More than 25 million people dying in agony without morphine every year

Concern over illicit use and addiction is putting morphine out of reach for millions of patients globally who need it for pain relief

More than 25 million people, including 2.5 million children, die in agony every year around the world, for want of morphine or other palliative care, according to a major investigation.

Poor people cannot get pain relief in many countries of the world because their needs are overlooked or the authorities are so worried about the potential illicit use of addictive opioids that they will not allow their importation.

Staring into this access abyss, one sees the depth of extreme suffering in the cruel face of poverty and inequity, says a special report from a commission set up by the Lancet medical journal.

In Haiti, for instance, says the report, there are no nursing homes or hospices for the dying and most have to suffer without pain relief at home.

Patients in pain from trauma or malignancy are treated with medications like ibuprofen and acetaminophen, says testimony from Antonia P Eyssallenne of the University of Miami School of Medicine. Moreover, nurses are uncomfortable giving high doses of narcotics even if ordered to do so for fear of being responsible for the patients death, even if the patient is terminal.

Death in Haiti is cruel, raw, and devastatingly premature. There is often no explanation, no sympathy, and no peace, especially for the poor.

A doctor in Kerala, India, which has a palliative care service, told of the arrival of a man in agony from lung cancer. We put Mr S on morphine, among other things. A couple of hours later, he surveyed himself with disbelief. He had neither hoped nor conceived of the possibility that this kind of relief was possible, said Dr M R Rajagopal.

But when he returned, morphine stocks were out. Mr S told us with outward calm, I shall come again next Wednesday. I will bring a piece of rope with me. If the tablets are still not here, I am going to hang myself from that tree. He pointed to the window. I believed he meant what he said.

The commissions three-year inquiry found that nearly half of all deaths globally 25.5 million a year involve serious suffering for want of pain relief and palliative care. A further 35.5 million people live with chronic pain and distress. Of the 61 million total, 5.3 million are children. More than 80% of the suffering takes place in low and middle-income countries.

Jim Yong Kim, president of the World Bank, said things had to change. Failure of health systems in poor countries is a major reason that patients need palliative care in the first place. More than 90% of these child deaths are from avoidable causes. We can and will change both these dire situations.

Morphine is hard to obtain in some countries and virtually unobtainable in others. Mexico meets 36% of its need, China meets 16%, India 4% and Nigeria 0.2%. In some of the worlds poorest countries, such as Haiti, Afghanistan and many countries in Africa, oral morphine in palliative care is virtually non-existent.

Oral and injectable morphine is out of patent, but costs vary widely and it is cheaper in affluent countries like the USA than in poor countries. A second issue is opiophobia the fear that allowing the drugs to be used in hospitals will lead to addiction and crime in the community.

The world suffers a deplorable pain crisis: little to no access to morphine for tens of millions of adults and children in poor countries who live and die in horrendous and preventable pain, says Professor Felicia Knaul, co-chair of the commission from the University of Miami, calling it one of the worlds most striking injustices.

Knaul says she only realised that many people suffered without pain relief when she was working to improve access to cancer treatment in low-income countries. I was shocked. I had no idea. When people were showing me the data I thought it cant be in this world, she told the Guardian.

She had also experienced the need for morphine herself after a mastectomy for breast cancer. When I woke up I couldnt breathe because the pain was so bad. If they hadnt arrived with the morphine I dont know how I would have got through it. And as a young girl in Mexico, she had to watch her father suffer as he died without pain relief.

I dont think that we have cared enough about poor people who have pain, she said. It doesnt make them live any longer. It doesnt make them more productive. It is simply the human right of not suffering any more pain and we dont care about that for people who are poor.

The commission recommends that all countries put in place a relatively inexpensive package of effective palliative care for end of life conditions that cause suffering, including HIV, cancers, heart disease, injuries and dementia.

One of their most emphatic recommendations, says Knaul, is that immediate-release, off-patent, morphine that can cost just pennies should be made available in both oral and injectable formulations for any patient with medical need. The disparity and access abyss between the haves and have-nots is a medical, public health and moral injustice that can be effectively addressed by the commissions recommendations.

Read more: https://www.theguardian.com/science/2017/oct/12/more-than-25-million-people-dying-in-agony-without-morphine-every-year

How your blood may predict your future health

New research into bloodstream biomarkers aims to unlock the full impact of social status on peoples lifetime health outcomes. The key is exposure to stress

Health is a well-known inequality issue. While ageing is inevitable and most of us will get sick at some point, the rate of your decline is likely to be faster the lower down the socioeconomic ladder you started.

The intriguing thing is, nobody exactly knows why. Tempting though it is to blame the usual suspects poor diet, obesity, smoking they dont account for the whole story.

If you exactly knew somebodys diet, exercise level, smoking habit or alcohol consumption, you would be about 30 to 40% likely to accurately predict how long they are going to live, says Mel Bartley, professor emerita of medical sociology at University College London, who has dedicated her career to understanding the links between society and health. But whats the rest? Thats the big question.

Unpicking the biological connections between external socioeconomic forces and an individuals health is no easy task. But Bartley and others in her field believe important clues can be found in the very lifeblood of a nation.

The idea that measurable biological markers (biomarkers) in the bloodstream can reflect an individuals underlying health status and even offer some kind of prediction of their life expectancy gained popularity in the 1950s, as scientists started searching for tell-tale markers linked to the epidemic of heart disease spreading through the US.

High blood pressure was the obvious one, but they also discovered that the level of bad cholesterol in the bloodstream was a good indicator of risk. By monitoring blood cholesterol levels in healthy people before they show any outward signs of heart disease, doctors can predict who is most at risk. The resulting medical interventions, such as dietary changes and statin drugs, can demonstrably improve those peoples long-term health.

Now, researchers are using the same approach to measure the impact of social status on the body, in the hope of developing policies that can reduce the health toll on societys most deprived section (on average, the poorest people in the UK miss out on more than a decade of life compared with the richest).

One of the most ambitious projects, currently being undertaken by the University of Essexs Institute for Social and Economic Research (ISER), is looking at blood biomarkers from some of the 40,000 UK households taking part in its Understanding Society study, which covers the entire socioeconomic spectrum.

A biomarker is an objective measure of health, explains Professor Meena Kumari, the epidemiologist leading the study along with health economist Dr Apostolos Davillas. These chemicals are like molecular flags: they allow us to see what happens inside people as theyre going through their life course which they themselves might not be so aware of.

According to Kumari, Whats happened historically is that social scientists have tended to measure health in a simple way just asking people: How do you rate your health right now? But we wanted to bring together the biology and the social science.

Published in the journal Scientific Reports, the ISER teams initial analysis focused on measuring the levels of two molecules, fibrinogen and C-reactive protein (CRP), that are produced by inflammation the bodys response to infections, stress and other harmful stimuli. Chronic long-term inflammation is linked to poorer health outcomes including heart disease, diabetes and cancer.

According to Davillas and Kumari, measuring an individuals CRP and fibrinogen levels and matching them against their socioeconomic position starts to reveal the hidden mechanisms connecting social inequality and health. And the missing link appears to be stress.

The impact of chronic stress

When we experience something stressful, we activate the hypothalamic pituitary adrenal axis: a convoluted network involving the brain and the pituitary and adrenal glands. This results in the release of cortisol and other stress hormones such as adrenaline, which have a range of effects on the body.

The complex biological conversation between this stress response and the bodys inflammatory processes actually damps down inflammation in the short term. But this careful balance seems to shift in the face of chronic stress, resulting in more inflammation over time. Thus the levels of CRP and fibrinogen, as markers of chronic inflammation, are a proxy for the impact of long-term stress on a persons body.

CRP
CRP levels at different ages by household income, left, and education. Photograph: Davillas et al/Scientific Reports

For Kumari and Davillass biomarker study, blood samples were gathered from nearly 8,000 adults in the Understanding Society cohort. While CRP and fibrinogen levels increase in all of us as we age, the ISER team found that differences in the levels of CRP and fibrinogen between socioeconomic groups begin to show relatively early in life and on average rise faster and peak sooner in poorer people.

The research shows differences in CRP levels start around 30 years old and peak around the age of 55, Davillas says. Then the gap starts to narrow again theres not so much difference between the lowest and highest socio-economic groups in later life, although of course the social inequalities are still there. People in both groups end up with similar CRP readings by their mid-70s.

The analysis suggested people in lower socioeconomic groups have a demonstrably longer exposure to chronic inflammation with all its knock-on impacts on long-term health even once the team corrected for the usual suspects of health inequality, including diet and smoking. Theres clearly something else at work.

If you ask people about their health, you dont really see differences early in life people tend to become unhealthy later in life, Kumari says. But were starting to see these underlying biomarker differences in people in their 30s; so whats that about?

Fibrinogen
Fibrinogen levels at different ages by household income, left, and education. Photograph: Davillas et al/Scientific Reports

Kumari and Davillas are now considering the causes of chronic stress that might contribute to the patterns they have found, starting with employment or lack of it and the associated issues of poor pay, job insecurity, long hours and the burgeoning gig economy.

You have stressful life events such as bereavement or divorce, but were talking about understanding chronic long-term stresses, Kumari says. One of the things we think about is why is disadvantage stressful? For something like low income, it could be because you dont have the same levels of control over your life. Maybe you can manage it for a little while, but over the long term it becomes a chronic stress. These things are hard to measure and capture.

Bartley agrees more needs to be done to understand the financial causes of stress across society. Debt is deadly for people its the ultimate lack of control, she says. Housing is also a huge issue and it doesnt get researched enough living in poor situations is depressing, especially if youre bringing up children. People in poverty can end up in social isolation, and thats known to be associated with all kinds of unhealthy outcomes.

Changes in policy

Its all very well to be able to measure levels of inflammatory biomarkers, and link them to stress and worse health outcomes but the big question is what to do about it. If its as simple as lowering inflammation, then maybe we should just hand out anti-inflammatory drugs such as aspirin to poorer people?

I dont believe thats the answer, says Bartley. We need to understand what it is about living in a tougher social and economic situation that causes this underlying stress, in order to argue for more effective changes in policy.

From a policy perspective, if you know when health inequalities begin and when they peak, this can help you target these age groups and allocate resources more effectively, says Davillas, pointing to the example of retirement timing. If youre doing a stressful job and this impacts your health more compared to someone in a less stressful occupation, this is an important issue to consider from a public health perspective. Perhaps people in more stressful jobs should retire earlier.

Measuring biomarkers across society could also give researchers a way of monitoring the impact of policy interventions. But to do that effectively will require a lot more data. While the ISER teams findings suggest a link between inflammation, stress and poor health outcomes in the most disadvantaged sectors of society, the study is only a snapshot of biomarker levels in individuals of different ages at one point in time. Whats really needed is detailed, long-term research, monitoring and following people over decades as their lives change.

If we have 30-year-olds with high CRP, we want to know what happens to them five years later, says Bartley. We need to study people over their whole life course to find out if that early high CRP reading is fixed, and does high CRP at age 30 condemn someone to get sicker faster later on or does their health outcome change if they improve their situation and lower their stress levels?

The challenge with this long-term approach is finding ways of measuring biomarkers in large numbers of people across the full spectrum of society. It would be good if we could collect them by some electronic means, instead of having to stick needles in people for blood samples, Bartley speculates. Theres a lot of scope for improvements in technology such as mobile phones, in terms of understanding how society gets under the skin.

