Mukherjee highlights the complex nature between genes and identity through the story of his mother Tulu, and her identical twin, Bulu. Bulu, the older by several minutes, was born undernourished and weak and grew up timid, while Tulu was boisterous and chatty. Marriage marked a further divergence in their fortunes, with Tulu marrying Mukherjee’s father, “a penniless immigrant” (353) and Bulu wedding a wealthy lawyer in Calcutta. In another twist of fate, the fortunes of the sisters reversed, as Mukherjee’s father’s corporate job brought his family affluence and holidays abroad, while Tulu’s husband’s law practice dwindled. 

Mukherjee recalls that the sisters—born with near-identical features—even began to look different. At the same time, they continued to share an uncanny bond, leading him to believe that though the twins were no longer recognizably identical, “they shared the first derivative of identity” (355). Perhaps this first derivative is what an individual’s genetic structure gives them.

The greatest of such derivatives, of course, is biological sex. In 1903, Nettie Stevens located maleness to the Y chromosome, revolutionizing the theory of sex determination. Females were born with an XX configuration in each cell, and men with an XY pair. Scientists questioned which was the sex-determining gene. Peter Goodfellow, a geneticist in London, discovered the answer in the 1980s while studying women born with Swyer syndrome. In Swyer syndrome, women are anatomically female but have XY chromosomes in all their cells. It is almost as if the gene for maleness is switched off in such cases. Examining the genome of women with Swyer’s syndrome, Goodfellow found a mutation in the SRY gene, suggesting it was the gene linked with maleness.

In addition to sexual anatomy, genes also affect gender identity, as seen in cases where individuals have a sexual identity forced on them. An  example of the persistence of gender identity was David Reimer, a genetic male named Bruce at birth. Bruce’s penis was severely damaged in infancy. Psychiatrists convinced Bruce’s parents to raise him as a girl called Brenda, but Bruce was never happy with the forced lifestyle. At 14, Brenda switched her name to David and refused gender reassignment surgery. David lived as a male, but continued to have mental health issues and died by suicide in 2004.

Nowhere was the push to conflate genetic sex, gender identity, and sexuality more prominent than in the case of same-sex attracted people. Till the 1980s, most psychiatrists believed same-sex attraction was acquired, which is why gender reprogramming and conversion initiatives were common in this period. If “homosexuality” was acquired, it could also be programmed away. 

However, in 1993, a discovery by Dean Hamer, a researcher at the National Cancer Institute, changed the conversation around sexuality. Hamer, who happened to be gay, interviewed hundreds of gay men to construct their family trees. Concordance between twins and siblings was the expected finding, but Hamer also discovered that gay men tended to have gay uncles, but only on the maternal side. This strongly suggested that genes contributing to sexuality were located on the X chromosome. Hamer would even narrow down the heritable elements to a location near Xq28, although the specific genes are yet to be found.

Hamer’s findings galvanized the media, with one headline claiming mothers would now feel “guilty” about the sexuality of their sons. Though Hamer’s studies were twisted by the media, they are important in suggesting sexuality is an ingrained trait. The key difference from biological sex was that multiple gene systems—and not a single SRY—influenced sexual orientation and identity.

Since it is the interaction among chance, environment, and genetics that creates identity, there must be a mechanism by which chance or fate influences the cells. The controversial field of epigenetics may hold some answers. In the 1950s, English embryologist Conrad Waddington observed that a cell’s environment affected its use of genes, turning genes on and off. He coined the term epigenetics or “above genetics” for the phenomenon. 

Waddington’s theory was proven by a study of the family trees of the victims and survivors of the Hongerwinter, or the Hunger Winter, the famine northern Holland suffered in 1944 as occupying German forces stopped the northwards movement of food and coal. Children of women pregnant during the Hongerwinter were found to suffer from metabolic disorders, such as obesity and diabetes in their adulthood. Surprisingly, these conditions were even found in the third generation, suggesting that the famine had imprinted itself in the genetic memory of the victims.

Genetic memory challenges a key feature of Darwinian evolution in that it suggests experiences shape organisms in an heritable manner. However, Darwin had argued that heritable changes are the result of only mutation, survival, and selection. Epigenetics was reconciled with Darwin’s theories when it was found that environmental factors do not change the genes themselves, but append permanent stamps above genes.

The stamps are a methyl group that attaches to a part of DNA, signaling for the gene to switch off. When the stamps are appended to master-regulator genes (the most critical genes), whole metabolic functions are affected. For instance, in case of the Hongerwinter, prolonged starvation caused master-regulator genes to be stamped to slow down metabolism. Since even the germ cells were stamped, the memory of the starvation response carried to future generations.