24 April 2010

Dr. Weil: The Anti-Inflammatory Diet

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

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

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

22 April 2010

Medications Used in the Treatment of Alzheimer’s Disease

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


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

21 April 2010

Multiple Sclerosis: A Causative Analysis

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

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

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