caudoviral

Discussions and reflections on science and life

The failed promise of genomics

with 7 comments

Ironically, in certain circumstances, praise can do more damage than insult. One of my favourite television shows, Dylan Moran’s Black Books, has an episode in which the protagonist, Bernard Black, has a date ruined by one of his friends. However, instead of telling his date what a miserable bastard Bernard actually is, she does so by playing him up as impossibly brilliant (saying that he paints, and speaks seven languages, etc). Later, after things have begun to fall apart, he wheels on his friend and shouts: “You! What did you say to Kate? She thinks I’m the Renaissance!” I bring this up because an analogous relationship exists between Science, the Media, and the Public.

Perhaps in no place is this relationship so clear (in recent years at least) as it is with the subject of genetics & genomics. I often talk about “the failed promise of genomics”, and let me explain what I mean by that. If you ask a scientist: genomics is a fascinating field with a great many applications. It has been a vital step in understanding life and its tools will remain valuable in facing the challenges biology presents. It is the blueprint on which we will build many further endeavours. If you ask a journalist or (ugh) soft sci-fi author, genes are magic. Okay, maybe it isn’t that bad. But it’s close. And it becomes a problem when we look at scientific literacy and have to ask: who is the public getting their information from? Because it sure as hell doesn’t seem to be the scientist.

The Human Genome Project started in 1990. Even if there was a little bit of awareness before that, the HGP turned it into an obsession. Such is the vanity of H. sapiens. Suddenly genetics and genomics were catapulted from the scientists toolbox to the public eye. By the time the drafts were released in 2000 and 2003, we had genomania.

Genetic engineering and gene therapy had entered popular entertainment with films like Jurassic Park and Gattaca and games such as Metal Gear Solid and Bioshock. Our fiction portrayed genetics as mystically resurrecting dead species, fuelling dystopias, and granting abilities on par with magical powers. And the journalism on the subject hasn’t been much better. Over the past two decades we have been presented with everything from ‘obesity genes’ to ‘gay genes’ to a gene for every disease under the sun. Genes were suddenly the cause of and solution to everything.

But why does this happen?

Here we come upon one of the general principles involved in the distortion of science. Science is hard. It is a complicated field of study with a staggering amount of depth (biology with its irregularities and great breadth doubly so). Journalists have neither the training nor the time to accurately report on research. Genetics however has a simple, even elegant explanation. To the novice, a system of cause and effect presents itself. You can almost convince yourself there is a perfect little Mendelian world running with as much surety and clockwork as Newtonian physics. But once you reach the level of genomics (and  especially if you look into the newer studies of epigenetics and proteomics) this elegance breaks down. Such a breakdown isn’t pleasant. There is a parsimony and sense of ‘rightness’ to the “if I have gene A then I have trait A” paradigm. I have been in classes with students who have had total meltdowns over finding out that that is simply not true.

A full discussion of why that isn’t true is beyond the scope of this blog, but let me just throw out some examples: gene A might have multiple different alleles leading to multiple different products, each of those alleles might go through different processing, transcripts of gene A might be degraded by the protein product of gene B, the protein product of gene A might be degraded by the cell unless you also posses just the right amount of the protein product of gene C (or hell, maybe gene A doesn’t even get transcribed without gene C’s product promoting it!), maybe the protein product of gene D dimerizes with the protein product of gene A rendering it inactive (or maybe that is the only way to render it active), etc. And reasons like these just scratch the tip of the iceberg. The number of possible snafus in the pathway from genome to phenotype are so numerous that there is no such thing as a classic Mendelian single phenotype genetic disorder (something I will discuss in greater length if I ever get around to doing a write up on one of my favourite journal articles: Loscalzo, et al. 2007)

So what we have here, is an incredibly complex system with an enticing misconception just waiting to be picked up and ran with. It is a misconception that makes sense, it is a misconception that makes people happy, and it is a misconception that promises power over and easy solutions to all of the ills that surround us. The problem is that it doesn’t exist. And the scary part comes when you realise that it is kind of like crying wolf. How long until the public says: “Oh, geneticists, bah, they promised to cure my cancer and let me grow wings and have a dog-opus and make me not fat. I didn’t get none of that. And now scientists are asking for more money? Screw em.”

The human genome gives us a blueprint. Nothing more and nothing less. And don’t get me wrong. That is huge. But it is not the finished product. You can’t sit down and fly a jet, just because you have the blueprints. Hell, you can’t even necessarily build a jet just because you have the blueprints. But it is a vital step, and a really solid start. The problem is that “the failed promise of genomics” is really a misnomer. Because genomics never made these promises (well…perhaps we should say that it never made these promises outside of over-enthusiastic grant proposals). The media made promises for it, and the public becomes disappointed and disillusioned with the field when scientists can’t deliver on promises they never made in the first place. And without the support and funding of the public, science is going to fall flat.

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Written by Caudoviral

01/11/2011 at 18:05

Posted in Biology, Uncategorized

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7 Responses

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  1. Well, I wouldn’t call that a “misconception” as much as an “approximation”. While claiming that there exists an obesity gene is technically inaccurate (for all the reasons you outlined), existence of single-gene mutations that predispose for obesity appears, indeed, quite plausible .
    Some “traits” are indeed quite modular (though this is easier to find in microorganisms, which can be readily forced into producing human insulin with but a single gene), which off course does not mean that all of them are (which of course tends to be glossed over in literature)

    It’s much like when we tell another person (possibly a friend ;-) ) something along the lines of “I know how you feel”, we are being technically inaccurate (possibly grossly so) and gloss over a great deal of important details.

    Of course, public tends to treat such approximations overly literally…but then, sometimes friends do take our “know how you feel” claims completely at face value, don’t they?

    Val

    01/14/2011 at 14:56

    • I still think the distinction is a little finer than that, let me lay it out a little. I have two problems with the notion of declaring any gene the “X gene”:

      Genes are information, they do not actually do anything. Possessing a gene means that you possess a potential and merely possessing the gene itself does not speak to the realisation of that potential. For instance, every gene in your entire genome is contained within every cell of your body. But the presence of many of these genes is irrelevant because they are completely silenced (any given human cell actually expresses between a minimum of ~30% and a maximum of ~70% of the genome). Gene expression, does do things. So there may well be a single protein or functional RNA that leads to a predisposition for obesity (for instance, cortisol is putatively linked to a predisposition to obesity). But the presence of the gene does not necessitate the presence of that protein. The genomics revolution was great! But we need the current revolution in proteomics to fully use that information. Because the proteome (and to a lesser extent the transcriptome) determines phenotype directly.

      My second concern is more pragmatic and less pedantic, as well as being less solidly founded. Predisposition is of dubious use and may well harm patients. If people become too focused on what genes they have and don’t have, they may well forget environmental causes and risks (or alternately overreact to them). If people screen themselves for the “obesity gene” find out that they don’t have it, and as a result care less about diet, exercise, and other healthy habits, they are most likely going to suffer for it. On the flip side we have people taking it too far the other direction. On the Diane Rehm show late last year (November 3rd, 2010) Dr Arthur Caplan spoke about his encounter with a father who wanted his young daughter tested for the “breast cancer gene” so that he could force her into a prophylactic mastectomy if she had the potential. Now fortunately no surgeon in his right mind would do so, but it serves as a graphic illustration of why diagnosing with potentials is a dangerous game. The fact that the so called “personal genomics revolution” wants to put such capability into the corner drug store is, to my mind a cause for alarm.

      Wait till we nail down the proteomics. Wait till we have a full chain of cause and effect from genome -> transcriptome -> proteome -> phenotype rather than mere correlation between gene and phenotype. In my opinion, such uses of genomics for anything but family planning is really jumping the gun.

      Caudoviral

      01/15/2011 at 00:20

      • I still think the distinction is a little finer than that, let me lay it out a little. I have two problems with the notion of declaring any gene the “X gene”:

        Genes are information, they do not actually do anything. Possessing a gene means that you possess a potential and merely possessing the gene itself does not speak to the realisation of that potential. For instance, every gene in your entire genome is contained within every cell of your body. But the presence of many of these genes is irrelevant because they are completely silenced (any given human cell actually expresses between a minimum of ~30% and a maximum of ~70% of the genome). Gene expression, does do things. So there may well be a single protein or functional RNA that leads to a predisposition for obesity (for instance, cortisol is putatively linked to a predisposition to obesity). But the presence of the gene does not necessitate the presence of that protein. The genomics revolution was great! But we need the current revolution in proteomics to fully use that information. Because the proteome (and to a lesser extent the transcriptome) determines phenotype directly.

        Well, that is true (and, if we decide to be really pedantic, we should probably distinguish between genes that are silent in ontogenetically mature humans and non-coding DNA, which never ends up as a protein product ever, and then between various types of non-coding DNA ;-) ) however, when people say “X genes” they of course ;-) mean genes that are likely to be actively expressed in their “carriers”.
        In fact, given how current medical genetics research works, you are exceedingly unlikely to even get to deal with a gene that is not expressed in a typical patient at least at some point of patient’s life (unless you get good correlations between presence of a gene and a clinical phenomenon X, you don’t get to claim any clinical importance and thus don’t get any additional funding, besides, the concept of “penetrance” is around since longer than one could care to recall…)

        Most certainly, saying that “product of gene X, if and when expressed, and if not neutralized via other genetic or environmental factors, affects the likelihood of condition Y” is more informative and accurate. It’s just that we are yet to discover any associations between diseases and non-coding sequences (AFAIK), so all that verbosity actually does, from a strictly clinical perspective, is wasting bandwidth to illustrate speaker’s superiority at all things biochemical.

        Oh, and if we intend to be even more pedantic, even the utterly nonfunctional non-coding DNA (like that 0.1% of mouse genome which was experimentally removed without ill effects for the rodent) does at least two things – it physically occupies space (which can play role in interactions with viruses) and it takes ATP and nutrients to replicate, which, across an entire organism and during an entire lifespan, is gonna amount to something.

        My second concern is more pragmatic and less pedantic, as well as being less solidly founded. Predisposition is of dubious use and may well harm patients. If people become too focused on what genes they have and don’t have, they may well forget environmental causes and risks (or alternately overreact to them). If people screen themselves for the “obesity gene” find out that they don’t have it, and as a result care less about diet, exercise, and other healthy habits, they are most likely going to suffer for it. On the flip side we have people taking it too far the other direction. On the Diane Rehm show late last year (November 3rd, 2010) Dr Arthur Caplan spoke about his encounter with a father who wanted his young daughter tested for the “breast cancer gene” so that he could force her into a prophylactic mastectomy if she had the potential.

        Methinks that your real issue is not with (somewhat) sloppy use of molbio lingo in medicine, but with the abstraction known as “risk factor”

        Genes certainly can be claimed to be risk factor, and you don’t even need to know anything about the underlying biochemistry to claim that – you just need sufficiently reliable statistics.
        And that, by the way, is pretty accurate – after all, there are very few mutations that guarantee the development of a condition, and risk factors are a concept that describes exactly such phenomena – things that increase the probability of a condition but not guarantee it.

        Yes, people will overreact to having risk factors.

        Yes, people will overreact to learning about not having them.

        But those reactions do not have anything to do with molecular biology.

        They would be exactly the same if the medical claims were made with full and explicit account of proteomic issues involved.

        Also, such reactions are not entirely irrational – there is nothing particularly irrational about Mr.Lucky indulging in more pleasant alimentary excesses if Mr.Lucky knows that he has a genotype that is associated with capacity to handle that (of course, it would be somewhat more prudent to wait till the entire molecular-biological cascade is unveiled and analyzed, so that we can be sure that some peculiar epigenetic shtick will not suddenly cut Mr.Lucky’s joy at the knee, but frankly, mere correlations are sufficient to make a moderate claim about Mr.Lucky’s comparatively lower probability of developing a disease due to his excess)

        Now fortunately no surgeon in his right mind would do so, but it serves as a graphic illustration of why diagnosing with potentials is a dangerous game. The fact that the so called “personal genomics revolution” wants to put such capability into the corner drug store is, to my mind a cause for alarm.

        I think that the father’s peculiar obsession with proactive surgery for his daughter only appears “unwholesome” because of the fact that most genes “implicated in breast cancer development” have a relatively mild effect on probability of eventual disease development.

        Let’s engage in a bit of a thought experiment here – let’s imagine that there exists a risk factor (not necessarily a gene, but something that cannot be removed at this level of technological development) that, when present, gives one a probability of developing a malignant mammary tumor of no less than 65% over first thirty years of lifetime .

        Would proactive surgical removal of the gland that is most certainly not vital, which can be emulated with very little fuss as far as primary physiological function is concerned, and the social/cosmetic function of which can be restored completely and trivially, make sense than?

        If no, how strong must a risk factor be to justify such measures, given the relatively mild surgical risks and relatively small effects not having a mammary gland would have?

        Or are you in principle opposed to interventions that are justified by anything less than utmost certainty?

        Wait till we nail down the proteomics. Wait till we have a full chain of cause and effect from genome -> transcriptome -> proteome -> phenotype rather than mere correlation between gene and phenotype. In my opinion, such uses of genomics for anything but family planning is really jumping the gun.

        True ideal determinism doesn’t even exist in computer systems (there are random variations in transistor counts in CPUs, random impurities in MOSFETs that affect thermal endurance, and random impurities and leaks in RAM, and that’s just from the top of my head), so most our claims about world are really probabilistic, just sometimes probabilities of unexpected outcome are so futile that we can safely make a claim to certainty.

        Generally, I see no problem with “diagnosing potentials” as long as people understand that we are talking about probabilities and potentials, and if someone is too stupid to understand what “increased probability” means, than it is honestly not the fault of personal genomics (okay, maybe it might, at least to a degree, be a fault of the transcriptional products of some his very own genes, but it weren’t the PG people who put those genes there, right? :-) )

        Val

        01/15/2011 at 14:57

  2. Damn, I need the edit button so bad :-(

    Val

    01/15/2011 at 15:04

  3. Most certainly, saying that “product of gene X, if and when expressed, and if not neutralized via other genetic or environmental factors, affects the likelihood of condition Y” is more informative and accurate. It’s just that we are yet to discover any associations between diseases and non-coding sequences (AFAIK), so all that verbosity actually does, from a strictly clinical perspective, is wasting bandwidth to illustrate speaker’s superiority at all things biochemical.

    No, what that verbosity actually does is lay out vital routes of understanding disease that both affect risk factors and guide therapy. A couple of years back, I had the opportunity to speak with Dr. Betty Pace on her research regarding novel treatments for sickle-cell disease and I believe it might be helpful to look at the sort of thing she and her lab teams do. Sickle-cell disease has long been considered one of those “classic Mendelian single phenotype genetic disorders” that I just finished asserting didn’t exist. And here is why I say that:

    If we were to use your schema, we would do genomic analysis and say “Oh, look there, you are homozygous for HbS. That means you most likely will have sickle cell this is the likely progression of the disease.” And we would be right. There is a probability, but that is the limit of our ability with genomics alone. But this isn’t what clinicians and researchers actually do. They do actual blood draws and bone marrow aspirations. They look at the determinants of phenotype directly. Why? Precisely because we can and do actually say “You are producing sickle haemoglobin, this is because your HbS gene is active, and if not neutralised via gene therapy or the gene products of the HbF gene will certainly lead to sickle-cell disease. If it is neutralised by the presence of foetal haemoglobin (which depends on the level of expression of the HbF gene) or through gene therapy then it will certainly not. If you are producing the gene product of HbC then the disease will certainly assume the Hb SC disease phenotype. If you have a beta thalassemia mutation then the disease will certainly assume the haemoglobin S/thalassemia phenotype.” All of these factors can be determined by taking the genomic data as a base and investigating the phenotype with observational and proteomic methods. It is only by looking past the simple gene = phenotype paradigm that teams like Dr. Pace’s have opened up paths for both plotting disease course and providing cures.

    Why would you use meteorology to determine whether it is raining when you can open the window and take a sample of the liquid falling from the sky for analysis? Why would you rely on genomics and risk factors alone when you can take blood and examine the structure and composition of the haemoglobin directly? Let’s say you use genetic analysis and diagnose someone with sickle cell, but an environmental factor has induced the reactivation of their foetal haemoglobin (note: even if the gene had not been re-activated it would still be there and look identical on purely genomic studies). He never gets it. You can run genetic test after test after test and it will always tell you: HbS! Sickle-cell disease! And it will be wrong.

    There is a black box of nigh infinite complexity between the genome and the proteome. It is currently impossible to accurately predict one from the other. This is why it is so vital to know both through their independent techniques and technologies.

    Methinks that your real issue is not with (somewhat) sloppy use of molbio lingo in medicine, but with the abstraction known as “risk factor”

    I have two issues with risk factor.

    (1) As expressed above, in a growing number of cases we do not have to rely on statistics. We can assay fact directly. This is a new capability, that’s why proteomics is the breakthrough that it is. To be clear, we are no longer talking about predispositions and such not, but rather are gaining the capability to assay the molecular machinery of the disease itself. We have the ability to cast out a net and draw in the proteome of a disease state versus a standard state and the difference between those two, that Δstate is the disease.

    (2) That is not how the media has been portraying genetics & genomics. People do not understand that we are talking about probabilities and potentials. That is not what they are given in their news or fiction, and the recent scientific literacy polls make it pretty clear that they are not educating themselves. In America for instance the majority doesn’t even know what DNA is, how do you expect them to gain a functional understanding of what their genome means? A quick google news search for “gene” tosses up three articles about genes on the first page:
    -an absurd simplification of the genetics for thalassemia (which fails to mention that thalassemia results from numerous different mutations of numerous different genes and just declares people with thalassemia have “the thalassemia gene”)
    -a Christian group excited about a British study that claims to have found a “believer gene” and discussing how they can spread their faith through breeding (…moving on).
    -and my favourite “Gene Found Responsible for Brain Cell Destruction in Alzheimer’s Disease” (not only perpetuates the myth that genes have activity on their own, but completely fails to bring up that there are multiple theories on the etiology of Alzheimer’s, also fails to even name the gene or provide any information on a putative mechanism).

    And that’s just the first page. Not only do these articles blindly perpetuate the myth of certainty vs. risk factor, only one of them links to supplemental information (Wikipedia on genes), and only one of them actually cites its source as a journal article and gives the author and journal title. So, people vastly undereducated, news media not helping, people not educating themselves, news media not supplementing their watered down message with references = not good.

    Remember, as I said in the initial post, the failed promise of genomics is not a promise genomics itself made, but rather a promise that the media made for it, and that society will expect it to deliver on. Genomics is good. I am making it one of my topics of study this semester. It is just important that we try not to endow it with power that it doesn’t have.

    Or are you in principle opposed to interventions that are justified by anything less than utmost certainty?

    I do realise that I am not addressing your hypothetical in depth, I have already gone on way too long in this comment. However, to get to the core of the matter: as I have already suggester earlier, I am in principle opposed to interventions justified by any less than the utmost possible certainty. Which is limited by our technology, technique, and intelligence. So no, I am not holding out for 99.99%, but if we could get it that would sure be nice. But I won’t say much beyond that. I am not up to the philosophical exercise of ‘pin the percentage point on the hypothetical’ just now.

    I will re-iterate that I do think genetic risk analysis is appropriate and even welcome in family planning. I myself have decided not to have kids based on genetic considerations. The dividing line here is that playing probability games with possible people is much more ethically consequence-less than doing so with actual ones.

    Damn, I need the edit button so bad :-(

    Hmmm…I am not sure I can turn that on for you, but I will certainly check.

    EDIT: As far as I can tell, no. There isn’t a way for me to enable that. Sorry.

    Caudoviral

    01/15/2011 at 18:38

  4. Ah yeah, blockquotes.
    Should feel better.

    No, what that verbosity actually does is lay out vital routes of understanding disease that both affect risk factors and guide therapy. A couple of years back, I had the opportunity to speak with Dr. Betty Pace on her research regarding novel treatments for sickle-cell disease and I believe it might be helpful to look at the sort of thing she and her lab teams do. Sickle-cell disease has long been considered one of those “classic Mendelian single phenotype genetic disorders” that I just finished asserting didn’t exist. And here is why I say that:

    If we were to use your schema, we would do genomic analysis and say “Oh, look there, you are homozygous for HbS. That means you most likely will have sickle cell this is the likely progression of the disease.” And we would be right. There is a probability, but that is the limit of our ability with genomics alone. But this isn’t what clinicians and researchers actually do. They do actual blood draws and bone marrow aspirations.

    But you don’t loose that knowledge just because you use a somewhat imperfect (but convenient) turn of phrase.

    I suspect we might be having a mite of misunderstanding here.

    See, my claim is not “genomics is enough for all our needs to come” (Why would one limit oneself so?)
    My claim is “using turns of phrase that are less than perfectly biochemically accurate does not diminish a professional’s capacity for understanding the complexities involved”.

    Much like when people say “app X BSODed my PC”, they are glossing over a lot of details, but as far as human communication goes it is usually enough (and a professional most certainly understands that there are numerous complexities involved there, like, for one, as far as immediate cause goes, it is not the misbehaving application that brings up the blue screen, but the OS’s error handling functions)

    It’s a little bit like the (in?)famous saying about guns that don’t kill people (with proteome being the bullet in this lame analogy ;) )

    Why would you use meteorology to determine whether it is raining when you can open the window and take a sample of the liquid falling from the sky for analysis?

    Well, that wasn’t what I intended to convey (see above).

    Also, whether or not to rely on genetic tests actually depends on a lot of circumstances. For one, screening is far easier to implement with measly genetic tests, so you need to only use the more complex (and sometimes more invasive) procedures only on those who have a significant likelihood of needing them. But then again, my only point originally was that verbose pedantic phrase building does not directly affect a professional’s understanding (and laypeople have rather poor understanding of the issues anyways)

    There is a black box of nigh infinite complexity between the genome and the proteome. It is currently impossible to accurately predict one from the other. This is why it is so vital to know both through their independent techniques and technologies.

    Well, it’s not like anyone is proposing to stick with only one branch of research or something, methinks?

    That is not how the media has been portraying genetics & genomics. People do not understand that we are talking about probabilities and potentials. That is not what they are given in their news or fiction, and the recent scientific literacy polls make it pretty clear that they are not educating themselves.

    Most people (even majority of programmers, I would endeavor to say) have less than perfect idea of how personal computers actually work, let alone pay attention to immense complexity of those systems carefully concealed under layers upon layers of programming (“high” languages, virtual machines) and functional (“just grab it and drag it, gramps!”) abstractions.
    Not to mention the peculiar myth of “perfect determinism” of modern real-world computers (bollocks! Demonstrably so!)

    Yes, it would be somewhat tidier if we have explained genes to the public with something like nuclear missile metaphor (genes are little bit like people who order the launch) instead of just saying “X gene does Y”, but if the majority of public isn’t even sure what DNA is, that would be somewhat of a wasted effort, no?

    -and my favourite “Gene Found Responsible for Brain Cell Destruction in Alzheimer’s Disease” (not only perpetuates the myth that genes have activity on their own, but completely fails to bring up that there are multiple theories on the etiology of Alzheimer’s, also fails to even name the gene or provide any information on a putative mechanism).

    Well, again, IMHO “genes having action on their own” is a linguistic convenience approximation. Much like “Stalin killed millions of people” is a linguistic convenience approximation (Stalin most certainly didn’t have a killing action of his own. His activity was that of writing orders and giving speeches).
    And the article basically aims to inform people who aren’t certain what DNA is that scientists have discovered some “gene” that seems to have something to do with Alzheimer’s, which is good and will allow scientists to invent a way of doing something about Alzheimer’s some time down the line. That is more than enough for an average non-bioscience minded person.

    Yes, that person might get some odd “gene causes Alzheimer’s” idea. Being more accurate or verbose would not helped him in all likelihood (maybe bored him, though), because he doesn’t care about biology and medical science that much.

    And that’s just the first page. Not only do these articles blindly perpetuate the myth of certainty vs. risk factor, only one of them links to supplemental information (Wikipedia on genes), and only one of them actually cites its source as a journal article and gives the author and journal title.

    “popular science” articles not giving sources are a blight, here I agree most utterly.

    Remember, as I said in the initial post, the failed promise of genomics is not a promise genomics itself made, but rather a promise that the media made for it, and that society will expect it to deliver on.

    Methinks you are a bit exaggerating/dramatizing here.

    “society at large” (much like your average pulp scifi) doesn’t “go” into distinctions between genomics, proteomics, prophylactics and therapeutic applications.
    The idea that (by definition) it will not be “genomics” that will be dealing with the issue of what to do about people with a pesky high-risk gene is just a bit too fine for the mass media and for people without life-sciences interest.

    They just lump it all into one giant ball of “medical biology/medical genetics/(my favorite) high-tech medicine” because it is not like they can tell the difference, so they don’t expect “specifically genomics” to “pay up”, that would be to fine a target.

    They expect this giant ball of “high tech medicine” to pay up. Eventually.

    As long as “pills happen”, they’re happy ;-)

    Which, methinks, isn’t that bad.

    The dividing line here is that playing probability games with possible people is much more ethically consequence-less than doing so with actual ones.

    Hmmmmmmmmm….
    Asking person you care about to quite smoking is a probability game (smoking does not guarantee cancer or any other disease)

    ;-)

    Val

    01/16/2011 at 17:50

    • It’s late here, but I wanted to get in a brief reply before I head to sleep. I think I have a much better idea of what you are saying now. I agree that we have been misunderstanding each other. What this boils down to, I think, is that we disagree about acceptable levels of ignorance in society.

      I am just reluctant to, as a for instance, let patients off the hook re: things like so called “informed consent”. And maybe we should just do away with that pretence. I mean, if the patient was capable of understanding the medicine fully, why would they need the doctor? But as long as they want to play this game of having a choice and making the decisions, then I feel the Med/Sci community has every right to expect them to shape up and actually inform themselves properly.

      Perhaps this is a uniquely American issue, but my observation has been that it seems a lot of people here want the freedom to make decisions without the burden of actually having to understand them. I just think it should be a package deal: either make your own decisions and be forced to understand it, or give up the right to make the decision because you couldn’t be bothered to educate yourself. One or the other leads to bad decisions. Take for instance the whole antibiotic issue. People go to doctors begging antibiotics for viral infections. They don’t want to actually know how antibiotics work or the difference between a bacteria and a virus, they just want a pill to make everything better. Doctors cave just to get the patients off their backs. In the end, not only is medicine wasted, but you potentially have a paradigm that is contributing to the resistant bacteria crisis (which notably, is not nearly as much of a crisis as some alarmists will tell you, but the point still holds). If nothing else it is sorely grating, at least in my opinion.

      And I am not saying that we shouldn’t play probability games with actual people, just that the stakes are higher.

      Thanks though, I think I have a better idea of where you are coming from, and as long as we are solid on the facts behind the science I won’t hound you about differences in opinion on society ^_^

      Re: Sourcing. Yeah, I really need to make sure I source this blog a little better. I was biting my tongue about how non-sourced my own post was today (the whole thing was written very spur of the moment). I used to have this brilliant book filled with collected journal articles on telomeres ranging from the original publications in the 70s to present day, and I tore my bookshelves apart looking for it today. Wonder if I accidentally sold it or lost it in a move…

      Also I suck at brevity.

      Caudoviral

      01/18/2011 at 02:17


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