NHS understaffing may have effect on baby mortality rate, says top doctor

‘Legitimate to ask’ whether number of staff is contributing to death of 300 babies a year, says Dr David Richmond


Doctor holding stethoscope

Nearly three hundred babies a year are dying during or soon after their birth with a further 1,200 ending up with brain damage or other serious health problems. Photograph: Richard Gardner/Rex Features

Britain’s leading obstetrician says it is legitimate to ask whether understaffing of maternity care and labour wards is contributing to Britain’s stubbornly high rates of baby death and brain damage.

Dr David Richmond, president of the Royal College of Obstetricians and Gynaecologists, has voiced alarm that nearly 300 babies a year are dying during or soon after birth with a further 1,200 ending up with brain damage or other serious health problems.

The infant deaths, Richmond said, were due to a range of issues. But with maternity units struggling to cope with a baby boom over the past 10 years and a shortage of midwives and doctors, Richmond said it was “a legitimate question to ask” whether pressure on resources was contributing to the tragic toll.

“We need to look at the possibility that understaffing, labour wards that are under pressure and busy, and stretched facilities may be a factor in some of these poor outcomes,” Richmond told the Guardian in his first interview since taking up the post.

The obstetrician, who represents the UK’s 6,000 maternity doctors, also conceded that errors by doctors and midwives were to blame for some of the terrible outcomes.

There were instances where staff made “small, relatively innocuous mistakes [which], when combined, lead to a disaster”, he added.

Richmond said that Britain’s high rate of stillbirth – almost 4,000 a year or about 10 a day – was an “appalling” and largely preventable loss of life. He voiced particular concern about the 144 babies who died during labour in 2009, the last year for which figures are available, and the 134 who died within the week after birth, despite not having a major congenital anomaly.

The UK had the third-worst stillbirth rate among 35 high-income countries, according to a study in the medical journal the Lancet in 2011. While the numbers of stillbirths had gone down slightly, “it’s still a lot of mums in the 21st century that are losing their babies unnecessarily”, Richmond added.

Data from the Office for National Statistics show that there were 4.9 stillbirths for every 1,000 live births in England and Wales in 2012.

The royal college’s new president said the 22% increase in births over the past decade meant maternity units were being “squeezed” because midwife and doctor numbers have not been increasing at the same rate.

Labour wards are having to cope with too few midwives and 800 fewer consultants than are needed to provide 24-hour care in the 62 units that handle at least 5,000 births a year in which complications arise.

“If you need to have a consultant there at three in the afternoon, why is it not equally important to have a consultant there at three o’clock in the morning? In my view, it is,” Richmond added.

But the NHS‘s tight finances meant there was no realistic possibility of consultant numbers rising from 2,200 to the ideal of 3,000, he said.

Action was also needed, Richmond said, to reduce the 1,200-a-year rate of “near misses”, in which complications occur during labour and birth that often leave the baby temporarily but dangerously deprived of oxygen. Babies who become “severely hypoxic” face the risk of brain damage and profound lifelong disability.

“These are babies that are born in very poor condition and may have a very slow heartbeat or very restricted breathing or not respond to stimulation,” he said.

Each such case can leave the NHS having to find millions of pounds in compensation to pay for the substantial cost of providing lifetime care for the child.

The loss of life and very serious medical consequences for newborns in all these deaths and near-misses, totalling almost 1,500 a year, constituted “an ongoing tragedy involving potentially avoidable very serious outcomes” and represented “1,500 individual tragedies”, said Richmond.

Asked why the baby deaths occur, Richmond replied: “The best analogy is to describe them as plane crashes.

“Lots and lots of women travel through pregnancy and labour safely but occasional tragedy occurs. These tragedies are always ‘multifactorial’ and require thorough investigation to establish why.

“It is not uncommon that a series of small relatively innocuous mistakes, when combined, lead to a disaster. There are often no easy fixes.

“The challenge is to be willing to share these experiences, to learn from each other and invest in safety. There is a big difference: flights are often cancelled for safety reasons – medical emergencies during pregnancy and labour can’t be cancelled,” he said.

Sands, a stillbirth and neonatal deaths charity, said the often chronic shortage of midwives in the NHS, in which some hospitals have almost one in five posts unfilled, and potentially inferior care at weekends, when often less experienced doctors are on duty, were factors in the UK’s relatively high baby death rates.

“It is a travesty that so many babies die every year in labour in the UK, devastating the lives of families,” said Charlotte Bevan, the charity’s senior research and prevention adviser.

“In many cases, these are tragedies that happen at term, when the baby is ready to start new life outside the womb, and they should never happen. We need more midwives so that women can have continuity of care in pregnancy and one-to-one care in labour.”

