Einstein’s gravity theory passes toughest test yet.



“Official EU research verifies bee holocaust caused by dangerous man-made poisons, Big Ag and Big Government do nothing”

A class of insecticide chemicals commonly applied to rapeseed, also known as canola here in the U.S., as well as sugar beets, corn, and various other crops is killing off bee populations across the globe, and a prominent environmental watchdog group is now demanding that these insecticides be immediately pulled from the market. As reported by the U.K.’s Daily Mail, a report issued by the U.K.’s Environmental Audit Committee (EAC) confirms that neonicotinoid insecticides are to blame for mass bee die-offs.

The declaration by this prominent government advisory group comes following the release of data out of the E.U. showing that neonicotinoids contain compounds that interfere with bees’ central nervous systems, and thus cause them to become confused while pollinating. Eventually, bees affected by these chemicals lose their ability to navigate back to the hive, forgetting where they are and how to get home, which results in them starving and dying en masse.

Back in January, the European Food Safety Authority (EFSA) determined that neonicotinoids, which have been in use since the early 1990s, are directly responsible for triggering an epidemic of Colony Collapse Disorder (CCD) all around the world. The agency went on to express opposition to the further use of neonicotinoid insecticides, particularly with regards to plants that are attractive to bees. But the European Commission was ultimately unable to garner enough votes to successfully implement a two-year ban on the chemicals, which has prompted EAC to issue its own call for a ban.

“If farmers had to pollinate fruit and vegetables without the help of insects, it would cost hundreds of millions of pounds and we would all be stung by rising food prices,” says Joan Walley MP, chair of EAC, referring to the devastating losses that will occur in the absence of pollinating bees. “Defra (Department for the Environment Food and Rural Affairs) Ministers have refused to back EU efforts to protect pollinators and can’t even come up with a convincing plan to encourage bee-friendly farming in the U.K.”

UK, Germany primarily responsible for enabling continued ‘armageddon’ on bees

According to earlier reports, the European Commission was roadblocked in its attempt to protect bee populations by both the U.K. and Germany, which at the last minute failed to vote in favor of a two-year moratorium. The winners in the proposal’s defeat, of course, are chemical companies like Syngenta and Bayer CropScience, both of which have a vested interest in neonicotinoids. The losers are not only bees, but the global population at large, which will suffer from crop failures and eventually starvation.

“Britain and Germany have caved in to the industry lobby and refused to ban bee-killing pesticides,” Iain Keith from the non-profit environmental group Avaaz is quoted as saying by the U.K.’s Guardian. “[The] vote flies in the face of science and public opinion and maintains the disastrous chemical armageddon on bees, which are critical for the future of our food.”301946_563684540338331_1499555076_n

LED streetlamp aims to improve public’s view of stars.

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Researchers believe they have come up with a new type of LED-powered streetlamp that could radically reduce light pollution.

Current designs “leak” large amounts of light in unwanted directions, obscuring views of the stars, wasting energy and making it harder for drivers to see.

The team, based in Mexico and Japan, said they believed their solution was the “best ever reported”.

However, they have yet to turn their theory into a working prototype.

The study – carried out by scientists in Mexico and Taiwan – appears in the open-access journal Optics Express.

LED lens

According to the researchers, conventional street lamps – which use high-pressure sodium or mercury vapour – scatter up to 20% of their energy horizontally or vertically because it is difficult to control their beams.

It is easier to direct light from LEDs because it is being emitted from a smaller area.

So, while manufacturers controlled the direction of the light rays from older lamps using a reflector typically made out of polished aluminium, they can now take advantage of lenses to be more precise.

The researchers say the best LED (light-emitting diode) streetlamps on the market direct about 10% of their energy horizontally or vertically.

But they claim their own invention could further reduce the amount to just 2%.

Their proposed lamp uses three features to ensure the vast majority of its light is limited to a pre-determined rectangular shape covering the road:

The researchers suggest that the set-up would also save on electricity costs since it should require between 10 and 50% less power to illuminate a section of road than current LED streetlamps.

They added that they were now working to build a prototype and hoped to have it completed by October.

LED revolution

London-based light design firm Speirs and Major unveiled anLED-based streetlamp design of its own last year.

The firm’s associate director, Andrew Howis, said the latest study was just one of several efforts under way aimed at tackling the problem of stray light.

“As a result of LEDs it is now possible to place light exactly where it is needed and to greatly reduce spill light and energy wastage,” he said.

“This new research is an example of the innovation in LED optics – of which there are many – which uses a fairly sophisticated optical system to produce an optimised distribution for street lighting.

“It sounds like an advance on what is already available, but of itself is not revolutionary. The change from conventional light sources to LED is the revolution.”

The Campaign to Protect Rural England (CPRE) also gave the new work a qualified welcome.

The lobby group carries out an annual star count to publicise the problem of light pollution which it says disrupts wildlife and people’s sleep.

It noted that the new technology would only be of use if councils were willing to invest in it.

“From 1993 to 2000, light pollution in England increased by 26%, which shows the huge amount of energy and money wasted,” said campaigner Emma Marrington.

“It should be seen as an investment for local authorities to install more efficient street lighting, which will save money and energy waste in the long-term.

