Insomnia and Sleep Medicine
Have a moment you want to sleep but your eyes will not shut? It sucks, Time was so slow and so boring. Morning? Fatigue did not go away and when the need for high concentrations of employment, the sleep attack. Read more
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Pronunciation: ox-A-zeh-pam (also pronounced ox-AZ-eh-pam)
Chemical Abstracts Service Registry Number: 604-75-1
Formal Names: Anxiolit, Serax, Serenid D
Type: Depressant (benzodiazepine class).
Federal Schedule Listing: Schedule IV (DEA no. 2835)
USA Availability: Prescription
Pregnancy Category: C Read more
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Pronunciation: NIK-uh-teen (also pronounced NIK-uh-tin)
Chemical Abstracts Service Registry Number: 54-11-5
Formal Names: Habitrol, Nicoderm, Niconil, Nicorette, Nicotiana rustica, Nicotiana tabacum, Nicotrol, Prostrop, Tobacco
Informal Names: Chip (cigarette mixed with PCP), Fry Daddy (cigarette mixed with crack cocaine)
Type: Stimulant (pyridine alkaloids class).
Federal Schedule Listing: Unlisted
USA Availability: Generally available to adults as a component of tobacco products; nonprescription and prescription in pharmaceutical format
Pregnancy Category: C or D (depending on pharmaceutical format) drugsencyclopedia.net/nicotine/nicotine-habitrol-nicoderm-niconil-nicorette-nicotiana-rustica-nicotiana-tabacum-nicotrol-prostrop-tobacco/#more-28″ class=”more-link”>Read more
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Pronunciation: pen-toh-BAR-bi-tal
Chemical Abstracts Service Registry Number: 76-74-4
Formal Names: Cafergot, Nembutal, Pentobarbitone, Phenobarbitone
Informal Names: Nebbies, Nembies, Nemmies, Nimbies, Yellow Bullets, Yellow Dolls, Yellow Jackets, Yellows
Type: Depressant (barbiturate class).
Federal Schedule Listing: Schedule II (oral and parentral, DEA no. 2270), Schedule
III for suppositories (DEA no. 2271)
USA Availability: Prescription
Pregnancy Category: D
Uses.
This short-acting substance has sedative qualities but is considered ineffective in treating nervous apprehension. Because of the drug’s sleepinducing characteristics, it is used as a preliminary to administering anesthesia and as a short-term treatment for insomnia. Pentobarbital has been observed to lower blood pressure, body temperature, and muscle tone. The compound can be used as an emergency anticonvulsant when a person has seizures, and
has been used to treat alcohol addicts undergoing withdrawal. Pentobarbital has been found effective in reducing pressure that fluid creates in the brain after severe head injury. Pentobarbital reduces a type of nerve cell death called neuronal apoptosis, and this reduction may help prevent stroke. Animal studies indicate that pentobarbital can help protect brain tissue against radiation, which might have practical application during treatment of brain tumors. Veterinarians use the substance for euthanasia: An unusual demonstration of the drug’s strength occurred when a lion was poisoned by eating meat from a horse that had been killed with pentobarbital.
Drawbacks.
Although the drug is a sedative, it can cause hyperactivity in children. Sudden stoppage of combined pentobarbital and benzodiazepine therapy in an infant caused temporary chorea (involuntary jerking). A feline experiment showed that tremors reminiscent of Parkinson’s disease can occur when pentobarbital is administered with chlorpromazine (also called Thorazine, often used to treat psychotic behavior). Persons with porphyria, a body chemistry affliction that can provoke violence, are supposed to avoid pentobarbital. Examination of epileptic children receiving pentobarbital shows elevated readings for total cholesterol, though levels of high-density lipoprotein (so-called good cholesterol) and triglycerides (associated with heart attack and stroke) seem unaffected.
In a monkey experiment pentobarbital interfered with time perception, ability to learn, short-term memory, attention span, and interest in tasks. The substance impeded task performances in a human experiment, with performance getting worse as the amount of thinking necessary for a chore increased.
Such a drug is unlikely to be welcome in the workplace. Although children using the substance apparently have trouble with language skills, a study found language development to be normal two years after the medication ceased.
Abuse factors.
