Genes are not destiny

Way back, Art Devany had a post about two twins who, while having very similar genes ended up looking very different. One trained as a long distance runner and one in field events. One looked, well like a marathon runner and the other like a bodybuilder.

He explains:

Genes are not destiny; they are if/then off/on switches capable of enormous variation in output (proteins) when combined in signal cascades;

Rob Wolf commented on this idea Exercise and Gene Expression

We are not only born into this world with genes wired for certain types and ratios of foods but our genes are also best expressed when we are active. VERY active.

I recalled these posts today when I saw this story:

Lifestyle Can Alter Gene Activity, Lead To Insulin Resistance

A Finnish study of identical twins has found that physical inactivity and acquired obesity can impair expression of the genes which help the cells produce energy. The findings suggest that lifestyle, more than heredity, contributes to insulin resistance in people who are obese.

The story refers to this new article:

Acquired obesity and poor physical fitness impair expression of genes of mitochondrial oxidative phosphorylation in monozygotic twins discordant for obesity


Defects in expression of genes of oxidative phosphorylation in mitochondria have been suggested to be a key pathophysiological feature in familial insulin resistance. We examined whether such defect can arise from lifestyle-related factors alone. Fourteen obesity-discordant (BMI difference 5.2 ± 1.8 kg/m2) and 10 concordant (1.0 ± 0.7 kg/m2) MZ twin pairs aged 24-27 yr were identified among 658 MZ pairs in the population-based FinnTwin16 study. Whole body insulin sensitivity was measured using the euglycemic hyperinsulinemic clamp technique. Transcript profiles of mitochondrial genes were compared using microarray data of fat biopsies from discordant twins. Body composition of twins was determined using DEXA and maximal oxygen uptake (VO2max) and working capacity (Wmax) using a bicycle ergometer exercise test with gas exchange analysis. The obese co-twins had lower insulin sensitivity than their non-obese counterparts (M-value 6.1 ± 2.0 mg/kgLBM·min vs. 9.2 ± 3.2 mg/kgLBM·min, P<0.01). Transcript levels of genes involved in the oxidative phophorylation pathway (GO:0006119) in adipose tissue were lower (P<0.05) in the obese as compared to the non-obese co-twins. The obese co-twins were also less fit, as measured by VO2max (50.6 ± 6.5 ml/kgLBM·min vs. 54.2 ± 6.4 ml/kgLBM·min, for obese vs. non-obese, P<0.05), Wmax (3.9 ± 0.5 W/kgLBM vs. 4.4 ± 0.7 W/kgLBM, P<0.01) and also less active, by the Baecke leisure-time physical activity index (2.8 ± 0.5 vs. 3.3 ± 0.6, P<0.01). This would imply that acquired poor physical fitness is associated with defective expression of the oxidative pathway components in adipose tissue mitochondria.

"These data suggest that physical inactivity may have contributed to the defects in mitochondrial oxidative phosphorylation described in type 2 diabetic patients and prediabetic subjects," the authors wrote. The authors also noted that, although environment plays a role in how these genes work, there still may be a hereditary component.

You can't blame it all on your genes.....