May 31th
2008
8:48 PM
Prednisone
I am 17yrs old and i take prednisone. I was diagnosed with kidney falier when i was 13. i had my transplant at 15. well I have come to hate prednisone, I use to be 127lbs and now well lets just say i am way above that. Today i went online to find out how to reverse the side effects of the stupid medication but i can't.If you take the time to read this you should really look up cushing disease because you might want to know what that is if you are taking prednisone.No matter what i do i still gain weight.One time i went to on of my Ann Arbor checkup's and my food doctor said i was not eating enough i was on the line of developing an eating disorder.I have asked my doctors how to get rid of these horrible side effects and all they say is exercise,exercise.Well i am always active and still no results.They always check me for some of the side effects that i read above like the yellow in your eye, the lumps in your armpits swelling in my legs etc. well i hope you never have to take this medication if you do then you know what i am saying.
January 13th
2007
4:16 PM
Anxiety and Psychiatric Disorders
Magnesium deficiency causes increased levels of adrenaline, which can lead to a feeling of anxiety. Rats who become magnesium deficient have an increased level of urinary catecholamine excretion (a by-product of adrenaline).
People who have mitral valve prolapse have also been found to have an increased state of anxiety and have an increased level of urinary catecholamine excretion, the exact same condition found in rats who are Mg deficient.
It is not surprising then, to find that people with mitral valve prolapse are usually low in magnesium, and that magnesium supplementation alleviates the symptoms of mitral valve prolapse and reduces the level of urinary catecholamine excretion, i.e. it also reduces the anxiety symptoms.
Researchers in Spain found a correlation between anxiety disorders and hypermobility. In fact, they found that patients with anxiety disorder were over 16 times more likely than control subjects to have joint laxity. If you put the study results together, then there's a link between anxiety and hypermobility, a link between anxiety and mitral valve prolapse, and a link between mitral valve prolapse and hypermobility.
These studies tell us that anxiety disorders occur in many people who simply have mitral valve prolapse and/or joint hypermobility, meaning anxiety disorders are not specific to EDS or any particular connective tissue disorder. Marfans also have mitral valve prolapse and joint hypermobility which would lead one to conjecture that they, too, have anxiety related disorders. As it turns out, a connection between Marfans and anxiety related disorders has been noted.
A study in Bulgaria also found magnesium abnormalities in patients with schizophrenia and depression. The authors thought the schizophrenia and depression caused the magnesium deficiencies, but I disagree that that was necessarily the case. When you look at this study within the context of all the other studies mentioned in this section, it is more likely that the magnesium abnormalities caused the mental illness. (There are quite a few studies on magnesium and mental illness on Medline. I just included a few to highlight my points.)
In a study from England, there was a strong association for more disturbed and excitable patients to have abnormal (either high or low) magnesium levels. The authors thought that the patients who seemed most disturbed may have some abnormality of magnesium metabolism.
To read up on the link between cholesterol levels and anxiety and depression, see my web page on low cholesterol levels.
For more on this topic, see my section on Anxiety and Depression - overlooked nutritional causes.
-- By jpisano | Reply | Private Message me
November 6th
2005
12:09 AM
Coincidence....I think not. A 15 day dose of Levaquin was prescribed for a recurrent sinus infection despite the documented effectiveness of Augmentin in past occurences. Within the first eight days there was no change in my inability to breath through my nasal passage. In addition to the Levaquin I took Benadryl Maximum Strength Allergy and Sinus in order to breathe with less difficulty. During the fifteen day treatment, I experienced, insomina and short term memory lapses, stiffness in both knees, diarrhea, extreme gas pains, and constipation. I actually think my rectal muscles were affected. After two days of incessant diarrheal woes, my body constantly felt as though excretion was necessary. Mucuous began to fill my tear ducts and affected my vision. My primary physician of ten years directed me to visit the emergency room....wow, now there's a thought....go to primary...go to emergency room....follow up with primary...Needless to say, my HMO may have saved me over $200, but it actually cost me four days away from the office and a weekend in bed.
-- By doc2u | Reply | Private Message me
June 12th
2008
1:33 AM
The Journal of Immunology, Vol 146, Issue 4 1294-1302, Copyright © 1991 by American Association of Immunologists
ARTICLES
Urinary nitrate excretion in relation to murine macrophage activation. Influence of dietary L-arginine and oral NG-monomethyl-L-arginine
DL Granger, JB Hibbs Jr and LM Broadnax
Division of Infectious Diseases, Duke University School of Medicine, Durham, NC 27710.
Murine macrophage oxidation of L-arginine guanidino nitrogen to nitrite/nitrate yields an intermediate effector, possibly nitric oxide, with antimicrobial activity. Total body nitrogen oxidation metabolism (NOM) was measured in vivo by determining the urinary nitrate excretion of mice ingesting a chemically defined nitrite/nitrate-free diet. As reported previously, mycobacterial infection with bacillus Calmette- Guerin led to a large increase in urinary nitrate excretion. This increase was temporally related to macrophage activation in vivo. The substrate for macrophage nitrogen oxidation metabolism in vitro, L- arginine, was deleted from the diet without ameliorating the urinary nitrate excretion response induced by BCG. This suggested that L- arginine was synthesized endogenously because there are no other known natural substrates for NOM. A competitive inhibitor of NOM, the L- arginine analog, NG-monomethyl-L-arginine was fed to mice in their drinking water. NG-monomethyl-L-arginine ingestion blocked both basal and bacillus Calmette-Guerin-induced urinary nitrate excretion over a 2- 4 week time span. These experimental conditions should prove useful for further investigation on the role of macrophage NOM in host defense against intracellular microorganisms.
-- By concernedcitizen | Reply | Private Message me