Americans Are Retiring Later, Dying Sooner and Sicker In-Between

The U.S. retirement age is rising, as the government pushes it higher and workers stay in careers longer.

But lifespans aren’t necessarily extending to offer equal time on the beach. Data released last week suggest Americans’ health is declining and millions of middle-age workers face the prospect of shorter, and less active, retirements than their parents enjoyed.

Here are the stats: The U.S. age-adjusted mortality rate—a measure of the number of deaths per year—rose 1.2 percent from 2014 to 2015, according to the Society of Actuaries. That’s the first year-over-year increase since 2005, and only the second rise greater than 1 percent since 1980.

 

At the same time that Americans’ life expectancy is stalling, public policy and career tracks mean millions of U.S. workers are waiting longer to call it quits. The age at which people can claim their full Social Security benefits is gradually moving up, from 65 for those retiring in 2002 to 67 in 2027.

Almost one in three Americans age 65 to 69 is still working, along with almost one in five in their early 70s.

Postponing retirement can make financial sense, because extended careers can make it possible to afford retirements that last past age 90 or even 100. But a study out this month adds some caution to that calculation.

Americans in their late 50s already have more serious health problems than people at the same ages did 10 to 15 years ago, according to the journal Health Affairs.

University of Michigan economists HwaJung Choi and Robert Schoeni used survey data to compare middle-age Americans’ health. A key measure is whether people have trouble with an “activity of daily living,” or ADL, such as walking across a room, dressing and bathing themselves, eating, or getting in or out of bed. The study showed the number of middle-age Americans with ADL limitations has jumped: 12.5 percent of Americans at the current retirement age of 66 had an ADL limitation in their late 50s, up from 8.8 percent for people with a retirement age of 65.

At the current retirement age of 66, a quarter of Americans age 58 to 60 rated themselves in “poor” or “fair” health. That’s up 2.6 points from the group who could retire with full benefits at 65, the Michigan researchers found.

Cognitive skills have also declined over time. For those with a retirement age of 66, 11 percent already had some kind of dementia or other cognitive decline at age 58 to 60, according to the study. That’s up from 9.5 percent of Americans just a few years older, with a retirement age between 65 and 66.

While death rates can be volatile from year to year, Choi and Schoeni’s study is part of a raft of other research showing the health of Americans deteriorating.

Researchers have offered many theories for why Americans’ health is getting worse. Princeton University economists Anne Case and Angus Deaton, a Nobel Prize winner, have argued that an epidemic of suicide, drug overdoses and alcohol abuse have caused a spike in death rates among middle-age whites.

Higher rates of obesity may also be taking their toll. And Americans may have already seen most of the benefits from previous positive developments that cut the death rate, such as a decline in smoking and medical advances like statins that fight cardiovascular disease.

Declining health and life expectancy are good news for one constituency: Pension plans, which must send a monthly check to retirees for as long as they live.

According to the latest figures from the Society of Actuaries, life expectancy for pension participants has dropped since its last calculation by 0.2 years. A 65-year-old man can expect to live to 85.6 years, and a woman can expect to make it to 87.6. As a result, the group calculates a typical pension plan’s obligations could fall by 0.7 percent to 1 percent.

    Read more: http://www.bloomberg.com/news/articles/2017-10-23/americans-are-retiring-later-dying-sooner-and-sicker-in-between

    Trump Officials Dispute the Benefits of Birth Control to Justify Rules

    When the Trump administration elected to stop requiring many employers to offer birth-control coverage in their health plans, it devoted nine of its new rule’s 163 pages to questioning the links between contraception and preventing unplanned pregnancies.

    In the rule released Friday, officials attacked a 2011 report that recommended mandatory birth-control coverage to help women avoid unintended pregnancies. That report, requested by the Department of Health and Human Services, was done by the National Academies of Sciences, Engineering and Medicine — then the Institute of Medicine — an expert group that serves as the nation’s scientific adviser.

    “The rates of, and reasons for, unintended pregnancy are notoriously difficult to measure,” according to the Trump administration’s interim final rule. “In particular, association and causality can be hard to disentangle.”

    Multiple studies have found that access or use of contraception reduced unintended pregnancies. 

    Claims in the report that link increased contraceptive use by unmarried women and teens to decreases in unintended pregnancies “rely on association rather than causation,” according to the rule. The rule references another study that found increased access to contraception decreased teen pregnancies short-term but led to an increase in the long run.

    “We know that safe contraception — and contraception is incredibly safe — leads to a reduction in pregnancies,” said Michele Bratcher Goodwin, director of the Center for Biotechnology and Global Health Policy at the University of California, Irvine, School of Law. “This has been data that we’ve had for decades.”

    Riskier Behavior

    The rules were released as part of a broader package of protections for religious freedom that the administration announced Friday.

    The government also said imposing a coverage mandate could “affect risky sexual behavior in a negative way” though it didn’t point to any particular studies to support its point. A 2014 study by the Washington University School of Medicine in St. Louis found providing no-cost contraception did not lead to riskier sexual behavior.

    The rule asserts that positive health effects associated with birth control “might also be partially offset by an association with negative health effects.” The rule connects the claim of negative health effects to a call by the National Institutes of Health in 2013 for the development of new contraceptives that stated current options can have “many undesirable side effects.” 

    The rule also describes an Agency for Healthcare Research and Quality review that found oral contraceptives increased users’ risk of breast cancer and vascular events, making the drugs’ use in preventing ovarian cancer uncertain.

    Federal officials used all of these assertions to determine the government “need not take a position on these empirical questions.”

    “Our review is sufficient to lead us to conclude that significantly more uncertainty and ambiguity exists in the record than the Departments previously acknowledged.”

      Read more: http://www.bloomberg.com/news/articles/2017-10-06/trump-officials-dispute-birth-control-benefits-to-justify-rules

      Trump’s New Obamacare Killer to Cost Uncle Sam $194 Billion

      President Donald Trump is halting some Obamacare subsidies. A big money saver for taxpayers, right? Wrong. The move could actually force the government to dole out almost $200 billion more on health insurance over the next decade.

      Here’s why: The insurer payouts Trump cut off aren’t the only government funds financing the program. Consumers also can get help with their insurance premiums. When the insurer subsidies are discontinued, those premiums are pushed higher — and because the consumer subsidies are far bigger than those given to insurers, that’s a costly trade.

