Nutrigenetics
Variants associated with nutrient metabolism and with dietary traits. The level of evidence is stated on each card: not all the associations have the same support, and they are worth reading with that label attached.

All 15 of your dietary traits, with their support stated
Your summary: 15 traits read — 4 with established clinical use, 2 with solid support and 9 with weaker support. Each card states its level of evidence.
Lactose tolerance
G/AYou carry one copy of the lactase persistence variant. Lactose is generally tolerated, although symptoms may occur with high loads. A G/G result would indicate non-persistence. This position explains lactase persistence in European ancestry; in African or Middle Eastern ancestry other variants are involved that this chip does not measure, so there a G/G is not enough to claim non-persistence.
Genetic risk of celiac disease
DQ2.5 negativo · DQ8 negativoMore than 99% of people with celiac disease carry DQ2.5 or DQ8, so not having them makes the diagnosis very unlikely. It does not rule it out: these haplotypes are inferred from tag variants on the chip rather than from HLA typing, and cases with DQ2.2 or with a half heterodimer do exist. If there are symptoms, the diagnosis is made with serology and biopsy, not with this result.
Alcohol metabolism
G/GWithout the ALDH2 deficiency variant (facial flushing). This does not imply that alcohol consumption is harmless.
Iron overload (hemochromatosis)
G/GYou do not carry the C282Y variant, which is responsible for most cases of hereditary hemochromatosis.
How quickly you break down alcohol
C/TOne copy of the fast variant. The first step of the breakdown speeds up and acetaldehyde builds up sooner, so discomfort from alcohol tends to appear with a smaller amount. It goes hand in hand with the ALDH2 result: if that enzyme also works slowly, the effects add up.
Triglycerides and blood fats
A/GOne copy of the variant. It is associated with higher fasting triglycerides and with a larger rise after high-fat meals. This is an average tendency: the actual value is measured with a lipid panel.
Caffeine metabolism
A/CCaffeine is cleared more slowly. It has been associated with greater sensitivity to its effect on sleep and, in some studies, with higher cardiovascular risk at high intakes. The evidence is consistent but the effect is small.
Folate metabolism
C/TVery common in the general population. On its own it does NOT justify supplementing with methylfolate or ordering additional testing. Maintaining an adequate folate intake is the standard recommendation, the same as for anyone else.
Plant-based omega-3 conversion
G/TIntermediate capacity to convert ALA (of plant origin) into EPA/DHA. In diets without fish, a direct source of EPA/DHA may be favored.
Circulating vitamin D
A/CAssociated with a lower concentration of vitamin D binding protein. The clinically useful measure remains 25-OH-vitamin D measured in blood, not the genotype.
Caffeine, sleep, and jitteriness
C/TOne copy of the variant associated with more jitteriness and worse sleep at the same dose. The effect is small and is noticeable mainly with coffee in the afternoon.
Appetite and feeling of fullness
T/COne copy of the variant. On average it is associated with somewhat more hunger and slightly higher body weight. The measured effect is a few hundred grams: it is real at the population level and very small at the level of an individual.
Bitter taste perception
C/GA trait with no clinical implication. It may influence preference for cruciferous vegetables (broccoli, cauliflower).
Preference for sweet foods
G/AOne copy of the variant associated with higher consumption of sugar and candy. FGF21 is a hormone involved in macronutrient preference; the association is consistent but the effect is small.
Salt sensitivity
A/GOne copy of the variant. The studies associating it with higher blood pressure on high-sodium diets do not always replicate, and the effect is small.
Read each card with its evidence level in view, because this section mixes two kinds of result. Level A and B traits have established clinical support — lactose tolerance, alcohol metabolism or iron overload are not curiosities, and what those cards say holds. This warning is for the level C and D ones: for those, no study has shown that adjusting your diet according to the genotype improves a health outcome; the effects are small and are buried under everyday diet, weight, physical activity, and personal history. Anyone selling you a «DNA-based diet» built on that class of traits is selling you something the evidence does not support.