Growing Pains: first person account of growth hormone
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L.A. Weekly on March 21, 1997 written and provided by David DavisLike an old home movie, memory reveals itself to me in jerky, flickering images.
I see myself, a slight 10-year-old boy with light-red hair and freckles, sitting alone in the kitchen of my parents Manhattan apartment. I am fiddling with the place settings and waiting for my mom. She enters the room carrying a syringe, a needle, saline solution and a glass vial containing a small chunk of white matter. After placing these objects on the kitchen counter, she walks to the sink to wash her hands.
With her back to me, my mom tears the wrapping off the syringe and attaches a needle to it. A pediatrician, she knows the routine. She expertly measures out some saline into the syringe and injects the liquid into the vial, shaking it up to dissolve the nugget. She turns the bottle upside down to measure out a dose, and then she's finished.
She puts down the needle and asks me if I'm ready. I nod because I cannot trust my voice. She pulls up my sleeve and swabs my upper arm to sterilize it. In one fluid motion, she picks up the needle, steadies it above me and pushes it in. I watch as she empties the contents of the syringe into me. It is a scene both alien and achingly familiar.
Afterward, I walk down the hallway to my room, where I pick up a Nerf basketball and resume playing an imaginary game between the New York Knicks and the Los Angeles Lakers. It is a game I have played again and again. Though my arm is sore, I lead my team to victory.
Back then, in 1973, I couldn't have explained the precise medical reason for my shortness. But I knew that I had always been by far the smallest child in my class. When my parents eventually took me to a specialist, they were told I was a hypopituitary dwarf, that my pituitary gland was failing to produce sufficient growth hormone. But there was also good news. Doctors had been getting remarkable results from injecting children like me with human growth hormone recovered from the pituitary glands of cadavers. I began getting thrice-weekly injections of the stuff.
I dreaded the shots, but I endured them: I was going to grow taller.
As I played my silent game of basketball each night, I thought a lot about how much taller I'd soon be. And while I never thought I'd play center against the 7-footer Wilt Chamberlain, it seemed not impossible that I'd grow to 6-foot-something, tall enough to play alongside my man Walt "Clyde" Frazier, the Knicks superstar guard.
The injections continued, off and on, from 1973 to 1977. As my doctor predicted, they worked. By the time I went away to college in 1980, I stood 5-foot-4 -- not tall enough to start in the NBA, but not abnormal either.
I put those shots out of my mind until about a year after I graduated from college. I had been staying with my parents for a few weeks prior to leaving for an extended trip to Australia. One night my father called me into the dining room: He and my mother had something to discuss with me. They seemed unusually somber.
My father handed me a letter from the National Institutes of Health. I read it, not entirely comprehending its meaning. My mom explained it in simpler terms. "Three people who took the same type of growth-hormone injections you did when you were younger have died of something called Creutzfeldt-Jakob disease," she said. "They don't know if you or anybody else who took the shots is in any danger, but it's very possible that the injections are the reason for the deaths."
The letter went on to describe the symptoms of Creutzfeldt-Jakob disease. The human equivalent of Mad Cow Disease, CJD is an extremely rare degenerative illness that eats spongelike holes in the brain. The first symptom is usually loss of balance, followed by memory loss and, finally, within about a year, dementia and death. It is always fatal. The letter also noted ominously that no one can predict how long CJD lurks in the body -- perhaps as long as 30 years -- before it strikes, and that no test exists that detects CJD during its incubation.
I sat quietly, digesting the news. Then I asked my parents about the odds of my getting CJD. They could only restate the NIH's numbers. Out of approximately 8,000 children who had received the growth-hormone injections, only three had contracted the disease. In other words, 1 in 2,500 recipients had died.
"I'll take those odds," I said.
Since I first heard of the situation, things have grown steadily worse. In 1987, I learned that five patients were now affected by CJD, bringing the odds down to 1,600-to-1. In 1989, after two new cases were discovered, the odds fell to 1,150-to-1. In 1994, the death toll had reached 11, or about 725-to-1.
But I had other things to think about. I concentrated on partying hard, traveling around the world and trying out a couple of different careers. Except for the few days after I received an update from the NIH every year or so, I thought very little about CJD and my chances of getting it.
The most recent NIH update came in April 1996, and for some reason it preyed on me. Perhaps it was because of the two broken bones and the emergency eye surgery I'd recently experienced. Perhaps it was the continuing string of failed relationships whose unravelings I couldn't fathom. Or maybe I was a little uncomfortable with the updated odds: With a total of 14 confirmed deaths from CJD in the United States, I was now approaching a 500-to-1 shot.
Whatever the reason, that letter sparked something. I began examining the role of height in my life, looking at how it shaped me as a child. I wanted to know more about the growth-hormone injections and why my parents worried about my shortness. And I wanted to know about the development of human-growth-hormone treatment and about what went so horribly wrong as to cause 14 people to die (plus two additional confirmed cases where the patients are still alive).
Like a good journalist, I would arm myself with facts. Maybe the flickering memories would be stilled. And maybe, just maybe, I'd find myself with a future.
The 1940s and '50s were heady times for the U.S. scientific community. America had just emerged from World War II as the unchallenged leader of the free world, and it was technology that had brought victory. In making the atomic bomb, scientists had proved their mastery of the elements. Now that they could turn their attention to peaceful applications, the future seemed limitless.
The baby boom and the atomic age -- what a marriage it was to be. At first, the triumphs and discoveries came quickly, almost effortlessly, thanks in part to the largess of the federal government, which supplied unprecedented sums for scientific research. Such innovations as cortisone (1948), the polio vaccine (1955) and birth-control pills (1960) were tested, perfected and distributed. In 1961, when President John F. Kennedy said we would land a man on the moon before the end of the decade, nobody doubted.
Researchers became increasingly specialized, looking to solve the previously unsolvable through knowledge. It was perhaps inevitable, in an era when nothing was blindly accepted as unalterable, that doctors would begin to look for ways to make their short patients taller.
There was much to understand, but through the early and mid-'50s, work progressed. The hormone that causes growth was isolated in the pituitary gland, and scientists -- without success -- injected humans with growth hormone from rats, cows and pigs. Toward the end of the decade, Tufts University physician and chemist Dr. Maury Raben began experimenting with ways of harvesting and purifying human growth hormone.
Raben was an excellent and versatile clinician and researcher. He conducted important studies of anti-thyroid drugs, and he developed the first device used for detecting and measuring radiation. Later, he served as director of cardiovascular research at the New England Center Hospital in Boston.
