thousands of enzymatic and chemical reactions. By all means, if you don't do dairy, take a QUALITY calcium supplement with magnesium and vitamin D in the very least.
My family?? Dad chemoed and radiated to death. Uncle received umpteen laser surgeries for retinopathies but not once was told about pycnogenol for retinopathies.
Brother? put on cholesterol lowering meds only to have joint problems thereafter. There are a DOZEN different proven nutritional interventions for borderline hypercholesteremia. DOZENS, but what do they play with???? Frigging Lipitor, Zochor and the like that not only have debilitating effects on joints but they also can cause a Coenzyme Q10 deficiency since they also stop the liver from producing Coenzyme Q10.
Mom?? Kidney failure after being put on several meds most of which she didn't need. Second doc confirmed this.
What are they trying to deal with the kidney inflammation with??? Frigging prednisone and NOTHING ELSE. "Specialist stated: I don't want you to take ANYTHING, NOTHING AT ALL regarding supplements.
Of course, what do I know, I'm not a kidney specialist however I have read Dr. McCully's book on Homocysteine and how it is metabolized with B-Vitamins. Imagine that. I suggest you read and then understand my disdain for the disregard the all knowing and all seeing hold regarding nutritional medicine.
http://www.lef.org/protocols/prtcl-065a.shtmlHomocysteine
Discovered in 1932, homocysteine is a sulfur-containing amino acid normally found in small amounts in the blood of healthy persons. Homocysteine is derived from dietary protein (meat, milk, eggs) and is metabolized in the liver using vitamins B6 and B12. High levels of homocysteine can result from genetic disease (homocystinuria); kidney disease; hyperthyroidism; psoriasis; systemic lupus erythemotosus; drug treatment for chronic diseases; and dietary vitamin deficiencies (folic acid, B6, B12) (Welch et al. 1998).
Homocysteine levels tend to increase with age and are higher in men than in women. High levels of homocysteine can be very damaging to the kidneys and the vascular system (Dierkes et al. 1999; Marangon et al. 1999; Levin et al. 2002). Accumulation of toxic homocysteine has been associated with the development of cardiovascular disease (artherosclerosis, stroke, heart attack); pulmonary embolism and deep venous thrombosis; dementias (Alzheimer's disease, multi-infarct dementia); and kidney disease ESRD (Joosten et al. 1997; McCaddon et al. 1998; Welch et al. 1998; Dierkes et al. 1999; Levin et al. 2002; Seshadri et al. 2002). Cardiovascular disease (CVD) is common in patients with chronic kidney disease (CKD) and is responsible for the majority of morbidity and mortality in patients (Levin et al. 2002).
As early as 1969, researchers began to make clinical observations linking elevated homocysteine to vascular diseases (McCully 1969). Subsequent investigations confirmed these observations (Clarke et al. 1991; Ueland et al. 1992; Stampfer et al. 1992; 1995; Selhub et al. 1995; Welch et al. 1998). In CVD, there is evidence that elevated levels of homocysteine are related to arterial wall damage, but the mechanism is unclear (Welch et al. 1998). It may be that homocysteine has a toxic effect on the endothelial (cellular) lining of blood vessels. Data from a study on healthy U.S. physicians (14,916) with no prior history of heart disease demonstrated that highly elevated homocysteine levels are associated with a more than threefold increase in the risk of heart attack over a 5-year period. This finding was published in 1992 in the Journal of the American Medical Association (JAMA) as part of the Physicians' Health Study (Stampfer et al. 1992). The Framingham Heart Study (1041 elderly subjects) (Selhub et al. 1995) and other studies have also confirmed that elevated homocysteine is an independent risk factor for heart disease (Chaveau et al. 1993; van Guldener et al. 2000; Hoffer et al. 2001; Suliman et al. 2001).
In kidney disease, homocysteine levels in the blood increase because the kidneys do not properly filter homocysteine. Elevated levels of homocysteine are commonly seen in renal patients, sometimes three or four times higher than normal levels (van Guldener et al. 2000; Friedman et al. 2001; Herrmann et al. 2001; Suliman et al. 2001). Homocysteine is consistently elevated to very high levels in patients who require dialysis (Levin et al. 2002). Plasma homocysteine concentrations often decrease after dialysis (Welch et al. 1998). Therefore, to further help lower homocysteine levels, dialysis patients often require high levels of nutrients, including folic acid, vitamin B12, TMG (also known as betaine or trimethylglycine), and vitamin B6 (Bostom et al. 1996; Chauveau et al. 1996; Robinson et al. 1996; Sadava et al. 1996; Tucker et al. 1996; Welch et al. 1998; van Guldener et al. 2000; Herrmann et al. 2001; Levin et al. 2002).
Folic acid was used in a study conducted in 82 patients undergoing dialysis 3 times a week for 4 weeks (hemodialysis, 70 patients; peritoneal dialysis, 12 patients) (Dierkes et al. 1999). The results demonstrated that in both groups, homocysteine concentration was reduced by 35% after taking 2.5-5 mg of folic acid after each dialysis treatment.
As noted earlier, although dialysis has the effect of lowering homocysteine levels, folic acid further reduced homocysteine levels and, more importantly, had long-term effects even after supplementation was withdrawn (Dierkes et al. 1999).
Although the relationship between CVD and CKD is convincing, therapeutic strategies appear to be underused in the care of patients with kidney disease. CVD and CKD have similar traditional risk factors (diabetes, hypertension, dyslipidemia, obesity) as well as nontraditional risk factors (hyperhomocysteinemia, anemia, disturbed mineral metabolism, parathyroid excess). Because these risk factors are also specific to kidney disease and are modifiable, they should be identified and treated in persons with CKD (Levin et al. 2002). Patients with mild hyperhomocysteinemia have no clinical signs and are typically asymptomatic until the third or fourth decade of life (Welch et al. 1998).
For some time, physicians have recognized the danger of homocysteine and they recommend use of vitamin supplements to lower homocysteine levels (Tucker et al. 1996; Welch et al. 1998). The "normal range" used by commercial laboratories is 5-15 micromoles/L of blood. However, epidemiological data reveal that homocysteine levels above 6.3 result in a steep, progressive risk of heart attack, with each three-unit increase equaling a 35% increase in risk for heart attack (Verhoef et al. 1996; Robinson et al. 1996). There may be no safe "normal range" for homocysteine. A survey in Cardiologia reported that the average American's level of homocysteine is 10 (Andreotti et al. 1999).
For many persons, daily intake of TMG (500 mg), folic acid (800 mcg), vitamin B12 (1000 mcg), vitamin B6 (100 mg), choline (250 mg), inositol (250 mg), and zinc (30 mg) will keep homocysteine levels in a safe range. Unfortunately, without a homocysteine blood test, it is impossible to know if the proper amounts of nutrients are being taken. Therefore, the only way to be certain is to have a blood test to ascertain that your homocysteine level is below 7. Sometimes treatment must be individualized for complicated conditions. High levels of homocysteine can require up to 6 grams of TMG or vitamin B6 (in cystathione-B synthase deficiencies).
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