Posts
An unholy alliance
Excellent documentary about CIA, Afghanistan, Freedom Fighters
Thanks to Cult Of The Dead Fish blog for bringing attention to it!
Movie: The Fiddler On The Roof
I posted this because it was freely available here, so if some studio dude gets mad just ask me to take it down ill take it down.
Image: Something beautiful for spring
Click the picture to visit the photographer's online album, he has other pretty ones too (^.^)
Article: Bird Flu
The Chicken
Littles Were Wrong
The bird flu threat flew the coop.
by Michael Fumento
12/25/2006, Volume 012, Issue 15
It's that time of year again--avian flu panic season. As the weather turns colder in the northern hemisphere and the flu starts making its annual rounds, the media and their anointed health experts are chirping and squawking once again about how we could be blindsided by a pandemic that some have estimated could kill a billion persons worldwide. New books like The Coming Avian Flu Pandemic join last year's The Monster at Our Door: The Global Threat of Avian Flu.
A year ago in these pages I clucked at all this, laying out the evidence that the alarmists were wrong, that avian influenza type H5N1 would not become readily transmissible from human to human and therefore not become pandemic--meaning a global epidemic. (See "Fuss and Feathers: Pandemic Panic over the Avian Flu," November 21, 2005.) Some of the arguments I made have quietly caught on. For instance, health officials, including National Institute of Allergy and Infectious Diseases director Dr. Anthony Fauci, no longer talk about an "overdue pandemic" (because there is no pattern to when pandemics occur; they are never "due" or "overdue"). But the damage has been done. A Harvard School of Public Health survey of adults who have children revealed that 44 percent think it "likely" or "somewhat likely" there will be "cases of bird flu among humans in the U.S. during the next 12 months." Less than a fifth of respondents considered it "not at all" likely.
Not coincidentally, an avian flu bureaucracy has become entrenched. Like all bureaucracies, it will fight to survive and thrive, egging on governments to provide ever more money. The alarmingly titled 2006 Guide to Surviving Bird Flu is published by no less than the Department of Health and Human Services. Never mind that no one in this country has yet even contracted bird flu. Congress last year allocated $3.8 billion to prevent the ballyhooed catastrophe (Bush requested almost twice that amount). The latest "scary news," promulgated in the November 23 issue of the New England Journal of Medicine by über-alarmist Robert Webster of St. Jude Memorial Children's Hospital, is that human cases of H5N1 contracted from birds are continuing to increase. Indeed, confirmed cases for 2006 are running ahead of those for last year. But the difference is slight; 97 worldwide for all of last year versus 111 through the end of November 2006. This difference could be entirely explained by better surveillance. Moreover, the real concern is not sporadic bird-to-human transmission, but human-to-human transmission. Far more people die of tuberculosis in an hour than all those known to have died from H5N1.
So it's time to revisit the allegations and show that as small as the risk was a year ago, it's nevertheless dropped considerably since.
Mutation and Reassortment
A flu pandemic can come about in two ways. One way is for the virus to randomly mutate to become easily transmissible between humans. "Randomly" is the key word here. There are no evolutionary pressures to make H5N1 adapt better to humans. Given enough time, H5N1 might mutate so that it could under the right conditions become pandemic. But that could take millions of years, during which time it would be more likely to mutate itself out of existence. H5N1 was first identified in Scottish chickens in 1959. It has been flying around the globe for close to half a century and hasn't done a number on us yet. There's absolutely no reason to think it will pick this year or next to do so.
Another scenario is that somebody with human flu could contract avian flu at the same time and the two flus could "reassort" into hybrid avian-human flu. The last two flu epidemics in the 20th century--1957-58 and 1968-69--were caused by such hybrids. We can help reduce this possibility by vaccinating as many people as possible (especially Southeast Asian poultry farmers) against human flu, thus reducing the potential number of "mixing vessels." Programs underway to keep farmers away from poultry droppings and spittle (birds don't sneeze or cough) will also help.
Ferreting Out the Truth
A fascinating study in the August 8, 2006, issue of Proceedings of the National Academy of Sciences would seem to indicate we're already pretty safe from a human-avian hybrid. Researchers from the U.S. Centers for Disease Control and Prevention conducted three separate studies with ferrets, which are among the few animals known to suffer from and transmit human flu. The ferrets were infected with several H5N1 strains in addition to a common human influenza virus (H3N2) that circulates almost every year. The infected animals were then either placed in the same cage with uninfected ferrets to test transmissibility by close contact or in adjacent cages with perforated walls to test spread of the virus from respiratory droplets.
The research showed that the H3N2 virus passed easily by droplets (ferrets do sneeze and do not use handkerchiefs) but the H5N1 virus did not spread--the same thing we're seeing in humans infected with H5N1 from birds.
Separately, the scientists used gene splicing to create a hybrid H5N1/H3N2 virus. In other words, rather than letting nature take its course and seeing if the viruses would reassort, they guaranteed that reassortment occurred. They found these hybrids also did not pass easily between the animals. Moreover, ferrets injected with the reassorted virus showed symptoms less severe than those with the pure avian flu. Reassortment appears to have weakened the virus.
In a final study, CDC researchers passed a hybrid virus through a series of ferrets to see if it would accumulate genetic changes necessary to transmit more easily. This tested the mutation factor. The scientists found this introduced only one genetic change in the virus but didn't enhance its transmissibility.
Other researchers have found the explanation for a phenomenon that was already clear but unexplained--that H5N1 virtually never spreads from human to human and, if it does, it's only after prolonged contact. This contrasts with human flu, which can be contracted via a single cough or sneeze. A Nature magazine study published last March found that while avian flu can infect human lungs, it cannot infect most of the cells lining the nose, throat, and sinuses. Moreover, it tends not to penetrate deeply into the lungs. "It has been an enigma why people get sick and die from H5N1 avian flu virus, but the virus does not spread well in humans," study leader and University of Wisconsin virologist Yoshihiro Kawaoka told WebMD. "Our finding explains it."
That Allegedly Horrendous Death Rate
Ersatz experts like Laurie Garrett, a renowned pandemic panic-monger, warn of a horrific mortality rate from the bird flu virus. "Right now in human beings, it kills 55 percent of the people it infects," she told ABC News's Primetime last year. St. Jude's alarmist Webster referred to a similar death rate in his New England Journal of Medicine article, and the media routinely parrot it. By comparison, the devastating 1918-1919 Spanish flu is believed to have killed 2.5 percent to 5 percent of those it infected. The death rate in a typical flu season is less than 1 percent. It's true that, of bird flu cases recorded by the World Health Organization, 59 percent have died. But this is a mere artifact with an obvious explanation: Only people with the most severe cases go to the hospital and become part of the dataset.
As to what the true mortality rate is, over a three-month period in 2004, Swedish and Vietnamese researchers studied 45,478 residents in a rural district in Vietnam that had H5N1 outbreaks to find out how many had contact with sick birds and how many had flu-like illnesses. They published their results in January 2006 in the Archives of Internal Medicine. They found that of 8,149 who had a flu-like illness, 650 to 750 probably caught it from birds. Yet for all of 2004, the World Health Organization data indicated only 29 Vietnamese cases with 20 deaths. Thus what might seem to be a horrific mortality rate of almost two in three, or 69 percent, appears to be actually around one in 140 or 0.71 percent. This, in the rural portion of a Communist country with a state-run medical system. That 0.71 percent is in the same range as seasonal human flu.
More good news from Vietnam, incidentally, is that it has reported zero cases in 2006. Why? As I wrote last year, "Vietnam appears to be making a heroic effort to inoculate all of its poultry." If you can keep poultry from getting flu, you've knocked down the chance of a human pandemic from close to zero to absolute zero.
Antivirals: Preventing Infection, Preventing Spread
Another risk-reducing development over the past year is the increased availability and evident reliability of Roche's Tamiflu and GlaxoSmithKline's drug Relenza. These drugs interfere with neuraminidase (the 'N' in H5N1), a protein on the surface of the virus that must multiply in order for the virus to multiply. Research at St. Jude's has shown that H5N1 appears to express the highest level of neuraminidase of any flu since 1957, and studies continue to appear showing both drugs can kill two birds with one stone. That is, they are effective both in preventing a person from getting the flu and, if they do get it, from transmitting it.
