Κυριακή, 20 Ιουλίου 2014

VTEC O117:H7 VT1 (Verotoxinogenic Escherichia coli O157:H7) circulating amongst the MSM community O VTEC O117:H7 VT1 κυκλοφορεί στη gay κοινότητα στην Αγγλία 17 Ιουλίου 2014

Public Health England have detected seven cases of VTEC O117: H7 VT1 circulating amongst the men who have sex with men (MSM) community.

Οι φορείς δημόσιας υγείας στην Αγγλία εντόπισαν επτά περιστατικά VTEC O117:H7 VT1 μεταξύ των ανδρών της gay κοινότητας

VTEC O117:H7 is a serogroup usually reported at low levels in England with 1-2 cases annually. 
These cases are generally in adults reporting foreign travel to destinations outside of Europe and North America.

Ο VTEC O117:H7 VT1 είναι ένας ορότυπος που συνήθως αναφέρεται σε χαμηλά επίπεδα στην Αγγλία με 1-2 περιστατικά ετησίως. 
Αυτά τα περιστατικά καταγράφονται συνήθως σε ενήλικες που αναφέρουν ταξίδια εκτός Ευρώπης και Β.Αμερικής.

However, there has been a recent shift in the epidemiology of VTEC O117:H7, with seven cases reported between October 2013 and 16 July 2014. 
All seven cases are adult males with a mean age of 39 years. 
One case reported travel to South America, but no travel was reported for the other six cases. 
Four cases are reported as MSM, while MSM status is currently unknown for the remaining three cases.

Εν τούτοις υπήρξε πρόσφατη μεταβολή στην επιδημιολογία του VTEC O117:H7 VT1 με επτά περιστατικά που αναφέρθηκαν μεταξύ Οκτωβρίου 2013 και Ιουλίου 2014. 
Και τα επτά περιστατικά είναι ενήλικες άνδρες με μεση ηλικιά τα 39 έτη. 
Ενας απο αυτούς ανέφερε οτι ταξίδεψε στη Ν.Αμερική αλλά οι άλλοι εξι δεν ανέφεραν κανένα ταξίδι. 
Για τους 4 από τα περιστατικά αναφέρεται οτι είναι gay ενώ δεν είναι γνωστός προς το παρόν ο σεξουαλικός προσανατολισμός για τα υπόλοιπα 4 περιστατικά

These cases will be interviewed by specialists in sexually transmitted infections in order to allow more detailed epidemiological data to be collected and possible routes of transmission to be identified.

Αυτά τα περιστατικά θα εξετασθούν από ειδικούς στα ΣΜΝ προκειμένου να συλλεγούν πιό λεπτομεή επιδημιολογικά δεδομένα και να εντοπισθούν οι πιθανοί τρόποι μετάδοσης

Γενικές πληροφορίες

Από το 2007, έχουν αναφερθεί 99 περιατατικα..

Είναι σπάνιος ορότυπος στην Ε.Ε. 

Τα συμπτώματα του Verotoxinogenic E. coli O117:H7 (VTEC O117:H7) μπορεί να μη υπάρχουν καθόλου (ασυμπτωματικά άτομα) να είναι μια μέτρια υδαρής διάρροια, αιμορραγική διάρροια έως και σοβαρές επιπλοκές όπως το αιμορραγικό αιμολυτικό σύνδρομο ή και ο θάνατος.

Η περίοδος επώασης είναι περίπου 3 ημέρες 
(μπορεί να ποικίλει από 1-8 ημέρες) όπου 
τα άτομα που έχουν μολυνθεί εμφανίζουν διάρροια (30-60%) και κοιλιακό πόνο. 

Περίπου το 30% των ασθενών έχουν ήπιο πυρετό. 
1-3 ημέρες μετά την έναρξη των συμπτωμάτων το 70% των ασθενών εμφανίζουν αιμορραγική διάρροια ποικίλης έντασης.

Η μετάδοση του νοσήματος απο άνθρωπο σε άνθρωπο γίνεται μέσω της στοματοπρωκτικής οδού. 

Ανεπαρκή μέτρα υγιεινής μετά τη χρήση τουαλέτας διευκολύνει τη μετάδοση που παρατηρείται σε μέλη της ίδιας οικογένειας καθώς και σε ιδρύματα.

Σάββατο, 19 Ιουλίου 2014

After MH17 Ukraine Crash, Global AIDS Researchers Mourn Lost Colleagues / July 18, 2014

The cause of HIV/AIDS research will be set back because of experts lostin the Malaysia Airlines Ukraine disaster

[UPDATE: 7/18/14, 11:52 AM EDT]
There was a pall over the 20th annual International AIDS Conference in Melbourne even before the crash of Flight MH17 in eastern Ukraine, which killed an estimated 100 delegates who were en route to the meeting. [Update: Later reports suggest that the number of delegates lost is much lower.]
In the past couple of years the vibrant showcase event—part serious science, part activist networking and carnivalhas been headily optimistic, as HIV treatments improved and the possibility of a cure no longer seemed so far off. 
“The mood is always an important part,” says Professor Mike Toole, an international communicable diseases veteran with Melbourne’s Burnet Institute who has been at the HIV/AIDS front line since the pandemic began some 30 years ago.
Toole remembers that the landmark Durban International AIDS Conference back in 2000 demonstrated to this eclectic crowd—a disparate crew of laboratory researchers, front-line health workers, activists and people living with the infection—their powerful potential. 
It was in Durban that the commitment to deliver then-prohibitively expensive antiretroviral drugs to the world’s poorest populations ignited, and was carried through over the next few years by organizations like The Global Fund and the U.S. President’s Emergency Fund for Aids Relief.
The past two International Aids Society (IAS) meetings, in Vienna and Washington DC, have been buoyed by signals that a breakthrough was close, and the expectation was that the momentum would continue into Melbourne.
Then, barely a week ago, came a serious blow.
 For over a year many members of the HIV/AIDS community had been pinning their hopes for a breakthrough on the so-called Mississippi baby, an HIV-positive infant that had apparently been cured through aggressive drug treatment soon after birth. But on July 10, news came, that the child was showing symptoms that the virus had returned.
Although there are other programs that indicate that it might be possible to eliminate HIV infection from a human body, the apparent relapse of the Mississippi baby “depressed people incredibly,” says Toole.
Then came yesterday’s tragedy. 
For Toole and others HIV/AIDS experts the crash summoned up ghosts. 
“It reminds me of the Swissair flight, New York to Geneva, when Jonathan Mann died,” he says. 
Mann then the founding director of the World Health Organization’s global AIDS program was killed with several other researchers, including his wife Mary-Lou Clements-Mann, en route to AIDS meetings when the plane crashed in Canada, September 3, 1998. 
“I lost five friends on that flight.”
In Sydney, at a pre-conference gathering on July 18, about 200 delegates spent the day closely monitoring Twitter and exchanging snippets of news, desperate for updates on who would and would not be joining them in Melbourne. 
The word there was that a substantial number of the 100-plus delegates reported to be on the downed aircraft were part of the global network of activists and people living with AIDS.
With only a handful of names of the deceased confirmed by Friday, it’s difficult to measure the overall impact on HIV/AIDS research and advocacy. 
But the loss of internationally renowned Dutch researcher Joep Lange—a former president of the IAS—would be a massive blow. 
“It will have a big psychological effect,” says Toole.
“He was one of the leaders in the field.”
Another known casualty was Glenn Thomas, a British media officer working for WHO in Geneva. 
Thomas was to be part of a media launch on July 20 revealing new tools to reduce harm to users of intravenous drugs. 
He was also recognized as a particularly effective communicator on the links between HIV/AIDS and tuberculosis, says Toole. 
(The risk of developing TB is up to 20 times greater in people infected with HIV, and in 2012, of the 8.6 million new cases of TB diagnosed internationally, 1.1 million were among people with HIV.)
“And the other hundred [on board]—we don’t know who they are, what it means.”
The annual AIS conferences are like no other medical gathering, says Professor Rob Moodie of the University of Melbourne, a former senior WHO official and longtime Australian public health specialist. 
“You have this incredible mixture of scientists and clinicians, public health people, civilian organizers, human rights activists, people who have the virus … who all have some sort of sense of ownership and collective leadership.”
The energy and collaborations of these gatherings have helped drive the huge advances achieved in understanding and responses to HIV/AIDS in a relatively short time. 
“We learned more about HIV in the first 10 years than we did in a century with other diseases,” says Moodie. 
The involvement of grassroots activist groups—as well as lab researchers—has been key to that success. 
MH17’s toll would not only be measured in the loss of medical expertise, but of advocacy, understanding and hard-won personal experience.
“There is a black cloud on this conference,” says Toole.
Still, Toole was confident that delegates would be driven to achieve as much as they could in memory of their colleagues. 
He welcomed the move by the City of Melbourne on July 18 to cancel fireworks that had been scheduled to kick off the conference, but was disappointed that that’s night fixture in the Australian Football League competition—to which AIDS2014 delegates had been given tickets as part of the cultural program—did not pause for a minute of silence.

