Scientists are redesigning bacteria like these to “speak” a new language.

All living things pretty much use the same language to read their genes. That is about to change.

Scientists in Boston are close to teaching a strain of bacteria a new dialect of the genetic code. In combination with some work done by a different group in 2010, we are now getting to the point where we can actually think about (re)designing life. Which is a big step from what we have been able to do up until now.

The genetic engineering we have done in the past has been pretty crude. We have mostly added pre-existing genes to cells to give the cells new properties or to have the cells make something for us.

So we add a human gene to bacteria so they will make insulin for us. Or we add a gene from bacteria to a plant to make the plant resistant to an herbicide like Round Up. Or we even add two genes to cause rice to make vitamin A like in golden rice.

Now we aren’t always this unsophisticated. We have managed to do some pretty elegant things with genes in mice. There we have tinkered with mouse genes to slightly change how they work or to control how they are expressed.

But these new experiments are different. This is changing the language of life so we can make a living thing do things nothing living has yet been able to do. Maybe this is even the start of intelligent design…

A big reason this is all possible is because nature has given us a very simple template to work with. Not only does the genetic code have just four letters and 64, three letter words, but many of its words also have the same meaning. It is this last point that has allowed researchers to futz with the code.

The researchers plan to teach bacteria a new language by co-opting one of the words in the genetic code and giving it a new meaning. There are two things scientists need to do to make this happen.

The first is to replace all instances of one word in the bacteria’s genes with an equivalent word. Now the bacteria’s genes all still code for all the same things but a word has been freed up so it can be given a new meaning.

The second step is to redefine the replaced word. This will probably be done by mutating the cell’s reading machinery using some pretty well established genetic techniques.

Church’s group has nearly finished the first step. They managed to create four strains of bacteria each with ¼ of all 314 instances of TAG changed to TAA. They are now in the process of combining these four strains in such a way to generate a single strain with no functional TAG’s. After this first step is done (which should be soon), this group of researchers will be ready to teach these bacteria a new language.

An easy first thing they can do is to change the definition of the TAG so it means the same thing as one of the other words. So the TAG will no longer mean STOP but instead will mean Met or Lys or some other amino acid. (The genetic words or codons really just tell a cell which amino acid to put where in a protein.)

Done correctly, this would probably make the bacteria immune to viral infection.* Which would be a boon for the biotech industry as it loses millions of dollars every year because of infected bacterial strains.

This is pretty pedestrian stuff though. The cool thing will be when they redefine TAG as a word that isn’t already in the genetic code. Then we’ll be able to easily create different proteins with properties useful as medicines, industrial enzymes or who knows what else. At least that is the hope.

And this is just one word. There are another 30-40 codons that may be able to be freed up and given new meanings as well.

We are stepping into a whole new area of research. We are retraining life to do what we want. Let’s hope we know what we’re doing…

*This is because viruses use a cell’s machinery to read its own genes. If the machinery changes, the virus will misread its own genes and die.

Scientists are finally unraveling enough of the mystery of
human DNA to help individual patients.

In the last few months, a couple of stories have come out that show the promise of the upcoming genetic revolution. In each case, doctors found a patient’s best treatment by looking at every last letter of that patient’s DNA.

In the first case, a young boy had all the hallmarks of an immune problem but there was no conclusive diagnosis. Without knowing for sure what was wrong, doctors weren’t comfortable treating the boy with a risky bone marrow transplant.

Then scientists sequenced the boy’s DNA. Lo and behold there was a never-before-seen mutation in a known gene. This nailed down the diagnosis of a potentially life-threatening form of irritable bowel disease (IBD).

The doctors went ahead with the bone marrow transplant. The boy not only survived the treatment, but his symptoms cleared up as well. He is now essentially cured because he had his DNA sequenced.

The second case involves a set of boy-girl twins. They suffer from a movement disorder called dopamine-responsive dystonia (DRD).