A review of four of these studies appeared online in the American Journal of Epidemiology in November. It showed that preventive administration of Relenza, which is given with an inhaler, reduced the chance of becoming infected by 75 percent, reduced the chance of transmission by 19 percent, and reduced the severity of illness by 52 percent. For Tamiflu, taken as tablets or liquid, preventive administration reduced the chance of becoming infected by 81 percent, reduced the chance of transmission by 80 percent, and reduced the severity of illness by 56 percent. Mind you, these were tests against human seasonal flu strains. But because H5N1 expresses such high levels of neuraminidase, there's an excellent chance it would be even more vulnerable to these two antivirals than is human flu. Last year three cases of Tamiflu-resistant H5N1 set off warning bells, but there have been no such cases reported this year.
Naturally all this is great news if you have the drug and take it in time. But the drugs can also be used to prevent a pandemic outbreak. Even a year ago, the World Health Organization had a program in place to quickly detect any outbreak of human avian flu, offering hope of smothering it with antivirals. Writing in Nature, researchers predicted that such an outbreak in the area most likely to have one, Southeast Asia, could be snuffed with "a stockpile of 3 million courses" depending on "how quickly cases are diagnosed and the speed with which antiviral drugs can be distributed." The World Health Organization had such a stockpile by early 2006, and assuredly it's much larger now.
A year ago, people and governments were flocking to get Tamiflu in the same way they've recently stampeded to get the new Sony PlayStation. But according to maker Roche, production will have been expanded to a rate of 400 million treatment courses annually by the end of this year, a more than ten-fold increase since 2004. Currently there are only 10,000 treatments of Relenza available in pharmacy channels, says a company spokesman, "However, next year we will have approximately 20 million treatments available. The deliveries will begin in January 2007 and the majority of the initial shipments will be for the U.S. government pandemic stockpiling efforts."
Vaccines: Birds in the Bush and in the Hand
Although much of the $3.8 billion Congress allocated to fight pandemic H5N1 will be a complete waste, legislators wisely dedicated a billion of that to developing an entirely new way of making flu shots. (Although vaccine makers might have done the same with their own funds at the same pace.) This entails growing the vaccine in mammalian cell cultures rather than eggs. Six companies are now working on such vaccines using federal funds. Cell cultures can cut the usual nine-month period for making vaccine batches in chicken eggs to a mere 90 days. Although the current rabies vaccine has been grown from a cell culture since 1980 and two drug companies have cell-cultured H5N1 vaccines in clinical trials, such vaccines have not yet received FDA or E.U. approval.
In fact, no human H5N1 vaccine has yet received official approval, but companies are pumping them out anyway in the confidence that their drugs will be found both safe and effective. Switzerland has ordered enough vaccine from GlaxoSmithKline for one inoculation of each of its eight million citizens if a pandemic erupts. The U.S. government has ordered 2.7 million doses from three makers, which would be enough to vaccinate first responders so they could take care of those who did become ill. Eventually the country plans to stockpile 20 million doses and then presumably will increase that as well, but since the vaccines aren't yet available, even that amount is still academic.
It's common to hear that stockpiling vaccines is futile since it's impossible to say what the effectiveness of a vaccine based on the virus presently in humans exposed to birds will be when it's altered to a point where it's going from human to human. But there was already evidence last year that such a mutation shouldn't be a problem. Scientists tested blood from people who had received an experimental vaccine against a 1997 strain of H5N1 and found it provoked a powerful cross-reaction from a strain that killed several Vietnamese in 2004.
Newer research by Dr. John Treanor and colleagues at the University of Rochester, presented on October 13 at a meeting of the Infectious Diseases Society of America supports these findings. Treanor's team studied people who'd been vaccinated against the Hong Kong strain of the H5N1 virus in 1998. Each was vaccinated again this year with a booster shot to fight the strain found in Vietnam. A second test group received only shots for the Vietnam strain in 2005. Those who received shots back in 1998 developed better protection than those with just the 2005 vaccination. Thus for all the talk about how rapidly H5N1 mutates, injections from 1998 were still protective. On the other hand, a seasonal human flu injection from 1998 would be worthless.
This is both evidence that H5N1 is not mutating like gangbusters and that we can quite possibly amass enough vaccine to protect every reachable person on the planet without having to build a new stockpile each year. Hysteria over an avian flu pandemic has been very good for the Chicken Little media, authors, ambitious health officials, drug companies, and even Bush bashers. (An alarmist fantasy published by Nature magazine in May 2005 concluded by predicting a pandemic outbreak in December of last year, laying the blame entirely at the president's feet.) But even as many of the panic-mongers have begun to lie low, the vestiges of hysteria remain--as do the misallocations of billions of dollars from more serious health problems. Too bad no one ever holds the doomsayers accountable for the damage they've done.
Michael Fumento is a writer based in Washington, D.C.
Source: The Weekly Standard
Littles Were Wrong
The bird flu threat flew the coop.
by Michael Fumento
12/25/2006, Volume 012, Issue 15
It's that time of year again--avian flu panic season. As the weather turns colder in the northern hemisphere and the flu starts making its annual rounds, the media and their anointed health experts are chirping and squawking once again about how we could be blindsided by a pandemic that some have estimated could kill a billion persons worldwide. New books like The Coming Avian Flu Pandemic join last year's The Monster at Our Door: The Global Threat of Avian Flu.
A year ago in these pages I clucked at all this, laying out the evidence that the alarmists were wrong, that avian influenza type H5N1 would not become readily transmissible from human to human and therefore not become pandemic--meaning a global epidemic. (See "Fuss and Feathers: Pandemic Panic over the Avian Flu," November 21, 2005.) Some of the arguments I made have quietly caught on. For instance, health officials, including National Institute of Allergy and Infectious Diseases director Dr. Anthony Fauci, no longer talk about an "overdue pandemic" (because there is no pattern to when pandemics occur; they are never "due" or "overdue"). But the damage has been done. A Harvard School of Public Health survey of adults who have children revealed that 44 percent think it "likely" or "somewhat likely" there will be "cases of bird flu among humans in the U.S. during the next 12 months." Less than a fifth of respondents considered it "not at all" likely.
Not coincidentally, an avian flu bureaucracy has become entrenched. Like all bureaucracies, it will fight to survive and thrive, egging on governments to provide ever more money. The alarmingly titled 2006 Guide to Surviving Bird Flu is published by no less than the Department of Health and Human Services. Never mind that no one in this country has yet even contracted bird flu. Congress last year allocated $3.8 billion to prevent the ballyhooed catastrophe (Bush requested almost twice that amount). The latest "scary news," promulgated in the November 23 issue of the New England Journal of Medicine by über-alarmist Robert Webster of St. Jude Memorial Children's Hospital, is that human cases of H5N1 contracted from birds are continuing to increase. Indeed, confirmed cases for 2006 are running ahead of those for last year. But the difference is slight; 97 worldwide for all of last year versus 111 through the end of November 2006. This difference could be entirely explained by better surveillance. Moreover, the real concern is not sporadic bird-to-human transmission, but human-to-human transmission. Far more people die of tuberculosis in an hour than all those known to have died from H5N1.
So it's time to revisit the allegations and show that as small as the risk was a year ago, it's nevertheless dropped considerably since.
Mutation and Reassortment
A flu pandemic can come about in two ways. One way is for the virus to randomly mutate to become easily transmissible between humans. "Randomly" is the key word here. There are no evolutionary pressures to make H5N1 adapt better to humans. Given enough time, H5N1 might mutate so that it could under the right conditions become pandemic. But that could take millions of years, during which time it would be more likely to mutate itself out of existence. H5N1 was first identified in Scottish chickens in 1959. It has been flying around the globe for close to half a century and hasn't done a number on us yet. There's absolutely no reason to think it will pick this year or next to do so.
Another scenario is that somebody with human flu could contract avian flu at the same time and the two flus could "reassort" into hybrid avian-human flu. The last two flu epidemics in the 20th century--1957-58 and 1968-69--were caused by such hybrids. We can help reduce this possibility by vaccinating as many people as possible (especially Southeast Asian poultry farmers) against human flu, thus reducing the potential number of "mixing vessels." Programs underway to keep farmers away from poultry droppings and spittle (birds don't sneeze or cough) will also help.
Ferreting Out the Truth
A fascinating study in the August 8, 2006, issue of Proceedings of the National Academy of Sciences would seem to indicate we're already pretty safe from a human-avian hybrid. Researchers from the U.S. Centers for Disease Control and Prevention conducted three separate studies with ferrets, which are among the few animals known to suffer from and transmit human flu. The ferrets were infected with several H5N1 strains in addition to a common human influenza virus (H3N2) that circulates almost every year. The infected animals were then either placed in the same cage with uninfected ferrets to test transmissibility by close contact or in adjacent cages with perforated walls to test spread of the virus from respiratory droplets.
The research showed that the H3N2 virus passed easily by droplets (ferrets do sneeze and do not use handkerchiefs) but the H5N1 virus did not spread--the same thing we're seeing in humans infected with H5N1 from birds.