UNAIDS in shock over tragic loss of life / MELBOURNE/GENEVA, 18 July 2014 / Press statement

—UNAIDS expresses deep sadness over the loss of life of the passengers and crew of flight MH17, which crashed over eastern Ukraine on Thursday, 17 July 2014.
While the full details are still unclear, it is believed that many of the passengers were on their way to participate in the International AIDS Conference in Melbourne, Australia. 
It has been confirmed that the United Nations has lost a colleague from the World Health Organization.
It seems that some of the finest academics, health-care workers and activists in the AIDS response may have perished while travelling to take part in the international gathering of experts and advocates. 
Professor Joep Lange, the former President of the International AIDS Society, was among the victims. 
Professor Lange was a leading light in the field since the early days of HIV and worked unceasingly to widen access to antiretroviral medicines around the world.
“We are bracing ourselves to hear of the deaths of others who worked in the AIDS response as their names are officially released,” 
said Michel Sidibé, Executive Director of UNAIDS. 
“The UNAIDS family is in deep shock. Our hearts go out to the families of all the victims of this tragic crash. The deaths of so many committed people working against HIV will be a great loss for the AIDS response.”
The UNAIDS family stands in solidarity with the families, friends and colleagues of all who have perished in this tragedy.


The Joint United Nations Programme on HIV/AIDS (UNAIDS) leads and inspires the world to achieve its shared vision of
zero new HIV infections, 
zero discrimination and 
zero AIDS-related deaths. 

UNAIDS unites the efforts of 11 UN organizations—UNHCR, UNICEF, WFP, UNDP, UNFPA, UNODC, UN Women, ILO, UNESCO, WHO and the World Bank—and works closely with global and national partners to maximize results for the AIDS response. 
Learn more at unaids.org and connect with us onFacebook and Twitter.

Παρασκευή, 18 Ιουλίου 2014

HIV: 'the WHO is perpetuating gay stereotypes' The World Health Organisation has recommended that all gay men take antiretroviral drugs to stop the spread of HIV, but surely education - not more drugs - is the answer

The HIV virus
'A more relaxed attitude to HIV is not exclusive to the gay community' 
Photo: Alamy
Anything else you’d like us to take responsibility for? Famine in Africa? Umemployment statistics? Binge drinking in Magaluf? 
Being gay can often feel like the world is against you, and yet again the planet’s HIV epidemic is being firmly placed on our shoulders. 
I’m talking about the news that the World Health Organisation has announced for the first time that men who have sex with men should take antiretroviral drugs, in a bid to try and contain the growing rates of HIV in gay communities around the world. 
That’s all men who have sex with men
No mention of men who have sex with women. 
Are they all suddenly having safe sex? 
In guidelines published last Friday, the WHO said that it “strongly recommends men who have sex with men consider taking antiretroviral medicines as an additional method of preventing HIV infection”. 
Gottfried Hirnschall, the head of WHO’s HIV department, said that infection rates among homosexual men are increasing again, 33 years after the epidemic first hit. 
According to the report, men who have sex with men are 19 times more likely to have HIV than the general population. 
I'm not arguing with those statistics, but I do believe it's important to challenge the constant message that binds all gay men to the rising HIV epidemic. 
Worryingly, this latest recommendation does nothing to dispel the myth that all gay men are promiscuous, irresponsible or ignorant and regularly play Russian roulette with their sexual health. 
Hirnschall highlighted the fact that HIV doesn’t hold as much fear to a younger generation because of the availability of effective drugs to live with the condition, but are more drugs really the answer? 
Doesn’t the fact that people have become complacent about HIV imply that what we really need is to address is the severe lack of education around contracting it and other STDs, rather than funding and promoting yet another expensive treatment? 
This education needs to start with young people, both gay and straight. 
However, we first have to address the fact that many adults believe that it is inappropriate to talk to young people about sex in full and frank detail, out of fear that doing so will encourage them to indulge in risky behaviours. 
In many situations, these attitudes are based on moral or religious views rather than any real evidence, and as a result have severely limited HIV and AIDS education in the UK. 
It is simply wrong to assume that talking to young people about safer sex and the importance of using condoms leads to an increase in sexual activity. 

Young people, gay and straight, are having sex, and they are experimenting with drugs and alcohol, just as their parents did. 
It’s a fact that we, and especially parents, shouldn't ignore. 
Some experiment more than others, some play it very safe. 
Some experiment with behaviour that some adults would view as "immoral"
We of course need to protect children from potential harm, but in teaching them about sex we need to ensure we don't focus on the negatives, the dangers, and reduce it to argument about what's moral or immoral. 

There is still an assumption among many in our society, which is being passed on to the younger generation, that indulging in "immoral" sex and illegal drug use will lead to HIV infection. 
This simply perpetuates the stigmatisation of people who are living with HIV, and risks implying that anyone who has HIV is therefore involved in "immoral" activities, and has got what was coming to them. 

The WHO guidelines feel like a step backwards, promoting a negative gay stereotype that I thought we were moving away from. 
Let's be clear: a more relaxed attitude to HIV is not exclusive to the gay community. 
It's an attitude that's become prevalent across all communities. 
The report will encourage straight people to believe that HIV is simply a gay problem, and that they themselves are off the hook.

I am not against antiretroviral drugs where they are needed. 
The report correctly highlights that antiretroviral drug use can reduce the chance of passing on HIV by up to 92 per cent. 
However, other studies tell us that, when used correctly, a condom is about 98 per cent effective. 
Shouldn't we be focusing our efforts on educating people to use condoms (which are cheaper than drugs and side-effect free) instead? 

A fraction of the cost of investing in vast amounts of antiretroviral drugs would go a long way to creating a programme that educates us all - gay and straight - about responsible sexual health. 

Instead, the WHO appears to have created a situation with a very clear winner (drugs companies) and a very clear loser (gay men). 

Τρίτη, 15 Ιουλίου 2014

Italy not fingerprinting many migrants despite law

Posted: Friday, July 4, 2014 11:27 am | Updated: 
11:45 pm, Fri Jul 4, 2014.

Every day, boatloads of refugees arrive on Italian shores. 
European Union law requires Italy to fingerprint them, so that if they apply for asylum in another country they can be sent back to their port of entry. 
Instead, Italy is letting thousands of migrants slip quietly into northern Europe, with no record of their time in Italy.

An Associated Press analysis of EU and Italian data suggests that as many as a quarter of the migrants who should have been fingerprinted in the first half of the year were not.
While EU law required Italy to share fingerprints for about 56,700 of the migrants, only 43,382 sets were sent.
Even accounting for possible delays in sending fingerprints to Brussels, it's clear that thousands of refugees are slipping through the cracks.
"It's a very serious problem," 
European Home Affairs Commissioner Cecilia Malmstroem told the Swedish newspaper Dagens Nyheter this week. 
After complaints from member states, the European Commission is studying whether Italy is living up to its EU obligations. 
The Italian government didn't respond to repeated requests for comment.
EU countries are angry that they can't send migrants back to their first port of entry when there is no record of where that was. Human rights officials also worry that the refugees can't benefit from U.N. protections for refugees if they don't officially exist.
Italy, by not fingerprinting migrants, avoids the possibility that they'll be sent back. 

It is already spending 9.5 million euros ($13 million) a month to rescue thousands of migrants making the perilous crossing from North Africa aboard smugglers' boats in an operation launched after 360 migrants drowned off Sicily last year, and feels it's doing more than its share already.
The refugees themselves are happy not to be fingerprinted. 
With unemployment at 12.6 percent and youth unemployment at 43 percent, new arrivals have little interest in staying in Italy, and would rather settle in northern Europe where there are better job opportunities and more established refugee communities.
Aided by Rome's blind eye, Syrian migrants in particular are falling off Italy's radar, making their way to Milan's central train station in groups of 100 or more. 

They are met by railway police, aid workers and city officials who offer food, a bed and — for those who ask — advice on asylum.
Of the 10,500 who arrived in Milan since October, only eight requested asylum in Italy, city officials said. Many others, after a few hours or days in Milan, headed north with no record of ever having set foot in Italy.
"No Syrian wants to get fingerprinted," 
said Shadi Howara, a doctor from Damascus passing through Milan.
The Italian Interior Ministry reported 60,435 migrants arrived by boat in Italy this year through June 30. 
A number of those are accompanied children who by EU rules shouldn't be fingerprinted; Save the Children estimates there were 3,700. 
During the same time period, the EU said Italy shared 43,382 sets of fingerprints.
As more Syrians began to arrive and officials spotted children sprawled out on stone benches, the city of Milan set up a welcome desk in the train station in October, according to the city's top immigration official, Pierfrancesco Majorino.
The welcome desk, a table on the mezzanine of the cavernous station, sits behind yellow plastic barriers marked 
"Syrian Emergency."
The scene is surreal: 
As a nearby escalator ferries fashionable commuters to and from work in Italy's financial capital, Syrian war refugees mill about in donated clothes and little more than a plastic bag's worth of belongings, waiting for the next train north.
Why haven't they been fingerprinted?
"You have to ask the Interior Ministry," 
Majorino said, adding that only law enforcement agencies — not city workers — are authorized to carry out the task.
The Interior Ministry declined repeated requests for comment on Italy's application of the EU fingerprinting directive.

Syrian refugee Issam Zarai, 35, spent 30 hours in a packed boat with his wife and two children, 6 and 7, before being rescued at sea. 
On his way to Sweden, he had no problem with Italy's lax application of the EU directive.
"They took no fingerprints," he said, "and no names."
Associated Press writers Kavitha Surana and Nicole Winfield contributed from Rome.

BBC: Why do we have blood types? By Carl Zimmer

(Science Photo Library)
(Science Photo Library)
More than a century after their discovery, we still don’t know what blood groups like O, A and B are for. Do they really matter? Carl Zimmer investigates.
When my parents informed me that my blood type was A+, I felt a strange sense of pride. 
If A+ was the top grade in school, then surely A+ was also the most excellent of blood types – a biological mark of distinction.

It didn’t take long for me to recognise just how silly that feeling was and tamp it down. 
But I didn’t learn much more about what it really meant to have type A+ blood. 
By the time I was an adult, all I really knew was that if I should end up in a hospital in need of blood, the doctors there would need to make sure they transfused me with a suitable type.

And yet there remained some nagging questions. 
Why do 40% of Caucasians have type A blood, while only 27% of Asians do? Where do different blood types come from, and what do they do? 
To get some answers, I went to the experts – to haematologists, geneticists, evolutionary biologists, virologists and nutrition scientists.
We all know we have a blood type, but what we don't know is exactly why we have them in the first place. (Science Photo Library)
In 1900 the Austrian physician Karl Landsteiner first discovered blood types, winning the Nobel Prize in Physiology or Medicine for his research in 1930. 
Since then scientists have developed ever more powerful tools for probing the biology of blood types. 
They’ve found some intriguing clues about them – tracing their deep ancestry, for example, and detecting influences of blood types on our health. 
And yet I found that in many ways blood types remain strangely mysterious. Scientists have yet to come up with a good explanation for their very existence.

“Isn’t it amazing?” says Ajit Varki, a biologist at the University of California, San Diego. 
“Almost a hundred years after the Nobel Prize was awarded for this discovery, we still don’t know exactly what they’re for.”

Transfusion confusion

My knowledge that I’m type A comes to me thanks to one of the greatest discoveries in the history of medicine. 
Because doctors are aware of blood types, they can save lives by transfusing blood into patients. 
But for most of history, the notion of putting blood from one person into another was a feverish dream.

Renaissance doctors mused about what would happen if they put blood into the veins of their patients. 
Some thought that it could be a treatment for all manner of ailments, even insanity. 
Finally, in the 1600s, a few doctors tested out the idea, with disastrous results. 
A French doctor injected calf’s blood into a madman, who promptly started to sweat and vomit and produce urine the colour of chimney soot. 
After another transfusion the man died.

Such calamities gave transfusions a bad reputation for 150 years. 
Even in the 19th Century only a few doctors dared try out the procedure. 
One of them was a British physician named James Blundell. 
Like other physicians of his day, he watched many of his female patients die from bleeding during childbirth. 
After the death of one patient in 1817, he found he couldn’t resign himself to the way things were.
“I could not forbear considering, that the patient might very probably have been saved by transfusion,” he later wrote.
Transfusions weren't a routine procedure until the discovery that we have blood types (Science Photo Library)
Blundell became convinced that the earlier disasters with blood transfusions had come about thanks to one fundamental error: transfusing “the blood of the brute”, as he put it. 
Doctors shouldn’t transfer blood between species, he concluded, because “the different kinds of blood differ very importantly from each other”.

Human patients should only get human blood, Blundell decided. But no one had ever tried to perform such a transfusion. 
Blundell set about doing so by designing a system of funnels and syringes and tubes that could channel blood from a donor to an ailing patient. 
After testing the apparatus out on dogs, Blundell was summoned to the bed of a man who was bleeding to death. 
“Transfusion alone could give him a chance of life,” he wrote.

Several donors provided Blundell with 14oz (0.4kg) of blood, which he injected into the man’s arm. 
After the procedure the patient told Blundell that he felt better – “less fainty” – but two days later he died.

Still, the experience convinced Blundell that blood transfusion would be a huge benefit to mankind, and he continued to pour blood into desperate patients in the following years. 
All told, he performed 10 blood transfusions. 
Only four patients survived.

While some other doctors experimented with blood transfusion as well, their success rates were also dismal. 
Various approaches were tried, including attempts in the 1870s to use milk in transfusions (which were, unsurprisingly, fruitless and dangerous).

Prize discovery
Blundell was correct in believing that humans should only get human blood. 
But he didn’t know another crucial fact about blood: that humans should only get blood from certain other humans. 
It’s likely that Blundell’s ignorance of this simple fact led to the death of some of his patients. 
What makes those deaths all the more tragic is that the discovery of blood types, a few decades later, was the result of a fairly simple procedure.

The first clues as to why the transfusions of the early 19th Century had failed were clumps of blood. 
When scientists in the late 1800s mixed blood from different people in test tubes, they noticed that sometimes the red blood cells stuck together. 
But because the blood generally came from sick patients, scientists dismissed the clumping as some sort of pathology not worth investigating. 
Nobody bothered to see if the blood of healthy people clumped, until Karl Landsteiner wondered what would happen. 
Immediately, he could see that mixtures of healthy blood sometimes clumped too.

Landsteiner set out to map the clumping pattern, collecting blood from members of his lab, including himself. 
He separated each sample into red blood cells and plasma, and then he combined plasma from one person with cells from another.
By experimenting on his lab members' and himself, Karl Landsteiner discovered blood types (Science Photo Library)
Landsteiner found that the clumping occurred only if he mixed certain people’s blood together. 
By working through all the combinations, he sorted his subjects into three groups. 
He gave them the entirely arbitrary names of A, B and C. (Later on C was renamed O, and a few years later other researchers discovered the AB group. 
By the middle of the 20th Century the American researcher Philip Levine had discovered another way to categorise blood, based on whether it had the Rhesus (Rh) blood factor. 
A plus or minus sign at the end of Landsteiner’s letters indicates whether a person has the factor or not.)

When Landsteiner mixed the blood from different people together, he discovered it followed certain rules. 
If he mixed the plasma from group A with red blood cells from someone else in group A, the plasma and cells remained a liquid. 
The same rule applied to the plasma and red blood cells from group B. 
But if Landsteiner mixed plasma from group A with red blood cells from B, the cells clumped (and vice versa).

The blood from people in group O was different. 
When Landsteiner mixed either A or B red blood cells with O plasma, the cells clumped. 
But he could add A or B plasma to O red blood cells without any clumping.

Distinguishing features

It’s this clumping that makes blood transfusions so potentially dangerous. 
 If a doctor accidentally injected type B blood into my arm, my body would become loaded with tiny clots. 
They would disrupt my circulation and cause me to start bleeding massively, struggle for breath and potentially die. 
But if I received either type A or type O blood, I would be fine.

Landsteiner didn’t know what precisely distinguished one blood type from another. 
Later generations of scientists discovered that the red blood cells in each type are decorated with different molecules on their surface. 
In my type A blood, for example, the cells build these molecules in two stages, like two floors of a house. 
The first floor is called an H antigen. 
On top of the first floor the cells build a second, called the A antigen.

People with type B blood, on the other hand, build the second floor of the house in a different shape. 
And people with type O build a single-storey ranch house: they only build the H antigen and go no further.
Different blood types arise as a result of different molecules on the surface of red blood cells (Science Photo Library)
Each person’s immune system becomes familiar with his or her own blood type. 
If people receive a transfusion of the wrong type of blood, however, their immune system responds with a furious attack, as if the blood were an invader. 
The exception to this rule is type O blood. 
It only has H antigens, which are present in the other blood types too. 
To a person with type A or type B, it seems familiar. 
That familiarity makes people with type O blood universal donors, and their blood especially valuable to blood centres.

Landsteiner reported his experiment in a short, terse paper in 1900. “It might be mentioned that the reported observations may assist in the explanation of various consequences of therapeutic blood transfusions,” he concluded with exquisite understatement. 
Landsteiner’s discovery opened the way to safe, large-scale blood transfusions, and even today blood banks use his basic method of clumping blood cells as a quick, reliable test for blood types.

But as Landsteiner answered an old question, he raised new ones. What, if anything, were blood types for? 
Why should red blood cells bother with building their molecular houses? 
And why do people have different houses?
Solid scientific answers to these questions have been hard to come by. 
And in the meantime, some unscientific explanations have gained huge popularity. 
“It’s just been ridiculous,” sighs Connie Westhoff, the Director of Immunohematology, Genomics and Rare Blood at the New York Blood Center.

Crash diet

In 1996 a naturopath named Peter D’Adamo published a book called Eat Right 4 Your Type. D’Adamo argued that we must eat according to our blood type, in order to harmonise with our evolutionary heritage.
Blood types, he claimed, “appear to have arrived at critical junctures of human development.” 
According to D’Adamo, type O blood arose in our hunter-gatherer ancestors in Africa, type A at the dawn of agriculture, and type B developed between 10,000 and 15,000 years ago in the Himalayan highlands. Type AB, he argued, is a modern blending of A and B.

From these suppositions D’Adamo then claimed that our blood type determines what food we should eat. 
With my agriculture-based type A blood, for example, I should be a vegetarian. 
People with the ancient hunter type O should have a meat-rich diet and avoid grains and dairy. 
According to the book, foods that aren’t suited to our blood type contain antigens that can cause all sorts of illness. 
D’Adamo recommended his diet as a way to reduce infections, lose weight, fight cancer and diabetes, and slow the ageing process.
Test card and samples being used to determine a patient's blood type as part of what is known as the blood type diet (Science Photo Library)
D’Adamo’s book has sold seven million copies and has been translated into 60 languages. 
It’s been followed by a string of other blood type diet books; D’Adamo also sells a line of blood-type-tailored diet supplements on his website. 
As a result, doctors often get asked by their patients if blood type diets actually work.

The best way to answer that question is to run an experiment. 
In Eat Right 4 Your Type D’Adamo wrote that he was in the eighth year of a decade-long trial of blood type diets on women with cancer. 
Eighteen years later, however, the data from this trial have not yet been published.

Recently, researchers at the Red Cross in Belgium decided to see if there was any other evidence in the diet’s favour. 
They hunted through the scientific literature for experiments that measured the benefits of diets based on blood types. 
Although they examined over 1,000 studies, their efforts were futile. 
“There is no direct evidence supporting the health effects of the ABO blood type diet,” says Emmy De Buck of the Belgian Red Cross-Flanders.

After De Buck and her colleagues published their review in the American Journal of Clinical Nutrition, D’Adamo responded on his blog. 
In spite of the lack of published evidence supporting his Blood Type Diet, he claimed that the science behind it is right. 
“There is good science behind the blood type diets, just like there was good science behind Einstein’s mathmatical [sic] calculations that led to the Theory of Relativity,” he wrote.

Different strokes

Comparisons to Einstein notwithstanding, the scientists who actually do research on blood types categorically reject such a claim. 
“The promotion of these diets is wrong,” a group of researchers flatly declared in Transfusion Medicine Reviews.

Nevertheless, some people who follow the Blood Type Diet see positive results. 
According to Ahmed El-Sohemy, a nutritional scientist at the University of Toronto, that’s no reason to think that blood types have anything to do with the diet’s success.

El-Sohemy is an expert in the emerging field of nutrigenomics.
He and his colleagues have brought together 1,500 volunteers to study, tracking the foods they eat and their health. 
They are analysing the DNA of their subjects to see how their genes may influence how food affects them. 
Two people may respond very differently to the same diet based on their genes.
Scientists say there's no reason to think that blood types have anything to do with what you should eat (Science Photo Library)
“Almost every time I give talks about this, someone at the end asks me, ‘Oh, is this like the Blood Type Diet?’” says El-Sohemy. 
As a scientist, he found Eat Right 4 Your Type lacking. “None of the stuff in the book is backed by science,” he says. 
But El-Sohemy realised that since he knew the blood types of his 1,500 volunteers, he could see if the Blood Type Diet actually did people any good.

El-Sohemy and his colleagues divided up their subjects by their diets. 
Some ate the meat-based diets D’Adamo recommended for type O, some ate a mostly vegetarian diet as recommended for type A, and so on. 
The scientists gave each person in the study a score for how well they adhered to each blood type diet.

The researchers did find, in fact, that some of the diets could do people some good. 
People who stuck to the type A diet, for example, had lower body mass index scores, smaller waists and lower blood pressure. 
People on the type O diet had lower triglycerides. 
The type B diet – rich in dairy products – provided no benefits.
“The catch,” says El-Sohemy, “is that it has nothing to do with people’s blood type.” 
In other words, if you have type O blood, you can still benefit from a so-called type A diet just as much as someone with type A blood – probably because the benefits of a mostly vegetarian diet can be enjoyed by anyone. 
Anyone on a type O diet cuts out lots of carbohydrates, with the attending benefits of this being available to virtually everyone. 
Likewise, a diet rich in dairy products isn’t healthy for anyone – no matter what their blood type.

Monkey business

One of the appeals of the Blood Type Diet is its story of the origins of how we got our different blood types. 
But that story bears little resemblance to the evidence that scientists have gathered about their evolution.

After Landsteiner’s discovery of human blood types in 1900, other scientists wondered if the blood of other animals came in different types too. 
It turned out that some primate species had blood that mixed nicely with certain human blood types. 
But for a long time it was hard to know what to make of the findings. 
The fact that a monkey’s blood doesn’t clump with my type A blood doesn’t necessarily mean that the monkey inherited the same type A gene that I carry from a common ancestor we share. 
Type A blood might have evolved more than once.

The uncertainty slowly began to dissolve, starting in the 1990s with scientists deciphering the molecular biology of blood types. 
They found that a single gene, called ABO, is responsible for building the second floor of the blood type house. 
The A version of the gene differs by a few key mutations from B. 
People with type O blood have mutations in the ABO gene that prevent them from making the enzyme that builds either the A or B antigen.
Our blood may have more in common with gibbons than you may think (Science Photo Library)
Scientists could then begin comparing the ABO gene from humans to other species. 
Laure Segurel and her colleagues at the National Center for Scientific Research in Paris have led the most ambitious survey of ABO genes in primates to date. 
And they’ve found that our blood types are profoundly old. Gibbons and humans both have variants for both A and B blood types, and those variants come from a common ancestor that lived 20 million years ago.

Our blood types might be even older, but it’s hard to know how old. Scientists have yet to analyse the genes of all primates, so they can’t see how widespread our own versions are among other species. 
But the evidence that scientists have gathered so far already reveals a turbulent history to blood types. 
 In some lineages mutations have shut down one blood type or another. 
Chimpanzees, our closest living relatives, have only type A and type O blood. Gorillas, on the other hand, have only B. 
In some cases mutations have altered the ABO gene, turning type A blood into type B. 
And even in humans, scientists are finding, mutations have repeatedly arisen that prevent the ABO protein from building a second storey on the blood type house. 
These mutations have turned blood types from A or B to O. 
“There are hundreds of ways of being type O,” says Westhoff.

