Nutrigenetic Profile

People differ in their responses to food and physical activity. Body weight is influenced by many genes, habits, sleep, diseases, medicines and social conditions. Nutrigenetics studies interactions between inherited variants and nutrition, but a small set of DNA variants cannot reliably select an ideal diet for everyone or guarantee permanent weight loss.

Weight-management programs usually combine suitable nutrition, physical activity and behavioral changes. Suspected endocrine or other disease requires clinical assessment. Medicines and surgery have separate indications. A diet that helped someone else may not suit you; this alone does not establish a need for genetic testing.

A polymorphism is a DNA sequence variant occurring in a population. It does not necessarily cause disease. A research association between a variant and a trait is not proof that it can guide treatment or diet. Current expert recommendations regard evidence supporting routine genotype-guided nutrition as limited.

What the Profile Includes

Diagen Plus offers testing of five polymorphisms in four genes: FABP2, PPARG2, ADRB2 and ADRB3. Results describe the variants tested. Computer interpretation can provide additional information but does not replace nutritional and health assessment or professional advice. This panel has not been shown to reliably determine the best nutrient balance or type and amount of exercise.

The sample is venous blood. The original service description specifies no special preparation and a price of 30000 drams including recommendations. Testing arrangements should be checked with the laboratory. Inherited genotype generally does not change, but test scope and interpretation may be revised. The claim that all molecular genetic tests are performed only once in a lifetime is incorrect: somatic-change testing, for example, may be repeated.

Genes and Variants Tested

FABP2: G163A (Ala54Thr)

Possible genotypes: G/G, G/A, A/A. FABP2 encodes an intestinal long-chain fatty acid-binding protein involved in intracellular transport and metabolism. Ala54Thr has been studied in relation to protein properties, lipid metabolism, insulin resistance and obesity. Its presence does not diagnose diabetes or obesity or prescribe a particular diet.

PPARG2: C34G (Pro12Ala)

Possible genotypes: C/C, C/G, G/G. In this nomenclature, C corresponds to Pro and G to Ala: C/C is Pro/Pro, C/G is Pro/Ala, and G/G is Ala/Ala. PPARG is a nuclear receptor regulating adipocyte differentiation, lipid metabolism and insulin sensitivity. Associations with metabolic traits do not reliably predict an individual response to a low-calorie diet or exercise.

ADRB2: C79G (Gln27Glu) and A46G (Arg16Gly)

C79G genotypes are C/C, C/G and G/G; A46G genotypes are G/G, G/A and A/A. ADRB2 encodes the β2-adrenergic receptor involved in catecholamine responses. These variants have been studied in relation to receptor expression, asthma, body weight and metabolic syndrome. The direction and magnitude of associations vary between studies; they cannot assign an individual asthma or metabolic-syndrome risk or a training type.

Metabolic syndrome is a combination of cardiometabolic factors, including central obesity, impaired glucose metabolism, blood pressure and lipid measurements. It is assessed by clinical criteria, not ADRB2.

ADRB3: T190C (Trp64Arg)

Possible genotypes: T/T, T/C, C/C. ADRB3 encodes the β3-adrenergic receptor involved in catecholamine signaling, lipolysis and thermogenesis. Studies of Trp64Arg and obesity do not establish a universal risk ratio or a guaranteed dietary recommendation for a carrier.

Variant frequencies depend on ancestry and the sample studied. These common variants should not be described as separate autosomal dominant diseases. Diet and activity choices should reflect clinical status, preferences, accessibility and the sustainability of changes.