She meant well, to be sure. My friend, one of the most supportive people I know, had come to visit me in the hospital as I cuddled my prematurely born son, who was still hooked up to various tubes and looking more like an alien fetus than a baby.
“Oh,” she cooed when she saw him, “he’s a little monkey baby!”
About 12% of American babies are born prematurely — a half-million babies a year — posing quandaries to all who know the parents. If a baby is still facing myriad, potentially life-threatening complications, is it right to say “Congratulations”? On the other hand, will you offend the parents by not saying it? What about commenting on a baby’s size or looks? Mentioning possible silver linings?
At our request, nearly a dozen of the mothers in the Inspire Preemie Support Community have kindly boiled their insights down into their top 10 don’ts, drawing on the report and multitudes of comments in their discussion strings. (At the end of this post, we’ll also share their top 10 most welcome remarks.)
WHAT NOT TO SAY
1. “You’re so lucky that you didn’t have to go through the end of pregnancy!”
2. “At least, with the baby in the NICU (Neonatal Intensive Care Unit), you can get rest at night!”
3. “He’s so small!”
4. “When will she catch up?”
5. “What did you do, that he was born so early?”
6. “Everything happens for a reason.”
7. “Now that you have her home and off all that medical equipment, everything will be fine.” Continue reading →
[Note: This is a “good news” story. It describes the scientific road to the first drug that successfully attacks the underlying defect in cystic fibrosis, bringing dramatic improvements. But the drug appears to work for only 4% of cystic fibrosis patients. CommonHealth plans to write next about the remaining majority, their lives and their prospects.]
The snowdrifts towered before her, taller than she was, dumped by yet another of last winter’s blizzards. The snowblower was broken. Her husband has a bad back. So Roe Van Epps picked up her shovel. When she had cleared her entire driveway, she turned to find her husband behind her, tears in his eyes.
Her first thought was that he was going to critique her shoveling. “What’s wrong?” she demanded.
Nothing was wrong. “Oh my God, you’re shoveling!” he said.
It sank in. “Oh my God!” she echoed.
In her entire 41 years, Roe had never been able to shovel snow. Or to run. Or to go a full winter without getting ill enough to need weeks of intravenous antibiotics.
She was born with cystic fibrosis, a genetic disease that affects 30,000 Americans, gumming up their lungs with dangerously thick mucus that tends to breed bacteria. At birth, doctors told her parents that her life expectancy was age five. Along with school and play, her youth consisted of hospital beds and piles of pills and hours each day of inhalation therapy.
Medical treatments that continually improved in small steps, from new antibiotics to improved enzymes, kept her alive. But she remained a person without a future, told at each life stage not to expect the next. Her husband planned for retirement. She did not.
Now, because of a still-experimental drug called VX-770, made by Cambridge-based Vertex Pharmaceuticals, that has changed.
Roe clearly has a spirit as sparkly-bright as a Roman candle. When she came to speak to the cystic fibrosis team at Children’s Hospital Boston recently, she wore zebra-print stilettos that made the same fun-wild statement as the many shades of red in her hair. But she is openly bewildered by the new possibility of living out a full lifespan.
“Now I’m like, holy cow, I might be 80!” she said. “Maybe I should start using some face cream!” It’s almost like she’s a different person: “I still have cystic fibrosis but I can do things, I can live my life.”
Roe does not use the word “cure.” No one does when they talk about VX-770. Dr. Greg Sawicki, a cystic fibrosis specialist at Children’s, says he would definitely call it a “major advance,” the first drug to come this far that attacks the basic defect in cystic fibrosis. More cause for optimism? Yes. But a cure? No.
Roe still takes antibiotics and does hours of inhalation therapy every day. She doesn’t dare stop. But “this is life-changing,” she said. “I’m very, very careful, I’m trying not to get excited, but I really am, at the same time.”
This is two stories, intertwined. One is Roe’s life with cystic fibrosis and then on VX-770. The other is a tale of amazing science — and a gamble of hundreds of millions of dollars that hit the medical jackpot. Researchers tell it with a hint of disbelieving awe in their voices: For once, nature played no tricks. For once, everything came together just as it was supposed to, from theory to test-tube to human patients. Continue reading →
I’m sure my boyfriend doesn’t have herpes, a patient recently told Dr. Lydia Shrier, an adolescent medicine specialist at Children’s Hospital Boston.
