no great salt debate: we should be consuming less

The human body needs a tiny amount of sodium to function properly and this is typically found in salt (sodium chloride). But today most people consume way too much salt, increasing the burden of cardiovascular disease around the world.

Health professionals have been trying to tackle this problem for decades, but face several barriers, including research that muddies the water about what safe levels of salt intake are. This has cast unnecessary doubt on the importance of reducing intakes. But our latest research has found flaws in these studies and suggests that salt intake should be reduced even further than current recommendations.

The World Health Organisation (WHO) recommends that people consume less than 5g of salt a day, but global intakes average 10g a day. Excess salt consumption raises blood pressure, which increases the risk of heart attacks, heart failure and stroke.

Many studies show a linear relationship between salt intake and cardiovascular disease: as salt intake increases, the risk of cardiovascular disease and premature death increases. But other studies suggest that the relationship between salt consumption and disease is not linear. They posit that consuming both less than 7.5g and more than 12.5g of salt per day could lead to an increased risk of cardiovascular disease and early death. But there are flaws in the methods used in these studies.

Cheaper but less accurate

We excrete most of the salt we consume in our urine (90%). And there is a large variation in the amount of salt we consume each day, so the gold standard for measuring salt intakes is to collect urine over at least three non-consecutive 24-hour periods. Although this is the most accurate way of measuring salt intake, it is also the most expensive and is more work for both the participant and the researcher.

Some studies have estimated salt intake using spot urine measurements rather than 24-hour urine collection because it is easier to do, cheaper and less hassle for the participants. Participants only have to provide one small urine sample from which daily salt intake is then calculated.

The studies that suggest that the relationship between salt intake and cardiovascular disease is not linear, used data from spot urine measurements. This way of measuring, however, is not accurate as it represents salt intake from a very short period of time and is also affected by the amount of fluid the participant drank and the time of day the sample was taken. Estimates from spot urine measurements are therefore unreliable reflections of habitual daily salt intake.

We found that calculating salt intakes from spot urine samples can alter the linear relationship seen between salt intake and mortality. We analysed data from Trials of Hypertension Prevention, which used the gold standard method for assessing salt intake (several 24-hour urine measurements) in nearly 3,000 adults with prehypertension (high normal blood pressure) over periods ranging from 18 months to four years.

When we analysed the data, we found a direct linear relationship between salt intake and the risk of death down to a salt intake level of 3g a day.

To mimic spot urine sampling, we then applied the formulas developed for these samples on the sodium concentration of the 24-hour urine samples. The results showed the same non-linear relationship that were reported in the controversial studies. This implies that their findings could be explained by the method they used to estimate salt intake, as spot urine measurements are unreliable reflections of habitual daily salt intake and it also appears that the formulas themselves are problematic.

So the message remains clear: salt reduction saves lives, and the findings from studies that use a less reliable assessment of salt intake should not be used to derail critical public health policy or divert action.

A gradual reduction in salt intake across the whole population, as recommended by WHO, remains an achievable, affordable, effective and important strategy to prevent cardiovascular diseases and premature death worldwide. Even a small reduction in salt intake will have an enormous benefit on people’s health.

Feng He is a member of Consensus Action on Salt, Sugar and Health (CASSH) and World Action on Salt & Health (WASH). Both CASSH and WASH are nonprofit charitable organisations, and Feng does not receive any financial support from CASSH or WASH.
Feng has received funding from the National Institute of Health Research (NIHR) using Official Development Assistance funding (16/136/77).

Source: The Conversation: Health

http://theconversation.com/there-is-no-great-salt-debate-we-should-be-consuming-less-120874

Being left-handed doesn’t mean you are right-brained — so what does it mean?

There have been plenty of claims about what being left-handed means, and whether it changes the type of person someone is – but the truth is something of an enigma. Myths about handedness appear year after year, but researchers have yet to uncover all of what it means to be left-handed.

