Nelson Vergel
Founder, ExcelMale.com
I am hoping hydroxychloroquine works for prevention of infection or symptoms in these large placebo controlled studies. Some are using once per week dosing.
Coronavirus COVID-19 Update: Hydroxychloroquine and Other Treatments
- Thread starter Rock H. Johnson
- Start date
The death rate at hospital from coronavirus in US is well above 11%: just go to coronavirus tracker and calculate for US: 46.6K dead, 77.8K recovered, death rate = 46.6/(46.6 + 77.8) = 37% !
So where exactly these "smart medical professionals" got a non-treated group with a death rate of only 11%? The explanation is very simple - that group is SELF SELECTED - people with a light case of coronavirus chose not to take any drug for it.
The people in the hydroxychloroquine group are most probably patients in a more serious condition so they chose hydroxychloroquine as a treatment.
So they are comparing light cases with severe cases and claim the treatment drug killed the patients. This is an utmost medical stupidity - it's like they never took statistics. However this "study" is being wildly critisized on the preprint archive where it is "published".
So where exactly these "smart medical professionals" got a non-treated group with a death rate of only 11%? The explanation is very simple - that group is SELF SELECTED - people with a light case of coronavirus chose not to take any drug for it.
The people in the hydroxychloroquine group are most probably patients in a more serious condition so they chose hydroxychloroquine as a treatment.
So they are comparing light cases with severe cases and claim the treatment drug killed the patients. This is an utmost medical stupidity - it's like they never took statistics. However this "study" is being wildly critisized on the preprint archive where it is "published".
Nelson Vergel
Founder, ExcelMale.com
ACEI/ARBs linked with survival in hypertensive, Chinese COVID-19 patients
A study drawing from 1,128 hypertensive, Chinese patients with COVID-19 suggested that those on an ACEI or ARB had better 28-day survival.
www.mdedge.com
DragonBits
Well-Known Member
I think the true death rate is below 1%.
Death rate is determined by number infected / number dying.
There are more and more studies indicating many people have been infected and recovered without ever getting tested so they aren't in the statistics until we have wide spread antibody testing.
NY was the most recent state to have conducted a 3000 person study where they estimate 21.2% of NY City has had the virus and recovered, statewide is 13.9%.
If you included all those who never went to a doctor, never got tested while they had Covid, the death rate is much lower, which also makes intuitive sense.
New York antibody study estimates 13.9% of residents have had the coronavirus, Gov. Cuomo says
The state's mortality rates remains persistently high at about 7.4%. The antibody testing indicates the actual death rate may be far lower.
If you look at the death rate of only those put on a ventilator, it's more like an 80% death rate. If you look at those admitted to a hospital, and labeled "recovered" then you are probably right.
But recovered is a bogus number. Because ....the critira is so rigid for recovered.
Why have so few people officially recovered in the U.S.?
This is a dangerous virus, so the Centers for Disease Control and Prevention is being extremely careful when deciding what it means to recover from COVID-19. Both medical and testing criteria must be met before a person is officially declared recovered.
Medically, a person must be fever-free without fever-reducing medications for three consecutive days. They must show an improvement in their other symptoms, including reduced coughing and shortness of breath. And it must be at least seven full days since the symptoms began.
In addition to those requirements, the CDC guidelines say that a person must test negative for the coronavirus twice, with the tests taken at least 24 hours apart.
Here’s what determines who has recovered from coronavirus — and it includes two more tests
COVID-19 recovery is about more than just feeling better.
www.marketwatch.com
---------------------------------------------------------------
You can't get a test for covid unless you are admitted to a hospital, or meet rigid rules for a test, such as travel to china or exposure to a known proved Covid positive person, but they again because of hippa secrecy how do you know who has been tested?
This is in Illinois.
I am pretty familiar with this because I am 98% certain my wife had covid, but despite two virtual visits with two different doctors, they said it's quite likely she has covid, but can't write an order to get the test and without the order you can't get a test. She isn't sick enough, hasn't traveled, etc.
Now yesterday her company said one employee she worked closely with has tested positive, because this person was pregnant and admitted to a hospital. So she could probably get the test now, but it's been nearly 3 weeks from her first symptoms, so she now might test negative.
What surprised me, I either didn't get sick enough to bother me, or never got it despite sleeping in the same bed as her. AND my mother who is 93 also live with us, and she didn't seem to get sick. I had a runny nose for a few weeks, so maybe that was it, maybe not.
We will get the antibody test once it becomes more widely available.
BTW, I had worked 20 years doing statistical analysis in telecommunications ,before that I as a chemist, what is your background in stats?