      More than eight in ten individuals who buy Obamacare plans get help paying their premiums directly from the federal government. Those subsidies effectively cap how much people have to pay for insurance as a percentage of their income. 

      Even if premiums climb, people who receive those benefits won’t pay more out of their own pockets. The subsidies are available to people making as much as four times the federal poverty level, or just over $97,000 for a family of four.

      That means that those most likely to be hurt by the president’s action aren’t low-income people who will still get help with their costs. Instead, consumers who make too much money to qualify for subsidies will now have to pay a much higher price for their health plans.

      It all adds up to a hefty bill for taxpayers for as long as the Affordable Care Act is the law of the land. The Congressional Budget Office estimated that ending the cost-sharing payments would increase the U.S. fiscal shortfall by $194 billion over the next decade as subsidy outlays jump.

        Read more: http://www.bloomberg.com/news/articles/2017-10-13/trump-s-latest-obamacare-killer-will-cost-uncle-sam-194-billion

        The shorter your sleep, the shorter your life: the new sleep science

        Leading neuroscientist Matthew Walker on why sleep deprivation is increasing our risk of cancer, heart attack and Alzheimers and what you can do about it

        Matthew Walker has learned to dread the question What do you do? At parties, it signals the end of his evening; thereafter, his new acquaintance will inevitably cling to him like ivy. On an aeroplane, it usually means that while everyone else watches movies or reads a thriller, he will find himself running an hours-long salon for the benefit of passengers and crew alike. Ive begun to lie, he says. Seriously. I just tell people Im a dolphin trainer. Its better for everyone.

        Walker is a sleep scientist. To be specific, he is the director of the Center for Human Sleep Science at the University of California, Berkeley, a research institute whose goal possibly unachievable is to understand everything about sleeps impact on us, from birth to death, in sickness and health. No wonder, then, that people long for his counsel. As the line between work and leisure grows ever more blurred, rare is the person who doesnt worry about their sleep. But even as we contemplate the shadows beneath our eyes, most of us dont know the half of it and perhaps this is the real reason he has stopped telling strangers how he makes his living. When Walker talks about sleep he cant, in all conscience, limit himself to whispering comforting nothings about camomile tea and warm baths. Its his conviction that we are in the midst of a catastrophic sleep-loss epidemic, the consequences of which are far graver than any of us could imagine. This situation, he believes, is only likely to change if government gets involved.

        Walker has spent the last four and a half years writing Why We Sleep, a complex but urgent book that examines the effects of this epidemic close up, the idea being that once people know of the powerful links between sleep loss and, among other things, Alzheimers disease, cancer, diabetes, obesity and poor mental health, they will try harder to get the recommended eight hours a night (sleep deprivation, amazing as this may sound to Donald Trump types, constitutes anything less than seven hours). But, in the end, the individual can achieve only so much. Walker wants major institutions and law-makers to take up his ideas, too. No aspect of our biology is left unscathed by sleep deprivation, he says. It sinks down into every possible nook and cranny. And yet no one is doing anything about it. Things have to change: in the workplace and our communities, our homes and families. But when did you ever see an NHS poster urging sleep on people? When did a doctor prescribe, not sleeping pills, but sleep itself? It needs to be prioritised, even incentivised. Sleep loss costs the UK economy over 30bn a year in lost revenue, or 2% of GDP. I could double the NHS budget if only they would institute policies to mandate or powerfully encourage sleep.

        Why, exactly, are we so sleep-deprived? What has happened over the course of the last 75 years? In 1942, less than 8% of the population was trying to survive on six hours or less sleep a night; in 2017, almost one in two people is. The reasons are seemingly obvious. First, we electrified the night, Walker says. Light is a profound degrader of our sleep. Second, there is the issue of work: not only the porous borders between when you start and finish, but longer commuter times, too. No one wants to give up time with their family or entertainment, so they give up sleep instead. And anxiety plays a part. Were a lonelier, more depressed society. Alcohol and caffeine are more widely available. All these are the enemies of sleep.

        But Walker believes, too, that in the developed world sleep is strongly associated with weakness, even shame. We have stigmatised sleep with the label of laziness. We want to seem busy, and one way we express that is by proclaiming how little sleep were getting. Its a badge of honour. When I give lectures, people will wait behind until there is no one around and then tell me quietly: I seem to be one of those people who need eight or nine hours sleep. Its embarrassing to say it in public. They would rather wait 45 minutes for the confessional. Theyre convinced that theyre abnormal, and why wouldnt they be? We chastise people for sleeping what are, after all, only sufficient amounts. We think of them as slothful. No one would look at an infant baby asleep, and say What a lazy baby! We know sleeping is non-negotiable for a baby. But that notion is quickly abandoned [as we grow up]. Humans are the only species that deliberately deprive themselves of sleep for no apparent reason. In case youre wondering, the number of people who can survive on five hours of sleep or less without any impairment, expressed as a percent of the population and rounded to a whole number, is zero.

        The world of sleep science is still relatively small. But it is growing exponentially, thanks both to demand (the multifarious and growing pressures caused by the epidemic) and to new technology (such as electrical and magnetic brain stimulators), which enables researchers to have what Walker describes as VIP access to the sleeping brain. Walker, who is 44 and was born in Liverpool, has been in the field for more than 20 years, having published his first research paper at the age of just 21. I would love to tell you that I was fascinated by conscious states from childhood, he says. But in truth, it was accidental. He started out studying for a medical degree in Nottingham. But having discovered that doctoring wasnt for him he was more enthralled by questions than by answers he switched to neuroscience, and after graduation, began a PhD in neurophysiology supported by the Medical Research Council. It was while working on this that he stumbled into the realm of sleep.

        Matthew
        Matthew Walker photographed in his sleep lab. Photograph: Saroyan Humphrey for the Observer

        I was looking at the brainwave patterns of people with different forms of dementia, but I was failing miserably at finding any difference between them, he recalls now. One night, however, he read a scientific paper that changed everything. It described which parts of the brain were being attacked by these different types of dementia: Some were attacking parts of the brain that had to do with controlled sleep, while other types left those sleep centres unaffected. I realised my mistake. I had been measuring the brainwave activity of my patients while they were awake, when I should have been doing so while they were asleep. Over the next six months, Walker taught himself how to set up a sleep laboratory and, sure enough, the recordings he made in it subsequently spoke loudly of a clear difference between patients. Sleep, it seemed, could be a new early diagnostic litmus test for different subtypes of dementia.

