md_a
Member
- Joined
- Aug 31, 2015
- Messages
- 468
Donnay Detoxicology LLC: humans make more CO naturally in response to lung infections of all kinds.. It comes from Heme oxygenase-1 induced catabolism of heme proteins like hemoglobin, myoglobin, and cytochromes which releases CO along with equal amounts of iron (which is converted to ferritin form) and biliverdin (which reduces to bilirubin). Both ferritin and bilirubin are reported to be high in COVID -19 patients, and ferritin is even considered the primary biomarker of their cytokine storms. But COVID clinicians are not yet testing for CO via blood, breath or skin, which they don't suspect because the pulse oximeters they are using to monitor oxygen saturation are mislabeled with a display says "O2Sat" but is actually the sum of Oxyhemoglobin + Carboxyhemoglobin + Methemoglobin (O2Hb + COHb + MetHb) . Doctors also don't realize that mechanical ventilators cause an increasing level of CO to buildup in the blood and tissues of people who are on them for any reason [see Chawla 2019], which causes an falling level of oxygen [see Ascha 2018] that ends in multi-organ failure and acute hypoxic death [see Simonsen 2018].
Oxygen is extremely toxic, and inhaling high concentration at high flow rate as is typically done in ambulances and EDs via non-rebreather mask that prevents CO2 accumulation actually causes humans to make more CO naturally in response, and it drives this CO from arterial blood into plasma and from there into tissues. Problem is that free CO is much more toxic in tissues, where it causes acute hypoxic multiorgan failure.
CO-oximeter - Wikipedia
....
Title COVID-19 morbidity and mortality caused by endogenous carbon monoxide poisoning, with recommendations for testing and treatment
Abstract
To test our hypothesis that abnormal levels of endogenous carbon monoxide (CO) produced naturally by heme oxygenase-1 (HO-1) in response to infections of all kinds may be contributing to the morbidity and mortality associated with COVID-19, we searched PubMed for peer-reviewed literature on carbon monoxide and each of eleven abnormal blood tests, fourteen signs and symptoms, and five fatal complications of COVID-19 infection reported in a case series from a hospital in Wuhan, China: acute respiratory distress syndrome (ARDS), acute kidney injury, acute cardiac injury, arrhythmia, and shock. We found reports of acute exogenous CO poisoning causing all the same signs, symptoms and complications, and all the abnormal blood tests except D-dimer and procalcitonin. Our search also found endogenous HO-1 and CO levels correlated with these complications, independent of any inhaled CO exposure. In sharp contrast to the CO poisoning literature, most studies of endogenous CO interpret its close positive correlation with these acute conditions as protective, with some going so far as to recommend treating ARDS with inhaled CO. We conclude with new recommendations for testing endogenous CO poisoning in COVID-19 cases using devices approved by the US Food and Drug Administration that can distinguish CO coming from the lungs, arteries, veins, and average of all tissues, unlike current protocols for CO poisoning that only measure CO in arteries or veins but not both. Based on these findings, we appeal to clinicians to start testing CO levels in COVID-19 patients and to stop monitoring oxygen saturation with conventional pulse oximeters that overestimate oxygen saturation by the sum of carboxyhemoglobin and methemoglobin. We conclude by reviewing FDA-approved treatments that may help COVID-19 patients with endogenous CO poisoning.
These include zinc-based drugs that lower the rate of endogenous CO production by inhibiting HO-1, and drug-free devices and methods that reduce the total body burden of CO after exogenous CO poisoning.
Conclusions
We have shown that 14 signs and symptoms and 5 frequently fatal complications of COVID-19 infection reported in a representative series of hospitalized cases from Wuhan, China, are all also reported in the peer-reviewed literature on CO poisoning. All the complications are each also independently associated with increases in endogenous CO. These findings are consistent with the hypotheses that endogenous carbon monoxide is causing the signs, symptoms and complications of COVID-19 but they do not prove it, which will require appropriate testing of cases and controls. Fortunately, FDA-approved devices for non-invasive spot and continuous testing of CO levels in real time are already widely distributed among hospitals and fire departments.
We conclude that people with COVID-19 who have labs, signs, symptoms, and complications consistent with endogenous CO poisoning should be tested for this possibility with any device that can measure CO reproducibly in lungs, blood and tissues.
We also urge clinicians worldwide to stop relying on conventional pulse oximeters to monitor oxygen saturation since the display is always overestimated by unknown fractions of COHb and MetHb.
For people with abnormally high levels of CO in their lungs, blood, and/or tissues, we recommend treatments that either quickly lower the total body burden of CO without drugs, or which quickly reduce the rate of endogenous CO production, while boosting ventilation if needed with carbon dioxide mixtures. This should exclude mechanical ventilation, high-flow hyperoxygenation, and hyperbaric because all increase the level of CO in tissues.
Our approach will not cure COVID-19 infections but we predict it will reduce morbidity and mortality and eliminate the need for mechanical ventilators.
….
From Ray Peat:
“Not all the oxygen we consume is put to good use, and we sometimes produce exhalation of gases other than carbon dioxide and water vapor.
Under stressful conditions, people may exhale measurable amounts of pentane, ethane, isoprene, carbon monoxide, and other substances with potential toxicity.
In hyperventilation, so much carbon dioxide is lost in the breath that our tissue respiration is impaired, creating a partial ‘tissue suffocation.’
If cells consume oxygen without producing carbon dioxide generously, a situation analogous to hyperventilation/tissues suffocation exists.
Oxygen deprivation is one of the signals that stimulates the production of new red blood cells, and this involves the production of porphyrin, heme, and hemoglobin.
The elimination of heme by oxidation produces carbon monoxide, which can block the respiratory production of energy.”
"The exhaled breath is being used to diagnose inflammatory lung disease, since so many of the mediators of inflammation are volatile, but systemic diseases such as cancer and arthritis, and relatively minor stress can be detected by changes in the chemicals found in the breath. Polyunsaturated fats and their breakdown products-- aldehydes, prostaglandins, isoprostanes, hydrocarbons, and free radicals--and carbon monoxide, nitric oxide, nitrite, and hydrogen peroxide are increased in the breath by most stresses."
"The mitochondria are responsible for the efficient production of energy needed for the functioning of complex organisms, and especially for nerves. The enzyme in the mitochondria that reacts directly with oxygen, and that is often rate limiting, is cytochrome c oxidase.
This enzyme is dependent on the thyroid hormone and is inhibited by nitric oxide, carbon monoxide, estrogen, polyunsaturated fatty acids, serotonin, excess or free iron, ionizing radiation, and many toxins, including bacterial endotoxin.”
“The heme group (of hemoglobin and the respinitory enzymes, for example) is the iron-binding oily molecule that interacts with oxygen, and it is called a porphyrin.”
“The presence of porphyrin poisoning, with its associated free radical toxins, can lead to the activation of heme oxygenase, the enzyme which produces carbon monoxide, which I have discussed elsewhere as a cause of the respiratory defect that characterizes cancer. Both ammonia and porphyria have been implicated in the production of cancer.”
“Excess heme is destroyed by the enzyme heme oxygenase, which converts heme into biliverdin and carbon monoxide. Both of these factors have effects on the cell which are characteristic of cancer.”
“Any hypoxic tissue, including inflammations of any sort, will express the heme oxygenase enzyme, producing carbon monoxide.”
“This enzyme degrades the heme molecule, which is released from hemoglobin and other proteins in injured tissues, and which in the free state is toxic (Kumar and Bandyopadhyay, 2005). In degrading heme, this enzyme releases free iron atoms and biliverdin, as well as carbon monoxide. Although free iron atoms can cause harmful oxidation, biliverdin, and the bilirubin that's produced from it, can have beneficial antioxidant effects.”
“Carbon monoxide increases the formation of cortisol, by stimulating ACTH release from the pituitary.
The stress response is self-sustaining on several levels.