Nelson Vergel
Founder, ExcelMale.com
Plea for multitargeted interventions for severe COVID-19
April 20 2020 The Lancet Inf Dis - Benjamin Jean Gaborit, Jean-François Bergmann, Cristina Mussini, Jose Ramon Arribas, Georg Behrens, Sharon Walmsley, Anton Pozniak, *François Raffi
Severe coronavirus disease 2019 (COVID-19) is not just a serious respiratory viral disease, as influenza is, but rather a systemic multiorgan viral invasion. It is frequently complicated by overwhelming immunological reactions, with overactivation of T cells, leading to acute respiratory distress syndrome and multiorgan failure, secondary to immunopathological processes. The viral load of severe acute respiratory syndrome coronavirus 2 is not correlated with worsening symptoms, but it is the host inflammatory response that is a major cause of lung damage and subsequent mortality. 1, 2
Hyper-inflammatory responses in patients with COVID-19 are associated with a cytokine storm that is characterised by an increase in proinflammatory cytokines, including tumour necrosis factor, interleukin (IL)-1β, IL-6, and other chemokines in serum.3, 4
Overwhelming secretion of cytokines causes severe lung damage, which manifests as extensive damage to pulmonary vascular endothelial cells and alveolar epithelial cells, as well as increased pulmonary vascular permeability, leading to pulmonary oedema and hyaline membrane formation.2, 3, 4
Most clinical trials to date have evaluated various strategies of antivirals, immunomodulators, host-targeted drugs, immune-based therapies, or immunosuppressive drugs, including steroids, IL-6 or IL-1 antagonists, and selinexor; all have assessed single drugs with a clinical endpoint using the WHO seven-point ordinal scale.5 Although some of these drugs might have clinically meaningful effects on viral burden or some of the immune-related signs, it is highly improbable that a single drug will be enough to control and improve the most severe forms of COVID-19. It is likely that both antivirals and blockage of inflammatory pathways are needed to optimise responses. For example, it would be relevant to understand the role of steroids in combination with or sequential to antiviral treatments. Without studying combinations, and their potential synergies or additive effects, potentially useful agents could be disregarded. Furthermore, in the absence of synergistic combinations, single drugs might cause more harm—for example, mass killing of the virus might enhance inflammatory responses. Because of the urgency of the current situation and, so far, an absence of clear evidence of a clinically meaningful effect of any monotherapy strategy, investigators should join their efforts in proposing, rather than adaptive or sequential studies of a single strategy, combined approaches through multifactorial designs. This approach will enable determination of the risks and benefits of combinations versus monotherapies. Such trials with multifactorial designs (eg, with randomisation first to antivirals and then to adjunctive immune-based therapy) are urgently needed and could provide more rapidly clinically meaningful results.
Furthermore, with improving knowledge of the various clinical presentations of COVID-19, better definitions of patient populations at highest risk of poor outcomes, based not only on clinical status but also on biomarkers (eg, C-reactive protein, D-dimer, ferritin, and IL-6), should be incorporated into inclusion criteria and stratifications.6 Finally, the optimal timing or sequence of administration of the components of therapy during a worsening COVID-19 disease course need to be explored. We call for collaboration between pharmaceutical companies, institutions, and policy makers to either allow individuals to be enrolled simultaneously in trials of different investigational drugs with distinct targets or to collaborate on trials that include study arms that investigate combination therapy.
April 20 2020 The Lancet Inf Dis - Benjamin Jean Gaborit, Jean-François Bergmann, Cristina Mussini, Jose Ramon Arribas, Georg Behrens, Sharon Walmsley, Anton Pozniak, *François Raffi
Severe coronavirus disease 2019 (COVID-19) is not just a serious respiratory viral disease, as influenza is, but rather a systemic multiorgan viral invasion. It is frequently complicated by overwhelming immunological reactions, with overactivation of T cells, leading to acute respiratory distress syndrome and multiorgan failure, secondary to immunopathological processes. The viral load of severe acute respiratory syndrome coronavirus 2 is not correlated with worsening symptoms, but it is the host inflammatory response that is a major cause of lung damage and subsequent mortality. 1, 2
Hyper-inflammatory responses in patients with COVID-19 are associated with a cytokine storm that is characterised by an increase in proinflammatory cytokines, including tumour necrosis factor, interleukin (IL)-1β, IL-6, and other chemokines in serum.3, 4
Overwhelming secretion of cytokines causes severe lung damage, which manifests as extensive damage to pulmonary vascular endothelial cells and alveolar epithelial cells, as well as increased pulmonary vascular permeability, leading to pulmonary oedema and hyaline membrane formation.2, 3, 4
Most clinical trials to date have evaluated various strategies of antivirals, immunomodulators, host-targeted drugs, immune-based therapies, or immunosuppressive drugs, including steroids, IL-6 or IL-1 antagonists, and selinexor; all have assessed single drugs with a clinical endpoint using the WHO seven-point ordinal scale.5 Although some of these drugs might have clinically meaningful effects on viral burden or some of the immune-related signs, it is highly improbable that a single drug will be enough to control and improve the most severe forms of COVID-19. It is likely that both antivirals and blockage of inflammatory pathways are needed to optimise responses. For example, it would be relevant to understand the role of steroids in combination with or sequential to antiviral treatments. Without studying combinations, and their potential synergies or additive effects, potentially useful agents could be disregarded. Furthermore, in the absence of synergistic combinations, single drugs might cause more harm—for example, mass killing of the virus might enhance inflammatory responses. Because of the urgency of the current situation and, so far, an absence of clear evidence of a clinically meaningful effect of any monotherapy strategy, investigators should join their efforts in proposing, rather than adaptive or sequential studies of a single strategy, combined approaches through multifactorial designs. This approach will enable determination of the risks and benefits of combinations versus monotherapies. Such trials with multifactorial designs (eg, with randomisation first to antivirals and then to adjunctive immune-based therapy) are urgently needed and could provide more rapidly clinically meaningful results.
