Medicines and Bladder Control

Your Medicines and Bladder Control

On this page:
Do you have a bladder control problem?
How does bladder control work?
How can medicines cause leaking?
What can you do about your bladder control problem?
Points to Remember
Do you have a bladder control problem?
If so, one cause of your problem may be sitting in your medicine cabinet. Medicines (drugs) can cause people to lose bladder control.
Do not stop taking any medicine without talking to your doctor. If your medicine is causing your bladder problem, your doctor may find another medicine. If you need to keep taking the same medicine, your doctor can help you find another way to regain bladder control.

Parts of the bladder control system.
How does bladder control work?
Your bladder is a muscle shaped like a balloon. While the bladder stores urine, the muscle relaxes. When you go to the bathroom, the bladder muscle tightens to squeeze urine out of the bladder.
Two sphincter (SFINK-tur) muscles surround a tube called the urethra (yoo-REE-thrah). Urine leaves your body through this tube.
The sphincters keep the urethra closed by squeezing like rubber bands. Pelvic floor muscles under the bladder also help keep the urethra closed.
When the bladder is full, nerves in your bladder signal the brain. That's when you get the urge to go to the bathroom.
Once you reach the toilet, your brain tells the sphincter and pelvic floor muscles to relax. This allows urine to pass through the urethra. The brain signal also tells the bladder to tighten up. This squeezes urine out of the bladder.
Bladder control means you urinate only when you want to. For good bladder control, all parts of your system must work together:
Pelvic muscles must hold up the bladder and urethra.
Sphincter muscles must open and shut the urethra.
Nerves must control the muscles of the bladder and pelvic floor.

Medicine for high blood pressure can cause bladder control problems.
How can medicines cause leaking?
Leaking can happen when medicines affect any of these muscles or nerves. For instance, medicines to treat high blood pressure may make the sphincter muscles too tight or too loose. Medicines to treat colds can have the same effect.
You may take medicine to calm your nerves so that you can sleep or relax. This medicine may dull the nerves in the bladder and keep them from signaling the brain when the bladder is full. Without the message and urge, the bladder overflows. Drinking alcohol can also cause these nerves to fail.
Water pills (diuretics) take fluid from swollen areas of your body and send it to the bladder. This may cause the bladder to leak because it fills more quickly than usual. Caffeine drinks such as coffee and cola have the same effect. Some foods such as chocolate also can cause bladder problems.

What can you do about your bladder control problem?
Your doctor needs to know what medicines you take.
Before your next doctor visit, make a list of all the prescription medicines you take. Also list medicines you buy without a prescription. Or you can bring all your medicines with you to show the doctor. Ask your doctor if any of the medicines could cause your bladder problem. Your pharmacist can also give you information about your medicines.
You may have to continue taking a medicine that causes a bladder control problem. Ask your doctor to help you find another way to control your bladder.
Other ways might include
exercises for the muscles that close the bladder
devices to stimulate the muscles
training the bladder to hold more urine
Points to Remember
Never stop taking a prescribed medicine without first talking to your doctor.
Certain medicines, foods, and drinks can cause bladder control problems.
Make a list of your medicines—both prescription and nonprescription—to show your doctor. Take the list to talk about bladder control.
You may have to keep taking important medicines, even if they cause some bladder control problems.

Medicines and Bladder ControlMedicines and Bladder ControlMedicines and Bladder ControlMedicines and Bladder ControlMedicines and Bladder ControlMedicines and Bladder ControlMedicines and Bladder ControlMedicines and Bladder ControlMedicines and Bladder ControlMedicines and Bladder Control

Abortion, Miscarriage, and Breast Cancer Risk

Abortion, Miscarriage, and Breast Cancer Risk

IntroductionA woman’s hormone levels normally change throughout her life for a variety of reasons, and these hormonal changes can lead to changes in her breasts. Many such hormonal changes occur during pregnancy, changes that may influence a woman’s chances of developing breast cancer later in life. As a result, over several decades a considerable amount of research has been and continues to be conducted to determine whether having an induced abortion, or a miscarriage (also known as spontaneous abortion), influences a woman’s chances of developing breast cancer later in life.
Current KnowledgeIn February 2003, the National Cancer Institute (NCI) convened a workshop of over 100 of the world’s leading experts who study pregnancy and breast cancer risk. Workshop participants reviewed existing population-based, clinical, and animal studies on the relationship between pregnancy and breast cancer risk, including studies of induced and spontaneous abortions. They concluded that having an abortion or miscarriage does not increase a woman’s subsequent risk of developing breast cancer. A summary of their findings, titled atBackgroundThe relationship between induced and spontaneous abortion and breast cancer risk has been the subject of extensive research beginning in the late 1950s. Until the mid-1990s, the evidence was inconsistent. Findings from some studies suggested there was no increase in risk of breast cancer among women who had had an abortion, while findings from other studies suggested there was an increased risk. Most of these studies, however, were flawed in a number of ways that can lead to unreliable results. Only a small number of women were included in many of these studies, and for most, the data were collected only after breast cancer had been diagnosed, and women’s histories of miscarriage and abortion were based on their “self-report” rather than on their medical records. Since then, better-designed studies have been conducted. These newer studies examined large numbers of women, collected data before breast cancer was found, and gathered medical history information from medical records rather than simply from self-reports, thereby generating more reliable findings. The newer studies consistently showed no association between induced and spontaneous abortions and breast cancer risk.
Ongoing Research Supported by the National Cancer InstituteBasic, clinical, and population research will continue to be supported which investigate the relationship and the mechanisms of how hormones in general and during pregnancy influence the development of breast cancer.
Important Information About Breast Cancer Risk FactorsAt present, the factors known to increase a woman’s chance of developing breast cancer include age (a woman’s chances of getting breast cancer increase as she gets older), a family history of breast cancer, an early age at first menstrual period, a late age at menopause, a late age at the time of birth of her first full-term baby, and certain breast conditions. Obesity is also a risk factor for breast cancer in postmenopausal women. More information about breast cancer risk factors is found in NCI’s publication What You Need To Know About™ Breast Cancer.
Important Information About Identifying Breast CancerNCI recommends that, beginning in their 40s, women receive mammography screening every year or two. Women who have a higher than average risk of breast cancer (for example, women with a family history of breast cancer) should seek expert medical advice about whether they should be screened before age 40, and how frequently they should be screened.

Abortion, Miscarriage, and Breast Cancer RiskAbortion, Miscarriage, and Breast Cancer RiskAbortion, Miscarriage, and Breast Cancer RiskAbortion, Miscarriage, and Breast Cancer RiskAbortion, Miscarriage, and Breast Cancer RiskAbortion, Miscarriage, and Breast Cancer Risk

Investigational Drugs

Investigational Drugs: Questions and Answers

Key Points
An investigational drug is one that is under study and is not approved by the U.S. Food and Drug Administration for sale in the United States (see Question 1).
The most common way patients receive investigational drugs is by taking part in clinical trials (see Question 2).
Patients sometimes receive investigational drugs through mechanisms such as expanded access protocols and special exception programs (see Question 3).
Specific criteria must be met to receive an investigational drug outside a clinical trial (see Questions 3 and 7).
Patients interested in receiving investigational drugs should talk to their physician (see Question 8).
In general, investigational drugs are provided free of charge (see Question 9).
What is an investigational drug?
An investigational drug is one that is under study but does not have permission from the U.S. Food and Drug Administration (FDA) to be legally marketed and sold in the United States.
FDA approval is the final step in the process of drug development. The first step is for the new drug to be tested in the laboratory. If the results are promising, the drug company or sponsor must apply for FDA approval to test the drug in people. This is called an Investigational New Drug (IND) Application. Once the IND is approved, clinical trials can begin. Clinical trials are research studies to determine the safety and measure the effectiveness of the drug in people. Once clinical trials are completed, the sponsor submits the study results in a New Drug Application (NDA) or Biologics License Application (BLA) to the FDA. This application is carefully reviewed and, if the drug is found to be reasonably safe and effective, it is approved.
How do patients get investigational drugs?
By far, the most common way that patients get investigational drugs is by taking part in a clinical trial sponsored under an IND. A patient’s doctor may suggest a clinical trial as one treatment option. Or a patient or family member can ask the doctor about clinical trials or new drugs available for cancer treatment.
Another way patients and their families can learn about new drugs being tested in clinical trials is through the National Cancer Institute’s (NCI) PDQ® database. This database contains information on a large number of ongoing studies. Individuals can search this database at http://www.cancer.gov/clinicaltrials/search, or they can call the NCI’s Cancer Information Service at 1–800–4–CANCER (1–800–422–6237). Information specialists can search the database and provide a list of trials for individuals to discuss with their doctor.
Are there other ways to get investigational drugs?
Less common ways that patients can receive investigational drugs include mechanisms such as an expanded access protocol or as special or compassionate exception. The sponsor must agree to provide the drug for this use.
Investigational drugs given under these mechanisms must meet the following criteria:
There must be substantial clinical evidence that the drug may benefit persons with particular types of cancer.
The drug must be able to be given safely outside a clinical trial.
The drug must be in sufficient supply for ongoing and planned clinical trials.
Expanded Access The purpose of an expanded access protocol is to make investigational drugs that have significant activity against specific cancers available to patients before the FDA approval process has been completed. Expanded access protocols allow a larger group of people to be treated with the drug.
The sponsor must apply to the FDA to make the drug available through an expanded access protocol. There must be enough evidence from studies already completed to show that the drug is likely to be effective against a specific type of cancer and that it does not have unreasonable risks. The FDA generally approves expanded access only if there are no other satisfactory treatments available for the disease.
The NCI’s Treatment Referral Center (TRC) protocols are one type of expanded access protocol. The NCI establishes a TRC protocol when clinical evidence suggests that an investigational drug should be made more widely available to patients, even though the FDA approval process has not been completed. The TRC protocol is made available at NCI-designated cancer centers and other institutions selected to provide wide geographic availability of the drug to patients.
Special Exception/Compassionate ExemptionPatients who do not meet the eligibility criteria for a clinical trial of an investigational drug may be eligible to receive the drug under a mechanism known as a special exception or a compassionate exemption to the policy of administering investigational drugs only in a clinical trial. The patient’s doctor contacts the sponsor of the investigational agent and provides the patient’s medical information and treatment history. The sponsor (the drug company or NCI) evaluates the requests on a case-by-case basis. There should be reasonable expectation that the drug will prolong survival or improve quality of life.
In some cases, even patients who qualify for treatment with an investigational drug on a compassionate basis might not be able to obtain the drug if the supply is limited and the demand is high.
Are all investigational drugs available through an expanded access or special exception mechanism?
No. The sponsor decides whether to provide an investigational drug outside a clinical trial. Availability may be limited in part by drug supply, patient demand, or other factors.
What is the NCI’s role in providing access to investigational drugs?
The NCI acts as the sponsor for many, but not all, investigational drugs. When acting as sponsor, the NCI provides the investigational drug to the physicians who are participating in clinical trials or TRC protocols. A physician who wishes to treat a patient with the investigational drug as a special exception must request the drug from the NCI. These requests are reviewed on a case-by-case basis.
Who can provide access to investigational drugs being developed by pharmaceutical companies?
In the case of investigational drugs sponsored by a drug company, the drug company in collaboration with the FDA provides access to the drug. The process is similar to that described above.
The patient’s physician must submit a request to the drug company and to the FDA. The drug company can provide the name of the appropriate reviewing division at the FDA. (FDA reviewing divisions are prohibited from divulging proprietary information such as whether a sponsor has filed an IND or the status of an IND.)
Are there specific criteria used to determine whether patients can receive an investigational drug outside a clinical trial?
To be considered for treatment with an investigational drug outside a clinical trial, generally patients must meet the following criteria:
have undergone standard treatment that has not been successful
be ineligible for any ongoing clinical trials of this drug
have no acceptable treatment alternatives
have a cancer diagnosis for which the investigational drug has demonstrated activity
be likely to experience benefits that outweigh the risks involved
What should patients do if they are interested in receiving an investigational drug through a special exception or expanded access mechanism?
Patients interested in gaining access to investigational drugs should talk to their physician about available options. Physicians can make requests for special exceptions by contacting the study sponsor. Physicians will be required to follow strict guidelines, including gaining approval from their Institutional Review Board and obtaining informed consent from the patient. Informed consent is a process that includes a document to be signed by the patient which outlines the known risks and benefits of the treatment, as well as the rights and responsibilities of the patient.
What are the costs involved in receiving an investigational drug?
In general, the drug is provided free of charge. However, there may be other costs associated with the treatment. Before beginning treatment, patients should check with their insurer about coverage of these costs.
What are some of the potential drawbacks to receiving an investigational drug?
It is not known whether an investigational drug is better than standard therapy for treating a disease, and a patient may not receive any benefit. Side effects (both long-term and short-term) from the drug may not be fully understood, especially if the drug is in early phases of testing. Finally, a patient’s health insurance company may not pay expenses associated with receiving the investigational drug.

