News And Updates
Newsletter - October 13th, 2021
Registration Now Open! Upcoming Workshop Event
In our last newsletter we announced a one of a kind provider workshop on February 25th, 2022 in partnership with Neurobiologix and how to save a spot early. Now registration is officially open! Join GX Sciences Founder and Medical Director Kendal Stewart, MD in-person here in Austin, TX and virtually live where he will provide invaluable insight into clinical case studies utilizing advanced nutrigenomic testing to enhance provider treatment protocols.
Lab Status Update - September 2021
Last month we started including a special update for our providers of monthly Lab Turnaround Time statuses, and we continue this month with September’s numbers. The monthly average and the monthly median turnaround time (TAT) is measured in business day.
Important reminder that lab turnaround time does not include lead time of patients needing to submit required Questionnaire Forms for Specialty Panels (TrichoTest™, NutriGen™, and the upcoming TeloTest™). The sooner patients submit their questionnaires, the faster their reports can be delivered.
![](https://gxsciences.com/wp-content/uploads/2021/10/TAT-Indicator-sept-768x256.png)
GX Sciences’ Average Turnaround time in July 2021 was 7.4 business days, while the Median was 7 business days. Our goal is 5-7 business days.*
*Lab turnaround time is calculated starting at the time a valid sample is received and all subsequent forms are received correctly. Low concentrations in a sample adds time required to prevent sample recollection. Accounts for potential for one or more SNPs to be rerun to rectify NOAMP or UND calls.
Why is it relevant?
Prescription drugs can be a major health risk if misused and abused, ranking fourth as the leading cause of death in the past few years. Nearly 840,000 hospitalized patients are given drugs that cause serious adverse reactions for a total of 2.74 million serious adverse drug reactions. PharmacoGenomics (aka PGx) revolutionizes the world of pharmaceuticals by combating the “one-size-fits-all” approach. PharmacoGenomics is the study of how a person’s genes affect their response to drugs. It combines pharmacology (the science of drugs) and genomics (the study of genes and their functions) to develop a highly accurate method of determining medication specifics that are tailored to a patient’s genetic makeup. Patients no longer need to engage in a trial-and-error process to find the best medicine with the least amount of side effects. GX Sciences strives to educate our practitioners about the genetic factors that could explain symptoms associated with adverse reactions to pharmaceuticals.
Why is it important?
Roughly 81 million adverse reactions are experiences by the 1170 million Americans taking drugs, specifically the elderly and those taking multiple medications. Our comprehensive panel, Pharmacogenomic (PGx), identifies specific genetic variants that can influence a drug’s metabolism, drug to drug interactions, side effect potential, expected efficacy and clot risk. Genetic results will be able to provide insight of medication choice and proper dosage. Patients that might benefit from our Pharmacogenomic (PGx) panel include those who have or have experienced:
- Previous Drug Reactions
- Family History of Drug Reactions
- Chemical Sensitivities
- Multiple Health Issues
- Taking Multiple Medications
- Poor Communication Skills
Key Genes Related to PGx
Cytochrome P450 Genes
Cytochrome P450 (CYP) part of phase I detoxification in the liver. Cytochrome P450 (CYP) enzymes are membrane-bound hemoproteins that play an essential role in detoxifying xenobiotics, cellular metabolism, and homeostasis. Cytochrome P450 is one of the most important classes of enzymes involved in drug metabolism. It is estimated that more than 60% of current drugs undergo metabolism by Cytochrome P450 enzymes. Cytochrome P450 enzymes are found in the liver, small intestine, and other tissues of the body.
In general, Cytochrome P450 (CYP) genes are divided into two groups: CYP1 and CYP2 families. The members of both gene clusters share a highly conserved structural organization consisting of 3 domains; Cytochrome P450 proteins contain approximately 440 amino acids that form an internal cavity binding site for oxygen or other reducing equivalents (Takatashi, 2007). Cytochromes P-450 perform their catalytic function associated with NADPH-dependent reductase while metabolizing drugs/xenobiotics through transferases reaction involving two electrons.
Foundation-related Genetic Variants for MTHFR
There are two MTHFR variants called C677T and A1298C that have been actively studied. It is estimated that about 30-40% of Americans have a mutation in the population frequency of MTHFR C677 Tallele. In the US, about 25% of people who are Hispanic and 10-15% of people who are Caucasian have two copies of the C6722T variation. Studies have shown that people with two variants for C6722T gene and elevated homocysteine are at an increased risk of blood clots. Women with two copies of the variant of C6722T are at increased risk of having a child with a neural tube defect. MTHFR variants can impact our ability to detoxify. Genetic variants such as MTHFR, and Phase 2 liver defects, lead to increased toxins exposure within the extracellular space. This is where hormones, immune cells, and neurotransmitters communicate with one another. With the extra toxin exposure present communication is interrupted. (Source)
COMT
Worrier or warrior? The COMT gene has instructions for making an enzyme responsible for the breakdown of dopamine and other catechol’s such as norepinephrine and epinephrine. There are two variants of this gene known as the worrier and the warrior. The homozygous SNP, or the “worrier,” can result in reduced dopamine degradation leading to altered stress response. In contrast, the “warrior” mutation breaks down these neurotransmitters quickly. In white populations, the estimated genotype frequencies are25% for high enzymatic activity, 50% for intermediate, and 25% for low enzymatic activity. The low enzymatic activity variation is less common in black populations, measuring at only 7% for the mutation. (Source 1, Source 2)
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