While researching more of the scientific articles I came to find an interesting article relating to anti-inflammatory drug use and the risk for Parkinson's disease.

Evidence from studies suggests a role of neuroinflammation in the pathogenesis of Parkinson's disease (PD). This study takes advantage of the well established American Cancer Society's Cancer Prevention Study II (CPS-II) Nutrition Cohort, and was able to further examine the relation between NSAID use and PD risk with more detailed information on different types of NAIDs. The cohort is a study that was initiated in 1992 to investigate the factors for cancer. Participants were from a cohort who replied to a mailed survey in 1982. In 1992 they answered a questionnaire on four types of common used analgesics. Follow-up surveys were conducted in 1997,1999, and 2001. In 2001's survey a specific question on the lifetime occurrences of PD was asked. Follow-up started on the date of return of the 1992 questionnaire and ended on the date when the first symptoms of PD were noticed for PD cases or September 30, 2001 for participants without PD.

In the '92 questionnaire, participants were asked whether they took the following analgesics regularly during the past year: aspirin, acetaminophen, ibuprofen, or other nonsteroidal analgesics. They were also asked how many days per month they took each drug, how many tablets they took per day, and the duration of use. The '97 survey asked about "baby or low dosage aspirin" and "regular or extra strength aspirin". Four baby aspirin was counted as one tablet. Users were categorized according to dosage: fewer than 2 tablets/ week; 2 to 6.9 tablets/week; and 1 or more tablets a day. Results of the study showed significant inverse association was suggested between the cumulative updated dosage of ibuprofen use and PD risk. Overall, ibuprofen users had a lower PD risk than nonusers. Unlike ibuprofen, the use of aspirin and other NSAIDs, or acetiminophen was not associated with PD risk. Non aspirin NSAID users had a 26% lower risk than nonusers.

Results were consistent with previous findings that users of non aspirin NSAIDs but no aspirin, had a lower risk for PD than nonusers. This study also further suggested that only certain non-aspirin NSAIDs such as ibuprofen reduce the risk for PD. However there is insufficient information on the optimal dosage, and it remains uncertain whether this effect is mediated by COX inhibition or through other mechanisms specific to ibuprofen and possibly some other selected NSAIDs.

The full article can be found on PubMed, the title of the article is: Nonsteroidal Antiinflammatory Drug use and the Risk for Parkinson's Disease.

Aspirin Decreases the Risk of Breast Cancer Deaths

It was revealed in February 2010 that the use of anti-inflammatory drugs such as aspirin (and other NSAIDs such as ibuprofen and naproxen) has shown to decrease the risk of dying from breast cancer. This information comes out of the Nurses’ Health Study which has followed 4,164 registered nurses who were diagnosed with stages I, II, or III breast cancer between 1976 and 2002 until their death or June 2006, whichever came first. This study has looked at a wide range of health issues in these women. In particular, they started in 1976 looking at which of the women took aspirin on a regular basis (often to reduce risk of heart attack and stroke) and have attempted to draw correlations in other health areas.

The researchers looked at the breast cancer mortality risk and the number of days per week of aspirin use (0,1,2 etc.). They found that women who took aspirin two to five days a week had a 60 percent reduced risk of their cancer spreading and a 71 percent lower risk of breast cancer death. Six to seven aspirins a week lowered the risk of spread by 43 percent and the risk of breast cancer death by 64 percent. In the end they concluded that among women living at least 1 year after a breast cancer diagnosis, aspirin use was associated with a decreased risk of distant recurrence and breast cancer death. The researchers state that more information is needed but the use of aspirin could affect tumor growth or recurrence through a decrease in inflammation.

Interestingly, it was revealed in January 2009 based on data from the Nurses’ Health Study that the use of aspirin or other NSAIDs does not decrease the risk of getting breast cancer among premenopausal women. The information from both of these papers is intriguing and points to the role of inflammation at different stages of a variety of disease states. It is likely that a baby aspirin does more than treat muscle pains, headaches and offer protection from heart disease. More information is needed however, it is promising that anti-inflammatories may have a beneficial role in decreasing mortality risk after cancer.

Holmes MD, Chen WY, Li L, Hertzmark E, Speigelman D, Hankinson SE. Aspirin intake and survival after breast cancer. J Clin Oncol 28(9): 1467-72, 2010.

Eliassen AH, Chen WY, Spiegelman D, Willett WC, Hunter DJ, Hankinson SE. Use of aspirin, other nonsteroidal anti-inflammatory drugs, and acetaminophen and risk of breast cancer among premenopausal women in the Nurses’ Health Study II. Arch Intern Med 169(2): 115-21, 2009.