The NHS had to provide “a maternity service that works as well at the weekend as it does during the weekday, that can respond to an increasingly complex pregnancy population”, she added.

Dr Dan Poulter, the health minister, said childbirth on the NHS was safe and perinatal mortality was declining.

“The numbers of stillbirths and infant mortalities are at the lowest levels since 1993, but there is still more to do. The NHS is a safe place to give birth, with women reporting high levels of trust and confidence in staff,” said Poulter, who is also an obstetrician.

The NHS in England has more than 1,500 more midwives than in 2010 and a record 6,000 more in training, he added.

Since 2012, the NHS has measured hospitals on their progress in reducing stillbirths and baby deaths, and is trying to better identify unborn babies who are smaller than average for their gestational age. Many babies who are stillborn are of below normal size.

5 Osteoporosis Assumptions: Myth or Fact?

Sadly, the first time many people think about osteoporosis is after their first bone fracture.

Even though this disease of weakened bones is highly common — affecting as many as 200 million people worldwide — many myths prevent people from seeking the treatment or risk-reduction strategies they need. Below are just a few common assumptions.

1. Men don’t get osteoporosis

Myth. Although osteoporosis is five times more common in women, 20 to 25 percent of men will experience a bone fracture because of osteoporosis or reduced bone mass during their lives. Men typically develop osteoporosis a little later in life, after age 65. Women may develop it as early as their 50s because of the effects of menopause.

“Even if you have already been diagnosed with osteoporosis, you can increase your bone density — but probably not without help.”

Scott Burg, DO

Department of Rheumatologic and Immunologic Disease

2. You may never notice symptoms

Fact. Osteoporosis can be a silent disease. It typically doesn’t come with pain or other symptoms. To further complicate things, even a fracture may be painless. You will notice a broken leg or hip, of course, but vertebral fractures can happen over time with very little discomfort.

The silent nature of this disease is all the more reason to talk to a doctor about risk factors and whether you would benefit from a DEXA scan — a simple test that measures bone density. For women after menopause, we typically recommend having one every two years. Men may not need them as frequently, but it’s absolutely worth working out a schedule recommendation with your doctor.

3. Osteoporosis is a natural part of aging

Myth. Aging is a factor, but there’s so much more to osteoporosis. In addition, most people will lose bone mass over time, but that doesn’t necessarily mean you have osteoporosis.

Other factors play a part, including genetics and family history, a lack of vitamin D, high caffeine intake, smoking, a lack of exercise, and even medications such as those used to treat acid reflux and prostate cancer.

4. You don’t need to think about osteoporosis when you’re young

Myth. Establishing good exercise and nutrition habits at any age will help you reduce your risk. Exercise may help you prevent losing as much bone as you would if you were a couch potato.

Smart eating habits can help you get the vitamins and minerals that help fight bone loss. For example, both calcium and vitamin D play a major role in bone health. If you’re not getting enough in your diet or through sunlight, ask a doctor about supplementation.

5. You can regain bone mass

Fact. Even if you have already been diagnosed with osteoporosis, you can increase your bone density — but probably not without help.

Exercise alone won’t do it. Calcium and vitamin D supplements alone won’t do it. The best way to approach bone loss is through a combination of these plus medications designed to treat osteoporosis. These include traditional drugs such as bisphosphonates as well as newer options such as teriparatide and denosumab.

The bottom line: Don’t ignore osteoporosis. The more you know about it, the more you can work to prevent it — or treat it if you’ve been diagnosed.

Stephen Sutton ‘coughs up tumour: Terminal inspirational cancer campaigner recalls hospital drama in latest blog update .

Inspirational teenager Stephen Sutton has told how he coughed up a tumour that had caused his lung to collapse.

Updating well-wishers about his condition on his Facebook page, the 19-year-old said he felt “bloody fantastic”.

He said he suffered a violent coughing fit and felt like he was suffocating.

But he revealed his condition dramatically improved when he “forced out an oval red stained solid object through my mouth”.

The teen is now breathing without the help of oxygen and X-rays have shown his collapsed lung has slightly inflated.

Writing on his Facebook account, Stephen’s Story, he said he felt better than when he was admitted to hospital a week ago on Easter Sunday.

Stephen said: “This whole week has been pretty unbelievable and I can barely fully get my head round everything that has gone on, but yesterday there was perhaps the most bizarre but fortunate twist in the tale yet.

“From around mid afternoon yesterday I developed a slight cough which slowly got worse as the day went on.

“Amongst frantic hand pointing and panicking I felt like I was like suffocating.