In a test, alcohol drinkers who were not alcoholics found pentobarbital less appealing than a placebo and experienced no euphoria from pentobarbital, a finding consistent with other studies of persons who do not abuse drugs. When given choices of assorted substances, monkeys chose pentobarbital less often than water, which indicates the compound has low addictive potential. In contrast, drug abusers participating in an experiment found effects of pentobarbital and diazepam to be similar. Those two drugs thus had comparable appeal even though scientists running the experiment found pentobarbital possessing only 10% of diazepam’s strength. A study testing various effects on former drug addicts found pentobarbital to be 15 times
stronger than meprobamate, but morphine acted 6 times stronger than pentobarbital.
Cross-tolerance among chlordiazepoxide, pentobarbital, and alcohol has been observed in rats. A study of sedative drug abusers found alcohol and pentobarbital to deliver similar effects, with pentobarbital possibly having more appeal. A monkey experiment indicates that alcohol increases the attractiveness of pentobarbital. Dependence can develop, and in humans the
pentobarbital withdrawal syndrome can duplicate the delirium tremens of alcohol withdrawal. A mice study found that tolerance to pentobarbital developed more rapidly if assorted drugs of abuse were also being administered (morphine, amphetamine, alcohol, or cocaine).
Drug interactions.
A case report notes that pentobarbital can almost double the speed with which theophylline (commonly used to treat asthma and other breathing difficulties) disappears from the bloodstream, requiring changes in normal theophylline dosage. In a mice experiment alcohol boosted pentobarbital’s potency. A human study found that chronic alcohol ingestion reduces
the effective length of a pentobarbital dose. Grapefruit juice extends the amount of sleep produced by pentobarbital in rats, and in mice the drug inhibits caffeine effects. At one time researchers suspected that taking pentobarbital along with MDMA would reduce organic brain damage caused by MDMA, but rat experiments indicate that any apparent benefit comes simply
from the lower body temperature produced by pentobarbital. Although cocaine is a stimulant, in a rat experiment it increased the sleep-inducing quality of pentobarbital.
Cancer.
In animal experimentation pentobarbital has caused cancer. In humans long-term usage is associated with cancer of the ovaries and bronchi, but that finding is weakened by the patients also smoking cigarettes. Pregnancy. A large survey of pregnancy outcomes found that pentobarbital does not appear to cause birth defects. Nonetheless pregnant women are supposed
to avoid the drug.
Additional information.
Some capsule formats of Nembutal (pentobarbital sodium CAS RN 57-33-0) contain FD&C Yellow No. 5 (tartrazine), which can cause asthma attacks or other allergic responses in sensitive persons, particularly if someone has adverse reactions to aspirin. Cafergot PB is a combination
of bellafoline, caffeine, and ergotamine tartrate. The combination was tested with and without pentobarbital sodium to determine effect on migraine headache. Presence of pentobarbital not only enhanced reduction of pain but also helped treat anxiety, nausea, vomiting, poor appetite, and low tolerance of light.
Additional scientific information may be found in:
Cole-Harding, S., and H. de Wit. “Self-Administration of Pentobarbital in Light and
Moderate Alcohol Drinkers.” Pharmacology, Biochemistry, and Behavior 43 (1992):
563–69.
Hambly, G., C. Frewin, and B. Dodd. “Effect of Anticonvulsant Medication in the Preschool
Years on Later Language Development.” Medical Journal of Australia 148
(1988): 658, 661–62.
Mintzer, M.Z., et al. “Ethanol and Pentobarbital: Comparison of Behavioral and Subjective
Effects in Sedative Drug Abusers.” Experimental and Clinical Psychopharmacology
5 (1997): 203–15.
Pickworth, W.B., M.S. Rohrer, and R.V. Fant. “Effects of Abused Drugs on Psychomotor
Performance.” Experimental and Clinical Psychopharmacology 5 (1997): 235–41.
Pierce, James I. “Drug-Withdrawal Psychoses.” American Journal of Psychiatry 119
(1963): 880–81.
