Our genetic makeup determines our appearance (the colour of our hair and eyes, if we are tall or short) and how we respond to different external factors (nutrients, physical activities, medications). Our DNA can explain how we metabolize certain substances and how our body can lose and gain weight.
It refers to the ability to move objects, expressed in terms of absolute weight. For example: “She can squat 80 kilos for one repetition”.
A natural substance that is found in plants and has bitter taste.
One of the variants of genetic material on a specific location (locus) of the chromosome. An individual has a chromosome pair where there are two alleles, which can be identical or not, and this is called homozygosis or heterozygosis. Different alleles in a human population can be the reason for inherited characteristics, such as blood type or hair colour.
A gene variant that dominates in the expression over the other allele and therefore appears more often in the population. According to classical Mendelian genetics, the dominant allele is the reason for a 3-fold larger incidence of one phenotype, which is the consequence of allele forms A/A, A/a and a/A where A denotes the dominant allele.
Gene variant that is expressed only if both alleles are recessive. It appears less frequently in the population. According to classical Mendelian genetics, the probability of the presence of a phenotype which results from two recessive alleles (a/a) is 0.25.
A basic structural unit, from which protein is built. Different combinations of amino acids represent different proteins. The exact combination of amino acids is encoded in DNA with three sequential nucleotides: GCU is the code for amino acid alanine, UGU for cysteine, etc.
Prevents the development of cancer.
Substances which protect us from oxidative stress.
A blood vessel that carries blood away from the heart. The main artery is the aorta.
An overview of variations in the human genome with the aim of finding the genetic links to human diseases such as asthma, high blood pressure, etc. In order to figure out these links, the genomes of the disease-free individuals must be compared to the genomes of the people who have the disease. In both groups, known sites for SNPs are checked in the genomes in order to see if some SNPs appear more often in the diseased group than in the healthy group. If certain SNPs occur mainly in the patient group, it can be assumed that they are linked to the occurrence of disease. The strength of this association is revealed by the result of the association study. Given the SNPs in his genome and the incidence of disease in the population, we can use this association to calculate the risk of the disease occurrence for a random individual whom we assume to originate from the same population. The data of association studies, published in prestigious scientific journals, are used by GenePlanet to calculate the risk of disease on the basis of personal genotyping.