“Then I forced out an oval red stained solid object through my mouth.

“Since then, my breathing has dramatically improved.”

Terminally ill Stephen has already raised more than £2.8 million for the Teenage Cancer Trust, and a comedy gig that sold out in just four minutes is set to raise even more cash.

Celebrities have urged the public to dig deep and help a terminally-ill teenager raise £5 million for charity.

The teenager has spoken of his astonishing charity legacy as he bravely prepares to die, saying: “I’m cool with it. I’ll go knowing I’ve helped others.”

But while it seemed Stephen may not have long left to live last week his health has actually improved slightly over the weekend.

He wrote: “Physiologically a tumour breaking away like this is possible, but it all just seems incredibly surreal- mind, I’m not complaining!

“My lungs are still pretty messy with other tumours, clots and potential infections/inflammations/etc affecting my overall condition but, for now at least, I am in a good stable state.

“I have no immediate problems and in fact feel better than I did when I first came into hospital last Sunday!

“The general oncologist and team I’ve been seeing will discuss the events with my professor in the morning and we will see where we go from there.

“It’s still a case of taking each day as it comes, but at the moment the days just keep on coming!!”

Does Water Really Speed Up Weight Loss?

We asked experts if drinking H20 can affect the number on the scale.

The question: I’ve heard the rumor that you should drink water to lose weight. But can simple H20 really help you shed pounds? It sounds too good to be true.

The experts: Brooke Alpert, R.D., founder of B Nutritious, and Keri Peterson, M.D., a physician at Lenox Hill Hospital in New York City and a medical advisor for Women’s Health

The answer: “I don’t think that water directly affects weight loss,” says Alpert. “However, I think water consumption is directly correlated with weight loss.” As in: Water does not have some magical property that burns fat (sorry!), but it definitely can help you with your weight-loss efforts (hooray!).

First off, staying hydrated could help you avoid overeating. “A lot of people confuse thirst for hunger,” says Peterson. “So they’ll tend to eat rather than drink water.” If you’re craving a midday snack and want to make sure your pangs are caused by hunger, not hydration, have a glass of water first. Then see if you’re still hungry 30 minutes later, says Peterson.


Also important to keep in mind: “If you’re continually staying well hydrated, that false cue won’t happen,” says Peterson. To make sure you’re getting enough H20 in general, the key is your pee (seriously): You want it to be a pale yellow.

Of course, drinking water also means you’re not drinking something else—such as sugary, caloric beverages or even potentially diet-breaking diet soda.


That said, this doesn’t mean that you should go around guzzling water nonstop to avoid dehydration. (Though it is rare, it’s actually possible to drink too much water, particularly if you’re forcing yourself to drink regularly even when you’re not thirsty.)

So what’s the moral here? “Water is a great accessory for weight loss,” says Alpert. “Drinking enough water and staying properly hydrated is part of a healthy weight-loss system and healthy weight in general.”  We’ll raise a glass of H20 to that!

MERS May Be A Concern But It’s Not SARS.

Unlike SARS, MERS is no pandemic virus
Source: Wikipedia; Modifications: Jason Tetro

Over the last week, the number of human patients suffering from Middle East Respiratory Syndrome (MERS) has grown significantly bringing fears of a possible SARS-like spread of the disease and the potential for the development of a pandemic.  Although this may be perceived as crying wolf, the concern is indeed justified albeit not to that extent.  The problem lies in the apparent unanswered questions with respect to this epidemic.  Without information on epidemiology, transmission, route of entry and infection control, public health officials simply cannot offer a perspective on the future of this disease.

Yet there are answers to be found.  Over the nearly two years since the causative virus, the MERS coronavirus (MERS-CoV) was identified, researchers have gained significant insight into the ongoing epidemic.  They have also seen just how this virus compares with SARS and the answer always appears to be the same.  While MERS is a bad actor, it is no SARS and most likely will not cause a pandemic.

The first comparison is epidemiological. MERS appears to be a respiratory disease with the potential for other complications including diarrhea, muscle and joint pain, kidney injury and organ failure.  There are quite a few similarities with SARS however a closer look at the progression of infection shows these two are not at all alike.

SARS is a two-stage infection requiring up to several weeks of incubation before symptoms begin.  When they hit, the person remains ambulatory for upwards of ten days to three weeks.  Then, when the second stage occurs, the patient inevitably requires hospitalization and in some 10% of cases, death occurred.  MERS, on the other hand, requires only about 5 days for onset of symptoms (although periods of up to two weeks have been seen) and there appears to be only one stage.  When symptoms begin, especially in severe cases, the person is all but debilitated and requires rapid medical attention.  Death occurs in about a quarter of the population although those numbers continue to drop.

The reason for this reduction in mortality stems from the rise of either mild or asymptomatic MERS infection in healthy individuals. The median age of death is about 52 years of age and most severe cases occur in people with underlying conditions such as diabetes, renal failure, heart disease and immunosuppression.  This suggests MERS may not be a perfect pathogen and normal healthy individuals may be able to fight off infection.  In comparison, SARS infected people uniformly and equally as deadly; the median age of death was closer 43 years. Some did exhibit lower levels of infection, possibly due to prior infection and there were some who simply did not exhibit any symptoms.

The next comparison lies in the spread of the two viruses and how best to control it.  SARS was easily transmitted in the environment while MERS continues to require close contact with an infected person or animal.  Some may feel this might change allowing MERS to be spread just as rapidly.  Yet the biological differences between the two means of infection suggest this may be unlikely.

SARS and other less virulent coronaviruses rely on receptors found throughout the respiratory tract.  They can easily cause infection through aerosols and droplets.  MERS on the other hand, infects through interaction with a protein called dipeptidyl peptidase 4 (DPP4) although it is also known as adenosine deaminase complexing protein 2 (ADCP2) and cluster of differentiation 26 (CD26).  As the multiple aliases suggest, this molecule is found in many locations within the body and performs a variety of functions including cell movement as well as regulation of blood sugar and cardiac functions.

There is, however, one place DPP4 cannot be found:  the upper respiratory tract.  Studies have shown the protein can only be found in the lower respiratory region including the bronchi, blood vessels and submucosal glands. As a result of this, MERS infection simply cannot happen in the same way as SARS.  The only means possible– at least via this route – is through deep inhalation of the virus, achievable solely through close contact with an infected person or animal.  With this light shed on the situation, it is easy to see that this interaction can easily be prevented through either social distancing or by wearing a mask.

MERS does have another possible route for infection leading to an even greater concern. The virus may still gain entry through the gastrointestinal tract where DPP4 can be found in abundance. To date there is only limited data on the impact of ingestion of viruses in laboratory cell cultures.  Yet a recent case in Malaysia linked to drinking camel milk may suggest this link may have credence.  Should this be the case, the virus may spread systemically through the body without the involvement of the lungs.  This would, however, change the focus of the virus from airborne to primarily foodborne.  Control would be more intensive than wearing a mask yet could be achieved by ensuring the virus is killed either through cooking or pasteurization prior to being consumed.

The final aspect of MERS biology relevant to its spread is its survival in the environment.  Studies on other coronaviruses have shown survival on surfaces for hours to days. That being said, it’s also relatively easy to kill with heat, disinfectants and even detergents.  This clearly shows the importance of infection control measures, such as hand hygiene and regular surface cleaning to prevent spread.

The data suggest the pandemic fears regarding MERS may not be necessary.  Due to the biological nature of the virus, its receptor for infection, its routes for spread and the relative ease of necessary disinfection measures, there is every indication this virus can be controlled and infections prevented.  Yet, while the science is relatively clear, the future of MERS remains in doubt.

Research can only offer the best means possible to keep the virus at bay.  But ensuring that these actions are taken requires an even harder threshold and one that may be the root cause of the problems:  behavior.  As seen before with SARS, avian flu and Ebola, promoting and enforcing human actions to minimize the risks is nearly impossible, even in trained individuals.  Yet as long as compliance remains poor, whether in healthcare or in public, the chances for infection will continue.  While the current spike in cases is most likely not indicative of a future trend, it is a reminder that even a virus not entirely suited for humans, such as MERS, can indeed cause significant disease burden and unfortunately cause a number of needless deaths.

One plus to wearing stripes.

Scientists have long wondered what benefit zebras might get from their fancy black-and-white coats. Those snazzy stripes may be most useful as protection from biting flies, a study now concludes.

Biologists studied zebras and other closely related African animals. They tested five popular ideas about how the stripes might function. No evidence emerged to support most of these notions, Tim Caro told Science News. A wildlife biologist, he works at the University of California, Davis.

Some scientists had proposed those stripes help zebras hide from predators, such as lions, or confuse them. Still others suggested that those stripes might offer some cooling or help the animals in forming social groups.

None of those ideas hold up, Caro’s team reported April 1 in Nature Communications. Instead, the stripes appear to help the animals avoid the bite of bloodthirsty flies. This finding supports some studies had found signs that flies prefer solids to stripes when hunting for a landing place.

To test all of the theories, Caro’s group used geographic information. They looked at where in Africa the 20 different types of animals belonging to the genus Equus lived. Some of these equines have stripes, including zebras and asses with striped legs. Others are stripe-free. These include other asses and wild horses.

The scientists found no connection between stripes and whether the animals lived in woodsy areas. That suggests stripes don’t camouflage zebras in those places.

The scientists also saw no link between where striped animals lived and where lions hunted. In other studies, researchers found that lions ate plenty of zebras. The new observations suggest stripes don’t confuse the predators.

The experts also looked for — and found — no evidence that stripes cool the zebras or help them recognize each another when forming social groups.

Striped animals often live in places where the environment is just right much of the year for biting flies to flourish. In those areas, horseflies, tsetse (TSET see) flies and other biting flies spread fatal diseases to zebras and horses. That connection now suggests stripes may help zebras reduce the number of bites — and the infections they can spread.

The study doesn’t answer how the zebra got its stripes in the first place, Caro admits. Science may never know.

Innes Cuthill is a biologist at England’s University of Bristol. He finds the new study “compelling.” Until now, Cuthill’s favorite hypothesis had been that zebra stripes confused predators. It’s too soon to say the mystery of the zebra’s stripes has been solved, he notes. But he says that keeping flies away is now probably “the leading contender.”


Neonicotinoid pesticides harm honeybees while failing to improve crop yields.

The immune systems of honeybees are being compromised. Bees are being slaughtered in droves. Piles of these pollinators are gathered by the handfuls at farms across the Western Hemisphere. This isn’t a small-scale problem that the bee populations can easily adapt to and overcome. This has been a growing problem since 2006, when commercial bee colony collapse was first observed. Now, beekeepers consistently report an average loss of one-third of bee populations each year.


This isn’t the complaint of some poser environmental cause. This travesty is affecting each and every person on the planet in tremendous ways. Without honeybees, important nutritious vegetable crops cannot be pollinated. Without honeybees, one of nature’s most valuable antibiotics — honey — falls into limited supply. Important medicinal resources like beeswax and bee propolis are becoming scarcer. Honeybees play an integral role in a healthy human experience.

Neonicotinoids harm honeybee immune systems at the molecular level

The honeybee fallout comes at the hands of people who invest in chemical manufacturers — most significantly, pesticide manufacturers.

The speculation over the dangers of neonicontinoid pesticides is over. New findings from scientists in Italy suggest that neonicotinoid pesticides exert a molecular trigger in honeybees that damages their immune response. By compromising the bees’ immune system, the chemicals make the pollinators more susceptible to viruses. As a synthetic nicotine chemical, these pesticides are intended to destroy the nervous system of insects like aphids; however, this study breaks new ground, showing how these pesticides exert an immunosuppressant effect on honeybees.

Imidacloprid and clothianidin suppress protein signals involved in immune system regulation

The study, led by Francesco Pennacchio of the University of Naples Federico II, identified a specific gene in the honeybees containing a code for a protein that regulates immune response. This leucine-rich repeat (LRR) protein family is responsible for suppressing activities of a key protein involved in immune signals. When a class of neonicotinoid pesticides called clothianidins was applied at sublethal doses, the LRR protein was expressed at increased levels, ultimately suppressing the immune system pathway of the honeybees.

Another class of neonicotinoid called imidacloprid had the same effect on the bees’ immune system. In contrast, an organophosphate insecticide called chlorpyrifos did not signal the LRR gene codes, leaving the bees unharmed.

Therefore, clothianidin and imadacloprid scientifically suppress the honeybees’ immune system. When the scientists exposed the compromised bees to a common field pathogen called the deformed wing virus, the virus replicated unchecked, overwhelming the bees’ immune systems. When no neonicotinoid pesticides were applied, bees were much healthier and could ward off the deformed wing virus more effectively.

New report finds that honeybee-harming neonicotinoids actually fail to improve crop yields

To make matters worse for neonicotinoid pesticides and their primary manufacturer, Bayer CropScience, a new report finds that these honeybee-harming chemicals don’t even help farmers improve their crop yields.

The Center for Food Safety compiled new evidence showing how this class of pesticide actually fails to improve crop yields on a consistent basis. In some instances, the pesticides have an opposite effect, attacking the wrong insects that are needed to control the aphids!

As the go-to pesticide in America, neonicotinoids are doused on the 170 million acres of GMO corn and soybean crops across the country. This insect neurotoxin is absorbed by the growing crop and becomes chemical warfare for insects and spiders that are naturally present in the field.

In many instances, neonicotinoids have a reverse effect

The Center for Food Safety review included 19 scientific peer-reviewed studies that evaluated whether the pesticides were effective for increasing a crop’s bushels-per-acre yield. In the conclusion, 11 studies were inconsistent and eight showed no improvement in crop yields at all.

