Category Archives: medicine

Fury as experts say Ecstasy is harmless | Mail Online

I have been having this long (and interesting) debate with my teenage daughter about whether or not drugs should be legalised. She is adamant that MDMA is harmless. The Daily Mail think otherwise…..

one pill makes you larger and one pill makes you small
molly, e, mdma: one pill makes you larger and one pill makes you small

Controversial claims that Ecstasy may not be dangerous and that its adverse effects could be imaginary caused outrage yesterday.
A research team criticised ‘biased’ studies which said the drug causes long-term brain damage and mental problems.
But other experts and parents of Ecstasy victims were horrified by the claims, made in The Psychologist magazine, pointing out that dozens of people die after taking the drug every year.
Paul Riddell, whose 23-year-old son Graham died last year after taking the drug, said their conclusions are ‘ridiculous’.
‘Ecstasy boils the blood and organs,’ said Mr Riddell, 48, of Normanton, West Yorkshire.
‘If it is doing that to the organs, what is it doing to the brain? My son lost his life after taking it on a night out – how can it possibly not be dangerous?’
In July, the Daily Mail told how deaths from the Class A drug have doubled to 56 in the past year, with some young people dying after a single tablet.
The shocking figures, compiled by the independent drug monitoring unit at St George’s Hospital in London, came as Ecstasy claimed its youngest victim, ten-year-old Jade Slack, from Lancaster. She accidentally swallowed five pills she found at a friend’s house.
But researchers Dr Jon Cole and Harry Sumnall, of Liverpool University, and Professor Charles Grob, a director in psychiatry at the Harbor-UCLA medical centre in California, claim the adverse effects of Ecstasy could be imaginary and brought about by the widely held belief that the drug causes long-term harm.
They say this belief has come about through flawed research.
They say that many psychological problems begin in adolescence anyway, Continue reading Fury as experts say Ecstasy is harmless | Mail Online

Metre long alien worms burst from your body

I found this amazing article in New Scientist magazine. It’s about a parasitic worm that lives in your body for a year, grows to a meter in length then bursts out of your body just like in the film Alien. And you thought you had it bad.

guinea worm infection

IT STARTS with a painful blister – a very painful blister. It feels, people say, like being stabbed with a red-hot needle. When the blister bursts, the head of a worm pops out, thin, white and very much alive.
The rest of the worm, about a metre long, remains inside your body. It can take up to two months to pull it out, inch by agonising inch, during which time it may be impossible to walk. In extreme cases, you may host up to sixty of them, anywhere on your body. The worms can cause paralysis or lethal bacterial infections, and even if you survive mostly unscathed, next year it can happen all over again.
The guinea worm (Dracunculus, or little dragon) is probably the closest living equivalent to the monsters in the Alien movies – except we’re beating this enemy. Guinea worm was once widespread in Africa, the Middle East and many parts of Asia. In 1986, there were nearly 4 million cases a year in 20 countries across south Asia and Africa. Last year, there were just 3142 in four countries in Africa. The worm could be extinct by 2012, making dracunculiasis the second human disease ever to be eradicated – the first being smallpox.
Guinea worms start out as minuscule larvae living inside water fleas of the genus Cyclops. These millimetre-long crustaceans live in stagnant water, and people can swallow them when they drink from ponds, ditches or shallow wells. Stomach acids dissolve the water fleas but can leave the larvae untouched. The free larvae then burrow out of the intestine and cross to the chest or abdominal wall, where the male and female worms mature and mate. The males eventually die, but the growing females tunnel imperceptibly to, and then under, the skin.
Even as the females grow up to a metre long, their hosts remain unaware of their presence. The worms prevent pain by secreting opiates and dodge the immune system by coating themselves with human proteins. It may be just as well people don’t know they are infected as nothing can help at this stage. Continue reading Metre long alien worms burst from your body

Talking to people in a coma. I do it all the time.

We have all seen and heard this story about successful attempts at communicating with people in a Vegetative State – this is a very well informed article about the topic from the New Scientist this week written by Celeste Biever.

THE inner voice of people who appear unconscious can now be heard. For the first time, researchers have struck up a conversation with a man diagnosed as being in a vegetative state. All they had to do was monitor how his brain responded to specific questions. This means that it may now be possible to give some individuals in the same state a degree of autonomy.

“They can now have some involvement in their destiny,” says Adrian Owen of the University of Cambridge, who led the team doing the work.

In an earlier experiment, published in 2006, Owen’s team asked a woman previously diagnosed as being in a vegetative state (VS) to picture herself carrying out one of two different activities. The resulting brain activity suggested she understood the commands and was therefore conscious.

Now Owen’s team has taken the idea a step further. A man also diagnosed with VS was able to answer yes and no to specific questions by imagining himself engaging in the same activities.

The results suggest that it is possible to give a degree of choice to some people who have no other way of communicating with the outside world. “We are not just showing they are conscious, we are giving them a voice and a way to communicate,” says neurologist Steven Laureys of the University of Liège in Belgium, Owen’s collaborator.

When someone is in a VS, they can breathe unaided, have intact reflexes but seem completely unaware. But it is becoming clear that some people who appear to be vegetative are in fact minimally conscious. They are in a kind of twilight state in which they may feel some pain, experience emotion and communicate to a limited extent. These two states can be distinguished from each other via bedside behavioural tests – but these tests are not perfect and can miss patients who are aware but unable to move. So researchers Continue reading Talking to people in a coma. I do it all the time.

Don’t get ill in August. A new doctor might see you.

The second medical story of the week. If you fall ill in August your chances of recovery are significantly less. Because that’s when the newly qualified doctors are on the wards. So BBC news and The Guardian would have us know.

There is never a good time to have a heart attack, but the wise person afflicted with clogging arteries might want to be especially careful in future to avoid stress and watch the diet as August rolls around.

The NHS, it is revealed today, has its very own black Wednesday, when death rates go up by an average of 6%; and there is a somewhat disturbing underlying cause – the arrival on the wards of a new intake of junior doctors.

On the first Wednesday in August every year, a freshly qualified set of junior doctors arrives on the wards. Pristine and eager and brilliant they no doubt are, but while they are finding their way around something unexplained and slightly perplexing appears to happen.

Researchers from the Dr Foster unit and the department of acute medicine at Imperial College London say there has been a suspicion for years that more people die on the day the new doctors arrive, but for the first time they have established that it happens – although they say the rise in deaths is very small.

They do not blame the doctors’ inexperience or confusion in the hospital and say it is also possible that only the severest cases are admitted in that week, because of the changeover.

Their study has international implications, the researchers say. “A similar effect has been recorded in the US (known as the ‘July phenomenon’),” they write in their paper, published today in the open-access journal PloS (Public Library of Science) One. But previous studies have looked only at a few hospitals.

The Imperial study is far bigger, scrutinising data from nearly 300,000 patients in 175 hospital trusts between 2000 and 2008. It compared death rates on the first Wednesday in August with the last Wednesday in July. The difference was most marked in medical cases, such as heart attacks and strokes, where there was an 8% increase in deaths; there was no difference in surgical cases.

“We wanted to find out whether mortality rates changed on the first Wednesday in August, when junior doctors take up their new posts,” said senior author Paul Aylin. “What we have found looks like an interesting pattern and we would now like to look at this in more detail to find out what might be causing the increase.

“Our study does not mean that people should avoid going into hospital that week. This is a relatively small difference in mortality rates, and the numbers of excess deaths are very low. It’s too early to say what might be causing it.”