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Oxazepam (Anxiolit, Serax, Serenid D)
Pronunciation: ox-A-zeh-pam (also pronounced ox-AZ-eh-pam)
Chemical Abstracts Service Registry Number: 604-75-1
Formal Names: Anxiolit, Serax, Serenid D
Type: Depressant (benzodiazepine class).
Federal Schedule Listing: Schedule IV (DEA no. 2835)
USA Availability: Prescription
Pregnancy Category: C
Uses.
This substance is a metabolite of diazepam, temazepam, chlordiazepoxide, and clorazepate dipotassium. Oxazepam’s primary medical usage is to fight insomnia, hostility, and anxiety. Some researchers have found the drug also works against depression. Studies show oxazepam, diazepam, and flunitrazepam to have about the same therapeutic effects, though not the same
strengths (oxazepam being the weakest). In the 1990s a survey of pharmacies in Cracow, Poland, illustrated oxazepam’s worldwide popularity; around 14% of benzodiazepine prescriptions were for oxazepam, predominantly to women. One advantage of the drug is its safe “therapeutic ratio,” meaning that the amount needed to produce a desired medical effect is far below the amount needed to produce a poisonous effect. Thus medical practitioners have
considerable flexibility in adjusting dosage to an exact amount needed by a patient.
Experimental use against tinnitus (ringing in the ears) has been promising. Sometimes oxazepam is the preferred antianxiety medicine for alcoholics suffering from cirrhosis, because a fully functioning liver is unnecessary to flush the substance from the body. Oxazepam is used to alleviate alcohol withdrawal syndrome and has been used to treat neuroses and schizophrenia.
Oxazepam is considered appropriate for short-term treatment of agitation in elderly persons suffering from dementia. Tests indicate the drug can reduce hostility as well as anxiety, an ability that would set oxazepam apart from other benzodiazepines. In a cat experiment, however, the drug increased predator behavior. The drug makes mice more combative. Rats kill more mice when dosed with oxazepam, but researchers interpret that result as illustrating
potency of the drug rather than indicating it would promote aggression in humans. Human oxazepam reactions that increase hostility and combativeness are unusual and unexplained, although factors may include size and frequency of dose along with inherent personalities of users. Hostile human reactions are “paradoxical” effects, meaning they are the opposite of what
normally happens after taking an oxazepam dose.
Drawbacks.
While under the drug’s influence people exhibit memory trouble. Oxazepam lowers body temperature in mice and rats. Case reports tell of oxazepam causing blisters or other skin eruptions on people. In mice the substance boosts the poisonous action of the cancer medicine ifosfamide. Some experiments using oxazepam to induce sleep find no hangover effect on persons’ performance the next day, but that result is not invariable; size of dose appears relevant. An experiment testing the drug’s effect on vigilance (an important ability when driving a car) found normal ability while persons were under the influence of a low dose. Another experiment using a dose four times greater did find vigilance impairment. Still another experiment showed slower movements.
Abuse factors.
One reviewer of the drug’s characteristics reported that it may have less addictiveness than diazepam. In one study opiate addicts found oxazepam no more attractive than a placebo. In another study sedative abusers judged the drug less attractive than diazepam and indeed mistakenly identified oxazepam as a placebo one third of the time (a mistake they almost
never made with diazepam) and even considered a placebo more appealing than oxazepam about one fifth of the time (a preference never occurring with diazepam). A similar experiment in which drug abusers compared oxazepam, diazepam, and placebo produced comparable results.
An animal research study found no tolerance produced by the drug. Monkeys, however, exhibit signs of tolerance, dependence, and withdrawal after taking the drug for a week or two. One human study found tolerance but no withdrawal symptoms. Nonetheless, melancholy, mood swings, confusion, anxiousness, panic, and seizures have been observed when doses of the drug
stopped abruptly. Some of those “withdrawal symptoms,” however, are also conditions for which the drug is prescribed; so emergence of those conditions upon stopping the drug may simply mean the underlying conditions were not cured. A case report recounts a rare instance of someone having visual hallucinations while undergoing oxazepam withdrawal. Tapering oxazepam does not necessarily prevent abstinence symptoms, but symptoms have been controlled by substituting another drug. One authority warns that stopping oxazepam can be as touchy as stopping barbiturates. In the 1980s a health official in Australia portrayed oxazepam dependence as a growing problem. In contrast, another authority reviewing oxazepam’s history for a medical journal found only four accounts of human dependence on the drug and declared
withdrawal symptoms to be unusual upon sudden stoppage. This reviewer speculated that oxazepam’s slow delivery of drug effects and its tendency to make people dizzy if a lot is consumed help discourage abuse.
