Hot tubs have been shown to be associated with disease. A well documented example of this is Hot Tub Lung (Mycobacteria induced respiratory illness) as a result of hot tub use.
Hot tubs are a favorable environment for these thermophillic bacteria and their disinfectant-resistant nature can make them a potential health risk for bathers. Once established, a Mycobacteria infection can also be very difficult to treat with antibiotics. The Center for Biofilm Engineering at Montana State University has developed hot tub simulations to study the efficacy of chlorine as a disinfectant against Mycobacterium fortuitum.
Bacterial samples were taken from three locations: from the bulk water, from coupons mimicking hot tub surfaces such as walls, and from inline hot tub filters. In the control, it was determined that colonies were particularly prevalent in the bulk water and on the inline filters. The main result was that while chlorine worked fairly well in a clean system inoculated with an organism, if fouled filters were moved to a clean system (analogous to a poor cleaning or just a spray down of the filter) with no new inoculation, M. fortuitum would not just survive but would actually GROW in the presence of chlorine. This enhances the chances for a user to experience repeat exposure and eventually develop a Type III Immunopathology response, hypersensitivity pneumonitis.
Chronic hot tub use can lead to inoculation of the bacterium resulting in the development of antibodies circulating in the blood stream. At a certain threshold, an individual may enter the hot tub and develop an immune response to the bacteria, as the circulating antibodies bind to the antigen. When the antibodies bind to the antigen large immune complexes form that cannot be cleared and they are subsequently deposited in vessel walls and there is an inflammatory response.
The center at MSU suggested that hot tub filters are really tricky to effectively clean due to all of the folds and even an aggressive cleaning could result in this occurrence.
All that said and I will be hot tubbing sometime this winter season!
05 December 2008
Cell Death
Last February there was a series of three papers in Immunity on the contraction of the T cell response and the mechanisms of the two major cell death pathways. I have always found the process of cell death fascinating. Apoptosis: the programmed cell death brought about by signals that trigger the activation of a cascade of ‘suicide’ proteins in the cells destined to die. This was the first definition of cell death I learned, but as my education continued and as the scientific literature advanced the science of the cellular death pathway the definition has become more complex.
There are two known pathways of apoptosis; extrinsic and intrinsic. Extrinsic apoptosis: death ligands (FasL) bind to associative death receptors (Fas) on the cell surface triggering recruitment of varying molecules and eventual autocatalysis and subsequent cell degradation. Intrinsic apoptosis: Bcl-2 proteins, one of which is Bim, is an apoptosis pathway occurring near or within the mitochondria. Bim is a trigger of the mitochondrial pathway of apoptosis and plays a prominent role in cell death caused by cytokine deprivation of T cells. When these mechanisms of cell death do not operate properly autoimmune disease can result and have accelerated progression.
Hughes et. al. (2008) discovered overlapping roles for Fas and Bim in T cell death. Mice lacking both Fas and Bim mediated death had enhanced and accelerated fatal lymphadenopathy (disease or swelling of the lymph nodes) and autoimmunity relative to those lacking only one of the death proteins. Hutcheson et. al. (2008) focused on the progression of systemic lupus erythematosus (SLE) as it related to the balance of the two cell death pathways. Mice with defects in the two pathways developed severe SLE-like disease. Weant et. al. (2008) came to the similar conclusion that both death pathways concurrently prevent autoimmunity and regulate T cell response.
Green (2008) in his review of these three articles poses the question; there is a redundancy in the cell-death process, but who is backing up whom? He reviews literature that suggested the process of T cell clonal contraction during an immune response was due to limited growth and survival factors rather than active ligation of death receptors. These new studies highlight the essential combination of each pathway in the T cell clonal contraction process.
There are two known pathways of apoptosis; extrinsic and intrinsic. Extrinsic apoptosis: death ligands (FasL) bind to associative death receptors (Fas) on the cell surface triggering recruitment of varying molecules and eventual autocatalysis and subsequent cell degradation. Intrinsic apoptosis: Bcl-2 proteins, one of which is Bim, is an apoptosis pathway occurring near or within the mitochondria. Bim is a trigger of the mitochondrial pathway of apoptosis and plays a prominent role in cell death caused by cytokine deprivation of T cells. When these mechanisms of cell death do not operate properly autoimmune disease can result and have accelerated progression.
Hughes et. al. (2008) discovered overlapping roles for Fas and Bim in T cell death. Mice lacking both Fas and Bim mediated death had enhanced and accelerated fatal lymphadenopathy (disease or swelling of the lymph nodes) and autoimmunity relative to those lacking only one of the death proteins. Hutcheson et. al. (2008) focused on the progression of systemic lupus erythematosus (SLE) as it related to the balance of the two cell death pathways. Mice with defects in the two pathways developed severe SLE-like disease. Weant et. al. (2008) came to the similar conclusion that both death pathways concurrently prevent autoimmunity and regulate T cell response.
Green (2008) in his review of these three articles poses the question; there is a redundancy in the cell-death process, but who is backing up whom? He reviews literature that suggested the process of T cell clonal contraction during an immune response was due to limited growth and survival factors rather than active ligation of death receptors. These new studies highlight the essential combination of each pathway in the T cell clonal contraction process.
03 December 2008
Epstein-Barr Virus, Complement Receptor 2, and Immortal B Cells
In class this past Tuesday, Dr. Cohen mentioned Epstein-Barr virus (EBV) and its role in triggering Burkitt lymphoma. He mentioned briefly how EBV infects B lymphocytes; I thought I would share how our lab uses this phenomenon as part of our research.
I work in a lab dedicated to researching the pathogenesis of the autoimmune disease systemic lupus erythematosus. We are specifically focused on the role of Complement Receptor 2 (CR2), a receptor found primarily on the surface of B cells. This receptor is actually involved in both innate and adaptive immune responses due to the variety of ligands with which it interacts. Among these ligands are gp 350/220, found on EBV. Once EBV has entered the B cell, it acts as an internal mitogen and the infected cell begins to proliferate.
Our lab actually cultivates EBV from a special cell line. We periodically collect supernatant from this cell culture and then use it to “transform” human peripheral blood mononuclear cells into immortalized B cell lines. After infection with EBV, the B cells begin to proliferate and within a week form visible “clumps.” The cells will usually continue to divide as long as I add fresh “cell chow.” Once I have a sufficient number of healthy B cells, I freeze them using a special freezing media. The cells can later be thawed and grown in culture again!
I work in a lab dedicated to researching the pathogenesis of the autoimmune disease systemic lupus erythematosus. We are specifically focused on the role of Complement Receptor 2 (CR2), a receptor found primarily on the surface of B cells. This receptor is actually involved in both innate and adaptive immune responses due to the variety of ligands with which it interacts. Among these ligands are gp 350/220, found on EBV. Once EBV has entered the B cell, it acts as an internal mitogen and the infected cell begins to proliferate.
Our lab actually cultivates EBV from a special cell line. We periodically collect supernatant from this cell culture and then use it to “transform” human peripheral blood mononuclear cells into immortalized B cell lines. After infection with EBV, the B cells begin to proliferate and within a week form visible “clumps.” The cells will usually continue to divide as long as I add fresh “cell chow.” Once I have a sufficient number of healthy B cells, I freeze them using a special freezing media. The cells can later be thawed and grown in culture again!
Booze your way to a healthier heart?
Many people were wondering what was so great about red wine and why was it good for the heart, the answer is resveratol. Resveratrol is a chemical compound found in certain plants. It is called a phytoalexin because plants naturally produce it as an antibiotic substance to fight both bacteria and fungi. Plants containing resveratrol include the grapes and skins of grapes that produce wine, raspberries, mulberries, blueberries and cranberries. However, the amount of resveratol in red wine is minimal. Probably the best common food source if one wants to consume resveratrol in its natural state is peanuts. Peanuts have significantly higher resveratrol content than do any berries or grapes that produce the chemical. This idea of drinking moderate consumptions of red wine is called the "French paradox" because French people have low cardiovascular mortality rates even though they eat foods high in fats. I found an article from the mayo clinic website that lays out the benefits of resveratol in layman's terms. I also found an article from a study that uses resveratol to reduce infarct size and improving ventricular function after myocardial ischemia in rats. The study proves that resveratol is a cardioprotective agent. I will post both the article and the study for those of you that are interested in drinking red wine to save your ticker.
This is the article:
http://www.mayoclinic.com/health/red-wine/HB00089
This is the study:
http://zp9vv3zm2k.ssscom.ezproxy2.library.arizona.edu/OpenURL_local?sid=Entrez:PubMed&id=pmid:18639559
This is the article:
http://www.mayoclinic.com/health/red-wine/HB00089
This is the study:
http://zp9vv3zm2k.ssscom.ezproxy2.library.arizona.edu/OpenURL_local?sid=Entrez:PubMed&id=pmid:18639559
Omega 3 and 6 fatty acids
I wanted to shed some light on omega-3 fatty acids since they have been mentioned on and off throughout the semester. The key to getting the most benefit from polyunsaturated fatty acids is balance between omega-3 and 6. The typical American consumes approximately 20 to 25 times more omega-6 fatty acids (linoleic acid) than omega-3 fatty acids. Predominant sources of omega-6 include soy, corn, safflower, and sunflower oils. In contrast there is a relatively low amount of omega-3 fatty acids (alpha-linolenic acid) in the western diet as its predominant sources include dark leafy green vegetables and flaxseed. Linoleic acid(LA) is converted to arachidonic acid (AA) while alpha-linolenic is converted to eicosapentaenoic acid (EPA). Cold, water fatty fish such as salmon and trout are good sources of dietary EPA. Both omega-6 and 3 are considered to be essential fatty acids as they are not synthesized endogenously.
Increasing dietary omega-3 fatty acids can shift the balance of the eicosanoids produced to a less inflammatory mixture through EPA competing with AA pathway. I have included a schematic below:
Increasing dietary omega-3 fatty acids can shift the balance of the eicosanoids produced to a less inflammatory mixture through EPA competing with AA pathway. I have included a schematic below:
There is also a good journal article on polyunsaturated fatty acids in the American Journal of Clinical Nutritoin.
Ref:
James, M et al. Dietary Polyunsaturated fatty acids and inflammatory mediator production. Am J Clin Nutr 2000, 71(suppl):343s-8s.
02 December 2008
Vegan and Vegetarian Diets
Vegan and vegetarian diets are both great in fighting inflammation. Eating a diet rich in vegetables and excluding meat (vegetarian) is associated with a lower risk of developing cancer, heart disease, obesity, and diabetes. Vegetarians also tend to weigh less, have lower cholesterol and lower blood pressure.
A vegan diet (vegetarian diet but excludes ALL animal products including eggs, cheese, yogurt, and milk) is also very beneficial in reducing inflammation, especially in people with rheumatoid arthritis. It decreases risk of heart attack and stroke in RA patients as well as reduces the severity of the disease. In one study, it was discovered that RA patients following a vegan diet had lower levels of C-reactive protein as well as RA factor, thus decreasing inflammatory markers.
Although both of these diets show promising anti-inflammatory effects, vegans and vegetarians must make sure they are getting proper nutrition. A don't forget about omega-3s! Look to supplement fish oils for flaxseed and other plant or nut oils.
01 December 2008
The Wonder Herb Has A Sidekick?
In discussion today someone mentioned that they would be curious to see the effect of a combination of anti-inflammatories such as omega-3 fatty acids and curcumin. I happened to be researching some more studies on curcumin and came across a study dealing with the prevention and treatment of pancreatic cancer with the use of curcumin and omega-3 fatty acids. The study was actually very interesting and is the first study done of its kind. Pancreatic adenocarcinoma is the fourth most common cause of cancer-related deaths and occurs in both men and women. It kills very quickly, patients usually die within 6 months of being diagnosed. Pancreatic cancer has upregulation of inflammation mediators suchs as those we have already discussed including nuclear factor kappa B, inductible nitric oxide synthase (iNOS), cycloxygenase-2 (COX-2) and 5-lipoinase (5-LOX). The study was done in vitro and in vivo models. This study shows that dietary administration of omega-3 fatty acids and curcumin suppresses the pancreatic tumor bettter than either one alone. The study overall shows many different things dealing with iNOS, COX-2, 5-LOX mediators. If you care to check out the study more I have provided the link to the article. I figured this article would tie in great with the omega-3 exercise article we discussed today in class.
Here is the link to the article:
http://www.informaworld.com.ezproxy1.library.arizona.edu/smpp/section?content=a905311628&fulltext=713240928
Here is the link to the article:
http://www.informaworld.com.ezproxy1.library.arizona.edu/smpp/section?content=a905311628&fulltext=713240928
Follow-up to last week's lay article on cognitive function and anti-inflammatories
After last week's lay article and discussion on cognitive function and the use of anti-inflammatories I wanted to follow-up with more specifics on the research study and the complete reference for the paper if you wanted to read further.
Study Design:
2528 participants randomized in 1:1:1.5 fashion to either 200mg of celecoxib twice daily, 220mg naproxen sodium twice daily or placebo (n= 726, 719, 1083) respectively.
Participant eligibility:
Participants were recruited from 6 sites around the country (Boston,MA, Rochester, NY, Balitmore, MD, Seattle, WA, Tampa, FL, Suncity, AZ) through mailers to medicare beneficiaries in targeted age and zip code ranges. Paticipants were then sub-divided into age groups (70-74, 75-79 and >80 years)and also had to have a first degree relative with Alzheimer's disease type dementia, score satisfactorily on cognitive battery test, and did not regularly take NSAIDs (with the exception of 81mg aspirin).
Data collection:
Participants completed a series of cognitive tests prior to randomization, including modified mini-mental state examination, the Hopkins learning verbal test revised and the informant rated dementia severity rating scale. After randomization the following tests were also administered the Digit Span Test, a generative verbal fluency of naming as many supermarket items as possible in 1 minute, narratives
from the Rivermead Behavioral Memory Test, the Brief Visuospatial Memory Test–Revised, self-rating of memory functions, and the Geriatric Depression Scale. The cognitive battery was then administered annually there after.
Study results:
The study was designed to last for 7 years, however was stopped after 4 years due to the fear of increased risk of cardiovascular events in participants taking celecoxib after observations from another trial reported increases in cardiovascular events for participants on celecoxib. In these 4 years study investigators saw no difference in cognitive function between the 3 study groups.
Reference:
ADAPT Research Group, Cognitive function over time in the Alzheimer's disease anti-inflammatory prevention trial (ADAPT), Arch Neurol, 2008;65(7):896-905.
Study Design:
2528 participants randomized in 1:1:1.5 fashion to either 200mg of celecoxib twice daily, 220mg naproxen sodium twice daily or placebo (n= 726, 719, 1083) respectively.
Participant eligibility:
Participants were recruited from 6 sites around the country (Boston,MA, Rochester, NY, Balitmore, MD, Seattle, WA, Tampa, FL, Suncity, AZ) through mailers to medicare beneficiaries in targeted age and zip code ranges. Paticipants were then sub-divided into age groups (70-74, 75-79 and >80 years)and also had to have a first degree relative with Alzheimer's disease type dementia, score satisfactorily on cognitive battery test, and did not regularly take NSAIDs (with the exception of 81mg aspirin).
Data collection:
Participants completed a series of cognitive tests prior to randomization, including modified mini-mental state examination, the Hopkins learning verbal test revised and the informant rated dementia severity rating scale. After randomization the following tests were also administered the Digit Span Test, a generative verbal fluency of naming as many supermarket items as possible in 1 minute, narratives
from the Rivermead Behavioral Memory Test, the Brief Visuospatial Memory Test–Revised, self-rating of memory functions, and the Geriatric Depression Scale. The cognitive battery was then administered annually there after.
Study results:
The study was designed to last for 7 years, however was stopped after 4 years due to the fear of increased risk of cardiovascular events in participants taking celecoxib after observations from another trial reported increases in cardiovascular events for participants on celecoxib. In these 4 years study investigators saw no difference in cognitive function between the 3 study groups.
Reference:
ADAPT Research Group, Cognitive function over time in the Alzheimer's disease anti-inflammatory prevention trial (ADAPT), Arch Neurol, 2008;65(7):896-905.
30 November 2008
NSAIDs, Your Bones, and Surgery
Fractures and Surgery:
Non-steroidal anti-inflammatory drugs are a large class of compounds that inhibit cyclo-oxygenase and thus the formation of prostaglandins, which are involved in bone metabolism. However, the effect of these drugs on bone metabolism is often overlooked. They inhibit osteoblasts at the endosteal bone surface and also reduce both the immune response and the inflammatory response. PGs have been shown to elicit and participate in inflammatory responses, increase osteoclast activity and subsequent bone resorption, and increase osteoblast activity and new bone formation. This apparent integral role for PGs in the process of bone healing, coupled with the knowledge that NSAIDs act by inhibiting the production of PGs, results in an understanding of the likely mechanism through which NSAIDs impart their deleterious effects on bone healing. By inhibiting the COX enzymes and the subsequent production of PGs, NSAIDs not only achieve their desired anti-inflammatory effects but also inhibit the increased production of PGs that is necessary for bone healing to occur.
On studies strong argues, the harmful effects of NSAIDs on bone: 'Despite animal studies which have highlighted the harmful effects of these drugs on the healing of fractures and spinal fusion, they continue to be used commonly for the relief of postoperative pain in the absence of well designed human trials. A random survey of the type of analgesia received by patients undergoing hip arthroplasties on our elective orthopaedic ward showed that 95% (18/19) were being treated with these drugs.' Based on this site ibuprofen has been shown to have an irreversible effect on the healing of fractures. Also the inhibitory effect of these drugs on fracture healing is greater the longer the duration of use.
Hip Surgery:
Another site argues that NSAIDs are good after hip surgery due to prevention of abnormal bone formation. 'Abnormal bone formation in the muscles around the hip occurs after about one third of all hip replacements. Use of an NSAID (apart from low dose aspirin) around the time of surgery reduces the risk of such bone developing by between one half and two thirds with little risk of side effects from treatment. Prevention of abnormal bone formation is likely to reduce the risk of long-term pain, stiffness and disability after hip replacement. However, the effects of treatment on these outcomes needs to be proved in a large-scale trial.'
It seems that NSAIDs have the ability to inhibit bone formation. This could be a good thing after hip surgery or a bad thing after a fracture or spinal fusion. However, more studies are needed.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1113091
http://www.cochrane.org/reviews/en/ab001160.html
Non-steroidal anti-inflammatory drugs are a large class of compounds that inhibit cyclo-oxygenase and thus the formation of prostaglandins, which are involved in bone metabolism. However, the effect of these drugs on bone metabolism is often overlooked. They inhibit osteoblasts at the endosteal bone surface and also reduce both the immune response and the inflammatory response. PGs have been shown to elicit and participate in inflammatory responses, increase osteoclast activity and subsequent bone resorption, and increase osteoblast activity and new bone formation. This apparent integral role for PGs in the process of bone healing, coupled with the knowledge that NSAIDs act by inhibiting the production of PGs, results in an understanding of the likely mechanism through which NSAIDs impart their deleterious effects on bone healing. By inhibiting the COX enzymes and the subsequent production of PGs, NSAIDs not only achieve their desired anti-inflammatory effects but also inhibit the increased production of PGs that is necessary for bone healing to occur.
On studies strong argues, the harmful effects of NSAIDs on bone: 'Despite animal studies which have highlighted the harmful effects of these drugs on the healing of fractures and spinal fusion, they continue to be used commonly for the relief of postoperative pain in the absence of well designed human trials. A random survey of the type of analgesia received by patients undergoing hip arthroplasties on our elective orthopaedic ward showed that 95% (18/19) were being treated with these drugs.' Based on this site ibuprofen has been shown to have an irreversible effect on the healing of fractures. Also the inhibitory effect of these drugs on fracture healing is greater the longer the duration of use.
Hip Surgery:
Another site argues that NSAIDs are good after hip surgery due to prevention of abnormal bone formation. 'Abnormal bone formation in the muscles around the hip occurs after about one third of all hip replacements. Use of an NSAID (apart from low dose aspirin) around the time of surgery reduces the risk of such bone developing by between one half and two thirds with little risk of side effects from treatment. Prevention of abnormal bone formation is likely to reduce the risk of long-term pain, stiffness and disability after hip replacement. However, the effects of treatment on these outcomes needs to be proved in a large-scale trial.'
It seems that NSAIDs have the ability to inhibit bone formation. This could be a good thing after hip surgery or a bad thing after a fracture or spinal fusion. However, more studies are needed.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1113091
http://www.cochrane.org/reviews/en/ab001160.html
Exercise: Anti-inflammatory
We have discussed in almost every class the importance of a balanced diet and exercise. It seems fit to discuss how exercise acts as an anti-inflammatory. Regular exercise offers protection against chronic, low-grade systemic inflammation. We have talked about many different types of chronic inflammatory diseases; obesity/type II diabetes, stroke, inflammatory bowel diseases, arthritis, and neurodegenerative diseases.
Chronic, low-grade systemic inflammation has been introduced as a term for conditions in which there is typically a two to threefold increase in the systemic concentrations of TNF-α, IL-1, IL-6, IL-1ra, sTNF-R, and CRP is reflected.
Typically, IL-6 is the first cytokine present in the circulation during exercise. Plasma-IL-6 increases in an exponential fashion with exercise and is related to exercise intensity, duration, the mass of muscle recruited, and endurance. It has been demonstrated that the IL-6 protein is expressed in contracting muscle fibers, and that IL-6 is released from skeletal muscle during exercise.
The anti-inflammatory effects of IL-6 are demonstrated by stimulating the production of anti-inflammatory cytokines and cytokine inhibitors such as IL-1ra and IL-10 and
TNF-R. Furthermore, IL-6 stimulates the release of soluble TNF-α receptors, but not IL-1β or TNF-α.
Chronic, low-grade systemic inflammation has been introduced as a term for conditions in which there is typically a two to threefold increase in the systemic concentrations of TNF-α, IL-1, IL-6, IL-1ra, sTNF-R, and CRP is reflected.
Typically, IL-6 is the first cytokine present in the circulation during exercise. Plasma-IL-6 increases in an exponential fashion with exercise and is related to exercise intensity, duration, the mass of muscle recruited, and endurance. It has been demonstrated that the IL-6 protein is expressed in contracting muscle fibers, and that IL-6 is released from skeletal muscle during exercise.
The anti-inflammatory effects of IL-6 are demonstrated by stimulating the production of anti-inflammatory cytokines and cytokine inhibitors such as IL-1ra and IL-10 and
TNF-R. Furthermore, IL-6 stimulates the release of soluble TNF-α receptors, but not IL-1β or TNF-α.
Figure 1: A marked increase in IL-6, which is followed by IL-1ra, TNF-R, and IL-10.
IL-10 acts as an anti-inflammatory by inhibiting the synthesis of pro-inflammatory cytokines like IL-1β, IL-1-α, and TNF-α along with the production of chemokines, all of which play a critical role in the activation of granulocytes, monocytes/macrophages, natural killer cells, and T and B cells and, in their recruitment to the sites of inflammation.
http://jap.physiology.org/cgi/reprint/98/4/1154
As I researched, I found many different websites that demonstrated how exercise can prove beneficial to those suffering from inflammatory diseases.
Heart Disease/Stroke:
- increase strength of heart muscle
- decrease blood pressure
- increase HDL
- decrease LDL
- improve blood flow
Obesity/Type II Diabetes:
- decrease body fat
- increase muscle mass
- increase body’s ability to use calories
Rheumatoid Arthritis/Osteoarthritis:
- increase muscle strength
- decrease pain and fatigue
- increase grip strength
- replenishment of lubrication to joint
- promotion of bone formation
- prevention of bone loss with aging
Crohn’s Disease (mild only)
- improved symptoms
- increased ratings of quality of life
Multiple Sclerosis:
- improved bowel and bladder function
- increased coordination
- increased ratings of quality of life
- decreased risk of CAD
- increased endurance
Parkinson’s Disease:
- decreased incidence of muscle cramps, rigidity of joints
- decreased aches/pains associated with staying still
- maintained control of gross movement (not tremors)
- heighten sense of achievement kept stress and anxiety levels low
In conclusion, regular exercise protects against diseases associated with chronic low-grade systemic inflammation.
http://www.medicinenet.com/benefits_of_exercise/article.htm
http://www.heuga.org/articles/benefits_of_exercise_for_people_with_ms
http://www.ccfa.org/reuters/excercise
http://www.worldwidehealth.com/health-article-The-Benefits-of-Exercise-for-People-Who-Suffer-From-Parkinsons-Disease.html
http://www.nutristrategy.com/health.htm
http://www.hopkins-arthritis.org/patient-corner/disease-management/exercise.html
Top 10 Anti-Inflammatory Foods
Hope everyone's Thanksgiving was wonderful!! Now that everyone ate a bunch of food, let's see if anyone got in their anti-inflammatories. Here are the Top 10 Anti-inflammatory Foods in no particular order...according to dlife.com.
Cold Water Fish and Grass Fed Animals.
This includes Salmon, Free-Range Chicken, and Grass Fed Beef. The thing that all three have in common is the super healthy fats, omega-3s. Although your cold water fish like salmon is going to give the most omega-3s, Grass Fed Cows and Chickens are going to have way more than grain fed, which have next to none. Grass fed beef may be a little tougher though so cook it ground or slow!!
Olive Oil
Olive oil is another great source of an anti-inflammatory fat. This one is called oleic acid. According to the American College of Nutrition, those who consume more oleic acid have better insulin function and lower blood sugar. Extra Virgin is the least processed so it is better for you. Other "cold-pressed" or "expeller-pressed" can be good for you too!
Salads
Dark green lettuce, spinach, tomatoes, and other salad veggies that are rich in vitamin C are anti-inflammatories. They are also rich in anti-oxidants and nutrients that also dampen inflammation. Use olive oil and vinegar for the dressing for even more anti-inflammatory action!!
Cruciferous Vegetables
What are they? Vegetables like broccoli, cauliflower, brussel sprouts, and kale. These veggies contain anti-oxidants as well as sulfur which which allows the body to make another much needed, high powered anti-oxidant, glutathione.
Cherries
According to the Journal of Nutrition, cherries are once again packed with anti-oxidants and if eaten daily, significantly reduce inflammation. Not in season? Frozen are just as good.
Blueberries
Not only do they have natural compound that reduce inflammation, they may also protect the brain from the effects of aging (Alzheimer's?). Again, frozen are just as good as fresh, and maybe a little cheaper.
Tumeric
A revisited spice. According to Biochemical Pharmacology, it is a powerful, natural anti-inflammatory. Pan fry curry seasoned, free range chicken in some extra virgin olive oil...very anti-inflammatory!!
Ginger
Here is another East Asian flavor that has anti-inflammatory benefits. Studies have shown that ginger can be used to help control blood sugar.