Separately, the scientists used gene splicing to create a hybrid H5N1/H3N2 virus. In other words, rather than letting nature take its course and seeing if the viruses would reassort, they guaranteed that reassortment occurred. They found these hybrids also did not pass easily between the animals. Moreover, ferrets injected with the reassorted virus showed symptoms less severe than those with the pure avian flu. Reassortment appears to have weakened the virus.
In a final study, CDC researchers passed a hybrid virus through a series of ferrets to see if it would accumulate genetic changes necessary to transmit more easily. This tested the mutation factor. The scientists found this introduced only one genetic change in the virus but didn't enhance its transmissibility.
Other researchers have found the explanation for a phenomenon that was already clear but unexplained--that H5N1 virtually never spreads from human to human and, if it does, it's only after prolonged contact. This contrasts with human flu, which can be contracted via a single cough or sneeze. A Nature magazine study published last March found that while avian flu can infect human lungs, it cannot infect most of the cells lining the nose, throat, and sinuses. Moreover, it tends not to penetrate deeply into the lungs. "It has been an enigma why people get sick and die from H5N1 avian flu virus, but the virus does not spread well in humans," study leader and University of Wisconsin virologist Yoshihiro Kawaoka told WebMD. "Our finding explains it."
That Allegedly Horrendous Death Rate
Ersatz experts like Laurie Garrett, a renowned pandemic panic-monger, warn of a horrific mortality rate from the bird flu virus. "Right now in human beings, it kills 55 percent of the people it infects," she told ABC News's Primetime last year. St. Jude's alarmist Webster referred to a similar death rate in his New England Journal of Medicine article, and the media routinely parrot it. By comparison, the devastating 1918-1919 Spanish flu is believed to have killed 2.5 percent to 5 percent of those it infected. The death rate in a typical flu season is less than 1 percent. It's true that, of bird flu cases recorded by the World Health Organization, 59 percent have died. But this is a mere artifact with an obvious explanation: Only people with the most severe cases go to the hospital and become part of the dataset.
As to what the true mortality rate is, over a three-month period in 2004, Swedish and Vietnamese researchers studied 45,478 residents in a rural district in Vietnam that had H5N1 outbreaks to find out how many had contact with sick birds and how many had flu-like illnesses. They published their results in January 2006 in the Archives of Internal Medicine. They found that of 8,149 who had a flu-like illness, 650 to 750 probably caught it from birds. Yet for all of 2004, the World Health Organization data indicated only 29 Vietnamese cases with 20 deaths. Thus what might seem to be a horrific mortality rate of almost two in three, or 69 percent, appears to be actually around one in 140 or 0.71 percent. This, in the rural portion of a Communist country with a state-run medical system. That 0.71 percent is in the same range as seasonal human flu.
More good news from Vietnam, incidentally, is that it has reported zero cases in 2006. Why? As I wrote last year, "Vietnam appears to be making a heroic effort to inoculate all of its poultry." If you can keep poultry from getting flu, you've knocked down the chance of a human pandemic from close to zero to absolute zero.
Antivirals: Preventing Infection, Preventing Spread
Another risk-reducing development over the past year is the increased availability and evident reliability of Roche's Tamiflu and GlaxoSmithKline's drug Relenza. These drugs interfere with neuraminidase (the 'N' in H5N1), a protein on the surface of the virus that must multiply in order for the virus to multiply. Research at St. Jude's has shown that H5N1 appears to express the highest level of neuraminidase of any flu since 1957, and studies continue to appear showing both drugs can kill two birds with one stone. That is, they are effective both in preventing a person from getting the flu and, if they do get it, from transmitting it.
A review of four of these studies appeared online in the American Journal of Epidemiology in November. It showed that preventive administration of Relenza, which is given with an inhaler, reduced the chance of becoming infected by 75 percent, reduced the chance of transmission by 19 percent, and reduced the severity of illness by 52 percent. For Tamiflu, taken as tablets or liquid, preventive administration reduced the chance of becoming infected by 81 percent, reduced the chance of transmission by 80 percent, and reduced the severity of illness by 56 percent. Mind you, these were tests against human seasonal flu strains. But because H5N1 expresses such high levels of neuraminidase, there's an excellent chance it would be even more vulnerable to these two antivirals than is human flu. Last year three cases of Tamiflu-resistant H5N1 set off warning bells, but there have been no such cases reported this year.
Naturally all this is great news if you have the drug and take it in time. But the drugs can also be used to prevent a pandemic outbreak. Even a year ago, the World Health Organization had a program in place to quickly detect any outbreak of human avian flu, offering hope of smothering it with antivirals. Writing in Nature, researchers predicted that such an outbreak in the area most likely to have one, Southeast Asia, could be snuffed with "a stockpile of 3 million courses" depending on "how quickly cases are diagnosed and the speed with which antiviral drugs can be distributed." The World Health Organization had such a stockpile by early 2006, and assuredly it's much larger now.
A year ago, people and governments were flocking to get Tamiflu in the same way they've recently stampeded to get the new Sony PlayStation. But according to maker Roche, production will have been expanded to a rate of 400 million treatment courses annually by the end of this year, a more than ten-fold increase since 2004. Currently there are only 10,000 treatments of Relenza available in pharmacy channels, says a company spokesman, "However, next year we will have approximately 20 million treatments available. The deliveries will begin in January 2007 and the majority of the initial shipments will be for the U.S. government pandemic stockpiling efforts."
Vaccines: Birds in the Bush and in the Hand
Although much of the $3.8 billion Congress allocated to fight pandemic H5N1 will be a complete waste, legislators wisely dedicated a billion of that to developing an entirely new way of making flu shots. (Although vaccine makers might have done the same with their own funds at the same pace.) This entails growing the vaccine in mammalian cell cultures rather than eggs. Six companies are now working on such vaccines using federal funds. Cell cultures can cut the usual nine-month period for making vaccine batches in chicken eggs to a mere 90 days. Although the current rabies vaccine has been grown from a cell culture since 1980 and two drug companies have cell-cultured H5N1 vaccines in clinical trials, such vaccines have not yet received FDA or E.U. approval.
In fact, no human H5N1 vaccine has yet received official approval, but companies are pumping them out anyway in the confidence that their drugs will be found both safe and effective. Switzerland has ordered enough vaccine from GlaxoSmithKline for one inoculation of each of its eight million citizens if a pandemic erupts. The U.S. government has ordered 2.7 million doses from three makers, which would be enough to vaccinate first responders so they could take care of those who did become ill. Eventually the country plans to stockpile 20 million doses and then presumably will increase that as well, but since the vaccines aren't yet available, even that amount is still academic.
It's common to hear that stockpiling vaccines is futile since it's impossible to say what the effectiveness of a vaccine based on the virus presently in humans exposed to birds will be when it's altered to a point where it's going from human to human. But there was already evidence last year that such a mutation shouldn't be a problem. Scientists tested blood from people who had received an experimental vaccine against a 1997 strain of H5N1 and found it provoked a powerful cross-reaction from a strain that killed several Vietnamese in 2004.
Newer research by Dr. John Treanor and colleagues at the University of Rochester, presented on October 13 at a meeting of the Infectious Diseases Society of America supports these findings. Treanor's team studied people who'd been vaccinated against the Hong Kong strain of the H5N1 virus in 1998. Each was vaccinated again this year with a booster shot to fight the strain found in Vietnam. A second test group received only shots for the Vietnam strain in 2005. Those who received shots back in 1998 developed better protection than those with just the 2005 vaccination. Thus for all the talk about how rapidly H5N1 mutates, injections from 1998 were still protective. On the other hand, a seasonal human flu injection from 1998 would be worthless.
This is both evidence that H5N1 is not mutating like gangbusters and that we can quite possibly amass enough vaccine to protect every reachable person on the planet without having to build a new stockpile each year. Hysteria over an avian flu pandemic has been very good for the Chicken Little media, authors, ambitious health officials, drug companies, and even Bush bashers. (An alarmist fantasy published by Nature magazine in May 2005 concluded by predicting a pandemic outbreak in December of last year, laying the blame entirely at the president's feet.) But even as many of the panic-mongers have begun to lie low, the vestiges of hysteria remain--as do the misallocations of billions of dollars from more serious health problems. Too bad no one ever holds the doomsayers accountable for the damage they've done.
Michael Fumento is a writer based in Washington, D.C.
Source: The Weekly Standard
Just Listen: Pavarotti - Recondita armonia - Tosca, Puccini
Italian
Dammi i colori...
Recondita armonia di bellezze diverse!
È bruna Floria, l'ardente amante mia.
E te, beltade ignota, cinta di chiome bionde,
Tu azzurro hai l'occhio,
Tosca ha l'occhio nero!
L'arte nel suo mistero,
le diverse bellezze insiem confonde...
Ma nel ritrar costei,
Il mio solo pensiero,
Il mio sol pensier sei tu,
Tosca, sei tu!
Pass me the colors...
Concealed harmony of contrasting beauties!
Floria, my ardent lover, is dark haired.
And you, unknown beauty, crowned with blond hair,
You have blue eyes,
Tosca has black eyes!
Art, in its mysterious way,
blends the contrasting beauties together...
But while I'm painting her,
My only thought,
My only thought is of you,
Tosca, it is of you!
Film/Documentary: The Strecker Memorandum
The sound track is a few seconds slow later on in the film but it is still the best full length quality version I can find at this time.
Image/Document: Sir Frank Macfarlane Burnet
Sir Frank Macfarlane Burnet Order of The British Empire, Order of Austrailia, Order Of Merit, Nobel Prize winner, Royal Society Award Winner
Discusses spreading diseases by air in a declassified document.
[So this is what you have to be involved in to get knighted eh?]
Marked Secret,to be passed by hand
http://naa12.naa.gov.au/scripts/imagine.asp?B=3039064&I=1&SE=1
Discusses spreading diseases by air in a declassified document.
[So this is what you have to be involved in to get knighted eh?]
Marked Secret,to be passed by hand
http://naa12.naa.gov.au/scripts/imagine.asp?B=3039064&I=1&SE=1
Documentary: The Living Dead
Adam Curtis- The Living Dead 1/3: On the Desperate Edge of Now
Adam Curtis- The Living Dead 2/3: You Have Used Me as a Fish Long Enough
Adam Curtis- The Living Dead 3/3: The Attic
Adam Curtis- The Living Dead 2/3: You Have Used Me as a Fish Long Enough
Adam Curtis- The Living Dead 3/3: The Attic
Documentary: Pandora's Box
Pandora's Box Part 1 of 6
The Engineer's Plot
Pandora's Box Part 2 of 6
To The Brink of Eternity
Pandora's Box Part 3 of 6
Pandora's Box Part 4 of 6
Goodbye Ms.Ant
Pandora's Box Part 5 of 6
Black Power
Pandora's Box Part 6 of 6
A is for Atom
The Engineer's Plot
Pandora's Box Part 2 of 6
To The Brink of Eternity
Pandora's Box Part 3 of 6
Pandora's Box Part 4 of 6
Goodbye Ms.Ant
Pandora's Box Part 5 of 6
Black Power
Pandora's Box Part 6 of 6
A is for Atom
Documentary: The power of nightmares
The Power Of Nightmares Part 1 of 3
Baby Its Cold Outside
The Power Of Nightmares Part 2 of 3
The Phantom Victory
The Power Of Nightmares Part 3 of 3
The Shadows In The Cave
This is a three part documentary done by Adam Curtis which was aired on the BBC
Baby Its Cold Outside
The Power Of Nightmares Part 2 of 3
The Phantom Victory
The Power Of Nightmares Part 3 of 3
The Shadows In The Cave
This is a three part documentary done by Adam Curtis which was aired on the BBC
Just Watch: Pinky & The Brain [intro]
What are we going to do tonight brain?
The Same thing we do everynight pinky, try to take over the world!
One Million Views and counting, looks like the brain may be accomplishing his goal after all.........
Short Report: Genetic markers used by historians to account for Kazarian issue
European Journal of Human Genetics (2005) 13, 388–391. doi:10.1038/sj.ejhg.5201319 Published online 3 November 2004
Y chromosome evidence for a founder effect in Ashkenazi Jews
Almut Nebel1,2,4, Dvora Filon2, Marina Faerman3, Himla Soodyall1 and Ariella Oppenheim2
1. 1MRC/NHLS/Wits Human Genomic Diversity and Disease Research Unit, Division of Human Genetics, School of Pathology, National Health Laboratory Service and University of the Witwatersrand, Johannesburg, South Africa
2. 2Department of Hematology, Hebrew University – Hadassah Medical School and Hadassah University Hospital, Jerusalem, Israel
3. 3Laboratory of Biological Anthropology and Ancient DNA, Hebrew University – Hadassah School of Dental Medicine, Jerusalem, Israel
Correspondence: Dr M Faerman, Department of Biological Anthropology and Ancient DNA, Faculty of Dental Medicine, Hebrew University, POB 12272, Jerusalem 91120, Israel. Tel: +972 2 6757608; Fax: +972 2 6757451; E-mail: marinaf@pob.huji.ac.il
4Current address: Institute for Clinical Molecular Biology – Christian-Albrechts-University Kiel, Germany
Received 8 January 2004; Revised 24 August 2004; Accepted 17 September 2004; Published online 3 November 2004.
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Abstract
Recent genetic studies, based on Y chromosome polymorphic markers, showed that Ashkenazi Jews are more closely related to other Jewish and Middle Eastern groups than to their host populations in Europe. However, Ashkenazim have an elevated frequency of R-M17, the dominant Y chromosome haplogroup in Eastern Europeans, suggesting possible gene flow. In the present study of 495 Y chromosomes of Ashkenazim, 57 (11.5%) were found to belong to R-M17. Detailed analyses of haplotype structure, diversity and geographic distribution suggest a founder effect for this haplogroup, introduced at an early stage into the evolving Ashkenazi community in Europe. R-M17 chromosomes in Ashkenazim may represent vestiges of the mysterious Khazars.
Keywords:
Y chromosome haplotypes, Ashkenazi Jews, founder effect
Top of page
Introduction
Ashkenazi Jews, who have resided in various European countries during the Diaspora, traditionally trace their origin to the Jewish people that lived in the Holy Land before the Roman exile. However, some studies claimed that a substantial part of Ashkenazim were descendants of Eastern European non-Jews. In particular, according to Middle Age historians, the Khazars from a small kingdom near the Caspian Sea converted en masse to Judaism1 and therefore might have contributed to the composition of the emerging Ashkenazi community. Yet, recent genetic studies, based on Y chromosome polymorphic markers, clearly showed that Ashkenazim are more closely related to other Jewish and Middle Eastern groups than to their host populations in Europe.2, 3, 4 Those findings argue against large-scale male-mediated gene flow into the Ashkenazi community during the Diaspora. The male admixture proportion of Europeans in Ashkenazi Jews was estimated to be 0.5% per generation,3 indicating that Ashkenazim remained, to a large extent, genetically isolated throughout their history.
Ashkenazim were found to have a significantly higher frequency of the R-M17 haplogroup compared with Sephardic and Kurdish Jews.4, 5 Interestingly, Behar et al6 reported R-M17 to be the dominant haplogroup in Ashkenazi Levites (approx52%), although rare in Ashkenazi Cohanim (1.3%) and Israelites (4%). R-M17, the most common haplogroup in Eastern Europe, was suggested to have originated and started to expand in the Ukraine, probably in a Paleolithic population after the Last Glacial Maximum about 13 000 years ago.5, 7
Our present study demonstrates that R-M17 is a distinctive feature of the Ashkenazim in general and not only of Levites, as reported previously.6 Furthermore, we provide evidence for a founder effect of this haplogroup in Ashkenazim, dated to the first millennium CE.
Top of page
Subjects and methods
A total of 495 DNA samples, from different sources (Table 1), were collected from paternally unrelated male Ashkenazi Jews, irrespective of their religious status (Cohen, Levite, Israelite).
Table 1 - Frequencies of haplogroup R-M17 in Ashkenazi Jews sampled from various DNA collections.
Table 1 - Frequencies of haplogroup R-M17 in Ashkenazi Jews sampled from various DNA collections - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact help@nature.com or the authorFull table
The typing of the Y chromosome biallelic marker M17 and the six microsatelllite loci (DYS19, DYS388, DYS390, DYS391, DYS392 and DYS393) was conducted following Thomas et al.8 Statistical analyses were performed as previously described.4 The study was approved by the ethics review committees of the respective institutions.
Top of page
Results and discussion
In total, 495 DNA samples from different collections (Table 1) were screened for the Y chromosome polymorphism M17. The average frequency of the haplogroup R-M17 in Ashkenazi Jews (11.5%, 57 individuals) is significantly higher (P<0.05) than that in Sephardic Jews (3.9%), Kurdish Jews (4%) and Palestinian Arabs (1.4%). To date, comparable frequencies of R-M17 in other Middle Eastern populations have been reported in Moslem Kurds, Syrians and Lebanese (Table 2). However, the haplotype distribution within R-M17, available only for Moslem Kurds, is very different from that of Ashkenazim.4 These data suggest that the increase in R-M17 in Ashkenazim occurred after they had gone into the Diaspora.