“Design is great but councils have to follow through with investment.”


Gout chemical slows Parkinson’s.

goutThe chemical urate, which is known to cause gout, appears to slow the progression of Parkinson’s disease, US researchers have concluded.

The team found that a study confirmed their previous suspicions about urate, which occurs naturally in the blood.

Urate is a potent antioxidant and so counteracts oxygen-related cell damage thought to contribute to Parkinson’s, they report in Archives of Neurology.

Trials are under way to find a safe way to raise urate levels as a therapy.

With support from the Michael J Fox Foundation, the researchers will recruit 90 recently diagnosed Parkinson’s patients for treatment with a chemical which helps to produce urate – called inosine – to see if this can raise urate levels so as to slow or halt disease progression.

Diets which are rich in foods like liver, seafood and dried beans and peas, as well as alcohol, can also increase blood urate levels.

But too much urate in the blood can cause gout, a painful joint disease.

Dr Michael Schwarzschild and colleague Dr Alberto Ascherio originally made the link between urate and Parkinson’s when analysing data from a previous clinical trial.

Their latest work confirms their hunch that urate is protective, they say.

New lead

They looked at samples of both blood and cerebrospinal fluid – the fluid that surrounds the brain and spinal cord – and measured urate levels.

Among the 800 Parkinson’s patients in the study there was a clear trend linking higher urate levels and slower disease progression.

Dr Schwarzschild, associate professor of neurology at Massachusetts General Hospital in Boston, said: “Urate is a major antioxidant and it can protect brain cells in the lab, which makes this a compelling possibility; but we don’t yet know if it’s urate itself or some urate-determining factor that helps people with Parkinson’s.”

He said people should not take the findings to mean they should eat more urate-rich foods to guard against Parkinson’s.

“Because elevated urate levels have known health risks, including gout and kidney stones, urate elevation should only be attempted in the context of a closely monitored clinical trial in which potential benefits and risks are carefully balanced,” he said.

Dr Kieran Breen of the Parkinson’s Disease Society said more research was needed.

“This tells us that it is possible to influence the rate of disease progression. It’s a new lead to follow.”

He said the findings might help find a therapy and markers to help track the disease.

He added that people treated for gout should not be concerned that the treatment would inadvertently increase their risk of Parkinson’s.

“There is no evidence to suggest it would,” he said.


Source: BBC


Worm could offer Parkinson’s clue.

_46859149__1207401_celegansa300-1Scientists believe that worms could hold the key to why some people develop Parkinson’s Disease.

Worms share 50% of their genes with humans, including those involved with inherited Parkinson’s.

Dundee University researchers will study a simple worm called C. elegans to try to work out why the condition causes patient’s brain cells to die.

The Parkinson’s Disease Society has given the university £190,000 to carry out the research.

Eventual cure

There are about 120,000 people with Parkinson’s in the UK. In up to 5% of those cases, the disease is believed to be directly inherited.

Parkinson’s is a progressive neurological condition affecting movements such as walking, talking and writing. It occurs as a result of a loss of nerve cells in the brain.

Dr Anton Gartner, who is leading the study, said: “Research leading to an eventual cure for Parkinson’ s disease is a daunting task and requires a very broad and multidisciplinary approach.

“I am grateful to the Parkinson’s society to recognise this and to so generously support our research.”

Worms will be used in the study as they are one of the simplest organisms with a nervous system.

The way worms’ nerve cells communicate with each other is also similar to how it works in humans.

Several genes, including one known as LRRK2, have been linked to the hereditary form of Parkinson’s Disease.

Dr Gartner’s team want to understand how changes or mutations in this gene lead to the development of Parkinson’s – and how drugs could stop the damage that these mutations cause to nerve cells.

Dr Kieran Breen, from the Parkinson’s Disease Society, said: “It’s fascinating that such a simple animal as a worm can be an excellent model for Parkinson’s researchers to study what happens in specific nerve cells.

“We are delighted to be funding this research with Dr Gartner in Dundee. It will help us to understand better what causes nerve cells to die in Parkinson’s, and will help us to develop new treatments for the condition.”

Source: BBC



Illegal loggers continue to threaten Amazonian tribe.

_67105288_awa1Campaigners say the Brazilian government is failing to protect one of the world’s most endangered tribes.

The Awa people are believed to number just 450, but their territory has attracted thousands of loggers and settlers.

Last year a judge ordered all outsiders should leave the area within 12 months.

But the deadline has passed and no evictions have taken place, says indigenous rights groupSurvival International.

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If their forest is being destroyed they will end up living on handouts from the government and lose their way of life”

The Awa live in north eastern Brazil and survive as hunter-gatherers in remote areas of rainforest. Of their number around 100 have never had contact with outsiders.

However, the tribe’s four protected territories have been whittled away over the years by settlers and loggers who are now said to outnumber the Awa by ten to one.

One territory of 120,000 hectares has had over 30% of the forest cover removed. Logging trucks are reported to enter and leave the area day and night.

“The Awa talk about hearing chainsaws and their game being scared away,” Alice Bayer, from Survival International, told BBC News.

“They find when they go to hunt there are less animals there because of all the noise.”