For example, stress increases the absorption of bacterial endotoxin from the intestine, which increases the estrogen level and synergizes with biliverdin and cortisol.
Biliverdin (F. Paradisi, 1975) activates betaglucuronidase, one of the main enzymes involved in the local release of estrogen.
In later stages, anemia and hemolysis are associated with CO and biliverdin production from the release of heme. (Anemia is seen in most patients with advanced cancer.)
Biliverdin, combined with estrogen and hypoxia, alters the cytoskeleton, producing chromosome imbalances, causing mutations and activating the "oncogenes."
Oxygen is extremely toxic, and inhaling high concentration at high flow rate as is typically done in ambulances and EDs via non-rebreather mask that prevents CO2 accumulation actually causes humans to make more CO naturally in response, and it drives this CO from arterial blood into plasma and from there into tissues. Problem is that free CO is much more toxic in tissues, where it causes acute hypoxic multiorgan failure.
CO-oximeter - Wikipedia
....
Title COVID-19 morbidity and mortality caused by endogenous carbon monoxide poisoning, with recommendations for testing and treatment
Abstract
To test our hypothesis that abnormal levels of endogenous carbon monoxide (CO) produced naturally by heme oxygenase-1 (HO-1) in response to infections of all kinds may be contributing to the morbidity and mortality associated with COVID-19, we searched PubMed for peer-reviewed literature on carbon monoxide and each of eleven abnormal blood tests, fourteen signs and symptoms, and five fatal complications of COVID-19 infection reported in a case series from a hospital in Wuhan, China: acute respiratory distress syndrome (ARDS), acute kidney injury, acute cardiac injury, arrhythmia, and shock. We found reports of acute exogenous CO poisoning causing all the same signs, symptoms and complications, and all the abnormal blood tests except D-dimer and procalcitonin. Our search also found endogenous HO-1 and CO levels correlated with these complications, independent of any inhaled CO exposure. In sharp contrast to the CO poisoning literature, most studies of endogenous CO interpret its close positive correlation with these acute conditions as protective, with some going so far as to recommend treating ARDS with inhaled CO. We conclude with new recommendations for testing endogenous CO poisoning in COVID-19 cases using devices approved by the US Food and Drug Administration that can distinguish CO coming from the lungs, arteries, veins, and average of all tissues, unlike current protocols for CO poisoning that only measure CO in arteries or veins but not both. Based on these findings, we appeal to clinicians to start testing CO levels in COVID-19 patients and to stop monitoring oxygen saturation with conventional pulse oximeters that overestimate oxygen saturation by the sum of carboxyhemoglobin and methemoglobin. We conclude by reviewing FDA-approved treatments that may help COVID-19 patients with endogenous CO poisoning.
These include zinc-based drugs that lower the rate of endogenous CO production by inhibiting HO-1, and drug-free devices and methods that reduce the total body burden of CO after exogenous CO poisoning.
Conclusions
We have shown that 14 signs and symptoms and 5 frequently fatal complications of COVID-19 infection reported in a representative series of hospitalized cases from Wuhan, China, are all also reported in the peer-reviewed literature on CO poisoning. All the complications are each also independently associated with increases in endogenous CO. These findings are consistent with the hypotheses that endogenous carbon monoxide is causing the signs, symptoms and complications of COVID-19 but they do not prove it, which will require appropriate testing of cases and controls. Fortunately, FDA-approved devices for non-invasive spot and continuous testing of CO levels in real time are already widely distributed among hospitals and fire departments.
We conclude that people with COVID-19 who have labs, signs, symptoms, and complications consistent with endogenous CO poisoning should be tested for this possibility with any device that can measure CO reproducibly in lungs, blood and tissues.
We also urge clinicians worldwide to stop relying on conventional pulse oximeters to monitor oxygen saturation since the display is always overestimated by unknown fractions of COHb and MetHb.
For people with abnormally high levels of CO in their lungs, blood, and/or tissues, we recommend treatments that either quickly lower the total body burden of CO without drugs, or which quickly reduce the rate of endogenous CO production, while boosting ventilation if needed with carbon dioxide mixtures. This should exclude mechanical ventilation, high-flow hyperoxygenation, and hyperbaric because all increase the level of CO in tissues.
Our approach will not cure COVID-19 infections but we predict it will reduce morbidity and mortality and eliminate the need for mechanical ventilators.
….
From Ray Peat:
“Not all the oxygen we consume is put to good use, and we sometimes produce exhalation of gases other than carbon dioxide and water vapor.
Under stressful conditions, people may exhale measurable amounts of pentane, ethane, isoprene, carbon monoxide, and other substances with potential toxicity.
In hyperventilation, so much carbon dioxide is lost in the breath that our tissue respiration is impaired, creating a partial ‘tissue suffocation.’
If cells consume oxygen without producing carbon dioxide generously, a situation analogous to hyperventilation/tissues suffocation exists.
Oxygen deprivation is one of the signals that stimulates the production of new red blood cells, and this involves the production of porphyrin, heme, and hemoglobin.
The elimination of heme by oxidation produces carbon monoxide, which can block the respiratory production of energy.”
"The exhaled breath is being used to diagnose inflammatory lung disease, since so many of the mediators of inflammation are volatile, but systemic diseases such as cancer and arthritis, and relatively minor stress can be detected by changes in the chemicals found in the breath. Polyunsaturated fats and their breakdown products-- aldehydes, prostaglandins, isoprostanes, hydrocarbons, and free radicals--and carbon monoxide, nitric oxide, nitrite, and hydrogen peroxide are increased in the breath by most stresses."
"The mitochondria are responsible for the efficient production of energy needed for the functioning of complex organisms, and especially for nerves. The enzyme in the mitochondria that reacts directly with oxygen, and that is often rate limiting, is cytochrome c oxidase.
This enzyme is dependent on the thyroid hormone and is inhibited by nitric oxide, carbon monoxide, estrogen, polyunsaturated fatty acids, serotonin, excess or free iron, ionizing radiation, and many toxins, including bacterial endotoxin.”
“The heme group (of hemoglobin and the respinitory enzymes, for example) is the iron-binding oily molecule that interacts with oxygen, and it is called a porphyrin.”
“The presence of porphyrin poisoning, with its associated free radical toxins, can lead to the activation of heme oxygenase, the enzyme which produces carbon monoxide, which I have discussed elsewhere as a cause of the respiratory defect that characterizes cancer. Both ammonia and porphyria have been implicated in the production of cancer.”
“Excess heme is destroyed by the enzyme heme oxygenase, which converts heme into biliverdin and carbon monoxide. Both of these factors have effects on the cell which are characteristic of cancer.”
“Any hypoxic tissue, including inflammations of any sort, will express the heme oxygenase enzyme, producing carbon monoxide.”
“This enzyme degrades the heme molecule, which is released from hemoglobin and other proteins in injured tissues, and which in the free state is toxic (Kumar and Bandyopadhyay, 2005). In degrading heme, this enzyme releases free iron atoms and biliverdin, as well as carbon monoxide. Although free iron atoms can cause harmful oxidation, biliverdin, and the bilirubin that's produced from it, can have beneficial antioxidant effects.”
“Carbon monoxide increases the formation of cortisol, by stimulating ACTH release from the pituitary.
The stress response is self-sustaining on several levels.
For example, stress increases the absorption of bacterial endotoxin from the intestine, which increases the estrogen level and synergizes with biliverdin and cortisol.
Biliverdin (F. Paradisi, 1975) activates betaglucuronidase, one of the main enzymes involved in the local release of estrogen.
In later stages, anemia and hemolysis are associated with CO and biliverdin production from the release of heme. (Anemia is seen in most patients with advanced cancer.)
Biliverdin, combined with estrogen and hypoxia, alters the cytoskeleton, producing chromosome imbalances, causing mutations and activating the "oncogenes."