Table 2 - Haplogroup R-M17 frequencies in Middle Eastern and European populations.
Table 2 - Haplogroup R-M17 frequencies in Middle Eastern and European populations - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact help@nature.com or the authorFull table
Variation within R-M17 was examined by analysing 56 of the 57 chromosomes for six microsatellite loci. Apart from one singleton (haplotype H9), the other 13 haplotypes form a compact network (Figure 1). The star-like pattern and the low level of diversity are indicative of a founder effect. The most common R-M17 haplotype in the total Ashkenazi sample (approx45%), haplotype 6 (H6), is most likely the ancestral haplotype of this haplogroup among Ashkenazim. The time to the most recent common ancestor of R-M17 in Ashkenazim9 was estimated to 62.7 generations ago (excluding H9), using the previously published mutation rate for the six microsatellite loci studied here (mu=1.8 times 10-3 with 95% CI 9.8 times 10-4–3.1 times 10-3).10 Assuming a generation time of 25 years, this amounts to 1567 years ago (95% CI 2877–910 years ago).
Figure 1.
Figure 1 - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact help@nature.com or the author
MJ network of haplogroup R-M17 in Ashkenazim. The network shows the relationships of the 14 haplotypes (56 individuals) found in Ashkenazi Jews. Haplotypes were constructed on the basis of six microsatellite loci (DYS19, DYS388, DYS390, DYS391, DYS392 and DYS393). The MJ (alt epsilon=0) was calculated on the data preprocessed by the RM algorithm (r=2). Circle size is proportional to haplotype frequency. Haplotype numbers refer to the supplementary information. At the centre of the network is H6 (16-12-25-10-11-13), the likely founding haplotype of this haplogroup in Ashkenazim. Those haplotypes marked with an asterisk were also observed in other Jewish groups and Moslem Palestinians4 (H6 and H7 – one Sephardic Jew each; H4 – one Moslem Palestinian; H1 – two Kurdish Jews and one Sephardic Jew).
Full figure and legend (13K)
If R-M17 had been present in substantial frequency in the pre-Diaspora Y chromosome pool, one would expect to observe the ancestral haplotype H6 in other Jewish groups and in Palestinians who share a large portion of their Y chromosomes with Jews.3, 4, 11 However, in a combined non-Ashkenazi sample of 320 individuals (Sephardic, Kurdish Jews and Palestinians),4 H6 was found only in a single Sephardic Jew (0.3%; Figure 1). This finding strongly suggests gene flow from an external population into the Ashkenazi gene pool.
Where did the R-M17 chromosomes in Ashkenazim come from? The haplogroup R-M17 has a wide geographic distribution in Europe, West Asia and the Middle East, with the highest frequencies in Eastern European populations (Table 2). Haplotype H6 is also present at considerable frequencies in various Eastern European populations,5, 12, 13 but is absent or found only at very low frequencies in Central and West Asians and in Middle Easterners.14, 15 Thus, R-M17 in Ashkenazi Jews could represent gene flow from Eastern European populations. This scenario is supported by the lower haplotype diversity measures (h) in Ashkenazim (0.735plusminus0.05) compared to those of Eastern European populations5 (ranging from 0.894plusminus0.022 to 0.919plusminus0.026), and by the fact that in a combined Ashkenazi–European network, Jews present only a subset of the haplotypes (not shown).
The widespread distribution of R-M17 in Europe might suggest multiple gene flow events from the European host populations into Ashkenazim. However, we observed that the frequencies of R-M17 in Jews from various countries (Germany, Lithuania, Czechoslovakia, Hungary, Romania, Poland, Russia and the Ukraine) ranged from 12–13% in Russia and Ukraine to 22% in Germany and Lithuania, and did not differ from one another (P>0.05). Likewise, the haplotypes of Jews from these countries showed very similar distribution patterns in a network (not shown). Furthermore, the frequencies of R-M17 in different Ashkenazi communities did not correspond to the east–west cline seen in Europeans. Altogether, these results support the hypothesis of a single male founder who introduced R-M17 into the Ashkenazi gene pool at the beginning of the Jewish Diaspora in Europe. Since then this haplogroup has expanded and spread among the Jewish communities across Europe.
Noteworthy, Behar et al,6 in their sample of Ashkenazi Levites, found R-M17 at a frequency of 52% and its modal haplotype (identical to H6 in the present study) at 74% within this haplogroup. They suggested a founder event specific to this particular group as a result of intrusion of one or a few European Y chromosomes into the forming Ashkenazi community. The present study does not necessarily contradict that of Behar et al,6 but rather indicates that R-M17 is characteristic of the general Ashkenazi population and not restricted to the Levites. The proportion of Levites in different Jewish populations has been estimated to range from 0.2516 to 3.4%.17 Thus, their contribution to the overall frequency of R-M17 in Ashkenazim could not exceed 2%, while the frequency observed in the present study is 11.5%. Similar frequency (9.7%) was also reported by Passarino et al.5 Furthermore, the haplotype diversity in the Ashkenazi Levites (0.451)6 is lower than in the sample of Ashkenazi Jews described here, suggesting that R-M17 drifted to high frequency in the Levites more recently than in the general Ashkenazi population.
It is historically well documented that the Khazar King Bulan and his court converted to Judaism at the end of the 8th century CE.1 The Khazars were originally a Turkic tribe from Central Asia who settled in the northern Caucasus and later spread to southern Russia and eastern Ukraine. Some authors argue that after the fall of their kingdom in the second half of the 10th century CE, the Khazar converts were absorbed by the emerging Ashkenazi Jewish community in Eastern Europe.18, 19 Since R-M17 haplogroup is also found at moderate to high frequencies in Central Asia20 and southern Russia/Ukraine,5 this haplogroup could have been present in the Khazars. However, if the R-M17 chromosomes in Ashkenazi Jews do indeed represent the vestiges of the mysterious Khazars then, according to our data, this contribution was limited to either a single founder or a few closely related men, and does not exceed approx12% of the present-day Ashkenazim.
Top of page
References
References
1. Dunlop D. The history of the Jewish Khazars Princeton: Princeton University Press 1954;.
2. Santachiara-Benerecetti SA, Semino O & Passarino G et al. The common Near Eastern origin of Ashkenazi and Sephardi Jews supported by Y-chromosome similarity. Ann Hum Genet 1993; 57: 55−64. | PubMed |
3. Hammer MF, Redd AJ & Wood ET et al. Jewish and Middle Eastern non-Jewish populations share a common pool of Y-chromosome biallelic haplotypes. Proc Natl Acad Sci USA 2000; 97: 6769−6774. | Article | PubMed | ChemPort |
4. Nebel A, Filon D, Brinkmann B, Majumder PP, Faerman M & Oppenheim A. The Y chromosome pool of Jews as part of the genetic landscape of the Middle East. Am J Hum Genet 2001; 69: 1095−1112. | Article | PubMed | ChemPort |
5. Passarino G, Semino O & Magri C et al. The 49a,f haplotype 11 is a new marker of the Eu19 lineage that traces migrations from the northern regions of the Black Sea. Hum Immunol 2001; 62: 922−932. | Article | PubMed | ChemPort |
6. Behar DM, Thomas MG & Skorecki K et al. Multiple origins of Ashkenazi levites: Y chromosome evidence for both Near Eastern and European ancestries. Am J Hum Genet 2003; 73: 768−779. | Article | PubMed | ChemPort |
7. Semino O, Passarino G & Oefner PJ et al. The genetic legacy of Paleolithic Homo sapiens sapiens in extant Europeans: a Y chromosome perspective. Science 2000; 290: 1155−1159. | Article | PubMed | ISI | ChemPort |
8. Thomas MG, Bradman N & Flinn H. High throughput analysis of 10 microsatellite and 11 diallelic polymorphisms on the human Y chromosome. Hum Genet 1999; 105: 577−581. | Article | PubMed | ChemPort |
9. Kittles RA, Perola M & Peltonen L et al. Dual origins of Finns revealed by Y chromosome haplotype variation. Am J Hum Genet 1998; 62: 1171−1179. | Article | PubMed | ISI | ChemPort |
10. Quintana-Murci L, Krausz C & Zerjal T et al. Y chromosome lineages trace diffusion of people and languages in southwestern Asia. Am J Hum Genet 2001; 68: 537−542. | Article | PubMed | ChemPort |
11. Nebel A, Filon D & Weiss D et al. High-resolution Y chromosome haplotypes of Israeli and Palestinian Arabs reveal geographic substructure and substantial overlap with haploytpes of Jews. Hum Genet 2000; 107: 630−641. | Article | PubMed | ChemPort |
12. Zerjal T, Pandya A & Santos FR et al. The use of Y-chromosomal DNA variation to investigate population history: recent male spread in Asia and Europe. In Papiha SS, Deka R, Chakraborty R (eds)Genomic diversity: applications in human population genetics New York: Plenum Press 1999; pp 91−101.
