Several blogs have been devoted to the awareness of anti-inflammatory foods and what they are. This blog is different. Today I’m going to inform all of you which foods are actually pro-inflammatory. You might think you know which foods cause inflammation, but you have no idea(haha).
According to Bonnie C. Minsky writer of “Inflammation = Degenerative Disease” the pro-inflammatory foods to avoid include:
* red meats from corn-fed, antibiotic/hormone laden animals
* saturated fats such as lard and meat fats
* fried foods
* partially hydrogenated (trans fats) found in margarines, chips, candies, cereals and baked goods
* cooking oils that are exclusively corn, safflower, sunflower or soy based
* soft drinks (both high sugar and diet varieties)
* excess sugar (both from heavily processed sources, such as candy and from naturally occurring sources such as fruit juice)
http://www.consciouschoice.com/2004/cc1706/healthconscious1706.html
Another site to look at is: http://www.oprah.com/presents/2005/young/life/life_inflammatory.jhtml
This site gives an extremely long and extremely depressing list of the foods that can cause inflammation. I don’t know what all of you eat, but I know what I eat and everything on that list I eat for breakfast, lunch, and dinner. Pretty much grass is the only thing not listed. Good luck with your diet!
14 May 2008
12 May 2008
Could chocolate be healthy?
To eat or not to eat chocolate, that is the question. Studies are popping up everywhere regarding the health effects of flavanol-rich cocoa on the body’s cardiovascular system. Such a study was performed by researchers from Harvard Medical School and the Brigham and Women’s Hospital in Boston. Participants included 15 healthy adults under the age of 50 and 19 healthy adults over the age of 50. As part of the study, the participants ingested a cocoa beverage every day for four to six days while the researchers documented the changes in function of their peripheral arteries. Overall, blood vessel function in the participants had significantly improved after consumption of the cocoa beverage.
The discovery made in this study shows that flavanol-rich cocoa can and does improve blood vessel function in healthy older people. According to Naomi Fisher, MD, Assistant Professor of Medicine at Harvard Medical School and the study’s co-author states, “Aging is typically associated with deterioration in vessel health, specifically related to function of the critical inner lining, or endothelium. Our findings demonstrate that consumption of this flavanol-rich cocoa can improve the function of blood vessels in a healthy elderly population.” However, she does seem uncertain about the effects of cocoa in elderly adults with already cardiovascular problems. "More research is needed to see if older adults with cardiovascular disease can also experience these improvements following consumption of this cocoa, but these initial findings certainly offer great promise." I guess we shall see in the near future how chocolate, specifically cocoa, can improve our way of eating leading to a healthier lifestyle.
http://www.naturalnews.com/019950.html
The discovery made in this study shows that flavanol-rich cocoa can and does improve blood vessel function in healthy older people. According to Naomi Fisher, MD, Assistant Professor of Medicine at Harvard Medical School and the study’s co-author states, “Aging is typically associated with deterioration in vessel health, specifically related to function of the critical inner lining, or endothelium. Our findings demonstrate that consumption of this flavanol-rich cocoa can improve the function of blood vessels in a healthy elderly population.” However, she does seem uncertain about the effects of cocoa in elderly adults with already cardiovascular problems. "More research is needed to see if older adults with cardiovascular disease can also experience these improvements following consumption of this cocoa, but these initial findings certainly offer great promise." I guess we shall see in the near future how chocolate, specifically cocoa, can improve our way of eating leading to a healthier lifestyle.
http://www.naturalnews.com/019950.html
11 May 2008
Lupus
Lupus has been my latest inquiry. A small, probably, unnoticeable segment connected to the very last page of the “Modulation of cell recruitment by anti-inflammatory agents in antigen-induced arthritis,” article had a memorable picture regarding a lupus case. The real eye catcher wasn’t the enormous butterfly tattoo on the 33 year old woman’s back, but the “ginormous” blotchy red lesion above it. This woman was diagnosed with cutaneous lupus. The cutaneous lupus lesion overlying her butterfly tattoo is one of many symptoms of lupus.
Definition
Lupus is an autoimmune disease in which chronic inflammation affects different parts of the body including the skin, joints, heart, lungs, blood, kidneys and brain.
The Attack
The role of the body’s immune system, normally, is to make antibodies that protect against invading viruses, bacteria, and other foreign materials. In such cases of autoimmune disorders like lupus, the body’s immune system isn’t able to distinguish between foreign substances and its own cells and tissues. So what happens is the immune system produces antibodies which act against its self. As a result, these antibodies cause inflammation, pain and damage to different portions of the body.
*Inflammation is considered the primary feature of lupus*
Who does it affect?
More than 90% of people with lupus are women. It is more common in African Americans, Latinos, Asians, and Native Americans than in Caucasians.
To learn more about this and in a cool way check out this video:
http://video.about.com/lupus/What-Is-Lupus--.htm
Definition
Lupus is an autoimmune disease in which chronic inflammation affects different parts of the body including the skin, joints, heart, lungs, blood, kidneys and brain.
The Attack
The role of the body’s immune system, normally, is to make antibodies that protect against invading viruses, bacteria, and other foreign materials. In such cases of autoimmune disorders like lupus, the body’s immune system isn’t able to distinguish between foreign substances and its own cells and tissues. So what happens is the immune system produces antibodies which act against its self. As a result, these antibodies cause inflammation, pain and damage to different portions of the body.
*Inflammation is considered the primary feature of lupus*
Who does it affect?
More than 90% of people with lupus are women. It is more common in African Americans, Latinos, Asians, and Native Americans than in Caucasians.
To learn more about this and in a cool way check out this video:
http://video.about.com/lupus/What-Is-Lupus--.htm
10 May 2008
Fibrin and Alzheimer's Disease
Going back to the neuro articles the thing that really stands out to me is how fibrin is concsidered the new target for Alzheimer’s disease. Fibrin correlates to beta-amyloid protein build-up in Alzheimer’s. As the beta-amyloid protein accumulates so does fibrin. According to Justin Paul, a graduate student, and Sidney Strickland, head of the Laboratory of Neurobiology and Genetics, fibrin could be an important fighting tool against Alzheimer’s. Sidney and Paul have discovered “that brains of Alzheimer’s patients have increased fibrin levels,” a finding that had previously been unexplored.
The function of Alzheimer’s is damage to the barrier that blocks blood from percolating into the brain. This damage allows fibrin and other blood proteins to seep through.
The Experiment
The researchers performed various experiments, either decreasing or increasing the deposition of fibrin in the brain’s of mice. An enzyme from snake venom called ancrod, which causes the liver to clear fibrin from the bloodstream, was used to decrease fibrin. To increase it, they used tranexamic acid, which prevents the breakdown of fibrin clots.
The Results
The effects of the experiment were as predicted. The only knew information gained from it was the fact that beta-amyloid protein plaques in the mice’s brain did not change with fluctuating levels of fibrin. However, the inflammatory cells surrounding them did. “The number of microglia associated with each plaque - the number of the little inflammatory cells that get excited by fibrin deposition - are reduced when there’s less fibrin around, and increased when you can’t degrade the fibrin,” Paul says. Also, a decrease in fibrin using ancrod decreased the blood-vessel deterioration in the brain. “So reducing inflammation might be the link to preventing blood-brain damage, as well,” says Paul.
Final Quote
“Fibrin is a critical component for increased inflammation in Alzheimer’s disease. And fibrin and fibrinogen, based on our study, should be considered a new therapeutic target. Although, beta-amyloid may be the cause of Alzheimer’s, alternative approaches need to be considered,” according to Paul.
The function of Alzheimer’s is damage to the barrier that blocks blood from percolating into the brain. This damage allows fibrin and other blood proteins to seep through.
The Experiment
The researchers performed various experiments, either decreasing or increasing the deposition of fibrin in the brain’s of mice. An enzyme from snake venom called ancrod, which causes the liver to clear fibrin from the bloodstream, was used to decrease fibrin. To increase it, they used tranexamic acid, which prevents the breakdown of fibrin clots.
The Results
The effects of the experiment were as predicted. The only knew information gained from it was the fact that beta-amyloid protein plaques in the mice’s brain did not change with fluctuating levels of fibrin. However, the inflammatory cells surrounding them did. “The number of microglia associated with each plaque - the number of the little inflammatory cells that get excited by fibrin deposition - are reduced when there’s less fibrin around, and increased when you can’t degrade the fibrin,” Paul says. Also, a decrease in fibrin using ancrod decreased the blood-vessel deterioration in the brain. “So reducing inflammation might be the link to preventing blood-brain damage, as well,” says Paul.
Final Quote
“Fibrin is a critical component for increased inflammation in Alzheimer’s disease. And fibrin and fibrinogen, based on our study, should be considered a new therapeutic target. Although, beta-amyloid may be the cause of Alzheimer’s, alternative approaches need to be considered,” according to Paul.
So Many Anti-inflammatory Products to Chose From
I am amazed at all the anti-inflammatory foods posted by my fellow classmates in this forum. I did some websuring just to see what other unusual things are claimed to have anti-inflammatory properties. Suprisingly and to my relief, I found that grass fed beef (as opposed to grain-fed) and other animal foods may offer some protection from inflammation. Meat from grass-fed animals supposedly has more omega-3 fatty acids while meat from grain-fed has none, but is not lacking in saturated fat. http://www.dlife.com/dLife/do/ShowContent/food_and_nutrition/top_10_anti_inflammatory_foods.html
Ashley F. mentioned green tea in her blog, but I am a white tea and aloe vera juice junkie.
There isn’t much difference between green and white tea. Tea leaves destined for white are just harvested earlier than green tea(before the leaves open). I have a preference for white tea because it tastes purer than its green counterpart, has less caffeine, and it undergoes less processing than green tea, therefore it retains much of its antioxidant and anti-inflammatory properties. Green tea is indicated for reduction of the inflammation associated with arthritis, cardiovascular disease, and skin diseases such as psoriasis. Unfortunately, scientific evidence of the anti-inflammatory benefits of white tea is very limited and is only based on consumption in cultural population.
Unfortunately, like the info on grass-fed livestock, I could not find any primary literature on aloe vera products. What I did find was that aloe vera juice (according to studies I couldn’t find) regulates some components of the Immune system by reducing the incidence of inflammation in the kidneys, and digestive tract, reducing blood flow to tumors, and preventing carcinogens from entering the liver. http://www.ageless.co.za/herb-aloe.htm
I am saddened by the fact that there is so mch hype about foods with anti-inflammatory properties, but not many physicians are taking heed to these benefits and are very quick to prescribe a pill. Instead they should place heavy emphasis on diet and lifestlye changes (if one's physical health can be salvaged-which is almost always the case).
Ashley F. mentioned green tea in her blog, but I am a white tea and aloe vera juice junkie.
There isn’t much difference between green and white tea. Tea leaves destined for white are just harvested earlier than green tea(before the leaves open). I have a preference for white tea because it tastes purer than its green counterpart, has less caffeine, and it undergoes less processing than green tea, therefore it retains much of its antioxidant and anti-inflammatory properties. Green tea is indicated for reduction of the inflammation associated with arthritis, cardiovascular disease, and skin diseases such as psoriasis. Unfortunately, scientific evidence of the anti-inflammatory benefits of white tea is very limited and is only based on consumption in cultural population.
Unfortunately, like the info on grass-fed livestock, I could not find any primary literature on aloe vera products. What I did find was that aloe vera juice (according to studies I couldn’t find) regulates some components of the Immune system by reducing the incidence of inflammation in the kidneys, and digestive tract, reducing blood flow to tumors, and preventing carcinogens from entering the liver. http://www.ageless.co.za/herb-aloe.htm
I am saddened by the fact that there is so mch hype about foods with anti-inflammatory properties, but not many physicians are taking heed to these benefits and are very quick to prescribe a pill. Instead they should place heavy emphasis on diet and lifestlye changes (if one's physical health can be salvaged-which is almost always the case).
07 May 2008
Rheumatoid Arthritis Patients At Higher Risk For Unrecognized Heart Disease And Cardiac Sudden Death
Doctors and researchers at Mayo Clinic in Rochester, Minn have proven studies that patients with rheumatoid arthritis are at a much greater risk for unrecognized heart disease and cardiac sudden death.
This may be because these two diseases have common origins, however the fact that the diseases are multifactoral, is the only known fact. Oftentimes, rheumatoid arthritis patients seek medical attention for unrelated symptoms, and upon ordering an electrocardiogram for a patient, revealed a past 'silent heart attack.' Perhaps patients with rheumatoid arthritis have such severe and constant joint pain, that prescribed medications are allowing them to not be as responsive to chest pains. "We suspect that the systemic inflammation that characterizes rheumatoid arthritis also promotes cardiovascular disease and cardiovascular death," says Sherine Gabriel, M.D. There are still ongoing studies and research to explain this phenomena and means to prevent increased risk.
For full article: http://www.sciencedaily.com/releases/2005/02/050204121639.htm
* The risk of heart attack is already there at the time a rheumatoid arthritis diagnosis is first made.
* Heart disease can remain silent in those with rheumatoid arthritis. Regular cardiac checkups are important, as is lowering traditional cardiac risk factors, such as taking care of blood pressure and cholesterol and quitting smoking.
* Heart disease in rheumatoid arthritis patients can manifest for the first time as a cardiac sudden death.
This may be because these two diseases have common origins, however the fact that the diseases are multifactoral, is the only known fact. Oftentimes, rheumatoid arthritis patients seek medical attention for unrelated symptoms, and upon ordering an electrocardiogram for a patient, revealed a past 'silent heart attack.' Perhaps patients with rheumatoid arthritis have such severe and constant joint pain, that prescribed medications are allowing them to not be as responsive to chest pains. "We suspect that the systemic inflammation that characterizes rheumatoid arthritis also promotes cardiovascular disease and cardiovascular death," says Sherine Gabriel, M.D. There are still ongoing studies and research to explain this phenomena and means to prevent increased risk.
For full article: http://www.sciencedaily.com/releases/2005/02/050204121639.htm
DAA, PPAR + MCP-1
After reading 'Active spice-derived components can inhibit inflammatory responses of adipose tissue in obesity by suppressing inflammatory actions of macrophages and release of MCP-1 from adipocytes' article, i found another article that talks about a substance inhibiting MCP-1 activity. Dehydroabietic acid (DAA) is an abietic acid derivative contained in Terpenoids of many herbal and dietary plant substances. An experiment done by M-S Kang et al showed that DAA acts as an agonist of PPARs (peroxisome proliferator-activated receptors), which is a ligand-activated nuclear transcription factor that regulate lipid metabolism and homeostasis. PPAR-gamma subtypes has been shown to mediate anti-inflammatory effects on macrophages once it is activated so if DAA stimulates PPAR-gamma subtypes release by binding to its receptor then it can induce anti-inflammatory response on macrophages thereby inhibiting the pro-inflammatory cytokine release from macrophages. From their experiment, they found that DAA does indeed inhibit the production of pro-inflammatory cytokines (TNF-alpha) and chemokine (MCP-1). Since DAA activates PPAR, which is important on lipid metabolism and homeostasis, its a valuable medicinal and food component for regulating the inflammatory changes in obese individual.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T99-
4RP0MX3-1&_user=56761&_rdoc=1&_fmt=&_orig=search&_sort=
d&view=c&_acct=C000059541&_version=1&_urlVersion=0&_userid=
56761&;md5=3f210d5eace7bc095185f91066c889ea
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T99-
4RP0MX3-1&_user=56761&_rdoc=1&_fmt=&_orig=search&_sort=
d&view=c&_acct=C000059541&_version=1&_urlVersion=0&_userid=
56761&;md5=3f210d5eace7bc095185f91066c889ea
Maybe we can learn from Ayurvedic medicine
After reading the article “Turmeric extracts containing curcuminoids prevent experimental Rheumatoid arthritis” by Janet Funk I wanted to find out a little more about Ayurvedic medicine. In particular I wanted find out what other herbs they believe to have helpful or healing powers. I found a list on Wikipedia called the “list of herbs and minerals in Aryuveda, and most of them have the therapeutic use that Aryuvedas are claiming. I think we could take notes from their culture on some things and not on other things.
For example camphor, is a herb that they use for thirst, obesity, burning sensations, throat problems, asthma, excessive sweats and a few other things. I personally identify it as the main ingredient in moth repellents, however; it has other uses such as embalming, fireworks and rust preventative coating.
It is amazing to see the use of this one herb from one spectrum to another, how it can “help” a person and how it can enhance man made materials in a completely unrelated way.
The website with the list
http://en.wikipedia.org/wiki/List_of_herbs_and_minerals_in_Ayurveda
Metal and Vitamin Toxicity
I have a strong interest in integrative medicine and I think complimenting modern medicine with Ayurvedic practices is a good idea. But upon doing some research I think there is an area where people should limit their intake. The Center for Disease Control found that, “Some Ayurvedic medicines contain metals and minerals that can lead to toxicity of the liver. “During 2000-2003, a total of 12 cases of lead poisoning among adults in five states associated with ayurvedic medications or remedies were reported to CDC.”
MMWR Morb Mortal Wkly Rep. 2004 Jul 9;53(26):582-4.
Another study found that herbs, minerals and metals have led to cases of, “status epilepticus,5 fatal infant encephalopathy,6 congenital paralysis and sensorineural deafness,7 and developmental delay.8 Since 1978, at least 55 cases of heavy metal intoxication associated with Ayurvedic HMPs in adults and children have been reported in the United States and abroad. JAMA. 2004 Dec 15;292(23):2868-73.
The medicines that were found to contain it were; Bal Chamcha, Bala Guti, Bala Sogathi, Balguti, Kersaria, Gesari, Karela, Maha Sudarshan Churna, Mahalakshmi Vilas Ras, Navratna Rasa, Safi, Shilajit, Swarna.
So I would take some caution taking more than the prescribed dosage on these medications.
Also I think this applies to any vitamin or mineral. People have the same problem when they take too much vitamin D. It can lead to vitamin toxicity. Sometimes people think the more vitamins the better but that is not true in this case.
MMWR Morb Mortal Wkly Rep. 2004 Jul 9;53(26):582-4.
Another study found that herbs, minerals and metals have led to cases of, “status epilepticus,5 fatal infant encephalopathy,6 congenital paralysis and sensorineural deafness,7 and developmental delay.8 Since 1978, at least 55 cases of heavy metal intoxication associated with Ayurvedic HMPs in adults and children have been reported in the United States and abroad. JAMA. 2004 Dec 15;292(23):2868-73.
The medicines that were found to contain it were; Bal Chamcha, Bala Guti, Bala Sogathi, Balguti, Kersaria, Gesari, Karela, Maha Sudarshan Churna, Mahalakshmi Vilas Ras, Navratna Rasa, Safi, Shilajit, Swarna.
So I would take some caution taking more than the prescribed dosage on these medications.
Also I think this applies to any vitamin or mineral. People have the same problem when they take too much vitamin D. It can lead to vitamin toxicity. Sometimes people think the more vitamins the better but that is not true in this case.
Turmeric: The Magical Antioxidant and Anti-inflammatory Spice
Since most of the articles this week focused on spices, I did some more research on anti-inflammatory spices. I found that the top 12 anti-inflammatory spices are Ginger, Turmeric, Black Pepper, Cinnamon, Rosemary, Basil, Cardamon, Chives, Cilantro ,Cloves, Garlic, and Parsley. There seemed to be the most information on Turmeric though. Turmeric is a spice that belongs to the ginger family and it is found in curry. Along with turmeric's role as an anti-inflammatory to treat arthritis, people also use it for other health conditions. Turmeric is an antioxidant that can help prevent cancer and can protect vital organs. It can also be used to treat digestive problems or be made into a paste to help treat skin problems such as cuts, scrapes, acne, and diaper rashes. The website suggested taking 1.5-3g of turmeric a day to help with digestive problems, but for the anti-inflammatory effects you need to take 3-5 g 3 times a day (that doesn't sound so pleasing to me). It's usually taken in by dissolving the powder in water or tea. It can also be dissolved in oils and applied to the skin where it penetrates through follicles and sweat glands. Turmeric has been used for a long time in Chinese medicine and many people believe it is effective. This is more of a recent subject in western medicine that should be studied a lot further. In the mean time we should start dumping turmeric powder in our drinks....who's gonna bring it to frog & firkin?
You can see the turmeric article here http://www.pureinsideout.com/turmeric-curcuma.html
Thanks for a great semester Dr. Cohen!
You can see the turmeric article here http://www.pureinsideout.com/turmeric-curcuma.html
Thanks for a great semester Dr. Cohen!
06 May 2008
Turmeric As An Antiinflammatory
Turmeric is a perennial native to Asia that has been used in traditional medicine for the treatment of inflammatory disorders. This experiment studied its efficacy of curcuminoid-containing turmeric extracts in prevention/treatment of Rheumatoid arthritis. An essential oil-depleted turmeric fraction(41% of the three major curcuminoids) was effective in preventing joint inflammation in both the acute and chronic destructive phases of arthritis when treatment was started before the onset of inflammation. The problem was that it had no significant impact when started after the onset of inflammation. Another sample containing 94% of the curcuminoids was better in preventing arthritis. Daily low doses inhibited joint inflammation in both the acute and chronic phases. The arthritic inhibition was close to that caused by a six-fold higher dose of the turmeric fraction. The results suggest that the “extra” components of the turmeric fraction, other than the major curcuminoids, may work against the protective action of the curcuminoids. The curcuminoids appear to be responsible for the antiarthritic effect. Take home message=if you have arthritis, Asia is the place to be….just kidding. I made this short and sweet due to exhaustion but if you have any questions, feel free to post...Have a great summer! Happy Graduation to all who have completed!!!
05 May 2008
Strawberry, bitter melon juices + anti-inflammatory
Since we're doing anti-inflammatory for the last weeks of the semester i thought id look up easily accessible foods that has anti-inflammatory effects. I found an article by J-Y. Lin and C-Y Tang who conducted an experiments on strawberries, loquat, mulberry and bitter melon juices to examine their anti-inflammatory effects on LPS-stimulated peritoneal macrophages cultures taken from mice. Lin and Tang chose these fruits/vegetable because of their properties that exhibit anti-inflammatory responses from previous experiments. It has been found that fruits such as strawberries contain compounds that inhibits COX activity and have demonstrated that it has an anticancer activity as well while mulberry fruit extracts inhibit atherosclerosis on rats in cholesterol-rich diets and bitter melon are used in traditional medicine by Asian countries as treatment for diabetes. What they found was that
The fruit juice extracts were taken from strawberry, loquat, mulberry and bitter melon bought from a supermarket in Taiwan. Peritoneal macrophages were taken from mice and divided into 3 different LPS-induced inflammation models. Model A was an inflammation-prophylactic cell culture (peritoneal macrophages were exposed to 0, 10 and 500 microgram/ml concentration of fruit juices before LPS stimulation), model B was designed where peritoneal macrophage cell cultures were first stimulated with LPS then administered 0, 10 and 500 microgram/ml concentration of fruit juices and model C was designed to examine the effects of fruit juice administration to cell upon cytokine production clearance with simultaneous acute LPS stimulation. What they found was that loquat, bitter melon and mulberry administration significantly decreased levels of pro-inflammatory cytokines while strawberry (along with the other fruits/veg.) increased IL-10 production in dose-dependent experiment model A. Administration of bitter melon and loquat also significantly increased IL-10 production in model C, suggesting that strawberry, loquat, mulberry and bitter melon all have prophylactic anti-inflammatory properties by decreasing pro-inflammatory cytokines (IL-1beta, IL-6 and TNF-alpha) and increasing anti-inflammatory cytokine (IL-10) production in LPS-induced inflammation in mice peritoneal macrophages.
So, eat your fruits and vegetables :)!
http://web.ebscohost.com.ezproxy1.library.arizona.edu/ehost/detail?vid=2&hid=114&sid=194fc15b-49fb-421c-a4b9-411eb893a794%40sessionmgr107
The fruit juice extracts were taken from strawberry, loquat, mulberry and bitter melon bought from a supermarket in Taiwan. Peritoneal macrophages were taken from mice and divided into 3 different LPS-induced inflammation models. Model A was an inflammation-prophylactic cell culture (peritoneal macrophages were exposed to 0, 10 and 500 microgram/ml concentration of fruit juices before LPS stimulation), model B was designed where peritoneal macrophage cell cultures were first stimulated with LPS then administered 0, 10 and 500 microgram/ml concentration of fruit juices and model C was designed to examine the effects of fruit juice administration to cell upon cytokine production clearance with simultaneous acute LPS stimulation. What they found was that loquat, bitter melon and mulberry administration significantly decreased levels of pro-inflammatory cytokines while strawberry (along with the other fruits/veg.) increased IL-10 production in dose-dependent experiment model A. Administration of bitter melon and loquat also significantly increased IL-10 production in model C, suggesting that strawberry, loquat, mulberry and bitter melon all have prophylactic anti-inflammatory properties by decreasing pro-inflammatory cytokines (IL-1beta, IL-6 and TNF-alpha) and increasing anti-inflammatory cytokine (IL-10) production in LPS-induced inflammation in mice peritoneal macrophages.
So, eat your fruits and vegetables :)!
http://web.ebscohost.com.ezproxy1.library.arizona.edu/ehost/detail?vid=2&hid=114&sid=194fc15b-49fb-421c-a4b9-411eb893a794%40sessionmgr107
Bee Venom; Antinociceptive and Anti-inflammatory?
I remember reading an article earlier in the semester that used Bee Venom as an alternative treatment for patients suffering with MS. Now it's potentially helpful in arthritis?
The paper "Bee Venom Pretreatment Has Both an Antinociceptive and Anti-inflammatory Effect of Carrageenan-Induced Inflammation", Lee et.al. provided some very interesting informmation that under normal conditions, bee venom is nociceptive. This statement seems very vague for reasons as follows. Does the bee venom have to bee administered directly to the site of inflammation or does it have peripheral effects as well? I was under the impression that there is most likely always inflammation occurring somewhere in every person at any given time so would this deter the bulk of individuals from being under normal conditions?
On another note, I would like to thank SarahD for better defining Fos and Carrageenan (CR); I wasn't too sure what they were, so thanks for clearing that up.
Researchers used CR to induce inflammation in rat models proceeding Bee Venom injection. To my surprise they acutally found that bee venom was successful in suppressing inflammation; aside from creating a small response of its own such as irriation at the injection site, etc.
It just tickles me to think that cures for some common diseases could be right under our noses or in our gardens.
The paper "Bee Venom Pretreatment Has Both an Antinociceptive and Anti-inflammatory Effect of Carrageenan-Induced Inflammation", Lee et.al. provided some very interesting informmation that under normal conditions, bee venom is nociceptive. This statement seems very vague for reasons as follows. Does the bee venom have to bee administered directly to the site of inflammation or does it have peripheral effects as well? I was under the impression that there is most likely always inflammation occurring somewhere in every person at any given time so would this deter the bulk of individuals from being under normal conditions?
On another note, I would like to thank SarahD for better defining Fos and Carrageenan (CR); I wasn't too sure what they were, so thanks for clearing that up.
Researchers used CR to induce inflammation in rat models proceeding Bee Venom injection. To my surprise they acutally found that bee venom was successful in suppressing inflammation; aside from creating a small response of its own such as irriation at the injection site, etc.
It just tickles me to think that cures for some common diseases could be right under our noses or in our gardens.
Carrageenan and Fos
While reading the article outlining the antinociceptive and anti-inflammatory effects of bee venom, I realized I had no idea what carrageenan or Fos were. These were both key components of the paper and so I decided to define both terms as best I could in order to clarify for any other uniformed people like myself. :)
Carrageenans are a group of substances composed of linear sulphated polysaccharides extracted from red seaweed. This group of items is utilized in many varying fields. One use of carrageenan is as a thickening, gelatin like substance in many foods. There are three main commercial classes of carrageen, which include the lota gels, kappa gels, and lambda gels. This latter type of carrageen forms a gel when mixed with proteins, and is also the type of carrageen used in the experiments regarding the anti-inflammatory properties of bee venom. Lambda carrageenan solution of 1-2% causes inflammation, swelling, and pain in when injected into animal experimental models.
I had a hard time finding a definition for Fos. What I did find is that Fos is a protein found within the body that is usually at a low concentrations until a neuron is activated by an external stimulus, such as pain. I also found that Fos expression can increase with other factors as well, such as metabolic changes. I am actually wondering if anyone can give me a clearer definition on what Fos actually is.
Carrageenans are a group of substances composed of linear sulphated polysaccharides extracted from red seaweed. This group of items is utilized in many varying fields. One use of carrageenan is as a thickening, gelatin like substance in many foods. There are three main commercial classes of carrageen, which include the lota gels, kappa gels, and lambda gels. This latter type of carrageen forms a gel when mixed with proteins, and is also the type of carrageen used in the experiments regarding the anti-inflammatory properties of bee venom. Lambda carrageenan solution of 1-2% causes inflammation, swelling, and pain in when injected into animal experimental models.
I had a hard time finding a definition for Fos. What I did find is that Fos is a protein found within the body that is usually at a low concentrations until a neuron is activated by an external stimulus, such as pain. I also found that Fos expression can increase with other factors as well, such as metabolic changes. I am actually wondering if anyone can give me a clearer definition on what Fos actually is.
Popularity of Bee Venom Treatment
I find it very interesting that so many people are willing to be treated with bee venom to cure their ailments. Many people even prefer it to western medicine, or at least many people, especially in Asia find it an affordable alternative to mainstream health care. I'd like to encourage everyone to read the information on the alternative medicine of bee sting venom and its popular use at the following website: http://www.msnbc.msn.com/id/16751949/
I find the topic of alternative medications quite interesting, because I really believe that at least some of what people have found over time to work against disease must have a foundation. I am definitely not stating that every all natural cure out there is THE cure to all diseases, but I like that the papers this week look into spices and bee venom as possible means to curing or preventing disease.
I find the topic of alternative medications quite interesting, because I really believe that at least some of what people have found over time to work against disease must have a foundation. I am definitely not stating that every all natural cure out there is THE cure to all diseases, but I like that the papers this week look into spices and bee venom as possible means to curing or preventing disease.
04 May 2008
Oil Pulling Therapy: Effective Natural Detoxification, Stimulation of Elimination, Self-Help Cure and Prevention of Many Diseases Including Cancer?
Over the weekend I was talking to a friend that told me about an oil detox treatment. I was curious about it and decided to investigate more on this treatment. The name of the treatment is Oil Pulling Therapy.
Oil Pulling Therapy consists of thoroughly sloshing certain types of common oils (sunflower or sesame) in the mouth for approximately 20 minutes. Swishing is believed to activate the enzymes that draw toxins from the blood. This practice is believed to remove toxins and destroy natural mouth germs while stimulating the body's eliminatory system and increasing metabolism which leads to improved health. According to Dr Karach, a naturopath, the therapy has both preventative and curative effects.
Lothar Hirneise’s, a new cancer treatment center in Germany, prescribes oil pulling as part of the daily morning routine in conventional and alternative cancer treatment
Dr. Karach claims that oil pulling has healed illnesses such as bronchitis, tooth pain, diseased teeth, headaches and migraines, eczema, thrombosis, chronic sleeplessness, arthritis & related illnesses, diseases of stomach and intestines (ulcers, peritonitis), kidney, liver, and heart disease, blood disorders (chronic blood disease like leukemia), woman’s diseases and hormonal disorders, and disease affecting the nervous system (such as encephalitis, meningitis, neuro-physiological paralysis). It has been also claimed to prevent the growth of malignant tumors, to be a heart attack preventative, to cure disease brought about toxic drugs, and it is also thought to cure diabetes. Dr. Karach claims to have cured a patient with chronic blood disease of 15 years using this oil therapy. He also claims it increases human lifespan. And, in terminal diseases such as cancer, Aids and chronic infections, this therapy has helped symptoms disappear without side effects.
Patients with more than one disease tend to experience a worsening of the symptoms initially which is a sign (according to naturopaths) that the disease is disappearing.
Oilpulling.com claims that the therapy can cure acute diseases in two to four days, while chronic disease will take more time. Some times even more than a year.
According to the article, in 1996 the Indian Daily Newspaper, conducted a survey among its reader regarding the effect of oil pulling. 1041 readers responded, 927 of them reported healing effects (one of more diseases), 114 did not report any disappearance of disease. Some of the chronic diseases reported cured were:
-Diseases like polio, cancer, leprosy, polycystic kidney, neural fibroma, paralysis: 72 cases.
-Female reproductive diseases: 21 cases
-Diabetes: 56 cases
-Heart Disease and blood pressure: 74 cases
-Arthritis and joint pains: 91 cases
-Digestive system: 155 cases
-Allergy and respiratory diseases: 191 cases, and more.
According to the article, no one has done any placebo-controlled double-blind studies on the benefits of oil pulling so any published material on this topic can easily be dismissed a as simple anecdotes based on the powerful placebo effect.
There is a lot of information regarding OP but non of the articles that I found explained the physiological effect of this therapy.
Here are some of the articles I found related to this topic (and there is a lot more):
http://www.healingcancernaturally.com/detoxification-oil-pulling.html
http://www.earthclinic.com/Remedies/oil_pulling.html
http://www.oilpulling.com/
http://www.thecolonet.com/colonet_newsletter.pdf
http://www.americanchronicle.com/articles/24247
Oil Pulling Therapy consists of thoroughly sloshing certain types of common oils (sunflower or sesame) in the mouth for approximately 20 minutes. Swishing is believed to activate the enzymes that draw toxins from the blood. This practice is believed to remove toxins and destroy natural mouth germs while stimulating the body's eliminatory system and increasing metabolism which leads to improved health. According to Dr Karach, a naturopath, the therapy has both preventative and curative effects.
Lothar Hirneise’s, a new cancer treatment center in Germany, prescribes oil pulling as part of the daily morning routine in conventional and alternative cancer treatment
Dr. Karach claims that oil pulling has healed illnesses such as bronchitis, tooth pain, diseased teeth, headaches and migraines, eczema, thrombosis, chronic sleeplessness, arthritis & related illnesses, diseases of stomach and intestines (ulcers, peritonitis), kidney, liver, and heart disease, blood disorders (chronic blood disease like leukemia), woman’s diseases and hormonal disorders, and disease affecting the nervous system (such as encephalitis, meningitis, neuro-physiological paralysis). It has been also claimed to prevent the growth of malignant tumors, to be a heart attack preventative, to cure disease brought about toxic drugs, and it is also thought to cure diabetes. Dr. Karach claims to have cured a patient with chronic blood disease of 15 years using this oil therapy. He also claims it increases human lifespan. And, in terminal diseases such as cancer, Aids and chronic infections, this therapy has helped symptoms disappear without side effects.
Patients with more than one disease tend to experience a worsening of the symptoms initially which is a sign (according to naturopaths) that the disease is disappearing.
Oilpulling.com claims that the therapy can cure acute diseases in two to four days, while chronic disease will take more time. Some times even more than a year.
According to the article, in 1996 the Indian Daily Newspaper, conducted a survey among its reader regarding the effect of oil pulling. 1041 readers responded, 927 of them reported healing effects (one of more diseases), 114 did not report any disappearance of disease. Some of the chronic diseases reported cured were:
-Diseases like polio, cancer, leprosy, polycystic kidney, neural fibroma, paralysis: 72 cases.
-Female reproductive diseases: 21 cases
-Diabetes: 56 cases
-Heart Disease and blood pressure: 74 cases
-Arthritis and joint pains: 91 cases
-Digestive system: 155 cases
-Allergy and respiratory diseases: 191 cases, and more.
According to the article, no one has done any placebo-controlled double-blind studies on the benefits of oil pulling so any published material on this topic can easily be dismissed a as simple anecdotes based on the powerful placebo effect.
There is a lot of information regarding OP but non of the articles that I found explained the physiological effect of this therapy.
Here are some of the articles I found related to this topic (and there is a lot more):
http://www.healingcancernaturally.com/detoxification-oil-pulling.html
http://www.earthclinic.com/Remedies/oil_pulling.html
http://www.oilpulling.com/
http://www.thecolonet.com/colonet_newsletter.pdf
http://www.americanchronicle.com/articles/24247
Green Tea, Does it increase efficacy of antibiotics???
To add to the previous post of natural alternatives as anti-inflammatory, here is an article discussing a natural healthy approach to increasing the efficacy of antibiotics. I happened to come across this article from discoveryhealth.com and thought it might be of some interest since there have been many encouraging words from multiple sources about the benefits of green tea in ones daily diet.
Green Tea Boosts Antibiotics for Superbugs (3-21-2008)
Green tea can help antibiotics be three times more effective in fighting drug-resistant bacteria, even superbugs, according to a study by researchers at Alexandria University in Egypt.
Green Tea Boosts Antibiotics for Superbugs (3-21-2008)
Green tea can help antibiotics be three times more effective in fighting drug-resistant bacteria, even superbugs, according to a study by researchers at Alexandria University in Egypt.
Green tea is common in Egypt, and it's likely that many people there drink it while taking antibiotics.Therefore, the researchers wanted to determine if green tea would decrease or increase the effectiveness of antibiotics or have no effect.
"We tested green tea in combination with antibiotics against 28 disease-causing microorganisms belonging to two different classes," Dr Mervat Kaseem, of the university's pharmacy faculty, said in a prepared statement. "In every single case, green tea enhanced the bacteria-killing activity of the antibiotics. For example, the killing effect of chloramphenicol was 99.99 percent better when taken with green tea than when taken on its own in some circumstances."
Kaseem and colleagues also found that green team made 20 percent of drug-resistant bacteria susceptible to cephalosporin antibiotics, an important type of antibiotics to which new drug-resistant strains of bacteria have evolved resistance.
In almost every case and for all types of antibiotics they tested, the researchers found that drinking green tea at the same time as taking the antibiotics appeared to increase the action of the antibiotics and reduce drug resistance in bacteria. In certain cases, even low concentrations of green tea were effective.
The study was to be presented Monday at a meeting of the Society for General Microbiology in Edinburgh, Scotland.
"Our results show that we should consider more seriously the natural products we consume in our everyday life," Kaseem said. "In the future, we will be looking at other natural herb products such as majoram and thyme to see whether they also contain active compounds which can help in the battle against drug resistant bacteria."
article taken from: http://health.discovery.com/news/healthscout/article.html?article=614042&category=3&year=200803 May 2008
8 Natural Alternatives for anti inflammatories
I was interested in seeing what other alternatives there are out there as far as ant inflammatories go so I googled it. I came upon an interesting article. The article had the following suggestions:
1. Omega-3 Fatty Acids From Fish Oils: The omega-3 fats EPA and DHA found in fish oil have been found by many animal and clinical studies to possess anti-inflammatory properties that promote joint lubrication and decrease joint inflammation. Animal based omega-3 fats form the precursors to the molecules that actually produce or inhibit inflammation in your body (prostaglandins). That is why it is essential to make sure you are getting enough. It is also vital to understand that you need to reduce omega-6 fats like vegetable oils seeds and nuts, as it is actually the ratio of omega 6:3 fats that determines how much inflammation is present. You could theoretically consume enough omega-3 fish oils to work but then ruin the effect by consuming too many omega-6 fats.
2. Ginger: This herb is anti-inflammatory and offers pain relief and stomach-settling properties. Fresh ginger works well steeped in boiling water as a tea or grated into vegetable juice.
3. Bromelain Enzymes: This enzyme, found in pineapples, is a natural anti-inflammatory. It can be taken in supplement form, but eating fresh pineapple may also be helpful.
4. Cetyl Myristoleate (CMO): This oil, found in fish and dairy butter, acts as a "joint lubricant" and an anti-inflammatory. In one study of 106 people with various types of arthritis who did not respond to NSAIDs, 63.5 percent of those who took CMO orally and applied the cream topically (it's available both in oral supplement and cream forms) improved, compared to only 14.5 percent of those taking a placebo.
5. Boswellia: aka “boswellin” or "Indian frankincense," this herb contains specific active anti-inflammatory ingredients, referred to as boswellic acids that animal studies have shown significantly reduce inflammation. In a study of 175 patients with rheumatic disorders such as rheumatoid arthritis, 122 participants had reduced stiffness and inflammation just two to four weeks after starting on boswellia.
6. Evening Primrose Oil (or borage oil or black current oil): These contain the essential fatty acid gamma linolenic acid (GLA), which is useful for treating arthritic pain. In one study of 37 rheumatoid arthritis patients, those who received 1.4 grams of GLA per day reduced the number of tender joints by 36 percent, the tenderness of the joints by 45 percent, the number of swollen joints by 28 percent, and the degree of joint swelling by 41 percent. The placebo group showed no significant improvements.
7. Cayenne Pepper: (capsaicin) in the form of cayenne cream: Also called capsaicin cream, this spice comes from dried hot peppers. It alleviates pain by depleting the body's supply of substance P, a chemical component of nerve cells that transmits pain signals to the brain.
8. White Willow Bark: Aspirin is made from the bark of the white willow. People have been using white willow bark for centuries as a mild pain reliever. White willow bark does not destroy the stomach lining on contact the way aspirin does, however, it does have the same blood thinning effect as aspirin and caution is indicated.
here's the link to the article if anyone wants to check it out
http://ezinearticles.com/?Eight-Natural-Alternatives-to-Anti-Inflammatory-Medication&id=131679
1. Omega-3 Fatty Acids From Fish Oils: The omega-3 fats EPA and DHA found in fish oil have been found by many animal and clinical studies to possess anti-inflammatory properties that promote joint lubrication and decrease joint inflammation. Animal based omega-3 fats form the precursors to the molecules that actually produce or inhibit inflammation in your body (prostaglandins). That is why it is essential to make sure you are getting enough. It is also vital to understand that you need to reduce omega-6 fats like vegetable oils seeds and nuts, as it is actually the ratio of omega 6:3 fats that determines how much inflammation is present. You could theoretically consume enough omega-3 fish oils to work but then ruin the effect by consuming too many omega-6 fats.
2. Ginger: This herb is anti-inflammatory and offers pain relief and stomach-settling properties. Fresh ginger works well steeped in boiling water as a tea or grated into vegetable juice.
3. Bromelain Enzymes: This enzyme, found in pineapples, is a natural anti-inflammatory. It can be taken in supplement form, but eating fresh pineapple may also be helpful.
4. Cetyl Myristoleate (CMO): This oil, found in fish and dairy butter, acts as a "joint lubricant" and an anti-inflammatory. In one study of 106 people with various types of arthritis who did not respond to NSAIDs, 63.5 percent of those who took CMO orally and applied the cream topically (it's available both in oral supplement and cream forms) improved, compared to only 14.5 percent of those taking a placebo.
5. Boswellia: aka “boswellin” or "Indian frankincense," this herb contains specific active anti-inflammatory ingredients, referred to as boswellic acids that animal studies have shown significantly reduce inflammation. In a study of 175 patients with rheumatic disorders such as rheumatoid arthritis, 122 participants had reduced stiffness and inflammation just two to four weeks after starting on boswellia.
6. Evening Primrose Oil (or borage oil or black current oil): These contain the essential fatty acid gamma linolenic acid (GLA), which is useful for treating arthritic pain. In one study of 37 rheumatoid arthritis patients, those who received 1.4 grams of GLA per day reduced the number of tender joints by 36 percent, the tenderness of the joints by 45 percent, the number of swollen joints by 28 percent, and the degree of joint swelling by 41 percent. The placebo group showed no significant improvements.
7. Cayenne Pepper: (capsaicin) in the form of cayenne cream: Also called capsaicin cream, this spice comes from dried hot peppers. It alleviates pain by depleting the body's supply of substance P, a chemical component of nerve cells that transmits pain signals to the brain.
8. White Willow Bark: Aspirin is made from the bark of the white willow. People have been using white willow bark for centuries as a mild pain reliever. White willow bark does not destroy the stomach lining on contact the way aspirin does, however, it does have the same blood thinning effect as aspirin and caution is indicated.
here's the link to the article if anyone wants to check it out
http://ezinearticles.com/?Eight-Natural-Alternatives-to-Anti-Inflammatory-Medication&id=131679
30 April 2008
BOTOX to treat arthritis??
New studies show that maybe Botulinium type A (Botox) may help pain and function of arthritic patients. There was a study conducted in 2006 published in Neurotoxicity Research that tested Botox injection efficacy among 11 patients with different forms of arthritis. The subject group was given one or more Botox injections within the afflicted joint, and then followed for a year post-treatment.
All 11 participants reported improvements of pain and function, these results differing among patients, with different degree of improvements anywhere from three to twelve months afterward. However, there was no placebo test group, and the amount of injection was not standardized, leading to more studies to further investigate. The treatment seems promising, as no patient trial was complicated with adverse effects.
Mayo Clinic in Rochester, Minnesota is beginning a trial to test the results of Botox injections of arthritic knees. Because Botox has been proven to paralyze muscle and nerve endings, there is a great chance that it may help subside severe pain in patients who no longer respond to cortisone treatments. Actually, several Botox trials are being looked into for pain and inflammation relief, so who knows what will happen!
South Beach Diet
After reading the Great Debate, I wanted to find out more about the south beach diet.
I read that it is a three phase plan and that its claim to fame is that you will loose the weight you need to loose and that it will improve your cardiovascular system. I really liked that the system was a life long program however; I thought that some things needed to be changed.
It states that phase 1 is two weeks in which you eat as much as you normally would however you eat three well balanced or healthy meals in order to subdue cravings. My problem is that it takes more than two weeks to learn how to eat healthy and maintain regularity in the process. Think of it in terms of a New Year’s resolution when you have to take baby steps and perform regularly for the new habit to stick. Two weeks has never made anyone’s New Years resolution stick.
Phase 2 is about loosing weight by continuing to eat healthy and with portion control in order to achieve your goal weight. This phase can go on as long as one pleases. Last is phase 3 were you are at your goal weight and you maintain it however the foods that you are allowed to eat are less restricted. The synopsis of phase three goes on to say that at this point in time you will improve your cardiovascular system. Any one who is clearly overweight and looses a significant amount of weight will improve, but the way it is described might have your average person thinking that it pertains specifically to this diet and not dieting in general. I personally think that they should elaborate on the idea so that people understand that that is common to weight loss.
Finally I see no mention about exercise, a crucial player in weight loss and improving health. Does anyone else have issues with that?
This is the website I got my info from
http://www.southbeach-diet-plan.com/index.html
I read that it is a three phase plan and that its claim to fame is that you will loose the weight you need to loose and that it will improve your cardiovascular system. I really liked that the system was a life long program however; I thought that some things needed to be changed.
It states that phase 1 is two weeks in which you eat as much as you normally would however you eat three well balanced or healthy meals in order to subdue cravings. My problem is that it takes more than two weeks to learn how to eat healthy and maintain regularity in the process. Think of it in terms of a New Year’s resolution when you have to take baby steps and perform regularly for the new habit to stick. Two weeks has never made anyone’s New Years resolution stick.
Phase 2 is about loosing weight by continuing to eat healthy and with portion control in order to achieve your goal weight. This phase can go on as long as one pleases. Last is phase 3 were you are at your goal weight and you maintain it however the foods that you are allowed to eat are less restricted. The synopsis of phase three goes on to say that at this point in time you will improve your cardiovascular system. Any one who is clearly overweight and looses a significant amount of weight will improve, but the way it is described might have your average person thinking that it pertains specifically to this diet and not dieting in general. I personally think that they should elaborate on the idea so that people understand that that is common to weight loss.
Finally I see no mention about exercise, a crucial player in weight loss and improving health. Does anyone else have issues with that?
This is the website I got my info from
http://www.southbeach-diet-plan.com/index.html
29 April 2008
Reduce LDL with a low carb diet?
In this weeks lay article, "The Great Diet Debate" two Dr's debated over The South Beach Heart Program. Dr. Agatston, the author of the book, claims this program will detect, prevent, and even reverse heart disease although a study showed this diet did not lower LDL cholesterol levels. Dr. Agatston also prescribes his patients drugs to lower their LDL cholesterol instead of advising them to eat less fat and exercise.
I think putting people on a low carb diet to help treat and prevent heart disease is, well, stupid. The south beach diet may help people with short-term weight loss which in turn can reduce the risk of heart disease, but this diet includes meats high in fat which are not the most heart-healthy foods. As stated in a previous blog, this issue goes back to the overall theme of the class: EAT HEALTHY AND EXERCISE. As Dr. Ornish stated in the article, diets that include omega-3 fatty acids can dramatically decrease cardiac events and reduce inflammation. So, eat less trans and saturated fats, eat more omega-3, and exercise!
I think putting people on a low carb diet to help treat and prevent heart disease is, well, stupid. The south beach diet may help people with short-term weight loss which in turn can reduce the risk of heart disease, but this diet includes meats high in fat which are not the most heart-healthy foods. As stated in a previous blog, this issue goes back to the overall theme of the class: EAT HEALTHY AND EXERCISE. As Dr. Ornish stated in the article, diets that include omega-3 fatty acids can dramatically decrease cardiac events and reduce inflammation. So, eat less trans and saturated fats, eat more omega-3, and exercise!
28 April 2008
Anti-Inflammatory Foods
A major cause of inflammation in our bodies is the food we eat. Inflammation can be aggravated by diets high in refined or hydrogenated vegetable oils such as those found in margarines, potato chips and baked goods and by diets high in sugars. Food can also be part of the solution to inflammation; anti-inflammatory foods, if eaten regularly, can reduce inflammation in the body.
Vegetables: Bell Peppers, Bok Choy, Broccoli, Broccoli Sprouts, Brussels Sprouts, Cabbage, Cauliflower, Chard Collards, Fennel Bulb, Garlic, Green Beans, Green Onions/Spring Onions, Kale, Leeks, Olives, Spinach, Sweet potatoes, Turnip, Greens
Oils: Avocado Oil, Extra Virgin Olive Oil
Drinks: Green Tea
Herbs & Spices: Basil, Cayenne Peppers/Chili Peppers, Cinnamon Cloves, Cocoa (at least 70% cocoa chocolate), Licorice, Mint, Oregano, Parsley, Rosemary, Thyme, Turmeric
Fruits: Acerola (West Indian) Cherries, Apples, Avocados, Black Currants,
Blueberries, Fresh Pineapple, Guavas, Kiwifruit, Kumquats, Lemons, Limes, Mulberries, Oranges, Papaya, Raspberries, Rhubarb, Strawberries, Tomatoes
Nuts & Seeds: Almonds, Flaxseed/Linseed, Hazelnuts, Sunflower Seeds, Walnuts
Fish: Cod, Halibut, Herring, Oysters, Rainbow Trout, Salmon, Sardines, Snapper Fish, Striped Bass, Tuna, Whitefish
List of Anti-inflammatory Foods from: http://www.metabolismadvice.com/
27 April 2008
Acupuncture
Another article that I read about anti-inflammatories discussed the benefits of acupuncture on different inflammatory diseases. I really liked this article because it went into pretty good detail about the different inflammatory diseases as well as the effect the acupuncture had on them. Their results showed that acupuncture mainly benefitted patients with asthma. The acupuncture also seemed to help with rhinitis after allergen provocation. Results seemed inconclusive for arthritis and inflammatory bowel disease. The article states that more studies need to be done in order to provide conclusive evidence but I thought it was still an interesting idea.
The full article can be seen here,
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1781596&blobtype=pdf
The full article can be seen here,
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1781596&blobtype=pdf
Stinging Nettle as an Anti-Inflammatory
As i was looking for different alternative anti-inflammatories, I came across a few articles that suggested the use of stinging nettles, particularly to ease the pain caused by rheumatoid arthritis. The stinging nettle is a plant whose stinging hairs on are sharp, polished spines that contain histamine and formic acid. Normally these stinging hairs are painful to the touch but when they come into contact with an area that is already in pain the chemicals can actually decrease the original pain.
Today the plant can also be used to treat urinary problems in the early stages of an enlarged prostate, eczema, gout, anemia, and kidney stones. It is available in many different forms; dried leaves, tea, root tincture (a solution of the herb in alcohol), cream, and in capsule form.
The full article can be found here,
http://www.healthandage.com/html/res/com/ConsHerbs/StingingNettlech.html
Today the plant can also be used to treat urinary problems in the early stages of an enlarged prostate, eczema, gout, anemia, and kidney stones. It is available in many different forms; dried leaves, tea, root tincture (a solution of the herb in alcohol), cream, and in capsule form.
The full article can be found here,
http://www.healthandage.com/html/res/com/ConsHerbs/StingingNettlech.html
Portions! Portions! Portions!...and content too
This week, all of the lay articles seemed to have a common theme: Watch what you eat, and you will succeed in your endevor to become a healthy individual. This is a concept that is not particularly striking and an idea we have previously discussed in class. As a recap, roughly 60% of the American public is clinically over weight, and from articles we have previously read in this class, reducing caloric intake of the general population seems capable of increasing life expectancy. This idea only seems logical for those 60% (or more) Americans.
In Snacking in the Line of Duty the author discussed the benefits of consuming small portion sizes despite the fact that many of these snacks lack any real nutritional value. It makes sense that the American public might benefit from only consuming 100 calories of chocolate rather than 250. In essence, the article states that these snacks are great for helping to portion meals. So, how much of a problem do our American portions present to our health. While on line, I looked up article that discussed the differeneces between the portion sizes in Japan and the US. At a McDonalds in the US, the Big Mac has 560 calories, and the largest drink size is a 32 oz, 310 calorie soda. In Japan, the same "Big Mac" has only 500 calories, and more surprisingly, the largest drink is only an 18 oz, 181 calorie drink. The article went on to say that in the US, an average serving of pasta at a restaurant is 480% of a recommended serving, and that an average cookie from a restaurant might be up to 700% of a recommended serving size. Wondering what that means in calorie world? Well, I went to an online calorie counter and found several values of portions sizes in popular family restaurants.
The results? Olive garden has a chicken (healthy, right?) dish that is over 1100 calories, chilie's has a salad that is almost 100o calories, and a breakfast at IHOP can cost you over 130o calories. So much for six small meals a day.
So what does this all mean? In essence this is just more proof that the epidemic of obesity in the US is largely a matter of large portion sizes. If portions were reduced, many of the maladies of obesity, inflammation included, could become a problem of the past. With reduced inflammation, the diseases that result therefrom could also be inhibited, leading to a healthier society in general. A solution? I say we keep portion sizes, and split meals for more cost effective dates. ;)
In Snacking in the Line of Duty the author discussed the benefits of consuming small portion sizes despite the fact that many of these snacks lack any real nutritional value. It makes sense that the American public might benefit from only consuming 100 calories of chocolate rather than 250. In essence, the article states that these snacks are great for helping to portion meals. So, how much of a problem do our American portions present to our health. While on line, I looked up article that discussed the differeneces between the portion sizes in Japan and the US. At a McDonalds in the US, the Big Mac has 560 calories, and the largest drink size is a 32 oz, 310 calorie soda. In Japan, the same "Big Mac" has only 500 calories, and more surprisingly, the largest drink is only an 18 oz, 181 calorie drink. The article went on to say that in the US, an average serving of pasta at a restaurant is 480% of a recommended serving, and that an average cookie from a restaurant might be up to 700% of a recommended serving size. Wondering what that means in calorie world? Well, I went to an online calorie counter and found several values of portions sizes in popular family restaurants.
The results? Olive garden has a chicken (healthy, right?) dish that is over 1100 calories, chilie's has a salad that is almost 100o calories, and a breakfast at IHOP can cost you over 130o calories. So much for six small meals a day.
So what does this all mean? In essence this is just more proof that the epidemic of obesity in the US is largely a matter of large portion sizes. If portions were reduced, many of the maladies of obesity, inflammation included, could become a problem of the past. With reduced inflammation, the diseases that result therefrom could also be inhibited, leading to a healthier society in general. A solution? I say we keep portion sizes, and split meals for more cost effective dates. ;)
26 April 2008
Chocolate May be good for you.
The most recent group of papers sent to us included two seperate papers making reference to chocolate and its anti-inflammatory effects. The first was "Snacking in the Line of Duty." Here was a very quick reference to flavanols which "relax blood vessels, improve blood flow, decrease blood clotting and redue inflammation." The second article was "Chocolate 'has health benefits'". After reading these articles idecided to look at this more closely. When I typed in "flavanol" in the Yahoo search engine 4 of the first 5 entries were from the Hershey Company. Looking at these entries they were using their website to explain the benefits of flavanol. Surprisingly they also mentioned flavanols could be found in berries, teas and red wines as well. Without disputing the positive effects of flavanol I think we can still say chocolate will not be changing it's status to "health food." As the Snacking in the Line of Duty article shows, having some benefits, such as flavanols, does not necessarily outweigh the downside, such as fat and sugar. The second article makes mention of diabetics eating chocolate. However, if you look at the ingredients in Hershey's Special Dark chocolate bar the first ingredient listed is still sugar. If the individual has Type 2 diabetes, the flavanols might help with the metabolizing of sugar but if the individual is a Type 1 diabetic, the pancreas is not producing insulin and the individual will need to inject higher doses of insulin to compensate for the higher intake of sugar.
Unfortunately for the many chocolate lovers in the world it looks like more evidence will be needed to say it actually has "benefits".
Unfortunately for the many chocolate lovers in the world it looks like more evidence will be needed to say it actually has "benefits".
Comparison of the Intestinal Toxicity of Celecoxib, a Selective COX-2 Inhibitor, and Indomethacin in the Experimental Rat
Gastrointestinal toxicity of NSAIDS appears to be due to a “topical” effect and inhibiting of COX-1; where as, selective COX-2 inhibitors show great GI tolerability. The “topical” component in the pathogenic mechanism for damage is thought to involve the uncoupling of mitochondrial oxidative phosphorylation with increasing intestinal permeability. (The "topical" effect may be due to the detergent-like action of NSAIDs, with the combination of their lipid soluble component and acidity.)The increase in permeability leads to mucosal inflammation. This inhibition may cause inflammation to turn into ulcers. COX-2 is thought to suppress PG synthesis in the areas of inflammation, while also controlling constitutive PG synthesis in the GI tract. This idea was tested using Celecoxib, a selective COX-2 inhibitor, and Indomethacin, which is a non-selective acidic COX inhibitor.
Celecoxib did not have a “topical” effect in their experiment assessing mitochondrial functioning, nor did it lead to changes that may be characteristic of uncouplers of oxidative phosphorylation. Indomethacin did both, while causing intestinal ulcers! Celecoxib did not show any significant damage to the small intestines though, and showed a lack of reduction in intestinal PGE; where as, Indomethacin reduced PGE levels 90%. Indomethacin clearly has damaging effects on the intestines, but Celecoxib does not. The combination of its selectivity and absence of a “topical” effect is thought to be the reason. I found this article interesting, as it went more in depth than I did here, in explaining the possible effects of these NSAIDs because many people around the world are on anti-inflammatory medications. Granted these experiments were done in rats, and one drug was shown to not be harmful, many people have complications with anti-inflammatory medications. They can be quite helpful but are they always worth the risk?!
Oh yeah....That gerbil is awesome!
Celecoxib did not have a “topical” effect in their experiment assessing mitochondrial functioning, nor did it lead to changes that may be characteristic of uncouplers of oxidative phosphorylation. Indomethacin did both, while causing intestinal ulcers! Celecoxib did not show any significant damage to the small intestines though, and showed a lack of reduction in intestinal PGE; where as, Indomethacin reduced PGE levels 90%. Indomethacin clearly has damaging effects on the intestines, but Celecoxib does not. The combination of its selectivity and absence of a “topical” effect is thought to be the reason. I found this article interesting, as it went more in depth than I did here, in explaining the possible effects of these NSAIDs because many people around the world are on anti-inflammatory medications. Granted these experiments were done in rats, and one drug was shown to not be harmful, many people have complications with anti-inflammatory medications. They can be quite helpful but are they always worth the risk?!
Oh yeah....That gerbil is awesome!
24 April 2008
NSAIDs & Asthma
I thought it was very interesting that Kerry brought up the adverse effects of NSAIDs on asthmatic people, so I did some research to see if a mechanism had been found.
I came across an article from the June 2007 edition of the journal Allergy (vol. 62). Wang, X.S. et al were able to culture mast cells (cells that are like basophil granulocytes and are involved in allergies) from peripheral blood progenitors into mature cells that resembled human lung mast cells. They cultured these cells from 3 groups of patients: normal/healthy patients, patients with aspirin tolerant asthma (ATA) and patients with aspirin exacerbated respiratory disease (AERD)--these are the ones at risk for increased bronchospasms due to NSAIDs.
Basically, the research group found that AERD patient mast cells are different from mast cells of the other 2 groups. AERD mast cells, when activated, can produce much more cysteinyl-leucotrienes (cys-LTs), which are chemical messengers involved in inflammation. cys-LTs help regulate the state of blood vessels and airways.
In addition, PGE2 decreases this overproduction of cys-LTs. So when AERD patients take NSAIDs and inhibit COX as well as PGE2 synthesis, this enables the increase in cys-LTs. More specifically, cys-LTs cause asthma attacks by allowing for bronchoconstriction, increased mucus secretion in the airway and infiltration of leukocytes in the airway. In fact, leucotriene receptor antagonists are used to treat asthma.
So...there you have it. =)
I came across an article from the June 2007 edition of the journal Allergy (vol. 62). Wang, X.S. et al were able to culture mast cells (cells that are like basophil granulocytes and are involved in allergies) from peripheral blood progenitors into mature cells that resembled human lung mast cells. They cultured these cells from 3 groups of patients: normal/healthy patients, patients with aspirin tolerant asthma (ATA) and patients with aspirin exacerbated respiratory disease (AERD)--these are the ones at risk for increased bronchospasms due to NSAIDs.
Basically, the research group found that AERD patient mast cells are different from mast cells of the other 2 groups. AERD mast cells, when activated, can produce much more cysteinyl-leucotrienes (cys-LTs), which are chemical messengers involved in inflammation. cys-LTs help regulate the state of blood vessels and airways.
In addition, PGE2 decreases this overproduction of cys-LTs. So when AERD patients take NSAIDs and inhibit COX as well as PGE2 synthesis, this enables the increase in cys-LTs. More specifically, cys-LTs cause asthma attacks by allowing for bronchoconstriction, increased mucus secretion in the airway and infiltration of leukocytes in the airway. In fact, leucotriene receptor antagonists are used to treat asthma.
So...there you have it. =)
23 April 2008
Most Recent Celebrex Side Effect
Celecoxib, marketed as Celebrex, is an NSAID commonly used in the treatment of rheumatoid arthritis. Celebrex hit the market just under 10 years ago as an “alternative” NSAID with the same pain relief but fewer adverse gastrointestinal effects than “conventional” NSAIDS like ibuprophen and naproxen. As an “alternative” NSAID, Celebrex is a highly selective COX 2 inhibitor, whereas the “conventional” NSAIDs inhibit both COX 1 and COX 2. Because Celebrex is a relatively new NSAID, the side effects, risks, and suggested dosages seem to be changing rather frequently. The most recent and detrimental risk that has been identified for Celebrex is heart attack and stroke. As recent as 2007, Celebrex was deemed a drug that should be used as a last result anti-inflammatory medication for those who are at risk of heart attack or related cardiovascular disease. It seems like every year that changes to the Celebrex label have to be made to add more side effects and risk factors. I don’t know how the typical FDA approval and initial marketing of new drugs usually plays out, but it seems like there have been a lot of detrimental effects caused by Celebrex, and the Pfizer company who markets the drug is trying to focus solely on the fact that it has decreased gastrointestinal risks. So until their large scale clinical trials are complete in 2010, my suggestion would be to steer clear of Celebrex and find another NSAID that has been around long enough to have all of its risks and benefits ironed out.
22 April 2008
The Bad and The Ugly of NSAIDs
In this week’s reading, “Comparison of the Intestinal Toxicity of Celecoxib, a Selective COX-2 Inhibitor, and Indomethacin in the Experimental Rat,” it mentions that non-steroid anti-inflammatories or NSAIDs are implicated in gastrointestinal and small bowel side effects. To put this into context, I looked up what exactly these side effects include, and found that NSAIDs can cause ulcers, diarrhea or constipation, loss of appetite, liver failure, kidney failure, and hemorrhaging. People with asthma can experience more exacerbated side effects, which can even lead to death because NSAIDs can induce bronchospasms. However, like with most things in science, it is not well understood why NSAIDs cause a more severe effects in asthmatic people. Maybe someone in our class has a guess as to why?
Comparison of Toxicity of Celecoxib vs. Indomethacin
There have been several factors that can lead to the damage of the gastrointestinal tract from NSAID's. There are two main mechanisms for the damage, one involves a the uncoupling of mitochondrial oxidative phosphorylation while the other is the inhibition of COX-1. For the peer review articles this week, it was suggested that the inhibition of COX-2 would suppress the prostaglandin synthesis at the sites of inflammation. To research this, the study used selective COX-2 inhibitors such as Celecoxib and Refecoxib while using Indomethiacin as the positive control in experimental rats.
The rats were treated with the drugs and such factors that were observed were in vitro which measured the liver mitochondria, in vivo which was measured through electron microscopy, intestinal permeability which was measured in urine excretion, the granulocyte marker protein which was taken by faecal samples, Intestinal prostaglandin determination which was taken by freezing the small bowel of the rat in liquid nitrogen and the prostaglandin was extracted from the sample and measured, and finally macroscopic damage which was done by performing a laparotomy on the rats and recording the amount of ulcers that were present upon dissection.
The results after gathering and assessing all the data was that the selective COX-2 inhibitor (Celecoxib) had no significant damage on the small intestine mucosa when compared to Indomethacin. This was probably due to the significantly less reduction that Celecoxib had on PGE levels when compared to Indomethacin which had a 90% reduction in PGE levels. Also to note is that Celecoxib did not lead to physiologic changes which is common with uncouplers of oxidative phosphorylation while Indomethacin showed all parameters of pathophysiologic changes and also caused intestinal ulcers which were present during the laparotomy. To summarize, when compared to Indomethacin, the Celecoxib showed no association with intestinal toxicity in the given study models.
The rats were treated with the drugs and such factors that were observed were in vitro which measured the liver mitochondria, in vivo which was measured through electron microscopy, intestinal permeability which was measured in urine excretion, the granulocyte marker protein which was taken by faecal samples, Intestinal prostaglandin determination which was taken by freezing the small bowel of the rat in liquid nitrogen and the prostaglandin was extracted from the sample and measured, and finally macroscopic damage which was done by performing a laparotomy on the rats and recording the amount of ulcers that were present upon dissection.
The results after gathering and assessing all the data was that the selective COX-2 inhibitor (Celecoxib) had no significant damage on the small intestine mucosa when compared to Indomethacin. This was probably due to the significantly less reduction that Celecoxib had on PGE levels when compared to Indomethacin which had a 90% reduction in PGE levels. Also to note is that Celecoxib did not lead to physiologic changes which is common with uncouplers of oxidative phosphorylation while Indomethacin showed all parameters of pathophysiologic changes and also caused intestinal ulcers which were present during the laparotomy. To summarize, when compared to Indomethacin, the Celecoxib showed no association with intestinal toxicity in the given study models.
21 April 2008
One for the Ages???
After reading this lay article I found several points that left a bad taste in my mouth. One of the key problems I found was the author's lack of significant proof. When he finally mentioned some numbers to back up the suggestions they were scarce and prove nothing. Out of the original 76 rhesus monkeys only 50 are still alive. There is no mention here about how many were from the experimental group and how many are from the control group. The difference in cancer of 5 to 3 (control vs. esperimental groups respectively) is not a significant difference. In addition the causes of cancer are still not fully understood so this is quite possibly due to the randomness of the disease.
The author also wrote about the "lower insulin levels". If we think back to PSIO 202 we can recall insulin is released by the pancreas in response to sugar levels. Now, if you are taking in less calories you are most likely taking in less sugar.
Another point that is not mentioned here is the quality of the diet. If someone were to reduce their caloric intake it would be necessary for them to maximize the amount of nutrients in their diet. To put it another way if you are going to eat less than a normal diet, that limited amount must be of a higher quality. With that in mind how much of the longevity observed is due to less calories and how much is due to a better quality diet.
Sorry to sound like a skeptic here but there just seemed to be too many gaps in the information to convince me.
The author also wrote about the "lower insulin levels". If we think back to PSIO 202 we can recall insulin is released by the pancreas in response to sugar levels. Now, if you are taking in less calories you are most likely taking in less sugar.
Another point that is not mentioned here is the quality of the diet. If someone were to reduce their caloric intake it would be necessary for them to maximize the amount of nutrients in their diet. To put it another way if you are going to eat less than a normal diet, that limited amount must be of a higher quality. With that in mind how much of the longevity observed is due to less calories and how much is due to a better quality diet.
Sorry to sound like a skeptic here but there just seemed to be too many gaps in the information to convince me.
20 April 2008
Possible Deaths due to Heparin
In class last week it was discussed about the safety of warfarin compared to heparin. I've recently looked up a article from the FDA stating that possible deaths related to heparin use could be higher than expected. I posted the link below and there is another link within the article that shows figures from Jan. '07 to March '08. My personal view of the article is probably the same as any other lay article, I cant say much on the accuracy and credibility, but could still be considered an interesting read.
http://www.medscape.com/viewarticle/572751
http://www.medscape.com/viewarticle/572751
17 April 2008
The Threat of Common Anticoagulants
Warfarin and Heparin are two common anticoagulants used to prevent thrombosis. They are both very effective at what they do, but come with some serious risks. Warfarin (market brand Coumadin) is a natural chemical found in plants that was originally marketed as a rat pesticide. Research uncovered Warfarin’s relatively safe and effective use as an anticoagulant not long after. If used at a safe dosage, Warfarin can prevent both thrombosis and embolism. The way Warfarin works is by inhibiting Vitamin K epoxide reducatase, therefore diminishing the amount of Vitamin K available in tissues and inhibiting the Vitamin K synthesis of many calcium dependent and regulator factors. This inhibition prevents the carboxylation activity necessary for coagulation factors to bind to blood vessel surfaces. The primary side effect of this effective clot-preventing drug is hemorrhage. Although the risk for hemorrhage is small, it is definite, which means that Warfarin derivatives should only be used if absolutely necessary.
Heparin (market brand Calciparine or Hep-lock) is an injectable anticoagulant, which makes it a much faster acting prevention for thrombosis than Warfarin. Heparin is derived from the mucosal tissues of slaughtered meat such as pigs and cows. It is a naturally occurring anticoagulant that is produced in basophils and mast cells. Heparin prevents clot formation and extension by binding to antithrombin 3 inhibitor, which then inactivates the body’s blood clotting response. The major side effect of this drug is known as Heparin-Induced Thrombocytopenia Syndrome, or HITS. This side effect makes the body’s blood platelets an immunological target, leading to the degradation of platelets.
Due to the considerable effectiveness of these two drugs, they are some of the most commonly used anticoagulants. Warfarin is typically administered as a prescription drug to patients who have already formed a blood clot. Because of its strong side effects, patients are required to submit a blood sample as often as once a day to ensure a proper dosage level is maintained. Heparin is restricted primarily to hospital use because it must be administered as a continuous infusion or as frequently as every half hour. Both of these treatments are very effective at preventing blood clots, but with side effects as severe as these, any patient considering starting Warfarin or Heparin should be cautious!
16 April 2008
Acetaminophen vs. Ibuprofen
Acetaminophen and Ibuprofen, the active ingredients contained in Tylenol and Advil respectively, are two of the most common over the counter pain analgesics. As with any medication, the side effects are dose-dependent, and may be elevated in conjunction with alcohol consumption. In a society that demands a disclaimer on our fast food coffee, it seems appropriate that these drugs should carry a warning label as well.
In large quantities, acetaminophen can induce acute hepatoxicity. The liver is an essential organ in digestive metabolism via the hepatic portal system, to reduce contaminants entering systemic circulation. For this reason, the combination of alcohol and Tylenol should be avoided, due to the extra stress placed on the liver.
In contrast, ibuprofen can induce gastric bleeding with inappropriate use. The mechanism of this drug inhibits the constitutively expressed COX-1 in the stomach, which may have protective effects on the stomach lining. Ibuprofen also has blood thinning effects, which also increases the chance of gastric bleeding.
The moral of the story? Ibuprofen and acetaminophen are effective analgesics when taken in moderation. Anything can be toxic to the body in large doses, so following dosage instructions is important in reducing the risk of developing side effects.
In large quantities, acetaminophen can induce acute hepatoxicity. The liver is an essential organ in digestive metabolism via the hepatic portal system, to reduce contaminants entering systemic circulation. For this reason, the combination of alcohol and Tylenol should be avoided, due to the extra stress placed on the liver.
In contrast, ibuprofen can induce gastric bleeding with inappropriate use. The mechanism of this drug inhibits the constitutively expressed COX-1 in the stomach, which may have protective effects on the stomach lining. Ibuprofen also has blood thinning effects, which also increases the chance of gastric bleeding.
The moral of the story? Ibuprofen and acetaminophen are effective analgesics when taken in moderation. Anything can be toxic to the body in large doses, so following dosage instructions is important in reducing the risk of developing side effects.
Use of NSAIDs--An Update
The articles for this week deal with the positive and negative actions of NSAIDs. This particular article primarily addressed a popular news topic: the increase in risk for cardiovascular and cerebrovascular events due to selective COX-2 inhibitors. These drugs looked promising for pain relief without the unwanted side affect of GI bleeding that occurs with COX-1 inhibition. However, in September 2004, Merck withdrew its product, Vioxx, from the market and the concerns for COX-2 inhibitors increased significantly.
The American Heart Association released this article as an update on the safety of using NSAIDs. An FDA joint meeting came to the conclusion that celecoxib (Celebrex), valdecoxib (Bextra) and rofecoxib (Vioxx), all selective COX-2 inhibitors, “significantly increase the risk of cardiovascular events in a dose-dependent manner.” Although celecoxib is still on the U.S. market, it comes with a strict “black box” warning.
The article by Antman et al. stated the hypothesis that the increased risk for CV events is due to a shift in the prothrombotic/antithrombotic balance on endothelial cells. The shift leans toward thrombosis. It is believed this occurs because platelet aggregation is COX-1-dependent and so this mechanism would still work. In addition, COX enzymes catalyze the production of prostacyclin in endothelial cells which can disrupt platelet aggregation. So selective COX-2 inhibition would keep COX-1 activated while decreasing prostacyclin production and thus decreasing antithrombotic activity. The hypothesis also includes the fact that COX-2 inhibition increases sodium and thus water reabsorption (which can cause edema) and can increase risk for heart failure and hypertension (since activation of COX ultimately causes “local smooth muscle cell relaxation and vasodilation” and this would be inhibited).
The article concludes basically by saying that patients who must have NSAID treatment should first try acetaminophen or aspirin, the least risky NSAIDs. If this doesn’t work, then they should be prescribed nonselective NSAIDs. Selective COX-2 inhibitors should only be prescribed if absolutely necessary, and in the lowest dose and for the shortest duration possible. Any patients with a medical history of CV problems should seriously weigh the risks and benefits.
The American Heart Association released this article as an update on the safety of using NSAIDs. An FDA joint meeting came to the conclusion that celecoxib (Celebrex), valdecoxib (Bextra) and rofecoxib (Vioxx), all selective COX-2 inhibitors, “significantly increase the risk of cardiovascular events in a dose-dependent manner.” Although celecoxib is still on the U.S. market, it comes with a strict “black box” warning.
The article by Antman et al. stated the hypothesis that the increased risk for CV events is due to a shift in the prothrombotic/antithrombotic balance on endothelial cells. The shift leans toward thrombosis. It is believed this occurs because platelet aggregation is COX-1-dependent and so this mechanism would still work. In addition, COX enzymes catalyze the production of prostacyclin in endothelial cells which can disrupt platelet aggregation. So selective COX-2 inhibition would keep COX-1 activated while decreasing prostacyclin production and thus decreasing antithrombotic activity. The hypothesis also includes the fact that COX-2 inhibition increases sodium and thus water reabsorption (which can cause edema) and can increase risk for heart failure and hypertension (since activation of COX ultimately causes “local smooth muscle cell relaxation and vasodilation” and this would be inhibited).
The article concludes basically by saying that patients who must have NSAID treatment should first try acetaminophen or aspirin, the least risky NSAIDs. If this doesn’t work, then they should be prescribed nonselective NSAIDs. Selective COX-2 inhibitors should only be prescribed if absolutely necessary, and in the lowest dose and for the shortest duration possible. Any patients with a medical history of CV problems should seriously weigh the risks and benefits.
15 April 2008
Warfarin or the generic form Coumadin is a commonly used prescription drug that is used to prevent stroke in patient suffering from chronic atrial fibrillation, a heart valve replacement, and/or a recent heart attack. Warfarin is usually referred to as a "blood thinner" or anticoagulant because it keeps blood flowing smoothly throughout the body by decreasing the amount of clotting proteins in the blood. This medication is classified has having a low therapeutic index(i.e. there is a small margin between a normal recommended dose and a potentially lethal dose).
Since the topic this week is Anti-inflammatories and warfarin has a extremely high level of protein binding, there is a possibility that Warfarin may interact with NSAIDs. Along with the affinity for protein binding, it also can cause partial metabolic inactivation by prehepatic and hepatic CYP2C9. The medications that can cause adverse reactions include aspirin, ibuprofen, naproxen, and celecoxib(Celebrex). The complications start because the NSAID's and the COX-2 inhibitor are also extremely prone to bind to proteins in the blood(~99%) and can therefore displace the protein binding for warfarin. This can then lead to free blood levels of non-binded warfarin which can lead to the increased risk of GI or other types of hemorrhagic diseases.
Another factor that could lead to the increased GI bleeding is that each of these drugs can have an effect of the clotting profile of the blood such as inhibition of potassium dependent clotting factors suppressed by the Warfarin and the inhibition of the COX-1 in the platelets and GI mucosa caused by the NSAID's. It could be recommended then that NSAIDs should be avoided while taking anticoagulants such as Warfarin and Coumadin and to use a mild pain reliever such as Acetaminophen or Tramadol as the alternative.
11 April 2008
Mechanism of Action of Aspirin-Like Drugs
The Cyclooxygenase enzyme, also known as COX, is responsible for prostaglandin synthesis. There are two isoforms that were studied in this paper, COX-1 and COX-2. COX-1 is constitutively expressed; whereas, COX-2 is known as the inducible isoform. These enzymes serve a variety of functions in several vital regions of the body, but for time sake I will just discuss a few examples of their functions, and some things I found interesting.
COX-1 is known for its importance in maintaining normal physiological function in the body, and to perform the housekeeping job in synthesis of protective prostaglandins, particularly important in the stomach. PGs are cytoprotective in the sense that they work to prevent gastric erosion and ulceration. For example, in the GI tract, COX-1 activation leads to the production of prostacyclin, which reduces secretions of gastric acid and causes vasodilation at the mucosa. Furthermore, the prostanoids stimulate the secretion of viscous mucus, gastric fluid, and duodenal bicarbonate. The mucus acts as a protective barrier in combination with the alkaline environment that helps neutralize any excess acid. Also, COX-1 in platelets causes thromboxane A2 production, leading to platelet aggregation (a clotting factor.) COX-2, on the other hand, is induced by inflammatory stimuli and cytokines, and functions more in inflammation situations. It is highly expressed in human and animal colon cancer cells, and in human colorectal adenocarcinomas. The increase in PG synthesis can be controlled by nonsteroid anti-inflammatory drugs selective to the particular COX enzyme.
Nonsteroid antiinflammatory drugs (NSAIDs) are aspirin-like drugs that inhibit the activity of the COX enzyme. Since the two isoforms are found at different levels of concentration at different sites in the body, and have various functions, inhibition of them also has different effects. Different NSAIDs are selective to the different isoforms. Among other functions, COX-2 inhibitors are used as anti-inflammatory agents, and have been used in the treatment of rheumatoid arthritis and osteoarthritis. They are also show promise in the inhibition of colorectal tumor cell growth and in delaying premature labor! COX-1 inhibitors are thought to cause some side effects, including GI and renal toxicity. NSAIDs that are selective to COX-2 may have less side effects that current ones used.
The COX enzymes serve a variety of functions and are found all over the body; they are especially important in the GI tract(as discussed), kidney, brain and spinal cord. To discuss all of these in detail would take up a ton of space, but if you have any questions regarding one of these areas, do not hesitate to ask….I have read all about it! =) However, here’s a brief description of some interesting info from some areas of study.
Kidney-"Prostaglandins are important for normal kidney function in both animal models of disease states and in patients with CHF, liver cirrhosis and renal insufficiency." Thus, when NSAIDs reduce PG synthesis, it can cause problems(e.g. increased risk for renal ischemia.) Kidney cells that produce PGs contain mostly COX-1.
Brain & SC- COX-1 is abundant in the forbrain, where PGs might be involved in complex integrative functions, like control of the ANS!
Gestation/Parturition-PGs are important for inducing uterine contraction, which is why NSAIDs are used to delay labor. COX-1 in the amnion may be essential for pregnancy maintenance via PG synthesis. COX-1 and COX-2 are expressed in the uterine epithelium at different times in early pregnancy and could be important during implantation of the ovum AND significant in angiogenesis important for the placenta!
COX-1 is known for its importance in maintaining normal physiological function in the body, and to perform the housekeeping job in synthesis of protective prostaglandins, particularly important in the stomach. PGs are cytoprotective in the sense that they work to prevent gastric erosion and ulceration. For example, in the GI tract, COX-1 activation leads to the production of prostacyclin, which reduces secretions of gastric acid and causes vasodilation at the mucosa. Furthermore, the prostanoids stimulate the secretion of viscous mucus, gastric fluid, and duodenal bicarbonate. The mucus acts as a protective barrier in combination with the alkaline environment that helps neutralize any excess acid. Also, COX-1 in platelets causes thromboxane A2 production, leading to platelet aggregation (a clotting factor.) COX-2, on the other hand, is induced by inflammatory stimuli and cytokines, and functions more in inflammation situations. It is highly expressed in human and animal colon cancer cells, and in human colorectal adenocarcinomas. The increase in PG synthesis can be controlled by nonsteroid anti-inflammatory drugs selective to the particular COX enzyme.
Nonsteroid antiinflammatory drugs (NSAIDs) are aspirin-like drugs that inhibit the activity of the COX enzyme. Since the two isoforms are found at different levels of concentration at different sites in the body, and have various functions, inhibition of them also has different effects. Different NSAIDs are selective to the different isoforms. Among other functions, COX-2 inhibitors are used as anti-inflammatory agents, and have been used in the treatment of rheumatoid arthritis and osteoarthritis. They are also show promise in the inhibition of colorectal tumor cell growth and in delaying premature labor! COX-1 inhibitors are thought to cause some side effects, including GI and renal toxicity. NSAIDs that are selective to COX-2 may have less side effects that current ones used.
The COX enzymes serve a variety of functions and are found all over the body; they are especially important in the GI tract(as discussed), kidney, brain and spinal cord. To discuss all of these in detail would take up a ton of space, but if you have any questions regarding one of these areas, do not hesitate to ask….I have read all about it! =) However, here’s a brief description of some interesting info from some areas of study.
Kidney-"Prostaglandins are important for normal kidney function in both animal models of disease states and in patients with CHF, liver cirrhosis and renal insufficiency." Thus, when NSAIDs reduce PG synthesis, it can cause problems(e.g. increased risk for renal ischemia.) Kidney cells that produce PGs contain mostly COX-1.
Brain & SC- COX-1 is abundant in the forbrain, where PGs might be involved in complex integrative functions, like control of the ANS!
Gestation/Parturition-PGs are important for inducing uterine contraction, which is why NSAIDs are used to delay labor. COX-1 in the amnion may be essential for pregnancy maintenance via PG synthesis. COX-1 and COX-2 are expressed in the uterine epithelium at different times in early pregnancy and could be important during implantation of the ovum AND significant in angiogenesis important for the placenta!
10 April 2008
Parkinson's, Nicotine and Caffeine
Since we learned in PSIO 480 that caffeine may play a role in decreasing the incidence of Parkinson’s Disease (PD), I wondered if there was any more recent research on this. I found this study by Singh et al published this past February in the journal Brain Research.
Although previous studies have shown neuroprotective effects of caffeine and nicotine against PD (see article’s references), no conclusion of the exact mechanism has been made. This study attempted to determine the effect of caffeine and nicotine on toxicant responsive enzymes and vesicular monoamine transporter-2 (VMAT-2), which are involved in chemically-induced PD. Since decreased expression of toxicant responsive genes such as CYP1A1 and VMAT-2 result in cellular damage and since this altered expression is seen in chemically-induced PD, the authors hypothesized that caffeine and nicotine may have an effect on these genes and proteins.
The study used an accepted model of chemically-induced PD that includes giving animals a chemical called MPTP, which is “a contaminant in synthetic heroin.” The study pre-treated mice with caffeine, nicotine, or saline (control) for 8 weeks. Then the animals were divided into subgroups, where some did not receive MPTP and other groups were co-treated with MPTP and caffeine or nicotine for 1 day to 4 weeks.
Biochemical analysis was performed on the striatum of the mice. Results showed that MPTP decreased dopamine in mice, but mice co-treated with MPTP and caffeine or nicotine had less of a decrease in dopamine compared to controls. Also, MPTP decreased CYP1A1 and VMAT-2 expression, while mice pre-treated with either caffeine or nicotine showed significant reversal of this decrease. All in all, caffeine and nicotine showed a reduction in toxicity of chemically-induced PD.
BUT, I am definitely not endorsing smoking or excessive caffeine-drinking!
Here's the journal article citation:
Singh S et al: Nicotine and caffeine-mediated modulation in the expression of toxicant responsive genes and vesicular monoamine transporter-2 in 1-methyl 4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's Disease phenotype in mouse. Brain Research, Feb. 2008
Although previous studies have shown neuroprotective effects of caffeine and nicotine against PD (see article’s references), no conclusion of the exact mechanism has been made. This study attempted to determine the effect of caffeine and nicotine on toxicant responsive enzymes and vesicular monoamine transporter-2 (VMAT-2), which are involved in chemically-induced PD. Since decreased expression of toxicant responsive genes such as CYP1A1 and VMAT-2 result in cellular damage and since this altered expression is seen in chemically-induced PD, the authors hypothesized that caffeine and nicotine may have an effect on these genes and proteins.
The study used an accepted model of chemically-induced PD that includes giving animals a chemical called MPTP, which is “a contaminant in synthetic heroin.” The study pre-treated mice with caffeine, nicotine, or saline (control) for 8 weeks. Then the animals were divided into subgroups, where some did not receive MPTP and other groups were co-treated with MPTP and caffeine or nicotine for 1 day to 4 weeks.
Biochemical analysis was performed on the striatum of the mice. Results showed that MPTP decreased dopamine in mice, but mice co-treated with MPTP and caffeine or nicotine had less of a decrease in dopamine compared to controls. Also, MPTP decreased CYP1A1 and VMAT-2 expression, while mice pre-treated with either caffeine or nicotine showed significant reversal of this decrease. All in all, caffeine and nicotine showed a reduction in toxicity of chemically-induced PD.
BUT, I am definitely not endorsing smoking or excessive caffeine-drinking!
Here's the journal article citation:
Singh S et al: Nicotine and caffeine-mediated modulation in the expression of toxicant responsive genes and vesicular monoamine transporter-2 in 1-methyl 4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's Disease phenotype in mouse. Brain Research, Feb. 2008
09 April 2008
Alzheimer's and Neurofibrillary Tangles
The articles we have read about Alzheimer's have focused on the amyloid-beta pathology. The other part of Alzheimer's disease is the formation of neurofibrillary tangles. Neurofibrillary tangles are composed of tau proteins that have abnormally formed because of overactive enzymes. Tau proteins are a microtubule associated protein. Tau proteins are important for assembling tubulin monomers into microtubules. Tau proteins also serve a structural purpose by maintaining the cytoskeleton and helping axonal transport. Neurofibrillary tangles form when there is a hyper-phosphorylation of tau protein and it becomes insoluble and forms aggregates. The tangles result in the death of cells and this is the role is plays in Alzheimer's disease.
Drink Apple Juice Now Before You Forget
I found this article of a study done. It says that eating aple related product could help with memory loss and alzheimer like symptoms.
Here the link to it
www.brightsurf.com/news/headlines/22731/Age-related_memory_improvement_linked_with_consumption_of_apple_products.html
For other neurological degenerative news here's another link
www.molecularneurodegeneration.com/news
Apitherapy
I was really interested in the Bee sting therapy of Multiple sclerosis which is also known as apitherapy. According to A Randomized Crossover Study of bee sting therapy for Multiple sclerosis, apitherapy has no significant affect on M.S. patients. So I tried to see if there were any other studies out there that say otherwise. Most of what is out there is proposed studies; very little research has already been done. What I found out was that apitherapy may be affective in treating other health problems such as tendonitis, fibromyositis and rheumatoid arthritis. These health problems appear ideal for this anti-inflammatory treatment. For the most part I found testimonials of those who swore by apitherapy. I noticed that those who swore by it would never have met the criteria that would allow them to participate in any study not being well enough to participate. If such people where allowed, I wonder how it would affect future studies.
07 April 2008
Leprosy and Neurodegeneration
In Anura Rambukkana's study, published in Nature Medicine, showed that the leprosy bacteria, Mycobacterium leprae, attaches to myelinated Schwann cells and induces rapid demyelination. This demyelination can occur in the absence of immune cells, which is the cause of demyelination in neurodegenerative diseases, but the process is chronic and relatively slow despite high levels of the M. Leprae.
Type-1 leprosy reactions are idiopathic episodes of strongly increased inflammation and cell-mediated immune reactivity which are frequently accompanied by acute inflammation of peripheral nerves. This peripheral inflammation often leads to extensive and irreversible nerve damage. Immunosuppressive drugs are often a treatment to prevent further nerve damage.
This information suggests that inflammatory immune reactions play an important role in leprosy nerve damage and that the mere presence of M. leprae does not explain the full extent of leprosy nerve damage. Inflammatory responses seem to be necessary for the complete manifestation of demyelination, like in other neurodegenerative diseases.
Though the mechanismas are not entirely clear, it is believed that there are two phases of M. leprae actions. The early phase consists of specific targeting of peripheral nerves and contact dependent demyelination. The other phase consists of increase immunity and inflammation, where acute and extensive nerve damage happens, mostly contributed by cytokines and immune effector cells.
The human immune response plays an important role in the full expression of leprosy nerve damage.
http://www.sciencemag.org/cgi/content/full/296/5569/927?ck=nck
Type-1 leprosy reactions are idiopathic episodes of strongly increased inflammation and cell-mediated immune reactivity which are frequently accompanied by acute inflammation of peripheral nerves. This peripheral inflammation often leads to extensive and irreversible nerve damage. Immunosuppressive drugs are often a treatment to prevent further nerve damage.
This information suggests that inflammatory immune reactions play an important role in leprosy nerve damage and that the mere presence of M. leprae does not explain the full extent of leprosy nerve damage. Inflammatory responses seem to be necessary for the complete manifestation of demyelination, like in other neurodegenerative diseases.
Though the mechanismas are not entirely clear, it is believed that there are two phases of M. leprae actions. The early phase consists of specific targeting of peripheral nerves and contact dependent demyelination. The other phase consists of increase immunity and inflammation, where acute and extensive nerve damage happens, mostly contributed by cytokines and immune effector cells.
The human immune response plays an important role in the full expression of leprosy nerve damage.
http://www.sciencemag.org/cgi/content/full/296/5569/927?ck=nck
06 April 2008
Randomized Cross Over Study For Bee Sting Therapy in MS
MS is a demyelinating disorder of the CNS (these axons unlike in the PNS cannot regenerate themselves) Treatment of MS does not invlove ridding the patient of the disease. Medical limitations allow only to alleviate the symptoms in hopes of the patient leading as normal a life as possible. Because of this, many people suffering with MS are open to trying alternative therapy, one includes bee sting venom. Bee sting venom contains anti inflammatory substances. Esentially, disease progression is characterized by an abnormal immune response in the central nervous system.
In relapse-remitting MS (85-90% of all cases) and secondary progressive MS. It showed no delay in disease progression and no improvement in bettering the quality of life.
Knowing how MS affects patients, it would be wise to experiment with different methods to somehow insert Na+ channels in areas of axons that have been demyelinated. Only then will action potentials propagate.
By stopping inflammation, I don't see how this would better the patient, they would remain diabled. What do you guys thinks???
In relapse-remitting MS (85-90% of all cases) and secondary progressive MS. It showed no delay in disease progression and no improvement in bettering the quality of life.
Knowing how MS affects patients, it would be wise to experiment with different methods to somehow insert Na+ channels in areas of axons that have been demyelinated. Only then will action potentials propagate.
By stopping inflammation, I don't see how this would better the patient, they would remain diabled. What do you guys thinks???
Fibrin Deposition Accelerates Neurovascular Damage and Neuroinflammation in Mouse Models of AD
A characterisitc of Alzheimer's Disease in neurofibrillary tangles and amyloid plaques. It is these amyloid plaques that are beleived to be the reason for neurodegenitive degradation by acting either as a neurotoxin or an inflammatory response. Fibrinogen (a precursor to and the inactive form of Fibrin) is a stabilizing component of blood clots. Typically it is not seen in the central nervous system because of its inability to penetrate the blood brain barrier. However, with neurological damage, fibrinogen in able to enter the brain's vascular system. In patients and mouse models with AD, researchers have noticed an increased deposition of fibrinogen. In those with an increase in the protein, wound healing is impaired and there seems to be a higher mortality rate. Because inflammation is seen in those patients with fibrinogen, it is beleived that fibrinogen either initiates or augments the degree of inflammation.
Paul et al. set out to examine this hypothesis by determining the blood brain barrier's permeability to fibrinogen in three mouse models. In mice with AD, they found both damage to the blood brain barrier (BBB) and fibrin, the active form of fibrinogen.
Paul et. al are confident that fibrin plays a role in AD progression. This is evident because they used a mouse model with AD to induce fibrin deposition and reduce fibrinolysis and the pathology worsened.
Paul et. al used Evan's Blue Dye (which binds to albumin; a protein found in the blood) to track the permeability of the blood brain barrier. Each of the three mice had different strains of AD which display different characteristics as far as disease progression and age of onset. It was consistent with each model that the BBB was comprimised due to the movement of this dye across the BBB. They biopsied portions of the cortex to determine endothelial cell health as well as its ability to repair itself upon inflicted damage. Endothelial cells showed reduced response to signaling indicating an inability to become aware of damage. The BBB showed to be permeable to albumin so it was assume that macromolecules such as fibrinogen would have access as well. So overtime, fibrinogen/fibrin would accumulate thereby increasing disease progression.
So based on this evidence, wouldn't it make sense to encourage fibrinolysis in the models to determine whether or not this slowed or halted disease progression? Paul et. al used this information to devise another experiment to test whether or not this would work. In the case of fibrinogen inhibition, the models seemed to have reduced inflammation and protected from degradation by plasmin (a protease). Plasmin works to destroy blood clots before the dislodge and become an embolism.
The only thing I found conclusive of the article was that fibrinogen/fibrin is an upstream mediator of inflammation. Does anyone know plasmin's role in AD. In this article it mentions that plasmin has damaging effects to the BBB as well.
Paul et al. set out to examine this hypothesis by determining the blood brain barrier's permeability to fibrinogen in three mouse models. In mice with AD, they found both damage to the blood brain barrier (BBB) and fibrin, the active form of fibrinogen.
Paul et. al are confident that fibrin plays a role in AD progression. This is evident because they used a mouse model with AD to induce fibrin deposition and reduce fibrinolysis and the pathology worsened.
Paul et. al used Evan's Blue Dye (which binds to albumin; a protein found in the blood) to track the permeability of the blood brain barrier. Each of the three mice had different strains of AD which display different characteristics as far as disease progression and age of onset. It was consistent with each model that the BBB was comprimised due to the movement of this dye across the BBB. They biopsied portions of the cortex to determine endothelial cell health as well as its ability to repair itself upon inflicted damage. Endothelial cells showed reduced response to signaling indicating an inability to become aware of damage. The BBB showed to be permeable to albumin so it was assume that macromolecules such as fibrinogen would have access as well. So overtime, fibrinogen/fibrin would accumulate thereby increasing disease progression.
So based on this evidence, wouldn't it make sense to encourage fibrinolysis in the models to determine whether or not this slowed or halted disease progression? Paul et. al used this information to devise another experiment to test whether or not this would work. In the case of fibrinogen inhibition, the models seemed to have reduced inflammation and protected from degradation by plasmin (a protease). Plasmin works to destroy blood clots before the dislodge and become an embolism.
The only thing I found conclusive of the article was that fibrinogen/fibrin is an upstream mediator of inflammation. Does anyone know plasmin's role in AD. In this article it mentions that plasmin has damaging effects to the BBB as well.
05 April 2008
Caffeine effects on PD in Men vs. Women
Parkinson’s Disease is a disease involving the degeneration of neurons in the substantia nigra. Many of these neurons contain the neurotransmitter dopamine. The degeneration of these neurons decreases the level of dopamine leading to an imbalance in the way muscles work and problems with movement.
Cures for Parkinson’s are idiopathic, however, studies have found treatments to the disease. One such treatment in reducing the symptoms of (PD) is caffeine intake. Caffeine is known as an antagonist to adenosine receptors which causes an increase in dopamine levels in the brain. There have been many large studies proving that caffeine intake does, in fact, reduce the risk of (PD) in men, however, in women it is questionable. One reason for the difference in effects of caffeine is the hormonal factor. Interesting discoveries were made from many studies: 1) Postmenopausal women taking hormone replacement therapy (HRT) who also drank five cups of coffee or more per day showed an increased susceptibility in developing PD 2) Women taking HRT and drank small amounts of coffee per day did not appear at risk to PD 3) And according to Dr. Ascherio, women not taking HRT who also drank less than half a cup of coffee per day had a PD risk similar to that of men. Interestingly, the combination of coffee and hormones shows a drastic increase in risk of PD development in women. Yet, each factor individually is proven to protect against PD. Hmmm!!!
Researchers suggest that estrogen levels in women have “neuroprotective effects in PD.” Dr. Schwarzschild believes that caffeine and estrogen are competing in the body, as a result, canceling each other’s effect. Another theory of his is that estrogen is interfering with the break down of caffeine in the body.
Cures for Parkinson’s are idiopathic, however, studies have found treatments to the disease. One such treatment in reducing the symptoms of (PD) is caffeine intake. Caffeine is known as an antagonist to adenosine receptors which causes an increase in dopamine levels in the brain. There have been many large studies proving that caffeine intake does, in fact, reduce the risk of (PD) in men, however, in women it is questionable. One reason for the difference in effects of caffeine is the hormonal factor. Interesting discoveries were made from many studies: 1) Postmenopausal women taking hormone replacement therapy (HRT) who also drank five cups of coffee or more per day showed an increased susceptibility in developing PD 2) Women taking HRT and drank small amounts of coffee per day did not appear at risk to PD 3) And according to Dr. Ascherio, women not taking HRT who also drank less than half a cup of coffee per day had a PD risk similar to that of men. Interestingly, the combination of coffee and hormones shows a drastic increase in risk of PD development in women. Yet, each factor individually is proven to protect against PD. Hmmm!!!
Researchers suggest that estrogen levels in women have “neuroprotective effects in PD.” Dr. Schwarzschild believes that caffeine and estrogen are competing in the body, as a result, canceling each other’s effect. Another theory of his is that estrogen is interfering with the break down of caffeine in the body.
03 April 2008
Dopamine and Memory Loss
In class the question was brought up about how depression affects memory loss. In the article "In Search of Lost Time," the author mentions how memory loss can be caused by depression, anxiety, and trouble sleeping. I looked back at the PSIO480 notes and found out how dopamine is involved in depression, anxiety, and trouble sleeping. The dopamine is a neurotransmitter and the pathway begins in the midbrain. The midbrain controls all our automatic functions including sleep. The dopamine pathway ends in the hypothalamus, basal ganglia, and mesolimbic area. The hypothalamus controls our short-long term memory. And the mesolimbic area influences goal-directed behavior and also anxiety. The main problem would be a disturbance in the dopamine pathway. And memory loss would be associated with depression, anxiety, and trouble sleeping.
02 April 2008
HLA-DR: Genetics and Autoimmune Conditions
In the "Inflammation in MS" review, the DR-17 haplotype was associated with autoimmune disorders such as diabetes, lupus, and thyroid disorders. In fact the more general Human Leukocyte Antigens (HLA) were found as the cell surface antigens mediating the rejection of tissue transplants in HLA mismatched donors. HLA-DR family is a major histocompatibility complex (MHC II) cell surface receptor and is a ligand for T-cell receptor.
HLA-DR is linked to many autoimmune conditions and disease susceptibility or resistance. In response to signalling, HLA-DR molecules are upregulated. In the instance of an infection, the peptide binds to a DR molecule and is presented to a few T-cell receptors found on T-helper cells. These cells then bind to antigens on the surface of B-cells stimulating B-cell proliferation. Upon activation, antibodies are produced, which can lead to autoimmune disorders or disease resistance.
Wikipedia has a very nice table of diseases associated with HLA-DR, displaying which specific DR is linked with which disease.
http://en.wikipedia.org/wiki/HLA-DR
HLA-DR is linked to many autoimmune conditions and disease susceptibility or resistance. In response to signalling, HLA-DR molecules are upregulated. In the instance of an infection, the peptide binds to a DR molecule and is presented to a few T-cell receptors found on T-helper cells. These cells then bind to antigens on the surface of B-cells stimulating B-cell proliferation. Upon activation, antibodies are produced, which can lead to autoimmune disorders or disease resistance.
Wikipedia has a very nice table of diseases associated with HLA-DR, displaying which specific DR is linked with which disease.
http://en.wikipedia.org/wiki/HLA-DR
01 April 2008
Neurodegenerative disease: Alzheimer’s synopsis
Alzheimer’s disease is a neurodegenerative disease that I took interest in because people spend their whole lives using cognitive function to create who they are. For some people the latter years of life are spent loosing all that function that was meticulously fostered to define them.
Alzheimer’s is the most common cause for Dementia, its cause and progression are not clearly known and there are no treatments for the disease. Despite a lack of options, there are a few things that are known about Alzheimer’s, such as the target population, the general symptoms and the plaque and tangle significance.
The disease targets people who are 65 and older. The progression can go from 5 years to 20 years and unless symptoms are displayed it the beginning stages can be overlooked. The most common symptom that brings the disease to light is memory loss becomes a concern to the individual. Other symptoms that follow are mood swings, confusion, anger and long-term memory loss. Individuals that have been diagnosed with Alzheimer’s are associated with having large numbers of plaques and tangles in the brain. Plaques are extracellular deposits in the gray matter of the brain that are surrounded by an abundance of immune cells microglia and astrocytes that are associated with neural degenerative disease. Tangles are protein aggregates also seen in those with Alzheimer’s however their role is unknown.
Perhaps with further research new strides can be made.
Alzheimer’s is the most common cause for Dementia, its cause and progression are not clearly known and there are no treatments for the disease. Despite a lack of options, there are a few things that are known about Alzheimer’s, such as the target population, the general symptoms and the plaque and tangle significance.
The disease targets people who are 65 and older. The progression can go from 5 years to 20 years and unless symptoms are displayed it the beginning stages can be overlooked. The most common symptom that brings the disease to light is memory loss becomes a concern to the individual. Other symptoms that follow are mood swings, confusion, anger and long-term memory loss. Individuals that have been diagnosed with Alzheimer’s are associated with having large numbers of plaques and tangles in the brain. Plaques are extracellular deposits in the gray matter of the brain that are surrounded by an abundance of immune cells microglia and astrocytes that are associated with neural degenerative disease. Tangles are protein aggregates also seen in those with Alzheimer’s however their role is unknown.
Perhaps with further research new strides can be made.
Sea Bathing???
I was researching cures/relief mechanisms for arthritis and something really caught my eye. Sea bathing. I really don’t know if it’s fact or fiction. I’ve searched high and low and all I’ve gotten are mixed theories and beliefs. Many articles state that sea bathing is a beneficial treatment for arthritis. The main constituent in the sea water valuable for pain relief of arthritis is iodine. Accordingly, iodine is known for its regulatory effects on the acid-alkaline balance in the blood and tissues. It is absorbed through the pores of the skin and enters into the thyroid gland’s secretion. It’s purpose is to restore worn out tissues and correct internal imbalances. If someone wants to check up on this subject please do and let me know what you find.
P.S. They say that if you’re not next to a body of sea water the next best thing is 30 minutes every night in a tub of warm water with a cup of sea salt. Hopefully, this home remedy really does do the trick for arthritis relief.
P.S. They say that if you’re not next to a body of sea water the next best thing is 30 minutes every night in a tub of warm water with a cup of sea salt. Hopefully, this home remedy really does do the trick for arthritis relief.
Calorie Restriction: Protecting From Neurodegeneration
Calorie restriction seems it may have a neuroprotective effect in ageing or age-related diseases, though the mechanism is not quite clear. In a study from the National Institute on Ageing found that adult mice showed an increase in neuron generation in the hippocampus, than mice on a normal diet. The dietary restriction boosts factors such as brain-derived neurotrophic factor (BDNF), which increases the brain's ability to produce neurons from stem cells and resist damage. This seems to mean that brain is more protected from degeneration, like Parkinson's and Alzheimer's diseases. More studies should be done to see if supplementing BDNF will produce the same results without calorie restrictions.
A study at the University of Florida showed that calorie restriction might prevent brain cell death. As seen in rats, apoptosis increases with age, however caloric restriction reduces this increase by 36%. This is possibly explained that the restrictive diet helps prevent age-related decline of ARC (Apoptotic Regulatory Protein) which represses apoptosis.
There are many other ways that caloric restriction can protect the brain. like affecting the endocrine system. A study in Neurobiology of Aging showed that this caloric restriction suppressed levels of specific hormones involved in high-energy processes, such as reproduction and growth (in mice). The hippocampus also seems affected through mechanisms that are mostly not understood.
http://websites.afar.org/site/PageServer?pagename=IA_b_cal_19_r_brain
However, as said in the article "One for the Ages: A Prescription That May Extend Life" there is very little proof that caloric restriction will have as substantial an effect on humans. Experts say that this may only increase lifespan by 2-7%. So is it really worth adopting such a severe diet, to live a little longer or to enjoy all the delicious calories and sacrifice a few years?
Mason, Michael: "One for the Ages: A Prescription That May Extend Life," New York Times, October 31, 2006
A study at the University of Florida showed that calorie restriction might prevent brain cell death. As seen in rats, apoptosis increases with age, however caloric restriction reduces this increase by 36%. This is possibly explained that the restrictive diet helps prevent age-related decline of ARC (Apoptotic Regulatory Protein) which represses apoptosis.
There are many other ways that caloric restriction can protect the brain. like affecting the endocrine system. A study in Neurobiology of Aging showed that this caloric restriction suppressed levels of specific hormones involved in high-energy processes, such as reproduction and growth (in mice). The hippocampus also seems affected through mechanisms that are mostly not understood.
http://websites.afar.org/site/PageServer?pagename=IA_b_cal_19_r_brain
However, as said in the article "One for the Ages: A Prescription That May Extend Life" there is very little proof that caloric restriction will have as substantial an effect on humans. Experts say that this may only increase lifespan by 2-7%. So is it really worth adopting such a severe diet, to live a little longer or to enjoy all the delicious calories and sacrifice a few years?
Mason, Michael: "One for the Ages: A Prescription That May Extend Life," New York Times, October 31, 2006
Histology 101: Synovial Joints, a Possible Explanation to their Susceptibility to Infection
A synovial joint consists of articulating bone surfaces that are covered with hyaline cartilage (aka articular cartilage) separated with a fluid filled space surrounded by a joint capsule. The lining of the joint space is covered with a synovial membrane. Synovial membranes are composed of cuboidal collagenous cells called synoviocytes, they function to secrete synovial fluid that aid lubrication.
This anatomical set-up seems pretty safe, a dense layer of cells surrounds the underlying vasculature to protect from infection. Well, not quite... in most epithelium, such as our stratified squamous epithelium of our skin, there are tight junctions and basal lamina that aid in keeping propagators of inflammation out. However, the layer of synoviocytes do not come with this protective shield. This fact has lead scientists to group synoviocytes separate from the tradition epithelium cell type.
What's the connection to arthritis? One of the many causes of arthritis is inflammation that can be caused by a septic infection that can eventually make its way to the synovial fluid of joints. Since there are no tight junctions or basal lamina within the synovium, bacteria have the ability to enter the highly vasculature tissue and initiate inflammatory processes. The body's reaction to joint inflammation often leads to joint destruction and therefore arthritis.
The important role of tight junctions and the basal lamina can be seen in the comparison between epithelium and synoviocytes and their ability to react to Staphylococcus aureus. Staphylococcus aureus is a very common bacteria strain seen within the mucus membranes of the respiratory tract and basically any outer surface of our body. Within the mucus membranes, for example, the bacteria are essentially trapped outside the body. However, within the synovial membrane, Staphylococcus aureus can easily enter. Staphylococcus aureus is the most commone infection seen within infectious or septic arthritis.
Young, Barbara, James Lowe, Alan Stevens, and John Heath. Wheater's Functional Histology, a Text and Colour Atlas. 5th ed. Churchill Livingstone Elsevier.
"Septic Arthritis." MayoClinic.Com. 31 July 2006. Mayo Clinic. http://www.mayoclinic.com/health/bone-and-joint-infections/
DS00545/DSECTION=3.
This anatomical set-up seems pretty safe, a dense layer of cells surrounds the underlying vasculature to protect from infection. Well, not quite... in most epithelium, such as our stratified squamous epithelium of our skin, there are tight junctions and basal lamina that aid in keeping propagators of inflammation out. However, the layer of synoviocytes do not come with this protective shield. This fact has lead scientists to group synoviocytes separate from the tradition epithelium cell type.
What's the connection to arthritis? One of the many causes of arthritis is inflammation that can be caused by a septic infection that can eventually make its way to the synovial fluid of joints. Since there are no tight junctions or basal lamina within the synovium, bacteria have the ability to enter the highly vasculature tissue and initiate inflammatory processes. The body's reaction to joint inflammation often leads to joint destruction and therefore arthritis.
The important role of tight junctions and the basal lamina can be seen in the comparison between epithelium and synoviocytes and their ability to react to Staphylococcus aureus. Staphylococcus aureus is a very common bacteria strain seen within the mucus membranes of the respiratory tract and basically any outer surface of our body. Within the mucus membranes, for example, the bacteria are essentially trapped outside the body. However, within the synovial membrane, Staphylococcus aureus can easily enter. Staphylococcus aureus is the most commone infection seen within infectious or septic arthritis.
Young, Barbara, James Lowe, Alan Stevens, and John Heath. Wheater's Functional Histology, a Text and Colour Atlas. 5th ed. Churchill Livingstone Elsevier.
"Septic Arthritis." MayoClinic.Com. 31 July 2006. Mayo Clinic. http://www.mayoclinic.com/health/bone-and-joint-infections/
DS00545/DSECTION=3
31 March 2008
Interleukin-1 and inflammatory degeneration
Inflammatory processes in the brain (and systemically) have been linked to neuron loss in CNS disease and injury, including Alzheimer’s Disease, Parkinson’s Disease, MS, stroke, etc. Inflammation in the brain can lead to increased expression of inflammatory mediators, cytokines being a primary one in the inflammatory response. The cytokine IL-1 has been shown to contribute to neuronal loss and may play an important role in neurodegenerative disease. IL-1 is expressed rapidly by microglia in response to injury, and increases brain injury by neutrophil mobilization and cell apoptosis by MMP-9.
Experimental brain insults, including ischaemia, trauma, inflammatory stimuli, etc, increased the expression of the IL-1 family. Administration of this cytokine causes a major increase in neuron cell death after brain injury. In models of Alzheimer’s in mice, B-amyloid- activated microglia produced IL-1, promoting the production of neurotoxic B-amyloid peptides. Furthermore, rat brains with high expression of IL-1 resulted in demyelinating lesions, similar to MS.
IL-1 is not toxic to pure neurons or when injected into healthy brains. Neurotoxicity typically requires cell contact interactions between astrocytes and neurons. IL-1 up-regulates genes in astrocytes that encode neurotoxic mediators, as well as survival-promoting factors. It also acts on endotheilial cells of the brain to up-reulate the expression of adhesion/chemoattractant substances and promote BBB breakdown, which are factors involved in leukocyte recruitment. There are many other examples in this paper of how IL-1 mediates neuron death, but the major focus should be on how we can modify or control this.
IL-1RA(receptor antagonist) is a major player , providing neuroprotection, that researchers are studying. It has been a success in treatment of rheumatoid arthritis, and has shown promise in the Phase II trial in stroke patients. It inhibits ischaemic, excitotoxic and brain injury in rats. There is still a lot of studying to be done on this but with high hopes. Brain injury creates a therapeutic challenge and it is still unclear whether inflammation promotes CNS diseases or is merely a coincidence. With the increased awareness of many neurodegenerative diseases today, I predict that we will know a lot more in the near future.
Experimental brain insults, including ischaemia, trauma, inflammatory stimuli, etc, increased the expression of the IL-1 family. Administration of this cytokine causes a major increase in neuron cell death after brain injury. In models of Alzheimer’s in mice, B-amyloid- activated microglia produced IL-1, promoting the production of neurotoxic B-amyloid peptides. Furthermore, rat brains with high expression of IL-1 resulted in demyelinating lesions, similar to MS.
IL-1 is not toxic to pure neurons or when injected into healthy brains. Neurotoxicity typically requires cell contact interactions between astrocytes and neurons. IL-1 up-regulates genes in astrocytes that encode neurotoxic mediators, as well as survival-promoting factors. It also acts on endotheilial cells of the brain to up-reulate the expression of adhesion/chemoattractant substances and promote BBB breakdown, which are factors involved in leukocyte recruitment. There are many other examples in this paper of how IL-1 mediates neuron death, but the major focus should be on how we can modify or control this.
IL-1RA(receptor antagonist) is a major player , providing neuroprotection, that researchers are studying. It has been a success in treatment of rheumatoid arthritis, and has shown promise in the Phase II trial in stroke patients. It inhibits ischaemic, excitotoxic and brain injury in rats. There is still a lot of studying to be done on this but with high hopes. Brain injury creates a therapeutic challenge and it is still unclear whether inflammation promotes CNS diseases or is merely a coincidence. With the increased awareness of many neurodegenerative diseases today, I predict that we will know a lot more in the near future.
Gold salts anyone?
Dr. David Pisetsky, chief of the division of rheumatology and immunology at Duke University Medical Center have recently found the curative property of gold salts for rheumatoid arthritis and other inflammatory diseases. Dr. Pisetsky, working with other scientists at Karolinska Institute in Sweden and the University of Pittsburg, have been studying the functional properties of HMGB1 molecules, which converts DNA to RNA inside the nucleus and is released from the cell either through normal processes or cell death. This molecule is released from the cell by the help of interferon-beta and nitric oxide. HMBG1 belongs to the High Mobility Group proteins that not only act on DNA transcription but also play a role on DNA repair. HMGB1, once released by the cell, attracts neutrophils and other inflammatory cells to infected tissue. This (HMGB1) molecule is found to be high in the synovial tissue and joint fluid where arthritis commonly occurs. Pisetsky and colleagues conducted their research on the properties of gold by stimulating mouse and human immune cells to release HMGB1 then treat them with gold salts. What they found was that when the immune cells were exposed to gold salts, there was an inhibition in the release of HMGB1 molecules from the nucleus. The implication is that if you block the release of HMGB1 molecules (which stimulates the aggregation of inflammatory cells in one location) then it should decrease the immune response. The gold salts inhibits the release of HMGB1 by blocking the helper molecules (interferon-beta and nitric oxide) so it is sequestered inside the nucleus and therefore cannot stimulate the immune system.
But like all the other treatments (for any disease), gold salts has its own side effects, which includes rashes, kidney damage and bone marrow's ability to synthesize blood cells and its ability to decrease immune system response via HMGB1 inhibition takes months to take effect. So until they figure out how to decrease some of the side effects and also decrease the time for gold salts to work, it could be awhile before this treatment would be as effective as one would hope. Still, it looks like Pisetsky and colleagues are going in the right direction in searching for another possible treatment for arthritis.
More information about HMGB1 protein:
HMGB1 proteins is secreted by macrophages and monocytes that were activated by IL-1 or TNF-alpha and act as a chemoattractant for myeloid and muscle cells. These proteins stimulates the expression of adhesion molecules in the endothelial cells, making it easy for inflammatory cells to bind and migrate to infected sites. This molecule also impairs the barrier function of intestinal epithelia (inhibiting the protective activity of intestine against pathogens). HMGB1 activity is initiated by binding to RAGE (receptor for advanced glycation end products), which is present in many immunoglobulin cells. The binding of HMGB1 to RAGE activates the chemoattractant capabilities of HMGB1 proteins thus stimulating the inflammatory response.
www.sciencedaily.com/releases/2007/10/071022153109.htm (from Science Daily)
'Role of Toll-like Receptors in HMGB1 release from Macrophages' by David Pisetsky and Weiwen Jiang (from Annals of the New York Academy of Sciences)
But like all the other treatments (for any disease), gold salts has its own side effects, which includes rashes, kidney damage and bone marrow's ability to synthesize blood cells and its ability to decrease immune system response via HMGB1 inhibition takes months to take effect. So until they figure out how to decrease some of the side effects and also decrease the time for gold salts to work, it could be awhile before this treatment would be as effective as one would hope. Still, it looks like Pisetsky and colleagues are going in the right direction in searching for another possible treatment for arthritis.
More information about HMGB1 protein:
HMGB1 proteins is secreted by macrophages and monocytes that were activated by IL-1 or TNF-alpha and act as a chemoattractant for myeloid and muscle cells. These proteins stimulates the expression of adhesion molecules in the endothelial cells, making it easy for inflammatory cells to bind and migrate to infected sites. This molecule also impairs the barrier function of intestinal epithelia (inhibiting the protective activity of intestine against pathogens). HMGB1 activity is initiated by binding to RAGE (receptor for advanced glycation end products), which is present in many immunoglobulin cells. The binding of HMGB1 to RAGE activates the chemoattractant capabilities of HMGB1 proteins thus stimulating the inflammatory response.
www.sciencedaily.com/releases/2007/10/071022153109.htm (from Science Daily)
'Role of Toll-like Receptors in HMGB1 release from Macrophages' by David Pisetsky and Weiwen Jiang (from Annals of the New York Academy of Sciences)
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