 1 Chicken Pox
 2 ARTERY DAMAGE by Chiropractors
 3 Athlete's foot
 4 Cholesterol
 5 Depression
 6 Infestation: Ticks
 7 Infestation: Fleas
 8 Infestation: Lice
 9 Infestation: Other
 10 Flies
 11 Mosquitos
 12 germs
 13 Kidney stones, and avoidance
 14 Stroke
 15 Insomnia
 16 Ulcers

\1 Chicken Pox

Chickenpox (Varicella) Shingles (Zoster) Postherpetic Neuralgia (PHN) Varicella Vaccine 

Chickenpox is caused by varicella-zoster virus (VZV) and is usually mild, but it may be severe in infants, adults, and persons with impaired immune systems. Almost everyone gets chickenpox by adulthood (more than 95% of Americans). Chickenpox is highly contagious. Approximately 4 million cases occur in the United States each year. The virus spreads from person to person by direct contact, or through the air. Approximately 90% of persons in a household who have not had chickenpox will get it if exposed t o an infected family member. The greatest number of cases of chickenpox occurs in the late winter and spring. Chickenpox has a characteristic itchy rash, which then forms blisters that dry and become scab  in 4-5 days. The rash may be the first sign of illness, sometimes coupled with fever and general malaise, which is usually more severe in adults. An infected person may have anywhere from only a few lesions to more than 500 lesions on his or her body during an attack (average 300-400). Adults are more likely to have a more serious case of chickenpox with a higher rate of complications and death. Chickenpox is contagious 1-2 days before the rash appears and until all blisters have formed scabs. Chickenpox develops within 10-21 days after contact with an infected person. Every year there are approximately 5,000-9,000 hospitalizations and 100 deaths from chickenpox in the United States. Varicella vaccine has been available since March 1995 and is approved for use in healthy children 12 months of age or older, and susceptible (i.e., no evidence of having had chickenpox in the past) adolescents and adults. Varicella vaccine is highly effective in protecting against severe chickenpox. Cases of disease caused by the wild virus, which may occur in a small  proportion of vaccinees, are typically very mild, with fewer than 50 skin lesions and no fever. It is recommended that all children be routinely vaccinated at 12-18 months of age and that all susceptible children receive the vaccine before their 13th birthday (CDC Advisory Committee on Immunization Practices, the American Academy of Pediatrics and the American Academy of Family Physicians). Many states will require vaccination for entry into pre-school or public school beginning in 1999. The vaccine is also approved for susceptible adolescents and adults, especially those with close contact with persons at high risk for serious complications (e.g., health-care workers, family contacts of immunocompromised persons). 

A history of chickenpox is considered adequate evidence of immunity. A blood test is avail to test immunity in persons who are uncertain of their history or who have not had chicken pox. Many of these persons will find that they are immune when tested and thus will not need to be vaccinated. 

Effective medications (e.g., acyclovir) are available to treat chickenpox in healthy and immunocompromised persons (e.g, those with cancer, human immunodeficiency virus/AIDS; those receiving meds that depress the immune system). 

Varicella zoster immune globulin (VZIG), an immune globulin made from plasma of healthy volunteer blood donors with high levels of antibody to VZV, is recommended after exposure for persons at high risk for complications (e.g., immunocompromised persons, pregnant women, premature infants <28 weeks gestation or <1000 grams at birth and premature infants whose mothers are not immune). For more information about varicella and other vaccine-preventable diseases, contact CDC's National Immunization Hotline at 1-800-232-2522 (English) or 1-800-232-0233 (Spanish). 

Shingles (Zoster)

VZV is associated with two distinct diseases: childhood chickenpox (varicella) and shingles (zoster). Chickenpox usually runs its course in about a week or two, but VZV is not eliminated from the body. The virus becomes dormant in sensory ganglia and may reactivate decades later to produce zoster (shingles) or herpes zoster. The incidence of herpes zoster in the United States is estimated to be 600,000 to one million cases per year. The virus may occasionally revert to its infectious state, but it is usually held in check by cell-mediated immunity (CMI). It is when CMI declines, such as in advanced age, lymphoma, or AIDS, that the virus reverts back to its infectious state and zoster results. It has been reported that blacks have a significantly lower  risk of developing zoster than whites, suggesting a racial difference in susceptibility to VZV reactivation (herpes zoster). It has also been reported that herpes zoster is an early manifestation of HIV infection in young Africans. The first symptom of z oster is usually pain and is caused by nerve damage due to VZV reactivation from latently infected ganglia. It is believed that the pain is usually at the site where the lesions are about to break out.

In rare episodes of zoster infection, pain is accompanied by flu-like symptoms (fever, malaise, chills, gastrointestinal distress, and/or headache). The pain, which can range from mild itching or tingling to severe pain, is followed, usually within 5 day s, by swelling or redness of the skin and clusters of clear vesicles, which soon develop into blisters. The eruption of zoster is unilateral and does not cross the midline. The zoster lesions resemble varicella, but unlike varicella they evolve less rapi dly and appear as grouped vesicles rather than single lesions. They may be scattered in patches or so numerous as to form a continuous band. Most commonly the regions affected are those supplied by the trigeminal nerve and thoracic ganglia. These areas i nclude those around the chest and abdomen, and the eyes (ophthalmic zoster). Normally, new zoster lesions continue to appear for 2-3 days, and within 14 days the lesions become pustular and crusty. At this point, they no longer contain the virus. Though  this is the normal course of zoster, complications can often occur. The most common and debilitating complication is postherpetic neuralgia (PHN). Another major complication of zoster is bacterial infection. This can cause severe complications because of
 the possibility of superficial gangrene and subsequent scarring. In the case of ophthalmic zoster, severe infection can cause corneal opacification or secondary bacterial infection. In general, approximately 10%-20% of the U.S. population will eventuall y develop one or more cases of shingles. However, herpes zoster is more common among immunocompromised persons. Immunocompetence declines with age, disease, and with some medical treatments, such as systemic corticosteroid therapy. Close to 50% of those  who live beyond the age of 80 can expect to develop shingles. Of those patients with HIV infection, AIDS, lymphoma, malignancy, and other immune deficiencies and those who are recipients of bone marrow and kidney transplants, 50% can be expected to devel op zoster. Therefore, otherwise healthy and young adults who develop zoster may wish to have themselves tested for an immunodeficiency or a malignancy (rarely, however, is zoster the only clue to such an illness). As the U.S. population ages, we may also
 expect an increase in the cases of herpes zoster. Diagnosis of Shingles There are two ways to diagnose herpes zoster—clinical diagnosis and laboratory diagnosis. Clinical diagnosis involves evaluating the various symptoms of the disease. Differentiating
 zoster from most diseases is rather clear-cut; the difficulty arises when attempting to differentiate herpes zoster from herpes simplex . Laboratory tests are necessary to accurately diagnose herpes zoster. Treatment of Shingles Acyclovir is a widely us ed drug for the treatment of herpes zoster. The drug reduces healing time, the appearance of new vesicles, the duration of pain and duration of viral shedding. Other drugs, including desciclovir, famciclovir, valaciclovir, and penciclovir--all variants o f acyclovir--have also been shown to provide adequate treatment of herpes zoster. Oral famciclovir (500 mg or 750 mg three times daily for 7 days) is an effective and well-tolerated therapy for herpes zoster. In addition, famciclovir decreases the durati on of PHN. [Top] Postherpetic Neuralgia (PHN) PHN is one of the major complications of herpes zoster (shingles). This is when the patient continues to feel pain even after the skin lesions have crusted. The pain is often severe in the areas where the bli sters occurred. The affected areas are also extremely sensitive to heat and cold. PHN is thought to result from nerve damage caused be the virus. Risk factors for the development of PHN may include severity of pain, significant sensory impairment and adv ancing age. Prompt treatment of acute zoster pain may decrease the incidence of PHN. In dealing with the chronic pain associated with PHN, analgesics can often be used. Steroid treatment is also used to reduce inflammation in the dorsal root ganglia and  nerves, but its use still remains controversial. [Top] Varicella Vaccine A live attenuated varicella virus (Oka strain) vaccine (VARIVAX) was licensed in 1995 in the United States and is manufactured by Merck & Co., Inc. This virus strain was isolated in
 Japan in the early 1970s from a child (Oka) with chickenpox. The virus was attenuated through sequential passages in human embryonic lung cells, embryonic guinea pig cells, and human diploid cells (WI-38). The attenuated virus was then used to immunize  children against chickenpox. Varicella vaccine is lyophilized (freeze dried). When reconstituted as directed by the package insert and stored at room temperature for 30 minutes, the virus contains more than 1,350 plaque forming units of Oka/Merck VZV in  each 0.5-ml dose. Each dose also contains 12.5 mg of hydrolyzed gelatin, trace amounts of neomycin and fetal bovine serum, 25 mg of sucrose, and trace residual components of MRC-5 cells, including DNA and proteins. The vaccine does not contain preservati ves. The seroconversion rate of varicella vaccine among susceptible children 12 months to 12 years of age is 97%. Among vaccinated persons 13 years of age or older, 78% seroconvert after the first dose of varicella vaccine, and 99% seroconvert after a se cond dose. The vaccine has proven to be effective for more than 10 years in preventing varicella. However, breakthrough infection (i.e., cases of chickenpox after vaccination) can occur (less than 1%-4.4%), usually resulting in mild illness. Healthy vacc inated persons have a minimal risk for transmitting vaccine virus to their contacts; this may be higher in vaccinees in whom a varicella-like rash develops following vaccination. Higher risk for transmission of vaccine virus has been documented among chi ldren who have both rash following vaccination and leukemia. In one study, varicella virus vaccine infection occurred in 15 (17%) of 88 exposed, healthy siblings of leukemic vaccine recipients; mild rash developed in 11 siblings. The incidence of herpes  zoster after vaccination among otherwise healthy children is 18 per 100,000 person years of follow-up. Distribution, Handling, and Storage of Vaccine The lyophilized vaccine (VARIVAX) must be stored at an average temperature of 5o F (-15o C) or lower. Th e vaccine should be reconstituted according to the package insert and only with the diluent supplied with the vaccine. The diluent should be stored separately either at room temperature or in the refrigerator. Once reconstituted, the vaccine should be us ed immediately to minimize loss of potency. If not used, the vaccine should be discarded (according to the guidelines for waste disposal of biohazard products) within 30 minutes after reconstitution. Recommendations for the Use of Varicella Vaccine Varic ella virus vaccine has been approved for use among healthy children 12 months to 12 years of age. • Children in this age group should receive one 0.5-ml dose of vaccine subcutaneously. • All children should be routinely vaccinated at 12-18 months of age.
 Varicella vaccine preferably should be administered routinely to children at the same time as MMR (Mumps, Measles, Rubella) vaccine at separate sites and with separate syringes. • Investigational vaccine studies have suggested no notable interactions be tween varicella and any other vaccines that are routinely administered to young children (e.g., measles, mumps, rubella, diphtheria, tetanus, pertussis, Haemophilus influenza type b, hepatitis B virus, live and inactivated polio viruses vaccines). • Simu ltaneous administration of most widely used live, attenuated and inactivated vaccines has not resulted in impaired antibody response or an increased rate of adverse events. Varicella virus vaccine is recommended for all susceptible children by their 13th
 birthday. Varicella virus vaccine is approved for use among healthy adolescents and adults. • Persons 13 years of age or older should be administered two 0.5-ml doses of vaccine, subcutaneously, 4-8 weeks apart. If more than 8 weeks elapse following the
 first dose, the second dose can be administered without restarting the schedule. • Vaccination is recommended for susceptible adolescents, adults, and health-care workers and family contacts of immunocompromised persons. • Vaccination should be consider ed for susceptible persons: teachers of young children, day-care employees, residents and staff of institutional settings, inmates and staff of correctional settings, military personnel, and women who are not pregnant but who may become pregnant in the f uture. • Vaccination should be considered for international travelers who are not immune to VZV infection. Varicella Virus Vaccine Adverse Reactions Pain and redness at the injection site were the only adverse reactions that occurred significantly more o ften in vaccine recipients in controlled clinical trials.

In uncontrolled clinical trials of 8,900 healthy children (12 months to 12 years of age) who received one dose of vaccine, 14.7% developed fever, 19.3% had complaints regarding the injection site, 3.4% had a mild varicella rash at the injection site, and
 3.8% had a non-localized varicella rash. In uncontrolled clinical trials of 1,600 persons age 13 years or older who received one dose, and 955 who received two doses of varicella vaccine: 10.2% and 9.5%, respectively, developed fever; 24.4% and 32.5% ha d complaints regarding the injection site; 3% and 1% developed a varicella-like rash at the injection site; and 5.5% and 0.9%, respectively, developed a non-localized rash. During the first 12 months following vaccine licensure, more than 2.3 million dos es of vaccine were distributed in the United States. The Vaccine Adverse Events Reporting System (VAERS) and the vaccine manufacturer have received a limited number of reports of serious medical events occurring within 6 weeks after vaccination, includin g 4 cases of encephalitis , 7 cases of ataxia, and 10 cases of erythema multiforme. Three cases of anaphylaxis have occurred within 10 minutes of vaccination. A causal relationship between the vaccine and these events has not been determined. Serious adv erse reactions regardless of whether they are or are not suspected to have been caused by varicella vaccine, should be reported to VAERS at 800-822-7967. In addition, in some states, serious adverse reactions should be reported to the State Health Depart ment. Contraindications and Precautions Varicella virus vaccine should not be administered to persons who have a history of anaphylactic reaction to any component of the vaccine, including gelatin and neomycin. Vaccination of persons who have severe illn ess should be postponed until recovery. Vaccination is not recommended for persons who have untreated and active tuberculosis. Varicella virus vaccine is not licensed for use in persons who have any malignant condition. Varicella vaccine should not be ad ministered to persons who have primary or acquired immunodeficiency, including immunosuppression associated with AIDS or other clinical manifestations of HIV infection, cellular immunodeficiency, hypogammaglobulinemia, and dysgammaglubulinemia. Varicella
 vaccine should not be administered to persons who have a family history of congenital or hereditary immunodeficiency in first degree relatives. Varicella virus vaccine should not be administered to persons receiving immunosuppressive doses of corticoste roids. Children who are receiving high doses of systemic steroids (2 mg/kg body weight or more of prednisone) for 2 weeks or longer may be vaccinated after the steroid therapy has been discontinued for at least 3 months. Vaccinees in whom vaccine-related
 rash develops should avoid contact with susceptible immunosuppressed persons. Varicella vaccine should not be administered for at least 5 months after administration of blood, plasma, immunoglobulins (IG), or VZIG. Vaccine recipient should avoid using s alicylates (aspirin) for 6 weeks after vaccination because of the association of aspirin use and Reye’s syndrome following varicella. Pregnant women should not be vaccinated. Non pregnant women who are vaccinated should avoid becoming pregnant for 1 mont h following each injection. Use of VZIG for Post Exposure Prophylaxis Varicella-zoster immune globulin (VZIG) prevents or modifies clinical illness in susceptible, immunocompromised persons who are exposed to varicella or zoster. VZIG is prepared from pl asma obtained from healthy volunteer blood donors who are identified by routine screening to have high antibody titers to VZV. VZIG is a sterile, 10%-18% solution of the globulin fraction of human plasma, primarily immunoglobulin G (IgG) in 0.3 M glycine
 as a stabilizer and 1:10,000 thimerosal as a preservative. VZIG is prepared by cold ethanol precipitation, which eliminates hepatitis B virus, HIV, and other known infectious agents from the product. VZIG is produced by the United States Biologics Labor atories (Massachusetts) and distributed by American Red Cross regional distribution centers. Administration of VZIG VZIG provides maximum benefit when administered as soon as possible after the presumed exposure, but it may be effective if administered a s late as 96 hours after exposure. The protection after VZIG administration may last for a period of approximately 3 weeks. Dosage of VZIG VZIG is supplied in two different dosages: the 125-U vial and the 625-U vial. The recommended dose is 125 U/10 kg ( 22 lbs) of body weight, up to a maximum dose of 625 U. The minimum dose is 125 U and 625 U should be sufficient to modify or prevent infection in healthy adults. Higher doses may be necessary for immunocompromised adults. VZIG should be administered intr amuscularly, as directed by the manufacturer’siinstructions. VZIG should never be used intravenously. Indications for the Use of VZIG The decision to administer VZIG to a person exposed to varicella should be based on whether: 1. The patient is susceptib le to VZV infection. 2. The exposure is likely to result in infection. 3. The patient is at greater risk for complications than the general population. Persons who receive bone-marrow transplants should be considered susceptible, regardless of prior hist ory of varicella or varicella vaccination in themselves or in their donors. Types of Exposure For the Use of VZIG Direct contact exposure of 1 hour or longer with an infectious person while indoors. Sharing the same hospital room with an infectious patie nt or prolonged direct face-to-face contact with an infectious person (e.g., health-care workers). Continuous exposure to household members who have varicella. Recommendations for the Use of VZIG Persons less than 13 years of age: • Immunocompromised chi ldren after substantial exposure to varicella. • Neonates whose mothers become infected with varicella shortly before delivery. • Postnatal exposure of neonates. Persons 13 years of age and older: • Immunocompromised persons who are considered susceptibl e and who have had substantial exposure to varicellashould receive VZIG. • pregnant women who are susceptible and who have been exposed to varicella. • Hospital personnel who are susceptible and are exposed to varicella. VZIG Associated Adverse Effects a nd Precautions The most frequent adverse reaction following VZIG administration is local discomfort at the injection site. Pain, redness, and swelling occur at the injection site in approximately 1% of patients. Less frequent adverse events (0.2%) includ


\2 ARTERY DAMAGE by Chiropractors

In Feb 1998  a 20-year-old woman from Saskatchewan lapsed into a coma on a chiropractor's table and died 24 hours later. She had sought treatment for a stiff neck and, after neck manipulation by the chiropractor, a dissection of a vertebral artery caused an aneurysm that interrupted blood flow to her brain.

Likewise, a 35-year-old mother of four in Seattle suffered a stroke precipitated by a dissected vertebral artery immediately after chiropractic manipulation. She survived but now struggles with simple everyday tasks like tying her shoes.

An arterial dissection starts with a tear inside one of the major arteries in the neck. This allows blood to enter the wall of the artery and split its layers, resulting either in the formation of a clot or in an aneurysm (a pouch sticking out from the blood vessel), possibly disrupting blood flow to the brain and damaging cranial nerves.

Why Does This Happen? Arterial dissections were once thought to be extremely rare and were usually detected only at autopsy. But with the aid of modern diagnostic techniques like CT scans and especially M.R.I.'s, neurologists are now discovering them more often. In a report March 22 in The New England Journal of Medicine, Dr. Wouter I. Schievink of the Cedars-Sinai Neurological Institute in Los Angeles reported an annual incidence of 1 per 100,000 to 1.5 per 100,000 people. While these dissections account for only about 2 percent of all nonhemorrhagic strokes, they are an important cause of stroke in young and middle-aged patients, accounting for as many as one-quarter of cases in these age groups.

Chiropractic spinal manipulation, estimated to cause strokes in as many as one in 20,000 patients who undergo it, is but one possible cause. Any sudden, abrupt neck movement or extreme neck position can cause an arterial dissection in a susceptible person. Other situations include getting one's hair washed in a beauty salon (the so- called beauty-parlor stroke) or drinking a shot of whiskey (dubbed the "bottoms-up dissection") or lifting heavy objects. A champion swimmer developed a dissected carotid from doing too much backstroke.

Dr. Schievink also lists precipitating events associated with hyperextension of the neck, including "practicing yoga, painting a ceiling, coughing, vomiting and sneezing," as well as medical procedures like receiving anesthesia or being resuscitated and traumatic causes like motor vehicle accidents or sports injuries.

An estimated one-fourth of patients who suffer an arterial dissection after chiropractic manipulation are believed to have an underlying connective tissue disorder or structural defect of the arterial wall that increases their vulnerability to arterial damage. In fact, it has been suggested that the early symptoms of vertebral-artery dissection, which commonly mimic musculoskeletal neck pain, may be what prompt people like the 20-year-old Canadian woman to visit a chiropractor in the first place.

There may also be an infectious factor in some cases, since the occurrence of carotid and vertebral artery dissections with no apparent cause peaks in the fall, when respiratory infections are most common.

It is critically important to respond quickly to the early warning signs of an arterial dissection. The spectrum of symptoms varies from patient to patient and is determined in part by which artery is affected. In patients with a dissection of the internal carotid artery, for example, typical symptoms include pain on one side of the head, face or neck accompanied by paralysis of one eye and followed hours or days later by brain or retinal symptoms. 

Other common symptoms of arterial dissections are pain in the back of the neck or head, a constant headache that develops suddenly on one side of the head and that may resemble a migraine, pain behind an eye, impaired ability to taste, tinnitus (pulsing noises in an ear), temporary visual loss and temporary loss of awareness (a kind of ministroke called a transient ischemic attack).

Anyone who develops two or more such symptoms should seek medical care without delay and, to enhance the likelihood of a speedy and correct diagnosis, perhaps even suggest that the doctor investigate the possibility of an arterial dissection by performing a magnetic resonance angiogram.

Carotid and vertebral artery dissections are fatal in fewer than 5 percent of cases, and about three-fourths of patients who suffer a stroke as a result of a dissection make a "good functional recovery," Dr. Schievink reported. Most dissections heal without surgery, blockages gradually resolve in 90% of cases and one-third of aneurysms decrease in size. There is, however, a small risk that once there has been an arterial dissection, the disorder will occur in another artery. 

Treatment involves preventing the complications of clots by administering anticoagulants, at first intravenously and then orally for three to six months. Patients must have their blood checked often to be sure it does not become too thin because overly thin blood can result in a hemorrhage.

When conservative treatment fails to correct the problem, a balloon may be inflated in the affected artery to compress the clot and a metal stent inserted to keep the artery open. With this modern therapy, surgery to bypass the damaged artery has become far less common.


\3 Athlete's foot

Why? Because athletes, like so many sporting groups tend to stand around shower/changing areas in their bare feet, spreading the little organism that causes the condition. So let’s talk about the condition. The correct name is Tinea, and we have several types depending upon the area of the body that is affected. If it is in your scalp we call it Tinea capitis, on the body - Tinea corporis, on the hands - Tinea manum, on the feet - Tinea pedis and in the groin we call it Tinea cruris, otherwise known as Dhobie itch or Crutch Rot! What a wonderful grab bag of conditions to say the least.

The organisms which cause all these are called Dermatophytes, and they have the ability to live in skin and so invade hair and even nails. The most common has the exciting name of Trichophyton rubrum, a noble name for an organism that can live in the soggy bits between your toes, I’m sure you’ll agree.

The symptoms generally consist of a spreading “rash” with reddened edges that becomes itchy and eventually quite painful as the infection goes into the deeper layers of the skin. This is the result of the organism putting out “tentacles” which extend deeper.

Unfortunately, there are a number of other conditions that can manifest themselves in a similar fashion, inc Psoriasis, eczema and some forms of dermatitis. This is the most usual reason for Athletes Foot preparations not working - it wasn’t Athlete's Foot to begin with!

There are various methods of clinching the diagnosis, including examination with a special Wood’s Light, which allows you to look at the affected region with UV light. The most accurate way however, is to take scrapings and examine under the microscope for the tell tale tentacles.

So what can you do if it really is our friend Tricho- phyton that is cropping up between your toes and other unmentionable places? The first thing to do is not use high powered steroid creams, but use a topical anti- dermatophyte preparation like Canesten cream. You can alternate with a weak steroid, but remember that the steroid does not cure the problem - it only masks it.

With some very stubborn cases it may be necessary to use medication by mouth to attack the organism through the blood stream, but these can have some fairly unpleasant and nasty side effects, especially on your liver. If your liver is having problems straining the blood out of the beer stream then you need extreme caution.

To prevent re-occurrence it is necessary to be very careful where you put your toes, never share towels and jump over communal bath mats - but even then you may find it comes back. Remnants of the organism start putting out their tentacles and the cycle is on again. And stop scratching!


\4 Cholesterol

Cholesterol is a white waxy substance (fat) naturally in the body including the blood and is essential toggood health (absorb fat soluble vitamins). When measured, several numbers are meaningful: the total, HDL (good), LDL (bad), and trigly- ceride level.

  Total less than 200 mg/dl
  HDL 50-75 is desirable
  LDL less than 130 is good
  sTrigly safe 200 or less

Discovered (2000) in Berlin MDC that gene #13 of 23 is responsible for cholesterol level in the blood. 

High blood levels of cholesterol (240 mg/dL and higher) greatly increase an individual's risk of heart disease. Cholesterol is a fatty substance that is used by the body to make cell membranes, hormones, and other substances. We get cholesterol from two sources: 1) our own bodies (it is produced primarily in the liver), and 2) by eating animal products such as meat (beef, chicken, fish), egg yolks, cheese and other whole milk products. Because the body can easily make all the cholesterol it needs, it doesn't need any additional cholesterol from foods. Do you know if your blood cholesterol level puts you at risk for heart disease? The table below details the standard breakpoints of total cholesterol levels. Total Cholesterol Levels 160 mg/dL optimal for people with a history of heart disease <200 mg/dL desirable for the general pop 200 mg/dL to 239 mg/dL borderline high blood cholesterol 240 mg/dL or greater high blood cholesterol Unlike sugar, cholesterol does not break down in the blood. Cholesterol is packaged as insoluble protein/fat particles called lipoproteins. These lipoproteins travel through the blood, delivering cholesterol to all the parts of our bodies. Excess cholesterol in the blood can be deposited in artery walls, contributing to a progressive disease called atherosclerosis or hardening of the arteries. As arteries narrow and harden, blood flow is restricted and the heart needs to pump harder to do its job. Hardened arteries can rupture, bleed, hemorrhage, or clot. Heart attacks and strokes occur when a blood clot completely blocks an artery, cutting off blood flow to the heart or brain.

The National Institutes of Health, National Heart, Blood and Lung Institute, devised two eating plans, the Step I and Step II Diets, aimed at lowering LDL cholesterol. The goals of the Step I Diet are to limit cholesterol intake to less than 300 mg per day and fat intake to 30 percent or less of the day's total calories, with only 8 percent to 10 percent of calories from saturated fat. The more aggressive Step II Diet limits cholesterol intake to less than 200 mg per day and fat intake to 30 percent or less of the day's total calories, with less than 7 percent of total calories from saturated fat. Saturated fats, which are solid at room temperature, derive from beef, pork, lamb, chicken, turkey, butter, egg yolks, coconut oil, palm oil and palm kernel oil. Bacon grease, for example, is saturated fat.

Additional Cholesterol-lowering Tips: The soluble fiber in some foods adheres to excess cholesterol in the intestines, blocks its absorption, and ushers it out of your body. Foods high in soluble fiber are oat bran, cooked dry beans, dry peas and lentils. Eat these foods to lower your overall cholesterol level. (Remember to drink six to eight glasses of water each day to help the fiber work.) Research has shown that the omega-3 fatty acids found in fish (sushi) will reduce cholesterol levels and decrease the likelihood of blood clotting. In general, the darker the meat of the fish, the higher the amount of omega-3. To reap the benefits of omega-3, try mackerel, lake trout, herring, fresh albacore tuna, sturgeon, whitefish, salmon or halibut for dinner once or twice a wk. Omega-3 fatty acids are also found in soybean oil, canola oil, nuts, soy, and flax seeds. If you need additional help to lower your cholesterol, your physician may prescribe medication. Take the medication as directed and make sure you follow your physician's advice about nutrition and physical activity. Steps You Can Take Today: If you don't know your cholesterol level, have it checked. Eat more whole grains, fruits and vegetables (at least five per day). They have no cholesterol. Avoid foods high in saturated fats and cholesterol. 

Understand Cholesterol... At Last By Health Pages We've been bombarded with so much complicated and conflicting information about cholesterol that it makes the head spin. But before you throw up your hands in disgust and dig into a four-egg-bacon-cheese-omelet with fries on the side, read this. It's important to understand how cholesterol and fat affect your health. If cholesterol is so bad for you, how can there be a "good" cholesterol? What's the difference between saturated, monounsaturated and polyunsaturated fat? What are triglyceridss and trans fatty acids? How do different types of fat impact cholesterol levels? It takes a bit of patience to understand all the ins and outs of fat metabolism but the basic principle is simple: Too much cholesterol in the blood is among the top four risk factors for heart disease (the other three are smoking, high blood pressure and lack of exercise). Excess blood cholesterol can cause arteries to become clogged and, in turn, may lead to a heart attack or stroke. Americans have received the cholesterol message loud and clear. Our national obsession to cut back has resulted in a 20 percent drop in the consumption of cholesterol since the mid-1970s. But fending off heart disease is not that simple. Why? Other types of fats influence cholesterol levels and they, too, need to be monitored in the diet. The biggest trouble-maker in the fight against elevated blood cholesterol and heart disease is saturated fat. What Is Cholesterol? Cholesterol is a lipid, a soft, fat-like substance that, in reasonable quantities, is critical to good health. It is a component of cell membranes, is found in all body tissues, and is converted into various hormones. Cholesterol comes from two sources: it's produced by the body, mainly in the liver. And it's found in food, especially animal products such as meat, poultry, seafood, dairy products and eggs. What Is Good & Bad Cholesterol? The answer to this question will become clear once you understand how cholesterol is shuttled around in the body. Like other nutrients, cholesterol has to travel to the body's cells through the blood. However, since it is not water soluble, the substance must be transported to organs by special carriers called lipoproteins. There are several kinds of lipoproteins, but low density lipoprotein (LDL) and high density lipoprotein (HDL) are the ones that get all the press when it comes to cholesterol. LDL is the major cholesterol carrier in the blood. It has been dubbed "bad" because it slowly builds up in the walls of arteries. Together with other substances, LDL-cholesterol can form plaque (a thick, hard deposit) that restricts the flow of blood through the arteries and can result in a heart attack or stroke. On the other hand, HDL carries about one-third to one-fourth of blood cholesterol. HDL cholesterol is touted as "good" because it not only carries cholesterol away from the arteries and back to the liver, where it's removed from the body, but it sweeps away the cholesterol dumped by LDL.

Studies have shown that, in adults with high blood cholesterol, for each one percent reduction in total cholesterol levels, there is a two percent reduction in the number of heart attacks. In other words, if you have been diagnosed with high cholesterol, reducing your cholesterol level by 15 percent, could drop your risk of coronary heart disease by 30 percent. What Role Do Other Fats Play? It may surprise you to find out that dietary cholesterol has only a modest impact on blood cholesterol levels for most of the population. When the body is working efficiently, the liver regulates itself to keep potentially harmful LDL-cholesterol from building up in the blood. And when we eat foods high in cholesterol, the small intestine absorbs less of it and the liver reduces its production of cholesterol. People called "cholesterol responders" have faulty cholesterol adjustment systems and teeir blood cholesterol is high, but this is quite rare. If this is true, you're probably wondering, what's all the fuss about? Well, cholesterol has accomplices in gumming up the arteries. Enter the role of fats we eat: saturated, polyunsaturated and monounsaturated. These three types of fat differ in their impact on cholesterol levels. Monounsaturated and polyunsaturated fats can help lower cholesterol levels. Monounsaturated fats are found in greatest amounts in food from plants, including olive, peanut and canola oil. When substituted for saturated fat, monounsaturated fat helps lower LDL's while leaving HDL's unchanged. Polyunsaturated fats are found in foods from plants, including safflower, sunflower, corn and soybean oils. When used instead of saturated fats, polyunsaturated fats tend to lower LDL's but they lower HDL's as well. Saturated fats are found mainly in foods from animals such as meat, poultry, and whole-milk dairy products like cream, milk, ice cream, and cheese. Saturated fat is also found in butter, lard and coconut, palm kernel, and palm oils. Saturated fats have the dubious distinction of raising cholesterol levels far more than anything else we eat. That's why, if you're trying to lower your blood cholesterol level through diet, you must curb the total amount of fat you eat, especially saturated fat. In addition, new evidence suggests that trans fats (formed when liquid vegetable oils are processed to make hard or semisoft table spreads and cooking fats) may be even worse for your heart than saturated fats. In an on-going study of 80,000 nurses, researchers found that the chance of suffering a heart attack was 53 percent higher for the women who consumed the largest amounts of trans fats than for those who consumed the least amount of them. But the women in the group with the largest consumption of total fat (46 percent of calories) had no greater risk of heart attack than those in the group with the lowest consumption of total fat (29 percent of calories). Does this mean as long as we eat the right fats we can eat as much as we like? Not at all. This is preliminary research, and health experts still underscore the importance of moderation when it comes to fat intake. A diet high in fat often leads to being over weight, which can have many negative effects on health, including increasing the risk of heart disease and diabetes. Does Dietary Cholesterol Matter at All? The main problem with cholesterol-rich foods is that they also tend to be high in dietary fat, particularly saturated fat. However, there are some foods that contain lots of cholesterol but little saturated fat. These include egg yolks, shellfish, such as shrimp and squid, and liver and other organ meats. If your cholesterol levels are well within the desirable range, you don't have to worry much about eating these foods. But be sensible. It's wise to follow the current public health recommendations, which include eating no more than three or four egg yolks per week, including those used in cooking, and only modest amounts of other animal foods. How Vigilant Should Senior Citizens Be about Cholesterol? Blood-cholesterol levels have a smaller impact on coronary risk in older people, so it's less important for them to watch cholesterol and saturated fat in foods. A greater concern for older people is to eat an adequate diet. One way to help insure this is by eating eggs, which are highly nutritious and inexpensive. Can Drinking Alcohol Be Heart Healthy? You may have heard that drinking one or two alcoholic beverages a day is linked to a lower incidence of heart disease in some studies. But you need to weigh certain risks before uncorking that bottle of wine. American Heart Association (AHA) warns that before continuing or starting to drink, you should check with your doctor. Alcohol can interact dangerously with certain medications, and it can worsen medical conditions such as liver disease, pancreatitis and uncontrolled hypertension. Heavy drinkers are at increased risk of cancers of the oral cavity, larynx and esophagus. As for breast cancer: Harvard researchers who analyzed six studies found that the risk of developing that disease rises 9 percent for every ten grams of alcohol a woman drinks per day. Women who average four glasses of wine daily have a 40 percent greater risk than nondrinkers. Pregnant women and people with a personal or family history of alcoholism should avoid alcohol. Are Fish Capsules Beneficial? Fish are rich in omega-3 fatty acids, a form of polyunsaturated fat that is different from the omega-6 fatty acids found in most vegetable oils. Omega-3 fatty acids lower blood levels of triglycerides and very low-density lipoproteins (VLDL). The AHA recommends eating fish regularly but thinks more studies need to be done to confirm any protective link fish oils have against heart disease. The use of fish oil capsules to lower cholesterol levels is not recommended. Can Antioxidants Help? A recent study at the University of Maryland Medical Center found that large doses of two antioxidants, vitamins C and E, may decrease the heart-disease risk posed by a high-fat diet. In the study, published in the Journal of the American Medical Association, 20 subjects ate a meal of Egg McMuffins and Sausage McMuffins with slabs of fried hash browns. After the fat-packed breakfast, they had impaired blood vessel function that lasted up to four hours. No such impairment was found when they swallowed 20 times the recommended daily dosage of vitamins C and E immediately before eating the same meal on a second occasion. Antioxidants are vitamins that protect cells from oxidation. The oxidation process is familiar: it causes metal to rust, fruit to turn brown and oils to go rancid. Inside the body, oxidation can severely damage cells and allow diseases to get a foothold. Destructive oxygen byproducts, called free radicals, are produced both in our bodies when oxygen is metabolized and in the environment by factors like cigarette smoke and polluted air. Antioxidants seem to deactivate free radicals, thus protecting cells from damage. Before rushing to the nearest vitamin store, keep in mind that the Maryland study was small and preliminary. Researchers have yet to determine whether there are any long-term benefits -- or dangers -- related to using such huge vitamin doses. Right now, the best thing is to enjoy foods high in vitamins C and E and continue to avoid a high-fat diet. Vitamin C is found in green and red peppers, collard greens, broccoli, spinach, tomatoes, potatoes, strawberries, oranges and other citrus fruits. Vitamin E is in vegetable oils, margarine, vegetable shortening, nuts, wheat germ and green leafy vegetables. What Is Considered High Blood Cholesterol? Your blood cholesterol levels are determined by your genetic makeup and by the amount of fat in your diet. To check cholesterol, a doctor will take a blood sample and measure the lipids in milligrams per deciliter (mg/dl). According to the American Heart Association (AHA), approximately 52 percent of adult Americans have Borderline-High blood cholesterol levels and 20 percent have High cholesterol levels (see chart). Though a blood cholesterol level of 240 mg/dl or greater is considered High, any level above 200 mg/dl increases your risk for heart disease. If your blood cholesterol is in the High category, you have more than twice the risk of someone whose cholesterol is 200 mg/dl. But total blood cholesterol is not enough to determine your risk. One out of every five heart attack victims has a total cholesterol level in the normal range, below 200 mg/dl. To really zero in on your risk for heart disease, you need to have a lipid analysis to determine your LDL, HDL and triglyceride levels.

Having less than 35 mg/dl of HDL-cholesterol is considered a risk factor for heart disease even when total cholesterol and LDL-cholesterol levels are normal. That is because you have less of this "good" cholesterol working in your system. Similarly, your LDL-cholesterol level greatly affects your risk of heart attack. In fact, LDL-cholesterol is a better predictor of heart attack risk than total blood cholesterol. When it comes to LDL-cholesterol levels, the lower your level the lower your risk. In addition to cholesterol, researchers have found that fat-like substances called triglycerides can increase the risk of heart disease by contributing to fatty deposits in the arteries. We get triglycerides primarily from the fat in our diet, but luckily, these lipids are much more responsive than cholesterol to lifestyle changes such as exercising and eating a low-fat diet.

Lowering your high blood cholesterol level will slow fatty buildup in the walls of the arteries and reduce your risk of a heart attack. Factors that will influence blood cholesterol levels include eating a low-fat diet, replacing saturated fat with unsaturated fat, shedding pounds if you're overweight, exercising regularly, and stopping smoking. Type of CholesterolDesirable Levels (in mg/dl)Borderline-High Levels (in mg/dl)High Levels (in mg/dl) TotalLess than 200200 to 239240 and above LDL ("bad")Less than 130130 to 159160 and above HDL ("good")More than 60*60 to 35Below 35 TriglycerideLess than 200200 to 399400-1,000 (high) 1,000 (very high) NOTE: These categories apply to anyone 20 years of age or older. *More than 60 mg/dl tends to lessen the risk posed by a high LDL. How Does Cholesterol Lead to Heart Disease? Most heart disease is caused by atherosclerosis, which occurs when cholesterol, fat, and other substances build up in the walls of the arteries that supply blood to the heart. These deposits, called plaque, narrow the arteries and can slow down or block the flow of blood. One of the most important functions of blood is to carry a constant supply of life-giving oxygen to the heart. Without oxygen, heart muscle tissues are gradually destroyed, resulting in chest pain (angina), a heart attack (myocardial infarction), or even death. In the same manner, a buildup in the arteries supplying blood to the brain can cause a stroke. Atherosclerosis is a slow progressive disease that may start very early in life yet might not show symptoms for many years. When high blood cholesterol is combined with other major risk factors, the chance that you'll suffer from heart disease increases even further. For example, if your cholesterol level is in the High category and your blood pressure is elevated, your risk for heart disease increases six times. If you also smoke, your risk increases more than twentyfold. What You Can Do Here are the current AHA recommendations: If you are a healthy adult over 20, test your blood cholesterol levels at least once every five years.

Eat no more than 300 milligrams of cholesterol a day. One egg yolk has about 213 milligrams of cholesterol. Egg whites, on the other hand, have no cholesterol or fat and are a great source of protein. You can substitute two egg whites for each egg yolk in many recipes that call for eggs.

Limit your total fat intake to less than 30 percent of calories, with less than 10 percent coming from saturated fats. You can accomplish this by: Choosing more fruits, vegetables and whole grains instead of fatty meats and bakery goods. Eating fish, poultry without skin and lean meats instead of fatty ones. Consuming low-fat or skim milk dairy products instead of whole milk dairy products. Can You Lower Your Cholesterol Too Much? Yes, it seems that you can. Studies suggest that while people with low cholesterol (less than 160 mg/dl) are at less of a risk for coronary heart disease, they are apparently more likely to die from noncardiac causes, ranging from cancer to physical trauma. What's more, people with high blood cholesterol who lower it have a high rate of noncardiac deaths too.

Although no one is sure why, the risk of lowering cholesterol seems to be greater when drugs are used. Based on these observations, many experts are calling for a cutback in the use of cholesterol-lowering drugs. What does all this mean to you? Cholesterol is not a matter of the lower the better.

So if you have normal cholesterol levels (between 160 and 200 mg/dl) you shouldn't get over-zealous and try to drive it down even further. If your doctor has suggested that you lower your cholesterol levels, don't rush into trying cholesterol-lowering drugs as an "easy fix." Try to whittle cholesterol levels down by exercising regularly, eating a low-fat diet, and stopping smoking. If that doesn't work and your doctor urges you to take medication, discuss the various drugs that are available. One option may be to take niacin, which can raise HDL (good cholesterol) and reduce LDL (bad cholesterol). Niacin is not appropriate for everyone who needs to lower cholesterol levels, but for those who are good candidates, it may give the best results at the lowest cost. A Fat Glossary Fats and oils are mixtures of fatty acids. Each one is designated saturated, monounsaturated or polyunsaturated, depending on what type of fatty acids is predominant in that one. Saturated Fatty Acids have all the hydrogen the carbon atoms can hold. The more saturated fatty acids in a fat, the harder it is at room temperature and, in general, the more damaging it is to your health. Saturated fats, abundant in meat, dairy products, palm and coconut oils, tend to increase "bad" LDL-cholesterol, thus raising the risk of heart disease.

Unsaturated Fatty Acids have at least one unsaturated bond -- that is, at least one place that hydrogen can be added to the molecule. There are two common types: Monounsaturated Fatty Acids have only one unsaturated bond. Monounsaturated oils are liquid at room temperature but start to solidify when chilled. Monounsaturated fatty acids, found in olive, peanut, and canola oils, seem to lower LDL-cholesterol without lowering HDL-cholesterol.

Polyunsaturated Fatty Acids have more than one unsaturated bond. And polyunsaturated oils (corn, soybean, safflower, sunflower) are liquid at room temperature and in the refrigerator. They easily combine with oxygen in the air to become rancid. Polyunsaturated fatty acids help to lower LDL-cholesterol, but may also reduce the "good" HDL-cholesterol.

Triglycerides are a type of blood fat derived directly from the fatty foods fats we eat or made by the body. They are important for transporting and storing fat in the body, but they may also play a role in cardiovascular problems. About half the people who get heart disease have low or normal cholesterol levels. For this population, experts suspect that high triglyceride levels may be the culprit. Excess triglycerides also appear to be associated with a greater risk of developing diabetes, which itself increases heart disease risk.

Trans Fatty Acids are formed when unsaturated fatty acids are subjected to a process called hydrogenation, which changes the structure of the unsaturated fatty acid molecules and makes them similar to saturated fatty acids. Since liquid oils spoil easily, manufacturers use hydrogenated oils in margarine, fast food, and processed food to keep their products fresher longer and give them a desirable consistency. But the so-called trans fats that are produced by hydrogenating oils increase the risk of a heart attack by raising blood levels of artery-clogging LDL cholesterol and triglycerides and lowering levels of HDL cholesterol. To avoid trans fatty acids, use tub margarines or liquid vegetable oils that are high in unsaturated fat instead of hydrogenated vegetable shortening, and cut down on commercially prepared and processed foods, including cookies, cakes and crackers. Getting an Accurate Reading Getting an accurate cholesterol reading can be tricky. The tests themselves -- particularly those done outside a doctor's office, laboratory, or other medical setting -- may be imprecise. But even with the best testing equipment, blood sample results can vary nearly 20 percent depending on the time of day, what you've eaten, and whether you've exercised recently. Here's how to maximize the chance of getting accurate readings: Ask if the laboratory processing your blood conforms to standards set by the Centers for Disease Control (CDC). If it doesn't, try to use a different lab.

Remind your doctor about any medications you're taking. Many drugs, such as blood-pressure medications and birth-control pills, can affect cholesterol levels.

Sit calmly for ten minutes before your blood is drawn. Your posture and any abrupt changes in position can affect the results. If you're having blood drawn from your arm, make sure the tourniquet stays on for no more than one minute. Any longer may boost cholesterol readings by as much as 15 percent.

In the 12 hours prior to your test consume only water. Avoid strenuous exercise for 24 hours before testing. Confirm any abnormal or borderline readings by taking a second test and averaging the findings. If the lower reading of total cholesterol is more than 14 percent below the higher reading, have a third test and average the results of all three. Do the same if the lower reading for HDL, LDL or triglycerides is more than 24 percent below the higher reading. Tests should be done at least one week apart, but within two months.

\5 Depression

All depressions are not alike. They can be one of three types, pychological, biological, or mixed. Not all depression require medical treatment and even the most severe cases eventually go away although about 15% of cases kill themselves before it does. These are the cases that can use Tofrannil or Prozac for awhile.

Psychological symtoms: Sadness and despair, irritability, low self esteem, apathy, no motivation, interpersonal problems, guilt and negative feelings. Suicidal thoughts.

Physical symptoms: sleep or appetite problems, loss of sex drive, fatigue and reduced energy, inability to experience pleasure. Family history of depression, suicide, insomnia or alchoholism. 

Other symptoms: Poor concentration, hypocondria, drug abuse, mood swings, panic attacks, or excessive emotional sensitivity as anger, irritability. 

5/25/99 -- Smoking And Depression Weakens Immune System Depressed persons who smoke cigarettes may be at increased risk of cancer and other diseases, according to new research. The combo of depression and cigarette smoking contributes to increased white blood cell count and a decline in the activity of natural killer cells (NK) that fight off tumours, the study demonstrated. The research was conducted by Waymund Jung MD, and Michael Irwin MD, at the Univ of CA, & Vets Affairs San Diego Healthcare Med Ctr. The results of their research are reported in the June issue of Psychosomatic Medicine. "The findings may have particular importance in view of the high rates of smoking among depressed persons reported in other research," Irwin said. "The immune changes in depressed smokers, along with the finding that depression and smoking interact to contribute in a unique way to elevated white blood cell counts and reduced NK activity, suggest that even moderate cigarette smoking can impact the immune system adversely.
 5/19/99 -- Effexor XR Produces Significant Relief From Depression In First Week of Treatment. Effexor XR (venlafaxine HCl) provides patients suffering from major depressive disorder significant relief from their sympms as early as the first week of treatment, according to a new study presented at 1999 Amer Psychiatric Assoc annual meeting. "Many antidepressant therapies take a few weeks to make a person feel and function better," said John Feighner, M.D., director, Feighner Research Institute. "These data are significant because they show it may be possible for a treatment to act more quickly, thereby shortening the length of time it would take a patient to feel well enough to resume their normal activities."
 5/18/99 -- Reboxetine Effective In Treating Depression Symptoms. Researchers presented the results of clinical studies during the 152nd annual meeting of the American Psychiatric Assoc (APA) show that reboxetine mesylate tablets, a new antidepressant, is effective in treating the symptoms of depression. Reboxetine, a selective norepinephrine reuptake inhibitor (NRI), is the first in this new class of meds. Researchers have long considered norepinephrine an important pathway in the treatment of depression because norepinephrine depletion has been demonstrated to affect most core symptoms of depression. Norepinephrine depletion in depressed patients is believed to be most closely assoc with several specific symptoms including lack of energy and interest and loss of motivation. Addressing these symptoms of depression is an important treatment goal for many patients.
 5/18/99 -- Drug-Psychotherapy Combo Effective For Chronic Depression. A new combo of drug treatment and psycho- therapy is much more effective than either med or therapy alone for treating chronic depression, according to preliminary results presented today at the annual meeting of the American Psychiatric Assoc. The combo treatment, involving Serzone (nefaoodone) and a form of psycho- therapy developed specifically to treat chronic depres- sion, also produced the highest response and remission rates for any reported study of chronic depression. The psychotherapy used in the study is a structured, intensive program, developed by James McCullough of Virginia Commonwealth University and called Cognitive Behavioral Analysis System of Psychotherapy (CBASP).
 5/17/99 -- Electromagnetic Stimulation Shows Promise For Treatment-Resistant Depression. An investigational treatment employing electromagnetic stimulation relieved depression in 25 patients whose depression failed to respond to conventional treatment, report Emory Univ resrchers at a Amer Psychiatric Assoc meeting. Scores on depression rating scales admin to study subjects before, during and after the new treatment were significantly improved at all time points compared to baseline, said first author Yvonne Greene, MD, a neurosciences fellow at the Emory Univ Sch of Med who collaborated on the open trial with William McDonald, MD, assoc prof of psychiatry at the Emory Univ Sch of Med, and others."64% of patients were rated very much improved or much improved on the [CGIC] Clinical Global Impression of Change and 40% of patients had an equal to or greater than 50% decrease in HDRS [Hamilton Depression Rating Scale] scores at the end of treatment week two," Greene writes. "40% of patients were rated very much improved or much improved on the CGIC and 32% of patients had an equal to or greater than 50% decrease in HDRS scores at the end of 4-week foll-up.
 5/13/99 -- Study Shows Psychotherapy As Effective As Drug Therapy For Atypical Depression. Psychotherapy can be just as effective for treating atypical major depression as the std drug treatment with phenelzine sulfate, reported Univ of TX SW Med Ctr at DAL researchers in today's Archives of General Psychiatry. Dr Robin Jarrett, assoc prof of psychiatry, said this is the first time researchers have compared medication and psychotherapy for atypical depression in a randomised, placebo-ctrl trial. It is only the second time cognitive therapy for major depression has been tested in a randomised study containing a pill placebo. "The implication of the study is that cognitive therapy is an effective alternative to MAO inhibitors for patients with major depressive disorder with affective features," she said. "These findings are important because clinicians and patients now have a tested and effective alt to pharmacotherapy."
 5/13/99 -- Researchers Look To Omega-3 Fatty Acid For Manic Depression Treatment. In a preliminary study, manic-depressive patient  given omega-3 fatty acid had significantly longer remissions and performed better on four symptom-severity scales than the placebo group, according to an article in this month's issue of the Archives of General Psychiatry. The researchers studied 30 patients with manic depressive illness in a four- month, double-blind, placebo-controlled study to compare the efficacy of omega-3 fatty acids (obtained from plant or marine sources, such as fish oil) versus placebo (olive oil) for treatment of manic depressive-illness. According to Andrew Stoll, MD, and colleagues, manic- depressive illness is a common neuropsychiatic illness with a high morbidity and mortality. "If further studies confirm their efficacy in bipolar disorder, omega-3 fatty acids may represent a new class of membrane-active psychotropic compounds and may herald the advent of a new class of rationally designed, mood-stabilising drugs," the researchers conclude.

5/11/99 -- Adolescent Depression Often Continues To Adulthood. Many depressed teenagers grow up to become depressed adults, with a significantly higher rate of suicide and suicide attempts, according to an article in The Journal of the AMA. Myrna Weissman, Ph.D., of the New York State Psychiatric Institute and Columbia Univ, and colleagues followed two groups of young people into adulthood. All were under 18 when they were initially selected for the study in the early 1980s. Ninety-one study participants were diagnosed with major depressive disorder (MDD) during adolescence; 73 of them were assessed in the follow-up. There also were 37 healthy adolescent subjects recruited from the community through newspaper advertising and word-of-mouth who were assessed in follow-up. The teenagers in the control group had no evidence of past or current psychiatric disorders.

An independent team of psychiatrists and psychologists without knowledge of the initial diagnosis conducted a follow-up 10-15 years later. The researchers found there was a high rate of suicide and suicide attempts among those who experienced depression as teenagers. Seven suicides (7.7%) occurred in the teen onset depressed subjects and more than half (50.6%) of the adolescent- onset MDD subjects made a suicide attempt over their lifetime -- 22% had made multiple attempts. Compared to the control subjects, those who were depressed as adolescents had more than a five-fold increased risk for a first suicide attempt in the follow-up period and a 14-fold increased risk over their lifetime.The depressed adolescents were at high risk (two-fold) to experience more depression as adults.
 Anxiety, Depression And Manic Depression
 An excellent primer from the Canadian Psychiatric Assoc.
 "Anxiousness and changing moods? So what? Aren't they something we all go through? Aren't they helpful in their own way? After all, anxiety can spur us on to prepare for an upcoming task. It can help us face danger. Depression can slow us down, offer us time to reflect and regroup. An energetic mood can help us accomplish necessary tasks. But when anxiety or depression, seem to come out of nowhere ... persist for many weeks without relief ... interfere with everyday life ... then we're not talking about ordinary moods anymore. We're talking about an illness.
 Depression and Cancer. "I had a recurrance of my Ovarian Cancer this past summer and finally had a hysterectomy (at age 37). I am on transdermal estrogen replacement therapy, Climara 0.1 mg. I have been dealing with what I call low-grade depression for a long time, but since the surgery it has gotten considerably worse. I've never taken medication for depression. I have days when I feel that I just can't function - I stay in bed or wander around, not able to work, concentrate or communicate well. I burst into tears at the slightest provocation. I even have trouble making art (I'm a visual artist) and journaling. I have no interest in sex and my body image is terrible (I work out 3-5 times a week and am not overweight). I either don't eat at all, or eat certain foods (chocolate, grains) somewhat compulsively during these times. Then, I have days when I swing back to the active, joyful, creative, productive person I usually am. It seems that the "down" days are getting worse, and the "up" days feel more frenetic than before.
 I went back to work 3 1/2 weeks after my surgery and do feel that I haven't dealt fully with the issues around the recurrance and surgery. My gynecologic oncologist's practice is starting a support group for women with gyencologic cancers within the next month, and I will be attending that. I have spoken with a male Ph.D. therapist friend, who suggested a short term anti-depressant regime combined with verbal therapy. Do any of you have any suggestions? Many thanks, Ginnie"
 Center for Current Research Report
 General Summary. Depression is more than a sadness that won't go away. It is a medical illness that is fairly common and fortunately treatable. Some of the symptoms of this illness include but are not limited to sleep and eating disturbances, a loss of energy, feelings of worthlessness and helplessness, problems concentrating, suicidal thoughts, and a loss of a sense of pleasure and interest in life (Weissman, 1992). It can range from mild to severe, depending upon the number and severity of the symptoms.
 Depression affects about one out of every 10-20 people (about 12-25 million people) in America each year (Klerman and Weissman, 1989).
 Twice as many women as men are affected by depression. It has also been found that more recent generations were more likely than their parents or grandparents to experience major depression sometime in their lives (Weissman, 1992). In other words, depression is showing up in younger people.
 Identification of biological markers in mental diseases would help resolve some of the problems associated with their diagnosis, treatment, prognosis, and prevention.
 Research in the area of biochemical markers has begun with the use of platelets as a readily accessible neurone model and by the application of neuroendocrinological dynamic tests (review: Ceskova, 1994).
 Another early marker is the childhood-onset of dysthymic disorder. Dysthymic children who have subsequent mood disorders are most likely first to have an episode of major depressive disorder (MDD), and that episode appears to be the "gateway" to recurrent mental illness. Researchers believe that the interval between the onset of dysthymia and the first major depression provides a window of opportunity for intervention and possible prevention of later episodes (Kovacs and others, 1994).
 If a person feels that he or she is depressed, the best thing to do is consult a mental health professional. A professional such as a social worker, psychologist, or psychiatrist has had the training to be aware of the symptoms of depression and to provide the necessary treatments. These treatments can include antidepressant drugs, psychotherapies, antidepressant drugs combined with psychotherapies and other treatments.
 Current Research. While there is no known single or specific biological cause of depression, there is little doubt that severe depression is a disease of the brain. This illness can be effectively treated with medication. There are many antidepressants currently avail and new ones are constantly being studied and marketed (review: Calabrese and Markovitz, 1991; review: Montgomery, 1994).
 A number of research projects involving experimental treatments have been reported in recently published medical journals. Some of these treatments, or the drugs involved, may not yet be available, however.
 The leading antidepressant being used is fluoxetine (or Prozac). People taking Prozac report that they feel much better with this drug, and do not complain of the side effects experienced with older, tricyclic antidepress- ants. Even high levels of dysfunctional attitudes (often associated with great severity of depression) have been successfully treated with Prozac (Fava and others, 1994).
 Several recent studies have looked at the serotonin- reuptake inhibitor, paroxetine (or Paxil) for long-term treatment and relapse prevention of depression. In clinical studies involving over 6,700 patients worldwide, the efficacy of Paxil has been shown consistently to be superior to placebo and comparable to tricyclic anti- depressant agents in the treatment of depression (Nemeroff, 1993; Duboff, 1993). During these trials, Paxil was used in a broad range of depressed patients, including the moderately to severely depressed, the elderly, and patients whose depressions were accompanied by symptoms of anxiety. In addition, it has been shown to be effective for the prevention of depressive relapse during long-term treatment.
 Paxil should not be co-administered with monoamine oxidase inhibitors or L-tryptophan, according to the author. Animal data and limited clinical experience suggest that Paxil is considerably safer in overdose than are tricyclic antidepressant drugs.
 In another study Paxil was effective in preventing the reappearance of depression following an acute illness (Montgomery, 1993). The author concluded that the results confirm the benefit of long-term pharmacotherapy for treating depressive illness.
 A new drug called "tianeptine" has been found to be beneficial in persons suffering from both depression and anxiety (Wilde and Benfield, 1995), with benefits noted also from its use in long-term therapy, particularly with the elderly. In any drug regimen, a doctor must be seen on a regular basis to monitor the dosage of medication and make dose adjustments when problems occur.
 Medication is not necessary for every patient diagnosed with depression. Some people choose not to take medication, and prefer a type of psychotherapy as first-line treatment instead.
 Some of the psychotherapies that have been studied for their effectiveness include behavioral, cognitive and interpersonal therapies, as well as multidisciplinary approaches (review: Okamura, 1994).
 Behavioral therapy looks at current behaviors; cognitive therapy focuses on thoughts and beliefs; and interpersonal therapy focuses on current relationships (DHHS, 1993).
 A recent study conducted in Pittsburgh has shown that interpersonal therapy, imipramine drug therapy, or a combination of the two, has significant (and cost-effective) outcomes on a patient's quality of life (Kamlet and others, 1995). 
 Researchers in New Zealand have reported favorable results from the use of venlafaxine in patients with major depression, finding that it also has fewer anticholinergic and central nervous system adverse effects than tricyclic antidepressants (Holliday and Benfield, 1995).
 Please remember to seek the advice of a mental health professional before you decide on a particular method of treatment.
 Bodily Effects. Antidepressant medications act on certain of the brain's neurotransmitter systems. Both Prozac and Paxil selectively enhance the action of serotonin, one such neurotransmitter. The drugs that zero-in on serotonin-containing cells avoid some unpleasant side effects that were common in earlier antidepressants, known as tricyclics and monoamine oxidase inhibitors.
 The earlier drugs are also more toxic, which makes it far easier for depressed patients to commit suicide by taking an overdose (Calabrese and Markovitz, 1991). The admin of bright light in a particular dosing schedule at the first signs of winter depression appears to prevent it from developing into a full-blown depression is currently being (Meesters and others, 1993).
 Two-thirds of all adults age 65 or older are either irregularly active or completely sedentary (Rooney, 1993). With this inactivity comes an increased risk of chronic diseases, including coronary heart disease, hypertension, diabetes, osteoporosis, and depression.
 Adequate aerobic exercise -- even when started as late as age 60 -- is associated with a 1- to 2-year increase in life expectancy, as well as increased functional independence.
 Even chairbound patients can benefit from a program of simple exercises. To help prevent injuries, your exercise prescription should include stretching exercises and exercises to strengthen the muscles surrounding weak joints, according to the authors.


\6 Infestation: Ticks

Ticks are found worldwide, often in brushy or leafy undergrowth or in caves. Before feeding they can be as small and dark as a freckle; when engorged they might be the size of a button. Adult ticks have 8 legs. Their jaws are built to latch onto skin as they feed, making them difficult to remove once they are in place. Before ticks can drink blood they have to inject saliva to thin it, and any organisms they carry can be transmitted to you. Ticks spread diseases such as typhus, relapsing fever, Lyme disease and encephalitis. It takes hours for ticks to get completely anchored, so don't assume they are fully embedded if you find them on you. To remove a tick, first flick or pull gently to see if it comes off. If the tick is already embedded, pull it up from its back end and work it out firmly until the mouth parts have disengaged. Any parts left in can cause infection. Reduce your chances of tick-related illness by closely following insect precautions. Cover as much skin as possible, wearing light-colored clothing so you can see ticks easily. Apply repellents with DEET to any exposed areas of skin and use permethrin on fabrics. Perform full-body checks for ticks every day; don't forget to check the scalp, behind the ears, the back and other hard-to-reach areas. You can use a mirror for this, or employ the buddy system with traveling companions.

TICKS: mostly not affected by repellants. The bite can be debilitating and sometimes fatal if the tick is not found and extracted. One method to extrace ticks is with dabs of gasoline so it will leave without breaking off its head causing infection. Book method: use tweezers to grip firmly close to the surface w/o squarshing the bugger and pull upward with steady even pressure. In Australia anti- venom may be needed against the common dog tick.

Ticks transmit Lyme disease found in brush/follage during summer and fall of western countries. Infection may not be for about 18 hours after contact, therefore after time in the bush, examine body for ticks. If found they may be extracted w/o infection.

Symptoms are an expanding red gash or ring (rash) at the site of the bite accompanied by head, muscle, joint aches with low grade fever 3-32 days later. Early cases may be treated orally. w/tetracyclines. Untreated, symptoms will disappear temporarily to recur with greater severity.

Other disease spread by ticks are Rocky Mountain Spotted Fever and encephalitis. Prevention can result in using repellent on light color trouser legs tucked in. Inspect and clean trousers before undressing. Best way to remove is to use tweezers or fingers and grip the tick as close to the skin as possible lift upward and pull away (parallell to skin) w/steady pressure until it detaches. Do not twist or jerk. Sanitize area.


\7 Infestation: Fleas

Adult fleas are small insects (under 1/4 inch) of dark reddish-brown color. They lack wings and have laterally compressed bodies enabling them to move easily through body hairs. They have three pairs of legs with the back pair modified for jumping.

There are several kinds of fleas. Adults of each live on the blood of animals and must have it to reproduce. Each species of flea prefers to live and feed on a certain kind of animal but when hungry will attack a wide variety of warm-blooded animals including humans. The cat flea is the most common and is usually the species found on cats and dogs and in homes. The dog flea looks and acts like the cat flea but is less common. The true human flea is the least common. Human fleas may occur in poorly cleaned homes. The occupants are then sources of infestation for neighbors and others with whom they may come in contact. Other species of fleas are associated with most other warm-blooded animals. There is no such thing as a sand flea which can live in the soil without having to feed on animals.

Female fleas deposit their eggs on their hosts, in pet bedding, on floor and furniture, or on other accessible places. Eggs laid on the host are not firmly attached and soon fall off. In a few days the eggs hatch into slender, white, legless larvae with bristly hairs. These tiny larvae are scavengers that feed on dirt, body wastes, and many kinds of debris. In about 12 to 15 days the full grown larvae change to pupae and then to adults. The adults immedi-ately search for animals upon which to feed. Pet owners returning from a vacation often find their home overrun with active adult fleas. Immature fleas present when the owners left have completed develop-ment, and the newly emerged hungry adults are searching for a blood meal. Also, homeowners or new tenants moving into vacant homes or apartments where previous tenants had dogs or cats may also experience an adult flea problem. Flea control should be directed to cats and dogs to kill adult fleas and to breeding sites to eliminate both young and adult fleas.

CONTROL ON DOGS AND CATS Pets can be treated for fleas by using insecticide sprays, dusts, foams, shampoos, collars, feed additives, and pills. Insecticides registered for pets include carbaryl (Sevin), chlorpyrifos (Dursban), malathion, naled, propoxur, pyrethrins, permethrin, a feed additive, cythioate (Proban), and a pill, lufenuron (Program). Check with a veterinarian for specific products containing these insecticides.

Always read and follow insecticide label directions. Do not use any insecticides on a pet unless the label specifically states that it can be used on that pet species. Follow restrictions such as age of animal to be treated, and precautions such as not treating sick animals or using in conjunction with other medications. Other products are available for flea control such as pet collars equipped with electronic sounding devices and combs for mechanical removal of fleas. These devices have not been proven to repel or control fleas and are not recommended.

CONTROL IN HOMES Before any insecticide is applied for flea control it is advised to vacuum the premises thoroughly, especially pet resting areas, to remove developing fleas. The entire house should be vacuumed, especially carpets, under furniture, in areas where pets frequent, in cracks and crevices along walls, and in all upholstered furniture. The vacuum bag contents should be destroyed by burning or should be placed in airtight plastic bags and discarded as soon as the house has been cleaned to get rid of the accumulated flea larvae and pupae. To control fleas on carpets and in furnished rooms, use a spray containing pyrethrins, malathion, or propoxur (Baygon). These sprays can be applied as a light mist to floors, carpets, upholstered furniture, and baseboards. Check label directions for proper mixing and use instruc-tions. Before spraying delicate fabrics, treat a small portion to be certain that the spray will not stain the fabric. Carbaryl (Sevin) can be applied as a dust treatment.

FLEAS Ralph E. Williams and Gary W. Bennett, Extension Entomologists PURDUE UNIVERSITY COOPERATIVE EXTENSION SERVICE  WEST LAFAYETTE, IN 47907 http://www.entm.purdue.edu/entomology/E-series/index.html

Ticks are any of the roughly 825 species of invertebrates of the suborder Ixodida, within the order Parasitiformes, subclass Acari (sometimes Acarina, or Acarida). Ticks, worldwide in distribution, are assigned to three families: Argasidae (soft ticks) and Nuttalliellidae and Ixodidae (together constituting the hard ticks). The family Nuttalliellidae is represented by one rare African species. Adults range in size up to 30 mm (slightly more than 1 inch), but most species are 15 mm or less. They may be distinguished from their close allies, the mites, by the presence of a sensory pit (Haller's organ) on the end segment of the first of four pairs of legs; eyes may be present or absent. Ticks are important parasites of large wild and domestic animals; they are also significant as carriers of serious human and animal diseases. Although no species is primarily a human parasite, some occasionally attack man. Hard ticks, such as the American dog tick, Dermacentor variabilis, attach to their hosts and feed continuously for several days. When engorgement is complete, the female drops from the host, finds a suitable site to rest, lays her eggs in a mass, and dies. Six-legged larvae hatch from the eggs, move up on blades of grass, and wait for a suitable host (usually a mammal) to pass by. The odour of butyric acid, emanated by all mammals, stimulates the larvae to drop onto and attach to a host. After filling themselves with the host's blood, the larvae detach and molt, becoming eight-legged nymphs. Nymphs also wait for a suitable host; after they have found one and engorged themselves, they fall off the host and molt into adult males or females. Adults may wait for a host as long as three years. Most hard ticks live in fields and woods, but a few, such as the brown dog tick, Rhipicephalus sanguineus, are household pests. Soft ticks differ from hard ticks by feeding intermittently, laying several batches of eggs, passing through several nymphal stages, and carrying on their developmental cycles in the home or nest of the host rather than in fields. Hard ticks damage the host by drawing large amounts of blood, by secreting neurotoxins (nerve poisons) that sometimes produce paralysis or death, and by transmitting disease. Such diseases include Lyme disease, Texas cattle fever, anaplasmosis, Rocky Mountain spotted fever, Q fever, tularemia, hemorrhagic fever, and a form of encephalitis. Soft ticks also are carriers of diseases.

NY Times Dr. Stephen K. Wikel, an entomologist at the Univ of Connecticut Health Center, is studying tick saliva to find a vaccine that could deter ticks.  Stephen K. Wikel pulled a little gauze-topped glass jar from a warm, damp incubator in his laboratory, and, with the heat from his palm and a puff of exhaled breath, roused the tiny blood-sucking creatures inside. "These are the beasts," he said. Bristly brown dots, each the size of a poppy seed, began to mill across the gauze, excited by the heat and gust of carbon dioxide that signaled the presence of a possible meal ticket on the other side. One dot was immobilized on some cellophane tape and placed under a microscope, revealing just a few of the myriad tools that enable Ixodes scapularis, the deer tick and the main carrier of Lyme disease, to detect, climb aboard and surreptitiously dine on a host. It is this diminutive eight-legged arachnid, a cousin of spiders, that has taken the carefree pleasure out of a summertime walk in the woods for millions of people in the Northeast. Other Ixodes species are spreading Lyme disease on the West Coast and in parts of Europe. The visible features of the tick are impressive enough, including forearm hooks that snag fur or fabric on a passing target, a pair of cutting mouth parts -- like scissor blades with the sharp edge outward -- and a serrated tube that serves both as an anchor and a drinking straw. Ticks are the "Inspector Gadget" of parasites. But it is the tick's invisible armamentarium, dozens of elaborate chemical weapons in its saliva, that have become the prime focus of Dr. Wikel, an entomologist at the University of Connecticut Health Center, which sits on a hilltop near Hartford overlooking wooded suburban yards that are prime tick habitat. He nnd other experts in tick biology have found that the seemingly primitive parasites use an array of sophisticated chemical strategies to subvert a host's immune defenses, to prevent blood from clotting, and to muffle any itch or pain that might elicit scratching that could dislodge a tick and ruin a vital blood meal. Ticks, which spend their lives stealthily avoiding detection, are beginning to give up some of their secrets. A central goal of the scientists is to develop a vaccine from some of the molecules pumped into a host when a tick bites, thereby turning its own weapons against it. A vaccine that deters the Ixodes tick, Dr. Wikel and other tick experts say, could prove more useful than the existing vaccine for Lyme disease, which only attacks the bacteria transmitted by the tick, not the tick itself. Recent research has shown that deer ticks carry at least two other diseases besides Lyme -- human granulocytic ehrlichiosis and babesiosis. So an "anti-tick" vaccine, Dr. Wikel said, could essentially be "a three-in-one" vaccine. Some preliminary work has shown that the strategy can be effective, and one anti-tick vaccine is being used against a different species that infests cattle in Australia -- sometimes with up to 20,000 ticks on a single host. But it will be years before scientists clearly identify the structure and purpose of the soup of molecules in tick spit, Dr. Wikel said, and years more before there is a marketable human vaccine. In the meantime, other scientists are finding that tick saliva is fertile territory for seeking potential new drugs, especially for controlling clotting and inflammation. "Ticks know everything we know and don't know about pharmacology," said Dr. Jose M. C. Ribeiro, a tick expert at the parasitology laboratory of the National Institutes of Health in Bethesda, Md. Dr. Ribeiro, Dr. Wikel and others studying ticks have practical ends in mind, but almost all of these scientists say they were drawn to these persistent pests mainly by their complex, often astonishing, abilities. "Biologically, a tick is a box inside a box inside a box," Dr. Ribeiro said. Another tick expert, Dr. James E. Keirans, recalled his wonderment 30 years ago when he was based in western Montana and hiked paths leading into the foothills of the Rockies in the spring, when adult dog ticks emerge. There, when you crouch down with the light behind you, he said, "you can see the ticks up on the grass blades, just sitting there attached by their third pair of legs. You can take off your hat and pass a shadow over them and see 60 or 70 ticks at once moving their legs." There are about 840 tick species, divided into two families, those with leathery bodies like the dog and deer tick -- which have three life stages and take only one big, momentous meal during each stage -- and others with soft bodies, which behave more like fleas, feeding repeatedly and often. Ticks feed on just about every kind of back-boned animal except fish, said Dr. Keirans, the curator of the National Tick Collection, which is owned by the Smithsonian Institution but is located at Georgia Southern University in Statesboro, Ga. He rattled off a few examples, including ticks that hopscotch continents on migrating seabirds, specialized ticks that may soon become extinct as the rhinoceroses on which they feed dwindle, even ticks that only feed on the Galapagos tortoise. The largest is a tick that feeds only on sloths in the American tropics. When fully engorged, he said, it is the size of a Ping-Pong ball. There is some debate, but many biologists say that ticks probably evolved more than 300 million years ago, possibly feeding on dinosaurs and amphibians. "For them, the mass extinction of dinosaurs just meant a menu change," said Dr. Ribeiro. A new target, the mammal, had a new feature in its blood, platelets, which aid clotting and would have thrown a roadblock at ticks. But, Dr. Ribeiro said, evolution carried on and ticks -- in the endless spy-versus-spy game of life -- developed ways to keep the blood flowing. "They have a very ancient wisdom about how to take blood," he said. The hard-bodied ticks have been the focus of most research in North America because they are the predominant carrier here of diseases that affect people and their livestock and pets. (Wildlife, of course, is not immune. Biologists have documented the presence in northern forests of "ghost moose" -- moose that have as many as 400,000 ticks feeding on them and that lose all their hair as they rub hopelessly against trees.) In its life cycle and habits, the deer tick is typical of many species, said Dr. Daniel E. Sonenshine, a biology professor at Old Dominion University in Norfolk, Va., and author of the two-volume "Biology of Ticks" (Oxford University Press, 1991 and 1993). A tick's prime goal is to find an appropriate host, climb aboard, find the ideal spot to latch on, and to dine on red blood cells, the source of the globin molecules needed to molt and mature and, in the end, for females to make and lay eggs. In each stage of life -- larva, nymph and adult -- the process of finding and feeding on a host is almost exactly the same. Only the targets change. The larvae almost always feed on mice, while the adult deer tick, which is big enough that it tends to be detected by a person and brushed or plucked off, targets mainly deer. For deer ticks, the nymph stage -- the stage milling around in Dr. Wikel's jar -- is the main transmitter of disease to people, with its peak of activity coming from late spring to late summer. A nymph's day generally starts in a moist, protected place, typically buried in leaf litter and only rarely out in the middle of a mowed lawn. Without adequate moisture it can quickly dry out and die. As the hours pass, it begins to "quest," in the parlance of tick biology, climbing instinctively in the opposite direction of gravity, usually up a blade of grass or a twig, and generally no more than a foot or two off the ground. It sits poised, waiting. In this posture, resumed daily, the tick is like a land mine, primed and ready and patient as can be, with weeks or even months passing before a potential target comes along. Most, Dr. Keirans said, never find a meal. But enough do. They detect a rustling vibration and a whiff of carbon dioxide and maybe a slight sensation of warmth. A shadow passes, triggering nerves attuned to changes in light. Holding onto the perch with that third pair of legs, they wave the rest of their appendages. Especially active are the forearms, which contain a sensory organ that is exquisitely tuned to sense chemical changes.

The legs are tipped with sharp hooks. The lucky ones snag a ride. But, Dr. Sonenshine said, for the tick, the job has only just begun. It begins to explore the host, he said, generally moving up against gravity until it either reaches an obstruction -- the elastic of underpants or a tight shirt collar -- or until it finds an ideal feeding spot, a place exuding sweat and warmth, indicating an ample blood supply. The sensory tools that led it to this place are now disregarded and it relies on its palps, paired arms next to its cutting mouth parts, to select an ideal dining spot. Once there, ticks do not bite like a horsefly or use a syringe like a mosquito. Unlike these insects, which eat and run, ticks have taken an evolutionary path requiring them to settle in for the long haul. Ticks dig a well. Using their serrated mouth parts, they excavate a pool beneath the host's skin from which they draw sustenance using the hypostome, a straw-like tube that resembles a drywall anchor and holds the animal almost as effectively. A tough, rubbery cement is released, helping hold the tick in place. The meal unfolds over up to five or even seven days, which is why people are generally not apt to acquire Lyme disease from a tick bite if the offender is removed within a couple of days of attachment, researchers say. The tick only sips tentatively at first, while steadily pumping into the wound saliva that carries a variety of ingredients that help it stay attached, avoid detection, suppress the immune system and keep blood flowing. The result is a pool brimming with just what the tick wants, red blood cells. The white blood cells that would normally flood a wound have been tricked to stay away. "Ticks are very finicky, like one of those brats who will only eat cookies," said Dr. Sonenshine. "The tick has this choice of all these wonderful things -- a big cafeteria of cells, muscle, other tissue. But it says no thanks. Just give me red blood cells." Finally, there comes what tick biologists call "the big sip," a binge of feeding reserved until the end so there is the least risk that the now rapidly growing parasite will be detected. As it ingests blood, it has to expel water, and it does so through its saliva, accelerating the passage of any hitchhiking Lyme bacteria into the host. Researchers stress that old methods for removing ticks -- like touching it with a burned match or daubing with alcohol -- probably cause it to expel even more spit into the wound. The best approach, they say, is to use steady pressure with small tweezers to draw the tick away from the skin until it pulls free. As the meal comes to a close, the tick grows sometimes a hundredfold in weight before finally dropping from the host and crawling into leaf litter and -- in the case of adult females -- laying thousands of eggs and starting the cycle all over again. Dr. Ribeiro has spent more than a decade hunting in tick saliva for all the hidden molecules used during feeding. A few have been identified by him or other researchers: •Apyrase, an enzyme that destroys substances released by injured cells that would normally cause platelets and white blood cells to accumulate. •Prostaglandin E2 , which suppresses some immune defenses and dilates capillaries, increasing blood flow. •Kininase, an enzyme that blocks several molecules that create the itch sensation and swelling when skin is injured. And there are probably dozens more, Dr. Ribeiro, Dr. Wikel and other researchers said. Increasingly, it appears that the infections transmitted by ticks take advantage of the conditions created by this chemical cocktail, Dr. Wikel said. All the more reason to find a way to vaccinate potential hosts so that the body -- instead of being tricked by the influx of weapons -- recognizes one of them and mounts a counterattack, he said. Dr. Wikel, who once enlisted a small army of students to dissect salivary glands out of 10,000 ticks, said that genetic sequencing techniques were accelerating the research. Even so, he said, "We probably have a lifetime of work ahead of us to look at all these products, develop the proteins and use them in vaccination trials." Dirty Secrets of Bloodthirsty Ticks by ANDREW C. REVKIN CDC; James Occi 

More Ticks. Thanks, El Nino




August 16, 1998


More Ticks. Thanks, El Nino PRACTICAL TRAVELER/ By SUSAN GILBERT L NIÑO may seem like a distant memory, but the mild, wet weather it brought to much of the country earlier this year has helped spawn outbreaks of several illnesses in popular vacation spots this summer. With lush vegetation for food and shelter, rodents are proliferating, according to public health experts, and so are the diseases that they spread. Hantavirus, a deadly infection, has returned to the Southwest, and tick-borne illnesses like Lyme disease are spreading in most states. No parks or other travel destinations have closed, and travel doctors have not been advising vacationers to cancel their plans. "But travelers might want to be extra cautious this year," said Dr. Clarence J. Peters, chief of the special pathogens branch of the Centers for Disease Control and Prevention in Atlanta. Before leaving home, he said, people should learn about the illnesses that are common or emerging in their destinations. To help, the C.D.C., the National Park Service and some state health departments have brochures and postings on their Web sites. Hantavirus in Southwest nyone traveling to rural areas of the Southwest should take precautions against hantavirus pulmonary syndrome, an incurable virus that can kill within hours of infection. The C.D.C. has counted 106 cases, including 35 deaths since 1994. There have been three deaths in Colorado and New Mexico this year, according to those states. All of the infections occurred in rural areas where the deer mice, which harbor the virus, live. People become infected when they inhale dust contaminated with mouse urine or feces. Travelers can guard against hantavirus by staying away from the rodents, as well as their burrows, which are small holes in the ground. Dr. Peters recommends that campers use a tent with a floor and lock food in a cooler. If you camp in a cabin, open the doors and windows half an hour before going inside. Doing so will clear the air of the rodents' urine spray and kill the viruses.

More information on preventing hantavirus is available on the C.D.C.'s Web site (www.cdc.gov) and in brochures from the National Park Service, which can be found at some national parks or on the Park Service's site (www.nps.gov). Recurrence of Plague he same weather that has promoted hantavirus has caused a rise in plague in the Southwest. Though people tend to think of plague as a disease from the history books, there are usually about 10 to 20 cases a year, mainly in New Mexico and Arizona, said Dr. Peters. Plague bacteria are carried by fleas and spread from rodents, rabbits and domestic animals to people. The number of people with plague has held steady this year so far, but public health officials are seeing a sharp increase in the number of rodents and domestic cats with the disease, which they fear could herald an increase in human infections. Frightening as that sounds, the threat to travelers is small, said Dr. Paul Ettestad, a public health veterinarian with the New Mexico Department of Health in Santa Fe. "People going to standard tourist areas, like national parks, are not at increased risk," he said. "There's more potential for infection if you're camping, but you can take precautions." As with hantavirus, Dr. Ettestad said, hikers and campers should avoid rodents and their burrows and protect themselves with an insecticide containing DEET. (Children should use preparations with no more than 10 percent DEET.) People traveling with their cats and dogs should dust them with flea powder and not let them roam free. Plague is curable if it is treated promptly. Symptoms include sudden fever, chills, headache and extremely swollen and tender lymph nodes. 2 New Tick-Borne Infections nfections spread by ticks appear to be on the rise this summer, experts say. By far the most prevalent one is Lyme disease, with nearly 13,000 cases reported to the C.D.C. last year. David Weld, executive director of the American Lyme Disease Foundation, a research and education group in Somers, N.Y., said that deer ticks, which transmit Lyme disease, are more abundant this summer in established trouble spots, like Long Island, the Hudson Valley and the shoreline from Connecticut to Massachusetts, as well as in the Midwest. In addition, he said, the ticks are spreading to new territories, including upstate New York, Florida and California. As with all tick-borne illnesses, the earlier Lyme disease is treated, the more easily it can be cured. Symptoms include a rash that looks like a red dot and then expands, as well as headache, fever and muscle aches.

Though far less common than Lyme disease, with just a few hundred cases a year, several other tick-borne illnesses that are spreading more rapidly are more dangerous, public health experts say. Ehrlichiosis occurs in the same areas as Lyme disease. Babesiosis is found mainly on the East Coast from Maryland to Maine and in Wisconsin, Minnesota and Michigan. Like Lyme disease, ehrlichiosis and babesiosis are transmitted by deer ticks. But the infections are harder to identify because there is no rash, and they can be fatal if they are not treated, Mr. Weld said. Ehrlichiosis symptoms include severe headache, chills, vomiting and high fever. Babesiosis symptoms are a spiking fever and sweats that come and go. These are fairly new diseases; there are no diagnostic tests and many doctors do not know about them, said Dr. Richard Falco, a scientific adviser to the American Lyme Disease Foundation. "If you get ill when you get back to your home state, let your doctor know that you were in an area where X tick-borne illness occurs." Another potentially deadly tick-borne illness is Rocky Mountain spotted fever, which occurs in most states, chiefly in the South and Southeast, said Dr. Falco. Several hundred people are infected each year, and the chance of dying is 25 percent without early treatment, he said. The first symptoms include fever, loss of appetite and a mild headache followed two to six days later by small pink spots on the wrists and ankles, which spread across the body. Rocky Mountain spotted fever is transmitted by the lone star tick and the American dog tick. Standard measures used against other tick-borne illnesses apply. For example, when hiking, walking or camping in grassy or wooded areas, apply a tick repellent that contains DEET to your shoes and legs. More information is available from the American Lyme Disease Foundation: (914) 277-6970. The best defense against tick-borne infections is to examine yourself and your children after being outdoors, Dr. Falco said. Remove ticks by pulling them out with tweezers or one of the tools designed for this purpose, like Ticked Off. Time is on your side: It takes 36 to 48 hours from the time a tick attaches itself to the body until it can transmit Lyme disease, 24 to 48 hours to transmit ehrlichiosis or babesiosis and 3 to 24 hours to transmit Rocky Mountain fever. Routine tick checks, said Dr. Falco, can reduce the chance of illness to almost nothing. 


\8 Infestation: Lice

LICE are of three types; HEAD LOUSE which are at home in the scalp. The CLOTHING LOUSE which infests clothing (seams), and the CRAB LOUSE that infests the beard, underarms and between your legs. All of them want to suck your blood on a regular basis. Infestation is by direct contact with low life and animals or exchanging use of clothing (towel). Their bites are a nuisance but long term infestation can lead to infection or allergy. The dried feces of clothing lice can cause typhus if inhaled or enters open wounds. 

Lice are small gray or brown bugs that live on blood and can pass disease to humans. Head lice and crab lice (which usually reside in the crotch) infest the roots of hair shafts, leaving tiny white eggs which are difficult to remove. They can cause itching and rash. Body lice usually live in the seams of clothing, taking frequent side trips to feed. You can acquire lice from contact with infested people or fabrics.

Lice can be combed out of hair using soap or vinegar and a fine-toothed comb, but the most efficient method is the use of chemical dusts, lotions or shampoos made for this purpose. Since some of the chemicals may be toxic if overused, it's important to follow directions exactly. Infested clothes, bedding and other fabrics must be cleaned thoroughly in very hot water (use the hottest cycle on washers and dryers), treated with insecticides or heated at 160°F (70C) for 30 min. Antihistamines can help control itching. Permethin (NIX) can be used to prevent and rid body of fleas and lice. Bedding & clothing must also be treated.

Lice can be combed out of hair using soap or vinegar and a fine-toothed comb, but the most efficient method is the use of chemical dusts, lotions or shampoos made for this purpose. Since some of the chemicals may be toxic if overused, it's important to follow directions exactly. Infested clothes, bedding and other fabrics must be cleaned thoroughly in very hot water (use the hottest cycle on washers and dryers), treated with insecticides or heated at 160°F (70°C) for 30 minutes. Antihistamines can help control itching.

Parasitic insects found on the heads of people. Having head lice is very common; as many as 6-12 million people worldwide get head lice each year.
 Anyone who comes in close contact with contaminated stuff as clothing, or belongings. Preschool and elementary-age kids, 3-10, and their families are infested most often. Gals get head lice more often than guys. In the US, blacks rarely get head lice.
 What do head lice look like? There are three forms of lice: the nit, the nymph, and the adult.
 Nit: Nits are head lice eggs. They are hard to see and are often confused for dandruff or hair spray droplets. Nits are found firmly attached to the hair shaft. They are oval and usually yellow to white. Nits take about 1 week to hatch.
 Nymph: The nit hatches into a baby louse called a nymph. It looks like an adult head louse, but is smaller. Nymphs mature into adults about 7 days after hatching. To live, the nymph must feed on blood.
 Adult: The adult louse is about the size of a sesame seed, has 6 legs, and is tan to greyish-white. In persons with dark hair, the adult louse will look darker. Females lay nits; they are usually larger than males. Adult lice can live up to 30 days on a person’s head. To live, adult lice need to feed on blood. If the louse falls off a person, it dies within 2 days.
 Head lice most commonly found on the scalp behind the ears and near the neckline at the back of the neck. Head lice hold on to hair with hook-like claws found at the end of each of their six legs. Head lice are rarely found on the body, eyelashes, or eyebrows.
 Signs and symptoms of head lice infestation?
  * Tickling feeling of something moving in the hair.
  * Itching, caused by the an allergic reaction to the bites.
  * Irritability.
  * Sores on the head caused by scratching. These sores can sometimes become infected.
 How did my child get head lice?
  * By contact with an already infested person. Contact is common during play at school and at home (slumber parties, sports activities, at camp, on a playground).
  * By wearing infested clothing, such as hats, scarves, coats, sports uniforms, or hair ribbons.
  * By using infested combs, brushes, or towels.
  * By lying on a bed, couch, pillow, carpet, or stuffed animal that has recently been in contact with an infested person.

How is head lice infestation diagnosed? By looking closely through the hair and scalp for nits, nymphs, or adults. Finding a nymph or adult may be difficult; there are usually few of them and they can move quickly from searching fingers. If lice are not seen, finding nits close to the scalp confirms that a person is infested. If you find nits more than 1/4 inch from the scalp, the infestation is probably an old one. If you are not sure if a person has head lice, the diagnosis should be made by a medic.

How can I treat a head lice infestation? By treating the individual, infested family members, and the household.
 Treat the individual/family: Requires using an OTC or prescription medication. Follow these treatment steps:

1. Remove all clothing.
 2. Apply lice medicine, also called pediculicide (peh-DICK-you-luh-side), according to label instructions. If your child has extra long hair, you may need to use a second bottle.
 WARNING: Do not use a creme rinse or combination shampoo/conditioner before using lice medicine. Do not re-wash hair for 1-2 days after treatment.
 3. Have infested person put on clean clothing after treatment.
 4. If some live lice are still found 8-12 hrs after treatment, but are moving more slowly than before, do not retreat. Comb dead and remaining live lice out of the hair. The medicine sometimes takes longer to kill the lice.
 5. If, 8-12 hours after treatment, no dead lice are found and lice seem as active as before, the medicine may not be working. See your health care provider for a different medication and follow their treatment instructions.
 6. Nit (head lice egg) combs, often found in lice medicine packages should be used to remove nits and lice from the hair shaft. Many flea combs made for cats and dogs are also effective.
 7. After treatment, check, comb, and remove nits and lice from hair every 2-3 days.
 8. Re-treat in 7-10 days.
 9. Check all treated persons for 2- 3 weeks until you are sure all lice and nits are gone. Treat the household:
 1. To kill lice and nits, machine wash all washable clothing and bed linens that the infested person touched during the 2 days before treatment. Use the hot water cycle (130o F) to wash clothes. Dry laundry using the hot cycle for at least 20 minutes.
 2. Dry clean clothing that is not washable, (coats, hats, scarves, etc.) OR
 3. Store all clothing, stuffed animals, comforters, etc., that cannot be washed or dry cleaned into a plastic bag and seal for 2 weeks.
 3. Soak combs and brushes for 1 hour in rubbing alcohol, Lysol*, or wash with soap and hot (130o F) water.
 4. Vacuum the floor and furniture. Do not use fumigant sprays; they can be toxic if inhaled.
 My child has head lice. I don't. Should I treat myself to prevent being infestated?
 No, although anyone living with an infested person can get head lice. Check household contacts for lice and nits every 2-3 days. Treat if lice and nits are found.
 Should my pets be treated for head lice? No. Head lice do not live on pets.
 My child is under 2 years old and has been diagnosed with head lice. Can I treat with prescription or OTC drugs?
 No. For children under 2 years old, remove nits, nymphs (immature adult lice), and adults by hand.
 What OTC medications are available to treat head lice? Many head lice medicines are available at your local drug store. Each OTC product usually contains one of the following active ingredients.
 1. Pyrethrins (Pie-WREATH-rins): (often combined with Piperonyl butoxide pie-PER-a-NIL beu-TOX-side):
 Brand name prods: A-200*, Pronto*, R&C*, Rid*, Triple X*

Pyrethrins are natural extracts from the chrysanthemum flower. Though safe and effective, pyrethrins only kill crawling lice, not unhatched nits. A second treatment is recommended in 7-10 days to kill any newly hatched lice. Treatment failures are common.
 2. Permethrins (per-meth-rin): Brand name product: Nix* Permethrins are similar to natural pyrethrins and are safe and effective and may continue to kill newly hatched eggs for several days after treatment. A second treatment may be needed in 7-10 days to kill any newly hatched lice.
 Treatment failures are common. A prescription drug used to treat head lice is Lindane (Kwell*): Lindane is one of the most common treatments used to treat head lice. When used as directed, the drug is probably safe. Overuse, misuse, or accidentally swallowing Lindane can be toxic to the brain an d nervous system.

Which head lice medicine is best? If you ain't sure, ask your pharmacist or health care provider. When using any medicine, always follow the instructions provided.
 When treating head lice: 1. Do not use extra amounts of the lice medication.
 2. Do not treat the infested person more than 3 times with the same medication if it does not seem to work. See your health care provider.
 3. Do not mix head lice medications. Should household sprays be used to kill adult lice? No. Spraying the house is NOT recommended. Fumigants and room sprays can be toxic if inhaled.
 Should I have a pest control company spray my house? No. Vacuuming floors and furniture is enough to treat the household.

Body and head lice (Pediculus humanus) can also be transmitted easily among tourists, either by direct contact or from clothing and headgear. They can even be transmitted from cloth-covered seats in cinemas or public transport. The lice lay small white eggs which are attached to hairs and can be located easily under Wood's light, when they fluoresce.

Symptoms include itching and sometimes a macular rash. Other symptoms can occur if the lice are carrying diseases such as typhus or relapsing fever, especially if the traveller picked up the infestation in Africa, Europe or Asia. Any fever associated with pediculosis should therefore be investigated.

Treatment, Piperonyl butoxide with pyrethrins (Lyban Foam) should be applied to the affected area, but not to the eyes. If eyelashes are infected, an ophthalmic ointment can be used two times a day for 10 days to smother the lice. Body and head lice can be treated with application of permethrin or maldison (Cleensheen, Lice Rid) and removal of the eggs using a fine-toothed comb.

Prevention: Insect repellents containing DEET (diethyl- oluamide), and sleeping sheets impregnated w/permethrin, are helpful in lowering the risk of pediculosis.


\9 Infestation: Other

Crabs can be quiet in your private places till their offspring overrun the neighborhood. They look like dandruff but won't brush off.

Fleas are tiny, wingless parasitic insects that live wherever there is blood to feed on. They usually feed on organic debris on the floor and breed on animal hosts. Usually found in transient bedding. Some types can jump several feet, so in addition to looking for moving dark spots on your ankles and bedding, check your knees and arms as well. Fleas are an uncomfortable nuisance, and can carry disease. Follow insect precautions carefully to avoid being bitten. Look for clean lodgings; vacuuming is helpful in getting rid of fleas, eggs and larvae. They can be seen easily on white background.

Flea bites are small, raised red spots that itch fiercely. Usually their harmless bites are a nuisance that cause small red raised itchy lesions and appear on the legs and ankles. The bites cause irritation for about two days. Use topical creams with hydrocortisone to control itching. Some fleas can transmit plague or murine typhus. 

To relieve itching apply 1% hydrocortisone cream twice a day. Use Permethrin (NIX) to treat and prevent. 

SCABIES is caused by a small mite that tunnels under the skin and is difficult to detect. Their unbearable itch can be relieved with antihistimine. Fortunately they carry no disease. Infestation comes from intimate contact with an infected person over time. Itching develops due to an allergic reaction in 6-8 wks on sides or between the legs usually at night and can be unbearable, but it does not carry disease.  A rash may be seen around the waist. Treatment: use ELIMITE.

Mites cause an intensely itchy, raised red rash called scabies. Mites burrow into human skin to lay their eggs and are spread among people through physical contact with skin or fabric. Because of the mite life cycle, it may be 6-8 weeks after contact before symptoms appear. These start with small itchy bumps, followed by the rash usually at the waist, underarms, inner thighs and/or backs of legs. Itching may increase at night. Various chemical lotions and creams are made to kill mites. They are applied over the entire body, left on for several hours, then washed off. Everyone living or traveling with an infested person must also be treated, even if they don't yet show any symptoms. Antihistamines help relieve itching, which can continue for up to 2 weeks after treatment. All clothing, bedding and other fabric should be cleaned thoroughly in very hot water (use the hottest cycle on washers and dryers), heated at 160F (70C) for 30 minutes or sealed tightly in plastic bags for 3-5 days until the mites are dead.


\10 Flies

Flies can transmit parasites and spread disease among humans and animals when they bite or sting. Even more common is their role in carrying bacteria, viruses and parasites from shit and filth to food products. Follow food, water and insect precautions carefully. Try to stay away from areas where flies congregate, such as garbage dumps and fields where shit is used as fertilizer.

Sandflies are found mainly in tropical and subtropical climates (Rio/Copacabana). The bite of the female spreads leishmaniasis and bartonellosis to humans. Sandflies are tiny, and the grid of most window screens and mosquito netting is not small enough to keep them out. Use a permethrin-based insecticide spray on screens and netting to kill sandflies on contact. Keep bed netting tucked in tightly around the base of the mattress at all times. Sandflies tend to breed in garbage and manure, so try to avoid disposal areas or fields where manure is being used as fertilizer. Sandflies are most active between dusk and dawn and hide in dark corners during the day. Follow insect precautions when traveling in areas where sandflies are responsible for spreading disease.


\11 Mosquitos

Found everywhere in the world. Mature female mosquitoes feed on blood to produce their eggs and are responsible for trans- mitting many disease causing parasites and viruses. Males do not bite. Of the three types: Aedes, Anopheles, and Culex, the aedes bites during the day.

Rubbing lime (any citrus) juice on mosquito bites makes them itch more temporarily, therafter they stop itching and heal faster. LP. 

Deodorants, shampoos, sweat, and colors will attract mosquitos. Wear long sleeves and trousers after sunset, cuffs laced with DEET. For restful sleep, spray room before sleep and/or use incense with ventilation.

Check condition & mend holes in netting during daylight. Use tape or fold around hole and pin. Spray solid lines and around patches with DEET before leaving room for evening. Mosquito borne disease is not a fun thing.

Humans really are the big cheeses of the animal kingdom -- at least  to the small, unloved mosquito. You know a creature is in deep, deep trouble when people don't think  twice about whacking it. Even animal rights activists aren't so  quick to leap to the mosquito's defense. The only good mosquito,  many people would say, is not just dead but well and truly dead,  reduced to a bit of insect juice on the wall. Why do mosquitoes bug us this way? And why some of us so much? (Why  me?) Considering our bad attitude, it's a wonder mosquitoes even come  near us -- an insanely risky proposition from their viewpoint.  That's probably why some mosquito species figured long ago they'd  rather tuck into an unconscious host, an unmovable feast as it were,  and voted by and large to nip at night. The nipping's done with a  proboscis, a sort of springy syringe with a hollow needle formed by  interlocking mouthparts and an outer sheath that rides up when the  needle slides through your skin and probes for blood. But hitting  the sweet spot isn't so easy--mask any intern drawing blood from a  patient for the first time. Or ask Jose Ribeiro, a medical  entomologist at the National Institutes of Allergy and Infectious  Diseases, who will gladly give you the gory details. "Less than 5  percent of skin is blood vessel, so the mosquito has to fish. It  casts its proboscis back and forth under your skin, sawing through  tissue and probing an area ten seconds at a time." 

After several  such "search castings" and no luck, the insect withdraws completely  and tries another patch of skin. But if it gets a good probe into  one of your small blood vessels, it freezes and sucks from the  hemorrhage, pumping in little spitballs of vessel dilators and blood thinners to keep its meal running freely. (An allergic reaction to mosquito drool is what produces those itchy red lumps, if you've  wondered.) A mosquito can suck two to three times its weight in blood, no trouble. That's like a 150 lb human vacuuming up 300-450 pounds of food.

At this point, stretch receptors in the mosquito's hugely bloated abdomen, sensing imminent blowout, initiate an urgent message to the  brain, saying in effect, "Whoa there, skeeter -- pull out!" It's a  pretty mechanical reflex, apparently. You can get mosquitoes to quit  feeding by pumping them up -- how can I put this delicately? -- from  the other end, with saltwater enemas or air. Marc Klowden, the  entomologist at the Univ of Idaho who did these insufflating  experiments, also has videos showing what happens when you prevent  the signal from the abdominal receptors from reaching the brain: too  much is never enough for these mosquitoes, and they eat until they explode.

Even under normal circumstances, once a mosquito has eaten its fill,  "it's so heavy it can barely fly," according to Ribeiro. Stuporous  and swollen as a blimp, it looks for a place to lie low and do what  anyone would do after going on the mother of all drinking binges --  it excretes like crazy. After a few hours the mosquito has reduced its blood meal by half into a supernutritious slush.

Thankfully, at any given time, in any population, less than half the mosquitoes are biters. That's because, first, only females are  hematophagous (Greek for "blood eaters"). Males are sweet nectar-loving types, peacefully sipping at nature's juice bar.  Second, most females feed on blood only when they need the extra  protein to finish making their eggs; for routine fuel they'll use  plant sugars, too. In fact, feeding on blood seems a pretty well orchestrated event, dangerous enough that females have built-in controls to switch it on and off --they don't seek out victims more than they have to. Remind yourself of this the next time you're being eaten alive. Things could be worse.

Which brings us back to that all-consuming question -- or rather, that question that consumes some of us more than others. How do  mosquitoes get wind of their prey, and why are certain people more preferable than others? You know who you are. You're the ones who make backyard barbecues safe well, tolerable -- 

for the rest of us by acting as live bait, the folks who get fed on right through their cotton T-shirts. You're the ones whose mothers dabbed lotion on bites and cheerfully consoled: "You just have sweet blood."

Entomologists are a blunter lot: they labor in the service of science, not in the warm, fuzzy business of sparing our inner child. 

Mosquitoes, they tell us, use various cues to find food -- color contrast and movement, skin temperature and humidity. But above all, experiments show they're olfactory creatures. Floral scents help steer them to their nectar meals. And breath and body vapors draw them to their animal hosts, including you and me. For mosquitoes our vapor trail is a no-brainer. It says: Fly this way. Make a right. Eat here. Just do it.

Each time you breathe out and blow off carbon dioxide, you're telling mosquitoes (and other nasty biting insects like ticks) that there's a vertebrate, a handy blood container, in the vicinity. 

Mosquitoes have CO[sub 2] receptors on little feelers called palpi and can detect a plume of the gas from about 50 feet away. This is bad news: there's a world of bloodsuckers waiting for you to exhale and no way you can hold your breath forever. Matters aren't helped,  either, by another vertebrate emanation of ours, a volatile chemical called lactic acid, which mosquitoes pick up on their bristly  antennae. Humans exude this compound from their hands, from their faces and shoulders -- in fact, from just about every pore of their  bodies, in secretions .like oil and sweat made by skin glands. 

Lactic acid escapes from our mouths too, whenever we go in for any heavy-duty exercise. As it happens, some of us are quite a bit more effusive than others.

That may begin to explain why everyone doesn't get bitten equally. "There's definitely a marked difference in people's skin exudations  and their effect on mosquitoes," says Dan Kline, a research  entomologist with the U.S. Department of Agriculture in Gainesville,  Florida. He recalled arriving at a lab some years ago when the  notion was in its early test stages: "People were walking in the  hallways with marbles in their hands, and I wondered what sort of  institution I'd come into. They were rubbing their marbles and then  seeing which ones attracted mosquitoes." Entomologists are pretty  sure that personal skin chemistry is the key. But skin exudes  hundreds of chemicals, and who's to say which ones are preferred?  Kline thinks diet may play a part. Among other things, he studies  octenol, a mosquito-attracting substance first found in ox breath  that's produced by grass fermenting in the ruminant's stomach.  Eating your greens, he mused, may make your skin ooze more octenol. It's also becoming clear that mosquitoes are quite fussy -- with  different species biting different hosts, and even particular bits  of their hosts, suggesting they respond to different cues. For  example, Anopheles gambiae, one of Africa's top malaria carriers, is  so inordinately fond of humans that it will fly by cattle, ignoring  all their bovine odors, to get to the herdsmen. It's also a foot  fetishist, according to a Dutch research group led by Willem Takken  at the Wageningen Agricultural University in the Netherlands. In  1993, Bart Knols, then a student with the group, demonstrated this  in a series of PG-rated experiments in which he used young men  wearing "only fight underwear" as target practice for hundreds of  avid mosquito females. Painstaking bite counts revealed that A.  gambiae nips at feet and ankles, while other mosquitoes seek out  heads and shoulders. From their flight patterns, it looked as if  each species was finding its favorite sites by tracking either  breath or foot aromas. Sure enough, piping the subjects' breath out  of the test area threw the headhunters into a tizzy, and they bit  other body parts instead. And feet freshly washed with antibacterial  soap left A. gambiae completely cold. Unwashed human feet, maybe you've noticed, have a rather distinctive  stinkyness. Nothing else springs to mind as smelling quite like  feet, except, well, cheese. That's what sprang to Bart Knols's mind,  too. In Holland they have a word for the odor, tenenkaas, or toe  cheese (not to be confused with the snack food Cheetos). In what  Knols admits is a rather anthropomorphic bit of scientific reasoning  (hey, whatever works), he decided to check his mosquitoes' response  to Limburger -- a famously pungent from age invented by Belgian  monks -- by conducting insect flight tests inside a small wind  tunnel. A. gambiae mosquitoes were released into the flight chamber  of this contraption some five feet downwind from two traps -- one  wafting Limburger fumes, the other clean air. The mosquitoes, good  little lab rats that they were, chose the cheese trap three times as  often as the odorless one. Of course, the Dutch have a theory to explain all this: what cheese  and feet have in common are odor-producing bacteria. Bacteria are  essential to making cheese -- the powers unseen that turn insipid  milk into a panoply of Bries, Goudas, Cheddars, Roqueforts,  Parmesans, Leer-dammers, and Limburgers. And we have loads of  bacteria growing on our feet. In fact, midway through his doctoral  thesis, Knols notes rather ominously that "it has even been  suggested that certain bacteria involved in cheese production  originate from human skin and therefore that 'cheese smells of feet  rather than the reverse.'" God knows how the good monks inoculated  the first Liraburger cheese; pray it was a miracle. As it happens -- just a coincidence, perhaps -- the bacterium used  for Lira-burger belongs to the same family as a bacterium that often  lurks on human feet. Brevibacterium linens is the cheese maker's  friend, and Brevibacterium epidermis is the one that hangs out on  the skin between people's toes. About 3 8 percent of people with normal feet harbor B. epidermis,  according to James Leyden, a professor of dermatology at the  University of Pennsylvania School of Medicine who (only  coincidentally?) happens to share his name with a famous Dutch city.  "But when it's there, it's there a lot" -- something like a million  per toe-web space. A lot of the sulfurous smells we associate with  stinky feet are produced by B. epidermis and a diminutive bacterium  called Micrococcus sedentarius, which break down proteins in skin  debris, Leyden elaborated. "But all feet have an odor," he added,  "mostly due to fatty acids" (from the breakdown of fat substances in  degenerating skin cells). Chalet Cheese Co-op, in Monroe, Wisconsin, is the last of the  Limburger makers in the United States. An oblong little cheese. with  a faintly orange rind, Limburger has a yellowish semisoft interior  and lots of funky flavor. Amazingly, though, every Limburger starts  life with no more character than a brick of cottage cheese. To begin  its transformation, it's placed on curing boards and repeatedly  wetted down and rubbed over with something Chalet manager Myron  Olson called "schmier." This is not the stuff New Yorkers spread on  bagels. In Wisconsin, "schmier," or smear water, is a cloudy mix of  water, salt, and proprietary organisms including B. linens cultured  from previous cheese batches. In a matter of days, smeared cheese  "has gone from white to golden," said Olson, but it's still "crumbly  and acidic like feta." Young Limburger is then put in cool cellars  where its surface coating of bacteria goes to work on its fats and  proteins, softening the cheese from the outside in, mellowing its  acidity, and developing its complex taste and aroma. At two months,  in Olson's view, "there's a sweetness to it and even the kids will  eat it." At three to four months it's at its flavor peak, with heady  whiffs of fatty acids -- especially butyric acid, the "barnyard  flavor you can also detect in Cheddar" -- as well as ammonia and  sulfur compounds. (It's really pretty tasty if you're game for  strong cheese.) By six months, though, you have to be a real  Limburgerlover to appreciate its whopping potency. The Dutch researchers, then, could be onto something with their  toe-cheese theory. Takken's group, however, wasn't content to trust  the human nose -- an unreliable stand-in, in any case, for mosquito  antennae and palpi, and a poor guide to what an insect can smell. So  the researchers proceeded to do gas chromatography studies. They  took parings of cheese and scrapings from under a volunteer's  toenails, analyzed the chemicals given off by both substances, and  found resemblances not only in their more obviously smelly sulfur  compounds but in their carboxylic fatty acids. These fatty acids are  something of a human trademark ("Bloodhounds follow our fatty-acid  fingerprint," according to Leyden). They're produced by bacteria  tirelessly breaking down triglycerides in the sebum coating our  skin. "Thus," the Dutch have concluded, "it is tempting to explain  the variations in attractiveness of individuals to A. gambiae on the  basis of the metabolic activity of their resident skin microflora."  You may take that to mean: Skin microbes make stuff that attracts  mosquitoes, but my microbes are not your microbes, and mine may make  more (or less) of the stuff mosquitoes find so irresistible. Whether  this theory will hold for other species of mosquito hasn't been  formally tested yet, but it couldn't hurt, could it, to pack your  Odor Eaters next time you leave home for mosquito-infested parts? 

And don't forget the Dial. There's a serious reason for all this work, of course. Malaria  mosquitoes are a scourge, and researchers like Knols would love to  come up with a simple trap, a Mosquito Motel, baited with the olfactory equivalent of a human. But as Knols pointed out, human skin produces hundreds of volatile chemicals. Comparing the volatiles produced by both cheese and feet is just one way to winnow out a few that are of interest to mosquitoes. Knols is now trying out a trap based on fatty acids, including butyric acid. But other chemicals might be blended with them in the future, including those sulfur compounds produced when bacteria break down proteins in skin residues.

In the meantime, if a mosquito does pick on you, there's always revenge -- or at least a really juicy malevolent fantasy. Remember  the explosive feeding experiment performed by Klowden? "Small boys  do something like that," a mosquito researcher let slip one day in  an unguarded moment, followed instandy by deep professional  misgivings. "Well, I've heard they do," the researcher said, when  pressed. "You're not going to quote me by name, are you? It's not  exactly, uh, scientific." Here's the trick: Once a mosquito has landed and begun feeding, you  stretch the skin taut on either side of it. Supposedly, if you're  deft, you can trap the proboscis in your skin in midfeed. Stuck in  the blood vessel, unable to pull out, its anticoagulants working  overtime to keep its blood meal coming, the mosquito sucks until it  pops. Maybe this method of entrapment works. Maybe it works only for small  boys. Maybe it's just a stupid pest trick or one of those urban legends i:hat shouldn't be put to the test. But, hey, it's prime time for mosquitoes. You be the judge.

ENCYCLOPÆDIA BRITANNICA mosquito  plural MOSQUITOES, OR MOSQUITOS (family Culicidae), any of the  familiar insects, numbering about 2,500 species, that are important  in public health because of the bloodsucking habits of the females.  Mosquitoes are known to transmit such serious diseases as yellow  fever, malaria, filariasis, and dengue. (See also dipteran.) The slender, elongated body of the adult is covered with scales; in  addition the mosquito is characterized by its long, fragile-looking  legs and its mouthparts, which are contained in an elongated  proboscis. The threadlike antennae of the male are generally bushier  than those of the female. The males, and sometimes the females, feed  on nectar and other plant juices. In most species, however, the  females require a blood meal in order to mature their eggs, which  are laid on the surface of water. Different species of mosquitoes  show preferences and, in many cases, narrow restrictions as to host  animals. The eggs laid by mosquitoes hatch into aquatic larvae, or wrigglers,  which swim with a jerking, wriggling movement and feed on algae and  organic debris; a few are predatory and may even feed on other  mosquitoes. Unlike most insects, mosquitoes in the pupal stage,  called tumblers, are active and free-swimming. The pupae breathe by  means of tubes on the thorax. The adults mate soon after emerging  from their pupal cases. The duration of the life cycle varies  greatly depending on the species. Mosquitoes are apparently attracted to host animals by moisture,  lactic acid, carbon dioxide, body heat, and movement. The mosquito's  hum results from the high frequency of its wingbeats; the female's  slightly lower frequency may serve as a means of sex recognition. Measures used to control mosquitoes include the elimination of  breeding sites, the application of surface films of oil to clog the  breathing tubes of wrigglers, and the use of larvicides. Synthetic  organic insecticides may be used to destroy adult mosquitoes  indoors. There are three important mosquito genera. Anopheles, the only known  carrier of malaria, also transmits filariasis and encephalitis.  Anopheles mosquitoes are easily recognized in their resting  position, in which the proboscis, head, and body are held on a  straight line to each other but at an angle to the surface. The  spotted colouring on the wings results from coloured scales.  Breeding usually occurs in water containing heavy vegetation. The  female deposits her eggs singly on the water surface. Anopheles  larvae lie parallel to the water surface and breathe through  posterior spiracular plates on the abdomen instead of through a  tube, as do most other mosquito larvae. The life cycle is from 18  days to several weeks. The genus Culex is a carrier of viral encephalitis and, in tropical  and subtropical climates, of filariasis. It holds its body parallel  to the resting surface and its proboscis is bent downward relative  to the surface. The wings, with scales on the veins and the margin,  are uniform in colour. The tip of the female's abdomen is blunt and  has retracted cerci (sensory appendages). Breeding may occur on  almost any body of fresh water, including standing polluted water.  The eggs, which float on the water, are joined in masses of about  100 or more. The long and slender Culex larvae have breathing tubes  that contain hair tufts; they lie head downward at an angle of 45º  from the water surface. The life cycle, usually 10 to 14 days, may  be longer in cold weather. C. pipiens pipiens is the most abundant  house mosquito in northern regions; C. pipiens quinquefasciatus is  abundant in southern regions. The genus Aedes carries yellow fever, dengue, and encephalitis. Like  Culex, it holds its body parallel to the surface with the proboscis  bent down. The wings are uniformly coloured. Aedes may be  distinguished from Culex by its silver thorax with white markings  and posterior spiracular bristles. The tip of the female's abdomen  is pointed and has protruding cerci. Aedes usually breeds in  floodwater, rain pools, or salt marshes, the eggs being capable of  withstanding long periods of dryness. The short, stout larvae have a  breathing tube containing a pair of tufts; the larvae hang head down  at a 45º angle from the water surface. The life cycle may be as  short as 10 days or, in cool weather, as long as several months. A.  aegypti, the important carrier of yellow fever, has white bands on  its legs and spots on its abdomen and thorax. This domestic species  breeds in almost any kind of container, from flower pots to  discarded car-tire casings. A. sollicitans, A. taeniorhynchus, and A. dorsalis are important salt-marsh mosquitoes. They are prolific breeders, strong fliers, and irritants to animals, including humans. 

PARIS -- Many passengers flying out of Africa are familiar with the ritual: the doors close and the flight attendants ask those wearing contact lenses to shut their eyes. Some passengers pull blankets over their heads. Then they pop the tops on two cans of a sickly sweet aerosol and walk quickly down the aisles, a white cloud billowing behind them which the air-conditioning quickly dissipates. 

This is mosquito control at the nexus between the poor, infected world and the rich, scared one. The spray is meant to kill any bugs that slipped in while the doors were open; a long-lasting fumigant is used in the luggage hold. 

There are 3,500 species of mosquitoes in this world; some even suck plants. Luckily for mankind, only a few relish human blood. No one knows how many germs and worms -- from viruses to bacteria to parasites -- are loose in the bloodstreams of other animals, but it's even luckier that only a few can survive back-to-back assaults by the mosquito digestive system and the human immune system and emerge as an illness. 

In the NY area, the arrival of the West Nile virus in 99 brought home just how unpleasant an unlucky series of coincidences can 
 be when the right mosquito for the job is around; of the 62 cases last 
 year, 7 were fatal. Seven cases have been reported this year. 
 If the indestructible cockroach is the Sherman tank of the insect 
 kingdom, the fragile mosquito is its DC-7, a pioneer in linking the 
 world by air. Most mosquitoes don't fly five miles in their lives, but 
 a few have joined the jet age. Just last month the World Health 
 Organization in Geneva issued a warning about "airport malaria." 
 France leads the world, with 26 cases since 1970, a few of them fatal, 
 among people who had never visited a malarious country but who lived 
 near airports or worked at them. They were probably bitten by 
 stowaways disembarking from flights from West Africa. In a 1994 
 outbreak, epidemiologists counted six malaria cases in three weeks 
 near Paris's Charles de Gaulle Airport, and calculated that 8 to 20 
 anopheles mosquitoes had been on each of 300 arriving flights. 
 "These are the dangers of globalization," said Dr. David L. Heymann, 
 director for communicable diseases at the World Health Organization, 
 although he was quick to point out that humans carry disease around 
 the globe more effectively than mosquitoes do. 

To stop mosquitoes, European nations have stepped up their spraying of airplanes; United States carriers hesitate, public health experts say, even on obviously dicey routes like some Caribbean flights because of fears of litigation from passengers claiming reactions to the aerosols, which the W.H.O. considers safe. 

Countries in northern climes have built-in barriers. As the old medical adage goes, "The world's best public health policy is winter." And until a cold snap arrives, rich nations have protection that citizens of poor tropical nations often cannot afford: air-cond, window screens, window glass and bug repellent. 

What poor nations have are trucks puffing out pesticide - something NYers are now enduring as West Nile reaches Central Park. Poor nations also still spray DDT on inside walls because it is cheap, persistent and lethal. 

If the US is not careful, the use of that old resource, now banned, could return, too. Americans forget that yellow fever was once endemic in the country and that mosquito species capable of spreading malaria are found as far north as Boston in summertime. Mosquito hitch- hikers predate not only the jet age but the steam age. 

The African species Aedes aegypti, an avid man-eater with the power to carry both yellow and dengue fever, probably reached S.America in slave ships. "The eggs lived in the water containers and the live ones fed on the populations on board," said Michael Nathan, an entomologist with the WHO. "A lot of slaves and a lot of crews died of yellow fever on the way over." 

Global commerce has sped up species transfers. Used tires sent for retreading are thought to be the vehicle for Aedes albopictus, the aggressive "tiger mosquito" that reached the US from SE Asia 20 years ago and is found as far north as Minnesota. It does not usually carry fatal diseases in the US, but can. Malaria is the riskiest candidate, but not the only one. Besides West Nile virus and its St Louis and Jap relatives, yellow fever, dengue fever and elephantiasis can all be injected by mosquito saliva. 

Agence France-Presse.  In Guatemala, fighting a mosquito that may have arrived from Africa on a slave ship. 


Mosquitoes are easy to hate, but there is no public health value in blaming them alone, particularly for West Nile. Since it survives in birds, West Nile could have entered in imported birds. Or in a gull blown far off course or, conceivably, one who shared a tick with a bird from Africa or the Middle East while both were summering near the Arctic Circle. 

But "the most likely transmission was in the blood of a tourist coming back from Israel," said Vincent Deubel, an arbovirus specialist at the Pasteur Institute here. There was an outbreak in rural Israel in 1998 and the New York strain is a close genetic match. 

Once it arrived, though, it still had to find a local mosquito to spread it around. According to Zdenek Hubalek of the Czech Academy of Sciences, 43 mosquito species can play that role. Night-biting culex pipiens obliged first; now day-biting Aedes japonicus has made the risk a 24-hour affair. 

Not all diseases need mosquito vectors for the animal- to-animal jump. Milkmaids caught cowpox on the job and became immune to smallpox. The AIDS virus, many scien- tists believe, jumped from chimpanzee blood to human in the 1940's when a hunter in central Africa nicked himself while butchering an ape. 

But because they are so effective at blood transfer, the flying syringes are the nearly perfect vector -- and the risk they pose is increasing. Not all that faint humming in the global village is from Internet connections.


\12 germs

How long can germs live on an object? Does the surface have to be moist? Sometimes when I get recurring colds or flu, I wonder if I am re-infecting myself.

A. Some disease-causing organisms, or pathogens, can thrive and multiply for some time on an object like a phone receiver spattered by the saliva of an infected person. But most bacteria and viruses quickly die when moisture disappears, usually after one or two hours for the saliva spray. 

Different pathogens have different survival times, ranging from a few minutes or hours to days or even months, and some might lurk for weeks or months on an object like a door handle in the house of someone with hepatitis A. In such cases, infectious disease specialists recommend frequent handwashing and avoiding touching your eyes or mouth; such measures would cut your infection risk to a very low level. 

Using the damp toothbrush of someone with some infectious diseases would be a very likely way to get sick yourself, but cold viruses are usually spread by hand-to- eye or hand-to-mouth contact. 

As for reinfecting yourself with the same illness by touching an object you yourself have touched, some experts think it is very unlikely, because you would probably have developed a resistance to a pathogen once you were recovering from it. You might become infected with a different organism with similar symptoms, however, and a second case of flu would probably be an unrelated strain. 


\13 Kidney stones

A very common disorder of the urinary tract affecting almost 5 out of every thousand Americans at some point in their life. In most cases (80%), the stone is small enough to pass from the kidney through the urinary tract spontaneously without requiring surgical intervention, but the process is often very painful. Fortunately, if surgical intervention is required to remove an obstructing urinary stone it can be done using instruments through the natural body channels (urethra, bladder and ureter) or using minimally invasive techniques.    Who Gets Kidney Stones? Anyone can develop kidney stones and at any age but generally it occurs during the 3rd, 4th and 5th decades of life. It tends to affect males more than females and also seems to occur more often to people living in warmer and/or mountainous regions of the country. It also appears to affect people who live relatively sedantary life styles whereas very active and athletic individuals seem to suffer less kidney stone problems.  There is much evidence that genetic predisposition plays an important role. In other words, if one of your parents, siblings or close relatives have suffered from kidney stones, you might also be predisposed to forming stones also. There are certain types of kidney stones that have a very clear and direct genetic correlation such as patients who are cystine stone formers.  Finally, people who tend to drink only small amounts of fluid every day or those who tend to over-indulge in certain types of foods and drinks on a regular basis are prone to kidney stone formation. Patients with chronic urinary tract infections may be susceptible to kidney stones.    What are the Symptoms of Kidney Stone Attacks? Stones that cause obstruction of the flow of urine from the kidneys results in very severe pain that is colicky in nature (thus the term 'renal colic'). This pain often starts in the flank or back region and radiates around to the lower abdominal area and into the genitalia region. It tends to come in waves of pain and may be associated with nausea, vomiting and sweating. Interestingly, people experiencing an attack of renal colic often are very restless and canít seem to find a comfortable position. Sometimes, the urine may have some blood in it that you might notice. In most cases, when the urine is examined under the microscope there is evidence of blood cells.  Because the stone causes obstruction, the tube draining the kidney (ureter) and the kidney interior itself become distended and this is what gives the pain associated with renal colic.  Associated fever and chills needs to be dealt with promptly in the Emergency room.  Fortunately, most stones will pass out of the kidney and ureter spontaneously, and the pain rapidly disappears. Generally stones less than 5 mm in size in the adult patient will pass spontaneously. Between 5 - 7 mm in size, surgical intervention may be required. Over 8 mm in size, these stones most likely will require active treatment.    How are Kidney Stones Diagnosed? In most cases, the history and physical exam which the patient presents with is typical. The microscopic urine exam often shows evidence of red blood cells and sometimes even stone crystals. The most important tests are X-rays. Because over 80% of stones contain some calcification, they can be seen on plain X-ray. However, to be certain of the diagnosis, an intravenous pyelogram (IVP) or computerized tomogram (CT scan) is usually ordered and are diagnostic.    How are Kidney Stones Managed? Once the diagnosis is made of an obstructing stone, patients are given pain medications and intravenous fluids. In most cases in stones less than 5 mm in size, the patient is encouraged to try to allow time for the stone to pass spontaneously, as it usually does. However, if the pain is poorly controlled or the patient demonstrates fever or signs of associated urinary tract infection, surgical intervention may be required. This is not common and requires placement of a temporary internal ureteral catheter (double J catheter) or a small tube placed directly into the kidney (percutaneous nephrostomy tube) so as to relieve the urinary obstruction, infection and/or severe pain. However, in most cases as mentioned previously, patients are carefully observed and given an opportunity to pass the stone spontaneously on their own.  If the stone is too large or is not passing through the urinary tract and causing significant obstruction to the kidney over time, the urologist will need to intervene. The size of the stone, its location in the kidney and/or ureter, and the suspected type of stone are important factors that determine how the urologist will manage the problem. Listed below are different surgical options and when they might be applicable.  Extracorporeal Shock Wave Lithotripsy (ESWL). This treatment involves administering electrohydraulic shock waves which travel through the back muscles and kidney tissue with direction to the targeted kidney or ureteral stone. Once the shock wave hits the stone it releases its energy and progressively pulverizes the obstructing stone. Then the stone fragments need to be passed through the urinary tract spontaneously.  Although this treatment is the most common and least invasive therapy for kidney stones, it is not optimal if the stone size is greater than 2.5 cm, is located in the middle ureter or lower pole region of the kidney or composed of cystine or other hard stone types.  Percutaneous Nephrolithotripsy. If the kidney stone is very large or not amenable to ESWL, percutaneous nephrolithotripsy is offered. Although this treatment options is more invasive than ESWL, it generally renders a higher success rate for the more difficult and larger kidney stone. It is strongly suggested for larger stones in the lower pole region of the kidney or those associated with infection.  Through a 1-2 cm incision in the back a tract is dilated directly into the kidney such that telescopic instruments may be passed into the kidney interior so as to visualize the obstructing stone(s). The stones may be extracted directly or may be fragmented with ultrasonic or laser energy probes. All fragments are suctioned out at the termination of the procedure. A small drainage tube is temporarily left in the kidney and then removed if follow-up X-rays show no residual stone particles. The tract into the kidney usually quickly closes off within 24 hours after the tube is removed.  Ureteroscopic Stone Fragmentation. Stones located anywhere in the ureter which are not amenable to ESWL can be removed using rigid or flexible ureteroscopic techniques. A ureteroscope is a very narrow telescopic instrument that is passed down the urethra into the bladder and then into the ureter in order to visualize the obstructing stone. Through the ureteroscope, instruments may be passed to extract the stone directly if it is not too big, or to fragment the stone into pieces if it is too large to pull out in one piece. Following the procedure, a small double J ureteral catheter is left in place which is ordinarily easily removed in the clinic a few days later.  Medical Therapy. Only select stones can be dissolved with medications. Specifically, pure uric acid stones may be slowly dissolved by increasing the pH of the urine (alkalinize) with drugs such as sodium bicarbonate or potassium citrate. Cystine stones may also be slowly dissolved by alkalinizing the urine. Short treatment attempts with these medications are worth while in select cases.  Unfortunately, antibiotic therapy may reduce the bacterial count in the urine of patients with infection-type stones but rarely dissolves the stone. In the vast majority of cases, the only way to get rid of the urinary tract infection is to get rid of all the stone which harbours bacteria in its inner matrix. Once all the stone is removed, however, suppressive antibiotic therapy is strongly suggested to maintain sterile urine and allow the kidney and ureteral tissues to heal.  Alternate Treatment Options. In rare cases where the obstructing stone(s) can not be successfully treated with minimally or non-invasive techniques as described above, more aggressive surgical intervention with laparoscopic surgery or open surgery may be required. However, this would account for less than 1% of cases performed in the Department of Urology at Stanford Health Services.    How to Prevent Kidney Stone Formation? There are a large number of causes to explain why kidney stones develop. As discussed above, sometimes there is a genetic predisposition and in certain cases urinary tract infections or other environmental factors are contributing to stone formation.  In certain cases the answer of why an individual is forming kidney stones may be as simple as he/she is not drinking enough fluids. Perhaps the person loves calcium, oxalate or uric acid containing foods which sets up the right urine chemistry to form a stone. In certain cases the problem may be more complicated in that the patient's intestines "hyperabsorb" too much calcium, oxalate or uric acid or alternatively the kidney tubules "leak" too much of these substances into the urine. Sometimes there may be a hormonal imbalance of the parathyroid or thyroid glands.  In order to determine where the abnormality lies, patients should be offered a "metabolic evaluation" after the stone is removed and he/she is back to normal diet and activities. This evaluation would consist of the following:  Stone analysis (assuming stone was recovered). Repeat urinalysis and culture. Blood for chemistry. Two 24-hour urine collections for chemical evaluation. Three-day dietary history.  Depending on the results of these tests, the patient will be counselled on dietary control and medication will be administered as required. The most important aspect of all preventative kidney stone therapy is encouraging fluid intake of at least 2 to 3 liters of clear water per day.   The Department of Urology offers all aspects of kidney stone evaluation, treatment and prevention under the direction of Howard N. Winfield, M.D. For an appointment please call 650-723-6024.      

Kidney Stone avoidance

Avoiding Kidney Stones By James Dillard Question: I've already had three kidney stone attacks and now I'm going for a lithotripsy (a noninvasive shock treatment) to break up another two stones. Are there any alternative methods to stop stones from forming? 

Answer: Jan. 8, 2001 -- Yes, but some of the best ways to prevent the formation of kidney stones are not so alternative. They involve basic lifestyle and dietary habit changes. The formation of stones in the urinary tract -- either in the kidneys or in the bladder -- affects 500,000 to 750,000 Americans a year. Men are afflicted four times as often as women, and the most common time to get the stones is in your 30s and 40s. Treating kidney stones generally requires the expertise of a urologist and may involve special X-rays or an ultrasound to look at the stone. Usually, the stones are allowed to pass while the patient takes pain medications. But sometimes it requires an operation -- or, for some, sound waves may be used to break up the stones, as you mentioned. 

As for preventing future stones, the surest approach may be to get an internist or a kidney specialist (known as a nephrologist) to do blood and urine tests to determine what's causing the stones. Though nothing is foolproof, here are a few prevention suggestions doctors may make. First, it's critical to get into the habit of drinking more fluids. Kidney stones are much more common in hot areas of the country, and people are more symptomatic during the summer months. People with recurrent urinary stones should try to roughly double their water intake, particularly after meals and before going to bed. You should have to get up during the night to hit the bathroom, and you should drink more water before you sack in again. Of course, if you have significant heart trouble like congestive heart failure, talk to your doctor before you start drinking a lot of extra water. 

We Americans generally eat way too much protein, which can injure the filtering tissue of the kidney itself. You should limit your intake to one gram of protein per kilogram (roughly two pounds) of body weight per day. Other dietary measures that seem to have good science behind them include eating a diet rich in vegetables, low in sugar and sodium, and rich in calcium, magnesium and potassium. 

It also seems that excessive consumption of grapefruit juice can contribute to stone formation, so keep this to a minimum. Supplementation with 50 to 100 milligrams of Vitamin B-6 (or this amount in a good B-complex), and 300 to 400 milligrams of magnesium citrate per day has also been shown to help. And drinking beer actually seems to reduce kidney stone risk. (For more information on this, see the American Journal of Epidemiology, July 15, 1999, Volume 150.) Obviously, moderation on this is advised. 

As for herbal remedies, I don't think the evidence is very good for this approach. Several major herbal texts do not list any recommended herbs for kidney stones, including the American Herbal Physicians Desk Reference. The German Commission E monographs of therapeutic herbs list 13 herbs that could possibly help. This tells me that none of the data is very solid, and most of this information probably comes from herbal traditions and folklore. Consultation with an experienced herbal practitioner would be recommended before you try any herbal remedies for kidney stones.


\14 Stroke

How to Stop a Stroke From Striking. Alcohol, Overexertion Could Trigger Strokes By Jeanie Davis Reviewed by Dr Jacqueline Brooks 

Feb 26 2001 - What sets off a stroke? Some surprisingly routine things, apparently. According to a preliminary study of stroke triggers, such commonplace activities as drinking alcohol, lifting a large box, and indulging in a vigorous romp in the hay have been tied to the onset of small "ischemic" strokes - the kind caused by a clot that blocks blood flow in an artery to the brain. 

Results from the Stroke Onset Pilot Study were presented at the American Heart Association's 26th International Stroke Conference, held recently in Fort Lauderdale, Fla. At the same meeting, another group of researchers reported that high blood pressure -- known to be a huge risk factor for stroke in people who have had a previous stroke -- remains largely uncontrolled in those seriously at-risk patients. 

While many studies have identified risk factors for stroke -- such as high blood pressure and high cholesterol -- "we don't have very good information about what immediately precipitates the stroke itself, what behaviors trigger it at that moment," says Murray Mittleman, MD, lead investigator of the Stroke Onset Pilot Study and director of cardiovascular epidemiology at Beth Israel Deaconess Medical Center in Boston. 

"Understanding the patterns in these triggers will hopefully tell researchers more about the underlying biological mechanisms that lead to a stroke," Mittleman tells WebMD. "From this new information, we can hopefully develop novel preventive measures." For the study, Mittleman and his colleagues recruited 50 patients who had been hospitalized for ischemic strokes. One-third of the participants were women, and the average age was just over 62 years. 

Each person was interviewed within two or three days after having their stroke, to pinpoint whether there were patterns in their habits in the days, weeks, and months before their stroke. Specifically, they were asked what medications they were taking, if they were drinking caffeinated beverages or alcohol, or if they were smoking or taking illicit drugs, including marijuana and cocaine.

Researchers also asked about times when people had meals (especially unusually large meals), whether they had strained to go to the bathroom, had sexual intercourse, exerted themselves physically (like lifting a large object), or become angry, anxious, or depressed. 

"We were especially looking at the period right before the stroke, looking at the person's behaviors [to see] whether that activity was unusual for that person," Mittleman tells WebMD. They found that 24 hours before having a stroke, one-third of the patients had engaged in various activities that may have triggered the stroke, including: 

28% drank alcohol 10% lifted an object that weighed more than 50 pounds 8% overly exerted themselves by doing things like shoveling snow 6% smoked marijuana 4% strained while trying to use the bathroom 4% had an angry outburst 2% had sexual intercourse 

Though the Stroke Onset study group was small, the researchers say they believe it demonstrates that triggers are involved when many patients suffer ischemic strokes. A larger study already is under way, Mittleman tells WebMD. "It's an interesting investigation, but very preliminary," says Owen Samuels, MD, assistant professor of neurology and director of the neurosciences critical care division at Emory University School of Medicine in Atlanta. 

"It certainly is an area that has not been looked at, that we know very little about," he says. "Certainly you would want to study this in more people. These are all very common activities. Right now, I don't think we can say there are any definite triggers based on this." 

In the second presentation, researchers conducting the Northern Manhattan Stroke Study followed a group of 655 survivors of ischemic stroke, whose average age was 69 years (55% were women). One year later, 107 had died; half of the remaining 548 had high blood pressure, and 19% had severely elevated blood pressure -- despite the fact that nearly half were prescribed blood pressure medications at the time of their discharge. 

Those most at risk of high blood pressure had less education, were Hispanic or black, were younger, and had few friends, says lead author Ralph L. Sacco, MD, associate chair of neurology at the Neurological Institute in New York City. 

"Although high blood pressure is very common, this underlines how enormously important it is as a risk factor for stroke," Samuels tells WebMD. "It also points to the fact that people without money are more vulnerable because they don't have the resources to take care of themselves. We really need to take another look at preventive measures and provide much better primary care." 

 Stroke Patients Get More Time to Reach Hospital Direct-to-Brain Drug Works More Than Six Hours Poststroke

By Daniel J. DeNoon Reviewed by Dr. Gary D. Vogin 

Mar 5, 2001 (San Antonio) -- The 85-year-old man got to the hosp too late for normal stroke treatment -- but he was in luck. It had been five hours since the man suffered a stroke, leaving him unable to speak or to use his right arm. If he had arrived a few hours earlier, injections of powerful drugs might have been able to dissolve the blood clot in his brain -- but it was far too late for that. Fortunately, interventional neuro- radiologist John D. Barr, MD, was on duty. 

Making a small incision in the man's groin, Barr ran a small tube all the way up into the artery in his neck. Dye injected through the tube allowed Barr to pinpoint the clot on an X-ray. Barr then ran an even smaller tube - barely thicker than a thread - up into the man's brain until it reached the clot. Then he put a small amount of a clot-dissolving drug into the tube and let it drip directly onto the clot. 

"His artery was opened in one hour, and he had a nearly complete recovery at three months,"Barr tells WebMD. "He is able to speak again, he can use his arm again, and he has returned to his previous level of independence." Barr reported his experience with the new technique here at the annual meeting of the Society of Cardiovascular & Interventional Radiology. So far, he's treated nine patients. 

"For the kind of patients we treated, only a very small percentage would be expected to have a good recovery and be able to go back to work or take care of themselves," Barr tells WebMD. "We had six of nine with a major recovery from the stroke -- much better than we would have expected. Three of the six had a complete or nearly complete return to normalcy. The other three did not fully recover but improved very significantly so they can still live independently and function rather well." 

Barr's patients reached the hospital an average of three-and-a-half hours after their stroke. For most of these patients, it was well past the three-hour window of opportunity for conventional use of clot-busting drugs. "The longest window anybody has seen with intravenous drug is three hours," Barr says. "One of our successfully treated patients was six-and-a-half hours out." 

Buddy Connors, MD, is director of interventional neuroradiology at Fairfax Hospital in Falls Church, Va. "The key is to be extremely fast and to be targeted in your approach," he tells WebMD. "The good thing is you don't saturate the body with massive doses -- you can put the drug into the place it is needed the most." 

The drug Barr used, Retavase, is approved only to break up blood clots in the heart when given by intravenous injection. Because such small doses are used for direct use in the brain, clinical trials are unlikely. 

"There are economic considerations that will prevent companies from running full-scale trials because the information is too expensive to derive," Barr says. This means that insurance companies consider the procedure to be experimental, and won't pay for it. "The lack of reimbursement has been hurting our patients," Barr says. 

 Nose Drops May Decrease Brain Damage After Stroke. Nasal Passages Provide Direct Route to the Brain By Peggy Peck Reviewed by Dr. Jacqueline Brooks 

Feb. 22, 2001 (Ft. Lauderdale) -- In films, you've seen actors mimic the rush that comes from snorting a drug. That "rush," says a Minnesota brain researcher, happens because the drug catches a ride on the nerve highway to the brain, so it reaches pleasure centers in the brain even before it can be detected in the bloodstream. 

The researcher says this same nonstop nerve highway can deliver healing drugs directly to the brain, and that simple proposal could someday revolutionize the treatment of stroke or Alzheimer's and Parkinson's diseases. William H. Frey II, PhD, explains that the nose contains nerve endings connected directly to two very powerful networks: the olfactory nerves, which control the sense of smell, and the trigeminal nerve, which sends sensations from the face and head to the brain. 

Those nerves, Frey tells WebMD, provide a "direct shot from the nose to the brain," without stopping first in the bloodstream. That means that a drug can reach the brain in less than 15 minutes, less than half the time it would take if the drug were injected into a vein. This is important, says Frey, because drugs that enter the bloodstream are often stopped short before making it to the brain by a natural protection mechanism called the "blood-brain barrier."

Many drugs for conditions such as stroke or Alzheimer's disease are promising in animal studies but flop when tested in humans because the drugs never make it past the hurdle of this barrier. 

He explains that any drug that was previously considered unable to "make it past the blood-brain barrier can be taken back down from the shelf, dusted off, and tried again with this method." But, according to several other researchers who met recently at the Amer Stroke Assoc's 26th Intl Stroke Conf, Frey's assessment is very optimi- stic. Frey did demonstrate the effectiveness of his nasal delivery system in a paper delivered at the conference -- but his demonstration was in rats, not people. 

He and his colleagues from the Alzheimer's Research Center of the Health Partners Research Foundation in Saint Paul, Minn., put a few drops of a natural substance called insulin-like growth factor-1 into the noses of rats that had had a stroke. 

Earlier experiments demonstrated that this substance can heal injured rat brains, but it had to be applied directly to the brain. In the past, says Frey, "the only way to get it to the human brain would be to drill a hole in the skull and put it in, so it is not considered a practical treatment for humans." 

Within hours of getting the drug, the rats showed signed of brain healing: Swelling was reduced, and movement improved, says Frey. Philip Gorelick, MD, prof and director of the Center for Stroke Research in Chicago, tells WebMD that "the std method of delivery for drugs to treat stroke is [via an injection into the vein]. So, if this were true, it would be novel." But after consulting with a number of colleagues who focus their research on animal studies, Gorelick's enthusiasm was dampened. 

The other researchers, says Gorelick, weren't that impre- ssed. He says that the method would have to be carefully tested in rats to see if the drug was adequately reaching all the areas in the brain it needed to. Larry B. Goldstein, MD, a member of the AHA's Stroke Council and an assoc prof of med at Duke Univ, says there is a very big difference between the olfactory nerves in rats and olfactory nerves in humans because a much larger part of a rat's brain is dedicated solely to the sense of smell. 

Frey agrees that rats have a more developed sense of smell but he adds that the trigeminal nerve, "is proportionally the same size in rats and humans." He says that "trigeminal nerves also hang down into the nasal cavity, and so the drug can just as easily travel along that [nerve] pathway." Goldstein does, however, agree that a nerve route could provide a speedy pathway to the brain. Speed is important to stroke researchers, whose motto is "Time is brain," meaning that the longer the blood supply to the brain is cut off, the more brain cells are destroyed. 

Frey, who says that the idea for the nose drops came to him "in a dream," says he has patented his "Method for Administering Neurologic Agents to the Brain" in the United States and several other countries. He says that more research needs to be done but suggests that he may pursue that research in partnership with a drug company. 

And, if you think that nose drops to treat stroke sound like something Dr. McCoy would use on Captain Kirk, what about a laser that takes aim at blood clots deep inside the brain and pulverizes them? That's exactly what a new device called an Endovascular Photo Acoustic Recanali- zation laser, or EPAR for short, is supposed to do. 

Helmi Lutsep, MD, of the Oregon Stroke Ctr at the Univ in Portland, is one of several researchers who tested the new laser in a safety trial. Based on that trial, the FDA has given the go-ahead for larger studies. Lutsep says the new laser, which was tested in 26 stroke patients, is small enough to be used in most blood vessels in the brain. Earlier lasers were too large or inflexible to be used in small vessels, she says. 

Goldstein says the EPAR laser is one of several lasers now being tested for what is called "mechanical clot disruption." While the devices are intriguing, he says there is a concern "that mechanical devices may acciden- tally dislodge other clots," thus causing additional damage while attempting to treat the original stroke. 

Another worry is that the devices, which have to be threaded through very tiny vessels using guide wires, may actually tear the delicate walls of blood vessels in the brain. Goldstein says, for example, that Lutsep's group reported three such tears in the 26 patients treated in their safety study. Lutsep says those three patients had no ill effects from the tears, but accord to Goldstein, "they were lucky." 

Lutsep, however, shrugs off criticism because she says that laser tech is likely to triumph in the end for a very simple reason: time. Once inside the brain, the EPAR laser "can dissolve a clot in 36 sec," she says, while it takes clot-busting drugs almost an hour," even if you deliver the drug directly to the site of the clot." 

 Lamotrigine Reduces Pain For Stroke Patients The drug lamotrigine can reduce the pain that affects some stroke patients, according to a study in the Jan 01 issue of Neurology, the scientific journal of the American Acad of Neurology. Central post-stroke pain occurs in eight% of stroke patients and is difficult to treat. The only current treatment, amitriptyline, doesn't work for many patients, and has many side effects.

The pain is felt in areas of the body that have sensory loss from the stroke. Researchers think the pain occurs when the stroke damages the fibers in the brain or in the spinal cord that lead to the thalamus area of the brain. The loss of sensory information to the brain creates a hyperexcitability, or excessive response to stimuli, in that area of the brain. Jan 23, 2001 -- 

Cholesterol-Lowering Drug, Pravastatin, Reduces Strokes A drug already being used to lower cholesterol and prevent heart attacks sharply reduced strokes in patients who already had heart disease, according to a study in the Jan. 23 issue of Circulation: Journal of the American Heart Assoc. The drug, pravastatin, reduced stroke by 20% compared to placebo, in patients with heart disease or high cholesterol, said Robt P. Byington, Ph.D., prof of public health sciences (epidemiology) at Wake Forest Univ School of Med, and colleagues in the Prospective Pravastatin Pooling Project. 

The study "offers a major new way to lower the stroke rate," Dr. Byington said. He said the drug reduced the risk of stroke over a wide range of cholesterol levels and among a wide spectrum of patients in pooled data from three similar clinical trials. The effect occurred primarily in the patients who already had coronary heart disease, where the reduction was 22%. 1/01

New Guidelines For Stroke Prevention Presented According to the ACCP (American College of Chest Physicians) Consensus Statement 2001 on Antithrombotic and Thrombo- lytic Therapy for Ischemic Stroke, the antiplatelet agent, aspirin/extended-release dipyridamole 25mg/200mg, is more effective than aspirin alone and may be more effective than clopidogrel for reducing the risk of secondary stroke in patients who have already experienced a stroke or Transient Ischemic Attack (or mini-stroke).

"The new ACCP stroke recommendations demonstrate that newer and more effective treatment options for stroke prevention are now available," said Dr. Gregory Albers, MD, director of the Stanford Stroke Center, Palo Alto, CA, and Chairman of the ACCP expert panel on stroke and atrial fibrillation of the 6th ACCP Consensus Conference on Antithrombotic Therapy. "New antiplatelet agents with improved efficacy over aspirin offer tremendous opps for stroke prevention and the reduction of stroke-related mortality and disability." 1/30/01 -- 

Low Dose Aspirin At Least As Effective As High Doses In Preventing Stroke Low doses of aspirin (80 to 325 mg) are at least as effective as higher doses (500 to 1,000 mg) in preventing stroke in patients with cerebrovascular disease, according to new guidelines released by the American College of Chest Physicians (ACCP). Entitled "The Sixth ACCP Consensus Conference on Antithrombotic Therapy," the guidelines represent expert consensus on various complications of atherosclerosis and related medical and surgical conditions.

A range of experts participated in reviewing all significant studies on the prevention and treatment of thrombosis and developed recommendations on specific conditions and approaches. The report was issued as a special supplement to January's issue of CHEST, ACCP's peer-reviewed journal.

Overview Stroke is the third-leading killer in the United States but few people recognize its early symptoms. According to Sidney C. Smith Jr., M.D., president of the AHA, "By recognizing the warning signs of stroke and seeking immediate medical attention, people can take steps to save their lives and reduce or even prevent disability." (Jan 1996.) 

Risk Factors for a Stroke - Stroke prevention is still the best medicine. The most important treatable conditions linked to stroke are: High blood pressure. Eat a balanced diet, maintain a healthy weight, and exercise to reduce blood pressure. Drugs are also available. Cigarette smoking. Medical help is available to help quit.

Heart disease. Your doctor will treat your heart disease and may also prescribe medication to help prevent the formation of clots. If you are over 50, National Institute of Neurological Disorders and Stroke, National Institutes of Health believes you and your doctor should make a decision about aspirin therapy. Diabetes. Treatment can delay complications that increase the risk of stroke. Transient ischemic attacks. These are brief episodes of stroke's warning signs and can be treated with drugs or surgery.  

Center for Current Research Report Summary: Nonvalvular atrial fibrillation (AF) is a strong, independent risk factor for stroke, but the absolute rate of stroke varies widely among AF patients, importantly influencing the potential benefit of antithrombotic prophylaxis. We explore factors associated with ischemic stroke in AF patients taking aspirin. 

Methods--We performed multivariate logistic regression analysis of 2012 participants given aspirin alone or in combination with low, inefficacious doses of warfarin in the Stroke Prevention in Atrial Fibrillation I-III trials followed for a mean of 2.0 years, during which 130 ischemic strokes were observed. Results--Age (relative risk [RR]=1.8 per decade, P<0.001), female sex (RR=1.6, P=0.01), history of hypertension (RR=2.0, P<0.001), systolic blood pressure >160 mm Hg (RR=2.3, P<0.001), and prior stroke or transient ischemic attack (RR=2.9, P<0.001) were independently associated with increased stroke risk. Regular consumption of >/=14 alcohol-containing drinks per week was associated with reduced stroke risk (adjusted RR=0.4, P=0.04). Among SPAF III participants, estrogen hormone replacement therapy was associated with a higher risk of ischemic stroke (adjusted RR=3.2, P=0.007). With the use of these variables, a risk stratification scheme for primary prevention separated participants into those with high (7.1%/y, 22% of the cohort), moderate (2.6%/y, 37% of the cohort), and low (0.9%/y, 41% of the cohort) rates of stroke. Ischemic strokes in low-risk participants were less often disabling (P<0.001). Conclusions-- Patients with AF who have high and low rates of stroke during treatment with aspirin can be identified. However, validation of our risk stratification scheme is necessary before it can be applied with confidence to clinical management. Postmenopausal estrogen replacement therapy and moderate alcohol consumption may additionally modify the risk of stroke in AF, but these findings require confirmation. 

Background Information Stroke, or "cerebrovascular accident," is the leading cause of neurologic disability in the western world. Half a million Americans suffer strokes each year, 95% of whom are over the age of 40. Over 20% can be traced to hereditary defects.

There are three major causes of strokes, all related to disturbances in the vessels that distribute blood to and within the brain: (1) narrowed arteries, resulting from atherosclerosis (hardening of the arteries); (2) blood clots originating in the chambers of the heart; and (3) ruptured arteries (hemorrhagic syndromes) or ruptured aneurysms. All people over 40, and family members of previous stroke victims, should have their blood pressure checked regularly (see articles on Hypertension and Arteriosclerosis).

There are several warning signs to watch for: sudden weakness, clumsiness, or numbness of a limb or face; transient loss of vision in one or both eyes, and difficulty speaking. These are characteristics of so-called mini-strokes or transient ischemic attacks (TIA), and should be reported to your doctor immediately. Symptoms of major strokes depend upon the part of the brain that has been deprived of blood flow and oxygen. 

These can range from partial paralysis of motor functions (including speech) to mild sensations of numbness in certain parts of the body. Similar symptoms, however, are also caused by such "space-occupying masses" as brain tumors and abscesses (see our page on Brain Cancer). Four out of five stroke victims survive, but damage to the brain is permanent.

A cranial computerized tomography or magnetic resonance image (MRI) can confirm whether or not a stroke actually occurred. Treatment of stroke is limited to anti- platelet (aspirin or ticlopidine) and anticoagulate (warfarin) therapies and preventive surgery (usually carotid endarterectomy). At least partial recovery is possible through physical therapy (that is, training other parts of the brain to assume new tasks). 

A number of research projects involving experimental preventive measures have been reported in the current medical literature. Some of these experiments may prove to be helpful either in reducing the risk of stroke, or perhaps preventing it altogether: (1) maintenance of blood pressure within the normal range (less than 140/90), with medication if necessary; (2) taking aspirin every day; (3) engaging in moderate exercise. Consult first with your physician before trying any of these procedures.


\15 Insomnia

Sleep is an alternate mode of consciousness and is influ- enced by circadian and biologic rhythms which may be reset by light behind the knee 2/98.

Enough regular sleep is as essential for good health as exercise, nutrition, and preventive medicine. Don't neglect it. Sleep deprivation can lead to: Diabetes, high blood pressure, obesity.

FITNESS Sharon Christine Riley 29 Dec 2000 Sleep is nature's way to recovery Your body needs `down time' to recharge your batteries, fight illness and keep you young We are continually told that we should exercise to maintain a fit and healthy lifestyle. But after doing all that exercise, how many of us are aware of the amount of rest (i.e. sleep) our body needs to allow it to recover to its best performance level?But, you say, I can put myself into "debt" during the week and catch up at the weekend by sleeping in on Sunday morning. Is this just a theory? Or does our body allow us to "repay" lost sleep by extending our sleep period once a week without any detrimental effects?Let's see what the experts say on these matters. Recent research into sleep-related disorders has uncovered some interesting facts that may explain why many of us have different sleep requirements to one another. 

OUR BODY'S SLEEP REQUIREMENTS There appears to be no substitute for sleep even though many of us continually participate in activities that lead to sleep deprivation. Completing a university course project on time, finishing a section report for the boss on schedule, finalising arrangements for that much needed holiday, can all lead to extra long hours for a period of days or possibly weeks. Many fitness fanatics even deny themselves much needed sleep to get in that daily workout after a hard day at the office. Most of these people operate on the principle of topping-up the "sleep bank" at the end of the busy period by spending a few extra hours, or even a day, in bed to catch up. 

But does this principle work? Well, according to the experts, to some extent yes. But before adopting this into your weekly activity schedule, consider the following points and activities that take place in our bodies while we are sleeping. 

The general consensus from sleep experts is that our bodies have a 2-for-1 ratio need for sleep. This means that for every two hours you are awake and active, you should have one hour of sleep. This is where we get the common figure of eight hrs sleep per day, eight hrs sleep plus eight times two hours of activity equals 24 hrs. 

If we do not get this eight hours of sleep, then we are usually causing our body to get less rest than is needed to allow it to fully recover to its optimum performance for the next day's activities. While sleeping, in addition to getting much needed rest, the body is going through a cycle of regeneration. New cells have a chance to develop and grow to replace those that we damage through exposure to the sun and other damaging elements during our day's activities. 

If we continually "short change" ourselves out of this rejuvenation period (i.e. sleep), the result will be premature aging!It is also this period of rest that the body goes through its "housekeeping" or cleansing processes _ similar to taking out the trash after a busy period in the kitchen after preparing a meal. The waste products building up in various parts of the body are given a chance to be further processed or repositioned to their next point of treatment or disposal. Without the time to allow these activities to take place, our body becomes "bogged down" in its own waste products _ thus that sluggish and heavy feeling when you wake up the next morning after a long day and short night. 

SUBSTITUTING FOOD FOR SLEEP Many of us tend to eat extra food when we deprive ourselves of sleep. Some see this extra food as a means of giving them the energy they failed to recoup by getting sufficient sleep. But what causes this reaction within our body where we actually feel like eating more with lack of sleep?In reaction to sleep deprivation, our body produces different hormones _ one being a substance called cortisol. 

This is a stress-related hormone and is the one primarily responsible for your waking period in the morning. With normal sleep patterns, cortisol levels within the body reach their peak at around five to six o'clock in the morning _ most people's natural waking period. As we go about our normal daily activities, cortisol levels drop and are normally at their lowest in the evening _ when you are ready to fall asleep. 

Cortisol also has an effect on muscle tissue. It can cause cellular breakdown. Therefore, if your cortisol levels are higher than normal, even though you may be able to get to sleep, your body will not be able to rejuvenate itself as efficiently. Your muscles will literally be weaker than if you were receiving sufficient sleep. This is the reason that your workouts do not seem as effective if you are suffering from a lack of sleep. You are not as strong as you should be. 

So where does the food come into this equation? This drained feeling tricks our body into thinking it is low on fuel. We therefore go into a "feeding frenzy" trying to satisfy this misinterpreted hunger. It is also thought amongst the experts that cortisol is one of the chemicals in our bodies that causes cravings for fatty foods such as high carbohydrate junk foods. 

CAFFEINE KICKS Need an early morning boost to get you going? Many of us turn to a strong cup of coffee or a diet cola to get us going after the "night before". Used on an irregular basis, this method of getting an early morning boost is not known to have long-term detrimental effects. But what is our body telling us here?In simple terms, you need more sleep. The caffeine jolt will be short lived. As the effects wear off, you drop back into your sleepy state. Why? Because caffeine merely stimulates the nervous system _ it is not a source of energy. The use of caffeine in these circumstances has been compared to someone being cold and yet refusing to put on a coat. What your body is actually saying is "Give me more sleep. I am not ready to do more work". 

SLEEP DEBT RISKS As has already been mentioned, a lack of sleep can lead to premature aging. This is a result of the body not having sufficient rest to rebuild damaged cells or generate new ones to replace those we destroy each day. 

But also consider the body's immune system. We constantly challenge it day in day out. Colds (or even influenza viruses), pollution, smog, bacteria _ all attack our body on a regular basis. Our immune system relies on a regular period of sleep to rejuvenate itself after this continual bombardment and to rebuild and repair the defence mechanisms it uses to fight off these attackers. If we do not give it a chance to recover and reload with ammunition against these enemies, our body will loose the battle and suffer from illnesses caused by these unwanted invaders. 

Another more serious consequence is the risk imposed on other people by those who insist on driving or operating transportation equipment whilst in a tired or fatigued condition. Many laws and regulations are now in place as a means of trying to limit this exposure. People such as truck drivers and pilots are monitored closely in an attempt to prevent them from operating in a fatigued or tired state. 

But how many times have you had a long day at the office just before a holiday weekend and then driven the family for many hours to spend the holiday with family or friends? Under these circumstances, you are placing the most important people in your life at unnecessary risk. Why not go to bed early and then depart early the next morning when you are rested? It may not only be your family that thank you but also the other innocent individuals that could be involved in a serious (or even fatal) accident because of your tiredness. 

GENDER CHARACTERISTICS Unfortunately, the females amongst us tend to lose out when it comes to sleep deprivation. Research into hormone changes during a woman's natural monthly cycle indicates that the changes in the levels of hormones (especially estrogen and progesterone) are at least partially responsible for sleep-related problems. 

In particular, body temperature varies with this hormone activity level. This can result in awakening in a sweat due to increases in body temperature, possibly in the middle of the most needed sleep period. The term commonly given to this phenomena is "hot flushes". 

These variations in the body temperature also cause discomfort and stress. What is the body's reaction to this stress? You guessed it. More cortisol being produced to magnify the sleeping problem even further! 

HINTS ON HOW TO SLEEP BETTER Most, if not all, of us will suffer from some form of sleep disorder through our lifetime. Following are a few points that may help you enjoy prolonged or possibly better sleep when your turn comes around. 

If you are waking up too early in the morning, try keeping your room as dark as possible. This can be done by using "black-out" curtains. If external noise disturbs you prematurely, try dampening out the noise by having the air conditioner on all the time, running just the fan. Soft ear plugs are another option. 

Make sure you have enough blankets on the bed during the cooler months so that you do not wake up with the pre-dawn shivers when the temperature drops in the early hours of the morning. If these fixes do not work, you may have a more serious underlying problem such as depression. Have this checked with your doctor. 

If you are waking up in the middle of the night, consider some of the following as the cause. It may even be a combination of several of these factors. Avoid drinking excessive amounts of fluids that could cause you to urinate during the night. Avoid excessive amounts of alcohol _ although it initially has a sedative effect, as this wears off it will then turn to stimulation that can cause arousal during the night. 

As a before-bed relaxation, try some quite music or yoga to wind down. If you suspect stress as the cause, address the issues causing the stress _ also, relate with people during the evening more often that make you feel good rather than causing you to engage in stressful conversation. 

If you are finding it difficult to go to sleep initially, give yourself a chance to wind down. Many people spend time on a relaxing hobby immediately before going to bed. Write up a diary while enjoying a warm sedative-type drink such as a herbal tea. Avoid reading or watching TV in bed _ try to preserve this area for sleep and sharing intimate times with your partner. 

Most of all, do not feel guilty about having to sleep. Your body needs it. If you have been running up a "debt" towards your required amount of sleep, remember that it is better to repay this debt earlier than later. By keeping the "books balanced" you will be able to live a longer, younger, healthier life. 

ÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄÄ There is probably no time of year when America's sleep debt is greater than it is right now. Starting with Thanksgiving week, holiday preparations and parties, gift shopping and packaging, family visits and extra hours of work to make up for days off prompt millions of Americans to cheat on their sleep even more than usual. Many are used to being tired and think, optimistically, that they'll catch up with lost sleep after the New Year. 

Losing Sleep Pt 1 - The value of naps Pt 2.

But few do. And new research suggests that the conseque- nces of chronic sleep deprivation may be far worse than simply diminished mental sharpness, shortened tempers and a tendency to doze off at every quiet moment. Rather, sleep scientists at the University of Chicago found that those who suffer from an accumulated sleep debt may develop serious health problems, including obesity, diabetes and high blood pressure. 

In a study inspired and partly financed by the MacArthur Foundation, D. Katrine Spiegal, Dr Eve Van Cauter and Rachel Leproult found that even in young, healthy people, as little as a weeklong sleep debt of three or four hours a night has adverse effects on the body's ability to process carbohydrates, manage stress, maintain a proper balance of hormones and fight off infections. 

Sleep Lost, Never Regained. Most previous studies looked only at short-term sleep deprivation - keeping people awake for 24 or 48 hours -- and explored only the effects on mental performance, alertness and mood, which do indeed suffer from a lack of sleep. In the new study, Dr. Van Cauter and colleagues examined the physiological effects of sleeping only four hours a night for six straight nights, a not uncommon practice, especially at this time of year. As one of millions trying each day to cram 36 hours' worth of activity into 24, I listened carefully to what Dr Van Cauter had to say, and I suggest you do too. 

"With prolonged sleep deprivation, we found effects much more relevant to health than result from the loss of one or two nights' sleep," Dr Van Cauter said in an inter- view. "We found that an accumulated sleep debt is potent- ially as detrimental to health as poor nutrition or a sedentary lifestyle. It may be as bad as smoking. People are sleeping less and less and becoming more and more tired. They may be very careful about exercise, good nutrition and vitamins, but they're sleeping only five hours a night." 

When Sleepless Nights Spell Trouble. James Maas, author of "Power Sleep" 1999, says an answer of "true" to two or more of the foll stmnts may be signs of a sleep problem. 
 •I need an alarm clock in order to wake up at the appropriate time.
 •It's a struggle for me to get out of bed in the morning. 
 •Weekday mornings I hit the snooze button several times to get more sleep. 
 •I feel tired, irritable and stressed out during the week. 
 •I have trouble concentrating and remembering. 
 •I feel slow with critical thinking, problem-solving and being creative. 
 •I often fall asleep watching television. 
 •I often fall asleep after heavy meals or after a low dose of alcohol. 
 •I often fall asleep while relaxing after dinner. 
 •I often fall asleep within five minutes of getting into bed. 
 •I often feel drowsy while driving. 
 •I often sleep extra hours on weekend mornings. 
 •I often need a nap to get through the day. 
 •I have dark circles around my eyes. 

Previous studies have indicated that the average adult needs eight to nine hours of sleep a night, but the typical American gets only seven and many get consider- ably less, without ever catching up. While it is true that individual sleep needs vary - there are natural "short sleepers" and "long sleepers" who fall well outside the average - it is also true that many short sleepers push themselves considerably beyond what is natural, staying up until midnight doing chores or watching tv, then rising to an alarm at 4:30 or 5am. These are the people who fall asleep on commuter trains and buses, at plays and concerts and, sometimes, behind the wheel. Some even doze off at business meetings or at the pc. 

A Physiological Toll - Dr Van Cauter and colleagues found that sleep deprivation caused "striking alterations in metabolic and endocrine function" that mimicked some of the hallmarks of aging. They conducted a very thorough study of 11 healthy men aged 18 to 27 who spent 16 consecutive nights in a clinical lab where the research- ers tightly controlled the amount of time they spent in bed. After three 8-hr nights, they were restricted to six consecutive 4-hour nights, followed by seven 12-hour nights. None were allowed to sleep during the day. 

Repeated blood and saliva samples enabled the researchers to gauge the metabolic and hormonal effects of the shortened nights. Striking deficits occurred in the participants' abilities to process glucose. This results in a rise in blood glucose, a condition that prompts the body to spew out more and more insulin, which ultimately leads to insulin resistance, the hallmark of adult-onset diabetes. Excess insulin also promotes the storage of body fat, thus increasing the risk of obesity and high blood pressure. 

The brain can use glucose for energy without the aid of insulin, but it too was less effective at processing glucose during the period of sleep deprivation. This would diminish the functioning of some areas of the brain and may explain why critical thinking, memory and mental sharpness are impaired by inadequate sleep. 

The researchers also found that blood levels of cortisol, a measure of stress, were higher in the afternoon and evening in the sleep-deprived subjects. Such rises in cortisol are typical of the aging process, and are assoc- iated with adverse health effects, including insulin resistance and memory impairment. 

Thyroid hormone levels were also distorted by sleep loss, but the researchers declined to speculate on the conse- quences of this abnormality. They also found evidence of immunological impairment during shortened nights. The participants were less responsive to flu vaccine. 

The Chicago team is now conducting further studies of sleep deprivation in women and older adults. Dr. Van Cauter says she expects the consequences in older people to be even worse, since the time spent in deep sleep, the most restful kind, normally declines drastically with age - from 100 mins a night in people aged 20-25 to less than 20 mins by middle age. When young people become sleep- deprived, they can make up for the loss of deep sleep, but older people may not be able to compensate adequately, she said. 

What You Can Do - "People have to become more reasonable about sleep if they want to stay healthy," Dr. Van Cauter said. She suggests that those who are cheating on their sleep should "go to bed one or two hours earlier" rather than turn off the morning alarm and arrive late for work. High school students are among the most sleep-deprived. "They go to sleep at midnight and get up at 6am and arrive at school like zombies," Dr Van Cauter said. 

"Our society seems to place a moral value on sleeping as little as poss," she noted. "In Europe, people are less impressed by short sleepers. Here we're almost embarras- sed to say that we are going to bed early. Saying 'I'm tired and I'm going to sleep' is viewed as being lazy." 

Studies by Dr. David Dinges, sleep researcher at the Inst of Penn Hosp and the Univ of Penn in Phila, found that after two weeks of chronic sleep loss, people may say they have adapted to less sleep and are not sleepy. But he showed that even those who think they have adapted performed poorly on tasks that are impaired by fatigue. 

"Clearly, there's a disconnect between objective and subjective sleepiness," Dr. Van Cauter said. "In our study, no one adapted." And in case you think you get more done by sleeping less, a study of how two adults used the extra time when their sleep was reduced to five and a half hours a night revealed that they got no more done: everything they did took longer. 

Paying the Price for Cheating on Sleep By JANE E. BRODY Dec 28 1999

------------------------------------ A Lack of Quality Sleep Contributes to Middle-Age Spread By THE AP Aug 16 2000
 CHICAGO -- Here's some news that could keep middle-aged men awake nights: A lack of quality sleep may contribute to love handles and double chins. Researchers at the University of Chicago found what appears to be a link between middle-age spread and men's sleep patterns as they get older. 

They found that the quality of men's sleep decreases with age along with the body's production of growth hormone. The drop in growth hormone, in turn, is thought to lead to flab. Now the researchers are working to see if new types of sleeping pills or hormone injections can slow signs of aging. "We actually know that if we increase deep sleep, we can increase growth hormone," said Eve Van Cauter, a prof of med who led the study, published in Journal of the AMA. The study of beauty sleep was limited to healthy men, and it is not clear whether the findings apply to women. 

Van Cauter and her team looked at sleep studies conducted on 149 men from 1985 to 1999. They found that by the time men reach age 45, they have nearly lost the ability to fall into deep sleep. Men produce growth hormone primarily during that kind of sleep. In studies of the elderly, growth hormone deficiency has been connected to obesity and the loss of muscle mass. 

The men involved in the sleep studies were of normal weight and ranged in age from 16 to 83. Researchers found that as the men moved into mid-life, from ages 35 to 50, their total amount of sleep remained fairly constant. The amount of deep, or slow-wave, sleep, however, decreased from nearly 20% of a normal night's sleep for men 25 or younger to less than 5% for those over 35. Growth hormone secretion declined by nearly 75%. 

The study also found that after age 50, men's total amount of sleep declined by about 27 minutes a decade. They awoke more frequently during the night and stayed awake longer. REM sleep, associated with dreaming, also declined after age 50 to c50% of a young man's level. 

In an accompanying editorial, Dr Marc R. Blackman of the Johns Hopkins in Baltimore said researchers do not know for certain whether sleep quality influences the produc- tion of hormones or if the change in hormone levels itself is responsible for changes in sleep. 

But Van Cauter said it is clear that more deep sleep produces more growth hormone. 

The research could be used to examine whether growth hormone injections could slow signs of aging in men during early mid-life, she said. Currently, such therapy is used mostly for men 65 or older. 

--------------------------------------------------------- Experts Explore Deep Sleep and the Making of Memories By SANDRA BLAKESLEE. Nov 14, 2000
 --------------------------------------------------------- Robert Burroughs for The NY Times  Dr. Terrence J. Sejnowski, at his laboratory at the Salk Institute in San Diego, suggests that people and animals sleep, in part, so they can remember. In the deepest sleep, links between brain cells may be formed. 
 NEW ORLEANS — By isolating slabs of tissue from the brains of sleeping cats and inspecting millions of cells at a time, scientists have discovered what they think may be a key element in the brain's machinery for making long-term memories.

It seems that during an extremely quiet phase of sleep, when researchers thought that nothing much was happening in the brain, groups of cells involved in the formation of new memories signal one another. The signals, discovered only a few years ago, appear to allow cells in many parts of the brain to form lasting links. Then, when a few of the cells are stimulated during waking hours, the links are activated and an entire memory is recalled.

The finding, described by a number of scientists at the Society for Neuroscience meeting in New Orleans in early November, is part of continuing research on the role of sleep in consolidating memories. The research results are being published in the December issue of Cerebral Cortex.

While many steps in this process have been worked out, it was not known how individual cells actually linked up to form memory networks that could last a lifetime.

The research also bears on one of the deepest mysteries of biology: why do all animals sleep?

One idea is that sleep is critical for the maintenance and storage of long- term memories. Indeed, for some time many neuroscientists have theorized that a phase of sleep, rapid eye movement or REM sleep, is when memories are stored. Though the new work calls that theory into question, it too suggests that people and animals sleep, at least in part, so they can remember, said Dr. Terrence J. Sejnowski, a neuroscientist at the Salk Institute in San Diego. 

"Why do almost all of us need eight hours of downtime each night?" he asked. "Our sensory systems are down, our muscles are paralyzed and we are very vulnerable. Evolution must have a purpose in mind."

During the day, he said, many bits of information enter short-term memory, but most of it is unimportant and can easily be discarded. But other information is important, Dr. Sejnowski said. So the brain needs to meld it with older memories, storing the new information as it updates older information.

The brain accomplishes this task by entering a series of different chemical and electrical states during the day and night, said Dr. Alexander Borbely, a researcher at the University of Zurich who studies sleep in people. 

When people are awake, he said, their brains produce a wide variety of fast electrical activity as many neurotransmitters — chemicals that help carry information — are released. Cells that are involved in paying close attention to an event are especially stimulated. This heightened level of activity seems to tag them for special attention during sleep.

As people fall asleep, their brains enter a different state, Dr. Borbely said. Neurotransmitters that help keep them awake are reduced to low levels. At the same time, whole brain regions begin to oscillate or fire rhythmically at slower frequencies. People grow drowsy. During the night, different patterns of spontaneous rhythms arise in what are called sleep stages.

One, called REM sleep, is what occurs when the brain becomes very active and produces dreams. Many researchers have argued that REM sleep is when memory consolidation occurs, Dr. Borbely said, but this may not be the case. Many popular antidepressant drugs essentially abolish REM sleep in people, he said, yet their memories are fine. 

One problem with studying sleep in whole brains is that everything happens so incredibly fast that it is difficult to see what groups of cells are doing, Dr. Sejnowski said. But the technique described last week has made it possible to study millions of cells at a time under slowed conditions. 

The technique, developed in the laboratory led by Dr. Mircea Steriade at Laval University in Quebec, involves severing the nerve cells around a section of tissue about the size of the tab button on a computer keyboard from the brains of anesthetized cats. The tissue is left in place, its blood supply intact. 

But because the clump of tissue is less complex than the whole brain, researchers can get a better handle on how the brain is wired up and oscillates during sleep.

When people first fall asleep, cells in the higher cortex are stimulated by waves of activity coming from the thalamus, deep in the brain, Dr. Steriade said. Cortical cells that carry weak memory traces seem to become particularly active. As these cells fire and burst repeatedly, Dr. Steriade said, it is likely that they are going over what has been learned during the day.

This rehearsal seems to go on all night as a region that encodes and holds short-term memories, called the hippocampus, relays what it has learned into the cortex. 

But the mystery remains: how do cells in the cortex physically lay down long-term memories? The answer seems to lie in another sleep stage called slow-wave sleep, when the cortex, where associations and memories reside, cuts itself off from other parts of the brain and basically listens to itself.

At first, cells fire rhythmically at the extremely low rate of one to four cycles per second, Dr. Sejnowski said. Then they seem to stop firing entirely, as if nothing was happening. It's in this ultraquiet state that cells randomly burst with activity and then go quiet, he said.

Using the slab technique, Dr. Steriade recently discove- red that cortical cells in this quiet state are in fact quite busy, leaking tiny amounts of chemical neurotransmitters in what are called miniature synaptic events, or minis.

Minis are the missing link to memory consolidation, Dr. Sejnowski said. The process involves the synapses, which are tiny gaps between cells, and those gaps contain a complex machinery for strengthening or weakening intercellular connections. When brain cells are especially active during the day, their synapses are highly stimulated.

At night, the few cells in a given bit of brain tissue that have been most active during the day will release the most minis. When just one of these cells releases enough minis to reach some sort of electrical threshold, it will fire a burst of signals that in turn activates synapses on all the cells it has been in contact with during the day.

A chain reaction gets under way, Dr. Sejnowski said. The relatively small number of cells that were involved in an act of paying attention to a particular event will fire together. In this heightened state, signals that turn on genes are released. New proteins are produced as cells involved in the memory make stronger bonds with one another. Days, weeks or even years later, when just a few of the cells in the strengthened circuit are activated, the entire memory is recalled.

Dr. Borbely said the new work showed that the parts of the brain that were most active during the day exhibited the slowest wave sleep at night. The process may help explain why sleeping on problems sometimes leads to creative solutions, Dr. Sejnowski said. Imagine that two memory traces use some of the same cells. "There has always been a close connection between sleep and creativity," he said, "which may be a byproduct of the way that nature chose to consolidate memories."


\16 Ulcers

A YOUNG AUSTRALIAN DOCTOR STUMBLED ON THE TRUE CAUSE OF ULCERS NEARLY 20 yrs AGO. INSTEAD OF BECOMING A HERO, HE WAS MOCKED AND HIS FINDINGS IGNORED. TODAY DOCS AND DRUG COMPANIES STILL AREN'T GIVING MOST PATIENTS THE CURE.
 The pain of an ulcer usually begins a few hours after eating--a stabbing sensation somewhere between your breastbone and your navel that bores through to your back. An ulcer is a raw red wound in your gut, between a nickel and a silver dollar in size, awash in stomach acid strong enough to dissolve shoe leather. Left untreated, it can eat into stomach arteries, triggering fatal bleeding, or perforate the gut entirely, spreading infection everywhere. 

An ulcer is not necessarily the mark of an overworked executive. Anybody can get one--and everybody should hope they don't. "It feels like I swallowed napalm," says one sufferer. "Like having a rabid tiger inside you," reports another.
 Thirteen years ago this summer, Dr Barry Marshall, a brash resident at an obscure hosp in w.Australia, swirled a beaker containing billions of bacteria that he suspected were the true, and hitherto unrecognized, cause of nearly all the peptic ulcers in the world.
 No trivial ailment, ulcers have long been a chronic, debilitating disease that affects about 10% of US adults. Expensive too. In the past five years Americans have spent nearly $25 billion on drugs to slow the production of acid thought to cause ulcers. Billions more have been spent on visits to entroenter-ologists when the ulcers, despite all that medicine, inevitably recurred. Marshall was convinced he could end the pain and expense if he could prove his hunch that the culprit was a species of bacteria he'd found in the stomach of nearly every ulcer patient he'd examined. He and colleague J. Robin Warren had gotten a lucky break two years before.
 They'd been frustrated at their failure to grow the bac- teria in a culture dish in the standard 48 hrs of incuba- tion. But by accident they had left a culture growing for five days during the 1982 Easter holidays, and bingo, there was a colony of the stuff when they returned.

Animal experiments with the bacteria had failed to gen- erate ulcers, so by 1984 Marshall was desperate to see whether he was right. He raised the beaker and gulped down the bacteria. "It tasted like swamp water," he later said. The move turned out to be one of the best and worst he ever made. Barry Marshall wound up revolutionizing the understanding of ulcers.

His work showed that they are not caused by stress or diet or acid. Ulcers are almost always the product of a corkscrew-shaped organism called Helicobacter pylori, which can be eradicated with as little as two weeks of antibiotic therapy. (His research also led to the disco- very that H. pylori triggers most stomach cancers too.) Marshall's work is momentous. It has been compared with the development of polio vaccine and the eradication of smallpox. He is a serious contender for the Nobel Prize.

And yet it is only now--13 years after Marshall drank the bacteria and a decade since his work first drew broad attention--that his controversial ideas and methods are finding their way, haltingly, into common medical practice. Even so, ulcers remain widespread, treatment of them with antibiotics is rare, and acid-blocking ulcer drugs are still the biggest-selling medicines on earth.

What happened? Isn't it a long time for a powerful idea to get digested by the med community? Yes and no. The story of Marshall's discovery provides a fascinating look at the economic, scientific, and personal forces that advance and retard a med breakthrough as it makes its way from the lab to the doctor's office.

Marshall's findings were propelled forward, at times, by his enthusiasm, by healthy greed, and by companies in search of new med therapies. A supermkt tabloid helped, as did rigorous, skeptical analysis by scientists eager, at first, to poke holes in an upstart's ideas. More often, though, the medical community resisted Marshall because his methods and brashness irritated researchers, and because his theories were so contrary to accepted wisdom that most ulcer scientists literally couldn't believe them.

Bad timing played a role too. Marshall and his H. pylori were competing for attention with two of the greatest pharmaceutical accomplishments of all time: the anti-acid ulcer medicines Tagamet and Zantac. These let doctors treat ulcers effectively as chronic problems and enabled drug companies and gastroenterologists to make such good money that they seemed less than thrilled at the prospect of eradicating ulcers.

The treatments that eventually grew out of Marshall's research often used generic, low-margin antibiotics whose manufacturers rarely spent money to educate doctors on their new use. Instead of seeing the world embrace his ideas, Barry Marshall got a hard lesson in med economics.

Ulcers seem to be a fairly recent phenomenon. They were rarely noted by doctors until the turn of the century but then swiftly became almost commonplace in industrialized countries. For decades a bland diet and low stress were seen as the way to manage them. In the 1940s and 1950s, a patient with an ulcer could expect to spend 4-6 weeks in bed, three months out of work, and years eating porridge, boiled eggs, and weak tea. Doctors used antacids to provide temporary relief, a treatment that often back- fired by prompting the stomach to produce even more acid.

And because a deep ulcer can be fatal-eroding and burst- ing big stomach arteries or causing massive infections surgery was often required. It was a drastic and unsatis- fying intervention, described years ago by a glum surgeon as "removing three-quarters of a person's stomach to remove a two-millimeter ulcer." By the 1960s, before Tagamet and Zantac, the state of the art in ulcer treat- ment was an operation called the vagotomy. Surgeons cut nerves to acid-secreting parts of the stomach, greatly reducing an ulcer's severity.

In 1976 came a breakthrough. After a decade of research, a struggling Philadelphia pharmaceuticals company, then called Smith Kline & French Labs, won approval for a completely new way to treat ulcers. Its scientists had learned that stomachs secrete acid in response to several stimuli, including a previously unknown histamine called H2. They had found a way to block that acid secretion response with the chemical cimetidine, which was given the brand name Tagamet. It slowed acid production so effectively that ulcer pain stopped in days; often ulcers seemed to heal after just a few wks of medication.

Tagamet was wildly successful. A year after its intro, ulcer surgeries in the U.S. dropped by one-third, to 66,000, and medical students were advised not to speci- alize in ulcers anymore. Tagamet's annual sales reached nearly $600 million by 1980. That year FORTUNE called it "one of the most stunningly successful products in the history of American business...up there with the Xerox 914 copier and the Ford Mustang." 

Tagamet soon surpassed venerable Valium to become the best-selling drug on earth. Smith Kline's earnings, which had been lackluster in the early 1970s, rose 266% in the four years after Tagamet was introduced.

In 1981 a British company, Glaxo, introduced a similar histamine-blocker drug, Zantac. It had slightly fewer side effects and was marketed very aggressively. It began outselling Tagamet in 1988 and has been the biggest- selling drug of any sort ever since. (Tagamet lost U.S. patent protection in 1994. Zantac is due to lose it this year, and sales are likely to plunge as low-priced generic clones come on the market. A new generation of acid blocker,

Prilosec, is expected to take over this year as the biggest-selling drug.)
 When Barry Marshall tried to talk about the bacteria cocktail he drank in 1984, he found the stomach doctors still cheering the anti-ulcer wonder drugs-and dismis- sing his findings. Because the new drugs worked by curbing stomach acid, med scientists were more certain than ever that excess acid caused ulcers. Research scientists knew the stomach could harbor bacteria, but it was widely believed the bacteria were a benign coloniz- ation more like a bird's nest in the eaves than termites in the basement.
 What had Marshall found? For a week after he drank the H. pylori, nothing happened. Then, suddenly, in the middle of the night, he became sick to his stomach. Within a week, he was pale, haggard, and foul of breath. A colle- ague performed an endoscopy by inserting a tiny video camera down Marshall's throat to inspect his gut. There to Marshall's excitement, was the telltale sign that accompanies virtually all ulcers: the redness and inflammation known as gastritis.

Armed with this "discovery," and his finding of H. pylori in nearly all the duodenal ulcer patients he had biopsied Marshall began traveling to conventions of gastroentero- logists. But after his exuberant speeches announcing that ulcers were caused by bacteria, he was practically laughed off stage. Worst of all, sober gastro researchers thought Marshall's decision to drink the beaker of bact- eria was highly unscientific: brave, maybe, but a stunt that didn't prove anything. 

Who was this guy anyway, a mere resident from Perth, Aust? He wasn't even a researcher, only a clinician examining biopsies of ulcerated stomachs and duodena. (The duodenum is the area where the stomach empties into the small intestine, and is the site of most ulcers.)

Marshall was undeterred and grew increasingly angry with his colleagues. "He'd get up and tell us we were criminal for not eradicating the bacteria," says Dr. David Y. Graham, a giant of gastroenterology research now at Baylor College of Medicine in Houston. "He was out of it--he was radical." 

He was way ahead of his data too, says Dr. James Freston, former president of the American Gastroenterological Association. Freston says he thought at the time that bacteria might cause stomach inflammation, but he felt Marshall was making an unforgivable leap to conclude that the gastritis caused ulcers. Freston later nominated Marshall for a prestigious medical prize, the Albert Lasker Award, citing his tenacity. But at first he was unimpressed. "Most people who make leaps like that are wrong," says Freston.
 It wasn't just Marshall's personality and research style that made the going rough. The emotions and economics arrayed against him were huge too. Dr. Cynthia Yoshida, a gastrointestinal researcher at the Univ of Virginia, describes how incomprehensibly foreign Marshall's ideas were to generations of doctors brought up to believe that ulcers were an acid problem.

 "I was raised a Christian in California," says Yoshida, "but when I was a teenager, my parents wanted me to understand my Japanese culture and told me to study Buddhism. Suddenly I was in a world of flowers, temples, and white elephants. That's how diff Barry's ideas were."

Marshall believes money was the main reason the medical community dismissed him--particularly the money made by companies producing the acid-blocking H2 medicines. To the delight, no doubt, of stockholders of Smith Kline and Glaxo, it soon became apparent that Tagamet and Zantac do not cure ulcers. Within a year of stopping H2's, 70% of patients have ulcers again. 

The medicines allow the ulcers to heal by blocking the acid aggravating them, but when the medicine is stopped, the ulcers resume their attack. Most people taking H2 blockers would have to use several dollars' worth every day for decades--tens of thousands of dollars over a lifetime. The drugs were poised to provide the manufact- urers with such a steady stream of revenues that they became known as annuity medicines. "I don't think anybody at Smith Kline or Glaxo thought they would get a promo- tion for saying, 'We've got to work on H. pylori so we can fix ulcers for good,'" says Marshall.
 Soon after he managed to culture the first of his bacteria, Marshall sent letters to Smith Kline and Glaxo asking them to support additional research. "I didn't explain distinctly what I had found," he says, "but they weren't interested. They sent letters back just saying, 'Keep up the good work' and 'We'd like to help, but research money is very tight.' They were making a fortune on H2 medicines. I can't believe money was tight."
 There is no evidence that any drug company actively tried to undermine Marshall or his research. In fact, says Graham, the Baylor scientist, Glaxo eventually became a major supporter of H. pylori research, altho Smith Kline never did. Nonetheless, notes Marshall, "They were fund- ing hundreds of research projects about their H2 meds. For every article on H. pylori, there were 100 on sup- pressing acid. Any doc looking at the scientific lit was convinced of the importance of acid, not bacteria."
 Gastroenterologists as well may have been ambivalent about eliminating ulcers. Patients with ulcers or acid problems make up about 25% of their practice. In any given year, about six million people in the U.S. have an active ulcer. Alas, many feel so much better taking Zantac or a cousin that they stop the medicine and the ulcer comes back, which usually means another visit to the doctor, who puts that expensive camera tube down the throat to look around.
 Developed in the early 1970s, endoscopies are still expensive--around $1,000--and lucrative. Says Dr. Martin Blaser, head of infectious diseases at Vanderbilt Univ and an H. pylori expert: "A doctor doing an endoscopy makes about ten times as much per hour as he would simply giving a patient advice." There was no conspiracy by docs to ignore Marshall, says Blaser, but no economic incen- tive for them to consider his controversial theories either. "To my way of thinking, there was a lot of enlightened self-interest," he says dryly.
 Marshall's fortunes eventually began to change, but only after a strange bit of publicity and some enlightened self-interest on the part of a huge, and unlikely, US corp. In 1984, Marshall described his findings on stomach inflammation and bacteria in the Lancet, a respected British med mag. The report was mostly ignored in medical circles but not by the inquiring tabloid minds at the National Enquirer, which ran a story that Nov.
 Soon the Cincinnati Enquirer ran a story too. A research scientist from Procter & Gamble saw the story in his Sunday paper and called Marshall. In his efforts to eradicate H. pylori, Marshall had had some success with compounds containing bismuth. The P&G scientist was intrigued. His company had recently purchased the Pepto-Bismol brand, that pink tummy medicine whose main ingredient is a bismuth compound.

Moreover, P&G had started a pharmaceuticals div and was looking for a big new product. By December, Marshall was discussing patent and business agreements with P&G. Over the next several years the company funded much of his research, holding H. pylori conventions and underwriting Marshall's move to the Univ of Virginia in 1986.

Marshall continued researching and proselytizing about H. pylori. Meanwhile, a handful of skeptical research scientists had begun to scrutinize his findings. Says Graham at Baylor, who would clash with Marshall for years: "I decided that if he were wrong, it would be easy enough to prove." 

The more Graham and others studied H. pylori, however, the more they became intrigued. Bacteria typically do not last long in the stomach, which secretes about a liter of extremely powerful hydrochloric acid every day. (A healthy stomach protects itself from the acid with a shielding layer of mucus.) The acid is strong enough to dissolve iron nails and fatal to most germs-another reason scientists had concluded that ulcers were caused by the acid system running amuck.
 As they studied H. pylori, scientists found it had an extraordinary ability to survive in that hostile environment. Its corkscrew shape helped it burrow through the protective mucous layer. In addition, it produced an enzyme, urease, that enabled it to make ammonialike compounds to neutralize the stomach acid. Voila! The bacteria could set up camp in tiny crevices of the stomach wall--creating safe, acid-free zones. 

Though the body's immune system would detect and respond to the bacteria, it often failed to kill them. Exactly how H. pylori causes ulcers still isn't clear; it appears to inflame and weaken the stomach wall, stimulate extra acid production, and perhaps diminish the protectiveness of the mucous layer.
 Scientists eventually realized that H. pylori is one of the world's most common infections--probably second only to tooth decay, says Graham. Infection rates in the U.S. are lower than in most countries but still high. The odds of getting H. pylori rise about one percentage point a year with age, so 50% of 50-year-old Americans have it, 60% of 60-year-olds, and so on. Just because you have H. pylori doesn't mean you will develop an ulcer. (Marshall didn't get one from his bacteria cocktail. 

To his surprise, his gastritis cleared up spontaneously after a few weeks.) Most people with the bug get an inflamed stomach and experience discomfort; just 20% develop an ulcer. It's not clear why; Blaser at Vander- bilt thinks there may be different strains of H. pylori. On the other hand, virtually everyone with an ulcer does have H. pylori, except for the 15% of ulcers caused by too much aspirin, ibuprofen, or similar analgesics.
 Researchers made more ominous findings too. H. pylori is far more dangerous elsewhere in the world, where it can be a leading cause of cancer. It spreads in crowded or unsanitary conditions, so in parts of Africa, Latin America, and even in Italy and Japan, H. pylori infection rates are extremely high. There, people usually catch it when they are infants or toddlers, which is especially dangerous, because the bacteria eventually destroy all the acid-secreting glands in the stomach, greatly increasing the risk of stomach cancer. 

(It's believed that stomach acid destroys many of the cancer-causing chemicals we eat.) In Peru, where nearly everyone has H. pylori, stomach cancer is the leading cause of death among men, and second among women. The U.S. has about 25,000 cases of stomach cancer, and 14,000 deaths, per year.
 Ever so slowly, Barry Marshall won his colleagues' grudging admiration. "He gets credit for starting this," says Blaser, "but where his scientific contributions stopped and others took over is a matter of controversy." For most of the 1980s, Marshall and Graham remained at each other's throats, engaging in rancorous public debates. "People would go to GI conventions just to see the fireworks," says one who saw them. In 1988, Graham wrote a scholarly article on H. pylori with the title: "Much Ado About Not Much?" 

Finding treatments to kill H. pylori infections proved about as difficult for Marshall as winning friends at gastroenterology conventions. Pepto-Bismol alone was not very useful; it eradicated the infection only 20% of the time. With backing from P&G, Marshall experimented with 20 different combinations, testing each on dozens of patients, and eventually came up with a regimen involving Pepto-Bismol and a common antibiotic, metronidazole, which worked about 70% of the time. Later, another researcher added tetracycline to the mix and boosted effectiveness to about 85%.

Marshall's lab at the University of Virginia gradually became a mecca for people with serious ulcer trouble. "He was getting calls from terrified people with severe problems," says Susie R. Hoffman, his research nurse. "They didn't respond to the H2 medicines and were at risk of dying from bleeding or perforated ulcers. They'd say, 'Help! They're about to cut out half my intestines. Can you help me?'" As reports of Marshall's success filtered out to researchers, and as other scientists looked for ways to attack H. pylori, his stature began to rise. 

By the late 1980s, scores of experiments were being done with antibiotics and antacid medicines--so many, in fact, that ordinary gastroenterologists became frustrated. They would attend conventions where they'd hear presentations by researchers on yet another mix of chemicals to kill H. pylori. But when they went home and tried the treatments on patients, few worked well. Many doctors gave up on eradication therapy.

      Eventually two powerful drugs emerged as the best combination
      against H. pylori and ulcers. One was the antibiotic Biaxin,
      developed by Abbott Laboratories and used primarily for lung
      infections. The other was a new kind of stomach-acid medicine called
      a proton pump inhibitor, or PPI, developed by Astra AB, a drug
      company in Sweden. Unlike Zantac and Tagamet, which keep stomach
      cells from reacting to histamine but don't stop them from gushing
      acid in response to other stimuli, the Astra product, Prilosec, stops acid production almost entirely.

Prilosec and Biaxin worked well together. In tests of earlier drug combinations, stomach acid had destroyed the antibiotics before they could work, but Prilosec kept the Biaxin intact long enough for it to be more successful. Abbott and Astra funded hundreds of H. pylori eradication experiments, including some by Graham, Marshall's doubter at Baylor. 

"The world changed with a Jan 93 paper in the JAMA," says Graham. "It had no new info but enough data to say that if you cure HP, you cure ulcers." Graham says Senator Edward Kennedy, whose main science adviser is a gastroen- terologist, then pushed for a definitive analysis of the debate, hoping to cut the cost of treating Medicaid patients with ulcers. 

In 1994 the NIH made an official proclamation: Ulcers are caused by H. pylori, and people with both an H. pylori infection and an ulcer should have the bacteria eradicated. "It wasn't until the NIH report that Barry finally got recognition," says Yoshida, who worked with Marshall in Virginia.
 Yet the thumbs up from the NIH did not bring about a sudden change in the treatment of ulcers. The Food and Drug Admin didn't approve any H. pylori medicine until April 1996, when it finally okayed the Biaxin/Prilosec combination. Last August a bismuth-Zantac-antibiotic combo from Glaxo, called Tritec, was approved. Procter & Gamble's Helidac, using Pepto-Bismol and two antibiotics, also got the green light.

FORTUNE; JUN 9 1997 WHY DOCTORS AREN'T CURING ULCERS By Brian O'Reilly, 

--------------------------------------------------------- America's doctors have been slow to change. IMS America, a research company in Plymouth Meeting, Pennsylvania, that analyzes prescription data, found that of the 3.8 million prescriptions written for ulcer patients last year, only 11,000 were for Tritec, 80,000 for Biaxin, and 48,000 for metronidazole. P&G's Helidac therapy didn't even show up. 

(The Helidac combination may be more popular than it appears: To P&G's frustration, its ingredients can be cobbled together from cheap generics for less than what P&G charges. Cost-conscious HMOs like Kaiser are doing just that.) Some therapies that were on the market for only part of 1996 will probably have better numbers in 1997, but no matter how the data are massaged, surprisingly few ulcer patients are on antibiotics.
 One reason is that Tagamet, Zantac, and similar brands like Pepcid and Axid are so easy to use. Side effects are rare, the pills need be taken only once or twice a day, and the drugs relieve symptoms quickly and effectively. Prilosec, the newest acid stopper, is just as easy and works even better. 

Do family doctors, squeezed by managed care, really want to take the time to treat H. pylori--which involves testing for it with blood and breath samples or sending patients to specialists for endoscopies, educating patients, worrying that they will react adversely to antibiotics, and bringing them back for follow-up tests?
 Another problem is that patient compliance with complex eradication regimens is poor. P&G's Helidac therapy requires taking 16 pills a day for two weeks. Often the acid-suppressant portion of the therapy makes patients feel so much better that they abandon the antibiotics after a few days. When the symptoms return, they treat themselves with over-the-counter versions of Zantac or Tagamet. 

Doctors' concerns about the overuse of antibiotics are an impediment too. H.pylori's natural resistance to Biaxin and other drugs is high, and many physicians are leery of the large doses needed to kill the bugs. If a strain survives weeks of treatment, the bugs that remain will be doozies.
 Finally, it is a fact of med life that most doctors learn about new treatments from pharmaceuticals companies, not scholarly journals or med conferences in HNL. Few drug companies have aggressively promoted eradication. 

"The longer I'm in this job, the more cynical I get," says Carl Seiden, a pharmaceuticals industry analyst at Sanford C. Bernstein in New York. "Doctors' habits don't change until you have a pharmaceuticals company with a financial incentive to change them. Except for Abbott with Biaxin, everybody is a net loser if eradication therapy catches on."
 James Culverwell, a Merrill Lynch analyst in London, says Glaxo doesn't have much credibility in ulcer eradication. "For years Glaxo was dismissive of the role of H. pylori. They had an enormous vested interest in not finding a role, with plenty of life left in Zantac.
 Now, with Zantac going off patent, they've come up with a treatment, but they're late." (Indeed, a Glaxo history of Zantac, written last Feb, barely acknowledges H. pylori. It notes "present evidence suggests" that ulcers "may" be caused by the bacteria, and never mentions that H. pylori can be eradicated.)
 Will ulcers eventually go the way of polio and smallpox? Not likely. In Peru most patients whose bugs are killed become reinfected in a year. Prospects are better in the U.S., where HMOs are almost certain to get religion about H. pylori if only because it costs less to kill the infection than to keep a patient on Zantac for a year.
 And what about Barry Marshall? He won the 1995 Lasker Award, which makes him a major contender for a Nobel. He has been on sabbatical in Australia since Aug and was spotted in Stockholm last Oct, the week the Nobel laureates were announced. (Marshall says his business there was unrelated.) Waiting to hear whether you've won a Nobel Prize has got to be stressful. But if Barry Marshall develops an ulcer, at least he'll know that's not what caused it. WHERE DOES IT HURT?
 What should you do if you have a severe stomachache? If it recurs often or doesn't go away, see your doctor, of course, even though managed care has made that about as much fun as a trip to the Motor Vehicles Dept. Just about anything can cause stomach pain, from a heart attack to a hiatal hernia to depression.
 The doctor will ask where it hurts. If you press your hands high on your stomach, he will suspect heartburn, which, if serious enough, is called gastric esophageal reflux disease, or GERD. It is not an ulcer but a disorder caused by stomach acid squirting back up into your esophagus, which lacks natural defenses against acid. GERD can be triggered by coffee, alcohol, fatty foods, tight clothes, being fat, or aging. More and more baby-boomers are getting it.
 Sometimes acid can rise high enough to trigger asthma attacks or irritate vocal cords, causing the sort of hoarseness that plagues Pres Clinton. Doctors commonly, and appropriately, treat GERD with acid reducers such as Zantac and Prilosec. In fact, acid-suppression medicines are probably prescribed for GERD more often than for ulcers. But years of GERD can damage the esophagus and even lead to cancer. Esophageal cancer is now one of the fastest-growing cancers in the U.S., affecting 10,000 people a year.

If your stomach pain typically comes a few hours after a meal, suspect an ulcer. If eating diminishes the pain, that's another ulcer sign (though eating can alleviate GERD too). Food neutralizes acid and speeds stomach emptying, which eases ulcer symptoms temporarily but also triggers acid secretions that can cause ulcer pain later. Try going easy on painkillers, even though your once magnificent body now creaks and aches with middle age. Aspirin and ibuprofen can directly damage the stomach wall, making it vulnerable to acid. Acetaminophen is far less irritating.

If your doctor suspects acid, not aspirin, he may put you on Zantac or Prilosec for a few weeks to see what happens. If the symptoms disappear and don't come back, great! Maybe it wasn't an ulcer. If they come back within a year, he should test for H. pylori. There are blood and breath tests that can detect the bacteria; endoscopy can be used to spot any ulcers and perform a painless biopsy for H.pylori. 

If you have an H. pylori infection, the NIH recommends eradication therapy even if no ulcer is present. There is no consensus on whether you should be tested to make sure the eradication was successful. But if the ulcer doesn't recur, you're probably cured.