13. Zerjal T, Beckman L & Beckman G et al. Geographical, linguistic, and cultural influences on genetic diversity: Y-chromosomal distribution in Northern European populations. Mol Biol Evol 2001; 18: 1077−1087. | PubMed | ChemPort |
14. Zerjal T, Wells RS, Yuldasheva N, Ruzibakiev R & Tyler-Smith C. A genetic landscape reshaped by recent events: Y-chromosomal insights into central Asia. Am J Hum Genet 2002; 71: 466−482. | Article | PubMed | ISI | ChemPort |
15. Weale ME, Yepiskoposyan L & Jager RF et al. Armenian Y chromosome haplotypes reveal strong regional structure within a single ethno-national group. Hum Genet 2001; 109: 659−674. | Article | PubMed | ChemPort |
16. Kosmin BA & Waterman S. The use and misuse of distinctive Jewish names. In Schmelz UO, Della Pergola S (eds)Papers in Jewish Demography 1985 Jerusalem: The Hebrew University of Jerusalem 1989; pp 1−10.
17. Della Pergola S.Alcuni aspetti quantitativi della distribuzione del cognome fra gli ebrei in Italia. Annu Studi Ebraici 1984; vol.10 Rome, Carucci pp: 65−86.
18. Brook KA. The Jews of Khazaria Northvale, NJ: Jason Aronson 2002;.
19. Koestler A. The thirteenth tribe: the Khazar Empire and its heritage New York, NY: Random House Trade Paperbacks 1976;.
20. Underhill PA, Jin L & Lin AA et al. Detection of numerous Y chromosome biallelic polymorphisms by denaturing high-performance liquid chromatography. Genome Res 1997; 7: 996−1005. | PubMed | ISI | ChemPort |
21. Nasidze I, Sarkisian T, Kerimov A & Stoneking M. Testing hypotheses of language replacement in the Caucasus: evidence from the Y chromosome. Hum Genet 2003; 112: 255−261. | PubMed |
22. Wells RS, Yuldasheva N & Ruzibakiev R et al. The Eurasian heartland: a continental perspective on Y-chromosome diversity. Proc Natl Acad Sci USA 2001; 98: 10244−10249. | Article | PubMed | ChemPort |
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Acknowledgements
We are grateful to Drs Ben Glaser, Deborah Rund, Avraham Shaag and Ms Ester Hyam for providing DNA samples of Ashkenazim. We thank Drs Silvana Santachiara-Benerecetti and Chris Tyler-Smith for sharing haplotype information on European populations. This work was supported by a research grant form the Israeli Ministry of Science, Culture and Sport to AO and MF, and jointly by the Medical Research Council of South Africa, the National Research Foundation, the National Health Laboratory Service and the University of the Witwatersrand to HS. AN was the recipient of the Hillel Friedland Postdoctoral Research Fellowship from the University of the Witwatersrand.
Supplementary Information accompanies the paper on European Journal of Human Genetics website (http://www.nature.com/ejhg)
Source Page:
http://www.nature.com/ejhg/journal/v13/n3/full/5201319a.html
Chart Page:
http://www.nature.com/ejhg/journal/v13/n3/fig_tab/5201319t2.html#figure-title
Y chromosome evidence for a founder effect in Ashkenazi Jews
Almut Nebel1,2,4, Dvora Filon2, Marina Faerman3, Himla Soodyall1 and Ariella Oppenheim2
1. 1MRC/NHLS/Wits Human Genomic Diversity and Disease Research Unit, Division of Human Genetics, School of Pathology, National Health Laboratory Service and University of the Witwatersrand, Johannesburg, South Africa
2. 2Department of Hematology, Hebrew University – Hadassah Medical School and Hadassah University Hospital, Jerusalem, Israel
3. 3Laboratory of Biological Anthropology and Ancient DNA, Hebrew University – Hadassah School of Dental Medicine, Jerusalem, Israel
Correspondence: Dr M Faerman, Department of Biological Anthropology and Ancient DNA, Faculty of Dental Medicine, Hebrew University, POB 12272, Jerusalem 91120, Israel. Tel: +972 2 6757608; Fax: +972 2 6757451; E-mail: marinaf@pob.huji.ac.il
4Current address: Institute for Clinical Molecular Biology – Christian-Albrechts-University Kiel, Germany
Received 8 January 2004; Revised 24 August 2004; Accepted 17 September 2004; Published online 3 November 2004.
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Abstract
Recent genetic studies, based on Y chromosome polymorphic markers, showed that Ashkenazi Jews are more closely related to other Jewish and Middle Eastern groups than to their host populations in Europe. However, Ashkenazim have an elevated frequency of R-M17, the dominant Y chromosome haplogroup in Eastern Europeans, suggesting possible gene flow. In the present study of 495 Y chromosomes of Ashkenazim, 57 (11.5%) were found to belong to R-M17. Detailed analyses of haplotype structure, diversity and geographic distribution suggest a founder effect for this haplogroup, introduced at an early stage into the evolving Ashkenazi community in Europe. R-M17 chromosomes in Ashkenazim may represent vestiges of the mysterious Khazars.
Keywords:
Y chromosome haplotypes, Ashkenazi Jews, founder effect
Top of page
Introduction
Ashkenazi Jews, who have resided in various European countries during the Diaspora, traditionally trace their origin to the Jewish people that lived in the Holy Land before the Roman exile. However, some studies claimed that a substantial part of Ashkenazim were descendants of Eastern European non-Jews. In particular, according to Middle Age historians, the Khazars from a small kingdom near the Caspian Sea converted en masse to Judaism1 and therefore might have contributed to the composition of the emerging Ashkenazi community. Yet, recent genetic studies, based on Y chromosome polymorphic markers, clearly showed that Ashkenazim are more closely related to other Jewish and Middle Eastern groups than to their host populations in Europe.2, 3, 4 Those findings argue against large-scale male-mediated gene flow into the Ashkenazi community during the Diaspora. The male admixture proportion of Europeans in Ashkenazi Jews was estimated to be 0.5% per generation,3 indicating that Ashkenazim remained, to a large extent, genetically isolated throughout their history.
Ashkenazim were found to have a significantly higher frequency of the R-M17 haplogroup compared with Sephardic and Kurdish Jews.4, 5 Interestingly, Behar et al6 reported R-M17 to be the dominant haplogroup in Ashkenazi Levites (approx52%), although rare in Ashkenazi Cohanim (1.3%) and Israelites (4%). R-M17, the most common haplogroup in Eastern Europe, was suggested to have originated and started to expand in the Ukraine, probably in a Paleolithic population after the Last Glacial Maximum about 13 000 years ago.5, 7
Our present study demonstrates that R-M17 is a distinctive feature of the Ashkenazim in general and not only of Levites, as reported previously.6 Furthermore, we provide evidence for a founder effect of this haplogroup in Ashkenazim, dated to the first millennium CE.
Top of page
Subjects and methods
A total of 495 DNA samples, from different sources (Table 1), were collected from paternally unrelated male Ashkenazi Jews, irrespective of their religious status (Cohen, Levite, Israelite).
Table 1 - Frequencies of haplogroup R-M17 in Ashkenazi Jews sampled from various DNA collections.
Table 1 - Frequencies of haplogroup R-M17 in Ashkenazi Jews sampled from various DNA collections - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact help@nature.com or the authorFull table
The typing of the Y chromosome biallelic marker M17 and the six microsatelllite loci (DYS19, DYS388, DYS390, DYS391, DYS392 and DYS393) was conducted following Thomas et al.8 Statistical analyses were performed as previously described.4 The study was approved by the ethics review committees of the respective institutions.
Top of page
Results and discussion
In total, 495 DNA samples from different collections (Table 1) were screened for the Y chromosome polymorphism M17. The average frequency of the haplogroup R-M17 in Ashkenazi Jews (11.5%, 57 individuals) is significantly higher (P<0.05) than that in Sephardic Jews (3.9%), Kurdish Jews (4%) and Palestinian Arabs (1.4%). To date, comparable frequencies of R-M17 in other Middle Eastern populations have been reported in Moslem Kurds, Syrians and Lebanese (Table 2). However, the haplotype distribution within R-M17, available only for Moslem Kurds, is very different from that of Ashkenazim.4 These data suggest that the increase in R-M17 in Ashkenazim occurred after they had gone into the Diaspora.
Table 2 - Haplogroup R-M17 frequencies in Middle Eastern and European populations.
Table 2 - Haplogroup R-M17 frequencies in Middle Eastern and European populations - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact help@nature.com or the authorFull table
Variation within R-M17 was examined by analysing 56 of the 57 chromosomes for six microsatellite loci. Apart from one singleton (haplotype H9), the other 13 haplotypes form a compact network (Figure 1). The star-like pattern and the low level of diversity are indicative of a founder effect. The most common R-M17 haplotype in the total Ashkenazi sample (approx45%), haplotype 6 (H6), is most likely the ancestral haplotype of this haplogroup among Ashkenazim. The time to the most recent common ancestor of R-M17 in Ashkenazim9 was estimated to 62.7 generations ago (excluding H9), using the previously published mutation rate for the six microsatellite loci studied here (mu=1.8 times 10-3 with 95% CI 9.8 times 10-4–3.1 times 10-3).10 Assuming a generation time of 25 years, this amounts to 1567 years ago (95% CI 2877–910 years ago).
Figure 1.
Figure 1 - Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, please contact help@nature.com or the author
MJ network of haplogroup R-M17 in Ashkenazim. The network shows the relationships of the 14 haplotypes (56 individuals) found in Ashkenazi Jews. Haplotypes were constructed on the basis of six microsatellite loci (DYS19, DYS388, DYS390, DYS391, DYS392 and DYS393). The MJ (alt epsilon=0) was calculated on the data preprocessed by the RM algorithm (r=2). Circle size is proportional to haplotype frequency. Haplotype numbers refer to the supplementary information. At the centre of the network is H6 (16-12-25-10-11-13), the likely founding haplotype of this haplogroup in Ashkenazim. Those haplotypes marked with an asterisk were also observed in other Jewish groups and Moslem Palestinians4 (H6 and H7 – one Sephardic Jew each; H4 – one Moslem Palestinian; H1 – two Kurdish Jews and one Sephardic Jew).
Full figure and legend (13K)
If R-M17 had been present in substantial frequency in the pre-Diaspora Y chromosome pool, one would expect to observe the ancestral haplotype H6 in other Jewish groups and in Palestinians who share a large portion of their Y chromosomes with Jews.3, 4, 11 However, in a combined non-Ashkenazi sample of 320 individuals (Sephardic, Kurdish Jews and Palestinians),4 H6 was found only in a single Sephardic Jew (0.3%; Figure 1). This finding strongly suggests gene flow from an external population into the Ashkenazi gene pool.
Where did the R-M17 chromosomes in Ashkenazim come from? The haplogroup R-M17 has a wide geographic distribution in Europe, West Asia and the Middle East, with the highest frequencies in Eastern European populations (Table 2). Haplotype H6 is also present at considerable frequencies in various Eastern European populations,5, 12, 13 but is absent or found only at very low frequencies in Central and West Asians and in Middle Easterners.14, 15 Thus, R-M17 in Ashkenazi Jews could represent gene flow from Eastern European populations. This scenario is supported by the lower haplotype diversity measures (h) in Ashkenazim (0.735plusminus0.05) compared to those of Eastern European populations5 (ranging from 0.894plusminus0.022 to 0.919plusminus0.026), and by the fact that in a combined Ashkenazi–European network, Jews present only a subset of the haplotypes (not shown).
The widespread distribution of R-M17 in Europe might suggest multiple gene flow events from the European host populations into Ashkenazim. However, we observed that the frequencies of R-M17 in Jews from various countries (Germany, Lithuania, Czechoslovakia, Hungary, Romania, Poland, Russia and the Ukraine) ranged from 12–13% in Russia and Ukraine to 22% in Germany and Lithuania, and did not differ from one another (P>0.05). Likewise, the haplotypes of Jews from these countries showed very similar distribution patterns in a network (not shown). Furthermore, the frequencies of R-M17 in different Ashkenazi communities did not correspond to the east–west cline seen in Europeans. Altogether, these results support the hypothesis of a single male founder who introduced R-M17 into the Ashkenazi gene pool at the beginning of the Jewish Diaspora in Europe. Since then this haplogroup has expanded and spread among the Jewish communities across Europe.
Noteworthy, Behar et al,6 in their sample of Ashkenazi Levites, found R-M17 at a frequency of 52% and its modal haplotype (identical to H6 in the present study) at 74% within this haplogroup. They suggested a founder event specific to this particular group as a result of intrusion of one or a few European Y chromosomes into the forming Ashkenazi community. The present study does not necessarily contradict that of Behar et al,6 but rather indicates that R-M17 is characteristic of the general Ashkenazi population and not restricted to the Levites. The proportion of Levites in different Jewish populations has been estimated to range from 0.2516 to 3.4%.17 Thus, their contribution to the overall frequency of R-M17 in Ashkenazim could not exceed 2%, while the frequency observed in the present study is 11.5%. Similar frequency (9.7%) was also reported by Passarino et al.5 Furthermore, the haplotype diversity in the Ashkenazi Levites (0.451)6 is lower than in the sample of Ashkenazi Jews described here, suggesting that R-M17 drifted to high frequency in the Levites more recently than in the general Ashkenazi population.
It is historically well documented that the Khazar King Bulan and his court converted to Judaism at the end of the 8th century CE.1 The Khazars were originally a Turkic tribe from Central Asia who settled in the northern Caucasus and later spread to southern Russia and eastern Ukraine. Some authors argue that after the fall of their kingdom in the second half of the 10th century CE, the Khazar converts were absorbed by the emerging Ashkenazi Jewish community in Eastern Europe.18, 19 Since R-M17 haplogroup is also found at moderate to high frequencies in Central Asia20 and southern Russia/Ukraine,5 this haplogroup could have been present in the Khazars. However, if the R-M17 chromosomes in Ashkenazi Jews do indeed represent the vestiges of the mysterious Khazars then, according to our data, this contribution was limited to either a single founder or a few closely related men, and does not exceed approx12% of the present-day Ashkenazim.
Top of page
References
References
1. Dunlop D. The history of the Jewish Khazars Princeton: Princeton University Press 1954;.
2. Santachiara-Benerecetti SA, Semino O & Passarino G et al. The common Near Eastern origin of Ashkenazi and Sephardi Jews supported by Y-chromosome similarity. Ann Hum Genet 1993; 57: 55−64. | PubMed |
3. Hammer MF, Redd AJ & Wood ET et al. Jewish and Middle Eastern non-Jewish populations share a common pool of Y-chromosome biallelic haplotypes. Proc Natl Acad Sci USA 2000; 97: 6769−6774. | Article | PubMed | ChemPort |
4. Nebel A, Filon D, Brinkmann B, Majumder PP, Faerman M & Oppenheim A. The Y chromosome pool of Jews as part of the genetic landscape of the Middle East. Am J Hum Genet 2001; 69: 1095−1112. | Article | PubMed | ChemPort |
5. Passarino G, Semino O & Magri C et al. The 49a,f haplotype 11 is a new marker of the Eu19 lineage that traces migrations from the northern regions of the Black Sea. Hum Immunol 2001; 62: 922−932. | Article | PubMed | ChemPort |
6. Behar DM, Thomas MG & Skorecki K et al. Multiple origins of Ashkenazi levites: Y chromosome evidence for both Near Eastern and European ancestries. Am J Hum Genet 2003; 73: 768−779. | Article | PubMed | ChemPort |
7. Semino O, Passarino G & Oefner PJ et al. The genetic legacy of Paleolithic Homo sapiens sapiens in extant Europeans: a Y chromosome perspective. Science 2000; 290: 1155−1159. | Article | PubMed | ISI | ChemPort |
8. Thomas MG, Bradman N & Flinn H. High throughput analysis of 10 microsatellite and 11 diallelic polymorphisms on the human Y chromosome. Hum Genet 1999; 105: 577−581. | Article | PubMed | ChemPort |
9. Kittles RA, Perola M & Peltonen L et al. Dual origins of Finns revealed by Y chromosome haplotype variation. Am J Hum Genet 1998; 62: 1171−1179. | Article | PubMed | ISI | ChemPort |
10. Quintana-Murci L, Krausz C & Zerjal T et al. Y chromosome lineages trace diffusion of people and languages in southwestern Asia. Am J Hum Genet 2001; 68: 537−542. | Article | PubMed | ChemPort |
11. Nebel A, Filon D & Weiss D et al. High-resolution Y chromosome haplotypes of Israeli and Palestinian Arabs reveal geographic substructure and substantial overlap with haploytpes of Jews. Hum Genet 2000; 107: 630−641. | Article | PubMed | ChemPort |
12. Zerjal T, Pandya A & Santos FR et al. The use of Y-chromosomal DNA variation to investigate population history: recent male spread in Asia and Europe. In Papiha SS, Deka R, Chakraborty R (eds)Genomic diversity: applications in human population genetics New York: Plenum Press 1999; pp 91−101.