Shree Datta, chair of the British Medical Association’s junior doctor committee, said the study had to be judged alongside others looking at mortality rates before and after junior doctors start their new jobs, but added: “Clearly even a small increase in death rates is of great concern and we need further research to see whether this is a real effect or an anomaly.”

You haven’t got cancer, don’t worry. Oh, hang on a minute….

I found this appalling story in The Independent this week. Fancy being told you were all clear then – oh surely some mistake, you have got cancer after all….

Fourteen women in Britain have been told they have breast cancer after a hospital radiologist wrongly gave them the all-clear.

The unnamed member of staff at Accrington Victoria Hospital, Lancashire, was responsible for 355 screenings that later came under scrutiny.

A total of 85 women were asked to have a second breast examination and of these the 14 were found to have cancer.

They have yet to learn whether the late diagnosis will affect their chances of survival.

A further four patients were found to have abnormal cells. However, health officials said the prognosis in each of these cases was unaffected by the radiologist’s errors.

Senior officials at East Lancashire NHS Trust have confirmed that the radiologist has since left the hospital.

Accrington Victoria carries out breast cancer screenings for the whole of East Lancashire.

The women affected by the error are understood to live in and around Burnley, Blackburn, Darwen, Accrington, Rossendale and the Ribble Valley.

Rineke Schram, the trust’s medical director, issued an apology “for any distress and anxiety caused.”

She went on: “The delay in identifying the women with breast cancer does mean there has been a delay in these cancers being treated.

“It is unfortunately not possible to state with certainty whether this delay in treatment has affected the prognosis, other than to state that early-stage breast cancers have a good prognosis.

“The cancers have been picked up through screening, albeit with a delay.”

Regional breast cancer experts were drafted in to Accrington after the initial concerns were raised last year.

An independent review concentrated its attention on the work carried out by a single radiologist over a period of three years.

Officials have refused to reveal the extent of the delay between the original scans and the eventual diagnosis in each case.

It is known that the radiologist involved in the alert carried out his last screenings in December. He left the trust in April.

Mrs Schram said: “The work of the trust’s other breast screening radiologists has been independently assessed and found to be of a high standard.

“The trust will be commissioning a further independent review to provide further assurance and ensure lessons are learned.”

Dr Ellis Friedman, director of public health for NHS East Lancashire, said: “The incident team, which I chaired, has thoroughly reviewed the incident and will ensure that lessons will be learned.”

Easter Island holds key to longer life.

I read this story this morning in the Independent written by Michael McCarthy. The soil in Easter Island appears to contain a substance that actually prolongs life. Is that what those lovely Modiliagni style heads have been trying to tell us all these years? Do you think maybe the ancients were showing us an emblem of people who were “longer”?  Geddit? OK call me stupid, you’re right…..

A drug originating on Easter Island, the mysterious South Pacific home of a lost statue-building people, may become the first substance to slow down human ageing, new research indicates.

Rapamycin, a pharmacological product used to prevent rejection in organ transplants, has been found to extend the lifespan of mice by up to 38 per cent, raising the possibility that it may delay ageing in people.

Hitherto a matter for science fiction, the idea of an anti-ageing drug which would allow people to prolong their natural lifespan and also to avoid age-related diseases is now being seriously considered for the first time as a result of the findings by American researchers.

Rapamycin is a bacterial product originally found in a soil sample from Easter Island, the Polynesian extinct volcano famous for its monumental statues erected hundreds of years ago by the island people, and known in the region as Rapa Nui – hence the drug’s name. Originally developed as an anti-fungal agent, rapamycin was soon found to have powerful immuno-suppressant properties and thus be valuable for preventing rejection of transplanted organs. It was also found to delay the ageing process when used experimentally with three sets of lower organisms: yeast, nematode worms and fruit flies.

Now, however, it has been shown to affect the ageing of mice – the first time that this has ever been shown with a mammal.

A team of 14 researchers from three institutions, led by David Harrison from the Jackson Laboratory at Bar Harbor in Maine, fed rapamycin to mice late in their life – at 600 days of age – and showed that both the median and maximal lifespan of treated animals were considerably extended. Currently, the only way to extend the life of a rodent is by severely restricting its diet, so this marks the first report of a pharmacological intervention that lengthens the life of mammals – with clear implications for humans.

The results, published today in an online paper on the website of the journal Nature, are attracting considerable excitement, and an accompanying article in Nature by two of the world’s leading experts on the ageing process, Matt Kaeberlein and Brian K Kennedy from the University of Washington, Seattle, headed “A Midlife Longevity Drug?” openly asks the question: “Is this the first step towards an anti-ageing drug for people?”

Their answer is that it may well be. Dr Kaeberlein and Dr Kennedy first issued a warning to people not to start taking rapamycin at once in the hope of prolonging their lives – “the potential immuno-suppressive effects of this compound alone are sufficient to caution against this,” they advised.

But they added: “On the basis of animal models, however, it is interesting to consider that rapamycin … might prove useful in combating many age-associated disorders. Also … it may be possible to develop pharmacological strategies that provide the health and longevity benefits without unwanted side-effects.

“So, although extending human lifespan with a pill remains the purview of science fiction writers for now, the results of Harrison et al provide a reason for optimism that even during middle age, there’s still time to change the road you’re on.”

Rapamycin was known to have an influence on ageing in the lower organisms by disrupting the influence of an enzyme known as TOR, which regulates cell growth. Dr Harrison and colleagues found that this was also the case with mice, and found that rapamycin feeding could extend mouse lifespan even when started late in life.

The maximum lifespan went up from 1,094 days to 1,245 days for female mice, and from 1,078 to 1,179 for male mice – a striking increase of life expectancy of 38 per cent for females and 28 per cent for males.

Dr Harrison and his colleagues conclude: “An effective anti-ageing intervention that could be initiated later than the midpoint of the lifespan could prove to be especially relevant to clinical situations, in which the efficacy of anti-ageing interventions would be particularly difficult to test in younger volunteers. Our data justify special attention to the role of the TOR pathway in control of ageing in mammals and in the pathogenesis of late-life illnesses.”

Also known as sirolimus, rapamycin was first discovered as a product of the bacterium Streptomyces hygroscopicus, which was found in an Easter Island soil sample.

Probably the world’s most remote and least-visited inhabited island, Easter Island is globally famous for its haunting monumental stone statues of human faces, set up around the coast, known as Moai. Weighing as much as 80 tonnes, they were carved by a lost people, whose society may have collapsed, according to the American environmental geographer Jared Diamond, when they overexploited their forests. Volcanic, hilly and now treeless, and a territory of Chile, the island is situated 2,180 miles west of Chile itself and 1,290 miles east of Pitcairn Island; its European name comes from its discovery on Easter Sunday 1722, by the Dutch explorer Jacob Roggeveen. Its oldest known Polynesian name is thought to be Te Pito O Te Henua, meaning “the navel of the world”. Rapa Nui is a name given to it by Tahitian sailors in the 19th century.

Health Secretary says swine flu cases could reach more than 100,000 per day by the end of August.

Today’s Daily Telegraph runs a short feature quoting the UK Health Secretary Andy Burnham predicting a real surge in the swine flu numbers. We’ve had this illness in our house already – but that doesn’t mean we’re immune as the virus mutates.

Andy Burnham has warned that swine flu could reach 100,000 cases a day by August

The UK has moved past the stage of containing the swine flu outbreak and into the “treatment phase”, he said.