Investigational DrugsInvestigational DrugsInvestigational DrugsInvestigational DrugsInvestigational DrugsInvestigational DrugsInvestigational DrugsInvestigational Drugs

Alcohol Abuse and Alcoholism

Alcohol Abuse and Alcoholism

Alcohol-Medication Interactions
Many medications can interact with alcohol, leading to increased risk of illness, injury, or death. For example, it is estimated that alcohol-medication interactions may be a factor in at least 25 percent of all emergency room admissions (1). An unknown number of less serious interactions may go unrecognized or unrecorded. This Alcohol Alert notes some of the most significant alcohol-drug interactions. (Although alcohol can interact with illicit drugs as well, the term "drugs" is used here to refer exclusively to medications, whether prescription or nonprescription.)
How Common Are Alcohol-Drug Interactions?
More than 2,800 prescription drugs are available in the United States, and physicians write 14 billion prescriptions annually; in addition, approximately 2,000 medications are available without prescription (2).
Ap proximately 70 percent of the adult population consumes alcohol at least occasionally, and 10 percent drink daily (3). About 60 percent of men and 30 percent of women have had one or more adverse alcohol-related life events (4). Together with the data on medication use, these statistics suggest that some concurrent use of alcohol and medications is inevitable.
The elderly may be especially likely to mix drugs and alcohol and are at particular risk for the adverse consequences of such combinations. Although persons age 65 and older constitute only 12 percent of the population, they consume 25 to 30 percent of all prescription medications (5) . The elderly are more likely to suffer medication side effects compared with younger persons, and these effects tend to be more severe with advancing age (5). Among persons age 60 or older, 10 percent of those in the community--and 40 percent of those in nursing homes--fulfill criteria for alcohol abuse (6).
How Alcohol and Drugs Interact
To exert its desired effect, a drug generally must travel through the bloodstream to its site of action, where it produces some change in an organ or tissue. The drug's effects then diminish as it is processed (metabolized) by enzymes and eliminated from the body. Alcohol behaves similarly, traveling through the bloodstream, acting upon the brain to cause intoxication, and finally being metabolized and eliminated, principally by the liver. The extent to which an administered dose of a drug reaches its site of action may be termed its availability. Alcohol can influence the effectiveness of a drug by altering its availability. Typical alcohol-drug interactions include the following (7): First, an acute dose of alcohol (a single drink or several drinks over several hours) may inhibit a drug's metabolism by competing with the drug for the same set of metabolizing enzymes. This interaction prolongs and enhances the drug's availability, potentially increasing the patient's risk of experiencing harmful side effects from the drug. Second, in contrast, chronic (long-term) alcohol ingestion may activate drug-metabolizing enzymes, thus decreasing the drug's availability and diminishing its effects. After these enzymes have been activated, they remain so even in the absence of alcohol, affecting the metabolism of certain drugs for several weeks after cessation of drinking (8). Thus, a recently abstinent chronic drinker may need higher doses of medications than those required by nondrinkers to achieve therapeutic levels of certain drugs. Third, enzymes activated by chronic alcohol consumption transform some drugs into toxic chemicals that can damage the liver or other organs. Fourth, alcohol can magnify the inhibitory effects of sedative and narcotic drugs at their sites of action in the brain. To add to the complexity of these interactions, some drugs affect the metabolism of alcohol, thus altering its potential for intoxication and the adverse effects associated with alcohol consumption (7).
Some Specific Interactions
Anesthetics. Anesthetics are administered prior to surgery to render a patient unconscious and insensitive to pain. Chronic alcohol consumption increases the dose of propofol (Diprivan)1 required to induce loss of consciousness (9). Chronic alcohol consumption increases the risk of liver damage that may be caused by the anesthetic gases enflurane (Ethrane) (10) and halothane (Fluothane) (11).
Antibiotics. Antibiotics are used to treat infectious diseases. In combination with acute alcohol consumption, some antibiotics may cause nausea, vomiting, headache, and possibly convulsions; among these antibiotics are furazolidone (Furoxone), griseofulvin (Grisactin and others), metronidazole (Flagyl), and the antimalarial quinacrine (Atabrine) (7). Isoniazid and rifampin are used together to treat tuberculosis, a disease especially problematic among the elderly (12) and among homeless alcoholics (13). Acute alcohol consumption decreases the availability of isoniazid in the bloodstream, whereas chronic alcohol use decreases the availability of rifampin. In each case, the effectiveness of the medication may be reduced (7).
Anticoagulants. Warfarin (Coumadin) is prescribed to retard the blood's ability to clot. Acute alcohol consumption enhances warfarin's availability, increasing the patient's risk for life-threatening hemorrhages (7). Chronic alcohol consumption reduces warfarin's availability, lessening the patient's protection from the consequences of blood-clotting disorders (7).
Antidepressants. Alcoholism and depression are frequently associated (14), leading to a high potential for alcohol-antidepressant interactions. Alcohol increases the sedative effect of tricyclic antidepressants such as amitriptyline (Elavil and others), impairing mental skills required for driving (15). Acute alcohol consumption increases the availability of some tricyclics, potentially increasing their sedative effects (16); chronic alcohol consumption appears to increase the availability of some tricyclics and to decrease the availability of others (17,18). The significance of these interactions is unclear. These chronic effects persist in recovering alcoholics (17).
A chemical called tyramine, found in some beers and wine, interacts with some anti-depressants, such as monoamine oxidase inhibitors, to produce a dangerous rise in blood pressure (7). As little as one standard drink may create a risk that this interaction will occur.
Antidiabetic medications. Oral hypoglycemic drugs are prescribed to help lower blood sugar levels in some patients with diabetes. Acute alcohol consumption prolongs, and chronic alcohol consumption decreases, the availability of tolbutamide (Orinase). Alcohol also interacts with some drugs of this class to produce symptoms of nausea and headache such as those described for metronidazole (see "Antibiotics") (7).
Antihistamines. Drugs such as diphenhydramine (Benadryl and others) are available without prescription to treat allergic symptoms and insomnia. Alcohol may intensify the sedation caused by some antihistamines (15). These drugs may cause excessive dizziness and sedation in older persons; the effects of combining alcohol and antihistamines may therefore be especially significant in this population (19).
Antipsychotic medications. Drugs such as chlorpromazine (Thorazine) are used to diminish psychotic symptoms such as delusions and hallucinations. Acute alcohol consumption increases the sedative effect of these drugs (20), resulting in impaired coordination and potentially fatal breathing difficulties (7). The combination of chronic alcohol ingestion and antipsychotic drugs may result in liver damage (21).
Antiseizure medications. These drugs are prescribed mainly to treat epilepsy. Acute alcohol consumption increases the availability of phenytoin (Dilantin) and the risk of drug-related side effects. Chronic drinking may decrease phenytoin availability, significantly reducing the patient's protection against epileptic seizures, even during a period of abstinence (8,22).
Antiulcer medications. The commonly prescribed antiulcer medications cimetidine (Tagamet) and ranitidine (Zantac) increase the availability of a low dose of alcohol under some circumstances (23,24). The clinical significance of this finding is uncertain, since other studies have questioned such interaction at higher doses of alcohol (25-27).
Cardiovascular medications. This class of drugs includes a wide variety of medications prescribed to treat ailments of the heart and circulatory system. Acute alcohol consumption interacts with some of these drugs to cause dizziness or fainting upon standing up. These drugs include nitroglycerin, used to treat angina, and reserpine, methyldopa (Aldomet), hydralazine (Apresoline and others), and guanethidine (Ismelin and others), used to treat high blood pressure. Chronic alcohol consumption decreases the availability of propranolol (Inderal), used to treat high blood pressure (7), potentially reducing its therapeutic effect.
Narcotic pain relievers. These drugs are prescribed for moderate to severe pain. They include the opiates morphine, codeine, propoxyphene (Darvon), and meperidine (Demerol). The combination of opiates and alcohol enhances the sedative effect of both substances, increasing the risk of death from overdose (28). A single dose of alcohol can increase the availability of propoxyphene (29), potentially increasing its sedative side effects.
Nonnarcotic pain relievers. Aspirin and similar nonprescription pain relievers are most commonly used by the elderly (5) . Some of these drugs cause stomach bleeding and inhibit blood from clotting; alcohol can exacerbate these effects (30). Older persons who mix alcoholic beverages with large doses of aspirin to self-medicate for pain are therefore at particularly high risk for episodes of gastric bleeding (19). In addition, aspirin may increase the availability of alcohol (31), heightening the effects of a given dose of alcohol.
Chronic alcohol ingestion activates enzymes that transform acetaminophen (Tylenol and others) into chemicals that can cause liver damage, even when acetaminophen is used in standard therapeutic amounts (32,33). These effects may occur with as little as 2.6 grams of acetaminophen in persons consuming widely varying amounts of alcohol (34).
Sedatives and hypnotics ("sleeping pills"). Benzodiazepines such as diazepam (Valium) are generally prescribed to treat anxiety and insomnia. Because of their greater safety margin, they have largely replaced the barbiturates, now used mostly in the emergency treatment of convulsions (2).
Doses of benzodiazepines that are excessively sedating may cause severe drowsiness in the presence of alcohol (35), increasing the risk of household and automotive accidents (15,36). This may be especially true in older people, who demonstrate an increased response to these drugs (5,19). Low doses of flurazepam (Dalmane) interact with low doses of alcohol to impair driving ability, even when alcohol is ingested the morning after taking Dalmane. Since alcoholics often suffer from anxiety and insomnia, and since many of them take morning drinks, this interaction may be dangerous (37).
The benzodiazepine lorazepam (Ativan) is being increasingly used for its antianxiety and sedative effects. The combination of alcohol and lorazepam may result in depressed heart and breathing functions; therefore, lorazepam should not be administered to intoxicated patients (38).
Acute alcohol consumption increases the availability of barbiturates, prolonging their sedative effect. Chronic alcohol consumption decreases barbiturate availability through enzyme activation (2). In addition, acute or chronic alcohol consumption enhances the sedative effect of barbiturates at their site of action in the brain, sometimes leading to coma or fatal respiratory depression (39).
Alcohol-Medication Interactions--A Commentary by NIAAA Director Enoch Gordis, M.D.
Individuals who drink alcoholic beverages should be aware that simultaneous use of alcohol and medications--both prescribed and over-the-counter--has the potential to cause problems. For example, even very small doses of alcohol probably should not be used with antihistamines and other medications with sedative effects. Individuals who drink larger amounts of alcohol may run into problems when commonly used medications (e.g., acetaminophen) are taken at the same time or even shortly after drinking has stopped. Elderly individuals should be especially careful of these potential problems due to their generally greater reliance on multiple medications and age-related changes in physiology.

