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È un test nutrigenetico che analizza in 22 geni la presenza di specifiche variazioni genetiche legate ai processi metabolici dei nutrienti e delle tossine. I risultati del test permettono di elaborare:

  1. il tuo fabbisogno nutrizionale: di quanti nutrienti hai bisogno?
  2. la tua dieta personale: quali alimenti aumentare o diminuire?
  3. la tua integrazione personalizzata: di quali integratori hai bisogno?

In questo modo il test ottimizza la tua nutrizione per supportare al meglio i processi metabolici e fisiologici in 12 aree critiche per la salute ed il benessere del tuo corpo.

Perché dovrei fare il test DNA-Wellness-Diet®?

La genetica ha rivelato che ciascuno di noi è un individuo unico diverso dagli altri tanto nell’aspetto esteriore quanto nei processi metabolici. Queste differenze sono causate da alcune variazioni genetiche puntiformi (SNP) che possono determinare la mancata produzione di proteine, o la produzione di proteine e recettori mal funzionanti o di enzimi che richiedono una quantità maggiore di vitamine o minerali per funzionare. In quest’ultimo caso, se le vitamine o i minerali sono insufficienti si ha un blocco o rallentamento del processo metabolico che può essere risolto dall’aumento delle vitamine o minerali coinvolte nel processo. Il DNA-Wellness-Diet permette di conoscere la presenza di blocchi o rallentamenti metabolici e di compensare tali situazioni con una nutrizione personalizzata.

Objectives: identifying genetic variants in 22 genes linked to metabolisms of food nutrients and xenobiotics that have been shown to have an impact on 12 functional areas relevant to the wellness state and that can be compensated by optimizing the individual nutritional intake through personalized food nutrients and food supplement schedule.

SNPs & Genes Role in the DNA-Wellness-Diet®


Gene: APOC3, Apolipoprotein C-III
SNP tested: C3175G;
Chromosome location: 11q23.1-23.2
Total publications on the gene: 195
Meta-Analysis: 30

Apolipoprotein C-III is a very low density lipoprotein (VLDL) protein. APOC3 inhibits lipoprotein lipase and hepatic lipase; it is thought to delay catabolism of triglyceride-rich particles. The APOA1, APOC3 and APOA4 genes are closely linked in both rat and human genomes. The A-I and A-IV genes are transcribed from the same strand, while the A-1 and C-III genes are convergently transcribed. An increase in apoC-III levels induces the development of hypertriglyceridemia.
The APOC3 3175 polymorphism (a.k.a. 'the SstI polymorphism') is located in exon 4 in the 3' untranslated region (3'UTR) of the gene encoding apolipoprotein C-III (apo C-III). The SNP tested in the DNA-Wellness-Diet has been demonstrated in numerous studies to be associated to high triglycerides levels.

Gene: LPL, Lipoproteinlipase
SNP tested: C1595G;
Chromosome location: 8p22
Total publications on the gene: 325
Meta-Analysis: 41

LPL encodes lipoprotein lipase, which is expressed in heart, muscle, and adipose tissue. LPL functions as a homodimer, and has the dual functions of triglyceride hydrolase and ligand/bridging factor for receptor-mediated lipoprotein uptake. The primary function of this lipase is the hydrolysis of triglycerides of circulating chylomicrons and very low density lipoproteins (VLDL): Triacylglycerol + H2O = diacylglycerol + a carboxylate. Binding to heparin sulphate proteogylcans at the cell surface is vital to the function. The apolipoprotein, APOC2, acts as a coactivator of LPL activity in the presence of lipids on the luminal surface of vascular endothelium. Severe mutations that cause LPL deficiency result in type I hyperlipoproteinemia, while less extreme mutations in LPL are linked to many disorders of lipoprotein metabolism. The variation tested in the DNA-Wellness-Diet has been found linked to reduced level of HDL and increased level of TG.


Gene: MTHFR, Methylentetrahydrofolate reductase
SNP tested: C677T
Chromosome location: 1p36.3
Total publications on the gene: 2205
Meta-Analysis: 282

The protein encoded by this gene catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine:
5,10-methylenetetrahydrofolate + NAD(P)H=5-methyltetrahydrofolate + NAD(P)+ (FAD is the cofactor). Genetic variation in this gene influences susceptibility to occlusive vascular disease, neural tube defects, colon cancer and acute leukemia, and mutations in this gene are associated with methylenetetrahydrofolate reductase deficiency (MTHFRD). The SNP tested in the DNA-Wellness-Diet is associated to an increased level of homocysteine that in turn has been found linked to an increased rate of deep vein thrombosis.