Drug interactions.
A driving skills test showed that oxazepam worsens impairment induced by alcohol. Cigarette smoking shortens the time span that an oxazepam dose stays in the body. A mouse study found that animals could withstand higher doses of morphine and methadone if oxazepam was also
used.
Cancer.
Findings about oxazepam’s potential for causing human cancer have been inconclusive. Gene mutations would be a possible sign that cancer might eventually emerge; some laboratory tests show that the drug does not cause gene mutations, but genetic mutations were apparent after a six-month administration of the drug to mice. Oxazepam is described as causing liver cancer in mice. Researchers testing the drug on rats concluded that an unclear potential for causing cancer exists, but their uncertain conclusion was partly based on some dosages so high that apparently they were fatal to various individual animals.
Pregnancy.
Experiments have exposed mice to oxazepam during fetal development, and assorted differences in their behavior (compared to mice with no exposure) have been documented, including decreased sociability and decreased interaction with surroundings. What those differences might mean in a human context is unclear. Experimental evidence indicates that prenatal exposure to oxazepam may harm a mouse’s learning ability and temporarily slow growth. In humans the drug passes from a pregnant woman into the fetus. A survey of 4,014 instances of birth defects in the Netherlands from 1981 to 1994 found an association between oxazepam and cleft lip. The same association was found in Finland a few years earlier. Mice experiments have also produced head and mouth malformations, but the doses involved were
far higher than humans would be expected to take.
Oxazepam is considered to have less impact than other benzodiazepines on a nursing mother’s milk supply. Two nursing mothers who had measurable levels of oxazepam in their blood had no evidence of the substance in their milk. A case report tells of a nursing mother whose milk contained about 4.7% of her oxazepam dosage, with no apparent effect on the infant. In other cases, not even 0.001% of the oxazepam dose taken by a mother passed into her milk.
Additional scientific information may be found in:
Ayd, F.J., Jr. “Oxazepam: Update 1989.” International Clinical Psychopharmacology 5
(1990): 1–15.
Bliding, A. “The Abuse Potential of Benzodiazepines with Special Reference to Oxazepam.”
Acta Psychiatrica Scandinavica. Supplementum, no. 274 (1978): 111–16.
Bucher, J.R., et al. “Toxicity and Carcinogenicity Studies of Oxazepam in the Fischer
344 Rat.” Toxicological Sciences 42 (1998): 1–12.
Fouks, L., et al. “The Clinical Activity of Oxazepam.” Acta Psychiatrica Scandinavica.
Supplementum, no. 274 (1978): 99–103.
Griffiths, R.R., et al. “Comparison of Diazepam and Oxazepam: Preference, Liking and
Extent of Abuse.” Journal of Pharmacology and Experimental Therapeutics 229
(1984): 501–8.
Mewaldt, S.P., M.M. Ghoneim, and J.V. Hinrichs. “The Behavioral Actions of Diazepam
and Oxazepam Are Similar.” Psychopharmacology 88 (1986): 165–71.
Vaisanen, E., and E. Jalkanen. “A Double-Blind Study of Alprazolam and Oxazepam
in the Treatment of Anxiety.” Acta Psychiatrica Scandinavica 75 (1987): 536–41.
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Pronunciation: NIK-uh-teen (also pronounced NIK-uh-tin)
Chemical Abstracts Service Registry Number: 54-11-5
Formal Names: Habitrol, Nicoderm, Niconil, Nicorette, Nicotiana rustica, Nicotiana tabacum, Nicotrol, Prostrop, Tobacco
Informal Names: Chip (cigarette mixed with PCP), Fry Daddy (cigarette mixed with crack cocaine)
Type: Stimulant (pyridine alkaloids class).
Federal Schedule Listing: Unlisted
USA Availability: Generally available to adults as a component of tobacco products;
nonprescription and prescription in pharmaceutical format
Pregnancy Category: C or D (depending on pharmaceutical format)
Uses.