Furthermore, with improving knowledge of the various clinical presentations of COVID-19, better definitions of patient populations at highest risk of poor outcomes, based not only on clinical status but also on biomarkers (eg, C-reactive protein, D-dimer, ferritin, and IL-6), should be incorporated into inclusion criteria and stratifications.6 Finally, the optimal timing or sequence of administration of the components of therapy during a worsening COVID-19 disease course need to be explored. We call for collaboration between pharmaceutical companies, institutions, and policy makers to either allow individuals to be enrolled simultaneously in trials of different investigational drugs with distinct targets or to collaborate on trials that include study arms that investigate combination therapy.
xqfq
Active Member
I am most excited about the trials of ARBs such as Losartan. 9 clinical trials of these drugs are now starting. Here is a writeup on one at University of Minnesota: University of Minnesota Launches COVID-19 Clinical Trials of Blood Pressure Drug Losartan
Mechanism described a bit here:
This does not mean someone who is on an ARB is immune. If someone is hypertensive and takes an ARB, then they are more or less at 'baseline' with respect to total number of unblocked AT1 receptors. I speculate they may require an additional ARB (e.g. if losartan proves effective, then add losartan twice a day), with twice-daily dosing.
It's possible this may not work, but I give it a 70% chance of working to stop the severity of the disease. The anti-viral approaches such as hydroxychloroquine and others would, I suspect, require treatment very early in the infection to show efficacy. For most people that is not possible. This is especially true of drugs like Remdesivir which require IV administration.
Convalescent plasma almost certainly works. The barrier to this treatment is logistics and competence of organizations, which is lacking in the US. Mass testing, including antibody testing, and plasma collection efforts should have started a month ago, but are still in very early stages. We can reduce the likelihood of death significantly by ensuring we have enough plasma on hand. If the majority of people (>= 80%) do not require hospitalization, those people can all donate plasma. Then we can give the plasma to the 20% requiring hospitalization. A previously infected person can donate plasma at least once every 28 days and likely more often than that. A given donation can save the lives of 2-4 people. If you do the math, it's clear that this method, if scaled up, can significantly reduce the risk of death if enough plasma is collected and deployed quickly.
Plasma can also be given prophylactically to healthcare workers and will likely be protective for a number of weeks. Less plasma may be required in these cases, too.
Mechanism described a bit here:
This does not mean someone who is on an ARB is immune. If someone is hypertensive and takes an ARB, then they are more or less at 'baseline' with respect to total number of unblocked AT1 receptors. I speculate they may require an additional ARB (e.g. if losartan proves effective, then add losartan twice a day), with twice-daily dosing.
It's possible this may not work, but I give it a 70% chance of working to stop the severity of the disease. The anti-viral approaches such as hydroxychloroquine and others would, I suspect, require treatment very early in the infection to show efficacy. For most people that is not possible. This is especially true of drugs like Remdesivir which require IV administration.
Convalescent plasma almost certainly works. The barrier to this treatment is logistics and competence of organizations, which is lacking in the US. Mass testing, including antibody testing, and plasma collection efforts should have started a month ago, but are still in very early stages. We can reduce the likelihood of death significantly by ensuring we have enough plasma on hand. If the majority of people (>= 80%) do not require hospitalization, those people can all donate plasma. Then we can give the plasma to the 20% requiring hospitalization. A previously infected person can donate plasma at least once every 28 days and likely more often than that. A given donation can save the lives of 2-4 people. If you do the math, it's clear that this method, if scaled up, can significantly reduce the risk of death if enough plasma is collected and deployed quickly.
