Most people don’t benefit from vaccination, but we still need it to prevent infections



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Everyone has to be vaccinated for immunisation programs to work.
from http://www.shutterstock.com

Allen Cheng, Monash University

A recent article in The Conversation questioned whether we should all get flu vaccinations, given 99 people would have to go through vaccination for one case of flu to be prevented.

But this position ignores the purpose of immunisation programs: whole populations of people need to take part for just a small number to benefit. So how do we decide what’s worth it and what’s not?




Read more:
The flu vaccine is being oversold – it’s not that effective


Decision-making in public health

When we consider a treatment for a patient, such as antibiotics for an infection, we first consider the evidence on the benefits and potential harms of treatment. Ideally, this is based on clinical trials, where we assume the proportion of people in the trial who respond represents the chance an individual patient will respond to treatment.

This evidence is then weighed up with the individual patient. What are the treatment options? What do they prefer? Are there factors that might make this patient more likely to respond or have side effects? Is there a treatment alternative they would be more likely to take?

In public health, the framework is the same but the “patient” is different – we are delivering an intervention for a whole population or group rather than a single individual.

We first consider the efficacy of the intervention as demonstrated in clinical trials or other types of studies. We then look at which groups in the population might benefit the most (such as the zoster vaccine, given routinely to adults over 70 years as this group has a high rate of shingles), and for whom the harms will be the least (such as the rotavirus vaccine, which is given before the age of six months to reduce the risk of intussusception, a serious bowel complication).

Compared to many other public health programs, immunisation is a targeted intervention and clinical trials tell us they work. But programs still need to target broad groups, defined by age or other broad risk factors, such as chronic medical conditions or pregnancy.




Read more:
Explainer: what is herd immunity?


Risks and benefits of interventions

When considering vaccination programs, safety is very important, as a vaccine is being given to a generally healthy population to prevent a disease that may be uncommon, even if serious.

For example, the lifetime risk of cervical cancer is one in 166 women, meaning one woman in 166 is diagnosed with this cancer. So even if the human papillomavirus (HPV) vaccine was completely effective at preventing cancer, 165 of 166 women vaccinated would not benefit. Clearly, if we could work out who that one woman was who would get cancer, we could just vaccinate her, but unfortunately we can’t.

It’s only acceptable to vaccinate large groups if clinically important side effects are low. For the HPV vaccine, anaphylaxis (a serious allergic reaction) has been reported, but occurs at a rate of approximately one in 380,000 doses.

An even more extreme case is meningococcal vaccination. Before vaccination, the incidence of meningococcal serogroup C (a particular type of this bacterium) infection in children aged one to four years old was around 2.5 per 100,000 children, or 7.5 cases for 100,000 children over three years.

Vaccination has almost eliminated infection with this strain (although other serotypes still cause meningococcal disease). But this means 13,332 of 13,333 children didn’t benefit from vaccination. Again, this is only acceptable if the rate of important side effects is low. Studies in the US have not found any significant side effects following routine use of meningococcal vaccines.

This is not to say there are no side effects from vaccines, but that the potential side effects of vaccines need to be weighed up against the benefit.

For example, Guillain Barre syndrome is a serious neurological complication of influenza vaccination as well as a number of different infections.

But studies have estimated the risk of this complication as being around one per million vaccination doses, which is much smaller than the risk of Guillain Barre syndrome following influenza infection (roughly one in 60,000 infections). And that’s before taking into account the benefit of preventing other complications of influenza.




Read more:
Is the end of Zika nigh? How populations develop immunity


High schools are bigger, so immunisation is easier than at primary schools.
from http://www.shutterstock.com

What other factors need to be considered?

We also need to consider access, uptake and how a health intervention will be delivered, whether through general practices, council programs, pharmacies or school-based programs.

Equity issues must also be kept in mind: will this close the gap in Indigenous health or other disadvantaged populations? Will immunisation benefit more than the individual? What is the likely future incidence (the “epidemic curve”) of the infection in the absence of vaccination?

A current example is meningococcal W disease, which is a new strain of this bacteria in Australia. Although this currently affects individuals in all age groups, many state governments have implemented vaccination programs in adolescents.

This is because young adults in their late teens and early 20s carry the bacteria more than any other group, so vaccinating them will reduce transmission of this strain more generally.

But it’s difficult to get large cohorts of this age group together to deliver the vaccine. It’s much easier if the program targets slightly younger children who are still at school (who, of course, will soon enter the higher risk age group).