        After this, sleep became his obsession. Only then did I ask: what is this thing called sleep, and what does it do? I was always curious, annoyingly so, but when I started to read about sleep, I would look up and hours would have gone by. No one could answer the simple question: why do we sleep? That seemed to me to be the greatest scientific mystery. I was going to attack it, and I was going to do that in two years. But I was naive. I didnt realise that some of the greatest scientific minds had been trying to do the same thing for their entire careers. That was two decades ago, and Im still cracking away. After gaining his doctorate, he moved to the US. Formerly a professor of psychiatry at Harvard Medical School, he is now professor of neuroscience and psychology at the University of California.

        Does his obsession extend to the bedroom? Does he take his own advice when it comes to sleep? Yes. I give myself a non-negotiable eight-hour sleep opportunity every night, and I keep very regular hours: if there is one thing I tell people, its to go to bed and to wake up at the same time every day, no matter what. I take my sleep incredibly seriously because I have seen the evidence. Once you know that after just one night of only four or five hours sleep, your natural killer cells the ones that attack the cancer cells that appear in your body every day drop by 70%, or that a lack of sleep is linked to cancer of the bowel, prostate and breast, or even just that the World Health Organisation has classed any form of night-time shift work as a probable carcinogen, how could you do anything else?

        There is, however, a sting in the tale. Should his eyelids fail to close, Walker admits that he can be a touch Woody Allen-neurotic. When, for instance, he came to London over the summer, he found himself jet-lagged and wide awake in his hotel room at two oclock in the morning. His problem then, as always in these situations, was that he knew too much. His brain began to race. I thought: my orexin isnt being turned off, the sensory gate of my thalamus is wedged open, my dorsolateral prefrontal cortex wont shut down, and my melatonin surge wont happen for another seven hours. What did he do? In the end, it seems, even world experts in sleep act just like the rest of us when struck by the curse of insomnia. He turned on a light and read for a while.

        Will Why We Sleep have the impact its author hopes? Im not sure: the science bits, it must be said, require some concentration. But what I can tell you is that it had a powerful effect on me. After reading it, I was absolutely determined to go to bed earlier a regime to which I am sticking determinedly. In a way, I was prepared for this. I first encountered Walker some months ago, when he spoke at an event at Somerset House in London, and he struck me then as both passionate and convincing (our later interview takes place via Skype from the basement of his sleep centre, a spot which, with its bedrooms off a long corridor, apparently resembles the ward of a private hospital). But in another way, it was unexpected. I am mostly immune to health advice. Inside my head, there is always a voice that says just enjoy life while it lasts.

        The evidence Walker presents, however, is enough to send anyone early to bed. Its no kind of choice at all. Without sleep, there is low energy and disease. With sleep, there is vitality and health. More than 20 large scale epidemiological studies all report the same clear relationship: the shorter your sleep, the shorter your life. To take just one example, adults aged 45 years or older who sleep less than six hours a night are 200% more likely to have a heart attack or stroke in their lifetime, as compared with those sleeping seven or eight hours a night (part of the reason for this has to do with blood pressure: even just one night of modest sleep reduction will speed the rate of a persons heart, hour upon hour, and significantly increase their blood pressure).

        A lack of sleep also appears to hijack the bodys effective control of blood sugar, the cells of the sleep-deprived appearing, in experiments, to become less responsive to insulin, and thus to cause a prediabetic state of hyperglycaemia. When your sleep becomes short, moreover, you are susceptible to weight gain. Among the reasons for this are the fact that inadequate sleep decreases levels of the satiety-signalling hormone, leptin, and increases levels of the hunger-signalling hormone, ghrelin. Im not going to say that the obesity crisis is caused by the sleep-loss epidemic alone, says Walker. Its not. However, processed food and sedentary lifestyles do not adequately explain its rise. Something is missing. Its now clear that sleep is that third ingredient. Tiredness, of course, also affects motivation.

        Sleep has a powerful effect on the immune system, which is why, when we have flu, our first instinct is to go to bed: our body is trying to sleep itself well. Reduce sleep even for a single night, and your resilience is drastically reduced. If you are tired, you are more likely to catch a cold. The well-rested also respond better to the flu vaccine. As Walker has already said, more gravely, studies show that short sleep can affect our cancer-fighting immune cells. A number of epidemiological studies have reported that night-time shift work and the disruption to circadian sleep and rhythms that it causes increase the odds of developing cancers including breast, prostate, endometrium and colon.

        Getting too little sleep across the adult lifespan will significantly raise your risk of developing Alzheimers disease. The reasons for this are difficult to summarise, but in essence it has to do with the amyloid deposits (a toxin protein) that accumulate in the brains of those suffering from the disease, killing the surrounding cells. During deep sleep, such deposits are effectively cleaned from the brain. What occurs in an Alzheimers patient is a kind of vicious circle. Without sufficient sleep, these plaques build up, especially in the brains deep-sleep-generating regions, attacking and degrading them. The loss of deep sleep caused by this assault therefore lessens our ability to remove them from the brain at night. More amyloid, less deep sleep; less deep sleep, more amyloid, and so on. (In his book, Walker notes unscientifically that he has always found it curious that Margaret Thatcher and Ronald Reagan, both of whom were vocal about how little sleep they needed, both went on to develop the disease; it is, moreover, a myth that older adults need less sleep.) Away from dementia, sleep aids our ability to make new memories, and restores our capacity for learning.

        And then there is sleeps effect on mental health. When your mother told you that everything would look better in the morning, she was wise. Walkers book includes a long section on dreams (which, says Walker, contrary to Dr Freud, cannot be analysed). Here he details the various ways in which the dream state connects to creativity. He also suggests that dreaming is a soothing balm. If we sleep to remember (see above), then we also sleep to forget. Deep sleep the part when we begin to dream is a therapeutic state during which we cast off the emotional charge of our experiences, making them easier to bear. Sleep, or a lack of it, also affects our mood more generally. Brain scans carried out by Walker revealed a 60% amplification in the reactivity of the amygdala a key spot for triggering anger and rage in those who were sleep-deprived. In children, sleeplessness has been linked to aggression and bullying; in adolescents, to suicidal thoughts. Insufficient sleep is also associated with relapse in addiction disorders. A prevailing view in psychiatry is that mental disorders cause sleep disruption. But Walker believes it is, in fact, a two-way street. Regulated sleep can improve the health of, for instance, those with bipolar disorder.

