Nutrition is Circulation | Betaine lowers homocysteine
Ischemia (low blood flow) and Apoptosis
Circulation of the blood is obviously vital for good health. What is not so obvious is that low blood flow (ischemia) can cause peroxidative damage and provoke programmed cell death by a mechanism called apoptosis. Apoptosis is the most common agent of aging because other mechanisms, such as peroxidation, glycosylation, protein cross-linking, DNA damage and nutrient deficiency, are more likely to damage but not kill the cell. Ischemia is a silent cause of aging: it kills cells in relatively small numbers, reduces their number, and gradually weakens tissue function. This is a progressive process, one that accelerates as the damaged and weakened tissues become ever more vulnerable.
The Sequence
Ischemia cuts down the amount of oxygen and nutrients that feed the cell. At first, the chemical reactions of the cell continue, thus using up the dwindling oxygen supply, and then shifting over to the less efficient anaerobic pathways which cannot support the mitochondria chemistry. The oxidative pathways in the mitochondria are quickly shut down, thus interrupting the production of hydrogen ions (H+) which normally provide reducing equivalents within the cell. With the loss of protons, hydroxyl ions can then accumulate within the cell (cytoplasm) and activate protease enzymes, (e.g. Caspases) that digest lysozymes, which ultimately digest cell membranes and destroy the cell.
Common Effects of Apoptosis
- Heart: gradual loss of cells leads to congestive failure, with or without actual infarct.
- Lung: weakening of alveoli and fibrosis leads to emphysema and oxygen debt.
- Pancreas: loss of cells leads to indigestion and malabsorption first, and diabetes later.
- Liver: destruction and fibrosis leads to cirrhosis.
- Brain: loss of cells leads to senile dementia with or without actual stroke. Localized damage can cause epilepsy.
- Bone: loss of cells and collagen leads to osteoporosis and fracture.
- Skin: loss of cells leads to senile atrophy.
- Sex Glands: loss of cells leads to involution and low hormone production.
Diagnosis of Blood Flow Status
Dark field Microscopy
Visualization of rouleaux, fibrin, platelet clumps.
ISAC (Immune Stimulated Activation of Coagulation)
Includes platelet receptors and response to ADP;
also thrombin-antithrombin complexes;
prothrombin fragments;
soluble fibrin monomers
fibrinogen.
Hereditary Coagulation Factors:
LDL 3a and 3b (small-dense LDL)
Homocysteine
Lipoprotein(a) (Lp(a))
PAli (Syndrome X-insulin resistance)
Protein S and Protein C.
Treatments can be Individualized:
Homocysteine:
TMG-Betaine, B6, B12, Folate, Serine, Glycine, N-Acetyl Cysteine
Lp(a):
Vitamin C, Lysine, Niacin, Proline, SSKI (potassium iodide).
Fibrinogen:
Bromelain, Pancreatin, Papain, Fungal-Derived Enzymes.
Prothrombin Fragments:
Magnesium, Vitamin E. Lapacho, Warfarin, Enzymes
Thrombin-Anti-Thrombin Complexes:
Low molecular weight Heparin; Warfarin.
Platelet Activation:
Ginkgo or Salicylate (aspirin), Curcumin, Ginger, et al.
LDL-3b (small dense type):
Vitamin E, Niacin, Bioflavonoids (chalcones), diet-low calorie and/or low carbohydrate diets
Pali:
Exercise, chromium, vanadium pancreatin, bromelain, testosterone, DHEA
Protein S (deficiency):
Vitamin K (phytanodione)
Low HDL:
Exercise, Niacin, Estrogen, Testosterone.
For more information, please see Dr. Kunin's article on Homocysteine: The Key to Heart Attack, Stroke, & Cancer.
To learn more about thick blood syndrome read Dr. Kunin's paper on Orthomoleclar Approach to Healthy Longevity available in our Books and Periodicals section.