Tobacco’s history is mentioned on page 18. Nicotine is the addictive drug component of tobacco and is found in other plants as well. Nicotine is one of the more hazardous drugs, and dosage via tobacco smoke adds still more peril. Although nicotine has medical uses, characteristics of the natural product tobacco fall within the criteria of a Schedule I controlled substance. Nonetheless, federal law explicitly excludes tobacco from such control, making the tobacco industry legal. At the time this book was written debate was under way about limiting adult access to nicotine products, a restrictive effort requiring changes in law.
Traditional medical uses of the drug include treatment of insect bites, skin and intestinal parasites, vomiting, earache, toothache, runny nose, hernia, and heart pain. Although tobacco smoking worsens a gastrointestinal inflammation called Crohn’s disease, medical practice uses nicotine skin patches, oral capsules, or suppositories to treat inflammation of the colon and rectum caused by ulcerative colitis. Nicotine chewing gum has been used successfully to treat finger or toe sores deriving from Buerger’s disease, an affliction in which blood vessels get blocked off (and which, despite the usefulness of pharmaceutical nicotine, seems to be worsened by smoking). Pharmaceutical nicotine helps some persons suffering from the tics of Tourette’s syndrome.
Researchers have found cigarette smoking to reduce the likelihood of getting preeclampsia, a potentially serious disease of late pregnancy in which women suffer fluid retention, high blood pressure, and too-high urine protein levels.
Cigarette smoking is also associated with a lower probability of getting Parkinson’s or Alzheimer’s disease. Even though “association” does not demonstrate cause and effect, some experiments using pharmaceutical nicotine to treat those afflictions show positive results. Such results, however, have not yet given nicotine a generally accepted role in treating those diseases. Nicotine reduces hunger pains and raises blood sugar, effects that help users eat less (Native Americans have traditionally chewed tobacco to better endure circumstances involving little food, water, or rest). Nicotine initially raises blood pressure, but continued dosage will lower it.
Drawbacks.
Tobacco smoking can lead to lung cancer and heart disease. Many other afflictions are attributed to tobacco smoking: bronchitis, emphysema, cataracts, mouth cancer, pancreas cancer, bone density loss (making broken bones more likely), abdominal aortic aneurysm (a sac ballooning out from the blood vessel wall), brain aneurysm, and gastroesophageal reflux (recurrent backward flow of acid and partially digested food from the stomach to the esophagus, making esophageal cancer more likely). One study noted that smoking tends to produce changes causing women to go through menopause at a younger age than nonsmokers. Laboratory tests imply that smokeless tobacco promotes tooth decay. Still more unwanted actions are known, partly because tobacco has simply been studied so intensively that more is known about it than is known about many other substances. Whether nicotine itself causes afflictions produced by tobacco is uncertain. For example, some investigators suspect that heart disease in smokers comes from carbon monoxide and tar constituents of smoke rather than the nicotine.
In adults 40 mg to 100 mg of pharmaceutical nicotine can produce fatal poisoning; an equivalent dose through cigarettes would require a person to quickly smoke several packs. Smaller dosages can be dangerous for children who play with nicotine patches or gum or who consume tobacco.
Abuse factors.
As with many drugs, persons often find nicotine unpleasant at first but learn to ignore bad sensations and focus upon effects that are enjoyed. Experiments examining differences that users perceive in various drugs find that some sensations from nicotine, amphetamine, and cocaine are similar, so similar that in one experiment persons receiving injections of nicotine typically identified it as cocaine. A user can establish a physical dependence
with nicotine, causing withdrawal symptoms if dosage stops:
nervousness, tenseness, crankiness, lightheadedness, broken sleep, weariness, distractedness, tremors. These symptoms often last a few days, sometimes longer, and can relate to a person’s expectations (a psychosomatic component).