        Ive mentioned deep sleep in this (too brief) summary several times. What is it, exactly? We sleep in 90-minute cycles, and its only towards the end of each one of these that we go into deep sleep. Each cycle comprises two kinds of sleep. First, there is NREM sleep (non-rapid eye movement sleep); this is then followed by REM (rapid eye movement) sleep. When Walker talks about these cycles, which still have their mysteries, his voice changes. He sounds bewitched, almost dazed.

        During NREM sleep, your brain goes into this incredible synchronised pattern of rhythmic chanting, he says. Theres a remarkable unity across the surface of the brain, like a deep, slow mantra. Researchers were once fooled that this state was similar to a coma. But nothing could be further from the truth. Vast amounts of memory processing is going on. To produce these brainwaves, hundreds of thousands of cells all sing together, and then go silent, and on and on. Meanwhile, your body settles into this lovely low state of energy, the best blood-pressure medicine you could ever hope for. REM sleep, on the other hand, is sometimes known as paradoxical sleep, because the brain patterns are identical to when youre awake. Its an incredibly active brain state. Your heart and nervous system go through spurts of activity: were still not exactly sure why.

        Does the 90-minute cycle mean that so-called power naps are worthless? They can take the edge off basic sleepiness. But you need 90 minutes to get to deep sleep, and one cycle isnt enough to do all the work. You need four or five cycles to get all the benefit. Is it possible to have too much sleep? This is unclear. There is no good evidence at the moment. But I do think 14 hours is too much. Too much water can kill you, and too much food, and I think ultimately the same will prove to be true for sleep. How is it possible to tell if a person is sleep-deprived? Walker thinks we should trust our instincts. Those who would sleep on if their alarm clock was turned off are simply not getting enough. Ditto those who need caffeine in the afternoon to stay awake. I see it all the time, he says. I get on a flight at 10am when people should be at peak alert, and I look around, and half of the plane has immediately fallen asleep.

        So what can the individual do? First, they should avoid pulling all-nighters, at their desks or on the dancefloor. After being awake for 19 hours, youre as cognitively impaired as someone who is drunk. Second, they should start thinking about sleep as a kind of work, like going to the gym (with the key difference that it is both free and, if youre me, enjoyable). People use alarms to wake up, Walker says. So why dont we have a bedtime alarm to tell us weve got half an hour, that we should start cycling down? We should start thinking of midnight more in terms of its original meaning: as the middle of the night. Schools should consider later starts for students; such delays correlate with improved IQs. Companies should think about rewarding sleep. Productivity will rise, and motivation, creativity and even levels of honesty will be improved. Sleep can be measured using tracking devices, and some far-sighted companies in the US already give employees time off if they clock enough of it. Sleeping pills, by the way, are to be avoided. Among other things, they can have a deleterious effect on memory.

        Those who are focused on so-called clean sleep are determined to outlaw mobiles and computers from the bedroom and quite right, too, given the effect of LED-emitting devices on melatonin, the sleep-inducing hormone. Ultimately, though, Walker believes that technology will be sleeps saviour. There is going to be a revolution in the quantified self in industrial nations, he says. We will know everything about our bodies from one day to the next in high fidelity. That will be a seismic shift, and we will then start to develop methods by which we can amplify different components of human sleep, and do that from the bedside. Sleep will come to be seen as a preventive medicine.

        What questions does Walker still most want to answer? For a while, he is quiet. Its so difficult, he says, with a sigh. There are so many. I would still like to know where we go, psychologically and physiologically, when we dream. Dreaming is the second state of human consciousness, and we have only scratched the surface so far. But I would also like to find out when sleep emerged. I like to posit a ridiculous theory, which is: perhaps sleep did not evolve. Perhaps it was the thing from which wakefulness emerged. He laughs. If I could have some kind of medical Tardis and go back in time to look at that, well, I would sleep better at night.

        Why We Sleep: The New Science of Sleep and Dreamsby Matthew Walker is published by Allen Lane (20). To order a copy for 17 go toguardianbookshop.com or call 0330 333 6846. Free UK p&p over 10, online orders only. Phone orders min p&p of 1.99

        Sleep in numbers

        Two-thirds of adults in developed nations fail to obtain the nightly eight hours of sleep recommended by the World Health Organisation.

        An adult sleeping only 6.75 hours a night would be predicted to live only to their early 60s without medical intervention.

        A 2013 study reported that men who slept too little had a sperm count 29% lower than those who regularly get a full and restful nights sleep.

        If you drive a car when you have had less than five hours sleep, you are 4.3 times more likely to be involved in a crash. If you drive having had four hours, you are 11.5 times more likely to be involved in an accident.

        A hot bath aids sleep not because it makes you warm, but because your dilated blood vessels radiate inner heat, and your core body temperature drops. To successfully initiate sleep, your core temperature needs to drop about 1C.

        The time taken to reach physical exhaustion by athletes who obtain anything less than eight hours of sleep, and especially less than six hours, drops by 10-30%.

        There are now more than 100 diagnosed sleep disorders, of which insomnia is the mostcommon.

        Morning types, who prefer to awake at or around dawn, make up about 40% of the population. Evening types, who prefer to go to bed late and wake up late, account for about 30%. The remaining 30% lie somewhere in between.

        Read more: https://www.theguardian.com/lifeandstyle/2017/sep/24/why-lack-of-sleep-health-worst-enemy-matthew-walker-why-we-sleep

        Are smartphones really making our children sad?

        US psychologist Jean Twenge, who has claimed that social media is having a malign affect on the young, answers critics who accuse her of crying wolf

        Last week, the childrens commissioner, Anne Longfield, launched a campaign to help parents regulate internet and smartphone use at home. She suggested that the overconsumption of social media was a problem akin to that of junk-food diets. None of us, as parents, would want our children to eat junk food all the time double cheeseburger, chips, every day, every meal, she said. For those same reasons, we shouldnt want our children to do the same with their online time.