13. Zerjal T, Beckman L & Beckman G et al. Geographical, linguistic, and cultural influences on genetic diversity: Y-chromosomal distribution in Northern European populations. Mol Biol Evol 2001; 18: 1077−1087. | PubMed | ChemPort |
14. Zerjal T, Wells RS, Yuldasheva N, Ruzibakiev R & Tyler-Smith C. A genetic landscape reshaped by recent events: Y-chromosomal insights into central Asia. Am J Hum Genet 2002; 71: 466−482. | Article | PubMed | ISI | ChemPort |
15. Weale ME, Yepiskoposyan L & Jager RF et al. Armenian Y chromosome haplotypes reveal strong regional structure within a single ethno-national group. Hum Genet 2001; 109: 659−674. | Article | PubMed | ChemPort |
16. Kosmin BA & Waterman S. The use and misuse of distinctive Jewish names. In Schmelz UO, Della Pergola S (eds)Papers in Jewish Demography 1985 Jerusalem: The Hebrew University of Jerusalem 1989; pp 1−10.
17. Della Pergola S.Alcuni aspetti quantitativi della distribuzione del cognome fra gli ebrei in Italia. Annu Studi Ebraici 1984; vol.10 Rome, Carucci pp: 65−86.
18. Brook KA. The Jews of Khazaria Northvale, NJ: Jason Aronson 2002;.
19. Koestler A. The thirteenth tribe: the Khazar Empire and its heritage New York, NY: Random House Trade Paperbacks 1976;.
20. Underhill PA, Jin L & Lin AA et al. Detection of numerous Y chromosome biallelic polymorphisms by denaturing high-performance liquid chromatography. Genome Res 1997; 7: 996−1005. | PubMed | ISI | ChemPort |
21. Nasidze I, Sarkisian T, Kerimov A & Stoneking M. Testing hypotheses of language replacement in the Caucasus: evidence from the Y chromosome. Hum Genet 2003; 112: 255−261. | PubMed |
22. Wells RS, Yuldasheva N & Ruzibakiev R et al. The Eurasian heartland: a continental perspective on Y-chromosome diversity. Proc Natl Acad Sci USA 2001; 98: 10244−10249. | Article | PubMed | ChemPort |
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Acknowledgements
We are grateful to Drs Ben Glaser, Deborah Rund, Avraham Shaag and Ms Ester Hyam for providing DNA samples of Ashkenazim. We thank Drs Silvana Santachiara-Benerecetti and Chris Tyler-Smith for sharing haplotype information on European populations. This work was supported by a research grant form the Israeli Ministry of Science, Culture and Sport to AO and MF, and jointly by the Medical Research Council of South Africa, the National Research Foundation, the National Health Laboratory Service and the University of the Witwatersrand to HS. AN was the recipient of the Hillel Friedland Postdoctoral Research Fellowship from the University of the Witwatersrand.
Supplementary Information accompanies the paper on European Journal of Human Genetics website (http://www.nature.com/ejhg)
Source Page:
http://www.nature.com/ejhg/journal/v13/n3/full/5201319a.html
Chart Page:
http://www.nature.com/ejhg/journal/v13/n3/fig_tab/5201319t2.html#figure-title
Video: Fritz Springmeier
The Illuminati is the continuation of the Mystery Religions System, hoarding knowledge, real and bogus.
The Satanic Bloodlines
http://theforbiddenknowledge.com/hardtruth/the_satanic_bloodlines.htm
Fritz Springmeier Writings Index
http://www.geocities.com/three_strikes_legal/fritz_springmeier_writings.htm
The Satanic Bloodlines
http://theforbiddenknowledge.com/hardtruth/the_satanic_bloodlines.htm
Fritz Springmeier Writings Index
http://www.geocities.com/three_strikes_legal/fritz_springmeier_writings.htm
Documentary: New Age Infiltration of the Truth Movement
There is no better explaination of this anywhere
KeithTruth did perfect movie, if you have a problem with his religion, GET OVER YOURSELF,
KeithTruth did perfect movie, if you have a problem with his religion, GET OVER YOURSELF,
Books: The Externalization of the Hierarchy
The Externalization of the Hierarchy
Alice Bailey & Djwhal Khul
http://www.bibliotecapleyades.net/sociopolitica/externalisation/contents.html
this book goes into the setting up of the evolution based religion
Alice Bailey & Djwhal Khul
http://www.bibliotecapleyades.net/sociopolitica/externalisation/contents.html
this book goes into the setting up of the evolution based religion
Film: It's A Wonderful Life [full]
I am very well aware now of the "subversive" nature of this film, but I still love old stuff
Video: Rage Against The Machine, Testify Video
From the looks of this video, seems like Rage was pretty awake in 2000
Wish List: Wood Cookstove
If you want to get off the grid, that means no gas prolly, so that means chopping wood n'stuff so need to get one of these stoves, it says it does not develop a lot of Creosote a good thing i guess since i didnt know what that was, so i looked it up Creosote
This website had the best ones though I got no monies for any of it ><
http://www.antiquestoves.com/general%20store/generalstore.index.htm
This website had the best ones though I got no monies for any of it ><
http://www.antiquestoves.com/general%20store/generalstore.index.htm
Image/Video: Orthodox Veiw
Long before I ever knew what hot was, I knew these dudes were hot. Yes im probably biased, I dig the curls.
They belong to an organization called Neturei Karta, for more information
visit their site, many things are explained therein.
Recipie: Paula Deen's Apple Strudel
Apple Strudel:
- 1/4 cup bourbon or apple juice
- 1/2 cup golden raisins
- 2 to 3 Granny Smith apples (about 1 pound), peeled, cored, halved, and thinly sliced
- 1/2 lemon, juiced
- 1 tablespoon lemon zest, finely chopped
- 1 teaspoon ground cinnamon, plus more for sprinkling
- 1/2 cup brown sugar, packed
- 1/2 cup crushed shortbread cookies
- 1/4 cup chopped pecans
- 2 tablespoons butter, cut into pieces
- 5 sheets phyllo dough from 1 pound package of frozen dough
- 2 tablespoons butter, melted, for brushing phyllo sheets, plus more if needed
- 1 tablespoon granulated sugar
- Confectioners' sugar
- Caramel sauce, purchased
Glaze:
- 2 cups confectioners' sugar
- 3 1/2 tablespoons milk
For the Strudel:
Directions
Preheat the oven to 350 degrees F. Line a baking sheet with parchment paper.
In a small bowl, pour the bourbon or apple juice over the raisins and microwave on high for 45 seconds. Let sit for 15 minutes.
Combine the raisins, apples, lemon juice, lemon zest, cinnamon, brown sugar, cookie crumbs, pecans, and butter in a large bowl.
Remove the phyllo dough from the box, unfold, and cover with a damp towel. Place 1 sheet of phyllo on the work surface and brush lightly with melted butter. Repeat with the remaining sheets, brushing each with melted butter, stacking when done, being sure to keep the unbuttered phyllo covered.
Place the apple mixture on the nearest third of the phyllo stack, being sure to leave a 2-inch border. Gently lift the bottom edge of the phyllo stack to cover the filling and fold the side edges over. Continue to roll the stack away from you until the filling is completely sealed in and the seam is on the bottom. Transfer to the prepared baking sheet. Brush the top with melted butter and sprinkle with granulated sugar.
Bake for 30 minutes, until golden brown. Pour over the glaze and sprinkle with cinnamon and confectioners' sugar. Pass warm caramel sauce, to drizzle over the strudel.
For the Glaze:
Mix ingredients thoroughly.
*Cook's Note: If too thick add a little bit of milk. If too thin add a little bit of confectioners' sugar.
http://www.foodnetwork.com/recipes/paula-deen/apple-strudel-recipe/index.html
Documentary: Nazis: The Occult Conspiracy
Nazis: The Occult Conspiracy Jan 1, 1998
Discovery Channel - imdb.com/title/tt0195938/
part 1of 2
part 2 of 2
Discovery Channel - imdb.com/title/tt0195938/
part 1of 2
part 2 of 2
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