Gene: ACE; Angiotensin I converting enzyme (peptidyl-dipeptidase A) 1
Variation tested: Ins/Del
Chromosome location: 17q23.3
Total publications on the gene: 1664
Meta-Analysis: 211

This gene encodes an enzyme involved in catalyzing the conversion of angiotensin I into a physiologically active peptide angiotensin II by release of the terminal His-Leu, this results in an increase of the vasoconstrictor activity of angiotensin. Angiotensin II is a potent vasopressor and aldosterone-stimulating peptide that controls blood pressure and fluid-electrolyte balance. This enzyme plays a key role in the renin-angiotensin system. Also able to inactivate bradykinin, a potent vasodilator. Has also a glycosidase activity which releases GPI-anchored proteins from the membrane by cleaving the mannose linkage in the GPI moiety.
Many studies have associated the presence or absence of a 287 bp Alu repeat element in this gene with the levels of circulating enzyme or cardiovascular pathophysiologies. Multiple alternatively spliced transcript variants encoding different isoforms have been identified, and two most abundant spliced variants encode the somatic form and the testicular form, respectively, that are equally active.
The Allele I tested in the DNA-Wellness-Diet is linked to an increased blood pressure with increased NaCl consumption. In addition to this, the allele D can negatively impact glycemic response to sugar.


Gene: PPARG; Peroxisome Proliferator-Activated Receptor Gamma
SNP tested: Pro12Ala
Chromosome location: 3p25
Total publications on the gene: 599
Meta-Analysis: 95

This gene encodes a member of the peroxisome proliferator-activated receptor (PPAR) subfamily of nuclear receptors. Three subtypes of PPARs are known: PPAR-alpha, PPAR-delta, and PPAR-gamma. It forms a heterodimer with the retinoic acid receptor RXRA called adipocyte-specific transcription factor ARF6 That regulate transcription of various genes.
This Receptor binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. It is a key regulator of adipocyte differentiation and glucose homeostasis. Genetic variation in PPARG may influence body mass index (BMI). Additionally, PPAR-gamma has been implicated in the pathology of numerous diseases including susceptibility to obesity, to type 2 insulin-resistant diabetes, hypertension, atherosclerosis (with increase of carotid intimal medial thickness-CIMT) and colon cancer. Alternatively spliced transcript variants that encode different isoforms have been described. The SNP tested influence the level of expression of the protein and the Ala version has been associated with a beneficial effect on the glycemic and insulin response to refined sugar.

Gene ACE: see above.


Gene: CYP1A2*1F; cytochrome P450 1A2
SNP tested: –163A>C
Chromosome location: 15q24.1
Total publications on the gene: 252
Meta-Analysis: 30

This gene encodes a member of the cytochrome P450 superfamily of enzymes. Cytochromes P450 are a group of heme-thiolate monooxygenases. The protein encoded by this gene localizes to the endoplasmic reticulum and its expression is induced by some polycyclic aromatic hydrocarbons (PAHs), some of which are found in cigarette smoke, but also in grilled meat. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. The enzyme's endogenous substrate is unknown; however It oxidizes a variety of structurally unrelated compounds, including steroids, fatty acids, and xenobiotics such as drugs (i.e. acetaminophen), Caffeine, Aflatoxin-B1, and PAHs. Most active in catalyzing 2-hydroxylation. Caffeine is metabolized primarily by cytochrome CYP1A2 in the liver through an initial N3-demethylation. Also acts in the metabolism of aflatoxin B1 and acetaminophen. Participates in the bioactivation of carcinogenic aromatic and heterocyclic amines. Catalizes the N-hydroxylation of heterocyclic amines and the O-deethylation of phenacetin. CATALYTIC ACTIVITY: RH + reduced flavoprotein + O(2) = ROH +oxidized flavoprotein + H(2)O. COFACTOR: Heme group.
The CYP1A2*1F allele which is quite common (40 to 50%) is due to a substitution of a base in the non-coding region of the CYP1A2 gene and has the effect of decreasing the enzyme inducibility. Individuals who are homozygous for the CYP1A2*1F allele are 'slow' caffeine metabolizers. Thus for these individual increased intake of caffeine seems to be associated with a concomitant increase in the risk of non-fatal myocardial infarction (MI). The SNP tested in the DNA-Wellness-Diet has been found associated to a change in the enzymatic rate that alters the production rate of bioactivated carcinogens and the metabolic clearance of caffeine.

