Health Tip: Giving Medications to People With Alzheimer's

(HealthDay News) -- As a caregiver of someone with Alzheimer's, administering their medication -- and preventing missed pills or the wrong dosages -- can be a daunting responsibility.


The Alzheimer's Association offers these suggestions:

• Learn about each medication before you administer it. Make sure you know exactly what each pill is for, and its possible side effects.


• In clear language, explain exactly what each pill is for, and why and how the person needs to take it.


• Keep good records of each medication taken, the dose, and when taken.


• Keep medications well-organized, and safely stored out of reach in a locked cabinet or drawer.


• Don't let taking medicine turn into a struggle. If the person doesn't want to take it at a particular moment, try again a bit later.


• Make the task as easy as possible. Ask your pharmacist for liquid, which may be easier to administer than a pill. Or ask the pharmacist if you can crush the pill and put it in food.

Green Tea Antioxidant May Help Prevent Alzheimer's

(HealthDay News) -- An antioxidant found in green tea appears to prevent the development of amyloid fibrils, a toxic protein associated with Alzheimer's and Parkinson's disease, a new study finds.

Amyloid plaque is commonly seen in the brains of Alzheimer's patients and appears to disrupt the function of cells. Strategies to prevent the development of amyloid plaque are one avenue being explored in the prevention and treatment of Alzheimer's.

Now, a German team says the tea antioxidant, called epigallocatechin gallate (EGCG), has potent anti-plaque ability.

"We can use small molecules like EGCG to convert certain misfolded structures of a protein into a new type of molecule, which is less toxic or not toxic for cells," said lead researcher Erich Wanker, from the Max Delbrueck Center for Molecular Medicine in Berlin.

The findings are published in the May 30 online edition of Nature Structural & Molecular Biology.

The accumulation of amyloid plaque in Alzheimer's and other neurodegenerative diseases, such as Parkinson's, are thought to be caused by the misfolding of certain proteins, which then become toxic to cells. The way proteins fold is key to their function, the researchers explained.

In experiments in the laboratory, the German team found that EGCG seems to change potentially harmful proteins into proteins that are not detrimental to brain cells. "We are able to convert a toxic structure into a less toxic structure," Wanker explained.

Because EGCG binds to unfolded proteins -- which are not associated with Alzheimer's -- the discovery could lead to medications that recognize the more troublesome proteins and convert them to harmless substances.

"This method could be more generally used to get rid of or remove the concentration of misfolded proteins in cells," Wanker said. "This strategy should be tested with patients. If treated early on, it could prevent the formation of amyloid plaque," he speculated.

Whether this type of treatment could reverse plaques that have already formed in the brain isn't known, Wanker said.

He noted that the study remains basic science, and he was cautious about recommending green tea as a way of preventing Alzheimer's disease. "I don't want to do a lot of speculating which could point people in the direction that could be harmful," Wanker said. "We have to go step-by-step."

One expert believes the approach could yield real results, however.

"Red wine, yellow curry and green tea have suspected health benefits because of high content of antioxidants," said Greg M. Cole, a neuroscientist at the Greater Los Angeles VA Healthcare System, and associate director of the Alzheimer's Disease Research Center at UCLA David Geffen School of Medicine. He was not involved in the study.

"This study provides evidence that a compound called EGCG, one of the major polyphenols in green tea, may be useful for diseases like Parkinson's and Alzheimer's, because it can block the formation of the filament-forming protein aggregates implicated in causing disease," Cole said.

One novel aspect of the study is the authors' demonstration that EGCG prevents toxic filament formation by redirecting the aggregating proteins to make non-toxic proteins, Cole said.

"This is surprising, because similar protein aggregate spheres called amyloid oligomers can be highly toxic to neurons and synapses," Cole said. "It will be important for the authors to prove that the EGCG-directed proteins also lack toxicity to synapses which were not present in the systems used to test toxicity," he said.

Assuming that the green tea compound has a stable effect and chronically blocks toxicity to real neurons and synapses, it could have genuine potential for Alzheimer's patients, Cole said.

"The major caveat is the very poor absorption and delivery of EGCG seen in some studies," Cole said. The fact that EGCG isn't available for patenting by pharmaceutical companies might be a problem, too, he said, since it could "limit the investment needed for clinical trials of sufficient size to prove that it really works."

In related research, a team of American scientists said that interrupting a key signaling pathway in immune system cells allowed those cells to enter the brain and attack and remove amyloid plaque.

Reporting May 30 in Nature Medicine, a team led by research scientist Terrence Town, of Cedars-Sinai Medical Center, Los Angeles, conducted their study in genetically engineered mice. The group blocked a molecule that typically suppresses a portion of the immune response. Once the system was freed up, immune cells called macrophages made their way to the brains and devoured up to 90 percent of amyloid plaques, the team said.

"If these experimental animals are representative of the clinical syndrome of Alzheimer's disease, we may have a therapeutic target that we did not have before," study co-author Dr. Jun Tan, of the University of South Florida, said in a statement.

More information
For more about Alzheimer's disease, visit the Alzheimer's Association.

Caffeine May Block High Cholesterol Linked to Alzheimer's

(HealthDay News) -- A little caffeine every day could offer some protection from Alzheimer's disease for people with high cholesterol.

Rabbits given the daily caffeine equivalent of one cup of coffee and fed a cholesterol-rich diet for 12 weeks suffered relatively little damage in their blood-brain barrier (BBB), which protects the central nervous system from the rest of the body's circulation, new research found.

The findings were published in the open-access publication Journal of Neuroinflammation.

Previous studies have shown that high levels of cholesterol break down the BBB, exposing the central nervous system to damage from blood-borne contamination. BBB leakage occurs in a variety of neurological disorders such as Alzheimer's disease.

"High levels of cholesterol are a risk factor for Alzheimer's disease, perhaps by compromising the protective nature of the blood-brain barrier. For the first time, we have shown that chronic ingestion of caffeine protects the BBB from cholesterol-induced leakage," Jonathan Geiger, of the University of North Dakota School of Medicine and Health Sciences, said in a prepared statement.

Caffeine appears to offer protection by helping proteins maintain the tight binding of the cells in the BBB, so they stop unwanted molecules from entering the central nervous system.

The findings also confirm previous studies showing that caffeine protects against memory loss in aging and in Alzheimer's disease.

"Caffeine is a safe and readily available drug, and its ability to stabilize the blood-brain barrier means it could have an important part to play in therapies against neurological disorders," Geiger said.

More information
The U.S. National Institute on Aging has more about Alzheimer's medications.

Scientists Turn Human Skin Cells Into Stem Cells

(HealthDay News) -- Two separate groups of scientists have succeeded in turning human skin cells into cells that are very similar -- but not identical -- to embryonic stem cells.

The two teams, one based in Japan and the other in Wisconsin, used slightly different methods to achieve essentially identical goals, researchers said.

"Embryonic stem cells can divide forever, and there has never been good evidence for such cells in adults, but this new paper shows a method to make cells essentially identical to embryonic stem cells," said James Thomson, senior author of the Wisconsin study and a professor in the departments of medicine and public health at the University of Wisconsin-Madison. "This will change the ethical debate," he said at a teleconference held Tuesday.

"We are now in a position to be able to generate patient- and disease-specific stem cells, without using human eggs or embryos," added Dr. Shinya Yamanaka, senior author of the first paper, who is affiliated with Kyoto University in Japan and the Gladstone Institute of Cardiovascular Disease in San Francisco. "These cells should be useful in understanding disease mechanisms, searching for effective and safe drugs, and treating patients with cell therapy," he said.

One outside exert agreed the achievement could shift research away from embryonic stem cells.
"Here's verification of another source of multipotent cells that could be useful for treating disease and would get around some of the ethical issues related to embryonic sources," Paul Sanberg, distinguished professor of neurosurgery and director of the University of South Florida Center for Aging and Brain Repair in Tampa, told HealthDay. "It also demonstrates that there are many cells that can be reprogrammed in the body, and this is not going to be the last time we hear of other types of cells and other ways we can make multipotent."

Multipotency or pluripotency refers to the ability of stem cells to grow into a variety of cell types.
However, the journey from laboratory to patient therapy is still a long one, experts said.
"This is a proof of principle, but, in terms of application, there are many steps in between," said Dr. Robert Tsai, assistant professor in the Center for Cancer and Stem Cell Biology at Texas A&M Health Science Center Institute of Biosciences and Technology in Houston.

The achievements followed closely on the heels of another breakthrough: Last week, U.S. scientists announced that they had created dozens of cloned embryos from a 10-year-old male macaque, a primate. This puts science one step closer to human cloning, those authors stated.

Embryonic stem cells are pluripotent, meaning they have the ability to develop into virtually any cell type in the body. The hope is that such cells may one day yield treatments or cures for diseases such as diabetes, liver failure, spinal injury, stroke, Alzheimer's disease and heart disease.

However, harvesting embryonic stem cells involves destroying a viable embryo, stirring much political debate. In the United States, embryonic stem cell research has been severely limited since August 2001, when President George W. Bush placed limits on federal funding of the field and restricted the number of embryonic stem cell lines that could be used.

Since that time, researchers have been racing to find other sources of viable stem cells. The approach documented in these two studies would circumvent the need for embryos and, thus, would bypass any controversy. The findings of Yamanaka's team are detailed in the Nov. 30 print issue of Cell, and the Wisconsin group's work was released online Tuesday by Science.

Last year, Yamanaka's team transformed mouse skin cells into pluripotent stem cells.

This year, the researchers tried the same method in humans: using a retrovirus to activate specific transcription genes in the skin cells. Transcription genes regulate gene expression, explained Yamanaka.

Using this method, his group generated about 10 cell clones from 50,000 human facial skin cells.
The new "induced pluripotent stem" (iPS) cells were identical to embryonic stem cells in terms of appearance and behavior in cell culture. They also expressed genetic markers that were the same as those observed in embryonic stem cells.

The iPS cells could also differentiate into other tissue types, the team found.

However, a screen of more than 30,000 genes showed that the iPS cells were not actually indistinguishable from embryonic stem cells. In fact, roughly 1,000 genes were expressed differently.

"Human iPS cells are similar, but not identical, to human embryonic stem cells, Yamanaka said. "DNA microarray analyses identified differentially expressed genes between the two stem cell lines. Further studies are required to determine whether human iPS cells can replace human ES cells."

The team at the University of Wisconsin-Madison also used human skin cells, then added two of the same genes as Yamanaka's team and two different genes in their approach. The outcome was essentially the same.

"The actual combination of the factors they put in are different, the rationale is the same," Tsai explained. "There are some tiny differences between the two different combinations."

The advent of the new cells does not render embryonic stem cells unnecessary, however.

"This does not mean that it is the end of embryonic stem cell research, if only that we need a gold standard to compare to," the University of Wisconsin's Thomson told reporters. "Over time, I believe embryonic stem cells will be used by fewer and fewer labs. These new stem cells would not have been derived if it had not been for the last 10 years of research on embryonic stem cell lines. I do, nonetheless, think that the world has changed."

Can the newly designed cells be used to clone humans? "Any cell in the body can do that," Thomson said. "It's probably true of these cells, if you manipulate them enough, but not if you put them in the body as they are."

It's not clear in either of the two new studies if the cells are completely pluripotent or if one line is more efficient than the other. "Will they have the ability to fully differentiate?" Tsai asked. "There's some evidence that they can move from a differentiated state to an undifferentiated state, but will they be able to reverse back?"

"We have to be sure the cells are safe," Yamanaka said. "One of the difficulties about human embryonic stem cells is their tumorigenicity [propensity to develop tumors]. Because of the usage of retroviruses, iPS cells may be more tumorigenic than human embryonic stem cells. We will have to find a way to avoid retroviruses."

But for the more immediate purposes of drug discovery and toxicology, the use of retroviruses is not a big problem, Yamanaka added.

iPS may present their own ethical concerns, however, if they are used to generate sperm and egg cells. "This might help people with infertility problems, but it will be essential to have proper regulation regarding the generation and usage of human iPS cells to avoid misusages of this technology," Yamanaka said.

More information
Learn more about stem cells at the International Society for Stem Cell Research.

Gene Mutation Linked to Parkinson's Disease

(HealthDay News) -- People who carry a certain gene mutation appear to have a greater risk for getting Parkinson's disease and for getting it at a relatively early age, new research suggests.

The study authors also found that because Ashkenazi Jews -- those with an Eastern European background-- are more likely to carry this gene mutation, this population may run an even higher risk for the disease. An estimated 90 percent of American Jews are of Ashkenazi lineage.

Study lead author Lorraine N. Clark, a researcher at Columbia University, described her team's findings as "unique and different."

"We specifically compared patients who had an early onset Parkinson's before age 50 with patients who had a later onset after age 50, and also with patients with and without Jewish ancestry," she said. "And we showed that mutations are twice as common among early onset Parkinson's and also that they're more frequent among patients with Jewish ancestry."

Clark serves as an assistant professor in the department of clinical pathology with the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, as well as the Center for Human Genetics, both at Columbia University.

The findings are published in the Sept. 18 issue of the journal Neurology.

Parkinson's disease is a brain disorder that affects 1.5 million Americans, according to National Parkinson Foundation estimates. Approximately 60,000 news cases occur each year, striking men and women equally, usually over the age of 65.

The disease is characterized by widespread damage to dopamine-producing nerve cells, impeding their ability to regulate body movement and muscle control. Key signs of the disease include tremors, stiffness, balance problems, and slowness of movement. Patients may also experience difficulty with speech and depression. There is no known cure.

To explore potential genetic underpinnings to the onset of Parkinson's, Clark and her colleagues decided to focus on the GBA gene. Mutations of this gene have already been identified as the cause of Gaucher disease, a rare fat-storage disorder that disrupts spleen and brain function.

Gaucher's and Parkinson's have some links, the study authors noted. In some cases, Gaucher's patients have a family history of Parkinson's, while others actually develop neurological features of Parkinson's. It is also one of the most prevalent genetic illnesses among Ashkenazi Jews.

For the new study, the researchers conducted a sequencing analysis of the GBA gene among 278 Parkinson's patients, 178 of who were of Jewish ancestry dating back to all four grandparents. A similar analysis was done among 179 men and women without Parkinson's.

Clark and her team found that 14 percent of the Parkinson's patients had GBA mutations, compared to just 5 percent of the healthy patients. And, while GBA mutations were found among 22 percent of Parkinson's patients who were diagnosed with their illness before the age of 50, only 10 percent of patients diagnosed after 50 had such abnormalities.

Teasing out information on Jewish patients, the researchers found that while nearly 17 percent of Jewish Parkinson's patients had GBA mutations, the figure was 8 percent among non-Jewish Parkinson's patients.

Clark called the study findings preliminary, and she cautioned that it remains unclear whether a single GBA mutation is a cause of Parkinson's or merely a part of a larger puzzle.

Still, she believes the findings could prove helpful in opening up new avenues of research into the disease.

"This is a gene we hadn't really thought about before," she said. "And it implicates new pathways that might be important in the pathogenesis of Parkinson's disease which could lead to the development of new treatment strategies. I do think, however, that further studies are needed in larger patient populations before we could use this work in diagnostic testing and counseling."

Robin Elliott, executive director of the Parkinson's Disease Foundation in New York City, called the new research "very interesting and very worthwhile, solid work in one of the most fruitful areas of Parkinson's research.

"Genetics and the study of genetics has been one of the most exciting areas of Parkinson's in the last 10 years," he said. "In 1996, we had not a single gene associated with the disease, and now it's up to 12 or 13. So, this is a very important study that pushes the science even further, and gives us the basis for more work."

More information
To learn more, visit the Parkinson's Disease Foundation.

First Skin Patch Sanctioned for Alzheimer's

(HealthDay News) -- The Exelon skin patch (rivastigmine transdermal system) has been approved by the U.S. Food and Drug Administration to treat dementia associated with mild-to-moderate Alzheimer's disease, maker Novartis Pharmaceuticals said Monday.

Exelon, approved in 2000 in capsule form to treat Alzheimer's dementia and in 2006 to treat Parkinson's dementia, can cause gastrointestinal side effects typical of its class of drug, called cholinesterase inhibitors.

The skin patch, while maintaining a steady supply of the drug over 24 hours, showed three times fewer reports of nausea and vomiting than the capsule form, Novartis said.

As with the capsule form, the company recommended that the medicated patch be used with caution in people with a history of so-called "sick sinus syndrome," ulcers, asthma and other chronic lung diseases, seizures, or urinary obstruction.

More information
For more information about this drug, visit the U.S. National Library of Medicine.

Marijuana-Like Compound May Slow Alzheimer's

(HealthDay News) -- A new U.S. study finds that marijuana may help slow the progression of Alzheimer's, while a second report suggests the "club drug" Ecstasy could yield insights into Parkinson's disease.

Both findings were presented Wednesday at the annual meeting of the Society for Neuroscience, in Atlanta.

In the first presentation, researchers from Ohio State University in Columbus found that marijuana may contain compounds that can slow memory loss associated with Alzheimer's disease.

In their study involving rats, a team led by psychology professor Gary Wenk searched for ways to reduce Alzheimer's-linked brain inflammation.

Wenk was already familiar with data that found that long-term marijuana users had lower rates of Alzheimer's disease than the general population. His team sought to find a compound that might reduce disease-linked brain inflammation but avoid the drug's psychoactive effects.
"We are using a component of marijuana that stimulates the same centers in the brain that marijuana does," Wenk said. The synthetic compound, which is very similar in composition to marijuana, is called WIN-55212-2 (WIN).

Experiments conducted on young and old rats revealed that WIN is "a very effective anti-inflammatory, it reduces brain inflammation," Wenk said.

What makes this discovery special is that this compound can cross the blood-brain barrier, Wenk explained. The results of a special rat "maze test" suggested that WIN "also reversed the memory impairment in the older rats," he said.

Brain inflammation is characteristic of many diseases other than Alzheimer's, including multiple sclerosis, ALS, AIDS, Huntington's and Parkinson's, Wenk noted. "We are beginning to notice that brain inflammation is always in the background as people get older," he said. "Inflammation doesn't cause the disease, it contributes to the pathology," he said.

WIN is not appropriate for use in humans because it still contains substances that may trigger a "high." However, Wenk hopes that some form of this compound might be used to benefit people with neurological diseases.

"We have the added advantage that millions of doses [of marijuana] have been taken by millions of people over the past centuries," he said. "We already know a lot about its actions in the body and its toxicity, or lack of toxicity. The only problem we have is that it's illegal."

Wenk is not suggesting that Alzheimer's patients start using marijuana. "Patients would have to be so careful not to get too much," he said. "That would only worsen the symptoms of their dementia."
The challenge is to find a dose that has an anti-inflammatory effect but does not make patients high, Wenk said. "It's hopeful," he said, "but it's not a therapy until we find a way to make it work in humans."

One expert believes it may be possible to derive therapeutic benefits from marijuana without inducing other effects that could be harmful to Alzheimer's patients.

"These are still early days for thinking about drugs derived from cannabis," said Dr. Samuel Gandy, director of the Farber Institute for Neurosciences at Thomas Jefferson University in Philadelphia.
"Still, we know the structure of tetrahydrocannabinol (THC) [the active ingredient in cannabis] in detail, and it is not inconceivable that helpful THC-based drugs could be created chemically that benefit brain function but lack the 'high' that currently stigmatizes the compound," Gandy added.

In the second report, researchers from the University of Cincinnati found that, in rats, MDMA (methylenedioxymethamphetamine) -- more commonly known as the illegal drug Ecstasy -- increases the survival of dopamine-releasing cells in the brain during fetal development.
"The club drug Ecstasy can cause dopamine neurons to grow and prevent them from dying off," explained lead researcher Jack Lipton, a professor of psychiatry.

Dopamine cells are critical to the regulation of voluntary movement. This discovery might lead to better therapies for neurological diseases such as Parkinson's, the researchers said.
Ecstasy, as is, is not beneficial for Parkinson's patients, Lipton cautioned. But a part of MDMA may be.

The trick now is to find the components of MDMA that have this effect on dopamine cells and develop ways to use it to help Parkinson's patients, Lipton said. It could also be used as an adjunct to stem cell transplantation, something that's now being studied in Parkinson's patients.
"It could help transplants take better and have more cells survive," Lipton said.

More information
There's more on Alzheimer's disease at the Alzheimer's Association.

'Quilt to Remember' Honors Those Struggling With Alzheimer's

(HealthDay News) -- The first stitches will soon be sewn in a giant U.S. "national quilt" to remember people affected by Alzheimer's disease and related illnesses, according to the project's sponsor, the Alzheimer's Foundation of America (AFA).

Inspired by the famous AIDS Memorial Quilt, the foundation's Quilt to Remember will be continuously added to over time with panels from individuals (four feet by four feet) and panels from organizations (eight feet by eight feet). Each panel will memorialize people who have either passed away from or are living with dementia, or family caregivers and health-care professionals committed to the cause.

Beginning next fall, the quilt will be displayed in cities across the United States.

"The AFA Quilt to Remember will be brought to the heart of America. Piece by piece, it will help our nation recognize the reality and the enormity of this disease, and affirm that we stand united for optimal care and a cure," AFA chief executive officer Eric J. Hall said in a prepared statement.

"Our desire is for the quilt to bring comfort and hope during the holiday season and throughout the year to families affected by this heartbreaking brain disorder," Hall said.

DMAE for Better Brainpower?

DMAE for Better Brainpower?
Provided by: DrWeil.com

Q: What are the benefits of DMAE, and is it safe to take daily? -- Devon

A: DMAE (dimethylaminoethanol) is a substance naturally produced in small amounts in the brain and also found in anchovies and sardines. DMAE supplements are promoted to boost brainpower, improve memory, and slow aging. The idea is that DMAE can improve memory stems from research suggesting it may increase levels of the neurotransmitter acetylcholine, which is believed to play an important role in learning and memory. Levels of acetylcholine decline among people with Alzheimer's disease, and the drugs used to treat Alzheimer's patients target the processes that break it down.

However, evidence that DMAE actually influences acetylcholine levels is contradictory, so I wouldn't count on supplements to yield positive effects. DMAE has also been studied as a means of relieving the symptoms of tardive dyskinesia, a spastic disorder that is a side-effect of long-term use of some anti-psychotic medications. Despite some promising preliminary studies, subsequent research failed to confirm that DMAE had any effect.

Reports that DMAE helps children with attention deficit disorder and short-term memory problems haven't been substantiated, either. And I've seen no evidence to support claims that DMAE in cream form removes age spots from skin or that supplements extend life or boost athletic performance.

Studies in which participants took high doses of DMAE haven't revealed any harmful side effects, although one study published in 1979 linked DMAE with depression and moderate symptoms of mania (hypomania).

DMAE may be safe, but I currently see no evidence that taking it will do anyone any good.
Andrew Weil, MD

More Proof Obesity and Alzheimer's Are Connected

Earlier this year, I told you about the strong correlation between a larger body mass index and the presence of beta-amyloid, the chemical associated with Alzheimer's disease. Makes sense, in light of new research that connects a patient's obesity in their 40s to a greater risk of Alzheimer's as they get older.

Researchers monitored the health of some 9,000 patients for up to three decades, measuring the thickness of their skin below their shoulder and behind their upper arms. By the numbers:

Patients with the thickest upper arms were 2.5 times more likely to develop Alzheimer's.
Thicker shoulders almost tripled a patient's risk of Alzheimer's.

If you're fighting obesity and need more direction, as well as side-stepping Alzheimer's, you'll want to review this must-read piece that covers a spectrum of safe, natural treatments that will help you win the battle over both.
Yahoo News April 6, 2006
Alzheimer Disease
DrEddyClinic.com

If ozone is so good why hasn't everyone heard about it?

If ozone is so good why hasn't everyone heard about it? Well, many have. I have been on over 700 radio and TV shows and speaking platforms telling people, but if I were to pick one word why ozone is not spoken of in the major media, it would be "Politics."

Although millions of people, including little babies, have AIDS, and ozone definitely solves the problem if applied correctly, for long enough, and early enough, the US medical establishment clings to the outmoded model of poisoning the body with toxic drugs to get rid of the disease instead of cleaning out the body and boosting immunity by flooding the body with oxygen (ozone treatments).

Most of the officials in the US medical and regulatory community are financially tied to the pharmaceutical industry which, through interlocking directorates within all major media outlets, does not allow unprofitable (for them) competing therapies to emerge into the public debate, no matter how successful they are.

Although this fact of life is a tragic and callous disregard of human suffering, this not allowing competing therapies to emerge is especially true - as in the case of ozone - if the patents have all run out on the therapies, and if the therapies are legally without owners and in the public domain.

In 1900 Nikola Tesla operated the "Tesla Ozone Company" in the US. Between 1958 and 1973 Dr. Robert Mayer and Dr. Edmund J. Ryan were granted 8 US ozone patents, and European physicians have reported successfully using ozone for over 50 years and to cure 33 major diseases. Quoting from the international MD's assembled at the May 1983 Sixth World Ozone Conference in Washington, D.C.:

Ozone eliminates... viruses and bacteria from blood, human and stored... Medical ozone is successfully used on AIDS, Herpes, Hepatitis, Mononucleosis, Cirrhosis of the liver, Gangrene, Cardiovascular Disease, Arteriosclerosis, High Cholesterol, Cancerous Tumours, Lymphomas, Leukaemia... Highly effective on Rheumatoid and other Arthritis, Allergies of all types...

Improves Multiple sclerosis, ameliorate Alzheimer's Disease, Senility and Parkinson's... Effective on Proctitis, Colitis, Prostate, Candidiasis, Trichomoniasis, Cystitis; Externally, ozone is effective in treating Acne, burns, leg ulcers, open sores and wounds, Eczema and fungus.

more info at:
http://www.dreddyclinic.com/integrated_med/ozone-therapy.htm

Dementia Rates To Double in 20 Years

I've been warning you for some time about the Alzheimer's epidemic waiting to happen in America. Based on the latest report from Alzheimer's Disease International on dementia, however, that epidemic has arrived, and on a worldwide scale too.

These numbers will shock you:

• A new dementia patient is diagnosed every 7 seconds.
• More than 24 million patients worldwide already have dementia and, almost 5 million new cases are reported annually.
• More than 20 percent of those suffering from dementia live in China, followed closely by Western Europe and North America.
• The number of dementia patients will exceed 80 million by 2040.

Folks, neither dementia or Alzheimer's are isn't a normal part of the aging process, and you can take steps to prevent their damage naturally, safely and without the need for a drug. Here's how:

• Get moving with an exercise program today!
• Eat a healthier diet, based on your body's unique metabolic type and be sure to increase your intake of fresh vegetables, high in folate.
• Challenge your mind by learning new things.
• Avoid aluminum and mercury at all costs.
• Consume a high quality fish or cod liver oil daily.
  

BBC News December 16, 2005

Integrated Medicine Forum

http://www.DrEddyClinic.com/
http://dreddyclinic.com/forum/viewforum.php?f=1

Established Drugs May Be More Lethal to Seniors Than New Ones

I told you about the growing realization among the medical establishment newer antipsychotic drugs aren't much better, if at all, than the older, cheaper ones they were meant to replace. Unfortunately, older drugs can be even more harmful, elevating a senior's risk of premature death, according to a new study.

Older antipsychotics, Haldol and Thorazine, were responsible for increasing a senior's mortality risks by 37 percent, based on a review of some 23,000 elderly patients in Pennsylvania.

About 15 percent of patients taking newer drugs like Risperdal or Zyprexa died within six months versus almost 18 percent taking older medications during a similar time frame.

This news may affect you more than think, especially if you have elderly relatives who live in nursing homes. As much as a quarter of the Medicare recipients living there take at least one antipsychotic drug.

By making some simpler and safer lifestyle changes, however, you and your loved ones can avoid lethal drugs -- old or new -- as well as dementia and Alzheimer's.

Modify your eating habits based on your body's unique metabolic type, while limiting, with the plan of eliminating, grains and sugars.

Get moving on an exercise program today.

Rebalance your intake of omega-3 fats by taking a high quality fish or cod liver oil daily.

New England Journal of Medicine, Vol. 353, No. 22, December 1, 2005: 2335-2341
Los Angeles Times December 5, 2005
U.S. News and World Report, December 2, 2005

Linking Your Cholesterol To Stress

An inability to handle stress can be devastating to your health in so many ways, as it can accelerate your risk of Alzheimer's disease and elevate your blood pressure. You can add high cholesterol to that growing list.

It's commonly known cholesterol rises for a short time in response to stress. Unfortunately, baby boomers whose cholesterol rose in reaction to stress, according to a UK study, were more prone to higher cholesterol years later.

Scientists monitored stress-related elevations in cholesterol among some 200 middle-age patients over three years. Patients completed two moderately stressful tasks, sandwiched in between blood tests before and after them. After follow-up blood tests were done later on, those whose cholesterol levels spiked due to stress before were more likely to have higher cholesterol.

In fact, patients who had the most elevated response to stress were a surprising 13 times more prone to high cholesterol than those in the lowest group. And, the high stress group was four times more likely to have elevated levels of LDL cholesterol. Just more evidence, stress can do great harm to your immune system.

The trick about stress, folks, is learning how to handle it, because you can never eliminate it, nor would you want to. One of the more effective methods I know of for managing stress -- the Emotional Freedom Technique -- isn't a useless drug or medical procedure. It's a form of psychological acupressure, based on the same energy meridians used in traditional acupuncture to treat physical and emotional ailments for over 5,000 years, but without the invasiveness of needles, that I use daily in my practice.

MSNBC November 29, 2005

Health Psychology, Vol. 24, No. 6, November 2005

Alzheimer's: Another Version of Diabetes?

An interesting follow-up study to research I posted earlier this year may go far toward explaining why diabetes elevates your risk of developing Alzheimer's disease.

The key hinges on your brain's ability to generate insulin. As Alzheimer's does its damage early on, according to the study, insulin levels in the brain as well as related cellular receptors fall dramatically and keep doing so as the severity of the disease increases. In the advanced stages of Alzheimer's, the lead researcher says, those receptors were functioning at about 20 percent the capacity of a normal brain.

Another tell-tale sign of this drop brain insulin: Low levels of acetylcholine.

The best way to ensure you'll never have to deal with Alzheimer's -- prevention -- is the simplest and you have plenty of free resources on my Web site to help you do just that.

Increase your intake of green, leafy vegetables based on your body's unique metabolic type.

Balance your intake of omega-3 fats, in part, by taking a high quality fish or cod liver oil daily.

Get moving on an exercise program today!

Journal of Alzheimer's Disease, Vol. 8, No. 3, December 2005

Parkinson's, Alzheimer's and the Placebo Effect

As of late, scientists have been digging deeper into how the placebo effect works in tandem with your brain to release endorphins -- the body's natural painkillers -- based solely on the belief an inert pill can relieve what ails you.

Some newer findings based on placebo research:

Once a patient succumbs to Alzheimer's and robs the mind of expectations that a conventional painkilling drug will work, it usually doesn't work as effectively.

In a test using an automated morphine injection machine, patients suffering from pain felt more relief when they knew a nurse was giving it to them, even if it was a placebo.

When told an implant that blocked tremors was activated in their brains, Parkinson's patients moved far better than when it was turned on without telling them.

More evidence the placebo effect is a very real one, considering an inert pill lowered one's blood pressure or almost as effectively as an antidepressant.

MSNBC November 28, 2005

Blood Test Gives Early Warning to Brain Injury

By Megan Rauscher
NEW YORK (Reuters Health) - A new test that detects fragments of broken brain cells that leak into the bloodstream may help doctors quickly detect and treat people with severe head injuries or brain diseases.

"The important thing about this work is that we can easily monitor the release of an axonal protein into serum for the first time," Dr. Gerry Shaw from the University of Florida College of Medicine in Gainesville told Reuters Health.

"It is useful to know this as you can decide whether an accident victim has a serious brain or spinal cord injury quickly without performing MRI, X-rays etc., and you should also be able tell if diseases such as amyotrophic lateral sclerosis, multiple sclerosis, or Alzheimer's are in their early, presymptomatic, stages."

Using their blood test, Shaw and colleagues observed that a brain protein called NF-H is readily detected in "surprisingly large amounts" in the blood of rats following experimentally induced spinal cord injury and, in smaller but still significant amounts, in rats given experimental traumatic brain injury. Since this protein is only found in axons -- nerve fibers that help brain cells communicate -- this indicates that axonal injury must have occurred, Shaw noted.

The discovery, reported in the current online issue of Biochemical and Biophysical Research Communications, could lead to tests for the clinic or battlefield to diagnose ailments with just a few drops of blood, bypassing more cumbersome, time-consuming, and expensive tests such as brain scans.

For example, shaken-soldier syndrome is a traumatic brain injury that can occur when a soldier survives a roadside blast, Dr. Douglas Anderson from the McKnight Brain Institute at the University of Florida who participated in the research explains. "In patients who are unconscious but with no penetrating head wounds, it would be extremely helpful for emergency medical technicians to test for a marker to see how severe the injuries are. Then perhaps something can be done early on," he said in a statement.

SOURCE: Biochemical and Biophysical Research Communications October 2005. More information’s here: