What is warfarin? How does it interact with other drugs?

Alfalfa

Effect: Possible Harmful Interaction

The herb alfalfa (Medicago sativa) is promoted for a variety of conditions. The relatively high vitamin K content in alfalfa could reduce the effectiveness of warfarin. Vitamin K directly counteracts warfarin’s blood-thinning effects. Since the amount of vitamin K in alfalfa varies widely, it is difficult to give an exact safe upper dose. As a precaution, avoid alfalfa supplements during warfarin therapy except under medical supervision.

Chamomile

Effect: Possible Harmful Interaction

The herb chamomile contains substances in the coumarin family. Some coumarins have blood-thinning actions that could interact with warfarin. One case report exists of a person in whom it appears that combined use of chamomile and warfarin led to internal bleeding.

Chondroitin

Effect: Possible Harmful Interaction

Based on chondroitin’s chemical similarity to the anticoagulant drug heparin, it has been suggested that chondroitin might have anticoagulant effects as well. There are no case reports of any problems relating to this, and studies suggest that chondroitin has at most a mild anticoagulant effect. Nonetheless, chondroitin should not be combined with warfarin except under physician supervision.

Coenzyme Q10 (CoQ10)

Effect: Possible Harmful Interaction

CoQ10 is a vitamin-like substance that plays a fundamental role in the body’s energy production. This substance is somewhat similar in structure to vitamin K, and reportedly, it too can reduce the therapeutic effects of warfarin. In three case reports, CoQ10 was found to interfere with warfarin’s blood-thinning effects. A double-blind study found no interaction between CoQ10 and warfarin. However, in view of warfarin’s low margin of safety, one should consult a physician before combining CoQ10 with warfarin.

Cranberry

Effect: Possible Harmful Interaction

Several case reports suggest that cranberry juice can increase warfarin’s action, causing dangerous and potentially fatal bleeding problems. However, formal studies have failed to find evidence of such an interaction. Nonetheless, one should be cautious, especially when taking cranberry juice in dosages higher than eight ounces daily.

Danshen

Effect: Possible Harmful Interaction

The herb danshen, the root of Salvia miltiorrhiza, is used in traditional Chinese medicine for treating heart disease. Preliminary evidence, including several case reports, suggests that danshen can dangerously increase the effects of warfarin and cause significant bleeding problems. Persons taking warfarin should avoid danshen except under a physician’s supervision.

Devil’s Claw

Effect: Possible Harmful Interaction

The herb devil’s claw (Harpogophytum procumbens) is used for various types of arthritis and digestive problems. According to one case report, devil’s claw might increase the risk of abnormal bleeding when taken with warfarin. As a precaution, one should not combine devil’s claw and warfarin except under a physician’s supervision.

Dong Quai

Effect: Possible Harmful Interaction

The herb dong quai (Angelica sinensis) is used for menstrual disorders. According to one case report, dong quai may add to the blood-thinning effects of warfarin, thus increasing the risk of abnormal bleeding. One should probably avoid combining dong quai and warfarin without medical supervision.

Feverfew

Effect: Possible Harmful Interaction

The herb feverfew (Tanacetum parthenium) is primarily used for the prevention and treatment of migraine headaches. In vitro studies suggest that feverfew thins the blood by interfering with the ability of blood platelets to clump together. This raises the concern that feverfew might increase the risk of abnormal bleeding when combined with warfarin. However, there is as yet no evidence that the blood-thinning effect of feverfew is significant in humans. Though an additive effect of feverfew and warfarin appears to be theoretical at this time, it may be best to avoid this combination except under medical supervision.

Garlic

Effect: Possible Harmful Interaction

The herb garlic (Allium sativum) is taken to lower cholesterol, among many other proposed uses. One of the possible side effects of garlic is an increased tendency to bleed. This blood-thinning effect has been demonstrated in a double-blind trial of garlic in sixty volunteers, as well as in other studies and one case report.

According to two other case reports, the blood-thinning effects of warfarin were greatly enhanced in persons taking garlic. This could amplify the risk of bleeding problems. Based on these findings, one should avoid combining garlic and warfarin except under a physician’s supervision.

Ginger

Effect: Possible Harmful Interaction

The herb ginger (Zingiber officinale) is used for nausea associated with motion sickness, morning sickness in pregnancy, and the postsurgical period. Ginger appears to thin the blood by interfering with the ability of blood platelets to clump together. As with feverfew, this raises the concern that ginger might increase the risk of abnormal bleeding when taken with warfarin. However, there is no evidence at present that the blood-thinning effect of ginger is significant in humans.

Though an additive effect of ginger and warfarin appears to be theoretical based on current evidence, it may be best to avoid this combination except under medical supervision. Ginger-flavored drinks should not present a problem, but candies containing whole dried ginger are potentially of concern.

Ginkgo

Effect: Possible Harmful Interaction

The herb ginkgo (Ginkgo biloba) has been used to treat Alzheimer’s disease and ordinary age-related memory loss, among many other uses. Inconsistent evidence suggests that ginkgo might reduce the ability of platelets (blood-clotting cells) to stick together. In addition, several case reports suggest that use of ginkgo may be associated with an increased risk of serious abnormal bleeding episodes in persons taking the herb. These findings raise concern that ginkgo might add to the blood-thinning effects of warfarin, and there is one report of abnormal bleeding in an individual who had been taking the herb and drug together. However, two double-blind studies found no interaction between ginkgo and warfarin. These findings are reassuring. Nonetheless, in view of warfarin’s low margin of safety, one should consult a physician before combining ginkgo with warfarin.

Ginseng

Effect: Possible Harmful Interaction

The herb ginseng (Panax ginseng) is promoted as an adaptogen, a treatment that is said to help the body adapt to stress of all types. A case report suggests that P. ginseng can reduce the anticoagulant effects of warfarin; however, three double-blind studies failed to find any interaction. In general, double-blind studies are far more reliable than case reports, and therefore, it would appear that there is not too much reason for concern regarding this potential interaction. However, another double-blind trial that evaluated the closely related American ginseng species (P. quinquefolius) found that use of the herb reduced the anticoagulant effects of warfarin, similar to what was seen in the case report. At this point, therefore, it is reasonable to suggest that caution should be exercised when combining ginseng and warfarin.

Low-Carbohydrate, High-Protein Diet

Effect: Possible Harmful Interaction

Low-carbohydrate, high-protein diets have been advocated for weight loss. According to two case reports, adoption of such diets may decrease the effectiveness of warfarin, possibly by increasing blood levels of a substance called albumin that might tend to bind and inactivate warfarin in the body.

Green Tea

Effect: Possible Harmful Interaction in Very High Doses

Dried green tea leaf contains significant levels of vitamin K on a per-weight basis. On this basis, it has been stated that people using blood thinners in the warfarin family should avoid green tea. However, green tea taken as a beverage provides such small amounts of the vitamin that the risk seems minimal for normal consumption. There is one case report of problems that developed in a person on warfarin who consumed as much as a gallon of green tea daily.

Ipriflavone

Effect: Possible Harmful Interaction

Ipriflavone, a synthetic isoflavone that slows bone breakdown, is used to treat osteoporosis. Warfarin use increases the risk of osteoporosis. Because ipriflavone has been found to help prevent osteoporosis in certain circumstances, one might be tempted to consider taking this supplement while also using warfarin. However, some evidence indicates that ipriflavone might interfere with the body’s normal breakdown of warfarin. This could raise the levels of warfarin in the body and could increase the risk of abnormal bleeding.

Papain, Bromelain

Effect: Possible Harmful Interaction

One case report suggests that papain, a digestive enzyme found in papaya extract (Carica papaya), might add to warfarin’s blood-thinning effect.

Vinpocetine

Effect: Possible Harmful Interaction

The substance vinpocetine is sold as a dietary supplement for the treatment of age-related memory loss and impaired mental function. Vinpocetine is thought to inhibit blood platelets from forming clots. For this reason, it should not be combined with medications or natural substances that impair the blood’s ability to clot normally, as this may lead to excessive bleeding. One study found only a minimal interaction between the blood-thinning drug warfarin and vinpocetine (and it actually involved an increased tendency for blood clotting), so one should use caution.

