Genetic Profiling for Epigenetic Health
The age of personalised medicine has arrived with the availability of personal DNA testing. While Naturopathic practitioners have long known that everyone is different, only recently have we been able to access an individual's genetic information to tailor treatment to their needs based on their unique genetic profile. The tailoring of treatment to patients has always been a fundamental feature of complementary, functional, holistic healthcare. Now, advances in genetic testing mean we can determine how a person's genes may influence their health (epigenetics0 as well as identify more suitable treatment protocols to optimise overall wellbeing.
Smart DNA Profile
Working with your genetic information to reduce the risk of common health issues that may affect you as you age. This program supports you to take the best health promotion measures to support the expression of your best self.
Using the Smart DNA Genomic Wellness Test the most affordable, scientifically up to date and comprehensive test around, we can use this information to understand and implement the best health and lifestyle measures for you. Going through the findings from your analysis report, current health care presentations and needs, this program will give you clear and insightful information that you can implement into your personalised optimal wellness program. Age more slowly, experience a higher quality of life, feel less stressed, avoid health problems down the track, improve genetic health for future generations.
Gene areas screened :
Lipid Metabolism :
The lipid panel is main hub for a heart health based diet. In particular Apolipoprotein E (APOE) genotyping maybe ordered by the practitioner when a patient has significantly elevated cholesterol and triglyceride levels that do not respond to dietary, exercise and lifestyle changes. A number of genetic variants have been identified that negatively impact the concentration of plasma lipids in response to the amount and type of fat consumed; total cholesterol, HDL-C, LDL-C and triglyceride levels. Genetic variants analysed include : APOA1, LPL, ABCA1, CETP, LIPC, APOB, APOB100, APOCIII, APOA5,LDL-R, eNOS3, FABP2 and LPA.The application and clinical benefit is for those patients with disorders of lipid metabolisms. The patient has an active role in lifestyle changes with specific nutrition based therapy. The selection of other genes involved in lipid metabolism is targeted to genes involved in HDL-C level, fat absorption, fat transport and the conversion and degradation of fat. Dyslipidemia can have various genetic causes which are influenced by nutrition, alcohol, smoking and sex-specific effects.
Metabolic Syndrome & Diabetes Risk
This is a genetic risk assessment for Type II Diabetes and Metabolic Syndrome (MetS). Diabetes is one of the major diseases of this century and genetics, lifestyle and nutrition are all equally important considerations. The long-chain acyl CoA synthetase 1 (ACSL1) and acetyl-CoA carboxylase (ACC2) play a key role in fatty acid synthesis and oxidation. Disturbance of these pathways is associated with impaired insulin responsiveness and metabolic syndrome (MetS). Moreover the ACSL1 and ACC2 gene polymorphisms are modulated by dietary fat intake. The individual being tested is genetically predisposed to normal, moderate or high level of Diabetes risk. Genetic variations detected in the TCF7L2,WFS1 and SLC30A8 genes have been reported to play a role in insulin function. The, FTO, G6PC2 and PPARG genes will indicate an increased likelihood of developing type 2 diabetes due to a higher BMI (FTO), reduced control of blood glucose levels (PPARG andG6PC2) or reduced pancreatic beta cell function (SLC30A8).
Inflammation has a key role to play in chronic disease, including diabetes, osteoporosis, obesity, aging and cardiovascular disease. Susceptibility to an increased inflammation response is genetically determined. Common variants found in the TNFA,IL6 and CRP genes are analysed.
High Blood Pressure
High blood pressure or hypertension is the leading cause of strokes and major risk factor for heart attacks. Two gene variants are analysed ACE and AGT which have been reported to be associated with sodium sensitivity.An individual with a “salt sensitive” genotype may result in higher plasma angiotensinogen levels and ultimately higher blood pressure leading to an increased risk of hypertension.
A nutrient vital for energy production, cardiovascular and nerve health, a variant in the NQO1 gene can affect uptake and utilisation of CoEnzyme Q10. If this is present, levels of this nutrient will want to be supported for future health and wellness.
Omega 3 and 6
A variant in the FADS1 gene can be associated with a decreased blood level of these essential nutrients. Individuals with this genotype may need to avoid the complications associated with a reduced blood level of these nutrients.
Vitamins - absorption and activation
There are genetic makers associated with lower levels of essential nutrients such as
vitamins B2, B6, B9, B12,
vitamin C, glutathione
vitamin D metabolism
Variants in genes such as MTHFR, NBPF3, FUT2, GSTT1, GSTM1, SLC23A1, INTERGENIC, GC, DHCR7 and CYP2R1, are markers which may signpost risk of lower levels of these essential nutrients.
