Back to week 3: Birth control pill is linked to heart disease?

Once again the "common folk" is a victim of the C-reactive protein (CRP) hype. A study done in 2003 showed pre-menopausal women that took birth control had twice as much CRP in their blood than women who did not take the pill. Since chronically high CRP has been linked to heart disease and inflammation and is believed to play a key role in narrowing and hardening of the arteries, it would be easy to believe the pill promotes inflammation (had we not all recently learned CRP is not the best indicator of inflammation)! However the pill has also been studied to reduce the risk of ovarian cancer due to the estrogen present.. But that's a whole other story. Pros and cons, pros and cons.

The same study revealed that even though levels of CRP were twice as high in the women who took the pill, both group's levels were considered to be in the "normal" range.

So what do we get from all this... Women currently on birth control pills shouldn’t throw them out strictly based on the fear of increased CRH levels and heart disease. Remember, heart disease is most commonly linked to other important factors such as SMOKING, diet, and genetics. Also, there are other important risk factors associated with the pill that we should be concerned with (as discussed in the discussion about stroke and blood clots linked to the pill). In conclusion, More research is necessary on this topic and hopefully next time it will include more factors besides good ol' CRP.

SOURCES: American Physiological Society annual meeting, San Diego. Darlene M. Dreon, DrPH, director of clinical research, Galileo Pharmaceuticals, Inc, Santa Clara, Calif. Trent MacKay, special assistant for obstetrics and gynecology in the Contraception and Reproductive Health Branch of the National Institute for Child Health and Human Development, National Institutes of Health.

Statistics on Countries using turmeric in food VS those that don't and the incidence of RA in these countries.

So, I was very curious after reading about turmeric being used as a spice in many Asian cultures, is there evidence showing a lower incidence in RA in these types of countries compared to the United States. I found an article with statistics of how many people are affected by RA in each country. The US has upwards of 2 millions, while some rural Asian countries are in the low thousands. I have to speculate this being because of the population difference, but it would make sense if these countries show a lower incidence of RA. The article I presented in class today shows that the curciminoids in the turmeric are very effective at inhibiting the inflammatory response causing RA problems before the RA has infected the patient. After the onset of RA there is no evidence shown that turmeric curciminoids will have any affect. So if the rural Asian countries have used turmeric as a spice in their cuisine for centuries then why wouldn't they be more prone to be effected by the inflammatory responses to RA. Maybe we should take this into account and start using more spices with turmeric. This could help our problem of millions of people in the US that suffer from RA. We could reduce this risk of RA in the US simply by putting this into our foods. This is not a totally proven way of decreasing RA but it seems to sure help. My only concern is that the turmeric curciminoids could have other effects on our body with it's inflammatory inhibitor response. It could cause us to inhibit inflammation when we really need it and just cause more problems for us. I guess this is always the issue when dealing with new ways to deal with inflammation and other diseases though.

Hey guys check out this link to an article that states that high altitude wines are more beneficial in repairing arteriole walls than low altitude wines!

http://www.jancisrobinson.com/articles/jr876

I only researched this because I recently sat next to a metabolic surgeon on an airplane and we talked the entire flight about inflammatory diseases and their relations to metabolic surgery. He was the one who informed me of the latest trends of wine drinking.

Polypharmacy

A random note about the topic of polypharmacy that we went over briefly last class:
I work at an optometrist office and sometimes I enter patient history information into the computer system, especially if we have a new patient. One of the questions on the patient history form asks the patient to list out any medication they are currently taking. This patient that I was working with needed help with that portion because she said she did not know all of the medication she was on. She said she was on "hundreds," and although that was an exaggeration, it is a good example of polypharmacy. When asked if she had some sort of list, she said "no."
Even though the likeliness of a complication arising when dealing with an eye exam is very slim, it was just a good example showing that if a patient is taking more medication than they can remember, they should always carry around a list with them.

Herbal Medicine

Herbal medicine relies on active plant chemicals with biological properties. Many conventional medicines are synthetic compounds designed to mimic the action of plant chemicals. For instance, the heart medication digoxin is derived from the foxglove plant. In herbal medicine, active chemicals are extracted from the plant parts (stems, seeds, roots, or leaves) that are the richest sources. The active chemicals can be quantitatively measured and prepared in the form of capsules, tinctures, teas, tonics, oils, or poultices. Aromatic herbs such as lavender can also benefit the immune system when used topically or as healing oils.

Inflammation is a key feature in autoimmune disease. In some conditions, such as Hashimoto's thyroiditis, inflammation contributes to the disease process. In other conditions, such as Crohn's disease, inflammation may occur as a result of the disease. Inflammation occurs as the immune system reacts to injury, infection, environmental agents, malignancy, and cellular changes. In skin, inflammation is most visible because it causes noticeable swelling, redness, discomfort and pain. The process leading to inflammation, which is known as the inflammatory response, also induces changes that aren't seen but influence the effects of inflammation and their severity.

The inflammatory response is a complex cascade of steps that include an activation of white blood cells, the release of immune system chemicals such as complement and cytokines, and the production and release of inflammatory mediators and prostaglandins. Inflammation may be acute or chronic or relapsing-remitting depending on the disease course. Most conventional treatments for autoimmune disease, including corticosteroids, work by reducing or suppressing inflammation.

Many herbs also possess anti-inflammatory (also known as antiphlogistic) characteristics. Herbs can be used as the sole therapy in autoimmune disease or as complementary corticosteroid-sparing therapies allowing patients to take smaller doses or shorter courses of corticosteroids. Treatment protocols today often rely on both alternative and conventional treatment options in a discipline known as integrative medicine.

Inflammation is a key feature in autoimmune disease. In some conditions, such as Hashimoto's thyroiditis, inflammation contributes to the disease process. In other conditions, such as Crohn's disease, inflammation may occur as a result of the disease. Inflammation occurs as the immune system reacts to injury, infection, environmental agents, malignancy, and cellular changes. In skin, inflammation is most visible because it causes noticeable swelling, redness, discomfort and pain. The process leading to inflammation, which is known as the inflammatory response, also induces changes that aren't seen but influence the effects of inflammation and their severity.

