magnesium is vital for health

Very few people are aware of how vital magnesium is for overall health. After oxygen, water, and basic food, magnesium may be the most important element needed by our bodies, activating over 300 different biochemical reactions necessary for your body to function properly. The U.S. minimum RDA for magnesium is about 320 mg per day for women and more than 400 mg per day for men, while optimum daily amounts are closer to 500 to 700 mg per day - yet studies show that most people regularly take in about half of that and that over 8 out of 10 people do not take enough daily magnesium for even the minimum daily amounts recommended. Recent research has revealed that this lack of magnesium may put your heart - and your health - at significant risk.

Magnesium protects against heart disease and heart attacks, high blood pressure and stroke, type II diabetes and much, much more. It is more important than calcium, potassium or sodium and regulates all three of them. Contrary to popular misconceptions, it is magnesium that is actually most important in building strong bones and preventing bone loss.

Magnesium is a muscle relaxant, while calcium is a muscle constrictor. Low magnesium intake is associated with muscle spasm, tremors and convulsions. Most Americans, particularly women, have been advised to consume 1200-1500 milligrams of calcium daily. Virtually none of these women have been told that calcium in single doses that exceed 500 milligrams are not absorbed and that they only need an additional 400-600 milligrams of supplemental calcium since their diet already provides about 800 milligrams of this mineral. Since 99 percent of magnesium resides inside living cells, blood serum levels are not a good indicator of magnesium deficiency. Blood tests for magnesium are notoriously inaccurate. Only 1 percent of the total body magnesium pool exists outside of living cells. So blood serum levels are notoriously inaccurate. [Clin Chem Lab Med 37: 1011-33, 1999]. In other words, your doctor can`t easily tell you by a blood test if your magnesium levels are low.

Most Americans, 8 in 10, do not consume enough magnesium. The countries that have the highest mortality rates in the world are the Scandinavian countries and New Zealand where more calcium is consumed from dairy products, while for comparison the lowest mortality rates in the world are in Portugal and Japan where calcium-rich dairy products are not consumed regularly. Americans consume about 800 milligrams of calcium daily (milk drinkers may get 1200-1500 mgs from their diet alone), but only consume about 275 milligrams of magnesium. Thus the dominance of calcium over magnesium produces symptoms of muscle spasm. Migraines, eyelid twitch, heart flutters, back aches, premenstrual tension, leg cramps and constipation are all linked to calcium overload. Excessive calcium may also result in kidney stones (1 in 11 Americans) and heart valve calcifications (mitral valve, 1 in 12 Americans). A significant percentage of American adults consume more than 2000 milligrams of daily calcium, the point where side effects of overdosage begin to be reported.

Magnesium has been called the "The Forgotten Mineral" and the "5-Cent Miracle Tablet" by medical researchers. Numerous researchers have reported that the provision of this mineral in the population at large would greatly diminish the incidence of kidney stones (1 in 11 Americans), calcified mitral heart valve (1 in 12 Americans), premenstrual tension, constipation, miscarriages, stillbirths, strokes, diabetes, thyroid failure, asthma, chronic eyelid twitch (blepharospasm), brittle bones, chronic migraines, muscle spasms and anxiety reactions. [Pediatric Asthma, Allergy Immunology 5: 273-79; Journal Bone Mineral Research 13: 749-58, 1998; Magnesium 5: 1-8, 1986; Medical Hypotheses 43: 187-92, 1994] That`s a lot of health benefits for a nickel. Sufficient provision of magnesium in the American population would likely reduce health care costs by billions of dollars.

When we get too low on oxygen, water or food, the consequences are serious. Yet, we often don`t realize the consequences of magnesium deficiency. The improper use of magnesium among health professionals and the population in general, is deeply responsible for many of the failures encountered daily in treating chronic health conditions nationwide. In addition to the ones listed above are:

Insomnia
Sleep-disorders
Fatigue
Body-tension
Headaches
Heart-disorders
Low energy

High Blood Pressure

PMS
Muscle tension

Backaches
Constipation
Kidney stones

Osteoporosis
Accelerated aging

Depression
Irregular-heartbeat
Anxiety
Muscle cramps

Spasms Irritability

and the list goes on.... It is reported that 90-95% of us are deficient in magnesium, including many of those who already supplement it. Why? Due to the misleading information presented in common magnesium texts. As a result, magnesium remains largely misunderstood, largely misused and the problem goes on undetected.

Magnesium and the Heart - One Mineral Can Make Or Break Your Heart`s Rhythm

Low blood levels of magnesium can significantly affect the way your heart pumps blood throughout your body. And even if you think you`re living a healthy lifestyle, you may not be getting enough of it.

Magnesium May Prevent Sudden Death Heart Attacks

More than 300,000 sudden-death heart attacks are reported annually in the US (more than 80 per day) which are believed to be related to excessive calcium and a shortage of magnesium. Modern medicine`s answer to the problem is to prescribe billions of dollars of calcium-blocker drugs. Magnesium is a natural calcium blocker, but this goes unrecognized by most physicians. Researchers warn that adults who consume excessive amounts of caffeine or alcohol, or who take water pills (diuretics), are prone to experience irregular heart beats and should consume more magnesium. The same is true for diabetics and people with low thyroid. Most Americans consume tap water that has been softened (sodium added) which worsens the problem. American adults need to supplement their diet with 200-400 milligrams of magnesium. The only side effect of too much magnesium is loose stool. Reducing dosage resolves this problem.

In the 1990s a preliminary report showed that intravenous magnesium reduced mortality rates following a heart attack. Unfortunately, this was apparently perceived as a threat to the sale of calcium-blocking drugs used for the same purpose. Medical researchers, financially backed by a pharmaceutical company that produces calcium-blocker drugs, deliberately chose to use an excessive dose of intravenous magnesium to prove it was of no value during the post-heart attack period. [Townsend Letter for Doctors, October 1998]

Magnesium is not limited to treating heart disease after a heart attack. A shortage of dietary magnesium has been repeatedly shown to be associated with an increased risk of sudden-death heart attack. Unequivocally, a shortage of magnesium from the American diet, in particular the absence or shortage of magnesium in drinking water, is directly related to sudden-death heart attack. [Epidemiology 10: 31-36, 1999; Heart 82: 455-60, 1999; American Journal Epidemiology 143: 456-62, 1996] Out of 750,000 heart attacks in the USA annually, an estimated 340,000 deaths occur within one hour of a heart attack. [Journal Nutrition Health Aging 5: 173-78, 2001]

One study showed the relative risk of sudden-death heart attack is more than 1.5 times higher among adults who consume on average 105 milligrams of magnesium a day compared to adults who consume 233 milligrams a day. [Magnesium Trace Element Research 9: 143-51, 1990]. In an animal experiment, no rodents experienced a sudden-death heart attack when magnesium levels were adequate, whereas 4 of 11 rodents with low magnesium levels experienced a sudden lethal heart muscle spasm. [Journal American Collage Cardiology 27: 1771-76, 1996]

Recently researchers reported on the effects of slowly withdrawing magnesium from the diet of postmenopausal women. Women began to exhibit abnormal heart rhythms as circulating magnesium levels declined. [American Journal Clinical Nutrition 75: 550-54, 2002] Of the minerals removed during water softening, magnesium is the only mineral found to be deficient in the heart muscle of sudden-death heart attack victims. [Science 208: 198-200, 1980]

Magnesium and High Blood Pressure

Magnesium helps signal muscles to contract and relax. And when the muscles that line the major blood vessels contract, your blood pressure rises.

When researchers studied the diets of 40,000 nurses and 30,000 male health professionals, they found lower blood pressures in people who ate more magnesium.

Magnesium and Diabetes

Eating more magnesium-rich foods, like green leafy vegetables and nuts, may reduce the risk of type-2 diabetes, suggests a meta-analysis of observational studies.

The analysis of prospective cohort studies, by researchers at Stockholm`s Karolinska Institutet, reports that for every 100 milligram increase in magnesium intake, the risk of developing type-2 diabetes decreased by 15 per cent. Larsson and Wolk identified seven studies looking at the link between magnesium intake from food or food plus supplements and the risk of type-2 diabetes. This gave the researchers a total of 286,668 participants and 10,912 cases of type-2 diabetes. Six of the studies showed a statistically significant inverse association, with every 100 mg per day increase in magnesium intake linked to a 15 per cent decrease in type-2 diabetes risk.

"The potential protective role of magnesium intake against type-2 diabetes may be due to improvement of insulin sensitivity," said the reviewers. "Studies in animals have demonstrated an adverse effect of magnesium deficiency on glucose-induced insulin secretion and insulin-mediated glucose uptake. In contrast, magnesium supplementation was shown to prevent fructose-induced insulin resistance and reduce the development of diabetes in a rat model of spontaneous type-2 diabetes."

They concluded that while it is too early to recommend magnesium supplements for type-2 diabetes prevention, increased consumption of magnesium-rich food "seems prudent."

While refusing to label the results of their meta-analysis definitive, authors Susanna Larsson and Alicia Wolk wrote in the Journal of Internal Medicine that the evidence that increased intake of magnesium may reduce the incidence of type-2 diabetes was "compelling."

Widespread Dietary Deficiency

Since the turn of last century, our depleted soils, processed foods and fast food diet lifestyles have led to a steady increase in mineral deficiencies. Nowhere is this more true than in Magnesium:

Progressive decline of dietary magnesium consumption

Magnesium intake in mg/day

1900-08 475-500

1909-13 415-435

1925-29 385-398

1935-39 360-375

1947-49 358-370

1957-59 340-360

1965-76 300-340

1978-85 225-318

1990-2002 175-225

[Magnesium Trace Elements 10: 162-28, 1997]

Dietary Sources of Magnesium by Standard Serving Size - Including Calories

Pumpkin and squash seed kernels, roasted - 1 oz contains 151 mg of magnesium and 148 calories

Brazil nuts - 1 oz contains 107 mg of magnesium and 186 calories

Bran ready-to-eat cereal (100%), - ~1 oz contains 103 mg of magnesium and 74 calories

 Halibut, cooked - 3 oz contains 151 mg of magnesium and 148 calories

Quinoa, dry - 1/4 cup contains 89 mg of magnesium and 159 calories

Spinach, canned - 1/2 cup contains 81 mg of magnesium and 25 calories

Almonds - 1 oz contains 78 mg of magnesium and 164 calories

Spinach, cooked from fresh - 1/2 cup contains 78 mg of magnesium and 20 calories

Buckwheat flour - 1/4 cup contains 75 mg of magnesium and 101 calories

Cashews, dry roasted - 1 oz contains 74 mg of magnesium and 163 calories

Soybeans, mature, cooked - 1/2 cup contains 74 mg of magnesium and 149 calories

Pine nuts, dried - 1 oz contains 71 mg of magnesium and 191 calories

Mixed nuts, oil roasted, with peanuts - 1 oz contains 67 mg of magnesium and 175 calories

White beans, canned - 1/2 cup contains 67 mg of magnesium and 154 calories

Pollock, walleye, cooked - 3 oz contains 62 mg of magnesium and 96 calories Black beans,

 cooked - 1/2 cup contains 60 mg of magnesium and 114 calories

Bulgur, dry - 1/4 cup contains 57 mg of magnesium and 120 calories

Oat bran, raw - 1/4 cup contains 55 mg of magnesium and 58 calories

Soybeans, green, cooked - 1/2 cup contains 54 mg of magnesium and 127 calories

Tuna, yellowfin, cooked - 3 oz contains 54 mg of magnesium and 118 calories

Artichokes (hearts), cooked - 1/2 cup contains 50 mg of magnesium and 42 calories

Peanuts, dry roasted - 1 oz contains 50 mg of magnesium and 166 calories

Lima beans, baby, cooked from frozen - 1/2 cup contains 50 mg of magnesium and 95 calories

Beet greens, cooked - 1/2 cup contains 49 mg of magnesium and 19 calories

Navy beans, cooked - 1/2 cup contains 48 mg of magnesium and 127 calories

Tofu, firm, prepared with nigaria (a) - 1/2 cup contains 47 mg of magnesium and 88 calories

Okra, cooked from frozen - 1/2 cup contains 47 mg of magnesium and 26 calories

Soy beverage - 1 cup contains 47 mg of magnesium and 127 calories

Cowpeas, cooked - 1/2 cup contains 46 mg of magnesium and 100 calories

Hazelnuts - 1 oz contains 46 mg of magnesium and 178 calories

Oat bran muffin - 1 oz contains 45 mg of magnesium and 77 calories

Great northern beans, cooked - 1/2 cup contains 44 mg of magnesium and 104 calories

Oat bran, cooked - 1/2 cup contains 44 mg of magnesium and 44 calories

Buckwheat groats, roasted, cooked - 1/2 cup contains 43 mg of magnesium and 78 calories

Brown rice, cooked - 1/2 cup contains 42 mg of magnesium and 108 calories

Haddock, cooked - 3 oz contains 42 mg of magnesium and 95 calories

Spirulina - 10 grams contains 40 mg of magnesium and 39 calories

(a)    Calcium sulfate and magnesium chloride.

Note: It is healthier to consume as many of the items on the list as possible in raw form. The soy products are not recommended due to the widespread use of GMO soy and other health concerns related to soy.

Supplementation Advised

Although you can see from the above chart that a person might be able to obtain enough minimum RDA of magnesium and perhaps even optimum amounts of magnesium through a very carefully planned and managed daily diet, it would be a difficult task since much of the above list are no longer staple parts of our Western diets. When processed food is added to the diet it can safely be assumed that, while anyone should be able to increase the magnesium they get from wise diet choices, it is exceedingly difficult for the general public to consume enough magnesium through dietary sources alone.

Only supplementation is likely to make up for such a widespread deficiency in magnesium. Foods cannot easily be fortified with magnesium because it is a bulky mineral that would alter the consistency and taste of flour and foods. Magnesium cannot be added to tap water because it would erode piping. Either magnesium pills or magnesium added to bottled water would make up for this mineral deficiency. Currently, only 5 major brands of bottled water provide a desirable measure of more than 75 milligrams of magnesium per liter and only one brand has a ratio of magnesium that exceeds that of calcium.

Since the same problems with soil depletion and diet causes deficiencies in many other vital minerals, it would be a good idea to supplement for magnesium and to also supplement with a wide range of minerals. The very best source of mineral supplements are plant derived minerals, because they are more readily absorbed than mined rock minerals. For maximum absorption, bromelain can be added. Bromelain is an all natural compound found in the stem of the pineapple plant and is a powerful binder that increases the absorption of many things.

Until now it was thought that the best forms of supplemental magnesium were the ones chelated to an amino acid (magnesium glycinate, magnesium taurate) or a krebs cycle intermediate (magnesium malate, magnesium citrate, magnesium fumarate). But now we have magnesium oil, a magnesium chloride, that can be applied directly to the skin, so dosage levels can be brought up safely to high levels without diarrhea and problems with absorption. Magnesium orotate is considered to be a superior form of oral magnesium supplementation. The only side effect of too much magnesium is loose stool. Reducing the dosage or dividing daily doses into smaller amounts resolves the problem.

Note: For optimum health, magnesium and calcium intake needs to be at about a 1 to 2 ratio. So, if you supplement with 500 mg of magnesium, you should supplement with 1000 mg of calcium (or less if you get plenty of dietary calcium and little dietary magnesium).

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junk food as street drugs

Scientists are increasingly becoming convinced that junk food can be just as physically addictive as street drugs like heroin
Researchers at Rockefeller University have found that foods high in fat and sugar cause the brain to release many of the same pleasure chemicals that produce drug addiction, including cortisol, dopamine, galanin and serotonin. Over time, regular consumption of junk food can create imbalances in these chemicals, leading us to eat more and more in order to restore normal levels.
"They cause us to have more cravings," said Rosa Lopez, of the New York Department of Health. "There are physiological changes."
A recent study by researchers from the Scripps Research Institute confirmed this long-term effect by feeding rats either a healthy diet, a healthy diet plus limited amounts of junk food, or a healthy diet plus unlimited amounts of junk food. While rats in the first two groups remained healthy, rats in the third group binged on junk food and quickly became obese.
"You lose control. It's the hallmark of addiction," researcher Paul Kenny said.

When researchers then directly stimulated the pleasure centers in the rats' brains, they found that the obese rats needed more stimulation than the other rats to achieve the same effect. This suggests that their junk food diet had actually dulled their brain's pleasure centers, creating dependency.
"This is the most complete evidence to date that suggests obesity and drug addiction have common neuro-biological foundations," researcher Paul Johnson said.Because ending a junk food addiction may be as difficult as quitting smoking, Lopez recommends tackling just one bad habit at first. Cutting out soda can be a good place to start.
"In some ways, you may have to view junk foods the way alcoholics anonymous views alcohol: one bite is too many, and a thousand is not enough," writes Jack Challem in his book The Food-Mood Solution.

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Archimedes' principle

Archimedes' principle can be stated as follows:
Any body completely or partially submerged in a fluid is buoyed up by a force equal to the weight of the fluid displaced by the body.
Everyone has experienced Archimedes' principle. As an example of a common experience, recall that it is relatively easy to lift someone if the person is in a swimming pool whereas lifting that same individual on dry land is much harder. Evidently, water provides partial support to any object placed in it. The upward force that the fluid exerts on an object submerged in it is called the buoyant force.
According to the Archimedes' principle,The magnitude of the buoyant force always equals the weight of the fluid displaced by the object.The buoyant force acts vertically upward through what was the center of gravity of the displaced fluid.
                  B = W
Where B is the buoyant force and W is the weight of the displaced fluid.
The units of the buoyant force and weight are newton ( N ) in SI and "pound force" ( lbf) in British Engineering units.
The buoyant force acting on the steel is the same as the buoyant force acting on a cube of fluid of the same dimensions. This result applies for a submerged object of any shape, size, or density.

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Thermodynamics

Thermodynamics is the study of relationship between energy and entropy, which deals with heat and work. It is a set of theories that correlate macroscopic properties that we can measure (such as temperature, volume, and pressure) to energy and its capability to deliver work. A thermodynamic system is defined as a quantity of matter of fixed mass and identity. Everything external to the system is the surroundings and the system is separated from the surroundings by boundaries. Some thermodynamics applications include the design of:
air conditioners and refrigerators
turbo chargers and superchargers in automobile engines
steam turbines in power generation plants
jet engines used in aircraft

Zeroth Law of Thermodynamics

The zeroth law of thermodynamics states that when two bodies have equality of temperature with a third body, they in turn have equality of temperature with each other. All three bodies share a common property, which is the temperature. For example: one block of copper is brought into contact with a thermometer until equality of temperature is established, and is then removed. A second block of copper is brought into contact with the same thermometer. If there is no change in the mercury level of the thermometer during this process, it can be said that both blocks are in thermal equilibrium with the given thermometer.

First Law of Thermodynamics

The first law of thermodynamics states that, as a system undergoes a change of state, energy may cross the boundary as either heat or work, and each may be positive or negative. The net change in the energy of the system will be equal to the net energy that crosses the boundary of the system, which may change in the form of internal energy, kinetic energy, or potential energy. The first law of   thermodynamics can be summarized in the equation:



Second Law of Thermodynamics

The second law defines the direction in which a specific thermal process can take place. The second   law of thermodynamics states that it impossible to construct a device that operates in a cycle and produces no effect other than the transfer of heat from a cooler body to a hotter body. The second law of thermodynamics is sometimes called the law of entropy, as it introduces the important property called entropy. Entropy can be thought of as a measure of how close a system is to equilibrium; it can also be thought of as a measure of the disorder in the system.

Vapor Compression Refrigeration Cycle

One of the applications that involves thermodynamic principles is the refrigerator. The figure below   is a schematic diagram of the components found in a typical refrigerator.

The refrigerant enters the compressor as a slightly superheated vapor at a low pressure. It then leaves the compressor and enters the condenser as a vapor at some elevated pressure, where the refrigerant is condensed as a result of heat transfer to cooling water or to the surroundings. The refrigerant then leaves the condenser as a high-pressure liquid. The pressure of the liquid is decreased as it flows through the expansion valve and, as a result, some of the liquid flashes into vapor. The remaining liquid, now at a lower pressure, is vaporized in the evaporator as a result of heat transfer from the refrigerated space. This vapor then enters the compressor.



Reversibility

A reversible process for a system is defined as a process that, once having taken place, can be reversed and leaves no change in either system or surroundings. The difference between a reversible and an irreversible process can be illustrated with the example below.

Suppose a gas under pressure is contained in a cylinder fitted with a piston. The piston is locked in place with a pin. If the pin is removed, the piston is raised and forced abruptly against the stopper. Work is done by the system during this process because the piston has been raised by a certain amount. If the system has to be restored to its initial state, force has to be exerted on the piston until the pin can be reinserted. Since the pressure on the face of the piston is greater on the return stroke than on the initial stroke, the work done on the gas is greater on the return stroke than the work done by the gas in the initial process. This caused an amount of heat to be transferred from the gas to the surroundings in order that the system have the same internal energy. The fact that work was required to force the piston down and that heat was transferred to the surroundings during the reverse process makes the system an irreversible process.



Another system has a number of weights loaded on the piston at the initial state. The weights are removed from the piston one at a time, allowing gas to expand and do work in raising the weight remaining. If the process is reversed, the weight can be placed back onto the piston without any work requirement, as for each level of the piston there will be a small weight that is exactly at the level of the platform. Such a process is a reversible process. There are many factors that render a process irreversible, such as friction and unrestrained expansion.

Thus, to summarize, reversible systems occur in situations when the system is essentially in equilibrium during the transition and at each step, and only an infinitesimal amount of work would be necessary to truly restore equilibrium.

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Well Thank God It Wasn't a Hydrogen Car Then!

Often I am concerned when I find that government bureaucrats, academics, and politicians assume that they are so wise, that they can create a business, which will automatically make money. Indeed, I find this fascinating because, more often than not they have no-experience in business. As a taxpayer, I worry when politicians and such think they can borrow the power of the free-market, modify regulations, put forth subsidies, and then march ahead with their pet projects.

Oh it's always in the name of a good cause, just as the "road to hell is always paved with the greatest intentions." I have an acquaintance who tells me the way to innovate is through government-private sector-academia-corporate partnerships, he swears by them. And yet, every time he gives me an example, all I see is waste, inefficiency, and silly mistakes that entrepreneurs using their own money would have seen coming a mile away.

There was an interesting article in the New York Times titled; "Batteries in Electric Cars Examined After Chevy Volt Fire," by Nick Bunkley on November 11, 2011. The article stated that;

"The US has put billions of dollars into programs aimed at promoting battery and electric-car manufacturing. The large, high-voltage batteries used in plug-in vehicles can be more easily damaged in a crash than traditional car batteries and create more potential to electrically shock occupants and rescuers. The Volt's 400-pound, T-shaped battery extends under the middle of the car and between the back seats rather than fitting under the hood with the engine of a gas-powered vehicle."

The article also noted the spontaneous fires in laptops with ion-lithium batteries as well. Okay so, my comments here as an automotive industry consultant is best summarized with a joke;

"Well Thank God It Wasn't a Hydrogen Car Then!"

"Sounds like a rolling Hindenburg Disaster to me!"

Look anytime you have new technology you are going to have challenges, for instance the Boeing 787 carbon composite airliner, it was delayed for 3-years as they worked though the bugs to make it perfectly safe, see that point? But still, I want to remind folks on this Chevy Volt, that we should have expected it to "flop" because anytime the government gets involved, subsidizes an industry, company, or their products, you can bet there will be problems; Solyndra for instance.

Okay so, let this be a lesson to all. And let's get government out of business, and out of the game of crony capitalism using our taxpayer's money. We don't need any more spontaneous combustions in the free-market place, we are dealing with enough blow-back from previous such mistakes as it is. Please consider all this and think on it.

Lance Winslow has launched a new provocative series of eBooks on Future Concepts. Lance Winslow is a retired Founder of a Nationwide Franchise Chain, and now runs the Online Think Tank; http://www.worldthinktank.net

Article Source: http://EzineArticles.com/?expert=Lance_Winslow

Article Source: http://EzineArticles.com/6688153

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Michael Jackson had just two doctors in the final months of his life

Entering the world of Dr Arnold Klein is an extraordinary experience.

That it happened in the slightly unreal setting of the glitzy mansion where they film 'The Real Housewives of Beverly Hills' was somehow fitting.

Dr Klein has been dermatologist to the stars for decades, medical royalty in a place where the search for youth and beauty is part of everyday life.

He can claim friendships with everyone from Elizabeth Taylor down - but it is his relationship with the star he calls his best friend that has put his reputation in the spotlight now.

His treatment of Michael Jackson has loomed over the trial of Dr Conrad Murray as the defence team have tried to push some of the blame for the pop superstar's drug issues on to Dr Klein.

He was not called to give evidence so agreed to speak to Sky News to defend himself against the allegations made in court.

And that's how we ended up under the chandeliers in the rarified atmosphere of a Beverly Park mansion on a chilly Friday evening.

Heiress and reality TV star Adrienne Maloof-Nassif and her plastic surgeon husband Paul Nassif were throwing a red-carpet party to mark the opening of Dr Klein's new offices.

The guest list included the likes Charlie Sheen, who married in the house three years ago, Warren Beatty and the Earl and Countess Spencer.

It is evident Dr Klein has some powerful and influential friends and clients - and a lot of them are willing to fight his corner right now.

We were pointed to testimonials from Sharon Stone and Carrie Fisher (pictured above with Jackson and the doctor). A friend of Dr Klein told me: "He is a truly nice person, a good friend to Michael and a truly amazing doctor."

The 66-year-old has some trouble walking due to a skiing accident but he made his way to the mansion's study to sit in a throne-like chair and talk about Jackson, Murray and his own reputation.

It is clear he is bothered by the allegations made in court, the use (misuse, he says) of his medical records, and by the damage being done to Jackson's memory.

He says he would never have done anything to harm the star and that he was merely putting right the wrongs done by others over the years.

He speaks lovingly of Jackson's three children - and then raves about his affection for the 'Queen of England' - it is obvious he is a man who relishes telling a story.

We departed before the celebrity party was in full-swing - crossing paths with a few Hollywood beauties of the 70s and 80s - to reflect on this strange twist.

Michael Jackson had just two doctors in the final months of his life - their predicaments are very different right now but both will be forever linked by the controversy over his death.

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Jason Thomas Scott convicted on federal counts; to be tried in Pr. George’s double murder

Jason Thomas Scott, who is charged in Prince George’s County in a grisly double homicide and who is suspected in other killings, was convicted Monday in federal court in Greenbelt on charges of committing a series of armed home invasions, molesting a teenage girl, stealing and selling firearms and other crimes.

After deliberating for about eight hours over two days, the jury of 11 men and one woman convicted Scott of each of the 11 offenses he was charged with.
Scott, 28, did not outwardly react as the verdict was read.

Maryland U.S. Attorney Rod J. Rosenstein, who helped prosecute Scott and delivered the government’s closing argument, said Scott faces a mandatory minimum sentence of 97 years in prison for the firearms and sexual molestation convictions.

“He’s a very dangerous man,” Rosenstein said after the verdict was announced. “Prince George’s County is much safer now that he’s off the streets. He became more brazen over time, going from burglaries to armed home invasions.”

Scott’s defense attorney, Kobie Flowers, declined to comment.

U.S. District Judge Peter J. Messitte scheduled sentencing for Oct. 31.

During a three-week trial, Rosenstein and Assistant U.S. Attorney Stacy D. Belf presented a raft of circumstantial evidence showing that Scott committed a series of violent crimes in 2008 and the first half of 2009. Most of them occurred in the Largo neighborhood where Scott lived at his mother’s home.

Victims of four home invasions testified for the government, but were unable to identify Scott. The attacker or attackers wore black masks which covered everything but their eyes, the victims testified.

But two accomplices testified that they had committed armed home invasions with Scott, and that he had planned the crimes and gave the orders.

One of the co-conspirators, Marcus D. Hunter, 25, testified that Scott was methodical in choosing which homes to attack and in covering his tracks.

Scott, who worked as a clerk at a UPS facility in Largo, used a computer there to scout target homes, Hunter testified. He looked for homes whose owners owned small businesses, according to court testimony.

In executing the home invasions, Scott wore gloves and a handgun in a belt holster, and carried a police scanner to listen for signs that officers were nearby, Hunter testified.

Scott was also methodical about not leaving evidence, going so far as to mop the floor of one victims’s home so that no shoe prints were left behind, according to court testimony.

Hunter testified that he and Scott burglarized a Carroll County gun shop in May 2009 and tried to sell some of the dozens of handguns, shotguns, rifles and Uzi-style assault weapons they took, Hunter said.

But their buyer turned out to be an informant, and agents with the Bureau of Alcohol, Tobacco, Firearms and Explosives launched an investigation.

Hunter has pleaded guilty to two firearms offenses and testified for the government under a plea deal in which he hopes to gain leniency at sentencing.

Flowers said in his opening and closing arguments that the testimony of Hunter and another accomplice was not credible.

But Scott provided some of the government’s best evidence — a series of confessions he made during three meetings with ATF agents. He provided a typed list of addresses of 28 homes he had burglarized and nine he had invaded; investigators learned that each home had been hit, Rosenstein said.

Flowers said in his opening and closing arguments that Scott “exaggerated” his criminality because he was struggling with his identity as a gay man.

In addition to the federal conviction, Scott is scheduled to be tried for murder in Circuit Court for Prince George’s in November in the killings of Delores Dewitt, 42, and her daughter Ebony, 20. Their burning bodies were found inside a stolen car that had been set on fire in Largo on March 16, 2009.

According to police, Scott is also a “person of interest” in the Jan. 16, 2009, slayings of Karen Lofton, 45, and her daughter Karissa, 16. They were shot inside their locked Largo home. Police have said that Scott is also being investigated for a 2008 killing in which a woman in Bowie was shot in her home, which was then set on fire.

source : http://www.washingtonpost.com/local/jason-thomas-scott-convicted-on-federal-counts-to-be-tried-in-pr-georges-double-murder/2011/07/18/gIQAXyyfMI_story.html

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Parkinson's Disease

Parkinson's disease may be one of the most baffling and complex of the neurological disorders. Its cause remains a mystery but research in this area is active, with new and intriguing findings constantly being reported.

Parkinson's disease was first described in 1817 by James Parkinson, a British physician who published a paper on what he called "the shaking palsy." In this paper, he set forth the major symptoms of the disease that would later bear his name. For the next century and a half, scientists pursued the causes and treatment of the disease. They defined its range of symptoms, distribution among the population, and prospects for cure.

In the early 1960s, researchers identified a fundamental brain defect that is a hallmark of the disease: the loss of brain cells that produce a chemical -- dopamine -- that helps direct muscle activity. This discovery pointed to the first successful treatment for Parkinson's disease and suggested ways of devising new and even more effective therapies.

Society pays an enormous

price for Parkinson's disease. According to the National Parkinson Foundation, each patient spends an average of $2,500 a year for medications. After factoring in office visits, Social Security payments, nursing home expenditures, and lost income, the total cost to the Nation is estimated to exceed $5.6 billion annually.

What is Parkinson's Disease?

Parkinson's disease belongs to a group of conditions called motor system disorders. The four primary symptoms are tremor or trembling in hands, arms, legs, jaw, and face; rigidity or stiffness of the limbs and trunk; bradykinesia or slowness of movement; and postural instability or impaired balance and coordination. As these symptoms become more pronounced, patients may have difficulty walking, talking, or completing other simple tasks.

The disease is both chronic, meaning it persists over a long period of time, and progressive, meaning its symptoms grow worse over time. It is not contagious nor is it usually inherited -- that is, it does not pass directly from one family member or generation to the next.

Parkinson's disease is the most common form of parkinsonism, the name for a group of disorders with similar features (see section entitled "What are the Other Forms of Parkinsonism?"). These disorders share the four primary symptoms described above, and all are the result of the loss of dopamine-producing brain cells. Parkinson's disease is also called primary parkinsonism or idiopathic Parkinson's disease; idiopathic is a term describing a disorder for which no cause has yet been found. In the other forms of parkinsonism either the cause is known or suspected or the disorder occurs as a secondary effect of another, primary neurological disorder.

What Causes the Disease?

Parkinson's disease occurs when certain nerve cells, or neurons, in an area of the brain known as the substantia nigra die or become impaired. Normally, these neurons produce an important brain chemical known as dopamine. Dopamine is a chemical messenger responsible for transmitting signals between the substantia nigra and the next "relay station" of the brain, the corpus striatum, to produce smooth, purposeful muscle activity. Loss of dopamine causes the nerve cells of the striatum to fire out of control, leaving patients unable to direct or control their movements in a normal manner. Studies have shown that Parkinson's patients have a loss of 80 percent or more of dopamine-producing cells in the substantia nigra. The cause of this cell death or impairment is not known but significant findings by research scientists continue to yield fascinating new clues to the disease.

One theory holds that free radicals -- unstable and potentially damaging molecules generated by normal chemical reactions in the body -- may contribute to nerve cell death thereby leading to Parkinson's disease. Free radicals are unstable because they lack one electron; in an attempt to replace this missing electron, free radicals react with neighboring molecules (especially metals such as iron), in a process called oxidation. Oxidation is thought to cause damage to tissues, including neurons. Normally, free radical damage is kept under control by antioxidants, chemicals that protect cells from this damage. Evidence that oxidative mechanisms may cause or contribute to Parkinson's disease includes the finding that patients with the disease have increased brain levels of iron, especially in the substantia nigra, and decreased levels of ferritin, which serves as a protective mechanism by chelating or forming a ring around the iron, and isolating it.

Some scientists have suggested that Parkinson's disease may occur when either an external or an internal toxin selectively destroys dopaminergic neurons. An environmental risk factor such as exposure to pesticides or a toxin in the food supply is an example of the kind of external trigger that could hypothetically cause Parkinson's disease. The theory is based on the fact that there are a number of toxins, such as 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine (MPTP) and neuroleptic drugs, known to induce parkinsonian symptoms in humans. So far, however, no research has provided conclusive proof that a toxin is the cause of the disease.

A relatively new theory explores the role of genetic factors in the development of Parkinson's disease. Fifteen to twenty percent of Parkinson's patients have a close relative who has experienced parkinsonian symptoms (such as a tremor). After studies in animals showed that MPTP interferes with the function of mitochondria within nerve cells, investigators became interested in the possibility that impairment in mitochondrial DNA may be the cause of Parkinson's disease. Mitochondria are essential organelles found in all animal cells that convert the energy in food into fuel for the cells.

Yet another theory proposes that Parkinson's disease occurs when, for unknown reasons, the normal, age-related wearing away of dopamine-producing neurons accelerates in certain individuals. This theory is supported by the knowledge that loss of antioxidative protective mechanisms is associated with both Parkinson's disease and increasing age.

Many researchers believe that a combination of these four mechanisms -- oxidative damage, environmental toxins, genetic predisposition, and accelerated aging -- may ultimately be shown to cause the disease.

Who Gets Parkinson's Disease?

About 50,000 Americans are diagnosed with Parkinson's disease each year, with more than half a million Americans affected at any one time. Getting an accurate count of the number of cases may be impossible however, because many people in the early stages of the disease assume their symptoms are the result of normal aging and do not seek help from a physician. Also, diagnosis is sometimes difficult and uncertain because other conditions may produce some of the symptoms of Parkinson's disease. People with Parkinson's disease may be told by their doctors that they have other disorders or, conversely, people with similar diseases may be initially diagnosed as having Parkinson's disease.

Parkinson's disease strikes men and women in almost equal numbers and it knows no social, economic, or geographic boundaries. Some studies show that African-Americans and Asians are less likely than whites to develop Parkinson's disease. Scientists have not been able to explain this apparent lower incidence in certain populations. It is reasonable to assume, however, that all people have a similar probability of developing the disease.

Age, however, clearly correlates with the onset of symptoms. Parkinson's disease is a disease of late middle age, usually affecting people over the age of 50. The average age of onset is 60 years. However, some physicians have reportedly noticed more cases of "early-onset" Parkinson's disease in the past several years, and some have estimated that 5 to 10 percent of patients are under the age of 40.

What are the Early Symptoms?

Early symptoms of Parkinson's disease are subtle and occur gradually. Patients may be tired or notice a general malaise. Some may feel a little shaky or have difficulty getting out of a chair. They may notice that they speak too softly or that their handwriting looks cramped and spidery. They may lose track of a word or thought, or they may feel irritable or depressed for no apparent reason. This very early period may last a long time before the more classic and obvious symptoms appear.

Friends or family members may be the first to notice changes. They may see that the person's face lacks expression and animation (known as "masked face") or that the person remains in a certain position for a long time or does not move an arm or leg normally. Perhaps they see that the person seems stiff, unsteady, and unusually slow.

As the disease progresses, the shaking, or tremor, that affects the majority of Parkinson's patients may begin to interfere with daily activities. Patients may not be able to hold utensils steady or may find that the shaking makes reading a newspaper difficult. Parkinson's tremor may become worse when the patient is relaxed. A few seconds after the hands are rested on a table, for instance, the shaking is most pronounced. For most patients, tremor is usually the symptom that causes them to seek medical help.

What are the Major Symptoms of the Disease?

Parkinson's disease does not affect everyone the same way. In some people the disease progresses quickly, in others it does not. Although some people become severely disabled, others experience only minor motor disruptions. Tremor is the major symptom for some patients, while for others tremor is only a minor complaint and different symptoms are more troublesome.

Tremor. The tremor associated with Parkinson's disease has a characteristic appearance. Typically, the tremor takes the form of a rhythmic back-and-forth motion of the thumb and forefinger at three beats per second. This is sometimes called "pill rolling." Tremor usually begins in a hand, although sometimes a foot or the jaw is affected first. It is most obvious when the hand is at rest or when a person is under stress. In three out of four patients, the tremor may affect only one part or side of the body, especially during the early stages of the disease. Later it may become more general. Tremor is rarely disabling and it usually disappears during sleep or improves with intentional movement.

Rigidity. Rigidity, or a resistance to movement, affects most parkinsonian patients. A major principle of body movement is that all muscles have an opposing muscle. Movement is possible not just because one muscle becomes more active, but because the opposing muscle relaxes. In Parkinson's disease, rigidity comes about when, in response to signals from the brain, the delicate balance of opposing muscles is disturbed. The muscles remain constantly tensed and contracted so that the person aches or feels stiff or weak. The rigidity becomes obvious when another person tries to move the patient's arm, which will move only in ratchet-like or short, jerky movements known as "cogwheel" rigidity.

Bradykinesia. Bradykinesia, or the slowing down and loss of spontaneous and automatic movement, is particularly frustrating because it is unpredictable. One moment the patient can move easily. The next moment he or she may need help. This may well be the most disabling and distressing symptom of the disease because the patient cannot rapidly perform routine movements. Activities once performed quickly and easily -- such as washing or dressing -- may take several hours.

Postural instability. Postural instability, or impaired balance and coordination, causes patients to develop a forward or backward lean and to fall easily. When bumped from the front or when starting to walk, patients with a backward lean have a tendency to step backwards, which is known as retropulsion. Postural instability can cause patients to have a stooped posture in which the head is bowed and the shoulders are drooped.

As the disease progresses, walking may be affected. Patients may halt in mid-stride and "freeze" in place, possibly even toppling over. Or patients may walk with a series of quick, small steps as if hurrying forward to keep balance. This is known as festination.

Are There Other Symptoms?

Various other symptoms accompany Parkinson's disease; some are minor, others are more bothersome. Many can be treated with appropriate medication or physical therapy. No one can predict which symptoms will affect an individual patient, and the intensity of the symptoms also varies from person to person. None of these symptoms is fatal, although swallowing problems can cause choking.

Depression. This is a common problem and may appear early in the course of the disease, even before other symptoms are noticed. Depression may not be severe, but it may be intensified by the drugs used to treat other symptoms of Parkinson's disease. Fortunately, depression can be successfully treated with antidepressant medications.

Emotional changes. Some people with Parkinson's disease become fearful and insecure. Perhaps they fear they cannot cope with new situations. They may not want to travel, go to parties, or socialize with friends. Some lose their motivation and become dependent on family members. Others may become irritable or uncharacteristically pessimistic.

Memory loss and slow thinking may occur, although the ability to reason remains intact. Whether people actually suffer intellectual loss (also known as dementia) from Parkinson's disease is a controversial area still being studied.

Difficulty in swallowing and chewing. Muscles used in swallowing may work less efficiently in later stages of the disease. In these cases, food and saliva may collect in the mouth and back of the throat, which can result in choking or drooling. Medications can often alleviate these problems.

Speech changes. About half of all parkinsonian patients have problems with speech. They may speak too softly or in a monotone, hesitate before speaking, slur or repeat their words, or speak too fast. A speech therapist may be able to help patients reduce some of these problems.

Urinary problems or constipation. In some patients bladder and bowel problems can occur due to the improper functioning of the autonomic nervous system, which is responsible for regulating smooth muscle activity. Some people may become incontinent while others have trouble urinating. In others, constipation may occur because the intestinal tract operates more slowly. Constipation can also be caused by inactivity, eating a poor diet, or drinking too little fluid. It can be a persistent problem and, in rare cases, can be serious enough to require hospitalization. Patients should not let constipation last for more than several days before taking steps to alleviate it.

Skin problems. In Parkinson's disease, it is common for the skin on the face to become very oily, particularly on the forehead and at the sides of the nose. The scalp may become oily too, resulting in dandruff. In other cases, the skin can become very dry. These problems are also the result of an improperly functioning autonomic nervous system. Standard treatments for skin problems help. Excessive sweating, another common symptom, is usually controllable with medications used for Parkinson's disease.

Sleep problems. These include difficulty staying asleep at night, restless sleep, nightmares and emotional dreams, and drowsiness during the day. It is unclear if these symptoms are related to the disease or to the medications used to treat Parkinson's disease. Patients should never take over-the-counter sleep aids without consulting their physicians.

What are the Other Forms of Parkinsonism?

Other forms of parkinsonism include the following:
Postencephalitic parkinsonism. Just after the first World War, a viral disease, encephalitis lethargica, attacked almost 5 million people throughout the world, and then suddenly disappeared in the 1920s.

Known as sleeping sickness in the United States, this disease killed one third of its victims and in many others led to post-encephalitic parkinsonism, a particularly severe form of movement disorder in which some patients developed, often years after the acute phase of the illness, disabling neurological disorders, including various forms of catatonia. (In 1973, neurologist Oliver Sacks published Awakenings, an account of his work in the late 1960's with surviving post-encephalitic patients in a New York hospital. Using the then-experimental drug levodopa, Dr. Sacks was able to temporarily "awaken" these patients from their statue-like state. A film by the same name was released in 1990.) In rare cases, other viral infections, including western equine encephalomyelitis, eastern equine encephalomyelitis, and Japanese B encephalitis, can leave patients with parkinsonian symptoms.


Drug-induced parkinsonism. A reversible form of parkinsonism sometimes results from use of certain drugs -- chlorpromazine and haloperidol, for example -- prescribed for patients with psychiatric disorders. Some drugs used for stomach disorders (metoclopramide) and high blood pressure (reserpine) may also produce parkinsonian symptoms. Stopping the medication or lowering the dosage causes the symptoms to abate.


Striatonigral degeneration. In this form of parkinsonism, the substantia nigra is only mildly affected, while other brain areas show more severe damage than occurs in patients with primary Parkinson's disease. People with this type of parkinsonism tend to show more rigidity and the disease progresses more rapidly.


Arteriosclerotic parkinsonism. Sometimes known as pseudoparkinsonism, arteriosclerotic parkinsonism involves damage to brain vessels due to multiple small strokes. Tremor is rare in this type of parkinsonism, while dementia -- the loss of mental skills and abilities -- is common. Antiparkinsonian drugs are of little help to patients with this form of parkinsonism.


Toxin-induced parkinsonism. Some toxins -- such as manganese dust, carbon disulfide, and carbon monoxide -- can also cause parkinsonism. A chemical known as MPTP (1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine) causes a permanent form of parkinsonism that closely resembles Parkinson's disease. Investigators discovered this reaction in the 1980s when heroin addicts in California who had taken an illicit street drug contaminated with MPTP began to develop severe parkinsonism.

This discovery, which demonstrated that a toxic substance could damage the brain and produce parkinsonian symptoms, caused a dramatic breakthrough in Parkinson's research: for the first time scientists were able to simulate Parkinson's disease in animals and conduct studies to increase understanding of the disease.


Parkinsonism-dementia complex of Guam. This form occurs among the Chamorro populations of Guam and the Mariana Islands and may be accompanied by a disease resembling amyotrophic lateral sclerosis (Lou Gehrig's disease). The course of the disease is rapid, with death typically occurring within 5 years.

Some investigators suspect an environmental cause, perhaps the use of flour from the highly toxic seed of the cycad plant. This flour was a dietary staple for many years when rice and other food supplies were unavailable in this region, particularly during World War II. Other studies, however, refute this link.


Parkinsonism accompanying other conditions. Parkinsonian symptoms may also appear in patients with other, clearly distinct neurological disorders such as Shy-Drager syndrome (sometimes called multiple system atrophy), progressive supranuclear palsy, Wilson's disease, Huntington's disease, Hallervorden-Spatz syndrome, Alzheimer's disease, Creutzfeldt-Jakob disease, olivopontocerebellar atrophy, and post-traumatic encephalopathy.

How do Doctors Diagnose Parkinson's Disease?

Even for an experienced neurologist, making an accurate diagnosis in the early stages of Parkinson's disease can be difficult. There are, as yet, no sophisticated blood or laboratory tests available to diagnose the disease. The physician may need to observe the patient for some time until it is apparent that the tremor is consistently present and is joined by one or more of the other classic symptoms. Since other forms of parkinsonism have similar features but require different treatments, making a precise diagnosis as soon as possible is essential for starting a patient on proper medication.

How is the Disease Treated?

At present, there is no cure for Parkinson's disease. But a variety of medications provide dramatic relief from the symptoms.

When recommending a course of treatment, the physician determines how much the symptoms disrupt the patient's life and then tailors therapy to the person's particular condition. Since no two patients will react the same way to a given drug, it may take time and patience to get the dose just right. Even then, symptoms may not be completely alleviated. In the early stages of Parkinson's disease, physicians often begin treatment with one or a combination of the less powerful drugs -- such as the anticholinergics or amantadine (see section entitled "Are There Other Medications Available for Managing Disease Symptoms?"), saving the most powerful treatment, specifically levodopa, for the time when patients need it most.

Levodopa

Without doubt, the gold standard of present therapy is the drug levodopa (also called L-dopa). L- Dopa (from the full name L-3,4-dihydroxyphenylalanine) is a simple chemical found naturally in plants and animals. Levodopa is the generic name used for this chemical when it is formulated for drug use in patients. Nerve cells can use levodopa to make dopamine and replenish the brain's dwindling supply. Dopamine itself cannot be given because it doesn't cross the blood-brain barrier, the elaborate meshwork of fine blood vessels and cells that filters blood reaching the brain. Usually, patients are given levodopa combined with carbidopa. When added to levodopa, carbidopa delays the conversion of levodopa into dopamine until it reaches the brain, preventing or diminishing some of the side effects that often accompany levodopa therapy. Carbidopa also reduces the amount of levodopa needed.

Levodopa's success in treating the major symptoms of Parkinson's disease is a triumph of modern medicine. First introduced in the 1960s, it delays the onset of debilitating symptoms and allows the majority of parkinsonian patients -- who would otherwise be very disabled -- to extend the period of time in which they can lead relatively normal, productive lives.

Although levodopa helps at least three-quarters of parkinsonian cases, not all symptoms respond equally to the drug. Bradykinesia and rigidity respond best, while tremor may be only marginally reduced. Problems with balance and other symptoms may not be alleviated at all.

People who have taken other medications before starting levodopa therapy may have to cut back or eliminate these drugs in order to feel the full benefit of levodopa. Once levodopa therapy starts people often respond dramatically, but they may need to increase the dose gradually for maximum benefit.

Because a high-protein diet can interfere with the absorption of levodopa, some physicians recommend that patients taking the drug restrict protein consumption to the evening meal.

Levodopa is so effective that some people may forget they have Parkinson's disease. But levodopa is not a cure. Although it can diminish the symptoms, it does not replace lost nerve cells and it does not stop the progression of the disease.

Side Effects of Levodopa

Although beneficial for thousands of patients, levodopa is not without its limitations and side effects. The most common side effects are nausea, vomiting, low blood pressure, involuntary movements, and restlessness. In rare cases patients may become confused. The nausea and vomiting caused by levodopa are greatly reduced by the combination of levodopa and carbidopa which enhances the effectiveness of a lower dose. A slow-release formulation of this product, which gives patients a longer lasting effect, is also available.

Dyskinesias, or involuntary movements such as twitching, nodding, and jerking, most commonly develop in people who are taking large doses of levodopa over an extended period. These movements may be either mild or severe and either very rapid or very slow. The only effective way to control these drug-induced movements is to lower the dose of levodopa or to use drugs that block dopamine, but these remedies usually cause the disease symptoms to reappear. Doctors and patients must work together closely to find a tolerable balance between the drug's benefits and side effects.

Other more troubling and distressing problems may occur with long-term levodopa use. Patients may begin to notice more pronounced symptoms before their first dose of medication in the morning, and they can feel when each dose begins to wear off (muscle spasms are a common effect). Symptoms gradually begin to return. The period of effectiveness from each dose may begin to shorten, called the wearing-off effect. Another potential problem is referred to as the on-off effect -- sudden, unpredictable changes in movement, from normal to parkinsonian movement and back again, possibly occurring several times during the day. These effects probably indicate that the patient's response to the drug is changing or that the disease is progressing.

One approach to alleviating these side effects is to take levodopa more often and in smaller amounts. Sometimes, physicians instruct patients to stop levodopa for several days in an effort to improve the response to the drug and to manage the complications of long-term levodopa therapy. This controversial technique is known as a "drug holiday." Because of the possibility of serious complications, drug holidays should be attempted only under a physician's direct supervision, preferably in a hospital. Parkinson's disease patients should never stop taking levodopa without their physician's knowledge or consent because of the potentially serious side effects of rapidly withdrawing the drug.

Are There Other Medications Available for Managing Disease Symptoms?

Levodopa is not a perfect drug. Fortunately, physicians have other treatment choices for particular symptoms or stages of the disease. Other therapies include the following:
Bromocriptine and pergolide. These two drugs mimic the role of dopamine in the brain, causing the neurons to react as they would to dopamine. They can be given alone or with levodopa and may be used in the early stages of the disease or started later to lengthen the duration of response to levodopa in patients experiencing wearing off or on-off effects. They are generally less effective than levodopa in controlling rigidity and bradykinesia.

Side effects may include paranoia, hallucinations, confusion, dyskinesias, nightmares, nausea, and vomiting.


Selegiline. Also known as deprenyl, selegiline has become a commonly used drug for Parkinson's disease. Recent studies supported by the NINDS have shown that the drug delays the need for levodopa therapy by up to a year or more. When selegiline is given with levodopa, it appears to enhance and prolong the response to levodopa and thus may reduce wearing-off fluctuations. In studies with animals, selegiline has been shown to protect the dopamine-producing neurons from the toxic effects of MPTP.

Selegiline inhibits the activity of the enzyme monoamine oxidase B (MAO-B), the enzyme that metabolizes dopamine in the brain, delaying the breakdown of naturally occurring dopamine and of dopamine formed from levodopa. Dopamine then accumulates in the surviving nerve cells. Some physicians, but not all, favor starting all parkinsonian patients on selegiline because of its possible protective effect. Selegiline is an easy drug to take, although side effects may include nausea, orthostatic hypotension, or insomnia (when taken late in the day). Also, toxic reactions have occurred in some patients who took selegiline with fluoxetine (an antidepressant) and meperidine (used as a sedative and an analgesic).

Research scientists are still trying to answer questions about selegiline use: How long does the drug remain effective? Does long-term use have any adverse effects? Evaluation of the long-term effects will help determine its value for all stages of the disease.


Anticholinergics. These drugs were the main treatment for Parkinson's disease until the introduction of levodopa. Their benefit is limited, but they may help control tremor and rigidity. They are particularly helpful in reducing drug-induced parkinsonism. Anticholinergics appear to act by blocking the action of another brain chemical, acetylcholine, whose effects become more pronounced when dopamine levels drop. Only about half the patients who receive anticholinergics respond, usually for a brief period and with only a 30 percent improvement. Although not as effective as levodopa or bromocriptine, anticholinergics may have a therapeutic effect at any stage of the disease when taken with either of these drugs.

Common side effects include dry mouth, constipation, urinary retention, hallucinations, memory loss, blurred vision, changes in mental activity, and confusion.


Amantadine. An antiviral drug, amantadine, helps reduce symptoms of Parkinson's disease. It is often used alone in the early stages of the disease or with an anticholinergic drug or levodopa. After several months amantadine's effectiveness wears off in a third to a half of the patients taking it, although effectiveness may return after a brief withdrawal from the drug. Amantadine has several side effects, including mottled skin, edema, confusion, blurred vision, and depression.

Is Surgery Ever Used to Treat Parkinson's Disease?

Treating Parkinson's disease with surgery was once a common practice. But after the discovery of levodopa, surgery was restricted to only a few cases. One of the procedures used, called cryothalamotomy, requires the surgical insertion of a supercooled metal tip of a probe into the thalamus (a "relay station" deep in the brain) to destroy the brain area that produces tremors. This and related procedures are coming back into favor for patients who have severe tremor or have the disease only on one side of the body. Investigators have also revived interest in a surgical procedure called pallidotomy in which a portion of the brain called the globus pallidus is lesioned. Some studies indicate that pallidotomy may improve symptoms of tremor, rigidity, and bradykinesia, possibly by interrupting the neural pathway between the globus pallidus and the striatum or thalamus. Further research on the value of surgically destroying these brain areas is currently being conducted.

Can Diet or Exercise Programs Help Relieve Symptoms?

Diet. Eating a well-balanced, nutritious diet can be beneficial for anybody. But for preventing or curing Parkinson's disease, there does not seem to be any specific vitamin, mineral, or other nutrient that has any therapeutic value. A high protein diet, however, may limit levodopa's effectiveness.

Despite some early optimism, recent studies have shown that tocopherol (a form of vitamin E) does not delay Parkinson's disease. This conclusion came from a carefully conducted study supported by the NINDS called DATATOP (Deprenyl and Tocopherol Antioxidative Therapy for Parkinson's Disease) that examined, over 5 years, the effects of both deprenyl and vitamin E on early Parkinson's disease. While deprenyl was found to slow the early symptomatic progression of the disease and delay the need for levodopa, there was no evidence of therapeutic benefit from vitamin E.

Exercise. Because movements are affected in Parkinson's disease, exercising may help people improve their mobility. Some doctors prescribe physical therapy or muscle-strengthening exercises to tone muscles and to put underused and rigid muscles through a full range of motion. Exercises will not stop disease progression, but they may improve body strength so that the person is less disabled. Exercises also improve balance, helping people overcome gait problems, and can strengthen certain muscles so that people can speak and swallow better. Exercises can also improve the emotional well-being of parkinsonian patients by giving them a feeling of accomplishment. Although structured exercise programs help many patients, more general physical activity, such as walking, gardening, swimming, calisthenics, and using exercise machines, is also beneficial.

What are the Benefits of Support Groups?

One of the most demoralizing aspects of the disease is how completely the patient's world changes. The most basic daily routines may be affected -- from socializing with friends and enjoying normal and congenial relationships with family members to earning a living and taking care of a home. Faced with a very different life, people need encouragement to remain as active and involved as possible. That's when support groups can be of particular value to parkinsonian patients, their families, and their caregivers.

A list of national volunteer organizations that can help patients locate support groups in their communities appears at the end of this brochure.

Can Scientists Predict or Prevent Parkinson's Disease?

As yet, there is no way to predict or prevent the disease. However, researchers are now looking for a biomarker -- a biochemical abnormality that all patients with Parkinson's disease might share -- that could be picked up by screening techniques or by a simple chemical test given to people who do not have any parkinsonian symptoms.

Positron emission tomography (PET) scanning may lead to important advances in our knowledge about Parkinson's disease. PET scans of the brain produce pictures of chemical changes as they occur in the living brain. Using PET, research scientists can study the brain's dopamine receptors (the sites on nerve cells that bind with dopamine) to determine if the loss of dopamine activity follows or precedes degeneration of the neurons that make this chemical. This information could help scientists better understand the disease process and may potentially lead to improved treatments.

What Research is Being Done?

In the last decade research has laid the groundwork for many of today's promising new clinical trials, technologies, and drug treatments. Scientists, physicians, and patients hope that today's progress means tomorrow's cure and prevention.

Parkinson's disease research focuses on many areas. Some investigators are studying the functions and anatomy of the motor system and how it regulates movement and relates to major command centers in the brain. Scientists looking for the cause of Parkinson's disease will continue to search for possible environmental factors, such as toxins that may trigger the disorder, and to study genetic factors to determine if one or many defective genes play a role. Although Parkinson's disease is not directly inherited, it is possible that some people are genetically more or less susceptible to developing it. Other scientists are working to develop new protective drugs that can delay, prevent, or reverse the disease.

Since the accidental discovery that MPTP causes parkinsonian symptoms in humans, scientists have found that by injecting MPTP into laboratory animals, they can reproduce the brain lesions that cause these symptoms. This allows them to study the mechanisms of the disease and helps in the development of new treatments. For instance, it was from animal studies that researchers discovered that the drug selegiline can prevent the toxic effects of MPTP. This discovery helped spark interest in studying selegiline as a preventive treatment in humans.

Scientists are also investigating the role of mitochondria, structures in cells that provide the energy for cellular activity, in Parkinson's disease. Because MPTP interferes with the function of mitochondria within nerve cells, some scientists suspect that similar abnormalities may be involved in Parkinson's disease.

Today, an array of promising research involves studying brain areas other than the substantia nigra that may be involved in the disease. One group of NINDS-supported scientists is studying the consequences of dopamine cell degeneration in the basal ganglia -- brain structures located deep in the forebrain that help control voluntary movement. In laboratory animals, MPTP-induced reduction of dopamine results in overactivity of nerve cells in a region of the brain called the subthalamic nucleus, producing tremors and rigidity and suggesting that these symptoms may be related to excessive activity in this region. Destroying the subthalamic nucleus results in a reversal of parkinsonian symptoms in the animal models.

Scientists supported by the NINDS are also looking for clues to the cause of Parkinson's disease by studying malfunctions in the structures called "dopamine transporters" that carry dopamine in and out of the synapse, or narrow gap between nerve cells. For example, one research group recently found an age-related decrease in the concentration of dopamine transporters in healthy human nerve cells taken from areas of the brain damaged by Parkinson's. This decline in transporter concentration means that any further threat to the remaining dopamine transporters could result in Parkinson's disease.

The search for more effective medications for Parkinson's disease is likely to be aided by the recent isolation of at least five individual brain receptors for dopamine. New information about the unique effects of each individual dopamine receptor on different brain areas has led to new treatment theories and clinical trials.

Scientists are also studying new methods for delivering dopamine to critical areas in the brain. NINDS-supported investigators, using an animal model of the disease, implanted tiny dopamine-containing particles into brain regions affected by the disease. They found that such implants can partially ameliorate the movement problems exhibited by these animals. The results suggest that similar techniques may one day work for people with Parkinson's disease.

A recent study revealed that when the experimental drug Ro 40-7592 is added to the standard drug treatment for Parkinson's disease, levodopa-carbidopa, symptom relief is prolonged by more than 60 percent. Although levodopa-carbidopa restores normal movement early in the disease's course, the treatment loses effectiveness as the disease progresses (wearing-off effect). NINDS scientists found, however, that patients treated with both levodopa-carbidopa and Ro 40-7592 experienced longer periods of improved movement. This promising new drug that blocks the breakdown of dopamine and levodopa would allow patients to take fewer doses and smaller amounts of levodopa-carbidopa and to decrease the problems of the wearing-off effect. At the present time, Ro 40-7592 is still in the experimental stage. Scientists are continuing to study the drug to learn whether it can be given in multiple daily doses to provide even further improvement.

Also under investigation are additional controlled-release formulas of Parkinson's disease drugs and implantable pumps that give a continuous supply of levodopa to help patients who have problems with fluctuating levels of response. Another promising treatment method involves implanting capsules containing dopamine-producing cells into the brain. The capsules are surrounded by a biologically inert membrane that lets the drug pass through at a timed rate.

Neural grafting, or transplantation of nerve cells, is an experimental technique proposed for treating the disease. NINDS-supported investigators have shown in animal models that implanting fetal brain tissue from the substantia nigra into a parkinsonian brain causes damaged nerve cells to regenerate. In January 1994, the NINDS awarded a research grant to a group of scientists from three institutions to conduct a controlled clinical trial of fetal tissue implants in humans. The treatment attempts to replace the lost or damaged dopamine-producing neurons with healthy, fetal neurons, and thereby improve movement and response to medications. A new and promising approach may be the use of genetically engineered cells -- that is, cells such as modified skin cells that do not come from the nervous system but are grown in tissue culture -- that could have the same beneficial effects. Skin cells would be much easier to harvest and patients could serve as their own donors.

What is the Role of the NINDS?

As a world leader in research on neurological disorders, including Parkinson's disease, the NINDS supports a wide range of basic laboratory studies and clinical trials at its Bethesda, Maryland, location and at grantee institutions around the world. Current research programs funded by the NINDS include using animal models to study how the disease progresses, developing new drug therapies, and implanting tissue in animals and humans. Through these and other research projects, scientists are moving ever closer to unraveling the mysteries of Parkinson's disease. For patients and families of patients, this research should offer encouragement and hope for the future.

The Institute also sponsors an active information program that provides patients and the general public with educational materials and research highlights. Among the NINDS publications that may be of interest to those concerned about Parkinson's disease is "Know Your Brain," an 8-page fact sheet that explains how the healthy brain works and what happens when the brain is diseased or dysfunctional. The Institute's address and phone number, as well as information on other organizations that offer various services to those affected by Parkinson's disease, are provided on the information resources card enclosed in the back pocket of this brochure.

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Early Alzheimer's Disease

Patient and Family Guide

Terms You Need to Know

Dementia is a medical condition that interferes with the way the brain works. Symptoms include anxiety, paranoia, personality changes, lack of initiative, and difficulty acquiring new skills. Besides Alzheimer's disease, some other types or causes of dementia include: alcoholic dementia, depression, delirium, HIV/AIDS-related dementia, Huntington's disease (a disorder of the nervous system), inflammatory disease (for example, syphilis), vascular dementia (blood vessel disease in the brain), tumors, and Parkinson's disease.

Alzheimer's disease is the most common form of dementia. It proceeds in stages over months or years and gradually destroys memory, reason, judgment, language, and eventually the ability to carry out even simple tasks.

Delirium is a state of temporary but acute mental

confusion that comes on suddenly. Symptoms may include anxiety, disorientation, tremors, hallucinations, delusions, and incoherence. Delirium can occur in older persons who have short-term illnesses, heart or lung disease, long-term infections, poor nutrition, or hormone disorders. Alcohol or drugs (including medications) also may cause confusion.

Delirium may be life-threatening and requires immediate medical attention.

Depression can occur in older persons, especially those with physical problems. Symptoms include sadness, inactivity, difficulty thinking and concentrating, and feelings of despair. Depressed persons often have trouble sleeping, changes in appetite, fatigue, and agitation. Depression usually can be treated successfully.



Purpose of this Booklet This booklet is about Alzheimer's disease and other types of dementia. It presents information for patients, family members, and other caregivers. It talks about the effects Alzheimer's disease can have on you, your family members, and your friends.

The booklet describes the early signs and symptoms of Alzheimer's disease. Sources of medical, social, and financial support are listed in the back of the booklet. This booklet is not about treating Alzheimer's disease.



What Is Alzheimer's Disease?

In Alzheimer's disease and other dementias, problems with memory, judgment, and thought processes make it hard for a person to work and take part in day-to-day family and social life. Changes in mood and personality also may occur. These changes can result in loss of self-control and other problems.

Some 2 to 4 million persons have dementia associated with aging. Of these individuals, as many as two-thirds have Alzheimer's disease.

Although there is no cure for Alzheimer's disease at this time, it may be possible to relieve some of the symptoms, such as wandering and incontinence.

The earlier the diagnosis, the more likely your symptoms will respond to treatment. Talk to your doctor as soon as possible if you think you or a family member may have signs of Alzheimer's disease.

Research is under way to find better ways to treat Alzheimer's disease. Ask your doctor if there are any new developments that might help you.



Who Is Affected? The chances of getting Alzheimer's disease increase with age. It usually occurs after age 65. Most people are not affected even at advanced ages. There are only two definite factors that increase the risk for Alzheimer's disease: a family history of dementia and Down syndrome.

Family History of Dementia Some forms of Alzheimer's disease are inherited. If Alzheimer's disease has occurred in your family members, other members are more likely to develop it. Discuss any family history of dementia with your family doctor.

Down Syndrome Persons with Down syndrome have a higher chance of getting Alzheimer's disease. Close relatives of persons with Down syndrome also may be at risk.

What Are the Signs of Alzheimer's Disease? The classic sign of early Alzheimer's disease is gradual loss of short-term memory. Other signs include:


Problems finding or speaking the right word.
Inability to recognize objects.
Forgetting how to use simple, ordinary things, such as a pencil.
Forgetting to turn off the stove, close windows, or lock doors. Mood and personality changes also may occur. Agitation, problems with memory, and poor judgment may cause unusual behavior. These symptoms vary from one person to the next.



Symptoms appear gradually in persons with Alzheimer's disease but may progress more slowly in some persons than in others. In other forms of dementia, symptoms may appear suddenly or may come and go.

If you have some of these signs, this does not mean you have Alzheimer's disease. Anyone can have a lapse of memory or show poor judgment now and then. When such lapses become frequent or dangerous, however, you should tell your doctor about them immediately.



Possible Signs of Alzheimer's Disease Do you have problems with any of these activities:


Learning and remembering new information. Do you repeat things that you say or do? Forget conversations or appointments? Forget where you put things?
Handling complex tasks. Do you have trouble performing tasks that require many steps such as balancing a checkbook or cooking a meal?
Reasoning ability. Do you have trouble solving everyday problems at work or home, such as knowing what to do if the bathroom is flooded?
Spatial ability and orientation. Do you have trouble driving or finding your way around familiar places?
Language. Do you have trouble finding the words to express what you want to say?
Behavior. Do you have trouble paying attention? Are you more irritable or less trusting than usual? Remember, everyone has occasional memory lapses. Just because you can't recall where you put the car keys doesn't mean you have Alzheimer's disease.



Consulting the Doctor Identifying mild cases of Alzheimer's disease can be very difficult. Your doctor will review your health and mental status, both past and present. Changes from your previous, usual mental and physical functioning are especially important.

Persons with Alzheimer's disease may not realize the severity of their condition. Your doctor will probably want to talk with family members or a close friend about their impressions of your condition.

The doctors first assessment for Alzheimer's disease should include a focused history, a physical examination, a functional status assessment, and a mental status assessment.

Medical and Family History Questions the doctor may ask in taking your history include: How and when did problems begin? Have the symptoms progressed in steps or worsened steadily? Do they vary from day to day? How long have they lasted?

Your doctor will ask about past and current medical problems and whether other family members have had Alzheimer's disease or another form of dementia.



Education and other cultural factors can make a difference in how you will do on mental ability tests. Language problems (for example, difficulty speaking English) can cause misunderstanding. Be sure to tell the doctor about any language problems that could affect your test results.

It is important to tell the doctor about all the drugs you take and how long you have been taking them. Drug reactions can cause dementia. Bring all medication bottles and pills to the appointment with your doctor.

Do you take any medications? Even over-the-counter drugs, eye drops, and alcohol can cause a decline in mental ability. Tell your doctor about all the drugs you take. Ask if the drugs are safe when taken together.

Physical Examination A physical examination can determine whether medical problems may be causing symptoms of dementia. This is important because prompt treatment may relieve some symptoms.

Functional Status Assessment The doctor may ask you questions about your ability to live alone. Sometimes, a family member or close friend may be asked how well you can do activities like these:


Write checks, pay bills, or balance a checkbook.
Shop alone for clothing, food, and household needs.
Play a game of skill or work on a hobby.
Heat water, make coffee, and turn off stove.
Pay attention to, understand, and discuss a TV show, book, or magazine.
Remember appointments, family occasions, holidays, and medications.
Travel out of the neighborhood, drive, or use public transportation. Sometimes a family member or friend is not available to answer such questions. Then, the doctor may ask you to perform a series of tasks ("performance testing").

Mental Status Assessment Several other tests may be used to assess your mental status. These tests usually have only a few simple questions. They test mental functioning, including orientation, attention, memory, and language skills. Age, educational level, and cultural influences may affect how you perform on mental status tests. Your doctor will consider these factors in interpreting test results.

Alzheimer's disease affects two major types of abilities:

1. The ability to carry out everyday activities such as bathing, dressing, using the toilet, eating, and walking.

2. The ability to perform more complex tasks such as using the telephone, managing finances, driving a car, planning meals, and working in a job.

When a person has Alzheimer's disease, problems with complex tasks appear first and over time progress to more simple activities.

Treatable Causes of Dementia Sometimes the physical examination reveals a condition that can be treated. Symptoms may respond to early treatment when they are caused by:


Medication (including over-the-counter drugs)
Alcohol
Delirium
Depression
Tumors
Problems with the heart, lungs, or blood vessels
Metabolic disorders (such as thyroid problems)
Head injury
Infection
Vision or hearing problems Drug reactions are the most common cause of treatable symptoms. Older persons may have reactions when they take certain medications. Some medications should not be taken together. Sometimes, adjusting the dose can improve symptoms.

Delirium and depression may be mistaken for or occur with Alzheimer's disease. These conditions require prompt treatment. See the inside front cover of this booklet for more information on delirium and depression.



Special Tests Gathering as much information as possible will help your doctor diagnose early Alzheimer's disease while the condition is mild. You may be referred to other specialists for further testing. Some special tests can show a persons mental strengths and weaknesses and detect differences between mild, moderate, and severe impairment. Tests also can tell the difference between changes due to normal aging and those caused by Alzheimer's disease.

If you go to a special doctor for these tests, he or she should return all test results to your regular family doctor. The results will help your doctor track the progress of your condition, prescribe treatment, and monitor treatment effects.



Getting the Right Care When the diagnosis is Alzheimer's disease, you and your family members have serious issues to consider. Talk with your doctor about what to expect in the near future and later on, as your condition progresses. Getting help early will help ensure that you get the care that is best for you.

When tests do not indicate Alzheimer's disease, but your symptoms continue or worsen, check back with your doctor. More tests may be needed. If you still have concerns, even though your doctor says you do not have Alzheimer's disease, you may want to get a second opinion.

Whatever the diagnosis, follow-up is important.

Report any changes in your symptoms. Ask the doctor what follow-up is right for you. Your doctor should keep the results of the first round of tests for later use. After treatment of other health problems, new tests may show a change in your condition.

Recognizing Alzheimer's disease in its early stages, when treatment may relieve mild symptoms, gives you time to adjust. During this time, you and your family can make financial, legal, and medical plans for the future.

Coordinating Care Your health care team may include your family doctor and medical specialists such as psychiatrists or neurologists, psychologists, therapists, nurses, social workers, and counselors. They can work together to help you understand your condition, suggest memory aids, and tell you and your family about ways you can stay independent as long as possible.

Talk with your doctors about activities that could be dangerous for you or others, such as driving or cooking. Explore different ways to do things.

Telling Family and Friends Ask your doctor for help in telling people who need to know that you have Alzheimer's disease members of your family, friends, and coworkers, for example.

Alzheimer's disease is stressful for you and your family. You and your caregiver will need support from others. Working together eases the stress on everyone.



Where To Get Help? Learning that you have Alzheimer's disease can be very hard to deal with. It is important to share your feelings with family and friends.

Many kinds of help are available for persons with Alzheimer's disease, their families, and caregivers. Turn to the back of this booklet for a list of resources for patients and families. These resources include:


Support groups. Sometimes it helps to talk things over with other people and families who are coping with Alzheimer's disease. Families and friends of people with Alzheimer's disease have formed support groups. The Alzheimer's Association has active groups across the country. Many hospitals also sponsor education programs and support groups to help patients and families.


Financial and medical planning. Time to plan can be a major benefit of identifying Alzheimer's disease early. You and your family will need to decide where you will live and who will provide help and care when you need them.


Legal matters. It is also important to think about certain legal matters. An attorney can give you legal advice and help you and your family make plans for the future. A special document called an advance directive lets others know what you would like them to do if you become unable to think clearly or speak for yourself.

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