Unusual Symptoms

Lab Test Genecept Assay Report Page 1 June 25, 2015



Sample Type: Buccal
Panel Ordered: Genecept Assay 1.1
Sample Collection Date: 6/25/2015

Results Report


A = Use caution with related therapies. B = Therapeutic options C = No known gene-drug interaction
Gene Result Therapeutic Implications Interaction Clinical Impact
Serotonin Transporter

L/S


[Intermediate risk of non-response]

 The serotonin transporter protein (SLC6A4) is a presynaptic transmembrane protein responsible for serotonin reuptake [1-9]
* Higher risk of poor response, slow response or intolerance to SSRIs and potentially higher rates of PTSD and reduced stress resilience
* Therapeutic options such as non-SSRIs may be used as clinically appropriate
A
 Use caution with SSRIs

Serotonin Receptor 2C

C/C

 5HT2C is antagonized by atypical antipsychotics and is involved in satiety [6,10-22]
A
 Use caution with atypical antipsychotics

[Highest weight gain risk]

 * Highest risk of weight gain with atypical antipsychotics that have a high binding affinity for this receptor
* Highest risk with clozapine, olanzapine, and risperidone
* Inositol acts downstream of 5HT2C to facilitate satiety signaling; supplementation may reduce metabolic effects of atypicals
B
 Therapeutic options: Inositol may be used if clinically indicated [20-22]

Dopamine 2 Receptor

INS/INS
[Normal]
 DRD2 is antagonized by most antipsychotics [23-26]
* This genotype confers normal activity
C
 There are no known gene-drug interactions for this genotype
Calcium Channel
C/C
 CACNA1C mediates excitatory signaling by regulating the influx of calcium into the cell [27-42]
* Abnormal calcium signaling may be clinically associated with conditions characterized by mood instability or lability
B
 Therapeutic options: atypical antipsychotics, mood stabilizers and/or omega-3 fatty acids may be used if clinically indicated [43-46]
Sodium Channel
C/C
[Normal]
 ANK3 belongs to a family of proteins known as the ankyrins and has a critical role in sodium ion channel function [27,29,47-54]
* This genotype confers normal activity
C
 There are no known gene-drug interactions for this genotype
Catechol-O-
Methyltransferase
Val/Val
[High activity]
 COMT is an enzyme responsible for breakdown of dopamine in the frontal lobes of the brain [55-69]
* Risk for heightened COMT enzyme activity and a parallel| in frontal lobe dopamine and working memory
* Dopaminergic agents may lead to greater improvements in executive function as compared to Val/Met or Met/Met patients
* Studies demonstrate a relationship between Transcranial Magnetic Stimulation (TMS) and dopamine in the brain
B
Therapeutic options: dopaminergic agents and/or TMS may be used if clinically indicated [60-69]
MTHFR (C677T)
C/T
[Intermediate activity]
 MTHFR is an enzyme responsible for catalyzing the conversion of folic acid to methylfolate. Methylfolate is a precursor to serotonin, norepinephrine and dopamine synthesis [76-83]
* Risk for reduced MTHFR enzyme activity and reduced methylfolate production
* Folic acid-based supplementation of SSRIs and SNRIs show superior symptom reduction and medication adherence compared to SSRIs/SNRIs alone in Major Depressive Disorder
B
 Higher intake of folic acid based interventions may be required [75-77]

Therapeutic options: L-methylfolate may be used if clinically indicated {80-83]
CYP2D6
EM
*1/*1
[Normal activity]
 Variations in the CYP2D6 liver enzyme can result in altered drug metabolism and unexpected drug serum levels [100,101]
* This genotype confers normal activity
C
 There are no known gene-drug interactions for this genotype
CYYP2C19
EM
*1/*1
[Normal activity
 Variations in the CYP2C19 liver enzyme can result in altered drug metabolism and unexpected drug serum levels [100,101]
* This genotype confers normal activity
C
 There are no known gene-drug interactions for this genotype
CYP3A4/5
*3/*3
[Normal activity]
 Variations in the CYP3A4/5 liver enzyme can result in altered drug metabolism and unexpected drug serum levels [100,101]
* This genotype confers normal activity
C
 There are no known gene-drug interactions for this genotype

This is based upon a review of the literature that is suggestive of treatments which may be appropriate and those that may be used with caution or avoided. Clinicians should review the full prescribing information of treatments being considered and should make their own treatment decisions based upon their knowledge as it relates to the patient. Medications in this report are listed in alphabetical order; listing of medications is not meant to imply comparable efficacy or safety. Brand names are listed for exemplary purposes only; additional brand names exist and Genomind does not endorse or support any particular product.
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