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DNA is the blueprint of all animal life (and almost all other life too). It is the code our cells use to build the proteins that keep us alive and make us who we are. 

DNA stands for deoxyribonucleic acid, so you can see why most people just say, “DNA.” Those nucleic acids that are referred to in the name are the letters in which the DNA code is written, and there are 4 different ones common to all animals. The names aren’t important to understand how they work, so we’ll just use their abbreviations, A, C, G, and T. Those 4 letters are strung along in a particular order that allows the cells to read them and make proteins. 

We have more in common with other animals than just the four letters. The order of those letters is very common as well. For instance we share over 84% of our DNA with our dogs (no matter what breed you have) and 90% with our cats. Our closest DNA relative is the Chimpanzee with whom we share almost 99% of our DNA. While there are 3 billion letters in the human DNA code, over 99.9% of them are the same no matter who you are. That makes it sound like we’re all pretty much the same, and we are. But 0.1% of 3 billion is still a very large number so there’s plenty of room for each of us to be unique.

It is those unique differences between us that determine how certain proteins are made. And it is those proteins that determine other effects. Of course, the environment plays a role, but studies of twins separated at birth show us that our genetic code determines a lot about who we really are.

In genetic studies, ethnicity has historically been used for a very good reason. Prior to high throughput methods to actually read the genetic data, a person’s ethnicity was a good shorthand for some commonality in their DNA. If a group of people were all living in the same place for thousands of years and intermarrying, they likely shared some genetic traits. If another group was isolated from them and lived in a different environment, they likely had some very different traits.

It was found early on in genetic studies that some changes in the genetic code (polymorphisms) meant different things in different ethnic groups. That just meant that the polymorphism we were looking at acted differently in different contexts determined by other genes. In some cases, the best shorthand for that is ethnicity.

The external markers for ethnicity have very little to say about the internal genetic changes that are important in determining your wellness. With modern genetics we can hope to get beyond those external markers and directly to the molecular changes that make each of us unique.

But GenEd can only tell you about the studies already done, and in some of those studies ethnicity is mentioned. The study may have been limited to a certain ethnicity or national origin, or two different studies in two different ethnicities showed conflicting results. We want you to know that we mention ethnicity only when the science mentioned it, and we look forward to the day when our studies are so precise, it need not be mentioned again.

We hear this from time to time, and the history of this attitude goes back a long way. It goes back so far, it pre-dates the science of genetics as we understand it. That’s one reason why generations of physicians have learned that addiction has nothing to do with genetics. The explanation they learned was made up before anyone knew much about human genetics.

Most addiction training today is centered on the diagnoses made in The Diagnostic and Statistical Manual of Mental Disorders (DSM) by the American Psychiatric Association. The DSM doesn’t mention addiction but divides it up into “substance use disorders” and ignores almost all the expressions of the illness involving other rewards (overeating, shopping, work, sex, etc). In the DSM model, people with addiction started out normal, used drugs because of a conscious decision, and those “addictive” drugs caused changes in the brain that led to a Substance Use Disorder. If that’s your model, genetics will have very little to do with it.

Under that model, there’s no explanation for the symptoms people with addiction have after they’ve stopped using the substance or behavior other than to suggest a different illness that they also had. This has led to a large industry of “dual-diagnosis” treatment where the substance use disorder is treated with psychosocial addiction rehab, and the co-occurring disorder is treated with an indicated medication. Dr. Wetsman has numerous blog posts and videos on the internet discussing the ramifications of this situation. 

Unfortunately almost all doctors being trained in addiction don’t get training in understanding addiction as primary illness that can occur before the first drug. So it may be that doctors you have spoken to don’t understand the ramifications of such a thing. Feel free to direct them to Dr. Wetsman’s videos, writings, and books, or have them contact him here. 

We don’t want to get between you and your doctor, and we aren’t a substitute for your doctor. It’s important to find a doctor that has a good understanding of the neurobiology of addiction that you trust. When looking for one, interview them. Any doctor who will spend time with you and give you personalized treatment will be willing to speak to you over the phone about your goals and their philosophy of treatment.

There could be several reasons that a polymorphism another company tests for didn’t make it into the GenEd panel. Our process was not to start with what others had been doing; it was to start with a model of the disease or condition, develop targets that were helpful in understanding the illness, and vet them thoroughly. It often happens that such critical educational targets are also the targets that clinicians need to make decisions because they are critical to understanding the process that occurs with the illness. 

The current academic standard is “publish or perish.” And the best way to get something published is to add to what “everyone already knows” or pile on with a finding all the reviewers of your paper agree with. New ideas are risky in the academic world. So the most accepted articles attract more researchers rather than the most challenging ideas attracting the most researchers. And if you want to take the safe academic way to creating a genetic panel, you’d pick the polymorphism with the most articles. That’s what most companies do. Not us.

