What causes headaches?

Health Check: what causes headaches?

We all get headaches from time to time. In fact, nearly every second person in the world had a headache at least once in the past year. But these can feel very different, depending on which of the nearly 200 types of headache you have.

More than half (52%) of people will have a tension-type headache at some point in their life, around 18% will get a migraine, and 4% will suffer from chronic daily headaches. These are the most common headache-related diagnoses. Although there are some variations globally, the figures seem remarkably consistent across populations.

Secondary headaches can be initiated by triggering factors such as medication overuse, medication side effects, neck pain, sinus disease or dental problems. These account for small percentages individually compared to the primary headaches, but may be more treatable if the predisposing problem can be sorted out.

Tension-type headache

Tension-type headaches (TTH) feel like a dull or heavy, non-pulsating band of pain, usually on both sides of the head. The name comes from an erroneous belief that overly tight muscles are the main reason for the headache.

TTH usually occurs in episodes, with each lasting from several hours up to a few days at a time. There is not usually much associated nausea, light sensitivity or sound sensitivity.

Chronic TTH is a less common form and is diagnosed when you have experienced at least 180 days with a headache per year. It is generally not aggravated by routine physical activity; it’s just there all the time.

Genetic tendencies explain some of the risk for developing TTH, with your own risk increased threefold if you have an immediate family member with the condition.

Infrequent episodic TTH does not appear to be strongly associated with psychological stress, despite this common belief. Chronic TTH has a stronger association with higher psychological distress, but it is unclear whether this is a cause or effect of having long-term disabling headaches.

Strangely for such a common and problematic condition, there is still little agreement about exactly how the pain is produced in TTH.

The most attractive hypothesis to me is that it represents a “virtual” pain whereby multiple low-grade inputs (likely including inputs that are “almost-painful”, or below the threshold for conscious pain) add up to produce sensitisation of the trigeminal nerve nuclei (the nerve shown in orange below).

stihii/Shutterstock

This turmoil registers as pain referred to the distribution of the head, usually the forehead, temple and back of the head locations. Examination of these areas doesn’t show any abnormalities because in TTH, there is no one driving mechanism of the headache.

Treatment remains almost trivially simple, despite years of research. It’s almost true to say that the proverbial “cup of tea, a Bex and a good lie down” sums it up. Aspirin, paracetamol or ibuprofen plus rest and possibly some cold packs seem to be the most reliable treatment. There is conflicting or negative evidence for almost every other, fancier therapy.

Migraine

Migraine alone is the sixth most disabling condition globally.

Migraines are usually one-sided, associated with nausea and light sensitivity (photophobia) and may also be preceded by idiosyncratic sensory experiences called an “aura”. Aura phenomena can include moods or emotions, such as deja vu, visual symptoms (flashing lights or jagged lines are common) or problems with speech.

Migraine is a clinical diagnosis; there is no objective test that can verify it with our current technology. But compared to the frustration of researching and treating tension-type headaches, migraine has been steadily giving up its secrets over the past decade.

Migraine physiology is extremely complex. The headaches seem to arise because of dysfunctional regulation of the tone of some of the blood vessels inside the skull.

Migraine sufferers – Migraineurs – may have genetic vulnerability to migraines because of overly responsive calcium channels in their nerve membranes or other mutations which result in them having overactive signalling pathways in the brain.

Environmental or internal triggers can provoke these nerves to over-react, resulting in the activation of a reflex pathway. This dysregulation of normal structures causes the headache, nausea, photophobia and phonophobia (sound sensitivity) typical of an attack.

Migraines are often associated with light sensitivity.
Rishi Bandopadhay/Flickr, CC BY-NC

The period of headache in a migraine attack corresponds with a rise in the blood levels in the head of a peptide called calcitonin gene-related peptide (CGRP). CGRP is one of the most common pain-inducing signal molecules in the body. When the CGRP falls, the headache goes away. Where the extra CGRP comes from is not clear but it probably is released from the overactive networks of cells in the brainstem.

The most effective group of drugs for migraine are the triptans. So effective and specific are these drugs that the diagnosis of migraine needs to be reconsidered if they don’t abort the headache attacks most of the time.

Triptans work by activating certain subtypes of serotonin receptors in the brain. Taking a triptan early in a migraine attack seems to directly lower the CGRP release and oppose its effects on blood vessels thereby stopping the attack. Triptans are not however useful to prevent frequent attacks of migraine.

Migraine prophylaxis is achieved by several drugs of different classes, with radically differing mechanisms of action. Some are anticonvulsants, which clearly work by suppressing the nerve overactivity typical of migraineurs. Others, such as the beta-blockers (propranolol) and calcium-channel blockers (verapamil) target the nerve endings on the blood vessels. Others which are known to be effective, such as botulinum toxin (Botox) and amitriptyline (Endep) work by means which are yet to be fully understood.

Severe migraineurs suffer years of disability and as a public service I would like to suggest that if you know someone who has severe migraines (you almost certainly do) please read this excellent list of what not to say to them when trying to be sympathetic or helpful.

Chronic daily headache

Imagine that you never had a day without headache. You can remember vaguely the time when you didn’t feel that pounding in the temples, squeezing in the back of the head or piercing pain above the eyes but it seems like another life. Such is the lot of sufferers of chronic daily headache (CDH).

Some headaches begin as as frequent but clearly episodic tension-type headache, or migraine, but then “transform” into what seems to be basically a continuous headache for at least some part of every day.

There are a number of rare headache types which may cause chronic daily headache and diagnosis of the these can lead to specific treatments which work well. This is the role of a neurologist or pain specialist with a special interest in headache.

If you have more than just the occasional headache, it pays to get a proper diagnosis.
Jared Earle/Flickr, CC BY-NC-ND

Possibly the most common reason why tension-type headache or migraine can transform is medication overuse, especially short-acting opioids such as codeine. The best solution to this problem is to avoid long-term regular use of codeine for headaches, though the evidence would suggest we may never achieve this goal except by making codeine prescription-only.

Frequent use of triptans is also believed to sensitise the trigeminovascular networks in the brainstem, thereby lowering the bar for triggering of migraine attacks. If the threshold for an attack becomes too low, they may never quite switch off, and one attack will run into the next one.

If you have more than just the occasional headache, it pays to get a proper diagnosis, as the reasons for your headache can be many and varied. Some have specific treatments for them, and others such as TTH seem quite difficult to find a specific treatment for. There are new classes of drug treatment under development, for migraine in particular, so it looks hopeful that future generations may not have to labour under the burden of poorly treated headaches.

Michael Vagg is Clinical Senior Lecturer at Deakin University School of Medicine & Pain Specialist at Barwon Health.

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

The next frontiers in maternal and child health post the millennium goals

Charles Anawo Ameh, Liverpool School of Tropical Medicine

With another deadline around the Millennium Development Goals (MDGs) reached, there is a renewed debate on how effectively they have helped shape the agenda and the strategies to improve health, reduce poverty and promote development across the globe.

Of the eight goals created in 2000 – which pledged member countries to reduce poverty and unacceptable global health disparities and improve the lives of poor people – there were two dedicated to maternal, reproductive, newborn and child health.

Goal four intended to reduce child mortality by two-thirds. Goal five was to reduce the maternal mortality rate by 75% by December 2015.

In absolute terms, there has certainly been a narrowing of the gap between countries. Significant progress has been made in all the MDGs.

It is widely accepted that both these goals have helped enormously in setting a clear agenda for maternal, reproductive and child health. The United Nations’ 2015 report released this week found the number of children dying before their fifth birthday has more than halved while the maternal mortality rate dropped by 45% worldwide.

But the goals are a classic case of missed opportunity for several reasons. The first is that they failed to address the disparities within countries. The national average data reported in these countries conceals these differences. The second is that there has been no focus on improving the health for sub-populations that are worse off within countries and to narrow the gap between countries.

How to fix the mistakes made last time

There is an argument that the MDGs failed to recognise the central role of existing health systems and the need to strengthen them. Instead, they placed more importance on measurable health outcomes related to vertical programmes. A vertical health programme is one that is managed, delivered and monitored outside the existing health care system. They are considered by many as parallel systems that weaken existing health systems.

The Sustainable Development Goals (SDGs) present an opportunity to correct this.

The end of the MDGs has renewed discussions on the concept of Universal Health Coverage, now firmly part of the post-2015 agenda. In 2014, UN member states asked the secretary-general to synthesise the full range of inputs into the post-MDG discussions. These were finalised by the end of the 2014 under the rubric: the road to dignity by 2030.

The proposed SDG related to health is to attain a healthy life for all at all ages. One target within this (3.6) is to achieve universal health coverage. This has the potential to reduce disparities and inequalities if implemented properly. The goal of universal health care is to make both preventative and curative health interventions accessible to the whole population – urban or rural, rich or poor.

The concept of universal health care is not new. It was discussed at the 2005 World Health Assembly. It was defined then as:

… access to key promotive, preventive, curative and rehabilitative health interventions for all at an affordable cost, achieving equity in access.

At the time, the discussion also emphasised the need to make access to health prevention and curative services affordable by ensuring that households did not risk financial hardship from unaffordable out-of-pocket payments. The suggested parameter was that no more than 40% of household non-food expenditure should be spent on health services.

New focus areas

While the new agenda seems to focus on strengthening health systems to take on the full responsibility of ensuring health for all, it will not specifically drive reproductive, maternal and newborn health.

It does, however, provide an opportunity to focus on specific targets within reproductive, maternal and newborn health. These focus areas include society, health providers and service delivery.

Within the society dimension is social and financial protection, under health provider dimension there is workforce quality, responsiveness and efficiency and around service delivery, there is affordability, acceptability, accessibility, efficiency and equity.

Addressing these three areas will ensure that quality reproductive, maternal and newborn health is accessible to the entire population with financial protection. Financial risk protection is the most popular but the other dimensions need to be defined to make sure it is successfully implemented.

Indicators covering all components of the three proposed areas will facilitate comprehensive coverage in the post-MDG era.

Implementing universal health care

There are several models of implementing universal health care. The most common is health insurance for the working population, starting with government employees. But this model will potentially exclude hard to reach populations.

Another increasingly popular approach is to provide free services for pregnant, lactating women and children under five years of age. But this needs to be properly funded, monitored, evaluated and has to include a wide range of quality preventive and curative services. The services must be accessible to both rich, poor and urban and rural women.

Countries that have struggled to meet the MDG targets will need a concrete framework to guide the implementation of universal health care to ensure inequalities and disparities in health care are closed fairly quickly.

Charles Anawo Ameh is Senior Clinical Lecturer at Liverpool School of Tropical Medicine.

