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April 9, 2001 Research Update |
James Bogash, D.C. Mesa, AZ
info@lifecarechiropractic.com
www.lifecarechiropractic.com
Topical Lidocaine Appears Promising as Treatment for Migraine
This is an interesting article because of its implications. A few things to consider. Migraines are believed to be related to some sort of electrical disturbance within the brain itself. If this is the case, then why would a topical anesthetic have an effect on these migraines? The author suggests that the lidocaine may affect the trigeminal ganglion, the housing for the cell bodies of the neurons going to many areas of the face. Could it be that many migraines are misdiagnosed, and the vast majority of them are truly tension-type headaches? There is still so much we do not understand about the human nervous system.
(Annual meeting, American Society for Clinical Pharmacology and Therapeutics) Dr. Frederick Freitag and Dr. E. Lockhart of the Diamond Headache Clinic in Chicago ran a placebo-controlled trial of 40 patients with migraine without aura. Among those using lidocaine, pain rated on a 10-point scale declined from a mean of 6.93 at baseline to 5.51 at 2 hours, and to 1.70 at 8 hours, a significant reduction compared with placebo. Seven patients who used lidocaine were pain-free at 2 hours and eight were pain-free at 8 hours. Some subjects reported a tingling or burning sensation, but there were no significant adverse effects. According to Dr. Freitag, previous studies have shown that IV and nasally administered lidocaine relieve migraine pain, most likely by desensitizing the trigeminal nerve. The lidocaine patch could be used on its own or as an adjunct to other medications, Dr. Freitag noted. "When patients get a migraine attack, it takes a while for the normal oral medication to work, while this provides relief very quickly." He added, "We foresee people using it primarily as a mainstay of therapy."
Heart Disease Risks Higher for All Asthma Patients
Still think our life expectency is going to increase? Look at the number of children developing asthma and how much those numbers are increasing. No we see that patients with asthma have a 33% increase in likelihood to develop or die from heart disease. Considering that evidence suggests that asthma is an inflammatory condition, and that inflammation has been linked to heart disease, this correlation is no great leap. What this does mean is that we must stop covering up the symptoms in all of todays chronic diseases and address the underlying biochemical faults.
(American Heart Association's 41st Annual Conference on Cardiovascular Disease Epidemiology and Prevention) Carlos Iribarren, MD, MPH, PhD, of Kaiser Permanente, found that nonsmoking patients with asthma were 33% more likely to develop — or die from — heart disease than nonsmoking patients without asthma. "This means that asthmatic patients and their doctors should be particularly careful," says Dr. Iribarren, "not only about managing their asthma, but also about managing cardiovascular risk factors such as blood cholesterol, blood pressure, and blood sugar."Dr. Iribarren's research was prompted by an interest in the "increasing realization," as he puts it, "that heart disease is an inflammatory process. Since asthma is an inflammatory disease as well, we were interested in finding out if asthma patients had an increased risk of heart disease."Earlier studies have indicated an excess cardiovascular mortality among patients with asthma. What is new is that the connection — and the risks — appear to be there even for nonsmokers. There have been prior studies of the link between asthma and heart disease, mostly in Europe, but none of them looked specifically at nonsmokers."The reason to study nonsmokers is to rule out the strong influence of smoking on both asthma and heart disease," says Dr. Iribarren. "This is an important question because asthma affects about 6% of the general population, and heart disease continues to be the leading cause of death in the US."
Empiric Folate Therapy Over Testing for Folate Levels in Macrocytosis
This is really a progressive article with a concept that I support wholeheartedly. Many times I can look at a CBC of a patient who has abnormally high or even normal levels at the high end and treat that patient with Vit B12 and folic acid without sending the patient back to get more blood drawn to check for serum levels. While this seems to make sense from a convenience (no need for additional bloodwork) as well as a cost factor, it is rarely done. This article gives an amazing cost savings of at least $82,900 for the number of patients examined at only two hospitals.
Am J Med 2001;110:88-90,149-150 Empiric supplementation with folic acid for patients with macrocytosis with or without anemia is preferable to routine testing for folate levels, report physicians from the HealthONE Presbyterian/St. Luke's Hospital in Denver. These investigators recommend that tests for folate deficiency be reserved for patients with persistent unexplained macrocytic anemia. Dr. Andrew R. Robinson and Dr. Jeanette Mladenovic reviewed all serum and erythrocyte folate assays performed during 1996 at three hospitals. Of 2998 folate levels measured, only 68 (2.3%) were low. Only 35 of these abnormal results were noted in the patients' records, and only 16 of these patients were treated with folic acid. In the investigators' cost analysis, $89,814 was spent on 1257 folate tests at two of the hospitals. On the other hand, the cost of empiric folic acid supplementation was estimated to be no more than $6914, which would have resulted in cost savings of at least $82,900. Added to the issue of cost effectiveness, according to Dr. Robinson and Dr. Mladenovic, is the unreliability of assays in detecting folate deficiency. Empiric folic acid supplementation would bypass the chance that some patients with true folate deficiency would go undiagnosed and untreated. Editorialist Dr. Nancy Berliner of Yale University in New Haven, Connecticut, points out the "apparent carelessness with which folate level tests were ordered" and the fact that half of the abnormal test results were ignored. She emphasizes, as do the study authors, that empiric folate therapy should be undertaken only after cobalamin deficiency has been ruled out. Dr. Berliner concludes, "Although it appears to be cost effective and clinically sound to choose empiric folate treatment over laboratory testing, such a course presupposes a more informed and conscientious approach to the patient than appears to be the case."
Influence of melatonin on glucose tolerance and insulin sensitivity
I've always been a little nervous about using any type of hormone replacement therapy be it estrogen, growth hormone, testesterone, insulin or melatonin. Precursers to these hormones may generally be considered safer because the body may only convert into the active hormone that which it needs. Melatonin was viewed as the "anti aging hormone of the week" several years ago after some studies in mice showed lower levels in aged mice when compared with younger mice. This study suggests a effect of meltonin on decreasing our bodies ability to use glucose efficiently. Synergy : Clinical Endocrinology 54 (3), 339-346
T lymphopaenia in relation to BMI and TNF-a in human obesity
This is a nice article suggesting one way to lower TNF-alpha levels via weight loss. With the new class of drugs used for rheumatoid arthritis and Crohn's disease that block TNF-alpha action this is a refreshing article showing natural, healthy ways to have the same effect. Synergy : Clinical Endocrinology 54 (3), 347-354
Maternal essential fatty acid deficiency depresses serum leptin levels
While this is a trial done in rats, if the same holds true in humans it puts even more responsibility on the mother to be to live a healthy lifestyle. This article suggests that the deficiency of essential fatty acids during gestation and nursing may predispose the infant to leptin dysregulation which can ultimately lead to obesity. Consider this in the context of young females getting pregnant--they typically do not have good nutritional status for their own growing bodies--let alone the developing fetus. J. Lipid Res. -- Abstracts: Korotkova et al. 42 (3): 359 http://www.jlr.org/cgi/content/abstract/42/3/359
Frequency of triggering bacteria in patients with reactive arthritis
The well known fact that certain organisms infecting the GI tract can cause systemic arthritic symptoms becomes lost on most clinicians when they consider such conditions as fibromyalgia and many of the autoimmune disorders causing joint pain. In talking with a gastroenterologist and a rheumatologist that I know, they would never entertain the idea that the GI tract could be a source of joint pain unless the "well know" organisms are present. Maybe that's why we're missing the boat on chronic pain in civilized health systems... Ann Rheum Dis -- Abstracts: Fendler et al. 60 (4): 337 http://ard.bmjjournals.com/cgi/content/abstract/60/4/337
Polycystic Ovary Syndrome Is Associated With Endothelial Dysfunction
In view of recent findings that insulin resistance can be a contributor to endothelial dysfunction; and knowing that high insulin levels can shunt hormone production into too much testosterone in the female to contribute to PCOS...then this study is merely proving that A=B and B=C so A must =C. But it's nice to see the studies done to prove what clinicians in the trenches use empirically every day. Circulation -- Abstracts: Paradisi et al. 103 (10): 1410 http://circ.ahajournals.org/cgi/content/abstract/103/10/1410