11/13/04 NEWSLETTER carlstonmd.com
Hello Patients HOME

The office will be closed until Thursday November 18 as I will be out of town.  Just a few quick notes this time and relatively unedited as it is late and I want to get this out to you before I leave. That is the blessing and curse of email correspondence.

Best, Michael Carlston, M.D.
www.carlstonmd.com 
707-545-1554

In This Issue: INDEX
  • EXCESS DOSES OF mEdia MAY BE HARMFUL TO YOUR HEALTH
  • VITAMIN E LEVELS LOW IN DEPRESSED PATIENTS
  • MAD COW-NO NEWS IS GOOD NEWS?
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    EXCESS DOSES OF mEdia MAY BE HARMFUL TO YOUR HEALTH TOP
    Several patients have called me out of concern over media headlines “Large Doses of Vitamin E May Be Harmful to Your Health”. Unfortunately the media can be like a child with ADD. The media has this annoyingly myopic or ill-informed habit of taking the newest study and treating it as if it is TRUTH - until the next one comes along.  All other studies conducted in the history medicine are abruptly cast aside.  Responsible journalists need to develop sufficient expertise to write responsibly rather than treating the latest informational tidbit as if the earth has opened up.
     
    Research accumulates and teaches us.  Some studies teach us more than others, however, a single study, no matter how good never outweighs a mass of other evidence.  
     
    The study raising all the fuss found an effect described variously as “extremely small” or “tiny” increase in the death rate of patient consuming more than 400 iu of vitamin E.  The New York Times quoted a UC Berkeley statistician "They may well be right, but as a statistician I find this paper unpersuasive".  Many experts believe the authors over-reached with their conclusions and doubt the reliability of the finding.
     
    I have not seen discussion of several, more fundamental flaws. Vitamin E has many forms and few supplements have any form other than the synthetic version of the poorest quality.  The i.u. measurement used with vitamin E to indicate its strength is very unreliable and we know for certain does not indicate activity in humans.  It applies to rats and we also know rats and humans metabolize it differently.

    There may be some kennel of truth in this finding, applicable in some specific circumstance but it is quite likely that will not be the case.

    I would not change your vitamin regimen based upon this study.

    VITAMIN E LEVELS LOW IN DEPRESSED PATIENTS TOP

    Another recent study of people suffering from depression found that they had low blood levels of vitamin E.  They also found that the lower the blood level of vitamin E the worse the patient’s depression score.  Interestingly, these results were independent of dietary intake of vitamin E (they were not taking vitamin supplementation).  So does this mean that vitamin E reduces depression? It could also mean that depression lowers blood levels of vitamin E.
    MAD COW- NO NEWS IS GOOD NEWS? TOP

    Following the latest flurry of excitement over the “mad cow” infection discovered in the American food supply, I decided it might be useful to summarize our knowledge about prion caused disease in a bit greater depth. Then again, recent non-news makes me wonder if that is necessary.
     
    The bad news comes in several packages.  First, to bring us all up to speed, the things we know
    Prion diseases occur in many different animal species
    Prion infections unpredictably cross from one species to another
    At this point, we have been operating on the assumption that all prion diseases have primarily neurologic effects
     
    The variant version (Mad Cow Disease) was identified in the UK in 1996.  Apparently British cattle (or maybe even just one cow) acquired the disease from a spontaneous mutation of its prion or from eating cattle feed made from sheep that suffered from the sheep version (scrapie).  That cow was then processed for food and fed to other cows. Those cows then were fed to humans or processed into feed for other cows and so the variant form of the disease spread.
     
    Some people get the disease much more slowly than others.  The 100+ cases of “mad cow disease” (aka - variant Creutzfeldt - Jakob Disease - vCJD) diagnosed in Britain have all been relatively rapid in appearance.  We know from regular CJD that some individuals do not become symptomatic for over 40 years.  There is no way to be certain that the disease is limited to those already diagnosed.
     
    One bit of bad news is that prions are very very tough. Sterilization procedures that kill bacteria and even virus have no impact on prions.  In fact there is currently no practical means of decontaminating surgical instruments.  The highest concentrations of prions in the body, in addition to the nervous system, are in the tonsils and small intestine (including appendix). Tonsil bx used as principle method of dx by the English National Prion Disease Clinic.  Tonsillar biopsy is only useful in the form of prion disease know as mad cow disease (vCJD).  Regular CJD is not detectable in this way. Because the tonsils are in the same neighborhood, dental procedures might theoretically spread prion disease.  The eye is another place prions accumulate.  tissues from those areas or instruments used to perform surgery on these body areas represent a very high risk. Have you ever had your appendix removed, tonsillectomy or for that matter any dental work?
     
    The first known medically caused case of prion disease was in 1974 from a corneal transplant.  This was from the “natural” sporadic form of the disease cased by a genetic mutation in the corneal donor.  Since then patients have developed the disease from human growth hormone until we learned to make it by genetic engineering.  At this time there are approximately 300 cases of prion disease in humans caused by medical “accidents”.
     
    It is clear that prion proteins are in muscle and urine.  They may also appear in blood.
     
    Well after all of that, you are undoubtedly wondering how I could write that no news might be good news.  I may be optimistic but there are real grounds for optimism.  
     
    There are still fewer than 150 recorded deaths in Britain with very few diagnosed cases still living.  Despite vigorous surveillance, very few new cases are being discovered. That could mean, as we have all been hoping, that it takes a heavy prion exposure to create prion disease. Given the fact that prion disease is a consequence of twisted misshapen proteins it may be ironic to suggest crossing our fingers, but why not?
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