Gene: ADH1C; Alcohol dehydrogenase 1C (class I), gamma polypeptide
SNP tested: Ile349Val
Chromosome location: 4q23
Total publications on the gene: 148
Meta-Analysis: 15

This gene encodes class I alcohol dehydrogenase, gamma subunit, which is a member of the alcohol dehydrogenase family. Members of this enzyme family metabolize a wide variety of substrates, including ethanol, retinol, other aliphatic alcohols, hydroxysteroids, and lipid peroxidation products.
Catalytic activity: An alcohol + NAD+ = an aldehyde or ketone + NADH. Cofactor: Zn ion.
Class I alcohol dehydrogenase, consisting of several homo- and heterodimers of alpha, beta, and gamma subunits, exhibits high activity for ethanol oxidation and plays a major role in ethanol catabolism. Three genes encoding alpha, beta and gamma subunits are tandemly organized in a genomic segment as a gene cluster.
The SNP tested is associate to a slower rate of ethanol oxidation and therefore to a reduced metabolic clearance.


Gene: GSTM1; Glutathione S-transferase mu 1
Variation tested: Ins/Del
Chromosome location: 1p13.3
Total publications on the gene: 1501
Meta-Analysis: 523

Eight distinct classes of the soluble cytoplasmic mammalian glutathione S-transferases have been identified: alpha, kappa, mu, omega, pi, sigma, theta and zeta. This gene encodes a glutathione S-transferase that belongs to the mu class. The mu class of enzymes functions in the detoxification of electrophilic compounds, including carcinogens, therapeutic drugs, environmental toxins and products of oxidative stress, by conjugation with glutathione. The genes encoding the mu class of enzymes are organized in a gene cluster on chromosome 1p13.3 and are known to be highly polymorphic. These genetic variations can change an individual's susceptibility to carcinogens and toxins as well as affect the toxicity and efficacy of certain drugs. Null mutations of this class mu gene have been linked with an increase in a number of cancers, likely due to an increased susceptibility to environmental toxins and carcinogens. Multiple protein isoforms are encoded by transcript variants of this gene. The Variation tested in the DNA-Wellness-Diet is associated with the loss of enzymatic function and impaired detoxification phase-II conjugation with glutathione.

Gene: GSTT1; Glutathione S-transferase theta 1
Variation tested: Ins/Del
Chromosome location: 22q11.23
Total publications on the gene: 1260
Meta-Analysis: 431

Glutathione S-transferase (GST) theta 1 (GSTT1) is a member of a superfamily of proteins that catalyze the conjugation of reduced glutathione to a variety of electrophilic and hydrophobic compounds. Human GSTs can be divided into five main classes: alpha, mu, pi, theta, and zeta. The theta class includes GSTT1 and GSTT2. The GSTT1 and GSTT2 share 55% amino acid sequence identity and both of them were claimed to have an important role in human carcinogenesis.
GSTT Conjugates reduced glutathione to a wide number of exogenous and endogenous hydrophobic electrophiles. Acts on 1,2-epoxy-3-(4-nitrophenoxy)propane, phenethylisothiocyanate 4-nitrobenzyl chloride and 4-nitrophenethyl bromide. Displays glutathione peroxidase activity with cumene hydroperoxide.
The catalytic reaction is: RX + glutathione = HX + R-S-glutathione
Found in erythrocyte. Expressed at low levels in liver. In lung, expressed at low levels in Clara cells and ciliated cells at the alveolar/bronchiolar junction. Absent from epithelial cells of larger bronchioles.
The GSTT1 gene is absent from 38% of the population. The presence or absence of the GSTT1 gene is coincident with the conjugator (GSST1+) and non-conjugator (GSTT1-) phenotypes respectively. The GSTT1+ phenotype can catalyze the glutathione conjugation of dichloromethane, a metabolic pathway that had been shown to be mutagenic in Salmonella typhimurium mutagenicity tester strains and was believed to be responsible for the carcinogenicity of dichloromethane in the mouse.
Individual differences in the metabolism of methyl bromide, ethylene oxide, and methylene chloride in human blood have been attributed to the genetic polymorphism of GSTT1. Genotoxic effects such as induction of sister chromatid exchanges (SCE) after exposure of human blood to methyl bromide and other agents in vitro were found to be more pronounced in non-conjugators. GST has been implicated in detoxifying mutagenic electrophilic compounds; patients with reduced ability to metabolize environmental carcinogens or toxins may be at risk of developing aplastic anemia. Among the aplastic anemia patients, 17.5% had chromosomal abnormalities at the time of diagnosis, and all aplastic anemia patients with chromosomal abnormalities showed GSTT1 gene deletions.
The Variation tested in the DNA-Wellness-Diet is associated with the loss of GSTT1 enzymatic function and impaired detoxification phase-II conjugation with glutathione.


