While they would consider my 8.05 still as high... (but much lower than the 9.83 on the 26th) I'm very happy to know that I have been reducing it...
But, you must ask: if homocysteine is a marker of atherosclerosis and heart disease, why is mine so good? I'm not taking Statins. I stopped taking the Beta Blockers because they also block the absorption of Magnesium... and now I know that they raised my triglycerides so high and dramatically lowered my HDL cholesterol. But, if you look at the rest of my blood tests, ALL that was related to a heart attack disappeared: AST, ALT, Bilirubina, LDH, C Reactive Protein... And, my lipid profile would still be almost perfect if the cardiologist hadn't given me Statins that Saturday night and if I hadn't taken his Beta Blockers...
And, I must inform you, returning to the reason why I want the genetic reading:
When I saw my triglycerides so high, knowing that I wasn't consuming sugar or any other refined carbs and was exercising at least an hour per day, I immediately google causes for a sudden rise in triglycerides. The Mayo Clinic explained that it is caused by too much consumption of refined carbs, sedentary lifestyle, certain diseases or certain medications. What medications? "Water pills" or Beta Blockers... However, they mentioned that this was an effect of older beta blockers... So, when I checked Lobivon (Nebivolol), it was stated that there was a risk of increased triglycerides and decreased HDL. However, it was rare that a person experienced those increases and decreases (like it being rare that a person be born with FAP/Gardners--1% of the U.S. population of colorectal cancer or rare that a person has histadelia or is an undermethylator) and that after a year, the lipid profiles would return... Granted, the cardiologists would say, "we wouldn't prescribe you a Beta Blocker without prescribing you a Statin" and that's what the cardiologist did... But, later on, what will they prescribe for me when I develop cancer for having cholesterol too low and for the Alzheimers caused by the same lack of sufficient cholesterol. And I know you don't want me to share with you why low cholesterol (below 160) puts you at high risk of Alzheimers... How cholesterol is needed for forming healthy sinapses... Isn't that what Alzheimers is about? Deterioration of brain synapses... the lack of ability of one part of the brain to communicate with another?
So, if my homocysteine is normal... as are all of the other markers for atherosclerosis (with the exception of what the Beta Blockers did to my triglycerides and HDL cholesterol), why throw in Statins? And, do I truly have a diagnosable problem? Or hasn't it always been something else...?
Dr. Gallagher (integrated healthcare specialist) and Dr. Julio Rodriguez (Cardiologist) explained to me why my BP remained low after the heart attack (not after the intervention). The Cardiologist said, "because you are a very healthy person..." (So, why so many pharmaceuticals? Why the heart attack if I'm so healthy?)... Dr. Gallagher said, "Because, when one of your heart arteries is blocked, your heart opens up other routes to move the blood." She gave it an actual name that I don't remember... What sounds most logical considering the treatment response. She says that we must address toxic stress in the body, heavy metal build-up in the liver, and toxins in the blood stream. Likewise, we must address a deficiency of anti-oxidants that are necessary for removing toxins from the body. We must address a deficiency of vitamins and minerals necessary for creating anti-oxidants or supplying anti-oxidants to the body. And we must address the deficiency of various enzymes necessary for metabolic purposes... Dr. Rodriguez says we must medicate and lower cholesterol... And, Dr. Gallagher says, "truthfully, you can't blame the doctors. That's what they were taught and is the only thing they know to do."
And I guess you would still trust the Cardiologist.
And here is what I found in the NIH Library of Medicine (although 8 years later, Homocysteine is being blamed more for cerebrovascular disease than cardiovascular disease). Please pay attention to the fact that they are not prescribing pharmaceuticals but nutrients... And, MTHFR is 5-methyl tetrahydro-folate...reductase. A deficiency of this causes an increase in Homocysteine. Jenny not only has Hashimotos Disease (the auto-immune form of hypo-Thyroidism, she also has MTHFR gene mutation:
Curr Atheroscler Rep. 2006 Mar;8(2):100-6.
Homocysteine: role and implications in atherosclerosis.
Guthikonda S1, Haynes WG.
Abstract
Hyperhomocysteinemia promotes atherosclerosis and is most commonly caused by B-vitamin deficiencies, especially folic acid, B(6), and B(12); genetic disorders; certain drugs; and renal impairment. Elevated homocysteine promotes atherosclerosis through increased oxidant stress, impaired endothelial function, and induction of thrombosis. Prospective studies have shown that elevated plasma homocysteine concentrations increase risk of cardiovascular disease by twofold and risk of cerebrovascular disease to a lesser degree. Hyperhomocysteinemia should be identified in patients with progressive or unexplained atherosclerosis and treated appropriately. Treatment of hyperhomocysteinemia is primarily through vitamin supplementation; folic acid and vitamins B(6) and B(12) are the mainstay of therapy. Betaine and 5-methyl tetrahydro-folate are also effective in lowering homocysteine levels. Treatment of moderately elevated plasma homocysteine in patients without atherosclerosis should be deferred until the completion of randomized outcome trials.
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