MENINGITIS

While I was researching online about anti-inflammation I came across Meningitis on the kids health website, a bacterial or viral disease. Meningitis is an inflammation of the meninges. Meninges cover the brain and spinal cord. Bacterial meningitis is very rare and can lead to death. Viral meningitis is less serious and more commonly seen. I have witnessed this disease twice in my life and have seen the viral and bacterial side affects. Meningitis is extremely serious with symptoms varying depending on the infection and the age of the person. The common symptoms include skin rashes, seizures, headache, photophobia, stiff neck, headache, irritability, lethargy, and fever. Viral meningitis being less serious can be treated at home by resting, getting enough fluids and over the counter pain medication. Bacterial meningitis being very serious is diagnosed by first giving an IV with antibiotics as soon as possible. Fluids may also be given. For inflammation reduction corticosteroids may be given depending on the cause. Wanting to know more about corticosteroids I proceeded to look them up on the mayo clinic website. These steroid hormones act as the hormones in the adrenal gland and are involved in many systems such as inflammation, carbohydrate metabolism, protein catabolism, immune response and stress response. The inflamed tissue around the brain can cause pressure within in the brain. Steroids reduce the inflammation causing the pressure to decrease. The sooner they are administered the faster they can work to reduce inflammation and improve chances of survival.
http://kidshealth.org/parent/infections/lung/meningitis.html#
http://www.mayoclinic.com/health/steroids/HQ01431

The Mind is an Amazing Healer

Acupuncture, bee stings, placebos: all treatment methods that are accepted by some and rejected by others. One common theme resonates throughout these types of treatments, and that is the power of believing in healing. Eastern cultures have been practicing spiritual healing for a very long time. The book "The Healing Power of the Mind" by a Tibetan Buddhist named Tulku Thondup Rinpoche explains some of the ideology of "awakening out inner wisdom." The main idea of the book is that when we hold onto the negative things that happen in our lives as well as the pain and suffering that comes with illness, we foster further pain and stress. However, when we open our mind to the warmth and sunlight all around us, we enable our body to release the pain and stress and begin to heal. According to "The Power of the Healing Mind," meditation is a technique that many western doctors have begun to adopt. There are quotations from several doctors:
Bernie Segal M.D., a surgeon and professor at Yale makes this statement: "It tends to lower and normalize blood pressure, pulse rate, and the levels of stress hormones in the blood."
Herbert Benson M.D. from Harvard states: "If you truly believe in your personal philosophy or religious faith-if you are committed mind, soul, and body to your world view-you may well be capable of achieving remarkable feats of mind and body that we may only speculate about."

While it would take a lot to convince our society as a whole that meditation can actually heal people, I feel that we should take it into consideration as a reasonable option. After all, before epidurals were available, women giving birth had to utilize meditation in order to get through the pain of childbirth. If it works for that, whose to say what other healing and protecting factors the mind may hold.

The Role of CD40 in Neuroinflammation

After going over the different factors that can lead to Alzheimer's Disease, I was interested in learning more about the role CD40 plays. The study, by Laporte et al, that I found looks at a transgenic mouse model that have an over-expressing tau phosphorylation, which leads to amyloid plaques and deposits. The study argues, if one genetically disrupts CD40, this will decrease cdk5 levels in mice, which will reduce tau phosphorylation. This is important, because this study alludes to that tau hyperphosphorylation is directly correlated with neuroinflammation, and that the dysregulation of cdk5 will lead to hyperphosphorylation of tau. The results of this study, looking to see if one disrupts CD40 will this decrease amyloid deposits, showed that by disrupting CD40 there is a relative loss of tau phosphorylation. So the study concludes by stating that, CD40 does not act directly on amyloid deposits, however there are inflammatory pathways, such as CD40, that have a direct effect on the phosphorylation of tau.

I thought this was a really good study and good article. It was very easy to understand what they were trying to do, and what their results were. Figure 3, which showed amyloid deposits in dystrophic neurites, was an excellent figure, it showed exactly what was going on, and pointed out where the amyloid deposits were. Overall, this was a good paper, I would be interested to see what you all thought of it.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6SYR-4SSY8XV-1&_user=9555371&_coverDate=09%2F22%2F2008&_alid=1733205199&_rdoc=4&_fmt=high&_orig=search&_origin=search&_zone=rslt_list_item&_cdi=4841&_sort=r&_st=13&_docanchor=&view=c&_ct=10&_acct=C000055186&_version=1&_urlVersion=0&_userid=9555371&md5=51a840abea7981ff101fc887e3f726fc&searchtype=a

Placebos and Nocebos

Hey Everyone!

When I was reading Jeff’s blog I realized he brought up an excellent point when asking about placebos and if they actually demerit a treatment such as acupuncture. I thought it was an interesting question and decided to look up some information about placebos. According to the American Cancer Society placebos have an effect in every 1 in 3 patients. Scientific research involving placebos has shown that these patients in particular have a change in brain activity due to the placebo. I think that in itself is pretty interesting and hopefully further research will determine its implications. While I don’t think a placebo necessarily demerits a treatment, I do think the treatment needs to be investigated and then explained as to what it truly does…not just what it is thought to do.

On another note, in addition to the placebo effect there is a nocebo effect. I was unaware of this and thought it was somewhat interesting. The placebo effect results in the positive outcome someone was hoping for, while the nocebo effect results in unpleasant symptoms as a result of the placebo. Together they are referred to as the expectation effects. If the patient expects to feel sick from a particular medicine they most likely will, and if they expect to gain relief from pain, they will most likely find their symptoms eased. I don’t think we can demerit placebos and the affect our brain, and our faith, have on our healing.

Brianna Cosentino

http://homeremedies.ygoy.com/updates/1753/home-remedies-for-inflammation-of-the-kidney/

While surfing the internet, I stumbled upon this little gem of a miracle cure. It discussed naturopathic ways in which nephritis can be cured. Nephritis is inflammation of the kidneys and has a 15/100k mortality rate. In addition, the condition has been steadily on the rise since the 1970's.

This websites recommends home remedies to combat inflammation of the kidneys through the consumption of avocados, coconut milk, and carrot juice with lime concentrate. While these may provide some placebo-type affects, no studies have been performed that connect these remedies with decreased inflammation. Furthermore, nephritis can cause permanent kidney damage that may result in death if not treated correctly. Therefore, if a reader does not read critically about a very serious condition, poor consequences may result. This website is another case-in-point of highly unverified websites disseminating information that may harm readers that do not take it with a grain of salt.

How Olive oil helps switch off genes which lead to conditions including heart disease and arthritis

After reading the article "How olive oil helps switch off genes which lead to conditions including heart disease and arthritis" I was very interested in all of the different kinds of foods that can help inflammation. When looking through many different articles I found similar foods in each and these foods are part of the Mediterranean diet which is stated in the article. They do not go into detail about the mediterranean diet so I thought this diagram would clearly illustrate the foods that can help inflammation http://www.drweil.com/ecs/images/anti-inflammatory-food-pyramid.jpg.

I really enjoyed reading about how olive oil can help inflammation but I feel as if the article need more information about monounsaturated fat (MUFAS) because this would allow for the general public to understand even though it has a lot of fat it is necessary for the body. Monounsaturated fat is a fat which is found in many different foods and oils. It has been shown through many different studies that monounsaturated fat improves blood cholesterol levels which can decrease your risk of heart disease. Like olive oil it does this by controlling LDL(bad) cholesterol levels while raising HDL (good) cholesterol levels. Studies also show that MUFAS may benefit insulin levels and blood sugar control which will help if you have type 2 diabetes. By adding this information the article would have had more supporting data.
What did everyone think about the information regarding omega-6 fatty acids after reading the article "Anti-inflammatory Agents: present and Future" ??

When Placebo Can't Be Controlled

Acupuncture has been practiced for thousands of years and with such age a practice gathers many strong believers. There are undoubtedly millions, possibly billions, of people in the world who believe that acupuncture administered by a knowledgeable practitioner can heal a wide variety of maladies... so how does the institution of Western intelligentsia scientifically evaluate a methodology that has produced results for millennia? There are plenty of theories concerning the pathway by which acupuncture effects its positive health results; some say acupuncture prevents pain perception by saturating certain neurological "gates"; others propose that stimulating the efferent vagus nerve elicits a parasympathetic down-regulation of inflammatory players like tumor necrosis factor alpha and proinflammatory interleukins; while always looming in the background is a crowd of critics screaming that acupuncture is pure placebo.

The majority of acupuncture research has been refuted by the scientific community as "poorly designed" or "biased." To be fair, it is not easy to put together a double-blind placebo-controlled study involving sticking people with sharp objects, but serious skepticism must be applied to every publication on acupuncture due to its inherently subjective nature. Challenges to the objectivity of testing acupuncture include the source which determines needle placement (Confucius says poke here versus Laozi says poke there), the concept of diffuse noxious inhibitory control (DNIC) set off by needle pricks at irrelevant sites, the possibility of a dose-response relationship, and the inadequate blinding via sham procedures.

DNIC is the scientific way of explaining counter-irritation, like when your dad offered to punch your arm to make your headache feel better. In acupuncture, it is proposed that needle pricks release endogenous opioid neuropeptides and monoaminergic neurotransmitters that send a message to the lower brain stem that result in anti-inflammatory actions. In the 1980's, Fauve et al. showed that in mice, local inflammation could reduce distant inflammation better than glucocorticoids. Cool concept... but there has yet to be a methodology set forth that is acceptable to the scholarly world as accounting for DNIC's potential reliance on the placebo effect. If acupuncture works because of DNIC, does needle placement matter? If placement doesn't matter, then any sham needle use will elicit a response that cannot be separated from the response to needle use in traditionally prescribed area.

Kavoussi's article begins with a quote from physicist/philosopher Thomas Kuhn, "There are many fields--I shall call them proto-sciences--in which practice does generate testable conclusions but which nevertheless resemble philosophy and the arts rather than the established sciences... incessant criticism and continual striving for a fresh start are primary forces, and need to be." So where is our fresh start on acupuncture? Is it reasonable to discard the obsession with ruling out placebo in our medical research paradigm? At some point, I think there has to be a concession by the scientific community that it cannot fully elucidate the incredibly complex interplay of physical, mental, emotional, and spiritual wellbeing in human subjects. The patient seeking acupuncture therapy must believe that acupuncture has some kind of power, be it physical or otherwise, but is that "placebo" necessarily a demerit to the efficacy of acupuncture?

Kavoussi, Ben, and B. Evan Ross. "The Neuroimmune Basis of Anti-inflammatory Acupuncture." Integrative Cancer Therapies. September 2007, vol. 6, no. 3. pp. 251-257.

Interestingly, after writing this article alongside a Licensed Acupuncturist, Ben Kavoussi has written extensively as a critic of acupuncture... a list of his articles can be found here: http://www.sciencebasedmedicine.org/?author=1346

Parkinsons Disease and Protective Nutrition

One theme that has been evident throughout most articles we read on inflammatory disease is that diet is of high importance when it comes to controlling and preventing increasing inflammation occurrence. There seems to be media coming from all angles on what type of foods help or hurt when it comes to all the inflammatory diseases. This made me wonder what research has been done on diet and Parkinson's and what type of diets are protective both prior to acquiring the syndrome and after.

One of the studies on Parkinson's and nutrition study the affects of nutritional urate in nueroprotection. The study started with 47,406 men of which 1,387 developed Parkinson's disease. It saw a protective effect with increased nutritional urate. It further explained the phenomena by adding, "Urate reduces oxidative stress primarily through its actions as an effective scavenger of peroxynitrite and hydroxyl radicals (1)." Increased urate is generally associated with causing gout and not commonly viewed as a positive nutritional aspect. This study believes that there are three mechanisms by which the urate was protective and states, "Possible mechanisms for a neuroprotective action of urate include suppression of oxyradical accumulation and preservation of mitochondrial function, inhibition of the cytotoxic activity of lactoperoxidase, and protection from dopamine-induced apoptosis (1).According to this study consuming more foods like fish and meat could decrease your chances of getting Parkinson's.

On the other hand, there is a study describing that increased protein ingestion while already having Parkinson's can be detrimental (2). The study explains that the reason for this is that there is a limited amount of transporters that cross the blood brain barrier. There is a dopamine protecting substance that competes with certain proteins to get transported (2). There was a correlation of decreased domapine protection with increase dietary protein after the onset of Parkinson's Disease.

Two other supplements that had a reverse relationship when it came to Parkinson's disease were Iron and Vitamin C. While heme-iron found in red meat products showed no association to Parkinson's in this studied fortified Iron products seemed to increase the instance of Parkinson's among individuals, and even more so in those who had Vitamin C deficiencies (3). The study also pointed out that grains from cereals fortified with Iron had a strong correlation with Parkinson's disease(3).

There were other dietary elements that were studied in relation to Parkinson's disease, however most had no strong correlations. Dairy specifically high fat dairy, is somewhat linked to increase risk of Parkinson's disease (2). Another slight correlation what found in the arachidonic acid, an Omega-6 fatty acid commonly found in peanut oil, was found to increase Parkinson's disease(2). Diets rich in fruits and vegetables like that of the Mediterranean diet seemed to decrease the incidences of Parkinson's (2). All and all it seems the best information on Parkinson's and diet says to eat natural fruits, vegetables,vitamins, proteins and leave out high fat foods to protect against getting Parkinson's Disease. Lastly, if you do get the disease it is better to lower your intake of Proteins.

References

(1)Gao, X., Chen, H., Choi, H. K., Curhan, G., Schwarzschild, M. A., & Ascherio, A. (January 01, 2008). Diet, urate, and Parkinson's disease risk in men. American Journal of Epidemiology, 167, 7, 831-8.

(2)Kones, R. (January 01, 2010). Review: Parkinson's Disease: Mitochondrial Molecular Pathology, Inflammation, Statins, and Therapeutic Neuroprotective Nutrition. Nutrition in Clinical Practice, 25, 4, 371-389.

(3)Logroscino, G., Gao, X., Chen, H., Wing, A., & Ascherio, A. (January 01, 2008). Dietary iron intake and risk of Parkinson's disease. American Journal of Epidemiology, 168, 12, 1381-8.

Updating Outdated Alzheimer's Diagnosing Techniques

I was on NPR and I stumbled upon a story published April 19, 2011 (serendipitously during Neurodegenerative week) about updating guidelines of diagnosing patients with Alzheimer's. Previously diagnosing those with the disease was done after the fact without any indication if a person was likely to develop the disease. Now an initiative being backed by the National Institute on Aging and the Alzheimer's Association, is urging doctors to tell patients whether or not they are likely to develop Alzheimer's by monitoring brain shrinkage, plaques in the brain, and modifications of CSF.

I think there are pros and cons.

One pro that is mentioned in the article is that those who are deemed highly likely to develop the disease, have more time to setup healthcare arrangements (i.e. hiring an at-home medical attendant, saving money, etc.). That way patients and their families will have more time to prepare for the subsequent series of unfortunate events.

Another pro mentioned in the article is that those who are placed in the "highly likely" category may be targets for experimental approaches at dealing with the disease down the road.

One con mentioned was that if people are labelled highly likely, then they may go through some deleterious psychological events.

Another con that I thought of, relates to insurance coverage. If someone is deemed highly likely to develop the disease he or she may be denied healthcare insurance coverage. This is extremely unfortunate but because of the recent economic decline, companies are trying to cut costs wherever they can and implementing stricter coverage guidelines. As a result, implementing this system of earlier Alzheimer diagnosis could potentially prohibit some patients from receiving care.

http://www.npr.org/2011/04/19/135548317/scientists-update-alzheimers-guidelines

T Regulatory Cell Therapy

I found the following review articles on T Reg cell therapy which pertains to the basic science article that we just read on Parkinson's Disease. I especially like the title: "Human T Regulatory Cell Therapy: Take a Billion or So and Call Me in the Morning". I have attached the link to the reviews so check them out. Basically, researchers believe that T reg cell transfer is a promising therapy for the treatment of many autoimmune, neurodegenerative, and inflammatory diseases due to the T reg cell's ability to suppress over-reactive immune states. They propose that a patients own T regs can be collected, proliferated ex-vivo and then reintroduced into the patient to increase the regulatory ability of the body's immune system. They also found that in some disease states, a patient's T regs have decreased ability to suppress immune responses, making it hard for adoptive transfer to have useful effects. It is still unknown why there is a depressed response from Tregs in many diseases. To overcome this, the authors propose using stem-cell therapy to create a new line of T regs that are functionally sound and can act to regulate autoimmunity. Most importantly, researchers are hoping that T reg therapy can be used following organ transplantation to suppress that immune response in Graft-Versus-Host Disease. Overall these review articles gives the pros and cons of research thus far into the area of T Regulatory Cell therapy.

http://www.cell.com/immunity/abstract/S1074-7613%2809%2900192-7

http://www.nature.com/nri/journal/v5/n4/full/nri1574.html

Memantine has been shown to be ineffective in the treatment of AD patients

Good afternoon All, a study was recently conducted that showed the drug memantine, or Namenda by its brand name, is ineffective for patients with moderate Alzheimers disease. The majority of doctors prescribe memantine coupled with a cholinesterase inhibitor, which prevents the breakdown of neurotransmitters which have been associated with memory, while memantine blocks NMDA glutamate receptors. The authors of the study argued that the combination of these drugs do not slow down the progression of the disease. Ultimately, there is no known cure for AD, the aforementioned medications are meant to help minimize the severity of symptoms and work differently for different people according to the study.

http://edition.cnn.com/2011/HEALTH/04/11/alzheimer.drug.ineffective/index.html

--I wanted to learn a little more about memantine, I was able to track down a very lengthy review article that discusses memantine in relation to AD and cholinesterase inhibitors. Memantine is a uncompetitive NMDA receptor antagonist. The overexcitation of these neurons is just one of many hypotheses that can explain the progression of AD. So the weak firing from low levels of glutamate will be blocked by the memantine and lead to overall improvement but will not effect stronger synaptice responese which are required for normal functioning. Overall, the review argues that memantine protects against neurodegeneration brought on by AB, however these were results from a mouse model. Overall, I liked the figures that the review included, the writing seemed straight forward, however while reading the review, the authors make a strong push for their medication. Even though this medication was cleared by the FDA, and showed strong results in mouse models, but from the study mentioned above, memantine has not been effective. Should they go back to the drawing board to research for other ideas on treating AD, or do you think uncompetitive NMDA receptor antagonists and cholinesterase inhibitors are the right direction we should be going?

http://onlinelibrary.wiley.com/doi/10.1111/j.1527-3458.2003.tb00254.x/pdf

More MS alternative therapies

Hey Everyone!

So after reading the article on bee sting therapy I decided to look up more alternative therapies for Multiple Sclerosis. Before I list these I should reiterate that none of them have been supported by any scientific findings, much like the bee sting therapy. Also the majority of these were described as “co-therapies” and were not meant to be the main course of treatment. The first co-treatment was massage. According to some massage therapy helps relieve stress and depression, which are both thought to progress MS. However, several websites cautioned against this form of treatment, since many of the mainline MS treatments can lead to bone thinning and osteoporosis. Depending on the severity of bone thinning, massage therapy has the possibility to be quite harmful. The next therapy suggested was acupuncture. According to some patients acupuncture relieves pain, lessens muscle spasms and helps with bladder and bowel control. However there is some research surfacing that acupuncture can actually be harmful. There is no hardcore scientific research pointing either way. The third alternative therapy was evening primrose oil also known as linoleic acid. Of the four studies I found, three of them were torn on the affects of linoleic acid and believed longer studies needed to be created to truly observe its affects on the myelin sheath. The last two alternative therapies were magnetism and marijuana. The magnetism studies I found were horribly designed and completely unscientific. Most of the information I found on marijuana strongly warned against its use since many MS patients already have cognitive impairments.

Possible drug targets for IBD and MS

I found an article that was covering new treatment possibilities for Inflammatory Bowel Disease (IBD) that were recently discovered. This possibility arose when the cytokine IL-23 was identified as playing a large role in the pathogenesis of this disease. It was found that IL-23 was being expressed in many different types of cells from the peripheral blood and intestinal mucosa of patients with IBD, demonstrating that new treatments of IBD may be aimed at limiting the damage caused by IL-23.

Having not heard of IL-23 as being a contributor to the disease in any of the articles we read in class, I did a little research on the cytokine. What I found out was that IL-23 assists in the pathogenesis of autoimmune inflammation as it induces CD4+ T cells which subsequently produces IL-17 and IL-6, both of which are known to act as proinflammatories. Interestingly, I also came across another article which stated IL-23 was also discovered in increased amounts in dendritic cells in patients that have Multiple Sclerosis. In the same article, it was shown that when inhibiting IL-23 along with IL-12, increased amounts of IL-10 and a decrease in TNF-α production were noticed; thus, presenting a possible drug treatment for MS aimed at IL-23 inhibition as well.

The articles mentioned can be found using the following links:

http://www.sciencedaily.com/releases/2011/03/110331114844.htm
http://www.jleukbio.org/content/89/4/597.full
http://www.jimmunol.org/content/176/12/7768.short
http://www.signaling-gateway.org/update/updates/200502/nri1559.html

Alzheimers Current Events

Here is an article in the New York Times today about new guidelines for Alzheimers diagnosis issued by the National Institute on Aging and the Alzheimers Association. The article talks about the newly implemented changes that are based on some of the research that we have been reading about.

http://www.nytimes.com/2011/04/19/health/19alzheimer.html?_r=1&hp

Testing for Alzheimer's

After all this talk about Alzheimer's Disease, I was curious about the ways in which people are tested for it. An early testing device is the cognitive testing process. There are a few commonly used tests that physicians use:

• Three word delayed recall: the patient is told three words (ex: blue, dog, pen) and asked to repeat them. About 5 minutes later the patient is asked to repeat them. If the patient cannot remember all three words, even after hints like one is an animal, they may need further evaluation.


• Mini cognition test combines with three word recall: the patient is given three simple nouns and asked to repeat them. Next, the patient is asked to draw the face of a clock on a piece of paper and put the hands at a specific time. After the clock is drawn, the patient is asked to recall the three words. If the patient remembers only two, one, or none of the words, the clock should be evaluated. If the clock is abnormal, the patient needs further evaluation. Also is the patient remembers all three words but makes an abnormal clock they would need further evaluation.


• Coin counting: The patient is asked "If i give you a nickel, a quarter, a dime, and a penny, how much money have I given you?" If the patient cannot come up with 41 cents as the answer, they need further evaluation.

These are just a few ways in which a person's cognitive ability can be evaluated. Check out these links below to read more about the testing methods and warning signs for Alzheimer's Disease.

Cognitive Testing: www.alz.org/professional_and_researchers_14306.asp

10 Warning signs: www.alz.org/alzheimers_disease_know_the_10_signs.asp

Ethnicity and Alzheimers

In class there was a little discussion on how ethnicity and race may play into the diagnosis of alzheimers, but nothing too concrete. This article I found discusses how racial and cultural differences can impact how individuals with early dementia are diagnosed. It looked into how varied bereavement across cultures is and analyzed the differences between the diagnoses in dementia between people of different races; emphasis was placed on African Americans, Latinos, Whites, and American Indians. Just some interesting information!

http://www.usatoday.com/news/health/2010-07-13-alzheimersculture13_ST_N.htm

Mice on Treadmill

Hey Everyone,

Just so you can have a visual for the "Chronic Exercise ameliorates the neuroinflammation in mice carrying NSE/htau23" article.... here is a link on mice subjected to treadmill excises. I'm thinking it may lead to improved cardiovascular fitness; however looks like it could induce a little chronic stress as well.

Mice on Treadmill link

Deep Brain Stimulation

• In class I had Mentioned that one of the treatments for Parkinson's Disease is deep brain stimulation. While it seems easy enough to understand that electrodes are placed in areas of the brain to stimulate and control movement, there is much more involved as far as placement and consequences of the treatment. Upon further exploration I found many interesting facts involving deep brain stimulations and even some videos of how the procedure works.





• In deep brain stimulation electrodes are placed in the sub cortical areas of the brain. There is a battery connected to the electrodes that is generally located in the collar bone region. Using a CT or MRI to monitor the surgery, a hole is drilled into the skull and the electrodes are carefully placed as well as tested for nerve stimulation. The job of the electrode is to stimulate neurons that have become dormant or less active. There are studies that have show that the use of deep brain stimulation paired with the common Parkinson's medication Levadopa has a greater response toward decreasing the movement issue symptoms in Parkinson's disease. While there is great success with the invasive procedure it does not come without consequences. Patients who have this implantation have seen a steep rise in infections compared to the Parkinson's patients just on the medication. Other side effects of the operation include stroke, change in mood, and overproduction of scar tissue. Patients who opt for this procedure must be willing to make a long term commitment to maintaining and monitoring the progress of the units within their brain. The battery must be changed regularly through surgery, and because of the sensitivity of the area stimulated by the electrodes progress must be continually monitored.






• Deep Brain Stimulation not only is a treatment for Parkinson's Disease, but has shown great potential in treating psychiatric disorders as well. Disorders such as depression, obsessive compulsive disorder, and phantom pain have also been exploring the world of deep brain stimulation with some pretty good results. While Parkinson's disease is a disease characterized by neuron death in the substancia nigra primarily as a result of inflammatory disease, it is interesting that a treatment for Parkinson's is transitional in other areas of medicine.






• There are some interesting videos showing the deep brain stimulation implantation on youtube. The one following I found interesting in explaining the implantation process.





• http://youtu.be/WW-SWAnphFU





• This other video is interesting because it shows a study that target the elderly which are predominately affected by the disease.





• http://youtu.be/WYDoHmg9ECl







• Other Sources and interesting articles on Deep Brain Stimulation:




• Pluta, R.M., Perazza, W.G.D., &Golub, R.M. (Feb 16, 2011). Deep Brain Stimulation. Jama-Journal of the American Medical Association, 305-7.





• Deuschl, G., Schade-Brittinger, C., Krack, P., Volkmann, J., Schafer, H., Botzel, K., Daniels, C,... German Parkinson Study Group, Neurostimulation Section. (Jan 1, 2011). A randomized trial of deep-brain stimulation for Parkinson's disease. The NEw England Journal of Medicine, 355-9, 896-908.

Play at Your Own Risk!

Neurodegenerative diseases, such as Alzheimer’s, Parkinson’s and Huntington’s disease, can be caused by many different factors. But from all the pathologies we discussed in class this past week, the one thing that sparked my interest into doing more research was how some of these diseases can be caused by high impact sports. This may include sports such as Hockey, Boxing, and Football.

Back in 2008, Boston University School of Medicine and Sports Legacy Institute partnered up to begin an intensive look into how chronic head injuries may cause neurodegenerative diseases later on in a players life. Thus the Center for the Study of Traumatic Encephalopathy was formed.

This center conducts state of the art research on Chronic Traumatic Encephalopathy (CTE), which is a disease that leads to a highly progressive dementia. Some of the early symptoms that may appear during the athlete’s career are memory loss, depression and personality changes. All of these symptoms get worse and worse over the years and eventually leads to dementia.

The continual onset of trauma to the brain triggers a progressive degeneration of the tissue, including the build up of an abnormal protein called tau. When a brain sample has been collected after the person has passed away, the researchers can stain for that specific protein and can visualize where dead brain matter has occurred.

For more information on this ongoing research, go to this website http://www.bu.edu/cste/

Here they have a nice video explaining overall research findings and what they hope to do in the future. There is also a review article that discusses CTE in more detail if you click on the About tab and then What is CTE. Its near the bottom of the page.

Music Therapy in Alzheimer's

In one of my neuroscience class we talked about the benefits of using Music Therapy (MT) in treating Parkinson's disease and how it could be applied to other neurodegenerative diseases. First off, MT is a field of scientific research that observes how a trained music therapist uses music (both passive listening and active participating) to improve symptoms of various disease states.

The article on AD observed the effects of passive MT, or the effects of just listening music on the behavior of patients with with moderate to severe Alzheimer's. The authors found that patients patients' daily activities were disturbed much less frequently, and that the patients displayed less aggressiveness and anxiety. The MT effects lasted for about a month after the therapy stopped.

While this therapy is clearly not going to cure AD, I think it is a great step in helping patients suffering for this disease to maintain a semblance of normalcy.

Alzheimer's Paper:

http://www.ncbi.nlm.nih.gov/pubmed/16618375

-Vinoo

Alzheimer's and DIet

So after learning about the different possible mechanisms that contribute to AD (described briefly below), it made me wondering what type of antioxidant intake research is out there regarding AD. Seems to be a mounting body of evidenced that flavonoids, particularly anthocyanin (responsible for the bright red/purple pigment in foods) maybe beneficial.

Possible mechanisms to produce AD:

1. reduced synthesis of acetylcholine (neurotransmitter)

2. hyperphosporlyation of tau proteins leading to neurofibrillary tangles

3. accumulation of amyloid beta plaques ---seems to be a connection to anthocyanins....

A paper published this past year looked at the affects of mulberry (ME), rich in anthocyanin ---(a flavonoid) on preventing AD in senescence-accelerated mice. Background evidenced indicated that antioxidant-rich berries can positively affect cognition and memory. Specifically, cyanidin-3-O-glycopyranoside (one of the most common anthocyanin) has been identified a "neuroprotective," by decreaseing amyloid beta peptide-medicated cytotoxicity in neurocytes. Other studies found that cyanidin-rich supplements improved lipid oxidation in the brain as well as spatial working memory tests in aged rats (via cAMP-response element).

This study examined 6-month old adult mice from SAMR1 (senescence-resistant) and SAMP8 (senescence-accelerated prone) strains. They found the following:

1. ME significantly improved memory deterioration

2. ME reduced oxidative stress-induced lipid oxidation (via isoprotane reduction)

3. ME improved MAPK cascade via lower levels of p38 and JNK as well as decreased nuclear Nrf2 levels (MAPK regulator), simular to that of the SAMR1 mice (control, not accelerated aging mice)

4. ME reduced the accumulation of amlyoid beta deposits in the hippocampus of the mice feed the extract.

Overall, they found the anthocyanins "promoted age-dependent antioxidant production and reduced oxidative stress-intduced damage."

Food for thought.

Shih P, et al. Antioxidant and cognitive promotion effects of anthocyanin-rich mulberry on senescence-accelerated mice and prevention of Alzheimer's disease. Science Direct. 2010;595-605

Psychoneuroimmunology

After reading more on stress and inflammation in the immune response I came across the term Psychoneuroimmunology which describes the relationship between the brain and the immune system. We had read a few lay articles on stress, particularly the study on how social stresses exacerbated the symptoms of Multiple Sclerosis. There is actually an organization committed to this specific field called the Psychoneuroimmunology Research Society and I have included their website below. Also, it seems that may medical schools and health care facilities have specific research units dedicated to this field. I have posted another paper on the concerns and difficulties that are involved in the field including measurement of psychological parameters and the effect of the environment on a subject.




http://en.wikipedia.org/wiki/Psychoneuroimmunology
http://www.apa.org/monitor/dec01/anewtake.aspx
pni.osumc.edu/KG%20Publications%20(pdf)/049.pdf

Living Long Time

Since we had the short discussion on longevity and ethics in medicine last time, I thought I would post this little quiz that I saw on Dr. Oz's website too.

http://inflammablog4.blogspot.com/

If you think about it most illnesses could be considered built in mechanisms to "weed out" or kill out certain disease states. Take diabetes for example. Too much visceral fat and intramuscular fat can (and more than likely will) lead to diabetes. This could be considered an evolutionary mechanism to decrease the prevalence of obesity in the human population. I know that sounds mean, but if you look at things from a biological and ecological standpoint, and it makes sense for other animals (remember the giant arthritic frogs)!

DR. OZ: Alzheimer's: Diabetes of the Brain

DR. OZ: Alzheimer's: Diabetes of the Brain

http://www.doctoroz.com/videos/alzheimers-diabetes-brain

Interesting points:

• Insulin is not only made in the pancreas, but also in the brain!
• As we know, the brain needs and metabolizes lots of glucose to function, and insulin helps it uptake that glucose into its cells. But in Alzheimer's, insulin function is impaired (insulin resistance)
• Since 1980, deaths of people with both diabetes and Alzheimer's have increased dramatically
• Visceral obesity is bad!!! LOL
• Processed foods are bad!!!

Not sure, but it seems like new treatments for diabetes have kept diabetics alive longer, and so now we see an increase in Alzheimer's in diabetic patients (especially elderly people). So would this link between diabetes and Alzheimer's be considered a coincidence???

Hey everyone!

So yesterday somebody posed the question of why MS is more common in women than in men. I found a few genotyping studies that confirmed the greater prevalence of certain MS-related genes in women, but it seems that the answer to this question is still largely unknown. Estrogen, though, seems to have some therapeutic effect on managing MS. Check these articles out: 
http://www.ncbi.nlm.nih.gov/pubmed/19539954
http://www.ncbi.nlm.nih.gov/pubmed/19591008
The second article is more recent, and even mentions various clinical trials that are currently testing the efficacy of estrogen therapy in MS treatment.

- Julia 

Homocysteine and its Role in Neurodegenerative Disorders

I stumbled across this article when doing some research for another course. I thought it was a relatively simple yet comprehensive article which addressed multiple components of disease that have been discussed in class (homocysteine levels, nutrient deficiency, etc.) in addition to corresponding with this weeks discussion of neurodegenerative disorders. Furthermore, upon reading this article, it brought to mind the discussion of stroke, which occurred at the beginning of the course. Increases homocysteine concentrations were directly correlated to an increase risk of stroke, which would subsequently exacerbate any cerebral vascular dysfunction experienced by the patient, causing further deleterious effects. As neurodegenerative diseases affect such a large group of people, and in my opinion impair one's quality of life, it would be amazing to decrease the severity of these diseases with something as accessible as a B-12 vitamin which can be found in any supermarket. However, it does appear that plasma homocysteine may not be a great indicator of a specific neurological disorder as it lacks specificity. In addition, use of homocysteine as a marker of disease my raise ethical questions, much like those discussed on Monday. Just though it was interesting! Note: While the abstract is listed below, the full article can be found at the provided link. Homocysteine: a biomarker in neurodegenerative diseases Abstract: Disease of the central nervous system are found in patients with severe hyperhomocysteinemia (HHcy). Epidemiological studies show a positive, dose dependent relationship between mild-to-moderate increases in plasma total homocysteine concentrations (Hcy) and the risk of neurodegenerative diseases such as Alzheimer's disease, vascular dementia, cognitive impairment or stroke. HHcy is a surrogate marker for B-vitamin deficiency (folate, B12, B6) and a neurotoxic agent. The concept of improving the patients clinical outcome by lowering of Hcy with B vitamins seems to be attractive. Recent B vitamin supplementation trials demonstrated a slowing of brain atrophy and improvement in some domains of cognitive function. Meta-analysis of secondary prevention trials showed that B vitamins supplementation caused a decrease in plasma Hcy and a trend for lowering the risk of stroke. HHcy is common in elderly people. Therefore, it seems prudent to identify B vitamin deficient subjects and to ensure sufficient vitamin intake. Therefore, recent evidence supports the role of Hcy as a potential biomarker in age-related neurodegenerative diseases. http://find.galegroup.com/gtx/retrieve.do?contentSet=IAC-Documents&resultListType=RESULT_LIST&qrySerId=Locale%28en%2C%2C%29%3AFQE%3D%28KE%2CNone%2C24%29Homocysteine+and+stroke+%24&sgHitCountType=None&inPS=true&sort=DateDescend&searchType=BasicSearchForm&tabID=T002&prodId=HRCA&searchId=R1&currentPosition=1&userGroupName=tusc83053&docId=A252447279&docType=IAC#

Diacerin

Last week during the arthritis discussion we analyzed an article that tested the effects of the drug Diacerin on osteoarthritic cells. The drug is unique because it inhibits interleukin-1 rather than acting on the cyclooxygenase enzymes like non-steroidal anti-inflammatory drugs do. However, this particular study only looked at chondrocytes in vitro and was not a human study. It got me wondering if there have been any human clinical studies on this drug and if it has any negative health effects. I found this article:

http://onlinelibrary.wiley.com/doi/10.1002/art.23056/pdf

Looks like they found Diacerin to be safe and well tolerated. No serious or
previously undocumented adverse events were observed
during the study. I'm interested to see where this drug will go in the future.

One last note on Arthritis

Last Monday we discussed the final segment of our arthritis block and covered a research article looking into the treatment of RA by breaking from the norm and not going with anti TNF alpha treatment, but rather an anti IL-1 treatment. It was believed that TNF drives most of the IL production, thus by targeting and block TNF, IL-1 would be suppressed as well. However they found that anti TNF treatment was only beneficial in reducing inflammation and that too when administered before or at onset of the disease. In studying using anti IL treatment, it was found that there was a significant effect seen in decreasing joint damage and destruction, and that too when given at onset or after induced arthritis.

The study did a good job in demonstrating how using this form of treatment as compared to what was previously thought, would be more beneficial in treating and reducing the effects of arthritis. The well formed and easy to read figures and graphs even demonstrate that anti TNF treatment does indeed only reduce some inflammation at onset of induced arthritis but has no beneficial physiological effect as the disease progresses. However use of anti anti IL treatment was beneficial in relieving inflammation and reducing joint destruction; which brings about a question as to why there was no test done in testing administering both drugs to the animal models and seeing the effect of both. Allowing anti TNF treatment to work in the early stages, and IL to become of use in the later developing and later processes.

However Dr. Cohen mentioned that still Il-1 treatment inst being used, so what is it about the study that they're leaving out that we need to know, or is it that in the 12 years that have passed since this paper has been published, more research has been shown that anti IL-1 isn't the best treatment after all.

Keep in mind arthritis costs the US economy over $86 billion per year. Thus cutting edge research will continue to find the most effective drug administered in the lowest amount.

