RWilly
Member
- Joined
- Aug 30, 2018
- Messages
- 479
COVID-19 causes sepsis:
"Now that more scientific data are available on COVID-19, the Global Sepsis Alliance can more definitively state that COVID-19 does indeed cause sepsis. Sepsis is “a life-threatening organ dysfunction caused by a dysregulated host response to infection.” In the case of COVID-19, the effects on the respiratory system are well-known, with most people requiring hospital admission developing pneumonia of varying severity; however, virtually all other organ systems can be affected. This is consistent with a combination of direct viral invasion and sepsis."
Update: Can COVID-19 Cause Sepsis? Explaining the Relationship Between the Coronavirus Disease and Sepsis — Global Sepsis Alliance
Here's an excerpt on a 2018 article about sepsis. (Sure sounds like what we see in COVID):
"Furthermore, it still does not give an answer to the key question of why some patients (for instance, in cases of severe pneumonia or meningitis due to Streptococcus pneumoniae) react excessively in terms of hyper-inflammation and “cytokine storm” (see below) whereas others have no symptoms although the same microbe can be detected on their skin or upper airways 8. The “old” theory is that the latter persons are simply “resistant” (that is, their inflammatory response keeps the contamination under control). However, there are two phenomena which contradict this theory. First, if carriers without symptoms have such a strong resistance, why are they still carriers? Second, if these persons have such a successful “inflammatory response”, why is it not possible to demonstrate this with serum biomarkers?
In a landmark article, Weis et al. describe a biological pathway for how this may be declared 9: it was found that blood glucose levels influence the mechanisms of “tolerance” against infections. “Tolerance” (or “resilience”) is a form of “defense strategy against infection that preserves host homeostasis without exerting a direct negative impact on pathogens” 9. In other words, the host organism coexists with the microbes; of course, this may change if this tolerance is disturbed (“dysregulated”) by, for example, other infections, pregnancy, splenectomy (in case of Streptococcus pneumoniae), or older age. Interestingly, in many of those cases where this disease tolerance fails, the clinical symptoms of sepsis often exert much more dramatic courses than “classical” infections. These recent findings about dysregulation in the pathogenesis of sepsis perfectly fit the new definition (see next section). Finally, the option to differentiate between the individual “type of host response” may foster research to enable the practice of more personalized medicine in patients with sepsis as was suggested for other life-threatening diseases such as acute respiratory distress syndrome/"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6173111/
And it looks like more lactate is being produced in sepsis:
"Septic shock occurs when there is insufficient circulation to maintain adequate metabolism because of sepsis. Increased lactate production caused by anaerobic metabolism can reflect shock status. The number of elderly patients and bed-ridden patients with cardiovascular complications such as stroke or myocardial infarction is increasing. Since these patients are at risk of chronic kidney disease and volume overload, too rapid replacement of fluid to elevate BP may be harmful in septic shock. The new definition of septic shock can affect the treatment modality, and thus physicians must prepare for the new therapeutic guideline according to cellular metabolism and cardiovascular complications."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4958885/
Increased lactic acid is what they are seeing in COVID as well:
"Lactate dehydrogenase (LDH) has been associated with worse outcomes in patients with viral infections. In this pooled analysis of 9 published studies (n = 1532 COVID-19 patients), we evaluated the association between elevated LDH levels measured at earliest time point in hospitalization and disease outcomes in patients with COVID-19. Elevated LDH levels were associated with a ~6-fold increase in odds of developing severe disease and a ~16-fold increase in odds of mortality in patients with COVID-19. Larger studies are needed to confirm these findings."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7251362/
And as Ray Peat says, CO2 production inhibits lactic acid production, and sugar intake increases CO2 production:
But many of those hospitalized have diabetes and have difficulty with sugar. Too bad most people don't know about fructose and potassium:
"Now that more scientific data are available on COVID-19, the Global Sepsis Alliance can more definitively state that COVID-19 does indeed cause sepsis. Sepsis is “a life-threatening organ dysfunction caused by a dysregulated host response to infection.” In the case of COVID-19, the effects on the respiratory system are well-known, with most people requiring hospital admission developing pneumonia of varying severity; however, virtually all other organ systems can be affected. This is consistent with a combination of direct viral invasion and sepsis."
Update: Can COVID-19 Cause Sepsis? Explaining the Relationship Between the Coronavirus Disease and Sepsis — Global Sepsis Alliance
Here's an excerpt on a 2018 article about sepsis. (Sure sounds like what we see in COVID):
"Furthermore, it still does not give an answer to the key question of why some patients (for instance, in cases of severe pneumonia or meningitis due to Streptococcus pneumoniae) react excessively in terms of hyper-inflammation and “cytokine storm” (see below) whereas others have no symptoms although the same microbe can be detected on their skin or upper airways 8. The “old” theory is that the latter persons are simply “resistant” (that is, their inflammatory response keeps the contamination under control). However, there are two phenomena which contradict this theory. First, if carriers without symptoms have such a strong resistance, why are they still carriers? Second, if these persons have such a successful “inflammatory response”, why is it not possible to demonstrate this with serum biomarkers?
In a landmark article, Weis et al. describe a biological pathway for how this may be declared 9: it was found that blood glucose levels influence the mechanisms of “tolerance” against infections. “Tolerance” (or “resilience”) is a form of “defense strategy against infection that preserves host homeostasis without exerting a direct negative impact on pathogens” 9. In other words, the host organism coexists with the microbes; of course, this may change if this tolerance is disturbed (“dysregulated”) by, for example, other infections, pregnancy, splenectomy (in case of Streptococcus pneumoniae), or older age. Interestingly, in many of those cases where this disease tolerance fails, the clinical symptoms of sepsis often exert much more dramatic courses than “classical” infections. These recent findings about dysregulation in the pathogenesis of sepsis perfectly fit the new definition (see next section). Finally, the option to differentiate between the individual “type of host response” may foster research to enable the practice of more personalized medicine in patients with sepsis as was suggested for other life-threatening diseases such as acute respiratory distress syndrome/"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6173111/
And it looks like more lactate is being produced in sepsis:
"Septic shock occurs when there is insufficient circulation to maintain adequate metabolism because of sepsis. Increased lactate production caused by anaerobic metabolism can reflect shock status. The number of elderly patients and bed-ridden patients with cardiovascular complications such as stroke or myocardial infarction is increasing. Since these patients are at risk of chronic kidney disease and volume overload, too rapid replacement of fluid to elevate BP may be harmful in septic shock. The new definition of septic shock can affect the treatment modality, and thus physicians must prepare for the new therapeutic guideline according to cellular metabolism and cardiovascular complications."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4958885/
Increased lactic acid is what they are seeing in COVID as well:
"Lactate dehydrogenase (LDH) has been associated with worse outcomes in patients with viral infections. In this pooled analysis of 9 published studies (n = 1532 COVID-19 patients), we evaluated the association between elevated LDH levels measured at earliest time point in hospitalization and disease outcomes in patients with COVID-19. Elevated LDH levels were associated with a ~6-fold increase in odds of developing severe disease and a ~16-fold increase in odds of mortality in patients with COVID-19. Larger studies are needed to confirm these findings."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7251362/
And as Ray Peat says, CO2 production inhibits lactic acid production, and sugar intake increases CO2 production:
But many of those hospitalized have diabetes and have difficulty with sugar. Too bad most people don't know about fructose and potassium:
