NYT: "The HapMap" and the *CORRECT* New Disease Paradigm
Mort Zuckerman
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Subject: NYT: "The HapMap" and the *CORRECT* New Disease Paradigm
Date: Jun 12, 2010 4:31 PM
ARTICLE BELOW
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Nope.
The New Disease Paradigm is not in
genetics but acquired modulations-
something only predictable with biosystem
changes due to global warming cuz that's
what we're talking about - exposures.
With the advent of The Lies of Allen
Steere, particularly his shenanigans
in Germany and Russia - and the Acquired
Russian Scientists who were also looking (
http://www.actionlyme.org/BOGUS_RUSSIAN_NYMC_ARTICLES.htm
"Some of the other Russian Scientists either publishing in
Dingleberry-Breath Durland's 'Journal", or New York Medical College-
Look closely at all of their publications. They're very interested in
genetic backgrounds of peoples of foreign nations:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=PureSearch&db=pubmed&details_term=%22Cabello%20FC%22%5BAuthor%5D
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=PureSearch&db=pubmed&details_term=%22Bakhvalova%20VN%22%5BAuthor%5D
- - - )
at genetic susceptibilities to diseases
(Hap or HLA) because that has bioweapons
value, we learned that, well, no, HLA
wasn't the critical mass. What happens
to B cells post-exposure is the main event.
It's all about dysimmunity, and it doesn't
seem to be anything any bioweaponeers
can capitalize on, especially since LYMErix
let the bioweapons cat out of the bag.
"Taken together, our results suggest that TLR4 signaling favors B
lymphocyte maturation, whereas TLR2 arrests/retards that process,
ascribing new roles for TLRs in B cell physiology."
http://www.ncbi.nlm.nih.gov/pubmed/15905502
But this could be as close as we can
get to the truth from the New York Times:
"Whoops - the haplotypes game wasn't it;
It's not about HLA-linked inflammation."
http://www.actionlyme.org/080924.htm
1992, Paul Duray:
"On occasion, these atypical-appearing large lymphocytes have been
misinterpreted in biopsy by several laboratories as cells of a
malignant lymphoma or leukemia. ***Bb antigens, then, may stimulate
growth of immature lymphocytic suibsets in some target organs, as well
as in the cerebrospinal fluid (Szyfelbein and Ross 1988).*** Usual
bacterial infections do not produce such lymphocytic infiltrates in
tissue. ***These immunoblastoid cells in Bb infections at times
resemble those found in Epstein-Barr virus infections.*** Does Bb
reactivate latent virus infections in tissues? Do some tick inocula
harbor simultaneous infectious agents (ixodid ticks can harbor
Rickettsiae, Babesia microti, and Ehrlichia bacteria, in addition to
Bb), producing multi-agent infections in some hosts? Further studies
can clarify these issues by mans of tissue-based molecular probe
analysis." -
-- Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor
Crooks' Conference, published in Steve Schutzer's Lyme Disease:
Molecular and Immunologic Approaches:
http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770/ref=sr_1_2?ie=UTF8&s=books&qid=1214848669&sr=1-2
Allow me to do the math:
18 years since Paul Duray described it in
a book and 21 years since he explained it
to IDSA directly, in their journal:
http://www.actionlyme.org/CHP_9_IDSA_REVIEWS.htm
Call it 20 years of lost lives and
research in every major disease because
the likes of the insurance companies put
a few tards up to the task of creating a
fake vaccine for Relapsing Fever, of all
things. And tards being tards, they took
the bait:
http://www.actionlyme.org/CRYME_DISEASE.htm
Kathleen M. Dickson
http://www.actionlyme.org
http://www.relapsingfever.org
=========================================
http://www.nytimes.com/2010/06/13/health/research/13genome.html?hpw=&pagewanted=print
12, 2010
A Decade Later, Human Gene Map Yields Few New Cures
By NICHOLAS WADE
Ten years after President Bill Clinton announced that the first draft
of the human genome was complete, medicine has yet to see any large
part of the promised benefits.
For biologists, the genome has yielded one insightful surprise after
another. But the primary goal of the $3 billion Human Genome Project —
to ferret out the genetic roots of common diseases like cancer and
Alzheimer’s and then generate treatments — remains largely elusive.
Indeed, after 10 years of effort, geneticists are almost back to
square one in knowing where to look for the roots of common disease.
One sign of the genome’s limited use for medicine so far was a recent
test of genetic predictions for heart disease. A medical team led by
Nina P. Paynter of Brigham and Women’s Hospital in Boston collected
101 genetic variants that had been statistically linked to heart
disease in various genome-scanning studies. But the variants turned
out to have no value in forecasting disease among 19,000 women who had
been followed for 12 years.
The old-fashioned method of taking a family history was a better
guide, Dr. Paynter reported this February in The Journal of the
American Medical Association.
In announcing on June 26, 2000, that the first draft of the human
genome had been achieved, Mr. Clinton said it would “revolutionize the
diagnosis, prevention and treatment of most, if not all, human
diseases.”
At a news conference, Francis Collins, then the director of the genome
agency at the National Institutes of Health, said that genetic
diagnosis of diseases would be accomplished in 10 years and that
treatments would start to roll out perhaps five years after that.
“Over the longer term, perhaps in another 15 or 20 years,” he added,
“you will see a complete transformation in therapeutic medicine.”