“We have reached the next stage in management of the disease,” Mr Burnham said on Thursday.

“The national focus will be on treating the increasing numbers affected by swine flu.

“We will move to this treatment phase across the UK with immediate effect.”

There are now 7,447 laboratory-confirmed cases in the UK, he said.

London and the West Midlands have already had sufficiently high numbers to move towards a policy of outbreak management, which saw people with swine flu clinically diagnosed rather than being confirmed by laboratory reports.

Mr Burnham said that last week saw a “considerable rise” in swine flu cases.

“There are now on average several hundred new cases every day,” he said.

“Our efforts during the containment phase have given us precious time to learn more about the virus.

“We have always known it would be impossible to contain the virus indefinitely and at some point we would need to move away from containment to treatment.”

He added: “We have now signed contracts to secure enough vaccine for the whole population.”

The first will become available next month, with 60 million doses available by the end of the year.

After surviving 6,000 ft fall, man threatened by Russian hospital hygiene.

This story from today’s Guardian should be fiction but isn’t.

A stunt skydiver and cameraman who survived a 6,000ft (1,829 metre) fall on to a remote Russian mountain when a parachute jump went wrong has told of his miraculous escape.

James Boole, 31, suffered a broken back, a cracked rib, a bruised lung and several chipped teeth following the jump last month when he hurtled to the ground at approximately 90 miles per hour, landing in a snowdrift.

Boole, a veteran of 2,500 skydives, was filming for a television documentary with another skydiver in the remote Russian region of Kamchatka when the accident happened. He and the other skydiver were disorientated by the snow and were unable to judge the altitude as they came to land on the final jump of their 10-day trip.

Boole said that in the two seconds before he hit the ground, he was aware that there was not enough time to open his chute and thought he was about to die.

“I didn’t panic or freak out,” he said. “In those two seconds I just thought of my wife and young baby and the sadness of not seeing them again plus the loneliness of my death.”

His parachute partially opened, but far too late, and he landed on his back and was briefly unconscious from the impact.

Then he faced an agonising half-hour wait in sub-zero temperatures before a helicopter was able to reach him. It was three hours before he was able to reach the nearest hospital.

“I opened my eyes and was immediately elated to be alive,” he said. “I did not think I would survive the fall. Breathing was incredibly difficult, there was blood in my mouth and I was in excruciating pain from my spine. My first three instincts were to breathe, vomit and scream.”

He was concerned as there was quite a lot of gurgling from his airways and about the difficulty of accessing medical treatment in such a remote area of Russia.

“There was no Hollywood moment of my life flashing in front of me as I fell, there was no glory that jumpers sometimes fantasise about if they are facing death,” he said.

“During that half hour, I was going through great highs and lows of emotion. I was glad to be alive and just wanted to see my wife and daughter but was thinking I wouldn’t ever be able to work again and would never recover from my injuries.

“In the end I thought those thoughts weren’t very useful and just had to focus on my immediate problems as my broken rib was making it difficult to breathe.”

Boole was taken by helicopter and ambulance to the nearest hospital at Kamchatsky city.

The hospital was primitive “with paint peeling off walls, the filaments visible in lightbulbs, patients in corridors, smoking allowed on wards and blood on the x-ray machines”. As for the food, he says it was “absolutely disgusting”.

Within 48 hours, he discharged himself from hospital and transferred to Moscow for further treatment. “I got to hospital and immediately had a CT scan, which was able to get a diagnosis.”

He flew back to the UK for further medical treatment at a hospital in London and is now home with his family in Tamworth, Staffordshire, where he is enjoying spending time with his daughter.

“Thanks to the back brace I was able to stand up after six days,” he says. “Over the last three weeks I have been taking my first tentative steps again.”

He has given up skydiving with a camera but will continue with the sport for fun. “I have re-evaluated my life and it is not something I want to ever do again with a camera,” he added.

“However, I have my own motivation to jump for fun and I will continue to do that.”

If you want to lose weight, just hang out in a cold room.

Today’s story is about fat that eats fat. Scientists thought this brown fat, or so it is called, disappeared from our bodies after childhood…………but no, according to the New York Times. What’s it got to do with cold and shivering? Read on…

Illustration showing where brown fat deposits appear in babies.

For more than 30 years, scientists have been intrigued by brown fat, a cell that acts like a furnace, consuming calories and generating heat. Rodents, unable to shiver to keep warm, use brown fat instead. So do human infants, who also are unable to shiver their muscles to stay warm. But it was generally believed that humans lose brown fat after infancy, no longer needing it once the shivering response kicks in.
That belief, three groups of researchers report, is wrong.
Their papers, appearing Thursday in The New England Journal of Medicine, indicate that nearly every adult has little blobs of brown fat that can burn huge numbers of calories when activated by the cold, like sitting in a chilly room that is between 61 and 66 degrees.
Thinner people appeared to have more brown fat than heavier people, younger people more than older people; people with higher metabolic rates had more than those whose metabolisms were more sluggish, and women had more than men. People taking beta blockers for high blood pressure or other medical indications had less brown fat.
“The thing about this brown fat is that it takes a very small amount to burn a lot of energy,” said Dr. C. Ronald Kahn, head of the section on obesity and hormone action at the Joslin Diabetes Center in Boston.
The fat really is brown, researchers say, because it is filled with mitochondria, cells’ tiny energy factories. Mitochondria contain iron, giving the tissue a reddish brown color.
The hope is that scientists may find safe ways to turn peoples’ brown fat on, allowing them to lose weight by burning more calories. But researchers caution that while mice lose weight if they activate brown fat, it is not clear that people would shed pounds — they might unwittingly eat more, for example. The data on global patterns of obesity are not good enough to say whether living in a cold climate makes people thinner.
The best evidence for the effects of brown fat is from earlier studies in mice, said Leslie P. Kozak, a professor of molecular genetics at the Pennington Biomedical Research Center of Louisiana State University.
Recently, Dr. Kozak put mice predisposed to obesity in a cold room, 41 degrees, for a week. The animals activated their brown fat. As a result, they lost 14 percent of their weight, which constituted 47 percent of their body fat, while eating a high-fat diet with two and a half times more calories than they had consumed at room temperature. “That’s just by going out in the cold, without any drug treatment,” Dr. Kozak said. But, he cautioned, mice, small animals with a comparatively huge surface area, are easily chilled. “Put the mouse in the cold,” he added, “and it becomes a heat producing machine.”
Jan Nedergaard of the University of Stockholm did the opposite of Dr. Kozak. He and Barbara Cannon, also at the University of Stockholm, studied mice that were genetically engineered so their brown fat could not burn calories. The animals became fat.
“Until very recently, we would have said that it is doubtful that differences in brown fat really could contribute to obesity,” Dr. Nedergaard said. Now, he said he had changed his mind, at least for mice.
The key to finding brown fat in humans was PET scans, which pinpoint areas where cells are actively burning glucose. Because brown fat rapidly burns glucose to produce heat, it lights up in the scans. In two of the three studies, investigators also studied samples of brown fat that were removed from a few subjects, confirming that the cells had a protein, UCP-1, that is unique to brown fat.
Brown fat in adult humans was in an unexpected place. Infants have it mostly as a sheet of cells covering their backs. Rodents have it mostly between their shoulder blades, just down from the neck. But in adult humans, it showed up in the upper back, on the side of the neck, in the dip between the collarbone and shoulder, and along the spine.
That may be one reason it was missed for so long, Dr. Kahn said.
“There was an interest in looking at humans 20 or 25 years ago with different scanning techniques, but people were always looking between the shoulder blades,” he said. And since there is so little brown fat — just a few grams of tissue — it can be hard to find, Dr. Kahn added.
His study, one of the three published Thursday, involved 1,972 people who had had PET scans for a variety of reasons. The scans showed brown fat in 7.5 percent of the women and 3 percent of the men — an underestimate, Dr. Kahn says, because the people had not deliberately activated brown fat by getting cold.
Dr. Kahn and his colleagues also examined biopsy samples taken from the necks of two patients. They concluded that what looked like brown fat in their scans was indeed brown fat.
A second study, led by Wouter D. van Marken Lichtenbelt of Maastricht University in the Netherlands, involved 24 healthy young men. Ten were lean, the rest overweight or obese.
The scans showed no brown fat when the men had been in a room that was a comfortable temperature. But after they were in a chilly room for two hours, scans showed brown fat in all but one, an obese man.
A third study, led by Dr. Sven Enerbäck of the University of Goteborg in Sweden, involved five healthy adults. Each had two PET scans — one after being in a room at a comfortable temperature, the other after being in a chilly room for two hours. The investigators saw brown fat in their chilled subjects. Three participants allowed the researchers to remove some white fat and some brown fat to demonstrate that what looked like brown fat in the scans really was that elusive substance.
The studies, investigators say, should stimulate research on safe ways to activate brown fat. It is known to be activated not only by cold but also by catecholamines, hormones that are part of the fight or flight response. That is why beta blockers, which block catecholamines, can suppress brown fat activation.
Epinephrine, or adrenaline, and ephedra, a herbal supplement containing epinephrine, can stimulate brown fat, said Dr. Rudolph Leibel, co-director of the Naomi Berrie Diabetes Center at the Columbia University Medical Center. But, he added, the drugs have too many side effects to be used for weight loss. While caffeine can boost ephedra’s effects, Dr. Leibel said, it is easy to eat your way out of a brown fat effect.
Brown fat, he said, “fits the fantasy — I eat what I want and burn it off.”
That, however, is still a fantasy, Dr. Leibel added.
If a drug that stimulates brown fat could be developed, said Dr. Claude Bouchard of the Pennington Biomedical Research Center, it would be the first obesity drug to affect energy expenditure rather than appetite.
Then there is the notion of simply hanging out in a cold room.
“We’re thinking of opening a frosty spa,” Dr. Kozak joked.