The ISER study also highlights another striking issue: the general lack of research focuses on people in midlife a time when life paths can become entrenched.

There are a lot of studies looking at older age groups, because thats when people get sick, and lots involving children because child development is interesting, but theres not a lot going on in the middle of the age span, Kumari says. And yet we found the difference between biomarker levels was biggest in working age groups, where we have the least amount of data.

Understanding the underlying biological pathways will help us to target what it is we should be focusing on. Our data suggest that it might be stress that we need to be thinking about, particularly for working age people. But this is just the beginning theres still a lot to do.

Share your experiences by emailing inequality.project@theguardian.com, or follow the Guardians Inequality Project on Twitter here

Read more: https://www.theguardian.com/inequality/2017/oct/10/how-your-blood-may-predict-your-future-health-biomarkers

‘Western society is chronically sleep deprived’: the importance of the body’s clock

The 2017 Nobel prize for medicine was awarded for the discovery of how our circadian rhythms are controlled. But what light does it shed on the cycle of life?

The cycle of day and night on our planet is age-old and inescapable, so the idea of an internal body clock might not sound that radical. In science, though, asking the questions why? and how? about the most day-to-day occurrences can require the greatest leaps of ingenuity and produce the most interesting answers.

This was the case for three American biologists, Jeffrey Hall, Michael Rosbash and Michael Young, who earlier this week were awarded the Nobel in medicine or physiology, for their discovery of the master genes controlling the bodys circadian rhythms.

The first hints of an internal clock came as early as the 18th century when the French scientist Jean-Jacques dOrtous de Mairan noticed that plants kept at a steady temperature in a dark cupboard unexpectedly maintained their daily rhythm of opening and closing their leaves. However, De Mairan himself concluded this was because they could sense the sun without ever seeing it.

It was only when Hall, Rosbash and Young used fruit flies to isolate a gene that controls the rhythm of a living organisms daily life that scientists got the first real glimpse at our time-keeping machinery that explains how plants, animals and humans adapt their biological rhythm so that it is synchronised with the Earths revolutions, the Nobel prize committee said.

Using fruit flies, the team identified a period gene, which encodes a protein within the cell during the night which then degrades during the day, in an endless feedback cycle.

Prof Robash, 73, a faculty member at Brandeis University in Waltham, Massachussetts, said that when his paper was published in the 1980s he had no grandiose thoughts about the importance of the discovery. During the intervening years, the picture has changed.

Its [now] pretty clear that it has its fingers in all kinds of basic processes by influencing an enormous fraction of the genome, he said.

Scientists discovered the same gene exists in mammals and that it is expressed in a tiny brain area called the suprachiasmatic nucleus, or SCN. On one side, it is linked to the retina in the eye, and on the other side it connects to the brains pineal gland, which pumps out the sleep hormone melatonin.

Modern lifestyles may no longer be constrained by sunrise and sunset, but light remains one of the most powerful influences on our behaviour and wellbeing. This realisation has fuelled a sleep hygiene movement, whose proponents point out that bright lights before bedtime and spending the whole day in a dimly lit office can dampen the natural circadian cycle, leaving people in a continual mental twilight dozy in the morning, and too alert to fall asleep promptly at night.

Rosbash welcomes this new awareness. Its been overlooked for a long time as a real public health problem, he said. All of western society is a little bit sleep deprived and, when I say a little bit, I mean chronically.

There is growing evidence that this decoupling from the natural circadian cycle can have long-term health consequences much more far-reaching than tiredness.

At first, it was assumed that the brains master clock was the bodys only internal timekeeper. In the past decade, though, scientists have shown that clock genes are active in almost every cell type in the body. The activity of blood, liver, kidney and lung cells in a petri dish all rise and fall on a roughly 24-hour cycle. Scientists have also found that the activity of around half our genes appear to be under circadian control, following undulating on-off cycles.

In effect, tiny clocks are ticking inside almost every cell type in our body, anticipating our daily needs. This network of clocks not only maintains order with respect to the outside world, but it keeps things together internally.

Virtually everything in our body, from the secretion of hormones, to the preparation of digestive enzymes in the gut, to changes in blood pressure, are influenced in major ways by knowing what time of day these things will be needed, said Clifford Saper, a professor of neuroscience at Harvard Medical School. The most common misconception is that people think that they do not have to follow the rules of biology, and can just eat, drink, sleep, play, or work whenever they want.

This discovery explains why jet lag feels so grim: the master clock adapts quickly to changing light levels, but the the rest of your body is far slower to catch up and does so at different speeds.

Jet lag is so awful because youre not simply shifted, but the whole circadian network is not aligned to each other, said Prof Russell Foster, chair of circadian neuroscience at the University of Oxford. If you were completely aligned but just five hours shifted you wouldnt feel so crappy.

It is also helps explain the extensive range of health risks experienced by shift workers, who are more likely to suffer from heart disease, dementia, diabetes and some cancers. Theyre having to override their entire biology, said Foster.

Obesity is also more common among those with irregular sleep patterns. Sapers team has found that animals that dont get enough sleep, but keep their circadian pattern, do not gain weight. But when they are placed on a 20-hour light-dark cycle, they eat more impulsively and develop glucose intolerance.

I would suggest that for humans, staying up late, watching video screens with high levels of blue light and eating high fat foods, is potentially a major cause of obesity and diabetes, said Saper.

Evidence is also emerging that our risk of acute illness rises and falls with a predictable regularity. People are 49% more likely to suffer a stroke between 6am and 12 noon than at any other time of the day and a similar pattern is true for heart attacks. This is linked to a circadian rise in blood pressure in the early morning, which happens even if youre lying in bed not doing anything.