Alcohol Abuse and Alcoholism Alcohol Abuse and Alcoholism Alcohol Abuse and Alcoholism Alcohol Abuse and Alcoholism Alcohol Abuse and Alcoholism Alcohol Abuse and Alcoholism Alcohol Abuse and Alcoholism Alcohol Abuse and Alcoholism Alcohol Abuse and Alcoholism

Analgesic Nephropathy

Analgesic Nephropathy (Painkillers and the Kidneys)
On this page:
Acute Kidney Failure
Analgesic Nephropathy
Treatment
For More Information Analgesic Nephropathy
An analgesic is any medicine intended to relieve pain. Over-the-counter analgesics—that is, painkillers available without a prescription—include aspirin, acetaminophen, ibuprofen, naproxen sodium, and others. These drugs present no danger for most people when taken in the recommended dosage. But some conditions make taking even these common painkillers dangerous for the kidneys. Also, taking one of these drugs regularly over a long period of time may increase the risk for kidney problems. Most drugs that can cause kidney damage are excreted only through the kidneys. That is, they are not broken down by the liver, as alcohol is, or passed out of the body through the digestive tract.
Analgesic use has been associated with two different forms of kidney damage: acute renal failure and a type of chronic kidney disease called analgesic nephropathy.

Acute Kidney Failure Analgesic Nephropathy
Some patient case reports have attributed incidents of sudden-onset acute kidney failure to the use of over-the-counter painkillers, including aspirin, ibuprofen, and naproxen sodium. Some of these patients experienced acute illnesses involving fluid loss or decreased fluid intake. Other patients in these reports had risk factors such as systemic lupus erythematosus, advanced age, chronic kidney disease, or recent heavy alcohol consumption. These cases involved a single dose in some instances and generally short-term analgesic use of not more than 10 days.
Acute kidney failure requires emergency dialysis to clean the blood. Kidney damage is frequently reversible, with normal kidney function returning after the emergency is over and the analgesic use is stopped.

Analgesic Nephropathy
A second form of kidney damage, called analgesic nephropathy, can result from taking painkillers every day for several years. Analgesic nephropathy is a chronic kidney disease that over years gradually leads to irreversible kidney failure and the permanent need for dialysis or a kidney transplant to restore kidney function. Researchers estimate that four out of 100,000 people will develop analgesic nephropathy. It is most common in women over 30.
The painkiller phenacetin has been taken off the market because of its association with analgesic nephropathy. Recent studies have suggested that longstanding daily use of analgesics such as acetaminophen or ibuprofen may also increase the risk of chronic kidney damage, but this evidence is not as clear.
In view of these findings, people with conditions that put them at risk for acute kidney failure should check with their health care provider before taking any analgesic medicine. People who take over-the-counter painkillers regularly should check with their primary care physician to make sure the drugs are not hurting their kidneys. The physician may be able to recommend a safer alternative and can order regular tests to monitor their kidney function.

Treatment Analgesic Nephropathy
If you have been taking analgesics regularly to control chronic pain, you may be advised to find new ways to treat your pain, such as behavior modification or relaxation techniques. Depending on how much your kidney function has declined, you may be advised to change your diet, limit the fluids you drink, or take medications to avoid anemia and bone problems caused by kidney disease. Your doctor will monitor your kidney function with regular urine and blood tests.

Analgesic Nephropathy Analgesic Nephropathy Analgesic Nephropathy Analgesic Nephropathy

cancer risk in women Oral contraceptive

Oral Contraceptives and Cancer Risk: Questions and Answers
Key Points
Some cancers depend on naturally occurring sex hormones for their development and growth. Researchers are interested in learning whether the hormones in oral contraceptives affect cancer risk in women (see Question 1).
Some studies have shown an increased risk of breast cancer in women taking oral contraceptives, while other studies have shown no change in risk (see Question 2).
Oral contraceptive use has been shown in multiple studies to decrease the risk of ovarian and endometrial cancer (see Question 3).
Oral contraceptives have been shown to increase the risk of cervical cancer; however, human papillomavirus is the major risk factor for this disease (see Question 4).
The risk of liver cancer is increased in women who take oral contraceptives and are otherwise considered low risk for the disease (see Question 5).
Introduction
Oral contraceptives (OCs) first became available to American women in the early 1960s. The convenience, effectiveness, and reversibility of action of birth control pills (popularly known as “the pill”) have made them the most popular form of birth control in the United States. However, concerns have been raised about the role that the hormones in OCs might play in a number of cancers, and how hormone-based OCs contribute to their development. Sufficient time has elapsed since the introduction of OCs to allow investigators to study large numbers of women who took birth control pills for many years.
This fact sheet addresses only what is known about OC use and the risk of developing cancer. It does not deal with other serious side effects of OC use, such as the increased risk of cardiovascular disease for certain groups of women. Recently, alternative methods of delivering hormones for contraception have been developed, including a topical patch, vaginal ring, and intrauterine delivery system, but these products are too new to have been tested in clinical trials (research studies) for long-term safety and other effects (1). They also are not covered in this fact sheet.

What types of oral contraceptives are available in the United States ? Why do researchers believe that oral contraceptives may influence cancer risk?
Currently, two types of OCs are available in the United States . The most commonly prescribed OC contains two man-made versions of natural female hormones (estrogen and progesterone) that are similar to the hormones the ovaries normally produce. This type of pill is often called a “combined oral contraceptive.” The second type of OC available in the United States is called the minipill. It contains only a type of progesterone.
Estrogen stimulates the growth and development of the uterus at puberty, causes the endometrium (the inner lining of the uterus) to thicken during the first half of the menstrual cycle, and influences breast tissue throughout life, but particularly from puberty to menopause.
Progesterone, which is produced during the last half of the menstrual cycle, prepares the endometrium to receive the egg. If the egg is fertilized, progesterone secretion continues, preventing release of additional eggs from the ovaries. For this reason, progesterone is called the “pregnancy-supporting” hormone, and scientists believe that it has valuable contraceptive effects. The man-made progesterone used in OCs is called progestogen or progestin.
Because medical research suggests that some cancers depend on naturally occurring sex hormones for their development and growth, scientists have been investigating a possible link between OC use and cancer risk. Researchers have focused a great deal of attention on OC users over the past 40 years. This scrutiny has produced a wealth of data on OC use and the development of certain cancers, although results of these studies have not always been consistent. The risk of endometrial and ovarian cancers is reduced with the use of OCs, while the risk of breast and cervical cancers is increased (1). A summary of research results for each type of cancer is given in Questions 2–5.
How do oral contraceptives affect breast cancer risk?
A woman’s risk of developing breast cancer depends on several factors, some of which are related to her natural hormones. Hormonal factors that increase the risk of breast cancer include conditions that may allow high levels of hormones to persist for long periods of time, such as beginning menstruation at an early age (before age 12), experiencing menopause at a late age (after age 55), having a first child after age 30, and not having children at all.
A 1996 analysis of worldwide epidemiologic data conducted by the Collaborative Group on Hormonal Factors in Breast Cancer found that women who were current or recent users of birth control pills had a slightly elevated risk of developing breast cancer. The risk was highest for women who started using OCs as teenagers. However, 10 or more years after women stopped using OCs, their risk of developing breast cancer returned to the same level as if they had never used birth control pills, regardless of family history of breast cancer, reproductive history, geographic area of residence, ethnic background, differences in study design, dose and type of hormone, or duration of use. In addition, breast cancers diagnosed in women after 10 or more years of not using OCs were less advanced than breast cancers diagnosed in women who had never used OCs. To conduct this analysis, the researchers examined the results of 54 studies. The analysis involved 53,297 women with breast cancer and 100,239 women without breast cancer. More than 200 researchers participated in this combined analysis of their original studies, which represented about 90 percent of the epidemiological studies throughout the world that had investigated the possible relationship between OCs and breast cancer (2).
The findings of the Women’s Contraceptive and Reproductive Experiences (Women’s CARE) study were in contrast to those described above. The Women’s CARE study examined the use of OCs as a risk factor for breast cancer in women ages 35 to 64. Researchers interviewed 4,575 women who were diagnosed with breast cancer between 1994 and 1998, and 4,682 women who did not have breast cancer. Investigators collected detailed information about the participants’ use of OCs, reproductive history, health, and family history. The results, which were published in 2002, indicated that current or former use of OCs did not significantly increase the risk of breast cancer. The findings were similar for white and black women. Factors such as longer periods of use, higher doses of estrogen, initiation of OC use before age 20, and OC use by women with a family history of breast cancer were not associated with an increased risk of the disease (3).
In a National Cancer Institute (NCI)-sponsored study published in 2003, researchers examined risk factors for breast cancer among women ages 20 to 34 compared with women ages 35 to 54. Women diagnosed with breast cancer were asked whether they had used OCs for more than 6 months before diagnosis and, if so, whether the most recent use had been within 5 years, 5 to 10 years, or more than 10 years. The results indicated that the risk was highest for women who used OCs within 5 years prior to diagnosis, particularly in the younger group (4).
How do oral contraceptives affect ovarian and endometrial cancer risk?
Studies have consistently shown that using OCs reduces the risk of ovarian cancer. In a 1992 analysis of 20 studies of OC use and ovarian cancer, researchers from Harvard Medical School found that the risk of ovarian cancer decreased with increasing duration of OC use. Results showed a 10 to 12 percent decrease in risk after 1 year of use, and approximately a 50 percent decrease after 5 years of use (5).
Researchers have studied how the amount or type of hormones in OCs affects ovarian cancer risk reduction. One of the studies used in the Harvard analysis, the Cancer and Steroid Hormone Study (CASH), found that the reduction in ovarian cancer risk was the same regardless of the type or amount of estrogen or progestin in the pill (6). A more recent analysis of data from the CASH study, however, indicated that OC formulations with high levels of progestin reduced ovarian cancer risk more than preparations with low progestin levels (7). In another recent study, the Steroid Hormones and Reproductions (SHARE) study, researchers investigated new, lower-dose progestins that have varying androgenic properties (testosterone-like effects). They found no difference in ovarian cancer risk between androgenic and nonandrogenic pills (8).
OC use in women at increased risk of ovarian cancer due to BRCA1 and BRCA2 genetic mutations has been studied. One study showed a reduction in risk, but a more recent study showed no effect (9, 10).
The use of OCs has been shown to significantly reduce the risk of endometrial cancer. This protective effect increases with the length of time OCs are used, and continues for many years after a woman stops using OCs (11).
How do oral contraceptives affect cervical cancer risk?
Evidence shows that long-term use of OCs (5 or more years) may be associated with an increased risk of cancer of the cervix (the narrow, lower portion of the uterus) (12). Although OC use may increase the risk of cervical cancer, human papillomavirus (HPV) is recognized as the major cause of this disease. Approximately 14 types of HPV have been identified as having the potential to cause cancer, and HPVs have been found in 99 percent of cervical cancer biopsy specimens worldwide (12). More information about HPV and cancer is available in Human Papillomaviruses and Cancer: Questions and Answers at http://www.cancer.gov/cancertopics/factsheet/risk/HPV on the Internet.
A 2003 analysis by the International Agency for Research on Cancer (IARC) found an increased risk of cervical cancer with longer use of OCs. Researchers analyzed data from 28 studies that included 12,531 women with cervical cancer. The data suggested that the risk of cervical cancer may decrease after OC use stops (13). In another IARC report, data from eight studies were combined to assess the effect of OC use on cervical cancer risk in HPV-positive women. Researchers found a fourfold increase in risk among women who had used OCs for longer than 5 years. Risk was also increased among women who began using OCs before age 20 and women who had used OCs within the past 5 years (14). The IARC is planning a study to reanalyze all data related to OC use and cervical cancer risk (12).
How do oral contraceptives affect liver cancer risk?
Several studies have found that OCs increase the risk of liver cancer in populations usually considered low risk, such as white women in the United States and Europe who do not have liver disease. In these studies, women who used OCs for longer periods of time were found to be at increased risk for liver cancer. However, OCs did not increase the risk of liver cancer in Asian and African women, who are considered high risk for this disease. Researchers believe this is because other risk factors, such as hepatitis infection, outweigh the effect of OCs (15).
What screening tests are available for the cancers described?
Studies have found that regular breast cancer screening with mammograms reduces the number of deaths from breast cancer for women ages 40 to 69. Women who are at increased risk for breast cancer should seek medical advice about when to begin having mammograms and how often to be screened. A high-quality mammogram, with a clinical breast exam (an exam done by a professional health care provider), is the most effective way to detect breast cancer early.
Abnormal changes in the cervix can often be detected by a Pap test and treated before cancer develops. Women who have begun to have sexual intercourse or are age 21 should check with their doctor about having a Pap test. Researchers are working on developing screening tests for ovarian and endometrial cancer.
Women who are concerned about their risk for cancer are encouraged to talk with their health care provider.

