The Miseries of My Father

ALBANY: How have you known the miseries of your father?

EDGAR: By nursing them, my lord.

—William Shakespeare, King Lear, act 5, scene 3

In the spring of 2014, my father had a fall. He was sitting on his favorite rocking chair—a hideous, off-kilter contraption that he had commissioned from a local carpenter—when he tipped over the back and fell off (the carpenter had devised a mechanism to make the chair rock, but had forgotten to add a mechanism to stop the chair from rocking over). My mother found him facedown on the veranda, his hand tucked under his body unnaturally, like a snapped wing. His right shoulder was bathed in blood. She could not pull his shirt over his head, so she took a pair of scissors to it, while he screamed in pain from his wound, and in deeper agony at having a perfectly intact piece of clothing ripped to shreds before his eyes. “You could have tried to save it,” he later groused as they drove to the emergency room. It was an ancient quarrel: his mother, who had never had five shirts for all five boys at a time, would have found a way to rescue it. You could take a man out of Partition, but you could not take Partition out of the man.

He had gashed the skin on his forehead and broken his right shoulder. He was—like me—a terrible patient: impulsive, suspicious, reckless, anxious about confinement, and deluded about his recovery. I flew to India to see him. By the time I arrived home from the airport, it was late at night. He was lying in bed, looking vacantly at the ceiling. He seemed to have aged suddenly. I asked him if he knew what day it was.

“April twenty-fourth,” he said correctly.

“And the year?”

“Nineteen forty-six,” he said, then corrected himself, groping for the memory: “Two thousand six?”

It was a fugitive memory. I told him it was 2014. Nineteen forty-six, I noted privately, had been another season of catastrophe—the year that Rajesh had died.

Over the next days, my mother nursed him back to health. His lucidity ebbed back and some of his long-term memory returned, although his short-term memory was still significantly impaired. We determined that the rocking-chair accident was not as simple as it had sounded. He had not tipped backward but had attempted to get up from the chair, then lost his balance and shot forward, unable to catch himself. I asked him to walk across the room and noticed that his gait had an ever-so-slight shuffle. There was something robotic and constrained in his movements, as if his feet were made of iron, and the floor had turned magnetic. “Turn around quickly,” I said, and he almost fell forward again.

Late that night, another indignity occurred: he wet his bed. I found him in the bathroom, bewildered and ashamed, clutching his underwear. In the Bible, Ham’s descendants are cursed because he stumbles on his father, Noah, drunken and naked, his genitals exposed, lying in a field in the half-light of dawn. In the modern version of that story, you encounter your father, demented and naked, in the half-light of the guest bathroom—and see the curse of your own future, illuminated.

The urinary incontinence, I learned, had been occurring for a while. It had begun with the feeling of urgency—the inability to hold back once the bladder was half-full—and progressed to bed-wetting. He had told his doctors about it, and they had waved it off, vaguely attributing it to a swollen prostate. It’s all old age, they had told him. He was eighty-two. Old men fall. They lose their memory. They wet their beds.

The unifying diagnosis came to us in a flash of shame the next week when he had an MRI of his brain. The ventricles of the brain, which bathe the brain in fluid, were swollen and dilated, and the tissue of the brain had been pushed out to the edges. The condition is called normal pressure hydrocephalus (NPH). It is thought to result from the abnormal flow of fluid around the brain, causing a buildup in the ventricles—somewhat akin to the “hypertension of the brain,” the neurologist explained. NPH is characterized by an inexplicable classic triad of symptoms—gait instability, urinary incontinence, dementia. My father had not fallen by accident. He had fallen ill.

Over the next few months, I learned everything I could about the condition. The illness has no known cause. It runs in families. One variant of the illness is genetically linked to the X chromosome, with a disproportionate predominance for men. In some families, it occurs in men as young as twenty or thirty. In other families, only the elderly are affected. In some, the pattern of inheritance is strong. In others, only occasional members have the illness. The youngest documented familial cases are in children four or five years old. The oldest patients are in their seventies and eighties.

It is, in short, quite likely to be a genetic disease—although not “genetic” in the same sense as sickle-cell anemia or hemophilia. No single gene governs the susceptibility to this bizarre illness. Multiple genes, spread across multiple chromosomes, specify the formation of the aqueducts of the brain during development—just as multiple genes, spread across multiple chromosomes, specify the formation of the wing in a fruit fly. Some of these genes, I learned, govern the anatomical configurations of the ducts and vessels of the ventricles (as an analogue, consider how “pattern-formation” genes can specify organs and structures in flies). Others encode the molecular channels that transmit fluids between the compartments. Yet other genes encode proteins that regulate the absorption of fluids from the brain into the blood, or vice versa. And since the brain and its ducts grow in the fixed cavity of the skull, genes that determine the size and shape of the skull also indirectly affect the proportions of the channels and the ducts.

Variations in any of these genes may alter the physiology of the aqueducts and ventricles, changing the manner in which fluid moves through the channels. Environmental influences, such as aging or cerebral trauma, interpose further layers of complexity. There is no one-to-one mapping of one gene and one illness. Even if you inherit the entire set of genes that causes NPH in one person, you may still need an accident or an environmental trigger to “release” it (in my father’s case, the trigger was most likely his age). If you inherit a particular combination of genes—say, those that specify a particular rate of fluid absorption with those that specify a particular size of the aqueducts—you might have an increased risk of succumbing to the illness. It is a Delphic boat of a disease—determined not by one gene, but by the relationship between genes, and between genes and the environment.

“How does an organism transmit the information needed to create form and function to its embryo?” Aristotle had asked. The answer to that question, viewed through model organisms such as peas, fruit flies, and bread molds, had launched the discipline of modern genetics. It had resulted, ultimately, in that monumentally influential diagram that forms the basis of our understanding of information flow in living systems:

But my father’s illness offers yet another lens by which we might view how hereditary information influences the form, function, and fate of an organism. Was my father’s fall the consequence of his genes? Yes and no. His genes created a propensity for an outcome, rather than the outcome itself. Was it a product of his environment? Yes and no. It was the chair, after all, that had done it—but he had sat on that same chair, without event, for the good part of a decade before an illness had tipped him (literally) over an edge. Was it chance? Yes: Who knew that certain pieces of furniture, moved at certain angles, are designed to jettison you forward? Was it an accident? Yes, but his physical instability virtually guaranteed a fall.

The challenge of genetics, as it moved from simple organisms to the human organism, was to confront new ways to think about the nature of heredity, information flow, function, and fate. How do genes intersect with environments to cause normalcy versus disease? For that matter, what is normalcy versus disease? How do the variations in genes cause variations in human form and function? How do multiple genes influence a single outcome? How can there be so much uniformity among humans, yet such diversity? How can the variants in genes sustain a common physiology, yet also produce unique pathologies?