This surgeon will nip off your love handles and use them to power his vehicle

I heard about this just before Christmas Eve and thought it was a joke, then found the story on – about the US surgeon (Mr Bittner) who used the fat he sucked from patients to power his vehicle – and his girlfriend’s SUV too. The writer has tagged his story “biofuels.” Only in America.

Liposuctioning unwanted blubber out of pampered Los Angelenos may not seem like a dream job, but it has its perks. Free fuel is one of them. For a time, Beverly Hills doctor Craig Alan Bittner turned the fat he removed from patients into biodiesel that fueled his Ford SUV and his girlfriend’s Lincoln Navigator. Love handles can power a car? Frighteningly, yes. Fat – whether animal or vegetable – contains triglycerides that can be extracted and turned into diesel. Poultry companies such as Tyson are looking into powering their trucks on chicken schmaltz, and biofuel start-ups such as Nova Biosource are mixing beef tallow and pig lard with more palatable sources such as soybean oil. Mike Shook of Agri Process Innovations, a builder of biodiesel plants, says this year’s batch of U.S. biodiesel was likely more than half animal-derived since the price of soybeans soared.A gallon of grease will get you about a gallon of fuel, and drivers can get about the same amount of mileage from fat fuel as they do from regular diesel, according to Jenna Higgins of the National Biodiesel Board. Animal fats need to undergo an additional step to get rid of free fatty acids not present in vegetable oils, but otherwise, there’s no difference, she says.Greenies like the fact that waste, such as coffee grounds and french-fry grease, can be turned into power. “The vast majority of my patients request that I use their fat for fuel–and I have more fat than I can use,” Bittner wrote on “Not only do they get to lose their love handles or chubby belly but they get to take part in saving the Earth.” Bittner’s lipodiesel Web site is no longer online.Using fat to fuel cars might be environmentally friendly, but it’s definitely illegal in California to use human medical waste to power vehicles, and Bittner is being investigated by the state’s public health department.

What a cough looks like.

The New York Times ran a story today about what a cough actually looks like. As everyone I know has one at the moment….I thought you should take a look. And there’s interesting stuff about Schlieren photography, which I had never heard of before…

The image, published online Oct. 9 by The New England Journal of Medicine, was created by schlieren photography, which “takes an invisible phenomenon and turns it into a visible picture,” said the engineering professor, Gary Settles, who is the director of the university’s gas dynamics laboratory.

Schlieren is German for “streaks”; in this case it refers to regions of different densities in a gas or a liquid, which can be photographed as shadows using a special technique.

“In my lab we use this technique a lot,” Dr. Settles said. “Often it’s used for other things, like in supersonic wind tunnels, to show shock waves around high-speed aircraft.”

The process involves a small, bright light source, precisely placed lenses, a curved mirror, a razor blade that blocks part of the light beam and other tools that make it possible to see and photograph disturbances in the air. In the world of gas dynamics, a cough is merely “a turbulent jet of air with density changes.” Though coughs spread tuberculosis, SARS, influenza and other diseases, surprisingly little is known about them. “We don’t have a good understanding of the air flow,” Dr. Settles said.

To map a cough, he teamed up with Dr. Julian Tang, a virus expert from Singapore. A healthy student provided the cough. The expelled air, traveling at 18 miles per hour, mixed with cooler surrounding air and produced “temperature differences that bend light rays by different amounts,” Dr. Settles said.

He went on: “The next thing is, you get a couple of people in front of the mirror talking, or one coughs on another, and you see how the air flow moves, how people infect one another. Or you look at how coughing can spread airborne infection in a hospital. This is really a suggestion for how we might study all that. The techniques used in wind tunnels can be used to study human diseases.”

Other schlieren images show the churning air and shock waves that emanate from a pistol’s firing; an Airedale sniffing a small flower; and the unseen, shimmering world around a candle burning in a breeze.

The final photograph, in a full-scale mock-up of an aircraft cabin, captures in microseconds the flash of an explosion under a mannequin in an airplane seat and the propagation of shock waves into the cabin. The blast was a re-creation of a terrorist’s attempt in 1994 to bring down a Philippine Airlines flight with a nitroglycerin bomb. The plane did not crash, but the explosion did kill the passenger seated over the bomb. The simulation used a less intense explosion than the actual bombing.

“The simulation helps to understand how the energy of an onboard blast reverberates around the cabin,” Dr. Settles said, “and it is also useful to check the results of computer blast simulations.”

Don’t shake hands with a Northerner.

The further north you go in England, the more likely you are to have faecal bacteria on your hands. And if you’re using the London Tube (underground railway) it’s an even bigger pile of sh*t than you ever thought. This story by the London School of Hygiene and Tropical Medicine shows that one in four commuters have faecal bacteria on their hands. So the North-South divide is perhaps more fundamental than we realised.  And I speak as a Northerner. Are my hands clean? Does a bear go to church? Does the Pope……..

The further north you go, the more likely you are to have faecal bacteria on your hands, especially if you are a man, according to a preliminary study conducted by the London School of Hygiene & Tropical Medicine.