Oral Contraceptives and Cancer Risk: Questions and Answers Key Points Some cancers depend on naturally occurring sex hormones for their development and growth. Researchers are interested in learning whether the hormones in oral contraceptives affect cancer risk in women (see Question 1). Some studies have shown an increased risk of breast cancer in women taking oral contraceptives, while other studies have shown no change in risk (see Question 2). Oral contraceptive use has been shown in multiple studies to decrease the risk of ovarian and endometrial cancer (see Question 3). Oral contraceptives have been shown to increase the risk of cervical cancer; however, human papillomavirus is the major risk factor for this disease (see Question 4). The risk of liver cancer is increased in women who take oral contraceptives and are otherwise considered low risk for the disease (see Question 5). Introduction Oral contraceptives (OCs) first became available to American women in the early 1960s. The convenience, effectiveness, and reversibility of action of birth control pills (popularly known as “the pill”) have made them the most popular form of birth control in the United States. However, concerns have been raised about the role that the hormones in OCs might play in a number of cancers, and how hormone-based OCs contribute to their development. Sufficient time has elapsed since the introduction of OCs to allow investigators to study large numbers of women who took birth control pills for many years. This fact sheet addresses only what is known about OC use and the risk of developing cancer. It does not deal with other serious side effects of OC use, such as the increased risk of cardiovascular disease for certain groups of women. Recently, alternative methods of delivering hormones for contraception have been developed, including a topical patch, vaginal ring, and intrauterine delivery system, but these products are too new to have been tested in clinical trials (research studies) for long-term safety and other effects (1). They also are not covered in this fact sheet. What types of oral contraceptives are available in the United States ? Why do researchers believe that oral contraceptives may influence cancer risk? Currently, two types of OCs are available in the United States . The most commonly prescribed OC contains two man-made versions of natural female hormones (estrogen and progesterone) that are similar to the hormones the ovaries normally produce. This type of pill is often called a “combined oral contraceptive.” The second type of OC available in the United States is called the minipill. It contains only a type of progesterone. Estrogen stimulates the growth and development of the uterus at puberty, causes the endometrium (the inner lining of the uterus) to thicken during the first half of the menstrual cycle, and influences breast tissue throughout life, but particularly from puberty to menopause. Progesterone, which is produced during the last half of the menstrual cycle, prepares the endometrium to receive the egg. If the egg is fertilized, progesterone secretion continues, preventing release of additional eggs from the ovaries. For this reason, progesterone is called the “pregnancy-supporting” hormone, and scientists believe that it has valuable contraceptive effects. The man-made progesterone used in OCs is called progestogen or progestin. Because medical research suggests that some cancers depend on naturally occurring sex hormones for their development and growth, scientists have been investigating a possible link between OC use and cancer risk. Researchers have focused a great deal of attention on OC users over the past 40 years. This scrutiny has produced a wealth of data on OC use and the development of certain cancers, although results of these studies have not always been consistent. The risk of endometrial and ovarian cancers is reduced with the use of OCs, while the risk of breast and cervical cancers is increased (1). A summary of research results for each type of cancer is given in Questions 2–5. How do oral contraceptives affect breast cancer risk?

Pregnancy

Pregnancy
Although many pregnant women with high blood pressure have healthy babies without serious problems, high blood pressure can be dangerous for both the mother and the fetus. Women with pre-existing, or chronic, high blood pressure are more likely to have certain complications during pregnancy than those with normal blood pressure. However, some women develop high blood pressure while they are pregnant (often called gestational hypertension).
The effects of high blood pressure range from mild to severe. High blood pressure can harm the mother's kidneys and other organs, and it can cause low birth weight and early delivery. In the most serious cases, the mother develops preeclampsia—or "toxemia of pregnancy"—which can threaten the lives of both the mother and the fetus.

Pregnancy Although many pregnant women with high blood pressure have healthy babies without serious problems, high blood pressure can be dangerous for both the mother and the fetus. Women with pre-existing, or chronic, high blood pressure are more likely to have certain complications during pregnancy than those with normal blood pressure. However, some women develop high blood pressure while they are pregnant (often called gestational hypertension). The effects of high blood pressure range from mild to severe. High blood pressure can harm the mother's kidneys and other organs, and it can cause low birth weight and early delivery. In the most serious cases, the mother develops preeclampsia—or "toxemia of pregnancy"—which can threaten the lives of both the mother and the fetus.

Premature Ovarian Failure

Premature Ovarian Failure
What is premature ovarian failure?
The term premature ovarian failure describes a stop in the normal functioning of the ovaries in a woman younger than age 40. Some people also use the term primary ovarian insufficiency to describe this condition. It is also known as hypergonadotropic hypogonadism.
Health care providers used to call this condition premature menopause, but premature ovarian failure is actually much different than menopause.
In menopause, a woman will likely never have another menstrual period again; women with premature ovarian failure are much more likely to get periods, even if they come irregularly.
A woman in menopause has virtually no chance of getting pregnant; a woman with premature ovarian failure has a greatly reduced chance of getting pregnant, but pregnancy is still possible.
What are the symptoms of premature ovarian failure?
The most common first symptom of premature ovarian failure is skipping or having irregular periods.
Some women with premature ovarian failure also have other symptoms, similar to those of women going through natural menopause. These may include:
Hot flashes and night sweats
Irritability, poor concentration
Decreased interest in sex or pain during sex
Drying of the vagina
Infertility
Premature ovarian failure also puts women at risk for some other health conditions, some of them serious, including:
Osteoporosis – loss of bone strength and bone density. Getting enough calcium, vitamin D, and weight-bearing physical activity can help reduce this risk.
Low thyroid function – affects metabolism and can cause very low energy. Replacing the thyroid hormone can treat the problem.
Addison’s disease – an autoimmune disorder in which the body has trouble handling physical stress, such an injury or illness, because of problems with the adrenal glands. About 3.2 percent of women with premature ovarian failure also have Addison’s disease. Addison’s can be dangerous for women who don’t know they have it. This condition can’t be prevented, but can be managed with help from your health care provider.
Heart disease – estrogen replacement therapy, along with keeping a healthy body weight and getting regular, moderate, physical activity, can help reduce this risk.
Also, it is important to know that people who are carriers for the gene for Fragile X syndrome, or who have the premutation for the condition, are more likely than other people to get premature ovarian failure. If you are a Fragile X carrier or have a premutation, it is important to get tested for premature ovarian failure.-->
Are there treatments for the symptoms of premature ovarian failure?
There is no proven treatment to make a woman’s ovaries work normally again. However, there are treatments that can help some of the symptoms of premature ovarian failure.
Estrogen replacement therapy (ERT), also called hormone replacement therapy (HRT) gives women the estrogen and other hormones their bodies are not making. HRT can help women have regular periods and lower their risk for osteoporosis.
Current research is looking into giving women the hormone testosterone to help prevent bone loss in women with premature ovarian failure.

