Vitamin K, in sufficient doses, was shown to decalcify soft tissue such as blood vessels, thus lowering blood pressure. Ray recommended up to 15 mg of vitamin K daily. 10 mg of vitamin K every other day for about six months reversed severe arterial calcification due to kidney disease. Japanese trials found that 90 mg daily could reverse osteoporosis.
It seems vitamin K is capable of negating the effects of cortisol. Since cortisol is known to be linked to osteopenia, vitamin K has an additional protective effect here.
#17 Feb 21, 2020
1:03:15, Georgi Dinkov
Pregnenolone was shown to provide clinically meaningful reductions in low back pain in veterans. Low back pain is a sign of endotoxemia, and pregnenolone is a toll-like receptor (TLR4, TLR2) antagonist. Dosages used were 100 mg, 300 mg, and 500 mg daily.
#16 Feb 8, 2020
1:39:22, Georgi Dinkov
“Insulin-resistant states of obesity and Type II diabetes show a multitude of metabolic abnormalities that could cause vascular dysfunction. Non-esterified fatty acid levels increase long before hyperglycaemia becomes present.” (Steinberg and Baron, 2002)
#16 Feb 8, 2020
41:00, Danny Roddy
The keto diet can directly cause diabetes and obesity.
When someone starts the keto diet and loses a lot of weight, it is usually water weight—not fat—because the keto diet acts as a diuretic.
After water weight is lost on a keto diet, there is excessive lipolysis and potentially ketosis, at which point there is some fat loss. However, the body interprets this as a stress signal, and much of what is eaten gets stored.
Additionally, because carbohydrates are not being provided and because lipolysis is so elevated, the liver is quickly overwhelmed. Anything that the liver cannot glucuronidate, it will try to re-esterify (convert back to triglycerides) and send back for storage in the adipose tissue.
But on a keto diet, the blood is already high in triglycerides, and the liver, sensing this, will not send as much fat back for storage as it normally would; instead, it will keep it.
This leads to fatty liver.
#16 Feb 8, 2020
30:55, Georgi Dinkov
Raising the NAD/NADH ratio may be a viable treatment for every autoimmune condition.
Most autoimmunity may be due to dysbiosis and excess nitric oxide (NO).
Estrogen and serotonin are also involved.
Cleaning the gut and lowering NO, estrogen, and serotonin would be effective in autoimmune conditions.
[𝘗𝘳𝘰𝘨𝘦𝘴𝘵𝘦𝘳𝘰𝘯𝘦, 𝘤𝘺𝘱𝘳𝘰𝘩𝘦𝘱𝘵𝘢𝘥𝘪𝘯𝘦, 𝘉𝘦𝘯𝘢𝘥𝘳𝘺𝘭 (𝘥𝘪𝘱𝘩𝘦𝘯𝘩𝘺𝘥𝘳𝘢𝘮𝘪𝘯𝘦), 𝘯𝘪𝘢𝘤𝘪𝘯𝘢𝘮𝘪𝘥𝘦, 𝘢𝘯𝘥 𝘵𝘩𝘺𝘳𝘰𝘪𝘥 𝘮𝘦𝘯𝘵𝘪𝘰𝘯𝘦𝘥]
#15 Jan 4, 2020
1:45:44, Danny Roddy, Georgi Dinkov
A 3:1 or 8:1 ratio of progesterone:DHEA with a small amount of pregnenolone (5-10mg) may be enough to restore libido in people with hypogonadism and could even act as an effective TRT (testosterone replacement therapy) substitute. This combination is very anti-catabolic.
#15 Jan 4, 2020
1:36:57, Georgi Dinkov
Ray took a high dose of T3 (active thyroid hormone) and his blood oxygen dropped very low, to about 87-88. His friend, a doctor, suggested they go to the hospital. Within a few hours at the hospital, his blood oxygen climbed back up to 92-93. The doctor at the hospital was perplexed, unaware of the Bohr effect.
#15 Jan 4, 2020
1:15:05, Georgi Dinkov
[𝘖𝘯 𝘱𝘺𝘳𝘶𝘷𝘢𝘵𝘦 𝘰𝘹𝘪𝘥𝘢𝘵𝘪𝘰𝘯, 𝘵𝘩𝘦 𝘴𝘵𝘦𝘱 𝘭𝘪𝘯𝘬𝘪𝘯𝘨 𝘨𝘭𝘺𝘤𝘰𝘭𝘺𝘴𝘪𝘴 𝘵𝘰 𝘵𝘩𝘦 𝘒𝘳𝘦𝘣𝘴 𝘤𝘺𝘤𝘭𝘦]
In order for pyruvate to get into the mitochondria, it needs to be converted into acetyl coenzyme A (acetyl-CoA) by an enzyme called pyruvate dehydrogenase (PDH). PDH is the rate-limiting step of glucose metabolism, and its cofactors are thiamine (B1), magnesium, and NAD+.
When you have a buildup of pyruvate and NADH but PDH is not working, the body needs NAD+. The problem is that NAD+ was used during glycolysis to generate NADH, and glycolysis is an anaerobic process, so oxygen is not an option for oxidation.
In the absence of any external help, pyruvate itself can be an oxidizing agent. Pyruvate is the keto acid of the amino acid beta-alanine, and ketones can serve an oxidizing function. So the enzyme lactate dehydrogenase (LDH) takes pyruvate and oxidizes NADH back into NAD+, but in the process, pyruvate is converted to lactate.
The cell does not like lactate and does everything it can to pump it into intercellular space, creating local hypoxia, meaning your tissues cannot properly extract oxygen from the blood.
When this lactic acid builds up, it can only be shuttled to the liver, where it is converted back to glucose through a process called the Cori cycle (aka the lactic acid cycle). If the liver is not working well, there is a risk of lactic acidosis, which has a high mortality rate. If the liver 𝘪𝘴 working well, then you just end up back at step one, turning that glucose into pyruvate again. This is how one can become “locked” into glycolysis.
Therefore, the primary things that determine the function of this process are the cofactors for PDH:
-Thiamine
-Magnesium
-NAD+/NADH ratio in the mitochondria.
The Krebs cycle and the electron transport chain have to be working well for this inter-mitochondrial NADH to be re-oxidized back into NAD+. Inside the mitochondria, there is not a backup oxidant to prevent bottlenecks (outside of things taken exogenously).
#15 Jan 4, 2020
1:03:36, Georgi Dinkov
ATP has an affinity for magnesium and ADP has an affinity for calcium, so if metabolism is not working well, the ADP/ATP ratio will rise and the cell will begin drawing calcium in and excluding magnesium. Restoring synthesis of ATP solves this. Supplementing magnesium may help, but if thyroid is low, magnesium will be difficult to retain.
#15 Jan 4, 2020
26:41, Georgi Dinkov
If someone suspects they are hypothyroid but their labs are “normal”, the next biomarkers to look for are elevated cholesterol, low vitamin D, and low CO2.
#15 Jan 4, 2020
17:43, Georgi Dinkov
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