Patients with DRD are usually treated with L-dopa. This can often clear up most symptoms but didn’t seem to help these twins as much. In particular, the twin sister still suffered severe enough symptoms to greatly diminish her quality of life.

Scientists sequenced the twins’ DNA and found out that they had a kind of DRD that responds best to both L-dopa and a medicine called 5-HTP. Once they both received this new treatment, their symptoms improved dramatically.

For example, the girl used to suffer from something called layngospasms that usually ended in vomiting. With the new treatment, this went away. An obvious improvement to her life!

Assuming prices keep dropping for sequencing and Congress keeps allocating money for basic research, there may come a day in the not too distant future when many more patients like these will be helped. People will have better lives because doctors can figure out what is wrong by looking at their DNA. As long as doctors have the tools they need to help patients that is.

Right now the information is so scattered and so specialized that most doctors can’t help without a scientist’s intervention. This greatly limits the number of patients who can be helped.

Getting this whole process streamlined enough so that more than just the wealthy, connected, or lucky can benefit won’t be easy. We need to generate lots more data. But we also need to collect and organize the data so doctors can take a patient’s DNA data and translate it into the right treatment without the help of a genetic scientist.

This last part is not exciting work but is absolutely necessary if the promise of the genomic revolution is to be fully realized. Here’s hoping someone funds something like this.

Great story about DRD and how L-dopa can help.

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Just because a trait is dominant does not mean it is common.
Each color represents different levels of light eyes.
Blue=80%+, teal=50-79%, olive=20-49%, brown=1-19%,
black=none.
Image courtesy of Dark Tichondrias

One of the first things we’re taught in genetics is that some traits are dominant and others are recessive. And that the dominant traits trump the recessive ones.

So brown eyes trump blue eyes. And red hair is always trumped by other hair colors. And so on.

From this, people often jump to the conclusion that the dominant trait is also the most common one. This isn’t always the case and there is no reason it should be.

Whether or not a trait is common has to do with how many copies of that gene version (or allele) are in the population. It has little or nothing to do with whether the trait is dominant or recessive.

Let’s take eye color as an example. The decision on whether to have brown eyes or not is pretty much controlled by a single gene, OCA2.

We can think of OCA2 as having two versions, brown and not-brown. The brown allele of OCA2 is dominant over the not-brown allele.

Nearly everyone in most of Africa has brown eyes. This isn’t because brown eyes are dominant over blue and green. Instead, it is because there are mostly brown alleles of OCA2 in the African population.

Northern Europe is a different story. In some parts of the continent, over 80% of the population has lighter colored eyes. Here the not-brown allele is more common even though it is recessive.

Now this allele isn’t exclusive, there are still brown-eyed folks in northern Europe. So why don’t their brown eyes dominate over time? Because in populations, dominant isn’t dominant over other people’s recessive gene versions. Your brown eyes can’t affect my kids’ eye color unless we get married.

Let’s do a thought experiment to make this clearer. To simplify things we’ll call brown eyes B and not-brown eyes b.

Without some sort of outside pressure,
the ratio of blue to brown eyes stays the same.Remember, you will have brown eyes if you are BB or Bb and blue or green if you are bb. This is because brown (B) is dominant over blue and green (b).

Imagine we start out with eleven bb people and one Bb person. The Bb person has 4 kids with one of the bb folks and each bb couple also has 4 kids.

Using regular old Mendelian genetics, we'll have 20 bb people from our 5 bb couples and 2 Bb and 2 bb from our mixed couple. This is 2 people with brown eyes and 22 people with blue or green. The same ratio as we started with. Brown did not become more common.

Now these folks all pair up randomly and have 4 kids each. Since we aren't going to allow incest, the Bb folks will find a bb for a mate. If they have 4 kids each, then we have 44 bb and 4 Bb. Again the same eleven blue to one brown ratio. Whether an allele is dominant or not does not affect how common a trait is.