Premature Ovarian Failure What is premature ovarian failure? The term premature ovarian failure describes a stop in the normal functioning of the ovaries in a woman younger than age 40. Some people also use the term primary ovarian insufficiency to describe this condition. It is also known as hypergonadotropic hypogonadism. Health care providers used to call this condition premature menopause, but premature ovarian failure is actually much different than menopause. In menopause, a woman will likely never have another menstrual period again; women with premature ovarian failure are much more likely to get periods, even if they come irregularly. A woman in menopause has virtually no chance of getting pregnant; a woman with premature ovarian failure has a greatly reduced chance of getting pregnant, but pregnancy is still possible. What are the symptoms of premature ovarian failure? The most common first symptom of premature ovarian failure is skipping or having irregular periods. Some women with premature ovarian failure also have other symptoms, similar to those of women going through natural menopause. These may include: Hot flashes and night sweats Irritability, poor concentration Decreased interest in sex or pain during sex Drying of the vagina Infertility Premature ovarian failure also puts women at risk for some other health conditions, some of them serious, including: Osteoporosis – loss of bone strength and bone density. Getting enough calcium, vitamin D, and weight-bearing physical activity can help reduce this risk. Low thyroid function – affects metabolism and can cause very low energy. Replacing the thyroid hormone can treat the problem. Addison’s disease – an autoimmune disorder in which the body has trouble handling physical stress, such an injury or illness, because of problems with the adrenal glands. About 3.2 percent of women with premature ovarian failure also have Addison’s disease. Addison’s can be dangerous for women who don’t know they have it. This condition can’t be prevented, but can be managed with help from your health care provider. Heart disease – estrogen replacement therapy, along with keeping a healthy body weight and getting regular, moderate, physical activity, can help reduce this risk. Also, it is important to know that people who are carriers for the gene for Fragile X syndrome, or who have the premutation for the condition, are more likely than other people to get premature ovarian failure. If you are a Fragile X carrier or have a premutation, it is important to get tested for premature ovarian failure.--> Are there treatments for the symptoms of premature ovarian failure? There is no proven treatment to make a woman’s ovaries work normally again. However, there are treatments that can help some of the symptoms of premature ovarian failure. Estrogen replacement therapy (ERT), also called hormone replacement therapy (HRT) gives women the estrogen and other hormones their bodies are not making. HRT can help women have regular periods and lower their risk for osteoporosis. Current research is looking into giving women the hormone testosterone to help prevent bone loss in women with premature ovarian failure.

Preterm Labor and Birth

Preterm Labor and Birth
What are preterm labor and birth?
Preterm labor (also called premature labor) is labor that begins before 37 weeks of pregnancy. Because the fetus is not fully grown at this time, it may not be able to survive outside the womb. Health care providers will often take steps to try to stop labor if it occurs before this time.
A baby born before 37 weeks of pregnancy is considered a preterm birth (or premature birth). Preterm births occur in about 12 percent of all pregnancies in the U.S. It is one of the top causes of infant death in this country.-->
Who is at risk for preterm labor and birth?
Health care providers currently have no way of knowing which women will experience preterm labor or deliver their babies preterm. But there are factors that place a woman at higher risk for preterm labor or birth:
Certain infections, such as bacterial vaginosis and trichomoniasis
Shortened cervix
Previously given birth preterm
What are the challenges to a baby born preterm?
Premature infants may face a number of health challenges, including:
Low birth weight
Breathing problems because of underdeveloped lungs
Underdeveloped organs or organ systems
Greater risk for life-threatening infections
Greater risk for a serious lung condition, known as respiratory distress syndrome
Greater risk for cerebral palsy (CP)
Greater risk for learning and developmental disabilities
They may need to stay in the hospital for several weeks or more, often in a neonatal intensive care unit (NICU).-->
What methods are used to prevent preterm delivery?
Research supported by the NICHD found that treating high-risk pregnant women (those who have previously had a spontaneous preterm baby) with a certain type of progesterone reduces the risk of another preterm delivery. The treatment worked among all ethnic groups in the study and improved outcomes for the babies. Efforts to find out whether the treatment works for other at-risk women, such as those having twins and triplets, are ongoing.
Bed rest and medications that relax the muscles in the uterus are also commonly used to try to stop preterm labor.

Preterm Labor and Birth What are preterm labor and birth? Preterm labor (also called premature labor) is labor that begins before 37 weeks of pregnancy. Because the fetus is not fully grown at this time, it may not be able to survive outside the womb. Health care providers will often take steps to try to stop labor if it occurs before this time. A baby born before 37 weeks of pregnancy is considered a preterm birth (or premature birth). Preterm births occur in about 12 percent of all pregnancies in the U.S. It is one of the top causes of infant death in this country.--> Who is at risk for preterm labor and birth? Health care providers currently have no way of knowing which women will experience preterm labor or deliver their babies preterm. But there are factors that place a woman at higher risk for preterm labor or birth: Certain infections, such as bacterial vaginosis and trichomoniasis Shortened cervix Previously given birth preterm What are the challenges to a baby born preterm? Premature infants may face a number of health challenges, including: Low birth weight Breathing problems because of underdeveloped lungs Underdeveloped organs or organ systems Greater risk for life-threatening infections Greater risk for a serious lung condition, known as respiratory distress syndrome Greater risk for cerebral palsy (CP) Greater risk for learning and developmental disabilities They may need to stay in the hospital for several weeks or more, often in a neonatal intensive care unit (NICU).--> What methods are used to prevent preterm delivery? Research supported by the NICHD found that treating high-risk pregnant women (those who have previously had a spontaneous preterm baby) with a certain type of progesterone reduces the risk of another preterm delivery. The treatment worked among all ethnic groups in the study and improved outcomes for the babies. Efforts to find out whether the treatment works for other at-risk women, such as those having twins and triplets, are ongoing. Bed rest and medications that relax the muscles in the uterus are also commonly used to try to stop preterm labor.

Chewing tobacco and snuff contain 28 cancer

Smokeless Tobacco and Cancer: Questions and Answers
Key Points
Snuff is a finely ground or shredded tobacco that is either sniffed through the nose or placed between the cheek and gum. Chewing tobacco is used by putting a wad of tobacco inside the cheek (see Question 1).
Chewing tobacco and snuff contain 28 cancer–causing agents (see Question 2).
Smokeless tobacco users have an increased risk of developing cancer of the oral cavity (see Question 3).
Several national organizations offer information about the health risks of smokeless tobacco and how to quit (see Question 8).
What is smokeless tobacco?
There are two types of smokeless tobacco––snuff and chewing tobacco. Snuff, a finely ground or shredded tobacco, is packaged as dry, moist, or in sachets (tea bag–like pouches). Typically, the user places a pinch or dip between the cheek and gum. Chewing tobacco is available in loose leaf, plug (plug–firm and plug–moist), or twist forms, with the user putting a wad of tobacco inside the cheek. Smokeless tobacco is sometimes called "spit" or "spitting" tobacco because people spit out the tobacco juices and saliva that build up in the mouth.
What harmful chemicals are found in smokeless tobacco?
Chewing tobacco and snuff contain 28 carcinogens (cancer–causing agents). The most harmful carcinogens in smokeless tobacco are the tobacco–specific nitrosamines (TSNAs). They are formed during the growing, curing, fermenting, and aging of tobacco. TSNAs have been detected in some smokeless tobacco products at levels many times higher than levels of other types of nitrosamines that are allowed in foods, such as bacon and beer.
Other cancer–causing substances in smokeless tobacco include N–nitrosamino acids, volatile N–nitrosamines, benzo(a)pyrene, volatile aldehydes, formaldehyde, acetaldehyde, crotonaldehyde, hydrazine, arsenic, nickel, cadmium, benzopyrene, and polonium–210.
All tobacco, including smokeless tobacco, contains nicotine, which is addictive. The amount of nicotine absorbed from smokeless tobacco is 3 to 4 times the amount delivered by a cigarette. Nicotine is absorbed more slowly from smokeless tobacco than from cigarettes, but more nicotine per dose is absorbed from smokeless tobacco than from cigarettes. Also, the nicotine stays in the bloodstream for a longer time.
What cancers are caused by or associated with smokeless tobacco use?
Smokeless tobacco users increase their risk for cancer of the oral cavity. Oral cancer can include cancer of the lip, tongue, cheeks, gums, and the floor and roof of the mouth.
People who use oral snuff for a long time have a much greater risk for cancer of the cheek and gum than people who do not use smokeless tobacco.
The possible increased risk for other types of cancer from smokeless tobacco is being studied.
What are some of the other ways smokeless tobacco can harm users' health?
Some of the other effects of smokeless tobacco use include addiction to nicotine, oral leukoplakia (white mouth lesions that can become cancerous), gum disease, and gum recession (when the gum pulls away from the teeth). Possible increased risks for heart disease, diabetes, and reproductive problems are being studied.
Is smokeless tobacco a good substitute for cigarettes?
In 1986, the Surgeon General concluded that the use of smokeless tobacco "is not a safe substitute for smoking cigarettes. It can cause cancer and a number of noncancerous conditions and can lead to nicotine addiction and dependence." Since 1991, the National Cancer Institute (NCI), a part of the National Institutes of Health, has officially recommended that the public avoid and discontinue the use of all tobacco products, including smokeless tobacco. NCI also recognizes that nitrosamines, found in tobacco products, are not safe at any level. The accumulated scientific evidence does not support changing this position.
What about using smokeless tobacco to quit cigarettes?
Because all tobacco use causes disease and addiction, NCI recommends that tobacco use be avoided and discontinued. Several nontobacco methods have been shown to be effective for quitting cigarettes. These methods include pharmacotherapies such as nicotine replacement therapy and bupropion, individual and group counseling, and telephone quitlines.
Who uses smokeless tobacco?
In the United States, the 2000 National Household Survey on Drug Abuse, which was conducted by the Substance Abuse and Mental Health Services Administration, reported the following statistics:
An estimated 7.6 million Americans age 12 and older (3.4 percent) had used smokeless tobacco in the past month.
Smokeless tobacco use was most common among young adults ages 18 to 25.
Men were 10 times more likely than women to report using smokeless tobacco (6.5 percent of men age 12 and older compared with 0.5 percent of women).
People in many other countries and regions, including India, parts of Africa, and some Central Asian countries, have a long history of using smokeless tobacco products

Smokeless Tobacco and Cancer: Questions and Answers Key Points Snuff is a finely ground or shredded tobacco that is either sniffed through the nose or placed between the cheek and gum. Chewing tobacco is used by putting a wad of tobacco inside the cheek (see Question 1). Chewing tobacco and snuff contain 28 cancer–causing agents (see Question 2). Smokeless tobacco users have an increased risk of developing cancer of the oral cavity (see Question 3). Several national organizations offer information about the health risks of smokeless tobacco and how to quit (see Question 8). What is smokeless tobacco? There are two types of smokeless tobacco––snuff and chewing tobacco. Snuff, a finely ground or shredded tobacco, is packaged as dry, moist, or in sachets (tea bag–like pouches). Typically, the user places a pinch or dip between the cheek and gum. Chewing tobacco is available in loose leaf, plug (plug–firm and plug–moist), or twist forms, with the user putting a wad of tobacco inside the cheek. Smokeless tobacco is sometimes called "spit" or "spitting" tobacco because people spit out the tobacco juices and saliva that build up in the mouth. What harmful chemicals are found in smokeless tobacco? Chewing tobacco and snuff contain 28 carcinogens (cancer–causing agents). The most harmful carcinogens in smokeless tobacco are the tobacco–specific nitrosamines (TSNAs). They are formed during the growing, curing, fermenting, and aging of tobacco. TSNAs have been detected in some smokeless tobacco products at levels many times higher than levels of other types of nitrosamines that are allowed in foods, such as bacon and beer. Other cancer–causing substances in smokeless tobacco include N–nitrosamino acids, volatile N–nitrosamines, benzo(a)pyrene, volatile aldehydes, formaldehyde, acetaldehyde, crotonaldehyde, hydrazine, arsenic, nickel, cadmium, benzopyrene, and polonium–210. All tobacco, including smokeless tobacco, contains nicotine, which is addictive. The amount of nicotine absorbed from smokeless tobacco is 3 to 4 times the amount delivered by a cigarette. Nicotine is absorbed more slowly from smokeless tobacco than from cigarettes, but more nicotine per dose is absorbed from smokeless tobacco than from cigarettes. Also, the nicotine stays in the bloodstream for a longer time. What cancers are caused by or associated with smokeless tobacco use? Smokeless tobacco users increase their risk for cancer of the oral cavity. Oral cancer can include cancer of the lip, tongue, cheeks, gums, and the floor and roof of the mouth. People who use oral snuff for a long time have a much greater risk for cancer of the cheek and gum than people who do not use smokeless tobacco