But Raben was most interested in his work with short-statured patients. "During the 1950s, when there was no treatment available, we saw a lot of adult patients who were 4-foot-5 or shorter," a Raben colleague recalls. "Their quality of life was very poor."
Then, in 1958, Raben published a groundbreaking paper called "Treatment of a Pituitary Dwarf With Human Growth Hormone." He had, he reported, injected a 17-year-old male pituitary dwarf with human growth hormone over a period of 10 months, and found the injections to be continuously effective and well-tolerated, producing no apparent side effects.
To the pediatric endocrinologists treating short-statured children, Raben's paper, published in the Journal of Clinical Endocrinology Metabolism, was thrilling, and they were eager to get hGH for their patients. But the growth hormone was in short supply. Initially, only Raben and Dr. Alfred Wilhelmi of Emory University, who used a slightly different extraction technique, were processing the hormone, and they couldn t keep up with demand.
The refining of growth hormone required large numbers of pituitary glands, which were then processed to extract, isolate and purify the hormone. Because pituitaries were routinely discarded after autopsy, Raben and Wilhelmi had to persuade pathologists to preserve the pituitaries and send them to their labs.
As word got out about Raben's findings, other physicians began begging their local pathologists to save pituitaries, oftentimes recruiting the parents of GH-deficient children to help them locate and obtain the now- valuable gland, which they'd ship off to Raben or Wilhelmi. To alleviate this haphazard arrangement, the National Pituitary Agency was created at Baltimore's Johns Hopkins Hospital in 1963. The NPA took over the laborious collection chores, while Raben, Wilhelmi and a third biochemist, Brij Saxena at Cornell University, were freed to handle the extraction and purification processes. The agency then distributed the hGH -- free of charge -- to doctors across the country, all of whom agreed to charge nothing for the hormone and use it only for patients with a clear-cut need.
In 1977, Harbor UCLA endocrinologist Albert Parlow began producing a superior form of hGH using a different purification process than Raben and Wilhelmi. After opening the contract to bidding, the NIH awarded Parlow exclusive rights to process hGH. Parlow would process as many as 60,000 pituitaries a year until the CJD crisis hit in 1985.
On June 17, 1984, Stanford University pediatric endocrinologist Raymond Hintz received word from the mother of a 20-year-old former patient. She was worried about her son, whom she said had just gotten back from visiting relatives. As her son got off the plane, the mother noticed that he was unsteady on his feet. His behavior seemed altered as well.
Hintz had seen the young man from the time he was very young and was diagnosed with deficiencies of thyroid, insulin and growth hormone. After 13 years of daily injections of purified growth hormone, the patient had grown to 5-foot-5. Now he was an adult, and Hintz was no longer technically his doctor. But he nevertheless offered to see the family. Worried by what he saw, he recommended further neurological testing.
The UC San Francisco doctors who evaluated the young man were puzzled, even after extensive examination. At a medical conference where the patient was presented, someone suggested that his symptoms, which now included an exceedingly unsteady gait and mild drooling, resembled that of Creutzfeldt-Jakob disease. But that notion was rejected due to the patient's young age.
Named after Hans Gerhard Creutzfeldt and Alfons Jakob, the two German neuropsychiatrists who first isolated the disease in 1920, CJD is known primarily for its rarity. Scientists estimate that it affects one in a million people in the overall population, usually men and women in their 50s. Among those under 40, CJD strikes at a one in a million rate.
In November, approximately six months after the onset of symptoms, the young man died. When UCSF physicians examined his brain, they found spongiform encephalopathy -- spongelike holes. It was a clearcut case of CJD.
The cause of the illness might have remained an unsolved puzzle had it not been for Hintz, who had attended a medical conference at which the difficulty of detecting slow-virus contamination in tissue transplants had been discussed. "Here was a boy who had received purified human tissue," Hintz recalls thinking. "What if there were a contamination?"
In February, soon after the autopsy, Hintz wrote to the NIH and other agencies raising "the possibility that [the hGH injections] were a factor in his getting Creutzfeldt-Jakob disease," and urging "careful follow-up of all patients treated with pituitary growth hormone in the past 25 years...looking for any cases of degenerative neurological disease."
Hintz's letter became the subject of heated debate.. Washington officials began notifying pediatric endocrinologists across the country about Hintz's concerns and requested their help in determining if other patients had suffered neurologixal problems. An April meeting was scheduled to plan strategy.
In the meantime, Hintz felt himself under extreme pressure. "Although my colleagues at Stanford were fully supportive of my actions," he recalled in a recent medical journal article, "many of my other pediatric endocrine colleagues clearly felt that I was an alarmist, and they did not hesitate to tell me so."
Events began moving quickly. Dr. Robert Blizzard, a former director of the National Pituitary Agency and a University of Virginia physician, heard from the parents of a 34-year-old former patient who'd recently died in Dallas. The man had received hGH from 1963-69. His parents told Blizzard that the man had displayed peculiar neurological symptoms before his death. The man s body was exhumed for an autopsy. He had died of CJD.
In Buffalo, Dr. Margaret MacGillivray learned that one of her former patients, a 22-year-old man, had been diagnosed with severe cerebeller syndrome. The patient was still alive, but his symptoms were similar tothose demonstrated by Hintz's patient. Additionally, two confirmed cases of CJD were reported in former hGH recipients in England.
More than 100 physicians and researchers gathered for the April meeting. Representatives from England and France attended, as did members of NIH, FDA, pharmaceutical companies and the prestigious Lawson Wilkins Pediatric Endocrine Society.
Now, with five CJD cases in two countries, and more than 3,000 patients currently receiving hGH, the NIH's course of action was clear. The agency immediately halted all distribution of the hormone. "This was a time of great concern because we often stay close to our patients even after they re adults," remembers one pediatric endocrinologist. "We didn't know what to expect."
The hGH crisis, like many in medicine, was born not of malice, but of unchecked enthusiasm. The physicians who prescribed the hormone believed, with an almost religious fervor, in what it could do for their patients with hypopituitary dwarfism. "We were happy to have hGH available," says Dr. Selna Kaplan, a UCSF professor of pediatrics and director of the pediatric endocrine unit. "We had all these children that were only 4 feet tall, and we were finally able to help them."
In the rush of excitement over the drug's possibilities, few doctors questioned its production and safety. Nor did government agencies, so certain were they that purification techniques were adequate to ensure patient safety. The NPA issued only perfunctory collection guidelines: Pituitaries from those suffering from known systemic infections were banned, but pituitaries taken from those who died of chronic neurological diseases and other illnesses were accepted. A 1965 NPA memo to pathologists entitled Directions for Storing Pituitary Glands states, "The pituitary glands should be removed as soon as possible after death. The age of the patient and the disease process are immaterial."
