alternative medicine for arthritis pain relief

Natural, herbal remedies can help arthritis sufferers who have tried traditional pain medications without success. Many natural remedies and supplements have been found to actually reduce cartilage deterioration and even rebuild a patient’s lost cartilage. Many people are also seeking natural remedies because of the increasing cost of prescription medication. Conventional over-the-counter pain relievers, such as acetaminophen and ibuprofen, can be very helpful in decreasing joint pain, but they do produce side effects and can cause problems in long-term users. Before adding any supplements to your daily routine, check with your healthcare advisor, as supplements can cause adverse reactions and may not be right for your situation. Before discontinuing a prescription medication, consult a physician.

However, with a doctor’s approval, there are many natural solutions, which may aid in managing arthritis. Acupuncture - This is a popular alternative to medication for pain relief. Although the pain-relieving effects may be temporary, these sessions can be very beneficial for those who find that drugs or supplements are insufficient or have unacceptable side effects

Aromatherapy - Aromatherapy focuses on using pleasurable aromatic botanical oils by either massaging them into the skin, adding them to the bath water, inhaling them directly or diffusing their scents into the surrounding environment. The oils have been known to affect moods, help with relaxation, lessen or end fatigue and anxiety, and help the brain and nervous system via olfactory nerves stimulation when inhaled. It is another holistic treatment used by some arthritic sufferers for pain relief and stress management.

Cayenne Cream - Cayenne peppers contain an substance called capsaicin which is responsible for their spicy effect. This also causes a burning sensation when it comes in contact with skin, and inhibits the body’s production of substance P which is heavily involved the relaying signals of pain to the brain. You may need to apply the cayenne cream to painful areas two to three times per day for at least one week before you find relief.

Chondroitin - The most popular dietary supplements for arthritis sufferers are chondroitin, fish oil and glucosamine. Chondroitin can draw fluid into the cartilage, improving shock-absorbing ability and weight control, as more weight equals more joint pressure.

Fish Oil - Fish oils help with controlling inflammation in the body and may provide relief when arthritis is caused by an immune system dysfunction as in lupus. A vegetarian alternative to fish oil is flax seed or borage oil. More information can be found at http://www.omega3fats.com

Glucosamine - Recent studies have shown that the cartilage-building substance called glucosamine is effective for the long-term relief of osteoarthritis pain. In some people, glucosamine appears to even slow the deterioration of joints over time and reinforce joint cartilage. Whether or not it can actually reverse the disease is still unclear. Glutathione

Glutathione - Glutathione is an antioxidant with anti-inflammatory properties and can be safely boosted by consuming its precursors available in the supplements, N-Acetyl-Cysteine (NAC) or undenatured whey protein. You can find out more about it here http://www.1whey2health.com

Magnets - Although magnets that are worn as jewelry or placed on bed linens have been reported by some to be effective pain relievers, results are still preliminary; doctors claim that these magnets are not strong enough.

MSM - Methyl-Sulfonyl-Methane is an organic sulfur supplement that appears to slow down the degeneration but is not yet proven and approved. It is used in the reduction of inflammation and can be used in conjunction with glucosamine, in some instances.

Nettle leaf - Nettles can reduce a patient’s need for NSAIDS (non-steroidal anti-inflammatory drugs) by up to 70 percent.

Vitamin B - It is an effective pain reliever. It works best on the knee and can help stop degeneration that is caused by free-radical molecules, not only in the joints but in other areas of the body as well.

Vitamin E - This antioxidant is used primarily for osteoarthritis.

Ginger - Ginger is an antioxidant that acts as an inflammatory with no major side effects.

These are merely a few examples of what an arthritis sufferer can use when seeking pain relief from natural remedies. Due to the lack of scientific study and testing on many of these alternate treatments, there is no proof of their effectiveness.

Nothing can cure osteoarthritis, but nutritional supplements, the application of heat or cold to affected joints, exercise, and weight loss can improve the function and flexibility of your joints, and perhaps even slow the progress of the disease.