Spasmodic Dysphonia

Spasmodic Dysphonia
On this page:
What is spasmodic dysphonia?
What are the types of spasmodic dysphonia?
What are the features of spasmodic dysphonia?
Who is affected by spasmodic dysphonia?
What causes spasmodic dysphonia?
How is spasmodic dysphonia diagnosed?
What treatment is available for spasmodic dysphonia?
Where can I get more information?
What is spasmodic dysphonia?
Spasmodic dysphonia (or laryngeal dystonia) is a voice disorder caused by involuntary movements of one or more muscles of the larynx or voice box. Individuals who have spasmodic dysphonia may have occasional difficulty saying a word or two or they may experience sufficient difficulty to interfere with communication. Spasmodic dysphonia causes the voice to break or to have a tight, strained or strangled quality. There are three different types of spasmodic dysphonia.


What are the types of spasmodic dysphonia?
The three types of spasmodic dysphonia are adductor spasmodic dysphonia, abductor spasmodic dysphonia and mixed spasmodic dysphonia.

What are the features of spasmodic dysphonia?
In adductor spasmodic dysphonia, sudden involuntary muscle movements or spasms cause the vocal folds (or vocal cords) to slam together and stiffen. These spasms make it difficult for the vocal folds to vibrate and produce voice. Words are often cut off or difficult to start because of the muscle spasms. Therefore, speech may be choppy and sound similar to stuttering. The voice of an individual with adductor spasmodic dysphonia is commonly described as strained or strangled and full of effort. Surprisingly, the spasms are usually absent while whispering, laughing, singing, speaking at a high pitch or speaking while breathing in. Stress, however, often makes the muscle spasms more severe.
In abductor spasmodic dysphonia, sudden involuntary muscle movements or spasms cause the vocal folds to open. The vocal folds can not vibrate when they are open. The open position of the vocal folds also allows air to escape from the lungs during speech. As a result, the voices of these individuals often sound weak, quiet and breathy or whispery. As with adductor spasmodic dysphonia, the spasms are often absent during activities such as laughing or singing.
Mixed spasmodic dysphonia involves muscles that open the vocal folds as well as muscles that close the vocal folds and therefore has features of both adductor and abductor spasmodic dysphonia.


Who is affected by spasmodic dysphonia?
Spasmodic dysphonia can affect anyone. The first signs of this disorder are found most often in individuals between 30 and 50 years of age. More women appear to be affected by spasmodic dysphonia than are men.


What causes spasmodic dysphonia?
The cause of spasmodic dysphonia is unknown. Because the voice can sound normal or near normal at times, spasmodic dysphonia was once thought to be psychogenic, that is, originating in the affected person¹s mind rather than from a physical cause. While psychogenic forms of spasmodic dysphonia exist, research has revealed increasing evidence that most cases of spasmodic dysphonia are in fact neurogenic or having to do with the nervous system (brain and nerves). Spasmodic dysphonia may co-occur with other movement disorders such as blepharospasm (excessive eye blinking and involuntary forced eye closure), tardive dyskinesia (involuntary and repetitious movement of muscles of the face, body, arms and legs), oromandibular dystonia (involuntary movements of the jaw muscles, lips and tongue), torticollis (involuntary movements of the neck muscles), or tremor (rhythmic, quivering muscle movements).
In some cases, spasmodic dysphonia may run in families and is thought to be inherited. Research has identified a possible gene on chromosome 9 that may contribute to the spasmodic dysphonia that is common to certain families. In some individuals the voice symptoms begin following an upper respiratory infection, injury to the larynx, a long period of voice use, or stress.


How is spasmodic dysphonia diagnosed?
The diagnosis of spasmodic dysphonia is usually made based on identifying the way the symptoms developed as well as by careful examination of the individual. Most people are evaluated by a team that usually includes an otolaryngologist (a physician who specializes in ear, nose and throat disorders), a speech-language pathologist (a professional trained to diagnose and treat speech, language and voice disorders) and a neurologist (a physician who specializes in nervous system disorders). The otolaryngologist examines the vocal folds to look for other possible causes for the voice disorder. Fiberoptic nasolaryngoscopy, a method whereby a small lighted tube is passed through the nose and into the throat, is a helpful tool that allows the otolaryngologist to evaluate vocal cord movement during speech. The speech-language pathologist evaluates the patient's voice and voice quality. The neurologist evaluates the patient for signs of other muscle movement disorders.


What treatment is available for spasmodic dysphonia?
There is presently no cure for spasmodic dysphonia. Current treatments only help reduce the symptoms of this voice disorder. Voice therapy may reduce some symptoms, especially in mild cases. An operation that cuts one of the nerves of the vocal folds (the recurrent laryngeal nerve) has improved the voice of many for several months to several years but the improvement is often temporary. Others may benefit from psychological counseling to help them to accept and live with their voice problem. Still others may benefit from job counseling that will help them select a line of work more compatible with their speaking limitations.
Currently the most promising treatment for reducing the symptoms of spasmodic dysphonia is injections of very small amounts of botulinum toxin (botox) directly into the affected muscles of the larynx. Botulinum toxin is produced by the Clostridium botulinum bacteria. This is the bacterium that occurs in improperly canned foods and honey. The toxin weakens muscles by blocking the nerve impulse to the muscle. The botox injections generally improve the voice for a period of three to four months after which the voice symptoms gradually return. Reinjections are necessary to maintain a good speaking voice. Initial side effects that usually subside after a few days to a few weeks may include a temporary weak, breathy voice or occasional swallowing difficulties. Botox may relieve the symptoms of both adductor and abductor spasmodic dysphonia

Spasmodic Dysphonia On this page: What is spasmodic dysphonia? What are the types of spasmodic dysphonia? What are the features of spasmodic dysphonia? Who is affected by spasmodic dysphonia? What causes spasmodic dysphonia? How is spasmodic dysphonia diagnosed? What treatment is available for spasmodic dysphonia? Where can I get more information? What is spasmodic dysphonia? Spasmodic dysphonia (or laryngeal dystonia) is a voice disorder caused by involuntary movements of one or more muscles of the larynx or voice box. Individuals who have spasmodic dysphonia may have occasional difficulty saying a word or two or they may experience sufficient difficulty to interfere with communication. Spasmodic dysphonia causes the voice to break or to have a tight, strained or strangled quality. There are three different types of spasmodic dysphonia. What are the types of spasmodic dysphonia? The three types of spasmodic dysphonia are adductor spasmodic dysphonia, abductor spasmodic dysphonia and mixed spasmodic dysphonia.
What are the features of spasmodic dysphonia? In adductor spasmodic dysphonia, sudden involuntary muscle movements or spasms cause the vocal folds (or vocal cords) to slam together and stiffen. These spasms make it difficult for the vocal folds to vibrate and produce voice. Words are often cut off or difficult to start because of the muscle spasms. Therefore, speech may be choppy and sound similar to stuttering. The voice of an individual with adductor spasmodic dysphonia is commonly described as strained or strangled and full of effort. Surprisingly, the spasms are usually absent while whispering, laughing, singing, speaking at a high pitch or speaking while breathing in. Stress, however, often makes the muscle spasms more severe. In abductor spasmodic dysphonia, sudden involuntary muscle movements or spasms cause the vocal folds to open. The vocal folds can not vibrate when they are open. The open position of the vocal folds also allows air to escape from the lungs during speech. As a result, the voices of these individuals often sound weak, quiet and breathy or whispery. As with adductor spasmodic dysphonia, the spasms are often absent during activities such as laughing or singing. Mixed spasmodic dysphonia involves muscles that open the vocal folds as well as muscles that close the vocal folds and therefore has features of both adductor and abductor spasmodic dysphonia. Who is affected by spasmodic dysphonia? Spasmodic dysphonia can affect anyone. The first signs of this disorder are found most often in individuals between 30 and 50 years of age. More women appear to be affected by spasmodic dysphonia than are men. What causes spasmodic dysphonia? The cause of spasmodic dysphonia is unknown. Because the voice can sound normal or near normal at times, spasmodic dysphonia was once thought to be psychogenic, that is, originating in the affected person¹s mind rather than from a physical cause. While psychogenic forms of spasmodic dysphonia exist, research has revealed increasing evidence that most cases of spasmodic dysphonia are in fact neurogenic or having to do with the nervous system (brain and nerves). Spasmodic dysphonia may co-occur with other movement disorders such as blepharospasm (excessive eye blinking and involuntary forced eye closure), tardive dyskinesia (involuntary and repetitious movement of muscles of the face, body, arms and legs), oromandibular dystonia (involuntary movements of the jaw muscles, lips and tongue), torticollis (involuntary movements of the neck muscles), or tremor (rhythmic, quivering muscle movements). In some cases, spasmodic dysphonia may run in families and is thought to be inherited. Research has identified a possible gene on chromosome 9 that may contribute to the spasmodic dysphonia that is common to certain families. In some individuals the voice symptoms begin following an upper respiratory infection, injury to the larynx, a long period of voice use, or stress. How is spasmodic dysphonia diagnosed? The diagnosis of spasmodic dysphonia is usually made based on identifying the way the symptoms developed as well as by careful

Spit Tobacco

Spit Tobacco
Spit tobacco, also known as dip and chew, snuff, chewing tobacco, and smokeless tobacco, comes in two forms. Chewing tobacco comes as loose leaves of tobacco, as plug tobacco (brick form), or in a twist form. Snuff is finely ground (powdered) tobacco that is sold moist, dry, or in tea bag-like pouches called sachets. But no matter what it’s called, spit tobacco is highly addictive and can harm your health. Here’s why:
Spit tobacco is still tobacco. Tobacco contains cancer-causing chemicals called nitrosamines.
Like cigarettes, spit tobacco also contains nicotine—an addictive drug. In fact, holding an average-size dip in the mouth for just 30 minutes can deliver as much nicotine as smoking three cigarettes. Nicotine addiction can make quitting difficult.
Spit tobacco may cause mouth cancer and other health problems.
If I Want to Quit…
Quitting spit tobacco is not easy. The most effective way to quit chewing tobacco is to have a quit date and a quitting plan. Successful quitters also include support teams in their plan— friends, family, and co-workers who can help during the difficult times when urges and temptations are strongest.

Spit Tobacco Spit tobacco, also known as dip and chew, snuff, chewing tobacco, and smokeless tobacco, comes in two forms. Chewing tobacco comes as loose leaves of tobacco, as plug tobacco (brick form), or in a twist form. Snuff is finely ground (powdered) tobacco that is sold moist, dry, or in tea bag-like pouches called sachets. But no matter what it’s called, spit tobacco is highly addictive and can harm your health. Here’s why: Spit tobacco is still tobacco. Tobacco contains cancer-causing chemicals called nitrosamines. Like cigarettes, spit tobacco also contains nicotine—an addictive drug. In fact, holding an average-size dip in the mouth for just 30 minutes can deliver as much nicotine as smoking three cigarettes. Nicotine addiction can make quitting difficult. Spit tobacco may cause mouth cancer and other health problems. If I Want to Quit

Taking Care of Your Voice

Taking Care of Your Voice
On this page:
What is voice?
What are some causes of voice problems?
How do you know when your voice is not healthy?
Tips to Prevent Voice Problems
What research on voice is NIDCD supporting?
Additional Resources
PubMed Database Search
Where can I get more information?
What is voice?
We rely on our voices to inform, persuade, and connect with other people. Your voice is as unique as your fingerprint. Many people you know use their voices all day long, day in and day out. Singers, teachers, doctors, lawyers, nurses, sales people, and public speakers are among those who make great demands on their voices. Unfortunately, these individuals are most prone to experiencing voice problems. It is believed that 7.5 million people have diseases or disorders of voice. Some of these disorders can be avoided by taking care of your voice.

What are some causes of voice problems?
Causes of vocal problems may include upper respiratory infections, inflammation caused by acid reflux, vocal misuse and abuse, vocal nodules or laryngeal papillomatosis (growths), laryngeal cancer, neuromuscular diseases (such as spasmodic dysphonia or vocal cord paralysis), and psychogenic conditions due to psychological trauma. Keep in mind that most voice problems are reversible and can be successfully treated when diagnosed early.

How do you know when your voice is not healthy?
Has your voice become hoarse or raspy?
Have you lost your ability to hit some high notes when singing?
Does your voice suddenly sound deeper?
Does your throat often feel raw, achy, or strained?
Has it become an effort to talk?
Do you find yourself repeatedly clearing your throat?
If you answer "yes" to any of these questions, you may be experiencing a voice problem. You should consult a doctor. An otolaryngologist (oh-toe-lar-in-GAH-luh-jist) is the physician and surgeon who specializes in diseases or disorders of the ears, nose, and throat. He or she can determine the underlying cause of your voice problem. The professional who can help you with improving the use of your voice and avoiding vocal abuse is a speech-language pathologist.
Tips to Prevent Voice Problems
Limit your intake of drinks that include alcohol or caffeine. These act as diuretics (substances that increase urination) and cause the body to lose water. This loss of fluids dries out the voice. Alcohol also irritates the mucous membranes that line the throat.
Drink plenty of water. Six to eight glasses a day is recommended.
Don't smoke and avoid second-hand smoke. Cancer of the vocal folds is seen most often in individuals who smoke.
Practice good breathing techniques when singing or talking. It is important to support your voice with deep breaths from the diaphragm, the wall that separates your chest and abdomen. Singers and speakers are often taught exercises that improve this breath control. Talking from the throat, without supporting breath, puts a great strain on the voice.
Avoid eating spicy foods. Spicy foods can cause stomach acid to move into the throat or esophagus (reflux).
Use a humidifier in your home. This is especially important in winter or in dry climates. Thirty percent humidity is recommended.
Try not to overuse your voice. Avoid speaking or singing when your voice is hoarse.
Wash your hands often to prevent colds and flu.
Include plenty of whole grains, fruits, and vegetables in your diet. These foods contain vitamins A, E, and C. They also help keep the mucus membranes that line the throat healthy.
Do not cradle the phone when talking. Cradling the phone between the head and shoulder for extended periods of time can cause muscle tension in the neck.
Exercise regularly. Exercise increases stamina and muscle tone. This helps provide good posture and breathing, which are necessary for proper speaking.
Get enough rest. Physical fatigue has a negative effect on voice.
Avoid talking in noisy places. Trying to talk above noise causes strain on the voice.
Avoid mouthwash or gargles that contain alcohol or irritating chemicals. If you still wish to use a mouthwash that contains alcohol, limit your use to oral rinsing. If gargling is necessary, use a salt water solution.
Avoid using mouthwash to treat persistent bad breath. Halitosis (bad breath) may be the result of a problem that mouthwash can't cure, such as low grade infections in the nose, sinuses, tonsils, gums, or lungs, as well as from gastric reflux from the stomach.
Consider using a microphone. In relatively static environments such as exhibit areas, classrooms, or exercise rooms, a lightweight microphone and an amplifier-speaker system can be of great help.
Consider voice therapy. A speech-language pathologist who is experienced in treating voice problems can provide education on healthy use of the voice and instruction in proper voice techniques.

Taking Care of Your Voice On this page: What is voice? What are some causes of voice problems? How do you know when your voice is not healthy? Tips to Prevent Voice Problems What research on voice is NIDCD supporting? Additional Resources PubMed Database Search Where can I get more information? What is voice? We rely on our voices to inform, persuade, and connect with other people. Your voice is as unique as your fingerprint. Many people you know use their voices all day long, day in and day out. Singers, teachers, doctors, lawyers, nurses, sales people, and public speakers are among those who make great demands on their voices. Unfortunately, these individuals are most prone to experiencing voice problems. It is believed that 7.5 million people have diseases or disorders of voice. Some of these disorders can be avoided by taking care of your voice.
What are some causes of voice problems? Causes of vocal problems may include upper respiratory infections, inflammation caused by acid reflux, vocal misuse and abuse, vocal nodules or laryngeal papillomatosis (growths), laryngeal cancer, neuromuscular diseases (such as spasmodic dysphonia or vocal cord paralysis), and psychogenic conditions due to psychological trauma. Keep in mind that most voice problems are reversible and can be successfully treated when diagnosed early.
How do you know when your voice is not healthy? Has your voice become hoarse or raspy? Have you lost your ability to hit some high notes when singing? Does your voice suddenly sound deeper? Does your throat often feel raw, achy, or strained? Has it become an effort to talk? Do you find yourself repeatedly clearing your throat? If you answer "yes" to any of these questions, you may be experiencing a voice problem. You should consult a doctor. An otolaryngologist (oh-toe-lar-in-GAH-luh-jist) is the physician and surgeon who specializes in diseases or disorders of the ears, nose, and throat. He or she can determine the underlying cause of your voice problem. The professional who can help you with improving the use of your voice and avoiding vocal abuse is a speech-language pathologist. Tips to Prevent Voice Problems Limit your intake of drinks that include alcohol or caffeine. These act as diuretics (substances that increase urination) and cause the body to lose water. This loss of fluids dries out the voice. Alcohol also irritates the mucous membranes that line the throat. Drink plenty of water. Six to eight glasses a day is recommended. Don't smoke and avoid second-hand smoke. Cancer of the vocal folds is seen most often in individuals who smoke. Practice good breathing techniques when singing or talking. It is important to support your voice with deep breaths from the diaphragm, the wall that separates your chest and abdomen. Singers and speakers are often taught exercises that improve this breath control. Talking from the throat, without supporting breath, puts a great strain on the voice. Avoid eating spicy foods. Spicy foods can cause stomach acid to move into the throat or esophagus (reflux). Use a humidifier in your home. This is especially important in winter or in dry climates. Thirty percent humidity is recommended. Try not to overuse your voice. Avoid speaking or singing when your voice is hoarse. Wash your hands often to prevent colds and flu. Include plenty of whole grains, fruits, and vegetables in your diet. These foods contain vitamins A, E, and C. They also help keep the mucus membranes that line the throat healthy. Do not cradle the phone when talking. Cradling the phone between the head and shoulder for extended periods of time can cause muscle tension in the neck. Exercise regularly. Exercise increases stamina and muscle tone. This helps provide good posture and breathing, which are necessary for proper speaking. Get enough rest. Physical fatigue has a negative effect on voice. Avoid talking in noisy places. Trying to talk above noise causes strain on the voice. Avoid mouthwash or gargles that contain alcohol or irritating chemicals. If you still wish to use a mouthwash that contains alcohol, limit your use to oral rinsing. If gargling is necessary, use a salt water solution. Avoid using mouthwash to treat persistent bad breath. Halitosis (bad breath) may be the result of a problem that mouthwash can't cure

Basics: Disorders of Vocal Abuse and Misuse

Basics: Disorders of Vocal Abuse and Misuse
Have you "lost" your voice?
When you abuse or misuse your voice, you can damage your vocal folds, causing temporary or permanent voice changes such as
Laryngitis
Vocal nodules
Vocal polyps
Contact ulcers
Who is at risk?
Anyone who uses his or her voice excessively may develop a vocal abuse or misuse disorder. These problems are fairly common among
Lawyers
Teachers
Clergy
Cheerleaders
Singers
Actors
Children
Diagnosis
If you've had vocal change or hoarseness for more than 2 weeks, see a doctor, preferably an otolaryngologist.
Treatment
Most disorders of vocal abuse and misuse can be cured. The best treatment is to eliminate the vocal behavior that caused the problem.

Basics: Disorders of Vocal Abuse and Misuse Have you "lost" your voice? When you abuse or misuse your voice, you can damage your vocal folds, causing temporary or permanent voice changes such as Laryngitis Vocal nodules Vocal polyps Contact ulcers Who is at risk? Anyone who uses his or her voice excessively may develop a vocal abuse or misuse disorder. These problems are fairly common among Lawyers Teachers Clergy Cheerleaders Singers Actors Children Diagnosis If you've had vocal change or hoarseness for more than 2 weeks, see a doctor, preferably an otolaryngologist. Treatment Most disorders of vocal abuse and misuse can be cured. The best treatment is to eliminate the vocal behavior that caused the problem.

