How was Katniss's decorating Rue's body a noble act in The Hunger Games by Suzanne Collins?

Let's try to define what a noble act is first.  A noble act is a chivalrous act.  It is an act or action in which the welfare of another person is put before the person doing the act.  The act might involve courage, but it doesn't always have to.  For example, giving up your seat on a bus for an elderly person isn't brave, but it is noble.  You are treating the person with respect...

Let's try to define what a noble act is first.  A noble act is a chivalrous act.  It is an act or action in which the welfare of another person is put before the person doing the act.  The act might involve courage, but it doesn't always have to.  For example, giving up your seat on a bus for an elderly person isn't brave, but it is noble.  You are treating the person with respect and dignity.  It might even be at your own expense, because the act might cost you time, energy, or money.

Thinking of Katniss's decoration of Rue's body as a noble act is interesting because Rue is no longer alive.  She cannot benefit from Katniss's action.  Nonetheless, Katniss's action is noble, because she is treating Rue (her body) with respect and dignity at the possible expense of her own safety.  Katniss is leaving herself vulnerable to attack and/ or wasting precious time that could be spent gathering supplies to help herself stay alive.  Katniss's act is noble because she doesn't gain anything (immediately, anyway) from it, nor does she expect to gain anything from it.  

What picture of Minnie Foster (after her marriage) does her conversation with Mrs. Peters help the reader develop? What does hiding the bird say...

Mrs. Hale is a dynamic and round character in the story "A Jury of Her Peers." Even though she always suspects something is not entirely clear at the scene of the crime, her discoveries continuously make her more sure of her assertions, and about her views on the case.

As such, she is able to create a mental tableau of the life of Minnie Wright. She already knew Minnie, whose maiden name was "Foster" before...

Mrs. Hale is a dynamic and round character in the story "A Jury of Her Peers." Even though she always suspects something is not entirely clear at the scene of the crime, her discoveries continuously make her more sure of her assertions, and about her views on the case.

As such, she is able to create a mental tableau of the life of Minnie Wright. She already knew Minnie, whose maiden name was "Foster" before Minnie married John Wright. She describes a very different person from the nervous, anxiety-ridden woman now being held at the county jail because she is expected of murdering her husband.

Mrs. Hale explains that Minnie Foster, the name she prefers to use for Minnie Wright, was a much happier woman before she married.

She used to wear pretty clothes and be lively—when she was Minnie Foster, one of the town girls, singing in the choir. But that—oh, that was twenty years ago."

Still, Mrs. Hale is able to show compassion toward the woman who now awaits her fate by a future jury of her peers; a woman who is a mere memory of who she was. She no longer has any of her former youth or beauty as a result of an unhappy and abusive marriage.

I s'pose she felt she couldn't do her part; and then, you don't enjoy things when you feel shabby.

When Mrs. Hale and Mrs. Peters discover the dead bird and busted canary cage, they are able to piece together the night's events. John Wright must have killed Minnie Foster's only source of joy, her canary, and that caused her to snap and kill him.

Because of their mutual understanding of Minnie's sad situation, Mrs. Hale and Mrs. Peters silently agree to hide the evidence of the bird. This is because it could have been used as evidence to establish a motive for murder. Since this could incriminate Minnie, and the women knew that a jury of her peers is likely to find Minnie guilty and put her to death, they choose to hide it. They believe Minnie murdering her husband was justified.

What are pancreatic cancers? |

Related conditions:
Acinar cell carcinoma, insulinoma, gastrinoma, glucoganoma

Definition:

Pancreatic cancers are malignant tumors occurring anywhere in the pancreas. The pancreas is an organ behind the stomach containing exocrine and endocrine glands. The exocrine glands, where most pancreatic cancer occurs, release digestive juices, which break down fats, proteins, and carbohydrates, and neutralize stomach acids. The endocrine glands produce insulin and glycogen, hormones used by the body to metabolize, or break down, sugar to use as energy.

Risk factors: Factors implicated in the development of pancreatic cancer include advanced age, diabetes, cigarette smoking, chronic pancreatitis, and a family history of the disease. About two-thirds of patients who develop pancreatic cancer are older than age sixty-five, according to the National Cancer Society's 2014 statistics.

Diabetes and pancreatic cancer have been linked, but it is not clear whether diabetes is a cause or a symptom of pancreatic cancer. The American Cancer Society reported in 2014 that pancreatic cancer is more common in those who have diabetes, especially in those who have type II diabetes.

According to the American Cancer Society in 2014, an estimated 20 to 30 percent of exocrine pancreatic cancer cases can be attributed to cigarette smoking. The cancer-causing chemicals in cigarette smoke are thought to enter the bloodstream and damage the pancreas, creating a two to three times greater risk among smokers.

The role of diet in developing pancreatic cancer is inconclusive, although diets high in fat and processed meats appear to present some increased risk, and diets high in fruit, vegetables, and fiber appear to protect against cancer. Obesity and lack of physical activity are also risk factors, as is occupational exposure to chemicals and pesticides.

Long-term inflammation of the pancreas, or chronic pancreatitis, is a risk factor, but the majority of people with this condition do not develop cancer of the pancreas without the presence of other risk factors. However, having a family history of pancreatitis at a young age has been implicated in the development of pancreatic cancer years later. Individuals who have had peptic ulcer surgery with a partial gastrectomy (partial removal of the stomach) may be at increased risk of developing pancreatic cancer.
Helicobacter pylori
infection also has been linked to pancreatic cancer.

According to the American Society of Clinical Oncology in 2013, the National Institutes of Health has estimated that the risk of developing pancreatic cancer is increased four to five times for someone who has a first-degree relative with the cancer. Particularly among those with two or more relatives who have had pancreatic cancer, inherited deoxyribonucleic acid (DNA) mutations are believed to play a part. People of Ashkenazi Jewish descent may be at greater risk because of the presence of an inherited mutation in the breast cancer gene BRCA2 (each individual inherits two such genes, one from the mother and one from the father). However, the presence of one defective BRCA2 does not increase an individual’s risk of developing pancreatic cancer in the absence of other genetic and environmental factors.

Further, individuals with a rare hereditary disease, Peutz-Jeghers syndrome, in which affected family members develop polyps from the surface of the intestine, may be at increased risk of developing pancreatic cancer. Individuals with hereditary nonpolyposis colorectal cancer (HNPCC) also may be at increased risk of developing cancer of the pancreas.

Etiology and the disease process: Pancreatic cancer occurs when abnormal cells grow in pancreatic tissue. The vast majority of abnormal cells occur in the ducts carrying pancreatic juices from the exocrine glands. Although the exact cause of pancreatic cancer is not known, inherited or acquired changes in DNA are believed to be behind most cases. Many pancreatic cancers are not detected until they are locally advanced and have invaded the vascular system or have spread to lymph nodes. If the tumor blocks the common bile duct and bile cannot be released into the digestive system, the patient’s skin and whites of the eyes become jaundiced and the urine may become darker. The cancer may spread and cause pain in the upper abdomen and sometimes the back.

Incidence: As of 2014, according to the National Cancer Institute, pancreatic cancer is the fourth-leading cause of cancer death in the United States because it grows aggressively and causes few symptoms in the initial stages. However, it is relatively rare compared with other forms of cancer. About 46,420 new cases were diagnosed in 2014, as compared with 232,670 new cases of breast cancer and 224,210 of lung cancer. According to the American Cancer Society, rates of pancreatic cancer increased slightly throughout the first decade of the 2000s. The National Cancer Institute reported that the incidence rate of pancreatic cancer was 12.3 per 100,000 men and women between the years of 2007 and 2011, although this type of cancer is more prevalent among men than women. The incidence of pancreatic cancer is higher in the African American population than in other racial or ethnic groups in the United States, probably because of the higher rates of obesity, poverty, cigarette smoking, and type II diabetes in this group.

Symptoms: Many people do not experience symptoms of pancreatic cancer until the tumor has spread to the lungs, liver, or lymph nodes. The majority of pancreatic cancers occur in the head of the organ, creating symptoms associated with blockage of this area closest to the bile duct. One common symptom is jaundice, a yellowing of the skin and the whites of the eyes resulting from an accumulation of bilirubin in the blood. At least half of those with pancreatic cancer will experience jaundice. Other symptoms include nausea and diarrhea, a swollen gallbladder or liver, pain in the midback, fatigue, a slow metabolism, light-colored stools, and itchy skin.

The smaller percent of pancreatic cancers occurring in the tail of the pancreas often obstruct the vein draining the spleen, resulting in an enlarged spleen and pressure in varicose veins around the stomach and esophagus. An individual may experience this as pain in the midback, pain in the stomach several hours after a meal, blood clots in the legs, and loss of appetite. Tumors or cystadenocarcinoma affecting the hormone-secreting functions of the pancreas, though rare, can produce symptoms of fatigue, dizziness, chills, diarrhea, or muscle spasms.

If the pancreatic cancer occurs in the islet cells, which produce insulin and other hormones, the cells may produce too much insulin, causing the affected individual to feel dizzy and weak and to experience chills, muscle spasms, and diarrhea. This type of endocrine pancreatic cancer is considered highly treatable.

Screening and diagnosis: A high blood level of cancer antigen 19-9 (CA 19-9), a product released into the blood by pancreatic cancer cells, serves as a marker indicating the presence of a pancreatic tumor. However, this marker is used only to assess response to therapy and not as a screening test.

Because there is no screening test for pancreatic cancer, people should report any sudden onset of abdominal pain, loss of appetite, or unexplained weight change to their physician. If pancreatic cancer is suspected, the physician will palpate for presence of an abdominal tumor and order blood tests that will indicate changes in blood sugar or the presence of anemia. However, the pancreas is hidden behind other organs and cannot be felt during a routine physical exam. A differential diagnosis should rule out any liver-related causes of jaundice.

If a pancreatic tumor is present, diagnostic tests such as ultrasound, computed tomography (CT) scans, and endoscopic retrograde cholangiopancreatography (ERCP), a type of X ray, will be ordered to stage the progression of the disease. An ultrasound has been shown to be more useful than a CT scan in detecting the presence of small tumors. A CT scan can be used to guide a needle in obtaining a biopsy. During a positron emission tomography (PET) scan, a form of sugar that is readily absorbed by cancer cells is injected into the patient’s blood to assess the location and spread of cancer cells. A combination PET/CT scan has been found useful in detecting the spread of cancer that surgery cannot remove, for staging, and even for detecting early-stage cancer. ERCP can be used to examine the pancreatic duct while a tissue biopsy is taken to study the cancer cells. An angiogram can be used to show any blockage or impediment of blood flow in vessels caused by the tumor or abnormality of blood vessels to assess the likelihood of removing the cancer surgically.