So why are people left-handed? The truth is we don’t fully know that either. What we do know is that only around 10% of people across the world are left-handed – but this isn’t split equally between the sexes. About 12% of men are left-handed but only about 8% of women. Some people get very excited about the 90:10 split and wonder why we aren’t all right-handed.

But the interesting question is, why isn’t our handedness based on chance? Why isn’t it a 50:50 split? It is not due to handwriting direction, as left-handedness would be dominant in countries where their languages are written right to left, which it is not the case. Even the genetics are odd – only about 25% of children who have two left-handed parents will also be left-handed.

Read more:
How children’s brains develop to make them right or left handed

Being left-handed has been linked with all sorts of bad things. Poor health and early death are often associated, for example – but neither are exactly true. The latter is explained by many people in older generations being forced to switch and use their right hands. This makes it look like there are less left-handers at older ages. The former, despite being an appealing headline, is just wrong.

Positive myths are also abound. People say that left-handers are more creative, as most of them use their “right brain”. This is perhaps one of the more persistent myths about handedness and the brain. But no matter how appealing (and perhaps to the disappointment of those lefties still waiting to wake up one day with the talents of Leonardo da Vinci), the general idea that any of us use a “dominant brain side” that defines our personality and decision making is also wrong.

Brain lateralisation and handedness

It is true, however, that the brain’s right hemisphere controls the left side of the body, and the left hemisphere the right side – and that the hemispheres do actually have specialities. For example, language is usually processed a little bit more within the left hemisphere, and recognition of faces a little bit more within the right hemisphere. This idea that each hemisphere is specialised for some skills is known as brain lateralisation. However, the halves do not work in isolation, as a thick band of nerve fibres – called the corpus callosum – connects the two sides.

Interestingly, there are some known differences in these specialities between right-handers and left-handers. For example, it is often cited that around 95% of right-handers are “left hemisphere dominant”. This is not the same as the “left brain” claim above, it actually refers to the early finding that most right-handers depend more on the left hemisphere for speech and language. It was assumed that the opposite would be true for lefties. But this is not the case. In fact, 70% of left-handers also process language more in the left hemisphere. Why this number is lower, rather than reversed, is as yet unknown.

Read more:
Why is life left-handed? The answer is in the stars

Researchers have found many other brain specialities, or “asymmetries” in addition to language. Many of these are specialised in the right hemisphere – in most right-handers at least – and include things such as face processing, spatial skills and perception of emotions. But these are understudied, perhaps because scientists have incorrectly assumed that they all depend on being in the hemisphere that isn’t dominant for language in each person.

In fact, this assumption, plus the recognition that a small number of left-handers have unusual right hemisphere brain dominance for language, means left-handers are either ignored – or worse, actively avoided – in many studies of the brain, because researchers assume that, as with language, all other asymmetries will be reduced.

How some of these functions are lateralised (specialised) in the brain can actually influence how we perceive things and so can be studied using simple perception tests. For example, in my research group’s recent study, we presented pictures of faces that were constructed so that one half of the face shows one emotion, while the other half shows a different emotion, to a large number of right-handers and left-handers.

Usually, people see the emotion shown on the left side of the face, and this is believed to reflect specialisation in the right hemisphere. This is linked to the fact that visual fields are processed in such a way there is a bias to the left side of space. This is thought to represent right hemisphere processing while a bias to the right side of space is thought to represent left hemisphere processing. We also presented different types of pictures and sounds, to examine several other specialisations.

Our findings suggest that some types of specialisations, including processing of faces, do seem to follow the interesting pattern seen for language (that is, more of the left-handers seemed to have a preference for the emotion shown on the right side of the face). But in another task that looked at biases in what we pay attention to, we found no differences in the brain-processing patterns for right-handers and left-handers. This result suggests that while there are relationships between handedness and some of the brain’s specialisations, there aren’t for others.

Left-handers are absolutely central to new experiments like this, but not just because they can help us understand what makes this minority different. Learning what makes left-handers different could also help us finally solve many of the long-standing neuropsychological mysteries of the brain.