Priya Shah is the editor of The Glutathione Report and Health Naturale. For a comprehensive report on arthritis.

How Superbug Staph Aureus Resists Our Natural Defenses

Researchers at the University of Washington have uncovered how the bacterium Staphylococcus aureus, including the notorious MRSA (methicillin-resistant Staph aureus) "superbug" strains, resists our body's natural defenses against infection. The work, which was featured on the cover of the March 21 issue of Science, could lead to new ways to fight the bacteria.

Dr. Ferric Fang, UW professor of laboratory medicine and microbiology, and his UW colleagues Dr. Anthony Richardson and Dr. Stephen Libby set out to determine what makes Staph aureus a better pathogen than other bacteria. They focused on a chemical compound called nitric oxide (NO), a natural antibiotic that our cells excrete to protect us from pathogens. For most bacteria, NO creates an environment that keeps invading microbes from undergoing respiration or fermentation, vital chemical processes that allow bacteria to grow.

The researchers found that Staph aureus has a mechanism that allows it to produce lactic acid in the presence of NO, which allows it to maintain its chemical balance and keep growing and thriving in the harsh host environment. When Staph aureus is exposed to NO, it produces the novel enzyme responsible for lactic acid production, along with another enzyme that converts NO to non-toxic products. NO is commonly found in the nose and nasal passages, and is meant to protect people against disease-causing microbes. But Staph aureus is commonly found in the nose despite the presence of NO, the researchers explained.

When the researchers modified Staph aureus to take away its ability to make lactic acid, the bacteria could no longer tolerate NO. The modified bacteria also lost their ability to survive in host immune cells and cause lethal disease in mice.

"MRSA has become an enormous public health problem, by causing both hospital- and community-acquired infections," explained Fang. "Staph aureus has already colonized about one-third of the world's population, so traditional antibiotics will probably not be the complete answer to the MRSA problem."

However, the researchers added, trying to make Staph aureus more susceptible to our natural defenses might lead to new strategies to de-colonize the population and prevent staphylococcal infections.

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Adapted from materials provided by University of Washington, via EurekAlert!, a service of AAAS.

Blue Light Destroys Antibiotic-resistant Staph Infection

Two common strains of methicillin-resistant Staphylococcus aureus, commonly known as MRSA, were virtually eradicated in the laboratory by exposing them to a wavelength of blue light, in a process called photo-irradiation.

Antibiotic-resistant bacterial infections represent an important and increasing public health threat. At present, fewer than 5% of staphylococcal strains are susceptible to penicillin, while approximately 40%-50% of Staph aureus isolated have developed resistance to newer semisynthetic antibiotics such as methicillin as well.

Chukuka S. Enwemeka, Deborah Williams, Sombiri K. Enwemeka, Steve Hollosi, and David Yens from the New York Institute of Technology (Old Westbury, NY) had previously demonstrated that photo-irradiation using 405-nm light destroys MRSA strains grown in culture. In the current study, "Blue 470-nm Light Kills Methicillin-Resistant Staphylococcus aureus (MRSA) in Vitro," the authors exposed bacterial colonies of MRSA to various doses of 470-nm light, which emits no UV radiation.

The two MRSA populations studied—the US-300 strain of CA-MRSA and the IS-853 strain of HA-MRSA—represent prominent community-acquired and hospital-acquired strains, respectively.

The authors report that the higher the dose of 470-nm blue light, the more bacteria were killed. High-dose photo-irradiation was able to destroy 90.4% of the US-300 colonies and the IS-853 colonies. The effectiveness of blue light in vitro suggests that it should also be effective in human cases of MRSA infection, and particularly in cutaneous and subcutaneous infections.

"It is inspiring that an inexpensive naturally visible wavelength of light can eradicate two common strains of MRSA. Developing strategies that are capable of destroying MRSA, using mechanisms that would not lead to further antibiotic resistance, is timely and important for us and our patients," says Chukuka S. Enwemeka, PhD, FACSM, Co-Editor-in-Chief of the Journal and first author of the study.