This article describes the use of plant chemicals with anti-inflammatory properties as complementary therapies for patients with autoimmune disease. Also this article I found it interesting because it gives another alternative to the consumption of NSAIDS or other drugs; the alternative way is the use of herbal products that will eventually treat the symptoms.

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.

Dr. Weil: The Anti-Inflammatory Diet

This week’s topic is anti-inflammatories. Many of you may have heard of Dr. Andrew Weil. He is a Harvard Medical school graduate who has been at the forefront of popularizing Integrative Medicine. He is the program director of the Arizona Center for Integrative Medicine here at the University of Arizona which he founded in 1994. Since his undergraduate career he has been interested in botany and the role plants can play in health. Interestingly, he wrote his thesis on the narcotic properties of nutmeg. However, in recent years he has concentrated his focus on different lifestyle interventions that may assist in medical treatment. One of these is the Anti-Inflammatory Diet.

Dr. Weil credits the Anti-Inflammatory diet as more of a lifestyle than an actual diet. However, he claims that “it is the blueprint for optimum nutrition”. He continues to say that simple changes in eating habits can counteract inflammation which is at the root of diseases such as: heart disease, Alzheimer Disease, Parkinson Disease, age related disorders including cancer and autoimmune diseases such as rheumatoid arthritis and lupus. At the heart of his diet plan is variety and a balance. The diet strives to balance omega-6 fatty acids (said to promote inflammation) and omega-3 fatty acids (anti-inflammatory). It recommends that we eat less meat and poultry which contain omega-6 fatty acids and eat more fish with have omega-3 fatty acids. It also aims to decrease refined and processed foods which often contain pro-inflammatory compounds called AGEs (advanced glycation end products) and have a high glycemic index. Dr. Weil’s modified version of the food pyramid depicts the Anti-Inflammatory diet’s key points very well.

I can definitely see the benefit in eating a healthy diet in order to maintain balance in our body and optimum functioning. I would say that the Anti-Inflammatory diet is a wonderful lifestyle to promote. However, I as being “anti-inflammatory”, I am still on the fence. But, it is all comparative: it is anti-inflammatory compared to the fast food nation we have become with diets high in saturated fat. Looking over the pyramid, the way of eating appears to be much more similar to our hunter/gatherer past with a greater emphasis on fruits, vegetables and fish and sparse consumption of poultry, red meat and sweets. Take a look for yourself and let me know what you think: http://www.drweil.com/drw/u/ART02012/anti-inflammatory-diet

Medications Used in the Treatment of Alzheimer’s Disease

I had discussed in the class the research that is being conducted regarding the relationship between fibrin and Alzheimer’s Disease. I was interested in finding the current medications that are used in the treatment of AD, and came across an article from a PhD student, Carrie Hill. We know that there is no current cure for AD, which is why studies like I discussed in class are being performed. There are, however, medications that improve symptom management of the disease. When developing treatment plans, the cognitive and behavioral symptoms are considered.
I wanted to focus on cognitive symptoms, which include problems with thought processes like memory, language, and judgment. Cholinesterase inhibitors and Namenda are two kinds of medications that have been approved by the FDA for treating these symptoms. Cholinesterase inhibitors increase the levels of acetylcholine in the brain, which plays a key role in memory and learning. Surprisingly, this alone can postpone the worsening of symptoms for 6 to 12 months in about half of the people who take it. Cholinesterase inhibitors are most commonly prescribed for mild to moderate Alzheimer’s disease. Namenda, known as memantine, regulates glutamate in the brain, which plays a key role in processing information. This drug is used to treat moderate to severe Alzheimer’s disease and may delay the worsening of symptoms in some people.
Cholinesterase inhibitors can be started as soon as Alzheimer’s symptoms appear, and are most effective in the early stages of disease. When a physician determines that the cholinesterase inhibitor is no longer effective, memantine is usually introduced. Sometimes, memantine and a cholinesterase inhibitor are taken simultaneously during the moderate stage of the disease. I wonder if this combination with the addition of anti-inflammatory drugs would show a decrease in the progression of Alzheimer’s Disease?

http://alzheimers.about.com/od/treatmentofalzheimers/a/treatments.htm

Multiple Sclerosis: A Causative Analysis

As we've already read in class, many researchers are looking at what they believe is/are the cause/s for the development and full expression of multiple sclerosis. We read a paper on microglia changing its phenotype to a cell somewhat identical to a phagocyte, and past research focuses have been on T cells. This condition is commonly referred to as an autoimmune response to some protein of the myelin sheaths, though this is still debatable. Current treatment can attenuate the response and lesson the symptoms, but there is no way to target any chemical treatment to the nervous tissue without effecting the entire immune system and its cells--so attenuating the cells of the immune system pharmacologically if a patient with MS also attenuates any immune response (depending on the compound used). The research of MS is further confounded by research models. Currently, rate or mice are generally used; however, since the cause of the disease is unknown, we cannot accurately say that the animal models are expressing the disease to the same or similar extent.

The affected tissue lies deep within the brain, forbidding any manual intervention that would not cause unknown irreversible consequences. Recent research has been done on the assumption that MS spontaneously begins with auto-reactive T cells, and this is supported by the mice models which much be injected with nervous tissue to develop the disease. Countering this idea is a group of scientists who have developed a murine which spontaneously develops MS. All murine models of MS have not been able to show B cell involvement, except this new model. The group found that yes, T cells are active in the model, but they are not actually inducing disease...B cells induce MS (shown by general good health in these models when B cells are removed). This is not to say that B cells are the prime player. T cells can do plenty of damage in the brain, but antibodies may be needed to sustain and develop the disease.