Plasma can also be given prophylactically to healthcare workers and will likely be protective for a number of weeks. Less plasma may be required in these cases, too.
Last edited:
Nelson Vergel
Founder, ExcelMale.com
Coronavirus Pandemic Update 60: Hydroxychloroquine Update; NYC Data; How Widespread is COVID-19?
The baseline characteristics were very different in the different groups in the VA hydroxychloroquine study that showed higher mortality in the hydroxycholoroquine + azithromycin arm.
Here are the hydroxychloroquine placebo-controlled studies being done right now in the US:
Search of: hydroxychloroquine, placebo | COVID | United States - List Results - ClinicalTrials.gov
The baseline characteristics were very different in the different groups in the VA hydroxychloroquine study that showed higher mortality in the hydroxycholoroquine + azithromycin arm.
Here are the hydroxychloroquine placebo-controlled studies being done right now in the US:
Search of: hydroxychloroquine, placebo | COVID | United States - List Results - ClinicalTrials.gov
Vince
Super Moderator
Researchers studying a common heartburn drug as treatment for Covid-19
Hospitals in New York are giving Covid-19 patients the heartburn medicine famotidine to see if it helps fight the virus, according to the doctor who initiated the trial.
amp-cnn-com.cdn.ampproject.org
Nelson Vergel
Founder, ExcelMale.com
Closely watched arthritis drug disappoints as a Covid-19 treatment, studies show
Statnews.com. April 27, 2020
An arthritis drug that was seen as a promising treatment for some Covid-19 patients delivered disappointing results in clinical studies, its makers, the drug firms Regeneron and Sanofi, said Monday.
The result could have an impact not only for their treatment, Kevzara, but also for a similar drug from Roche, Actemra, that is being used off-label in many hospitals. It also may lower the odds that other repurposed medicines used against autoimmune diseases like rheumatoid arthritis will benefit Covid-19 patients.
“When you try everything under the kitchen sink, most of the time it’s not going to deliver the results that you want, no matter what the small 20-patient or 30-patient studies say,” said George D. Yancopoulos, Regeneron’s co-founder and chief scientific officer.
Kevzara was not expected to directly block the coronavirus, SARS-CoV-2, that is causing a global pandemic. But it was hoped that the drug would help ease the immune system’s overreaction to the virus — a “cytokine storm” that causes inflammation and fluid buildup in the lungs of many of the sickest patients — potentially helping to keep patients off of ventilators or saving their lives. Early data from a 21-patient study in China using Actemra had appeared promising.
But there was no benefit in the group of patients most like those in that Chinese study: those termed “severe,” meaning they needed oxygen, but not with air pressure that is faster than normal breathing and certainly not those on ventilators. A 276-patient study in this group was stopped because there was no chance it would succeed.
There is still a glimmer of a positive result in sicker patients, whom the companies call “critical.” These patients need what is called high-flow oxygen, or are on ventilators. In that group, an extra 1 in 10 patients who received high-dose Kevzara was discharged from the hospital compared to those who received placebo. A larger study is continuing in the hopes of proving this benefit.
“It’s not, unfortunately, black and white that’s going to cure everybody,” said Yancopoulos. But he said that such a difference, if confirmed, would still be important. For that 1 person in 10, “it’s all the difference in the world.”
The Kevzara trial had been designed to be run in two stages: a Phase 2 study in which researchers would try to understand which measures of the disease were important, and a larger Phase 3 study in which they would try to confirm those results with the rigor necessary to achieve regulatory approval. In both stages, patients were randomly assigned to receive one of three options: a placebo; a 200-milligram dose of Kevzara; or a 400-milligram dose of Kevzara. Going forward, the patients in Phase 3 will receive either a placebo or the 400-mg. dose of Kevzara.
When it came time to analyze the Phase 2 results, there had been no apparent benefit for patients taking the drug when the severe and critical groups were combined. But in the severe group, it appeared that patients who received Kevzara were actually doing worse. This led a panel of outside experts who were looking at the data for the larger Phase 3 study to look at the severe group. They found that patients were not, in fact, being harmed by Kevzara. But there was also no hope the study would show a benefit for the severe patients.
Part of the reason: The results in the Kevzara arms were similar to those seen in the 21-patient study that had been published in China, which had lacked a control group of patients who had received a placebo or standard treatment. But the patients in the new study’s placebo arm did as well.
Overall, all of these patients, though hospitalized, did better than researchers had expected. In the severe group, 80% of patients were discharged from the hospital, 10% died, and 10% are still hospitalized.