Emma Karlsson does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Source: The Conversation: Health

http://theconversation.com/being-left-handed-doesnt-mean-you-are-right-brained-so-what-does-it-mean-121711

How development of the ‘self’ in infants provides clues to the breakdown of memory in dementia

When we look in the mirror we see “me”: a particular combination of features that matches our idea of who we are. We also feel the sensation that the movement of the self in the mirror is under our control – we have a sense of agency and ownership of the mirror image.

But the self we connect with in the mirror extends beyond the moment. Although our features age, we perceive the self in the mirror to be intimately connected to the child, the teenager, the young adult, that once stood before us in our reflection. We see them as the same person who will move forward into the future – the main character in the story of our lives.

This is surprising, since the self in the mirror is not only physically distinct from the self of the past, or the self of the future (our cells constantly age and replace), but cognitively distinct. Our mental processes mature, our choices, dreams and aspirations change – even our personalities are in constant flux.

So our perception of the self as a stable entity is illusory. The human mind is designed to tell us a coherent story of the world, consistent with past experience. Where there are gaps to be filled, the mind fills them. This is what leads some researchers and philosophers to think of the self as the ultimate illusion. But how does the “self-illusion” develop, and what happens when it dissolves?

Infancy and memory

We are born subjective agents, capable of feeling sensations, experiencing positive and negative emotions and intentionally guiding our own actions. But it is not until the end of infancy that we are able to step outside of this first-hand experience of the self, cognitively reflecting on ourselves from a second-person perspective, as neatly illustrated by the onset of mirror self-recognition at two years of age.

The idea of “me” first captured by mirror recognition is made up of factual self-knowledge (including information about our physical features and personality traits) and autobiographical self-knowledge (including information about events which have happened to us in the past, and events planned for the future).

The “me” inherent in memory was recognised by early philosophers including Hume and Locke, and the relation between self and memory continues to guide modern theories of autobiographical processing. The close link between self and memory provides one explanation for the riddle of “childhood amnesia” – the fact that adults have no enduring memories prior to the age of two years.

Until children have an idea of “me” that enables them to anchor event memories, they are unlikely to be able to start to build and retrieve a personal life narrative. Our research measured four to six-year-old children’s factual self-knowledge by asking them to provide self-descriptions, alongside their ability to “label” memories as their own (for example by recalling which of a set of actions they had performed, or which pictures had appeared with their own face). Together, these capacities were predictive of their ability to retrieve specific, autobiographical details of their lives (such as a full narrative of their first day of school or nursery).

Our research therefore provides strong support for the idea that the development of autobiographical memory is dependent on the wider development of self-representation. But what does this close relationship between self and memory mean for the sense of self in old age, when memory may decline?

Dementia and the breakdown of self-recognition

Around one in three people born in 2019 will suffer from dementia in their lifetime. One of the most distressing symptoms of this condition is the feeling of identity loss associated with the decline of autobiographical and/or factual self-knowledge.

Fundamental breakdowns in self-recognition have been reported in late-stage dementia. Some sufferers fail to recognise themselves in photographs or mirrors, unable to connect their current experience of self to the self of the past. Does this breakdown in the self-illusion suggest that the self is lost? Not if we use the model of development to recognise the importance of agency – the first building block of the self.

The majority of dementia studies have focused on the link between conceptual self-recognition or autobiographical processing and identity, neglecting the idea of agency. However, behaving intentionally and having our intentions recognised by others is fundamental to our first experience of selfhood.

Despite infants’ relatively limited social repertoire, positive interactions that reinforce agency (such as soothing emotions and engaging in early conversations) are easily supported by parents and caregivers and are thought to be at the root of secure attachment relationships. Could this nurturing approach also be applied at the other end of the lifespan to maintain connections between people?

We are currently planning a series of studies to explore this possibility. The first step is to establish whether the dissolution of self follows the same steps as its development. If access to higher level self-representation (such as factual and autobiographical self-knowledge) is lost first, feelings of agency may be the last remaining facet of self.