If surgery such as a laparoscopy is performed, a biopsy may be taken to determine the location and spread of the disease. Laparoscopy is a diagnostic procedure in which an incision is made in the abdomen and a laparoscope, or lighted tube, is inserted to view the pancreas. Alternatively, the physician may choose to perform a laparotomy, a diagnostic surgical procedure in which a large incision is made to examine organs in the abdomen for extent of disease.

Staging for pancreatic cancer is as follows:

• Stage IA: Tumor is confined to pancreas and is no larger than 2 centimeters (cm).





• Stage IB: Tumor is confined to pancreas and is larger than 2 cm.





• Stage IIA: Cancer has metastasized to nearby organs and tissues but not into large blood vessels or to lymph nodes.





• Stage IIB: Cancer has metastasized to nearby lymph nodes and may have spread to nearby tissues and organs but not distant sites.





• Stage III: Cancer has reached blood vessels near the pancreas and may have spread to lymph nodes but not distant sites.





• Stage IV: Cancer, regardless of tumor size, has metastasized to distant organs, and may also be in tissues near the pancreas or in lymph nodes.

Alternatively, some physicians stage the pancreatic cancer on the basis of the likelihood that the tumor can be removed surgically according to the following stages: resectable (can remove entire tumor); locally advanced, unresectable (wherein complete removal of the tumor is not possible); and metastatic (where the cancer has spread and surgery would be undertaken only to relieve symptoms or complications).

Treatment and therapy: The Whipple procedure, or pancreatectomy, a major surgery with a high risk of complications, is used when it is likely that surgery will cure the individual of the entire pancreatic tumor. The head of the pancreas and parts of the stomach and small intestine, bile duct, and gallbladder are removed. After this surgery, the pancreas is still able to produce insulin and digestive juices. A total pancreatectomy involves removal of the entire pancreas, part of the stomach and small intestine, the common bile duct, and the gallbladder, spleen, and nearby lymph nodes.

Palliative surgery may relieve pain and complications associated with the impact of the cancer on digestion, particularly blockage of the bile duct. When surgery cannot remove the entire tumor, during the course of an ERCP, a biliary stent is placed to relieve biliary obstruction and allow vessels to move bile. Inserting an endoscopic or percutaneous biliary stent can relieve jaundice, particularly for those with cancer in the head of the pancreas.

Radiation therapy may be administered five times a week for several weeks or months before surgery, after surgery, or as a primary treatment in conjunction with chemotherapy when the cancer is isolated in the pancreas but cannot be removed surgically.

Chemotherapy alone, particularly gemcitabine, is often used for palliative care of metastatic pancreatic cancer that has spread distally to other organs or body parts. Gemcitabine (Gemzar) has resulted in clinical improvement in some of these patients. The use of erlotinib (Tarceva), which stops signals that instruct cancer cells to multiply, in combination with gemcitabine has proved to be more effective than using gemcitabine alone. However, patients must be healthy and functioning well enough to be able to tolerate the side effects of chemotherapy. Common side effects of chemotherapy treatment with gemcitabine include fatigue, lowered production of blood cells, increased incidence of infection, tiredness, breathlessness, and bruising.

Ongoing clinical trials involve a vaccine for pancreatic cancer that is used to treat existing disease by causing an immune response to the pancreatic cancer.

Prognosis, prevention, and outcomes: The mortality rate for pancreatic cancer based on National Cancer Institute data collected between 2007 and 2011 is 10.9 deaths per 100,000 men and women per year. According to the American Society of Clinical Oncology's data for 2013, the overall five-year survival rates for this cancer are 6 percent. The majority of pancreatic cancers are diagnosed when they have already metastasized.

According to the American Cancer Society in 2014, the five-year survival rate following diagnosis for those with cancers of the exocrine pancreas, the most common type, is 12 to 14 percent when the cancer is localized. However, when it has spread to nearby organs and tissues, the survival rate falls to between 3 and 7 percent, and 1 percent when the cancer has spread to distant organs.

Recommendations for preventing pancreatic cancer include health education to reduce tobacco consumption and referring those at increased risk for familial reasons to genetic counseling and possibly genetic testing.

Azmi, Asfar S, ed. Molecular Diagnostics and Treatment of Pancreatic Cancer: Systems and Network Biology Approaches. London: Academic, 2014. Print.

Hassan, M. N., et al. “Risk Factors for Pancreatic Cancer: Case-Control Study.” American Journal of Gastroenterology 102.12 (2007): 2696–2707. Print.

Reber, Howard, ed. Pancreatic Cancer: Pathogenesis, Diagnosis, and Treatment. Totowa: Humana, 1998. Print.

Risch, H. A. “Etiology of Pancreatic Cancer, with a Hypothesis Concerning the Role of N-Nitroso Compounds and Excess Gastric Acidity.” Journal of the National Cancer Institute 9512 (2003): 948–960. Print.

Wiederpass, E., et al. “Occurrence, Trends and Environment Etiology of Pancreatic Cancer.” Scandinavian Journal of Environmental Health 243 (1998): 165–174. Print.

Wolfgang, Christopher L., et al. "Recent Progress in Pancreatic Cancer." CA: A Cancer Journal for Clinicians 63.5 (2013): 318–48. Print.

Yadav, Dhiraj, and Albert B. Lowenfels. "The Epidemology of Pancreatitis and Pancreatic Cancer." Gastroenterology 144.6 (2013): 1252–61. Print.

Describe the White Witch's manipulation of Edmund in The Lion, the Witch, and the Wardrobe.

I think that the White Witch's manipulation of Edmund is done in three styles.  

The first form of manipulation is addiction.  The White Witch lured Edmund to her sleigh by acting nice and friendly.  She offered him any food that he wanted, and Edmund chose Turkish Delight.  It was the best Turkish Delight he had ever had, and he ate all of it while she quizzed him up and down about his brother and sisters.  The reader is eventually told that the Turkish Delight was magic Turkish Delight that created an uncontrollable hunger for more of it. 

Probably the Queen knew quite well what he was thinking; for she knew, though Edmund did not, that this was enchanted Turkish Delight and that anyone who had once tasted it would want more and more of it, and would even, if they were allowed, go on eating it till they killed themselves.

Essentially Edmund is addicted to the Turkish delight and is willing to do anything just to get another "fix" of it.  

The second form of manipulation is done through temptation.  The White Witch offers Edmund fame, fortune, and power, if he brings Peter, Susan, and Lucy to her.  

"You are to be the Prince and - later on - the King; that is understood. But you must have courtiers and nobles. I will make your brother a Duke and your sisters Duchesses."

Of course Edmund would be tempted with that.  He would get to be king, eat more Turkish Delight, and rule over his brothers and sisters.  Edmund sees that as a win, win, win situation.  

The final form of manipulation is manipulation through fear.  During chapter eleven, Edmund witnesses the White Witch turn a group of forest animals into stone.  The sight terrifies Edmund, but he barely has enough time to consider what he just saw because the White Witch turns and hits Edmund.  She then threatens to do the same to Edmund if he tries to interfere with her again. 

"As for you," said the Witch, giving Edmund a stunning blow on the face as she re-mounted the sledge, "let that teach you to ask favour for spies and traitors. Drive on!"

At the very end of the chapter, she threatens to kill Edmund.  Edmund has no other choice than to obey.  

What is glutathione as a therapeutic supplement?

Overview

Dangerous naturally occurring substances in the body called free radicals
pose a risk to many tissues. The body deploys an antioxidant defense system to
hold free radicals in check. Glutathione, a protein made from the amino acids
cysteine, glutamic acid, and glycine, is one of the most important elements of
this system.

Glutathione does much of its work in the liver, although it is also found elsewhere in the body. Besides fighting free radicals, it helps keep various essential biological molecules in a chemical state called reduced (as opposed to oxidized). In addition, glutathione can act on toxins such as pesticides, lead, and dry cleaning solvents, transforming them in such a way that the body can excrete them more easily.

Nutrients such as vitamin C and vitamin E
also help neutralize free radicals. In the 1990s, such antioxidant supplements
were widely promoted for preventing a variety of diseases, including cancer and
heart disease. During this period, oral glutathione became popular as an
additional antioxidant supplement. Glutathione is not absorbed when taken by
mouth, so such supplements are almost certainly useless. It may be possible,
however, to raise glutathione levels in the body by taking other supplements, such
as vitamin C, cysteine, lipoic acid, and N-acetylcysteine. Whether doing so would offer any health
benefits remains unclear.

Requirements and Sources

There is no dietary requirement for glutathione. The body makes it from scratch, utilizing vitamins and common amino acids found in food. Glutathione levels in the body are reduced by cigarette smoking. Various diseases are associated with reduced levels of glutathione, including cancer, cataracts, diabetes, and human immunodeficiency virus (HIV) infection.

Therapeutic Dosages

A typical recommended dose of oral glutathione is 50 milligrams twice daily. However, as noted above, when glutathione is taken by mouth it is destroyed. Therefore, no matter what the dose, it will not make any difference. It is possible that some glutathione may be absorbed if it is held in the mouth and allowed to dissolve, but this has not been well studied.

A more promising method for raising glutathione levels in the body involves
taking supplemental cysteine or antioxidant supplements. Evidence
suggests that cysteine (often supplied in the form of whey protein, which is high
in cysteine) can raise glutathione levels in people with cancer, hepatitis, or
HIV.

In addition, because vitamin C has overlapping functions with glutathione,
vitamin C supplements may spare some of the body’s glutathione from being used up,
thereby increasing its levels in the body. The antioxidant supplement lipoic acid
appears to raise glutathione levels as well. Other supplements that might raise
glutathione levels include N-acetylcysteine, glutamine,
methionine, and S-adenosyl methionine (SAMe).

Therapeutic Uses

Various Web sites promote glutathione for a wide variety of health problems, from preventing aging to enhancing sports performance. However, oral glutathione supplements are almost certainly useless for any condition, since they are not absorbed.

