From several different inheritance studies, it appeared that the genetic component of overweight or fat mass appears to be between 20% and 90%. However, it should be noted that while such studies can measure the effect of all genes, they do not identify the genes that are responsible. The genes we analyze are certainly only part of that 20% to 90%.
Here are some examples:
In a meta-analysis of 97 studies and 44,833 participants, it was shown that the bad gene variant here explained a variation in BMI of 0.24 or approximately 700 g body weight. (Kurokawa et al 2008. →)
“Maes et al. has provided a comprehensive review of this literature, the results of which indisputably support a heritable component of BMI and fat mass. Heritability estimates fall in the 20 to 80 percent range when estimated from family studies that compared parent-child and sibling correlations, 20 to 60 percent when estimated from adoption studies, and 50 to 90 percent when estimated from twin studies. For example, in an analysis of more than 3,500 pairs of twins who were 4 years old, shared environmental influences accounted for 24 percent of the weight differences adjusted for length in boys and 25 percent of the variance in girls.”
So from these two genes (out of 8 that we have) explain a BMI variation of 1.28. Thus, individuals with the unfavorable gene profile have an average BMI 1.28 points higher than individuals with the favorable profile in only these two genes. This is only a brief overview of 2 out of 8 genes. For an overweight of 10 kg (variation of 2.9 BMI points), only these two of eight gene variations cause 1.28 points, or 43% of the variation. At 20 kg overweight it is 22% of variation and at 30 kg overweight it is 14%. Genes are therefore not solely responsible for obesity, but they certainly have a relevant influence on it.
Caution is advised
The predisposition to obesity may be interesting, but it has few actual applications. More importantly, what influence do genes have on how effective certain weight loss strategies (exercise or calorie reduction) are in a person? In a quick research regarding our genes, we came up with the following numbers:
FTO-Gen und Fettempfindlichkeit:
Individuals who consume a lot of fat and carry the unfavorable gene variation of this gene have a BMI 2.4 points higher than individuals who consume a lot of fat and have the favorable gene variation. That’s a difference of about 8 kg! →
PPARG Gen und Einfluss auf Fettempfindlichkeit:
Individuals with the unfavorable gene variant who had particularly high dietary fat intake had an average of 1.9 BMI points more than individuals with the favorable gene variant who had particularly high dietary fat intake. That’s a difference of 6.6 kg! →
PPARG-Gen Einfluss auf Gewichtsreduktion bei Kalorienreduktion und sportlicher Betätigung:
Individuals with the favorable genetic variation lost 4.9% more weight than individuals with the unfavorable genetic variation. →
ADRB3-Gen Einfluss auf Gewichtsreduktion durch sportliche Betätigung:
Individuals who participate in sports have a 2.98-fold higher risk (298%) of being overweight with the unfavorable gene variant. →
ADRB3-Gen Einfluss auf Sport und Kalorienreduktion:
Individuals with the unfavorable gene variant lost 0.73 kg less weight than individuals with the favorable gene variant. →
APOA5-Gen Einfluss auf Gewichtsreduktionseffektivität:
Individuals with the favorable gene variant reduced their BMI by 13.4%, whereas individuals with the unfavorable gene variant reduced their BMI by 0.4% with the same effort. →
APOA2-Gen und Fettempfindlichkeit:
People who eat a lot of fat and have the unfavorable gene variant have on average a 6.2% higher BMI than people who eat a lot of fat and carry the favorable gene variant. That’s a variation of about 6.3 kg again! →
Learn more from our study