Debate exists about how addictive nicotine is. A study published in 1994 noted that about 33% of tobacco smokers become addicted. A study published in 2000 found that 20% to 60% of adolescent smokers are addicted. Many smokers with no interest in quitting can nonetheless substantially reduce their cigarette consumption with little difficulty. In contrast, many smokers wanting to stop find themselves unable to cease, and for them even pharmaceutical
nicotine can be an insufficient replacement for tobacco. Among such persons the persistence of a smoking habit suggests that something more than the drug nicotine is involved. Tobacco smoke contains thousands of chemical ingredients besides nicotine; perhaps some of the less-studied ones are important. In addition, the paraphernalia and mechanics of cigarette smoking provide a psychological buffer to users, allowing continual brief respites in interactions with other persons (such as breaking eye contact during a puff). Nicotine itself is a mild stimulant able to release adrenaline and increase pulse rate and blood pressure, with the physiological arousal produced by the drug masking physical arousal provoked by life’s tensions, thereby making smokers feel less nervous despite the stimulant effects. Smokers tend to have lower levels of body chemicals that are supplemented by antianxiety and antidepressant drugs.
Such pharmaceuticals, unfortunately, seemingly have little ability to help smokers quit their tobacco addiction.
As with any addiction, the power of nicotine and tobacco depends upon needs met by those substances. People do not smoke simply to avoid temporary withdrawal symptoms. If a person’s life is filled with situations that smoking eases like nothing else can, breaking the addiction is hard. If a person finds other ways of dealing adequately with those situations, desire for cigarettes can go away and never be bothersome again. Contrary to expectations of researchers, a laboratory test found nicotine to be no more appealing to exsmokers than to persons who have never smoked—a finding implying that life circumstances, and not just chemistry, determine this drug’s appeal.
Alcohol and illicit drug abusers reliably tend to be tobacco cigarette smokers, so reliably that the amount of tobacco use can be used to estimate the amount of cocaine and opiate usage by persons in drug abuse treatment programs.
An experiment found that persons smoked less tobacco when they had access to marijuana, suggesting that those persons used the two substances for similar purposes. Nonsmokers tend to avoid drug abuse, implying that smokers and nonsmokers use different strategies to cope with life’s challenges.
Cigarette smoking is more prevalent among schizophrenics, seriously depressed persons, and persons with low-grade psychiatric disturbance that may lack outward symptoms. Almost two thirds of smokers in one research project turned out to have a history of present or past psychiatric abnormality.
Among such individuals smoking may be a strategy of self-medication. One study found that withdrawal symptoms can depend on the extent to which the drug is used for self-medication.
Improvement has been measured in alertness, energy, and happiness as cigarette smokers start their day’s consumption in the morning. Conversely, cutting off a smoker’s supply of cigarettes produces measurable increases in fatigue, irritation, sadness, stress, and disorientation. New users do not get favorable effects sought by experienced users but instead have measurable nausea and general uneasiness. Among new users nicotine reduces job performance skills such as physical coordination and accuracy in memory tasks the opposite of what happens with experienced users.
Although pharmaceutical nicotine has various medical applications, its main use is for treatment of addiction to tobacco smoking. One authority aptly described nicotine chewing gum as the methadone of cigarettes, meaning that such a treatment strategy is intended to switch addicts from tobacco to pharmaceutical nicotine, just as treatment personnel seek to switch heroin addicts to methadone. Although such programs may have an official goal of eliminating a person’s addiction, in practice simply switching a person from a more harmful drug to a less harmful drug is often considered a success.Drug interactions. Nicotine interacts with commonly used medical drugs.
Antipsychotic drugs and the anti–blood clot medicine heparin flush from the body faster if a person uses nicotine. Nicotine also reduces the sedative effect of benzodiazepines and reduces pain relief from various opioids. Cigarette smoke acts as a monoamine oxidase inhibitor (MAOI), a type of chemical found in some antidepressants and that can have serious adverse effects when
used simultaneously with some medicines (though acute danger from cigarette interactions may be small). Caffeine seems to make nicotine more pleasurable.
Rat studies show that nicotine increases alcohol’s appeal and worsens pancreas inflammation caused by both drugs. Birth control pills increase the boost that nicotine gives to pulse rate, and some researchers speculate that such increase is related to the elevated risk of heart disease found among smokers who use birth control pills.
Cancer.
Tests indicate that pure nicotine (as opposed to smoke containing nicotine) does not cause cancer.
Pregnancy.