There is a bit of evidence that injected glutathione might offer a few health benefits, such as preventing blood clots during surgery, reducing the side effects and increasing the effectiveness of cancer chemotherapy drugs such as cisplatin, treating male infertility, and alleviating symptoms of early Parkinson’s disease. Although oral glutathione is not likely to provide the same benefits, it is at least theoretically possible that taking the nutrients described in the previous section (and thereby raising glutathione levels indirectly) could offer similar benefits. However, there is no direct evidence to indicate that this hypothesis is true.

Safety Issues

Oral glutathione should be entirely safe, since it is not absorbed.

Bibliography

Bharath, S., et al. “Glutathione, Iron, and Parkinson’s Disease.” Biochemical Pharmacology 64 (2002): 1037-1048.

Bounous, G. “Whey Protein Concentrate (WPC) and Glutathione Modulation in Cancer Treatment.” Anticancer Research 20 (2000): 4785-4792.

De Rosa, S. C., et al. “N-Acetylcysteine Replenishes Glutathione in HIV Infection.” European Journal of Clinical Investigation 30 (2000): 915-929.

Droge, W., and R. Breitkreutz. “Glutathione and Immune Function.” Proceedings of the Nutrition Society 59 (2000): 595-600.

Hultberg, B., et al. “Lipoic Acid Increases Glutathione Production and Enhances the Effect of Mercury in Human Cell Lines.” Toxicology 175 (2002): 103-110.

Lenzi, A., et al. “Lipoperoxidation Damage of Spermatozoa Polyunsaturated Fatty Acids (PUFA): Scavenger Mechanisms and Possible Scavenger Therapies.” Frontiers in Bioscience 5 (January, 2000): E1-E15.

Packer, L., et al. “Molecular Aspects of Lipoic Acid in the Prevention of Diabetes Complications.” Nutrition 17 (2001): 888-895.

Describe how Holden feels in Mr. and Mrs. Spencer's house?

Holden is not very comfortable to be in the Spencer home. He's glad that he isn't out in the frozen world, but he feels depressed and anxious to be around sick and old people. Holden behaves properly, though. For being on edge and uncomfortable, he keeps his speech and behavior respectful. When Mr. Spencer reads his history report out loud, Holden feels embarrassed and ashamed because he didn't do a very good job with it. He...

Holden is not very comfortable to be in the Spencer home. He's glad that he isn't out in the frozen world, but he feels depressed and anxious to be around sick and old people. Holden behaves properly, though. For being on edge and uncomfortable, he keeps his speech and behavior respectful. When Mr. Spencer reads his history report out loud, Holden feels embarrassed and ashamed because he didn't do a very good job with it. He also feels a little disrespected that Mr. Spencer would embarrass him like that. Holden says the following about how he is treated by Mr. Spencer:

"He put my goddam paper down then and looked at me like he'd just beaten hell out of me in Ping-Pong or something. I don't think I'll ever forgive him for reading me that crap out loud" (12).

Again, Holden keeps his thoughts to himself and doesn't disrespect the old and sickly Mr. Spencer after he feels disrespected. Holden understands that Mr. Spencer is doing his best to help him, but it isn't a very nice experience for him.

What is elephantiasis? |

Causes and Symptoms

Elephantiasis is characterized by gross enlargement of a body part caused by the accumulation of fluid and connective tissue. It most frequently affects the legs but may also occur in the arms, breasts, scrotum, vulva, or any other body part. The disease starts with the slight enlargement of one leg or arm (or other body part). The limb increases in size with recurrent attacks of fever. Gradually, the affected part swells, and the swelling, which is soft at first, becomes hard following the growth of connective tissue in the area. In addition, the skin over the swollen area changes so that it becomes coarse and thickened, looking almost like elephant hide. The elephant-like skin, along with the enlarged body parts, gave the disease the name elephantiasis.

Elephantiasis is found worldwide, mostly in the tropics and subtropics. About 90 percent of cases of elephantiasis are a result of infection with a parasitic worm called Wuchereria bancrofti (W. bancrofti). W. bancrofti belongs to a group of
worms called filaria, or roundworms, and infection with a filarial worm is called filariasis. Filariasis caused by W. bancrofti is the most common and widespread type of human filarial infection and is often called Bancroft’s filariasis; filarial infections that can cause elephantiasis are known in general as lymphatic filariasis. Elephantiasis is the advanced, chronic stage of lymphatic filariasis, and only a small percentage of persons with the infection will develop elephantiasis. During Bancroft’s filariasis, adult forms of W. bancrofti live inside the human lymphatic system, and it is the person’s reaction to the presence of the worm that causes the symptoms of the disease. The worm’s life cycle is important in understanding how the disease is transmitted from one person to another, how the symptoms develop, and how to prevent and reduce the incidence of the disease.

The adult worms live in human lymphatic vessels and lymph nodes and measure about 4 centimeters in length for the male and 9 centimeters in length for the female. Both are threadlike and about 0.3 millimeters in diameter. After mating, the female releases large numbers of embryos or microfilariae (microscopic roundworms), which are more than one hundred times smaller in length and ten times thinner than their parents. They make their way from the lymphatic system into the bloodstream, where they can circulate for two years or longer. Interestingly, most strains of microfilariae exhibit a nocturnal periodicity, in which they appear in the peripheral blood system (the outer blood vessels, such as those in the arms, legs, and skin) only at night, mostly between the hours of 10 p.m. and 2 a.m., and spend the remainder of the time in the blood vessels of the lungs and other internal organs. This nighttime cycling into the peripheral blood is somehow related to the patient’s sleeping habits, and although it is unknown exactly how or why the microfilariae do this, it is necessary for the survival of the worms. The microfilariae must develop through at least three different stages (called the first, second, and third larval stages) before they are ready to mature into adults; these stages take place not within humans but within certain types of mosquitoes, which bite at night. Thus, the microfilariae appear in the peripheral blood just in time for the mosquitoes to bite an infected human and extract them so that they can continue their life cycle. It is important to note, therefore, that both humans and the proper type of mosquito are needed to keep a filariasis infection going in a particular area.

Female night-feeding
mosquitoes of the genera Culex, Aedes, and Anopheles serve as intermediate hosts for Wuchereria bancrofti. The mosquitoes bite an infected person and ingest microfilariae from the peripheral blood. The microfilariae pass into the intestines of the mosquito, invade the intestinal wall, and within a day find their way to the thoracic
muscles (the muscles in the middle part of the mosquito’s body). There they develop from first-stage to third-stage larvae in about two weeks, and the new third-stage larvae move from the thoracic muscles to the head and mouth of the mosquito. Only the third-stage larvae are able to infect humans successfully, and the third stage can mature only inside humans. When the mosquito takes a blood meal, infective larvae make their way through the proboscis (the tubular sucking organ with which a mosquito bites a person) and enter the skin through the
puncture wound. After they enter the skin, the larvae move by an unknown route to the lymphatic system, where they develop into adult worms. It takes about one year or longer for the larvae to grow into adults, mate, and produce more microfilariae.

A person contracts Bancroft’s filariasis by being bitten by an infected mosquito. Various forms of the disease can occur, depending on the person’s immune response and the number of times the person is bitten. The period of time from when a person is first infected with larvae to the time microfilariae appear in the blood can be between one and two years. Even after this time some persons, especially young people, show no symptoms at all, yet they may have numerous microfilariae in their blood. This period of being a carrier of microfilariae without showing any signs of disease may last several years, and such carriers act as reservoirs for infecting the mosquito population.

In those patients showing symptoms from the infection, there are two stages of the disease: acute and chronic. In acute disease, the most common symptoms are a recurrent fever and lymphangitis or lymphadenitis in the arms, legs, or genitals. These symptoms are caused by an inflammatory response to the adult worms trapped inside the lymphatic system. Lymphangitis, an inflammation of the lymph vessels, is characterized by a hard, cordlike swelling or a red superficial streak that is tender and painful. Lymphadenitis is characterized by swollen and painful lymph nodes. The attacks of fever and lymphangitis or lymphadenitis recur at irregular intervals and may last from three weeks up to three months. The attacks usually become less frequent as the disease becomes more chronic. In the absence of reinfection, there is usually a steady improvement in the victim, each relapse being milder. Thus, without specific therapy, this condition is self-limiting and presumably will not become chronic in those acquiring the infection during a brief visit to an area where the disease is endemic.

The most obvious symptoms caused as a result of W. bancrofti infection, such as elephantiasis, are noted in the chronic stage. Chronic disease occurs only after years of repeated infection with the worms. It is seen only in areas where the disease is endemic and only occurs in a small percentage of the infected population. The symptoms are the result of an accumulation of damage caused by inflammatory reactions to the adult worms. The inflammation causes tissue death and a buildup of scar tissue that eventually results in the blockage of the lymphatic vessels in which the worms live. One of the functions of lymphatic vessels is to carry excess fluid away from tissues and bring it back to the blood, where it enters the circulation again as the fluid portion of the blood. If the lymphatic vessels are blocked, the excess fluid stays in the tissues, and swelling occurs. When this swelling is extensive, grotesque enlargement of that part of the body occurs.

Treatment and Therapy

One way in which doctors can tell whether a person has Bancroft’s filariasis is by taking a sample of peripheral blood at night and looking at the blood under a microscope to try to find microfilariae. Sometimes, the ability to find microfilariae is enhanced by filtering the blood to concentrate the possible microfilariae in a smaller volume of liquid. Many persons infected with W. bancrofti have no detectable microfilariae in their blood, so other methods are available. In the absence of microfilariae, a diagnosis can be made on the basis of a history of exposure, symptoms of the disease, positive antibody or skin tests, or the presence of worms in a sample of lymph tissue. It is important to note that in addition to W. bancrofti, a few other filarial worms and at least one bacteria can also cause elephantiasis; therefore, if symptoms of elephantiasis are observed, it is important to discover the correct cause so that the proper treatment can be given. Since chronic infection occurs after prolonged residence in areas where the disease occurs, patients with acute disease should be removed from those areas. They also should be reassured that elephantiasis is a rare complication that is limited to persons who have had constant exposure to infected mosquitoes for years. The best way to avoid contracting filariasis when traveling to an affected area is to avoid being bitten by mosquitoes. Insect repellent, mosquito netting, and other methods are helpful in this regard.

