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“GATTACA” turned out to be personal bust—for Ars Technica editor

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Remember the film? Editor Cyrus Farivar decided to get tested at both 23andme and a much more expensive outfit, due to heightened risk of Alzheimer. His article provides a wealth of information about how such tests work, but he concludes,

What I learned from the process, in short, is that they’re not quite ready for prime time. It may be helpful to know about a slightly elevated risk for one disease or another, but the genetics behind the results—for average consumers at least, perhaps not those purchasing full genome sequencing—is still lagging. I wouldn’t have paid my own money for these tests. (Ars covered the 23AndMe fees, Gentle offered up its trial as Science Editor John Timmer has previously worked with the company’s CEO.)

The current scientific limits are why the FDA forced 23andMe to pull their health risks section from their site for new customers. It’s why Gentle backtracked on my Alzheimer’s risk factor during a follow-up call. Today’s DTC genetic testing distills complex biology—like the presence of a certain SNP—into a fixed, digestible number. I can understand what a 12.6 percent risk for Alzheimer’s (according to 23andMe) might mean. But the fact that there are so many contributing factors both known and unknown is complicated at best and deceptive at worst.

“If you try to give someone a risk figure, you’re really not giving them an accurate risk picture,” Laura Hercher, a genetics counselor and faculty member at Sarah Lawrence College, told me. “What they should say is that the part of your risk explained by this one thing we’re looking for goes up two percent, but we don’t really know what your global risk is. It would be like if you had a stock portfolio, [and your financial advisor] looked at two or three stocks and said: these are up, and so your [overall performance] is up. The advisor wouldn’t be lying but would be very misleading.”

Remember that scene from GATTACA where the delivery room nurse reads off information that shows that our hero will die young of heart issues?

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What you wanna bet the biggest factor in all types of senile dementia (most Alzheimer sufferers are old) will turn out to be just your chances of living to an advanced age? We tend to assume that northern Europeans are more at risk, and no doubt genetics support this. But northern Europeans were also among the first groups to benefit from medical advances that caused a much greater proportion of the population to “qualify for” late life illnesses.  Let’s see what happens if lifespans lengthen in other parts of the world.