A 1991 study conducted by NIH researchers found, "At least 140 infected pituitary glands may have been processed and randomly distributed among lots of hGH." The NIH has ruled out the possibility that one bad batch infected all 14 of those who died plus two others now suffering from CJD. But the agency still doesn't know exactly what did happen. It's possible that many vials of hGH contained the virus, but that only a few contained enough of the infectious material to cause death. It's also possible that many of us were exposed to CJD, but that our bodies are somehow resistant to it. And it's likely that other deaths will occur.
To date, the patients who have died of CJD all began receiving hGH, as I did, before purification techniques were refined in 1977. No patient treated exclusively with post-1977 hGH has contracted CJD. (After 1985, a safe, synthetic form of growth hormone was used.)
The post-1977 techniques upped the purity of the product from 40 percent hGH to 95 percent hGH. But, more important, they greatly reduced the chance of a contaminants like CJD. Writing in the New England Journal of Medicine shortly after the CJD outbreak, Dr. Clarence Gibbs and his team concluded, "Neither [pre-1977] method used procedures that would have excluded the agent of Creutzfeldt-Jakob disease from the final product or sterilized the Creutzfeldt-Jakob disease virus."
As one researcher recalls, "When you mixed up their compound it looked like Coca-Cola, because there was so much protein matter floating around. (Wilhelmi and Raben have both died; Saxena, who referred all questions to his attorney, refused to discuss these events because of potential legal ramifications.)
Whether or not more precautions should have been taken with hGH is a question that will be debated by medical ethicists for decades. But along the way there were certainly warning signs that were ignored. In 1974, writing in the New England Journal of Medicine, Dr. Philip Duffy and his colleagues at Columbia University warned about CJD transmission after learning of a case that had resulted from a corneal transplant from an infected corpse: "Aside from the importance of this report to the transmission of Creutzfeldt-Jakob disease, there are wider implications to be considered in all transplantation programs with relation to the transmission of slow-virus diseases."
But no researcher directly connected hGH to CJD, and certainly nobody warned the 8,000 or so hGH recipients about this possibility. "There may have been a certain amount of hubris in this," says one pediatrician. "CJD had been suggested as a vague possibility, but most physicians thought hGH was absolutely safe."
I am perhaps too close to the hGH disaster, but I can't help but see it as an echo of other medical experiments gone wrong. Before the early 1970s, when the federal government finally delineated strict protocol regarding human research and experimentation, there were few strictures on the largely self- governing medical community. And, as it turned out, there were many excesses. As medicine pushed toward new frontiers, its sins grew in number, with things like the Tuskegee study, the radiation-exposure experiments, Willowbrook and DES.
These experiments involved many more victims than did the hGH injections. But they share a common denominator: the status of the subjects. Hypopituitary dwarfs don t lead normal lives, and thus were perfect candidates for a virtually untested drug. Not unlike the black men in the Tuskegee study, who went untreated for the syphilis they had contracted. Or the terminally ill patients who were injected with plutonium. Or the retarded children of Willowbrook who were used as subjects in hepatitis experiments. Or the women given DES to prevent miscarriages during pregnancy who later saw their daughters contract a rare form of vaginal cancer.
The hGH injections were experiments under the banner of therapy, and physicians used their own patients as subjects. Only -- only -- 14 of us have died from CJD in the United States. The rest of us are a little taller and a lot luckier.
Linda Ann Sluder Shipman was one of the unlucky ones. She received hGH injections from 1966 to 1972. She died of CJD in July of 1995.
When Linda was first diagnosed as a hypopituitary dwarf, her parents, Lucille and Roland Sluder, enthusiastically threw themselves into the hGH enterprise. They were among the founding members of a group called the Human Growth Foundation, which served as a combination support group for families of hGH recipients and collection agency of pituitary glands from local pathologists. Roland, a meat cutter at the local A&P, played Santa every Christmas for 13 years in an effort to raise money for the foundation.
The Sluders were true believers in hGH, especially after Linda grew into a cute, 4-foot-10-inch woman. The injections, they felt, had made a normal life possible for their daughter, who eventually moved to Florida, got a good job as a mortgage-loan processor and got married.
Then, in the fall of 1994, Linda suffered several falls and complained of being cold. By February 1995 she needed a wheelchair, and her mother became increasingly certain that her daughter had CJD, which she'd become aware of through her involvement with the Human Growth Foundation. By April Linda could no longer speak. In May, after the CJD diagnosis became official, she had several violent seizures. Toward the end, Lucille had to feed her daughter with an eyedropper. On July 23, 1995, Linda died in her sleep.
"I still haven't had a good cry about this," says Lucille Sluder. "I get choked up, but I haven't really let go. Everything was okay with her life -- after all those shots -- and then this."
Last year, the Sluders sued the National Human Pituitary Program, Johns Hopkins School of Medicine, the U.S. Department of Health and Human Services, and others for damages. In the opening salvo of the product-liability case, the Sluders attorney charged, "The [hGH] was dangerous and defective in its formulation and in lack of warning labeling to anticipate or avoid [Creutzfeldt-Jakob disease], by reason of which the product was unreasonably dangerous to decedent as a child between 1966 and 1972."
The Sluders' case is one of three filed by U.S. victims of hGH-CJD in the last two years. In Brooklyn, the family of Stacey Crair has sued, among others, biochemist Brij Saxena, Johns Hopkins University and the United States of America for damages. In Washington state, the family of Tracia Hagy has sued following Hagy s death in 1993. Defendants in all the cases have denied liability.
Despite the lawsuits, virtually nothing about growth hormone and its connection to CJD has made it into the U.S. popular press. In England, though, where 17 hGH recipients have died of CJD, the newspapers reported the scandal widely, even before Mad Cow Disease hit. Last summer, in a much-anticipated decision, a London court ruled that Britain s Department of Health was negligent in not heeding experts advice about the transmissibility of CJD. In Britain, these warnings had come as early as 1977, and the court awarded monetary compensation to the families of those post-1977 hGH recipients who died from CJD. In France, the situation is even worse. Some 50 hGH recipients (from a pool of about 2,000) have died. Worse, health officials have been charged with knowingly distributing banned hGH to French children in 1985, after the initial CJD cases were reported.
In South Carolina, Lucille Sluder is not optimistic that she'll win her daughter's case. "We're fighting the government, and I don t have my hopes up," she says by telephone. But she is equally determined that someone take responsibility for her daughter's death. "Someone should have known better," she says.
I had hoped the NIH would help me get in touch with other hGH recipients who, like me, must live with the specter of CJD. I asked the agency to mail a letter, at the Weekly s expense, to all of the hGH recipients on its mailing list. The letter was straightforward. I identified myself as a reporter who had also received hGH injections, and invited anyone willing to be interviewed for a newspaper article to call me. But Dr. Judith Fradkin, chief of the endocrinology and metabolic-diseases programs branch of the National Institute of Diabetes and Digestive and Kidney Diseases, a division of the NIH, turned me down. "We don't want to upset anyone," she said.
In the end, I found other hGH recipients despite the NIH. In response to a blurb about my research in the newsletter of the Human Growth Foundation, I eventually heard from three people (one of whom was Lucille Sluder). They were as curious to talk to me as I to them. And though I thought we'd talk mostly about CJD, what we ended up connecting on was the more abstract notion of height.
When I first spoke with Gina Banick over the phone and told her that I was 5-foot-4, she said in a Southern accent, "Oh, that's tall." I liked her immediately. Raised in Tennessee, Banick traveled to Emory University to get injections after being diagnosed as a hypopituitary dwarf. In addition to the shots, Banick endured several long hospital stays for further testing. "It screwed up my school life," she says. "I was like a guinea pig, taking very useless and humiliating tests."
Even with the injections, Banick only grew to 4-foot-7. Her height, she says, made high school very difficult. "Kids are the meanest little things," she says. "You never forget the bad stuff, everything that was ever said. Walking down the halls with guys screaming nicknames and calling me cruel words -- it was real hard to feel normal."
Banick, now 42 years old, lives near Atlanta and works as a legal secretary for a major corporation. Because she had such high expectations for hGH, Banick admits that she felt somewhat let down by her experience. "Everybody had built up hGH for years, so it was like a dream to me," she says. "I thought maybe I'd grow to 5 feet or at least to 4-foot-10 -- which is what they call petite -- so I could buy clothes."
Banick is single and often feels despair about finding a husband. "It's hard for me to meet men. Men are looking for tall, pretty women, like what's on TV and in the movies. I accept being short, but I'm always reminded that it's a tall people's world," she says. "There's a sense of sadness in my life. I'm not depressed, but I've always wanted to live the typical American dream of job, children and husband."
Banick says she rarely dwells on CJD. "I think taking the interstate to work is more dangerous, but it's always in the back of your head," she says. "It only bothers me when I get those little newsletters. I can forget about it for a year, and then I'll be reminded of everything."
Susie Goione, now 32, grew up in New Jersey. As a child, soon after beginning the shots, she was about the same height as her brother, who was four years younger. When her mother took the two of them to the supermarket, people would gush, "Oh, what beautiful little twins."
At school, Goione was teased mercilessly. "I used to be known as the biter," she says with a laugh. "All the kids would tease me, and the only way I knew how to fight back was to bite them. Then they made fun of the biting, but I didn't care about that."
As Goione grew older, she began having other physical problems. Her body didn't produce estrogen; at 15, she hadn't had her first period. "I never got to go through puberty with other girls -- you know, when other girls are comparing their breasts in the locker room," she says. "I felt very isolated. And that's how my parents explained it to me: 'We want you to be normal, we want you to be like other kids.'"
Goione stopped taking hGH at 18, when she went to college. She had reached 4-foot-10, her present height, but she still felt abnormal. At one point Goione sought psychiatric help, but even this backfired. In 1991, she took all of the antidepressants she had been prescribed. She then drove herself to Johns Hopkins, the hospital where she had received hGH as a child, and had her stomach pumped.
Since the aborted suicide attempt, Goione has regrouped. She's adopted her own personalized brand of spirituality, and she works as a freelance painter. She also hopes to eventually have a more well-rounded social life. "I haven't been a nun or anything, but it's hard being alone, Goione says, noting that she's had just one serious boyfriend in her life. "Until I establish a relationship with myself, I can't be with other people."
Goione found out about CJD only in 1995. She reacted to the information with macabre humor. "I thought, This isn t going to happen to me," she says. "And then I was reading about all of the symptoms, and I'm, like, I have that, I have that. I mean, I bump into things all the time, and I have the worst memory." But the larger issue for her is still height. "I do feel disappointed in Johns Hopkins in not offering psychological support through the whole thing," she says. "I m not angry and I m not vindictive, but I feel very stranded."
I've feared CJD only once. When I had my vision problems last year, the thought entered my mind that this might be the beginning of the end: One of the first symptoms of the disease is the loss of sight. The diagnosis of a detached retina -- and the subsequent two months of recovery time spent thinking on my couch -- forced me to re-evaluate how I've been living my life.
I don't remember my first visit to Dr. Edna Sobel, the pediatric endocrinologist who prescribed growth hormone for me. But the files show that it took place on March 18, 1968, when I was 5. Dr. Sobel wrote that my mother was "concerned about her son's height since he was less than 1 year old because he has grown more slowly than the other children in the family." As she noted, at 3-foot-2 and 31 pounds, I was "three standard deviations below the average in height. Height is about average for 31/2 years and weight is average for 21/2 years."
In 1972, after my diagnosis as a hypopituitary dwarf, she and my parents first began to discuss growth-hormone injections. "I now have the opportunity to treat a limited number of short children with growth hormone," Dr. Sobel wrote in my files. According to her notes, I didn t initially want to take the shots. But I soon changed my mind. Dr. Sobel writes that I began three-times-a-week injections on April 2, 1973. I was 10 years old, stood exactly 4 feet tall and weighed 48 pounds.
My visits with Dr. Sobel took on a familiar, if slightly uncomfortable, routine. Every three months, I'd take a taxi after school to her office at the Albert Einstein College of Medicine in the Bronx. There, my mother would meet me. She and Dr. Sobel would talk awhile, and then, after I had stripped to my underpants, Dr. Sobel would give me a physical. She'd bang my knees with that little rubber mallet, take my blood pressure and pulse, and reach inside my drawers to check my genital area. Then, the big moment: She d measure my height and weigh me.
Nine years after the initial consultation, when I was 14 and had just begun to sexually mature, I took my last hGH injection. I was now 4-foot-8 and weighed 73 pounds. At my final examination, Dr. Sobel predicted that I would grow to around 5-foot-3, and said, "We now know that he should have no problem producing children when he reaches the appropriate age and if he wishes to be a father."
