Exo-toxins are produced and emitted by bacteria in both acute and chronic infections. Microbes produce endo-toxins when they die. Body cells that die also produce toxins. Toxins act to cause anti-oxidants to lose one or more electrons and toxins become deactivated in part by this action. The anti-oxidant AA converts to oxidant DHA and must be excreted or it will kill body cells. Allergens and other immune cells, recognizing infections, cause immune mast cells to produce products that kill microbes and body cells, that oxidize cholesterol and lipids, and that produce more toxins. Oxidation of lipids make neurotoxins. Peroxides rapidly deplete free vitamin C. Intake of enough antioxidant AA stops this toxin/oxidation cascade.
Vitamin C is ascorbic acid (AA). It is present and stored in the body as ascorbate. It has three forms: anti-oxidant, single-oxidized and double oxidized. The double oxidized form is dehydroxy ascorbic acid. (DHA, or sometimes, DHAA) AA takes part in many life-critical chemical pathways, where it is recycled.
AA is an essential molecule; we must eat it; we do not make it. We can store a limited amount of it, but when that amount is depleted by ever increasing toxins, we get very sick. Indeed, the sickness, pain, itching, irritation, inflammation that we feel are the feelings of AA depletion. If we quickly replace enough AA, we immediately feel better, until the toxins deplete that new AA, and we need to intake more.
AA rapidly converts to DHA, systemically, in the presence of reactive oxidative stress (ROS), of all toxin overloads, of vaccine induced stress, of chronic and acute infections, of antibiotic produced endo-toxemia, of Jarish Herxheimer reactions, of snake and insect venoms, of environmental toxin/allergen intake, of smoke inhalation and carbon monoxide poisoning, of sinus headache inflammation, of sunburn and heatstroke toxins, etc. See: Dr. Levy's AA Antitoxin Chapter 3
When free AA is depleted, and the amount of toxins is still large compared to the amount of systemic AA, most free AA converts to DHA, and the life-giving chemical pathways dependent on AA are blocked. Vital chemical reactions stop. The ratio of AA/DHA nears unity or below, histamine is produced by immune mast cells and blood levels of histamine rise exponentially. Histamine poisons the system, and the blood vessels start to leak blood and other fluids. Extreme allergic respiratory tract distress reactions occur, itching, pain and inflammation can and do result.
As a last life saving measure, an emergency injection of adrenaline can cause release of a few (~5 grams) of AA from the adrenal glands. When that is converted to DHA the AA/DHA ratio again plummets. If no supplemental AA is provided by injection, anaphylaxis and death can result. The adrenaline injection would not be needed if AA was supplied IV in large enough (multi tens of grams per hour) quantities. Along with a need for an adrenaline shot, goes the need for repeated supplemental AA intake. See:
An autoimmune cascade of toxins is the result of AA/DHA <1 and declining.
DHA is an oxidant and must be excreted, requiring water intake, and free flow of urinary functions.
High intake of supplementary anti-oxidants is needed. IV Glutathione intake can act to reduce the DHA, but this is not usually provided. Frequently-repeated supplemental multiple (2-3) gram quantities of AA intake are an economical way to improve and maintain the high values of the AA to DHA ratio and improve the chemical pathways operation. This applies both during emergency crisis and to speed recovery. Additional antioxidants like CoQ10, vitamin A and vitamin E should also be supplemented during recovery.
If the AA/DHA ratio is in the range 4-10 vitality is good and toxemia risks are low. However, the blood half-lifetime of AA is ½ hour. So with systemic toxemia, the AA/DHA ratio can change dynamically in just a few minutes or hours. After 6 hours the AA level can deplete to ½ to the 12th power, i.e. 1/4000th of the starting value, to a negligible, not protective amount. Oral AA intake, gut-to-blood transfer-efficiency is less than 15% for water soluble AA.
Low systemic AA, chronic respiratory/gut infections, endotoxins, vaccinations, and low AA/DHA ratio, all acting together, have been identified as causes of sudden infant death syndrome (SIDS), shaken baby syndrome (SBS), asthmatic allergic reactions, COPD exacerbations, and anaphylaxis symptoms which can include congestive heart dysfunctions. See Baby Yurkos Autopsy
Forms of AA intake are Oral, parenteral (injection) and Intra-Venous (IV) sodium ascorbate.