The Awa have tried to fight back, using the courts to enforce their rights to their territories that are guaranteed by the Brazilian constitution. A judge, Jirair Aram Meguerian ordered that all the loggers, ranchers and other settlers who have come into the area should leave by the end of March this year.

But the authorities haven’t done anything to evict invaders. Campaigners say that responsibility for the issue has fallen between different government departments. And because the rainy season is now finishing, more loggers are expected into the area.

“We’re very worried, more and more, that the Awa are going to find less food in the forest and become dependant on government handouts in the end,” said Alice Bayer.

“If their forest is being destroyed they will end up living on handouts and lose their way of life.”

At the end of the 1960s geologists discovered some of the world’s richest reserves of iron ore in the region where the Awa lived. In the 1980s a railway line was built to transport the ore from the Carajas mine. The development brought outsiders who exposed the Awa to disease and violence. Their population was decimated.

Despite the lack of progress in meeting the judicial deadline, there is hope that if pressure can be brought to bear on the authorities to act, the future for the Awa can be secured.

“If the settlers are evicted and the areas are protected, they should be fine,” said Alice Bayer.

“We have lots of other examples of indigenous people in Brazil who do have protected areas and their numbers are recovering and they are doing very well. It doesn’t really take that much.”

Brazil’s National Indian Foundation (FUNAI) estimates there are around 77 isolated indigenous tribes in the Amazon region – only 30 of these have been located as yet.

Source: BBC




Space debris collisions expected to rise.

debrisUnless space debris is actively tackled, some satellite orbits will become extremely hazardous over the next 200 years, a new study suggests.

The research found that catastrophic collisions would likely occur every five to nine years at the altitudes used principally to observe the Earth.

And the scientists who did the work say their results are optimistic – the real outcome would probably be far worse.

To date, there have been just a handful of major collisions in the space age.

The study was conducted for the Inter-Agency Space Debris Coordination Committee.

This is the global forum through which world governments discuss the issue of “space junk” – abandoned rocket stages, defunct satellites and their exploded fragments.

The space agencies of Europe, the US, Italy, the UK, Japan and India all contributed to the latest research, each one using their own experts and methodology to model the future space environment.

Simulated futures

They were most concerned with low-Earth orbit (that is, below 2,000km in altitude). This is where the majority of missions returning critical Earth-observation data tend to operate.

All six modelling groups came out with broadly the same finding – a steady increase in the numbers of objects 10cm and bigger over the 200-year period.

This growth was driven mostly by collisions between objects at altitudes between 700km and 1,000km.

The low-end projection was for a 19% increase; the high-end forecast was for a 36% rise. Taken together, the growth was 30%. These are averages of hundreds of simulations.

For the cumulative number of catastrophic collisions over the period, the range went from just over 20 to just under 40.

Somewhat worryingly, the forecasting work made some optimistic assumptions.

One was a 90% compliance with the “25-year rule”. This is a best-practice time-limit adopted by the world’s space agencies for the removal of their equipment from orbit once it has completed its mission.

The other was the idea that there would be no more explosions from half-empty fuel and pressure tanks, and from old batteries – a significant cause of debris fragments to date.

Concept development

“We’re certainly not at 90% compliance with the 25-year rule yet, and we see explosion events on average about three times a year,” explained Dr Hugh Lewis, who detailed the research findings at the 6th European Conference on Space Debris in Darmstadt, Germany, on Monday.

“It is fair to say this is an optimistic look forward, and the situation will be worse than what we presented in the study,” the UK Space Agency delegate to the IADC told BBC News.

“So one message from our study is that we need to do better with these debris-mitigation measures, but even with that we need to consider other approaches as well. One of the options obviously is active debris removal.”

Research groups around the world are devising strategies to catch old rocket bodies and satellites, to pull them out of orbit.

Previous modelling work has indicated that removing just a few key items each year could have a significant limiting effect on the growth of debris.

Most ideas include attaching a propulsion module to a redundant body, perhaps via a hook or robotic clamp.

Harpoon idea

One UK concept under development is a harpoon. This would be fired at the hapless target from close range.

A propulsion pack tethered to the projectile would then tug the junk downwards, to burn up in the atmosphere.

When the BBC first reported this concept back in October, the harpoon was being test-fired over a short range of just 2m.

The latest testing, to be reported at the Darmstadt conference this week, has seen the harpoon fired over a much longer distance and at a more realistic, rotating target.

“Our tests have progressed really well, and everything seems to be scaling as expected,” explained Dr Jaime Reed, from Astrium UK.

“We’ve now upgraded to a much more powerful gun and have been firing the harpoon over 10m – the sort of distance we’d expect to have to cover on a real debris-removal mission.

“Our harpoon also now has a shock absorber on it to make sure it doesn’t go too far inside the satellite, and we’ve been firing it with the tether attached. It’s very stable in flight.”

Chinese test

There are some 20,000 man-made objects in orbit that are currently being monitored regularly. About two-thirds of this population is in Low-Earth orbit.

These are just the big, easy-to-see items, however. Moving around unseen are an estimated 500,000 particles ranging in size between 1-10cm across, and perhaps tens of millions of other particles smaller than 1cm.