Full of medical jargon and facts, the files are helpful on a basic, informational level. But words can't reproduce feelings. It's the fall of 1968, the first day of first grade. My mom drops me off outside the school, and I stand in my blue-and-gold uniform shirt and gray slacks, watching as other similarly attired students gather in front of a red-brick building on Manhattan's Upper East Side. I don't recall them converging on me, but I am soon surrounded. It's like a scene out of Lord of the Flies, a book we'd all write reports on in sixth grade. They loom over me, pointing and laughing, marveling at my size. I'm in tears for much of the morning.
Being short -- and the concomitant experience of feeling short -- was so painful and humiliating that I made myself learn to fit in. I was always one of my class's fastest runners, and my grades were decent. And because I attended all-boys schools through high school, I never had to deal with the social pressures that girls brought to the classroom -- until high school.
The first mixer I ever went to was memorable only for the two bowls of potato chips I ate while watching my friends dance to Earth Wind & Fire's "Serpentine Fire." When I came home and my sister opened up the front door to the apartment, she only had to glance at my anguished face to know how badly the evening had gone.
I prayed every day that I'd get a girlfriend, but the Big Guy upstairs apparently didn't get the messages. Instead, I got Randy Newman singing, "Short people got no reason to live." Listening to the song on the radio -- and listening as classmates and strangers sang it to my face -- I wondered if anybody else felt as small as I did.
Until I began doing research on hGH and CJD, I had forgotten about these incidents. Or, to be accurate, I had buried them. These are the bad memories the NIH wants to shield me from. And they re the reason my parents and my doctor urged me to take human growth hormone. A 4-foot-something adult lives a severely restricted existence, because this is a society that values height. We elect presidents because they 're taller than their opponents. In Hollywood, during the filming of love scenes, we make our leading men stand on boxes so that they're taller than their love interests.
Talking with other hGH recipients has made me realize that I m thankful I took the injections. I'll always be self-conscious about my height, but gaining several inches gave me a shot at a normal life. Or at least a life that has all the trappings of normality. Being 5-foot-4 is undeniably better than being 4-foot-anything.
But it was clear from talking to the others that the inches we gained didn't necessarily translate into "normal" lives. Rather, the treatment underscored our pervasive sense of being abnormal and raised expectations (perhaps unattainable) about the outcome.
Our conversations often came back to relationships and the problems we've encountered in establishing and maintaining them. Our issues were somewhat different: They're female and I'm male. But I've since found that many of our common experiences echo the findings of several psychosocial studies conducted of hGH recipients.
In a study of peer and social relations among hGH recipients published in "Slow Grows the Child: The Psychological Aspects of Growth Delay," Dr. C.M. Mitchell writes, "The two most commonly reported effects of short stature on the relationships with peers were the lack of adequate relationships with peers of the same sex and age, and difficulties with heterosexual social relationships." Dr. Heather Dean reports in the same book, "Although educational achievements are similar to the general population and siblings, the rates of employment and marriage of hGH recipients are significantly lower than the general population and siblings." Dr. Maria Kusalic and Claire Fortin, in the Canadian Psychiatric Association Journal, state, "Treatments with hGH helped them to grow taller, but their long-lasting emotional and family problems persisted and jeopardized their adjustment to growth."
Without blaming all of my social and personal inadequacies on the acronyms in my life, hGH and CJD, I've come to realize that I'd never stopped to consider a future. I barged into and out of relationships without much forethought, and I shied away from thinking about a wife and kids. Children, especially, have been a charged issue for me. Even though medical evidence suggests that I won't pass on short stature or CJD (hypopituitary dwarfism and this form of CJD aren't genetic), I've feared having kids in case they'd have to endure what I have suffered.
A humiliating past, an uncertain future -- this is not a good combination for a healthy present. And the overwhelming feeling I took from my interviews with the others was one of abandonment: The people who got us into this mess have completely abandoned us. Once a year -- tops -- they send us an updat
Meanwhile, the doctors and organizations that made their reputations treating me and my ilk have never arranged for any type of "survivor" counseling services, nor have they encouraged any discussion about the issues we face. They've never arranged for reunions with other hGH recipients. In all probability, they won't send this article to the other 8,000 hGH recipients. "It'll bring up too many bad memories," they'll say.
The son in me is nervous about the call the journalist needs to make. But there is still a piece of the puzzle missing. My mother is a prominent geneticist-pediatrician. We are close, and I understand completely the decision she and my father made on my behalf. But I need to know how she now feels about hGH and what it did or didn't do for me.
When I catch up with her, she is, as usual, traveling on business. She is speaking by phone from her hotel room in Bethesda, Maryland, where she's attending an NIH conference. I ask her how she felt on the day the letter came informing her about the CJD risk.
"I was devastated," she says. "I was the person who injected you with the stuff, and I asked myself all sorts of questions: Did I cause harm? Did I make a crummy decision?"
Despite years of professional practice breaking bad news to parents, she says, she had difficulty handling her emotions regarding bad news affecting me. "You and I were connected at the womb," she says. "I was wide awake at the time you were born. We all laughed and had a wonderful time at your birth. All I 've wanted you to have -- and I hate to use the word 'normal' -- is a healthy, productive life. When this news happened, I was so sorry. I thought, 'What have I done?'"
And then my mom turns the tables, asking me about height and CJD and the role they've played in my life. "If you've lived with something during the formative stages of your life, how do you come to grips with who you are now?" she asks. "Are you ever going to be free of it? Does it weigh on you so that you can't embrace life?"
I don t have a definitive answer for her. I thought that by writing this article and finding answers to my many questions, I might resolve some issues. But I realize that closure may not be possible. All I can do is make peace with my past and allow myself to have a future. And I think I'm now big enough to do both.
BYLINE: Gray, RobertUK consumers are looking at the risks of BSE and are again adding beef to their shopping baskets. Robert reports on the PR efforts helping to restore public confidence Of all the public relations crises endured by the last government, there can be few that rival the debacle that surrounded the BSE scare when it spiralled out of control in March 1996.
After a decade of stating otherwise, the administration announced that its scientific advisers believed there might possibly be a link between BSE and the gruesome human brain condition Creutzfeldt-Jakob disease (CJD) after all.
The about-face precipitated a collapse in confidence in British beef. Domestic sales plummeted and a worldwide export ban was introduced. For weeks uncertainty prevailed, fanned by the apparent absence of any government emergency strategy worthy of the name. The outlook for the beef industry seemed exceptionally gloomy. Yet, two years on, UK sales volumes have recovered to a mere 7% or 8% below pre-1996 levels, even though the export ban remains and BSE keeps returning to the headlines.
