Autoimmune Thyroid Disease

An Unfortunate and Lengthy Adventure in Misdiagnosis

Salicylates block folate?

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I had another “duh!” moment when I stumbled across this useful website about cerebral folate deficiency. According to the website:

Numerous drugs are known to inhibit the body’s ability to utilize folate including: 1) aspirin, 2) cholesterol lowering drugs, 3) oral birth control pills, 4) antacids, and 5) methotrexate when used for rheumatoid arthritis. Folinic Acid

According to the Linus Pauling Institute:

When taken in very large therapeutic dosages, for example in the treatment of severe arthritis, nosteroidal anti-inflammatory drugs (NSAIDs) such as aspirin or ibuprofen may interfere with the metabolism of folate. Routine low dose use of NSAIDs has not been found to adversely affect folate status. Folic Acid

But what if they interact with your genes? One symptom I particularly associate with salicylates is a “trapped nerve” sensation in my neck. Folic acid is very important for proper nerve functioning and in myelin formation. I also get this symptom if I take too much B12 for too long.

The end results of folate or B12 deficiency is megaloblastic anaemia and high homocysteine levels. Both of these are associated closely with Parkinson’s, Alzheimer’s, and stroke. My paternal grandmother, the probable proband for my condition, developed Alzheimer’s before she died.

One of the weirder symptoms associated with folic acid deficiency is restless legs syndrome. It’s also a food chemical intolerance symptom. Aspirin use has long been associated with anaemia, though the cause is thought to be gastrointestinal bleeding. Aspirin use and the ingestion of toxic chemicals including benzene, are both associated with aplastic anaemia, a different type of anaemia.

There are studies on aspirin and folate balance:

To clarify the effect of aspirin on folate balance, we studied serum concentration, protein binding, and urinary excretion of endogenous folate. A healthy woman twice followed an 11-day protocol of constant diet, blood sampling twice daily, collection of all urine, and 650 mg of aspirin by mouth every 4 hours on the middle 3 days. As determined by equilibrium dialysis and Lactobacillus casei assay, aspirin induced a brisk, significant but reversible fall in total and bound serum folate and a small but insignificant rise in urinary folate excretion. Aspirin in vitro also displaced significant amounts of bound serum folate. Thus, aspirin in therapeutic doses can contribute to subnormal serum folate values, and if it increases urinary folate excretion even slightly, may impair folate balance. Aspirin and Folate Binding

Many non-steroidal anti-inflammatory drugs (NSAIDs) (including sulphasalazine, sulindac, indomethacin, naproxen, salicylic acid, ibuprofen, piroxicam and mefenamic acid) were found to be competitive inhibitors (with respect to folate) of avian liver phosphoribosylaminoimidazolecarboxamide formyltransferase (AICAR transformylase, EC 2.1.2.3) and bovine liver dihydrofolate reductase (EC 1.5.1.3). In contrast, aspirin and the antipyretic-analgesic drugs acetaminophen and antipyrine were weak inhibitors of these enzymes. Structure-activity correlation suggests that an aromatic ring with a side chain containing a carboxylic acid is a requirement for competitive inhibition of the transformylase. The above-listed NSAIDs also inhibited the folate-coenzyme-mediated biosynthesis of serine from glycine and formate (i.e., the C1 index) by human blood mononuclear cells (BMCs) in experiments where the drug was added to a culture of BMCs. Acetaminophen had a weak inhibitory effect on the C1 index. Consistent with the results obtained in vitro is the observation that the C1 index of BMCs from rheumatoid-arthritis patients treated with drugs which possess little antifolate activity (e.g. acetaminophen) is higher than the C1 index of BMCs from rheumatoid-arthritis patients treated with NSAIDs possessing more potent antifolate activity (e.g. sulindac, sulphasalazine, naproxen and ibuprofen). The mean activity of the transformylase in BMCs taken from healthy humans was 1.98 nmol of product/h per 10(6) cells and the activity was positively correlated with BMC folate levels. These results are consistent with the hypothesis that (1) the antifolate activity of NSAIDs, and hence cytostatic consequences, are important factors in producing anti-inflammatory activity and (2) aspirin exerts its anti-inflammatory effects after its conversion into salicylic acid, which possesses greater antifolate activity than its parent compound. Inhibition of folate-dependent enzymes by non-steroidal anti-inflammatory drugs

It seems to me that many of the mental symptoms of food chemical intolerance could be explained through a “blocking” effect of salicylates on folate. It explains why methylcobalamin helps my brain fog symptoms. It also explains why some autistics seem to respond to certain types of folate and to methylcobalamin. I had thought that autism was a more complicated condition, but it may simply be caused by genes combined with various food chemicals. For example a common MTHFR mutation or a DHFR mutation that makes autistics genetically more vulnerable.

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Written by alienrobotgirl

23 January, 2007 at 3:27 pm

Posted in The Science of FCI

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