The article will appear in the April 2009 issue (Volume 27, Number 2) of the peer-reviewed journal Photomedicine and Laser Surgery.

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Adapted from materials provided by Mary Ann Liebert, Inc./Genetic Engineering News.

Turning Down Gene Expression Promotes Nerve Cell Maintenance

Anyone with a sweet tooth knows that too much of a good thing can lead to negative consequences. The same can be said about the signals that help maintain nerve cells, as demonstrated in a new study of myelin, a protein key to efficient neuronal transmission.

Normal nerve cells have a myelin sheath, which, much like the insulation on a cable, allows for rapid and efficient signal conduction. However, in several diseases – the most well-known being multiple sclerosis – demyelination processes cause the breakdown of this "insulation", and lead to deficits in perception, movement, cognition, etc. Thus, in order to help patients of demyelinating disease, researchers are studying the pathways that control myelin formation and maintenance.

A new study by University of California scientists examines the role of a structural protein, called lamin, in maintaining myelin. They found that, while lamin is necessary in the initial stages of myelin formation, too much lamin promotes myelin breakdown. Further investigation led the researchers to the discovery of a signal that fine-tunes lamin expression. This signal, a microRNA called miR-23, can turn down lamin gene expression, and thereby prevent demyelination due to lamin overexpression.

This new work reported in Disease Models & Mechanisms (DMM), adds another piece to the puzzle that is understanding myelin formation and maintenance. Additionally, the identification of miR-23 as a myelin regulator introduces a new potential drug target in developing treatments for demyelinating illness.

The report was written Shu-Ting Lin and Ying-Hui Fu at the Department of Neurology, University of California San Francisco. The report is published in the March/April issue of Disease Models & Mechanisms (DMM), a research journal published by The Company of Biologists, a non-profit based in Cambridge, UK.

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Adapted from materials provided by The Company of Biologists/Disease Models & Mechanisms, via EurekAlert!, a service of AAAS.

Chemists Shed Light On Health Benefits Of Garlic

A Queen's-led team has discovered the reason why garlic is so good for us

Researchers have widely believed that the organic compound, allicin – which gives garlic its aroma and flavour – acts as the world's most powerful antioxidant. But until now it hasn't been clear how allicin works, or how it stacks up compared to more common antioxidants such as Vitamin E and coenzyme Q10, which stop the damaging effects of radicals.

"We didn't understand how garlic could contain such an efficient antioxidant, since it didn't have a substantial amount of the types of compounds usually responsible for high antioxidant activity in plants, such as the flavanoids found in green tea or grapes," says Chemistry professor Derek Pratt, who led the study. "If allicin was indeed responsible for this activity in garlic, we wanted to find out how it worked."

The research team questioned the ability of allicin to trap damaging radicals so effectively, and considered the possibility that a decomposition product of allicin may instead be responsible. Through experiments with synthetically-produced allicin, they found that an acid produced when the compound decomposes rapidly reacts with radicals.

Their findings are published in the January 2009 issue of the international chemistry journal Angewandte Chemie.

"Basically the allicin compound has to decompose in order to generate a potent antioxidant," explains Dr. Pratt, who is Canada Research Chair in Free Radical Chemistry. "The reaction between the sulfenic acid and radicals is as fast as it can get, limited only by the time it takes for the two molecules to come into contact. No one has ever seen compounds, natural or synthetic, react this quickly as antioxidants."

The researcher is confident that a link exists between the reactivity of the sulfenic acid and the medicinal benefits of garlic. "While garlic has been used as a herbal medicine for centuries and there are many garlic supplements on the market, until now there has been no convincing explanation as to why garlic is beneficial," says Dr. Pratt. "I think we have taken the first step in uncovering a fundamental chemical mechanism which may explain garlic's medicinal benefits."