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

Garden eggs not only for the poor but everyone

By ROBERT MURIISA

Many homes and restaurants have garden eggs (intoryi) on their menus. Fortunately, a few people know their nutritional benefits and strive to eat them as often as possible. However some people, especially the middle class and rich, loathe garden eggs arguing that they are for the poor.
The truth
Garden eggs, contrary to what some people think, have numerous health benefits and should be enjoyed by everyone – not just the poor. According to nutritionists, garden eggs are essential for the overall development of our body.
Dr Rene Tabaro, a senior nutritionist and a dietitian at King Faisal Hospital, Kigali, says: “This natural fruit (intoryi) is rich in vitamins and other nutrients. Garden eggs provides the body with both soluble vitamins and water soluble vitamins; they are rich in vitamin C, moderate quantity of carbohydrates and potassium that is used for normalising the liver and B.P (Beat Pressure) i.e. pressure of the heart.”
Furthermore, intoryi are very essential in the fight against cancer and other diseases. Tabaro says garden eggs can reduce the rate at which cancer cells develop. He, however, explains that they are not good for people suffering from goiter.
Garden eggs are also good for weight reduction. “This is the perfect recipe for achieving weight loss within a short period of time because it’s very low in calorie content. I encourage all people that want to lose weight to eat garden eggs a lot. They are also key in reducing the risk of developing heart complications,” Tabaro says.
And Dr Ndubuisi Nkakakwa, a physician/consultant Acupuncturist at Green Leaves Clinic and Acupuncture Centre in Nigeria, shares Tabaro’s view.
“A high level of blood cholesterol level, more particularly low-density lipoprotein cholesterol, is a primary risk factor for cardiovascular diseases such as stroke and heart diseases and garden egg has the power of reducing such risks,” Nkakakwa writes in an article.
Garden eggs are also said to be good for sight. A study titled “Effects of Garden Egg on some visual functions of visually active Igbos of Nigeria” established that eating plenty of garden eggs can help lower eye pressure in persons with glaucoma.

Garden eggs should not be overcooked in order to preserve the nutrients. (Robert Muriisa)
Tabaro said garden eggs are important for sight as they have a very good effect on visual functions. Garden eggs are also excellent to the growth of the unborn baby since they contain Iodine that contributes to the growth of baby’s brain and making it active and functioning normally.
How to prepare garden egg/intoryi,
Nutritionists advise against overcooking intoryi since it kills very useful nutrients like Vitamin C. Tabaro says garden eggs should be half-cooked if one is to fully benefit. For maximum benefit, it is recommended that they be half-cooked.
*******************
Benefits of garden egg
1. A good source of dietary fibre
2 Flexibility of blood vessels
3. Cardio protective
4. Regulate blood sugar
5. Natural source of B vitamins like thiamin, niacin, B6 and
pantothenic acid
6. Cholesterol control
7. Improves digestive system
8. Low calorie good for weight management
9. Good for skin and hair
10. High in folate, manganese, Vit k
magnesium, vitamin c & copper
11. A source of nasunin ( a powerful and rare antioxidant for the brain
12. Bone strengthening minerals
14. Improves blood circulation
15. Beneficial for constipation
due to high fibre
16. Good for colon health
17. Good amount of phenolic acid, anthocyanins and flavonoids. These antioxidants help protect the body from health risks, like aging, inflammations, and neurological diseases
Agencies

Originally published in The New Times Rwanda

You should really be nicer to your colleagues rude behavior is contagious

You should really be nicer to your colleagues – rude behavior is contagious

Trevor Foulk, University of Florida

We experience rudeness and incivility all the time. From simple insults and offhand remarks to purposely excluding others from groups, these behaviors are largely tolerated in our daily lives and in the workplace. The question is, what effect do these behaviors have on us?

It’s pretty clear that high-intensity negative behaviors like abuse, aggression and violence are harmful. But what’s the harm in just being rude and uncivil?

A growing body of research offers compelling evidence that experiencing rudeness, and even simply witnessing rudeness, can have surprisingly harmful effects on performance, creativity and even helpfulness. However, it might not even end there.

What if rudeness was actually contagious? This would mean that rudeness may not only hurt those who experience or witness it, but also have secondary effects. People who’ve experienced rude behavior from others are now “infected” with rudeness themselves, and will be rude to the people they interact with next.

Office rudeness is contagious, just like the common cold

To explore this phenomenon, my colleagues and I at the University of Florida (Andrew Woolum and Amir Erez) conducted a study to find out if rudeness was contagious from one person to another.

Over the course of a seven-week period, the participants (students engaged in a negotiations course) engaged in 11 negotiations exercises with various partners.

After each negotiation, participants had the opportunity to rate how rudely their negotiation partner had behaved. The structure of this exercise allowed us to explore how rudeness could be contagious by examining how the rudeness experienced in one negotiation influenced rude behaviors in the next negotiation. We didn’t instruct participants to be rude; we simply measured the normal rudeness that was present in the negotiation setting.

We found that rudeness is in fact contagious. If negotiators felt that their negotiation partner was rude, when they went on to their next negotiation, their new partner in turn perceived them as rude.

Another surprising finding was how long this effect lasted. Some of the negotiations took place one after another, and some took place up to seven days apart. We found that the time between negotiations didn’t seem to matter. Even if negotiations were a week apart, the rudeness experienced in the previous negotiation still caused participants to be rude in their next negotiation.

Is it catching?
Office workers via www.shutterstock.com.

Why does rudeness spread from one person to another?

Prior research has shown that both emotions and behaviors can be socially contagious.

For example, when people around you are feeling happy, it is likely that you will start to feel happy too. Similarly, when people around you tap their toes or fold their arms, often you will start doing the same thing. Since these effects are usually described as simple subconscious mimicry, they probably can’t describe why rudeness can make us more rude. So how does it happen?

To tackle this question, we explored whether a process occurring in a subconscious part of the brain was responsible. When we experience social stimuli (like a conversation with a coworker), they can activate concepts deep in the subconscious part of our brains.

A concept could be anything. We have a concept for anger, happiness, sadness, power, and, of course, rudeness. The activation of concepts is automatic – meaning when it happens, we aren’t aware of it. And when concepts are activated, this changes the way we perceive the world a little bit.

Happy concept activated.
Smiley face via www.shutterstock.com

For example, just seeing a happy face could activate the happiness concept, causing us to perceive future stimuli as more happy. Furthermore, researchers have found that when people write a short vignette about power, that can activate the power concept, causing people to feel more powerful.

So if that rude concept is activated, it causes us to perceive stimuli as a little bit more rude. And that’s what we found in two experimental studies. When people experienced (or even witnessed) rudeness, they noticed rudeness in their environment more, making them more likely to perceive things as rude, and this perception of rudeness caused them to respond with rudeness.

For example, imagine someone walking by you and saying “Hey, nice shoes!” You might interpret that as a compliment, or you might interpret it as an insult – it’s sort of hard to tell, and your brain has to decide. Well, when you’ve recently experienced rudeness, you are more likely to perceive that comment as rude even if it wasn’t meant that way. Then, subsequently, you will respond to the perceived rudeness with more rudeness.

What is so scary about this effect is that it’s an automatic process – it takes place in a part of your brain that you are not aware of, can’t stop, and can’t control. So, you would not necessarily be aware that the reason you (mis)interpreted the “nice shoes” comment is that you had recently experienced rudeness. This means you can’t temper the process.

Just don’t be rude

This evidence that rudeness is contagious really underscores how harmful these behaviors can be, particularly in organizational settings.

While prior evidence showed that rudeness could be harmful to performance, creativity and helpfulness, this research shows that the effects are not limited to the parties of the rude interaction.

In this way, rudeness can spread out like a virus, not only harming the performance of those who experience it but also making them carriers likely to pass the harm on to those with whom they interact next.

This means that maybe we need to rethink what behaviors are acceptable in the workplace. Behaviors like aggression, abuse, and violence are not tolerated at work, but sometimes rudeness tacitly is – but maybe it shouldn’t be. Up to 98% of workers report that they have experienced rudeness in the office, and 50% say they experience it weekly. So just be nice.

Trevor Foulk is Doctoral Student at University of Florida.

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

Four challenges we have to crack before immune therapy can revolutionize how we fight cancer

Sri Krishna, Arizona State University

Most of us know about the conventional treatment of cancer: surgery to remove tumors, chemotherapy and radiation. But within the last five years, a new class of drugs that use our immune systems to fight cancer are gaining traction in cancer treatment. This is called “immunotherapy.” Instead of killing cancer cells with radiation or chemotherapy, immunotherapy mobilizes the immune system to fight against cancer much like it does against bacteria and viruses.

For a training immunologist like myself, immune therapies have opened new doors to understanding and treating cancers. In the future, immunotherapy could mean a personalized treatment, entirely tailored to an individual. As exciting as that sounds, we still have plenty of work to do, as there remains a lot we don’t know about the immune system. Here are some of the challenges we need to overcome to create these personalized treatments.

Challenge #1: Tumors don’t want the immune system to know they are tumors

In the late 1980s, researchers started to wonder if the immune system could fight tumors the same way it fought foreign invaders. Studies in mice and in humans showed that when immune cells were extracted from a body, reprogrammed and transferred back into the same body, they caused tumors to temporarily shrink, giving first indications of immunotherapy at work.

In turns out that tumors are pretty vicious in avoiding the immune system. In the 1990s, researchers discovered that tumors can actively put “brakes” on the body’s immune system to evade detection by T-cells, a special kind of immune cell. T-cells search for signs of infection within cells by looking for specific protein codes on the cell surface. When T-cells decide that protein codes displayed on a cell don’t look like they belong to normal cells, they attack these abnormal cells and kill them (as shown in this fantastic video).

Cytotoxic (Killer) T-cells in action destroying a cancer cell.

Tumors can block T-cells from recognizing these protein codes. By doing this, tumors essentially go into stealth mode, flying under the radar of immune detection.

We’ve figured this challenge out – sort of. Extensive research on the T-cell brakes eventually led to drugs that block the effects of these brakes – allowing the immune system to detect and attack tumors that would otherwise be invisible to it – and present-day cancer immunotherapy was born.

A cancer patient receives an intravenous dose of Pembrolizumab during a promising cancer treatment clinical trial at UCLA Medical Center in Los Angeles, California, August 19 2013.
David McNew/Reuters

Challenge #2: Immunotherapy drugs are highly effective, but not in everyone

Today there are three drugs approved as immune therapies – Ipilumimab, Nivolumab and Pembrolizumab. All three drugs act by releasing the T-cell brakes in different ways, freeing T-cells to look for the small protein codes characteristic of tumor cells.

These drugs have provided long-term remissions in patients with metastatic relapses in cancers such as melanoma and lung cancer. This means that patients whose cancers came back after an initial chemotherapy treatment (often a 3-month death sentence) remarkably survived, in some cases for several years, after their T-cells were rebooted to attack cancer. Very few conventional treatments can offer a comparable second chance after relapse.