In the critical group, the results were more positive, but still subtle. In the placebo group, 55% of 77 patients died or were on a ventilator; this compared to 46% of the 94 who received 200 mg. of Kevzara, and 32% of the 88 who received 400 mg. of Kevzara. Similarly, 41% of the placebo patients were discharged from the hospital, compared to 39% in the 200-mg. group and 53% in the 400-mg. group. Those differences would be positive if shown in a larger study, but in the current study they could be the result of the play of chance.
Regeneron and Sanofi said that they would share the results with the data monitoring committee of a study of Kevzara they are running outside the U.S. Roche is conducting its own study of Actemra in Covid-19 patients.
Yancopoulos said that the experience with Kevzara holds a lesson for other drugs being tested against Covid-19: Data from large, randomized trials where a defined group of patients are assigned to get an experimental drug or the best treatment available are necessary to know what works and what doesn’t.
“It shows how hard it is,” he said. “It shows that a lot of times when people think they’re seeing things in desperate situations, when they’re just trying whatever they can, that a lot of times that leads to misleading hypotheses and misleading results. Which is why it’s so important, so crucial, to get this sort of data to really guide physicians and patients in terms of which drugs are really working, in what setting, and for what patients.”
Yancopoulos expressed hope regarding Regeneron’s other effort at developing a Covid-19 drug: creating synthetic antibodies against the virus, an approach that had positive results against the Ebola virus. Those studies, he said, are expected to begin in June.
Statnews.com. April 27, 2020
An arthritis drug that was seen as a promising treatment for some Covid-19 patients delivered disappointing results in clinical studies, its makers, the drug firms Regeneron and Sanofi, said Monday.
The result could have an impact not only for their treatment, Kevzara, but also for a similar drug from Roche, Actemra, that is being used off-label in many hospitals. It also may lower the odds that other repurposed medicines used against autoimmune diseases like rheumatoid arthritis will benefit Covid-19 patients.
“When you try everything under the kitchen sink, most of the time it’s not going to deliver the results that you want, no matter what the small 20-patient or 30-patient studies say,” said George D. Yancopoulos, Regeneron’s co-founder and chief scientific officer.
Kevzara was not expected to directly block the coronavirus, SARS-CoV-2, that is causing a global pandemic. But it was hoped that the drug would help ease the immune system’s overreaction to the virus — a “cytokine storm” that causes inflammation and fluid buildup in the lungs of many of the sickest patients — potentially helping to keep patients off of ventilators or saving their lives. Early data from a 21-patient study in China using Actemra had appeared promising.
But there was no benefit in the group of patients most like those in that Chinese study: those termed “severe,” meaning they needed oxygen, but not with air pressure that is faster than normal breathing and certainly not those on ventilators. A 276-patient study in this group was stopped because there was no chance it would succeed.
There is still a glimmer of a positive result in sicker patients, whom the companies call “critical.” These patients need what is called high-flow oxygen, or are on ventilators. In that group, an extra 1 in 10 patients who received high-dose Kevzara was discharged from the hospital compared to those who received placebo. A larger study is continuing in the hopes of proving this benefit.
“It’s not, unfortunately, black and white that’s going to cure everybody,” said Yancopoulos. But he said that such a difference, if confirmed, would still be important. For that 1 person in 10, “it’s all the difference in the world.”
The Kevzara trial had been designed to be run in two stages: a Phase 2 study in which researchers would try to understand which measures of the disease were important, and a larger Phase 3 study in which they would try to confirm those results with the rigor necessary to achieve regulatory approval. In both stages, patients were randomly assigned to receive one of three options: a placebo; a 200-milligram dose of Kevzara; or a 400-milligram dose of Kevzara. Going forward, the patients in Phase 3 will receive either a placebo or the 400-mg. dose of Kevzara.
When it came time to analyze the Phase 2 results, there had been no apparent benefit for patients taking the drug when the severe and critical groups were combined. But in the severe group, it appeared that patients who received Kevzara were actually doing worse. This led a panel of outside experts who were looking at the data for the larger Phase 3 study to look at the severe group. They found that patients were not, in fact, being harmed by Kevzara. But there was also no hope the study would show a benefit for the severe patients.
Part of the reason: The results in the Kevzara arms were similar to those seen in the 21-patient study that had been published in China, which had lacked a control group of patients who had received a placebo or standard treatment. But the patients in the new study’s placebo arm did as well.
Overall, all of these patients, though hospitalized, did better than researchers had expected. In the severe group, 80% of patients were discharged from the hospital, 10% died, and 10% are still hospitalized.