PC-SPES

Effect: Possible Harmful Interaction

PC-SPES is an herbal combination that has shown promise for the treatment of prostate cancer. One case report suggests that PC-SPES might increase risk of bleeding complications if combined with blood-thinning medications. Subsequent evidence has indicated that PC-SPES actually contains warfarin, making this interaction inevitable.

Policosanol

Effect: Possible Harmful Interaction

Policosanol, derived from sugarcane, is used to reduce cholesterol levels. It also interferes with platelet clumping, creating a risk of interactions with blood-thinning drugs.

For example, a thirty-day, double-blind, placebo-controlled trial of twenty-seven persons with high cholesterol levels found that policosanol at 10 milligrams (mg) a day markedly reduced the ability of blood platelets to clump together. Another double-blind, placebo-controlled study of thirty-seven healthy volunteers found evidence that the blood-thinning effect of policosanol increased as the dose was increased: the larger the policosanol dose, the greater the effect. Another double-blind, placebo-controlled study of forty-three healthy volunteers compared the effects of policosanol (20 mg daily), the blood-thinner aspirin (100 mg daily), and policosanol and aspirin combined at these same doses. The results again showed that policosanol substantially reduced the ability of blood platelets to stick together, and that the combined therapy exhibited additive effects. Based on these findings, persons should not combine warfarin and policosanol except under medical supervision.

Reishi

Effect: Possible Harmful Interaction

One study suggests that reishi impairs platelet clumping. This creates the potential for an interaction with any blood-thinning medication.

Royal Jelly

Effect: Possible Harmful Interaction

One case report indicates that use of royal jelly can increase the effectiveness of warfarin, creating risk of bleeding.

Soy

Effect: Possible Harmful Interaction

One case report indicates that soy milk might decrease warfarin’s effectiveness.

St. John’s Wort

Effect: Possible Harmful Interaction

The herb St. John’s wort (Hypericum perforatum) is primarily used to treat mild to moderate depression. Evidence suggests that St. John’s wort may interfere with warfarin, possibly requiring an increased dosage of the drug to maintain the proper therapeutic effect. Seven cases have been reported in which the blood-thinning effects of warfarin have been impaired in persons taking St. John’s wort. A hidden risk lies in this type of interaction. If taking warfarin, one should avoid St. John’s wort except under a physician’s supervision.

Vitamin A

Effect: Possible Harmful Interaction

Supplemental vitamin A might increase the blood-thinning effects of warfarin, and this could potentially lead to an increased risk of abnormal bleeding. For this reason, it may be best to avoid combining vitamin A with warfarin unless supervised by a physician.

Vitamin C

Effect: Possible Harmful Interaction

Vitamin C taken in high dosages (more than 1,000 mg daily) has been reported to reduce the blood-thinning effect of warfarin. In one case, the person was taking 1,000 mg of vitamin C daily; another involved megadoses (about 16,000 mg daily). As a precaution, if taking warfarin, one should consult with a physician before taking high-dose vitamin C supplements.

Vitamin E

Effect: Possible Harmful Interaction

On the basis that vitamin E thins the blood, it has been suggested not to combine vitamin E with warfarin. However, a four-week, double-blind study of twenty-five persons taking warfarin found no additive effect. None of the participants taking vitamin E at a daily dose of 800 or 1,200 IU showed an increased risk for abnormal bleeding.

In contrast, a case report indicated that vitamin E (800 IU daily) added to the effects of warfarin and resulted in abnormal bleeding. Because this effect did not become apparent until the fourth week, it is possible that problems might take longer to develop than the four-week period covered by the double-blind study, or that certain persons might be more prone to an interaction. An unpublished, thirty-day study of three volunteers taking a warfarin-like drug also found an additive effect with only 42 IU of vitamin E daily.

Though the evidence supporting a possible interaction is scanty, it is best not to risk serious bleeding problems. One should avoid combining vitamin E with warfarin except under the supervision of a physician.

Vitamin K

Effect: Possible Harmful Interaction

Vitamin K is an antidote to warfarin; it directly counteracts warfarin’s blood-thinning effects. This is true for both supplemental vitamin K and foods high in vitamin K. For this reason, eating more vitamin K-rich vegetables can decrease warfarin’s therapeutic effect, and eating less of these foods can increase the drug’s effect. Either situation can lead to potential life-threatening complications.

Therefore, once established on a certain dose of warfarin, one should not change one’s usual intake of vitamin K without consulting a physician.

One study suggests a novel way of using this effect deliberately. Researchers gave people on warfarin a fixed daily dose of vitamin K to override the changes in warfarin action caused by the natural variation in day-to-day dietary vitamin K consumption. The results were positive: INR values (the standard measurement of warfarin’s blood-thinning effect) became more stable. However, this method should not be used except under close physician supervision.

White Willow

Effect: Possible Harmful Interaction

The herb white willow (Salix alba), also known as willow bark, is used to treat pain and fever. White willow contains a substance that is converted by the body into a salicylate similar to the blood-thinner aspirin. Because white willow, like aspirin, may enhance the blood-thinning effects of warfarin, this combination should be avoided unless medically supervised.

Other Herbs and Supplements

Effect: Possible Harmful Interaction

One case report suggests that a combination of the herbs boldo and fenugreek increased the effects of warfarin. Another isolated case report suggests that the same can happen when fish oil is combined with warfarin.

Based on their known effects or the effects of their constituents, the following herbs and supplements might not be safe to combine with warfarin, though this has not been proven: chamomile (Matricaria recutita), Coleus forskohlii, ginger (Zingiber officinale), horse chestnut (Aesculus hippocastanum), papaya (Carica papaya), red clover (Trifolium pratense), reishi (Ganoderma lucidum), mesoglycan, fish oil, oligomeric proanthocyanidins (OPC’s), and phosphatidylserine.

Bibliography

Beatty S. J., B. H. Mehta, and J. L. Rodis. “Decreased Warfarin Effect After Initiation of High-Protein, Low-Carbohydrate Diets.” Annals of Pharmacotherapy 39 (2005): 744-747.

Buckley, M. S., et al. “Fish Oil Interaction with Warfarin.” Annals of Pharmacotherapy 38 (2004): 50-52.

Greenblatt, D. J., et al. “Interaction of Flurbiprofen with Cranberry Juice, Grape Juice, Tea, and Fluconazole.” Clinical Pharmacology and Therapeutics 79 (2006): 125-133.

Jiang, X., et al. “Effect of Ginkgo and Ginger on the Pharmacokinetics and Pharmacodynamics of Warfarin in Healthy Subjects.” British Journal of Clinical Pharmacology 59 (2005): 425-432.

Lee, N. J., and J. D. Fermo. “Warfarin and Royal Jelly Interaction.” Pharmacotherapy 26 (2006): 583-586.

Lee, S. H., et al. “Interaction Between Warfarin and Panax ginseng in Ischemic Stroke Patients.” Journal of Alternative and Complementary Medicine 14, no. 6 (2008): 715-721.

Pham, D. Q., and A. Q. Pham. “Interaction Potential Between Cranberry Juice and Warfarin.” American Journal of Health-System Pharmacy 64 (2007): 490-494.

Welch, J. M., and K. Forster. “Probable Elevation in International Normalized Ratio from Cranberry Juice.” Journal of Pharmacy Technology 23 (2007): 104-107.

Yuan, C. S., et al. “American Ginseng Reduces Warfarin’s Effect in Healthy Patients.” Annals of Internal Medicine 141 (2004): 23-27.

What is malaria? |

Causes and Symptoms

Malaria



in humans is caused by transfer into the bloodstream, through the saliva of the Anopheles mosquito, of the protozoan (single-cell) Plasmodium parasite. There are several different strains of the malaria parasite, all belonging to the phylum Sporozoa, a classification connected with the importance of spores in the organism’s reproductive cycle. Serious and potentially lethal malarial infections in humans are primarily associated with P. falciparum. Other Plasmodium parasites that can produce infection are P. vivax (formerly present in temperate climate zones but now found only in the subtropics), P. malariae (also only subtropical), and P. ovale (quite rare, and mainly limited to West Africa). Other Plasmodium parasites infect only nonhuman primates (P. knowlesi and P. cynomolgi, for example),
only rodents (four different species), or only birds (P. cathemerium and P. gallinaceum). The latter two species have been used widely in experimental testing of antimalarial vaccines.

