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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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| My guess is that your cholesterol rose because your body is under stress and it not as inhibited as it was when you were on a higher PUFA diet. If I had your cholesterol level, I would try to eliminate stressors and see if the TC goes down. I haven't had a test for a few years now, but last time it was 209, which I consider to be ideal. |
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| I second the stress, I should definitely go easier on my lifestyle. But do you think that exercise like weightlifting can also raise TC? Exercise is generally recommended to lower rather than raise cholesterol. |
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| | | Sent: 11/29/2007 11:10 PM |
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| The generalizations are what has led to this mess in the first place, so unless you have found good evidence about weightlifting and TC, I wouldn't worry about what "experts" have to say about it. I tell people to remove all known stressors, eat truly essential items, an give it a few months. In other words, try to "normalize" your body. And at that point, if you TC is 220, that is fine. If it's well over TC at that point, then there is likely a stressor that has not been detected and removed, though older people might "naturally" have TCs in the mid to upper 200s. |
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Something related to competitive bodybuilders which are restricting carbs and perhaps also what they think is "saturated" fat prior to competition. They are "stressing" their bodies to a great extent by the training regime. Intererstingly their cholesterol is not high at all:
J Am Coll Nutr. 1990 Apr;9(2):136-42.
Nutrient intake, body fat, and lipid profiles of competitive male and female bodybuilders.
Bazzarre TL, Kleiner SM, Litchford MD.
Department of Nutrition, University of North Carolina, Greensboro 27412-5001.
The purpose of this research was to measure nutrient intake, body fat, [estimated from seven skinfolds: chest, axilla, triceps, subscapular, abdominal, suprailiac, and thigh (Jackson and Pollock, 1985)], total cholesterol (TC), HDL-cholesterol (HDL-C), HDL2-C, and HDL3-C of 19 male and 8 female bodybuilders competing in the National Physique Committee's USA Bodybuilding Championships (Raleigh, NC, April 1988). Casual blood samples and anthropometric data were collected 18 hours prior to competition, whereas 7-day diet records were completed 1 week prior to competition. Only 11 males and 2 females provided blood samples. Competitors were not tested for steroid use. These data are unique because the measurements were collected on site at the competition. Data are presented as means and standard deviations. Estimated body fat for males (6.0 +/- 1.8%) and females (9.8 +/- 1.5%) was quite low. Blood lipids (mg%) for males (TC = 187 +/- 11, HDL-C = 37 +/- 6, HDL2-C = 13 +/- 4, and HDL3-C = 24 +/- 4) were not indicative of increased coronary heart disease (CHD) risk. Data for the 2 females (TC = 190, 205; HDL-C = 56, 56; HDL2-C = 22, 8; and HDL3-C = 34, 48) could only be evaluated on an individual basis. Body fat was significantly correlated with HDL-C (r = 0.63; p = 0.04) and HDL3-C (r = 0.65; p = 0.03), but not TC nor HDL2-C. Of the dietary variables, only saturated fat was significantly correlated with HDL2-C (r = 0.60; p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 2338462
J Sports Med Phys Fitness. 1998 Sep;38(3):245-52.
Effect of a precompetition bodybuilding diet and training regimen on body composition and blood chemistry.
Too D, Wakayama EJ, Locati LL, Landwer GE.
Department of Physical Education and Sport, State University New York, Brockport 14420-2989, USA.