Identical Twins and Multiple Sclerosis

Using extremely fine-grained analytical tools, scientists compared genetic information in three sets of identical twins. One of each pair had Multiple Sclerosis, and the other didn’t — yet their genes proved essentially identical. The research cost $1.5 million, and the scientists took 18 months to sequence 2.8 billion DNA units in each twin, and determine whether they came from the mother or father. Most genomic comparisons look for differences in a just handful of suspect genes, and even whole-genome approaches don’t differentiate between parental contributions. The researchers also analyzed the twins' CD4 cells because of their central role in the development of MS. The absence of genetic differences doesn’t mean that genetics are irrelevant to multiple sclerosis. Identical twins, who are descended from the same egg, are six times more likely to develop MS than non-identical twins, who come from two different eggs. It’s still possible that some as-yet-unknown genetic factor, undetectable by even the most advanced tools, may explain the discordance in the study. However, geneticist Stephen Kingsmore thinks the culprit is probably an unknown environmental influence. This unknown factor could combine with other known genetic risks of developing multiple sclerosis. This study was a pioneering effort and the researchers are looking forward to studying more twins and other cells.

Head Trauma Linked To Alzheimer's Disease

Researchers at the University of Pennsylvania in Philadelphia are working to find out more about Alzheimer's Disease. The findings back previous studies that suggested brain trauma increases the risk of Alzheimer's disease, a leading cause of dementia, later in life. Trauma to the head may trigger a cascade of biochemical events in the brain, in time resulting in neurodegenerative changes similar to those found in patients with Alzheimer's disease. Dr. Douglas Smith says his findings support "several epidemiologic reports (that have suggested) a link between a single episode of brain trauma and the development of Alzheimer's disease later in life." Smith's team induced brain injury in anesthetized pigs via very rapid acceleration/deceleration of the animals' heads without direct impact, similar to what humans often experience in an automobile accident. Brain trauma is one of the only environmental risk factor for Alzheimer's disease, so there is something about brain trauma that might initiate these insidious neurodegenerative cascades. The analyses of the brain tissue revealed a remarkable and consistent accumulation of amyloid beta and tau proteins in damaged brain cells following trauma. In Alzheimer's disease, changes in tau protein lead to the disintegration of microtubules in brain cells disintegrating the neuron's transport system for nutrients. In the study animals, these changes were evident as early as 3 to 10 days post-injury. The team concluded that microscopic injury to the brain caused by trauma can be linked to the development of Alzheimer's disease many years after the injury. The findings may also lead to new drugs aimed at preventing the process. "This study adds to the body of knowledge that might aid us in the development of an anti-plaque-making compound," Smith said in a statement.

8 Alternative ways to reduce Inflammation without the chance of adverse effects of NSAIDs.

These are all ways of reducing inflammation without using NSAID's or other anti-inflammatory drugs. We talked about in class how COX-2 inhibitors could be linked to increased MI, and COX-1 inhibitors cause damage to you gastrointestinal system. So, why take the chance when you can just eat the right things to help you out. Omega-3 fatty acids can be consumed by taking in fish oil. There have been many studies done that show the omega-3 fatty acids make the precursors to prostaglandins, which can start or inhibit inflammation. But, remember to reduce you omega-6 fatty acid intake or you increased omega-3 fatty acid intake will not work for inflammation. The second food for you to consume is ginger. It has been proven to be a slight anti-inflammatory and helps with stomach aches and pain. The third is to take bromelain enzymes. These are seen in pineapples or you can buy them as a supplement. They are a naturally occurring anti-inflammatory. Another is Cetyl Myristoleate oil, which is seen in butter and fish. It will help with lubricating your joints and also is a natural anti-inflammatory. There was a study conducted with this oil and 63.5 % of the patients that did not respond to NSAID's for arthritic pain responded to this oil. Number five is Boswellia, which is boswellic acids that ares said to reduce inflammation. This was agreed with in a study of 175 patients with rheumatic disorders and 122 patients found reduced stiffness and inflammation in four weeks. Evening Primrose Oil was used in a study with 37 rheumatoid arthritis patients and significantly reduced tenderness swelling of the patients when only taking 1.4 g a day. Cayenne Peppers in a cream form can reduce pain by depleting a chemical component of the nerve cells that give signals to the brain about pain. The last one is White Willow Bark, in which aspirin is made out of. It gives mild pain relief and does not have the adverse effects on the gastrointestinal tract as aspirin does.

So, there's eight more things you can try to reduce inflammation before jumping the list and going straight to the medicine cabinet for your NSAIDs.

CHERRIES as treatment for inflammatory diseases

We've blogged this week about the anti-inflammatory diet, complementary and alternative medicine, and the use of NSAIDs in the treatment of inflammatory diseases... but now CHERRIES??

While looking more into the new and upcoming treatments of inflammatory diseases I was shocked to see cherries as one of these remedies!

On April 27th, 2010 a team of Michigan researchers presented a new study at the Experimental Biology annual meeting sayig there is more evidence of tart cherries' powerful anti-inflammatory benefits.

