Social environments can trigger a metamorphosis in a number of different species, but is there any evidence that social environments regulate human genes in a similar way? The example of the common cold helps to address the question. Social environments increase our susceptibility to the common cold but also influence how we fight it. Colds are more common in the winter months, not because of the lower temperatures (contrary to popular belief) but through the transmission of the virus between people. One reason why the virus may be more prevalent in the winter months is that we tend to congregate closer as the nights draw in, enabling the virus to transmit more readily from one to another. Viruses are small packets of DNA made up of about 10–100 genes that enter our cells and hijack the protein production to make copies of themselves. As this infection multiplies, the normal function of the cells and ultimately the whole of the body comes under attack. However, a virus’s ability to express and duplicate its own DNA is regulated by our own body’s reaction to social stress.
Social stress and isolation have long been known to affect viral infections, which is why we can all do with a little TLC along with our chicken soup when it comes to nursing a cold.41 All this sounds like common sense, but what this folk wisdom reflects is an increasing understanding of the role of social factors in illness. An analysis of the DNA in the white blood cells or leukocytes of lonely adults revealed different levels of gene expression in comparison to adults who were not lonely.42 Specifically, the genes responsible for producing antibodies to infection were downgraded, making their immune response less effective. This may explain why lonely adults are more vulnerable to diseases. What is remarkable is that the different gene expression is only found in those individuals who feel they are lonely and is not related to the actual number of social contacts they have. Even some of the most popular people can still be the loneliest in a crowd because it is how they feel that is more important, rather than the extent of their actual social circles.
If social factors can regulate the expression of viral genes, then our own complement of roughly 20,000 genes is likely to be regulated in biologically significant ways by social factors as well.43 It is not only our biology but also our psychology that affects how we cope with illness.
Lamarck’s daft idea
What is the evidence for epigenetic processes in humans? After all, humans do not spontaneously change sex when a dominant female leaves the group, but critical events can trigger changes in how our genes operate and sometimes the resulting changes in behaviour can be passed on to subsequent offspring. This is an astonishing idea but is not new. In the early nineteenth century a minor French noble, Jean-Baptiste Lamarck, proposed that characteristics acquired during a lifetime could be passed on to the next generation.
In support of this idea, he showed that the sons of blacksmiths had larger arm muscles than the sons of weavers before they ever took part in the family business, which he interpreted as an inherited characteristic. As another example, he suggested that giraffes’ necks became long through their constant reaching up to high branches to eat leaves – a physical trait that they then passed on to their young.
Contrast this Lamarckian notion to Darwinian natural selection. In Darwin’s theory there are two mechanisms that lead to change. The first is spontaneous mutation that generates variations among members of the group. Today, we now understand that this variation arises from genetic processes. Second, the environment operates to select those variations that endow the individual with a competitive advantage to breed and pass on the variation. With successive generations, the variant becomes stable in the population. In the case of giraffes, those born with a mutation that resulted in them having longer necks were more successful in breeding. It was not the experience of trying to reach leaves that was passed on to the offspring, but rather the genes that increased the length of the neck.
Darwin originally suggested that long necks would provide an advantage for reaching more leaves, but it turns out that there are a number of competing explanations.44 What is known is that the mechanism of inheritance is not Lamarckian. Rather, long necks originated as a genetic mutation that was passed on while giraffes with short necks did not get the same opportunity to reproduce for some reason. Lamarckian theory has been roundly denounced as daft in scientific circles but epigenetics is casting new light on his ideas. Maybe experiences during a lifetime can influence the biology of the next generation.
There are so many problems and errors with Lamarck’s evidence that it would be all too easy to consign the notion to the dung heap of bad ideas. Moreover, Darwin’s theory of evolution by natural selection is simply better at explaining and predicting the data. And yet aspects of Lamarck’s daft idea have been resurrected with the rise of epigenetics. Sometimes events during one’s lifetime can affect the next generation. Epigenetics explains how environmental signals change the activity of genes without altering the underlying sequence of the DNA. The process of natural selection will ultimately correct any epigenetic influences of the environment. Rather, the effects are more to do with the switches that are being flipped by epigenetic processes. So Lamarck may have gained a minor battle, but Darwin has won the war in explaining how we pass on characteristics from one generation to the next. Epigenetics may even explain why humans traumatized as infants grow up with an emotional legacy that can stay with them for the rest of their lives. Once again, studies of the rearing practices of generations of laboratory rats have shown how early experiences shape the bond between mother and daughters.
Licking rats
What could be worse than licking a rat? For many people, rats are disgusting abhorrent pests associated with poverty, disease and death. This is rather unfair, as the female rat is an intelligent and social animal with a strong maternal instinct. When she is rearing her pups in the nest, the female rat will invest time licking and grooming her brood like an attentive mother. Some mother rats are much more conscientious, with very high rates of licking, whereas others are less so – a trait these mothers share with all their sisters.45
What is remarkable is that if you take female pups from a low-licking mother and have them raised in the litter of a high-licking mother, they will acquire this attentive trait. Likewise, if you cross-foster in the opposite direction, you get the opposite effect.46 Is this rat example simply a case of learning how to raise your pups? There is more to it than that. Grooming and licking appears to regulate the baby rat’s response to stress. Those mothers with a high licking rate produce offspring who cope much better with stress than those from a low-licking mother. They also grow up into more resilient adult rats and, if female, pass this behavioural trait on to the next generation.47 They are better adapted to reproduce.
You can even generate this effect if rat pups are reared by humans and given different levels of handling during the early days. This activity changes the baby rats’ HPA response by altering their reactivity to stress. The grooming and licking releases the ‘feel-good’ neurotransmitter serotonin that regulates the gene that controls for GR in the hippocampus. In contrast, this gene is switched off in the under-stimulated pups, whereas it is almost never methylated in the pups of high-licking grooming mothers. With higher levels of GR expressed in the hippocampus, the rat is better able to regulate the HPA effectively. Even though DNA methylation patterns tend to be stable, if you cross-foster the pups of high- and low-licking mothers during the critical period, you can reverse the methylation of the gene in the hippocampus. In short, the early grooming experience is turning the genes on or off.48