All of this material is travelling at several kilometres per second – sufficient velocity for even the smallest fragment to become a damaging projectile if it strikes an operational space mission.

Two key events have added significantly to the debris problem in recent years.

The first was the destructive anti-satellite test conducted by the Chinese in 2007 on one of their own retired weather spacecraft.

The other, in 2009, was the collision between the Cosmos 2251 and Iridium 33 satellites.

Taken together, these two events essentially negated all the mitigation gains that had been made over the previous 20 years to reduce junk production from spent rocket explosions.

Source: BBC


Orbital’s Antares rocket makes test flight.

_67155140_67154099A new rocket has launched from the US eastern seaboard to prove its readiness to help service the International Space Station (ISS).

The 40m-tall Antares vehicle lifted clear of the Wallops Flight Facility in Virginia at 1700 local time (2100 GMT).

The apparently flawless 10-minute ascent should lead to it being allowed to propel an unmanned cargo ship towards the ISS later this year.

Antares has been developed by the Orbital Sciences Corporation (OSC).

The Dulles-based company is one of a number of commercial outfits that have partnered with the US space agency (Nasa) to create cheaper technologies for getting payloads and astronauts into orbit.

The agency has so far invested some $275m (£180m) in OSC to help it advance its rocket and cargo-vessel concepts.

A contract worth $1.9bn (£1.2bn), covering eight re-supply missions to the station, will be triggered once the company has satisfactorily demonstrated its designs.

Sunday’s test-flight required the two-stage Antares rocket raise itself to an altitude of about 255km where it jettisoned a dummy payload.

That 3.8-tonne test mass was intended to simulate the Cygnus cargo ship, which will make its maiden outing on the next launch of the rocket.

Orbital is an established Nasa contractor, which has been building satellites and smaller rockets for more than 30 years.

The company was chosen by the agency to pick up some of the ISS servicing capability lost by America when it retired its space shuttles two years ago.

A second firm, SpaceX of California, is further along in its development schedule, having already completed its test flights and begun commercially contracted missions to the ISS.

OSC packed Sunday’s Antares full of sensors to gather as much data as possible on its performance.

Everything on the flight appeared to proceed extremely smoothly. All the major events such as rocket-stage separation, fairing separation, and the ejection of the dummy payload occurred on cue.

“We will obviously go in and analyse it much more carefully in the coming days and replay everything to make sure we get maximum information from the data. But at first glance, it all looked really good,” observed Frank Culbertson, an Orbital executive vice-president and a former astronaut.

Nasa too will want to review the flight data before deciding whether to release more seed funding to Orbital, and to clear the company for a Cygnus freighter demonstration mission to the ISS. All being well, this next demonstration could occur in late June or early July.

The early message from the agency was that it was very happy with Sunday’s outcome.

“It was an amazing achievement for Orbital today,” said Alan Lindenmoyer, the manager of Nasa’s Commercial Crew and Cargo Program.

“The flight was just beautiful. It looks like – the preliminary data says – that all the objectives we established for the flight were 100% met.”

Italian job

One interesting aspect of the Antares design is its use of two Aerojet AJ-26 engines on its liquid-fuelled first stage.

These are modified, Russian-built power units that were originally developed for the ill-fated Soviet Moon rocket, the N-1.

The Antares second-stage – the segment that deploys the payload at the target altitude – is powered by a solid-fuel motor. This was provided by ATK, the company that used to make the solid-fuelled boosters for the shuttles.

OSC hopes to use the Antares for other ventures besides keeping the space station stocked with food and equipment.

It has worked with an economic development agency in Virginia to bring the Wallops launch facility up to a standard that would permit many more flights from the coastal spaceport, which in the past has been used for small research rockets.

OSC has developed its Cygnus freighter with Italian company Thales Alenia Space (TAS).

The pressurised segment of this cargo ship is based on TAS’s Multi-Purpose Logistics Module, or MPLM. This was the “packing box” put in the back of space shuttles when they hauled supplies to the ISS.

Two versions of Cygnus are being built. One can carry two tonnes, the other nearly three tonnes.

Unlike SpaceX’s Dragon capsule, the OSC freighter cannot bring materials back to the Earth’s surface.

Instead, Cygnus will be filled with rubbish from the ISS and allowed to burn up in the planet’s atmosphere.

Sunday’s demonstration flight also released three “nano-satellites” controlled by smartphones. These mini-spacecraft, which only measure 10cm across, will operate for a few weeks before falling back to Earth.

The dummy Cygnus will also begin its descent to Earth in about a fortnight.

Source: BBC

Worm therapy: Why parasites may be good for you.

Early trials suggest a host of allergies and autoimmune ailments could be treated with worm therapy, or infection with live worm-like parasites. But will it ever reach the clinic?

Jim Turk initially put his symptoms down to stress. The self-described “health nut” who was in training to run marathons suddenly found himself unable to jog for more than a couple of minutes before coming to a gasping, staggering halt. His speech began to slur. Turk, then in his early thirties, blamed the combined pressures of juggling a full-time job, studying for a master’s degree and his parenting responsibilities. When he collapsed in the middle of a baseball field one sunny afternoon in 2008 while coaching his son’s team, he realised it was time to seek help.

At the hospital, magnetic resonance imaging (MRI) scans revealed plaques peppered throughout Turk’s brain and spine. The diagnosis was obvious: multiple sclerosis, the autoimmune condition in which the body eats away at its own nerve cell casings. The cure: not known yet.

A month later, Turk saw an ad on the news seeking multiple sclerosis patients to try out an unusual new treatment at the University of Wisconsin, in his hometown of Madison. Patients were being asked to infect themselves with live pig whipworm eggs to see if the parasites alleviated any of their symptoms or slowed the spread of telltale brain and spine lesions. “I’ve always had a research interest so I decided to put my money where my mouth is,” Turk says. “Plus I was terrified and didn’t know what to do.”

When Turk arrived at the clinic, John Fleming, a professor of neurology, presented him with a vial of clear liquid. “It tasted a little bit salty but otherwise it was just water,” says Turk. “I couldn’t see the eggs or anything.”

For the next three months, he and four others visited the lab every two weeks to swallow doses of 2,500 parasite eggs. At the start of the trial, MRI scans showed patients had an average of 6.6 active lesions – scars on the protective layer around nerve cells that disrupt the transmission of electrical messages in the brain and spinal cord. By the end of the study, that number had dropped to two. Two months after discontinuing the worm treatment, the lesions rebounded to an average of 5.8. “The beauty of this is that the number of new lesions is really an objective, brutally honest answer,” Fleming says. “It’s not proof, it’s not definitive, but at least it’s promising.”

Old friends

Fleming’s trial in 2008 was the first to infect multiple sclerosis patients with live parasitic worms, also known as helminths, but others were also investigating their therapeutic potential. The field has its origins in the early 1990s. Joel Weinstock, now chief of the division of gastroenterology/hepatology at Tufts Medical Center in Boston, struck upon the idea during a six-hour delay on the runway at Chicago’s O’Hare airport.

“Over the years, people had looked for environmental factors that caused inflammatory bowel disease and hadn’t found anything,” Weinstock says. “While on the plane, I decided to play a game and pretend that it’s caused by the loss of something rather than the addition of something.” It was as if “a light suddenly went off”, Weinstock says, as parasites came to mind. Hygiene does wonderful things, he realised, but there’s always a price for change.

The price might be the surge in cases of asthma and allergies we’ve seen in western countries over the past 40 years. Likewise, rates of autoimmune and immunoregulatory conditions such as Crohn’s diseases, type 1 diabetes, inflammatory bowel disease and multiple sclerosis have been on the rise. Yet in developing countries, such conditions remain .

In 1989, David Strachan, an epidemiologist at St. George’s University in London, published a landmark study proposing that improved hygiene in the developed world could explain trends in hay fever incidence. Strachan’s idea was that changes to sewage treatment, availability of clean water and food, and a shift away from farming lifestyles decreased our contact with soil, faeces and contaminated food where bacteria and parasites like helminths live.

The so-called “hygiene hypothesis” quickly took off, but in recent years a growing number of scientists have said the picture is more complex. The rise in allergies and inflammatory diseases may not necessarily be caused by a general lack of microbes in hygienic environments, but rather by a lack of certain organisms that have, over the course of evolution, trained our immune system to be more tolerant.

One of those organisms could be the worm-like parasite. Many of our human ancestors would have been infected with helminths, as are large numbers living in developing nations today. When helminths infect individuals and attach themselves in their hosts’ gastrointestinal tracts, the immune system launches an attack, while at the same time issuing a chain of anti-inflammatory orders to ensure the response does not get out of hand. People who survived infection have passed on immune advantages to future generations. In the modern, developed and sterile West, the theory goes, immunoregulatory effects no longer develop normally, leaving some particularly vulnerable to allergies and inflammatory diseases. “It’s not that you’re diseased or abnormal, it’s just that the world has changed,” says David Elliott, hepatologist at the University of Iowa, and Weinstock’s research colleague.

Market forces

In 1999, when Elliott and Weinstock first found that helminths protected mice against colitis, news spread fast. Six years later, the group published the result of two preliminary trials in humans. In one, involving 54 ulcerative colitis patients, 43% of those given pig whipworm eggs improved, compared with only 17% who received placebos. In a second trial 29 patients with Crohn’s disease took whipworm eggs every three weeks. By the end of 24 weeks, 79% had reduced disease activity and 72% had gone into remission. Researchers and biomedical companies around the world began to investigate the potential of helminthic therapy for treating conditions ranging from asthma to autism to psoriasis.

Helminthic therapy is still at the experimental stage, but some patients are unwilling to wait. In 2007, self-infected entrepreneurs Garin Aglietti and Jasper Lawrence founded a worm therapy start-up called AutoimmuneTherapies in the US by harvesting hookworms plucked and sterilised from their own faeces, and charging between $2,000 to $3,000 per dose. However in 2009, the Food and Drug Administration defined helminths as biological products that could not be sold before having undergone a series of clinical trials, which they had not. Aglietti set up his own WormTherapy operation to Tijuana, Mexico, and Lawrence returned to his native England.

Herbert Smith, a financial analyst in New York bought hookworms, and pig and human whipworms from WormTherapy and AutoimmuneTherapies, either travelling to Mexico or receiving mail-order worms from Lawrence. Smith was diagnosed with Crohn’s disease in 1996, and lost a foot of his intestines to surgeries before he stumbled on one of Weinstock’s papers. Today, he maintains a healthy population of hookworms, which he says have caused a complete remission. “This therapy could help people who don’t have any other treatment options,” Smith says.

Not everyone responds so well, however. Moises Velasquez-Manoff, a journalist, also visited Aglietti’s Tijuana clinic to receive a dose of 30 hookworms for his allergies and asthma, and to chronicle the experience in his book, An Epidemic of Absence. Once infected, he suffered diarrhoea and a dull, constant gut pain, and his allergies failed to improve. After a year and a half he took medication to flush out the invaders. “The idea is very, very powerful,” Velasquez-Manoff says. “They just weren’t doing anything for me.”

Researchers across the board are keen to discourage self-infection, which they say puts patients at risk of taking the wrong dose or purchasing contaminated batches. Fleming says he advises the multiple sclerosis patients who email him at a rate of around one a week against self-infecting with helminths. “People might say they’re getting better or worse, but they don’t really know,” he says. “Outside a scientific trial, it’s a muddle.”

Testing stage

Nowadays, most researchers investigating helminthic therapies have abandoned blood-sucking hookworms in favour of pig whipworms, as they have evolved to colonise swine and therefore cannot complete their life cycle within humans. Patients must re-infect themselves every few weeks but do not risk a chronic infection potentially spiralling out of control, or of accidentally infecting family members. “Pig whipworm is very kosher,” Weinstock says.

At New York University, immunologist P’ng Loke found monkeys suffering from chronic diarrhoea not only got better after receiving a dose of pig whipworms but also had significantly different gut microbes post-infection. He is currently enrolling ulcerative colitis patients to repeat the experiment in humans.

Gastroenterologist John Croese, at the Prince Charles Hospital in Brisbane, is inoculating 12 coeliac disease patients, who suffer from gluten intolerance, with hookworms. Gluten is slowly introduced into their diets to see if the hookworms will suppress the disease’s inflammatory response.

Back in Wisconsin, Fleming is continuing his studies on multiple sclerosis. He has enrolled another 15 patients for a longer trial with pig whipworms, the results of which are expected at the end of this year. As for Weinstock and Elliott, they have returned to mouse models, seeking to understand how helminths inhibit disease.

Coronado Biosciences, a Massachusetts-based company, hopes to have results from two large studies being carried out in the US into the use of pig whipworm eggs to treat Crohn’s disease by the end of the year. Meanwhile, German firm Dr Falk Pharma is collaborating with Coronado in a similar trial.

Coronado also expects results from its multiple sclerosis trials next year. Trials on adults with autism are underway, and the firm is planning studies on psoriasis, ulcerative colitis, type 1 diabetes and children with autism. “Our most important task now is to identify which diseases to pursue and which patient populations to target,” says Karin Hehenberger, Coronado’s chief medical officer.

Worm factory

None of these trials have reached phase 3, the final testing stage required to gain approval. Even if they are successful it is likely to be a few more years before treatments are made available to patients. Frustrating though it may be for some, developing new modes of therapies simply takes a long time. Gaining approval for trials, recruiting patients and waiting to evaluate the effects are all time-consuming.

It’s not just a case of demonstrating helminthic therapy is safe and effective, researchers will also have to figure out how to administer it. A live organism’s many complex molecular interactions with its host may be key to triggering the desired immune-suppressing reaction. It may therefore make sense to administer helminths as “living probiotics”. In the case of whipworms this means patients swallowing doses of live eggs; in the case of hookworms they apply gauzes containing live larvae to their skin. “When you give someone a live worm, it’s like giving them the factory that makes the products and letting the factory do what it needs to do,” Elliott says. “Evolution has already created this thing.”

Others oppose this approach. “These worms are not benign,” says Peter Hotez, dean of the National School of Tropical Medicine at Baylor College of Medicine, Houston. “We can design better, bona fide treatments based on the biology of the worms that can be scaled up and manufactured without the complexities or safety issues that go along with administering live parasites.”

Hotez and others including Weinstock’s group are working on identifying the molecules responsible for the effects of treatment with worms so they can be purified and synthesised as pharmaceuticals, just as scientists did with penicillin. Several discoveries have already been made with hookworms, such as a protein that inhibits white blood cell activity and another with anticoagulant properties.

Back in Wisconsin, Turk, who has no desire to travel to Mexico or England to attain illicit worms, awaits the trial results. He occasionally speaks to multiple sclerosis support groups about his experiences, encouraging others to take part in research to speed the discovery of better medications. He is taking interferon beta-1a, a drug that reduces relapse rates, but he hopes the trials of helminthic therapy prove successful, and would gladly switch to it if it gained approval. Without a tried and tested cure, Turk says he has good days and bad days. “A lot of people look at me and don’t think there’s anything wrong, but that’s just because I do a good job at hiding it,” he adds.

Source: BBC




Stress and illness: The decades-long search for a link.

Common sense tells us that stress makes us prone to illness, but proving any connection has been virtually impossible. Until now, perhaps.