But there is a problem: these drugs do not work for everyone. They are approved only to treat melanoma and certain types of lung cancer, and even in these cancers, these drugs only work in some patients. For instance, in about 20% of people with metastatic melanoma, Ipilimumab can double the long-term survival. For the other 80%, the drug is much less effective.

Scientists say that part of the reason why immunotherapy drugs can be amazingly effective in some patients, and much less effective is others, boils down to differences in our DNA.

Although we share 99.9% of our DNA with each other, there is massive variation from one individual to the next, partly because of our genetics and partly due to the environment. This variation extends to our tumors and our immune system. Because of this genetic variation that makes us who we are, our immune systems, and thus our cancers, have their own life story.

To try to solve this problem, researchers are trying to understand the genetic basis of clinical response to immunotherapies, and developing techniques to identify whether a patient who walks into the clinic with cancer will benefit from these drugs before going under treatment.

Challenge #3: Survival of the fittest tumors

In recent years we’ve learned that one of the reasons tumors are hard to treat is because they evolve. Some researchers believe that tumors exist only because they have evolved to hide from the immune system. This process takes years of natural selection, where only the fittest tumor cells, which effectively hide from or actively fight against the immune system, manage to survive, grow and cause major complications.

This means that we can expect that at least in some patients undergoing immune therapy, their tumors can evolve resistance to immune system detection and can come back. Although our immune system is capable of constantly evolving to counter viruses and bacteria, tumor evolution is a formidable enemy to overcome, and we are just beginning to understand this aspect of the disease.

Challenge #4: The immune system ‘blind spot’

Our immune system carries out a fine balancing act between hunting down and attacking cells that can harm us, such as viruses and bacteria, and leaving healthy “self” cells in our bodies (or good bacteria) alone. Immune cells that recognize our own normal “self” cells are killed off early during development, which prevents us from developing autoimmune disorders.

But most tumors result from our own cells. So how do we get the immune system to fight “self” cells it is supposed to ignore, and how do we make sure the immune system targets tumor cells, but not healthy cells? This is a big challenge for immune therapies.

Immunotherapies let T-cells do their job.
Healthy human T-cell via NIAID, CC BY

By freeing T-cell brakes, current immunotherapies often work by overcoming these blind spots: immune cells suddenly start seeing our own “self” cells, which is very effective against tumors disguised as our own normal cells. The downside, however, is that this often upsets the delicate balance between autoimmunity and cancer.

As a result, some patients treated with immunotherapy experience autoimmune reactions.
Some melanoma patients undergoing immunotherapy have been known to develop Vitiligo, a condition where that leads to the loss of skin color. Other patients undergoing treatment also report gastrointestinal distress as a common side effect from the immune system being overactivated. In extreme cases, severe life-threatening autoimmune reactions such as organ rejection can happen, indicating that immunotherapy drugs need careful examination and regulation.

Overcoming the challenges

Researchers are starting to sequence the DNA of tumors to get a better understanding of how they work at the genetic level. We have just begun to understand how different they are from other cells of our body.

Tumor DNA sequencing, along with emerging technologies, like liquid biopsies on the blood to diagnose and monitor tumors, will help us understand how cancers evade the immune system and who will actually benefit from these treatments. In patients who do not respond to regular immunotherapies, it has been proposed that immunotherapies might be combined with conventional chemotherapies (“immunochemotherapy”) to improve potency of treatment.

We are also at the beginning of personalized immune therapies. This treatment involves designing vaccines made of engineered immune cells from a patient’s own body, to treat their own tumors. In the not too distant future, a patient may walk into a clinic, have their tumors sequenced and their immune system analyzed to decide on the best course of personalized immune therapy.

For now, though, we have to be careful in regulating immune therapies, and get better at understanding the intricate dance between cancers and our immune systems.

Sri Krishna is PhD Candidate, Biological Design, School of Biological and Health Systems Engineering at Arizona State University.

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

Why Honey Bees Are Essential to a Healthy Lifestyle

Healthy food and honey bees are greatly intertwined – they have been for thousands of years. In fact, large-scale honey bee cultivation has been traced back to the 10^th century BCE in Israel, where beekeepers harvested honey, honeycomb, and beeswax. Of course, taste had a lot to do with it, but honey bee products such as propolis are still used today to treat topical infections. Even bee venom is being investigated for its potential use to relieve the symptoms associated with Parkinson’s disease.

Yet when people think of the many health benefits of honey bees, they don’t often consider their role when it comes to balanced nutrition. As one of the most prolific pollinators, honey bees are an integral aspect of modern sustainable agriculture, pollinating roughly one-third of the world’s crops. In other words, without honey bees, it wouldn’t be possible for us to enjoy some of our favorite fruits and vegetables—both of which are important components of a balanced meal.

It’s a big responsibility for such tiny creatures. And because we largely rely on honey bees for our collective livelihood, it’s important to keep them healthy. That is why Monsanto is proud to be a member of the Honey Bee Health Coalition which is working with beekeepers, farmers, researchers, conservation groups, governmental agencies, and a variety of others to collaboratively implement solutions to improve honey bee health. This coalition—and others like it—are focusing their efforts on finding solutions to address the multiple factors impacting honey bee health and ensure that honey bees can thrive.

from Webmd.com

Posted by Mike Urinzwenimana

2Easy Meals for Families

Make time for dinner

children-mother-healthy-meal-400x400 — Children mother healthy meal

Eating meals together as a family has a range of benefits. Research shows that it boosts kids’ grades, leads to healthier eating habits, and (believe it or not) helps relieve parental stress.

