>> 10,000mg of NAC/ALA/(Lead chelator)I
First off, if you get 10k take some then wait ten minutes and check again first making sure you are actually getting the correct amount...
Then, neither are Lead chelatos, if anything NAC mobilzes Lead so taking more while in a dump stage makes it worse
>> Anyone else experiencing high dumps,
Yup, but the doctrine should take care of what could otherwise take a week in just a few minutes...
>> I had to give a time frame, like a dwell time for the commandemnt.
You where not talking to your guides then, check yourself before doing stuff like that.
(ex Fix B1 pathway) Would I be able to use any verb other than FIX.
Depends, you can't actually fix B1 pathways. The body with a perfect digestive track can ony absorb a tiny amount of B1. Add that Candida turns that into pyruvic acid, Lead destroys it and Legionella eats it then its a miracle there is enough left to make a tiny amount of CoA.
But don't worry because one Ethylene dump will chew up all CoA that is if you still have some after all those fuel additives which are manufacturered to require CoA to detox.
If you can't sleep then due to BeriBeri you can go to yoru Medico Mafia Agent and start on the slippery slope of Benzo and Fluoridated SSRIs..
- Lead Poisoning requires huge doses of B1
- Candida requires thiamine for growth, and produce pyruvic acid, best to use Benfotiamine
- Wet beriberi affects the heart; it is sometimes fatal, as it causes a combination of heart failure and weakening of the capillary walls, which causes the peripheral tissues to become waterlogged.
- Dry beriberi causes wasting and partial paralysis resulting from damaged peripheral nerves. It is also referred to as endemic neuritis.
- It protects against the damaging effect of lead poisoning, and prevents oedema or fluid retention in connection with heart ailments.
- It also reduces fatigue, increases stamina, and prevents premature ageing and senility by increasing mental alertness.
- high levels of acetylcholine suggest inability to convert to acetyl CoA due to B1 deficiency
Vitamin B1 Deficiency Symptoms
A lack of sufficient thiamine in the diet can cause loss of appetite, poor digestion, chronic constipation, loss of weight, mental depression, nervous exhaustion, and insomnia. It can lead to muscular weakness, leg cramps, slow heartbeat, irritability, defective hydrochloric acid production in the stomach and consequent digestive disorders. In case of insufficient supply of thiamine in the body, the heart muscles become lazy and fatigued, and the auricles or the upper chambers of the heart lose their strength and gradually enlarge. This may lead tto a condition known as hypertrophy of the heart. Prolonged gross deficiency can cause beriberi, neuritis, and oedema. Lack of vitamin B1, can slow down circulation to the scalp to the extent that hair may fall and new hair may grow very slowly. Deficiency of thiamine can be induced by excessive use of alcohol, dietary sugar, and processed and refined foods.
NOTE: Thiamine is absorbed from the small intestine. The capacity of the human intestine to absorb this vitamin is limited to about 5 mg per day.
This may mean that some with Chrohn's or IBS need Benfotiamine.
Thiamine deficiency and malaria in adults from southeast Asia.
Beriberi or thiamine deficiency is common in countries where malaria is endemic. The hypotheses that subclinical thiamine deficiency complicates malaria and may be associated with lactic acidosis and coma were investigated in a prospective study conducted in Kanchanaburi, Thailand. 77 consecutive patients who presented to Paholpolpayuhasena Hospital between May and July 1992 with malaria or other febrile illnesses and 50 healthy relatives and volunteers were enrolled. The activation coefficient for transketolase activity in erythrocytes was used to measure thiamine deficiency. The mean Box-Cox transformed coefficients were 0.166 among cases with severe malaria (n = 23), 0.145 in cases with uncomplicated malaria (n = 54), 0.138 in healthy volunteers (n = 27), 0.137 in febrile controls (n = 10), and 0.122 in healthy relatives of patients (n = 13). 12 patients (52%) with severe malaria and 10 (19%) of those with uncomplicated malaria had coefficients above the normal range. Thiamine deficiency occurred in significantly more patients with cerebral malaria than in those with uncomplicated malaria (odds ratio, 4.8; 95% confidence interval, 1.68-13.8). The 12 patients who died from severe malaria had higher coefficient values than the 115 patients and controls who survived. Finally, the 15 patients with lactic acidosis had significantly higher coefficient values than those without this complication. A study of thiamine administration to patients with cerebral malaria is recommended to allow distinctions between the findings recorded in this study and the possibility of a causal link.