In November 2001 my husband Mike began to feel ill. The first time he mentioned it to me we were at his cousin’s wedding. I guessed he’d had too much to drink and wasn’t especially worried. But days later, Mike still felt unwell. He was unusually tired. We attributed it to his work, long-distance runs and the sleepless nights we often had with our baby, Tom. But as weeks and then months passed, other things felt wrong, too. Mike was constantly thirsty. He drank orange juice not by the glass but by the litre. He drank milkshakes and cola throughout the day. And though he’d never had a sweet-tooth before, he began to eat enormous quantities of chocolates, cakes and biscuits – he even drank the syrup from a can of fruit cocktail.
Yet despite his gigantic calorie intake, Mike was losing weight. He thought that the weight loss could be the result of long-distance running. Then his feet went numb and his vision blurred. That’s when he went to the doctor.
He was diagnosed with Type 1 diabetes, formerly known as childhood, juvenile or insulin-dependent diabetes, an autoimmune disorder that destroys beta cells, the insulin-producing cells of the pancreas. Insulin is the hormone that allows glucose to move from the bloodstream into the cells, where its energy is put to use. Without insulin, the glucose remains locked outside the cells and they starve. So people with Type 1 diabetes must inject themselves with insulin before each meal. They must also test their blood throughout the day to check their glucose levels.
According to Diabetes UK, diabetes affects around 5 per cent of the world’s population, and its prevalence is doubling every generation. There are 430,000 children under 14 with diabetes (almost all of these will have Type 1 diabetes). The other diabetics have Type 2, or adult-onset, whose rise to epidemic levels in recent years has been attributed to obesity and lifestyle factors. Type 1 is also increasing in prevalence – the number of new diagnoses has doubled every 20 years since the mid-20th century – though not at the alarming rate of Type 2. And in the case of Type 1, no one knows exactly why. Moreover, while Type 2 can sometimes be reversed by weight loss and exercise, there is no cure for Type 1.
Mike took the news of his diagnosis in his stride. He began to prick his fingertips to check his blood sugar up to 10 times a day. I knew the pricking was painful, but I never heard him complain. He swore off sugar, and when I ordered dessert in restaurants, which he insisted I continue to do, he sat politely and watched me eat. I began to think of him as a version of Kafka’s protagonist in “The Hunger Artist”. He resisted food with ease.
At home we drastically modified our diet, cutting out sweets and most carbohydrates. But one night, tired, hungry and facing an empty refrigerator, we ordered pizza. In anticipation, Mike took more insulin than usual. Shortly after eating, he began to shake and sweat. Then he turned angry over nothing and seemed confused. It was clear to me that this was a severe hypoglycemic attack, the result of an insulin overdose. To correct the problem Mike needed sugar, as fast as possible. I begged him to drink some juice, but in his rage, he initially refused. When he did finally drink and his blood sugar rose, he went right back to normal, as if nothing had happened. He was the same, but I wasn’t. Seeing Mike’s fragility struck emotions I thought I’d buried long ago.
In 1978 my mother was diagnosed with multiple sclerosis, an autoimmune disease that affects the central nervous system. At that time there were no treatments for MS. As a five-year-old, I witnessed what happened to her, the way, piece by piece, she lost control of her body, but I wasn’t old enough to understand the medical terminology of an autoimmune disease. My grandmother told me that my mother’s body was attacking itself, but the idea was impossible to conceive. I wanted an outside agent to blame, something concrete to be responsible for my mother’s condition; Snow White had a poisoned apple and Sleeping Beauty pricked her finger on a spindle, after all.
Facing Mike’s autoimmune disease, I found myself wishing once again for something that could be overcome. The body attacking itself, although I now understood the words, seemed as strange to a young wife as it had to a child. As a five-year-old I had tried to wish away my mother’s illness; that hadn’t worked and I began to realise that if I was going to help my husband, I had to move beyond the sense of helplessness I’d known as a child. I could not stop his body from attacking itself, so I tried to figure out what I could do.
I put my energy into research. Reading about diet and meal planning, however, wasn’t enough for me; even studying how to try to avoid hypoglycemic attacks seemed inadequate in the face of a disease with long-term complications like renal failure and blindness.
As I skimmed through medical literature, I knew I was reading with the eyes of someone looking for a way out of Type 1. Like a lot of people who haven’t yet come to terms with a chronic disease, I was reading for a cure. As it turned out, at the time I was reading, it looked like a cure for Type 1 diabetes might finally be within reach.
In 1972, Paul Lacy, a researcher at Washington University in St Louis, had discovered he could rid rats of Type 1 diabetes by taking islet cells (the pancreatic tissue composed of insulin-producing beta cells) from healthy animals and transplanting them into their diabetic counterparts. From the moment Lacy published his results, the scientific and medical communities began the effort to replicate them in humans. But after two decades of failed attempts, most scientists began to consider it a pointless endeavour. In reports from the International Islet Transplant Registry from 1990-1998, only 12 per cent of patients with Type 1 who underwent islet transplants developed insulin independence for more than seven days. Some scientists speculated that the islet cells were damaged during extraction from the donor pancreas and during implantation. Others suggested that exposure to the immunosuppressive drugs necessary for transplant was destroying the beta cells. Another possibility was that despite the use of immunosuppressive drugs, the body continued to attack the newly transplanted cells.