Here’s an example of a polymorphism almost everyone else uses that didn’t make our cut, rs686. This is a SNP of the dopamine type 1 receptor (DRD1) and it’s been associated in the literature with nearly every syndrome known to man. If you want to pad your report with scary results and a lot of “info” you’ll want to add rs686. But there are some problems. This SNP is actually quadrallellic. Unlike most SNPs that can be one of two different bases, any of the four bases can be found here. Yet none of the clinical literature acknowledges that, so how can we count on any of it? It’s so poorly understood in spite of the vast amount of study, even the “laboratory standard” that we used from the 1000 Genomes Study was labeled wrongly as a homozygote. Our heterozygous result gave us fits until we went back and looked at their data. It was heterozygous. That experience taught us to go back to the original work on everything rather than just accept what is “known” like everyone else.

At GenEd, we didn’t seek to pad our panel with a lot of fluff. We didn’t want to find the most published SNP so that we could put a lot of references on the report. We looked for polymorphisms that could teach you about the illness you want to learn about, how it works, why it does what it does. So it’s quite likely that we don’t have a SNP that another company reported on. We’re okay with that. And if you want to send us a suggestion on what to include, we’d be happy to hear it.

Well, because we’re not your doctors. Our job is to give you education in the biology of the bodily process you have an interest in and to give you high quality genotyping results to make that educational experience more interesting to you. We are not in the business of making medical recommendations.

In fact we don’t think anyone should be in that business except your licensed healthcare practitioner.  Once you know how the biology of your body works, and can see it in the context of your own life, we think your conversations with your medical provider will be fuller and more useful to you both. We just want to facilitate the conversation so you can find out who you really are.

Quite simply, education. 

Since our first product is about addiction, we’ve heard the question, “Will your test tell me if I have addiction?” The answer is, “No.” Addiction is a clinical diagnosis that should be made by the appropriate medically trained practitioner along with the patient. An IGR for addiction education is not intended to diagnose or treat addiction or any other condition. It will help you understand the nature of addiction in humans with the added interest provided by your own genetics as an example. If you believe you have addiction and you wish to use the information provided by us in your treatment, please share the information with a licensed professional who you trust. Don’t act on anything you see in our reports without first checking with an appropriate medical professional. 

We’ve also gotten the question, “Will this tell me if I’m at risk for addiction?” There are those out there who have suggested that their genetic testing will give you a definitive “risk score” for addiction. As you will see from our education on addiction, the actual illness risk is far more complex than one can get from a small screening test in which each gene is weighted the same. Furthermore, whatever genetic risk an individual has is moderated or enhanced by the environment in which they live. Genetics is not destiny. We only seek to educate you so that we can all have a fuller understanding of addiction as we aim to end it as a problem in our society. If the referenced symptoms you read in our report spark a recognition in your own life and you wish to understand that better, discuss the results with a competent addiction medicine specialist who is knowledgeable regarding the neurobiology of addiction risk.

GenEd wants to give you the best education possible on the factors you can base your wellness choices on. Many people know of the importance of the Dopamine Reuptake Pump (DAT) in dopamine tone, but Monoamine Oxidase B (MAOb) is just as important. Here’s a brief synopsis.

After dopamine is released at the Nucleus Accumbens, it is taken back up by the DAT so it can be recycled by the dopamine producing cells. Once it’s taken back up, and before it’s repackaged into a vesicle for release, it is liable to be broken down by MAOb. To understand this better, lets create a metaphor for it.

Imagine a large group of deer moving quickly through a valley. There’s a hunter in the valley and he has a single shot rifle. As the deer move through the valley, he will certainly get one or more of them.

There is a polymorphism of MAOb that gives the enzyme extra speed. Think of this like the hunter now having a much faster rifle. Under otherwise normal circumstances, the hunter will kill more deer before they reach the end of the valley. In the dopamine producing cell that would be MAOb chewing up more dopamine molecules before they reached the safety of the vesicle. This leads to fewer dopamine molecules in each vesicle. There are medications doctors can use to slow MAOb, which is one reason why it is important to measure this polymorphism.

But there’s another reason. DAT also has polymorphisms that make it run faster than normal, and sometimes doctors use medication to slow it down. These medications have the effect of putting a barrier at the front of the valley so the deer can only enter slowly. This gives a hunter with a single shot rifle more time to kill more deer. If the hunter had a faster rifle, imagine how few deer would get through.

So careful doctors need to know a person’s status at both DAT and MAOb before suggesting blockade of DAT for clinical purposes. If they didn’t, and the person had a fast MAOb, the person may feel better with initially higher dopamine tone only to feel worse in a few days to weeks as dopamine release fell with fewer dopamine molecules in each vesicle.