OBJECTIVE: The purpose of this investigation was to document the effect of a 10-wk precompetition bodybuilding diet and training, on blood chemistry and body composition. PARTICIPANT: One adult male, steroid and drug free, preparing for a first competition. MEASURES: Average daily dietary intake consisted of 2263 calories (71% protein, 16% carbohydrate, 13% fats), with a protein intake of 5.0 gm.kg-1 body mass (BM). Initial body weight of 76.3 kgf (16% body fat) decreased to 63.4 kgf (4.4% body fat). Blood samples for electrolytes, TP, Alb, bilirubin, LDL-C, TG, UA, and amylase were normal. HDL-C levels increased from 65 to 89 mg.dL-1. RESULTS: Decreased glucose levels (< 50 mg.dL-1), indicated hypoglycemia. Increased Mg, LD, and CK levels indicated intense training. Increased inorganic phosphorus from 3.7 to 8.2 mg.dL-1 suggested lactic acidosis. Increased BUN levels from 16 to 53 mg.dL-1 and creatinine from 1.1 to 1.8 mg.dL-1 may be attributed to a high protein diet. However, heart muscle enzyme (CK-MB) was not elevated. CONCLUSIONS: Substantial changes in body composition and blood chemistry suggest adequate nutrition be ensured, and caution taken to avoid excessive physiologic stresses on the body during precompetition diet and training.
PMID: 9830833
BTW at the time of my last cholesterol measurement I was trying a Tribulus terrestris supplement which is supposed to raise testosterone and lower TC. I am neither competitive bodybuilder (perhaps recreational we can say) nor restricting carbs or saturated fat in any way. |
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| Well, it depends upon what "high cholesterol" means, and what factors they controlled. With an omega 6 PUFA-rich diet and assuming they are young and in apparent good health, their TCs were within the range I would expect. I'd like to know the ages of the people in the study. |
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| Hans, what was your diet like before you started being the vegan? How much corn oil had you been ingesting daily? |
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| No way to know for sure. My mom used corn oil for cooking, and we had meat at least twice a day. Antioxidant-rich foods were not common either. My investigations into nutrition began while I was in my teens, because I had intestinal problems. The vegan diet seemed to work, but if I ate greasy falafel (and similar things), the intestinal issues came back, which now makes sense, of course, but at the time I didn't know about the lipid peroxidation studies. Basically, the vegan diet was very low in fat, so I avoided lipid peroxidation to a large degree (especially compared to most Amercans). However, the food did not satisfy for long, and it also caused bloating and gas (probably the high fiber content and/or legumes). |
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Here's a new report about something I learned "the hard way:"
"A new study suggests that low levels of gastric acid in the stomach can increase one's likelihood of getting a foodborne infection..."
http://www.sciencedaily.com/releases/2008/02/080221200040.htm |
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| Hans, have you ever had your glycosylated hemoglobin (http://en.wikipedia.org/wiki/HbA1c) levels tested? My rose recently, still within the limits of <=5.8 but makes me worried about the unrestricted consumption of carbohydrates combined with mostly sedentary lifestyle. I am getting significantly less PUFAs than previously when it was just in the middle. |
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| Well, it's been quite a while since I've had a blood test, so even if that was tested (which I don't think it was), it would be "outdated" at this point. With Mead acid in my cells, a diet with a good amount of antioxidant-rich food items, and not much UFAs, I'm not concerned. I do try to observe any signs that my body is not "working right," but there hasn't been anything worthy of note over the last few years or more. |
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Hans, you have mentioned most of your grandparents lived into their 90. Did they have any eye problems like the senile cataracts? Most of my relatives now in their early 70ties are developing the age-related cataracts and one of them had it already surgically removed. Strange enough even the pets are suffering from this disease now. The doctors say it's because people and their pets are living much longer than before these days ...
http://en.wikipedia.org/wiki/Cataract
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"...Lipid peroxidation (LPO) is a causative and pathogenic factor in cataract. Increased concentrations of primary molecular LPO products (diene conjugates, lipid hydroperoxides, oxy-derivatives of phospholipid fatty acids) and end-fluorescent LPO products have been detected in the lipid moieties of aqueous humour samples and human lenses obtained from patients with senile and complicated cataracts as compared with normal donors..."
Source: Drugs in R&D, Volume 6, Number 6, 2005 , pp. 345-369(25)
http://www.ingentaconnect.com/content/adis/rdd/2005/00000006/00000006/art00004
I think my great grandfather may have had some cataract issues, though that was when he was in his 90s. There's nothing to lose by avoiding lipid peroxidation as much as possible, is there? |
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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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