It is important to note that only one mosquito genus, Anopheles, and only the female Anopheles mosquito, serves the vector function in transmitting malaria. The explanation of the female’s role is surprisingly simple: Only the female Anopheles nourishes itself (usually in the night hours) by piercing the skin of its victim and sucking small quantities of blood. The male of the species feeds mainly on fruit juices.

In the most common scenario, the mosquito ingests the Plasmodium parasite when it sucks the blood of an already infected human. This phase is followed by several others—all connected with the reproductive processes of the same organism (both sexual and asexual)—until subsequent generations of the parasite are passed on by the mosquito to another human host, who then becomes infected. The protozoan’s first, sexual stage of reproduction occurs when male gametes emit flagella that seek out and join their female counterpart, producing a fertilized zygote. Once lodged in the gut tissue of the mosquito in the form of an oocyst, a further, asexual stage of reproduction occurs through what is called sporogony: the release from the oocyst of myriad spores. They spread rapidly throughout the body of the mosquito. Many enter the insect host’s salivary glands, from which they are transferred into the blood of the next human bitten by the mosquito. It is the further development of the spores in the human organism that produces the disease symptoms associated with malaria.

Once transmitted into the human host through the mosquito saliva, the parasite spores flow quickly through the blood, entering the liver. Their next transformation occurs once they lodge themselves in the cells of the liver, becoming what are called hepatic trophozoites. As they feed off of the liver cells, the trophozoites grow and burst open. This process of asexual multiplication in the liver is referred to as hepatic schozogony. At that stage, the parasite has multiplied many hundreds of times, producing the actual agent of malarial disease, merozoites. If the parasite is P. vivax, then this phase may not occur immediately, as a result of a state of dormancy in the parasitic trophozoites. In this case, months or even years can pass before the merozoites are released. Even then, the delayed release is still not final. This explains why some malaria-infected individuals experience a cyclical disappearance of symptoms, followed some time later by a resurgence of the latent disease.

When released from the trophozoites, the merozoites quickly invade the red blood cells of the host. The damage that they inflict leads to anemic reactions as the number of healthy blood cells in the organism decreases. It is not only the liver that is affected; the disease can also spread to the spleen.

Once the effects of malaria begin to take hold in the blood and various organs of the body, certain symptoms will appear. There is an onset of fever, probably caused by the release of a pyrogen (a fever-inducing agent) by the white blood cells reacting to the diseased situation of red blood cells that have been attacked by the malaria parasite. Since this release of pyrogens may follow an irregular pattern, fever can come and go, seemingly sporadically. Meanwhile, as the number of parasitized red blood cells increases, infected red blood cells begin to attach themselves to the inside tissue of capillaries of the internal organs. The effect is blockage of the necessary free flow of blood. If pressure builds because of this blockage, then blood vessels themselves may burst. Such internal hemorrhages allow the directionless dispersion of infected blood within the body, increasing the anemic symptoms that are characteristic of malaria. Perhaps the most dramatic sign of blocked blood vessels occurs if and when the parasitized
cells affect the blood flow to the brain. In such cases, convulsions occur, eventually leading to coma.

Treatment and Therapy

Long before researchers were able to explain the causes of malaria, treatment of its symptoms, primarily manifested in spells of fever, involved giving the patient doses of quinine. As knowledge of the disease increased, different forms of treatment evolved. Such developments occurred not only as new discoveries emerged; they also became necessary as the malaria parasite itself evolved genetically, in effect developing its own immunity to quinine-based treatment.

Several compounds were developed in the later decades of the twentieth century to complement or, more recently, to replace complete dependence on quinine.

Depending on the Plasmodium species coming into contact with it, the alkaloid quinine could kill the parasitical organism at key stages in its reproductive activity. Sometimes, however, toxic side effects accompanied the use of quinine in malaria cases. These negative effects eventually sparked research aimed at producing synthetic drugs that could be as effective as quinine in preventing malaria, even though they might not be as effective in treating the disease once contracted. The earliest synthetic antimalarials, introduced between 1926 and the early 1950s, included pamaquine, the first synthetic; mepacrine; and chloroquine and primaquine, two well-known drugs from the mid-1940s through the 1950s. These synthetic agents intervened to stop reproduction of the malaria parasite at different points in its life span. Depending on which preventive drug was taken, treatment might have to begin well before expected exposure, during the period of exposure, or for a certain period after being present in a malaria-infected area. Several generations of antimalarial drugs are on the market, but such progress in pharmaceutical options has not effectively resolved the problem of endemic malaria in regions of the world where those most in need lack either public health information programs or the financial means to obtain necessary drugs.

Research involving vaccination to protect against malarial infection has tended to follow one of two main approaches: vaccines to combat the diffusion of spores directly, and vaccines to block one or several stages of the parasite’s life cycle. Some vaccines have been developed by extracting spores from the blood of infected patients and using methods such as radiation to reduce their potency. Injection of these weakened agents into the blood can induce formation of antibodies that are able to fight invasive spores coming from an outside source (mosquito saliva) into a potential host organism. Commercial production of such vaccines, however, would require finding an economically viable way of obtaining and treating large quantities of Plasmodium spores, not only from P. falciparum but also from other malaria parasites that are less deadly but an important threat to large numbers of people around the world. For this reason, researchers have tended to concentrate more on isolating antigens that the body produces naturally to fight invasive spores and merozoites, analyzing them, and attempting to use biotechnology to produce effective synthetic antigens.

Observation over a long period of time has provided statistical evidence that, in a number of subtropical areas where malaria is endemic, fatalities from the disease are more frequent among children than among adults. The reason for this is linked to the adult population’s prior exposure to one or more nonlethal malarial infections. In essence, the adult body’s production of natural antigens seems to neutralize the effects of blood cells that have become carriers. If they remain in the bloodstream, these antigens reduce the susceptibility to what, in children, takes the form of a sudden invasion of infected and (for the body’s immune system) unrecognizable blood cells transmitted through Anopheles mosquito bites.

There is, therefore, an entire field of malaria research dealing with the body’s own immune responses. Where malaria is concerned, researchers pay particular attention not only to the challenge of understanding how immunity can build in populations living in endemic zones but also to the possibility of increasing the efficiency of certain body organs that naturally affect the bloodstream in ways that can impede the spread of the parasite’s damage. Attention has focused, for example, on the internal functions of the spleen. The spleen can prevent the progress of intravascular pathogens in general by reducing the flow of infected red blood cells to other organs and isolating them in a chemical state that renders them less directly dangerous to the body. This capacity is called splenic filtration. Although research has not yet identified an effective way to use externally applied medications to enhance this facet of the spleen’s natural defense system, it is agreed that here there is a serious prospect for another area of treatment to complement, if not replace, preventive drugs and synthetic antigens.

Once it was clear that malaria was transmitted by mosquitoes, the most logical tactic to prevent spread of the disease involved campaigns to eradicate, or at least diminish the life chances of, Anopheles. Thus, drainage of swamp areas (a costly but effective measure where possible), public health measures to guard against insalubrious concentrations of stagnant water, and insecticide spraying have been practiced throughout the world to combat Anopheles. During World War II and until the late 1950s, DDT was the insecticide of choice. When the harmful side effects of DDT for humans and the environment became apparent, legislation in most but not all countries banned the chemical. Research has since aimed at, but not fully succeeded in, developing safer insecticides that can approach DDT’s levels of efficiency.

Perspective and Prospects

Research in the field of malarial disease and its biological origins advanced rather slowly, with most major advances occurring fairly late in the nineteenth century. It was in 1897 that a surgeon in the British Indian army, Sir Ronald Ross, following British tropical disease expert Sir Patrick Manson’s suggestions, announced his discovery that malaria was transmitted to humans by mosquitoes. There had been earlier theories concerning the role of mosquitoes, some going back as far as the early eighteenth century in Italy (where the term “malaria,” meaning “bad air,” had originated). It took the work of a French military doctor in Algeria, Alphonse Laveran, to show, under a microscope, the ongoing activity of parasites in the blood of malaria patients. Laveran also did postmortem studies of malaria victims’ blood and organs and found a dark pigment composed mainly of iron which came from the parasites’ apparent digestion and waste disposal of vital hemoglobin in the red blood cells. He became the first to posit that malaria was a disease of red blood cells and that it was caused by an invasion of parasites.

From there, it was a question of finding how the parasites entered the human bloodstream. This was the result of Ross’s observation in India of a particular variety of mosquito larvae (later identified as the small brown Anopheles, distinct from Culex varieties commonly observed in the daytime) collected from stagnant waters in the region. When Ross followed Manson’s suggestion that mosquitoes hatched from these larvae should be induced to feed from a known malaria patient, he found that only a few insects survived the next few days. When these were dissected, he found oocysts embedded on the wall of the mosquitoes’ gut. Microscopic analysis showed that they contained the same dark pigment that Laveran had found in the blood of malaria victims in Algeria.

Both Ross (in 1902) and Laveran (in 1907) received Nobel Prizes in recognition of their work, Ross in medicine and Laveran in physiology or medicine. Other contributors, notably the Italian Giovanni Batista Grassi, carried on significant work in the same first decade of the twentieth century that paralleled (or, according to Grassi, may have been accomplished before) Ross’s studies. The most important suggestion by Grassi—which was correct but which took much more work to prove in the laboratory—was that there must be significant transformations, in fact multiple stages of reproduction, between the sporozoite phase of dissemination of the parasite via mosquito saliva and the merozoite phase, when the actual attacking parasite can destroy red blood cells in the human host. Later researchers finally provided, in 1934, convincing evidence that there was a sequence of sexual and asexual phases of reproduction (the later labeled “schizogony”) in the life cycle of the Plasmodium parasite.

Over the years, other researchers helped broaden the understanding of malaria, its causes, and treatment. Despite the obvious costs paid during the first half of the twentieth century involving debilitation and loss of human lives in areas where malaria was endemic, truly major breakthroughs occurred only during the extraordinary conditions created by World War II. The fact that large numbers of troops were sent to areas in East, South, and Southeast Asia as well as Africa meant that the danger of widespread malarial infection could hamper strategic operations. Distribution of all forms of preventive equipment, including both mosquito nets and insect repellents, was destined to become standard procedure in tropical zones. Doses of quinine were also part of each soldier’s medical supply packet.

Bibliography

Carlton, Jane M., Susan L. Perkins, and Kirk W. Deitsch. Malaria Parasites: Comparative Genomics, Evolution, and Molecular Biology. Norfolk, England: Caister Academic Press, 2013.

Farmer, Paul. Infections and Inequalities: The Modern Plagues. Berkeley: University of California Press, 2001.

Honigsbaum, Mark. The Fever Trail: In Search of the Cure for Malaria. New York: Farrar, Straus and Giroux, 2002.

Malaria Foundation International. http://www.malaria .org.

Rocco, Fiammetta. “Corrections and Clarification: The Global Spread of Malaria in a Future, Warmer World.” Science 289 (September, 2000): 2283–284.

Rocco, Fiammetta. The Miraculous Fever-Tree: Malaria and the Quest for a Cure That Changed the World. New York: HarperCollins, 2003.

World Health Organization. Defeating Malaria in Asia, the Pacific, Americas, Middle East, and Europe. New York: Author, 2013.

What are anxiety disorders? |

Introduction

The concept of anxiety is one of the most often used and loosely defined concepts in psychology. It can be used to describe a temporary state (“You seem anxious today”) or an enduring personality trait (“He is an anxious person”). It is used to assign cause (“He stumbled over the words in his speech because he was anxious”) and to describe an effect (“Having to give a speech sure makes me anxious”). It is seen as the result of discrete objects or situations such as snakes or heights or as evolving from basic existential problems such as the trauma of birth or the fear of death. All major theories in psychology in some way confront anxiety.

Because of the preeminence of anxiety in the field of psychology, there are many different theories about the nature and origin of anxiety disorders. Anxiety disorders include generalized anxiety disorder, social anxiety disorder, panic disorder, obsessive-compulsive disorder, post-traumatic stress disorder, and specific phobias. The two most important and influential viewpoints on anxiety are the Freudian and the behavioral viewpoints. Although these theories attempt to explain many anxiety disorders, an examination of how they apply to
phobias presents a good indication of how they work. A specific phobia can be defined as an anxiety disorder involving an intense fear of a particular thing (such as horses) or situation (such as heights).

Freudian Approach

Sigmund Freud, who said that understanding anxiety “would be bound to throw a flood of light on our whole mental existence,” had two theories of anxiety, an early one in 1917 and a later one in 1926. In the early theory, libido
(mental energy, often equated with sexual drive) builds up until it is discharged by some pleasurable activity. Sometimes the energy cannot be discharged, for example, when the sexual object is not attainable or is morally unacceptable. This undischarged energy is anxiety, and it remains even when its original, unacceptable object is repressed or eliminated from conscious awareness. This anxiety may attach itself to an otherwise harmless object, resulting in a phobia. This theory is best illustrated in one of Freud’s most famous cases, that of “Little Hans,” a five-year-old who developed a phobia of horses. Freud believed that Hans had a sexual desire for his mother and wanted his father dead so that he could have his mother to himself. This desire for his mother and hatred of his father were unacceptable impulses and so were repressed from consciousness, resulting in anxiety. This anxiety attached itself to horses, Freud thought, because the black blinders and muzzle of the horse symbolized his father’s glasses and mustache.

In Freud’s first theory, repression
causes anxiety. In psychoanalytic theory, repression is a defense mechanism that keeps unacceptable thoughts and impulses from becoming conscious. In the later theory, the relationship between them has changed: anxiety causes repression. In this theory, anxiety acts as a signal to the ego (in Freud’s theory, the rational, conscious part of the mind) that a forbidden impulse (such as Little Hans’s desire for his mother) is trying to force its way into consciousness. This signal alerts the ego to try to repress the unwanted impulse. If the ego cannot successfully repress the forbidden impulse, it may try to transfer the forbidden impulse to an irrelevant object (horses, in Little Hans’s case). This object can arouse all the emotions associated with the forbidden impulse, including the signal anxiety. In this way, it becomes a phobic object.

Two-Factor Theory

One influential behavioral approach to anxiety is O. Hobart Mowrer’s
two-factor theory. It uses the principles of Pavlovian learning—in which two stimuli are presented one after the other, and the response to the first changes because of the response automatically elicited by the second stimulus—and operant conditioning—learning in which a behavior increases or decreases depending on whether the behavior is followed by reward or punishment—to explain fear and phobic avoidance, respectively. Fear is acquired through Pavlovian conditioning when a neutral object or situation is paired with something painful or punishing. For example, having an automobile accident can result in a fear of driving. At this point, operant learning principles take over to explain phobic avoidance. In operant learning, any action that leads to a reward is likely to be repeated. The person who is anxious about driving might avoid driving. Because this avoidance is rewarded by reduced anxiety, the person is more likely to avoid driving in the future. Continued avoidance makes it harder to get back behind the wheel again.

Many problems were found with two-factor theory, and many modifications have been made to it. Two problems will be discussed here to illustrate these changes. First, the theory predicts that people will be likely to fear things that are most often associated with pain. There are very few people in modern society, however, who are phobic of electrical sockets and end tables, even though almost everyone has received a shock from the former and stubbed a toe on the latter. On the other hand, many people are afraid of snakes and spiders, even if they have never been bitten by one. This has been explained through the concept of preparedness: Evolutionary history has prepared people to learn that some things—such as reptiles, insects, heights, darkness, and closed spaces—are dangerous. These things are “easy” to learn to fear, and they account for a large proportion of phobias. On the other hand, people’s evolutionary ancestors had no experience with electric sockets or guns, so people are not prepared to become phobic of these objects even though they cause much more pain in modern society than do snakes or spiders.