I just found this research interesting, and linked the paper's title above. I still feel it's important to take this with a grain of salt, simply because this is one study, published recently, in a species other than our own with a disease that is still not understood fully and may not completely represent how we express the disease. There's obviously a lot of research to do, but it's so very interesting to read about these finds which go against what the topic's body of research says.

The role of glial cells in Parkinson's Disease

The glial reaction is generally considered to be a consequence of neuronal death in neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and Parkinson's disease. In Parkinson's disease, postmortem examination reveals a loss of dopaminergic neurons in the substantia nigra associated with a massive astrogliosis and the presence of activated microglial cells. Recent evidence suggests that the disease may progress even when the initial cause of neuronal degeneration has disappeared, suggesting that toxic substances released by the glial cells may be involved in the propagation and perpetuation of neuronal degeneration. Glial cells can release deleterious compounds such as proinflammatory cytokines (TNF-α, Il-1β, IFN-γ), which may act by stimulating nitric oxide production in glial cells, or which may exert a more direct deleterious effect on dopaminergic neurons by activating receptors that contain intracytoplasmic death domains involved in apoptosis. In line with this possibility, an activation of proteases such as caspase-3 and caspase-8, which are known effectors of apoptosis, has been reported in Parkinson's disease. Yet, caspase inhibitors or invalidation of TNF-α receptors does not protect dopaminergic neurons against degeneration in experimental models of the disease, suggesting that manipulation of a single signaling pathway may not be sufficient to protect dopaminergic neurons. In contrast, the antiinflammatory drugs pioglitazone, a PPAR-γ agonist, and the tetracycline derivative minocycline have been shown to reduce glial activation and protect the substantia nigra in an animal model of the disease. Inhibition of the glial reaction and the inflammatory processes may thus represent a therapeutic target to reduce neuronal degeneration in Parkinson's disease.

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AD-Cholesterol Connection

As I had mentioned in class, there has been an establishment of cholesterol as a risk factor in the pathogenesis of Alzheimer’s disease (AD). This is a major focus of current research for AD. I came across a review article from PubMed titled, Alzheimer’s disease: the cholesterol connection, and found that in the past few years, this link has been supported through genetic, epidemiological and biochemical data. The review was from Harvard Medical School’s Neurobiology of Disease Laboratory and Genetics and Aging Research Unit.

In all forms of Alzheimer’s disease (AD) there is an abnormal accumulation of the beta-amyloid protein in specific brain regions, which is regulation by cholesterol. It was found that elevated levels of cholesterol increase the beta-amyloid protein in cellular and most animal models of AD, and that drugs that inhibit cholesterol synthesis lower the beta-amyloid levels. Recent studies have shown that the total amount and distribution of cholesterol within neurons impact the beta-amyloid biogenesis. I mentioned in class the role of the apolipoprotien E gene, the identification of a variant of this gene as a major genetic risk factor for AD is consistent with a role for cholesterol in the pathogenesis of AD.

The review describes its recent findings concerning the molecular mechanisms underlying the cholesterol-AD connection. Drugs that lower cholesterol levels are currently being considered and tested as potential therapies for the treatment of AD. Statins, which are relatively safe and have been used for a long time against high cholesterol levels, are now being directly tested in clinical trials for efficacy against AD. Some of the potentially beneficial effects of statins might also represent improved cardiovascular health, resulting in a reduction in ischemic events that are also considered risk factors for AD. An effective therapy for patients whose cognitive function does not benefit from statin treatment may ultimately consist of a combination of lipid regulating products, perhaps in combination with statins. Alternative products for cholesterol management so far include extended-release niacin, cholesterol absorption inhibitiors, ACAT inhibitors and cholesteryl ester transfer protein (CETP) inhibitors. Results from in vitro studies suggest that ACAT inhibitors are good candidates for regulating beta-amyloid biogenesis, but more research is needed to understand the exact molecular mechanisms underlying the AD-cholesterol connection. Also, it is necessary to gain an in-depth understanding of brain cholesterol metabolism. With new technology that is developing, we may be able clarify how plasma and brain cholesterol contribute to AD.

Full PDF text found at EBSCHOhost:
Title: Alzheimer's disease: the cholesterol connection.
Author: Puglielli, Luigi; Tanzi, Rudolph E.; Kovacs, Dora M.;http://web.ebscohost.com/ehost/pdfviewer/pdfviewer?vid=2&hid=106&sid=86523406-21ed-4ee6-8f03-87d50b8af3df%40sessionmgr110

Sunlight (UV) and Multiple Sclerosis?

As I mentioned in class, the 2010 CDC study found a correlation between areas of highest MS prevalence and greater UV exposure. I've chosen to explore this idea and I've found an article which I've referenced below which discusses an exploration of this trend:

For some time now, the observation that MS prevalence increases with latitude, meaning the further from the equator one gets, the higher likelihood of MS in the environment. Researchers in this article therefore look at Vitamin D and how its levels may in these different latitudes may help explain the differences in prevalence.

The article notes that 400,000 people in the U.S. have MS, of nearly 309, 055, 803 people in the U.S. (U.S. Census Bureau). UV exposure, as well as vitamin D levels can effect immune responses, but the question which arises is whether immunoregulation is done via UV exposure, or indirectly via vitamin D levels, or the two? As referenced in the article, research somewhere (not cited) has shown that increased levels of the active form of vitamin D can "block" the disease in animals.

The experiment uses mice which are genetically predisposed to an MS-like disease state, and the mice are injected with nerve antigen to initiate the disease. After initiation, one group of animals were exposed to "moderate" UV strength (equal to 2 hours of direct summer sun) for one week and the other group was irradiated every 2nd or 3rd day. They found that the exposure reduced the expression of symptoms for MS, but not the prevalence, especially in those mice irradiated every other day. The researchers also deduced that although vitamin D levels were increased with UV exposure, that factor alone could not explain the results.

The groups next area of study is to see what role skin may play with UV exposure to the production and expression of compounds involved in inflammation and the inflammatory response. The article identifies two possibilities of usefulness:

1. In the short term, if they can identify the specific active wavelength at which these same results can be obtained, this can be used as a therapy for those people suffering from MS.

2. In a more long term goal, if the group can discover the compound or compounds that the skin may be producing, the may be able to isolate or synthesize the compound and market a drug treatment.

The group does caution that this information is in the early experimental stages of development, and that results of a similar treatment may not lead to intentions.

Article

Food Allergies linked to RA???

In class we discussed the possibility (mentioned in one of our lay articles) that RA may be linked to an "allergic" type of response to certain foods.

I did a little bit of research on the subject and found an article that suggests that RA symptoms may be caused by an "allergic" immune response to foods such as milk and other dairy products. The basic premise of the study the article mentions is that your body may produce antibodies to certain foods. These antibodies form immune complexes in your intestines and from there, these complexes can travel throughout your body and become inflammatory mediators.

This article mentions a study done by an individual doctor who noticed that up to a third of his RA patients felt improvement in their symptoms when they eliminated most allergy-causing foods and reverted to a basic "Stone Age" diet of fruits, vegetables, fish, and plain meat.

Here is a link to the article :http://www.arthritistoday.org/conditions/rheumatoid-arthritis/healthy-living/ra-food-allergies-2.php

Neurodegenerative Disease

This week, we will be discussing inflammation associated with neurodegenerative disease. Neurodegenerative disease is the umbrella term that encompasses diseases that involve progressive dysfunction and loss of neurons in the central nervous system. Some examples of neurodegenerative diseases include Parkinson disease, Alzheimer disease, multiple sclerosis, Huntington's disease, amyotrophic lateral sclerosis or Lou Gherig's disease, and Friedreich's ataxia. These diseases may cause decline of motor functioning and cognitive functioning, and eventually death. The impact of these diseases can be devastating to patients and their family members, not only functionally and emotionally but also economically. Thousands of dollars are spent on medical care provided by physicians, nurses, pharmacists, physical therapists, occupational therapists, speech-language pathologists, dietitians, and social workers. Thousands of dollars are also spent on research focused on preventing or remediating these diseases.

The articles for this week's discussion indicated that, while researchers are making progress toward understanding the mechanisms behind these diseases, effective treatment approaches for these diseases have not yet been discovered. Even when treatment approaches seem to work in the early phases of research, they later prove to be ineffective and even sometimes result in lethal side effects. As economic times become even more challenging, fewer and fewer studies will be approved, and the progress toward finding effective therapeutic approaches will likely be stalled even more.

What are your suggestions for improving the system for research that we have now to facilitate progress toward finding effective treatments for neurodegenerative diseases?

Arthritis and Intereukin 1

One of the presented articles this week compared anti-TNF treatments with anti-IL-1 treatments in the CIA model. The article showed many more benefits when using the anti-IL-1 treatment, but did not have much information regarding human clinical trials. This article was from 1999, so I was very curious to see what some of the current anti-IL-1 treatments were.

I found the review article "Actual status of antiinterleukin-1 therapies in rheumatic diseases," which reviews some of the current clinical options for arthritis and rheumatic diseases. The article summarizes the pathophysiologic role of IL-1 and also goes over the three major types of anti-IL-1 treatments including Anakinra, Canakinumab, and Rilonacept. Anakinra is a treatment which prevents the binding of IL-1 by occupying the IL-1 receptors. Canakinumab is a fully human monoclonal anti-IL-1 beta antibody, which works by binding and neutralizing IL-1 beta. This was recently granted orphan drug status in Europe and the United States for the treatment of systemic juvenile idiopathic arthritis. Rilonacept is a dimeric fusion protein that consist of the ligand-binding domain of IL-1RI and its accessory protein, which is designed to bind and neutralize circulating IL-1.

Many of the studies have so far concluded short-term benefits in terms of biochemical markers, joint damage, and inflammation, but data for long-term use is still being collected. The advancement of these types of treatments in the past decade has really helped fight arthritis by increasing therapeutic options, but continued observation for long-term effects and further advancement is still necessary.

The full article and description of the reviewed studies can be found here:

http://www.ncbi.nlm.nih.gov.ezproxy2.library.arizona.edu/pubmed/20150813

Biological Agents for Relief of RA

Several people in my life (including my mother) have struggled with RA and have now found relief with so-called "biological agents." I was interested in finding out exactly what these "agents" are and how they work (immunologically speaking . . . . )

These treatments are currently marketed as Enbrel, Remicade, and Humira. They are each a slightly different type of TNF (tumor necrosis factor) blocker. As we all know, TNF is a pro-inflammatory cytokine. These medications (which must be given as an injection or as an intravenous infusion) work by completely blocking the action of TNF. This provides great relief to many RA sufferers. For some, it even stops the progression of rheumatoid arthritis.

This may seem to be a perfect treatment! But . . . A major downside to this type of treatment (an issue that we discussed on Monday) is that our immune systems manufacture TNF for a reason. By blocking TNF completely, the immune systems of the RA patients are compromised and the patients are therefore highly susceptible to infectious diseases. I suspect that research in this area will continue until a treatment is found that inhibits progression of RA without compromising the immune system in the process.

Vitamin D and Rheumatoid Arthritis

So I was looking around at studies done on treatments for arthritis and ran across this article on Vitamin D. The article is called "Vitamin D intake is inversely associated with rheumatoid arthritis: results from the Iowa Women's Health Study". The point of their study was to evaluate the association between vitamin D intake and incidences of rheumatoid arthritis. They picked women between 55 and 69 who previously had no history of rheumatoid arthritis. Their diet and vitamin D intake were evaluated using a questionnaire. The women were then followed up for 11 years to check possible cases of the disease. Their results showed that a greater intake of Vitamin D lead to a decreased risk of RA.

An issue with this study is that it was only done on women. We really have no data then on how Vitamin D intake affects men. It might also be interesting to see what affect Vitamin D has on people who already have rheumatoid arthritis.

http://www.ncbi.nlm.nih.gov/pubmed/14730601

Psoriatic Arthritis

Many articles about arthritis mention that there are hundreds of types of arthritis. The most common types that we have been discussing in class are rheumatoid arthritis and osteoarthritis, which are also the only 2 out of hundreds that I have heard of before. So I decided to learn about another type of arthritis.

I found an article containing information about a type of arthritis that occurs in people with psoriasis, called psoriatic arthritis. It is defined as "an inflammation of the joints that occurs in 10 to 30 percent of patients with psoriasis. It is not a type of psoriasis, but a symptom of psoriasis which is classified as a type of arthritis." The article I found stated that "Approximately 1 million people in the United States suffer from psoriatic arthritis. Most of them are adults between the ages of 30 to 50. However, psoriatic arthritis can affect juveniles and young people." I thought that it was very interesting that this type of arthritis is known to occur in children, because arthritis is usually said to occur in older people.

Psoriatic arthritis is suspected to be caused by genetics, but the cause is unknown. Therapy for this condition includes psoriasis treatment and progress that is being made in a type of medication made from human and animal proteins, called biologics.

http://www.omnimedicalsearch.com/conditions-diseases/psoriatic-arthritis.html

Arthritis and Heredity?

One of you asked whether arthritis is hereditary so I decided to try to find some information on it. Discovery Health posted an article titled “Arthritis and Heredity” in which it talked about the many forms of arthritis and which ones tend to run in families. The most common varities of arthritis are osteoarthritis and rheumatoid arthritis with arthritis affecting one in seven Americans. While the article did not talk very much about the heredity of arthritis too much it did provide a lot of information on how arthritis can develop and what types of people are most affected. In osteoarthritis may be due to inactivity caused by muscle weakness and obesity. This form of arthritis is more common in women and in older people. Rheumatoid arthritis involves the body’s immune system attacking its own tissues. Women are much more likely than men (2 times more) to have this form of arthritis. Unlike osteoarthritis, rheumatoid arthritis tends to affect people of all ages and can travel throughout the body.

Here is the link to the site:

http://health.discovery.com/centers/arthritis/arthritis_qa/arthritis_hered.html

Hydrotherapy and Tai Chi effects on Osteoarthritis

As I was looking around for arthritis related topics to blog on, I came upon an interesting study that looked at two different activities and their effect on symptoms of OA.

The study done in 2007 ran a 12 week test, with a 12 week follow up, on 152 elderly sufferers of osteoarthritis of the hip or knee. Subjects needed to be about 70 years of age and classified as inactive. 55 subjects were placed in a 12 week hydrotherapy class, 56 subjects were placed in a 12 week Tai Chi course and, 41 were placed in a control (wait list). Each session was 1 hour long and held twice a week, making a total of 24 classes.
Results showed a decrease in joint pain for patients in both hydrotherapy and Tai Chi groups based on the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) scores. Physical function also improved in these two groups and was tested using the "Up and Go" test, 50-foot walk time, and timed stair climb. The "Up and Go test" is a measure of a patient's ability to get up out of a chair without arm support, walk several paces out and back, and sit back down without arm support. These improvements were sustained by most subjects for an additional 12 weeks after the classes.


http://www.arthritiswa.org.au/documents/PAFORMmainresultsACR.pdf

The article "What A Pain," from The Boston Globe, referenced the Arthritis Foundation a few times, so I decided to learn more about it. I went to the website and found that it was actually very helpful and informative about arthritis. The website has information about many types of arthritis, events to raise awareness, and current research.

One of the topics that is currently being researched that I found interesting was in an article called, "Clarifying the Role of Fat in Osteoarthritis." It mentions how obesity is thought to increase the risk of arthritis due to increased weight and force on joints. The article goes on to say, "excess fat may take a toll in another way, too. Fat is a metabolically active tissue that secretes cytokines, or signaling molecules, that can trigger inflammation. An increase in cytokines may help to explain why, for example, obesity increases the risk not only for osteoarthritis in the knees, which would be directly impacted by the increased load, but also in the wrist, which is not a weight-bearing joint."

Research is currently being done on this topic. Here is the website to the Arthritis Foundation webpage
http://www.arthritis.org/

Different Categories of Crohn's Disease

Interestingly I stumbled on a website that contained alot of really interesting information about Crohn's Disease. A lot of the material was, more or less, a review of things that we have seen in the various papers we have read; however, I did find a couple of interesting things that we have not really talked about. The first is different categories of Crohn's. The following table was taken from the website Crohns.net and lays out various forms of the disease mostly based on the origin of the symptoms.

Subcategory	Area Affected
Ileocolitis	The most common form of Crohn's Disease, affecting the ileum and colon
Ileitis	Affects only the ileum; fistulas or inflammatory abscesses possible
Gastroduodenal Crohn's Disease	Affects the stomach and duodenum; bowel obstruction possible
Jejunoileitis	Patchy areas of inflammation in the jejunum; fistulas possible
Crohn's (Granulomatous) Colitis	Affects only the colon and anus; anal fistulas, abscesses, and ulcers possible

Adapted from Crohn's and Colitis Foundation of America, Inc. 2004
http://www.ccfa.org/research/info/aboutch

There is also some interesting information about diseases that can arise from Crohn's. Of these one of the most common is osteoporosis. This comes about for two reasons; the first is a lack of nutritional absorption of vitamins d and k and the second is the treatment of the disease with corticosteroids. Both of these lead to decreased bone density and thus the condition of osteoporosis. Some other major medical problems that could occur either as a result of the different therapies or the disease state itself are colorectal cancer, infertility, bacterial infections, even a higher possibility of ischemic stroke. The increase in risk for stroke is thought to be because of a vitamin B deficiency and a hypercoaguable state brought on as an effect of the disease.

If you would like to to read more about this or see more about Crohn's in general visit crohns.net.

Information taken from
http://www.crohns.net/Miva/education/articles/Potential_Sequelae_of_Crohns_Disease.shtml\
http://www.crohns.net/Miva/education/articles/Crohns_Disease_Table_1.shtml

Stress and IBD

There was an interesting correlation mentioned while I was researching about inflammatory bowel disease (IBD). This article examined the association between stress and IBD. In the past, there were several studies done that illustrated how IBD is affected by psychological components such as stress. With recent findings, research has shown that stress does not induce IBD; however, because of the past association between stress and IBD, the general public believes this false correlation. Often times, diseases such as IBD bring about stress and manifest effects through symptoms. In IBD, irritability, depression, or panic attacks can occur due to stress making IBD worse.

Another article I found on PubMed looked into the psychological aspects of inflammatory diseases and mentioned that stress does play a factor in IBD. Not only does it aggravate IBD, some believe that stress can cause IBD. Stress can affect the functions of secretion, vascular structure, and motility of the GI tract.

To examine if stress is associated with IBD, another case study evaluated stress by life even occurrences in Crohn’s disease and ulcerative colitis patients along with two control groups. Various questionnaires were utilized to assess stress in patients. It was concluded in this paper that stress such as life event is not considered an independent risk factor for the cause of IBD.

It appears to me that there is varying knowledge of the association of stress and IBD. The general public seems to relate the two as one causing the other while medical researchers do not categorize it as a risk factor but a factor that aggravates onset of the disease.

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=3765643&ordinalpos=237&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=3765643&ordinalpos=237&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Some Interesting and Recent Studies on IBD

Today, as I was searching the web for some fun facts we may not have touched on regarding IBD, I came across a recent news article that caught my attention. Published only yesterday, the lay article citing a very recent study on IBD spoke of a vaccine currently in development which, “can delay IBD development, control inflammation and thereby reduce the risk of future cancers.” The vaccine targets the MUC1 protein produced by the body which is found in large amounts in a patient with IBD. When tested in animal models the vaccine was shown to delay the onset of IBD symptoms which then reduced the risk of colon cancer. This recent finding could lead to a possible therapeutic option to lesson or delay the symptoms of IBD in a patient. I attempted to find the original article published in Cancer Prevention Research but was unable to do so due to the recent date of the publication.

Here is the link to the lay article I found online:

http://news.xinhuanet.com/english2010/sci/2010-03/25/c_13223568.htm

Here is a website with more information and specifics about the MUC1 protein:

http://www.genecards.org/cgi-bin/carddisp.pl?gene=Muc1

Also when I was scouring the web for different IBD tid-bits I came across a nice question and answer site with a good general overview of what is known today about IBD. It contains much of the terminology covered throughout the articles we have read over the past two weeks. Here it is:

http://www.ittakesmorethanguts.com/media/faq.htm

The final article that caught my eye on my search proposed a connection between IBD and venous thromboembolisms. The study shows that patients suffering from IBD are sixteen times as likely to have a venous thromboembolism than people who do not have IBD. The study followed 13,756 patients with IBD and 71,672 healthy controls. Of the subjects, 139 IBD patients reported a venous thromboembolism and 165 reported cases in the control group.

Here is a link to the lay article:

http://www.medpagetoday.com/Gastroenterology/InflammatoryBowelDisease/18362

Here is a link to the journal article:

Grainge M, et al "Venous thromboembolism during active disease and remission in inflammatory bowel disease: a cohort study" Lancet 2010; DOI: 10.1016/S0140-6736(09)61963-2.

The main page where I found this article has quite a few articles about IBD. Here is the link to that if you would like to read more:

http://www.medpagetoday.com/Gastroenterology/InflammatoryBowelDisease/

IBD Management

While going through my daily browsing through Yahoo Health, I stumbled upon an article relating to Inflammatory Bowel Disease (IBD). Since many of the articles we read touched upon treatments targeting the initiation of inflammation before tissue damage occurs, I thought it would be interesting to read about various treatments. Treatment is individualized based upon each patient. The physician and the patient work closely to develop which treatment goal is most effective. The goals are developed based upon the intensity of IBD and the side effects of a treatment. Managing IBD serves to improve quality of life by either reducing symptoms or eliminating them. This article discusses the use of corticosteroids for IBD to reduce the inflammatory response in ulcerative colitis and Crohn's disease. Typically, corticosteroids are used by people with severe symptoms because they stop symptoms by putting patients in remission. Long term use is not encouraged because they have side effects which limit treatment. Using systemic corticosteroids causes side effects such as acne and severe mood changes, adrenal insufficiency, visual changes, cataract formation, and aseptic joint necrosis.

Pregnant women use corticosteroids to manage IBD as well. They are considered as a safe means of treatment when symptoms flare up. Before, women with IBD were advised not to have children because they are more at risk for having a miscarriage, to deliver prematurely and to have a low birth weight infant. Medications have been used to help manage this problem in order for women to have a more successful pregnancy.

One common factor that develops with IBD is depression. This coexistence further decreases the “fair and poor” quality of life many IBD patients have described. Nearly 30-50 percent of people with IBD also suffer from depression and of these people, 30 percent develop a dependence on medication and alcohol.

Sources:
http://www.aafp.org/afp/980101ap/botoman.html
http://health.yahoo.com/digestive-medications/corticosteroids-for-inflammatory-bowel-disease/healthwise--hw40876.html;_ylt=AhI4dhx_I93e9ODpBwFreVFLvs8F

UA Live Fit

During several of our class discussions regarding inflammatory diseases, we have mentioned the importance of diet and exercise in preventing and remediating some of these diseases. We have also discussed the lack of education in the U.S. specifically about diet and exercise. I just learned that UA Campus Health is introducing a new web-based program to educate students about living healthy, active lives. Apparently, everyone with a UA net ID and password will have access to this web-based service, which is described in the UA News (see link below) as “kind of like having an online personal trainer and nutrition adviser that’s available to you 24/7.” The website provides information about preparing nutritious food with limited resources, finding nearby restaurants that serve nutritious food, implementing new exercise programs, and even tracking fitness goal progress. For more information, follow this link to the UA news article:

http://uanews.org/node/30533

Surgical Options for Crohn's Disease/Ulcerative Colitis

Alright so we talked about many of the different treatment options available for people suffering with Ulcerative Colitis or Crohn's Disease including immunosuppressants, steroids, anit-inflammatories, and probiotics; however I thought that I would post about the surgeries available for these people. The problem with surgery is that the Crohn's & Colitis Foundation of America have found that about 50% of patients that have surgery will see a recurrence of the disease, but they do state that medication (like the ones listed before) taken after the surgery can help the patient avoid, or at least delay, a recurrence.

