The Genetic Health Testing approach helps the healthcare professional establish the optimal nutrition necessary for good health, longevity, and disease risk mitigation. Diet is a key factor in determining genomic stability, as it affects all relevant pathways: exposure to dietary carcinogens, biotransformation, DNA repair and synthesis, and apoptosis. Current recommended dietary amounts of vitamins and minerals are largely based on the prevention of deficiency diseases. However, because lifestyle diseases are caused in part by DNA damage, it stands to reason that we should focus our attention on defining optimal requirements for key minerals and vitamins to prevent genomic instability.
Particular attention should be paid to individuals with genetic polymorphisms that alter the bioavailability of specific micronutrients and the affinity of specific key enzymes for their micronutrient cofactor.
Clinical value
- Highlights specific metabolic pathways that may require additional support
- Provides recommendations that involve optimizing amounts of certain nutrients, vitamins and minerals.
- It suggests whether an individual is better able to reduce their cholesterol levels through diet, rather than through medication.
- It provides an indication of the degree of susceptibility to the harmful effects of carcinogens ingested in the diet.
The Genetic Health Test report provides:
- The level of impact of any genetic variants identified.
- An explanation of its impact on health.
- Appropriate nutritional and lifestyle recommendations
The results are divided into key metabolic function sections, so that genetic weaknesses and strengths within a functional area can be easily identified.
Analytes measured:
Lipid metabolism
LPL: Removes lipids from the circulation by hydrolyzing triglycerides into free fatty acids.
CETP: Plays a key role in HDL metabolism and mediates lipid exchange between lipoproteins.
APOC3: Plays an important role in cholesterol metabolism.
APOE: It is essential for the normal catabolism of the constituents of lipoproteins rich in triglycerides. Affects the requirement for antioxidants.
B Vitamins/Methylation
MTHFR: It directs dietary folate to DNA synthesis or homocysteine remethylation.
MTR: Catalyzes the remethylation of homocysteine to methionine.
COMT: It catalyzes the transfer of a methyl group from S-adenosylmethionine to catecholamines, including the neurotransmitters dopamine, epinephrine, and norepinephrine.
MTRR: It catalyzes methylcobalamin, which is essential for maintaining adequate intracellular stores of methionine. It is also responsible for maintaining homocysteine concentrations at non-toxic levels.
CBS: It catalyzes the conversion of homocysteine to cystathionine and is directly involved in the removal of homocysteine from the methionine cycle.
detox
CYP1A1: The cytochrome P450 enzyme converts environmental procarcinogens into reactive intermediates, which are carcinogenic.
GSTM1: Influences Phase II detoxification. It is responsible for the elimination of xenobiotics, carcinogens and oxidative stress products.
GSTP1: It influences the metabolism of many carcinogenic compounds.
GSTT1: Member of a superfamily of proteins that catalyzes the conjugation of reduced glutathione.
NQO1: Quinone reductase is primarily involved in the detoxification of potentially mutagenic and carcinogenic quinones derived from tobacco smoke, diet, and estrogen metabolism.
Inflammation
IL-6: It plays a crucial role in inflammation by regulating the expression of C-reactive protein (CRP).
TNF-A: TNFα is a proinflammatory cytokine, secreted by both macrophages and adipocytes, that has been shown to disrupt whole-body glucose homeostasis and has been implicated in the development of obesity, obesity-related insulin resistance, and dyslipidemia. .
Responsiveness and sensitivity to food
MCM6: Associated with hypolactasia in adults.
FADS1: It influences blood fat concentrations by affecting the efficiency of the desaturase enzyme.
CYP1A2: This detoxifying enzyme influences the ability to metabolize caffeine.
ACE and AGT: Part of the renin-angiotensin system and response to salt.
HLA DQ2/DQ8: Main genetic predisposition to celiac disease
Vitamin metabolism
BC01: Retinal carotenoid catalyst (vitamin A)
CYP2R1: Conversion of vitamin D to 25(OH)D
FUT2: Absorption and transport of vitamin B12
G STT1: Contributes to the antioxidant cycle of glutathione-ascorbic acid (vitamin C)
iron overload
HFE: Regulates iron absorption, regulating the interaction of the transfer receptor with transferrin. Hereditary hemochromatosis results from defects in the HFE gene.
Oxidative stress
eNOS: It influences vascular tone and peripheral vascular resistance. It also has vasoprotective effects by suppressing platelet aggregation, leukocyte adhesion, and smooth muscle cell proliferation.
MnSOD/SOD2: It has vital antioxidant activity within the cell, especially within the mitochondria. Destroys radicals that are normally produced within cells.
bone health
VDR: It has a profound influence on bone density.
COL1A1: It influences the proportion of collagen alpha chains produced by bone cells, affecting bone mineralization and bone resistance.
Insulin Sensitivity
PPARG: Involved in the differentiation of adipocytes. It is a transcription factor activated by fatty acids, and is also involved in the regulation of glucose and lipid metabolism.
TCF7L2: It influences blood glucose homeostasis, both insulin secretion and resistance.
FTO: It influences susceptibility to obesity and the risk of type 2 diabetes.
SLC2A2: It facilitates glucose-induced insulin secretion and participates in food intake and regulation.
Privacy Policy:
The DNA and original sample material are destroyed after 3 months so that no names or other identifiers remain in the samples. Samples are analyzed only for the SNPs included in DNALife tests, and no other investigations or analyzes are performed without separate permission from the patient. We do not give or sell the results to third parties.