Now of course traits can become more common over time. The changes just don’t have anything to do with whether the trait is dominant or not.

If brown eyes gave an advantage, then it would start to become more common. Brown eyes would also become more common if a bunch of Africans moved in or many of the blue-eyed people were killed for some reason (witch burning?). And there are other ways too of getting more brown eyes in Europe. Or more blue eyes in Africa (see South Africa for example).

Dominant does not mean common. Which in some ways is a good thing considering diseases like Huntington’s disease that are dominant.

Why some gene versions are dominant and some are recessive.

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As I have blogged about before, a big part of sexual preference is biological. Research shows that some people are hardwired to prefer the same sex. This is true in animals as well.

What scientists haven’t had much luck at yet is finding out why this is. There have been studies that have implicated the X chromosome (although not convincingly). And others that have pointed to brain structure. But none of these studies really gets at what is going on in these folks’ brains that makes them prefer relationships with the same sex.

A new study out suggests that, at least in mice, the neurotransmitter serotonin may play a big role. Scientists created a strain of mice that lacked most of a certain kind of serotonin receptors in the brain (central serotonin receptors). These mice were healthy and happy. And the males were not at all fussy about whom they hooked up with.

When scientists put wild type* male mice in a cage with other males, they mostly ignored the other mice. The male mice lacking their central serotonin receptors reacted differently. They got busy with the male mice almost every time.

These mice aren’t homosexual though. Given a choice of a male or female, they didn’t really care; they went after both at about the same rate. The genetically altered mice were more bisexual than homosexual.

The researchers did lots of other experiments as well that showed that these mice were not oversexed or lacking anything in particular. They just liked the boys as much as the girls.

What this study tells us is that in mice, serotonin plays a big role in sexual preference through these particular brain neurons. What it doesn’t tell us is if the same thing is true in people. After all, picking a mate is very different in mice as compared to people.

But there are hints that serotonin works differently in the brains of bisexual and homosexual men. For example, certain selective serotonin reuptake inhibitors (or SSRIs) have different effects in bisexual and homosexual men compared to heterosexual men. Still, this isn’t yet enough to finger serotonin use as the main driver of sexual preference in people.

What it does do though is provide scientists some direction for their research. Instead of wading through all 20,000+ genes, they can start out focusing on those that deal with serotonin. This will greatly simplify the research and if serotonin does play a role, then scientists will find the genetic variations involved sooner rather than later.

And frankly, given the slow progress thus far, focusing on serotonin genes won’t set the field back too far. It is probably worth taking the research in this direction.

* Wild type just means a mouse (or any living thing) that hasn’t been tampered with. In this case, it is a run of the mill lab mouse.

A more in depth look at the story from blogger Ed Yong at Not Exactly Rocket Science.

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The gene CMAH is needed to induce human-like diabetes in mice. Image courtesy of AlicePopkorn.

New research suggests that rodents and other mammals might not be ideal for studying type 2 diabetes because of a gene that was deleted from the human genome millions of years ago.

Virtually all mammals produce specific sugar molecules that aid cells in interacting with their environment. That is, all except humans. Around 2 to 3 million years ago humans lost CMAH, a gene that codes for an enzyme that produces the sugar Neu5Gc.

To test the role of this gene, researches compared two sets of mice. One group had a normal CMAH function and Neu5Gc production, the other group did not—just like humans. Both groups of mice were fed a diet that normally induces obesity and insulin resistance (metabolic syndrome), and both groups experienced these symptoms. However, only the mice missing the CMAH gene had lost the ability to produce insulin in the pancreas.

These findings suggest that while normal mice can exhibit some of the symptoms of type 2 diabetes in the lab, they do not mimic the full effects of metabolic syndrome experienced by humans exposed to a similar diet.

Future diabetes research may be better served using mice with a genetic background more similar to humans and missing the CMAH gene.