Why is this? Is it simply down to the perversity of the British consumer, or has the British beef industry worked wonders to allay public concerns? To find the answer, one must first look back at those emotionally charged events of March 1996. As the government dithered, the Meat and Livestock Commission (MLC) went into crisis mode, immediately hiring Sir Tim Bell1s PR outfit Lowe Bell with a remit to shore up the reputation of British beef.
In truth, there was little except fire-fighting that could be done in the short term, as the media went to town with the hysterical zeal that typifies health scare stories in this day and age. Inevitably, any industry would have been unprepared for the level of media attention, says MLC marketing director Gwyn Howells.
It went from being a consumer issue to a political one, and as the consumer dimension started to diminish the political one grew. Amid the clamour from special interest groups and those with a political axe to grind, it proved difficult for the MLC to make much of a PR impact. To manage the crisis as best it could, it set up a strategy group comprising senior MLC figures such as Howells and director-general Colin Maclean as well as key agencies, including Lowe Bell and advertising agency BMP DDB.
At first, there was little more that could be done than respond to the specific questions raised by the government1s announcement. The position taken was that the link between BSE and CJD had not been proven, that the British beef industry had improved its hygiene and quality standards and consequently British beef remained a safe product.
The MLC has faced an extraordinarily difficult time throughout the BSE crisis, says Brook Wilkinson PR managing director Rosemary Brook, who numbers the National Dairy Council among her clients. I think that their responses on the whole have been good. Few industries have had such a long-running and difficult issue to deal with for which there are no easy answers. I don1t think they were well served by the government.
In the year from March 1996, the MLC upped its marketing and communications budget to about [pounds]15m and spent another [pounds]12m in the following 12 months. Rather than throwing money at the problem, the MLC commissioned consumer research which found that confidence was returning relatively quickly for prime cuts such as steaks and joints.
The launch of the British Meat Quality Standard for Minced Beef in June 1996 was supported by [pounds]2m worth of PR and advertising activity. In the wake of its introduction, beef sales rose by an estimated [pounds]40m.
The Commission also sought PR capital by using the ongoing debate about food safety as a platform for its messages, launching its Assured British Meat quality initiative on the same day as the government published its White Paper on the Food Standards Agency.
The MLC was in a very difficult situation and did the best it could, says Bill Hamilton, director of public affairs at supermarket chain Safeway. But retailers have also played a fundamental role in maintaining confidence in British beef.
Beef sales at Safeway have almost returned to pre-1996 levels, says Hamilton, and the stores are stocking 100% British beef again, having reduced the proportion to 85% at the height of the crisis. There has been a silver lining to the recent upsurge in farmer militancy, adds Hamilton, in that it has allowed Safeway to discuss its support of the industry with beef suppliers.
But the head of one PR company with a meat industry client is scathing of the National Farmers Union (NFU). My view of the NFU is that they were far too soft for too long. It1s only in the past couple of months that the NFU has been stirred into positive action because of the grassroots activities of its members.
The same source claims that the feed companies seem to have escaped scot-free while farmers have suffered. If this had been the US, he muses, they would surely be facing the same kind of lawsuits for damages as the tobacco companies do.
More recently, in the wake of the media coverage of the escaped pigs dubbed the Tamworth Two , the Society tried to subvert National Bacon Week by sending out thousands of rashers of vegetarian bacon.
As well as retaining Lowe Bell, the MLC has given other PR agencies specific briefs during the crisis. Scope Ketchum worked to restore confidence among meat-trade buyers in key European markets; Richmond Towers is retained to work with the UK catering trade; and Shandwick is currently working in a political capacity.
The Labour government is pragmatic, says Shandwick director Jon McLeod. Its consumer-driven agenda is upfront and it is nor going to do the meat industry's bidding. But in that context, it is in listening mood when it feels it1s getting genuine, constructive suggestions.
McLeod suggests that there is one silver lining to come out. of BSE making the headlines so frequently: it allows the MLC to put over fairly technical issues, such as the latest processes and procedures for hygiene control, to the government and its advisors. It is to the MLC1s credit that it has managed to get some of its own messages across rather than just reacting to developments in the BSE saga.
This is reflected in its ads, such as the latest TV campaign depicting an amorous old couple with the implication that red meat has kept their love life going, as well as its below-the-line work.
It might be enough for the MLC to give up the ghost, were it not for one thing: the reaction of the public. Consumers are judging the risks of eating beef for themselves, and many are finding them to be minimal, certainly in comparison with many other activities in which they happily indulge. For a significant number of the buying publicO, the Cunningham beef-on-the-bone ban goes too far.
A sector of society out there is saying to hell with this, says Ross Muir, PR managing partner of Ross Muir, whose clients include the Scotch Quality Beef and Lamb Association, and Guild of Q Butchers. There is still no positive link between BSE and new-variant CJD.
The last government failed on all counts in the beef crisis. It was slow to respond in identifying and slaughtering sick cows and pursuing the causes of the outbreak. It was a mistake to pay farmers only half the market price for infected cattle. Half measures don't work.
Public concern about the risk to humans from BSE was consistently refuted by government spokespeople. While there was no certainty either way, such confident reassurance was imprudent and subsequently compounded public cynicism.
The stunt in 1992 by John Gummer, then agriculture minister, of feeding a beef burger, unsuccessfully, to his four-year-old daughter in front of TV Cameras now looks ludicrous. The old government was driven by pressure and panic to make policy decisions on the hoof. Labour's beef-on-the-bone ban was a patronising over-reaction.
With the government there is communication interruptus all the time, which means it's always going to be issues-driven and reactive, the worst possible position to be in.
It needs to pursue long-term communication campaigns rather than relying on press notices. And it needs to build networks so that relevant organisations know what is going on before press notices are released.
Tue, Dec 1, 1998 By Eileen Murphy, Consumer Affairs Correspondent, PA NewsFormer Conservative Agriculture Minister John MacGregor is set to tell the inquiry investigating the mad cow disease crisis that his Government decided to keep a "low profile" on the BSE outbreak until it had scientific details. Mr MacGregor, who was Minister between 1987 and July 1989, is due to give evidence to the London inquiry tomorrow (Wednesday).
In a written statement, he said: "BSE was, of course, a very important issue, identified early on as a high priority and took up a great deal of time, particularly once we believed that we had identified its likely cause." He first became aware of the disease in July 1987 in a Parliamentary submission, six months after it first became properly identified in the UK.
Mr MacGregor said: "The submission informed us of an emerging disease amongst cattle, what was being done to investigate the problem and how any publicity was being handled to ensure that it was responsible and well-informed. "The cause of the disorder was unknown. It was not yet known whether it was transmissible but the submission stated there was no evidence that it was transmissible to humans."