Two-factor theory states that for something to cause fear, it must be paired with a painful or punishing experience. Yet people sometimes become phobic of objects or situations with which they have never had a bad experience. Indeed, many people who have never seen a live snake are afraid of snakes. Thus, there must be other ways in which fear is acquired. One of these is vicarious transmission: seeing someone act afraid of something can lead to acquiring that fear. For example, whether an infant becomes afraid of being in a high place depends on whether its mother is smiling or has an expression of fear on her face. In an ingenious set of experiments, Susan Mineka and her colleagues showed that vicarious transmission of fear is influenced by preparedness. She showed that rhesus monkeys that watched a videotape of other monkeys acting afraid of a snake became afraid of snakes themselves. Monkeys that watched other monkeys act afraid of rabbits, however, did not become afraid of rabbits because they were not evolutionarily prepared to fear rabbits. Human beings also can acquire fear by being told that something is dangerous. Children can learn to avoid running in front of oncoming cars by being told not to do this by their parents; luckily, they does not have to be hit by a car or watch someone get hit to acquire this information.

Treating Anxiety

All theories of anxiety disorders attempt to explain and organize what is known about fear and anxiety. Some of the theories, including the ones described here, also have been applied in developing treatments for anxiety disorders. As might be expected, clinical psychologists with very different ideas about the cause of anxiety will recommend very different treatments to eliminate it.

In the case of Little Hans, Freud thought that his anxiety about horses was caused by repressed sexual impulses toward his mother and hatred of his father. From this, it follows that these repressed impulses would need to be brought out into the open and resolved before his anxiety about horses would diminish. This was the basic goal of the psychoanalytic therapy Freud recommended for Hans.

On the other hand, if Little Hans’s parents had taken him to
behavioral therapy, the therapist would have assumed that the child’s fear stemmed from a fright he suffered in the presence of a horse. In fact, Freud stated that the phobia began when Hans saw a horse fall while pulling a bus. Further, the therapist would assume that now Hans was rewarded for avoiding horses by anxiety reduction and by getting extra attention from his parents. Treatment would involve having the boy gradually think about, look at, and even pet horses, and it would include being rewarded for approaching (rather than avoiding) horses.

Presented with these vastly different theories and treatments, the question arises: which is right? The theoretical issues are still debated, but it is clear that treatments based on a behavioral model of anxiety have been much more successful in reducing fear than have treatments based on the theories of Freud or his followers.

Cognitive Theories

Cognitive theories of anxiety also illustrate how theory is applied to develop a treatment. There are many different cognitive models of anxiety, but all are similar in that they assume that there is a cognitive cause of the fear state. This cognitive step is sometimes called an "irrational belief." A cognitive theorist might explain Little Hans’s fear in the following way: Hans is afraid of horses because he has some irrational belief that horses are dangerous. The specific belief might be “The horse will bite me,” or “The horse might get spooked and run into me,” or even “Horses have germs, and if I go near one, I’ll catch its germs and get sick.” The theory assumes that anxiety will stop when the irrational belief is eliminated. Thus, a cognitive therapist would first carefully question Hans to find out the specific irrational belief causing his fear. Once that is determined, the therapist would use persuasion, logical reasoning, and evidence to try to change the belief. (Little Hans was used here only to continue with the same example. A therapist probably would not try to reason with a five-year-old, and a different treatment would be used. Cognitive therapies are more commonly used with adults.)

Physiological Theories

Physiological theories of anxiety are increasing in importance. As with behavioral, psychodynamic, and cognitive theories, there are many physiological theories. They differ with respect to the brain areas, pathways, or chemicals implicated in anxiety. It is likely that many physiological theories contain an element of truth. Anxiety is a complex state, involving multiple interacting parts of the nervous system, and it will take much additional research to develop a complete model of the brain’s role in anxiety.

One physiological variable that has been integrated into many theories of anxiety is the panic attack. This is a sudden and usually short-lived attack that includes trouble with breathing, heart palpitations, dizziness, sweating, and fear of dying or going crazy. These attacks appear purely physiological at first in that they seem to come “out of the blue”; however, psychological factors determine whether they progress into a full-blown disorder. People can become anxious about having panic attacks, and this added anxiety leads to more attacks, producing panic disorder. Some people become afraid of having an attack in a place where they will be unable to cope or receive help. These people may progressively avoid more and more places. This is known as agoraphobia, which at its worst can result in people who are afraid to leave their homes.

The development of physiological theories also illustrates an important point in the relationship between theory and therapy. Thus far, it has been stressed that theories of anxiety help determine treatment. This relationship also works in reverse: success or failure of treatments adds information used in theory development. This is most clear in physiological theories. For example, the physiological mechanisms of different types of anxiety-reducing tranquilizers have been investigated to provide clues as to how the brain is involved in anxiety.

Impact on Field of Psychology

Just as most theories in psychology have a view of anxiety, anxiety is an important concept in many areas of psychology. Obviously, anxiety is very important in the fields of psychopathology and psychotherapy. It also has been very important in learning theory; experiments with conditioned fear have advanced knowledge about Pavlovian and operant conditioning. Anxiety is also an important trait in theories of personality, and it figures in theories of motivation. It might be said that anxiety is everywhere in psychology.

Theoretical developments in anxiety have been incorporated into other areas of psychology. For example, in the early 1960s, Peter Lang described fear and anxiety as being composed of three systems—that is, there are three systems in which fear is expressed: verbal (saying “I’m anxious”), behavioral (avoiding or running away from a feared object), and physiological (experiencing an increase in heart rate or sweating). An important point in understanding the three systems of fear is that the systems do not always run along parallel tracks. A person may speak of being anxious about the condition of the world environment without any physiological arousal. Alternatively, a boy’s heart might pound at the sight of a snake in the woods, but he reports no fear and does not run away in the presence of his friends. Describing fear in a three-systems framework presents an important challenge to any theory of anxiety. An adequate theory must explain why the three systems sometimes give the same information and sometimes do not. The three-systems approach not only has been very influential in anxiety theory and research, but also has been applied to many other areas of psychology, such as studying emotion, stress, and pain. This approach is an important concept in behavioral formulations of anxiety, stating that anxiety has behavioral, physiological, and verbal components and that they do not necessarily provide the same information.

Another major challenge for theories of anxiety is to begin to integrate different positions. The present theories are not all mutually exclusive. The fact that a behavioral theory of anxiety has some validity does not mean that cognitive approaches are wrong. Also, psychological theories need to be integrated with physiological theories that describe brain activity during anxiety. Although theory and research in anxiety has a long and fruitful history, there is much work to be done, and many important developments lie ahead.

Bibliography

Antony, Martin M., Susan M. Orsillo, and Lizabeth Roemer, eds. Practitioner’s Guide to Empirically Based Measures of Anxiety. New York: Kluwer Academic, 2002. Print.

"Anxiety Disorders." Psychiatry.org. Amer. Psychiatric Assn., 2014. Web. 25 Feb. 2014.

Barlow, David H. Anxiety and Its Disorders: The Nature and Treatment of Anxiety and Panic. 2nd ed. New York: Guilford, 2004. Print.

Freud, Sigmund. “Analysis of a Phobia in a Five-Year-Old Boy.” The Standard Edition of the Complete Psychological Works of Sigmund Freud. Ed. James Strachey. Vol. 10. London: Hogarth, 1955. Print.

Freud, Sigmund. “Inhibition, Symptoms, and Anxiety.” The Standard Edition of the Complete Psychological Works of Sigmund Freud. Ed. James Strachey. Vol. 20. London: Hogarth, 1959. Print.

Hall, Kirsty. The Stuff of Dreams: Fantasy, Anxiety, and Psychoanalysis. London: Karnac, 2007. Print.

Kase, Larina, and Deborah Roth Ledley. Anxiety Disorders. Hoboken: Wiley, 2007. Print.

Marks, Isaac Meyer. Living with Fear: Understanding and Coping with Anxiety. 2nd ed. New York: McGraw-Hill, 2001. Print.

Scholten, Amy. "Anxiety Disorders." Health Library. EBSCO Information Services, 26 Sept. 2012. Web. 25 Feb. 2014.

Stahl, Stephen M., and Bret A. Moore, eds. Anxiety Disorders: A Guide for Integrating Psychopharmacology and Psychotherapy. New York: Routledge, 2013. Print.

Stein, Dan J., Eric Hollander, and Barbara Rothbaum. Textbook of Anxiety Disorders. 2nd ed. Washington, DC: American Psychiatric, 2009. Print.

Storch, Eric A., and Dean McKay, eds. Handbook of Treating Variants and Complications in Anxiety Disorders. London: Springer, 2013. Print.

Tuma, A. Hussain, and Jack D. Maser, eds. Anxiety and the Anxiety Disorders. New York: Erlbaum, 1985. Print.

Wolpe, Joseph, and Stanley Rachman. “Psychoanalytic 'Evidence': A Critique Based on Freud’s Little Hans.” Journal of Nervous and Mental Disease 131.2 (1960): 135–48. Print.

What food item became currency for the trade system among the confederate prisoners?

Most people don't consider rats a food item, but if they were among the over 400,000 soldiers held prisoner during the U.S. Civil War, they might change their mind. Desperation led to desperate schemes in POW camps in both the North and the South. One soldier at  Camp Lawton, near Millen, Georgia, wrote that prisoners were “obsesses with food, sometimes consuming rats or boiling grass to ward off scurvy” (quoted in CNN.com/us/civil war/150th anniversary-prisons).

Of all the prison camps, Andersonville Prison in the Confederate State of Georgia is the most well known, and it was considered the worst of all camps. About 45,000 soldiers went through Andersonville. The peek population, in a prison built to house only 10,000, was over 33,000. And when the prisoner swap between the Northern and Southern Armies stopped because the South refused to exchange “negro troops the same as white soldiers,” the overcrowded conditions continued (civilwar.org). Food was scarce for everyone in the prisons, prisoners and guards alike. However, the guards were fed more of the scarce rations than the prisoners, so prisoners ate whatever they could find — including rats. Lack of adequate food, medical care, and sanitation took the lives of many at the Andersonville Prison Camp.

Overcrowding was an issue in almost all prison camps during the war, in both the North and the South. Thus, insufficient food was also a problem for overcrowded Northern POW camps. The Elmira Camp in the Union State of New York, with barracks space for only 5,000, had 12,000 prisoners residing there between July 6,1864, and July 11,1865. Hence, the prisoners in Northern camps also ate whatever they could find. Rats were a big problem at the camps, so the Elmira Camp officials used a small dog to catch rats that they then sold to prisoners for 5 cents. Most of the Confederate soldiers could not afford the 5 cents, though, leading two Elmira prisoners to capture the dog and cook it. They were, of course, sent to the guardhouse for 30 days for punishment.

Countless soldiers on both sides died from malnutrition and disease, especially since there was little medical care available. At Elmira about one-fourth (3,000) of the prisoners died. At Andersonville, over 12,000 died (almost as many as the whole prison population at Elmira). Approximately 56,000 deaths, nearly 10% of the total Civil War death toll, were due to the horrible conditions in prison camps.

What is the relationship between birds and infectious disease?

Definition

Wild and domestic birds are at risk for infections with pathogens
that may lead to disease in other birds and in humans. Each type of bird may carry
infections that lead to different clinical diseases. Wild birds have adapted to
urban environmental settings, increasing the risk of domestic infections.

Even though infections may be spread from birds to humans, a resulting human illness is rare. Newborns, young children, and immunocompromised persons are at greatest risk for disease transmission.

Avian Flu

Avian
flu, or bird flu, is typically found in asymptomatic wild birds.
However, domestic birds such as farm chickens and ducks may become sick and spread the disease through saliva or
droppings. The avian flu does not pass easily from bird to human or from human to
human. Typically, the avian flu is spread to pigs and other animals that can
contract both bird and human flu strains. The bird and human flu strains combine
to form a new mutant strain to which humans are susceptible. The avian flu is
caused by strain H5N1.

Mild symptoms resemble the seasonal flu: fever, sore throat, and muscle aches. More severe symptoms include eye infection and pneumonia and other respiratory difficulties. The risk for mortality is high because humans have no immunity to the avian flu strains. More than one-half of all persons who have been diagnosed with the avian flu have died.

Certain antiviral medications are effective, but the seasonal influenza vaccine
cannot protect against avian flu. Newer vaccine combinations appear promising.

West Nile Virus

West Nile virus is a flavivirus that is spread by a mosquito that first bites an infected bird and then, newly infected, bites a
human. West Nile
virus was first documented in the United States in 1999, and
it spread rapidly. Urban communities have a higher risk than rural populations.
Symptoms may be mild, with a rash, muscle weakness, and flulike symptoms, or they
may be more severe, with meningitis, encephalitis,
or a lack of cognitive clarity.

In 2004, 2,200 human cases were reported; 73 of these cases ended in death.
Although the virus is not as prevalent in the human population now as it was
during the original outbreak, West Nile virus remains a subject of medical
research. Scientists continue to work on identifying the types of birds that carry
the disease and on what mechanism causes the disease to infect both humans and
birds. Antibiotics are not effective, and antiviral medication
trials are ongoing.

Bacterial Infections

Psittacosis
. Parrots and parakeets often carry the bacterium Chlamydophila psittaci. The disease is rare in humans; only a few hundred cases are reported each year in the United States. Veterinarians, pet-store employees, and bird owners between the age of thirty and sixty years are at greatest risk; the disease is rarely reported in children. Symptoms are usually flulike, with a cough, and are treated with antibiotics. Rarely, the presentation is more severe and includes pneumonia, infection of the heart, hepatitis, and death.

Salmonellosis. Baby chicks and ducklings often have the bacterium
Salmonella in their intestines, hence they shed it in their
droppings. Salmonella is also found on the feathers and beaks of
birds. Chicks will not typically display signs of infection. Humans may develop
salmonellosis either by holding the bird or by touching a
contaminated object. Children are at greatest risk because of their improper
handwashing technique and because of their tendency to put their fingers in their
mouths after petting birds. Persons who are immunocompromised, elderly, or
pregnant should avoid touching birds, especially chicks and ducklings.
Salmonellosis results in diarrhea, fever, stomach pain, and other flulike symptoms
within a few days of exposure. The symptoms typically resolve within one week.

Fungal Diseases

Cryptococcosis. Cryptococcosis is a disease transmitted to humans from pigeons and chickens. The fungi Cryptococcus neoformans, which causes
the disease, is found in soil droppings or in roosts, such as in attics and on
ledges. Inhaling the spores causes the disease. Infections are usually
asymptomatic or mild and include flulike symptoms, a cough, and a skin rash. In
more severe forms, infection in the lungs may spread to the central nervous system
and cause brain damage or become fatal. Cryptococcosis is treated with antifungal
medication.

Histoplasmosis. Histoplasmosis, a disease transmitted to humans commonly from pigeons, starlings, blackbirds, and bats, is caused by the fungus Histoplasma capsulatum.
Humans may contract the disease by inhaling air near affected soil, near roosts
that have been maintained for several years, or near droppings (from bats). The
spores may be airborne too and can travel great distances. Construction workers,
gardeners, and those in other outdoor occupations
are at highest risk because of the disruption of soil at work sites.
Infections are typically mild with flulike symptoms. Rarely, the infection may
lead to fever, blindness, and death. Young children, the elderly, and persons with
lung disease are at greatest risk for these more significant symptoms.

Impact

Perhaps the greatest impact to global public health and the world economy can be found in the experiences of the bird flu pandemic of 1997. For example, government officials in Hong Kong who feared outbreaks and a significant number of deaths had ordered the slaughter of all poultry in that region (about 1.5 million birds) within three days. This slaughter led to economic problems in Hong Kong and elsewhere. The virus spread rapidly to other Asian countries, and with bird migration, the disease spread to Europe.

Continuing research into vaccines and proper education about bird handling and care are vital to reducing the amount of human infections and preventing avian-disease-related pandemics. However, a balance should exist between preserving the wild and domestic bird populations and protecting humans.

Bibliography

Clark, Larry, and Jeffrey Hall. “Avian Influenza in Wild Birds: Status as Reservoirs and Risks to Humans and Agriculture.” In Current Topics in Avian Disease Research: Understanding Endemic and Invasive Diseases, edited by Rosemary K. Barraclough. Washington, D.C.: American Ornithologists’ Union, 2006. A good outline of the problem. Also considers human health, agricultural concerns, and the potential effect on wild bird populations.