A bereaved man suffers a heart attack. An unemployed graduate is plagued by eczema. A divorced woman develops high blood pressure. Are these situations connected… or mere coincidences?

Of all the influences on our health and well-being, chronic stress is among the most ubiquitous. And because the misery of stress is often experienced as much in the body as the mind – tiredness, headaches, tense muscles and the like – common sense tells us that psychological stress leaves us prone to physical illness.

While most people outside medicine happily accept this view, it has been viewed with a much greater degree of scepticism within the field. And that’s partly on account of the difficulty in proving exactly how stress might work, not to mention understanding why some people succumb to it but others do not. There are plenty of ideas and intuitive hunches, but rather less incontestable evidence.

But a recent finding from a team led by Sheldon Cohen at Carnegie Mellon University in Pittsburgh could finally have revealed a link, offering perhaps the best evidence so far of how stress operates at the biological level. What Cohen thinks stress is doing – a surprise, perhaps, to many of us – is undermining the body’s capacity to deal with inflammation.

It’s not the only possible stress mechanism; nor is it likely to be the whole truth. But the work represents an important step in understanding the mechanism of stress. It not only adds plausibility to claims about its role in promoting ill health, it’s a mechanism that fellow researchers find plausible and convincing.

Seeking proof

Cohen has been working on stress for 30 years, and despite a fair amount of epidemiological evidence accumulated during this time, he and other professionals have been cautious about accepting a link without firm evidence about a possible mechanism. In a 2007 review of psychological stress published in the Journal of the American Medical Association, Cohen said: “Despite widespread public belief that psychological stress leads to disease, the biomedical community remains [sceptical] of this conclusion.” But speaking now, little more than half a decade later, he takes a rather more positive view. There’s been a shift, he says. A plausible mechanism to explain the effects stress will reinforce it.

The issue is how you design an experiment that proves any ill-effects are caused by stress. Up until now, the real hard evidence has had to come from animal studies. “With humans you can bring them to a lab and expose them to stress, and you can get elevations in heart rate and blood pressure,” he says. Physiological changes, in other words, that often play a role in disease. But, for ethical reasons what you can’t do is give human subjects an illness and see if stress makes it worse.

Well, not quite. An upper respiratory tract infection like a cold is an illness, but it is mild enough to make it ethically acceptable to break the rule, and do human experiments.

Cohen began the research that propelled him to the forefront of this field back in the early 1990s. His approach, originally developed at Britain’s (now defunct) Common Cold Research Unit, relied on giving measured doses of cold virus to volunteers and checking to see if they developed symptoms. Before infecting his subjects with the virus Cohen rated their stress levels using standard questionnaires. The higher his subjects’ stress scores, he found, the greater the likelihood they would catch a cold.

Further studies showed that the principal enduring and stressful life events that rendered people susceptible to the cold virus were problems with family and friends, overwork, and unemployment. The longer these events lasted, the greater the susceptibility.

British stress researcher Andrew Steptoe, a professor of psychology at University College, London, describes these experiments as probably the most elegant of all the studies of stress and infection done to date. “What you don’t usually know under everyday circumstances is exactly when people were exposed to an infectious organism,” he says. “There are bugs floating around all the time.” Thanks to those experiments, stress levels could be linked precisely to the time of infection.

Prime suspect

While this work confirmed the association between stress and illness, it left Cohen little wiser about the mediating influence. Part of the explanation is quite likely behavioural. Stressed people smoke and drink more. They sleep badly and often take less exercise. All these things have detrimental consequences on your health. But Cohen worked on the assumption that as well as lifestyle issues there are also specific biochemical pathways linking stress and health.

One of the key molecular players in these pathways is also among the most familiar of the body’s signalling chemicals: cortisol, a steroid commonly referred to as a “stress hormone”. Produced by the adrenal gland in response to stress, the original view of cortisol was straightforward: more stress prompts your body to make more cortisol, and the higher the level of cortisol in your circulation, the worse the outlook for your health.

However, many studies have undermined this simple idea, says Professor Phil Evans, a psychologist at the University of Westminster with a long established interest in stress and cortisol. “Generally, levels of cortisol in naturalistic studies [i.e. those carried out in the real world] do not predict health outcomes strongly, or with any great consistency,” he says.

So if cortisol is involved, but not in the simplistic sense of “the more, the worse”, what is the nature of the link? Cohen’s view is that what matters more than the level of circulating cortisol is the body’s response to it. Cortisol molecules exert their effects on the body’s cells via a set of specific receptor sites: the glucocorticoid receptors, to give them their full name. When a cortisol molecule attaches itself to a receptor it triggers a chain of chemical events within the cell. Stress, says Cohen, changes the sensitivity of these receptors; they become resistant to the activating effects of cortisol.

One of cortisol’s key roles in the body is the suppression of inflammation. This is why its synthetic equivalent, hydrocortisone, is used in treating a range of inflammatory conditions, from eczema to ulcerative colitis. It’s Cohen’s contention that if the glucocorticoid receptors on the cells of the immune system fail to respond as they should to the presence of cortisol –“glucocorticoid resistance”, as it’s known – the body’s arrangements for keeping inflammation in check break down.