But women living in the South and Wales have little to feel smug about. In London, they are three times as likely as their men folk to have dirty hands, and in Cardiff, twice as likely. The men of London registered the most impressive score among all those surveyed, with a mere 6% found to have faecal bugs on their hands. Overall more than one on four commuters have bacteria which come from faeces on their hands.

The Dirty Hands Study was conducted in order to provide a snapshot of the nation’s hand hygiene habits, as part of the world’s first Global Handwashing Day today. Commuters’ hands were swabbed at bus stops outside five train stations around the UK (Newcastle, Liverpool, Birmingham, Euston and Cardiff).

The results indicated that commuters in Newcastle were up to three times more likely than those in London to have faecal bacteria on their hands (44% compared to 13%) while those in Birmingham and Cardiff were roughly equal in the hand hygiene stakes (23% and 24% respectively). Commuters in Liverpool also registered a high score for faecal bacteria, with a contamination rate of 34%.

In Newcastle and Liverpool, men were more likely than women to show contamination (53% of men compared to 30% of women in Newcastle, and 36% of men compared to 31% of women in Liverpool), although in the other three centres, the women’s hands were dirtier. Almost twice as many women than men in Cardiff were found to have contamination (29% compared to 15 %) while in Euston, they were more than three times likelier than the men to have faecal bacteria on their hands (the men here registered an impressive 6%, compared to a rate of 21% in the women). In Birmingham, the rate for women was slightly higher than the men (26% compared to 21%).

The bacteria that were found are all from the gut, and do not necessarily always cause disease, although they do indicate that hands have not been washed properly.

Dr Val Curtis, Director of the Hygiene Centre at the London School of Hygiene & Tropical Medicine, comments: ‘We were flabbergasted by the finding that so many people had faecal bugs on their hands. The figures were far higher than we had anticipated, and suggest that there is a real problem with people washing their hands in the UK. If any of these people had been suffering from a diarrhoeal disease, the potential for it to be passed around would be greatly increased by their failure to wash their hands after going to the toilet’.

For more information, or to interview the investigators, please contact Gemma Howe in the London School of Hygiene & Tropical Medicine Press Office on 0207 927 2802 or

Notes to Editors:

Global Handwashing Day was initiated by the Public-Private Partnership for Handwashing (, which is dedicated to promoting handwashing with soap to reduce diarrhoea in developing countries and implement large-scale handwashing interventions by combining the expertise and resources of the soap industry with the facilities and resources of governments. Global Handwashing Day activities are being implemented in more than forty countries and focus on raising awareness among policymakers and the public about the role handwashing plays in public health.

For more information about Global Handwashing Day, please go to: All materials on the website are available to be downloaded, or can be used in publication.

Heath Ledger was not alone. Self-medication deaths have risen by over 3,000 percent in recent years

I found this story published by UCSD – San Diego, University of California – with the story written by Paul Mueller – the first thorough study looking at what happens when we, the general public, are left to monitor our own medications. The answer is simple, thanks to a variety of causes including (and I’m not saying this is what happened with Heath Ledger because there is no evidence) accidental combinations with street drugs or alcohol – which happens a lot with ordinary people apparently – stands to reason really.

Asking patients to monitor their own medications can be fatal, as exemplified by the recent death of actor Heath Ledger. In the first large-scale study of home medication consumption, sociologists at the University of California, San Diego have found a 3,196 percent increase in fatal domestic medication errors involving alcohol and/or street drugs.

Their study examines nearly 50 million U.S. death certificates from 1983 to 2004, and focuses on a subset of 200,000 deaths from medication errors. The study appears in the July 28 issue of the Archives of Internal Medicine, an official journal of the American Medical Association.

“The decades-long shift in the location of medication consumption from clinical to domestic settings,” the authors say, “is linked to a dramatic increase in fatal medication errors.”

“Increasingly,” says principal author David P. Phillips, professor of sociology at UC San Diego, “people take their medications at home, away from hospitals and clinics. But most studies of fatal medication errors have focused on those clinical settings. We wanted to know three things: how many of these fatal errors happen at home; how many involve alcohol and/or street drugs; and are these numbers going up?”

Phillips and his co-authors Gwendolyn E.C. Barker and Megan M. Eguchi, all at UC San Diego, examined trends in four types of fatal medication errors. They note that the increase in fatal errors varies by astonishing amounts based on where the errors occur and the particular combinations of drugs.

Type 1 errors – deaths at home from combining medications with alcohol and/or street drugs – skyrocketed by 3,196 percent.

In sharp contrast, type 4 errors – non-domestic fatal errors not involving alcohol or street drugs – show the smallest increase, just 5 percent.

The intermediate types of errors increased by intermediate amounts. Type 2 errors – domestic medication fatalities not involving alcohol or street drugs – increased by 564 percent. Type 3 errors – non-domestic medication fatalities involving alcohol and/or street drugs – increased by 555 percent.

“Thus,” the sociologists say, “domestic fatal medication errors, combined with alcohol and/or street drugs, have become an increasingly important health problem.”

In addition to possible changes in policy and clinical practice, Phillips says, “it also seems advisable to expand research on medication errors. Much of this research has focused on elderly patients and clinical settings. The present findings suggest that more research should be devoted to middle-aged patients and domestic settings.”

The study was supported in part by a grant from the Marian E. Smith Foundation.

Ledger, the actor, was cast as the Joker in the current hit movie “The Dark Knight,” shortly before dying, on January 22, 2008, from an accidental prescription-drug overdose at age 28.

A PDF of the paper is available here

Is it OK to use brain-boosting drugs to enhance your academic performance?

I first heard this story on BBC Radio 4 when they were discussing the use of cognitive brain enhancers to boost academic performance. It appears to first come from an article in Nature magazine by Barbara Sahakian and Sharon Morein-Zamir – but I found a version published here.Basically, you’re about to take an exam – would you like an espresso with a double shot of methylphenidate…..or just soft brown sugar?

Would you boost your own brain power? Cognitive-enhancing drugs are increasingly being used in non-medical situations such as shift work and by active military personnel. This is where the debate about their use begins
in earnest. How should the use of cognitive-enhancing drugs be regulated in healthy people? Should their use always be monitored by healthcare professionals? If offered by a friend or colleague, would you, the reader, take a pill that would help you to better focus, plan or remember? Under what conditions would you feel comfortable taking a pill, and under what conditions would you decline? The answers to such questions hinge on many factors, including the exact drug being discussed, its short-term and long-term benefits and risks, and the purpose for which it is used. There are instances in which most people would agree that the use of cognitive-enhancing drugs should be prevented or at least regulated and monitored, such as by healthy children or in competitive settings (including entrance exams to university). There are also situations in which many would agree that the use of drugs to improve concentration or planning may be tolerated, if not encouraged, such as by air-traffic controllers, surgeons and nurses who work long shifts. One can even imagine situations where such enhancing-drug-taking would be recommended, such as for airport-security screeners, or by soldiers in active combat. But there are no straightforward answers and any fruitful debate must address each situation in turn.
How would you react if you knew your
colleagues — or your students — were
taking cognitive enhancers?
In academia, we know that a number of our scientific colleagues in the United States and the United Kingdom already use modafinil to counteract the effects of jetlag, to enhance productivity or mental energy, or to deal with demanding and important intellectual challenges . Modafinil and other drugs are available online, but their non- prescription and long-term use has not been monitored in healthy individuals. For many, it seems that the immediate and tangible benefits of taking these drugs are more persuasive than concerns about legal status and adverse effects. There are clear trends suggesting that the use of stimulants such as methylphenidate on college campuses is on the rise, and is becoming more commonplace in ever younger students.
Universities may have to decide whether to ban drug use altogether, or to tolerate it in some situations (whether to enable all-night study sessions or to boost alertness during lectures).
The debate over cognitive-enhancing drugs must also consider the expected magnitude of the benefits and weigh them against the risks and side effects of each drug. Most readers would not consider that having a double shot
of espresso or a soft drink containing caffeine would confer an unfair advantage at work.
The use of caffeine to enhance concentration is commonplace, despite having side effects in at least some individuals
Often overlooked in media reports on cognitive enhancers is the fact that many of the effects in healthy individuals are transient and small-to-moderate in size. Just as one would hardly propose that a strong cup of coffee could be the secret of academic achievement or faster career advancement, the use of such drugs does not necessarily entail cheating. Cognitive enhancers with small or no side effects but with moderate enhancing effects that alleviate forgetfulness or enable one to focus better on the task at hand during a tiring day at work would be unlikely to meet much objection.
And does it matter if it is delivered as a pill or a drink? Would you, the reader, welcome a cognitive enhancer delivered in a beverage that is readily obtainable and affordable, and has a moderate yet noticeable effect
on your concentration and alertness?……
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I will be looking for more threads on this story in coming weeks.