Methyation is essential to efficient and safe detoxification of chemicals and substaces in the body, as well as the production of neurotransmitters important for mood and function. The ability to reduce homocysteine to cysteine and methionine, for example, is influenced by genetics, environmental factors especially vitamins B2, B6, B9 and B12, as well certain medications and lifestyle factors. Variants in the MTHFR, MTRR, MTR, CBS, TCN2 and SLC19A1 genes can be associated with elevated homocysteine levels, giving rise to an increased risk of vascular disease (including peripheral and cerebral vascular disease, coronary artery disease and thrombosis), neurological and mood disorders.
Genetic variations in the MTHFD1 gene can be associated with an increased risk of developing choline-deficiency induced nerve / organ dysfunction, and/or having a child with a neural tube defect. This is due to the role choline plays as an important methyl group donor in the methylation of nerves, cells and detoxification processes. Low dietary choline has been reported to contribute to higher homocysteine levels, which can also increase the risk of cardiovascular disease and dementia.
A variant in the CYP1A2 gene can be associated with slowed caffeine metabolism. This genotype is associated with an increased risk of hypertension and heart attack when caffeine consumption exceeds two cups of coffee per day. People with this gene variant will want to reduce the intake of caffeine for better health.
Genetics is the most powerful known risk factor for glutent metabolism and the risk of coeliac disease. The analysis of DQ8and DQ2.5 genetic variants provides information on the likelihood that an individual is at greater risk of ceoliac disease or gluten sensitivity.
The MCM6 gene analysis provides information on lactose metabolism and the risk of intolerance caused by non-persistence of the lactase enzyme into adult life.
Oxidative Stress Risk
Oxidative stress is a major cause of premature ageing and cell damage. The major enzymes involved in anti-oxidative defence SOD2, GPX1 and CAT are assessed. Issues found with these genes will want to be supported with nutritional and lifestyle measures to reduce the likelihood of damage to body cells, tissues and organs, and accelerated ageing.
Drugs (including caffeine), metals and hormones are transformed in the Phase I process of liver detoxification. The enzymes CYP1B1, CYP1A1 and COMT are involved in this process, and need to be operating optimally for safe removal of toxins and metabolites that have the potential of doing harm. Assessment of the enzyme function is useful in relation to the processing of compounds such as xeno-estrogens, drugs, toxins and chemicals. Metabolites from Phase I detoxification are transformed into water soluble compounds which are then excreted in urine. A reduced clearance through Phase II detoxification can lead to the accumulation of toxic metabolites and these related issues. The glutathione transferase enzymes GSTT1, GSTM1 and GSTP1 are involved in this process and if these genes are not optimally blueprinted, this process will want to be supported by other means.
Knowing what exercise to do which supports your strengths can help greatly with getting the most out of your exercise and recovery program, as well as other factors that are helpful to understand. This section of the report includes genetic variants whose activities are modified by nutrition and exercise such as saturated fat (APOA2) and monounsaturated fat (APOA5 and PPARG), predisposition to higher total cholesterol (NPY) or attenuated improvement in HDL-C level (PPARD). Genetic information in relation to satiety or feelings of fullness (FTO), Bitter taste perception (TAS2R38) which may increase salty food intake,resistance to weight loss (ADRB2 and ADRB3), increased snacking (MC4R), circulating levels of adiponectin and weight regain (ADIPOQ), increased consumption of sugary foods (SLCA2) and food addiction (DRD2), increased metabolic rate (LEPR) and exercise in relation to weight loss maintenance and benefits of weight loss in relation to protein intake (FTO).
Exercise & Physiogenomics
Physiogenomics integrates genotypes, phenotypes and functional variability amongst individuals to help identify which exercise is best suited for your metabolic type. A phenotype is a measurable physiological, morphological, biological, biochemical or clinical characteristic. Genotype refers the genetic composition of that individual. The section of the report covers increased risk of obesity, depression and episodic memory (BDNF), blood pressure response to exercise (EDN1), KIBRA and working memory, HPA axis stress responses in particular elevated ACTH and cortisol levels (TH and MR), seasonal variation in sleep, mood, appetite, social activity (NPAS and CLOCK), increased plasma ghrelin level and weight gain (CLOCK) and exercise in relation to reducing injury and developing a personalised exercise and recovery plan (COL1A1, VDR (FOK1), ACTN3, HIF1, MCT1, VEGFR2,eNOS3 and ACE).