In the following slideshow, we’ve assembled 20 healthy, easy-to-prepare meals that families can enjoy together. There’s enough pizza and pasta dishes to keep the kids happy, yet the interesting twists on old favorites will appeal to moms and dads.

Wagon Wheel Beef Soup

beef-soup-oh-1733687-l-400x400 — beef soup

On a cold night, this quick recipe is a crowd-pleaser for a family meal. Hearty and seasoned to perfection, the kids will love the wagon wheel pasta and spaghetti sauce, while lean ground round provides a rich salty flavor.

Ingredients: Wagon wheel pasta, ground round, onion, beef broth, spaghetti sauce, kidney beans.

Other way coming soon

From:HEALTH.COM

Mike urinzwenimana/Kigalihe.com

A dark night is good for your health

Richard Stevens, University of Connecticut

Today most people do not get enough sleep. The Centers for Disease Control and Prevention (CDC) has called insufficient sleep an epidemic. While we are finally paying attention to the importance of sleep, the need for dark is still mostly ignored.

That’s right. Dark. Your body needs it too.

Being exposed to regular patterns of light and dark regulates our circadian rhythm. Disruption of this rhythm may increase the risk of developing some health conditions including obesity, diabetes and breast cancer

Light regulates our sleep and wake patterns

The physiological processes that control the daily cycle of sleep and wake, hunger, activity levels, body temperature, melatonin level in the blood, and many other physiological traits are called the endogenous circadian rhythm.

Sunrise.
Mathilde AUDIAU, CC BY-NC-ND

On its own, the endogenous circadian rhythm is nearly, but not exactly, 24 hours. Our bodies rely on the Sun to reset this cycle and keep it at precisely 24 hours, the length of our days. The light – and the dark – are important signals for the cycle. This circadian rhythm has developed over three billion years as life evolved on Earth in the context of the Sun’s day/night cycle. It is built deeply into our genetic makeup.

During the night, in the dark, body temperature drops, metabolism slows, and the hormone melatonin rises dramatically. When the Sun comes up in the morning, melatonin has already started falling, and you wake up. This natural physiological transition into and out of night is of ancient origin, and melatonin is crucial for the process to proceed as it should.

If you were to put someone in a dark cave with no time cues at all, the cycle will last about 24 hours, but not exactly. Without time cues like those from the Sun, eventually that person would become out of sync with people outside. In fact many profoundly blind people, who cannot perceive light, must cope with this de-synchronization in their daily lives.

Dark is good.
Sign image via www.shutterstock.com.

What does your body do in the dark?

Many things happen to our bodies during the dark. Levels of the hormone leptin, which helps control hunger, go up. High levels of leptin mean we do not feel hungry while low levels make us hungry.

Why does leptin go up in the dark? Since we evolved without artificial light at night, one theory holds that leptin goes up at night because it would be good to not be hungry during the night, rather than needing to forage in the dark and possibly get into trouble.

This fasting that should happen every night, and why we call the first meal in the morning “breakfast.” Experiments in human beings have shown that sleep disruption and turning on lights lowers leptin levels which makes people hungry in the middle of the night.

In the last decade or two it has become clear that the genes which control the endogenous circadian rhythm (the “clock genes”) also control a large part of our entire genome including genes for metabolism (how we process the food we eat), DNA damage response (how we are protected from toxic chemicals and radiation), and cell cycle regulation and hormone production (how our cells and tissues grow).

Light at night disrupts these processes. The changes that result from exposure to electric light at night have biological connections to disease and conditions that are common in the modern world today including obesity, diabetes, cancer and depression.

Blue light from tablets can make it hard to fall asleep.
Boy with tablet via www.shutterstock.com

Blue light, red light, no light

Not all light is the same – some kinds of light make you more alert and more awake, and others have less of an effect.

Light from the Sun is strong in blue, short wavelength light, although it includes all other colors as well. That’s important in the morning when we need to be alert and awake. But when it comes in the evening or during the night, it fools the body into thinking it’s daytime. We now know that this bright blue light has the strongest effect on lowering melatonin during the night.

Your tablet, phone, computer or compact fluorescent lamp (CFL) all emit this kind of blue light. So using these devices in the evening can prevent that primordial physiological transition to night from occurring. This makes it harder to sleep and might also increase the longer term risk of ill-health.

Other kinds of light, like dimmer long wavelength yellow and red light, have very little effect on this transition. This is the kind of light from a campfire or a candle; even the old fashioned incandescent light bulb is dimmer and redder than the new CFL.

Only in the last 20 years have we acquired a basic biological understanding of how the eye’s retina tells the circadian system it is daytime. Now we know that blue, short wave-length light is captured by the newly discovered photopigment melanopsin in the retina, and that when blue light stops, we start our physiological transition to nighttime mode.

It’s hard to find dark, even at night.
NASA Earth Observatory, CC BY

Electricity changed the way we sleep

Before electricity, people experienced bright, full-spectrum days of sunlight and dark nights. We slept in a different way than we do now. The dark lasted about twelve hours and during this time people slept for eight or nine hours in two separate bouts, and were awake, but in the dark, for another three or four hours.

