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By "popular demand," I wrote up the following post, explaining exactly what happened to me which led me to doing medical/biological/nutritional research:
In 2000, I began to lose weight and had bouts of food-poisoning like episodes. My doctor thought it was "malabsorption," but the question was why and what could be done about it. He didn't have an answer, the upper G.I. series was fine. I went to see a gastroenterologist. He said everything looked fine, that my vegan diet was not the cause, and that I should have an endoscopy, which I decided not to do. One doctor, who called me about the test results, said he would prescribe anti-acid medication for me, but since I never had "heart burn," I didn't see the need to try this. In the meantime, I tried to figure out what was wrong, but there were several possibilities: Celiac disease, not enough stomach acid, not enough digestive enzymes, "leaky gut syndrome," etc. At the time, I didn't really know what to do first, for how long, and in what amounts.
The food-poisoning like episodes continued, and by mid 2001, I was at my worst, weighing less than 100 pounds (at 5'9" tall). Nobody ever suggested an "HIV test," and since I had engaged in no "high risk behavior," I would not have taken one even if a doctor had suggested it. I also had a nasty case of oral thrush in 2000, which was treated successfully with anti-fungal wafers that you let dissolve in your mouth (don't remember which medication it was), and that took 2-3 weeks or so.
Another thing I had was a weird fungal growth in my navel, which I dealt with myself, since it was possible to remove it without specialized instruments.
Over time, I developed other problems, such as severe osteoporosis, a nasty facial rash, raised EBV levels, borderline B12 deficiency, tendonosis in the shoulder, hypotension problems, constant back pain, and fatigue/migraines.
Eventually, I learned a couple of very important things. The main issue was likely Protein Energy Malnutrition, which may have occurred due to a diet too low in salt. I needed to take more stomach acid for a longer period of time than I initially did, because I didn't know and neither did the doctors, though I found the same issue in an old medical book (circa 1919). When I learned of the osteoporosis, I took the wrong form of calcium (carbonate), which probably made the stomach acid problem worse while doing little if anything for the osteoporosis.
I was mislead for a while, thinking that I had Celiac disease, but even though I felt better after taking gluten out of my diet, the problems continued, and after about 2-3 weeks, I felt similar to before. However, I had two gluten sensitivity tests done, and the less specific one showed a clear sensitivity, so I stayed away from gluten for about two years. Now I have no problems with gluten. It took stomach acid supplementation as well as eating enough high-quality protein to clear things up, and I also took supplements of magnesium citrate, calcium citrate, and a few other things. It took a few months before I started gaining weight and feeling a little better, then I started eating enough high-quality protein, and felt much better after 6 months or so.
Old history:
1. Plantar's wart on foot was successfully treated with large doses of water-soluble vitamin A (early 1980s).
2. PVCs (irregular heart beats) treated successfully with magnesium citrate (mid 1990s).
3. Keloid on shoulder, which kept growing and was red until switching to very low PUFA diet (started in late 1970s).
4. Digestive disorders since birth. Switching to whole grain vegan diet in late 1980s seemed to work, though greasy food, like falafel, caused recurrence.
5. I had chalazions as a young child, and every once in a while I used to get them again as an adult. I have yet to have one over the last several years.
6. I was raised on a diet rich in corn oil, which I now realize, from my research, was very bad, making me prone to various "inflammatory" conditions.
7. I had a growth on my neck as a teenager, which the doctor said not to worry about unless it got larger. Over the last few years it shrunk, and now I can no longer feel it.
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Thanks Hans, that's very interesting paper. Actually, carnosine the LPO quencher is protecting the lens, brain tissue and muscle from LPO damage in healthy tissues -
http://en.wikipedia.org/wiki/Carnosine
and it is used in the eye drops to slow down the cataracts!
But the experts keep telling us that cataracts are caused by sugar-derived AGEs because they develop earlier during diabetes etc. ... |
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The reason, I suppose, that many "experts" talk about sugar or something else that clearly makes no sense, is that they are unfamiliar with the literature, and won't "think outside the box," for whatever reason. I was taught to just look at the evidence, and not to make assumptions about what "experts" say. Here's an important piece of evidence that most of the anti-sugar crowd probably has never read:
THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 271, No. 17, Issue of April
26, pp. 9982-9986, 1996
© 1996 by The American Society for Biochemistry and Molecular Biology,
Inc. Printed in U.S.A.
"The Advanced Glycation End Product, Ne-(Carboxymethyl)lysine, Is
a Product of both Lipid Peroxidation and Glycoxidation Reactions*"
QUOTE: "CML is also formed during
metal-catalyzed oxidation of polyunsaturated fatty
acids in the presence of protein... We also report that CML, heretofore
described as a gly-coxidation
product, is formed during peroxidation of polyunsat-urated
fatty acids (PUFA) in the presence of ribonuclease A (RNase), a protein
that contains neither enzymatically nor
nonenzymatically attached carbohydrate... oxidation of fatty acid is
clearly a more efficient source of CML, despite the fact that the
glucose is in solution throughout the course of the experiment,
while the PUFA are only progressively solubilized. Further,
after 6 days of incubation, a large fraction of the arachidonate
was oxidized based on its solubilization in the aqueous phase,
while 2% of the glucose is oxidized during this same time
period... The observations described above indicate that CML,
previ-ously
described as a glycoxidation product or AGE, may, in fact,
be derived from PUFA during lipid peroxidation reactions. UNQUOTE.
UNQUOTE. |
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