The World Health Organization (WHO) recommends treating lymphatic filariasis through mass drug administration to at-risk populations. The preferred regimen consists of a single dose of two combined drugs: albendazole and either ivermectin or diethylcarbamazine citrate (DEC). These drugs kill the parasites with the body. Generally, in the treatment of acute disease, excellent results are obtained when the proper dosages of the drugs are given. Side effects include nausea or vomiting, usually relatively mild, and fever and dizziness, the severity of which depends on the number of microfilariae a person has in his or her blood; the more microfilariae, the more severe the reaction. Other drugs have been used in the treatment of filariasis, including suramin, metrifonate, and levamisole, but they are generally less effective or more toxic than the WHO's recommended regimen. Additional treatment measures include bed rest and supportive measures, such as using hot and cold compresses to reduce swelling. The administration of antibiotics for patients with secondary bacterial infections and painkillers as well as anti-inflammatory agents during the painful, acute stage is helpful. Sometimes, swollen limbs can be wrapped in pressure bandages to force the lymph from them. If the distortion is not too great, this method is successful. It should also be noted that although drugs such as DEC, albendazole, and ivermectin might be effective in killing W. bancrofti, the chronic lesions resulting from the infection are mostly incurable. Signs of chronic filariasis, such as elephantiasis of the limbs or the scrotum, are usually unaffected or only incompletely cured by medication, and it sometimes becomes necessary to apply surgical or other symptomatic treatments to relieve the suffering of the patients. Chronic obstruction in less advanced stages is sometimes improved by surgery. The surgical removal of an elephantoid breast, vulva, or scrotum is sometimes necessary.

Theoretically, it should be possible first to control and eventually to eliminate Bancroft’s filariasis. Conditions that are highly favorable for continued propagation of the infection include a pool of microfilariae carriers in the human population and the right species of mosquitoes breeding near human habitations. Thus, control can be effected by treating all microfilariae carriers in an affected area and eliminating the necessary mosquitoes. It is important to note that eliminating the mosquitoes alone will not control the disease, especially in tropical areas, since the breeding period and season in which the disease can be transmitted is so extensive. In some temperate areas, where Bancroft’s filariasis used to be endemic, measures that removed the mosquitoes alone aided in the elimination of the disease from that area, since in temperate areas the breeding period and thus the season for transmission is so short. In tropical areas, both drug therapy and mosquito control must be applied in order to control the disease.

The mosquito population can be controlled in four ways. First, general sanitation measures such as draining swamps can be carried out in order to reduce the areas where the mosquitoes are breeding. Second, insecticides can be used to kill the adult mosquitoes. Third, larvacides can be applied to sources of water where mosquitoes breed in order to kill the mosquito larvae. Finally, natural mosquito predators, such as certain species of fish, can be introduced into waters where mosquitoes breed to eat the mosquito larvae. Numerous problems stand in the way of eradication, such as poor sanitation, persons who do not cooperate with medical intervention, mosquitoes that become resistant to all known insecticides, increasing technology that yields increasing water supplies and therefore places for mosquitoes to breed, large populations, ignorance of the cause of the disease, and lack of medicine and distribution channels.

Perspective and Prospects

Dramatic symptoms of elephantiasis, especially the enormous swelling of legs or the scrotum, were recorded in much of the ancient medical literature of India, Persia, and the Far East. The embryonic form of microfilariae was first discovered and described in Paris in 1863. The organism was named for O. Wucherer, who also discovered microfilariae in 1866, and Joseph Bancroft, who discovered the adult worm in 1876. Two important facts about W. bancrofti—namely, its development in mosquitoes and the nocturnal periodicity of the microfilariae—were discovered by Patrick Manson between 1877 and 1879. This was the first example of a disease being transmitted by a mosquito, and its discovery earned for Manson the title of founder of tropical medicine. These and most of the other essential facts of the disease were discovered before the end of the nineteenth century. Progress in the epidemiology and control of filariasis came after World War II. In 1947, DEC was shown to kill filariae in animals, and this result was followed by the successful use of DEC in the treatment of humans. The first promising results in the control of Bancroft’s filariasis by mass administration of DEC were reported in 1957 on a small island in the South Pacific. Through subsequent studies, it has become clear that effective control of the infection can be achieved if sufficient dosages of DEC and related drugs are administered to infected populations.

Filariasis is a serious health hazard and public health problem in many tropical countries. Infection with W. bancrofti has been recorded in nearly all countries or territories in the tropical and subtropical zones of the world. The infection occurs primarily in coastal areas and islands that experience long periods of high humidity and heat. Infections have also been noted in some temperate zone districts, such as mainland Japan, central China, and some European countries. In early 2013, the WHO estimated that more than 120 million people worldwide were infected and more than 1.4 billion were at risk.

Bibliography

Beaver, Paul C., and Rodney C. Jung. Animal Agents and Vectors of Human Disease. 5th ed. Philadelphia: Lea & Febiger, 1985.

Biddle, Wayne. A Field Guide to Germs. 2d ed. New York: Anchor Books, 2002.

Frank, Steven A. Immunology and Evolution of Infectious Disease. Princeton, N.J.: Princeton University Press, 2002.

Global Health, Division of Parasitic Diseases and Malaria. "Lymphatic Filariasis." Centers for Disease Control and Prevention, February 1, 2012.

Joklik, Wolfgang K., et al. Zinsser Microbiology. 20th ed. Norwalk, Conn.: Appleton and Lange, 1997.

MedlinePlus. "Lymphatic Diseases." MedlinePlus, April 23, 2013.

Ransford, Oliver. “Bid the Sickness Cease.” London: John Murray, 1983.

Roberts, Larry S., and John Janovy, Jr., eds. Gerald D. Schmidt and Larry S. Roberts’ Foundations of Parasitology. 7th ed. Boston: McGraw-Hill Higher Education, 2005..

Salyers, Abigail A., and Dixie D. Whitt. Bacterial Pathogenesis: A Molecular Approach. 2d ed. Washington, D.C.: ASM Press, 2002.

World Health Organization. "Lymphatic Filariasis." World Health Organization, March 2013.

What does Hannah Arendt say about freedom?

Though not grounded in a careful reading of any particular text or set of texts, Arendt convincingly argues in "What Is Freedom?" that political liberty has become—in modern philosophical and theological discourse—“a potential freedom from politics” (149) defined in terms of a “guaranty of security” (ibid.). Though not specifically channeling Hobbes, Arendt points to the Hobbesian security state as the example par excellence of this negative freedom: “security, in turn, made freedom possible, and the word ‘freedom’ designated a quintessence of activities which occurred outside the political realm” (ibid.). Freedom, here, appears not so much the goal of politics or its founding principle, but rather as a kind of byproduct of the security state. Political subjects are only minimally free to preserve their own lives in the realm of biological necessity; as Arendt puts it, “the total domain of the political, was now considered to be the appointed protector not so much of freedom as of the life process” (150), the biopolitical aspirations of the security state effectively quashing freedom through the political.

Against what she terms the modern age’s insistence on the “separ[ation] [of] freedom and politics” (ibid.), Arendt wishes to found a conception of freedom that is thoroughly imbricated within the political itself. Put briefly at the end of the essay’s first section, Arendt states “that the raison d’etre of politics is freedom and that this freedom is primarily experienced in action” (151). This freedom—against the negative freedom of the security state—is a positive one, grounded in the political subject’s right to act in the public (political) realm beyond the mere necessities of biological life, a freedom to politics rather than a freedom from it. In fact, she goes so far as to claim: “Freedom as a demonstrable fact and politics coincide and are related to each other like two sides of the same matter” (149), effectively conflating freedom-in-action and the political as such. 

Arendt is able to argue that freedom constitutes the essence of politics rather than its marginalized byproduct by emphasizing the importance of action, community, and (implicitly) natality to her conception of freedom. Action, here, by being free from both the intellect and the will (152), becomes the means through which humans actualize what (through Montesquieu) she calls principles (e.g. “honor or glory, love of equality … but also fear or distrust or hatred” (ibid.), which, due to their abstract character, can enter the political only through action. As she puts it: “Men are free—as distinguished from their possessing the gift for freedom—as long as they act, neither before nor after; for the be free and to act are the same” (153). Moreover, this actualization of principles through action depends entirely on a common, public space in which multiple political subjects act simultaneously, what Arendt calls at one point “a kind of theater where freedom could appear” (154). Extending the metaphor further, she likens the political actor to a performance artist who “depend[s] upon others for the performance itself” (ibid.). What Arendt finds so valuable about this positive freedom to politics—in contradistinction to the negative freedom lying at the heart of the security state—is its capacity “to call something into being which did not exist before” (151) or, to use the term we have been teasing out of The Human Condition, its ability to bring about the event of natality. Freedom—characterized by action, community, and natality—becomes in Arendt’s hands the very stuff of politics, an intersubjective acting together in the public realm to initiate the new and open up the possibility of new futures for the polis.

Despite the seemingly wholly secular character of Arendt’s new definition of freedom which constitutes the first two parts of the essay, grounded in Kant, everyday experience, and scientific views of causality, Arent devotes the second half of the essay almost exclusively to issues of political theology. On the one hand, she levels a critique against a certain strain of Pauline and Augustinian theology. On the other, however, she subsequently reads into them at the very least a kernel of her freedom to politics.

Beginning in Section III, Arendt takes up the issue of “the Christian and modern notion of free will” (157) to analyze (what she sees as) its negative effects on ideas of political freedom. The importance of this Christian tradition for Arendt almost cannot be understated. As she writes: “For the history of the problem of freedom, Christian tradition has indeed become the decisive factor” (157). Locating in Christian theology a fundamental split between what she calls the “I can” and the “I will,” a split unknown and incomprehensible to the ancient philosophers, Arendt contends that freedom becomes interiorized, thought in terms of the individual subject rather than the collective of the polis. As a result, “will, will-power, and will-to-power are for us almost identical notions; the seat of power is to us the faculty of the will as known and experienced by man in his intercourse with himself” (160). This resignation of freedom to the realm of the individual subject and his will, Arendt argues, has “fatal consequences for political theory” (162). More specifically, freedom “became sovereignty, the ideal of a free will, independent from others and eventually prevailing against them” (163). The interiorized freedom of Christian theology thus becomes the grossest suppression of freedom in the forms of, for example, the Hobbesian state and the rise of totalitarianism. Succinctly put: “If men wish to be free, it is precisely sovereignty they must renounce” (165).