The most telling example of failed crop yields was explained by Jonathan Lundgren, an agricultural scientist at the North Central Agricultural Research Laboratory in Brookings, S.D.

In the peer-reviewed study, two different kinds of soybean seeds were planted in opposite fields. One was coated with pesticides, and the other was not. For two years in a row, the crop yields were evaluated. Both crops yielded generally the same amount of soybeans. After studying the insects affected, Lundgren found that the targeted aphid wasn’t even harmed, since the pesticide dried up before the bug appeared in mid-July.

The pesticide actually targeted the wrong insects. Ladybugs, lacewings and spiders that prey on the aphid were affected the most.

In trying to control the natural world, the pesticide actually had the opposite effect, killing the aphid’s predators, allowing the bug to go unchecked and do more harm to crops.

In summary, the Center for Food Safety’s attorney Peter Jenkins said, “In most cases they [neonicotinoids] are totally unnecessary and are causing tremendous harm.” Mr. Jenkins represents beekeepers and is taking on the EPA to address the environmental challenges imposed by neonicotinoids.

Sources for this article include




Why Bill Gates Fights Diseases Abroad, Not At Home.

This week in Seattle, Bill and Melinda Gates are attending a meeting of the minds.

Five hundred of the world’s top innovators in global health have gathered for the , an annual event in which scientists, engineers, policymakers and activists work to develop new tools for fighting diseases.

By ensuring vaccines are invented and distributed, Bill Gates says, his foundation is dramatically reducing the number of childhood deaths in poor countries.

Since the Bill & Melinda Gates Foundation began in 2000, the nonprofit has invested a lot of money in education in the U.S. But even more money has gone toward ending diseases in developing countries. Last year, the foundation dedicated to eradicate polio worldwide.

NPR’s Morning Edition host David Greene recently spoke with Gates about why he and his wife have chosen to focus their efforts abroad and less here at home — and whether he thinks the world is still on track for eradicating polio by 2018.

We note that the Gates Foundation supports NPR programming. And the interview has been edited for length and clarity.

Why have you chosen to invest billions of dollars on diseases that the U.S. eradicated decades ago?

Our view on health is that we have a lot of interventions where we’re saving lives for less than $2,000 per life saved.

By making sure new vaccines are invented, making sure they get out to all the kids on the planet, we’re taking diarrheal deaths, pneumonia deaths and bringing those down pretty dramatically.

Any country where we can save a life for a few thousand dollars, we’ll do it. It turns out the place you can do that — really make dramatic reductions in the number of children who die — is the really poor countries.

One area the foundation focuses on is eradicating. Why did you choose that disease?

I was stunned when I found out that malaria, when we got started [in 2000], was killing a million children a year; most of that’s in Africa.

Way back in 2000, we gave a $30 million grant, and we became one of the largest funders in the area. It was stunning to me that a problem of such magnitude wasn’t getting huge focus. …

For Africa to move forward, you’ve really got to get rid of malaria.

Nobel Prizes have been given for work on malaria. Governments and foundations have spent a flood of money on it. But the disease has persisted. Why do you think this is the moment when you can make a difference with malaria?

Those Nobel Prizes were given a long time ago. The thing that’s magical now is that we’re able to look at the malaria genetics and understand how it’s spreading. …

It’s fair to say that there have been failures in the past. The year I was born, 1955, the first big disease-eradication program in the world was declared for malaria. After about a decade of work, they realized that at least in the tropical areas, they did not have the tools to get it done.

We’re going to have to be a lot smarter this time.

We’re able to model the disease dynamics in a way that wasn’t possible before. We actually have a [now]. It’s not a 100-percent-effective vaccine. But that looks like it will be a very helpful tool.

Do you think there will ever be moment when you might start thinking that maybe money would be better spent on something outside health or vaccines, such as infrastructure?

I don’t think that’s likely to happen. We want to be realistic. [But] people do care a lot about [malaria]. They see their children dying. They see the effects of cerebral malaria even on kids that survive.

So I don’t think this is one where we’ll run into much resistance, too much apathy. This is a big killer.

Development is a series of things. If you could only pick one thing, I think you would pick health because it’s so catalytic.

But then education, good governance, infrastructure — all of those things are part of the magic things that have allowed countries like China, Brazil, Thailand, Mexico to become middle-income.

So now we can focus on the remaining countries, the low-income countries, and have a goal that within 20 years, the number of people living in extreme poverty could get close to zero.

The foundation also works on wiping out. The goal is to finish the job by 2018. Do you think that’s still realistic after recent?

