OK, when all is "said and done" it comes down to dollar$. Look at the topic and tell me how you think genetic testing (whole genome) will impact healthcare costs. Try to be broad thinking here.

I know that adverse effects of some drugs may be avoided and that can have an impact on healthcare costs. Let's try to put together a list of "impact factors" and how genetic testing will be positive in saving costs or negative in increasing costs.

The topic of this post was raised by a Law professor and is very thought provoking. So I was thinking about this and I am not sure that genetic information is really different. For instance, if my blood pressure was elevated, I would be at increased risk of cardiovascular, renal and other diseases, but it does not mean I will experience the diseases. If an insurer knows I have high blood pressure and have related risks, would that information be different than if I was at risk for some disease based on genetics?

Why are we, apparently, treating this so differently?

For discussion (I am withholding my opinion):

If genome testing is available to the consumer and provides some information about the potential risk of disease and drug sensitivity, then why shouldn't the physician, pharmacist, nurse and other healthcare providers utilize the information?

Not looking at the information is negligent isn't it?

For instance, people are prescribed clopidogrel as an antiplatelet drug even though the prescriber and related healthcare providers have no idea if it will work for a given patient. You can check the patient's genetics...so why not check? The pharmacist discusses the drug with the patient and explains how it works and the potential adverse effects, looks for drug interactions to see if there is a potential problem. Why not check the genetics to see if it will work for a patient?

Is there liability?

OK, the data that is available right now for me in the form of 'raw data' consists of 960,544 pieces of genetic information. These are the SNPs from the parts of my DNA that were evaluated. A list of rs (reference SNPs; see http://pgxcheck.com/?s=my-disease-risk-prostate-cancer for an explanation of what a SNP is) information.

So, based on some information in the discussions (Blog topic 'Questions Part 1)', I have copied and pasted my SNP data onto a 'thumb drive'. I can now take it with me whenever I see a healthcare provider.

Below is an example list of five SNPs from my raw data (chosen randomly from 960,544 SNPs; the number (rs) is the reference SNP and the genotype follows):

rs12210179 CT

rs2341362 CC

rs2395185 GG

rs16908853 TT

rs28391282 GG

I decided to act as if this data got into the hands of my medical insurance company. I am going to see what I can find on the Internet relative to each SNP above. Here, I am cutting out detail and 'boiling it down'. This is not a 'sophisticated search':

rs12210179 genotype CT; What I found - the rare GG genotpye is associated with an increased risk of breast cancer. OK, no problem with this SNP as I have the genotype CT.

rs2341362 genotype CC; What I found - not much on this one except that, if I have this correct, 94% of people have the CC genotype. I am in the majority for...I don't know what!

rs2395185 genotype GG; What I found - The G allele and I have two of them, imparts an increased risk of ulcerative colitits. I am 5,1 and I do not have ulcerative colitis (UC). I may get late onset UC or I may not.

rs16908853 genotype TT; What I found - less than not much!

rs28391282 genotype GG; What I found - significant increase risk of writing a blog about genetic information. Amazing! No, not much here either.

Obviously, this little test of my raw data yielded little information that would be of potential for use in a less than optimal way. However, this approach in no way resembles what would likely be done with the data. What I see as a potential approach would be to have a database with significant SNP data (the SNPs with substantiated relationship to disease risk, drug sensitivity etc.) that could be used to 'merge' data from an individual to look for the significant SNPs in the given individual.

It is the 'raw data', the SNP list that is in need of protection as discussed in an earlier post topic.

So, here is a challenge. I am going to provide three SNPs and my genotype for each. Tell me what you find! If someone posts the information before you do, confirm the previous post or add to or debate the information. Here they are:

rs7216389 CT

rs9273363 CC

rs762551 AA

and a bonus SNP: rs2153271 TT

Let me know what you find!!!

I think everyone has seen enough of the data and we have done a pretty good job at discussing it. There may be new information coming and I will share it when I get it.

Now, let us start working our way through some 'big picture' questions. I think these will stimulate more discussion. We will have some general questions, and then will move into some ethical, legal, and business questions that will expand our view on the topic of personal genome information.

So, here is question #1 (actually a couple of questions), with a 'pre-question' statement:

At the point when the cost of complete sequencing of the genome is reasonable, as compared to other medical laboratory tests, I believe that every newborn should have their genome sequenced and the information stored securely in a database that is accessible to healthcare providers.