Smoking reduces female fertility according to most studies of the topic, and studies of Canadian farm couples and of men in the Netherlands found an apparent reduction in male fertility as well. Pregnant women who smoke tobacco increase the chance of miscarriage, premature birth, smaller full-term infants, and sudden infant death syndrome (SIDS or “crib death”).
The children are more likely to have muscle tone abnormalities. Smoking harms male and female gametes, damages chromosomes, and can change DNA in ways linked with childhood cancer. Nicotine usage by a pregnant woman changes movements and heart action of a fetus. One researcher warns that nicotine patches or chewing gum may deliver even more nicotine to a
fetus than smoking would. Nicotine enters the milk of nursing mothers. Rat experiments indicate that fetal exposure to nicotine combined with newborn exposure to nicotine in milk increases the risk of offspring developing lung trouble similar to emphysema. Human birth defects have been attributed to tobacco smoking. Although a study of teenage tobacco smokers did not see
any increased incidence of birth defects in their infants, research based on animal experimentation and published in 1998 declared that nicotine causes defects in fetal brain development leading to problems in thinking and learning that may not become apparent until years after birth. The children tend to have lower scores on psychological measurements, somewhat reminiscent of “cocaine babies,” deficits that continue for years. Some investigators see a link between pregnant smokers and offspring with psychological problems.
Investigators tracking mothers and daughters for three decades found that daughters were more likely to take up smoking if their mothers smoked during pregnancy.
Additional information.
Scientific studies find that “passive smoking” threatens health of bystanders who inhale smoke from tobacco products and exhalations of smokers. A study of spontaneous abortions found them more likely in pregnant nonsmoking women who inhale environmental smoke and use a lot of caffeine or a moderate amount of alcohol. Infants from nonsmoker women who were exposed to tobacco smoke during pregnancy are more likely to have lower birth weight and persistent pulmonary hypertension. Offspring also exhibit the same kinds of lower psychological test scores that are seen in children of active smokers. Inhalation of smoke by infants is suspected of
contributing to SIDS. For sure, compared to children in nonsmoking households, infants of smokers are hospitalized more often for pneumonia and bronchitis. The level of environmental smoke necessary for ill effects is often unclear in scientific studies; a person working in a poorly ventilated smokey bar for eight hours a day will have a considerably different exposure than
someone in a nonsmoking household who sits outside once a week with a friend who smokes a couple of cigarettes.
Additional scientific information may be found in:
Brown, C. “The Association between Depressive Symptoms and Cigarette Smoking in an Urban Primary Care Sample.” International Journal of Psychiatry in Medicine 30 (2000): 15–26.
Brown, K.G. “Lung Cancer and Environmental Tobacco Smoke: Occupational Risk to Nonsmokers.” Environmental Health Perspectives 107 (1999, Suppl. 6): 885–90.
Colby, S.M., et al. “Are Adolescent Smokers Dependent on Nicotine? A Review of the
Evidence.” Drug and Alcohol Dependence 59 (2000, Suppl. 1): S83–S95.
Dursun, S.M., and S. Kutcher. “Smoking, Nicotine and Psychiatric Disorders: Evidence
for Therapeutic Role, Controversies and Implications for Future Research.” Medical
Hypotheses 52 (1999): 101–9.
Haustein, K.O. “Cigarette Smoking, Nicotine and Pregnancy.” International Journal of
Clinical Pharmacology and Therapeutics 37 (1999): 417–27.
Parrott, A.C., and F.J. Kaye. “Daily Uplifts, Hassles, Stresses and Cognitive Failures:
In Cigarette Smokers, Abstaining Smokers, and Non-smokers.” Behavioural Pharmacology
10 (1999): 639–46.
Robinson, J.H., and W.S. Pritchard. “The Role of Nicotine in Tobacco Use.” Psychopharmacology
108 (1992): 397–407.
Stolerman, I.P., and M.J. Jarvis. “The Scientific Case That Nicotine Is Addictive.” Psychopharmacology 117 (1995): 2–10.
Van Gilder, T.J., P.L. Remington, and M.C. Fiore. “The Direct Effects of Nicotine Use
on Human Health.” Wisconsin Medical Journal 96 (1997): 43–48.