Inflammation in this context refers not to the sudden burst of activity you get following acute infection or injury – a protective attempt to deal with some form of harm to the body and to initiate the healing process – but to a low level elevation of chemical processes that are there all the time. “We know that stress, acutely and chronically, increases inflammation,” says Steptoe. If Cohen is right, we now know how. Stress reduces the sensitivity of the receptors (in effect chemical switches) which are supposed to control the level of inflammation in the body.

Detecting resistance

This possibility has actually been under consideration for some time. Cohen himself published some of the early work on glucocorticoid resistance. One study looked at parents of children with cancer: an extremely stressed group. “Our argument was that when you look at people who are under chronic, extreme stress you should find an increase in glucocorticoid resistance. And in comparison with matched control parents that’s exactly what we did find.” But this work didn’t set out to demonstrate any subsequent link between glucocorticoid resistance and illness in those parents.

Back to the common cold. Cohen realised that data from two of his previous studies could be used to test this glucocorticoid resistance theory. In one of these studies he’d assessed 276 volunteer subjects for major stressful life events, exposed them to common cold viruses, and then checked over the next five days for signs and symptoms of a cold. Although he didn’t have any direct measurements of the sensitivity of their receptors, he did have details of the proportions of the various types of immune cells present in their blood. Other research has shown that this acts as a surrogate measure of glucocorticoid resistance.

The experiment revealed that prolonged stress is correlated not only with the likelihood of developing a cold, but also with higher levels of glucocorticoid resistance. In other words, the people whose receptors responded inadequately to the cortisol in their blood were the ones who got the colds.

In a second study, Cohen had made direct measurements of glucocorticoid resistance in a group of 79 subjects before exposure to cold viruses. His hope was that it would allow him to predict which of his subjects would catch a cold and which wouldn’t. In fact the group wasn’t large enough to make a statistically significant prediction about actual colds; but he was able to predict which subjects showed a pattern of biological activity of the kind associated with the symptoms of a cold.

The findings of both studies point in the same direction. What counts is not the amount of cortisol circulating in the body, but how much our cells react to it.

Health predictor

Colds may be unpleasant but, in the scheme of things, they’re hardly a big deal. So what of more serious disease? The real importance of the work, says Cohen, lies in its relevance to the many other conditions in which inflammation is a factor. “It’s a model that can be applied to many diseases. Cardiovascular disease, asthma, autoimmune disease, diabetes…The regulation of inflammation plays a big role in the progression of all of them.”

Steptoe agrees. “People are already interested in inflammation in relation to chronic diseases such as diabetes and coronary heart disease,” he says. And Phil Evans too joins the chorus of acceptance. Cohen’s conclusions, he says, are “potentially generalisable to a range of other inflammatory illnesses”.

At University College London, Steptoe works with the epidemiologist Professor Michael Marmot, who’s spent many years studying peoples’ health in relation to their socioeconomic class and their status at work. Some of the variation that Marmot has identified is clearly attributable to differences in peoples’ material circumstances and behaviour. But when it comes to the health effects of their status in a hierarchy, the forces at work are more subtle.

One possibility is that people fare less well when they find themselves unable to determine their own actions and make their own choices. The crossover with stress is obvious. Professor Steptoe is investigating the cortisol biochemistry associated with their predicament, especially as it affects their risk of heart disease.

Definitive proof

Cohen readily admits that proving his hypothesis will be difficult, at least for now. One of the classic methods of studying a biological system in animal models is to disturb it in some way – stimulate it or inhibit it, for example – and see what happens. “There’s no way at present we could directly manipulate glucocorticoid resistance without upsetting all kinds of other systems as well,” he says. While animal work showing that chronic stress affects glucocorticoid resistance is persuasive, it is not definitive. “And we can’t do this in humans,” he adds. “We can’t randomly assign people to chronic stressful and non-stressful conditions.”

Steptoe agrees. We’re reliant on the differing stress levels that people themselves report, he says. “And in an observational study in humans there’s always the possibility that some other factor is involved which you can’t avoid. For example, it could be that a certain type of person chooses a job that puts them under higher work stress, so any changes aren’t necessarily to do with the stress per se, but with the type of person who’s attracted to that kind of occupation.”

In the meantime, Cohen wants to know if there is evidence that other forms of ill health can be linked to stress-induced resistance in the glucocorticoid receptors. He talks of finding opportunities “to examine the role of glucocorticoid resistance in predicting the onset and progression of other inflammatory diseases, probably in epidemiological studies.” And he’s not alone. He knows, for example, of another group of researchers planning a study of the role of glucocorticoid resistance in asthma.

There is always the possibility that the definitive experiment will always remain out of reach, in which case stress researchers might find themselves in the position of doctors trying to demonstrate a causal link between lung cancer and smoking. Unable to do the definitive experiment they have had to rely on an accumulation of observational studies, animal experiments, and studies of the physiological mechanisms most likely involved.

After thirty years of exploration, Cohen says he remains undaunted by the prospect that definitive experiment might elude him, and he laughs off any suggestion of frustration. “When you work in chronic stress,” he says, “you don’t expect to be able to do experiments like that.”

Source: BBC