What do you think?

What are the advantages of this approach?

What are the disadvantages of this approach?

We have a number of faculty that  will respond to your comments...so, let's hear it!

Well, I may not benefit from clopidogrel because my genetic make-up includes a less active form of the enzyme that converts clopidogrel to its active form.

Let's look at another drug, this time warfarin (Coumadin is a brand name). My results indicate that I have the 'normal' form of the metabolizing enzyme. Here the enzyme is CYP2C9 and my genotype is *1/*1. So, my designation is a 'normal' or 'extensive' metabolizer (CYP2C9*1/*1). Warfarin is NOT a prodrug as it does not have to be converted to an active form. So, I would most likely respond to a 'normal', standard dose. Below is information from the warfarin package labeling:

Daily Dose of warfarin based on genotypes for VKORC1 and CYP2C9

VKORC1                                         CYP2C9

                        *1/*1        *1/*2        *1/*3        *2/*2        *2/*3        *3/*3

GG                   5-7mg    5-7mg    3-4mg    3-4mg    3-4mg     0.5-2mg

AG                   5-7mg    3-4mg    3-4mg    3-4mg    0.5-2mg  0.5-2mg

AA                   3-4mg    3-4mg   0.5-2mg 0.5-2mg  0.5-2mg  0.5-2mg

If the table above does not look 'lined up' sorry about that. I tried to paste the table in, but was unable to do so.

For CYP2C9, the *2 and *3 forms mean there is decreased metabolism. Therefore individuals with these forms need lower doses. * 3 being the 'least active' if you will.

As it turns out, you see another influence with warfarin dosing. Here, VKORC1, which is the target of warfarin, that is, the way that warfarin works is by inhibiting VKORC1, which leads to anticoagulation when dosed correctly. So I need to provide another peice of information relative to my genetics. My results indicate that I have the AA genotype for VKORC1, meaning that it will take less warfarin to inhibit my VKORC1. Based on this information I am going to ask you to tell me what dose should I receive if I need to start taking warfarin? I will count on my anticoagulation clinic to get me in the therapeutic range, but, what dose do I start with if I am *1/*1 and AA?

A large study looked at genotyping patient for CYP2C9 and VKORC1. When this information was utilized in dosing, there was a 31% decrease in all cause hospitalization and a 28% decrease in hospitalization due to bleeding or clotting.

If I went to the physician and was diagnosed with an illness requiring warfarin therapy, I would receive standard care and likely a less than optimal warfarin dose to start with. Again, I would utilize this information and tell my physician.

Tell me, should the use of gentic information in this scenario be the standard of care? When will it be the standard of care? The same question applies to clopidogrel from the earlier post! What will make it the standard of care???

As we start to discuss "Drug Sensitivity", I need to say that this topic is the real driving force for the overall discussion of direct to consumer genetic testing. While disease risk is covered from a relative point, I believe that drug sensitivity comes from more of a ‘mechanistic’ point of view.

Let’s start with the drug known by its trade name Plavix and the generic name clopidogrel (this is the generic name, but the drug is not yet available in generic form in the United States). I will use clopidogrel as the name from here on out.

Clopidogrel is a drug that keeps platelets from being ‘sticky’ and is used in people who have certain heart diseases including people that have had placement of a ‘stent’ which is a small tube used to keep arteries open to allow blood flow. The effectiveness of clopidogrel is seen in prevention of clot formation by keeping the platelets from sticking together. A clot formation can result in a heart attack which can damage heart muscle and can be fatal.

Where does genetics come into play with clopidogrel? The drug is a ‘pro-drug’, meaning that the body has to activate the drug for it to work. The enzyme responsible for the conversion of clopidogrel to its active form is called CYP2C19. This is a name based on a system for defining this type of drug metabolizing enzyme. It is pronounced ‘SIP-2-C-19’. As it turns out, CYP2C19 activity can be varied and is a result of single DNA base changes (see the earlier post on prostate cancer risk where the DNA change is described). In this case, there are a number of different variant forms of the enzyme:

CYP2C19*1 is termed the ‘wild-type’ allele and people with these alleles are termed ‘normal’ or ‘extensive metabolizers’ (remember we get information from mom and dad, so *1/*1 is the normal or extensive metabolizer (EM)).

CYP2C19*2, CYP2C19*3, CYP2C19*4, CYP2C19*5, CYP2C19*6, CYP2C19*7, and CYP2C19*8 are termed ‘reduced function’ alleles and people with combinations of these alleles (e.g. *2/*2) are termed “poor metabolizers (PM)” in that they do not convert the pro-drug to the active form readily and do not benefit from the drug’s effects on platelets.

People that have one normal function allele and one reduced function allele (e.g. *1/*2) are considered intermediate metabolizers (IM) and convert some of the prodrug to the active form.

While more rare, there are some people that have the *17/*17 genotype and the individuals are termed 'ultra-rapid metabolizers (UM)' being extremely efficient at converting the pro-drug to the active form. An individual who is *1/*17 also readily converts the pro-drug to the active form.

So, here is what I am thinking...If I have the therapeutic need for this drug, I want to let my doctor know whether or not I am a ‘normal metabolizer’, ‘intermediate metabolizer’, ‘poor metabolizer’ or an 'ultra rapid metabolizer (which would be unusual because I am not ultra rapid at anything!) and if I am a ‘poor metabolizer’ I can look to get a different drug than clopidogrel because I will not convert the pro-drug to the active drug.

The next time you see a clopidogrel (Plavix) commercial you may see the statement ‘certain genetic factors...reduce the effects of clopidogrel (Plavix)’. Here they are talking about the ‘reduced function alleles’ and people that are intermediate or poor metabolizers.

Here are my results: CYP2C19*1/*2

Of importance here is the following information about the frequency of the metabolizer types:
Caucasian 2% - 6% PM
Asian 13% - 19% PM
African 10% - 20% PM
Overall 24% - 36% IM
Overall ~5% UM

So, I fit into the most 'frequent' group IM as a *1/*2 individual. Here, if I need the drug, I won't convert as readily the pro-drug to the active form. One solution here is to give me a bigger dose...maybe 150 mg instead of the more common 75 mg. If I was a 'PM', I would likely need a different drug.

Recently, December 2011, in the Journal of the American Medical Association, there was an article that APPARENTLY showed that identifying a patient's genetic make-up relative to CYP2C19 had no bearing on the clinical outcome with the use of clopidogrel relative to effects on the heart. The capitalizing of (APPARENTLY) was done to point out that in this study, the investigators excluded a population of patients for which there is substantial evidence that genotype is related to clopidogrel effectiveness. That population consists of patients with stent placements as noted above. So studies published, even in the most reputable journals need to be looked at very closely.

This is an issue of the mechanism of drug activation and not relative risk of disease as discussed previously. Consider this from the 'Black-Box Warning' from the Plavix (clopidogrel) label:

'Effectiveness of clopidogrel (Plavix) depends on activation to an active metabolite by the cytochrome P450 (CYP) system, principally CYP2C19.'

Your thoughts?

The implications of Alzheimer's disease (AD) are of concern, especially early onset. My anxiety has now 'peaked' as I scroll down to see my results. I was not anxious at all until I got to the actual point of looking at the results.

The APOE gene has been associated with risk of AD. There are three variants of the gene that infer different risk. These variants are determined by two single nucleotide changes (polymorphisms (SNPs)).

For me, the results indicate that for the first SNP of interest, my genotype is CC (remember one from each parent). The second SNP of interest indicates a genotype of TT.

Ok, what does this mean? The combination of SNPs is used to determine the APOE variant. For me, the C + T (in both cases, I had two Cs and two Ts) = the variant E3, so with a C and T from mom and a C and T from dad, I am an E3/E3.

As it turns out, this variant inparts 'normal' risk. While I am a bit relieved that I was not E3/E4 or E4/E4, because E4 imparts increased risk of earlier onset AD, I know that more than 50% of people with AD do not have the E4 variant. The E4 variant, again, appears to impart increase risk of early onset AD. The E2 variant may be 'protective'.

In a study of over 3400 individuals, the frequency of the different APOE variants were:

E3/E3 - 63.9%

E3/E4 - 19%

E2/E3 - 13.7%

E4/E4 - 1.7%

E2/E4 - 1.3%

E2/E2 - 0.4%

So I ask...do you want to know your risk of AD based on genetic markers (SNPs and gene variants)? If so, why? If not, why not? What are some of the ethical, legal, and social implications?

With my disease risk results, I am provided with information that is supported by different levels of data. Previously, for my prostate cancer risk (increased) and coronary heart disease (decreased), the results were supported by multiple studies that included at least 750 people in each study. With similar supporting data, I have the following results:

Increased risk:

Rheumatoid Arthritis - My risk 2.9%     Average (Ave.) risk 2.4%

Exfoliation Glaucoma; flaky material causing glaucoma (increased pressure in the eye) - My risk 2.2%    Ave. risk 0.7%

Ulcerative Colitis - My risk 1%     Ave. risk 0.8%

Scleroderma (Limited Cutaneous; a skin disease) - My risk 0.08%     Ave. risk 0.07%

Here, the average risk is low in the population and my risk, while increased is still rather low. So, how does someone interpret/evaluate this information? Should I be concerned about these risks, even though the average risk in the population is low?

Let's hear it! If these were your results, what would your evaluation be?

Based on the information from 23andMe, I am in a group of individuals (those with similar genetics relative to markers for CHD) in which 32.8 out of 100 would develop coronary heart disease, where as an overall group of similar age and ethnicity would have 46.8 out of 100 develop CHD. So in this case, my odds of developing CHD are lower. Here the odds ratio relative to CHD is 0.7 (<1 is better than >1 and a value of ~1 would mean average risk).

We are going to try something different here. Tell me how you would interpret the above information. Then I will follow up after we get some comments!

P.S. don't forget to go back once in a while and check to see some of the newer comments from the previous topics. They are very insightfeul. For instance, check out post #22 in the "Getting part of my genome tested".

With the many different people reading this blog, I thought it best to have a baseline with the discussions starting with the disease risk information. (Please note that this is generalized for folks who do not have a background with this information. Also, while the results presented below are from 23andMe, the rest of the information was taken from various sources.)

The human genome is made up of a sequence of four chemicals, called nucleotide bases and include adenine (A), guanine (G), thymine (T), and Cytosine(C). This sequence is our DNA and it is found in every cell of the body on 23 chromosomes. We get a set of chromosomes from each parent, so there are 46 chromosomes in each cell. The sequence of DNA from each parent is about three (3) billion bases long...the four chemicals in a long sequence. Based on DNA we are about 99.9% the same. Differences between individuals can be described as genetic variation. In some cases the genetic variation can be a result of a change in the sequence by one nucleotide base replacing another, such as an A replacing a G. For instance:

A sequence that is the most “common” sequence may be TCC CAG CTG GAA TCC GGT GTC

The variation may be: TCC CAG CAG GAA TCC GGT GTC, where A (adenine) replaced T (thymine).

This is called a single nucleotide change or single nucleotide polymorphism (SNP, pronounced “snip”), since one chemical replaced another. This change may result in a difference from one individual to another. We will have some examples of this over the coming weeks.

Disease Risk: The information provides information about increased risk of disease, average risk of disease and decreased risk of disease. Let’s start with increased risk of disease. According to 23andMe, I have 1.5 x the average risk of getting prostate cancer.

How was this information provided to me? Through what is called the “odds calculator”, where 26.7 men with a genetic make-up like, according to 23andMe will develop prostate cancer where as with average risk 17.8 men out of 100 will develop the disease. The 1.5 x risk value is simply 26.7 divided by 17.8.

So what is the genetic basis for this increased relative risk of getting prostate cancer? I received genetic information from my mother and father that shows, on a region on chromosome number 8 (something called band 24) from each parent, I have a certain sequence of those four chemicals mentioned above and at one specific point I have a certain chemical base (remember one from my mother and one from my father), here being G and T. We typically write this as GT and this is termed the “genotype”. People that have a T from their mother and a T from their father, with the genotype being TT have average risk for prostate cancer. However, one of my parents passed along a G, where the T would be. This is a SNP or “snip”, one chemical replacing another. It turns out that this SNP is related to an increase in the risk of prostate cancer.

How is this SNP related to increased risk of prostate cancer? This SNP (G for T on one of the number 8 chromosomes) was shown to be related to an increase risk of prostate cancer in a study of more than 2300 Caucasian males. This study is called a “Genome Wide Association Study” (GWAS...we have abbreviations for everything!)

It turns out from other studies that there are other SNPs (single base difference at other places on DNA) that have been related to increased risk for prostate cancer in middle-to-late age Caucasian males. In a study of over 3600 male Caucasians, the SNP mentioned above, along with four other SNPs (snips) and family history was related to the increased risk. So, we can say that the group of five SNPs and the family history provides the cumulative (here for discussion) risk.

Here are my genotypes for the five potential SNPs (in general terms here) making up the cumulative risk relative to the normal risk genotype:

SNP 1 (from above) – Normal risk genotype TT, my genotype GT – increased risk

SNP 2 – Normal risk genotype CC, my genotype CC – normal risk

SNP 3 – Normal risk genotypes AG or GG, my genotype AA – increased risk

SNP 4 – Normal risk genotype GT, my genotype GT – normal risk

SNP 5 – Normal risk genotype CC, my genotype CC – normal risk

Family history – unknown (I am adopted)

So, out of the five SNPs that make up the cumulative risk, I have two SNPs that are related to increased risk.

What does this mean to me. I will talk to my doctor about this and I will look into “prostate health”. What if I did not know this information? Well, I did not know this information last year when I turned 50, so I followed the American Cancer Association recommendations and talked to my physician. Am I going to get prostate cancer? I do not know, but I will be diligent in my healthcare.

Again, we have such a diverse audience reading this. I hope that the presentation of the information makes sense. I went to a great deal of work to go to this level of understanding my relative risk as presented in my data. Most individuals will look at the summary data and not look at this technical level. Again risk does not mean it will happen. The genetic-based risk must be looked at in the context of overall risk that includes diet, and the environment among other potential risk factors.

What are your thoughts?

First, I must say there is considerable information provided by 23andMe for the testing and test result interpretation. As many of the comments were related to what 23andme should provide, here are some section headings from the "Terms and Conditions", which are freely available from their website and a comment about each:

>Risks and Considerations Regarding 23andMe Services:

- Once you obtain your Genetic Information, the knowledge is irrevocable. Comment: There are some results with more substantiation than others.

- You may learn information about yourself that you do not anticipate. Comment: This is part of the intrigue.

- You should not change your health behaviors solely on the basis of information from 23andMe. Comment: I plan to use it in this way. If I have a reported increase risk for a given disease, I will try to change the other risk factors I can change.

- Genetic research is not comprehensive. Comment: This is not a sequencing of my entire genome...just bits and pieces of which some may be more important than others.

- Genetic Information you share with others could be used against your interests. Comment: Please don't! 

There is a lot of information you can get from their website (again, not an endorsement; click here). The disclaimers are there, but so is the plethora of information. It can be a lot to try and digest for the average individual. I see the questions coming to healthcare providers.

Later this week, we will start looking at the disease risk information.

I think we need to get some opinions on this comment. We will get to more results and what they mean, but it is a concern to many people that the DNA information can invoke anxiety. You will see later that there are some test results that I will talk about that certainly could be cause for anxiety...until they are put into perspective. So, here is what Mark stated:

'I would like to return to Brittany's comment.

(From Brittany: 'One could debate whether or not having genetic testing done is good for the public if as you said, some of the traits that the company says you should express are not indeed the ones that you do express? I feel that if it says "likely for some disease" that the general public may gain concern, anxiety, or depression (for example) over what their health could be, leading them to make lifestyle changes etc. that may not be necessary if they do not actually get the disease?')

The principal audience here consists in individuals who understand a considerable amount about both the test process and how to interpret the results. As a philosopher I know little about the technical details, nor how to interpret the results. So how do we deal with the fact that people who might use a service like 23andme would not have the skills to put the information into perspective? When it comes to disease and illness the most common reaction is an emotional one - I'm going to get cancer!!! As the old adage has it a little knowledge can be more dangerous that no knowledge at all. Do companies like 23andme have an obligation to educate the user's of the service about how to interpret the data?'

What are your thoughts?

As I debated getting my genome tested, here not looking at all of the sequence of my DNA, but only some of the current variations (single nucleotide polymorphisms SNPs, pronounced snips), I went in search of the direct to consumer companies and ended up looking at three (here I am not endorsing any one of them). Navigenics appeared to require the testing be done through a physician or wellness program, both of which I had access to, but neither that I wanted to bother. Certainly, and I may do this, I would like to work with both my physician and wellness program as we can all move along the learning curve. Decodeme was a second company and for me at this time, for reasons you will see later, was too expensive, so I chose a third company, 23andme.

I went online, and reviewed the procedure. Here, pick the service and pay via credit card, then wait for the kit to arrive. In about a week, I received the test sample kit and promptly read the directions. Following the directions, I provided the saliva sample, which took about five minutes of spitting into the tube to obtain the correct volume. The tube cap has a preservative that automatically mixes with the saliva when you close the cap. At this point I put the shipping cap on the tube, placed it in the provided zip-lock bio-bag and placed that into the already addressed return container.

The fact that saliva was used is key to a consumer product. I think the other two services mentioned above ask for a cheek swab. With DNA in every cell of the body I guess it really doesn't matter...I just do not see the public drawing an arterial blood sample! And, I would struggle supplying a hair sample!

Now, at this point, I hesitated as I thought do I really want to know all this. I would receive information about my physical traits, RISK OF DISEASE, "drug sensitivity", and DISEASE CARRIER STATUS. The capital letters show the information I was questioning. Well, I though "go ahead the DNA is there regardless of whether or not I know what is says"...into the mailbox it went...I could now wait for the results, which I should see in 4 to 6 weeks.

I don't know if business was slow or if the laboratory folks were just super-efficient because I got the results in three weeks...here we go!

Now some of you may be thinking let's get to the good stuff. What diseases is he at risk for, what disease does he carry to pass along...not so fast! We are going to start with the simple things, what my DNA states about my physical traits. We'll cover this over the first week or two. Take a look at "About DFK". Check the link on the menu at the left. Some questions come to mind right away: 1. I know I can taste bitter substances, my genetic make-up says otherwise. (Note to self #1 My DNA does not get it correct all the time. Note to self #2 ask 23and me for a refund!). Really, it is all relative. my DNA is not saying I absolutely will not taste bitter substances. Green eyes versus brown...My DNA states that I "Likely Brown"...well, the person who set up the 23andme automated results put in the term "likely brown" or someone did, because while DNA tells us something, it does not speak!

So why doesn't my DNA match up with my expressed trait all the time...years and years of environment plus some other reasons. Let me know!

Why is this blog here? With the responsibility of keeping our students on the forefront of pharmacy education, I felt obligated to present, from a public point of view, where "things" are at with personal genetic information. As I have talked about patients who eliminate drugs from their body slowly (poor metabolizers) versus those who remove drugs rapidly (extensive and ultra rapid metabolizers) in class for years, I felt that this needed to be placed in the context of the "bigger picture". With the advent of direct to consumer (DTC) genetic testing, I saw the opportunity to investigate the "bigger picture".

I looked at a number of direct-to-consumer “personal genome” companies (deCODEme, Navigenics, and 23andme; This is not an endorsement of any of them) and sent my DNA sample (saliva) to arguably the most commercial of the DTC "personal genome" companies so I could delve into this new world of personal genetic information.

Being in pharmacy education, I specifically was looking at this information to see the drug-genetic connections (pharmacogenetic) side of things. I wanted to know how my body handled certain drugs. This term, pharmacogenetics was defining what I wanted to know. That is, I wanted to study my genetic makeup in order predict how I would respond to certain drugs and to understand how certain drugs should be prescribed for me.

So, I am checking my pharmacogenetics, hence this PGxCheck.com blog...but it is much bigger than just drug response. I will learn what disease risk I have, what disease(s) I may be a carrier of and what my DNA says about physical traits. The bigger picture includes legal issues, such as discrimination, ethics, healthcare, business and broader personal questions. We all need to be thinking about the use of genetic information in this era of easy access to DNA information.

For me, there is another reason for looking at this information. Being adopted, I do not know anything about my family medical history. It made sense to me to look at my “predisposition” relative to disease risk. When offering a family history you should go back three generations to put in perspective potential inherited diseases and inherited risk, if you will. I couldn’t come close to doing that, so after I see my results from the personal genome company, I can offer that to the clinicians…as my family history.

So, I will start with the traits my genetics says I have. Certainly, I know how I express some of the defined traits (and some, frankly, are not pretty!). It will be interesting to see if my expression of the traits, my phenotype, matches what my genetics say I should express as a trait, my genotype.

To get us all at a starting point, click on “About DFK” at the left. You will see the trait that was tested by the personal genome company, how I express that trait and I will start looking at the results and enter the results from my DNA testing. We will see if they match…and discuss why they may not!

Ok, that is the first entry for the blog. I will be putting a notice out, via Twitter to let everyone know when I am posting comments and results of the testing. For the students that are following along, I will also send an e-mail when there is a post. If you wish, you can follow me through Twitter (@pgxcheck).