As a result, it makes sense to take certain blood pressure medications first thing, before getting out of bed. By contrast, cholesterol is made more rapidly by the liver at night. So, statins, which lower cholesterol, work best if taken before going to bed.

Foster said that a failure to consider the circadian influence in past animal experiments may even have led to promising drug candidates being shelved. Toxicity can change from 20% to 80% depending on the time of the day you test a drug, he said.

As the impact of scientific advance slowly trickles down, the medical profession and society at large are waking up to the power of the biological clock.

A paper last year showing that jet lag impairs baseball performance, prompted some professional sports teams to take on circadian biologists as consultants on schedules for training and travel. The US Navy has altered its shift system to align it with the 24-hour clock, rather than the 18-hour day used in the old British system. Schools are experimenting with later school days, better aligned with the teenage body clock, which runs several hours later than that of adults.

As circadian rhythms have journeyed from obscure corner of science to part of the zeitgeist, companies are launching an increasing number of products on the back of a new anxiety around sleep and natural cycles. This is the western world; if somebody can make a buck theyre going to try to do it, said Rosbash.

The 73-year-old, who describes his own relationship with sleep as borderline problematic, prefers low- tech remedies, however.

I havent quite figured out how to do better, he said. I try not to take sleep medication. I dont drink alcohol too late in the evening, I read a good book. The common sense things, I think they help.

Read more: https://www.theguardian.com/science/2017/oct/06/western-society-is-chronically-sleep-deprived-the-importance-of-the-bodys-clock

Could a drug that mimics a zero-carb diet help us live longer, healthier lives?

Researchers hope to develop a medication that mimics a diet stripped of carbohydrate, after two studies showed clear benefits in mice

A drug that mimics a zero-carbohydrate diet could help people live longer, healthier lives and have better memories in old age, US researchers claim.

Scientists hope to develop a medication after two independent studies showed that mice fed on a diet stripped of all carbohydrate lived longer and performed better on a range of physical and mental tasks than those that had regular meals.

Because the diet is hard to stick to, the researchers are working on a compound that aims to deliver the same benefits for humans. If they are successful, it would amount to an extra seven to ten years of life on average, and protection against the weakening muscles and faltering memories that are defining aspects of human ageing.

Im excited about this, and its hard not to be after what weve seen that it does. These are pretty profound effects, said Eric Verdin, a physician who led one of the studies at the Buck Institute for Research on Aging in California.

The zero carb diet was designed to induce a dramatic change in metabolism, by fooling the mice into thinking they were fasting. When deprived of carbohydrate, the body shifts from using glucose as its main energy source to burning fat and producing chemicals in the liver known as ketone bodies.

In 2013, Verdin showed that a ketone body called BHB served as fuel in the body and might also protect animals against the microscopic damage that builds up in cells as part of the natural ageing process.

In a new study published in the journal Cell Metabolism, Verdin and his colleagues describe how they fed one-year-old mice either a normal high-carbohydrate diet; a high-fat, low-carb diet; or a high-fat, zero-carb diet, also known as a ketogenic diet. They found that mice on the zero-carb diet were more likely to reach old age and scored better on memory tasks than those on the other diets.

Similar benefits of the ketogenic diet were seen in a separate study by scientists at the University of California in San Diego. Megan Roberts and others found that mice fed on a zero-carbohydrate diet lived 13% longer, reaching an average age of 1,003 days compared with 886 days for mice given standard meals.

But while the zero-carb diet appeared to benefit mice, its health effects have yet to be proven in humans. To make up the calories, the mouse diet contained 90% fat, which could be dangerous for humans to adopt.

Stephen ORahilly, director of the Metabolic Research Laboratories at Cambridge University, said high-fat diets drive up LDL or bad cholesterol in humans, and so raise the risk of heart disease. Mice dont really use LDL cholesterol in the first place, so it doesnt have that bad impact on them, he said.

The work could still lead to valuable insights though. We may be able to learn from these studies what some of the pathways are that this sort of diet influences to keep mice somewhat generally healthier as they age. But for it to be useful in humans we would have to somehow dissociate these effects from the adverse effects on circulating LDL cholesterol, ORahilly added.

Verdin said that the difficulty of sticking to the diet was a major reason his team was searching for drugs to mimic the its effects. Tests are underway on a compound that produces BHB in the body in the hope that it could be taken as a supplement, he said.

The biggest problem with the diet is that it is difficult to maintain as a lifestyle, Verdin said. Its an antisocial diet. You can hardly eat anything that most of us like.

Read more: https://www.theguardian.com/science/2017/sep/05/could-a-drug-that-mimics-a-zero-carb-diet-help-us-live-longer-healthier-lives

New heart treatment is biggest breakthrough since statins, scientists say

US researchers find heart attack survivors given anti-inflammatory injections have fewer future episodes and lower cancer risk

Anti-inflammatory injections could lower the risk of heart attacks and may slow the progression of cancer, a study has found, in what researchers say is the biggest breakthrough since the discovery of statins.

Heart attack survivors given injections of a targeted anti-inflammatory drug called canakinumab had fewer attacks in the future, scientists found. Cancer deaths were also halved in those treated with the drug, which is normally used only for rare inflammatory conditions.

Statins are the mainstay drugs for heart attack prevention and work primarily by lowering cholesterol levels. But a quarter of people who have one heart attack will suffer another within five years despite taking statins regularly. It is believed this is because of unchecked inflammation within the hearts arteries.

The research team, led from Brigham and Womens hospital in Boston, tested whether targeting the inflammation with a potent anti-inflammatory agent would provide an extra benefit over statin treatment.

The researchers enrolled more than 10,000 patients who had had a heart attack and had a positive blood test for inflammation into the trial, known as the Cantos study. All patients received high doses of statins as well as either canakinumab or a placebo, both administered by injection every three months. The trial lasted for four years.

For patients who received the canakinumab injections the team reported a 15% reduction in the risk of a cardiovascular event, including fatal and non-fatal heart attacks and strokes. Also, the need for expensive interventional procedures, such as bypass surgery and inserting stents, was cut by more than 30%. There was no overall difference in death rates between patients on canakinumab and those given placebo injections, and the drug did not change cholesterol levels.

Dr Paul Ridker, who led the research team, said the study ushers in a new era of therapeutics.

For the first time, weve been able to definitively show that lowering inflammation independent of cholesterol reduces cardiovascular risk, he said.

This has far-reaching implications. It tells us that by leveraging an entirely new way to treat patients targeting inflammation we may be able to significantly improve outcomes for certain very high-risk populations.

The hospital said the reductions in risk were above and beyond those seen in patients who only took statins.

Ridker said the study showed that the use of anti-inflammatories was the next big breakthrough following the linkage of lifestyle issues and then statins.

In my lifetime, Ive gotten to see three broad eras of preventative cardiology, he said. In the first, we recognised the importance of diet, exercise and smoking cessation. In the second, we saw the tremendous value of lipid-lowering drugs such as statins. Now, were cracking the door open on the third era. This is very exciting.

But there were some downsides to the treatment. The researchers reported an increase in the chances of dying from a severe infection of about one for every 1,000 people treated, although this was offset by an unexpected halving of cancer deaths across all cancer types. In particular, the odds of succumbing to lung cancer were cut by over 75%, for reasons the team do not yet understand. The researchers are planning further trials to investigate canakinumabs potentially protective effect against cancer.

Prof Martin Bennett, a cardiologist from Cambridge who was not involved in the study, said the trial results were an important advance in understanding why heart attacks happen. But, he said, he had concerns about the side effects, the high cost of the drug and the fact that death rates were not better in those given the drug.

Treatment of UK patients is unlikely to change very much as a result of this trial, but the results do support investigation of other drugs that inhibit inflammation for cardiovascular disease, and the use of this drug in cancer, he said.

Prof Jeremy Pearson, associate medical director at the British Heart Foundation, was optimistic about the trial opening the door to new types of treatment for heart attacks.

Nearly 200,000 people are hospitalised due to heart attacks every year in the UK, Pearson said. Cholesterol-lowering drugs like statins are given to these people to reduce their risk of another heart attack and this undoubtedly saves lives. But we know that lowering cholesterol alone is not always enough.

These exciting and long-awaited trial results finally confirm that ongoing inflammation contributes to risk of heart disease, and [lowering it] could help save lives.

Read more: https://www.theguardian.com/science/2017/aug/27/anti-inflammatory-drugs-may-lower-heart-attack-risk-study-finds

Forget five a day, eat 10 portions of fruit and veg to cut risk of early death

Scientists say even just 2.5 portions daily can lower chance of heart disease, stroke, cancer and premature death

Five portions of fruit and veg a day is good for you, but 10 is much better and could prevent up to 7.8 million premature deaths worldwide every year, say scientists.

The findings of the study led by Imperial College London may dismay the two in three adults who struggle to manage three or four portions perhaps some tomatoes in a sandwich at lunchtime, an apple and a few spoonfuls of peas at dinner.

All of that is good because a daily intake of even 200g, or two and a half standard 80g portions, is associated with a 16% reduced risk of heart disease, an 18% reduced risk of stroke, a 13% reduced risk of cardiovascular disease, 4% reduced risk of cancer and a 15% reduction in the risk of premature death.

But the study suggests we should be piling up platefuls of vegetables and raiding the fruit bowl every day if we want the best chance of avoiding chronic diseases or an early death.

We wanted to investigate how much fruit and vegetables you need to eat to gain the maximum protection against disease, and premature death. Our results suggest that although five portions of fruit and vegetables is good, 10 a day is even better, said Dr Dagfinn Aune, lead author of the research from the School of Public Health at Imperial.

Eating up to 800g of fruit and vegetables equivalent to 10 portions and double the recommended amount in the UK was associated with a 24% reduced risk of heart disease, a 33% reduced risk of stroke, a 28% reduced risk of cardiovascular disease, a 13% reduced risk of total cancer, and a 31% reduction in premature deaths.

What does 800g look like?

And not all fruit and veg are created equal. Apples and pears, citrus fruits, salads and green leafy vegetables such as spinach, lettuce and chicory, and cruciferous vegetables such as broccoli, cabbage and cauliflower were found to be best at preventing heart disease and stroke.

To reduce the risk of cancer, however, the menu should include green vegetables, such as green beans; yellow and orange vegetables such as peppers and carrots; and cruciferous vegetables.

The researchers did not find any difference between the protective effects of cooked and raw fruit and vegetables.

Fruit and vegetables have been shown to reduce cholesterol levels, blood pressure, and to boost the health of our blood vessels and immune system, said Aune. This may be due to the complex network of nutrients they hold. For instance they contain many antioxidants, which may reduce DNA damage, and lead to a reduction in cancer risk.

Compounds called glucosinolates in cruciferous vegetables, such as broccoli, activate enzymes that may help prevent cancer. Fruit and vegetables may also have a beneficial effect on the naturally occurring bacteria in our gut, he said.

Toddler
Most people struggle to eat three or four portions a day, the study shows. Photograph: Simon Masters/Getty Images/Vetta

And it will not be possible to bottle the effects of fruit and vegetables or put them in a pill, he said. Forget the supplements. Most likely it is the whole package of beneficial nutrients you obtain by eating fruits and vegetables that is crucial to health, he said. This is why it is important to eat whole plant foods to get the benefit, instead of taking antioxidant or vitamin supplements (which have not been shown to reduce disease risk).

The analysis in the International Journal of Epidemiology pooled the results from 95 different studies involving a total of approximately 2 million people. They assessed up to 43,000 cases of heart disease, 47,000 cases of stroke, 81,000 cases of cardiovascular disease, 112,000 cancer cases and 94,000 deaths.

Aune said more research was needed, but it is clear from this work that a high intake of fruit and vegetables hold tremendous health benefits, and we should try to increase their intake in our diet.

Sarah Toule, from the World Cancer Research Fund, said: This interesting research shows just how incredibly important vegetables and fruit are as part of a healthy diet. In fact, theyre essential for maintaining a healthy weight, which our own evidence has shown reduces the risk of 11 common cancers.

People should aim to eat at least five portions of vegetables and fruit a day but the more the better. If people find this hard, why not start by adding an extra portion of fruit or veg a day to your lunch or try swapping one of your naughty snacks for a piece of fruit?

Read more: https://www.theguardian.com/society/2017/feb/23/five-day-10-portions-fruit-veg-cut-early-death

Eating cheese does not raise risk of heart attack or stroke, study finds

Consumption of even full-fat dairy products does not increase risk, international team of experts says

Consuming cheese, milk and yoghurt even full-fat versions does not increase the risk of a heart attack or stroke, according to research that challenges the widely held belief that dairy products can damage health.

The findings, from an international team of experts, contradict the view that dairy products can be harmful because of their high saturated fat content. The experts dismiss that fear as a misconception [and] mistaken belief.

The results come from a new meta-analysis of 29 previous studies of whether dairy products increase the risk of death from any cause and from either serious heart problems or cardiovascular disease. The study concluded that such foodstuffs did not raise the risk of any of those events and had a neutral impact on human health.

This meta-analysis showed there were no associations between total dairy, high- and low-fat dairy, milk and the health outcomes including all-cause mortality, coronary heart disease or cardiovascular disease, says the report, published in the European Journal of Epidemiology.

Ian Givens, a professor of food chain nutrition at Reading University, who was one of the researchers, said: Theres quite a widespread but mistaken belief among the public that dairy products in general can be bad for you, but thats a misconception. While it is a widely held belief, our research shows that thats wrong.

Theres been a lot of publicity over the last five to 10 years about how saturated fats increase the risk of cardiovascular disease and a belief has grown up that they must increase the risk, but they dont.

However, the governments health advisers urged consumers to continue to exercise caution about eating too many products high in saturated fat and to stick to low-fat versions instead.

Dairy products form an important part of a healthy balanced diet; however, many are high in saturated fat and salt. Were all consuming too much of both, increasing our risk of heart disease, said a spokesman for Public Health England. We recommend choosing lower-fat varieties of milk and dairy products or eating smaller amounts to reduce saturated fat and salt in the diet.

Givens and colleagues from Reading, Copenhagen University in Denmark and Wageningen University in the Netherlands analysed 29 studies involving 938,465 participants from around the world undertaken over the last 35 years, including five done in the UK.

No associations were found for total (high-fat/low-fat) dairy and milk with the health outcomes of mortality, CHD or CVD, they said. In fact, they added, fermented dairy products may potentially slightly lower the risk of having a heart attack or stroke.

Doctors, public health experts and official healthy eating guidelines have for many years identified saturated fats as potentially harmful for heart and cardiovascular health and advised consumers to minimise their intake.

That has led to consumers increasingly buying lower-fat versions of dairy products. For example, 85% of all milk sold in the UK is now semi-skimmed or skimmed.

Givens said consumers were shunning full-fat versions of cheese, milk or yoghurt in the mistaken view that they could harm their health. Young people, especially young women, were now often drinking too little milk as a result of that concern, which could damage the development of their bones and lead to conditions in later life including osteoporosis, or brittle bones, he said. Consuming too little milk can deprive young people of calcium.

Pregnant women who drank too little milk could be increasing the risk of their child having neuro-developmental difficulties, which could affect their cognitive abilities and stunt their growth, Givens added.

The most recent National Diet and Nutrition Survey, the governments occasional snapshot of eating habits, found that dairy products, including butter, accounted for the highest proportion of saturated fat consumption in British diets 27%, compared with meats 24%. But if butter was not counted then dairy products together were the second largest source of saturated fat, at 22%.

Saturated fat is a vital part of diet. The NDNS found that adults typically got 34.6% of their total energy from fats as a whole, just below the 35% the government recommends. However, while total fat consumption was just within target, saturated fats still made up an unhealthily large proportion of total food energy 12.6%, against the recommended maximum of 11%.

Givens said: Our meta-analysis included an unusually large number of participants. We are confident that our results are robust and accurate.

The research was part-funded by the three pro-dairy groups Global Dairy Platform, Dairy Research Institute and Dairy Australia but they had no influence over it, the paper said. Givens is an adviser to the Food Standards Agency.

Read more: https://www.theguardian.com/society/2017/may/08/consuming-dairy-does-not-raise-risk-of-heart-attack-or-stroke-study

We can cure Alzheimers if we stop ignoring it | Joseph Jebelli

Given focus and funding, Alzheimers will yield to science and reason, writes neuroscientist and author Joseph Jebelli

The terror of Alzheimers is that it acts by degrees, and can therefore bewilder family members as much as its victims. Those who first notice the onset of Alzheimers in a loved one tell of forgotten names and unsettling behaviour, of car keys found in the fridge and clothing in the kitchen cabinet, of aimless wanderings.

Naturally, they want to understand the boundaries of normal ageing and whether these are being crossed. Often, the answer arrives when theyre greeted as complete strangers, when the patients mind becomes irrevocably unmoored from its past. The disease is terrifying for its insidiousness as well as its long-term manifestations.