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This redwood, in Henry Cowell Redwoods State Park near Santa Cruz, might be genetically identical to some of its neighbors. Photo: kqedquest.

QUEST has an inordinate fondness for albino redwoods. It all started with the Science on the SPOT video Albino Redwoods, Ghosts of the Forest. Then there was a radio story, and a few blog posts. And last week QUEST revisited the research in two new Science on the SPOT videos about the ghosts of the forest. The video Revisiting Albino Redwoods, Cracking the Code focuses on QUEST blogger Barry Star and Stanford professor Ghia Euskirchen’s research on how the albinos are genetically different from “normal” coast redwoods. In Revisiting Albino Redwoods, Biological Mystery, Santa Cruz Professor Jarmila Pitterman wonders how albino redwoods’ total lack of chlorophyll affects their physiology and ecology. After producing all these videos, QUEST Producer Chris Bauer still had questions.

Chris saw three albino redwoods, arranged in a straight line, a short distance from one another. He wondered if these three redwoods, yards apart, might be genetically identical. Maybe they sprung from the same individual. To understand how this is even possible, you need to know about the numerous ways that redwoods can reproduce—some of which involve cloning themselves.

New redwood trees can come about in four ways: through seeds, cuttings, stump sprouts, and root sprouts.

QUEST on KQED Public Media.

Like all plants, redwoods can grow from seeds. Redwood seeds come from those tiny, inch-long redwood cones that fall from the branches in autumn. Each cone contains one to two dozen tiny seeds. These seeds were fertilized with redwood pollen; they are mix of genetic material from the parent that made the seed and the parent that made the pollen. However, redwood seeds have a notoriously low germination rate. Hardly any of them will grow into a plant. Which brings us to the next method of redwood tree generation: cuttings.

Redwood trees that you buy from a nursery probably began as cuttings—branches that were cut from a tree. To make a good redwood cutting, horticulturists will cut a branch from a young tree, or sapling, because cuttings from young trees tend to survive better. They treat the cutting with hormones to encourage growth, and plant the cutting in a special blend of soils. After a few months, about 25-35% of the cuttings have formed roots; the others do not survive. Once the cuttings have established, they can grow quite quickly—up to 7 feet in height in a single growing season. Regeneration from existing branches doesn’t just happen in the nursery—it happens in nature too. When a branch falls off a redwood tree, say in a storm, the branch can come in contact with the soil and develop roots. These provide the branch with nutrients and water, and before long the branch has grown into a tree. Trees grown from cuttings or from branches are genetically identical of the tree that donated the branch. (For the same reason, California’s vineyards are very low in genetic diversity; see this article in the New York Times.)

Stump sprouts on a coast redwood. Photo: kqedquest.

Many a majestic redwood tree began as a stump sprout. Stump sprouts are tiny growths from the base of existing trees. They can grow out of a healthy tree, or a tree that has been logged or damaged by fire. Redwoods have extensive underground root systems, which are impervious to trifling things like lumberjacks’ axes and fire. Trees that grow from stumps grow quickly and have a good chance of success, because the trees are automatically connected to a large root system. Multiple stump sprouts from a single trunk form what is called a fairy ring: a ring of trees, with a circular clearing in the middle, because the original tree breaks down. Stump sprouts are generally genetic clones of the original tree. However, the albino redwoods are stump sprouts with a mutation (or two, or three…). The genomic research happening Stanford will hopefully shed some light on how this mutation happens.

A fairy ring. The ring of trees has sprouted from the moss-covered trunk in the middle. Photo: Swiv.

Redwoods don’t just sprout from stumps; they can also sprout new growth from their roots. Redwood roots extend horizontally under the soil. Many redwoods live in flood-prone ecosystems, on the banks of rivers. When redwood forests become flooded, sediment piles up on the surface of the soil, burying the roots a bit deeper than they were before. Redwoods will grow another set of horizontal roots, a little closer to the surface. By digging deep into the ground and counting the horizontal layers of roots, people can tell how many floods a redwood has endured. When new growth sprouts from the surface roots, the original tree soon has a neighbor that is basically an identical twin. This is what Chris thinks is going on with the three albino redwoods, all in a row.

