Party with red wine and chocolate!

Red Wine

The researchers from the University of Barcelona studied the difference between red wine and gin (gin represented for any other type of alcoholic beverage) and found that red wine contains many complex compounds including polyphenols which induces a much greater anti-inflammatory effect than other alcoholic beverages.
Dr. Emanuel Rubin, a distinguished professor of pathology at Jefferson Medical College in Philadelphia said that consumption of any form of alcohol will help in lowering inflammatory markers; however, red wine has a much greater effect.

Red wine has long been associated with a lowered risk of heart attack and stroke. An experiment was performed by the Jefferson-led team[1], they measured inflammatory biomarkers in the blood to compare the different effects of red wine and gin on heart health.
The results of this study confirmed that red wine significantly lowered the level of inflammatory molecules such as adhesion molecules (inflammatory markers), proteins that cause white blood cells to stick to the walls of the arteries, which can lead to the formation of atherosclerotic plaques.

The benefits of red wine to a person’s health have been well documented. Numerous research suggesting that a moderate consumption of red wine could help to reduce the chance of getting heart diseases, various cancers, as well as reducing blood pressure and cholesterol levels.

Red wine has a number of antioxidant compounds, one of them is resveratrol --- a compound which has been linked with cancer prevention.
Scientists have been doing research on resveratrol’s role as a potential treatment against sepsis, appendicitis and peritonitis. Severe sepsis is known to have few effective treatments and a high percentage of mortality; however, scientists and research groups have found positive effects of resveratrol and its role of down regulating inflammation. Although further understanding and research is required, resveratrol may play an important role as an effective anti-inflammatory drug in the future.[2]


Chocolate

There is a review article which discussed the anti-inflammatory impact of cocoa flavanols. The article mentioned that cocoa-based products are the richest functional foods based upon flavanols. Flavanols modify the production of pro-inflammatory cytokines, the synthesis of eicosanoids, the activation of platelets and NO-mediated mechanisms. There have been studies suggesting that the regular or occasional consumption of cocoa-rich compounds result in beneficial effects on blood pressure, insulin resistance, vascular damage, and oxidative stress.[3]

Similar to red wine, polyphenols are also found in chocolate which makes it beneficial for health as well. Polyphenols are found in beverages (wine, coffee and tea), fruits and vegetables (apples, broccoli, onions, blueberries, blackberries, cherries, strawberries, plums and red grapes). [4] Although the best way to get plenty of polyphenols is to consume lots of fruits and vegetables, having chocolate every once a while will not hurt!

MODERATE consumption of red wine + MODERATE consumption of chocolate = FUN anti-inflammatory protection




[1] Red Wine Has Greater Anti-Inflammatory Action Than Other Alcohols. NUTRA ingredients.
http://www.nutraingredients.com/Research/Red-wine-has-greater-anti-inflammatory-action-than-other-alcohols
[2] Scientists Uncork Anti-Inflammatory Secrets of Red Wine. Family Health Guide. http://www.familyhealthguide.co.uk/scientists-uncork-anti-inflammatory-secrets-of-red-wine.html
[3] Chocolate at heart: The anti-inflammatory impact of cocoa flavanols. Carlo Selmi, Claudio A. Cocchi, Mario Lanfredini, Carl L. Keen, and M. Eric Gershwin. http://www.worldcocoafoundation.org/scientific-research/research-library/documents/Selmi2008.pdf
[4] Cocoa in Chocolate May Be Good for the Heart. Bio-Medicine http://www.bio-medicine.org/medicine-news-1/Cocoa-in-Chocolate-May-Be-Good-for-the-Heart-59974-1/

FX125L

Article: "New Anti-Inflammatory Molecule Safe" from Medpage Today.

I tried to do some research to find the original article that this article by Michael Smith from Medpage Today was referencing based on the citation at the end, but it turns out that it is actually an oral presentation by P. Wiesel and associates at the American College of Allergy, Asthma, and Immunology Conference in July 2009. This article describes a new and innovative drug, FX125L, that is considered an oral anti-inflammatory and is targeted for the treatment of mainly asthma and COPD. They claim that at even relatively high doses, the medication is safe. Based on the article, a very recent study was performed with 66 volunteers regarding the drug and doses ranging from 0.3 to 3,000 mg. I don't know about you, but that is a VERY large range of dosing. According to the abstract of the presentation, there were no serious side effects, but some effects were adverse with the most common side effect being headache (4 on FX125L and 2 on placebo), dizziness (1 on FX125L and 1 on placebo), and nausea (1 on FX125L and 1 on placebo).

According to the 6th edition of Immunology - A Short Course by Coico, et.al, asthma involves cytokine-induced recruitment of inflammatory cells (mainly eosinophils) that can cause tissue injury due to toxic substances released by these cells that can include oxygen radicals, nitric oxide, and cytokines. Cytokines released by TH2 cells and mast cells (IL-4, IL-13, and TNFalpha) upregulate expression of leukocyte and endothelial adhesion molecules such as ICAM-1 and E-selectin. Because of these adhesion molecules, there in an increase in eosinophil-endothelial cell adhesion that causes migration and prolonged survival within lung tissue.

So, what is FX125L? It seems to be a broad-spectrum chemokine receptor inhibitor. FX125L acts similar to a corticosteroid, but the article claims that it doesn't have as adverse effects as corticosteroids. According to theasthmacenter.org, corticosteroids (like Advair and Pulmicort) in asthma suppress the inflammatory reaction that causes swelling and narrowing of the bronchi. It is normally used when asthma can't be controlled with bronchodilaters like albuterol. The most significant side effects with corticosteroids is usually caused by a high daily oral dose over a period of months to years.

The exact molecular action of FX125L was hard to find. The only thing I could find was that it blocked migration of inflammatory cells. This would obviously prevent the inflammation from occuring if the cells associated with inflammation are unable to chemotax to the site. Also, according to the presentation abstract, FX125L inhibits neutrophil recruitment to the lung. Neutrophils are the first line of defense against fungal and bacterial infections, but when recruited to the lung, can release chemokines and cytokines that enhance inflammation such as IL-6, IL-8, IL-1beta, andTNFalpha.

The term "broad-spectrum" usually refers to being effective over a wide range. It would be interesting to know exactly how this is accomplished. If FX125L targets a specific receptor, how can it be broad-spectrum? I think about antibiotics and how there are broad-spectrum ones that are used to treat a number of strains of bacteria that cause infections so it can be prescribed for many infections. How does FX125L target chemokine receptors in general and manage to target a particular one? Maybe it targets a specific receptor that is associated with inflammation in general or in most to all cases. This is one of many questions that I hope will be explained soon as the research progresses.


"ACAAI: New Anti-Inflammatory Molecule Safe" Medpage Today. Ed. Michael Smith. 9 Nov. 2009. Web. 16 Nov. 2009. .
Presentation - Wiesel P, et al "First clinical experience with FX125L, an anti-inflammatory oral small molecule with an entirely novel mechanism of action" Ann Allergy Asthma Immunol 2009; 103(5)(suppl 2): Abstract 5
Corticosteroids - http://www.theasthmacenter.org/manual/part2-12.html
Neutrophils - http://www.springerlink.com/content/j71781x837m85n12/fulltext.pdf

Strenuous Exercise linked to memory Loss

This study was presented at the Alzheimer’s Association 2009 International Conference on Alzheimer’s disease. Long-term strenuous physical activity has been shown to decrease lifetime exposure to ovarian hormones in women and has been found to play a protective role against breast cancer. However a decrease in ovarian hormone exposure has been associated with increased risk of cognitive impairment. Also, long-term physical activity is associated with improved cognition but the intensity required to preserve cognition is not known. Mary C. Tierney, PhD, and professor at the University of Toronto wanted to examine the relations between both long-term strenuous and moderate activity and cognition in recently postmenopausal women. The study had 90 women aged 50-63 years old who gave details on the amount of their strenuous and moderate physical activities from high school to menopause. Eight memory and brain function tests were administered to all participants. The researchers found that long-term strenuous activity was always associated with poorer performance on all eight of the tests. Moderate physical activity was always associated with better performance on all eight of the tests. The results suggest that long-term strenuous activity may increase the risk of cognitive impairment in recently postmenopausal women, but moderate long-term physical activity may improve later life cognition. Dr. Tierney says that further study is needed.

Don't Sneeze On Your Cat!

As a self-proclaimed “cat lady” I decided that the recent confirmation of the transmission of the H1N1 influenza virus from humans to cats is appropriate to blog about. On November 4, 2009, it was reported and confirmed that a 13-year old cat in Iowa contracted the H1N1 influenza virus. Since then, more cats have been diagnosed with H1N1 and there has been one presumed, yet not confirmed, death.

When two members of an Ames, Iowa, family came down with the H1N1 flu, the family pet, a 16-pound orange tabby, became lethargic, lost his appetite, and was showing signs of respiratory discomfort. Fortunately they were able to call a family friend, Dr. Brett A. Sponseller, who is a specialist in large animal internal medicine and molecular virology at the College of Veterinary Medicine at Iowa State University. Dr. Sponseller and his colleague Dr. Albert Jergens conducted many tests and concluded that the cat indeed had H1N1 influenza.

This story is unique because it is the first case of a feline contracting influenza from a human, which has created concern for health officials and pet owners alike. There have been cases of companion animals acquiring the flu from other species. The canine influenza (H3N8) began in horses, and cats have been known to contract avian influenza (H5N1) from eating birds. However, the feline H1N1 case in Iowa remains the first time a cat has contracted influenza from a human. To date this virus has been confirmed in three pet ferrets, turkeys in Chile and Canada, and has also been transmitted between humans and pigs.

Since then, there have been more confirmed cat H1N1 cases. On November 17th 2009, a cat in Park City, Utah became the second confirmed H1N1 feline case. The owner contracted the H1N1 flu and noticed flu-like symptoms in the cat – similar to the Ames family. On November 18^th, 2009, the Oregon State public health veterinarian reported that a pet cat died from presumed H1N1 influenza virus infection approximately one week after a child in the household had flu-like symptoms. The cat shared a household with three other cats – all of which became ill with less severe sneezing and coughing symptoms.

Even though veterinarians and health care officials are uncertain of how the cats contracted the virus, it is known that the flu is easily transmitted between family members, and it is not surprising that a sociable cat would come into contact with the virus making it more susceptible. It is important to note that according to Dr. Sponseller, there is no evidence that a cat can transfer the H1N1 virus to a person because cats with flu typically don’t cough or sneeze.

This situation has fostered more “swine” flu panic and has raised many questions. How can a cat get H1N1 from humans? What makes this influenza virus transmittable to cats? Can a cat transfer H1N1 to humans? Can other companion animals such as dogs get H1N1? Will there be a H1N1 vaccine for pets? Until more is learned about the transmission of the H1N1 influenza virus, many of these questions will remain unanswered.

Parker-Pope, Tara, “The Cat Who Got Swine.” The New York Times. The New York Times Company. November 5th, 2009. Web. November 17^th, 2009. <http://well.blogs.nytimes.com/2009/11/05/the-cat-who-got-swine-flu>.

“2009 H1N1 Flu Virus Outbreak” AVMA. American Veterinary Medical Association. November 18^th, 2009. Web. November 20^th, 2009. <http://www.avma.org/public_health/influenza/new_virus/>.

Alzheimer’s Disease- Oral hygiene

Disclaimer: This post may come off as insensitive.
I just finished reading an article titled “Trouble Thinking? Better See the Dentist” found here http://www.reuters.com/article/newsOne/idUSTRE5AC06O20091113.
Let me start off by saying I worked in a dental office for 2 years.
The patients who came in with the WORST cases of Periodontitis & Calculus were usually the most uneducated and apathetic patients we would see. For some, a lifetime of calculus would cake onto their teeth so badly that they thought their teeth were simply growing. That’s what I said: THEY THOUGHT THEIR TEETH WERE GROWING!
For these patients, the only thing more painful than seeing the dentist would be reading The Great Gatsby. But I digress.
The Amyloid Hypothesis associated with chronic inflammation has been questioned as a causative factor in the pathogenesis of Alzheimer’s disease. Granted, I saw plenty of inflamed gum tissue in my time working in a dental office. But these epidemiological studies are simply telling me that the less health conscious individuals are showing early signs of Alzheimer’s disease for the sake of being unhealthy. What frustrates me is the scientific spin on it “those with the highest levels of the gum disease-causing pathogen Porphyromonas gingivalis were three times more likely to have trouble recalling a three-word sequence after a period of time.” When a dentist assesses gum disease, they stick a probe in your gums and measure the depth. It takes 5 seconds, less if you don’t have gum disease. This article makes it sound like they cultured the Porphyromonas gingivalis and really narrowed it down as a pathogen for Alzheimer’s disease.
Growing up, my dad would always tell me “Sit mens sana in corpore sano”, which is Latin for “a healthy mind in a healthy body” (my mom is Latina; dad is from New York…he says it in Latin to look cool). I think we should continue looking into the Amyoloid Hypothesis as a pathophysiological factor in the progression of Alzheimer’s Disease. However, I think there are things we control on a day to day basis that can make our brains healthier and more useful.

Clean Pigs and Diabetes

I came across this cool report in Science about a group looking to use pig pancreatic islet cells in human patients. You can check it out here:

Science 20 November 2009:
Vol. 326. no. 5956, p. 1049
DOI: 10.1126/science.326.5956.1049-a

Basically there are a few centers in the world raising pigs in sterile environments for islet cell harvest. By transplanting the pig islet cells into human autoimmune diabetes patients the hope is that the pig cells will not be susceptible to the autoimmune response to human islet cells. Hopefully, these cells will act as a near-term solution while the bugs are being worked out of a similar human stem cell approach.

Since pig tissue in a human will obviously mount a strong immune response the New Zealand group is "encapsulating the islets in material that will fend off immune attack while allowing insulin out. The Minnesota team is still working on an immunosuppression regimen that will allow the use of "naked islets," says Schuurman, which the scientists think will have better access to nutrients. Further down the road, scientists at the University of Pittsburgh and elsewhere are working on techniques for shuffling pigs' genes or conditioning patients' immune systems to narrow the species gap."

Obviously the biggest hurdles will be working out the regulatory issues related to grafting living pig tissue into humans to permit clinical trials. An interesting and kind of crazy idea.

What do you guys think about this? What are some of pros and cons you can think of with this approach?

Scale for the Severity of Disease State in EAE

During our discussion on multiple sclerosis last class we discussed the animal model of multiple sclerosis called Experimental Autoimmune Encephalomyelitis (EAE) as a tool to determine the effectiveness of treatments for multiple sclerosis. In the paper by Tsutsui et al. it was mentioned that the animals were assessed daily for EAE severity but it did not elaborate on how this was quantified in a consistent manner.
By tracing back through the references I found in the journal Natural Medicine (Liu et. al.) that severity of EAE was determined on a scale from 0-5 according to function. A score of 0 indicates that the disease is not apparent in the mobility of the animal. A score of 1 indicates mild physical signs including weight loss and tail weakness. 2 indicates mild paralysis in the hind limbs, a 3 indicates complete paralysis of the hind limbs. A 4 indicates hind limb paralysis with fore limb weakness or paralysis and finally a 5 indicates moribund (approaching death) or death.
As useful as this scale is it is unfortunate that the limit to its usefulness is limited to very advanced degrees of disease state. In humans with multiple sclerosis we know that there is a range of other problems in the early stage that manifest themselves early before obvious motor problems are manifested that this model could not be used to investigate.