Everything changed when electric lighting was invented in the latter part of the 19th century. Since then there has been an ever increasing assault on dark. Outdoor environments are relentlessly lit, and more and more people use computer tablets and smart phones at all hours, bathing their faces in bright blue light at times of day when they should be transitioning to nighttime physiology.

When people get away from the city and its artificial light to go camping, they often notice a marked improvement in their sleep. A recent study has verified this effect.

Today, most of us get too little light during the day and too much at night for our circadian rhythm to function at its best. It is the rare person who sleeps in a completely dark bedroom, and many people get very little sunlight because they work inside all day long.

What can you do for your circadian health? Get bright, blue light in the morning (preferably from the Sun), and use dim, longer wavelength light (more yellow and red like incandescent) in the evening. And sleep in the dark.

This will certainly improve sleep, and may reduce risk of later disease.

Richard Stevens is Professor, School of Medicine at University of Connecticut.

This article was originally published on The Conversation.
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How long does it take to get an autism diagnosis?

Laura Crane, City University London and Elisabeth L Hill, Goldsmiths, University of London

Receiving a diagnosis of an autism spectrum disorder (ASD) has a major impact on an individual and their family. As well as providing an explanation for why a child might be experiencing certain difficulties, the diagnosis is generally thought of by parents as the point at which they can access support for themselves and their child.

But despite increased rates of autism, coupled with heightened public awareness of Autism Spectrum Disorder, our research shows that often it is actually getting the diagnosis which is proving to be a difficult and lengthy process.

We surveyed more than 1,000 parents in the UK who had experienced the diagnostic process for their child. We found that on average, parents had to wait three and a half years before their child got a confirmed diagnosis of ASD.

Given these lengthy delays, it is perhaps not surprising that just over half the parents we surveyed were dissatisfied with the diagnostic process as a whole – and most found the process stressful.

A stressful process

Children and adults with ASD have difficulties interacting socially and show unusually repetitive behaviours, interests or routines. ASD can affect different people in different ways.

Until very recently, children and adults on the autism spectrum received different labels, such as “classic autism” or “Asperger syndrome”, to explain their behaviours. However, in recent years – and not without controversy – there has been a move towards providing a more generic label to anyone displaying the key signs of ASD.

ASD is not rare. UK figures estimate that it affects around one in 100 people. More recent statistics from the US suggest this figure could be as high as one in 68. Public awareness of ASD is increasing too – from high-profile celebrities revealing that they or their children are on the autism spectrum, to popular awareness-raising campaigns led by charities, almost everyone feels they know about autism. So if many of us now know much more about it, why does diagnosis take so long?

‘Autism’ or ‘Asperger syndrome’

Although our results showed that some parents waited around three and a half years to get their child’s ASD diagnosis confirmed, this varied widely – some parents were able to get their child diagnosed almost straight away, whereas others had to wait several years. Looking at our results more closely, this seemed to be linked to the type of ASD that the children had.

Children assigned the label “autism’ were diagnosed much quicker than children with the label “Asperger syndrome”. This is probably because the signs of Asperger syndrome are more subtle than the signs of autism.

When a parent flags that their child isn’t talking at the age of two, and they aren’t engaging socially with their parents (as is often the case for those with autism), alarm bells start to ring. But when a child is speaking fluently and achieving their developmental milestones (as commonly found in children with Asperger syndrome), parents and professionals may overlook their social awkwardness or dismiss their autistic behaviours as “quirks”. It may not be until several years later, perhaps when the child starts school, that the challenges associated with their autism become apparent.

What needs to be done?

Although our survey showed that parents were very astute to the early signs that their child was developing differently, healthcare professionals didn’t always act on these concerns.

Labelling issues.
Label by Shutterstock

In many cases this was due to service inefficiencies. Occasionally, it was in the child’s best interests to wait and see whether the behaviours changed over time – effectively delaying a diagnosis – to avoid the risk of labelling a child who later outgrows these behaviours.

This is at odds with the views of parents, who want the diagnostic process to be quicker and easier. This is because parents feel that the autism label will get them the help and support that their child needs. This emphasises the need for parents and professionals to have a more open dialogue during the diagnostic process.

From label to need

Moving towards a system where the provision of services is based on addressing the specific needs of the child, rather than relying on a label, would help overcome this. This is perhaps easier to implement in the UK than in other parts of the world; in the US, for example, a diagnosis is needed in order to access healthcare insurance for any interventions.

We also mustn’t forget that autism is not a childhood condition. A growing number of adults are recognising that they might be on the autism spectrum and are seeking a diagnosis later in life. The same issues still apply. Although there is some indication that the situation is improving for autistic adults (for example the process is getting quicker), we still have a long way to go.

In a parallel survey that we ran, considering the diagnostic experiences of adults, the lack of awareness of autism among front-line healthcare professionals was also highlighted. One woman who took part in this survey recalled how she approached her doctor to suggest she was on the autism spectrum and was met with the response: “Why would a nice lady like you want a diagnosis like that?”

Moving forward

Efforts are being made to improve the diagnostic process here in the UK. The Autism Act 2009, which aimed to improve services for the autism community, was heralded as a landmark piece of legislation. It led to the subsequent autism strategy for England in 2014, which provides statutory guidance concerning the autism diagnostic process. This includes the need for specialist autism training to be provided for key staff (for example, family doctors), and for the development of a clear pathway to diagnosis and assessment for children and adults with autism. Guidelines from NICE also aim for a consistent approach to referral and diagnosis across the UK.