Hopefully Chris can test his hypothesis in a year or two, when the redwood genome is sequenced and we know what mutation (or mutations) cause albinism. Are the three neighboring albino redwoods mutants that sprung from genetically identical trees? Maybe that tree’s genotype is just a little different from that of an albino—and the mutation that causes albinism is very likely to occur. Or maybe the three albinos are a series of chlorophyll-free coincidences. We’ll have to wait patiently for the genome data. But, for a coast redwood that can live for 2,000 years, the wait won’t be long at all.

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Universal genetic testing may cause the break up of some families.

What became clear to me at a recent meeting I attended is that most everyone is going to have his or her DNA read in the near future. Another thing that became obvious is that scientists aren’t doing enough thinking about what impact this will have on society.

Here’s a seemingly trivial example. In most scenarios I have seen, children‘s DNA is read as soon as they are born. This will definitely have some huge health benefits especially as we learn more and more about how our DNA works and what it means. But this will also have some big unintended consequences too.

Parents will know both their kids’ and their own DNA. From that it will be pretty easy for most anyone to piece together whether or not a child is related to them. In other words, if everyone knows their family’s DNA, then every family will automatically undergo a paternity test. And if some statistics I have seen are true, then a whole lot of people are in for a nasty surprise.

The most recent numbers that I have seen are that something like 3-4% of fathers are unknowingly raising kids who are not their own*. Universal DNA testing will undoubtedly spill the beans in these cases causing many families to break apart.

This “misattributed paternity” is not an unknown problem today…genetic counselors deal with this sort of thing in their practice on occasion. Genetic counselors struggle with what to do with this collateral information and have the option of not revealing it to their patients. Withholding this information won’t be an option in a future where families know their DNA.

So in the not too distant future, up to one million dads in America will find out that little Susie or Jimmy isn’t theirs. Some will be able to deal with this but it will tear many families apart. This will obviously have a huge impact on society.

There will be more subtle effects too. Both men and women will quickly figure out that paternity won’t ever be a secret any more. If you have an affair and have a child, you will be found out.

Will this knowledge work as a sort of moral police, preventing people from having affairs? (Probably not.) Will people be more careful about contraception? Will abortions increase to cover up affairs?

As you can see, just knowing this little bit about our DNA will have profound effects on society. And I haven’t even talked about how medical care and the insurance industry might be restructured. Or how it will affect who you decide to have kids with. Or…

* This is the latest estimate I could find which is much less than the 10-30% number that med school students used to be taught. We won’t have an accurate number until more genetic testing of families is done.

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If you’re an adult and you can drink milk, then you are a mutant. Image courtesy of Collectie Willem van de Poll, via Nationaal Archief.

Over the last couple of weeks it has become obvious that my daughter is lactose intolerant. In most of the world, that wouldn't be a big deal. One study I saw claimed that at least 3 in 4 adults worldwide are lactose intolerant. And in some countries (like Thailand), over 99% of adults can’t drink milk as an adult.

This makes sense since lactose intolerance is the norm for mammals. Humans are one of the few animals where a sizable minority of adults are lactose tolerant. Scientists have noted this and have renamed the Eurocentric "lactose intolerance," lactase persistence.

Sigh, scientists never make things easy do they? Why not call it lactose tolerance so everyone understands?

They named it lactase persistence because of how lactose is digested in our bodies. Lactose is digested by the enzyme lactase and lactase persists longer in people that are lactose tolerant. Hence, lactase persistence.

Our cells make lactase by reading the lactase gene. In most mammals, this gene gets shut off in adulthood.