There are really three options depending on the severity of symptoms. The first surgery is called a strictureplasty. This procedure is used to widen the narrowed diseased areas of the small intestine. FYI the diseased areas are called strictures and are a result of scarring brought on by the chronic inflammation of the disease. The surgery is as simple as cutting open the stricture then sewing it back up crosswise.

The second option is called a resection. This surgery is used when strictures are very long or there are many of them within a close vicinity and simply cuts away the diseased section then the healthy ends to the intestine are reattached. Finally if the damage done by Crohn's is really bad then a colectomy or proctocolectomy may be needed. The colectomy procedure removes the whole colon while the proctocolectomy does the same but also removes the rectum which means that another procedure (ileostomy) would be needed to create a stoma that would allow the patient to pass stool.

There are two quality of life issues that are presented to a patient; especially with a surgery like the proctocolectomy. The first is that a colostomy bag is needed when the rectum is removed; which means that it will have to be emptied multiple times a day and obviously would have to be worn all day. Also if too much of the intestine is taken it is possible to end up with short bowel syndrome. Essentially this can lead to malnutrition/dehydration and diarrhea. This happens because the decreased length of intestine does not provide adequate room for absorption of nutrients, minerals, and water. To counteract this people with short bowel syndrome have to take supplements and eat very small meals at a much more frequent pace then normal.

All in all it may seem as though surgery is a bad option; however it is essential when medications no longer control the symptoms.

Here are the websites where I found this info:
http://www.ccfa.org/info/surgery/surgerycd
http://digestive.niddk.nih.gov/ddiseases/pubs/shortbowel/
http://www.umm.edu/patiented/articles/what_surgical_procedures_crohns_disease_000103_10.htm

IBD in Children and the Difference Between IBD and IBS

As a volunteer in the Pediatric Unit at the Tucson Medical Center over the past year something I find interesting is the communication between doctors and their child patients. It made me think about my topic this week and how I would go about explaining to a child who has IBD exactly what was going on inside of their bodies. The most common age range for this disease is 15 to 30, however, there are reported cases of even younger children who are affected. So how do you bring up a “sensitive” issue like this to a child? I have seen some pretty interesting techniques from the use of puppets to doctors addressing a child as if they were another doctor. You would be surprised what some kids can remember! So I found a couple of internet sites dedicated to the discussion of IBD in a way children would understand. The links are below:

http://kidshealth.org/parent/medical/digestive/ibd.html#

http://kidshealth.org/kid/health_problems/stomach/IBD.html

Here is also a site where kids explain their disease in their own words:

http://growingupibd.org/

The last link is important in that it shows the diversity of the symptoms present in a population of children. Each kid’s story is different and so are their needs as a patient. That is probably the biggest thing I have learned as a volunteer. What might work on one child may totally backfire with another. I have seen the puppet trick give a child a better understanding of their illness in one case while bringing a different child completely to tears. This is an important aspect of medicine to keep in mind for anyone in the field. The needs of patients both young and old should be examined on an individual bases. There is no one correct way to address a child about their illness.

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I also thought it would be good to address the difference between IBD and IBS for those of us who needed clarification. Both IBD and IBS have similar symptoms that may cause confusion to a patient. Symptoms of both include: alteration of bowel habits, pain, discomfort, bloating and increased urgency to use the restroom. The difference between the two illnesses is that IBS does not involve inflammation of the GI tract where IBD is identified by the inflammation of the mucosal tissue in the intestines. IBS is also known as a spastic colon or bowel and is an example of a functional disorder. A functional disorder is defined as “a disorder of physiological function having no known organic basis.” (http://medical-dictionary.thefreedictionary.com/functional+disorder). In other words there is an abnormality in the function of the GI tract but there are no physical signs of a problem. All in all, IBD is a more serious illness than IBS, The physical toll that the chronic inflammation can take on the GI tract can lead to ulcers as well as anemia from stool blood loss.

Probiotics

One of the lay articles assigned for this week had said that Americans consume fewer fermented products that any other developed country and I agree with that author. Americans tend to turn to drugs when dealing with health issues, while Asian and European cultures stick to the more "natural" remedies. After reading that lay article that talked about probiotics in things like yogurt and fermented milk, I was curious because we had recently done an experiment to isolate microbes from yogurt in micro lab. So, I decided to try and search for the "best" brands of yogurt to eat. Instead I came across another article which talks about Kimchi, which is a spicy Korean dish that contains a strain of the probiotic Lactobacillus that was found to help reduce cancer cell growth. I'm not saying you should go and eat lots of Kimchi (because it's definitely not for everyone. I personally don't like it), but I just found this pretty surprising and interesting that such unexpected foods have promising health benefits, so I decided to share. Enjoy!


The full article can be found here:
http://www3.interscience.wiley.com/cgi-bin/fulltext/123206305/HTMLSTART.

Stroke Symptoms

Hey guys! Here is a great way that I found from the National Stroke Association to remember the symptoms of a stroke! It's called "Act F.A.S.T."

FACE	Ask the person to smile. Does one side of the face droop?
ARMS	Ask the person to raise both arms. Does one arm drift downward?
SPEECH	Ask the person to repeat a simple sentence. Are the words slurred? Can he/she repeat the sentence correctly?
TIME	If the person shows any of these symptoms, time is important. Call 911 or get to the hospital fast. Brain cells are dying.