In the critical group, the results were more positive, but still subtle. In the placebo group, 55% of 77 patients died or were on a ventilator; this compared to 46% of the 94 who received 200 mg. of Kevzara, and 32% of the 88 who received 400 mg. of Kevzara. Similarly, 41% of the placebo patients were discharged from the hospital, compared to 39% in the 200-mg. group and 53% in the 400-mg. group. Those differences would be positive if shown in a larger study, but in the current study they could be the result of the play of chance.
Regeneron and Sanofi said that they would share the results with the data monitoring committee of a study of Kevzara they are running outside the U.S. Roche is conducting its own study of Actemra in Covid-19 patients.
Yancopoulos said that the experience with Kevzara holds a lesson for other drugs being tested against Covid-19: Data from large, randomized trials where a defined group of patients are assigned to get an experimental drug or the best treatment available are necessary to know what works and what doesn’t.
“It shows how hard it is,” he said. “It shows that a lot of times when people think they’re seeing things in desperate situations, when they’re just trying whatever they can, that a lot of times that leads to misleading hypotheses and misleading results. Which is why it’s so important, so crucial, to get this sort of data to really guide physicians and patients in terms of which drugs are really working, in what setting, and for what patients.”
Yancopoulos expressed hope regarding Regeneron’s other effort at developing a Covid-19 drug: creating synthetic antibodies against the virus, an approach that had positive results against the Ebola virus. Those studies, he said, are expected to begin in June.
Can Estrogen and Other Sex Hormones Help Men Survive Covid-19?
Last week, doctors on Long Island in New York started treating Covid-19 patients with estrogen in an effort to increase their immune systems, and next week, physicians in Los Angeles will start treating male patients with another hormone that is predominantly found in women, progesterone, which has anti-inflammatory properties and can potentially prevent harmful overreactions of the immune system.
Last week, doctors on Long Island in New York started treating Covid-19 patients with estrogen in an effort to increase their immune systems, and next week, physicians in Los Angeles will start treating male patients with another hormone that is predominantly found in women, progesterone, which has anti-inflammatory properties and can potentially prevent harmful overreactions of the immune system.
DragonBits
Well-Known Member
We do seem to be in a free fire zone, try whatever we have in the drug cabinet, the kitchen sink approach.
I haven’t seen any data that differentiates between older and younger females, as older female have much less estrogen.
But I do believe estrogen (and or progesterone) does enhance the immune system, based on my own personal experience.
After stating TRT this time, I became allergic to penicillin type drugs and several glaucoma eye drops. The immune system is involved in allergies. It seems like it was because my E2 went up from below 5 (unmeasurable) to much higher, 15-40, (it varies quite a bit). I also tied exogenous progesterone, mostly to see if it helped sleep. For a while, I believe I had too much progesterone because it was making me dizzy at times. I measured progesterone, it was 0.5 ng/ml, the top of the range for men, who knows how high it might have gone, I only measured twice and kept lowing the dose.
That said, it probably takes longer than a few weeks for higher estrogen / ? to change the immune system, and that might not be the only reason women have a better immune system.
It could be likely that there are two phases, one positive, one negative, the immune system gets involved, stopping the spread to the lungs and other organs, but once the viruses gets too prevalent, there is the possibility of an overreaction.
And not to put too fine a point on it, they are also trying immunosuppression drugs because a cytokine storm”, which is an over-reaction of the immune system and kills quickly.
THE SCIENTIFIC REASON WHY MEN MAY RECOVER FROM FLU QUICKER THAN WOMEN
“Man flu”, a term that refers to the concept of men exaggerating their symptoms when feeling under the weather, is supposedly a real phenomenon.
While research has claimed that a number of men do in fact have weaker immune systems than was previously supposed, a new study has discovered that when afflicted with influenza, there may be scientific reason why men recover at a faster rate than women.
Researchers from Johns Hopkins Bloomberg School of Public Health decided to investigate the various effects that influenza can have on men and women.
Amphiregulin is a growth factor that has been found to play a role in tissue repair and development.
The increased production of amphiregulin in the male mice and male human cells is believed to have enabled a faster recovery time from the influenza strain, as the male mice who produced less of the growth factor were found to have similar recovery times to the female mice.
“The novel finding here is that females also have slower tissue-repair during recovery, due to relatively low production of amphiregulin,” said lead author Sabra Klein, PhD, who works as an associate professor at Bloomberg School.
The scientific reason why men may recover from flu quicker than women
Women are more likely to suffer serious symptoms from influenza, a study has claimed
www.independent.co.uk
It's an understatement to say, it's complicated.
DragonBits
Well-Known Member
Study Links Low Vitamin K Levels to Severity in COVID-19 Outcomes
Vitamin K, is generally accepted as an inhibitor of vascular calcification, and vitamin K deficiencies are linked to "high-risk" comorbidities.