While this rejection of both the notion of sovereignty and the individual subject of Christian theology might appear to be an outright rejection of political theology on Arendt’s part, she also finds in the very same tradition an underground current (to channel Althusser) of “a freedom which is not an attribute of the will but an accessory of doing and acting” (165). She finds in Augustine’s only political writing, The City of God, “an entirely differently conceived notion” (167) of freedom than that which he champions in his strictly theological writings. In City of God, Arendt argues, freedom is both “a character of human existence in the world” and the “faculty of beginning” reaffirmed in “the birth of each man” (ibid.), a definition approximating Arendt’s own by emphasizing both being-in-the-world and natality. She goes on to locate a similar tendency in the New Testament which, to her reading, exhibits “an extraordinary understanding of freedom” (168). This extraordinary freedom manifests itself in the decidedly theological concept of the miracle which serves as an “interruption of some natural series of events, of some automatic process, in whose context they constitute the wholly unexpected” (ibid.). The miracle, then, becomes yet another example of natality and, when secularized at the hands of Arendt, an example of political freedom itself.

What is existential psychology? |

Introduction

Existential psychology was inspired by the original insights of the philosophy of existentialism. By examining situations of great horror (such as the concentration camps of the Nazis) and of great beauty or joy (such as a father seeing his little girl happily skipping down the sidewalk), existentialism posited that human existence is without absolutes: There are no limits either to human cruelty or to human love. Existentialism removes all presuppositions, abstractions, and universal rules. It attacks the conformity and complacency caused by the illusion that a human is only a predetermined cog in a completely ordered, mechanical universe.

Modern culture can be alienating, with its huge bureaucratic and technological structures that do not recognize one’s concrete existence. In spite of the pervasiveness of this alienation, existentialism holds that the possibility of existing as an authentic individual is never lost. Existentialism depicts the “absurdity” (the sense that there is no inherent basis for conferring meaning to life) of the lack of preestablished systems of meaning, but it rejects the artificiality of schemes that try to account for meaning as somehow produced by systems “out there,” beyond the individual. Instead, existentialism returns to concretely lived situations as the birthplace of whatever meaning may be found in life. In that sense, life is an adventure that unfolds as one lives it. As William Barrett has said, “Life is not handed to us on a platter but involves our own act of self-determination.”

Mainstream psychology has not, for the most part, addressed this existentialist outlook. Instead, it has borrowed from natural science the viewpoint that human life is essentially mechanistic and causally determined—that personal life can be reduced to a bundle of drives, stimuli, or biochemical reactions. The problem with those approaches, notes existential psychologist Rollo May, is that “the man disappears; we can no longer find 'the one’ to whom this or that experience has happened.” Thus, the crucial innovation offered by existential psychology is its aim to understand the personal, experienced reality of one’s free and meaningful involvement in one’s world. This is accomplished by analyzing the experiential situations and concerns of persons as the most fundamental dimension of their existence. This approach has been especially evident in the areas of personality theory and psychotherapy. It is in those areas that psychologists are most directly confronted with real human problems and are therefore unable to settle for abstract laboratory experiments as a basis for knowledge.

Emergence of Study

Psychologists began to turn to existentialism in the 1940s. The pioneers of existential analysis were psychoanalysts originally influenced by the ideas of Sigmund Freud. As analysts, they already stood outside mainstream experimental psychology and so were not as influenced by its presumptions. Furthermore, as therapists, their overriding purpose was to assist people who were experiencing real distress, anxiety, and conflict. Abstract theories and dogmas about stimuli and responses were more easily recognized as insufficient in that context, and an approach that focused on patients’ actual existence was welcome.

The first practitioners were the Swiss psychiatrists Ludwig Binswanger and Medard Boss, whose early writings date from the late 1940s. They were inspired by the existential philosophy of Martin Heidegger’s key book Sein und Zeit (1927;
Being and Time
, 1962). They believed that analysis needed to be broadened beyond the limits that Freud had established. In place of Freud’s psychoanalysis—the aim of which was to understand an interior mental apparatus—they developed existential analysis, with the aim of understanding the person’s existence, that is, the person’s “being-in-the-world.” This term, developed by Heidegger, was meant by its hyphens to indicate that the relation of person and world is not merely one of the person being located “in” the world (as a pencil is located in a drawer). Rather, the person is always “worlded” in the sense that one’s existence is a network of meaningful involvements—relationships that are specifically and uniquely one’s own. Heidegger had called this the “care” structure, and he saw it as the very core of what it means to be a human being: that people care and that the people, places, and things with which one is involved inevitably matter.

Being-in-the-world as involvement is revealed by the ways in which such basic dimensions of the world as time and space are experienced. Time is not lived as a clock would record it, in equal minutes and hours. Rather, some hours drag on and on, whereas others zip by, depending on one’s involvements. Similarly, the space of a strange place looms differently when it has become familiar. Even one’s own body reflects this understanding of existence as being-in-the-world. A great variety of symptoms, from cold feet to high blood pressure, disclose one’s involvements, as do gestures, both habitual and spontaneous.

Other continental European psychiatrists who advanced the development of existential psychology include Karl Jaspers, Eugene Minkowski, Henri Ey, Erwin Straus, Frederik Jacobus Buytendijk, and Viktor Frankl. In England, R. D. Laing, a brilliant young psychiatrist originally influenced by the British “object relations” school of psychoanalysis, developed an existential account of schizophrenic
persons, beginning around 1960. He sought to show “that it was far more possible than is generally supposed to understand people diagnosed as psychotic.” He proceeded to do so by examining their “existential context.” In books such as The Divided Self: An Existential Study in Sanity and Madness (1965), Laing attempted to unravel the mystery of schizophrenic speaking and symptoms by revealing how their apparently nonsensical quality does have a sense when seen in terms of the person’s own experience of the totality of his or her relationships and existence.

Existential analysis came to the United States at the end of the 1950s mainly through the influence of May, who introduced the writings of the European analysts. May provided both a scholarly background to the approach and an examination of its role in psychotherapy. His later books, such as Man’s Search for Himself (1953), Psychology and the Human Dilemma (1967), and Love and Will (1969), did much to popularize existential psychology in the United States without trivializing its philosophical depth.

Appreciating Personhood

Existential therapists, such as May, have generally argued that they are not seeking to establish a new type of therapy with new techniques. Rather, they have developed a different approach, one that can be used with any specific therapeutic system. They developed a different way for the therapist to “be present” for the patient or client. This distinctive way of being present is well illustrated in Laing’s therapeutic work; it hinges on the type of relationship that exists between the therapist and the patient. Laing pointed out the difference between two ways of relating to a patient: as a biochemical organism (and a diseased organism at that) or as a person. He cited, as an example, the difference between listening to another’s speaking as evidence of certain neurological processes and trying to understand what the person is talking about. When a therapist sees a patient as an “it,” the therapist cannot really understand that patient’s desire, fear, hope, or despair. Seeing the patient as a person, however, implies seeing the patient “as responsible, as capable of choice, in short, as a self-acting agent.”

This undiluted respect for the personhood of the patient is well exhibited in Laing’s work with schizophrenic persons. In place of the usual medical model, Laing offered them a “hospital” in the original sense of that word: a place of refuge, of shelter and rest for a traveler. Their experience was respected there, however different it appeared. They were allowed to complete their journey through madness, accompanied by another person (Laing) who was always respectful that it was real.

May similarly asserted that “the central task and responsibility of the therapist is to seek to understand the patient as a being and as being-in-his-world.” That understanding does not deny the validity of any psychodynamic insights; rather, it holds that any such dynamics “can be understood only in the context of the structure of existence of the person.” Indeed, the very aim of existential therapy is to help the patient experience his or her existence as real. What makes it possible for the patient to change, said May, is ultimately this experience of being treated, in the moment, as the real person that the person is. That is why existential therapy emphasizes a sense of reality and concreteness above a set of techniques.

Being-in-the-World Dilemmas

While each person’s reality is unique, there are certain basic dilemmas that arise by virtue of one’s being-in-the-world. Because existence is fundamentally a relationship with a world, the givens of existing provide what Irvin D. Yalom
has called the “ultimate concerns of life.” He has identified four: death, freedom, existential isolation, and meaninglessness. Yalom notes that the confrontation with any of these existential issues can become a serious conflict for a person. Specifically, to the extent that a person begins to become aware of these conflicts without yet facing them fully, that person will experience anxiety and so will seek to defend against the experience by turning away from the underlying concern. The task of the existential therapist is to use that experience of anxiety as a clue to help the patient find a way back to the ultimate concern and then, by fully facing it, discover the positive transformation it offers for authentic living. The first two of these ultimate concerns, death and freedom, can serve as illustrative examples.

The first of these conflicts is that one’s life will end in death even though one wishes it could continue. Death therefore holds a terror that may leave one anxious. One may even try to evade any awareness of death, living as though one would live forever. For the existential therapist, however, this awareness of death can be used to propel the patient to live his or her life authentically. Because life’s preciousness is most evident when one is aware that one will lose it, becoming authentically aware of one’s mortality can give one a powerful commitment not to waste one’s life. In that sense, the anxiety of trying to evade death can be turned around and transformed into a clue to help patients discover what it is that they would be most anxious about dying without having experienced.

The second of these conflicts has to do with freedom. Though it seems to be a positive value, realizing one’s freedom fully can be terrifying, for it entails accepting responsibility for one’s life. One is responsible for actualizing one’s own true self. Experiences such as anxiety, guilt, and despair reveal the dilemma of trying to hide from oneself the fact that one was not willing to be true to oneself. They then provide the basic clue by which the patient can uncover the self.

Roots of Existentialism

Existentialism arose in the mid-nineteenth century with Søren Kierkegaard. He opposed the Hegelian philosophy dominant during his time with the criticism that its formalism and abstractness omitted the individual. He insisted that the existing person was the most basic starting point for philosophy, that the authentic acceptance of being an individual is the basic task of one’s life, and that “the purpose of life is to be the self which one truly is.” Through analyses of such experiences as passion and commitment, Kierkegaard showed the important truths of subjective life.

At the beginning of the twentieth century, Edmund Husserl
established phenomenology
as a philosophical method by which to investigate actual experience. This provided a powerful boost to existentialism, especially evident in Heidegger’s subsequent analysis of the “care structure” as the meaning of being human. The next developments in existentialism arose in France, during and immediately after World War II. In a country occupied by the Nazis for five years, people who worked in the French Resistance movement became intimately acquainted with their own mortality. Death awaited around every corner; one never could know that this day was not the last. Such direct experience had a powerful impact on the French existential philosophers who participated in the Resistance movement, of whom Jean-Paul Sartre
, Albert Camus, Simone de Beauvoir, and Maurice Merleau-Ponty are the best known.