The pharmaceutical industry has spent billions of dollars to reap
genomic secrets and is starting to bring several genome-guided drugs
to market. While drug companies continue to pour huge amounts of money
into genome research, it has become clear that the genetics of most
diseases are more complex than anticipated and that it will take many
more years before new treatments may be able to transform medicine.
“Genomics is a way to do science, not medicine,” said Harold Varmus,
president of the Memorial Sloan-Kettering Cancer Center in New York,
who in July will become the director of the National Cancer Institute.
The last decade has brought a flood of discoveries of disease-causing
mutations in the human genome. But with most diseases, the findings
have explained only a small part of the risk of getting the disease.
And many of the genetic variants linked to diseases, some scientists
have begun to fear, could be statistical illusions.
The Human Genome Project was started in 1989 with the goal of
sequencing, or identifying, all three billion chemical units in the
human genetic instruction set, finding the genetic roots of disease
and then developing treatments. With the sequence in hand, the next
step was to identify the genetic variants that increase the risk for
common diseases like cancer and diabetes.
It was far too expensive at that time to think of sequencing patients’
whole genomes. So the National Institutes of Health embraced the idea
for a clever shortcut, that of looking just at sites on the genome
where many people have a variant DNA unit. But that shortcut appears
to have been less than successful.
The theory behind the shortcut was that since the major diseases are
common, so too would be the genetic variants that caused them. Natural
selection keeps the human genome free of variants that damage health
before children are grown, the theory held, but fails against variants
that strike later in life, allowing them to become quite common. In
2002 the National Institutes of Health started a $138 million project
called the HapMap to catalog the common variants in European, East
Asian and African genomes.
With the catalog in hand, the second stage was to see if any of the
variants were more common in the patients with a given disease than in
healthy people. These studies required large numbers of patients and
cost several million dollars apiece. Nearly 400 of them had been
completed by 2009. The upshot is that hundreds of common genetic
variants have now been statistically linked with various diseases.
But with most diseases, the common variants have turned out to explain
just a fraction of the genetic risk. It now seems more likely that
each common disease is mostly caused by large numbers of rare
variants, ones too rare to have been cataloged by the HapMap.
Defenders of the HapMap and genome-wide association studies say that
the approach made sense because it is only now becoming cheap enough
to look for rare variants, and that many common variants do have roles
in diseases.
At this point, some 850 sites on the genome, most of them near genes,
have been implicated in common diseases, said Eric S. Lander, director
of the Broad Institute in Cambridge, Mass., and a leader of the HapMap
project. “So I feel strongly that the hypothesis has been vindicated,”
he said.
But most of the sites linked with diseases are not in genes — the
stretches of DNA that tell the cell to make proteins — and have no
known biological function, leading some geneticists to suspect that
the associations are spurious.
Many of them may “stem from factors other than a true association with
disease risk,” wrote Jon McClellan and Mary-Claire King, geneticists
at the University of Washington, Seattle, in the April 16 issue of the
journal Cell. The new switch among geneticists to seeing rare variants
as the major cause of common disease is “a major paradigm shift in
human genetics,” they wrote.
The only way to find rare genetic variations is to sequence a person’s
whole genome, or at least all of its gene-coding regions. That
approach is now becoming feasible because the cost of sequencing has
plummeted, from about $500 million for the first human genome
completed in 2003 to costs of $5,000 to $10,000 that are expected next
year.
But while 10 years of the genome may have produced little for
medicine, the story for basic science has been quite different.
Research on the genome has transformed biology, producing a steady
string of surprises. First was the discovery that the number of human
genes is astonishingly small compared with those of lower animals like
the laboratory roundworm and fruit fly. The barely visible roundworm
needs 20,000 genes that make proteins, the working parts of cells,
whereas humans, apparently so much higher on the evolutionary scale,
seem to have only 21,000 protein-coding genes.
The slowly emerging explanation is that humans and other animals have
much the same set of protein-coding genes, but the human set is
regulated in a much more complicated way, through elaborate use of
DNA’s companion molecule, RNA.
Little, if any, of this research could have been done without having
the human genome sequence available. Every gene and control element
can now be mapped to its correct site on the genome, enabling all the
working parts of the system to be related to one another.
“Having a common scaffold on which one can put all the information has
dramatically accelerated progress,” Dr. Lander said.
The genome sequence has also inspired many powerful new techniques for
exploring its meaning. One is chip sequencing, which gives researchers
access to the mysterious and essential chromatin, the complex protein
machinery that both packages the DNA of the genome and controls access
to it.
The data from the HapMap has also enabled population geneticists to
reconstruct human population history since the dispersal from Africa
some 50,000 years ago. They can pinpoint which genes bear the
fingerprints of recent natural selection, which in turn reveals the
particular challenges to which the populations on different continents
have had to adapt.
As more people have their entire genomes decoded, the roots of genetic
disease may eventually be understood, but at this point there is no
guarantee that treatments will follow. If each common disease is
caused by a host of rare genetic variants, it may not be susceptible
to drugs.
“The only intellectually honest answer is that there’s no way to
know,” Dr. Lander said. “One can prefer to be an optimist or a
pessimist, but the best approach is to be an empiricist.”
Next: Drug companies stick with genomics but struggle with information
overload.
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci