Cystic Fibrosis Quotes

Human touch, we need that touch from the one we love almost as much as we need air to breathe. I never understood that until I couldn’t have it. This is my life with cystic fibrosis.

Cystic fibrosis will steal no more from me. From now on, I am the thief.

They tell us race is an invention, that there is no genetic variation between two black people than there is between a black person and a white person. Then they tell us black people have a worse kind of breast cancer and get more fibroid. And white folk get cystic fibrosis and osteoporosis. So what’s the deal, is race an invention or not?

We should forgive God . . . For making us too short. Fat. Poor. We should forgive God our baldness. Our cystic fibrosis. Our juvenile leukemia. We should forgive God’s indifference, His leaving us behind: Us, God’s forgotten Science Fair project, left to grow mold. God’s goldfish, ignored until we’re forced to eat our own shit off the bottom".

I don't know that I ever planned on having children, but it's one thing to decide you aren't going to do something and another thing to be told that you can't do something.

Cystic fibrosis will steal no more from me. From now on, I am the thief.

Examples of those genetic defenses include the protections (at a price) that the sickle-cell gene, Tay-Sachs gene, and cystic fibrosis gene may confer on African blacks, Ashkenazi Jews, and northern Europeans against malaria, tuberculosis, and bacterial diarrheas, respectively.

The second thing that can be said with regard to life expectancy is that it is not a good idea to be an American. Compared with your peers in the rest of the industrialized world, even being well-off doesn’t help you here. A randomly selected American aged forty-five to fifty-four is more than twice as likely to die, from any cause, as someone from the same age-group in Sweden. Just consider that. If you are a middle-aged American, your risk of dying before your time is more than double that of a person picked at random off the streets of Uppsala or Stockholm or Linköping. It is much the same when other nationalities are brought in for comparison. For every 400 middle-aged Americans who die each year, just 220 die in Australia, 230 in Britain, 290 in Germany, and 300 in France. These health deficits begin at birth and go right on through life. Children in the United States are 70 percent more likely to die in childhood than children in the rest of the wealthy world. Among rich countries, America is at or near the bottom for virtually every measure of medical well-being—for chronic disease, depression, drug abuse, homicide, teenage pregnancies, HIV prevalence. Even sufferers of cystic fibrosis live ten years longer on average in Canada than in the United States. What is perhaps most surprising is that all these poorer outcomes apply not just to underprivileged citizens but to prosperous white college-educated Americans when compared with their socioeconomic equivalents abroad.

In 1993, a New York hospital launched an aggressive program to screen Ashkenazi Jews for three genetic diseases, including cystic fibrosis, Gaucher’s disease, and Tay-Sachs disease (mutations in these genes are more prevalent in the Ashkenazi population). Parents could freely choose to be screened, to undergo amniocentesis for prenatal diagnosis, and to terminate a pregnancy if the fetus was found to be affected. Since the launch of the program, not a single baby with any of these genetic diseases has been born at that hospital.

The real key to human gene mapping, Botstein had realized, was not finding the gene, but finding the humans. If a large-enough family bearing a genetic trait-any trait-could be found, and if that trait could be correlated with any of the variant markers spread across the genome, then gene mapping would become a trivial task. If all the members of a family affected by cystic fibrosis inevitably "co-inherited" some variant DNA marker, call it Variant-X, located on the tip of chromosome seven, then the cystic fibrosis gene had to sit in proximity to this location.

Until recently, three unspoken principles have guided the arena of genetic diagnosis and intervention. First, diagnostic tests have largely been restricted to gene variants that are singularly powerful determinants of illness—i.e., highly penetrant mutations, where the likelihood of developing the disease is close to 100 percent (Down syndrome, cystic fibrosis, Tay-Sachs disease). Second, the diseases caused by these mutations have generally involved extraordinary suffering or fundamental incompatibilities with “normal” life. Third, justifiable interventions—the decision to abort a child with Down syndrome, say, or intervene surgically on a woman with a BRCA1 mutation—have been defined through social and medical consensus, and all interventions have been governed by complete freedom of choice. The three sides of the triangle can be envisioned as moral lines that most cultures have been unwilling to transgress. The abortion of an embryo carrying a gene with, say, only a ten percent chance of developing cancer in the future violates the injunction against intervening on low-penetrance mutations. Similarly, a state-mandated medical procedure on a genetically ill person without the subject’s consent (or parental consent in the case of a fetus) crosses the boundaries of freedom and noncoercion. Yet it can hardly escape our attention that these parameters are inherently susceptible to the logic of self-reinforcement. We determine the definition of “extraordinary suffering.” We demarcate the boundaries of “normalcy” versus “abnormalcy.” We make the medical choices to intervene. We determine the nature of “justifiable interventions.” Humans endowed with certain genomes are responsible for defining the criteria to define, intervene on, or even eliminate other humans endowed with other genomes. “Choice,” in short, seems like an illusion devised by genes to propagate the selection of similar genes.

Of course there is no doubt that some diseases, like Huntington’s chorea, beta thalassemia, and cystic fibrosis, can be blamed entirely on one faulty gene. But single-gene

I need not point out that being redheaded is not a maladaptive condition. It’s a very lovely condition. It is an absurdity, offensive to both redheads and geneticists—a group that contains both family and friends—to suggest that red hair might be subject to a force of natural selection so powerful that oblivion awaits. Even actually maladaptive genetic traits, actual diseases with well-understood modes of inheritance, such as cystic fibrosis or Duchenne muscular dystrophy are not likely to go extinct, because carriers of a single copy live healthily and pass the faulty gene on to their children.

Cystic fibrosis,” Kira rasped. “She was born with it.” The irony of that stabbed a fresh spurt of pain in Kira. According to what Mencheres just revealed, Kira might also have been born with a genetic mutation, but though hers might steal her freedom, it wouldn’t grow deadlier until it killed her, like Tina’s. “She is dying,” Mencheres said, still with that same indecipherable expression. “Don’t say that.” Kira gave the vampire a look filled with all her impotent rage over her sister’s condition as she stood up. She knew it was true. All her instincts warned that this time, Tina wouldn’t recover. She’d felt that dread growing in her all day even though she’d tried to discount it. His black eyes were hard. “As she is now, that is fact, but what are you prepared to do to change that fact?” Did he mean . . . ? Kira looked at Tina, at Mencheres, then at the EKG machine monitoring her sister’s weak pulse. A pulse that Mencheres no longer had. “Nothing quite that drastic,” Mencheres said, with the barest hint of a nod at the heart monitor. “My blood healed your injuries. It cannot cure your sister’s disease permanently, but it could heal the complications that cause her to be in this condition.

Poor posture and flexibility are common features in patients with CF. CF-related bone disease and abnormal respiratory mechanics lead to a high incidence of musculoskeletal pain, thoracic kyphosis, and vertebral fracture rates. All patients should have an annual musculoskeletal and postural assessment from childhood (age ~8 years), with monitoring and treatment of any musculoskeletal issues (see Chapter 9).

In the years to come, some of our best minds will try to dig deeper into that computer program, to figure out its individual lines of code (the IF-THENS that we call genes), the products of those lines (what we call proteins), how all those lines of biological code fit together, and how they make room for nurture. In the long run, the effects on society will be profound. Take, for example, the advances that our increasing understanding of genes will lead to in medicine. Because, as we have seen, the brain is built like the rest of the body, it is also amenable to many of the same types of treatment. For example, stem cell therapies originally developed for leukemia are being adapted to treat Parkinson's disease and Huntington's disease. Gene therapies developed for cystic fibrosis may someday help treat brain tumors. Both work by harnessing the body's own toolkit for development.

A Family Affair: Essential Fatty Acids More chemical clues to the nature of alcoholism come from research focusing on alcoholics with at least one grandparent who was Welsh, Irish, Scottish, Scandinavian, or native American. Typically, these alcoholics have a history of depression going back to childhood and close relatives who suffered from depression or schizophrenia. Some may have relatives who committed suicide. There also may be a family history of eczema, cystic fibrosis, premenstrual syndrome, diabetes, irritable bowel syndrome, or benign breast disease. The common denominator here is a genetic abnormality in the way the body handles certain essential fatty acids (EFAs) derived from foods. Normally, these EFAs are converted in the brain to various metabolites such as prostaglandin E1 (PGE1), which plays a vital role in the prevention of depression, convulsions, and hyperexcitability. When the EFA conversion process is defective, brain levels of prostaglandin E1 are lower than normal, which results in depression. In affected individuals, alcohol acts as a double-edged sword. It activates the PGE1 within the brain, which immediately lifts depression and creates feelings of well-being. Because the brain cannot make new PGE1 efficiently, its meager supply of PGE1 is gradually depleted. Over time, the ability of alcohol to lift depression slowly diminishes. Several years ago, researchers hit upon a solution to this problem. They discovered that a natural substance, oil of evening primrose, contains large amounts of gamma-linolenic acid (GLA), which can help the brain convert EFAs to PGE1. The results are quite dramatic. In a recent study in Scotland, researcher David Horrobin, M.D., matched two groups of alcoholics whose EFA levels were 50 percent below normal. The first group got EFA replacement, the second, a placebo. Marked differences between the two groups emerged in the withdrawal stage. The group that got EFA replacement had far fewer symptoms, while the placebo group displayed the full range of withdrawal symptoms associated with prostaglandin deficiency: tremors, irritability, tension, hyperexcitability, and convulsions. At the outset of the study, members of both groups had some degree of alcohol-related liver damage. Three months later, the researchers found that liver function among the EFA replacement group was almost normal. There was no significant improvement among the placebo group. A year later, the placebo group was still deficient in the natural ability to convert essential fatty acids into PGE1. What’s more, only 28 percent of this group had remained sober; the rest had resumed drinking. Results were dramatically better among the EFA replacement group: 83 percent remained sober and depression free.

Tom's parents were growing old and one of his sisters had cystic fibrosis, so he moved back to Denver to spend some precious time with his family. I moved into town where I shared a house with a businesswoman, her son, and a foreign student from the university.

The New Jersey State Organization of Cystic Fibrosis was founded in 1977 to provide financial assistance to cystic fibrosis patients throughout the state. NJSOCF also provides referrals and educational materials to patients and their families. NJSOCF is committed to helping those born with cystic fibrosis. We use our donated dollars to purchase the daily necessities of living for patients with the disease. These include prescription drugs, medical equipment, nutritional supplements and extra nutritious foods. Services are available to patients from birth to adulthood.

Tissue doesn't lie.

Cystic fibrosis was the most common genetic disease in Caucasian populations—about one in twenty-nine Caucasians carried a single copy of the mutant CF gene, or in terms of the US population,

cystic fibrosis

the pet health interests of rich people may or may not line up with what society overall should give priority to in seeking medical breakthroughs. As the Times warned: “The philanthropists’ war on disease risks widening that gap, as a number of the campaigns, driven by personal adversity, target illnesses that predominantly afflict white people—like cystic fibrosis, melanoma and ovarian cancer.

Becoming Animals" is a very interesting, enjoyable, and thought-provoking read; a brilliant addition to the libraries of science fiction and fantasy fans, as well as anyone who simply enjoys a good story.

Incredibly, given the astounding progress in other areas of medicine over the last twenty years—think cancer or HIV/AIDS or cystic fibrosis or cardiovascular disease—as I write this in 2017 not only is there no cure for Alzheimer’s disease, there is not even anything that reliably prevents or slows Alzheimer’s disease.

I want to sit with my best friend and ask about bras, scars, tingling sensations and numb nipples. Instead, I’m stuck having clinical conversations.

cystic fibrosis

was a picture of hospital doors and above them read, The Sarah Gunderson Cystic Fibrosis Center.