While Merleau-Ponty wrote books of particular relevance for a psychology of perception and behavior, it was Sartre who most fully depicted the foibles of human life that are relevant to the psychotherapist. In philosophical books such as L’Être et le néant (1943; Being and Nothingness, 1956), as well as in plays and novels, Sartre lucidly revealed the ways people dodge rather than face their own freedom and their own responsibility to choose. For him, this living as if one were not really free (inauthentic living) was “bad faith.” Sartre contrasted his “existential analysis” of phenomena such as bad faith with the Freudian psychoanalysis of the unconscious. In doing so, he replaced Freud’s conceptions of a theoretical construct (the unconscious) with descriptions of experiences of living inauthentically.

These developments in France led to a burst of expanded interest in existentialism throughout the 1950s, in both Europe and the United States. By the 1960s, many new books, journals, and even graduate programs began to emphasize existential philosophy and psychology. Graduate programs that focused on existential psychology appeared at Duquesne University, West Georgia College, and Sonoma State University.

Existentialism became one of the primary sources of inspiration for an alternative to the dominant psychoanalytic and behavioristic psychologies that began to gather momentum in the 1960s under the name “ humanistic psychology.” By offering the perspective that people’s experiences of their own situations are vitally important to an understanding of their behavior, this view posed a central challenge to mainstream experimental psychology. This existential insight did not sway most psychologists, however; instead, the rise of cognitive psychology in the 1970s and 1980s established a new paradigm. It, too, offered the key notion that a person’s involvement was crucial to understanding behavior, but cognitive psychology defined that involvement in terms of a computational model: The person “takes in” the world by “processing information.” That model preserved the mechanistic assumption so important to mainstream psychology—the very assumption that existential psychology most decisively disputed. As a result, existential psychology remains a lively critic on psychology’s periphery rather than being an equal partner with more traditional approaches.

Bibliography

Boss, Medard. Psychoanalysis and Daseinsanalysis. New York: Da Capo, 1982. Print.

Diamond, Stephen A. “What Is Existential Psychotherapy?” Psychology Today. Sussex, 21 Jan. 2011. Web. 19 May 2014.

Frankl, Viktor Emil. Man’s Search for Meaning. New York: Washington Square, 2006.Print.

Frankl, Viktor Emil. Man’s Search for Ultimate Meaning. Cambridge: Perseus, 2000. Print.

Jacobsen, Bo. Invitation to Existential Psychology: A Psychology for the Unique Human Being and Its Applications in Therapy. Hoboken: Wiley, 2008. Print.

Laing, Ronald David. The Divided Self: An Existential Study in Sanity and Madness. 1965. Rpt. New York: Routledge, 2001. Print.

May, Rollo. The Discovery of Being. 1983. Rpt. New York: Norton, 1994. Print.

May, Rollo, Ernest Angel, and Henri F. Ellenberger, eds. Existence. 1958. Rpt. Northvale: Aronson, 1995. Print.

Russo-Netzer, Pninit, and Alexander Batthyany. Meaning in Positive and Existential Psychology. New York: Springer, 2014. eBook Collection (EBSCOhost). Web. 19 May 2014. Print.

Valle, Ronald S., and Steen Halling, eds. Existential-Phenomenological Perspectives in Psychology. New York: Plenum, 1989. Print.

Welsh, Talia. The Child as Natural Phenomenologist: Primal and Primary Experience in Merleau-Ponty’s Psychology. Evanston: Northwestern UP, 2013. Print.

Yalom, Irvin D. Existential Psychotherapy. New York: Basic , 1980. Print.

What are four symbols in The Great Gatsby by F. Scott Fitzgerald? Why are they significant, and what do they teach us about society and the...

The green light at the end of Daisy's dock is symbolic, in many ways, of the American Dream.  It represents hope for the future, that if a person works hard enough and long enough, they can prosper and be happy.  Nick sees Gatsby reaching out toward the light at the end of the first chapter, and in the final lines of the novel, he calls the light "the orgastic future that year by year recedes before us.  It eluded us then, but that's no matter -- to-morrow we will run faster, stretch out our arms farther. . . . And one fine morning--."  We can, put simply, never actually reach the light.  No matter how hard we work or try or dream, we can never really reach that American Dream, and its elusiveness ought to make us pity Gatsby, and even Myrtle and George Wilson, as victims of its unattainability.

In Chapter IV, having been reunited with Daisy after five years, Gatsby almost breaks a clock at Nick's house when Nick invites them both for tea at Gatsby's request.  Gatsby longs, and believes that it is possible, to repeat the past.  He tells Nick this very thing later in the story.  However, it is not possible to stop time or to revisit the past, and the fact that he almost breaks the clock represents his desire to stop time, while the fact that he doesn't break the clock symbolizes his inability to do so.

The valley of ashes, where the Wilsons live, is a place where everything is so covered in ashes that the houses and people and landscape appear to be made of ashes.  It is the product of industry, the industry that makes just a few very, very wealthy and leaves the majority with so very little.  Wilson, for example, works so hard, but he cannot earn enough money even to be able to afford to move elsewhere.  The valley, therefore, symbolizes the great gulf between those few individuals who prosper and the vast majority who are used up, reduced to ash, by the demands of the prosperous.  It certainly helps us to understand and sympathize with someone like George Wilson.

The deaths of Gatsby and the Wilsons is symbolic of the death of the American Dream.  When Gatsby tries to reach it honestly, he finds that it is impossible, and so he attempts to reach it illegally (which means that he does not actually achieve it).  Then, George and Myrtle each try to better their situations, in different ways, and neither is successful either.  No one can really get what they want in a world that is corrupt enough to give all the privilege to terrible people like Tom and Daisy simply because they possess "old money" and status.

What is imprinting? |

Introduction

Imprinting is an important type of behavior by which an animal learns specific concepts and identifies certain objects or individuals that are essential for survival. Imprinting events almost always occur very early in the life of an animal, during critical periods or time frames when the animal is most sensitive to environmental cues and influences. The phenomenon occurs in a variety of species, but it is most pronounced in the homeothermic (warm-blooded) and socially oriented higher vertebrate species, especially mammals and birds.

Imprinting is learned behavior. Most learned behavior falls within the domain of exogenous behavior, or behavior that an animal obtains by its experiences with fellow conspecifics (members of the same species) and the environment. Imprinting, however, is predominantly, if not exclusively, an endogenous behavior
, which is a behavior that is genetically encoded within the individual. An individual is born with the capacity to imprint. The animal’s cellular biochemistry and physiology will determine when in its development the imprinting will occur. The only environmental influence of any consequence in imprinting is the object of the imprint during the critical period. Ethologists, scientists who study animal behavior, debate the extent of endogenous and exogenous influences on animal behavior. Most behaviors involve a combination of both, although one type may be more pronounced than the other.

The capacity for an animal to imprint is genetically determined and, therefore, is inherited. This type of behavior is to the animal’s advantage for critical situations that must be correctly handled the first time they occur. Such behaviors include the identification of one’s parents (especially one’s mother), the ability to navigate, the ability to identify danger, and even the tendency to perform the language of one’s own species. Imprinting behaviors generally are of high survival value and hence must be programmed into the individual via the genes. Biological research has failed to identify many of the genes that are responsible for imprinting behaviors, although the hormonal basis of imprinting is well understood. Most imprinting studies have focused on the environmental signals and developmental state of the individual during the occurrence of imprinting.

Maternal Imprinting

These studies have involved mammals and birds, warm-blooded species that have high social bonding, which seems to be a prerequisite for imprinting. The most famous imprinting studies were performed by the animal behaviorists and Nobel laureates Konrad Lorenz
and Nikolaas Tinbergen. They and their many colleagues detailed analyses of imprinting in a variety of species, in particular waterfowl such as geese and ducks. The maternal imprinting behavior of the newborn gosling or duckling on the first moving object that it sees is the most striking example of imprinting behavior.

The maternal imprint is the means by which a newborn identifies its mother and the mother identifies its young. In birds, the newborn chick follows the first moving object that it sees, an object that should be its mother. The critical imprinting period is within a few hours after hatching. The chick visually will lock on its moving mother and follow it wherever it goes until the chick reaches adulthood. The act of imprinting not only allows for the identification of one’s parents but also serves as a trigger for all subsequent social interactions with members of one’s own species. As has been established in numerous experiments, a newborn gosling that first sees a female duck will imprint on the duck and follow it endlessly. On reaching adulthood, the grown goose, which has been raised in the social environment of ducks, will attempt to behave as a duck, even to the point of mating. Newborn goslings, ducklings, and chicks can easily imprint on humans.

In mammals, imprinting relies not only on visual cues (specific visible physical objects or patterns that an animal learns to associate with certain concepts) but also on physical contact and smell. Newborn infants imprint on their mothers, and vice versa, by direct contact, sight, and smell during the critical period, which usually occurs within twenty hours following birth. The newborn and its mother must come into direct contact with each other’s skin and become familiarized with each other’s smell. The latter phenomenon involves the release of special hormones called pheromones from each individual’s body. Pheromones trigger a biochemical response in the body of the recipient individual, in this case leading to a locked identification pattern for the other involved individual. If direct contact between mother and infant is not maintained during the critical imprinting period, then the mother may reject the infant because she is unfamiliar with its scent. In such a case, the infant’s life would be in jeopardy unless it were claimed by a substitute mother. Even in this situation, the failure to imprint would trigger subsequent psychological trauma in the infant, possibly leading to aberrant social behavior in later life.

Bird Migration and Danger Recognition

Although maternal imprinting in mammal and bird species is the best-documented example of imprinting behavior, imprinting may be involved in other types of learned behavior. In migratory bird species, ethologists have attempted to explain how bird populations navigate from their summer nesting sites to their wintering sites and back every year without error. Different species manage to navigate in different fashions. The indigo bunting, for example, navigates via the patterns of stars in the sky at night. Indigo bunting chicks imprint on the celestial star patterns for their summer nesting site during a specific critical period, a fact that was determined by the rearrangement of planetarium stars for chicks by research scientists.

Further research studies on birds also implicate imprinting in danger recognition and identification of one’s species-specific call or song. Young birds of many species identify predatory birds, such as hawks, falcons, and owls, by the outline of the predator’s body during flight or attack and by special markings on the predator’s body. Experiments also have demonstrated that unhatched birds can hear their mother’s call or song; birds may imprint on their own species’ call or song before they hatch. These studies reiterate the fact that imprinting is associated with a critical period during early development in which survival-related behaviors must become firmly established.

Human Imprinting

Imprinting is of considerable interest to psychologists because of its role in the learning process for humans. Humans imprint in much the same fashion as other mammals. The extended lifetime, long childhood, and great capacity for learning and intelligence make imprinting in humans an important area of study. Active research on imprinting is continually being conducted with humans, primates, marine mammals (such as dolphins, whales, and seals), and many other mammals, as well as with a large variety of bird species. Comparisons among the behaviors of these many species yield considerable similarities in the mechanisms of imprinting. These similarities underscore the importance of imprinting events in the life, survival, and socialization of the individual.

With humans, maternal imprinting occurs much as with other mammals. The infant and its mother must be in direct contact during the hours following birth. During this critical period, there is an exchange of pheromones between mother and infant, an exchange that, to a large extent, will bond the two. Such bonding immediately following birth can occur between infant and father in the same manner. Many psychologists stress the importance of both parents being present at the time of a child’s delivery and making contact with the child during the critical hours of the first day following birth. Familiarization is important not only for the child but for the parents as well because all three are imprinting on one another.

Failure of maternal or paternal imprinting during the critical period following birth can have drastic consequences in humans. The necessary, and poorly understood, biochemical changes that occur in the bodies of a child and parent during the critical period will not occur if there is no direct contact and, therefore, no transfer of imprinting pheromones. Consequently, familiarization and acceptance between the involved individuals may not occur, even if intense contact is maintained after the end of the critical period. The psychological impact on the child and on the parents may be profound, perhaps not immediately, but in later years. Studies on this problem are extremely limited because of the difficulty of tracing cause-and-effect relationships over many years when many behaviors are involved. There is some evidence, however, that indicates that failure to imprint may be associated with such things as learning disabilities, child-parent conflicts, and abnormal adolescent behavior. Nevertheless, other cases of imprinting failure seem to have no effect, as can be seen in tens of thousands of adopted children. The success or failure of maternal imprinting in humans is a subject of considerable importance in terms of how maternal imprinting affects human behavior and social interactions in later life.

Different human cultures maintain distinct methods of child rearing. In some cultures, children are reared by family servants or relatives from birth onward, not by the mother. Some cultures wrap infants very tightly so that they can barely move; other cultures are more permissive. Child and adolescent psychology focuses attention on early life experiences that could have great influence on later social behavior. The success or failure of imprinting, along with other early childhood experiences, may be a factor in later social behaviors such as competitiveness, interaction with individuals of the opposite sex, mating, and maintenance of a stable family structure. Even criminal behavior and psychological abnormalities may be traceable to such early childhood events.

Experiments

Imprinting studies conducted with nonhuman mammals and bird species are much easier than those with humans because the researcher has the freedom to conduct controlled experiments that test many different variables, thereby identifying the factors that influence an individual animal’s ability to imprint. For bird species, a famous experiment is the moving ball experiment. A newly hatched chick is isolated in a chamber within which a suspended ball revolves around the center of the chamber. The researcher can test not only movement as an imprinting trigger but also other variables, such as critical imprinting time after hatching, color as an imprinting factor, and variations in the shape of the ball as imprinting factors. Other experiments involve switching eggs between different species (for example, placing a duck egg among geese eggs).

For mammals, imprinting has been observed in many species, such as humans, chimpanzees, gorillas, dolphins, elephant seals, wolves, and cattle. In most of these species, the failure of a mother to come into contact with its newborn almost always results in rejection of the child. In species such as elephant seals, smell is the primary means by which a mother identifies its pups. Maternal imprinting is of critical importance in a mammalian child’s subsequent social development. Replacement of a newborn monkey’s natural mother with a “doll” substitute leads to irreparable damage; the infant will be socially and sexually repressed in its later encounters with other monkeys. These and other studies establish imprinting as a required learning behavior for the successful survival and socialization of all birds and nonhuman mammals.

Biology and Behavior

Animal behaviorists and psychologists attempt to identify the key factors that are responsible for imprinting in mammalian and avian species. Numerous factors, including vocal cues (specific sounds, frequency, and language that an animal learns to associate with certain concepts) and visual cues, are probably involved, although the strongest two factors appear to be direct skin contact and the exchange of pheromones that are detectable by smell. The maternal imprinting behavior is the most intensively studied imprinting phenomenon, though imprinting appears to occur in diverse behaviors such as mating, migratory navigation, and certain forms of communication.

Imprinting attracts the interest of psychologists because it occurs at critical periods in an individual’s life; because subsequent developmental, social, and behavioral events hinge on what happens during the imprinting event; and because imprinting occurs at the genetic or biochemical level. Biochemically, imprinting relies on the production and release of pheromones, molecules that have a specific structure and that can be manufactured in the laboratory. The identification and mass production of these pheromones could possibly produce treatments for some behavioral abnormalities.

As an endogenous (instinctive) form of learning, imprinting relies on the highly complex nervous and endocrine systems of birds and mammals. It also appears limited to social behavior, a major characteristic of these species. The complex nervous systems involve a highly developed brain, vocal communication, well-developed eyes, and a keen sense of smell. The endocrine systems of these species produce a variety of hormones, including the pheromones that are involved in imprinting, mating, and territoriality. Understanding the nervous and endocrine regulation of behavior at all levels is of major interest to biological and psychological researchers. Such studies may prove to be fruitful in the discovery of the origin and nature of animal consciousness.

Imprinting may be contrasted with exogenous forms of learning. One type of exogenous learning is conditioning, in which individuals learn by repeated exposure to a stimulus, by association of the concept stimulus with apparently unrelated phenomena and objects, or by a system of reward and punishment administered by parents. Other exogenous learning forms include habituation (getting used to something) and trial and error. All learned behaviors are a combination of endogenous and exogenous factors.

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Wilson, Edward O. Sociobiology: The New Synthesis. 25th anniv. ed. Cambridge: Belknap, 2000. Print.

What is hypoglycemia? |

Causes and Symptoms

The condition known as hypoglycemia exists when the concentration of glucose in the bloodstream is too low to meet bodily needs for fuel, particularly those of the brain. Ordinarily, physiological compensatory mechanisms are called into play when the circulating concentration of glucose falls below about 3.5 millimoles. Activation of the sympathetic nervous system and the secretion of glucagon are especially important in promoting glycogenolysis and gluconeogenesis. Symptoms of sympathetic nervous activation normally become apparent with glucose concentrations that are less than about 3 millimoles. Brain function is usually demonstrably abnormal at glucose concentrations below about 2 millimoles; sustained hypoglycemia in this range can lead to permanent brain damage.

Some of the symptoms of hypoglycemia occur as by-products of activation of the sympathetic nervous system. These symptoms include trembling, pallor, palpitations and rapid heartbeat, sweating, abdominal discomfort, and feelings of anxiety and/or hunger. These symptoms are not dangerous in themselves; in fact, they may be considered to be beneficial, as they alert the individual of the need to obtain food. Meanwhile, the sympathetic nervous system signals compensatory mechanisms. The manifestations of abnormal brain function during hypoglycemia include blunting of higher cognitive functions, disturbed mentation, confusion, loss of normal control of behavior, headache, lethargy, impaired vision, abnormal speech, paralysis, neurologic deficits, coma, and epileptic seizures. The individual is usually unaware of the appearance of these symptoms, which can present real danger. For example, episodes of hypoglycemia have occurred while individuals were driving motor vehicles, which can lead to serious injury and death. After recovery from hypoglycemia, the patient may have no memory of the episode.

There are two major categories of hypoglycemia: fasting and reactive. The most serious, fasting hypoglycemia, represents impairment of the mechanisms responsible for the production of glucose when food is not available. These mechanisms include the functions of cells in the liver and brain that monitor the availability of circulating glucose. Additionally, there is a coordinated hormonal response involving the secretion of glucagon, growth hormone, and other hormones and the inhibition of the secretion of insulin. The normal consequences of these processes include the addition of glucose to the circulation, primarily from glycogenolysis, as well as a slowing of the rate of utilization of circulating glucose by many tissues of the body, especially the liver, skeletal and cardiac muscle, and fat. Even after days without food, the body normally avoids hypoglycemia through breakdown of stored proteins and activation of gluconeogenesis. There is considerable redundancy in the systems that maintain glucose concentration, so the occurrence of hypoglycemia often reflects the presence of defects in more than one of these mechanisms.

The other category of hypoglycemia, reactive hypoglycemia, includes disorders in which there is disproportionately prolonged and/or great activity of the physiologic systems that normally cause storage of the glucose derived from ingested foods. When a normal person eats a meal, the passage of food through the stomach and intestines elicits a complex and well-orchestrated neural and hormonal response, culminating in the secretion of insulin from the beta cells of the islets of Langerhans in the
pancreas. The insulin signals the cells in muscle, adipose tissue, and the liver to stop producing glucose and to derive energy from glucose obtained from the circulation. Glucose in excess of the body’s immediate needs for fuel is taken up and stored as glycogen or is utilized for the manufacture of proteins. Normally, the signals for the uptake and storage of glucose reach their peak of activity simultaneously with the entry into the circulation of glucose from the food undergoing digestion. As a result, the concentration of glucose in the circulation fluctuates only slightly. In individuals with reactive hypoglycemia, however, the entry of glucose from the digestive tract and the signals for its uptake and storage are not well synchronized. When signals for the cellular uptake of glucose persist after the intestinally derived glucose has dissipated, hypoglycemia can result. Although the degree of hypoglycemia may be severe and potentially dangerous, recovery can take place without assistance if the individual’s general nutritional state is adequate and the systems for activation of glycogenolysis and gluconeogenesis are intact.

Diagnosis and Treatment

The diagnostic evaluation of an individual who is suspected of having hypoglycemia begins with verification of the condition. Evaluation of a patient’s symptoms can be confusing. On one hand, the symptoms arising from the sympathetic nervous system and those of neuroglycopenia may occur in a variety of nonhypoglycemic conditions. On the other hand, persons with recurrent hypoglycemia may have few or no obvious symptoms. Therefore, it is most important to document the concentration of glucose in the blood.

To establish the diagnosis of fasting hypoglycemia, the patient is kept without food for periods of time, up to seventy-two hours, with frequent monitoring of the blood glucose. Should hypoglycemia occur, blood is taken for measurements of the key regulatory neurosecretions and hormones, including insulin, glucagon, growth hormone, cortisol, and epinephrine, as well as general indices of the function of the liver and kidneys. If there is suspicion of an abnormality in an enzyme involved in glucose production, the diagnosis can be confirmed by measurement of the relevant enzymatic activity in circulating blood cells or, if necessary, in a biopsy specimen of the liver.

Fasting hypoglycemia may be caused by any condition that inhibits the production of glucose or that causes an inappropriately great utilization of circulating glucose when food is not available. Insulin produces hypoglycemia through both of these mechanisms. Excessive circulating insulin ranks as one of the most important causes of fasting hypoglycemia, most cases of which result from the treatment of diabetes mellitus with insulin or with an oral drug of the sulfonylurea class. If the patient is known to be taking insulin or a sulfonylurea drug for diabetes, the cause of hypoglycemia is obvious; appropriate modification of the treatment should be made. Hypoglycemia caused by oral sulfonylureas is particularly troublesome because of the prolonged retention of these drugs in the body. The passage of several days may be required for recovery, during which time the patient needs continuous intravenous infusion of glucose.

Excessive insulin secretion may also result from increased numbers of pancreatic beta cells; the abnormal beta cells may be so numerous that they form benign or malignant
tumors, called insulinomas. The preferred treatment of an insulinoma is surgery, if feasible. When the tumor can be removed surgically, the operation is often curative. Unfortunately, insulinomas are sometimes difficult for the surgeon to find. Magnetic resonance imaging (MRI), computed tomography (CT) scanning, ultrasonography, or angiography may help localize the tumor. Some insulinomas are multiple and/or malignant, rendering total removal impossible. In these circumstances, hypoglycemia can be relieved by drugs that inhibit the secretion of insulin.

Malignant tumors arising from various tissues of the body may produce hormones that act like insulin with respect to their effects on glucose metabolism. In some cases, these hormones are members of the family of insulin-like growth factors, which resemble insulin structurally. Malnutrition probably has an important role in predisposing patients with malignancy to hypoglycemia, which tends to occur when the cancer is far advanced.

Fasting hypoglycemia can be caused by disorders affecting various parts of the endocrine system. One such disorder is adrenal insufficiency; continued secretion of cortisol by the adrenal cortex is required for maintenance of normal glycogen stores and of the enzymes of glycogenolysis and gluconeogenesis. Severe hypothyroidism also may lead to hypoglycemia. Impairment in the function of the anterior pituitary gland predisposes a patient to hypoglycemia through several mechanisms, including reduced function of the thyroid gland and adrenal cortices (which depend on pituitary secretions for normal activity) and reduced secretion of growth hormone. Growth hormone plays an important physiologic role in the prevention of fasting hypoglycemia by signaling metabolic changes that allow heart and skeletal muscles to derive energy from stored fats, thereby sparing glucose for the brain. Specific replacement therapies are available for
deficiencies of thyroxine, cortisol, and growth hormone.

Hypoglycemia has occasionally been reported as a side effect of treatment with medications other than those intended for treatment of diabetes. Drugs that have been implicated include sulfonamides, used for treatment of bacterial infections; quinine, used for treatment of falciparum malaria; pentamidine isethionate, given by injection for treatment of pneumocystosis; ritodrine, used for inhibition of premature labor; and propranolol or disopyramide, both of which are used for treatment of cardiac arrhythmias. Malnourished patients seem to be especially susceptible to the hypoglycemic effects of these medications, and management should consist of nutritional repletion in addition to discontinuation of the drug responsible. In children, aspirin or other medicines containing salicylates may produce hypoglycemia.

Alcohol hypoglycemia occurs in persons with low bodily stores of glycogen when there is no food in the intestine. In this circumstance, the only potential source of glucose for the brain is gluconeogenesis. When such an individual drinks alcohol, its metabolism within the liver prevents the precursors of glucose from entering the pathways of gluconeogenesis. This variety of fasting hypoglycemia can occur in persons who are not chronic alcoholics: It requires the ingestion of only a moderate amount of alcohol, on the order of three mixed drinks. Treatment involves the nutritional repletion of glycogen stores and the limitation of alcohol intake.

Severe infections, including overwhelming bacterial infection and malaria, can produce hypoglycemia by mechanisms that are not well understood. Patients with very severe liver damage can develop fasting hypoglycemia, because the pathways of glycogenolysis and gluconeogenesis in the liver are by far the major sources of circulating glucose in the fasted state. In such cases, the occurrence of hypoglycemia usually marks a near-terminal stage of liver disease. Uremia, the syndrome produced by kidney failure, can also lead to fasting hypoglycemia.

Some types of fasting hypoglycemia occur predominantly in infants and children. Babies in the first year of life may have an inappropriately high secretion of insulin. This problem occurs especially in newborn infants whose mothers had increased circulating glucose during pregnancy. Children from two to ten years of age may develop ketotic hypoglycemia, which is probably related to insufficient gluconeogenesis. These disorders tend to improve with time. Fasting hypoglycemia is also an important manifestation of a variety of inherited disorders of metabolism characterized by the abnormality or absence of one of the necessary enzymes or cofactors of glycogenolysis and gluconeogenesis or of fat metabolism (which supplies the energy for gluconeogenesis). Most of these disorders become evident in infancy or childhood. If there is a hereditary or acquired deficiency of an enzyme of glucose production, the problem can be circumvented by provision of a continuous supply of glucose to the affected individual.

There are several other rare causes of fasting hypoglycemia. A few individuals have had circulating antibodies that caused hypoglycemia by interacting with the patient’s own insulin or with receptors for insulin on the patient’s cells. Although the autonomic (involuntary) nervous system has an important role in signaling recovery from hypoglycemia, diseases affecting this branch of the nervous system do not usually produce hypoglycemia; presumably, hormonal mechanisms can substitute for the missing neural signals.

Reactive hypoglycemia can occur with an unusually rapid passage of foodstuffs through the upper intestinal tract, such as may occur after partial or total removal of the stomach. Persons predisposed to maturity-onset diabetes may also have reactive hypoglycemia, probably because of the delay in the secretion of insulin in response to a meal. Finally, reactive hypoglycemia need not indicate the presence of any identifiable disease and may occur in otherwise normal individuals.

Diagnosis of reactive hypoglycemia is made difficult by the variability of symptoms and of glucose concentrations from day to day. Adding to the diagnostic uncertainty, circulating glucose normally rises and falls after meals, especially those rich in carbohydrates. Consequently, entirely normal and asymptomatic individuals may sometimes have glucose concentrations at or below the levels found in persons with reactive hypoglycemia. Therefore, the
glucose tolerance test, in which blood samples are taken at intervals for several hours after the patient drinks a solution containing 50 to 100 grams of glucose, is quite unreliable and should not be employed for the diagnosis of reactive hypoglycemia. Proper diagnosis of reactive hypoglycemia depends on careful correlation of the patient’s symptoms with the circulating glucose level, preferably measured on several occasions after ingestion of ordinary meals. Some persons develop symptoms such as weakness, nausea, sweating, and tremulousness after meals, but without a significant reduction of circulating glucose. This symptom complex should not be confused with hypoglycemia.

When rapid passage of food through the stomach and upper intestine causes reactive hypoglycemia, the administration of drugs that slow intestinal transit may be helpful. When reactive hypoglycemia has no evident pathological cause, the patient is usually advised to take multiple small meals throughout the day instead of the usual three meals and to avoid concentrated sweets. These dietary modifications can help avoid hypoglycemia by reducing the stimulus to secrete insulin.

Two rare inherited disorders of metabolism can produce reactive hypoglycemia after the ingestion of certain foods. In hereditary fructose intolerance, the offending nutrient is fructose, a sugar found in fruits as well as ordinary table sugar. In
galactosemia, the sugar responsible for hypoglycemia is galactose, a major component of milk products. Management of these conditions, which usually become apparent in infancy or childhood, consists of avoidance of the foods responsible.

Perspective and Prospects

Fasting hypoglycemia is uncommon, except in the context of treatment of diabetes mellitus. The most serious public health problem associated with hypoglycemia is that it limits the therapeutic effectiveness of insulin and sulfonylurea drugs. Evidence suggests that elevation of the circulating glucose concentration (hyperglycemia) is responsible for much of the disability and premature death among patients withdiabetes. In many of these patients, therapeutic regimens consisting of multiple daily injections of insulin or continuous infusion of insulin through a small needle placed under the skin can reduce the average circulating glucose to normal. Frequent serious hypoglycemia is the most important adverse consequence of such regimens. Persons with diabetes seem to be at especially high risk for dangerous hypoglycemia for two reasons. First, there is often a failure of the warning systems that ordinarily cause uncomfortable symptoms when the circulating glucose concentration declines, a situation termed hypoglycemic unawareness. As a consequence, when a patient with diabetes attempts to control his or her blood sugar with more frequent injections of insulin, there may occur unheralded episodes of hypoglycemia that can lead to serious alterations in mental activity or even loss of consciousness. Many patients with diabetes also have hypoglycemic unresponsiveness, an impaired ability to recover from episodes of hypoglycemia. Also, diabetes can interfere with the normal physiologic responses that cause the secretion of glucagon in response to a reduction of circulating glucose, thus eliminating one of the most important defenses against hypoglycemia. If both hypoglycemic unawareness and hypoglycemic unresponsiveness could be reversed, intensive treatment of diabetes would become safer and more widely applicable.

Reactive hypoglycemia, although seldom a clue to serious disease, has attracted public attention because of its peculiarly annoying symptoms. These symptoms, which reflect activation of the sympathetic nervous system, resemble those of fear and anxiety. The symptoms are not specific, and many patients with these complaints do not have hypoglycemia.

In summary, hypoglycemia indicates defective regulation of the supply of energy to the body. When severe or persistent, hypoglycemia can lead to serious behavioral disorder, obtunded consciousness, and even brain damage. Fasting hypoglycemia may be a clue to significant endocrine disease. Reactive hypoglycemia, while annoying, usually responds to simple dietary measures. The study of hypoglycemia has led to many important insights into the regulation of energy metabolism.

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