Is it possible for a country to have a mixture of more than just one type of government?

A mixed government is indeed possible. It also may be called a mixed constitution or a balanced government. Nevertheless, by definition, mixed government combines elements of democracy, aristocracy, and monarchy. Thus, it embraces the views, desires, and impact of the many (democracy) with those of the few (aristocracy) and a singular person's (monarchy). Because of the structure of a mixed government, issues are decided in a variety of ways as well. For instance, democracy requires participation of the people (demos), so some decisions are made by popular vote with majority rule. Aristocracy implies that some decisions are made by the few (aristocracy). Then lastly, the one (monarch) makes some decisions. In the English form of government, under which the British North American Colonies resided prior to the War of Independence, the House of Commons, the House of Lords, and the Monarchy (a mixed/balanced government) addressed the “the differing ‘Ranks and Interests’ of the society at large” (The Founders Constitution).

When studying the Enlightenment, Montesquieu’s ideas about balanced government may be the first political theory presented in this regard. Classical writers like Plato, Aristotle, Polybius, and Cicero also believed a balanced/ mixed government was better than dictatorship or absolute monarchy. Also, James Harrington, who wrote during Oliver Cromwell’s Commonwealth period in England, championed the idea of a mixed government with popular sovereignty. During the Renaissance, Niccolo Machiavelli reiterated the classical basis of mixed government in his works. 

Montesquieu used the British government as an example of balanced government, but made no distinction between mixed/ balanced government and the separation of powers. James Harrington’s idea of “a system whereby one part debates and divides, yet another part resolves or chooses, and still another executes” was more influential in American government than Montesquieu's writings (The Founders Constitution). The United States Constitution's institutional checks and balances were the result of creatively tweaking the classical and enlightenment ideas of balanced/ mixed government. The outcome: three separate but equal branches (legislature, judiciary, and executive) whose powers checked and balanced one another became another iteration of mixed government.

What happened to Annemarie's sister, Lise in Number the Stars?

Annemarie refers to her older sister, Lise, with a sense of sadness throughout the book Number the Stars.  It soon is revealed to the reader that Lise died, but it is unclear exactly how.  The reader learns that Lise "died in an accident two weeks before her wedding" when she was eighteen.  Lise had looked forward to marrying Peter and starting a family with him.  

As the story goes on, Annemarie reveals to the reader bits and pieces about the circumstances surrounding her sister's death.  In chapter five, Annemarie tells Ellen how her parents went to the hospital on a rainy night when Lise was in the accident.  They came back "in the middle of the night" to inform Anniemarie that "Lise had died."  They told her that a car had hit her, and Annemarie assumed it was because of the rainy weather.

It is not until the end of the book that the reader finds out exactly how Lise died.  It is two years after the events in the book when Annemarie learns these details.  Annemarie discovers from her parents that Lise was part of the Danish Resistance movement with Peter.  She was at a meeting, which was raided by the Nazis.  Lise ran away, but was purposely run over by a military car. 

What are migraine headaches?

Causes and Symptoms

Migraine is the name given to a particularly severe, chronic, and painful headache that occurs often on one side but sometimes on both sides of the head, usually just behind or above one or both eyes. Until the early twenty-first century, migraines were medically described as vascular headaches resulting from the dilation of blood vessels that supply nervous tissue in the brain. Further research has indicated that the primary source of migraines may be neurological rather than vascular. It appears that neuron messages that control the size of blood vessels in the brain are interrupted as a result of chemical changes in the brain. The dilated vessels become swollen and press on adjacent nerves, neurons, and other brain tissue, which in turn become irritated and inflamed. The result is a throbbing headache that is often debilitating.

Many Americans suffer from migraines, although the actual number may be even higher as many cases remain undiagnosed or are mistaken for sinus headaches or bouts of colds or influenza. Migraines are three times more common in women than in men. More than half of the women experiencing migraines have more headaches near or during their menstrual cycle; these are referred to as menstrual migraines. The peak incidence of migraines occurs between the ages of thirty to forty and wanes after the age of fifty, but they also occur in some children and elderly people. The incidence of migraine headaches is increasing in all age groups, and it is estimated that at least one out of every four individuals suffers from migraines at some point in life. Some medical research has linked certain genes to migraines, indicating that the source might be genetic. This correlates with the fact that 70 to 80 percent of migraine sufferers have family members who also experience migraines.

At least fourteen distinct types of migraine headaches are recognized by the International Headache Society. They can be grouped broadly into three categories: classical migraines, which are preceded by a warning aura; common migraines, which are not preceded by an aura; and atypical migraines.

Migraine symptoms often vary greatly from patient to patient and sometimes from one migraine episode to another. Warning aura symptoms of classic migraines occur within an hour of migraine onset and may include sensitivity to bright lights and sound, especially flashing lights, strobe lights, and laser lights. Some people are disturbed by loud or unexpected noise. Other aura symptoms may include hallucinations, hot flashes, a tingling of limbs that may extend in the hands and feet, numbness or weakness on one side of the body, and cravings for certain kinds of foods. Women experience classic migraines less often than do men.

Aura symptoms are followed by the onset of migraine headache. In most types of migraines, the pain is concentrated on one side of the head and then may radiate into the face, eyes, and sinuses. As the migraine becomes increasingly severe, nausea, vomiting, and dizziness are manifested, along with increased urination and sometimes diarrhea. Some patients report vision problems including blind spots, sensitivity to bright and flickering lights, double vision, or tunnel vision.

Three types of migraines occur mostly in children: hemiplegic, basilar, and retinal migraines. Sufferers of hemiplegic migraines sometimes experience temporary paralysis on the same side of the head as the migraine pain. Basilar migraine may last several days, and the pain is centered in the eye and the nerves that control vision. The patient may experience double vision, hearing loss, vertigo, and a bulging, enlarged eye. In both basilar migraine and retinal migraine, temporary blindness or vision blurring may occur.

Two other atypical types of migraines are complicated migraines, in which both symptoms and aura persist for a week or more, and abdominal migraines, in which migraine pain is transferred to the abdominal area. Abdominal migraine is a recurrent disorder that occurs mainly in children. Moderate to severe abdominal pain and nausea may last for up to three days. The source of this type of migraine is unknown. Most children who experience abdominal migraines suffer migraine headaches later in life.

The causes of migraines are varied. Heredity, lifestyle, environmental factors, and changes in hormone levels have all been implicated, and probably all contribute to some degree to the onset and severity of migraines. Some specific migraine triggers include lights, weather changes, certain foods, food additives, certain beverages, odors, lack of sleep, loud noises, and stress. In many patients, a single factor may trigger a migraine, while in other patients several factors may work in tandem, each contributing to the onset of the migraine. It is recommended that migraine victims keep a headache log or diary. This will help to identify individual triggers and narrow down the causes. As much as possible, these triggers should be avoided or limited. A few patients report no obvious triggers that initiate their migraine headaches.

Bright or strong lights, especially when glaring or flickering, are incipient migraine triggers in some patients. In others, the flickering of a television or computer screen or strobe lighting may start a migraine. Changes in weather also initiate migraines, at least in some patients, especially the rapid temperature and humidity changes during the fall/winter and spring/summer transition periods.

Foods that trigger migraines in some patients include dairy products, eggs, red wines and other alcoholic drinks, and caffeinated and carbonated drinks. Preserved foods that contain high levels of nitrates, such as hot dogs or pepperoni, and pickled foods have also been implicated as migraine triggers. Some migraine sufferers also react to foods that contain a high content of specific amino acids such as tyramine and tyrosine.

Probably the most compelling correlation can be made between the amount of stress in a person’s life and the onset and frequency of migraines. Emotional factors that have been implicated as migraine triggers include frustration, anger, and depression. In addition, emotional stress may exacerbate response to other migraine triggers as well.

Unlike tension headaches, migraines are so frequent and so painful that most patients seek medical attention. Migraines are clinically diagnosed by health care specialists who employ radiological and laboratory tests to ensure that other factors such as tumors or epilepsy are not the cause of headaches.

Treatment and Therapy

The treatment of migraines fall roughly into two categories: prescription drugs or changes in lifestyle to prevent migraines, and various strategies to alleviate the pain and duration of migraines. For many migraine sufferers, taking over-the-counter nonsteroidal anti-inflammatory drugs (NSAIDs) as needed (such as Advil, Motrin, Aleve, or Excedrin Migraine), drinking plenty of water, and eating regularly spaced meals helps to prevent or minimize the occurrence of migraines.

To prevent the onset of migraines, powerful antidepressants may be prescribed, particularly drugs that shut down terminal nerve receptors, thereby stopping further pain transmission sequences. Most effective are tricyclic antidepressants, such as amitriptyline, nortriptyline (Pamelor), and protriptyline (Vivactil). They appear to reduce the effect of migraines by changing the level of serotonin and other brain chemicals. These medications are considered to be first-line treatment agents. In some cases, these medical treatments have met with mixed success and have limited effectiveness.

Therapeutic strategies for sufferers of severe migraines employ some of the armamentarium of medically prescribed drugs now available, including beta-blockers, barbiturates, ergotamines, triptans, botulinum toxin type A (Botox) injections, antidepressants, serotonin inhibitors, and anticonvulsants. Of these drugs, some of the most powerful are ergotamines, which are derivatives of ergot alkaloids. They are injected into the muscle or vein or placed under the tongue. Ergot-derived drugs are potentially dangerous, however, and should be taken with caution. They should never be taken if the patient is pregnant or has a blood disease. Any medication that constricts blood vessels can be very dangerous if the victim already suffers from narrowing of the blood vessels, such as high blood pressure or coronary artery disease.

The triptans, including sumatriptan (Imitrix), rizatriptan (Maxalt), zolmitriptan (Zomig), almotriptan (Axert), naratriptan (Amerge), frovatriptan (Frova), and eletriptan (Relpax), can help to lessen the effects of migraines quickly. The first of the triptans to be used, Imitrix, acts to balance chemicals in the brain by binding to serotonin receptors and causing blood vessels to constrict. The others act similarly. Imitrix can be administered orally, by nasal spray, or by injection. Since triptans are not addictive narcotics or barbiturates, migraine pain can be relieved while the victim is still alert and in control. Side effects of triptans can include nausea, dizziness, and muscle weakness. On rare occasion, they can lead to stroke or heart attack. The triptan drugs should not be used with ergotamines or with antidepressants, particularly monoamine oxidase inhibitors (MAOIs) or selective serotonin reuptake inhibitors (SSRIs) such as Prozac. When used with antidepressants, triptans can produce serotonin syndrome, an excessive release of serotonin, which can result in weakness, tremors, and lack of coordination. A physician should be consulted before mixing any migraine drugs.

Self-care remedies aimed at preventing migraines include stress management, aerobic exercise, yoga, meditation, acupuncture, anger management, fasting, psychotherapy aimed at developing a positive attitude, emotional repair and stabilization, biofeedback, and the use of herbal and flower extracts. Magnesium supplements help some migraine victims.

A few migraine sufferers resort to folk remedies such as vinegar compresses, warm salt packs, herbal or ice footbaths, or headache tonics. One popular headache tonic consists of fresh ginger root, coriander seeds, diced garlic, and honey. Folk remedies should never be substituted for medical attention.

During and immediately following a migraine, most patients attempt to lessen or alleviate pain by ice packs and aspirin, acetaminophen (Tylenol), or other nonprescription drugs.

Perspective and Prospects

Although the pain is sometimes debilitating for short periods following attacks, migraines are not life-threatening. Furthermore, there are typically no serious afteraffects of migraine headaches, although the individual is often wan, fatigued, and sometimes confused following a migraine episode. Some recent medical studies have shown that some migraine sufferers are at increased risk of stroke.

The incidence and intensity of migraine headaches wanes with age; most patients report that migraines either disappeared or become infrequent after the age of fifty. Many female patients also report that migraines stopped following menopause.

Bibliography

American Council for Headache Education. Migraine: The Complete Guide. New York: Dell, 1994.

Davidoff, Robert A. Migraine: Manifestations, Pathogenesis, and Management. 2d ed. New York: Oxford University Press, 2002.

Evans, Randolph W., and Ninan T. Mathew. Handbook of Headache. 2d ed. Philadelphia: Lippincott Williams & Wilkins, 2005.

Henry, Katherine A., and Anthony P. Bossis. One Hundred Questions and Answers About Migraine. 2d ed. Sudbury, Mass.: Jones and Bartlett, 2009.

Mayo Clinic. "Migraine." Mayo Clinic, June 4, 2013.

MedlinePlus. "Migraine." MedlinePlus, August 15, 2013.

Milne, Robert D., and Blake More, with Burton Goldberg. Definitive Guide to Headaches: An Alternative Medicine. Tiburon, Calif.: Future Medicine, 1997.

Montemayor-Quellenberg, Marjorie. "Migraine—Child." Health Library, September 3, 2012.

National Institute of Neurological Disorders and Stroke. "NINDS Migraine Information Page." NIH National Institute of Neurological Disorders and Stroke, July 2, 2013.

Paulino, Joel, and Ceabert J. Griffith. The Headache Sourcebook. Chicago: McGraw-Hill/Contemporary Books, 2001.

Priedt, Robert. "Migraine Doctors in Short Supply Across U.S." MedlinePlus, June 28, 2013.

Wood, Debra. "Migraine—Adult." Health Library, October 24, 2012.

Young, William B., and Jefferson Headache Center. Jefferson Headache Manual. New York: Demos Medical, 2011.

How is alcohol advertised?

Alcohol as Image

Since the ancient Greeks celebrated Dionysus, the god of wine, theater, and ecstasy, a connection has endured among alcohol, media, and sensuality. In addition to sharing a profound appeal to the senses, alcohol, theater, and ecstasy offer an escape from the mundane and a sense of liberation. The view of intoxication as a celebration and a rite of passage continues to this day, anchored by the many messages modern society reflects in its depictions of alcohol through advertising.

Echoes of Dionysus reverberate throughout much modern advertising for alcohol, which often touts youth, sexual prowess, beauty, and athleticism. Initiation into manhood, quite often involving male bonding through modern-day sporting events, is rarely viewed as complete without alcohol. Alcohol advertisers carefully create their own myths about alcohol normalcy, portraying a world where the successful people drink and all drinkers are rewarded.

Through advertising, young people in particular learn to associate alcohol with social acceptance. Those who abstain are promptly left behind and dismissed. Young people are especially susceptible to the lure of alcohol advertising. The images depicting alcohol’s social benefits are wildly exaggerated and distorted by alcohol advertising, and many young people tend to accept the misconception that drinking will somehow improve their lives.

Instead of finding the advertised camaraderie and companionship, many will find themselves, years later, abusing alcohol alone. Alcohol advertising frequently sells one reality but delivers another.

Alcohol Advertising and Youth

The legal age to buy alcohol in all fifty US states is twenty-one years. Many people argue that some alcohol advertising campaigns are designed specifically to appeal to the youth market, despite the legal barriers to consumption. One such compelling argument was frequently made about the advertising mascot Spuds McKenzie, a highly appealing 1980s ad image of a bull terrier dog, the original “party animal.”

Wearing sunglasses, a bandana, a Hawaiian shirt, and headphones, and holding a Bud Light beer, Spuds was depicted in tropical locales and surrounded by beautiful, scantily clad young women. First appearing to acclaim in a 1987 Bud Light commercial during the broadcast of the Super Bowl, Spuds, throughout the late 1980s, rode skateboards, raced horses, drove convertibles, maneuvered surfboards, played Frisbee, and combed beaches.

Sales of Bud Light beer soared during the Spuds ad campaign, which not only marketed the alcoholic beverage but also sold millions of dollars of Spuds paraphernalia: everything from T-shirts to caps to plush toys. Antidrinking groups responded by arguing that the campaign targeted children and teenagers. In 1989, Mothers Against Drunk Driving claimed that Anheuser-Busch
, the maker of Bud Light, was deceptively marketing alcohol to children and demanded that Spuds ads cease promoting the beer. An investigation of the ad campaign by the Federal Trade Commission (FTC) ensued, and although the FTC found no wrongdoing by Anheuser-Busch, the company nevertheless terminated the campaign in 1989.

Anheuser-Busch again ignited controversy in the 1990s with its Budweiser Frogs ad campaign. First appearing as a Super Bowl television commercial in 1995, the Budweiser Frogs depicted three frogs, Bud, Weis, and Er, who lived on a log in a swamp behind a bar and croaked “Budweiser” rhythmically. In 1996, a study revealed that considerable numbers of nine- to eleven-year-old children could easily identify the Budweiser Frogs and associate them with beer, but were unable to recognize or identify various children’s cartoon figures. Antidrinking groups again accused the alcohol industry of targeting children.

Shortly thereafter, another study revealed that when asked to name US presidents, most eight- to twelve-year-old children could name few but had no difficulty naming a variety of brands of beer. In spite of these negative reports, the Budweiser Frogs campaign continued for many years; it is recognized in the adverting industry as one of most successful marketing campaigns in history.

A 2015 study published in JAMA Pediatrics found that exposure to alcohol ads predicted onset of underage drinking as well as binge and hazardous drinking in young people between the ages of fifteen and twenty-three. However, the same year, a study from the University of Texas at Austin found that while alcohol advertising increased 400% between 1971 and 2011, overall alcohol sales did not do so significantly, suggesting a weaker link between advertising and alcohol consumption.

Alcohol and Sporting Events

The alcohol industry is a frequent sponsor and promoter of sporting events, many of which appeal to a large percentage of fans who are minors. From the Super Bowl to the World Series to auto racing to college basketball, the alcohol industry spends billions of sponsorship and advertising dollars each year, specifically targeting an audience of sports fans, many of them younger than twenty-one years.

The alcohol industry provides a lucrative source of funding for collegiate sports, especially the National Collegiate Athletic Association’s (NCAA) annual basketball championships (known as March Madness), but some critics argue that the price for this funding is too high, owing to the toll it levies in the form of underage drinking. The NCAA’s playoff and championship games, for instance, welcome millions of children and minors as viewers each year, who are subjected to the same degree of intense alcohol advertising as adults. Although the alcohol industry maintains that it is advertising its products so rigorously during such sporting events only to establish brand loyalty among adults who already drink, March Madness nonetheless draws millions of underage viewers.

According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), studies reveal a greater propensity among young people to initiate drinking at a younger age if they are heavily exposed to alcohol advertising. Moreover, the NIAAA cites evidence demonstrating that the younger a person begins to drink, the greater the likelihood that he or she will become an alcoholic. For example, statistically, the NIAAA reports that a person who begins drinking by age fifteen years is four times as likely to become a heavy drinker and dependent on alcohol than a person who begins drinking at age twenty-one years.

Children, drawn to watch their favorite sports teams and athletes, are ill equipped to decipher the deceptive messages of alcohol advertising. Youths often come away from watching such sporting competitions with a false sense of normalcy, believing that alcohol consumption as portrayed by advertising is ubiquitous, harmless, fun, and inconsequential, regardless of age or circumstance. Fans attending both collegiate and professional sporting events sponsored by alcohol companies have recently become increasingly dismayed and alarmed at the escalation of public drunkenness and violence occurring among fans, an environment that is growing increasingly unsafe for children.

Bibliography

Bryant, Jennings, and Mary Beth Oliver. Media Effects: Advances in Theory and Research. 3rd ed. New York: Routledge, 2009. Print.

Lankford, Ronnie. At Issue: Alcohol Abuse. Farmington Hills: Greenhaven, 2007. Print.

Martin, Scott C. The SAGE Encyclopedia of Alcohol: Social, Cultural, and Historical Perspectives. Thousand Oaks: Sage, 2015. Print.

Richards, Katie. "Alcohol Ads Increased 400% over 40 Years, but Americans Aren't Drinking More." Adweek. Adweek, 25 Mar. 2015. Web. 27 Oct. 2015.

Sheehan, Kim. Controversies in Contemporary Advertising. Thousand Oaks: Sage, 2004. Print.

Tanski, Susanne E., et al. "Cued Recall of Alcohol Advertising on Television and Underage Drinking Behavior." JAMA Pediatrics 169.3 (2015): 264–71. Print.

Tardiff, Joseph. Teen Alcoholism. Farmington Hills: Greenhaven, 2008. Print.

Wechsler, Henry, and Bernice Wuethrich. Dying to Drink: Confronting Binge Drinking on College Campuses. Emmaus: Rodale, 2002. Print.

How did Veronica and Oupa solve their conflict?

Oupa’s discovery of a letter from Priscilla, Veronica's friend, inviting her to go to Johannesburg, marked the climax of the conflict between Oupa and Veronica. The letter from Priscilla was in response to Veronica’s request to move to Johannesburg, where Priscilla lived with her mother.

Veronica was opposed to her continued stay in the valley, where she worked as a servant for the white landowner. She had dreams of leaving the valley and pursuing music, among other ventures, in the city. Her grandfather, on the other hand, was opposed to this decision because of a previous tragedy in the family. Before Veronica was born, her mother ran away to the city. She later became terribly ill, forcing Veronica's grandmother to go to the city to stay with her. Unfortunately, Veronica's mother passed on, leaving behind Veronica as a little baby, who was raised by her grandparents.

Due to this terrible experience, Oupa feared for her granddaughter’s departure to the city. He prevented her from leaving, believing it would be the same mistake her mother made. However, Veronica had made up her mind, and to resolve the conflict, her reasons for leaving. She asserted that singing was her life, and she was obligated to tend to her passion and talent just as Oupa tended to his vegetables. In addition, she informed her grandfather that he raised her to be strong enough to survive in the bustling city. This convinced Oupa to yield to Veronica’s wishes, and he allowed her to leave for the city.

...Veronica comes to her Oupa to tell him that he must let her go. Like the pumpkin seeds he plants and tends so carefully, she tells him she, too, has grown up. She explains to him that her singing is her life, and she must tend it the way old Buks tends his vegetables. He warns her that it is a bad world outside of their little valley, but she insists that he has helped to make her strong, and the time for her to leave is now. Finally, old Buks gives Veronica his blessing...

What are natural treatments for sexual dysfunction in men?

Introduction

Impotence, or erectile dysfunction, is the inability to achieve an erection. Impotence has a minimum of fifteen possible causes, including diabetes, drug side-effects, pituitary tumors, hardening of the arteries, hormonal imbalances, and psychological factors. A few of these conditions respond to specific treatment. For example, if a blood pressure drug is causing impotence, the best approach is to change drugs. If a pituitary tumor is secreting the hormone prolactin, treating that tumor may result in immediate improvement. However, in most cases, conventional treatment of impotence is nonspecific.

The drugs Viagra and Cialis have revolutionized treatment for erectile dysfunction. These medications work by increasing tissue sensitivity to the blood-vessel-dilating substance nitric oxide (NO) in the penis. Older methods include mechanical devices that utilize a vacuum to produce an erection, drugs for self-injection, and implantation of penile prostheses.

Proposed Natural Treatments

Korean red ginseng. Two double-blind, placebo-controlled trials, involving about 135 people, found evidence that Korean red ginseng may improve erectile function. In the better of the two trials, 45 participants received either placebo or Korean red ginseng at a dose of 900 milligrams (mg) three times daily for eight weeks. After a one-week period of no treatment, the two groups were switched. The results indicate that while using Korean red ginseng, men experienced significantly better sexual function than while they were taking placebo.

In an analysis combining the results of six controlled trials, researchers found some evidence for the benefits of Korean red ginseng. However, the small size and generally low quality of the studies left some doubt about this conclusion.

L-arginine. Nitric oxide (NO) plays a role in the development of an erection. Drugs such as Viagra increase the body’s sensitivity to the natural rise in NO that occurs with sexual stimulation. A simpler approach might be to raise NO levels, and one way to accomplish this involves the use of the amino acid L-arginine. Oral arginine supplements may increase nitric oxide levels in the penis and elsewhere. Based on this, L-arginine has been advertised as “natural Viagra.” However, there is little evidence that arginine works. Drugs based on raising NO levels in the penis have not worked for pharmaceutical developers; the body seems to simply adjust to the higher levels and maintain the same level of response.

The main support for the use of arginine in erectile dysfunction comes from a small double-blind trial in which fifty men with erectile dysfunction received either 5 grams (g) of L-arginine or placebo daily for six weeks. More men in the treated group experienced improvement in sexual performance than in the placebo group.

A double-blind crossover study of thirty-two men found no benefit with 1,500 mg of arginine given daily for seventeen days; the much smaller dose and shorter course of treatment may explain the discrepancy between these two trials.

Arginine has also been evaluated with the drug yohimbine (made from the herb yohimbe). A double-blind, placebo-controlled trial of forty-five men found that one-time use of this combination therapy one or two hours before intercourse improved erectile function, especially in those with only moderate erectile dysfunction scores. Arginine and yohimbine were both taken at a dose of 6 g. One should not use the drug yohimbine (or the herb yohimbe) except under physician supervision, as it presents a number of safety risks.

Carnitine
. In a six-month double-blind trial of 120 men with an average age of sixty-six, carnitine (propionyl-L-carnitine, 2 g per day, plus acetyl-L-carnitine, 2 g per day) and testosterone (testosterone undecanoate, 160 mg per day) were separately compared with placebo. The results indicated that both carnitine and testosterone improve erectile function; however, while testosterone significantly increased prostate volume, carnitine did not.

Another double-blind, placebo-controlled study found that propionyl-L-carnitine at 2 g per day enhanced the effectiveness of sildenafil (Viagra) in forty men with diabetes who had previously failed to respond to sildenafil a minimum of eight times. In another double-blind study, a combination of the propionyl and acetyl forms of carnitine enhanced the effectiveness of Viagra in men who had erectile dysfunction caused by prostate surgery. Carnitine has also shown promise for treating male infertility.

Other treatments. A proprietary combination therapy containing arginine and Ginkgo biloba, ginseng, and vitamins and minerals has shown some promise in an unpublished study. Also, in a three-week, double-blind, placebo-controlled trial, twenty men with erectile dysfunction received either placebo or a special form of magnet therapy called pulsed electromagnetic field therapy (PEMF). PEMF was administered by means of a small box worn near the genital area and kept in place as long as possible during the study period; neither participants nor observers knew whether the device was actually activated or not. The results showed that the use of PEMF significantly improved sexual function compared with placebo.

A double-blind, placebo-controlled study enrolled forty men with difficulty achieving or maintaining an erection who also had low measured levels of dehydroepiandrosterone (DHEA). The results showed that DHEA at a dose of 50 mg daily improved sexual performance; however, the authors failed to provide a statistical analysis of the results, making the meaningfulness of this study impossible to determine.

Severe zinc deficiency is known to negatively affect sexual function. Because marginal zinc deficiency is relatively common, it is logical to suppose that supplementation with zinc may be helpful for some men. However, this hypothesis has only been studied in men receiving kidney dialysis. The results were promising.

The herb Butea superba has shown some promise for erectile dysfunction, according to a three-month randomized, double-blind study performed in Thailand. In other studies, weak evidence hints at potential benefit with pomegranate juice, melatonin, and oligomeric proanthocyanidins (alone or with arginine).

Based on preliminary evidence, the herb maca (Lepidium meyenii) has been advertised as an “herbal Viagra.” In one study in rats, the use of maca enhanced male sexual function. There is one published human trial too. In this small, twelve-week, double-blind, placebo-controlled study, the use of maca at 1,500 mg or 3,000 mg increased male libido. The study did not report benefits in male sexual function, just in desire. Because the loss of sexual function is a more common problem in men than loss of sexual desire, these results do not justify the “herbal Viagra” claim. Contrary to some reports, maca does not appear to affect testosterone levels.

Many other herbs are also reputed to improve sexual function in men, including ashwagandha, Avena sativa (oat straw), catuaba, Cordyceps, damiana, diindolylmethane, Eleutherococcus (Siberian ginseng), L-citrulline, Mucuna pruriens, molybdenum, muira puama (potency wood), pygeum, Polypodium vulgare, Rhodiola rosea, saw palmetto, schisandra, suma, traditional Chinese herbal medicine, and Tribulus terrestris. However, there is no real evidence that these herbs offer any benefits.

Numerous case reports and uncontrolled studies had indicated that the herb Ginkgo biloba offers dramatic benefits for male (and female) sexual disorders caused by antidepressants. However, double-blind, placebo-controlled studies are necessary to truly establish efficacy. When studies of this type were performed, it became clear that people had been misled about ginkgo’s efficacy by the power of suggestion: Ginkgo failed to improve sexual function to any greater extent than placebo.

In a small single-blind study, acupuncture proved superior to fake acupuncture for treatment of erectile dysfunction. However, because the treating practitioners administrating the control treatment were aware that they were providing sham acupuncture, it is quite likely that they unconsciously communicated lack of confidence as they provided it; this is an inherent limitation of single-blind studies.

Deer or antelope velvet antler is a popular treatment for sexual dysfunction. However, the one double-blind study performed on the subject failed to find benefit.

Herbs and Supplements to Use with Caution

The U.S. Food and Drug Administration has warned consumers not to purchase or consume several brands of dietary supplements after samples were found adulterated with the prescription drug tadalafil (Cialis), an analogue of sildenafil (Viagra). The products named in the warning are SIGRA, STAMINA Rx, STAMINA Rx for Women, Y-Y, Spontane ES, and Uroprin (all manufactured by NVE and distributed by Hi-Tech).

The herb yohimbe is the source of the drug yohimbine, which has been shown to be modestly better than placebo for impotence. However, because of many drug interactions and other risks, yohimbine is not recommend for use except under the supervision of a physician. Because there is no agency regulating the quality and labeling of herbal products, the herb yohimbe presents even more risks, such as unpredictable yohimbine content.

Soy or soy isoflavones, and the herb licorice, may reduce testosterone levels in men. For this reason, men with impotence, infertility, or decreased libido may want to avoid these natural products.

One report claims that both tea tree oil and lavender oil have estrogenic (estrogen-like) and antiandrogenic (testosterone-blocking) effects. If this were true, men with erectile dysfunction would be advised to avoid use of these herbs. However, a literature search failed to find any other published reports that corroborate this claim.

One case report suggests that a product containing the herb Epimedium grandiflorum (horny goat weed) caused rapid heart rate and symptoms similar to mania. The supplement androstenedione, often taken for male sexual dysfunction in the belief that it increases testosterone levels, actually appears to increase estrogen levels in men and might, therefore, increase problems with erectile function.

Bibliography

Cavallini, G., S. Caracciolo, et al. “Carnitine Versus Androgen Administration in the Treatment of Sexual Dysfunction, Depressed Mood, and Fatigue Associated with Male Aging.” Urology 63 (2004): 641-646.

Cavallini, G., F. Modenini, et al. “Acetyl-L-Carnitine plus Propionyl-L-Carnitine Improve Efficacy of Sildenafil in Treatment of Erectile Dysfunction After Bilateral Nerve-Sparing Radical Retropubic Prostatectomy.” Urology 66 (2005): 1080-1085.

Cherdshewasart, W., and N. Nimsakul. “Clinical Trial of Butea superba, an Alternative Herbal Treatment for Erectile Dysfunction.” Asian Journal of Andrology 5 (2003): 243-246.

Conaglen, H. M., J. M. Suttie, and J. V. Conaglen. “Effect of Deer Velvet on Sexual Function in Men and Their Partners.” Archives of Sexual Behavior 32 (2003): 271-278.

Engelhardt, P. F., et al. “Acupuncture in the Treatment of Psychogenic Erectile Dysfunction.” International Journal of Impotence Research 15 (2003): 343-346.

Forest, C. P., H. Padma-Nathan, and H. R. Liker. “Efficacy and Safety of Pomegranate Juice on Improvement of Erectile Dysfunction in Male Patients with Mild to Moderate Erectile Dysfunction.” International Journal of Impotence Research 19 (2007): 564-567.

Gentile, V., et al. “Preliminary Observations on the Use of Propionyl-L-Carnitine in Combination with Sildenafil in Patients with Erectile Dysfunction and Diabetes.” Current Medical Research and Opinion 20 (2004): 1377-1384.

Henley, D. V., et al. “Prepubertal Gynecomastia Linked to Lavender and Tea Tree Oils.” New England Journal of Medicine 356 (2007): 479-485.

Jang, D. J., et al. “Red Ginseng for Treating Erectile Dysfunction.” British Journal of Clinical Pharmacology 66 (2008): 444-450.

What is Williams syndrome?

Risk Factors

There are no known risk factors. The incidence of Williams syndrome is estimated to be less than 1 in 10,000 people. The disease almost always occurs sporadically. In the few reported examples of familial transmission, the deletion acts as an autosomal dominant mutation. Williams syndrome affects males and females equally.

Etiology and Genetics

Williams syndrome is caused by a loss of DNA from band 7q11.23 of chromosome 7. Therefore while the normal number of chromosomes is maintained, approximately twenty-five genes are lost because of the deletion. This region is referred to as the Williams-Bueren syndrome critical region (WBSCR). The deletion of the WBSCR in chromosome 7 is believed to be the result of unequal crossover events during meiosis. This region is flanked by low copy repeats that increase the likelihood of nonallelic homologous recombination. The deletion arises with equal frequency on the maternally or the paternally inherited chromosome 7. The size of the deletion can vary from 1.5 to 1.8 Mb pairs of DNA. Amongst the deleted genes is the elastin (ELN) gene. Loss of this gene is associated with the connective tissue abnormalities, cardiovascular disease (specifically supravalvular aortic stenosis), and facial dysmorphology found in people with this disease.

Other genes contained in this region include LIMK1 (lim kinase 1), GTF2IRD1 (part of the TFII-1 transcription family), and GTF2I (general transcription factor II, I). Their deletion may be responsible for the characteristic difficulties with visual-spatial tasks. Evidence also exists that the loss of the CLIP2 gene, among others, may contribute to the learning disabilities and other cognitive difficulties seen in Williams syndrome.

Most cases of Williams syndrome occur as random events during the formation of reproductive cells in a parent of an affected individual. These cases occur in people with no history of the disorder in their family. Williams syndrome is an autosomal dominant mutation. Williams syndrome should be distinguished from other syndromes that include developmental delay, short stature, distinctive facies, and congenital heart disease, such as Noonan syndrome
(deletion in chromosome 22q11) and Smith-Magenis syndrome (deletion in chromosome 17p11.2).

Symptoms

The onset of symptoms usually occurs just after birth or during infancy and begins with physical characteristics, irritability, colic, and feeding problems. Almost all cases of Williams syndrome have typical facial features that can be recognized even at birth. Williams patients usually have problems with spatial-visual tasks but have strong abilities in the area of music and spoken language. They often have outgoing and engaging personalities. Children often have delays in walking and speaking; however, the latter improves with age. Motor difficulties persist at all ages. Symptoms progress to abdominal pain in adolescents, diabetes, high blood pressure, heart failure (specifically supravalvular aortic stenosis, SVAS, and supravalvular pulmonary stenosis, SVPS), and hearing loss in adults.

Elastin arteriopathy is present in about 75 percent of Williams individuals, with the most common being SVAS. In most cases, morbidity is due to this aortic narrowing, which can lead to elevated left heart pressure, cardiac hypertrophy, and eventually cardiac failure.

Screening and Diagnosis

The clinical manifestations include a distinct facial appearance, which can be observed early after birth. Other characteristics such as cardiovascular anomalies and hypocalcemia, can be detected via electroencephalogram and routine blood examinations. The deletion in chromosome 7 is not detected through standard karyotyping but rather through fluorescence in situ hybridization (FISH). Testing is routinely performed on peripheral blood leukocytes. FISH testing and karyotype are performed in cytogenetics laboratories.

Prenatal testing is clinically available but is rarely used because most cases occur in a single family member only and no prenatal indicators exist for low-risk pregnancies.

Treatment and Therapy

There is currently no cure for Williams syndrome. Williams syndrome is a complex multisystem medical condition that requires the attention of multiple health care professionals. Initial care often centers on failure to thrive, hypocalcemia, or repair of the cardiac lesion. Physical therapy is helpful to patients with joint stiffness. Developmental and speech therapy can also help affected children; for example, verbal strengths can help make up for other weaknesses. Other treatments are based on a patient’s symptoms.

Prevention and Outcomes

There is no known way to prevent the genetic problem that causes Williams syndrome. Prenatal testing is available for couples with a family history of Williams syndrome who wish to conceive. About 75 percent of those with Williams syndrome have some intellectual disability. Most patients will not live as long as normal, due to complications. Most patients require full-time caregivers and often live in supervised group homes.

Bibliography

Bayes, M., et al. “Mutational Mechanisms of Williams-Beuren Syndrome Deletions.” American Journal of Human Genetics 73 (2003): 131–51. Print.

Cassidy, Suzanne B., and Judith E. Allanson. Management of Genetic Syndromes. 3rd ed. Hoboken: Wiley, 2010. Print.

Farran, Emily K., and Annette Karmiloff-Smith. Neurodevelopmental Disorders Across the Lifespan: A Neuroconstructivist Approach. Oxford: Oxford UP, 2012. Print.

Martens, Marilee. “Developmental and Cognitive Troubles in Williams Syndrome.” Pediatric Neurology. Ed. Olivier Dulac, Maryse Lassonde, and Harvey B. Sarnat. Edinburgh: Elsevier, 2013. 291–93. Print.

Morris, C., H. Lenhoff, and P. Wang. Williams-Beuren Syndrome: Research, Evaluation, and Treatment. Baltimore: Johns Hopkins UP, 2006. Print.

Morris, C. A., et al. “Natural History of Williams Syndrome: Physical Characteristics.” Journal of Pediatrics 113 (1988): 318–26. Print.