If this is the case, ultimately it will be important to find ways to positively reinforce dementia sufferers’ experience of their own actions (for example, by providing them with simple opportunities to have a positive effect on the world, such as moving their arms to activate music) and their emotional connection with caregivers (soothing negative emotions, laughing together), over and above conceptual aspects of self (such as prompts to recall self-knowledge).

Although our second-person perspective on self may be illusory and we all experience ageing, our bodily self and the sense of agency it entails is built to make connections with the world, and carry us from cradle to grave.

Josephine Ross has received funding from ESRC, Leverhulme, Carnegie, Nuffield foundations.

Source: The Conversation: Health

http://theconversation.com/how-development-of-the-self-in-infants-provides-clues-to-the-breakdown-of-memory-in-dementia-116452

Social media isn’t causing more eating disorders in young people – new study

There is ongoing debate about whether eating disorders are more common in modern society. Some say that as young people are both exposed to and share images of themselves in an unprecedented way on social media today, this affects their body image and may have an impact on their eating too. Others suggest that social media can help eating disorder recovery by providing platforms for people to talk about their experiences and treatment. So which one is correct?

We know that rates of eating disorders are high. According to a large survey conducted in 2017, about four in every 1,000 young people aged 5-19 years have an eating disorder in England alone. The most recent study to look at trends in eating disorders in primary care showed that more people were being diagnosed with eating disorders year on year too. It found that the number of people being diagnosed with eating disorders increased from 32 to 37 in every 100,000 people aged 10-49 years between 2000 and 2009. But the GP data used in this research is now more than ten years old – dating from before the launch of platforms such as Instagram.

For our newly published research, we decided to look again at these trends to find if the rise of social media had changed anything. We used a large primary care database covering about 7% of the population in England and specifically looked at the anonymised records of more than one million children and young people who visited their GP between 2004 and 2014.

We found that eating disorders recorded in primary care are nearly 11 times more common in females than males and twice as common in people aged 16–20 years old, than in the 11-15 or 21-24 age groups. They are also one and a half times as common in people from the most affluent areas compared to the least.

The most common type of eating disorder was not either of the two most well known – anorexia and bulimia nervosa – but eating disorders “not otherwise specified”. This means that they are eating disorders that don’t quite reach the threshold to be defined as anorexia or bulimia nervosa.

We also found that fewer young people are being diagnosed with eating disorders every year in primary care. Rates decreased most significantly for bulimia nervosa, less so for eating disorders not otherwise specified, and remained stable for anorexia nervosa. Decreases were seen in females, and the 16–24 age group too. Significant decreases were also found in young people from the most deprived areas, but not the most affluent (where rates are higher), further widening the difference between the two groups.

The numbers of males diagnosed with an eating disorder was too small for further breakdown, since less than 500 individuals were diagnosed over the 11-year study period. The number of both males and females with bulimia nervosa were particularly small too, although we did see a 50% decrease in females diagnosed.

Rates in context

It’s not easy to unpick what these findings may mean and whether social media has played a part in these changing trends. Looking at bulimia nervosa alone, some researchers suggest that bulimia nervosa is a Western phenomena, based on a pressure to be thin, while anorexia nervosa is less culture bound, and exists across time, cultures and even species.

They say that a decrease in bulimia nervosa could be attributed to the normalisation of being overweight, which reduces the pressure to be thin and leads to a decrease in bulimia nervosa. In which case, it could be argued that social media is affecting the trend, although not in the way that some might assume. Rather than increasing eating disorders, the body positivity and range of body shapes and sizes seen on social platforms is helping young people accept their own selves. This may also explain why the decrease is more evident in more deprived areas where the prevalence of obesity is higher.

But this concept is highly contested. And it’s hard to escape the rise in social media use and the increasing concerns about weight and body image. The mechanism where this might lead to eating concerns and disordered eating seems sensible. But our study doesn’t currently support that.

However, we did also find an increase in the number of people receiving in-patient care for eating disorders in England, which could suggest that people are being diagnosed with eating disorders at a later, more advanced stage than previously, requiring in-patient admission. Eating disorders can be problematic conditions for doctors to identify, refer and manage for several reasons.

Some studies have shown that diagnoses are less likely to be made if there are no specialist services in the area, for example. Greater availability of child and adolescent mental health services, and lower thresholds for acceptance of referrals than in adult services for eating disorders, could explain why eating disorder diagnosis rates for 11 to 15-year-olds have remained stable over the study period, yet decreased for 16 to 24-year-olds.

While more research must be done to work out whether, and how, social media influences the onset and continuation of eating disorders globally, studies like ours are starting to unpick assumptions we might make about the links between the two. And ultimately will help us to focus on creating better prevention and online therapeutic tools for young people with eating disorders and those who may go on to develop them.

Ann John receives/ed funding from MRC, MQ, HQIP and Welsh Government. Ann John is a Trustee of the Mental Health Foundation.

Sophie Wood receives/ed funding from MQ, HQIP, and the Department for Education.

Source: The Conversation: Health

http://theconversation.com/social-media-isnt-causing-more-eating-disorders-in-young-people-new-study-119959

Teens who hit puberty later could face bone health issues later in life, studies suggest

Puberty is a time of dramatic development for both boys and girls. Not only are those hormones raging, but there’s all the bodily changes to contend with.

Puberty is driven by the activity of sex hormones and its onset is announced by the appearance of pubic hair, beards and breasts. Along with the dramatic hormone-driven changes to a child’s body, another defining features of puberty is the adolescent growth spurt – children become taller and eventually physically mature into adults.

For boys and girls this growth spurt generally happens at different ages. And there can be big differences as to when the growth spurt happens. For girls, rapid growth generally occurs around age eleven and a half years but can begin as early as eight or as late as 14 while for boys it generally happens a year or two later than girls. Children continue to get taller during their growth spurt until the ends of their long bones fuse and stop increasing in length, which happens around the end of puberty.

Children’s bones develop rapidly during puberty. And our new findings published in JAMA Network Open suggest that teens who have their pubertal growth spurt later could have more problems with their bone health in the future. In essence our research shows that the timing of puberty might influence or at least signal a child’s bone strength throughout adolescence and into early adulthood.

Weak bones

Our study is not the first to report a link between the timing of puberty and bone strength. A 2016 study of British people born in 1946 showed that children who had their growth spurt at an older age had lower bone density near the end of their forearm bone when measured decades later in old age, making them more likely to get a broken wrist.

More recently, a study of adolescents and young adults from Philadelphia showed that people who were genetically predisposed to later puberty had lower bone density at the spine and hips sites which are known to be susceptible to osteoporosis in later life. This is an ageing-related condition where bones lose their strength and become more likely to break.

Our study tracked the development of bone strength in a group of British children through to adulthood and found that teens who hit puberty at an older age tend to have lower bone mineral density which is a strong indicator of having weaker bones. We found that this continued to be the case for up to several years of their adult life.

Measuring puberty

We analysed data from more than 6000 children from the Children of the 90s study. This is a multi-generational study that has tracked the lives of a large group of people born in the early 90s around Bristol in the south west of England.

We made use of multiple bone density scans taken from each child to assess their bone strength across a 15-year period between the ages of ten and 25 years.

To calculate the age when the children went through puberty, we tracked each child’s height and used this information to estimate the age when each child went through the adolescent growth spurt. We then assumed that children that had their growth spurt at an older age must have started puberty later. As a check, we repeated our analysis in girls using the age they reported getting their first period as a different indicator of when they hit puberty and we came to the same conclusions.

Rebuilding bone density

Our research adds to the growing evidence that children who mature later may be at increased risk of breaking a bone as they grow and mature. And that they may also have an increased risk of getting osteoporosis later in life.