Using a "whole fool" approach, reseachers found that a cherrt-enriched diet not only reduced overall body inflammation, but also reduced inflammation at key sites (belly fat, heart) known to affect heart disease risk in obese, at risk rats. At risk obese rats were fed a cherry- enriched "Western Diet" characterized by high fat & moderate carbohydrate- in line with the typical American diet- for 90 days.

Cherry-enriched diets, which consisted of whole tart cherry powder as 1 percent of the diet, reduced risk factors for heart disease including cholesterol, body weight, fat mass and know markers of inflammation. This study offers further promise that food rich in antioxidants, such as cherries, could potentially reduce inflammation and have the potential to lower disease risk.

A 2nd study found similar results in humans. Ten overweight or obese adults drank eight ouncesof tart cherry juice daily for a month. At the end of the trail, there were noteworthy reductions in quite a few markers of inflammation, in addition to lower levels of triglycerides, another key risk factor for hear disease. Researchers say both studies are encouraging and will lead to further clinical studies in humans to explore the link between diet, inflammation and lowering disease risk.

This is the latest linking cherries to protection against heart disease and inflammation. Researchers believe it's the anthocyanins- powerful antioxidant compounds in cherries- also responsible for the fruits bright red color, that connect cherries to reduced inflammation, even inflammation related to muscle recovery post-exercise. Since cherries are available year-round in dried, frozen and juice forms, they say it's easy to incorporate them into one's daily diet to help manage inflammation.

I'd personally like to see further research in this area. I could add cherries to my oatmeal or to my yogurt as preventative care, until its confirmed factual across the board. Why not?

Just a thought...

Article can be found at:

http://www.eurekalert.org/pub_releases/2010-04/wsw/-nrr042620.php

Use Complimentary and Alternative Medicine in the Treatment of Inflammatory Diseases

In the assigned review article Anti-Inflammatory Actions of Acupuncture, the authors discussed the use of acupuncture in the treatment of inflammatory diseases. Acupuncture is one type of complementary and alternative therapy used in the treatment of various diseases. Other types include use of herbal supplements, massage, chiropractic manipulation, hypnosis, and yoga. According the National Institutes of Health, 38.3% of American adults used complementary and alternative medicine approaches and spent $33.9 billion dollars out-of-pocket for these treatments in 2007. Interestingly, the number of Americans using complementary and alternative medicine therapies has been increasing across several years despite the limited evidence to support the use of these therapy approaches. What do you think might be the reason that these therapy approaches are utilized despite the lack evidence to support their use?

Role of IFN-gamma in Alzeihmers

Reactive gliosis surrounding amyloid beta (Abeta) plaques is an early feature of Alzheimer's disease pathogenesis and has been postulated to represent activation of the innate immune system in an apparently ineffective attempt to clear or neutralize Abeta aggregates. To evaluate the role of IFN-gamma-mediated neuroinflammation on the evolution of Abeta pathology in transgenic (Tg) mice, murine IFN-gamma (mIFN-gamma) was expressed in the brains of Abeta precursor protein (APP) Tg mice using recombinant adeno-associated virus serotype 1. Expression of mIFN-gamma in brains of APP TgCRND8 mice results in robust noncell autonomous activation of microglia and astrocytes, and a concomitant significant suppression of Abeta deposition. In these mice, mIFN-gamma expression upregulated multiple glial activation markers, early components of the complement cascade as well as led to infiltration of Ly-6c positive peripheral monocytes but no significant effects on APP levels, APP processing or steady-state Abeta levels were noticed in vivo. Taken together, these results suggest that mIFN-gamma expression in the brain suppresses Abeta accumulation through synergistic effects of activated glia and components of the innate immune system that enhance Abeta aggregate phagocytosis.

Anti-inflammatory drugs (NSAID's)

During class the following two weeks we are going to talk about anti-inflammatories. Many of all, if not all of us, have used over the counter drugs to reduce unpleasant symptoms such as pain. NSAIDS work by blocking the enzymes COX-1 and COX-2, these enzymes are responsible of the production of prostaglandins. Prostaglandins are produced in the cell and promote inflammation, pain and fever. These chemicals also play a role in blood clotting and help support the lining of the stomach. However, only the enzyme COX-1 produces prostaglandins to support platelets and protect the stomach lining. Since most NSAIDS block the COX enzymes, the excessive use or chronic use of these NSAIDS can lead to stomach ulcers and bleeding. The effect of NSAIDS is determined by the amount of time it takes to be eliminated from the body and how strong it inhibits the COX-1 and COX-2 enzymes. Thus, the more a drug blocks COX-1, the greater the chance of developing stomach ulcers. Not all NSAIDS will block the COX enzymes, for example "Celebrex" will block COX-2 and will have little effect on COX-1 blockage, then reducing the chance of developing stomach ulcers or bleeding; these types of drugs are called selective COX-2 inhibitors.