The former minister said that his recollection was at that time BSE was viewed as primarily an animal health problem with the focus on diagnosis and eradication.
Scientists had warned the Government that although there was no evidence the disease could be caught by humans it would take "many years" before it could definitely be established whether the disease was transmissible to man. According to the statement, by 1988 Government scientists had made the link that the disease was derived from animal material in feedstuff and submitted that the disease be made notifiable and the adoption of a policy of slaughter and compensation for infected animals.
Mr MacGregor said: "I indicated that I was cautious about action to be taken and that we needed to consider expenditure because it was clear that this would have to be taken into account not only in the first year estimates but also in future years." Mr MacGregor said the feeling at the time was to "maintain a low profile until the position was clearer".
Soon after Ministers were notified that meat and bonemeal derived from sheep material was the source of disease and in 1988 BSE became notifiable and the use of animal feed in ruminant feeds prohibited. A 50% compensation scheme for farmers was also introduced for the compulsory slaughter for infected cattle.
Mon, Nov 30, 1998 By Ralph T. King Jr. Staff Reporter of The Wall Street JournalAthena Neurosciences Inc. scored a coup last April, when an expert panel convened by the National Institutes of Health suggested that one of its tests for Alzheimer's disease was superior to rivals' tests in diagnosing the dementing illness. Athena wasted no time trumpeting the results to thousands of physicians. The report "has been very, very good for us," says David Hanak, a product manager at Athena, noting that sales of the genetic test are up 28% this year.
But in a flap that underscores the often-close ties between the pharmaceutical industry, government and academia, some Alzheimer's researchers are crying foul. Five of the panel's eight members had financial or research ties to Athena, a South San Francisco, Calif., unit of Ireland's Elan Corp. PLC. The panel's "consensus report," published in the journal Neurobiology of Aging, doesn't disclose these relationships. Some medical ethicists consider this a glaring omission.
In addition, Athena provided a $100,000 grant to fund the study and played a behind-the-scenes role in launching it. The company's unrestricted grant was disclosed in the report. But the nonprofit Alzheimer's Association, which used the funds to organize the panel on behalf of the NIH, now says it regrets accepting Athena's financial support. "It interferes with the perception of the credibility of the statement," concedes William Thies, vice president for medical and scientific affairs at the Alzheimer's Association.
While agreeing that Athena's ties to the panel should have been disclosed, Dr. Thies, NIH officials, the editor of Neurobiology of Aging and several panel members all insist that each panel member was aware of the others' ties. They also stress that the views expressed in the report are scientifically solid and not biased in favor of Athena. The NIH, while noting that its policies forbid product endorsements, says it has no jurisdiction over how Athena uses the report in its marketing.
The report wasn't an unqualified recommendation of Athena's test. It emphasized that there still is no way - short of an autopsy - to definitively diagnose Alzheimer's, which afflicts an estimated four million Americans. Still, the report did single out Athena's test as one that "can add confidence" to diagnosis in symptomatic, late-onset patients. For families desperate for answers - even imperfect ones - that distinction can be a strong selling point.
Doctors don't routinely use diagnostic Alzheimer's tests made by Athena or any other company, even though they have been available for years. Experienced neurologists can correctly diagnose the disease at least 70% of the time - mainly by ruling out other conditions. Tests specific to Alzheimer's seek to increase that degree of certainty, and at an earlier stage. Of the roughly 250,000 Alzheimer's diagnoses made annually by one estimate, fewer than 10% involve the $225 Athena test. [25,000 x $225 = $5.6 million]
None of the handful of Alzheimer's tests on the market is especially reliable. Athena's genetic test produces false or inconclusive readings about one-third of the time, a recent study showed. Even more importantly, there still is no cure or even effective treatment for the disease - though several drugs on the market can temporarily improve memory in a fraction of patients. Thus, many doctors feel that achieving 100% certainty in diagnosis is inconsequential.
"At the end of the day, unless you can tie this sort of diagnostic to a therapeutic, it's not clear where the value of testing is," says Walter Moos, chairman of MitoKor, a closely held San Diego company developing an Alzheimer's test, so far only for research purposes.
The Athena test spotlighted in the report is a blood test for a gene known as apolipoprotein E. The company says a faster, better diagnosis can improve physician care and potentially buy a patient time to prepare for the inevitable. But critics aren't persuaded. "I strongly disagree with Athena that it's an appropriate diagnostic test," says Hank Greely, a Stanford University law professor who co-wrote a recent study on the ethical implications of genetic testing for Alzheimer's. He believes any benefits are outweighed by the test's cost and its potential for unduly alarming genetically similar family members.
The field of Alzheimer's testing has been dogged by other controversies. In late 1996 another test maker, Nymox Pharmaceutical Corp., Montreal, ran mass-media advertisements stating that its test could definitively rule out the disease. The Alzheimer's Association retorted that the company didn't have published evidence to support its "highly objectionable" claims.
Today, a Nymox spokesman says: "The only people calling our ads controversial are our competitors or those people with commercial affiliations to our competitors." At around the time of the Nymox furor, while the Alzheimer's Association was pondering how to clear up public confusion over diagnostic testing, Athena came calling, recalls Zaven Khachaturian, an Alzheimer's research pioneer who directs the association's scientific programs as a paid consultant.
Athena suggested assembling a panel under the auspices of the association and the NIH. "They said they'd like to see a workshop done about the utility and scientific opportunity in diagnostic markers," Dr. Khachaturian says. "They gave an unrestricted gift of $100,000 with the understanding that they wouldn't control the meeting or have any say in who was invited or how it was conducted, and that's how the meeting was done."
Dr. Khachaturian, a member of the NIH panel, listed himself as an Athena consultant in an October 1997 article in the Journal of the American Medical Association. He did so, he says, because of indirect payments received by his firm for organizing the NIH Alzheimer's panel. But that affiliation wasn't listed in the panel's report, published six months later.
"There is an appearance of conflict," concedes Dr. Khachaturian. But the panel's purpose, he says, was to establish scientific criteria for evaluating Alzheimer's tests, not to promote a particular product. He adds: "I don't think in this case [disclosure] is relevant, but I could be mistaken." He stresses that he didn't contribute to the panel's written report.
Also on the panel was Teresa Radebaugh, Dr. Khachaturian's partner and, like him, an Alzheimer's Association consultant. Ms. Radebaugh says she acted merely as an administrator to the group and didn't contribute to its report.
Two other panel members had more direct financial stakes in Athena. Harvard researcher Dennis Selkoe is a board member and shareholder of Elan, Athena's parent. Allen Roses, a vice president at Glaxo Wellcome PLC and a professor at Duke University, was a consultant to Athena until mid-1997. He holds a patent on Athena's genetic test, and collects limited royalties.
A fifth panel member, John Trojanowski, had agreements with Athena in 1995 enabling him to receive proprietary research materials - including special strains of mice - from the company. Dr. Trojanowski says that because his Athena collaborations weren't financial, he sees no need to have disclosed them. In retrospect, Drs. Selkoe and Roses both now say that their affiliations should have been disclosed in the report. They both say that during the workshop they informed panel chairman John Growdon about those ties.
Dr. Growdon, a Harvard neurologist with no connection to Athena, calls the Athena ties of panel members "irrelevant." He adds, "Everyone had their academic hats on, not their company hats. The report is fair, honest, and not biased by any company affiliation."
Some medical ethicists disagree. "There is no doubt in my mind that you have to fully disclose what the ties are," says Arthur Caplan, director of the Center for Bioethics at the University of Pennsylvania, citing the increasingly pervasive connection between medical research and drug companies that stand to profit. "I don't believe the ties are necessarily distorting or necessarily bad, but people have a right to know what they are."
Wed, Dec 2, 1998 By Jackie Brown, PA NewsFormer Tory Agriculture Minister John MacGregor today told the inquiry investigating the crisis over mad cow disease that he went beyond the scope of scientific advice to ban beef offal from human food. Mr MacGregor and his deputy Sir Donald Thompson both decided to ignore the advice of officials and announced the offal ban in June 1989. They took the decision despite concern that it cause an outcry in the press that could result in the type of headlines which followed the recent ban on beef on the bone.
The inquiry, sitting in London, heard from Mr MacGregor that he originally took a cautious approach over BSE after taking up his role in 1987. He wanted scientific evidence before making decisions to protect the government from any threat of legal action. As a result of this in April 1988 he set up a working party of science experts under Sir Richard Southwood of Oxford University to report back to him on the issue. Their final report in February 1989 included a recommendation that offal should not be included in manufacturing baby food.
Mr MacGregor said that he grew increasingly concerned about this recommendation and decided to take a "belt and braces approach" by banning all beef offal, such as the spinal cord, brains, spleen and tonsils, from all human foods. He called a meeting of officials from his own department and the Department of Health in 1989 to tell them of this.
"It was controversial," Mr MacGregor told the inquiry today. "One reason my officials were concerned was because it put the issue up more strongly and could result in a flurry of concern, which we managed to avoid. "It was not popular with some of the industry. It was a very clear example of where the Ministry was acting in the best interests of food safety and not just taking the producers' line."
He met Sir Richard the following day to discuss the fact that there was not scientific evidence to support such a ban. The two men finally agreed on the move and decided that it would be presented as being the most effective way of dealing with the baby food issue because it would ensure that no such material got into the food chain.
Sir Donald, who was in charge of food safety at the time, told the inquiry they had expected an outcry. "We expected to get the same press as the ban on beef on the bone got just recently," he said. "At the end of the day it was an ultra-safe measure."
AP Worldstream, 30 Nov 1998The French Agriculture Ministry announced today a new case of mad cow disease - the third case reported this month in France - has been detected in the Pas de Calais region, near the English Channel.
It was the 15th case of bovine spongiform encephalopathy reported this year in France and the 46th case since 1990, the Ministry said.
Following existing regulations, the entire herd of 180 cows was incinerated over the weekend. The Ministry did not specify who owned the cows or when the illness in the one cow, a milk cow born in September 1994, was detected.
Tue, Dec 1, 1998 By Steve Stecklow Staff Reporter of The Wall Street JournalLISBON -- "Mad cow" disease isn't just a British problem. Consider Portugal. The European Union, which last week voted to lift its ban on British beef exports, only five days before imposed a ninemonth export ban on beef and cattle from Portugal. Cases of diseased cattle here are on the rise, thousands of suspect animals have been slaughtered, and consumers are shunning beef at butcher shops.
"Every day, we're speaking of this," says Fernando Agostinho Fonseca Nunes, a Lisbon butcher whose beef sales have dropped by half since 1996. "People don't eat it." Portugal's troubles still don't rival Britain's. To date, 168 Portuguese cattle are reported to have developed the deadly, rare brain disease, compared with more than 175,000 cases in Britain. Unlike in Britain, where 30 people have died of what many scientists believe is the human version of the disease, no cases have been reported in Portugal.
But Portugal, one of 14 countries outside of the United Kingdom that has reported the disease in cattle, is the only one where cases are steadily going up. Although the EU ban is mostly symbolic, since Portugal doesn't export much beef, the repercussions at home, both economic and psychological, are profound. In the northern town of Famalicao, butcher Aires Silva stuffs sausages into plastic. The traditional lining, local cow intestines, is now banned. So, too, are young cow brains, another once-popular delicacy. "There's no demand for it, anyway," he says.
In nearby Povoa de Varzim, Fernando Gomes Moreira, a third-generation dairy farmer, complains he has taken a financial beating since May, when one of his cows appeared frightened and suddenly collapsed. A local veterinarian diagnosed the condition as bovine spongiform encephalopathy, or BSE, the technical name of mad-cow disease. Mr. Gomes Moreira was instructed to kill and bury the cow on his farm, and the government ordered the destruction of the rest of the herd-140 cows in all.
Portuguese government officials say the country's BSE problem originated from imports of British cattle and animal feed in the 1980s. Between 1985 and 1989, when BSE was on the rise in Britain, Portugal imported 8,648 cows [perhaps15% or 1300 would have been infected -- webmaster] and more than 140 tons of animal feed, which often contained ground-up parts of diseased cattle. The first case in Portugal appeared in 1990, although the government at first denied there was a problem. By 1994, diseased cattle born in Portugal began to appear, apparently the result of the contaminated feed. The numbers have been rising since, with 77 cases this year to date.
The government maintains Portuguese beef has been safe all along, even though most of the cows imported from Britain were never accounted for, and certain animal parts more likely to carry infection weren't banned until last year. Asked how many infected cattle have entered the food chain, Ramiro Doutel Mascarenhas, vice director of the veterinary section of the Ministry of Agriculture in Lisbon, forms a circle with his fingers. "Zero," he says.
The proof, he says, is that farmers who report diseased animals are paid more than they are worth, so there is no financial incentive to send a sick animal to the slaughterhouse. The government also purchases the rest of the herd and destroys it, to make sure no other animals carry the disease. To date, more than 6,000 cattle have been destroyed.