Bombay puzzle

Being type A is not a legacy of my proto-farmer ancestors, in other words. 
It’s a legacy of my monkey-like ancestors. Surely, if my blood type has endured for millions of years, it must be providing me with some obvious biological benefit. 
Otherwise, why do my blood cells bother building such complicated molecular structures?
Yet scientists have struggled to identify what benefit the ABO gene provides. 
“There is no good and definite explanation for ABO,” says Antoine Blancher of the University of Toulouse, “although many answers have been given.”

The most striking demonstration of our ignorance about the benefit of blood types came to light in Bombay in 1952. 
Doctors discovered that a handful of patients had no ABO blood type at all – not A, not B, not AB, not O. 
If A and B are two-storey buildings, and O is a one-storey ranch house, then these Bombay patients had only an empty lot.

Since its discovery this condition – called the Bombay phenotype – has turned up in other people, although it remains exceedingly rare. 
And as far as scientists can tell, there’s no harm that comes from it. 
The only known medical risk it presents comes when it’s time for a blood transfusion. 
Those with the Bombay phenotype can only accept blood from other people with the same condition. 
Even blood type O, supposedly the universal blood type, can kill them.
Doctors discovered that a handful of patients in Bombay in the 1950s had no regular blood type (Getty Images)
The Bombay phenotype proves that there’s no immediate life-or-death advantage to having ABO blood types. 
Some scientists think that the explanation for blood types may lie in their variation. 
That’s because different blood types may protect us from different diseases.
Doctors first began to notice a link between blood types and different diseases in the middle of the 20th Century, and the list has continued to grow. 
 “There are still many associations being found between blood groups and infections, cancers and a range of diseases,” Pamela Greenwell of the University of Westminster tells me.

From Greenwell I learn to my displeasure that blood type A puts me at a higher risk of several types of cancer, such as some forms of pancreatic cancer and leukaemia. 
I’m also more prone to smallpox infections, heart disease and severe malaria. 
On the other hand, people with other blood types have to face increased risks of other disorders. 
People with type O, for example, are more likely to get ulcers and ruptured Achilles tendons.

Virus scan

These links between blood types and diseases have a mysterious arbitrariness about them, and scientists have only begun to work out the reasons behind some of them. 
For example, Kevin Kain of the University of Toronto and his colleagues have been investigating why people with type O are better protected against severe malaria than people with other blood types. 
His studies indicate that immune cells have an easier job of recognising infected blood cells if they’re type O rather than other blood types.

More puzzling are the links between blood types and diseases that have nothing to do with the blood. 
Take norovirus. 
This nasty pathogen is the bane of cruise ships, as it can rage through hundreds of passengers, causing violent vomiting and diarrhoea. 
It does so by invading cells lining the intestines, leaving blood cells untouched. 
Nevertheless, people’s blood type influences the risk that they will be infected by a particular strain of norovirus.

The solution to this particular mystery can be found in the fact that blood cells are not the only cells to produce blood type antigens. 
They are also produced by cells in blood vessel walls, the airway, skin and hair. 
Many people even secrete blood type antigens in their saliva. 
Noroviruses make us sick by grabbing onto the blood type antigens produced by cells in the gut.
What blood type you have influences the risk that you will be infected by a particular strain of norovirus (Science Photo Library)
Yet a norovirus can only grab firmly onto a cell if its proteins fit snugly onto the cell’s blood type antigen.
 So it’s possible that each strain of norovirus has proteins that are adapted to attach tightly to certain blood type antigens, but not others. 
That would explain why our blood type can influence which norovirus strains can make us sick.

It may also be a clue as to why a variety of blood types have endured for millions of years. 
Our primate ancestors were locked in a never-ending cage match with countless pathogens, including viruses, bacteria and other enemies. 
Some of those pathogens may have adapted to exploit different kinds of blood type antigens. 
The pathogens that were best suited to the most common blood type would have fared best, because they had the most hosts to infect. 
But, gradually, they may have destroyed that advantage by killing off their hosts. 
Meanwhile, primates with rarer blood types would have thrived, thanks to their protection against some of their enemies.

As I contemplate this possibility, my type A blood remains as puzzling to me as when I was a boy. 
But it’s a deeper state of puzzlement that brings me some pleasure. 
 I realise that the reason for my blood type may, ultimately, have nothing to do with blood at all.

This article was originally published by Mosaic, and is reproduced under a Creative Commons licence. 
For more about the issues around this story, visit Mosaic’s website here.