The programming for turning the gene off later in life is found in the DNA around the lactase gene. People with lactase persistence have a DNA change that messes with the programming. Now the lactase gene stays on so these folks can keep drinking milk and eating ice cream.

The “on” version is actually dominant over the normal one. In other words, lactose intolerant people need to get the normal lactase gene from both parents. So my wife and I are at least carriers—we can drink milk but carry one normal lactase gene.

I actually know that I am more than a carrier. I have two normal lactase genes even though I can still drink milk. This means that my gene hasn’t shut off yet but that it probably will at some point. Scientists don’t yet know why it shuts off early in some people like my daughter and later for others like me.

So how did some people end up able to drink milk as adults? Mutations and natural selection of course.

Most likely there is always a low level of lactase persistence in any mammalian population. Mutations (or new DNA changes) can and do happen and changes like this in the lactase gene are bound to be pretty neutral. In most situations there won’t be any advantage or disadvantage to having it and so it will stay rare.

This can all change if adults suddenly have to start drinking milk as happened in certain cultures in Europe and Africa. In these places, the few people with the right lactase mutation had an advantage and so did better than the lactose intolerant. Eventually, most people in these places could drink milk as an adult.

What is really interesting to me is the fact that European and African milk drinkers don’t share the same DNA difference. Each population had a distinct lactase mutation that became the norm. This is called convergent evolution—two populations arrive at a similar trait with different DNA changes.

However it happened, my daughter is now adjusting nicely to the milk-soaked culture she finds herself in. There are pills that let her drink milk as well as lactase-treated milk and ice cream. This means she can still have her favorite dessert in the world, chocolate ice cream.

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A few minor tweaks to genetic testing companies' websites could make their offerings more transparent to the public and the FDA.

The last couple of blogs I have been talking about direct to consumer (DTC) genetic tests. I talked about how the FDA has begun looking into them and why the FDA isn’t happy with what it sees.

In this blog I thought I'd propose a couple of different ways these DTC companies can present their data that might mollify the FDA. These changes will also let consumers know what they're really getting and whether they want it at all.

Before starting, I want to say that I will focus on 23andMe, a Bay Area company. I'm not picking on them. They are just the company I know best and one of the few that is good enough to survive the FDA's scrutiny. I also know a lot about them because I have taken their test.

23andMe has a very good website. They present complicated data in an understandable and easily searchable way. Their major weakness, though, is that they implicitly promise more than they can actually deliver. In essence, even though they are pretty good about disclaimers, they aren't good enough.

One of the first things the company should probably do is to reorganize the first page that potential customers see. They need to make sure that potential customers have a good idea about what they can and can't get from these sorts of genetic tests.

For example, right now a prominent feature is a box that lets the viewer search for the diseases 23andMe “covers” along with a list of popular topics. People may come away thinking 23andMe has useful tests for most of the diseases listed. They don't.

They have some useful tests for a few, rare genetic diseases. But the bulk of their tests are not at all useful yet in figuring out someone’s risk of getting a certain disease. What they have for the more complicated diseases is a way for people to compare their DNA to various studies in the scientific literature.

Maybe a study was done that found a DNA difference involved in diabetes. Customers can see whether or not they have this difference too but this tells them nothing about their risk for diabetes. It gives just one piece of a giant puzzle. They are not getting any meaningful results that can predict their risk for diabetes. This box should probably be heavily modified or even eliminated.

In fact, the website really should be organized into different sections that are labeled by how medically useful they are to the customer rather than by how strong the DNA study was scientifically. Maybe they could split their tests into three sections.

The first would be carrier testing. These tests can tell you if you have a hidden genetic disease that you could pass down to your child if your partner has it as well. This would get high marks for reliability, scientific validity, and usefulness.

The next section would be more fun related stuff. This would have ancestry and some of the traits testing. It would be able to tell you what your earwax is like, where your mother's, mother's, mother's, etc. mother came from, the odds that your child might have blue eyes, etc.

The final section would include the bulk of what is tested. These are the tests that compare your results to results in the scientific literature for complex diseases. Many of these tests would score high in scientific validity but get no points for usefulness. As I said before, most if not all of these tests will not give you an accurate risk assessment for the diseases they look at. Period.

There isn’t any reason these results shouldn’t be included, though. Maybe people enjoy seeing the results or want to use them to watch progress in the field or whatever. But the companies need to say upfront that these tests are not that useful for determining risk. This needs to be obvious enough that someone wouldn't buy the product just for that test.

As a last point, 23andMe (and all genetic testing companies) need to be much more upfront about what their tests can offer based on race. The carrier tests are probably pretty good for most everyone (although they may miss any nonwhite versions of many diseases). The fun section might be pretty useful to the nonwhite world for ancestry but probably less so for traits as they have mostly been determined for people of European descent.

Most of the rest of the tests they offer that deal with more complex diseases have only been validated for white people. This needs to be explicit on their website so nonwhite people know they aren't getting as much bang for their buck. Buyer of color beware!

These kinds of changes will go a long way towards making these sites more transparent to potential customers. And they may even keep the FDA at bay.

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Could you guess what this is from one of its hairs? That’s about how predictive current genetic tests are for complex diseases like prostate cancer or heart disease.

As I talked about in my last blog, direct to consumer (DTC) genetic tests are taking a beating right now from the FDA. Part of the problem has to do with some snake oil salesmen contaminating the whole field. But part of it has to do with the data that is available right now and how it is presented.

In this blog, I’ll deal with the data itself and why the FDA has such a problem with it. Next blog I’ll try to come up with ways to still get that data to consumers without ruffling any regulatory feathers.

A big problem with some of the current tests is that people will get different results based on the company they use. For example, the FDA reported that the same man was told he had an increased risk, the usual risk and a decreased risk for prostate cancer depending on the company he used. The FDA hates this kind of stuff.

To them (and many people), these kinds of results say that these tests aren’t working correctly. And given their experience with medical testing, they’re right.

A real medical test should give consistent results. If you take a test that looks at your cholesterol levels, your heart attack risk should be the same no matter who administers the test. Or if you take a genetic test to see if you are a carrier for sickle cell anemia, then again the results should be the same no matter who does the testing.

The genetic test for prostate cancer isn’t anything like these tests because it isn’t a medical test at all. It would be kind to even call it a work in progress. It is really just some interesting information at this point.

This is because we don’t have a good handle on the genetic risks for prostate cancer risk. There are almost certainly lots of different glitches in lots of different genes involved in increasing someone’s risks for getting prostate cancer. All of these variations need to be factored into a man’s risk for prostate cancer. And we only know about a few and those few have a pretty limited impact.

To add to the problem, different companies also look at different glitches or SNPs. So one company might look at one or two SNPs and say a man has a 1.2 fold increase in getting prostate cancer. And another might look at a different two and say he has a 1.1 fold decrease in getting prostate cancer. Different results but neither is particularly meaningful in predictive sort of way.

It is a little like trying to figure out what an elephant looks like from just the tip of its tail. And comparing that result to someone using an elephant’s eye lash to figure out the same thing. Odds are you’re not going to end up with the same animal. Just like you won’t end up with the same result from these kinds of genetic tests.

So when you have one of these tests done for complicated diseases like prostate cancer, diabetes, back pain, heart disease, etc., you’re only getting one piece of genetic information when you need 10 or 100 to figure out your actual risk. You have the eyelash or the tip of the elephant’s tail instead of the whole skeleton.

Now I don’t want you to walk away thinking that I am advocating that these companies shouldn’t give customers these results. I’m not. People should have a right to this information if they want it.

What I am advocating is that these companies come up with some way to explicitly state that these kinds of results are not useful medically. They need to be careful how they present the tests they offer and how they present the results. They don’t want to inadvertently lure customers into taking a test that can’t give them what they want.

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