In rolling out this vaccine program, even factors such as the size of schools (it is easier to vaccinate children at high schools rather than primary schools, as they are larger), the timing of exams, holidays and religious considerations (such as Ramadan) are also taken into account.




Read more:
What is meningococcal disease and what are the options for vaccination?


For government, cost effectiveness is an important consideration when making decisions on the use of taxpayer dollars. This has been an issue when considering meningococcal B vaccine. As this is a relatively expensive vaccine, the Pharmaceutical Benefits Advisory Committee has found this not to be cost effective.

This is not to say that meningococcal B disease isn’t serious, or that the vaccine isn’t effective. It’s simply that the cost of the vaccine is so high, it’s felt there are better uses for the funding that could save lives elsewhere.

While this might seem to be a rather hard-headed decision, this approach frees up funding for other interventions such as expensive cancer treatments, primary care programs or other public health interventions.

Why is this important?

When we treat a disease, we expect most people will benefit from the treatment. As an example, without antibiotics, the death rate of pneumonia was more than 80%; with antibiotics, less than 20%.

The ConversationHowever, vaccination programs aim to prevent disease in whole populations. So even if it seems as though many people are having to take part to prevent disease in a small proportion, this small proportion may represent hundreds or thousands of cases of disease in the community.

Allen Cheng, Professor in Infectious Diseases Epidemiology, Monash University

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

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The faster you walk, the better for long term health – especially as you age



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OK, you don’t need the poles. But you should pick up the pace.
from http://www.shutterstock.com

Emmanuel Stamatakis, University of Sydney

Some of us like to stroll along and smell the roses, while others march to their destination as quickly as their feet will carry them. A new study out today has found those who report faster walking have lower risk of premature death.

We studied just over 50,000 walkers over 30 years of age who lived in Britain between 1994 and 2008. We collected data on these walkers, including how quickly they think they walk, and we then looked at their health outcomes (after controlling to make sure the results weren’t due to poor health or other habits such as smoking and exercise).

We found any pace above slow reduced the risk of dying from cardiovascular disease, such as heart disease or stroke. Compared to slow walkers, average pace walkers had a 20% lower risk of early death from any cause, and a 24% lower risk of death from heart disease or stroke.

Australian Science Media Centre.



Read more:
We asked five experts: is walking enough exercise?


Those who reported walking at a brisk or fast pace had a 24% lower risk of early death from any cause and a 21% lower risk of death from cardiovascular causes.

We also found the beneficial effects of fast walking were more pronounced in older age groups. For example, average pace walkers aged 60 years or over experienced a 46% reduction in risk of death from cardiovascular causes, and fast walkers experienced a 53% reduction. Compared to slow walkers, brisk or fast walkers aged 45-59 had 36% lower risk of early death from any cause.

In these older age groups (but not in the whole sample or the younger age groups), we also found there was a linearly higher reduction in the risk of early death the higher the pace.

What it all means

Our results suggest walking at an average, brisk or fast pace may be beneficial for long term health and longevity compared to slow walking, particularly for older people.

But we also need to be mindful our study was observational, and we did not have full control of all likely influences to be able to establish it was the walking alone causing the beneficial health effects. For example, it could be that the least healthy people reported slow walking pace as a result of their poor health, and also ended up dying earlier for the same reason.

Fast walking for some might not seem it for others.
from http://www.shutterstock.com

To minimise the chances of this reverse causality, we excluded all those who had heart disease, had experienced a stroke, or had cancer when the study started, as well as those who died in the first two years of follow up.




Read more:
New study shows more time walking means less time in hospital


Another important point is that participants in our study self-reported their usual pace, which means the responses were about perceived pace. There are no established standards for what “slow”, “average” or “brisk” walking means in terms of speed. What is perceived as “fast” walking pace by a very sedentary and physically unfit 70-year-old will be very different from a sporty and fit 45-year-old.

For this reason, our results could be interpreted as reflecting relative (to one’s physical capacity) intensity of walking. That is, the higher the physical exertion while walking, the better health results.

For the general relatively healthy middle-aged population, a walking speed between 6 and 7.5 km/h will be fast and if sustained, will make most people slightly out of breath. A walking pace of 100 steps per minute is considered roughly equivalent to moderate intensity physical activity.

We know walking is an excellent activity for health, accessible by most people of all ages. Our findings suggest it’s a good idea to step up to a pace that will challenge our physiology and may even make walking more of a workout.

The ConversationLong term-health benefits aside, a faster pace will get us to our destination faster and free up time for all those other things that can make our daily routines special, such as spending time with loved ones or reading a good book.