Shorter arms, shorter memory.

I found this article in today’s Neurology magazine which amazingly for me anyway shows a strong link between the length of your arms and your likelihood of memory loss in later years. Basically those with shorter arms and legs are almost half as likely to get Alzheimer’s later in life. Almost 3,000 ordinary people were tested to get these results.

People with shorter arms and legs may be at a higher risk for developing dementia later in life compared to people with longer arms and legs, according to a study published in the May 6, 2008, bonus issue of Neurology, the medical journal of the American Academy of Neurology. Researchers say the association between short limbs and dementia risk may be due to poor nutrition in early life, which can affect limb growth.

Several studies have shown that early life environment plays an important role in susceptibility to chronic disease later in life. “Body measures such as knee height and arm span are often used as biological indicators of early life deficits, such as a lack of nutrients,” said Tina L. Huang, PhD, who was with Johns Hopkins University in Baltimore, MD, when the study started.

Huang is now with the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University in Boston, MA. “Because the development of the brain region most severely affected by Alzheimer’s disease coincides with the greatest change in limb length, we thought it was possible that men and women with shorter limbs could be at greater risk for developing dementia and Alzheimer’s disease.”

Researchers from the Cardiovascular Health Cognition Study followed 2,798 people for an average of five years and took knee height and arm span measurements. Most participants were white with an average age of 72. By the end of the study, 480 developed dementia.

Researchers found women with the shortest arm spans were 1.5 times more likely to develop dementia and Alzheimer’s disease than women with longer arm spans. For every inch longer a woman’s leg, the risk of dementia and Alzheimer’s disease was reduced by 16 percent.

In men, only arm span was associated with a lower risk of dementia. With every increased inch in arm span, men had a six-percent decrease in risk of dementia. The associations with such measures in men and women were stronger toward Alzheimer’s disease compared to other types of dementia.

Huang says there is a strong correlation between height and socioeconomic background, and trends are reflected as early as the first two years of life. “Reduced height for age, or stunting, is thought to be most closely tied to environment and the quality of diet in early life, which corresponds with periods of the fastest leg growth,” said Huang. “As a result, environment in the first years of life may play an important role in determining future dementia risk.”

“Our findings are consistent with other studies that have been done in Korean populations, where shorter limb length was associated with greater risk of dementia,” said Huang.

Sunbeds = skin cancer, Australia acts to ban them.

The ABCDs of melanoma skin cancer are:

* Asymmetry. One half doesn’t match the appearance of the other half.
* Border irregularity. The edges are ragged, notched, or blurred.
* Color. The color (pigmentation) is not uniform. Shades of tan, brown, and black are present. Dashes of red, white, and blue add to a mottled appearance.
* Diameter. The size of the mole is greater than 1/4 inch (6 mm), about the size of a pencil eraser. Any growth of a mole should be evaluated.

These are the classic signs of melanoma or skin cancer – if you’re worried about it yourself this is a useful source of information.
I heard this morning that sunbeds are to be totally banned in Australia, and that moves to put the legislation in place are actually happening. Further from the Sydney Morning Herald which puts more flesh on the bones of this story (sic) (k)

The Australian Medical Association and NSW Greens criticised the State Government this week for not acting sooner after both Victoria and South Australia introduced regulations earlier this year and Western Australia announced last week it would soon follow.

But yesterday the Minister Assisting the Minister for Health (Cancer), Verity Firth, said NSW would have “a comprehensive set of regulations in place for the solarium industry by the end of this year”.

A spokesman for Ms Firth said if the Radiation Health Committee did not speed up the process for national standards in the next few months, NSW would “jump ship”.

The spokesman said under-18s and those with sensitive “Type 1” skin would be banned from solariums. Type 1 includes those who burn and never tan.

The frequency of visits would also be limited, probably to no more than once every two days, he said. Coin-operated sunbeds would also be banned.

Research published in January showed that NSW teens were the highest users of solariums, with a prevalence rate of 12 per cent.

Below is a picture of Clare Oliver … the anti-solarium campaigner who died of sunbed-inspired cancer last year.

The study by the Queensland Institute of Medical Research also showed that solarium users aged under 35 had almost double the risk (98 per cent) of developing melanoma than those who did not.

The study’s co-author, Louisa Gordon, said yesterday there was no such thing as safe tanning.

“The sunbeds can emit very strong levels of radiation, stronger than the midday sun in Brisbane,” Dr Gordon said.

She said about 3 per cent of the population had used a solarium and less than 1 per cent of all UVR-caused melanoma deaths in Australia were attributable to solarium use each year.

Dr Gordon said there had been a fourfold growth in the solarium industry since 1992.

The Greens MP Lee Rhiannon said the Premier, Morris Iemma, was waiting too long to act.

Radio 4 are doing a feature on this this afternoon which I haven’t heard yet but you can access it here after 2pm today (21st April)

“If you think you are depressed, you probably are.”

I don’t usually go in for these “lifestyle” and “health” kind of stories, often finding them a bit limp and self-indulgent and wishy-washy – but reading this one, it turned into something a bit more real. It’s about a woman recognising the symptoms of depression and starting to deal with them. I suffered from depression just like the stuff she describes when I was sixteen and seventeen – and was fortunate enough to come through it – and have continued to do battle with it and found ways to defeat it as life went on. Churchill called it his Black Dog, always rocking up when you least needed it. If you’ve been unfortunate enough to ever get it yourself, I hope this article is useful for you.

It appeared at the start of the week in the Guardian.

After more than 20 years with depression, Zoe Lewis thought she would simply have to put up with her illness. But a friend persuaded her to try group therapy. What happened next changed her life.

‘Hello, I’m Zoe and I’m … depressed.” Twelve faces stare back at me, nodding sympathetically. I am in therapy for depression and I can’t believe I’m here. Why am I here?

I mean, I know I suffer from depression periodically and take antidepressants, but I’m not depressed depressed. I’m just not that bad. I’m a busy woman, and to take the time to attend to some silly little person like me seems to me the height of overindulgent selfishness.

I look around the room and imagine that the other people are all here for proper depression – bipolar or unipolar or compulsive disorders that mean they can’t leave the house. OK, so I get a bit down from time to time, but what’s the biggie?