Krauss, Hartmut, et al. Zoonoses: Infectious Diseases Transmissible from Animals to Humans. 3d ed. Washington, D.C.: ASM Press, 2003. Explores the myriad infections introduced by human-animal contact.

Ligon, B. “Avian Influenza Virus H5N1: A Review of Its History and Information Regarding Its Potential to Cause the Next Pandemic.” Seminars in Pediatric Infectious Diseases 16 (2005): 326-335. Examines the history of the bird flu and its possible future effects on global health.

Marquardt, William C., ed. Biology of Disease Vectors. 2d ed. New York: Academic Press/Elsevier, 2005. A biology text examining disease vectors, including bats and wild and domestic birds. Written for graduate students and researchers, but accessible to general readers.

National Association of State Public Health Veterinarians. “Compendium of Measures to Control Chlamydophila psittaci Infection Among Humans (Psittacosis) and Pet Birds (Avian Chlamydiosis).” 2010. Available at http://www.nasphv.org/documents/psittacosis.pdf.

Thomas, Nancy J., D. Bruce Hunter, and Carter T. Atkinson, eds. Infectious Diseases of Wild Birds. Ames, Iowa: Blackwell, 2007. A detailed description of the health risks to birds, other animals, and humans from avian-related infectious diseases.

What are logic and reasoning?

Introduction

Logical and reasoning tasks are typically classified as either deductive or inductive. In deductive reasoning, if the premises are true and a valid rule of inference is used, the conclusion must be true. In inductive reasoning, in contrast, the conclusion can be false even if the premises are true. In many cases, deductive reasoning also involves moving from general principles to specific conclusions, while inductive reasoning involves moving from specific examples to general conclusions.

Cognitive psychologists study deductive reasoning by examining how people reason using syllogisms, logical arguments comprising a major and a minor premise that lead to a conclusion. The premises are assumed to be true; the validity of the conclusion depends on whether a proper rule of inference is used. The classic example of deduction is as follows:
All men are mortal.



Socrates is a man.


Socrates is a mortal.

A more modern (and more controversial) example of deduction might be:
Abortion is murder.



Murder should be illegal.


Abortion should be illegal.

The second example prompts a distinction between “truth” and “validity.” Even though the second syllogism is logically valid, it may or may not be true. Broadly speaking, truth refers to content (that is, applicability of the conclusion to the real world), and validity refers to form (that is, whether the conclusion is drawn logically). It is thus possible to have a valid argument that is nevertheless untrue. For a clearer example, consider this syllogism:
All dinosaurs are animals.



All animals are in zoos.


All dinosaurs are in zoos.

The conclusion is valid but is not true, because one of the premises (all animals are in zoos) is not true. Even though a valid rule of inference was applied and a valid conclusion was drawn, the conclusion is not true. If a valid conclusion has been drawn from true premises, however, the argument is called “sound.”

With inductive reasoning, the validity of the conclusion is less certain. The classic example of induction is as follows:

Every crow I have seen in my life up to this time has been black.


All crows are black.

Other examples of induction include a child who begins to say “goed” (from “go”) instead of “went,” a detective piecing together evidence at the scene of a crime, and a stock analyst who, after observing that prices have fallen during the past two Septembers, urges clients to sell in August. In all these cases, a conclusion is drawn based on evidence observed before the conclusion. There remains the possibility, however, that additional evidence may render the conclusion incorrect. It does not matter how many positive instances (for example, black crows, September stock declines) have been observed; if one counterexample can be found (a white crow, a September stock rise), the conclusion is incorrect.

Heuristics

The study of induction spans a variety of methods and topics. In this article, most of the consideration of induction involves cases in which people rely on heuristics
in their reasoning. Heuristics involve rules of thumb that yield ballpark solutions that are approximately correct and can be applied across a wide range of problems.

One common heuristic is representativeness, which is invoked in answering the following questions: What is the probability that object A belongs to class B, event A originates from process B, or that process B will generate event A? The representativeness heuristic suggests that probabilities are evaluated by the degree to which A is representative of B, that is, by the degree to which A resembles B. If A is representative of B, the probability that A originates from B is judged to be high; if A does not resemble B or is not similar to B, the probability that A originates from B is judged to be low.

A second heuristic is availability, which is invoked in judgments of frequency; specifically, people assess the frequency of a class by the ease with which instances of that class can be brought to mind. Factors that influence the ability to think of instances of a class, such as recency, salience, number of associations, and so forth, influence availability in such a way that certain types of events (such as recent and salient) are more available. For example, if several people one knows have had car accidents recently, one’s subjective probability of being in a car accident is increased.

Rules of Inference

Before examining how people reason deductively, two rules of inference must be considered: modus ponens (the “method of putting,” which involves affirming a premise) and modus tollens (the “method of taking,” which involves negating a premise). Considering P and Q as content-free abstract variables (much like algebraic variables), modus ponens states that given “P implies Q” and P, one can infer Q. In the following example, applying modus ponens to 1 and 2 (in which P is “it rained last night” and Q is “the game was canceled”), one can infer 3.
1. If it rained last night, then the game was canceled.


2. It rained last night.


3. The game was canceled.

Modus tollens states that given “P implies Q” and ~Q (read “not Q”; “~” is a symbol for negation), one can infer “~P.” Applying modus tollens to 1 and 4, one can infer 5.
4. The game was not canceled.


5. It did not rain last night.

In general, people apply modus ponens properly but do not apply modus tollens properly. In one experiment, four cards showing the following letters or numbers were placed in front of subjects:
E K 4 7

Subjects saw only one side of each card but were told that a letter appeared on one side and a number on the other side. Subjects judged the validity of the following rule by turning over only those cards that provided a valid test: If a card has a vowel on one side, then it has an even number on the other side. Turning over E is a correct application of modus ponens, and turning over 7 is a correct application of modus tollens (consider P as “vowel on one side” and Q as “even number on the other side”). Almost 80 percent of subjects turned over E only or E and 4, while only 4 percent of subjects chose the correct answer, turning over E and 7. While many subjects correctly applied modus ponens, far fewer correctly applied modus tollens. Additionally, many subjects turned over 4, an error called affirmation of the consequent.

When stimuli are concrete, reasoning improves. In an analogous experiment, four cards with the following information were placed before subjects:
beer Coke 16 22

One side of each card showed a person’s drink; the other side showed a person’s age. Subjects evaluated this rule: If a person is drinking beer, that person must be at least nineteen. In this experiment, nearly 75 percent of the subjects made the correct selections, showing that in some contexts people are more likely to apply modus tollens properly.

When quantifiers such as “all,” “some,” and “none” are used within syllogisms, additional errors in reasoning occur. People are more likely to accept positive conclusions to positive premises and negative conclusions to negative premises, negative conclusions if premises are mixed, a universal conclusion if premises are universal (all or none), a particular conclusion if premises are particular (some), and a particular conclusion if one premise is general and the other is particular. These observations led to the atmosphere hypothesis, which suggests that the quantifiers within the premises create an “atmosphere” predisposing subjects to accept as valid conclusions that use the same quantifiers.

Influence of Knowledge and Beliefs

Prior knowledge or beliefs can influence reasoning if people neglect the form of the argument and concentrate on the content; this is referred to as the belief-bias effect. If a valid conclusion appears unbelievable, people reject it, while a conclusion that is invalid but appears believable is accepted as valid. Many people accept this syllogism as valid:
All oak trees have acorns.



This tree has acorns.


This tree is an oak tree.

Consider, however, this logically equivalent syllogism:
All oak trees have leaves.



This tree has leaves.


This tree is an oak tree.

In the first syllogism, people’s knowledge that only oak trees have acorns leads them to accept the conclusion as valid. In the second syllogism, people’s knowledge that many types of trees have leaves leads them to reject the conclusion as invalid.