In a study published in Preprints.org, researchers examined the link between outcomes in COVID-19 patients and their vitamin K status. Patients with vitamin K deficiencies had less favorable outcomes compared to patients with better vitamin K status and other healthy controls, based on the results of comparing 123 patients with 184 healthy controls.
The study was conducted by researchers from the Netherlands-based Canisius-Wilhelmina Hospital, Maastricht University Medical Center, and the Cardiovascular Research Institute Maastricht (CARIM).
Vitamin K status was determined by the amount of inactive vitamin K-dependent protein, MGP. Research has shown that vitamin K2 activates vitamin K-dependent proteins, which are beneficial to cardiovascular and bone health.
“This study presents an amazing finding,” Prof. Leon Schurgers, Professor of Biochemistry of Vascular Calcification and Vice Chair of Biochemistry at the Cardiovascular Research Institute Maastricht, and co-author of the study, said. “While we do not suggest that vitamin K2 is a treatment for COVID-19, this study illustrates that a poor vitamin K status- deduced from low dp-ucMGP levels- is linked to poor prognosis. Thus, hypothesizing that improving vitamin K2 status is linked to better health outcomes including cardiovascular, and perhaps even lung health.”
While COVID-19 is predominantly known for the presentation of severe acute respiratory syndrome, it also may progress beyond the lungs. Incidences of coagulopathy, a condition in which the blood’s ability to coagulate is impaired, and thromboembolism, the obstruction of a blood vessel by a clot that has become dislodged from another site in circulation, have been observed in COVID-19 cases. Another factor researchers took into account was a previous finding that in COPD patients, the body uses vitamin K stores at an accelerated rate, which was highlighted as a potential reason for vitamin K deficiency in patients with severe COVID-19.
Vitamin K status was evaluated in 123 patients, and measurements showed that du-ucMGP levels were lower in COVID-19 patients compared to controls (signifying low levels of vitamin K), and that dp-ucMGP levels were lower in patients with unfavorable outcomes compared to those whose disease was less severe, suggesting a potential link between vitamin K deficiency and disease severity. An important variable, researchers acknowledged, was the link between vitamin K deficiencies and comorbidities such as heart disease, hypertension, and type 2 diabetes, all of which are known to place COVID-19 patients at a greater risk of developing severe or fatal cases of the disease.
MGP is generally accepted as an inhibitor of vascular calcification, and, according to this study, there are scientific leads suggesting that MGP plays a role in the pathogenesis of lung fibrosis.
Researchers concluded that this study warrants an investigation into what effects, if any, administering vitamin K to current COVID-19 patients might have on disease progression and outcomes.
“It might be tempting to speculate that vitamin K administration has an improving effect on vitamin K status in severe COVID-19 patients; however, this has never been studied in this patient group,” they wrote. “Additionally, whether improving vitamin K status would correlate with better prognosis in SARS-CoV-2-infected individuals has to be tested. Preliminary evidence was provided suggesting a potential mechanistic link between reduced vitamin K status and accelerated tissue degradation. An intervention trial is now needed to assess whether vitamin K administration improves outcome in patients with COVID-19.”
Vitamin K, is generally accepted as an inhibitor of vascular calcification, and vitamin K deficiencies are linked to "high-risk" comorbidities.
In a study published in Preprints.org, researchers examined the link between outcomes in COVID-19 patients and their vitamin K status. Patients with vitamin K deficiencies had less favorable outcomes compared to patients with better vitamin K status and other healthy controls, based on the results of comparing 123 patients with 184 healthy controls.
The study was conducted by researchers from the Netherlands-based Canisius-Wilhelmina Hospital, Maastricht University Medical Center, and the Cardiovascular Research Institute Maastricht (CARIM).
Vitamin K status was determined by the amount of inactive vitamin K-dependent protein, MGP. Research has shown that vitamin K2 activates vitamin K-dependent proteins, which are beneficial to cardiovascular and bone health.
“This study presents an amazing finding,” Prof. Leon Schurgers, Professor of Biochemistry of Vascular Calcification and Vice Chair of Biochemistry at the Cardiovascular Research Institute Maastricht, and co-author of the study, said. “While we do not suggest that vitamin K2 is a treatment for COVID-19, this study illustrates that a poor vitamin K status- deduced from low dp-ucMGP levels- is linked to poor prognosis. Thus, hypothesizing that improving vitamin K2 status is linked to better health outcomes including cardiovascular, and perhaps even lung health.”