Well, the biggie was that my best friend decided that she had had enough of my weirdness.

“You need help,” she told me, as she sat opposite me on the sofa, annoyingly entrenched.

“I’m fine.”

“You are not fine,” she persisted.

“OK, so I spend a lot of time alone,”

I snapped back. “I dislike the phone. I write every day. I’m driven to the point of obsession. OK, I want to be perfect – but don’t we all?”

“Er, no we don’t,” she said, following me into the kitchen. “You walk up to eight miles a day. You take an unnaturally long time to recover from the break-up of relationships. You feel safer being alone …”

“OK, OK, stop! I accept that I’m weird and I might need help for my weirdness but it’s my fault I’m weird. It’s not because I’m depressed.”

“You need group therapy,” she countered.

“Group what?” I shuddered at the thought.

I couldn’t help feeling that sitting in a sort of “depressives anonymous” would send even the most Mary Poppins-like of us over the edge, but being an extremely nosy person, as well as a writer, I decided to go along.

A few weeks later, confronted by a roomful of expectant people, I am desperate to be anywhere else. Frankly, burning in hell seems an attractive option.

“Would you like to tell the group a little about why you are here?” asks the counsellor.

“I get a bit depressed sometimes, but it’s just not that bad.”

“All depression is bad,” she says sympathetically. Like I deserve sympathy.

“I’m not depressed; I’m just not a very nice person. I get angry with people I don’t even know – like bus drivers and people in news-agents. When anyone ever asks me how I am, I am rude because I want to cry, because how I am is bad, always bad, and they should damn well know not to ask such a stupid question, and when people call, I don’t answer my phone. You see? I’m just a terrible person.”

“You’ve just described the classic symptoms of depression,” she says.

“No, no, no,” I say. “You don’t understand. This is what I’m like all the time.”

“Well, have you ever considered that you might be depressed all the time?”

“Oh no, I’ve always been like this – well, since I was about eight, I suppose.”

“Have you considered you might have been depressed since then?”

“No, no,” I smile at her patiently. “You don’t understand. I know when I’m depressed. When I’m depressed I can’t leave the house. It overwhelms me like a physically sickness. It comes in waves and often I just drive around or sit in the car and cry.”

“So could you possibly accept that these times you describe are serious major bouts of depression?”

I shrug and inspect my fingers, hoping that she’ll move on. She doesn’t.

“Do you know that a lot of people do not get out of bed for days in these bouts?”

My fingers are, at this stage, fascinating.

“The symptoms you describe are accurate for dysthymic depression – mild constant depression interrupted by occasional serious episodes.”

After that first session, I take a walk. It has become stunningly obvious that my noticeable traits of character – things I had put down to personal idiosyncrasies – are actually symptoms of depression: isolation, difficulty having relationships, feeling sad, rejecting affection.

I will save you the sob story, but my parents were unhappy together and finally divorced when I was eight. My childhood losses and my feelings of rejection and abandonment could have kick-started the depression.

From both my own experience and what I have learned from psychiatrists, depression is the same feeling as grief. Grief occurs naturally after a major trauma such as an accident, bereavement or physical or emotional abuse. A person can be genetically predisposed to depression (ie, the body doesn’t produce enough serotonin or some other “happy chemical”), but there is also a medical theory, to which I subscribe (promoted by Andrew Solomon in The Noonday Demon) that the brain, being a clever little sod, can learn to grieve all by itself. It says that lots of little traumas happening regularly throughout childhood and beyond (such as abandonment or the departure of a parent, or bullying or rejection) mean that the brain starts to recognise the feelings associated with grief and starts to repeat them whenever it feels like it, in the end not needing any traumatic event to stimulate it. Hence one starts to feel sadness and loss seemingly for no reason.

The knowledge that I am suffering from a depressive illness, coupled with my ability to discuss it with others in the same position, is nothing short of an epiphany. As the other people in the group talk, I find myself thinking, “My God, that’s me – that’s what I do” over and over again. Suddenly seeing that I am not alone in my weirdness is liberating. Perhaps I am not so terrible after all.

Then the group gives me feedback.

“I see a woman who is very hard on herself. Super-critical with impossibly high standards that she can never meet,” says one man.

“I see a woman who is sad and needs to show herself a little compassion,” says a lady with bipolar disorder.

Compassion? Me? Ha! That’s a load of bollocks. I don’t need compassion. I just need to do more, work harder – compassion is for other people.

My inner critic rages. Up to now I have relied on it to urge me forward, to keep me driven. Now I find that my negative voice is a manifestation of my illness, the lack of serotonin asserting itself, telling me I am bad and worthless.

“Are you ready to give yourself a break now?” The therapist smiles kindly. “It’s been 28 years – you deserve a bit of peace.”

I bite my lip and nod. Suddenly I feel like an eight-year-old again. I am made to write a letter from the adult me to the eight-year-old me, telling her that I love her.

I feel more than a little uncomfortable loving myself. I’m so used to hating myself.

You see, all those years, I thought it was normal to wake up in the morning and just see grey pointlessness. I thought it was normal to cry whenever you heard music. I thought it was normal to stare at people in the street and feel overwhelmed by sadness and futility at the sight of their pointless lives. I thought it was normal to avoid my friends most of the time. I’ve been seeing life in grey – like a rainy day in winter – and thinking this is what everybody sees. Happiness, whenever it has come, has been fleeting and so unfamiliar that it makes me sick with anxiety.

All of a sudden I can see that I have an illness that has gone untreated – perhaps dangerously so, because there are times I have felt so destructive or despairing that I have had no regard for my health. Now I am getting the help I need.

Of course, I am not the only person who has difficulty accepting this nebulous illness. Many people do not believe depression is real. There is no blood test that proves it, no physical handicap. Unless someone is crying in front of you how, can you tell they are depressed? They are probably just making it up, trying to get sympathy, attention, a day off work … But let’s turn this round. Why would someone want to be unable to get out of bed or go to the shops or talk on the phone or raise a smile?

I’m just thankful for the friend who loved me more than I loved myself, who stepped outside of her – and my – comfort zone and pointed it out. If you think you are depressed, you probably are – and there is no reason you should miss out on the everyday happiness that most people take for granted.

If you are a man suffering from depression, it can sometimes be a little harder to acknowledge, or to share with friends, because of all the stuff we are conditioned for – being men. This is a good source of advice if you would like to read more about help specifically aimed at men.

Pregnant man

This story ran in the Scotsman today. In the past I have shied away from those traditional “News of the World” style stories, but frankly I was fascinated by this and its implications. Mr Beatie appeared on Oprah Winfrey’s show and the footage was syndicated all over the world. What I was most taken with was Oprah’s statement at the end of her feature – saying it was a new definition of what diversity means for everybody. Maybe we will look back on this story in fifty years time and find it “everyday”- and not even worthy of comment.

A TRANSGENDER man who is six months pregnant said in a television interview yesterday that he had always wanted to have a child and considers it “a miracle”.
“It’s not a male or female desire to have a child. It’s a human desire,” said thinly bearded Thomas Beatie, who was once a teenage beauty queen.

“I have a very stable male identity,” he added, in an interview, broadcast on The Oprah Winfrey Show in the United States.

Mr Beatie, 34, who lives in Oregon, was born a woman but decided to become a man ten years ago.

He began taking testosterone treatment and had breast surgery to remove glands and flatten his chest.

“I opted not to do anything with my reproductive organs because I wanted to have a child one day,” he said.