Fear partly explains why Alzheimers has been ignored for so long. Yet it is now the leading cause of death among the oldest people, and according to Professor Sir Michael Marmot, an expert in health inequalities, it could be an important part of the stagnation in increases in life expectancy since 2010 that he has identified.

As a researcher, I have been struck by how many patients speak openly about their condition only after receiving a diagnosis. I knew something wasnt right. Sometimes I dont know what day of the week it is or what I have to do, one newly diagnosed patient told me. I look in my calendar but then I think: why am I looking at this? My husband was the one who made me see a GP. I was too frightened. I thought I might have it but I didnt want to hear it.

My grandfather suppressed his concerns and agreed to see a doctor only after being hassled by his five children. By that point he had forgotten where he lived and was mistaking his wife, Afsana, for his first wife, Parry. Raising the issue with him wasnt easy; hed insist his memory was fine, and then happily discuss the health concerns of others. When faced with the stark reality of dementia, patients can retreat into themselves and some opt for silence.

But another factor is undoubtedly at work. For most of history, Alzheimers was a deeply taboo subject; those who had it were mad or just foolish. Although we think of Alzheimers as a modern disease, early accounts of dementia were described by the Roman philosopher Cicero and the Greek physician Galen. And yet only in the past two decades have we begun to realise Alzheimers is an affliction no less urgent than cancer or stroke.

And if people with other diseases of old age deserve recognition and action, then so do people with Alzheimers. The crisis around the funding of social care, and the attention focused on this during the general election campaign, has only increased the sense of urgency.

Where memory used to be viewed as a spectral, intangible quality, impossible to pin down, Alzheimers research now demonstrates the precise opposite that memory is a material phenomenon, an exquisite product of healthy brain cells that appears to reside in a network of durable connections between those brain cells. To say that this needs protecting is an understatement. Memory forms an individuals autobiography. It defines who we are. As the noted cognitive neuroscientist Michael Gazzaniga once said: Everything in life is memory, save for the thin edge of the present.

Worried
We know now that a therapy must be given in the very early stages of the disease, before symptoms appear. Photograph: Alamy

This is why the more I consider the governments approach to Alzheimers the more frustrated I become. Alzheimers costs the UK an estimated 26bn a year the combination of spending on healthcare, social care and lost earnings and taxes from people who have taken up caring roles in place of paid employment.

This is more than cancer, heart disease and stroke combined. And yet, astonishingly, only a fraction of 1% of that amount is spent on research. A hallmark of the NHS constitution is to improve health and wellbeing. In his 1939 address as president of the American Psychiatric Association, Richard Hutchings warned: Our institutions promise to become in time vast infirmaries with relatively small departments for younger patients with curable disorders.

Indeed, if things continue this way, epidemiologists estimate that the total number of Alzheimers cases will double every 20 years, making dementia the next global pandemic. In that event, the current 850,000 patients in the UK would represent no more than the tip of a vast, society-crippling iceberg.

Increasing the overall health budget is an option. A smarter strategy would be to reassess how funding is allocated in the first place. Cancer now causes fewer deaths each year than Alzheimers, but receives on average 13 times more funding. Eliminating cancer is vital, but we shouldnt pour all our efforts into one pandemic only to then be met by another. Given the advances made in understanding Alzheimers the signs and symptoms, the causes and risk factors, the genetics and neurobiology the number of therapies awaiting discovery is limitless.

The task of developing such therapies lies with the pharmaceutical industry. The problem is that many in the industry feel uneasy: between 2000 and 2012, in more than 400 clinical trials, only one drug was approved (Namenda, a drug similar to the Aricept generation of drugs, and similarly insufficient). In total, Alzheimers drug candidates have racked up a lamentable 99.6% failure rate even higher than cancer, at 81%. The recent failure of Eli Lillys solanezumab and Merck & Cos verubecestat hasnt helped.

But things are changing. We know now that a therapy must be given in the very early stages of the disease, before symptoms appear. And so Lilly, Merck and other companies are now testing drugs on patients in the newly defined preclinica phase of Alzheimers, with results expected by 2025. The role of academic researchers and patient advocates in all this is to keep championing the issue, to keep applying pressure as well as encouragement.

The word incurable is often used to describe Alzheimers. I have never liked the term because it is freighted with hopelessness. And it is wrong. Alzheimers will yield to science and reason; it will one day be as treatable as diabetes and HIV. The choice in front of us is how many generations we are willing to lose before that day comes.

The remarkable patients I met during my research, each teaching us something new and profound about the disease, deserve our action, not our sorrow. It is time to abolish their fear and silence. Its time to foster a seriousness of purpose that defeats Alzheimers once and for all.

Read more: https://www.theguardian.com/commentisfree/2017/jul/19/alzheimers-disease-death-old-people-science

Coffee cuts risk of dying from stroke and heart disease, study suggests

Coffee a day keeps the doctor away? Perhaps, but benefits may be down to lifestyles rather than the brew itself, researchers say

People who drink coffee have a lower risk of dying from a host of causes, including heart disease, stroke and liver disease, research suggests but experts say its unclear whether the health boost is down to the brew itself.

The connection, revealed in two large studies, was found to hold regardless of whether the coffee was caffeinated or not, with the effect higher among those who drank more cups of coffee a day.

But scientists say that the link might just be down to coffee-drinkers having healthier behaviours.

It is plausible that there is something else behind this that is causing this relationship, said Marc Gunter, a co-author of one of the studies, from the International Agency for Research on Cancer.

But, he added, based on the consistency of the results he would be surprised if coffee itself didnt play a role in reducing the risk of death.