While COVID-19 is predominantly known for the presentation of severe acute respiratory syndrome, it also may progress beyond the lungs. Incidences of coagulopathy, a condition in which the blood’s ability to coagulate is impaired, and thromboembolism, the obstruction of a blood vessel by a clot that has become dislodged from another site in circulation, have been observed in COVID-19 cases. Another factor researchers took into account was a previous finding that in COPD patients, the body uses vitamin K stores at an accelerated rate, which was highlighted as a potential reason for vitamin K deficiency in patients with severe COVID-19.
Vitamin K status was evaluated in 123 patients, and measurements showed that du-ucMGP levels were lower in COVID-19 patients compared to controls (signifying low levels of vitamin K), and that dp-ucMGP levels were lower in patients with unfavorable outcomes compared to those whose disease was less severe, suggesting a potential link between vitamin K deficiency and disease severity. An important variable, researchers acknowledged, was the link between vitamin K deficiencies and comorbidities such as heart disease, hypertension, and type 2 diabetes, all of which are known to place COVID-19 patients at a greater risk of developing severe or fatal cases of the disease.
MGP is generally accepted as an inhibitor of vascular calcification, and, according to this study, there are scientific leads suggesting that MGP plays a role in the pathogenesis of lung fibrosis.
Researchers concluded that this study warrants an investigation into what effects, if any, administering vitamin K to current COVID-19 patients might have on disease progression and outcomes.
“It might be tempting to speculate that vitamin K administration has an improving effect on vitamin K status in severe COVID-19 patients; however, this has never been studied in this patient group,” they wrote. “Additionally, whether improving vitamin K status would correlate with better prognosis in SARS-CoV-2-infected individuals has to be tested. Preliminary evidence was provided suggesting a potential mechanistic link between reduced vitamin K status and accelerated tissue degradation. An intervention trial is now needed to assess whether vitamin K administration improves outcome in patients with COVID-19.”
Study Links Low Vitamin K Levels To Severity In COVID-19 Outcomes
Vitamin K, is generally accepted as an inhibitor of vascular calcification, and vitamin K deficiencies are linked to
www.nutraceuticalsworld.com
Nelson Vergel
Founder, ExcelMale.com
President Trump is taking one tab of hydroxychloroquine and zinc per day.
Wow. If you watch Fox News at night, you will hear from doctors all over the world successfully using hydroxy and zinc, even severe cases. "Every patient I've prescribed it to has been very, very ill and within 8 to 12 hours, they were basically symptom-free," said Los Angeles doctor Dr...
www.excelmale.com
Nelson Vergel
Founder, ExcelMale.com
Bad news. The study I was waiting for.
www.reuters.com
Malaria drug touted by Trump fails to prevent COVID-19 in high profile study
The malaria drug promoted by U.S. President Donald Trump as a treatment for COVID-19 was ineffective in preventing infection in people exposed to the coronavirus, according to a widely anticipated clinical trial released on Wednesday.
www.reuters.com
Nelson Vergel
Founder, ExcelMale.com
The story continues...
The WHO is resuming the hydroxychloroquine arm of the large Solidarity Trial. (Bloomberg)
And Sanofi is reviewing whether to resume recruiting COVID-19 patients for two hydroxychloroquine trials. (Reuters)
President Trump took 2 weeks of hydroxychloroquine with no effects on his ECG, White House physician Sean Conley confirmed in a report. (Reuters)
The WHO is resuming the hydroxychloroquine arm of the large Solidarity Trial. (Bloomberg)
And Sanofi is reviewing whether to resume recruiting COVID-19 patients for two hydroxychloroquine trials. (Reuters)
President Trump took 2 weeks of hydroxychloroquine with no effects on his ECG, White House physician Sean Conley confirmed in a report. (Reuters)
This pandemic just illustrates how unreliable medical studies are. "Conclusions" change every month to the exact opposite of before.
Hydroxychloroquine is known to be safe in the regular doses used by arthritis patients but they made everything possible to vilify it and it had to take the president himself to demonstrate safety.
Hydroxychloroquine is known to be safe in the regular doses used by arthritis patients but they made everything possible to vilify it and it had to take the president himself to demonstrate safety.
DragonBits
Well-Known Member
With covid, the drug was meant to be taken prophylactically by healthy people help prevent or reduce symptoms. Big difference between that and the small number of people who take if for things like lupus/malaria. Taking it for covid would have meant 10s of millions of people taking it if it worked, increasing the odds of dangerous side effects.
One guy taking this for two weeks means nothing, and I agree, it probably not going to hurt you, but does it help with Covid?
That is the key question.
And why did Trump stop taking it?
Yeah he heroically took it to prove it was safe. Jesus fuck how are you so stupid
That’s where you should stop reading
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