How successful have these initiatives been? Only time will tell. But more than anything else, we need to continue consulting parents and autistic people about how their needs can be met, while including healthcare professionals in this dialogue. It is only by addressing the concerns of different groups – along with the guidance – that we can continue to improve the autism diagnostic process.

Laura Crane is Research Fellow at City University London.
Elisabeth L Hill is Professor of Neurodevelopmental Disorders at Goldsmiths, University of London.

This article was originally published on The Conversation.
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How Nigeria beat the ebola virus in three months

Folasade Ogunsola, University of Lagos

The diagnosis of the first case of Ebola in Lagos, Nigeria in July last year set off alarm bells around the world. The fear was that it would trigger an apocalyptic epidemic that would make the outbreaks in Liberia, Sierra-Leone and Guinea, where 1322 cases were reported and 728 people had died within five months, pale in comparison.

This fear was very justifiable. Lagos has a population of over 21 million with a population density in built up areas of about 20 000 people per square kilometre. In some areas it is as high as 50 000 people per sq km.

But within three months, the most densely populated country on the continent had managed to contain the deadly virus with only eight deaths. By October 20 the World Health Organisation declared Nigeria ebola free.
In stark contrast, fourteen months after the first case of ebola was declared in Liberia, the country is celebrating the announcement that it is ebola free.

A combination of factors enabled Nigeria to contain the virus in such a short space of time. These included fast thinking on the part of government, a tried and tested tracking system, pooled expertise and assistance from national and international agencies.

The killer game plan

The disease was brought into the country on July 20 by Patrick Sawyer, a Liberian-American financial consultant. Sawyer initially denied exposure to ebola. He was treated for presumed malaria after suffering from a fever, vomiting and diarrhoea.

Sawyer died five days after his arrival. By then he had triggered a line of exposure. By September, 20 people had been infected. Twelve of whom were in Lagos state and eight in Rivers state. Seven more subsequently died.

In the week that Sawyer was diagnosed, an emergency operation centre was set up. At its core was the system Nigeria had developed for its war against polio and lead poisoning. The deputy manager of the polio campaign was brought in to head the Ebola response team and operations were rapidly scaled up.

The success of the system lies in a strong coordinating team that supervises house-to-house surveillance. A team of 40 trained epidemiologists and 150 contact tracers was mobilised. They drew up a list of all Sawyer’s contacts and those of the subsequent Ebola cases. Locations were mapped and hot spots identified. Fifty teams of contact tracers did house-to-house, in-person visits within a radius of each Ebola contact. In total, they visited 26 000 households in Lagos and Rivers States.

Aside from an initial case assessment, the team also managed the data, infection alerts and rumours, and implemented community-based surveillance.

Five other units backed up their work. These included strategy and coordination, case management and infection control, social mobilisation, laboratory services and points of entry.

The strategy team coordinated the activities of the ministries of health and the international partners, dealt with the media and ensured funding, administrative and logistic support. The social mobilisation team worked on advocacy, dealing with issues of stigma, the psychological and social well-being of contacts and the reintegration of discharged patients into their communities.

One of the six units that formed part of the incident manager system, was a social mobilisation team that ensured information leaving the Ebola operation centre was accurate.
Afolabi Sotunde/Reuters

All ports of entry were monitored. The temperature of everyone passing through airports, seaports and land borders were checked for potential exposure.

The case management and infection control team treated and managed every laboratory-confirmed or suspected case. Their job was also to prevent the infection being transmitted. This involved training health care workers at treatment centres and health care facilities on how to take precautions and set up screening centres. They also focused on ensuring safe burials.

Good fortune played a part

Good fortune also played a part in limiting the impact of the Sawyer case. Although he had contact with 72 people in the two days before the virus was suspected, only 20 became infected.

It was also fortunate that Sawyer arrived by plane rather than on congested public transport. If he had travelled by land he would have been in close proximity to a great many more people. Passengers would have got on and off at stops along the way, increasing the risk of exposure significantly.

His diplomatic status was also a major bonus. It meant that he was taken straight to a private hospital by diplomatic staff where he was nursed in a private room and diagnosed by an astute clinician.

It was also good fortune that Sawyer landed in Lagos state which has a disease surveillance system in place and facilities at the federal teaching hospital to make the laboratory diagnosis.

Managing the message to kill the panic

In the hours and days following news of Sawyer’s diagnosis, fear, myths and rumours spread like wild fire. Much of this was fanned by the press. This led to health care workers refusing to treat any bleeding or feverish patients.

The strategy team brought things under control by engaging the media, communities and key opinion leaders. A multi-pronged plan was put in place. Health care workers in communities were given hands on training about standard precautions and infection prevention. Protective equipment was also made available to health care centres in the communities.

Simple messages were developed that considered the available resources at health care facilities. In some instances, it was as basic as placing a chair at the end of a hospital corridor and cordoning off an area so that suspected cases could be isolated from other patients.

There was also a concerted effort to educate the media and to keep people informed. Daily briefings on patient recovery helped reduce fear.

Despite the tragedy, the ebola outbreak proved how important it is to rapidly respond to an outbreak with a unified plan, backed up with expertise, manpower and a health system with effective infection controls.

But equally important was the lesson in national unity evident in the unprecedented co-operation between the Nigerian public and private sectors, teaching hospitals, universities and volunteers. It was a massive team effort led by Nigerians assisted by the international agencies. Nigeria proved the pundits wrong.

Folasade Ogunsola is Professor of Clinical Microbiology at University of Lagos.

This article was originally published on The Conversation.
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