[Polio eradication] is our top priority. And things are looking pretty good in Nigeria. We’ve had only one case this year, which is way down from last year.

We have an outbreak that started in that has spread to some surrounding countries. We think we’ll be able to deal with that outbreak.

In Pakistan, we still have an area that the Taliban is not letting in vaccinators; and in fact, violence against vaccinators continues there. …

We’re still very committed to the eradication; 2018 still seems achievable. But we’re going to have to get a bit of political change in Pakistan, and we’re going to have to continue to do very good work in Nigeria.

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Hemophilia Treatments Have Come a Long Way.

Gone are the days when a hemophilia diagnosis meant you could not live a normal life. Now more treatments are approved by the Food and Drug Administration (FDA), and people with the condition can better manage bleeding. That’s good news as thousands observe World Hemophilia Day on April 17, 2014.

Hemophilia is a rare bleeding disorder. It is usually hereditary, but it can be acquired in rare cases if a person’s body develops antibodies that attack clotting factors in the bloodstream. Hereditary hemophilia usually occurs in males and currently affects about 23,500 Americans.

People with hemophilia are lacking one or more important clotting factors, which are proteins needed for blood clotting. Several types of clotting factors exist and there are two main types of hemophilia, says Nisha Jain, M.D., chief of the Clinical Review Branch in FDA’s Office of Blood Research and Review. Hemophilia A occurs when people have low levels, or missing, clotting factor VIII (8). Hemophilia B occurs when people have low, or missing, clotting factor IX (9).

People with hemophilia may bleed for a longer time than others after injury or surgery. They may also have internal bleeding—especially in knees, ankles, and elbows—that can damage organs and tissues and even be life-threatening.


Treatments for Hemophilia

Dr. Nisha Jain
“We have seen shifting toward the prevention of bleeds,” says Nisha Jain, M.D., chief of the Clinical Review Branch in FDA’s Office of Blood Research and Review.

At present hemophilia is not curable, but treatments have come a long way, Jain says.

Hemophilia is sometimes called the “Royal Disease” because it affected the royal family of England during the 1800s. By the 1960s, hemophilia was treated with whole blood or fresh plasma. But these treatments didn’t have enough factor VIII or IX proteins to stop serious internal bleeding.

Now the primary type of hemophilia treatment is replacement therapy: Concentrates of clotting factor VIII (for hemophilia A) or clotting factor IX (for hemophilia B) are injected into a patient’s vein to replace low or missing factor.

These concentrates have traditionally been made from human blood. Today, an increasing number are made using recombinant DNA technology (a form of artificial DNA), with some made without any material sourced from humans or animals. The final product is a powder that is mixed with sterile water before use.

Some people have regular preventive or “prophylactic” therapy to prevent bleeding. This can be done in less than five minutes, excluding prep time, Jain explains. Others have therapy only as needed.

The type and frequency of treatment varies depending on the severity of hemophilia, which can be classified as mild, moderate or severe.

People with mild hemophilia have 6% to 49% of the normal levels of clotting factors in their blood. They generally only have bleeding problems after serious injury or surgery.

Those with moderate hemophilia—about 15 percent of the hemophilia population, according to the
National Hemophilia Foundation—have 1% to 5% of normal clotting factor levels. They can have bleeding problems after injury and spontaneously.

Those with severe hemophilia—about 60% of the hemophilia population, per NHF—have less than 1% of normal clotting factor levels. They bleed after injury and may have frequent spontaneous bleeding, including bleeds into joints and muscles. In addition to factor replacement, pain medication and physical therapy are also used to lessen pain and swelling if joint bleeds occur.

“The mild patients rarely need treatment. And moderate patients are the same,” explains Jain. In certain situations, such as before dental work, patients with mild hemophilia receive Desmopressin (DDAVP) a man-made hormone that increases the level of factor in the blood. “Patients with severe hemophilia are those who really need treatment to prevent or resolve bleeds.”


A Shift Toward Prevention

Doctors, particularly hematologists who specialize in the study of blood, tend to identify people with severe hemophilia early. “Patients can be diagnosed as infants during circumcision,” says Jain. Then families can work with hematologists and hematology treatment centers.

“In recent times, we have seen shifting toward the prevention of bleeds,” Jain says. “You want to prevent bleeding that causes joint damage. Once joint damage starts, it is difficult to stop progression unless bleeding into joints is reduced.”

The treatments for hemophilia continue to improve, and FDA has approved many replacement factors in recent years. For instance, in March 2014 it approved Alprolix, the first Hemophilia B treatment designed to require less frequent injections when used to prevent or reduce the frequency of bleeding. It also recently approved Rixubis—a factor IX product—to control, prevent and reduce bleeding associated with hemophilia B. And the agency approved Novoeight, a factor VIII product, for control of bleeding and a routine prophylaxis treatment for adults, adolescents and children with hemophilia A.

