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October 24, 2002 Research Update |
James Bogash, D.C. Mesa, AZ
info@lifecarechiro.com
www.lifecarechiro.com
Coenzyme Q10 could slow functional decline in Parkinson's disease
A few interesting comments on this article. First, the highest therapeutic dose used in this study was 1200 mg...which is a pretty high dose as far as what I use in my office. Unfortunately, CoQ10 is not cheap and this would be prohibitive for many patients unless insurance covered some portion of it (dream on...). Interestingly, despite the fact that this study showed a clear benefit (44% reduction in worsening of symptoms) the authors still suggest "it would be premature for a PD patient to take these high doses until a phase III clinical trial is done." Do you think a Parkinson's patient who knows that progressive is inevitable would like to wait?
Effects of Coenzyme Q10 in Early Parkinson Disease: Evidence of Slowing of the Functional Decline
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Work stress and risk of cardiovascular mortality
It is well known that chronic states of stress lead to increased cortisol levels, and this increase in cortisol wreaks havoc on most body systems. One way it does this is by increasing insulin levels, producing abdominal obesity and increasing risk of heart disease. Insomnia, difficulty focusing and hormone disruptions can also be added to the list of detrimental effects of hypercortisolemia. Anyone care to take up a collection for billboards advertsing "stress kills?"
bmj.com Abstracts: Kivimäki et al. 325 (7369): 857
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Homocysteine and Risk of Ischemic Heart Disease and Stroke
This meta analysis finds an 11% increase in ischemic heart disease and 19% increase in stroke. While the authors were not jumping up and down about these results, I strongly disagree. First, one single solitary factor raised risk more than 10%. A single, solitary, VERY modifiable risk factor. (As far as cost, my office offers a 2,000 mcg B12 and 800 mg folic acid for about $8/month...that would equal to about $3,840 for forty years' worth...hardly the cost of diagnosing CVD). Remember, Western medicine rarely gets beyond the idea of "one cause, one cure." Natural approaches to CVD would attack multiple angles, with efficacy rising with a more broad scope approach. Lastly, this review accepts what is currently accepted as "normal" for homocysteine levels. It is highly possible (and we see it in many other lab values) that "normal" values are actually too broad. That would result in patients with "high normal" homocysteine that contributes to their CVD but would actually have counted against association.
Homocysteine and Risk of Ischemic Heart Disease and Stroke: A Meta-analysis
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MTHFR 677CtoT Polymorphism and Risk of Coronary Heart Disease
Chalk up another 16% risk for another modifyable risk factor (actually not modifyable, but rather compensatable). Here we see that genetic variants with a sluggish enzyme that converts oral folic acid to its active form increases risk of CHD. So up your level of folic acid (at no additional cost because you're already taking it to affect homocysteine levels...) to at least 400 mg (preferably 800 mg).
MTHFR 677CrarrT Polymorphism and Risk of Coronary Heart Disease: A Meta-analysis
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S-Adenosyl-L-methionine: its role in the treatment of liver disorders
When a nutrient seems to affect multiple conditions, we can assume two case scenarios. A. The nutrient is offerred by a multi level marketing company and is reported to fix everything from diabetes to cancer to my bald spot. B. The nutrient affects a basic metabolic defect/deficiency that leads to many downstream conditions. SAM-e falls into the second category. SAM-e is a strong methyl donor, and methylation is an incredibly important process that is essential for many biological processes such as homocysteine conversion, protecting DNA from damage and, in this study, protecting the liver by assisting in the production of glutathione (the liver's heavy hitter when it comes to detoxification). This would put SAM-e on the list along with milk thistle for any patients with liver problems.
AJCN -- Abstracts: Lieber 76 (5): 1183S
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Fructose, weight gain, and the insulin resistance syndrome
There are beliefs out there that fructose does not contribute to weight gain and alterations in insulin resistance. "Health" drinks contain glucose-fructose syrup and high fructose corn syrup is virtually ubiquitous in junk and processed food. Well, this study debunks these beliefs and supports the idea that fructose does get readily converted to fat in the liver, induces insulin resistance and increases blood pressure.
AJCN -- Abstracts: Elliott et al. 76 (5): 911
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Need for Mass Hepatitis A Vaccination of Indian Children
Hmmm....a worldwide organization suggesting that Hep A vaccine is unnecessary because most children have antibodies to the virus by age 10. And yet, here in the US, we are pushing hard to vaccinate everyone against Hep A (and B for that matter...just to ensure that those tiny little IV drug users don't get exposed via their sexual promiscuity...). Does this seem contradictory? We need to realize that our children are being USED in an attempt to prevent Hep A in adults. The vaccination has nothing to do with preventing the disease in children. In children the disease is hardly noticeable and self limiting. The truth would be nice for our parents--then let them decide if they still want their kids vaccinated.
Bulletin of the World Health Organization 2002;80:728-731
There may not be a need for universal vaccination of Indian children against hepatitis A, as a vast majority develop protective antibodies by 10 years of age, researchers from India report in the September Bulletin of the World Health Organization. Improvement in standards of living has led to a decreased prevalence of protective antibodies among children in various parts of the world. The result is an increased predisposition to severe forms of hepatitis A, but this mainly occurs in adults, Dr. Yogesh Batra and colleagues from the All India Institute of Medical Sciences in Delhi note. The paucity of specific data on hepatitis A seroprevalence in Indian children prompted the investigators to undertake a study of 500 school children between the ages of 10 and 17 years. The researchers tested for anti-hepatitis A antibodies using enzyme-linked immuno-sorbent assay (ELISA). A detailed clinical and biochemical evaluation was also conducted. Antibodies to hepatitis A were detected in 486 children (97.2%), indicating exposure to the virus, the researchers report. Anti-hepatitis A seroprevalence was 98.6% in children aged 10-12 years, 94.8% in children aged 13-14 years and 98.3% in children aged 15-17 years. There was no difference in anti-hepatitis A seroprevalence between boys and girls, Dr. Batra and colleagues report. A decline in the anti-hepatitis A seroprevalence among children is likely to result in an increase in incidence of hepatitis A infection among adults, Dr. Batra and colleagues warn. However, the incidence of hepatitis A in their hospital has more or less remained static between 1992 and 2000, so it is likely that anti-hepatitis A seroprevalence has changed little over the same period, the investigators believe. Similar results have been noted in other developing countries, where improvements in living conditions have not translated into a decline in the anti-hepatitis A seroprevalence, Dr. Batra comments. Thus, in endemic countries like India, where "exposure to hepatitis A virus is virtually universal" among children and the incidence of hepatitis A infection among adults has remained static, "mass vaccination against hepatitis A virus may not be cost-effective" or necessary, the Delhi team asserts.