THAT a gestating mother's environment can have a permanent effect on the physiology of her offspring is well established. The children of Dutch women who were pregnant during the “Hunger Winter” of 1944, for example, suffer much higher rates of obesity, diabetes and cardiovascular disease than those born a year or two earlier. Similar observations in other famines, together with experiments on rodents, suggest this is an accidental consequence of an evolutionary adaptation to food scarcity. The offspring of starving mothers, anticipating hard times during their own future lives, adjust their metabolisms to hoard calories. If the hard times then go away, the result is a tendency to put on weight, with the unpleasant consequences that entails.

Part of this adaptation is a response by the embryo to the nutrition it receives through the placenta. In some cases, though, the unfertilised ovum itself is believed to be affected. Its DNA is reprogrammed, the theory goes, by a process called cytosine methylation. This switches genes on and off in a way that is maintained when DNA replicates during the process of cell division—and can thus be passed down the generations. It is, moreover, a process that could apply equally to the sperm of putative fathers who were starved around the time of mating.

There are hints that it does. In particular, a recent paper by Sheau-Fang Ng of the University of New South Wales showed that gene activity in the pancreases of mice sired by fat fathers is abnormal. That is significant because the pancreas makes insulin, which regulates blood sugar. Abnormal insulin levels cause diabetes.

Oliver Rando of the University of Massachusetts and his colleagues have now looked at another metabolically crucial organ, the liver, and found a similar effect. To mimic starvation, they fed half of a group of male mice a diet that contained 11% protein, which is low for such rodents. The others were fed a normal diet, containing 20% protein. After between nine and 12 weeks on these diets, each male was given a couple of days' access to a female who had been raised on a normal diet, to allow him to mate. The males were then taken away from their females, to limit any influence they might have on their progeny. After birth, those progeny were reared by their mothers until they were three weeks old, at which point they were killed and their livers analysed to study the activity of genes involved in metabolism.

As they report in Cell, Dr Rando and his team found 445 genes whose expression appeared to depend strongly on the diet of the father. In particular, genes associated with fat and cholesterol synthesis were much more active in the offspring of fathers who had been fed low-protein diets than in those sired by males who had been on normal diets. That, it might reasonably be assumed, would have allowed the mice in question to lay down any surplus calories as fat more easily than the offspring of well-fed fathers could have done.

Whether cytosine methylation is the explanation for this difference has yet to be tested, but something is clearly happening. Fathers, as well as mothers, it seems, can pass on the benefits of their experiences by subtle tweaking of their genes.