Multiple Sclerosis Overview-Neurodegenerative

Multiple Sclerosis is an autoimmune disease affecting the central nervous system (CNS), which includes the brain, spinal cord, and optic nerves. When the immune system begins to attack the CNS, inflammation occurs, causing damage to the myelin sheath surrounding nerve fibers. While the myelin is being attacked, the nerve cell itself also becomes damaged. In addition to this, the cell and myelin develop scar tissue, also known as sclerosis, giving the disease its name. This damage leads to disruption in the signaling to and from the CNS. This disruption ranges from a slowing in the signal, to a complete halt in signaling, or cross-talk between signals.

Multiple sclerosis is more common among women and is generally diagnosed between the ages of twenty and thirty. The symptoms vary from patient to patient based on the severity and location of immune system attack. The symptoms of MS range everywhere from fatigue, numbness, pain and depression, to walking problems, balance and coordination problems, bowel and bladder dysfunction, impaired cognitive function, and spasticity. Other symptoms that are less common include things such as respiration problems, swallowing problems, speech disorders, tremors, and seizures.

There are four main categories, or courses, of MS: Relapsing-Remitting MS, Primary-Progressive MS, Secondary-Progressive MS, and Progressive-Relapsing MS. Relapsing-Remitting MS is the most common form and is “characterized by clearly defined acute attacks with full recovery or with residual deficit upon recovery”(NMSS). Typically in the periods between disease relapses, there is no disease progression. Primary-Progressive MS is a progression of the disease from its onset without acute attacks. Roughly 10% of people diagnosed with MS have the primary-progressive form. Secondary-Progressive MS can be thought of as a combination of relapsing-remitting and primary-progressive MS. In other words the patient starts with infrequent relapses and remissions and then moves towards a progressive worsening of the disease without remissions. According to several MS studies, “of the 85% who start with relapsing-remitting disease, more than 50% will develop SPMS within 10 years; 90% within 25 years” (NMSS). The last form, Progressive-Relapsing MS, is characterized by progressive worsening from the onset of the disease, but also acute relapses. This is the least common form and accounts for roughly 5% of patients with MS.

Quick Blurb about MS Review Article:

In the “Inflammation and MS Review” the authors contend that inflammation may not be completely detrimental to MS, as commonly thought, but may have beneficial roles as well. The review article continues on to describe the CNS and explain particularly beneficial roles of inflammation. In the CNS the brain is protected by the blood-brain barrier, which is composed of cerebral endothelial cells and tight junctions. In patients with MS the endothelial tight junctions of the blood-brain barrier are abnormal. As one might expect this allows for mononuclear cells and other detrimental factors to enter the brain. This breakdown in the blood-brain barrier is a main suspect as to how demyelination and axonal injury begins. The continuous influx of these cells and the inability to clear them leads to the activation of local immune cells and inflammatory mediators. The researchers of this article contend that while initial inflammation seems to play a large role in demyelination, it may be beneficial in the long run. When studying mice with the animal model of MS, they found that the morbidity rate increased 20% to 80% when treated with antibodies against proinflammatory cytokines. There research finds that inflammation may also be responsible for clearing toxins that are responsible for progressing the disease. There are clearly many details to the benefits and detriments of inflammation in MS so read the article and enjoy! Its very interesting!

(NMSS) "What Is Multiple Sclerosis? : National MS Society." Home : National MS Society. Web. 10 Apr. 2011. .

Osteoclasts + RA = ??

During class, one of the articles brought up the question of just what role osteoclasts have in RA. I spent quite some time searching for other supplementary reading that could provide an answer, but failed at finding any concrete information.

I did, however, come across a paper published in the journal, Rheumatology. In this research, a number of humoral and cellular factors that influence osteoclast formation from precursors in RA patients were analyzed and compared against controls. After the isolation, culturing, and analyzing of the specific osteoclasts had been completed, they found no difference between them and normal osteoclasts.

"...increased osteoclast functional activity rather than osteoclast formation is more likely to play a role in the generalized bone loss that occurs in RA, and that corticosteroids stimulate osteoclast formation and resorption", was the conclusion that was made by the team. Although this is not a very detailed finding, I still found it interesting because it applied to the comment in discussion.

Here is the rest of the paper :)

http://rheumatology.oxfordjournals.org/content/41/11/1232.full

Adiponectin: Friend or Foe?

So a couple weeks ago we were discussing Inflammatory Bowel Disease (IBD)and the possible role adiponectin played in its pathogenesis. As a just a quick recap, adiponectin is an adipocyte specific secretory protein that plays many different roles in the innate humoral immune system; in relation to IBD, and more specifically Crohn's Disease, it was proposed in one of the papers that it also has anti-inflammatory effects. In the study conducted, it was concluded that the adiponectin secreted from adipocytes in hypertrophied mesenteric adipose tissue could serve as a barrier, preventing the inflammation from spreading into the intra-abdominal space. In this case, adiponectin plays a positive role, limiting the damage done by the inflammation.

As is the case with many different inflammatory and anti-inflammatory proteins, adiponectin's roles are not limited of course to its actions in Crohn's Disease. What I wanted to know, however, was if adiponectin also has possible positive effects, if any, when it came to arthritis. When i did a little research, I was surprised to find out that in the case of Rheumatoid Arthritis (RA), adiponectin may actually play a significant role in the pathogenesis of RA. What was demonstrated in the study I found was that adiponectin stimulated the production of vascular endothelial growth factor (VEGF) and MMPS, which could lead to an increase in the joint inflammation and destruction. This study did state, however, that there must be more research conducted to prove these findings.

Toads and Humans

Hello everyone! When we first read the article about cane toads and arthritis in class I found it somewhat amusing. However, the more I thought about it, the more saddening I realized it really was. The toads in Australia are growing and evolving past their natural size. A huge part of this is due to that fact they have no naturals predators in Australia. Humans relocated them, and now they are becoming much larger in detriment to their own health.

After thinking about the toads for a while I began to think about diseases such as acromegaly, gigantism and marfans syndrome, which are all characterized by excessive growth and large size. From watching medical documentaries and odd history channel shows like “world’s tallest man”, I’ve heard that most people of increased stature and size, say eight feet, endure horrible arthritis. I remembered their joints being enlarged and put under horrendous stress due to the force applied to them. When I went online to search for more information, the thought of obesity popped into my mind and I realized I didn’t get much thought to it when it was mentioned in class. I thought about the billions of Americans who are obese, who weren’t born with a rare chronic metabolic disorder such as acromegaly, and who are by choice putting their body under massive stress. When I searched this topic I found countless websites stating an increased risk in osteoarthritis. According to the John Hopkins Arthritis Center, “being only 10 pounds overweight increases the force on the knee by 30-60 pounds with each step”. Imagine then what an extra 50 or 100 would do. While most of the research is still debating to what extent it increases your risk, “over five times the risk” and so on, it is clear that it is a large contributor to societal increase in osteoarthritis. In addition to increased stress and force there are also several “excess obesity hormones” being investigated for their roles in arthritis, such as leptin. Anyways, after feeling sorry for the toads, I realized it was even more sad that something so similar, yet something we as humans can control, is happening in our society.

What the heck are pannocytes?!?

While we were discussing the paper mentioning pannocytes in class, I realized I had no clue what those cells were. Here are some facts about these cell types based on an article I skimmed:

• These cells are found at the sites of RA cartilage injury but not in osteoarthritis cartilage.
• Morphologically, they are rhomboid in shape while fibroblasts are bipolar and chondrocytes are spherical.
• Chondrocytes are short lived (6-8 divisions) but pannocytes have a much longer life span (25 divisions)
• Both pannocytes and chondrocytes can produce collagenase and stromelysin, both of which are proteases that destroy the extracellular matrix. The kicker: pannocytes live much longer than chondrocytes...

For further info see: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1857892/pdf/amjpathol00027-0336.pdf

-Vinoo

Spinal Drug Administration

http://www.plosmedicine.org/article/info:doi/10.1371/journal.pmed.0030338

Here is a link to the lay article number two covered previously in class. We discussed the possible benefits, if any, and the logic behind administering drug through the spine to modulate peripheral response. The article in itself didn't do much to describe the full process or techniques for which this type of experiment would be conducted, that is why I have attached a link for those that are interested.

In reading the full research experiment and carefully critiquing the process and thought behind doing such a test, a few positive benefits arise as well some side affects, which could possibly be detrimental. By administering the doses through the spine, a smaller dosage of treatment would be required to reach the desired effect, thus resulting in a saving of money and possible better distribution and targeting of the drug. But also we must understand that all these tests were conducted on rats and not human samples. Though there are many parallels between systems, there is no guarantee that the results will be the same. The goal which was desired was to see whether CNS is essential to achieve a response even when administered as a systemic treatment. Which in turn means that there would be a change in the way that drugs are manufactured, in hoping to get to the CNS quicker and easier, to achieve lower doses while improving efficacy.

Glucosamine, any effect or just a placebo?

Everybody has heard of glucosamine as being the one-stop treatment for restoring cartilage and thus eliminating a lot of the pain associated with arthritis. The premise behind the supplement is that glucosamine is a precursor for glycosaminoglycans, which are a building-block in cartilaginous tissue. By providing glycosaminoglycans, it is assumed that cartilage can be rebuilt. However, no substantial evidence exists confirming its effectiveness.

In fact, studies performed at the University of Laval in Quebec indicate that over-consumption of glucosamine frequently happens, due to the fact that as no positive effects are felt, people are more inclined to take more until satisfied. Over consumption of glucosamine has been tied to developing type 2 diabetes by killing pancreatic cells. Furthermore, those that have allergies to shellfish have reacted badly to the supplement, due to glucosamine being an active factor in shellfish exoskeletons.

Of all the scientific studies performed on this supplement, many have been a little dubious in their findings. Of these studies, the primary sponsors were health supplement providers and low numbers of patients, with little or no controls, provided results that give the appearance that glucosamine does in fact treat arthritis. However by eliminating the studies that had loose guidelines, it was observed that glucosamine has no noticeable affects over a placebo.

Arthritis is a growing problem that plagues many young and old alike. But is it worth taking a supplement that has minimal scientifically-proven results, and even may be more detrimental to ones health than originally thought?

Gout: A historic disease of the "wealthy" transitions into the 21st century

Over the last few years I have noticed a substantial amount of men affected by gout; however it seems much less prevalent in women. I asked a few people and I really didn’t get a solid answer, so I did a little digging and found a really cool article published in the New England Journal of medicine in 2004 “Uric Acid and Diet — Insights into the Epidemic of Cardiovascular Disease"

Summary points:

· Gout has been described throughout history, as early as 4 B..C; originally thought to be a disease of the wealthy, affecting middle-aged men of wealthy upper class. It was associated with those that could afford the opportunity of overindulgence.

· “Humans are the only mammals which gout develops spontaneously.” This is thought to be because of mutations that occurred in the promoter region of the uricase gene. Uricase is the enzyme that converts uric acid to allatoin.

· This point addresses the men vs women factor: Estrogen stimulates urinary urate excretion, thus premenopausal women have lower serum uric acid levels.

· In the 1700’s it was proposed that a diet low in protein and high in dairy could decrease gout’s prevalence. Study in 2004 found gout was associated with diets high in meats and seafood and low in low-fat dairy. In fact they found an increase in risk of 21% per addition portion of meat per day. Populations with diets low in animal products and high in vegetables have a relatively low uric acid levels.

· Gout development is now following our current obesity trends. Higher populations of obesity have higher incidences of gout; even when these populations had lower rates throughout history, when obesity rates were lower (i.e. Maori of New Zealand).

· Recommend diets rich in fruits, vegetables and low-fat dairy foods (i.e. DASH diet)

So it seems that gout is following the obesity footsteps across the world, leaving behind the “wealthy” stereotype of the past and now affecting those at high risk of many other co-morbidities. Looks like it all comes back to a healthy diet…..

Johnson, R and Rideout B. Uric Acid and Diet--Insights into the epidemic of cardiovascular disease. N Engl J Med 2004; 350:1071-1073

Gouty Arthritis

Hey everyone! Most of what we're focusing on in this class as far as arthritis goes is OA and RA, but I had some questions about gout because I hear about it so often.
I found this lay article published today (http://www.medicinenet.com/gout/article.htm) that had some good info in it. Here are some of the main points from the article:
-Gout results from excess uric acid in the blood that can condense and form uric acid crystals that get caught in the joints, causing pain and inflammation (arthritis).
-The actual correlation between hyperuricemia and gout isn't clear because some people with hyperuricemia do not develop gout.
-Gout is more common in men than women; other risk factors are: obesity, diuretic intake, high alcohol intake, kidney problems, hypertension, and eating a lot of meat because meat contains more purines, which increases uric acid levels.
-Acute gouty arthritis is most common in the big toe (weird!).
-Treatment for gout includes anti-inflammatory use (but not aspirin, as this increases uric acid levels), weight loss, decreased alcohol consumption, decreased organ meat intake, and increased dairy consumption.

Read more for more info. Some of you may already know all this, but I thought it was pretty interesting, and it is clearly very preventable.