Emmanuel Stamatakis, Professor of Physical Activity, Lifestyle, and Population Health, University of Sydney

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

The bugs we carry and how our immune system fights them



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The immune system has to establish which cells belong to us and which are foreign, no mean feat.
http://www.shutterstock.com

Peter C. Doherty, The Peter Doherty Institute for Infection and Immunity

This article is part of a three-part package exploring immunity and infectious diseases around the world. Read the other articles here.


Human beings are large, complex, multicellular, multi-organ systems. We reproduce slowly and rely on a breadth of mechanisms that allow us to control the myriad of rapidly replicating, simple life forms that have evolved to live in or on us.

The system of defence is referred to collectively as immunity.

The word itself comes from the Latin immunis, describing the status of returned soldiers (Genio immunium) in the Roman state who were, for a time, exempt from paying taxes.

Our immunity protects us from many illnesses, including some forms of cancer. New cancer therapeutics, called immunotherapies, work by boosting our immune cells to fight cancer cells that have found ways to evade them.

The immune system is divided into two interactive spheres, the much older “innate” sphere, and the more recently evolved “adaptive” sphere. A primary challenge for the very specifically targeted cells that form the basis of adaptive immunity is to distinguish “self” (our own body cells and tissues) from “non-self” – the foreign invaders. When that goes wrong, we can develop autoimmune diseases such as multiple sclerosis or rheumatoid arthritis.




Read more:
Explainer: what are autoimmune diseases?


The organisms we carry around with us

The human body is host to many organisms over a lifetime. Some are dangerous to health (pathogens), some are benign, and some are necessary for proper functioning.

Most of the genetic material we carry around with us is “non-self”: principally harmless bacteria (called “commensals”) that live in the gastrointestinal tract.

Traditionally, studies focused on the “bad bugs” in our gut that cause diarrhoea and dysentery. But more recently, we’re learning there are also good guys. And there’s a general consensus we need to know more about the “microbiome”, the mass of bacteria in any “clinically normal” gut.

Gut bacteria provide essential vitamin B12 and when they die, release myriad proteins that will be broken down into amino acids, which the body needs. About 30% of our poo is comprised of dead bacteria.

Apart from our microbiome, normal human beings also have a substantial “virome”. Viruses differ from bacteria (which are cells in their own right) in that they are much simpler and can only replicate in living cells.

The greatest number of viruses we carry around are the “bacteriophages”, which infect the commensal bacteria in our gut. Not all “phages” are, however, benign. For example, the toxin that causes human diphtheria is encoded in the genome of a bacteriophage.

There’s also a spectrum of viruses that persistently infect our body tissues. The most familiar are herpes viruses, like those that cause cold sores (H. simplex) and shingles (H. zoster). Both viruses hide out in the nervous system and are normally under immune control. They re-emerge to cause problems as a consequence of tissue stress (such as a sunburnt lip) or as immunity declines with age (shingles). This is why a booster shingles vaccine is recommended for the elderly.




Read more:
Essays on health: microbes aren’t the enemy, they’re a big part of who we are


Our innate and adaptive immune systems

The innate system ranges from processes as basic as phagocytosis (ingestion of bacteria), to molecules like the interferons produced by any virus-infected cell that can limit replication. Such innate systems are found right across the evolutionary spectrum and don’t target specific pathogens.

The much younger adaptive immune system is what we stimulate with vaccines. A property of small white blood cells called lymphocytes, it divides broadly into two lineages: the B cells and T cells. These bear the extraordinarily diverse and very specific immunoglobulin (Ig) and T cell receptor (TCR) recognition molecules that detect invading pathogens (bacteria, virus, fungi and so on).

The immunoglobulins bind to “non-self” (foreign) proteins called “antigens”, while the T cell receptors are specifically targeted to “self” transplantation molecules.

The assassins of the immune system are then switched on; the killer T cells that eliminate virus-infected (or cancer) cells. Also activated are the “helper” T cells that secrete various molecules to “help” both the B cells and killer T cells differentiate and do their work.




Read more:
Explainer: what is the immune system?


How does our immune system learn and remember?

All lymphocyte responses work by massive cell division in the lymph nodes (the “glands” in our neck that swell when we get a sore throat). This process is started by small numbers of “naive” B and T cells that haven’t encountered the invader before, and only stops when the foreign invader is eliminated.

The B cells differentiate into large protein-secreting cells called plasma cells, which produce the protective antibodies (immunoglobulins) that circulate for years in our blood.