Mr Beatie’s wife, Nancy, said she inseminated him with a syringe, using sperm purchased from a sperm bank.

Now, he said, his size 32 jeans were getting a bit tight and his shirts a bit stretched.

Mrs Beatie, to whom he has been married for five years and who has two grown daughters by a previous marriage, also appeared on the show, saying the couple’s roles will not change once the baby, a girl, is born.

“He’s going to be the father and I’m going to be the mother,” she said.

Their marriage is legal and he is recognised under Oregon state law as a man.

“I can’t believe it. I can’t believe she’s inside me,” said Mr Beatie.

His obstetrician, Dr Kimberly James, who practises in the town of Bend, where the couple live, told Winfrey: “This is a normal pregnancy.

This baby is totally healthy.”

The Beaties said they decided to go public so they could control the way the news got out. “We’re just going to have the baby now,” Mrs Beatie said. “If we have to, we’ll go hide.”

Winfrey called the development “a new definition of what diversity means for everybody.”

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Shocking how much you can remember with a little help.

Loss of memory as one ages has been increasingly in the news. I found this superb story in the Independent today about an accidental discovery by scientists that electrically stimulating a deep part of the brain can improve memory radically.

Scientists performing experimental brain surgery on a man aged 50 have stumbled across a mechanism that could unlock how memory works.

The accidental breakthrough came during an experiment originally intended to suppress the obese man’s appetite, using the increasingly successful technique of deep-brain stimulation. Electrodes were pushed into the man’s brain and stimulated with an electric current. Instead of losing appetite, the patient instead had an intense experience of déjà vu. He recalled, in intricate detail, a scene from 30 years earlier. More tests showed his ability to learn was dramatically improved when the current was switched on and his brain stimulated.

Scientists are now applying the technique in the first trial of the treatment in patients with Alzheimer’s disease. If successful, it could offer hope to sufferers from the degenerative condition, which affects 450,000 people in Britain alone, by providing a “pacemaker” for the brain.

Three patients have been treated and initial results are promising, according to Andres Lozano, a professor of neurosurgery at the Toronto Western Hospital, Ontario, who is leading the research.

Professor Lozano said: “This is the first time that anyone has had electrodes implanted in the brain which have been shown to improve memory. We are driving the activity of the brain by increasing its sensitivity – turning up the volume of the memory circuits. Any event that involves the memory circuits is more likely to be stored and retained.”

The discovery had caught him and his team “completely by surprise”, Professor Lozano said. They had been operating on the man, who weighed 190kg (30st), to treat his obesity by locating the point in his brain that controls appetite. All other attempts to curb his eating had failed and brain surgery was the last resort.

The treatment for obesity was unsuccessful. But, while the researchers were identifying potential appetite suppressant points in the hypothalamus, the part of the brain associated with hunger, the man suddenly began to say that memory was flooding back.

“He reported the experience of being in a park with friends from when he was around 20 years old and, as the intensity of stimulation increased, the details became more vivid. He recognised his girlfriend [from the time] … The scene was in colour. People were wearing identifiable clothes and were talking, but he could not decipher what they were saying,” the researchers write in Annals of Neurology, published today.

The man, who has not been identified, was also tested on his ability to learn lists of paired objects. After three weeks of continuous hypothalamic stimulation, his performance on two learning tests was significantly improved. He was also much more likely to remember a list of unrelated paired objects with the electrodes turned on than when turned off.

Speaking to The Independent yesterday, Professor Lozano said: “His performance improved dramatically. As we turned the current up, we first drove his memory circuits and improved his learning. As we increased the intensity of the current, we got spontaneous memories of discrete events. At a certain intensity, he would slash to the scene [in the park]. When the intensity was increased further, he got more detail but, when the current was turned off, it rapidly decayed.”

The discovery surprised the scientists as the hypothalamus has not usually been identified as a seat of memory. The contacts that most readily produced the memories were located close to a structure called the fornix, an arched bundle of fibres that carries signals within the limbic system, which is involved in memory and emotions and is situated next to the hypothalamus.

Professor Lozano is a world authority on deep-brain stimulation who has undertaken 400 operations on Parkinson’s disease sufferers and is developing the technique as a treatment for depression, for which he has performed 28 operations. He said the discovery of its role in stimulating memory had wide implications.

“It gives us insight into which brain structures are involved in memory. It gives us a means of intervening in the way we have already done in Parkinson’s and for mood disorders such as depression, and it may have therapeutic benefit in people with memory problems,” he said.

The researchers are testing the approach in six Alzheimer’s patients in a Phase 1 safety study. Three have so far had electrodes surgically implanted. The electrodes are attached via a cable that runs below the skull and down the neck to a battery pack stitched under the skin of the chest. The “pacemaker” delivers a constant low-level current that stimulates the brain but cannot be perceived by the patient.

Professor Lozano said: “It is the same device as is used for Parkinson’s disease. We have placed the electrodes in exactly the same area of the hypothalamus because we want to see if we can reproduce the findings in the earlier experiment. We believe the memory circuits we are stimulating are close by, physically touching the hypothalamus.

“It is a very effective treatment for the motor problems associated with Parkinson’s disease and it has been used on 40,000 people. We are in the early stages of using it with Alzheimer’s patients and we don’t know if it will work. We want to assess if we can reach the memory circuits and drive improvement. It is a novel approach to dealing with this problem.”

British researchers welcomed the discovery. Andrea Malizia, a senior lecturer in psychopharmacology at the University of Bristol who is studying deep-brain stimulation as a treatment for depression, said: “If they had said let’s stick an electrode in the hypothalamus to modify Alzheimer’s disease, I would have said ‘Why start there?’ But, if they have had a serendipitous finding, then that is as good. Serendipitous findings are how a lot of discoveries in science have been made.”

Ayesha Khan, a scientific liaison officer at the Alzheimer’s Disease Society, said: “This is very cutting-edge research. It is exciting, but the initial result is in one person. It will need much further investigation.”

Deep -brain stimulation has been used for more than a decade to treat a range of conditions including depression, chronic pain, Parkinson’s disease and other movement disorders.

It has been so successful in treating Parkinson’s that 40,000 patients worldwide now have electrodes implanted in their brains driven by pacemakers stitched into their chests.

As the devices become smaller, requiring less risky surgery, and the target areas of the brain requiring stimulation are more precisely identified, demand for the treatment is expected to leap. Although it is expensive, the potential savings in care and treatment costs are immense. It does not lead to dependence on drugs and is reversible.

The electrodes are implanted under local anaesthesia while the patient is awake. Before the operation, the neurosurgeon performs an MRI scan and establishes the target location for the electrodes. He then carries out a craniotomy – lifting a section of the skull – and inserts the electrodes and leads. By stimulating the electrodes and checking the patient’s response, the surgeon can check that they are positioned in the right place.

Different areas of the brain are targeted for different conditions. For Parkinson’s disease, they are placed in the subthalamic nucleus; for depression, in area 25 of the cingulate cortex.

Deep-brain stimulation was developed in France and first licensed by the Food and Drug Administration in the US in 1997 as a treatment for tremor. In the UK, the surgery is performed at the National Hospital for Neurology and Neurosurgery in London, in Bristol, in Oxford and at a handful of other centres.

The name of the procedure is in some ways a misnomer as it often involves inhibiting electrical activity in an area of the brain rather than stimulating it. The technique is as much about restoring balance between competing brain areas which leads to the tremor characteristic of some types of Parkinson’s disease.