Gene: SOD2 ; Superoxide dismutase 2, mitochondrial
Variation tested: C-28T
Chromosome location: 6q25.3
Total publications on the gene: 298
Meta-Analysis: 58

This gene is a member of the iron/manganese superoxide dismutase family. It encodes a mitochondrial protein that forms a homotetramer and binds one manganese ion per subunit. This protein binds to the superoxide byproducts of oxidative phosphorylation and converts them to hydrogen peroxide and diatomic oxygen, destroying radicals which are normally produced within the cells and which are toxic to biological systems. Catalytic reaction: 2 superoxide + 2 H+ = O2 + H2O2 (cofactor: 1Mn ion per subunit)
Alternate transcriptional splice variants, encoding different isoforms, have been characterized. Mutations in this gene have been associated with idiopathic cardiomyopathy (IDC), premature aging, sporadic motor neuron disease, and cancer. Genetic variation in SOD2 is associated with susceptibility to microvascular complications of diabetes type 6 (MVCD6) [MIM:612634]. These are pathological conditions that develop in numerous tissues and organs as a consequence of diabetes mellitus. They include diabetic retinopathy, diabetic nephropathy leading to end-stage renal disease, and diabetic neuropathy. Diabetic retinopathy remains the major cause of new-onset blindness among diabetic adults. It is characterized by vascular permeability and increased tissue ischemia and angiogenesis.
The SNP tested in the DNA-Wellness-Diet is associated with a reduced anti-radical capacity of SOD2.


Gene: IL-6 ; interleukin 6 (interferon, beta 2)
Variation tested: G-174C
Chromosome location: 7p21
Total publications on the gene: 119
Meta-Analysis: 159

This gene encodes a cytokine that functions in inflammation and the maturation of B cells. The protein is primarily produced at sites of acute and chronic inflammation, where it is secreted into the serum and induces a transcriptional inflammatory response through interleukin 6 receptor, alpha. The functioning of this gene is implicated in a wide variety of inflammation-associated disease states, including susceptibility to diabetes mellitus and systemic juvenile rheumatoid arthritis (RASJ) [MIM:604302]. Genetic variations in IL6 may be correlated with bone mineral density (BMD). Low BMD is a risk factor for osteoporotic fracture. Osteoporosis is characterized by reduced bone mineral density, disruption of bone microarchitecture, and the alteration of the amount and variety of non-collagenous proteins in bone. Osteoporotic bones are more at risk of fracture.
The SNP tested in the Dna-Wellness-Diet is associated to an increased level of the cytokine and hence to an increased level of general inflammation.

Gene: TNF; Tumor Necrosis Factor (TNF-alpha)
Variation tested: G-308A
Chromosome location: 6p21.3
Total publications on the gene: 1932
Meta-Analysis: 245

This gene encodes a multifunctional proinflammatory cytokine that belongs to the tumor necrosis factor (TNF) superfamily. This cytokine is mainly secreted by macrophages and can induce cell death of certain tumor cell lines. It can bind to, and thus functions through its receptors TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. TNF-alpha is involved in the regulation of a wide spectrum of biological processes including cell proliferation, differentiation, apoptosis, lipid metabolism, and coagulation. It is a potent pyrogen causing fever by direct action or by stimulation of interleukin-1 secretion and is implicated in the induction of cachexia. This cytokine has been implicated in a variety of diseases, including autoimmune diseases, insulin resistance, and cancer. Knockout studies in mice also suggested the Neuroprotective function of this cytokine.
Genetic variations in TNF influence susceptibility to hepatitis B virus (HBV) infection [MIM:610424]. TNF it is also involved in disease and its Genetic variations are a cause of susceptibility to psoriatic arthritis (PSORAS) [MIM:607507]. PSORAS is an inflammatory, seronegative arthritis associated with psoriasis. It is a heterogeneous disorder ranging from a mild, non-destructive disease to a severe, progressive, erosive arthropathy.
The SNP tested in the DNA-wellness-Diet is in the promoter region and influence the level of TNF-alpha expression, hence having a direct impact on the general inflammation.


Gene: VDR; vitamin D (1,25-dihydroxyvitamin D3) receptor
Variation tested: C>T (taq1)
Chromosome location: 12q13.11
Total publications on the gene: 767
Meta-Analysis: 45

This gene encodes the nuclear hormone receptor for vitamin D3. This receptor also functions as a receptor for the secondary bile acid lithocholic acid. The receptor belongs to the family of trans-acting transcriptional regulatory factors and shows sequence similarity to the steroid and thyroid hormone receptors.
Regulates transcription of hormone sensitive genes via its association with the WINAC complex, a chromatin-remodeling complex. Recruited to promoters via its interaction with the WINAC complex subunit BAZ1B/WSTF, which mediates the interaction with acetylated histones, an essential step for VDR-promoter association. Plays a central role in calcium homeostasis though the receptor regulates a variety of other metabolic pathways, such as those involved in the immune response and cancer. Mutations in this gene are associated with type II vitamin D-resistant rickets. Genetic variations in VDR may determine Mycobacterium tuberculosis susceptibility [MIM:607948].
Defects in VDR are the cause of rickets vitamin D-dependent type 2A (VDDR2A) [MIM:277440]. A disorder of vitamin D metabolism resulting in severe rickets, hypocalcemia and secondary hyperparathyroidism.
A single nucleotide polymorphism in the initiation codon results in an alternate translation start site three codons downstream. Alternative splicing results in multiple transcript variants encoding different proteins.
The polymorphism tested in the DNA-Wellness-Diet is localized in the exon 9 of the VDR gene at the restriction site of the endonuclease Taq1; it consists of a nucleotide change from C to t; the allele T is also defined as Allele T, whereas the nucleotide C is also defined as Allele t. This polimorphism has been associated to a reduced bone mineral density (BMD).

Gene: COL1A1 ; Collagen, type I, alpha 1
SNP tested: G>T (S/s)
Chromosome location: 17q21.33
Total publications on the gene: 149
Meta-Analysis: 13

This gene encodes the pro-alpha1 chains of type I collagen whose triple helix comprises two alpha1 chains and one alpha2 chain. Type I is a fibril-forming collagen found in most connective tissues and is abundant in bone, cornea, dermis and tendon and ligaments. In bones the fibrils are mineralized with calcium hydroxyapatite.
Two transcripts, resulting from the use of alternate polyadenylation signals, have been identified for this gene.
Defects in COL1A1 are a cause of osteogenesis imperfecta type 1 (OI1) [MIM:166200], type 2A (OI2A) [MIM:166210], type 3 (OI3) [MIM:259420], and type 4 (OI4) [MIM:166220]. Mutations in this gene are associated with Ehlers-Danlos syndrome type VIIA, Ehlers-Danlos syndrome Classical type, Caffey Disease and idiopathic osteoporosis.Genetic variations in COL1A1 are a cause of susceptibility to osteoporosis (OSTEOP) [MIM:166710]; also known as involutional or senile osteoporosis or postmenopausal osteoporosis. Osteoporosis is characterized by reduced bone mass, disruption of bone microarchitecture without alteration in the composition of bone. Osteoporotic bones are more at risk of fracture. Reciprocal translocations between chromosomes 17 and 22, where this gene and the gene for platelet-derived growth factor beta are located, are associated with a particular type of skin tumor called dermatofibrosarcoma protuberans, resulting from unregulated expression of the growth factor.
The SNP tested in the DNA-Wellness-Diet is located at the polymorphic site Sp1 in the regulatory region 5-prime untranslated region (UTR) of the gene COL1A1 and it has been associated, both in homozygote (ss) and heterozygote forms (Ss) to an altered bone micro-architecture and increased relative risk of 2.97 (95% confidence interval 1.63-9.56) for vertebral fracture in individuals who carried the 's' allele. It has been reported that common polymorphic variants in the 5-prime UTR of COL1A1 regulate transcription by affecting DNA-protein interactions, and that increased levels of transcription correlated with reduced BMD values in vivo by altering the normal 2:1 ratio between alpha-1(I) and alpha-2(I) chains. While the mechanisms that underlie this association remained to be defined, the COL1A1 Sp1 polymorphism appeared to be an important marker for low bone mass and vertebral fracture, raising the possibility that genotyping at this site may be of value in identifying women who are at risk of osteoporosis.