Biases in Reasoning

A common bias in inductive reasoning is the confirmation bias, the tendency to seek confirming evidence and not to seek disconfirming evidence. In one study, subjects who were presented with the numbers (2, 4, 6) determined what rule (concept) would allow them to generate additional numbers in the series. In testing their hypotheses, many subjects produced series to confirm their hypotheses—for example, (20, 22, 24) or (100, 102, 104)—of “even numbers ascending by 2,’’ but few produced series to disconfirm their hypotheses—for example, (1, 3, 5) or (20, 50, 187). In fact, any ascending series (such as 32, 69, 100,005) would have satisfied the general rule, but because subjects did not seek to disconfirm their more specific rules, they did not discover the more general rule.

Heuristics also lead to biases in reasoning. In one study, subjects were told that bag A contained ten blue and twenty red chips, while bag B contained twenty blue and ten red chips. On each trial, the experimenter selected one bag; subjects knew that bag A would be selected on 80 percent of the trials. The subject drew three chips from the bag and reasoned whether A or B had been selected. When subjects drew two blues and one red, all were confident that B had been selected. If the probability for that sample is actually calculated, however, the odds are 2:1 that it comes from A. People chose B because the sample of chips resembles (represents) B more than A, and they ignored the prior probability of 80 percent that the bag was A.

In another experiment, subjects were shown descriptions of “Linda” that made her appear to be a feminist. Subjects rated the probability that Linda was a bank teller and a feminist higher than the probability that Linda was a bank teller. Whenever there is a conjunction of events, however, the probability of both events is less than the probability of either event alone, so the probability that Linda was a bank teller and a feminist was actually lower than the probability that she was only a bank teller. Reliance on representativeness leads to overestimation of the probability of a conjunction of events.

Reliance on representativeness also leads to the gambler’s fallacy. This fallacy can be defined as the belief that if a small sample is drawn from an infinite and randomly distributed population, that sample must also appear randomly distributed.

Consider a chance event such as flipping a coin (H represents “heads,” T represents “tails”). Which sequence is more probable: HTHTTH or HHHHHH? Subjects judge that the first sequence is more probable, but both are equally probable. The second sequence, HHHHHH, does not appear to be random, however, and so is believed to be less probable. After a long run of H, people judge T as more probable than H because the coin is “due” for T. A problem with the idea of “due,” though, is that the coin itself has no memory of a run of H or T. As far as the coin is concerned, on the next toss there is 0.5 probability of H and 0.5 probability of T. The fallacy arises because subjects expect a small sample from an infinitely large random distribution to appear random. The same misconceptions are often extended beyond coin-flipping to all games of chance.

In fallacies of reasoning resulting from availability, subjects misestimate frequencies. When subjects estimated the proportion of English words beginning with R versus words with R as the third letter, they estimated that more words begin with R, but, in fact, more than three times as many words have R as their third letter. For another example, consider the following problem. Ten people are available and need to be organized into committees. Can more committees of two or more committees of eight be organized? Subjects claimed that more committees of two could be organized, probably because it is easier to visualize a larger number of committees of two, but equal numbers of committees could be made in both cases. In both examples, the class for which it is easier to generate examples is judged to be the most frequent or numerous. An additional aspect of availability involves causal scenarios (sometimes referred to as the simulation heuristic), stories or narratives in which one event causes another and which lead from an original situation to an outcome. If a causal scenario linking an original situation and outcome is easily available, that outcome is judged to be more likely.

Evolution of Study

Until the twentieth century, deductive logic and the psychology of human thought were considered to be the same topic. The mathematician George Boole
entitled his 1854 book on logical calculus An Investigation of the Laws of Human Thought. This book was designed “to investigate the fundamental laws of those operations of the mind by which reasoning is performed.” Humans did not always seem to operate according to the prescriptions of logic, but such lapses were seen as the malfunctioning of the mental machinery. When the mental machinery functioned properly, humans were logical. Indeed, it is human rationality, the ability to think logically, that for many thinkers throughout time has separated humans from other animals (for example, Aristotle’s man as rational animal) and defined the human essence (for example, René Descartes’s “I think, therefore I am”).

As a quintessential mental process, the study of reasoning is an integral part of modern cognitive psychology. In the mid-twentieth century, however, when psychology was in the grip of the behaviorist movement, little attention was given to such mentalistic conceptions, with the exception of isolated works such as Frederic C. Bartlett’s studies of memory and Jerome Bruner, Jacqueline J. Goodnow, and George A. Austin’s landmark publication A Study of Thinking (1956), dealing with, among other topics, induction and concept formation. The development of the digital computer and the subsequent application of the computer as a metaphor for the human mind suggested new methods and vocabularies for investigating mental processes such as reasoning, and with the ascendancy of the cognitive approach within experimental psychology and the emergence of cognitive science, research on human reasoning has become central in attempts both to understand the human mind and to build machines that are capable of independent, intelligent action.

Involvement of Computers

In the latter part of the twentieth century, there were attempts to simulate human reasoning with computers and to develop computers capable of humanlike reasoning. One notable attempt involved the work of Allen Newell and Herbert Simon, who provided human subjects with various sorts of problems to solve. Their human subjects would “think out loud,” and transcripts of what they said became the basis of computer programs designed to mimic human problem solving and reasoning. Thus, the study of human logic and reasoning not only furthered the understanding of human cognitive processes but also gave guidance to those working in artificial intelligence. One caveat, however, is that even though such transcripts may serve as a model for computer intelligence, there remain important differences between human and machine “reasoning.” For example, in humans, the correct application of some inference rules (for example, modus tollens) depends on the context (for example, the atmosphere hypothesis or the belief-bias effect). Furthermore, not all human reasoning may be strictly verbalizable, and to the extent that human reasoning relies on nonlinguistic processes (such as imagery), it might not be possible to mimic or re-create it on a computer.

After being assumed to be logical or even being ignored by science, human reasoning is finally being studied for what it is. In solving logical problems, humans do not always comply with the dictates of logical theory; the solutions reached may be influenced by the context of the problem, previous knowledge or belief, and the particular heuristics utilized in reaching a solution. Discovery of the structures, processes, and strategies involved in reasoning promises to increase the understanding not only of how the human mind works but also of how to develop artificially intelligent machines.

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What is a Gamma Knife?

Cancers treated:
Brain tumors, cancerous tumors that originate elsewhere in the body but have spread to the brain

Why performed: Gamma Knife “surgery” is a noninvasive alternative to traditional open-brain surgery. The precisely focused radiation beams of the Gamma Knife allow surgeons to treat very small, deep-seated tumors without damaging nearby brain tissue.

Patient preparation: Patients should not eat or drink anything after midnight the night before the procedure. They should inform their doctor if they are taking medication to control diabetes, are allergic to shellfish or iodine, or have implanted medical devices in the body. Patients must remove glasses, contact lenses, jewelry, makeup, nail polish, wigs, and dentures.

Steps of the procedure: Surgeons apply a local anesthetic and use four screws to attach a lightweight frame to the patient’s head. The frame prevents the head from moving and allows surgeons to identify the treatment target accurately. With the head frame in place, surgeons take magnetic resonance images of the brain to establish the exact size, shape, and location of the target. From the images, surgeons develop a specific treatment plan.

For the treatment, the patient lies on a couch. A helmet is attached to the head frame. The couch slides into the Gamma Knife unit, where radiation destroys the tumor. The patient is awake during the procedure, which lasts from a few minutes to more than an hour, depending on the size and location of the tumor.

After the procedure: When the treatment is completed, the head frame is removed. In most cases, the patient goes home the same day and returns to a normal routine in a day or two.

Risks: Because surgeons make no incisions, the risk of complications from use of the Gamma Knife is low. Some patients feel minor soreness from the head frame. Temporary swelling and irritation are also possible. Some patients experience mild headache, dizziness, or nausea, which last only a short while.

The dose of radiation outside the target is very low and poses little risk. Occasionally, patients experience swelling in the brain, which is temporary and treatable.

Results: The effects of radiation treatments take time: weeks, months, or even years.

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"Gamma Knife—Cobalt-60 Therapy." American Brain Tumor Association. Amer. Brain Tumor Assn., 2014. Web. 6 Oct. 2014.

L'Annunziata, Michael F. Radioactivity: Introduction and History. Amsterdam: Elsevier, 2007. Digital file.

"Understanding Radiation Therapy." Cancer.org. Amer. Cancer Soc., 2 May 2014. Web. 6 Oct. 2014.