Most of the T cells die off after they’ve done their job, but some survive so they can remember how to target specific invaders. They can be rapidly recalled to their “killer” or “helper” function.

Prior infection or the administration of non-living or “attenuated” (to cause a very mild infection) vaccines sets up the memory so protective antibodies are immediately available to bind (and neutralise) pathogens like the polio or measles virus. While immune T cells are rapidly recalled to “assassin” status and eliminate pathogen-infected cells.

As you may have gathered from this very brief and far too simplified account, the immune system is extraordinarily complex. And it’s also very finely balanced with, for example, cross reactive responses to bacterial proteins sometimes setting us up for autoimmune diseases.




Read more:
No, combination vaccines don’t overwhelm kids’ immune systems


Another example of autoimmunity is rheumatoid arthritis, which can be triggered by blood-borne chemicals from tobacco smoke that modify “self” transplantation molecules in the joints.

The ConversationAnd when we talk about the possible effects of the microbiome, or the “too clean” hypothesis, we’re discussing how exposure to bacteria and viruses can modify that immune balance in ways that directly affect our wellbeing. This is a very active area of research which, given the underlying complexity, presents scientists with big challenges as we seek to reach verifiable conclusions.

Peter C. Doherty, Laureate Professor, The Peter Doherty Institute for Infection and Immunity

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

Health Check: why do we yawn and why is it contagious?



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Yawning increases our alertness.
from shutterstock.com

Mark Schier, Swinburne University of Technology and Yossi Rathner, Swinburne University of Technology

Consider the scenario. You’re driving on a long, straight stretch of country highway at about 2pm on a sunny afternoon, and you’re desperately keen to reach your destination. You’re trying to stay alert and attentive, but sleep pressure is building up.

In response you yawn, sit up straighter in your seat, possibly fidget around a little and engage in other mannerisms that may increase your level of arousal.

Is this the purpose of yawning? Yawning is generally triggered by several things, including tiredness, fever, stress, drugs, social and other psychological cues. These are generally well documented and vary between individuals.

The question of why we yawn evokes a surprising amount of controversy for what is a relatively minor field of study. We don’t have evidence that can point us to the exact purpose of yawning.

But there are several theories about the purpose of yawning. These include increasing alertness, cooling the brain, and the evolutionary theory of alerting others in your group that you’re too tired to keep watch, and someone else should take over.

1. Helps us wake up

Yawning is known to increase with drowsiness. This has led to the arousal hypothesis of yawning. Associated with the yawning are increased movement and stretching behaviour. The increased fidgeting behaviour may help maintain vigilance as sleep pressure builds.




Read more:
Health Check: how can I make it easier to wake up in the morning?


Also, specific muscles in the ear (the tensor tympani muscles) are activated during yawning. This leads to a resetting of the range of movement and sensitivity of the eardrum and hearing, which increases our ability to monitor the world around us after we may have tuned out before the yawn.

Yawning is usually accompanied by stretching behaviour.
from shutterstock.com

Additionally, the opening and flushing of the eyes will probably lead to an increase in visual alertness.

2. Cools the brain

Another theory for why we yawn is the thermoregulatory hypothesis. This suggests that yawning cools the brain. Yawning causes a deep inhalation that draws cool air into the mouth, which then cools the blood going to the brain.

Proponents of this theory claim a rise in brain temperature is observed prior to yawning, with a decrease in temperature seen after the yawn.

But the research report that gave rise to this theory only shows excessive yawning may occur during an increase in brain and body temperature. It doesn’t suggest this has a cooling purpose.

Increased yawning rates are seen when fevers have been experimentally induced, which does suggest a correlation between body warming and yawning. But there is no clear evidence it leads to body cooling – just that body warming seems to be a trigger for yawning.

3. Sentry duty

Yawning-like behaviour has been observed in almost all vertebrates, suggesting that the reflex is ancient. The evolutionary based behavioural hypothesis draws on humans being social animals. When we are vulnerable to an attack from another species, a function of the group is to protect each other.

Part of our group contract has included sharing sentry duties, and there is evidence from other social animals of yawning or stretching signals when individuals are becoming lower in arousal or vigilance. This is important for changing activities to prevent the watch from slipping, or to indicate the need for another sentry.

Neuroscience explanations

The yawning reflex involves many structures in the brain.

One study that scanned the brains of those who were prone to contagious yawning found activation in the ventromedial prefrontal cortex of the brain. This brain region is associated with decision-making. Damage to this region is also associated with loss of empathy.




Read more:
Understanding others’ feelings: what is empathy and why do we need it?


Stimulation of a particular region of the hypothalamus, which contains neurons with oxytocin, causes yawning behaviour in rodents. Oxytocin is a hormone associated with social bonding and mental health.

Injecting oxytocin into various regions of the brain stem causes yawning, too.
These include the hippocampus (associated with learning and memory), ventral tegmental area (associated with the release of dopamine, the happy hormone) and the amygdala (associated with stress and emotions). Blocking the oxytocin receptors here prevents that effect.

Patients with Parkinson’s disease don’t yawn as frequently as others, which may be related to low dopamine levels. Dopamine replacement has been documented to increase yawning.

Your dog could be yawning on long car trips because it is stressed.
from shutterstock.com

Similarly, cortisol, the hormone that increases with stress, is known to trigger yawning, while removal of the adrenal gland (which releases cortisol) prevents yawing behaviour. This suggests that stress might play a role in triggering yawning, which could be why your dog may yawn so much on long car trips.

So, it seems yawning is somehow related to empathy, stress and dopamine release.

Why is it contagious?

Chances are you’ve yawned at least once while reading this article. Yawning is a contagious behaviour and seeing someone yawn often causes us to yawn as well.
But the only theory that’s been suggested here is that susceptibility to contagious yawning is correlated with someone’s level of empathy.

It is interesting to note, then, that there is decreased contagious yawning among people on the autism spectrum, and people who have high psychopathic tendency. And dogs, considered to be highly empathetic animals, can catch human yawns too.




Read more:
Contagious yawns show social ties in humans and bonobos


Overall, neuroscientists have developed a clear idea of a wide range of triggers for yawning, and we have a very detailed picture of the mechanism underlying yawning behaviour. But the functional purpose of yawning remains elusive.

The ConversationBack to our road trip, the yawning may be a physiological cue as the competition between vigilance and sleep pressure begins to favour drowsiness. But the overwhelming message is that sleep is winning and encouraging the driver to pull over for a break, and it shouldn’t be ignored.

Mark Schier, Senior Lecturer in Physiology, Swinburne University of Technology and Yossi Rathner, Lecturer in Human Physiology, Swinburne University of Technology

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

We asked five experts: do I have to drink eight glasses of water per day?



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Eight seems like a lot…
from http://www.shutterstock.com

Alexandra Hansen, The Conversation

Everyone knows humans need water and we can’t survive without it. We’ve all heard we should be aiming for eight glasses, or two litres of water per day.

This target seems pretty steep when you think about how much water that actually is, and don’t we also get some water from the food we eat?

We asked five medical and sports science experts if we really need to drink eight glasses of water per day.

All five experts said no

Here are their detailed responses:

https://cdn.theconversation.com/infographics/248/5569e2081efba668022eb859f9f36a24735d7625/site/index.html


If you have a “yes or no” health question you’d like posed to Five Experts, email your suggestion to: alexandra.hansen@theconversation.edu.au


The ConversationDisclosure statements: Toby Mündel has received research funding from the Gatorade Sport Science Institute and Neurological Foundation of New Zealand, which has included research on hydration.

Alexandra Hansen, Section Editor: Health + Medicine, The Conversation

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

Health check: why do we get muscle cramps?



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Some people experience cramps frequently after vigorous, high-intensity exercise.
from shutterstock.com

Alan Hayes, Victoria University

Many of us know the feeling of a cramp – whether you’ve been struck down on the sports field or woken with a start in excruciating pain in the middle of the night. A cramp is the involuntary contraction of our skeletal muscle, and it hurts.

Some people often experience cramps after vigorous, high-intensity exercise, but there are also many who experience them with no exercise at all – mostly at night. These “nocturnal” cramps occur with increasing frequency as we age, and are common in pregnancy.

Interestingly, these cramps are usually restricted to the lower limb. This is generally the same as athletes experiencing exercise-associated muscle cramps. So, are the causes the same?

What causes cramps?

Actually, we don’t really know, but there are several theories.

We know cramps are rarely seen at the start of a sporting contest, but regularly seen at the end. So fatigue seems to be the defining factor in exercise. Some researchers have long suggested dehydration and electrolyte imbalance (such as decreased salt content) as a cause.

But recent reviews have downplayed this theory, as the evidence is mostly observational. This means while there may be an association between dehydration, salt depletion and cramps, we can’t prove one caused the other.

Also, in these studies, people who were prone to cramps didn’t have differences in hydration or electrolyte content compared to people who were not prone to cramps.




Read more:
Health Check: what happens to your body when you’re dehydrated?


And if electrolyte imbalance was implicated, then all the muscles in the body would be affected. But only muscles actively being used tend to cramp, particularly those that cross more than one joint, such as the calf muscle and hamstrings. These may be contracting from a shortened position when the knee is bent.

Mismatched reflexes

Muscles have an inbuilt reflex mechanism. When the muscle is tensed, or contracts, a reflexive message is sent to the spinal cord for the muscle to lengthen and relax. This protects the muscle from injury.

The recent reviews suggest what is called the altered neuromuscular control hypothesis to explain cramps. Here, the protective reflex action is disrupted, which usually happens when the muscle is tired. So, in this instance, the muscle contracts, but the usual signal to the spinal cord for it to relax is inhibited. There is now no protective relaxing of the muscle that follows, meaning it contracts for longer than you want it to.

When we tense our muscles a message is sent to the spinal cord for the muscles to relax.
From shutterstock.com

But the reason for neuromuscular fatigue, and why this inhibits the reflex, is not well understood. Cramps are also more common at the start of a sports season, when muscles are less conditioned. This is most likely due to higher levels of fatigue occurring in less trained muscles.

The altered neuromuscular control could also explain nocturnal cramps, as older muscles of inactive people are generally shorter. Whether this is the case in pregnancy is still debated.

Hot conditions have also been associated with increased cramping, but this likely relates to higher rates of fatigue when it’s hot. Despite what people may think, cold doesn’t increase the incidence of cramps, but may be likely to make the severity of cramps worse as reflexes are stronger in cold, stiff muscles.




Read more:
Health Check: how to exercise safely in the heat


Are certain people more susceptible?

Some people seem to experience cramps more often than others, which may be related to the sensitivity of their muscle reflexes.

Fatigue is a clear risk factor, both in long-term endurance athletes and in those participating in high-intensity activities. This is because high-intensity activities require the use of our powerful, fast-contracting fibres (fast fibres), as opposed to lower-intensity activities that use our slower fibres. Fast fibres are more susceptible to fatigue.

Cramps are more prevalent in males, which may be because males have more fast fibres, or because females demonstrate less fatigue when exercising at similar relative intensities.

Cramps may occur during the night, including commonly in pregnant women.
from shutterstock.com

Nocturnal cramps are more commonly reported in older age. There is also a particularly high prevalence of cramps in pregnancy, generally beginning in the second trimester and often worsening in the third.

No one really knows exactly why this occurs. It may be due to increased fatigue from carrying the extra body weight, or increased pressure on the leg muscles due to slowed return of blood to the heart.

Hormones could play a role too, and there have been suggestions that women taking the contraceptive pill could be more prone to cramping. Connective tissue stiffness is altered by sex hormones.

But, while reflex sensitivity does change with the phases of the menstrual cycle, the muscle stretch reflex is actually lowest at ovulation, and there is limited evidence that the pill affects this.




Read more:
Chemical messengers: how hormones change through menopause


How do we treat cramps?

Salt tablets and magnesium have been commonly used for cramps, but because electrolyte imbalance and dehydration don’t appear to be the cause, their usefulness is debatable.

Stretching is generally the best way to get rid of a cramp.
From shutterstock.com

The best way to get rid of a cramp is by stretching the muscle, since the reflex to do this is likely being inhibited. However, stretching a severely cramping muscle might cause a degree of damage to the muscle.

So, contracting the opposite muscle in the muscle pair (usually on the other side) may be a better approach. This involves, for example, contracting the quadriceps (at the front of the leg) when the hamstrings (at the back of the leg) are cramping.




Read more:
Health Check: do you need to stretch before and after exercise?


Given the overall lack of understanding of exactly how cramps occur, evidence-based prevention strategies are few and far between. If fatigue is one of the main causes of increased susceptibility to cramps, then methods to delay fatigue – such as fluid intake and salt replacement during exercise – may help prevent them. This can also aid performance.

The ConversationMassage (due to reduced nerve sensitivity) and stretching may also help decrease the incidence of cramps in older people and during pregnancy.

Alan Hayes, Assistant Dean, Western Centre for Health Research and Education, Victoria University

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

Six things you can do to reduce your risk of dementia



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Challenging and training your brain is important to prevent dementia risk.
Photo by rawpixel.com on Unsplash

Helen Macpherson, Deakin University

An ageing population is leading to a growing number of people living with dementia. Dementia is an umbrella term for a group of symptoms including memory impairment, confusion, and loss of ability to carry out everyday activities.

Alzheimer’s disease is the most common form of dementia, and causes a progressive decline in brain health.

Dementia affects more than 425,000 Australians. It is the second-ranked cause of death overall, and the leading cause in women.

The main risk factor for dementia is older age. Around 30% of people aged over 85 live with dementia. Genetic influences also play a role in the onset of the disease, but these are stronger for rarer types of dementia such as early-onset Alzheimer’s disease.




Read more:
What causes Alzheimer’s disease? What we know, don’t know and suspect


Although we can’t change our age or genetic profile, there are nevertheless several lifestyle changes we can make that will reduce our dementia risk.

1. Engage in mentally stimulating activities

Education is an important determinant of dementia risk. Having less than ten years of formal education can increase the chances of developing dementia. People who don’t complete any secondary school have the greatest risk.

The good news is that we can still strengthen our brain at any age, through workplace achievement and leisure activities such as reading newspapers, playing card games, or learning a new language or skill.

Even playing cards can strengthen your brain.
Photo by Inês Ferreira on Unsplash

The evidence suggests that group-based training for memory and problem-solving strategies could improve long-term cognitive function. But this evidence can’t be generalised to computerised “brain training” programs. Engaging in mentally stimulating activities in a social setting may also contribute to the success of cognitive training.




Read more:
What is ‘cognitive reserve’? How we can protect our brains from memory loss and dementia


2. Maintain social contact

More frequent social contact (such as visiting friends and relatives or talking on the phone) has been linked to lower risk of dementia, while loneliness may increase it.

Greater involvement in group or community activities is associated with a lower risk. Interestingly, size of friendship group appears less relevant than having regular contact with others.

3. Manage weight and heart health

There is a strong link between heart and brain health. High blood pressure and obesity, particularly during mid-life, increase the risk of dementia. Combined, these conditions may contribute to more than 12% of dementia cases.

In an analysis of data from more than 40,000 people, those who had type 2 diabetes were up to twice as likely to develop dementia as healthy people.

Managing or reversing these conditions through the use of medication and/or diet and exercise is crucial to reducing dementia risk.

Exercise is protective for heart health and diabetes, as well as against cognitive decline.
Photo by chuttersnap on Unsplash

4. Get more exercise

Physical activity has been shown to protect against cognitive decline. In data combined from more than 33,000 people, those who were highly physically active had a 38% lower risk of cognitive decline compared with those who were inactive.

Precisely how much exercise is enough to maintain cognition is still under debate. But a recent review of studies looking at the effects of taking exercise for a minimum of four weeks suggested that sessions should last at least 45 minutes and be of moderate to high intensity. This means huffing and puffing and finding it difficult to maintain a conversation.




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Australians generally don’t meet the target of 150 minutes of physical activity per week.

5. Don’t smoke

Cigarette smoking is harmful to heart health, and the chemicals found in cigarettes trigger inflammation and vascular changes in the brain. They can also trigger oxidative stress, in which chemicals called free radicals can cause damage to our cells. These processes may contribute to the development of dementia.

The good news is that smoking rates in Australia have dropped from 28% to 16% since 2001.

As dementia risk is higher in current smokers compared with past smokers and non-smokers, this provides yet another incentive to quit once and for all.

6. Seek help for depression

Around one million Australian adults are currently living with depression. In depression, some changes occur in the brain that may affect dementia risk. High levels of the stress hormone cortisol have been linked to shrinkage of brain regions that are important for memory.

High blood pressure can increase the risk of dementia.
Photo by rawpixel.com on Unsplash

Vascular disease, which causes damage to blood vessels, has also been observed in both depression and dementia. Researchers suggests that long-term oxidative stress and inflammation may also contribute to both conditions.




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A 28-year study of more than 10,000 people found that dementia risk was only increased in those who had depression in the ten years before diagnosis. One possibility is that late-life depression can reflect an early symptom of dementia.

Other studies have shown that having depression before the age of 60 still increases dementia risk, so seeking treatment for depression is encouraged.

Other things to consider

Reducing dementia risk factors doesn’t guarantee that you will never develop dementia. But it does mean that, at a population level, fewer people will be affected. Recent estimates suggest that up to 35% of all dementia cases may be due to the risk factors outlined above.

This figure also includes management of hearing loss, although the evidence for this is less well established.

The contribution of sleep disturbances and diet to dementia risk are emerging as important, and will likely receive more consideration as the evidence base grows.

The ConversationEven though dementia may be seen as an older person’s disease, harmful processes can occur in the brain for several decades before dementia appears. This means that now is the best time to take action to reduce your risk.

Helen Macpherson, Research Fellow, Institute for Physical Activity and Nutrition, Deakin University

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

Explainer: what is lupus and how is stress implicated?



File 20180312 30975 hd3c2u.jpg?ixlib=rb 1.1
Lupus is the body’s immune system attacking itself.
from http://www.shutterstock.com

Eric Morand, Monash Health

Thanks to Selena Gomez and Dr House, most of us have heard of lupus. But most of us don’t know what it is, and until recently, none of us were sure whether stress could be a risk factor.

The simplest way to understand lupus is “your immune system gone wrong”.

We have evolved powerful immune systems to detect, attack, and destroy invading microbes. But if the immune system makes an error in the “detect” stage – incorrectly recognising some part of us as foreign – it will attack it with all of the tools at its disposal.

This self-directed, or “auto”-immunity, is the basis of countless diseases, from juvenile diabetes to multiple sclerosis. But unlike those examples, in which the immune system attacks just one tissue, in lupus all tissues of the body can be targeted.




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This can mean anything from a rash and arthritis to the immune system disrupting the function of the brain, heart, and kidney. Some sufferers may have minor symptoms such as tiredness and joint pain that resolves within a few months, but for some the disease can last for years and require transplantation of damaged organs.

These symptoms can arrive in any order at any time, and cause a severe loss of quality of life and reduction in life expectancy. As lupus mostly affects young adult women, the impact of this is great.

Why does this happen?

We are much closer now to being able to answer this question, thanks in part to being able to analyse gene expression in people with the disease.

We know from genetic studies that at least some risk of lupus is inherited from our parents, but we also know that inheritance explains only a fraction of the risk of getting lupus. So other factors must contribute.

It now appears that a large subset of lupus patients’ disease is caused by mechanisms the immune system normally uses to combat viruses. The immune system produces virus-fighting hormones (called “cytokines”) such as interferon – which activates the production of antibodies and destructive inflammation intended to kill the infection. When this happens by error, and is directed at the self, tissue inflammation and damage occur.

Current treatments are limited to non-specific immune suppressant drugs “borrowed” from other diseases such as arthritis, and drugs used to stop an organ recipient’s body rejecting the donor organ. Although life-saving in many cases, these drugs have major side effects and don’t control all patients’ disease.




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How is stress related to lupus?

As a rheumatologist I treat patients in hospital with musculoskeletal diseases and autoimmune conditions. A patient of mine suffering from lupus had, some time prior to diagnosis, been the victim of an assault, which caused post-traumatic stress disorder (PTSD).

This case posed to me, and more importantly to the patient, the question of whether stress could have led to the development of lupus. Until recently this question has been effectively unanswerable.

A new study looked at data reporting on the association of trauma and PTSD with the incidence of lupus. It found that PTSD was associated with a nearly threefold increase in risk of subsequently developing lupus.

A study found a link between PTSD and auto-immune conditions in service personnel.
from http://www.shutterstock.com

A past history of trauma, regardless of carrying a PTSD diagnosis, was associated with a similar threefold increase in the risk of lupus.

These findings confirm a previous study of ex-service personnel, in which PTSD was both disturbingly prevalent and also a powerful risk factor for the development of autoimmune diseases, including lupus.




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The association of stress and the immune system dates back to the 1930s, when pioneering endocrinologist Hans Selye found that there are distinct changes in the body in response to a threat. The term “stress” was also attributed to Selye, albeit coined much later.

Crucially, Selye also observed that stress results in disturbances in steroid hormone production. As we now know, the body’s naturally occurring steroids act through the same pathway as steroid drugs used to treat lupus. This provides a possible mechanism for the connection between stress and the control of immunity.

Intriguingly, some organ manifestations of lupus, such as severe skin or blood disease, are notoriously resistant to steroids, and recent laboratory studies suggest interferon activation in lupus may be responsible for this steroid resistance. Thus, stress, changes in steroid production, and failure to suppress interferons may represent a chain of events influencing the development of lupus.

The ConversationSo this new study means we’re a little less unsure about the causes of auto-immune diseases. And while sufferers can’t change past life events, knowing the causes brings us closer to understanding, and to better treatments.

Eric Morand, Head, School of Clincial Sciences at Monash Health, Monash Health

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