How could she be so sure? Dr. Shrier asked. Because, the patient replied, she had scoped out his body and “there’s nothing irregular about him.”
Dr. Shrier, a researcher on sexually transmitted infections, goes through this kind of conversation all the time. Patients tell her that they’ve never had blisters or lesions or sores, and so cannot possibly have genital herpes. The same for their sexual partners.
It falls to her to disabuse them of these notions, saying: “You can have lesions or not, you can have symptoms or not, you should basically be operating the same way, which is to assume that everyone has herpes.” That means taking precautions, from limiting sexual contact to using condoms.
The study, led by Dr. Anna Wald of the University of Washington, found that people who’d had symptoms of herpes shed virus on about 20 percent of days, while people who test positive for herpes antibodies but have never had symptoms shed virus on only about 10 percent of days.
But here’s the kicker: When they’re shedding, people who’ve never had symptoms shed roughly the same amount of virus as people who’ve had symptoms. So it’s clearer than ever that lack of symptoms is no guarantee against infection. And in fact, Dr. Wald said, “Asymptomatic shedding may be the central phenomenon of transmission.”
In the old days, doctors would warn herpes patients to avoid sexual contact mainly when they had active lesions, believing that was the only time they were really contagious.
But evidence has long been growing that herpes can be transmitted even when no lesions are visible. The new study, by quantifying how much virus is shed even in the absence of symptoms, “is a real ‘aha!’ moment,” said Fred Wyand, spokesman for the American Social Health Association. “It’s really robust in terms of the number of subjects they enrolled and the length of time they were followed,” he said.
The study also helps explain how genital herpes has become so wildly common, infecting nearly one-fifth of the American adult population, given that it’s hard to imagine many people would want sex while they had the painful nether-regions equivalent of cold sores. Consider this stunning fact from the American Social Health Association:
In the United States, more people have genital herpes than all other sexually transmitted infections combined -– 50 million people in total.
A stroke patient at Spaulding Rehabilitation Hospital
Stroke eventually killed my biological father, But first it turned him from a successful doctor, author and professor into a Job-like figure who lost everything he loved.
He and my mother split up before I was born, and he went on to a second stormy divorce. He had finally found happiness in his third marriage, to a woman seventeen years his junior. But his youthful wife broke under the pressure of caring for him in his diminished, post-stroke form. She slit her own throat with a razor. He found her in the bedroom in a welter of blood and saved her life, pinching her artery closed to stop the spurting until the paramedics arrived. After she recovered, she divorced him, despite all his entreaties. Living on her own, she tried again to bleed to death, and there was no one there to save her.
My father had loved being a doctor. The stroke knocked out just enough of his memory and reasoning faculties to make him clearly unfit to practice. He had loved writing medical novels. The stroke left him unable to spell even the simplest words, and plotting that had once been complex and suspenseful now came out embarrassingly sophomoric, unpublishable. He had enjoyed public speaking and television appearances. Now he slurred his words. He was left, he said often, with nothing that he enjoyed in life except smoking — the very cigarettes that probably led to the stroke in the first place. Death had always been his nemesis, but when it finally came, four years after his stroke, I believe he welcomed it.
Stroke is the second-biggest killer worldwide, and the biggest disabler of American adults. It costs the American economy an estimated $74 billion each year. Among its surviving victims, 70% cannot work as they did before, and about one-third need help with basic self-care. Having seen its damage first-hand, I find myself always watching for word of progress on stroke as I scan the research news, and usually struck by how little there seems to be.
Why is there so very little good news, so few breakthroughs? What is so hard about stroke?
In answer, Dr. Randie M. Black-Schaffer, medical director of the stroke program at Spaulding Rehabilitation Hospital, offered this vivid analogy:
Say it’s wartime, and a bomb is dropped in a field. It’s relatively easy to fix, you just regrade the dirt and sprinkle some grass seed. That’s what happens when you get a skin wound. It’s not hard to get the cut to heal up almost as good as new.
World War Two bombing near Paris
Now say the bomb is dropped not on a field but on a town. A great many things have to happen for that town to start functioning again as a town. You start by clearing out the debris — which is like the inflammatory processes in the brain that clear out the cells killed by the stroke. Then you rebuild the buildings, but buildings alone do not make a town. You have to bring the people back, which is like bringing back the blood cells and the neurons. And then the town has to be connected to other towns, by road and by phone lines. And even then, the pattern of movements of goods and services to and from the town may never quite be the same.
In short, Dr. Black-Schaffer said, “It’s just so complex when you have damage in the brain. There are so many different components and systems involved in each functional area of the brain. They all have to be working right in order for the patient to be able to carry on the function.”
Given that image of a bombed town, it is amazing that researchers have made any progress at all. But they have. Lately there have been a couple of exciting findings, and they come against a longer-term background of growing, hard-won understanding of stroke’s effects in the brain. All in all, enough progress for a round-up of promising steps forward.
Herewith, ten relatively bright spots:
1. Overview: Treatment of stroke has advanced — though not as dramatically as hoped — and lab research has come a long way in recent years. Continue reading →
It was an explosive question: Might it be that the overuse of psychiatric medications is making many people sicker than they would have been, and preventing their recovery? Are the medications causing an epidemic of long-term psychiatric disability?
And it was about to be debated at a pinnacle of psychopharmacology, the top-rated psychiatry department in the country.
The match had drawn a full house to the fabled “Ether Dome” at Massachusetts General Hospital, the historic medical amphitheater where ether was first demonstrated as an anesthetic in 1846.
Against a vintage backdrop of glass cases holding a mummy and a well-used skeleton, the two adversaries were about to engage in a “grand rounds” debate — academic medicine’s intellectual equivalent of hand-to-hand combat.
“Thank you,” Massachusetts General Hospital psychiatrist Andrew Nierenberg said wryly, “for coming to the belly of the beast.”
The question is, author Robert Whitaker responded just as wryly, “Will I survive?”
End of humor. The stakes were too high for jokes. In his new book, “Anatomy of an Epidemic,” Whitaker doesn’t just ask whether long-term medication might often do harm. He presents study after mainstream study that inform his thesis, and he calls for the psychiatry establishment to discuss it openly.
‘The ‘Silent Spring’ of Psychiatry?
A science journalism maven at Harvard told me recently, “Mark my words, this book is going to be the ‘SIlent Spring’ of psychiatry” — a reference to the classic Rachel Carson book that opened the country’s eyes to the harmful effects of DDT.
“Anatomy of an Epidemic” only came out in April; it remains to be seen how widely its ripples will spread. But one thing is already clear: It has set Bob Whitaker, an award-winning local journalist and author of four books, on a personal journey into unexplored territory, to the Ether Dome and beyond.
It is taking him to a national conference on his hypothesis led by psychiatrists and providers of mental health services in Oregon next month. And to a line-crossing move for any journalist: the founding of a non-profit,“The Foundation for Excellence in Mental Health Care,” that will aim to present the science on various psychiatric treatments in a clear and unbiased way.
Most recently, that journey led him last week to stand in the Ether Dome beneath the curved rows of stadium-style seats, speaking upward to the full audience. Most of his listeners looked like students, except for a cluster of older men in the front whose bow-ties or suits gave them the look of staff.
Looking up at the Ether Dome
As the psychiatry establishment goes, this truly was “the belly of the beast”: Massachusetts General’s psychiatry is consistently ranked as the top department in the country by U.S. News and World Report. Sitting at the very front in a dark navy sweater was Jerrold Rosenbaum, the department chair.
Whitaker began with the plot-line about psychiatric drugs that tends to dominate in American society: The introduction of Thorazine in 1955 kicked off a “psychopharmacological revolution” that has included a march of new antipsychotics and antidepressants that are “sort of antidotes to these disorders.” They make it possible to empty institutions, and prevent people from becoming chronically ill. All in all, a positive picture of progress.
Except that there’s a troubling puzzle: Why, then, did the number of Americans on the disability rolls for mental health reasons triple between 1987 and 2007?
And more troubling questions: Yes, the drugs often help people short-term, and sometimes, longer term. But why do some data suggest that schizophrenics who take anti-psychotics fare worse, long-term, than those who don’t? Why do so many people with depression who take anti-depressants seem to flip into bipolar disorder? And why is the disability caused by bipolar disorder rising so sharply, anyway? Continue reading →