Oral (water soluble) AA can be in the form of AA, sodium ascorbate, calcium ascorbate (ester-C), magnesium ascorbate, and ascorbyl palmitate. Health supplement suppliers market these forms.
Another form of oral-intake AA, with superior pharmacokinetics and effectiveness, is Liposomal Vitamin C. Liposomal AA (L-AA) is AA nano-encapsulated (homogenized) with phospholipid lecithin. Its transport from gut to blood is more than 5 times better than for water soluble AA. Also, L-AA crosses the blood brain barrier better.
L-AA has an affinity (attraction) for microbes (bacteria and viruses) and body cells with lipid envelopes. L-AA delivers AA 7-11 times more effectively than water-soluble forms of AA to the cells, where the AA acts to kill microbes and microbe invaded cells.
L-AA thus can be taken orally, and produce pharmacokinetic concentrations equivalent or better than IV therapy, conveniently and at low cost. L-AA is available on Amazon.com. Users reviews of L-AA are found at Amazon.com and at the Vitamin C Foundation.
IV AA and parenteral AA is usually sodium ascorbate, sometimes with a small fraction of magnesium ascorbate and other critical electrolytes. Magnesium helps reduce the occurrences of heart fibrillations, because magnesium deficiency is associated with higher fibrillation risk. Orthomolecular MDs are familiar with IV AA administration. See Papers by Drs. Klenner and Cathcart.
Multi Toxemia Case History:
COPD Respiratory Polymicrobial Infections; Treatment is symptomatic. Responds positively to AA in levels over 8 grams per day 4-6x/d of 2 grams.
UTI Blockage, Infection & Toxemia: failure to void, always a full bladder, incontinence; Constant/recurring UTI infections. Urologist failed to see patient because his building lost electric power and facility was blacked out. Ultrasound room had power and full bladder was confirmed. Patient has had great difficulty obtaining urine sample of any quantity for period of many weeks. Cause of UTI blockage is unknown, blockage location below bladder. Hysterectomy? Structural degeneration of supporting cartilage resulting from Cipro? Stones? Effects of blockage on kidneys? Unknown, but worrisome. Never been catheterized. Should she be? Periodically?
Treatment of UTI with Cipro causing: Microbes die, Endotoxins release, Systemic Toxemia, AA oxidized to DHA, AA/DHA ratio shifts to critical range.
Extreme pain (plantar fasciitis) relieved overnight by higher afternoon and evening AA intake.
After oral Cipro: Extreme systemic muscle pains, Remedy for pains is 2-3 grams AA every 2-3 hours. Pain relief within a few hours, permanent muscle pain relief, if AA dosage is repeatedly kept high enough.
Cipro causes blockage of cartilage protein making and muscle regeneration. Cipro blocks DNA unzipping enzyme needed to transpose codes to RNA as part of protein making pathways.
First hospital visit with respiratory episode: AA intake was not given on late evening and at retiring, but vital signs were very good before retiring.
Next morning after ~10 hours of no AA intake no AA on arising: AA blood half lifetime is ½ hour. This is ½ to 20th power depletion of blood AA. ~1/500,000th.
Extreme breathing (shortness of breath) episode and chest pains. Heart Attack. Temp 99.2 degrees, some heart irregularities. Fibrillations in ER. Symptoms overlap some of those of anaphylaxis (AA depletion)
First-Aid 3 grams AA and 50 mg CoQ10, Then emergency room, IV Cipro, concurrent AA given by family with Drs’ permission. Other IV antibiotics not Cipro administered.
On return after 7-day hospital stay, continued 2 grams AA every 2-3 hours, at bedtime and on arising. Vitality improving each day. After 7 more days seems not to need much oxygen at all.
Bladder remains blocked; how and why undiagnosed. Waiting on new referral to see urologist.
Because of recurring bouts of toxemia need to find, diagnose and fix cause of urinary blockage.
KFP Copyright 2012 by KF & KM Poehlmann, all rights reserved.