Of course, there are things people can do to strengthen their bones. But given our findings, it is clear there is now a need for bigger and more detailed studies into the very complex relationships between puberty, growth and bone development. Continuing to track the lives of the people in our study will be crucial if we are to discover how puberty might impact people’s bones as they go through adult life and eventually move into old age. This will help to further understand the causes of osteoporosis and ultimately help people to maintain healthy bones throughout their lives.

Ahmed Elhakeem does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Source: The Conversation: Health

http://theconversation.com/teens-who-hit-puberty-later-could-face-bone-health-issues-later-in-life-studies-suggest-121470

Medical skin creams could be a lethal fire risk when soaked into fabric – here’s what you need to know

Care providers were alerted to a house fire involving one of their patients at 4am on May 30, 2015. The fire and rescue services discovered a 74-year-old lady who had succumbed to a blaze that developed rapidly while she was still lying in bed. She had been bed bound, known to smoke in bed and was being treated for a skin condition.

A year later, a 61-year-old man who was also a smoker, bed bound and had emollient applied to his skin by carers was found dead in his bed after an intense fire. A year after that, an 82-year-old man died with third degree burns when his dressing gown came into contact with a lighter. He was also receiving daily applications of a cream and ointment.

What do all of these tragic deaths have in common? The victims were all being treated with creams for their skin conditions. While the fires were caused by smoking, the authorities reported that they were made more intense by the presence of these emollients.

A hidden danger

In the UK, one in five children and one in 12 adults will suffer from eczema and 2-3% of the population have psoriasis. Medical creams, lotions and ointments are widely used to treat these conditions and can be prescribed or bought over the counter. They often include instructions to apply liberally, with multiple applications during the day. This results in the product soaking into clothing, dressings and bedding.

Several deaths from fires have been linked with the use of these skin emollients. A BBC freedom of information request revealed that 37 fire deaths since 2010 have been linked to creams that contain paraffin. But fire reports don’t require such information to be included and not all fire services responded to questions. So the actual number of deaths and injuries may be higher.

Read more:
Why batteries have started catching fire so often

It isn’t just products that contain lots of paraffin that pose a risk – those with a low paraffin content and even those without paraffin at all could be dangerous. Our research shows that all fabrics ignited quicker after contact with emollients – regardless of the paraffin level – than completely clean fabrics.

In our initial tests, we let a flame directly touch cotton sheeting that emollients had dried into for 24 hours. The fabric ignited too quickly to measure, but once we had the flame positioned 7cm from the edge of the soaked fabric, we found that ignition happened after only ten seconds, compared to over a minute with the same cotton sheeting that was completely clean.

The fabrics we tested included various thread counts of cotton and polyester blend sheeting and t-shirts – all are common in households and all ignite much quicker when skin creams are present. We also found that once the flame has extinguished, some of the fabrics smoulder for longer when the products are present – potentially burning for longer near the skin, causing significant burns and life-threatening injuries.

These findings have spurred the NHS and fire and rescue services to reassess their safety advice. Flammable residues are thought to be removed from fabrics if they’re washed at the highest temperature possible, but research is still ongoing.

It’s important to remember that these products – on their own and in containers – aren’t a fire risk. The risk emerges when fabrics are soaked with them and allowed to dry. As the creams have soaked into fabrics, reducing the time it takes for the garments to ignite, elderly and immobile victims haven’t been able to remove their clothing quickly enough to prevent injury or death.

People shouldn’t stop using much-needed medication, but they should know how to use the products safely. Our advice is to wash your clothes at high temperatures as often as you can to reduce the build up of the creams. Most importantly, keep any fabrics away from naked flames and cigarettes – you’re likely to have less time to react in the event of a fire than you think.

Sarah Hall conducted this work with research assistant Kirsty Blackburn.

Joanne Morrissey does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

Source: The Conversation: Health

http://theconversation.com/medical-skin-creams-could-be-a-lethal-fire-risk-when-soaked-into-fabric-heres-what-you-need-to-know-119784