In 2000, however, James Shapiro and his colleagues at the University of Alberta presented a breakthrough report describing the so-called Edmonton protocol. They described seven consecutive participants in their research programme who went without insulin injections for at least four months following one, two, or three islet infusions. The Edmonton protocol differed from the previous attempts at islet transplant in a number of ways: the islet cells were extracted from the donor pancreas with a new enzyme mixture that did not injure them; more than one procedure was performed on each patient using two or three different donors; and the Edmonton protocol used a new combination of immunosuppressive drugs.
By the time I learned about this, the procedure was already being tested elsewhere. I told Mike I had amazing news: people were being cured of diabetes. He was sceptical. Rather than setting his sights on getting rid of his disease, Mike had become an expert at managing it. He followed a strict diet, exercised and checked his blood glucose levels before and after every meal. His diabetes care was as routine as brushing his teeth. When I became pregnant, I had my own health issues to focus on. I was thinking about his cure less and less.
And so in 2006, when the New England Journal of Medicine reported that an international study conducted on the Edmonton protocol had found that insulin independence is not usually sustainable, I was disappointed but not crushed by the news.
I didn’t stop reading about diabetes, but I began to read with a new perspective. And the more I read the more apparent it was that in fact there has been a revolution in diabetes treatment. As is so often the case with complicated diseases the real revolutions don’t fall upon us like instant miracles.
This winter at the Tel Aviv University laboratory of Professor Shimon Efrat, I saw first-hand the quieter, more piecemeal diabetes research that is taking place in labs around the world. There are still many obstacles to overcome on the path towards successful islet cell transplants, but the major problem limiting the therapy is the lack of organ donors. Efrat, a soft-spoken Israeli, is attempting to solve this problem in two ways. He and his team are trying to expand and replicate adult human beta cells. Usually when beta cells are forced to replicate they lose the ability to secrete insulin. Efrat is also attempting to turn other cells, which are not destined to become beta cells, into insulin producers. He and his colleagues took human fetal progenitor liver cells, changed the gene expression and transformed them into insulin-secreting cells. These cells secrete only two-thirds as much insulin as a true beta cell, but most of the other research that has been done has not been as promising.
Efrat showed me beta cells he’d just received from a cadaver in Italy. In the microscope they looked golden, almost iridescent. “So far,” he said, “there’s not a safe bet on how to mass-produce beta cells so we can’t put all our eggs in one basket. We’re trying lots of approaches and hoping one will work out. In the meantime we’re learning a lot about these cells and beta cells are among the top priorities among almost every lab working on stem cells.”
Yet it’s fair to say that the greatest changes in the daily lives of diabetics aren’t just coming from scientific research, but from technological improvements. When Carlos Gordon* was diagnosed in 1965, at the age of 17, he was told he wouldn’t reach 50. For Gordon, now 60, life has been extended by a simple pocket glucometer, which became available in the early 1980s. “Glucose monitoring has truly saved me,” he says. “I check myself four times a day when in routine mode and about eight times a day when I travel.”
Today, even the pocket glucometer can seem outmoded. Tubeless insulin pumps and continuous glucose monitoring systems are already on the market. A small start-up company, Integrity Applications, has developed a product called GlucoTrack, now in clinical trials. GlucoTrack promises accurate non-invasive glucose monitoring via an iPod-like machine and a clip that attaches to the earlobe. And most exciting is the idea that somewhere down the line lies an artificial pancreas, a fully automated glucose monitoring and insulin delivery system. Like a pacemaker, the artificial pancreas would be implanted and the patient would live a normal life without the need for insulin injections.
Speculation abounds as to why the artificial pancreas has not yet been developed, and many blame the pharmaceutical companies, for whom – with the constant need for disposable test strips to check blood glucose levels – diabetes is a cash cow. But the artificial pancreas is on the way and if it succeeds, it will remove much of the pain, hassle, juggling and daily expense a diabetic faces.
Ironically, it’s only in the past few centuries that the word cure has taken on the meaning of remedy. Originally, cure meant care. And the near-flawless diabetes care that one can achieve with new technology is not all that far from a cure.
*name changed to protect privacy
This essay originally appeared in The Financial Times Magazine.
[…] the house. I also feel really good about ASweetLife and some of my other diabetes writing like this, and this where I shared some musings on whether or not to test my sons for […]
[…] week I put up an essay here that I wrote about Mike’s type 1 diagnosis. I wrote the essay before I knew about my own […]
What a poignant read filled with fact and emotion.
This is smart, touching, and spot-on.