Garlic
The jury is still out on this one, there has been inconsistent research. But garlic might have anti-inflammatory effects and glucose-regulating benefits. Also, it might help the body fight off infections.
Green Tea
Green Tea is like fruits and vegetables where it contains natural, anti-inflammatory compounds. Also, it may reduce the risk of heart disease and cancer. It is suggested to drink a cup a day.
So did you have a Free-Range turkey on Turkey Day?
Cold Water Fish and Grass Fed Animals.
This includes Salmon, Free-Range Chicken, and Grass Fed Beef. The thing that all three have in common is the super healthy fats, omega-3s. Although your cold water fish like salmon is going to give the most omega-3s, Grass Fed Cows and Chickens are going to have way more than grain fed, which have next to none. Grass fed beef may be a little tougher though so cook it ground or slow!!
Olive Oil
Olive oil is another great source of an anti-inflammatory fat. This one is called oleic acid. According to the American College of Nutrition, those who consume more oleic acid have better insulin function and lower blood sugar. Extra Virgin is the least processed so it is better for you. Other "cold-pressed" or "expeller-pressed" can be good for you too!
Salads
Dark green lettuce, spinach, tomatoes, and other salad veggies that are rich in vitamin C are anti-inflammatories. They are also rich in anti-oxidants and nutrients that also dampen inflammation. Use olive oil and vinegar for the dressing for even more anti-inflammatory action!!
Cruciferous Vegetables
What are they? Vegetables like broccoli, cauliflower, brussel sprouts, and kale. These veggies contain anti-oxidants as well as sulfur which which allows the body to make another much needed, high powered anti-oxidant, glutathione.
Cherries
According to the Journal of Nutrition, cherries are once again packed with anti-oxidants and if eaten daily, significantly reduce inflammation. Not in season? Frozen are just as good.
Blueberries
Not only do they have natural compound that reduce inflammation, they may also protect the brain from the effects of aging (Alzheimer's?). Again, frozen are just as good as fresh, and maybe a little cheaper.
Tumeric
A revisited spice. According to Biochemical Pharmacology, it is a powerful, natural anti-inflammatory. Pan fry curry seasoned, free range chicken in some extra virgin olive oil...very anti-inflammatory!!
Ginger
Here is another East Asian flavor that has anti-inflammatory benefits. Studies have shown that ginger can be used to help control blood sugar.
Garlic
The jury is still out on this one, there has been inconsistent research. But garlic might have anti-inflammatory effects and glucose-regulating benefits. Also, it might help the body fight off infections.
Green Tea
Green Tea is like fruits and vegetables where it contains natural, anti-inflammatory compounds. Also, it may reduce the risk of heart disease and cancer. It is suggested to drink a cup a day.
So did you have a Free-Range turkey on Turkey Day?
Turmeric and Inflammation
Is there a correlation between the Eastern Indian diet and cancer?
Compared to the United States, India has a significantly lower incidence of reported cancer cases. This is true for both men and women. There have been many studies performed in this area, all of which report that an Indian diet plays a major role in the health.
Turmeric is a spice used in Indian dishes, such as curry, that acts as an anti-inflammatory and an antioxidant. Turmeric is one of the 700 Ayurvic medications prescribed to promote good health and well-being. Ayurveda is traditional medicine native to India, which is practiced as a form of alternative medicine. Turmeric has been used for centuries in India to treat various diseases including cancer. The spice has been found to suppress and destroy blood cancer cell lines in humans.
Lastly, Indians may also have a decreased risk of cancer due to their vegetarian diets, which rely on legumes (beans, chickpeas, and lentils) as protein. Studies have shown that legumes are associated with a reduction in cancer.
Bottom line: Eat your veggies and curry!
Dealcoholized Red and White Wines Decrease Oxidative Stress Associated with Inflammation in Rats
When I read this article the first time (I ended up reading it 3 times!) I was very lost and so I thought it would be a good idea to do my blog this week on the article itself. Hopefully this sum up of the information will help you better understand the article.
This article looked at the antioxidant and anti-inflammatory affects of dealcoholized red and white wine. Both of theses affects are due to the polyphenols that are present in wine.
In the study they had three groups of rats, a control group that was fed standard food, a group that was fed food containing dealcoholized red wine (DRW), and a group that was fed food containing dealcoholized white wine (DWW). After 15 days the authors induced a granuloma with carrageenan (a component of red seaweed) in all the rats from all three groups. After 24 hours blood from the heart and exudate from the granuloma was taken from all the rats.
In the blood and exudate total phenols was measured. TBARS, or thiobarbituric acid-reactive substances were measured. This shows the amount of malondialdehyde in the blood plasma and the exudate which demonstrates the amount of lipid peroxidation. Lipid peroxidation is the break down of lipids via free radicals (see figure below courtesy of Wikipedia). They also measured the amount of NO in the plasma and exudate and the ratio of L-citrulline vs L-arginine. This ratio can be used as an indication of iNOS activity.
The authors also removed polymorphonuclear (PMN) leukocytes from each of the three groups of rats. When these cells are activated they cause the release of superoxide anion (O2-) which is generated by NADPH oxidase and xanthine oxidase. PMN cells also release NO, which is generated by iNOS activity. Once released O2- will cause damage while the effects of NO release depends on the amount released, the location of their release, and what other reactive species are present. With these removed cells, the authors could then measure O2- and NO production by the cells and the level of COX-2 activation. For the amount of NO they looked at both nitrites and nitrates, as well as the amount of L-citrulline formed from L-arginine which shows the iNOS activity as previously stated. To measure the amount of COX-2 activation the authors looked at the amount of PGE2 produced, which is a prostaglandin released due to COX-2 activation.
From all of these measurements the authors found that DRW had more polyphenolic compounds than DWW, which explained the slightly increased antioxidant abilities of DRW in comparison to DWW. They also found that with both DRW and DWW there was a decrease in the number of cells in the exudate, which they said was due to the fact that O2- will recruit leukocytes while NO inhibits this. Since there was a decrease in O2- and an increase in NO in the exudate for both of the wine groups then a decrease in cell number in the exudate was expected. One unexpected finding was that there was actually an increase in PGE2 in the DRW. The authors said that this might be due to something else in the wine that is interacting with the polyphenolic compounds. This was an important point in the paper, that though they see that polyphenolic compounds are the substances that are the most important in their rat model, in the human body the interactions of all the substances within metabolism make it hard to directly apply the results of the study to humans.
Hopefully this helps you with the reading the article, it sure helped me!
This article looked at the antioxidant and anti-inflammatory affects of dealcoholized red and white wine. Both of theses affects are due to the polyphenols that are present in wine.
In the study they had three groups of rats, a control group that was fed standard food, a group that was fed food containing dealcoholized red wine (DRW), and a group that was fed food containing dealcoholized white wine (DWW). After 15 days the authors induced a granuloma with carrageenan (a component of red seaweed) in all the rats from all three groups. After 24 hours blood from the heart and exudate from the granuloma was taken from all the rats.
In the blood and exudate total phenols was measured. TBARS, or thiobarbituric acid-reactive substances were measured. This shows the amount of malondialdehyde in the blood plasma and the exudate which demonstrates the amount of lipid peroxidation. Lipid peroxidation is the break down of lipids via free radicals (see figure below courtesy of Wikipedia). They also measured the amount of NO in the plasma and exudate and the ratio of L-citrulline vs L-arginine. This ratio can be used as an indication of iNOS activity.
The authors also removed polymorphonuclear (PMN) leukocytes from each of the three groups of rats. When these cells are activated they cause the release of superoxide anion (O2-) which is generated by NADPH oxidase and xanthine oxidase. PMN cells also release NO, which is generated by iNOS activity. Once released O2- will cause damage while the effects of NO release depends on the amount released, the location of their release, and what other reactive species are present. With these removed cells, the authors could then measure O2- and NO production by the cells and the level of COX-2 activation. For the amount of NO they looked at both nitrites and nitrates, as well as the amount of L-citrulline formed from L-arginine which shows the iNOS activity as previously stated. To measure the amount of COX-2 activation the authors looked at the amount of PGE2 produced, which is a prostaglandin released due to COX-2 activation.
From all of these measurements the authors found that DRW had more polyphenolic compounds than DWW, which explained the slightly increased antioxidant abilities of DRW in comparison to DWW. They also found that with both DRW and DWW there was a decrease in the number of cells in the exudate, which they said was due to the fact that O2- will recruit leukocytes while NO inhibits this. Since there was a decrease in O2- and an increase in NO in the exudate for both of the wine groups then a decrease in cell number in the exudate was expected. One unexpected finding was that there was actually an increase in PGE2 in the DRW. The authors said that this might be due to something else in the wine that is interacting with the polyphenolic compounds. This was an important point in the paper, that though they see that polyphenolic compounds are the substances that are the most important in their rat model, in the human body the interactions of all the substances within metabolism make it hard to directly apply the results of the study to humans.
Hopefully this helps you with the reading the article, it sure helped me!
Subscribe to:
Posts (Atom)