The Story of Fluoridation

The Story of Fluoridation
It started as an observation, that soon took the shape of an idea. It ended, five decades later, as a scientific revolution that shot dentistry into the forefront of preventive medicine. This is the story of how dental science discovered-and ultimately proved to the world-that fluoride, a mineral found in rocks and soil, prevents tooth decay. Although dental caries remains a public health worry, it is no longer the unbridled problem it once was, thanks to fluoride.
A Mysterious Disorder
In 1909 Dr. McKay (r) persuaded the Colorado State Dental Association to invite Dr. Green Vardiman Black (l), one of the nation's most eminent dental researchers, to attend 1909 convention where McKay's findings were to be presented. The two men began joint research and discovered other areas of the country where brown staining of teeth occurred.
Fluoride research had its beginnings in 1901, when a young dental school graduate named Frederick McKay left the East Coast to open a dental practice in Colorado Springs, Colorado. When he arrived, McKay was astounded to find scores of Colorado Springs natives with grotesque brown stains on their teeth. So severe could these permanent stains be, in fact, sometimes entire teeth were splotched the color of chocolate candy. McKay searched in vain for information on this bizarre disorder. He found no mention of the brown-stained teeth in any of the dental literature of the day. Local residents blamed the problem on any number of strange factors, such as eating too much pork, consuming inferior milk, and drinking calcium-rich water. Thus, McKay took up the gauntlet and initiated research into the disorder himself. His first epidemiological investigations were scuttled by a lack of interest among most area dentists. But McKay persevered and ultimately interested local practitioners in the problem, which was known as Colorado Brown Stain.
A Fruitful Collaboration
McKay's first big break came in 1909, when renowned dental researcher Dr. G.V. Black agreed to come to Colorado Springs and collaborate with him on the mysterious ailment. Black, who had previously scoffed that it was impossible such a disorder could go unreported in the dental literature, was lured West shortly after the Colorado Springs Dental Society conducted a study showing that almost 90 percent of the city's locally born children had signs of the brown stains. When Black arrived in the city, he too was shocked by the prevalence of Colorado Brown Stain in the mouths of native-born residents. He would write later:
"I spent considerable time walking on the streets, noticing the children in their play, attracting their attention and talking with them about their games, etc., for the purpose of studying the general effect of the deformity. I found it prominent in every group of children. One does not have to search for it, for it is continually forcing itself on the attention of the stranger by its persistent prominence. This is much more than a deformity of childhood. If it were only that, it would be of less consequence, but it is a deformity for life."
Black investigated fluorosis for six years, until his death in 1915. During that period, he and McKay made two crucial discoveries. First, they showed that mottled enamel (as Black referred to the condition) resulted from developmental imperfections in children's teeth. This finding meant that city residents whose permanent teeth had calcified without developing the stains did not risk having their teeth turn brown; young children waiting for their secondary set of teeth to erupt, however, were at high risk. Second, they found that teeth afflicted by Colorado Brown Stain were surprisingly and inexplicably resistant to decay. The two researchers were still a long way from determining the cause of Colorado Brown Stain, but McKay had a theory tucked away in the back of his head. Maybe there was, as some local residents suggested, an ingredient in the water supply that mottled the teeth? Black was skeptical; McKay, though, was intrigued by this theory's prospects.The water-causation theory got a gigantic boost in 1923. That year, McKay trekked across the Rocky Mountains to Oakley, Idaho to meet with parents who had noticed peculiar brown stains on their children's teeth. The parents told McKay that the stains began appearing shortly after Oakley constructed a communal water pipeline to a warm spring five miles away. McKay analyzed the water, but found nothing suspicious in it. Nonetheless, he advised town leaders to abandon the pipeline altogether and use another nearby spring as a water source.McKay's advice did the trick. Within a few years, the younger children of Oakley were sprouting healthy secondary teeth without any mottling. McKay now had his confirmation, but he still had no idea what could be wrong with the water in Oakley, Colorado Springs, and other afflicted areas. The answer came when McKay and Dr. Grover Kempf of the United States Public Health Service (PHS) traveled to Bauxite, Arkansas-a company town owned by the Aluminum Company of America-to investigate reports of the familiar brown stains. The two discovered something very interesting: namely, the mottled enamel disorder was prevalent among the children of Bauxite, but nonexistent in another town only five miles away. Again, McKay analyzed the Bauxite water supply. Again, the analysis provided no clues. But the researchers' work was not done in vain. McKay and Kempf published a report on their findings that reached the desk of ALCOA's chief chemist, H. V. Churchill, at company headquarters in Pennsylvania. Churchill, who had spent the past few years refuting claims that aluminum cookware was poisonous, worried that this report might provide fresh fodder for ALCOA's detractors. Thus, he decided to conduct his own test of the water in Bauxite-but this time using photospectrographic analysis, a more sophisticated technology than that used by McKay. Churchill asked an assistant to assay the Bauxite water sample. After several days, the assistant reported a surprising piece of news: the town's water had high levels of fluoride. Churchill was incredulous. "Whoever heard of fluorides in water," he bellowed at his assistant. "You have contaminated the sample. Rush another specimen." Shortly thereafter, a new specimen arrived in the laboratory. Churchill's assistant conducted another assay on the Bauxite water. The result? Photospectrographic analysis, again, showed that the town's water had high levels of fluoride tainting it. This second and selfsame finding prompted Churchill to sit down at his typewriter in January, 1931, and compose a five-page letter to McKay on this new revelation. In the letter, he advised McKay to collect water samples from other towns "where the peculiar dental trouble has been experienced... We trust that we have awakened your interest in this subject and that we may cooperate in an attempt to discover what part 'fluorine' may play in the matter." McKay collected the samples. And, within months, he had the answer and denouement to his 30-year quest: high levels of water-borne fluoride indeed caused the discoloration of tooth enamel.
New Questions Emerge
Hence, from the curious findings of Churchill's lab assistant, the mystery of the brown stained teeth was cracked. But one mystery often ripples into many others. And shortly after this discovery, PHS scientists started investigating a slew of new and provocative questions about water-borne fluoride. With these PHS investigations, research on fluoride and its effects on tooth enamel began in earnest. The architect of these first fluoride studies was Dr. H. Trendley Dean, head of the Dental Hygiene Unit at the National Institute of Health (NIH). Dean began investigating the epidemiology of fluorosis in 1931. One of his primary research concerns was determining how high fluoride levels could be in drinking water before fluorosis occurred. To determine this, Dean enlisted the help of Dr. Elias Elvove, a senior chemist at the NIH. Dean gave Elvove the hardscrabble task of developing a more accurate method to measure fluoride levels in drinking water. Elvove labored long and hard in his laboratory, and within two years he reported back to Dean with success. He had developed a state-of-the-art method to measure fluoride levels in water with an accuracy of 0.1 parts per million (ppm). With this new method in tow, Dean and his staff set out across the country to compare fluoride levels in drinking water. By the late 1930s, he and his staff had made a critical discovery. Namely, fluoride levels of up to 1.0 ppm in drinking water did not cause enamel fluorosis in most people and only mild enamel fluorosis in a small percentage of people.
Proof That Fluoride Prevents Caries
This finding sent Dean's thoughts spiraling in a new direction. He recalled from reading McKay's and Black's studies on fluorosis that mottled tooth enamel is unusually resistant to decay. Dean wondered whether adding fluoride to drinking water at physically and cosmetically safe levels would help fight tooth decay. This hypothesis, Dean told his colleagues, would need to be tested.In 1944, Dean got his wish. That year, the City Commission of Grand Rapids, Michigan-after numerous discussions with researchers from the PHS, the Michigan Department of Health, and other public health organizations-voted to add fluoride to its public water supply the following year. In 1945, Grand Rapids became the first city in the world to fluoridate its drinking water.The Grand Rapids water fluoridation study was originally sponsored by the U.S. Surgeon General, but was taken over by the NIDR shortly after the Institute's inception in 1948. During the 15-year project, researchers monitored the rate of tooth decay among Grand Rapids' almost 30,000 schoolchildren. After just 11 years, Dean- who was now director of the NIDR-announced an amazing finding. The caries rate among Grand Rapids children born after fluoride was added to the water supply dropped more than 60 percent. This finding, considering the thousands of participants in the study, amounted to a giant scientific breakthrough that promised to revolutionize dental care, making tooth decay for the first time in history a preventable disease for most people.
A Lasting Achievement
Almost 30 years after the conclusion of the Grand Rapids fluoridation study, fluoride continues to be dental science's main weapon in the battle against tooth decay. Today, just about every toothpaste on the market contains fluoride as its active ingredient; water fluoridation projects currently benefit over 200 million Americans, and 13 million schoolchildren now participate in school-based fluoride mouth rinse programs. As the figures indicate, McKay, Dean, and the others helped to transform dentistry into a prevention-oriented profession. Their drive, in the face of overwhelming adversity, is no less than a remarkable feat of science-an achievement ranking with the other great preventive health measures of our century.

The Story of Fluoridation It started as an observation, that soon took the shape of an idea. It ended, five decades later, as a scientific revolution that shot dentistry into the forefront of preventive medicine. This is the story of how dental science discovered-and ultimately proved to the world-that fluoride, a mineral found in rocks and soil, prevents tooth decay. Although dental caries remains a public health worry, it is no longer the unbridled problem it once was, thanks to fluoride. A Mysterious Disorder In 1909 Dr. McKay (r) persuaded the Colorado State Dental Association to invite Dr. Green Vardiman Black (l), one of the nation's most eminent dental researchers, to attend 1909 convention where McKay's findings were to be presented. The two men began joint research and discovered other areas of the country where brown staining of teeth occurred. Fluoride research had its beginnings in 1901, when a young dental school graduate named Frederick McKay left the East Coast to open a dental practice in Colorado Springs, Colorado. When he arrived, McKay was astounded to find scores of Colorado Springs natives with grotesque brown stains on their teeth. So severe could these permanent stains be, in fact, sometimes entire teeth were splotched the color of chocolate candy. McKay searched in vain for information on this bizarre disorder. He found no mention of the brown-stained teeth in any of the dental literature of the day. Local residents blamed the problem on any number of strange factors, such as eating too much pork, consuming inferior milk, and drinking calcium-rich water. Thus, McKay took up the gauntlet and initiated research into the disorder himself. His first epidemiological investigations were scuttled by a lack of interest among most area dentists. But McKay persevered and ultimately interested local practitioners in the problem, which was known as Colorado Brown Stain. A Fruitful Collaboration McKay's first big break came in 1909, when renowned dental researcher Dr. G.V. Black agreed to come to Colorado Springs and collaborate with him on the mysterious ailment. Black, who had previously scoffed that it was impossible such a disorder could go unreported in the dental literature, was lured West shortly after the Colorado Springs Dental Society conducted a study showing that almost 90 percent of the city's locally born children had signs of the brown stains. When Black arrived in the city, he too was shocked by the prevalence of Colorado Brown Stain in the mouths of native-born residents. He would write later: "I spent considerable time walking on the streets, noticing the children in their play, attracting their attention and talking with them about their games, etc., for the purpose of studying the general effect of the deformity. I found it prominent in every group of children. One does not have to search for it, for it is continually forcing itself on the attention of the stranger by its persistent prominence. This is much more than a deformity of childhood. If it were only that, it would be of less consequence, but it is a deformity for life." Black investigated fluorosis for six years, until his death in 1915. During that period, he and McKay made two crucial discoveries. First, they showed that mottled enamel (as Black referred to the condition) resulted from developmental imperfections in children's teeth. This finding meant that city residents whose