The subject of addiction isn’t one size fits all, and GenEd wants you to have all the information you can to understand the phenomenon.

The new definition of addiction put forth by the American Society of Addiction Medicine (ASAM), which sees addiction as a primary illness that occurs both when drugs are involved and when they are not, gives us a new perspective. By seeing addiction as primary, we can see what underlies it before the use of the first drug. By seeing other behaviors as being involved in addiction, we are able to see beyond the biology of drugs to the underlying biology of the brain.

The word addiction was coined by William Shakespeare from a Roman legal sentence, addicere. Addicere itself came from two roots, “ad” meaning together, and “dicere” meaning “I declare.” The magistrate would say “addicere” to mean “I declare these two together against their will.” It was what we call today debt slavery. Attachment against the will is the best description of addiction we have. As we hope you see on our site, what determines that level of attachment can be greatly affected by genetics.


Dopamine is a small molecule that’s used by your brain, along with other chemicals, to transmit messages from one nerve cell to another. Dopamine is important in addiction because it is the main messenger at the brain’s reward center. There are two actions of dopamine at that reward center that are important in addiction.

First, there is a dopamine tone created by the second by second release of small amounts of dopamine for normal functioning. The reward center senses this level and, if there is enough, sends a signal to the brain’s higher centers that everything is set for survival. The brain can think about other things like helping others, planning for the future, the right and wrong of any given choice, etc. If there isn’t enough dopamine tone, the brain becomes centered more on the here and now and the self. The higher centers slow down and there’s less computing power given to things like thoughts of others, the future, or moral questions.

Additionally, survival systems cut in to make it imperative to regain a higher dopamine tone and the memory centers are recruited to remember what raised dopamine in the past. Substances and behaviors that have raised dopamine in the past are sought to fix the problem. Hence, people with low dopamine tone tend to seek out things to raise the tone even if their judgment would tell them to do otherwise.

This brings about the first use of a drug, and the second major contribution of dopamine to addiction. When a reward is found that raises dopamine sufficiently, it rarely acts for long. Because the brain is focused on the now with a low dopamine state, the long-term effect is rarely calculated. Most behaviors and substances that raise dopamine work quickly and stop quickly creating a spike and a crash in dopamine levels. If the spike was sufficiently large, the crash will be deep enough to go below where the person started. So a low dopamine person who seeks a dopamine raising substance, may take the substance, feel momentary relief, and quickly be thrust back into an even lower dopamine state creating a loop of compulsive use of the substance. And the lower the dopamine tone, the higher the spike.

So both genetic determinants of dopamine tone and dopamine spike are important in understanding addiction. That’s why GenEd places so much emphasis on them.

The most common way in America to classify addiction is by the reward used. Instead of saying “addiction involving cocaine,” most Americans say “cocaine addiction.” This makes cocaine addiction sound like it is different from alcohol addiction or opioid addiction. This classification method defines differences but in a way that focuses away from the illness and toward a social issue. 
A less common and more useful classification was created by Robert Cloninger, working in people with addiction involving alcohol. He classified addiction into two types. Type I addiction came first because Cloninger thought this type more prevalent. Type I’s had addiction symptoms occur later in life, hated stimulants, loved sedative-hypnotics, rarely had family history of addiction, and had low levels of criminality. Type II’s, on the other hand, exhibited addiction earlier in life, loved stimulants, had a strong family history of addiction, and didn’t like rules. Most people who treat addiction today see far more Type II than Type I. Type II addiction generally maps to low dopamine tone at the Nucleus Accumbens from an early age either from genetics or early environmental effects. The story of how Type I’s get addiction is less straightforward.  

Some people are actually born with too much dopamine and are consequently anxious. They also don’t sit still, have trouble concentrating, and don’t sleep well; oddly, these are the same symptoms someone with low dopamine tone can have. Dopamine isn’t just acting at the reward center but is an activating neurotransmitter wherever it acts in the body. When you have too much dopamine, you feel anxious, fearful, and worried. A high dopamine syndrome most people are aware of is Obsessive-Compulsive Disorder. So, Type I people don’t use dopamine raising substances at first. They use sedative-hypnotics to try to lower dopamine in the anxiety areas of the brain, and at this point in their lives, they don’t have addiction. 

Unfortunately, most sedative hypnotics are also rewarding and cause a dopamine spike in the reward center. That spike is too high for the system to handle and can cause down regulation of dopamine receptors and early cell death in the cells that make the dopamine, a process called apoptosis. So, a Type I starts out with an anxiety problem, drinking (for instance) to lower dopamine, but ends up after decades of drinking having addiction from low dopamine in the reward center due to apoptosis. This lowered dopamine in the reward center doesn’t unfortunately go along with lowered dopamine elsewhere, so they often have both problems.

We understand why people want to upload their data from another company rather than go through testing all over again. We wish we could do that, but currently, it doesn’t work out well. First, our goal is to educate you about how various things work in your body and spice up the experience with your own genetic report. That means that we’ll be focused on what are the most important genetic changes that impact that area of the body or function. Other companies, that are using big machines to look at a large number of changes all at once, aren’t as focused and usually don’t have the data we’re looking for. Also, as the literature changes, so will we. We’ll keep you up to date on the latest findings. The larger companies maybe update their panels once a year, but we can update ours within a couple of weeks of deciding we should.

The second reason is accuracy. When you’re doing a test that’s 99.4% accurate and testing over 500,000 changes, you’re guaranteed to have around 3000 errors in your dataset. We don’t want to base our answers to you on erroneous data. That’s why we do the tests ourselves on a small scale that’s more controllable than the large genetic factories.

But now for the pluses. We hear that one of the reasons you’d like to upload your results from other companies is you’d like your answers fast. We understand. That’s why we will turn around your sample within a few days of its arrival in our lab and report your results on the portal instantaneously. We’ve also heard that you’d like not to incur the expense of additional testing. That’s why we’ve invested in technology that will keep our price low now and in the future.

We may one day, but we don’t think the PGx being sold today is very good, very reliable, or very useful. Can it help in some cases? Yes, of course. But the evidence is over generalized and misunderstood. Also, the testing is too limited.

It reminds us of the story of the man who lost his keys. His friend finds him on his hands and knees under a streetlight. The friend says, “Hey what’s up?” The man tells him that he lost his keys. The friend then asks, “Did you lose them here?” “No,” says the man, “but this is where the light is better.” PGx is where the light is right now, but it’s not where we’ll find the keys. When GenEd is ready with the keys, you’ll know it.

The answer is, it depends on who you are and what you want. 

Perhaps you have a friend or loved one who has addiction. Perhaps you’ve been confused and hurt by their behavior. Perhaps you’re angry and want to have a better understanding of why they feel how they feel and act how they act. 

Perhaps you have addiction and, whether you’ve been helped by treatment or not, never understood why you felt how you did and why your most effective reward did what it did for you. 

Perhaps you treat addiction and have been frustrated with the drug-based model you’ve found in DSM. Perhaps you’d like a better understanding of why some people need medication and some don’t and why one person uses one drug and his brother uses a different one. Perhaps you’ve been looking for an explanatory model of the illness that explains why symptoms don’t go away when the drugs stop. 

Perhaps you just like to learn and want to learn about this important illness that affects so many in America. Hopefully, you are asked to make policy on addiction, addiction treatment, or drugs and you’d like to learn what addiction is in nature before trying to make regulations about it. 

All these people and more have reason to get an IGR-AE. Thanks for letting GenEd be part of your journey of learning more about addiction.

No, there is no risk score for addiction. Addiction is a highly complex, chronic illness that can be caused by any of three factors, or any combination of the three: genetics, stress, and drug use. While it is the opinion of most of America that the last is the most common cause, science tells us it is actually hard to get a normal mammal to voluntarily take drugs that spike dopamine. It is unlikely that any more than a small minority of cases result from the voluntary use of drugs alone. 

The second factor, stress, can lower dopamine tone in even genetically normal constituted individuals. It is a powerful factor and powerfully present in the lives of Americans today. Two primary stresses, isolation and feeling less-than, have been shown to lower dopamine receptor density and, thereby, dopamine tone in primates. These two factors can stem from any number of environmental influences found in many Americans’ lives.

Finally, the genetic factors are far from straightforward. It would be wonderful if all the targets leading to low dopamine tone at the Nucleus Accumbens were known. That might account for the cases of Type II addiction, but would leave Type I cases unexplained. In addition that would not cover dopamine spike or cue-induced craving. 

In fact, every human is at risk for addiction, and that risk is multifactorial and not limited to genetics. If we tried to pick 5, 10, or even 20 polymorphisms and rate them on a scale of how far from normal they were to create a score, we would, at some point, find two people with the same score. Far from having the same risk, those two people would be the same at 20 polymorphisms within the context of being different at some 21st polymorphism. It is more important to understand the web of interactions that make up the neurobiology of addiction than assign a number to assuage someone’s anxiety. One day, we may know enough about genetics alone to assign risk (we doubt it), but even then, risk of what? Risk of having addiction without ever having a drug? Risk of having addiction if ever taking a drug? Which drug or drugs? How about gambling? Or sex? 

The idea of a risk score for genetics is not something GenEd endorses or wants to practice. What we want to offer people is the multifactorial picture of how the illness of addiction exists in the human brain. It is up to each individual to look at their lives, their reactions to the environment, and their own knowledge of themselves to come to an understanding of what constitutes risk for them. Should you be concerned that there is risk of addiction in your life, please see a licensed and trained addiction medicine specialist.

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