        A few days later, former GCHQ spy agency chief Robert Hannigan responded to the campaign. The assumption that time online or in front of a screen is life wasted needs challenging. It is driven by fear, he said. The best thing we can do is to focus less on the time they spend on screens at home and more on the nature of the activity.

        This exchange is just one more example of how childrens screentime has become an emotive, contested issue. Last December, more than 40 educationalists, psychologists and scientists signed a letter in the Guardian calling for action on childrens screen-based lifestyles. A few days later, another 40-odd academics described the fears as moral panic and said that any guidelines needed to build on evidence rather than scaremongering.

        Faced with these conflicting expert views, how should concerned parents proceed? Into this maelstrom comes the American psychologist Jean Twenge, who has written a book entitled iGen: Why Todays Super-Connected Kids Are Growing Up Less Rebellious, More Tolerant, Less Happy and Completely Unprepared for Adulthood and What That Means for the Rest of Us.

        If the books title didnt make her view clear enough, last weekend an excerpt was published in the American magazine the Atlantic with the emotive headline Have smartphones destroyed a generation? It quickly generated differing reactions that were played out on social media these could be broadly characterised as praise from parents and criticism from scientists. In a phone interview and follow-up emails, Twenge explained her conclusions about the downsides of the connected world for teens, and answered some of her critics.

        The Atlantic excerpt from your book was headlined Have smartphones destroyed a generation? Is that an accurate reflection of what you think?
        Well, keep in mind that I didnt write the headline. Its obviously much more nuanced than that.

        So why did you write this book?
        Ive been researching generations for a long time now, since I was an undergraduate, almost 25 years. The databases I draw from are large national surveys of high school and college students, and one of adults. In 2013-14 I started to see some really sudden changes and at first I thought maybe these were just blips, but the trends kept going.

        Id never seen anything like it in all my years of looking at differences among generations. So I wondered what was going on.

        What were these sudden changes for teens?
        Loneliness and depressive symptoms started to go up, while happiness and life satisfaction started to go down. The other thing that I really noticed was the accelerated decline in seeing friends in person it falls off a cliff. Its an absolutely stunning pattern Id never seen anything like that. I really started to wonder, what is going on here? What happened around 2011-2012 [the survey data is a year or two behind] that would cause such sudden changes?

        And you concluded these changes were being brought about by increased time spent online?
        The high-school data detailed how much time teens spend online on social media and games and I noticed how that correlated with some of these indicators in terms of happiness, depression and so on.

        I was curious not just what the correlations were between these screen activities, mental health and wellbeing, but what were the links with non-screen activities, like spending time with friends in person, playing sports, going to religious services, doing homework, all these other things that teens do?

        And for happiness in particular, the pattern was so stark. Of the non-screen activities that were measured, they all correlated with greater happiness. All the screen activities correlated with lower happiness.

        Youve called these post-millennials the iGeneration. What are their characteristics?
        Im defining iGen as those born between 1995 and 2012 that latter date could change based on future data. Im reasonably certain about 1995, given the sudden changes in the trends. It also happens that 1995 was the year the internet was commercialised [Amazon launched that year, Yahoo in 1994 and Google in 1996], so if you were born in that year you have not known a time without the internet.

        But the introduction of the smartphone, exemplified by the iPhone, which was launched in 2007, is key?
        There are a lot of differences some are large, some are subtle, some are sudden and some had been building for a while but if I had to identify what really characterises them, the first influence is the smartphone.

        iGen is the first generation to spend their entire adolescence with the smartphone. This has led to many ripple effects for their wellbeing, their social interactions and the way they think about the world.

        Psychology
        Psychology professor Jean Twenge. Photograph: Gregory Bull/AP

        Why are you convinced they are unhappy because of social media, rather than it being a case of the unhappy kids being heavier users of social media?
        That is very unlikely to be true because of very good research on that very question. There is one experiment and two longitudinal studies that show the arrow goes from social media to lower wellbeing and not the other way around. For example, an experiment where people
        gave up Facebook for a week and had better wellbeing than those who had not.

        The other thing to keep in mind is that if you are spending eight hours a day with a screen you have less time to spend interacting with friends and family in person and we know definitively from decades of research that spending time with other people is one of the keys to emotional wellbeing; if youre doing that less, thats a very bad sign.

        A professor at Oxford University tweeted that your work is a non-systematic review of sloppy social science as a tool for lazy intergenerational shaming how do you respond?
        It is odd to equate documenting teens mental health issues with intergenerational shaming. Im not shaming anyone and the data I analyse is from teens, not older people criticising them.

        This comment is especially strange because this researchers best-known paper, about what he calls the Goldilocks theory, shows the same thing I find lower wellbeing after more hours of screen time. Were basically replicating each others research across two different countries, which is usually considered a good thing. So I am confused.

        Your arguments also seem to have been drawn on by the conservative right as ammunition for claims that technology is leading to the moral degradation of the young. Are you comfortable about that?
        My analyses look at what young people are saying about themselves and how they are feeling, so I dont think this idea of older people love to whine about the young is relevant. I didnt look at what older people have to say about young people. I looked at what young people are saying about their own experiences and their own lives, compared to young people 10, 20, or 30 years ago.

        Nor is it fair or accurate to characterise this as youth-bashing. Teens are saying they are suffering and documenting that should help them, not hurt them. I wrote the book because I wanted to give a voice to iGen and their experiences, through the 11 million who filled out national surveys, to the 200 plus who answered open-ended questions for me, to the 23 I talked to for up to two hours. It had absolutely nothing to do with older people and their complaints about youth.

        Many of us have a nagging feeling that social media is bad for our wellbeing, but we all suffer from a fear of missing out.
        Teens feel that very intensely, which is one reason why they are so addicted to their phones. Yet, ironically, the teens who spend more time on social media are actually more likely to report feeling left out.

        But is this confined to iGeners? One could go to a childs birthday party where the parents are glued to their smartphones and not talking to each other too.
        It is important to consider that while this trend also affects adults, it is particularly worrisome for teens because their brain development is ongoing and adolescence is a crucial time for developing social skills.

        You say teens might know the right emoji but in real life might not know the right facial expression.
        There is very little research on that question. There is one study that looked at the effects of screens on social skills among 11- to 12-year-olds, half of whom used screens at their normal level and half went to a five-day screen-free camp.

        Those who attended the camp improved their social skills reading emotions on faces was what they measured. That makes sense thats the social skill you would expect to suffer if you werent getting much in-person social interaction.

        So is it up to regulators or parents to improve the situation? Leaving this problem for parents to fix is a big challenge.
        Yes it is. I have three kids and my oldest is 10, but in her class about half have a phone, so many of them are on social media already. Parents have a tough job, because there are temptations on the screen constantly.

        What advice would you give parents?
        Put off getting your child a phone for as long as possible and, when you do, start with one that doesnt have internet access so they dont have the internet in their pocket all the time.

        But when your child says, but all my friends have got one, how do you reply?
        Maybe with my parents line If your friends all jumped in the lake, would you do it too? Although at that age the answer is usually yes, which I understand. But you can do social media on a desktop computer for a limited time each day. When we looked at the data, we found that an hour a day of electronic device use doesnt have any negative effects on mental health two hours a day or more is when you get the problems.

        The majority of teens are on screens a lot more than that. So if they want to use Instagram, Snapchat or Facebook to keep up with their friends activities, they can do that from a desktop computer.

        That sounds hard to enforce.
        We need to be more understanding of the effects of smartphones. In many ways, parents are worried about the wrong things theyre worried about their kids driving and going out. They dont worry about their kids sitting by themselves in a room with their phone and they should.

        Lots of social media features such as notifications or Snapchats Snapstreak feature are engineered to keep us glued to our phones. Should these types of features be outlawed?
        Oh man. Parents can put an app [such as Kidslox or Screentime] on their kids phone to limit the amount of time they spend on it. Do that right away. In terms of the bigger solutions, I think thats above my pay grade to figure out.

        Youve been accused by another psychologist of cherry-picking your data. Of ignoring, say, studies that suggest active social media use is associated with positive outcomes such as resilience. Did you collect data to fit a theory?
        Its impossible to judge that claim she does not provide citations to these studies. I found a few studies finding no effects or positive effects, but they were all older, before smartphones were on the scene. She says in order to prove smartphones are responsible for these trends we need a large study randomly assigning teens to not use smartphones or use them. If we wait for this kind of study, we will wait for ever that type of study is just about impossible to conduct.

        She concludes by saying: My suspicion is that the kids are gonna be OK. However, it is not OK that 50% more teens suffer from major depression now versus just six years ago and three times as many girls aged 12 to 14 take their own lives. It is not OK that more teens say that they are lonely and feel hopeless. It is not OK that teens arent seeing their friends in person as much. If we twiddle our thumbs waiting for the perfect experiment, we are taking a big risk and I for one am not willing to do that.

        Are you expecting anyone from Silicon Valley to say: How can we help?
        No, but what I think is interesting is many tech-connected people in Silicon Valley restrict their own childrens screen use, so they know. Theyre living off of it but they know its effects. It indicates that pointing out the effects of smartphones doesnt make you a luddite.

        iGen: Why Todays Super-Connected Kids Are Growing Up Less Rebellious, More Tolerant, Less Happy and Completely Unprepared for Adulthood and What That Means for the Rest of Us by Jean Twenge is published by Simon & Schuster US ($27) on 22 August

        Read more: https://www.theguardian.com/technology/2017/aug/13/are-smartphones-really-making-our-children-sad

        It was all yellow: did digitalis affect the way Van Gogh saw the world?

        Extracted from foxgloves, digitalis was once used as a treatment for epilepsy. Could a side effect have triggered the artists yellow period?

        It was recently the 127th anniversary of the tragic death of Vincent van Gogh. His short life came to an untimely end two days after he shot himself in the chest; he had experienced mental health issues through much of his life. In the absence of a definitive diagnosis, speculation as to the true nature of his illness fills volumes.

        Although he came under the care of several doctors during his life time, knowledge of diseases of the mind was in its infancy in the late nineteenth century. As a result, many of the treatments used at the time would have been ineffective if not potentially dangerous. From our point of view, however, one drug that might have been given to Van Gogh is particularly interesting.

        Towards the end of his life, under the care of Dr Gachet, it seems that Van Gogh may have been treated with digitalis for the epileptic fits he experienced. Digitalis, extracted from foxglove plants, is a powerful medicine still in use today as a treatment for certain heart conditions, but not epilepsy. In Van Goghs day, and for a long time before then, digitalis was known to be an effective treatment of dropsy, or accumulation of fluid in the body. Dropsy could have been caused by inefficient beating of the heart or because of liver disease. But with little understanding of the underlying causes of many diseases, almost anything shown to have an effect on the body even if that was simply to induce vomiting was considered a medical benefit. If the treatment for one disease was successful, it was often tried out on a host of others, just in case it proved to be a panacea. Extracts of foxglove really would have been effective in treating dropsy caused by heart failure, but would have done nothing for Van Goghs epilepsy. However, it is just possible it may have contributed to his artistic output.

        Portrait
        Portrait of Dr Gachet, by Vincent van Gogh. Gachet holds a foxglove, seen by some to suggest that he treated Van Gogh with digitalis. Photograph: DEA / G. DAGLI ORTI/De Agostini/Getty Images

        Digitalis is, in fact, a mixture of several different compounds that today are separated and used individually to treat heart conditions. One of the compounds, digoxin, is listed by the World Health Organisation as an essential medicine because of its huge benefit in the treatment of abnormal heart rhythms such as atrial fibrillation. Digoxin has two effects on the heart. Firstly, it helps to control the electrical signals that are sent across the heart to trigger the cells to beat in a coordinated way producing a heartbeat. Secondly, it makes the individual heart cells contract more slowly and strongly, improving the efficiency of the pumping action to move blood round the body.

        To achieve these effects on the heart, digoxin and related compounds interact with the enzyme Na+/K+ ATPase. Digoxin is a very potent drug, the therapeutic dose is miniscule, and it is very close to the level that can also produce digitalis intoxication. Such a narrow gap between a therapeutic and potentially harmful dose would simply not be tolerated in a new drug being brought to market. However, the undoubted benefit of digoxin and its long history of use means it is a vital part of modern medicine. Because the drug has been in use for so long over 200 years, since the physician William Withering advocated its use in 1775 we have had plenty of time to understand how the drug works and the potential side-effects. Patients taking digoxin are carefully monitored and a number of antidotes have been developed to treat overdoses.

