Genetic Tests – What’s the big deal?

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Genetic-testGot a health issue?

Get a genetic test.

That seems to be the protocol of choice for any and all health issues these days.

However, genetic tests should play a supporting role not the starring role in treatment protocols.

If it was all about our genes, then we would see the same health outcomes in all nationalities with the same genetic defects – but that’s not the case.

Genetics may identify a weak link, but lifestyle, environment, and diet, determine whether or not that link is going to break or not.

Get the rest of the story below…


Is #genetic testing all that it’s cracked up to be? Where does it fit into treatment protocols? Find out!




Full Transcript:

Oh, Dr. Ben Lynch here. I want to talk with you about genetic testing and patients coming in your office and plopping down genetic test results. I know I’m probably causing a lot of patients coming in your office with genetic test results. I’m sorry for that. But I’m also glad for that, because as we know, the genetics of our patient, it allows us to dig in and identify why they are susceptible to certain things and why other patients are not.

Doctors love protocols. You go to a conference and you learn about the greatest nutrient possible. Let’s say it’s methylfolate. Okay? Methylfolate is like the next big nutrient and it deserves some spotlight. And you start giving it to all of your patients. But they do worse, some do fantastic. Why? Genetics. Genetics show susceptibility only. It’s a tool that you need to use only. It doesn’t dictate your treatment at all. It supports your treatment recommendation. It supports why your patients maybe not responding well to certain meds. It supports why they don’t respond to certain foods and it responds why they might do well in a certain environment. That’s what the genetics do for you and your patient.When a genetic test comes in, it doesn’t mean you drop everything else, you keep doing what you’re doing, and if the patient is not responding well, you can look at the genetics and see what’s going on. It doesn’t guarantee that there’s a problem in that gene, and it also doesn’t guarantee that there’s not a problem in that gene.

So let’s back up for a second. Let’s look at MTHFR, the mothership of all genetic issues, right? MTHFR is prevalent, it’s easy to test for, and it’s easy to support. Now, neural-tube defects, there’s a whole reason folic acid got in our food in the first place. We have folic acid in our food to support neural-tube defects to get rid of them, to reduce the incidents. Why is neural-tube defects around? Why is folic acid the answer? Well, first of all, it’s not the answer. Neural-tube defects are a methylation dysfunction problem. That’s first. You need support neural-tube defects in your patient with methylation.

Now, a big problem, the number one gene looked at for neural-tube defects is, right, MTHFR. That’s the number one research gene. Now, Americans and Chinese and Hispanics, if they have MTHFR, and they’re pregnant, and they have a child, their risk of having a baby with neural-tube defects is very high, if they’re not taking folate. Okay? Now, let’s fly overseas, land in gorgeous Italy where there’s sun, amazing food, amazing environment, family culture, right? Lifestyle, good diet. Bad genetics. No neural-tube defects, they have MTHFR just like the Hispanics and the Chinese, who are susceptible neural-tube defects. The Hispanics and Chinese are getting the neural-tube defects. The Italians aren’t, but they have the same gene. Why? Lifestyle and diet and environment, okay? So, you evaluate the entire lifestyle, the diet, and the environment of your patient. And if you do that, along with evaluating genetics, then you are going to be a much, much better clinician in understanding how to harness genetics with your patients.

Let’s give another example, vegetarians. Seventy-five percent of pregnant women are deficient in choline. It’s a big one; seventy-five percent of women are deficient in choline. Choline is a big methyl donor. So if someone is deficient in choline, and they have MTHFR, and they’re not eating their leafy greens, not only are they choline-deficient, but they’re also folate-deficient. You think neural-tube defects are going to go even higher? Yes. The gene which takes choline to make phosphatidylcholine is PEMT. So if you look at genetic thing and you see PEMT on there, like whoa, you have this variance as well. You have increase susceptibility in having methylation problems and some membrane problems, absolutely.

But, you support your methylation. You support their lifestyle and their diet. You identify their susceptibility. So, don’t worry about understanding what each gene does and prescribing meds and drugs and vitamins and lifestyle changes for every single snip. You’ve got to think big picture. You’ve got to think like this pathway planner here and how everything interacts. If you understand that, then you’ll be able to really calm down about genetic testing coming on your desk and harness it and identify where in these pathways are issues with your patient. If you do that, not only it would be announced any clinician, but your patients will get much, much better and will be reducing incidents of disease and unborn children which is my passion. Thank you.

Whoa! Wait, wait, wait. Sorry, I forgot about this. SHEICON2015, if you heard about it, you just enjoyed this video. I hope you’re excited about it. This information is very clinically relevant to you and your patients. SHEICON2015 is an upcoming conference in October that you can’t miss. There’s 400 like-minded people like me, like yourself, that want to know more about how to optimize the health of your patients. You got four days of it. You got 400 doctors who are wanting to get more information on thisand do what they need to do and transform medicine and transform the health of your patient and transform your practice. SHEICON2015. You can do it. Learn more at Thank you.

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Comments 1

  1. I’ve run my report through Strategene and Genetic genie and see differences in the MAO-A finding. Your report shows the T941G as -/- and the genetic genie shows MAO-A R297R rs6323 TT as +/+. Can you tell me why the differences in reporting? The raw data in 23andme shows + T variant for rs6323 but cannot find the raw data for T941G in 23andme. Any insight into this?

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