Along with onions, leeks and shallots, garlic is a species in the family Alliaceae. All of these other plants contain a compound that is very similar to allicin, but they do not have the same medicinal properties. Dr. Pratt and his colleagues believe that this is due to a slower rate of decomposition of the allicin analogs in the onions, leaks and shallots, which leads to a lower level of sulfenic acid available to react as antioxidants with radicals.

The study was funded by the Natural Sciences and Engineering Research Council of Canada (NSERC) and the Ontario Ministry of Innovation. Other members of the research team are Queen's Chemistry post-doctoral researcher Vipraja Vaidya and Keith Ingold, from the National Research Council of Canada.

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Adapted from materials provided by Queen's University.

DNA Component Can Stimulate And Suppress Immune Response

A component of DNA that can both stimulate and suppress the immune system, depending on the dosage, may hold hope for treating cancer and infection, Medical College of Georgia researchers say.

Low levels of CpG increase inflammation, part of the body's way of eliminating invaders. But high doses block inflammation by increasing expression of the enzyme indoleamine 2,3 dioxygenase, or IDO, an immunosuppressor, the researchers say.

"The same therapy can have two different effects," says Rusty Johnson, a fifth-year M.D./Ph.D. student in the MCG Schools of Medicine and Graduate Studies. "It was assumed that giving this treatment at higher doses would cause more stimulation, but it has the opposite effect."

The researchers hope that manipulating the dosage can help them optimize the role of inflammation in fighting invaders such as tumors and harmful bacteria. Mr. Johnson presented the findings at the Midwinter Conference of Immunologists this month in Asilomar, Calif. He is working with Drs. Andrew Mellor and David Munn, co-directors of the School of Medicine Immuno Discovery Institute, who discovered IDO's immunosuppressive capabilities more than a decade ago.

With the help of Drs. Babak Baban and Phillip Chandler, scientists in MCG's Immunotherapy Center, they've also learned IDO inhibits inflammation by blocking production of interleukin 6, a secreted factor that causes inflammation.

"This suggests that IDO is a counter-regulatory mechanism that serves as a balance to prevent too much inflammation," Mr. Johnson says. "Too much inflammation leads to destruction of normal body tissue, and this shows IDO's importance in preventing this from occurring."

The researchers already knew that IDO protects tumors from the immune system. While working with collaborators Drs. Alex Muller and George Prendergast at the Lankenau Institute in Philadelphia, they learned its role in tumor formation.

"Without it, a mouse becomes resistant to skin tumor formation, and tumors that do form are smaller and less malignant," Mr. Johnson says.

They've also learned that the cells IDO uses to suppress the immune system – IDO-competent dendritic cells – originate from B cells, which produce antibodies to fight infection.

Mr. Johnson was in his second year of medical school when he heard Dr. Munn lecture about his and Dr. Mellor's groundbreaking discovery of IDO's role in protecting a fetus from the mother's immune system. It was at that point that the Augusta native decided to pursue a career in immunology. Mr. Johnson earned a bachelor's degree in chemistry from the Georgia Institute of Technology and studied piano and voice at Augusta State University prior to coming to MCG.

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Adapted from materials provided by Medical College of Georgia.

Link Found Between Parkinson's Disease Genes And Manganese Poisoning

A connection between genetic and environmental causes of Parkinson's disease has been discovered by a research team led by Aaron D. Gitler, PhD, Assistant Professor in the Department of Cell and Developmental Biology at the University of Pennsylvania School of Medicine.

Gitler and colleagues found a genetic interaction between two Parkinson's disease genes (alpha-synuclein and PARK9) and determined that the PARK9 protein can protect cells from manganese poisoning, which is an environmental risk factor for a Parkinson's disease-like syndrome. The findings appear online this week in Nature Genetics.

Manganism, or manganese poisoning, is prevalent in such occupations as mining, welding, and steel manufacturing. It is caused by exposure to excessive levels of the metal manganese, which attacks the central nervous system, producing motor and dementia symptoms that resemble Parkinson's disease.