        The problem, as with all drugs, is side-effects. To achieve its effects on the heart, digoxin and related compounds interact with the enzyme Na+/K+ ATPase.Digoxins strong interaction with the enzyme means it is very potent, but Na+/K+ ATPase is distributed throughout the body. It is therefore the interaction between the drug and the enzymes located elsewhere in the body that is the cause of side-effects. The most common problems associated with digoxin are nausea and loss of appetite, but its other effects are more intriguing.

        Particularly high concentrations of digoxins target enzyme are found in the cone cells in retina of the eye. These are the cells that give us our colour perception. It is very rare, but some people taking digoxin and related drugs can experience haziness to their vision, or a yellow tinge to everything they see, known as xanthopsia. Occasionally, points of light may appear to have coloured halos around them. Rarer still are effects on pupil size, such as dilation, constriction or even unequal-sized pupils.

        The effects of digitalis intoxication have been suggested as the cause of Van Goghs yellow period and the spectacular sky he painted in The Starry Night. More circumstantial evidence comes from the two portraits Van Gogh produced of his doctor, Paul Gachet, showing him holding a foxglove flower. One of Van Goghs self portraits also shows uneven pupils.

        All of this is very interesting but it is pure speculation. Van Gogh may not have taken digitalis, and perhaps simply liked the colour yellow and the effect of swirling colours around the stars he painted. Unequal pupil size in his self-portrait may have been the result of a simple slip of the paintbrush.

        There are also many other factors to consider. Van Gogh was known to drink large quantities of absinthe (though not enough to produce yellow colour perception) as well as turpentine (which can affect vision but not colour perception). Whatever the reason for Van Goghs particular artistic choices, we can still appreciate his remarkable output from such a tragically short life.

        Read more: https://www.theguardian.com/science/blog/2017/aug/10/it-was-all-yellow-did-digitalis-affect-the-way-van-gogh-saw-the-world

        Rule that patients must finish antibiotics course is wrong, study says

        Experts suggest patients should stop taking the drugs when they feel better rather than completing their prescription

        Telling patients to stop taking antibiotics when they feel better may be preferable to instructing them to finish the course, according to a group of experts who argue that the rule long embedded in the minds of doctors and the public is wrong and should be overturned.

        Patients have traditionally been told that they must complete courses of antibiotics, the theory being that taking too few tablets will allow the bacteria causing their disease to mutate and become resistant to the drug.

        But Martin Llewelyn, a professor in infectious diseases at Brighton and Sussex medical school, and colleagues claim that this is not the case. In an analysis in the British Medical Journal, the experts say the idea that stopping antibiotic treatment early encourages antibiotic resistance is not supported by evidence, while taking antibiotics for longer than necessary increases the risk of resistance.

        There are some diseases where the bug can become resistant if the drugs are not taken for long enough. The most obvious example is tuberculosis, they say. But most of the bacteria that cause people to become ill are found on everybodys hands in the community, causing no harm, such as E coli and Staphylococcus aureus. People fall ill only when the bug gets into the bloodstream or the gut. The longer such bacteria are exposed to antibiotics, the more likely it is that resistance will develop.

        The experts say there has been too little research into the ideal length of a course of antibiotics, which also varies from one individual to the next, depending in part on what antibiotics they have taken in the past.

        In hospital, patients can be tested to work out when to stop the drugs. Outside hospital, where repeated testing may not be feasible, patients might be best advised to stop treatment when they feel better, they say. That, they add, is in direct contravention of World Health Organisation advice.

        Other experts in infectious diseases backed the group. I have always thought it to be illogical to say that stopping antibiotic treatment early promotes the emergence of drug-resistant organisms, said Peter Openshaw, president of the British Society for Immunology.

        This brief but authoritative review supports the idea that antibiotics may be used more sparingly, pointing out that the evidence for a long duration of therapy is, at best, tenuous. Far from being irresponsible, shortening the duration of a course of antibiotics might make antibiotic resistance less likely.

        Alison Holmes, a professor of infectious diseases at Imperial College London, said a great British authority, Prof Harold Lambert, had made the same point in a Lancet article entitled Dont keep taking the tablets as early as 1999. It remains astonishing that apart from some specific infections and conditions, we still do not know more about the optimum duration of courses or indeed doses in many conditions, yet this dogma has been pervasive and persistent.

        Jodi Lindsay, a professor of microbial pathogenesis at St Georges, University of London, said it was sensible advice. The evidence for completing the course is poor, and the length of the course of antibiotics has been estimated based on a fear of under-treating rather than any studies, she said. The evidence for shorter courses of antibiotics being equal to longer courses, in terms of cure or outcome, is generally good, although more studies would help and there are a few exceptions when longer courses are better for example, TB.

        But the Royal College of GPs expressed concerns. Recommended courses of antibiotics are not random, said its chair, Prof Helen Stokes-Lampard. They are tailored to individual conditions and in many cases, courses are quite short for urinary tract infections, for example, three days is often enough to cure the infection.

        We are concerned about the concept of patients stopping taking their medication midway through a course once they feel better, because improvement in symptoms does not necessarily mean the infection has been completely eradicated. Its important that patients have clear messages and the mantra to always take the full course of antibiotics is well known. Changing this will simply confuse people.

        The UKs chief medical officer, Prof Dame Sally Davies, said: The message to the public remains the same: people should always follow the advice of healthcare professionals. To update policies, we need further research to inform them.

        [The National Institute for Health and Care Excellence] is currently developing guidance for managing common infections, which will look at all available evidence on appropriate prescribing of antibiotics.

        The Department of Health will continue to review the evidence on prescribing and drug-resistant infections, as we aim to continue the great progress we have made at home and abroad on this issue.

        Read more: https://www.theguardian.com/society/2017/jul/26/rule-patients-must-finish-antibiotics-course-wrong-study-says

        Meningitis vaccine may also cut risk of ‘untreatable’ gonorrhoea, study says

        Bacteria causing two different illnesses belong to the same family and share much of the same genetic code providing unexpected cross protection

        Hopes to fight untreatable strains of gonorrhoea have risen after it emerged that a new vaccine against meningitis unexpectedly reduced the risk of people getting the sexually transmitted infection.

        Some strains of gonorrhoea are resistant to all available drugs, making vaccine development an urgent global health priority. But according to a study in The Lancet, a vaccine has offered protection against the sexually transmitted disease for the first time.

        Gonorrhoea spreads through unprotected vaginal, oral or anal sex and many of those who contract the disease experience no symptoms. If left untreated, the disease can cause infertility and can increase the transmission of HIV infection.

        A New Zealand meningitis epidemic in the early 2000s prompted the mass vaccination of a million people and fortuitously set the scene for the current study. The vaccine used, known as MeNZB, was designed to protect against meningococcal group B infection the cause of the most deadly form of meningitis.

        But intriguingly, over the next few years, scientists noticed fewer gonorrhoea cases than expected in those who had been vaccinated against meningitis.

        Dr Helen Petousis-Harris, a vaccine specialist from the University of Auckland who led the study, was optimistic: Some types of gonorrhoea are now resistant to every antibiotic we have, and there appeared [to be] little we could do to prevent the steady march of gonorrhoea to superbug status. But now theres hope, she added.

        The research team studied over 14,000 people aged 15-30 whod been diagnosed with gonorrhoea at sexual health clinics across New Zealand and who had been eligible for the MeNZB vaccine during the emergency vaccination programme. They found vaccinated individuals were over 30% less likely to develop gonorrhoea.

        Despite meningitis and gonorrhoea being very different illnesses, both are caused by bacteria from the same family and share much of the same genetic code, providing a possible explanation for the cross-protection that the team observed.

        More than 78 million people worldwide get gonorrhoea each year with most infections in men and women under the age of 25. It is the second most common bacterial sexually transmitted infection in the UK after chlamydia. In England alone, almost 35,000 people were affected in 2014.

        British Association for Sexual Health and HIVs President, Dr Elizabeth Carlin, who was not involved in the study, was more sceptical: These early findings are to be welcomed but its important to keep in perspective that the vaccine offered only moderate protection …. an individual receiving this vaccine remains susceptible to gonorrhoea but just less so than if unvaccinated.

        The MeNZB vaccine used in the current study is no longer manufactured, but Petousis-Harris has high hopes for a similar meningitis vaccine called 4CMenB, available in many countries.

        Petousis-Harris was clear about what needed to happen next. We need an urgent assessment of current meningitis vaccines to see if they protect against gonorrhoea. It may be possible to eliminate many gonorrhoea infections using a vaccine with only moderate protection. It does not need to be perfect, she added.

        Read more: https://www.theguardian.com/science/2017/jul/10/meningitis-vaccine-may-also-cut-risk-of-untreatable-gonorrhoea-study-says

        People taking heartburn drugs could have higher risk of death, study claims

        Research suggests people on proton pump inhibitors are more likely to die than those taking different antacid or none at all

        Millions of people taking common heartburn and indigestion medications could be at an increased risk of death, research suggests.

        The drugs, known as proton pump inhibitors (PPIs), neutralise the acid in the stomach and are widely prescribed, with low doses also available without prescription from pharmacies. In the UK, doctors issue more than 50m prescriptions for PPIs every year.

        Now researchers say the drugs can increase risk of death, both compared with taking a different type of acid suppressant and not taking any at all.

        We saw a small excess risk of dying that could be attributed to the PPI drug, and the risk increased the longer they took them, said Ziyad Al-Aly, an epidemiologist from the University of Washington and co-author of the study.

        The team say the study suggests those who take the drugs without needing to could be most at risk. They urged people taking PPIs to check whether this was necessary.

        Previous research has raised a range of concerns about PPIs, including links to kidney disease, pneumonia, more hip fractures and higher rates of infection with C difficile, a superbug that can cause life-threatening sepsis, particularly in elderly people in hospitals.

        But the latest study is the first to show that PPIs can increase the chance of death. Published in the journal BMJ Open, it examined the medical records of 3.5 million middle-aged Americans covered by the US veterans healthcare system.

        The researchers followed 350,000 participants for more than five years and compared those prescribed PPIs to a group receiving a different type of acid suppressant known as an H2 blocker. They also took into account factors such as the participants age, sex and conditions ranging from high blood pressure to HIV.

        The results show that those who took PPIs could face a 25% higher risk of death than those who took the H2 blocker.

        In patients on [H2 blocker] tablets, there were 3.3 deaths per 100 people over one year. In the PPI group, this figure was higher at 4.7 per 100 people per year, said Al-Aly.

        The team also reported that the risk of death for those taking PPIs was 15% higher than those taking no PPIs, and 23% higher than for those taking no acid suppressants at all.

        Similar levels of increased risk were seen among people who used PPIs but had no gastrointestinal conditions, a result which the authors speculated might be driving the higher risk seen overall.

        Gareth Corbett, a gastroenterologist from Addenbrookes hospital in Cambridge who was not involved with the study, cautioned against panic, pointing out that in most cases the benefits of PPI far outweighed any risk. What was more, he said, while the increased risk sounded high, it was still very low for each person.

        PPIs are very effective medicines, proven to save lives and reduce the need for surgery in patients with bleeding gastric and duodenal ulcers and several other conditions, he said.

        The studys authors said it was important that PPIs were used only when necessary and stopped when no longer needed.

        Corbett agreed that many people take PPIs unnecessarily. They could get rid of their heartburn by making lifestyle changes, such as losing weight and cutting back on alcohol, caffeine and spicy foods, he said.

        The authors said the study was observational, meaning it did not show that PPIs were the cause of the increased risk of death, and that it was unclear how the drugs would act to affect mortality. They said the drugs could affect components within cells, known as lysosomes, that help break down waste material, or shortening protective regions at the end of chromosomes, known as telomeres.

        Aly said people on PPIs should check with their GP whether the drugs were still needed, adding: In some cases we expect that PPIs can be safely stopped, particularly in patients who have been taking them for a long time.

        Read more: https://www.theguardian.com/science/2017/jul/04/people-taking-heartburn-drugs-could-have-higher-risk-of-death-study-claims