Of course, the agency continues to carry out its broad responsibility to regulate medicines made from blood and blood components, including clotting factors. Today, due to strengthened FDA safeguards and oversight, these products are safer than they have ever been.

“Patients should stay informed about various treatment options,” Jain adds, “and should consult with their health care providers to obtain, and follow, a comprehensive management plan.”

She says those with hemophilia tend to be well-educated about their health and notes, “With appropriate treatment and care, people with hemophilia can, and do, live normal lives.”

The robots will really take over this time


It’s no joke – the robots will really take over this time


Robot working in office

Welcome to the future: a robot working in an office.

Not often do you hear a Newsnight presenter using an arcane mathematical term, but last week was an exception. The culprit was David Grossman, who made an excellent film for Newsnight about the threat to employment from advanced robotics. In the course of this, he made the standard pilgrimage to MIT to interview Erik Brynjolfsson and Andrew McAfee, who have made much of the running in this area with a number of books, of which the most recent is The Second Machine Age. Their argument, said Grossman, was that our society has reached an “inflection point”, a concept beloved of those who studied differential calculus in their youth, but probably unfamiliar to the average viewer.

Still, that’s what Wikipedia is for. A point of inflection, it explains, is a point on a curve at which the curvature or concavity changes sign from plus to minus (or vice versa). Since this sounds like a smaller deal than the wholesale upheaval prophesied by Brynjolfsson and McAfee, Grossman might have got more mileage out of “tipping point”, which, though different to inflection, seems to me to get closer to the nub of the question.

In their book, Brynjolfsson and McAfee maintain that the combination of massive computing power, comprehensive networking, machine learning, digital mapping and the “internet of things” are bringing about a full-blown industrial revolution on the same scale as the transformations brought about by steam power and electricity. But whereas those earlier revolutions supplanted human (and horse) muscle, the new one will supplant much human cognition, in that work that involved employing people to do information-processing tasks will ultimately be done by computers. The implication is that even those in many white-collar occupations may find themselves unemployable.

At this point, many readers will yawn knowingly. We have, after all, heard this kind of heady talk before – in the 1960s, for example, when robots arrived on automobile assembly lines and there were dire predictions about mass unemployment caused by these new machines. It didn’t happen, or at any rate it didn’t happen as advertised. Many assembly-line jobs did disappear, but new kinds of enterprise appeared, and displaced workers found new employment and the prosperity machine rolled on. So are Grossman and his MIT interlocutors just winding us up?

Not so, they insist. The problem, they say, is that most people have no idea of the abilities of these new technologies. They point to the Google self-driving car as an example of a capability that – until recently – most people thought would be the exclusive preserve of human beings for a long time to come. Yet the cars now exist and are safer than human-controlled vehicles. And if computers can safely drive cars in crowded urban environments, they can certainly do a lot of the tasks currently performed by office workers. This time, in other words, is different. We really are standing on the brink of an inflection point.

There is a whiff of technological determinism to all this (although Brynjolfsson and McAfee vigorously deny the charge). It suggests that technology is the main – if not the only – force that drives history. In a variation on the “guns don’t kill people – people do” argument, critics point out that the social context in which technologies come into being, not technology itself, is the thing that determines change.

And that’s true. But, paradoxically, this time it may provide an argument that supports the determinist thrust of the Brynjolfsson/McAfee case. Because these new technologies have arrived at a time when the social context – neoliberal capitalism – seems purpose-built for furthering the extreme rationalisation of work that the new technologies enable. Do we seriously believe that an economic system that supports the massive outsourcing of jobs to low-wage countries would not jump at the opportunity of replacing expensive white-collar employees with robots that cost about $4 an hour to run, never answer back, don’t have unions and are never sick or depressed?

Then there is one other thing that Brynjolfsson and McAfee don’t really discuss, namely the four intrinsic properties of computing and networking technologies. They are: near-zero marginal costs (which confer massive advantages on early movers and investors); network effects (which lead to winner-takes-all outcomes, as has happened with search and social networking); the way in which online phenomena follow power law statistical distributions that apply when a few players capture the overwhelming bulk of the action, leaving everyone else scrabbling around in a “long tail”; and technical lock-in (of the kind that has enabled Amazon to exert an iron grip on cloud computing).

Put these together and you have technologies that have an in-built tendency towards monopolistic power. They are shaping the world into which we are heading. The inflection point of which David Grossman spoke might actually be the edge of a precipice.