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AVS @ 6
Stick to computer science.
Here's another good example of computer science professionals working in advanced biology-related research: Alberto Riva, PhD Assistant Professor, Department of Molecular Genetics and Microbiology and UF Genetics Institute Alberto Riva is a computer scientist whose research interests range from bioinformatics and computational biology to medical informatics, knowledge engineering and artificial intelligence. He is a faculty member with the Department of Molecular Genetics and Microbiology of the University of Florida since 2006, and is also affiliated with the UF Genetics Institute. Previously, he was an Instructor at the Children's Hospital Informatics Program of Harvard Medical School Dionisio
AVS @ 6 Notice the name "C J Tomlin" in bold text below. Also notice the subjects associated with advanced biological research. Planar Cell Polarity in Drosophila melanogaster Anil Aswani with R. Raffard, K. Amonlirdviman, J. Axelrod, C. Tomlin Amonlirdviman, K., Khare, N.A., Tree, D.R., Chen, W.S., Axelrod, J.D., and Tomlin, C.J. Mathematical modeling of planar cell polarity to understand domineering nonautonomy. Science 307, 423–426 (2005) Raffard, R., Tomlin, C. Parameter Identification via the Adjoint Method: Application to Protein Regulatory Networks. (2006) Modeling the control of planar cell polarity Jeffrey D. Axelrod and Claire J. Tomlin (2011) Here's Ms. Tomlin's CV (Résumé). Notice her background in electrical engineering and her work in advanced biology-related research. http://www.eecs.berkeley.edu/~tomlin/ Claire J. Tomlin Charles A. Desoer Chair in the College of Engineering Professor, Electrical Engineering and Computer Sciences UC Berkeley, Berkeley CA, 94720-1770 Ph.D. (EECS) U.C. Berkeley, 1998 M.Sc. (EE) Imperial College, London, 1993 B.A.Sc. (EE) University of Waterloo, 1992 How come this electrical engineer/computer science professional is working with biologists? couldn't the biologists themselves do her work? Well, not exactly. Neither could she do the work done by the biologists. Work specialization. Every specialist handles part of the entire research project. These days biology is becoming more complex. Professionals from different backgrounds joint their expertise and collaborate. However, they all have to learn a common set of technical terminologies so they could communicate with each other easily. Probably the engineers and computer scientists have to learn many biological terminologies and concepts. We can't get away without this kind of professional collaboration. c'est la vie mon ami. Let's be more respectful to others. Thank you. Dionisio
gpuccio @ 12 Molte grazie mio caro amico! Dionisio
Dionisio: Please, stick to biology! :) (By the way, never do what darwinists advice you to do, and you will live a happy life) :) . gpuccio
Dr JDD @ 7 Excellent explanation! Thank you, Sir. I really appreciate it. Have a good weekend. Dionisio
AVS @ 6
Garlic does have antimicrobial effects actually
My mother-in-law told me that too. She read it in a popular magazine she buys every week. ;-)
And you wouldn’t throw out the WBC idea just because your wife got sick and you didn’t one year.
My point was to show a simple example where different factors may affect our visible health condition. Can't just blame it all on one factor. Can't just look for quick simple explanations. System-wide explanations are better.
Stick to computer science.
Actually, my background is electrical engineering specialized in information management systems. I worked a number of years on software development for civil engineering design. The systems were conceived and designed by brilliant practicing civil engineers. I worked as a programmer for them. They never rejected me just because I did not have their background and did not understand their terminologies and concepts. On the contrary, they helped me to learn about their field, so that I could become a productive member of their teams. And that's what happened. Their products became successful and very appreciated by civil engineering organizations that used their software in those years. I think this is a very good time for other professionals to jump into the systems biology arena. The doors seem wide open for us these days. A few years ago I saw a presentation on cell polarity modeling given by a bright lady whose background is electronic engineering. She was the leader of a research team. As far as I remember the presentation took place at Stanford university. So now you know that you have to learn to be more tolerant of others around you, and treat others with more respect, even if they seem to know less than you. You may want to follow the example of other participants in these UD discussions, who have corrected my mistaken comments and have answered my questions in a very respectful and tolerant manner. So now you know I'm not the first non-biologist to join the biology party. More came before me and more will come after me. Just be ready to humbly accept this fact. Look around and see if this is really happening. Now, don't worry, engineers, mathematicians, computer scientists, won't replace the biologists (that's absurd), they just complement their work. I think -and here y'all can correct me- what's happening is that the big data coming out of research (done by brilliant scientists), is showing an extremely complex system that may require the joint work of professionals from different backgrounds. Does this make sense? I'm always willing to learn more everyday. I'm learning quite a bit from what many of you write on these pages. Remember each of us may look at the same problem from a different perspective. That's the beauty of team work. At the end of the day we want to know more about the ultimate reality, don't we? Let's work together towards that goal. Deal? Dionisio
Mung, there is certainly way more to it than old age. But some of us question a tendency to identify characteristics of a northern/western European (origin) population as predictive of old age illnesses, when those people were among the few worldwide who were in a position in previous generations to get old-age friendly disorders. There is Alzheimer in my family as well, but there is also the fact that those affected lived into their late eighties to late nineties. So the question arises, is it really one single genetic marker or would the number of affected patients with or without that marker increase simply due to the fact that aging brains get troubles like neuronal plaques that 18-yr-old brains don't? I say, wait and see what happens when populations whose current life expectancy is in the low sixties start to attain the low eighties, due to medical advances. Let's see which chronic illnesses become more commonly seen in clinical practice. News
Mung @ 5
Vampires are attracted to garlic and sucked the bad cold cells from your blood before you could get sick.
Didn't know that, but perhaps that's what happened. The vamps could've sneaked into the house when we opened the windows to ventilate the rooms ;-) If that's the case, they did a good work, keeping me from getting sick ;-) Any explanation is acceptable, as long as it is politically correct, i.e. it doesn't imply ID ;-) Dionisio
Dionisio - while there is a correlation some times with WBC count and resistance to infection, I am not sure how significant it always is. Like the old saying goes, quality not quantity! I work in the field of Immunology (well, Immunotherapy) and can guarantee that some healthy donors we take blood from will have 2-4x the number of WBCs per 1ml of blood than another person, yet on a like-for-like basis in a potency assay, are far inferior. It depends on your subtypes of cells, even within one population (e.g. T-cells) you have multiple sub-types with multiple effector properties and hence some people are better at clearing particular infections than others. Additionally, it is more likely to be down to your genotype differences between you and your wife - one example it that you may be a more common HLA-type thus present more common viral peptides than your wife (meaning evasion of viral infection is easier for your wife) or alternatively your wife is exposed to lower levels of infection more often and has a better built up immunity...the possibilities are near endless and just further demonstrate how little we know and understand about immunology (most Immunologists readily admit ro this fact!). JD Dr JDD
Garlic does have antimicrobial effects actually. And you wouldn't throw out the WBC idea just because your wife got sick and you didn't one year. Stick to computer science. AVS
yummm garlic Vampires are attracted to garlic and sucked the bad cold cells from your blood before you could get sick. Mung
Every winter I get sick with bad cold before my wife gets sick with a milder cold. Our annual physical reveals that I have half the WBC count of my wife. Apparently that difference explained the described situation. Or so I thought. However, this past winter my wife got sick but I didn't get sick at all. The WBC count theory was thrown out the window (or should I better say it got flushed down the toilet?). The only major difference with previous winters is that this time I ate large amounts of raw garlic! Was that it? No idea. I just know that no one dared to get close to me, because the garlic smell was felt all around me. Dionisio
Of somewhat related note, I was recently impressed with this tidbit from Michael Denton's background: Michael Denton Interview - March 2014 8. Q: Your retinal work has contributed to identifying several new disease genes, including a gene used in a successful gene-therapy trial at London’s Moorfields eye hospital. Would you elaborate a bit by explaining the nature of this gene-therapy trial and how it was successful? A: The gene was identified in a family from the city of Bangalore. We collected the family in the early 90’s, and the gene was identified in the late 90’s. The gene happens to be RPE65 which is mumbo-jumbo of course to a non-geneticist but that’s just the way genes are named. It’s a gene which is involved in regenerating the visual pigment. In the eye, the critical act of seeing, involves the visual pigment which changes slightly when the photon hits it, then it has to be regenerated, and it’s regenerated in the so-called retinal epithelial cells in the back of the eye. So in other words, basically, the gene we found is involved in that act of regeneration of the visual pigment. It’s a gene that causes a severe form of retinal degeneration which causes severe visual disability from birth and rapidly progresses in early childhood leaving most patients with very limited vision by age ten. So it was one of these very severe forms of retinal genetic disease, which cries out for something like gene therapy. And the group in Moorfields happened to select this gene for the first gene therapy trial in the retinal disease area. It turned out to be just about the first successful gene therapy trial in any area of biology, and any area of medicine. What this involves is you put a good copy of the gene into a viral vector and then you actually inject billions of copies of the viral vector containing the good gene in it into the back of the eye, and it automatically incorporates itself into the DNA of the retinal epithelial cells and corrects the defect. See, where you have a recessive disease you have two bad copies of the gene, so what you’re doing in this type of gene therapy is you’re putting in a good copy of the disease gene into the cells where it is used. In 2008 they gave six patients with quite advanced form of the disease (caused by defects in the RPE65 gene) and then they followed them over the next few months, and remarkably the vision in some of them improved in a striking way actually. And there is a video you can find on the web showing what happened. So basically the gene we found in Bangalore, was used in the first successful gene therapy trial that’s ever been done, certainly in the eye disease area. That was one of the high points of my career. I remember I was sitting in Australia watching the TV news and the second item in the news that night was the report of the successful gene therapy trial in Moorfields. Suddenly they said the magic word RPE65 and I said Wow! that was my gene! So that was one of the highlights of my career. I suppose overall, I have managed to make, with my colleagues, particularly with my Indian colleagues, a significant contribution to the genetics of human retinal disease. Discover magazine listed it in the top 30 scientific advances of 2008. http://successfulstudent.org/dr-michael-denton-interview/ BBC News Blindness gene therapy trial 'I don't trip over things any more' - video http://www.youtube.com/watch?v=JAJExpTj8ZY I remember quipping to myself (with the huge impact that Evolution: A Theory In Crisis had), well Dr. Denton has restored sight to both the spiritually blind and the physically blind! :) bornagain77
Genetic Explanations: Sense and Nonsense Mung
My mom has Alzheimer's and her sister did as well. There may be more to it than "old age." Her sister had no female children but three boys. I have two brothers and two sisters. Will be interesting to see what happens as we age. Mung

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