Gene: 5HTT(SLC6A4); solute carrier family 6 (neurotransmitter transporter, serotonin), member 4
Variation tested: 44bp ins
Chromosome location: 17q11.2
Total publications on the gene: 1162
Meta-Analysis: 116

This gene encodes an integral membrane protein that transports the neurotransmitter serotonin from synaptic spaces into presynaptic neurons. The encoded protein terminates the action of serotonin and recycles it in a sodium-dependent manner. Plays a key role in mediating regulation of the availability of serotonin to other receptors of serotonergic This protein is a target of psychomotor stimulants, such as amphetamines and cocaine, and is a member of the sodium:neurotransmitter symporter family. A repeat length polymorphism in the promoter of this gene has been shown to affect the rate of serotonin uptake and may play a role in sudden infant death syndrome, aggressive behavior in Alzheimer disease patients, and depression-susceptibility in people experiencing emotional trauma.
A polymorphism in the promoter region (5-HTT gene-linked polymorphic region, 5-HTTLPR) is located approximately 1 kb upstream of the transcription initiation site and is composed of 16 repeat elements. The polymorphism consists of a 44-bp insertion or deletion involving repeat elements 6 to 8. The short allele is associated with lower transcriptional efficiency of the promoter compared with the long allele. Over half of the Caucasian population has a short allele. Individuals with one or two copies of the short allele exhibit more depressive symptoms, diagnosable depression and suicidality in relation to stressful life events than individuals homozygous for the long allele. In addition, this polimorphism may play a role in sudden infant death syndrome and aggressive behavior in Alzheimer disease patients.
The polymorphism Val-425 seems to be linked to a susceptibility to obsessive-compulsive disorder (OCD) . Genetic variations in SLC6A4 determine the genetic susceptibility to alcoholism [MIM:103780].
The variation testes in the DNA-Wellness-diet is the presence or absence of the short allele (s), that is associated with susceptibility to depression in response to stressful events.


Gene: LCT; Lactase
Variation tested: -13910-CT
Chromosome location: 2q21
Total publications on the gene: 72
Meta-Analysis: -

The protein encoded by this gene belongs to the family 1 of glycosyl hydrolases. The protein is integral to plasma membrane, localized in the intestinal brush border, and has both phlorizin hydrolase activity and lactase activity.
Catalytic reactions of LCT are: 1) Lactose + H2O = D-galactose + D-glucose. 2)Glycosyl-N-acylsphingosine + H2O = N-acylsphingosine + a sugar.
Defects in LCT are the cause of congenital lactase deficiency (COLACD); also known as hereditary alactasia or disaccharide intolerance II. Congenital lactase deficiency is a an autosomal recessive, rare and severe gastrointestinal disorder. It is characterized by watery diarrhea in infants fed with breast milk or other lactose-containing formulas. An almost total lack of LCT activity is found in jejunal biopsy material of patients with congenital lactase deficiency. Opposite to congenital lactase deficiency, adult-type hypolactasia, also known as lactose intolerance, is the most common enzyme deficiency worldwide. It is caused by developmental down-regulation of lactase activity during childhood or early adulthood. The decline of lactase activity is a normal physiological phenomenon; however, the majority of Northern Europeans have the ability to maintain lactase activity and digest lactose throughout life (lactase persistence). The down-regulation of lactase activity operates at the transcriptional level and it is associated with a noncoding variation in the MCM6 gene, located in the upstream vicinity of LCT.
The SNP tested in the DNA-Wellness-Diet is the C/T(-13910) variant that occurs approximately 14 kb upstream of the LCT gene (603202) and affects a binding site of transcription factor AP-2 (see 107580). The C allele, associated with lactase non-persistence, is in the consensus binding motif, whereas the T variant disrupts this motif, allowing somehow gene expression. Note that this test is not a diagnostic test: a person with lactase deficiency may still be tolerant to lactose as a result of the gust lactobacilli flora. However, persons intolerant to lactose do have lack of LCT expression.