About 2.25bn cups of coffee are consumed worldwide every day. While previous studies have suggested coffee might have health benefits, the latest research involves large and diverse cohorts of participants.

The first study looked at coffee consumption among more than 185,000 white and non-white participants, recruited in the early 1990s and followed up for an average of over 16 years. The results revealed that drinking one cup of coffee a day was linked to a 12% lower risk of death at any age, from any cause while those drinking two or three cups a day had an 18% lower risk, with the association not linked to ethnicity.

We found that coffee drinkers had a reduced risk of death from heart disease, from cancer, from stroke, respiratory disease, diabetes and kidney disease, said Veronica Setiawan, associate professor of preventive medicine at the University of Southern California and a co-author of the research.

The second study the largest of its kind involved more than 450,000 participants, recruited between 1992 and 2000 across ten European countries, who were again followed for just over 16 years on average. We felt this analysis would capture some of [the] variation in coffee preparation methods and drinking habits, said Gunter.

After a range of factors including age, smoking status, physical activity and education were taken into account, those who drank three or more cups a day were found to have a 18% lower risk of death for men, and a 8% lower risk of death for women at any age, compared with those who didnt drink the brew. The benefits were found to hold regardless of the country, although coffee drinking was not linked to a lower risk of death for all types of cancer.

The study also looked at a subset of 14,800 participants, finding that coffee-drinkers had better results on many biological markers including liver enzymes and glucose control. We know many of these biological factors are related to different health outcomes, so it is another piece of the puzzle, said Gunter.

But experts warn that the two studies, both published in the Annals of Internal Medicine, do not show that drinking coffee was behind the overall lower risk, pointing out that it could be that coffee drinkers are healthier in various ways or that those who are unwell drink less coffee.

In addition, levels of coffee-drinking were self-reported, some participants consumed both caffeinated and decaffeinated coffee, and the European study only looked at coffee consumption levels at one point in time all factors which could have affected the results.

It is not necessarily the coffee drinking per se, it is that fact that there are other things about your lifestyle or the lack of ill-health that might be causing the association, said Naveed Sattar, professor of metabolic medicine at the University of Glasgow, pointing out that while coffee might have beneficial effects, it would take randomised trials to be sure.

Authors of both studies also agreed more work is needed, and said that it was unclear which of the many biologically active components within the coffee might potentially be driving the health benefits. This is an observational study, said Setiawan. We cannot say, OK, [if] you drink coffee it is going to prolong your life.

Gunter agreed. I wouldnt recommend people start rushing out drinking lots of coffee, but I think what it does suggests is drinking coffee certainly does you no harm, he said. It can be part of a healthy diet.

Sattar also urged caution. If people enjoy their coffee they can relax and enjoy their coffee, he said, adding that people should not imagine that drinking extra coffee would militate against other bad health behaviours.

Read more: https://www.theguardian.com/science/2017/jul/10/coffee-cuts-risk-of-dying-from-stroke-and-heart-disease-study-suggests

Is it really possible to live until you’re 146? The science of ageing

Scientists doubt that extreme natural longevity is feasible. But if lifespan is ruled by a genetic clock, that view could change

The grim reaper comes for everyone in the end, but sometimes he is in less of a rush. This was certainly true for Sodimedjo, an Indonesian man who died on Sunday, but whether he was the full 146 years he claimed remains doubtful not least because his purported birthdate is 30 years before local birth records began.

Scientists have their own reasons to be sceptical. A study published last year pointed to the existence of an upper ceiling on the natural human lifespan.

While the average life expectancy has steadily increased since the 19th century, data from the International Database on Longevity showed that the age of the very oldest people on the planet appeared to plateau in the mid-1990s at a mere 114.9 years. Since the apparent plateau happened at a time when the reservoir of healthy centenarians was expanding, scientists concluded that an intrinsic biological limit had been reached: even if you evade accidents and disease, your body will still steadily decline until it passes the point of no return, the data appeared to suggest.

Jan Vijg, a geneticist at Albert Einstein College of Medicine in New York City, who led this research, said: We simply provided evidence that humans do indeed have a ceiling that they really cannot go beyond. Thats part of being human.

There will be the occasional outlier the French supercentenarian and oldest woman to have lived, Jeanne Calment, was 122 when she died in 1997, but most of us have a shorter intrinsic shelf life. The probability of someone living to 146 is infinitesimal, Vijg said. If somebody told you that they saw a UFO yesterday but its gone now, youd probably be polite, but you wouldnt believe it, said Vijg. Thats my reaction with this story.

Before resigning yourself to the knowledge that you will almost certainly expire by the time you reach 115 years, it is worth noting that this ceiling could be moveable in the future.

Richard Faragher, professor of biogerontology at the University of Brighton, puts it this way: How long can a human live if you dont do anything to them? Probably around 120. But there is a separate question, how long do people last if you can do something to them?

Until now, the steady increase in average life expectancy (as distinct from lifespan) has been driven by fewer people smoking, better nutrition and antibiotics. Drugs and surgery for heart disease and cancer have also played a part.

However, scientists are only just beginning to explore the possibility of therapies designed to target the process of ageing itself, as well as the illnesses that come with advancing years. This field has recently taken an intriguing twist, as evidence has emerged that ageing is not simply the manifestation of environmental wear and tear. Instead, the latest work suggests that ageing is at least partly driven by an internal genetic clock that actively causes our cells and organs to grind to a halt.

This raises the intriguing possibility that ageing could be slowed or even reversed, and some animal studies have already claimed to do just this.

I wouldnt argue that the ceiling is unmoveable, said Vijg. But trying to say what the age limit is, science cant yet say, its predicting the future.

Read more: https://www.theguardian.com/science/2017/may/02/is-it-really-possible-to-live-until-youre-146-the-science-of-ageing