Dr. Henry Miller, physician and molecular biologist, a fellow at Stanford University's Hoover Institution, and Dr. Elizabeth Whelan, president of the American Council on Science and Health, have ended the vaccine autism wars.
Without providing any fancy explanations, or any substantial explanation at all, these learned figures have declared in Unlocking the Genetic Secrets of Autism that autism is 100% genetic and parents who resist this knowledge are fanatics particularly those who believe vaccines may play a role in causing vaccines. There ain't much science or logic in the declaration to confuse fanatic parents. The war is over. Autism is genetic. Let the parades begin:
Intense and even fanatical resistance to vaccination against childhood diseases is itself a significant public health problem. Opponents have blamed vaccines for everything from allergies and diabetes to cancer and autism. A recent study of abnormalities in the DNA of children with autism spectrum disorders (ASDs) should finally put to rest the claims of some activists, mainly parents of affected children, that vaccines cause these conditions.
Abnormalities in a small percentage of children with autism... They have no idea what genes do what or how or how severe or or or or or or....
ReplyDeleteBut that's ok, now they say we shouldn't have very many ultrasounds or x-rays, especially when pregnant and with my youngest I had 6??? Or more b/c I was in antenatal....
That long term use of cholesterol drugs will destroy your liver.
That long term use of blood pressure pills will increase your risk for cancer...
All except the vaccine one I have links via CBC news' health section online... and are supposedly "proven".
I'm not convinced.... anytime you put anything into your body that is not "natural", that changes how your body works... IMO... runs the risk of doing you harm.
And had I know then, what I know now... I too would probably have postponed my shots out of infancy.
That's repugnant. No other word I can think of than that. They should be ashamed of themselves for making that kind of sweeping generalization.
ReplyDeleteI just finished two very interesting articles.
ReplyDeleteNature 461, 747-753 (8 October 2009) | doi:10.1038/nature08494; Received 25 June 2009; Accepted 11 September 2009
Finding the missing heritability of complex diseases
Teri A. Manolio1, Francis S. Collins2, Nancy J. Cox3, David B. Goldstein4, Lucia A. Hindorff5, David J. Hunter6, Mark I. McCarthy7, Erin M. Ramos5, Lon R. Cardon8, Aravinda Chakravarti9, Judy H. Cho10, Alan E. Guttmacher1, Augustine Kong11, Leonid Kruglyak12, Elaine Mardis13, Charles N. Rotimi14, Montgomery Slatkin15, David Valle9, Alice S. Whittemore16, Michael Boehnke17, Andrew G. Clark18, Evan E. Eichler19, Greg Gibson20, Jonathan L. Haines21, Trudy F. C. Mackay22, Steven A. McCarroll23 & Peter M. Visscher24
Top of pageAbstract
Genome-wide association studies have identified hundreds of genetic variants associated with complex human diseases and traits, and have provided valuable insights into their genetic architecture. Most variants identified so far confer relatively small increments in risk, and explain only a small proportion of familial clustering, leading many to question how the remaining, 'missing' heritability can be explained. Here we examine potential sources of missing heritability and propose research strategies, including and extending beyond current genome-wide association approaches, to illuminate the genetics of complex diseases and enhance its potential to enable effective disease prevention or treatment.
and
Epigenetics as a unifying principle in the aetiology of complex traits and diseases
Arturas Petronis
Nature 465, 721–727 (10 June 2010) doi:10.1038/nature09230
Published online 09 June 2010
Abstract
Epigenetic modifications of DNA and histones might be crucial for understanding the molecular basis of complex phenotypes. One reason for this is that epigenetic factors are sometimes malleable and plastic enough to react to cues from the external and internal environments. Such induced epigenetic changes can be solidified and propagated during cell division, resulting in permanent maintenance of the acquired phenotype. In addition, the finding that there is partial epigenetic stability in somatic and germline cells allows insight into the molecular mechanisms of heritability. Epigenetics can provide a new framework for the search of aetiological factors in complex traits and diseases.
Here are some things I found interesting. It has been postulated that the paucity of genes found which are involved in the inheriting autism is because autistics lack reproductive fitness. This is not an insult it just means they are not likely to find a spouse and have children.
However in a characteristic such as height the 40 or so loci studied can only explain 5% of the inheritance of height which appears to be 80-90% inheritable.
In other autism is not unique in the discrepancy between the population with autism with known genetic variants and the much greater population with autism that lacks them
The error rate for DNA sequencing during mitosis is about 1 in 1 million, however methylation it is
about 1 in 1000. It is thought that most of these changes are random rather than environmental.
Finally I have lost the reference, but one of the people who is highly responsible for the decoding of the human genome stated that knowing his genetic profile does not allow him to predict the color of his own eyes.
I just finished two very interesting articles.
ReplyDeleteFinding the missing heritability of complex diseases
Nature 461, 747-753 (8 October 2009) | doi:10.1038/nature08494;
and
Epigenetics as a unifying principle in the aetiology of complex traits and diseases
Nature 465, 721–727 (10 June 2010) doi:10.1038/nature09230
Published online 09 June 2010
Abstract
Here are some things I found interesting. It has been postulated that the paucity of genes found which are involved in the inheriting autism is because autistics lack reproductive fitness. This is not an insult it just means they are not likely to find a spouse and have children.
However in a characteristic such as height the 40 or so loci studied can only explain 5% of the inheritance of height which appears to be 80-90% inheritable.
In other autism is not unique in the discrepancy between the population with autism with known genetic variants and the much greater population with autism that lacks them
The error rate for DNA sequencing during mitosis is about 1 in 1 million, however methylation it is
about 1 in 1000. It is thought that most of these changes are random rather than environmental.
Finally I have lost the reference, but one of the people who is highly responsible for the decoding of the human genome stated that knowing his genetic profile does not allow him to predict the color of his own eyes.