In Parkinson's patients, the alpha-synuclein protein normally found in the brain misfolds, forming clumps. Yeast cells, the model system in which Gitler studies disease proteins, also form clumps and die when this protein is expressed at high levels. These are the same yeast cells that bakers and brewers use to make bread, beer, and wine.

As a postdoctoral fellow at the Whitehead Institute in Cambridge, Massachusetts, Gitler and colleagues started looking for genes that could prevent the cell death caused by mis-folded alpha-synuclein in yeast. Eventually they found a few genes to test in animal models and some were able to protect neurons from the toxic effects of alpha-synuclein. "One of the genes that we found was a previously uncharacterized yeast gene called YOR291W. No one knew what it did back in 2006," he recalls.

In the meantime, researchers in Europe published studies about a family that had an early-onset form of a type of Parkinson's disease caused by mutations in the PARK9 gene. "When I read about this study, I wondered what the closest yeast gene was to the human PARK9 gene and it turned out to be YOR291W," explains Gitler. "It was one of the genes that could rescue alpha-synuclein toxicity from our yeast screen. That was the big Eureka! and completely unexpected. It suggested that Parkinson's disease genes could interact with each other in previously unexpected ways."

Because of its similarity to the human PARK9 gene, Gitler and colleagues renamed the yeast gene to YPK9 (which stands for Yeast PARK9). Researchers at Purdue University and The University of Alabama teamed up with Gitler and his colleagues to show that the PARK9 gene could also protect neurons from alpha-synuclein's toxic effects.

Next, the team set out to find the function of YPK9. Study co-first author, postdoctoral fellow Alessandra Chesi, PhD, discovered that YPK9 encodes a metal transporter protein. "Its sequence looks like other proteins that we know transport metals," says Chesi.

She deleted the YPK9 gene from yeast and the cells were fine. Then she exposed YPK9-deficient yeast cells to an excess of different metals -- zinc, copper, manganese, iron, etc. -- to determine which metal it might transport. Of all the metals Chesi tested, she found that in the presence of manganese, the YPK9-deficient yeast did not grow as well. They were hypersensitive to manganese.

"This was astonishing, because it was known for years that welders and miners that inhale manganese get a Parkinson's-like disease called manganese poisoning," says Chesi. "The specific neurons that are lost in the miners are from the globus pallidus, a brain motor center. The European parkinsonism patients with the PARK9 mutation also lose neurons in this region."

Gitler then found that the protein made by YPK9, the yeast gene equivalent of PARK9, is localized to the vacuole membrane in the yeast cell. Vacuoles are inner cell components that wall off toxic substances for later disposal. "Our hypothesis is that the vacuole, a bag in the cell that captures toxins, is sitting there and taking in manganese and sequestering it for detoxification, keeping it away from other cell organelles," explains Gitler. "But, having a mutation in the PARK9 gene causes problems for this process in yeast and possibly in humans".

"It's an interesting story that we've discovered in yeast and it will be important to see if it holds up in people. What's new is the connection between genetic and environmental causes of Parkinson's. How does PARK9 protect against alpha-synuclein toxicity and how does PARK9 help prevent manganese poisoning? This is what we will be investigating next."

This work was funded in part by a National Institute of Health Director's New Innovator Award.

Gitler is an inventor on patents and patent applications that have been licensed to FoldRx Pharmaceuticals, a company that investigates drugs to treat protein-folding diseases.

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Adapted from materials provided by University of Pennsylvania School of Medicine, via EurekAlert!, a service of AAAS.

Single Gene Lets Bacteria Jump From Host To Host

All life — plants, animals, people — depends on peaceful coexistence with a swarm of microbial life that performs vital services from helping to convert food to energy to protection from disease.

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Now, with the help of a squid that uses a luminescent bacterium to create a predator-fooling light organ and a fish that uses a different strain of the same species of bacteria like a flashlight to illuminate the dark nooks of the reefs where it lives, scientists have found that gaining a single gene is enough for the microbe to switch host animals.

The finding, reported this week (Feb. 1) in the journal Nature by a team of scientists from the University of Wisconsin-Madison, is important not only because it peels back some of the mystery of how bacteria evolved to colonize different animals, but also because it reveals a genetic pressure point that could be manipulated to thwart the germs that make us sick.

"It seems that every animal we know about has microbes associated with it," says Mark J. Mandel, the lead author of the study and a postdoctoral fellow in the UW-Madison School of Medicine and Public Health. "We pick up our microbial partners from the environment and they provide us with a raft of services from helping digestion to protection from disease."

In the Pacific, a species of bacteria known as Vibrio fischeri lives in luminescent harmony with two distinct hosts: the diminutive nocturnal bobtail squid and the reef-dwelling pinecone fish. In the squid, which feeds at night near the ocean surface, one strain of the bacterium forms a light organ that mimics moonlight and acts like a cloaking device to shield the squid from hungry predators below. In the pinecone fish, another strain of the bacterium colonizes a light organ within the animal's jaw and helps illuminate the dark reefs in which it forages at night. The fish light organ may also play a role in attracting the zooplankton that make up the pinecone fish's menu.

But how did a single species of bacteria come to terms with such different hosts?

Working in the UW-Madison laboratory of microbiologist Ned Ruby, Mandel and his colleagues scoured the genomes of the two different strains of V. fischeri and found that most of the bacterium's genetic architecture was conserved over the course of millions of years of evolutionary history, but with a key difference: The strain that colonizes the squid has a regulatory gene that controls other genes that lay down a biofilm that allows the microbe to colonize the animal's light organ.

"During squid colonization, this regulatory gene turns on a suite of genes that allow bacteria to colonize the squid through mucus produced by the animal," Mandel explains. "The mucus is the pathway to the light organ, but it also helps keep out the bad guys."

Both strains of bacteria, Mandel explains, have the same genes that produce the biofilms the bacterium needs to get established in its host. But the regulatory gene that sets the other biofilm genes in motion is absent in the strain that lives in the pinecone fish, the animal scientists believe was first colonized by V. fischeri before it moved in to the squid light organ when the squid family came onto the scene in the Pacific Ocean at least 30 million years ago.

"The regulatory gene entered the bacterium's lineage and allowed it to expand its host range into the squid," according to Mandel. "The bottom-line message of the paper is that bacteria can shift host range by modifying their capabilities with small regulatory changes."

The regulatory gene acquired by the bacterium, notes Ruby, is essentially a switch the organism uses to activate a set of genes that had been residing quietly in the V. fischeri genome. Such mechanisms, he says, are very likely at play in many other species of bacteria, including those that infect humans and cause illness.

"This is going to inform a question that has been around a long time in the area of pathogenesis," says Ruby. One line of thought is that "in order to become a pathogen, a whole suite of genes needs to be imported to a bacterium."

The new finding by his group, however, suggests that nature is far more parsimonious: Instead of requiring organisms to acquire many new genes to occupy a new host, the combination of a new regulatory gene and genes that already reside in a bacterium is enough to do the trick.

"Together, they can do something neither of them could do before. They can mix and match and open up new niches," says Ruby.

Knowing that a regulatory gene plays a key role in allowing an organism to fit a new host may prove useful in human medicine as many bacterial pathogens arose first in other animals before infecting humans. A single gene can be a much easier target for a drug or other intervention to prevent or mitigate infection, the Wisconsin scientists say.

In addition to Ruby and Mandel, authors of the new Nature report include Michael S. Wollenberg, also of UW-Madison; Eric V. Stabb of the University of Georgia; and Karen L. Visick of Loyola University Chicago. The study was supported by grants from the Betty and Gordon Moore Foundation, the National Institutes of Health and the National Science Foundation.