Gene: HLA-DQ2 and DQ8; major histocompatibility complex, class II
HLA-DQ alleles tested: DQA1*0201, DQA1*0501, DQA1*03, DQB1*02, DQB1*0301, DQB1*0302, DRB1*04, DRB1*07, DRB1*0301, DRB1*11, DRB1*12
Chromosome location: 6p21.3
Total publications on genes and celiac disease: 208
Meta-Analysis: 16
GWAS: 10

Celiac disease, also known as celiac sprue and gluten-sensitive enteropathy, is a multifactorial disorder of the small intestine that is influenced by both environmental and genetic factors. It is characterized by malabsorption resulting from inflammatory injury to the mucosa of the small intestine after the ingestion of wheat gluten or related rye and barley proteins. It is characterized by INFLAMMATION AND atrophy of the mucosa of the upper small intestine, loss of MICROVILLI structure, failed INTESTINAL ABSORPTION, and MALNUTRITION. Manifestations include diarrhea, malabsorption, steatorrhea, and nutritional and vitamin deficiencies.
Long regarded as gastrointestinal disorder of childhood, the disease is now considered to be a chronic systemic autoimmune disease and is more often diagnosed in adults than in children. Greater awareness of the presentation of celiac disease and the availability of accurate serologic tests led to the realization that the disorder is relatively common, affecting 1 of every 120 to 300 persons in both Europe and North America. The prevalence of celiac disease among Finnish schoolchildren is at least 1 case in 99 children. With a prevalence close to 1%, celiac disease is the most common food intolerance in general western populations.
A susceptibility to celiac disease has been found to be genetically determined by possession of specific HLA-DQ alleles (major histocompatibility complex, class II) on chromosome 6p21.3; this region has been designated CELIAC1. The class II MHC proteins are heterodimers of one alfa and one beta- transmembrane chains, with highly variable N-terminal domains (alfa-1 and beta-1) and two Ig-like conserved domains closed to the cell membrane. Class II MHC proteins play a central role in the immune system by presenting peptides derived from extracellular proteins and are expressed in antigen presenting cells (APC: B lymphocytes, dendritic cells, macrophages). On chromosome 6 there are three types of genes that encode for Class II MHC protein: DP (encodes for α and β), DQ (encodes for α and β), DR (encodes for α and 2 β). Depending on the parent allele contribution, there could be several types of MHC class II. HLA-DQ2 (heterodimer of DQA1*05:01/DQB1*02:01) is associated with more than 90% of celiac disease patients; a minority of patients displays HLA-DQ8 (heterodimer of DQA1*03/DQB1*03:02).
The DNA-Wellness-Diet test analyses the DNA-sample from oral mucosa by PCR-SSP (allele-specific primer) to determine the presence of the HLA alleles:
DQA1*0201, DQA1*0501, DQA1*03, DQB1*02, DQB1*0301, DQB1*0302, DRB1*04, DRB1*07, DRB1*0301, DRB1*11, DRB1*12.
On the whole, 11 HLA-alleles are tested. The result is visualized by agarose gel electrophoresis. The association of alleles defines the serological HLA DQ2 and DQ8 haplotypes which give predisposition to celiac disease. It has to be noted that this is not a diagnostic test of celiac disease and that the presence of DQ2 and DQ8 means an increased probability of having the disease; it is sensible to perform additional diagnostic analysis to verify the presence of the disease. On the contrary, the negativity to DQ2 and DQ8 let exclude the presence of the disease.


Gene: IL-6, GSTM1, GSTT1
Increased pro-inflammatory IL-6 level and impaired detoxification enzymatic activity may increase the sensitivity to the contact allergen nichel.
See IL-6, GSTM1, GSTT1

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