True clinical depression, like most illness these days, is considered largely the fault of a bad toss of the dice. The entire edifice of standard treatment for depression rests upon the theory that depression results from a chemical imbalance within the brain, considered to be largely hereditary.

The main genetic component for recurrent depression has to do with the serotonic transporter gene (STG). STG comes in two distinct varieties —the short and long allele.

The short allele, as its name suggests, represents the short straw.  This variation carries the major ‘on’ switch for depression; anyone with this gene who experiences a series of major life stresses is considered a prime candidate for major depression.

The Northwestern team is part of a new field called cultural neuroscience, which examines mental health across nations and individual social groups. One of the greatest distinctions in any culture is how someone thinks of himself in relation to other members of his society — and whether he mainly views himself as “individualistic” (a lone wolf) or “collectivistic” (a small cog in a greater whole).

The team examined health in relation to the cultural values of a cross-section of countries in most of the world’s continents, focusing on the degree to which each population places greater emphasis on the individual or the group.

In a nutshell, they found that Westerners define themselves by their individuality, while Easterners define themselves by the extent of their acceptance within a group.

“People from highly individualistic cultures like the United States and Western Europe are more likely to value uniqueness over harmony, expression over agreement, and to define themselves as unique or different from the group,” said Joan Chiao, the team leader.

In collectivistic societies, such as those of East Asia, on the other hand, higher value is placed on social harmony rather than individuality. The culture encourages behaviors and practices that endorse interdependence and group cohesion.

Chiao’s team made an unexpected discovery: the tighter knit the population, the higher percentage of the people who carried the gene for depression. East Asia, in particular, has a hugely disproportionate number of carriers of the short allele; at least 80 per cent of the population are genetically susceptible to depression.

According to the current genetic theory of depression, correspondingly high levels of depression should exist among these populations.

Instead, Chiao found the opposite: among these highly susceptible populations, the actual prevalence of depression was significantly lower than that of Western Europe or America.

The expectation of social support in these highly collectivist cultures seemed to buffer people from any environmental stressors that should have triggered depression. Even genetically inherited depression could be controlled by a social switch.

In the mid-eighties, John Cairns, a British-born geneticist at Harvard’s School of Public Health, carried out an experiment that would set off one of the biggest arguments in modern biology.

The plan of the experiment was simple enough — to place some bacteria in a tight spot.  He selected bacteria with a genetic defect rendering them unable to digest lactose, the sugar present in milk, then introduced them into a batch of Petri dishes containing cultures whose only food source was lactose. Without any digestible food, the bacteria faced death by slow starvation.

According to orthodox science and the neo-Darwinist view of natural selection, the bacteria would not be able to colonize; without a food source to drive metabolic processes, they could not carry out normal reproduction.  Nevertheless, in every Petri dish, Cairns found a goodly number of thriving colonies.

When Cairns tested for genetic changes in his colonies, he found that a single type of gene had changed – those preventing lactose metabolism. Identical changes in just those genes had occurred within every new colony in every Petri dish.

Cairns had confirmed that none of the original bacteria had contained a lactose-digesting mutation prior to the experiment. Through some unknown mechanism, the bacteria had activated life-saving mutations in direct response to an extreme environmental crisis, and these mutations had saved their lives.

The bacteria had defied the central dogma: they had evolved purposefully, not randomly, in order to restore balance and harmony with their environment. Somehow the extreme environmental conditions had caused changes in genes, enabling the bacteria to digest the only food available to them.

In 1988, Cairns published his findings in the prestigious journal Nature under the droll title “The Origin of Mutants,” a flippant nod to Darwin.  Cairns proposed that cells within organisms have the ability to orchestrate their own “directed mutation,” rapidly adapting to a changing environment. Although Cairns, the discoverer of the structure and replication of the E. coli genome, had great standing among his peers, his assertion that the environment changed genes sparked a decade-long protest in the medical literature. American journal Science dismissed his work as tantamount to “heresy.”

As other researchers looked closer, they discovered that, under environmental stress, a special enzyme in a bacterium cell gets activated, initiating a fevered copying process of cell DNA with a deliberate array of random mistakes, a mechanism now referred to as somatic hypermutation.

If any one of these mutated genes happens to be able to assemble a protein with the key to overcoming the environmental problem, the unthinkable occurs: the bacterium jettisons the original problem gene from its DNA and replaces it with the new gene.

This is the likely process by which bacteria continuously manage to outwit antibiotics. Although Darwin described mutation as random accident during the reproductive process, Cairns and other scientists after him have begun to show that the environment is constantly changing an organism, not simply through epigenetics but directly by changing genes.

This discovery is one explanation for why the Eastern populations with a depression gene didn’t express it. They were protected by their close community ties and expectation of support and their genes followed suit.

Their thoughts about support and family protected them from developing depression.