An additional method that can be used when one suspects a stroke is as follows: SUDDEN numbness/weakness of the face, arm, or leg, especially one side of the body. SUDDEN confusion, trouble speaking/understanding. SUDDEN trouble seeing in one or both eyes. SUDDEN trouble walking, dizziness, loss of balance or coordination. SUDDEN severe headache .

I also found some surprising statistics including the one which stated that twice as many women die from stroke every year than from breast cancer. I also found it interesting that strokes are preventable. Here are the guidelines offered on how to prevent a stroke:

Stroke Prevention Guidelines

Know your blood pressure. Find out if you have atrial fibrillation. If you smoke, stop. If you drink alcohol, do so in moderation. Find out if you have high cholesterol If you are diabetic... Exercise. Enjoy a lower sodium (salt), lower fat diet. Circulation (movement of the blood through the heart and blood vessels) problems. Know the Symptoms of Stroke.

All this information came from www.stroke.org.

"Deadly Inflammation, But No Sign of Infection"

Not necessarily relevant exactly, but interesting nonetheless:

A paper in the journal Nature published evidence that during systemic inflammatory response syndrome (SIRS), blood plasma was found to have large amounts of mitochondrial DNA (1000 times more than in normal plasma).

The study suggests from the data that when there is damage to many cells, they will release "mitochondrial debris" and the body will respond to these debris as if it were a foreign pathogen. The study tested the neutrophil response to increased mitochondrial debris in the plasma and found a similar response to the debris as one would see toward foreign invaders . If you choose to read, the study further tests the idea that these mitochondrial debris elicit an immune response by the neutrophils.

Link to Nature Article

Cardiovascular Disease

The four most common types of cardiovascular disease are coronary heart disease (which includes heart attack and angina pectoris or chest pain), stroke, high blood pressure and heart failure. Smoking, unhealthy diet, lack of physical acitvity, and over use of alcohol increase the risk for CVD. In 2000, CVD claimed over 945,000 lives, that’s one in every five deaths. In 2006, CVD claimed 831,272 lives which was 34.3% of all deaths or more than one of every four deaths! That’s way more than deaths due to cancer (559,888), accidents (121,599), and AIDS(12,113) combined. CVD occurs almost equally in men and women however, after menopause women have an increased risk.

Cardiovascular disease is the number one killer of people with diabetes, even when glucose levels are kept under control. People with diabetes are two to four times more likely to develop cardiovascular disease due to a variety of risk factors including high blood pressure, lipid disorders, high LDL, high triglycerides, low HDL, smoking, obesity, or high blood sugar levels. Recent studies have also shown that insulin resistance may be another risk factor.
Engaging in physical activity for at least 30 minutes every day, eating at least five servings of fruit and vegetables a day, and limiting your salt intake to less than one teaspoon a day of the week will help to prevent CVD.

Diet and Cardiovacular Disease

As we all know by now cardiovascular disease is a pretty important topic in today’s health news being THE top cause of death in the U.S as well as worldwide. It accounts for 40% of all deaths in the U.S. which is more than all forms of cancer combined! Not that this should scare people because it seems scare tactics rarely work but I just wanted to list a few top risk factors for CVD (as in introductory):
Age
High Blood Pressure *
Diabetes*
High cholesterol*
Cigarette smoking*

When I started background research I couldn’t help but keep going back to how four of the five of these are modifiable or manageable(*). Three are commonly linked to one’s diet and the other is smoking which to me is a voluntary act. Sure, some of these have been found to have a genetic influence however even if you don’t smoke that would cut your risk factor by one! The main idea I’m trying to get across is diet can play such a large role in this very serious disease and killer. You can’t avoid getting older but you can try avoiding foods that lead to disease.

Fatty plaque of course is what we know causes the narrowing of coronary arteries leading to blocks causing Heart attacks and strokes. These plaques accumulate from adolescents which means what we have been eating all these years MAY eventually catch up with us later in life. This might be why they call CVD the “silent disease” with little to no symptoms besides high blood pressure and why heart attacks seem to happen out of now where.

Since fatty plaque accumulates from adolescents wouldn’t it seem logical to start our younger generations on healthy eating and educating them in order to make a dent in this possible health epidemic? Nutrition education to me doesn’t seem to be a fix all but I find it to be a step in the right direction for reducing High Blood Pressure, type 2 diabetes, and high cholesterol ultimately cardiovascular disease!

It gives me great joy to see some big names in America take on this task of educating children on making healthier eating choices. The biggest example is Michelle Obama’s campaign against childhood obesity. She targets implementing heather foods in school systems where children receive majority of their meals. Check out http://www.whitehouse.gov/the-press-office/remarks-first-lady-event-surgeon-generals-report for more information and her thoughts and goals for the campaign.

Another similar movement I’ve recently discovered is Jaime Oliver’s Food revolution. Take a look at this famous chief’s moving T.E.D talk (a bit long but worth it) where he talks about bringing in fresh foods from local farms into schools as well as nutrition education for American youth. On a side note: He’s not even American and he cares this much about a serious topic affecting so many Americans.

http://joshpremuda.com/2010/02/12/jamie-oliver-wins-ted-prize/

Connection Between Gum and Heart Disease

Coronary heart disease is a narrowing of small blood vessels that supply blood and oxygen to the heart. It is usually caused by atherosclerosis, a condition which occurs when fatty material and plaques buildup on the walls of arteries. Its most common symptom is chest pain, however, in some cases no symptoms may be present. Treatment for heart disease can range from taking medication to surgery. Researchers have found that people with gum disease are almost twice as likely to suffer from heart disease. There are several theories that have shown a link between heart disease and periodontal disease. One theory is that oral bacteria effects the heart by entering the bloodstream and attaching to fatty plaques in the coronary arteries which contributes to clot formation. Another theory is that the inflammation caused by periodontal disease increases plaque buildup, which may contribute to swelling of arteries. There are more ongoing studies to further see the connection between gum and heart disease.