🚨💉MYOCARDITIS: Men vs Women X Exercise Intensity and Duration, and Myocarditis Frequency and Intensity involving mRNA COVID Injections Expanded Summary (this should be obvious by now):
Dr. Malone (how's it going?) has made statements that people who received the mRNA injections (I am paraphrasing) have subclinical damage to their hearts.
I want to expand on that please.
🚨💉Too long didn't read: mRNA COVID injections may cause subclinical myocarditis and full myocarditis (and worse) according to some doctors. This is due to inflammation, involving the LNP (lipids causing inflammation, DNA pieces and spike causing inflammation)--the immune system attacks the heart as part of this process. When we exercise, our immune system actually attacks the heart for a time! Women have some protective effects, such as estrogen and a difference in immune system activity, during working out. Women suffer less frequency and intensity of myocarditis due to estrogen effects, but a few other markers regarding immune system specifics.
In a nutshell, the heart gets inflamed at a level that is not noticeable after mRNA covid injections. Then, if you work out afterwards, a natural part of men and women working out, is the immune system inflaming the heart. Depending on the severity of inflammation, myocarditis (and worse), could occur.
Signs and symptoms of myocarditis during/after running in those who have received mRNA COVID injections, is probably due, to the immune system causing inflammation to the heart muscle because when we run, depending on if male or female, intensity and duration, different parts of our immune system become active, and cytokines come into the heart muscle, when running! If the heart muscle already has subclinical damage (that was due to different types of immune system effects--this has already been explained in all of these threads--cGAS STING activated by spike protein and DNA plasmid pieces and the lipids with macrophages [mononuclear phagocyte system]) then when we go for a run, our immune system gets activated (again) and inflames our heart. If we already have damage, this could lead to myocarditis, or worse.
(always see your doctor for medical advice. This is not medical advice. Not meant to treat, DX, or RX)
A bit longer summary (before the explanations):
Exercise-induced inflammation of the heart can exacerbate subclinical myocarditis, especially in individuals who experienced inflammation due to COVID mRNA injections.
(cGAS sting pathway is engaged in the heart if LNP entered with spike protein and pieces of DNA plasmid activating the cGAs STING pathway, that would activate the immune system, which would come into the area, and inflame the heart muscle. If the molar ratio of positively charged lipids to negatively charged nucleic acids like RNA and DNA is 10:1, this would make it EASIER for the LNP to enter the cardiomyocyte and "transfect it" compared to other ratios such as 20:1).
🚨💉High-intensity exercise poses a greater risk, as it triggers significant increases in pro-inflammatory markers like cytokines (e.g., IL-6, TNF-α) and white blood cells (WBCs), potentially leading to myocarditis exacerbation, acute cardiac events, or even sudden death. Men, who typically exhibit stronger inflammatory responses, may be at higher risk compared to women. Moderate exercise, on the other hand, induces a more balanced inflammatory response and is generally safer for individuals with subclinical myocarditis. Monitoring inflammatory markers and tailoring exercise recommendations based on gender and intensity can help mitigate risks and ensure safer exercise regimens.
So the heart is already in a state of subclinical inflammation, meaning the person is not showing signs, or might not realize or feel that anything is wrong, even though, they have had a COVID "vaccine" that was full of DNA pieces, lipids that inflame, and spike protein. All of these things are inflammatory, and our macrophage system does not like clearing these things out, and that in itself can become damaged with repeated injections of lipids (mps system damage).
So when we run, our immune system inflames the heart for a time--this is something that happens. But if we already have heart damage, and do not know it, then when we run, it can cause myocarditis.
Full breakdown:
Engaging in exercise, especially high-intensity exercise, can significantly impact those with subclinical myocarditis due to the following mechanisms:
1. Exercise induces the release of cytokines such as IL-6, TNF-α, and IL-1β. In people with subclinical myocarditis, this additional inflammatory load can aggravate heart muscle inflammation.
2. While IL-10 and other anti-inflammatory cytokines also increase, they may not sufficiently counterbalance the pro-inflammatory effects during intense exercise.
3.White blood cells increase (leukocytes).
Intense exercise leads to an increase in white blood cells: neutrophils and monocytes, which infiltrate the heart tissue and exacerbate inflammation in myocarditis.
4. CK and CRP: Markers of muscle damage and systemic inflammation, respectively, increase with exercise intensity. Elevated CK indicates muscle breakdown, which can parallel damage in cardiac muscle during myocarditis.
(CK stands for creatine kinase, an enzyme found predominantly in the heart, brain, and skeletal muscles. Elevated levels of CK in the blood can indicate muscle damage or stress, including damage to the heart muscle.
CRP stands for C-reactive protein, an acute-phase protein produced by the liver in response to inflammation. Elevated levels of CRP in the blood can indicate inflammation in the body, which can be caused by various factors, including infections, tissue injury, or chronic inflammatory conditions.)
5. Sex Class Differences
Men vs. Women
A. Inflammatory Responses
Men exhibit higher baseline and exercise-induced increases in cytokines such as IL-6 compared to women, which can make men more susceptible to exacerbation of subclinical myocarditis.
B. Myocarditis Prevalence
Men are more frequently diagnosed with myocarditis, potentially due to their more pronounced inflammatory response to physical stressors like exercise.
Exercise Intensity and Risk
Moderate Exercise
Moderate exercise tends to induce a balanced inflammatory response, with transient increases in cytokines and leukocytes returning to baseline relatively quickly.
Intense Exercise
High-intensity exercise results in significant and sustained increases in pro-inflammatory markers, potentially overwhelming the heart's capacity to manage inflammation in subclinical myocarditis.
This can lead to:
Myocarditis Exacerbation
Intensified inflammation can progress subclinical myocarditis to a more severe form, increasing the risk of complications.
6. Acute Cardiac Events
Elevated cytokine levels and WBC counts can precipitate arrhythmias or even myocardial infarction (heart attack).
7. Sudden Death
In severe cases, the acute inflammatory response combined with pre-existing myocardial inflammation can lead to catastrophic outcomes such as sudden cardiac death.
(extra data and sources):
Women's Immune Responses
Estrogen's Role: Estrogen enhances the production of anti-inflammatory cytokines like IL-10 and IL-1ra, while moderating the levels of pro-inflammatory cytokines like IL-1β and IL-6. This hormonal influence helps women to manage exercise-induced inflammation better, reducing the risk of myocarditis.
Cytokine Regulation
Women generally exhibit better regulation of IL-6 and IL-10 post-exercise, promoting an anti-inflammatory environment conducive to recovery and protection against myocarditis.
Men's Immune Responses
Higher Pro-inflammatory Tendency: Men tend to have higher baseline levels of pro-inflammatory cytokines and a less robust regulatory mechanism for anti-inflammatory cytokines like IL-10. This can lead to prolonged inflammation post-exercise, increasing the risk of myocarditis.
IL-1 and IL-6
Men may experience more pronounced and sustained increases in IL-1β and IL-6 post-exercise without the same level of counteracting IL-1ra and IL-10, leading to a higher risk of inflammation-related heart damage.
Cytokine Response to Exercise
IL-6: Exercise Response
Increases significantly post-exercise, with a greater increase observed in intense exercise (up to 26.79 times).
Myocarditis Implications: Elevated IL-6 is associated with inflammation and muscle damage, both of which are central to myocarditis pathology.
IL-8:Exercise Response
Rises after both moderate and intense exercise, peaking immediately and returning to baseline within hours.
Myocarditis Implications: Plays a role in neutrophil activation and migration, relevant in myocarditis where immune cell infiltration occurs.
IL-10:Exercise Response
Primarily increases after intense exercise, peaking within hours and returning to baseline within a day.
Myocarditis Implications: Acts as an anti-inflammatory cytokine, potentially modulating excessive inflammatory responses in myocarditis.
IL-1β:Exercise Response
Shows variable increases, more consistent in intense exercise.
Myocarditis Implications: A potent pro-inflammatory cytokine, contributing to the inflammatory milieu in myocarditis.
TNF-α:Exercise Response
Increases with intense, prolonged exercise.
Myocarditis Implications: Involved in systemic inflammation and has been implicated in the pathogenesis of myocarditis.
WBC: Increase
Observed immediately after intense exercise, including neutrophils, monocytes, and lymphocytes.
Duration: Levels generally return to baseline within 24 hours.
NK Cells Increase
Both number and activity increase with exercise intensity.
Impact: Enhanced immune surveillance transiently post-exercise.
Muscle Damage Indicators
CK:Increase
Seen in some studies after both moderate and intense exercise, with peaks varying (24 to 48 hours post-exercise).
Impact: Indicates muscle damage, though not consistently elevated across all studies.
Inflammatory Markers
CRP:Increase
Reported after both moderate and intense exercise, with peaks often observed 24 hours post-exercise.
Impact: Marker of inflammation, useful for assessing tissue injury and infection responses.
ncbi.nlm.nih.gov/pmc/articles/P…
frontiersin.org/journals/physi…
journals.physiology.org/doi/full/10.11…
ncbi.nlm.nih.gov/pmc/articles/P…
Dr. Malone (how's it going?) has made statements that people who received the mRNA injections (I am paraphrasing) have subclinical damage to their hearts.
I want to expand on that please.
🚨💉Too long didn't read: mRNA COVID injections may cause subclinical myocarditis and full myocarditis (and worse) according to some doctors. This is due to inflammation, involving the LNP (lipids causing inflammation, DNA pieces and spike causing inflammation)--the immune system attacks the heart as part of this process. When we exercise, our immune system actually attacks the heart for a time! Women have some protective effects, such as estrogen and a difference in immune system activity, during working out. Women suffer less frequency and intensity of myocarditis due to estrogen effects, but a few other markers regarding immune system specifics.
In a nutshell, the heart gets inflamed at a level that is not noticeable after mRNA covid injections. Then, if you work out afterwards, a natural part of men and women working out, is the immune system inflaming the heart. Depending on the severity of inflammation, myocarditis (and worse), could occur.
Signs and symptoms of myocarditis during/after running in those who have received mRNA COVID injections, is probably due, to the immune system causing inflammation to the heart muscle because when we run, depending on if male or female, intensity and duration, different parts of our immune system become active, and cytokines come into the heart muscle, when running! If the heart muscle already has subclinical damage (that was due to different types of immune system effects--this has already been explained in all of these threads--cGAS STING activated by spike protein and DNA plasmid pieces and the lipids with macrophages [mononuclear phagocyte system]) then when we go for a run, our immune system gets activated (again) and inflames our heart. If we already have damage, this could lead to myocarditis, or worse.
(always see your doctor for medical advice. This is not medical advice. Not meant to treat, DX, or RX)
A bit longer summary (before the explanations):
Exercise-induced inflammation of the heart can exacerbate subclinical myocarditis, especially in individuals who experienced inflammation due to COVID mRNA injections.
(cGAS sting pathway is engaged in the heart if LNP entered with spike protein and pieces of DNA plasmid activating the cGAs STING pathway, that would activate the immune system, which would come into the area, and inflame the heart muscle. If the molar ratio of positively charged lipids to negatively charged nucleic acids like RNA and DNA is 10:1, this would make it EASIER for the LNP to enter the cardiomyocyte and "transfect it" compared to other ratios such as 20:1).
🚨💉High-intensity exercise poses a greater risk, as it triggers significant increases in pro-inflammatory markers like cytokines (e.g., IL-6, TNF-α) and white blood cells (WBCs), potentially leading to myocarditis exacerbation, acute cardiac events, or even sudden death. Men, who typically exhibit stronger inflammatory responses, may be at higher risk compared to women. Moderate exercise, on the other hand, induces a more balanced inflammatory response and is generally safer for individuals with subclinical myocarditis. Monitoring inflammatory markers and tailoring exercise recommendations based on gender and intensity can help mitigate risks and ensure safer exercise regimens.
So the heart is already in a state of subclinical inflammation, meaning the person is not showing signs, or might not realize or feel that anything is wrong, even though, they have had a COVID "vaccine" that was full of DNA pieces, lipids that inflame, and spike protein. All of these things are inflammatory, and our macrophage system does not like clearing these things out, and that in itself can become damaged with repeated injections of lipids (mps system damage).
So when we run, our immune system inflames the heart for a time--this is something that happens. But if we already have heart damage, and do not know it, then when we run, it can cause myocarditis.
Full breakdown:
Engaging in exercise, especially high-intensity exercise, can significantly impact those with subclinical myocarditis due to the following mechanisms:
1. Exercise induces the release of cytokines such as IL-6, TNF-α, and IL-1β. In people with subclinical myocarditis, this additional inflammatory load can aggravate heart muscle inflammation.
2. While IL-10 and other anti-inflammatory cytokines also increase, they may not sufficiently counterbalance the pro-inflammatory effects during intense exercise.
3.White blood cells increase (leukocytes).
Intense exercise leads to an increase in white blood cells: neutrophils and monocytes, which infiltrate the heart tissue and exacerbate inflammation in myocarditis.
4. CK and CRP: Markers of muscle damage and systemic inflammation, respectively, increase with exercise intensity. Elevated CK indicates muscle breakdown, which can parallel damage in cardiac muscle during myocarditis.
(CK stands for creatine kinase, an enzyme found predominantly in the heart, brain, and skeletal muscles. Elevated levels of CK in the blood can indicate muscle damage or stress, including damage to the heart muscle.
CRP stands for C-reactive protein, an acute-phase protein produced by the liver in response to inflammation. Elevated levels of CRP in the blood can indicate inflammation in the body, which can be caused by various factors, including infections, tissue injury, or chronic inflammatory conditions.)
5. Sex Class Differences
Men vs. Women
A. Inflammatory Responses
Men exhibit higher baseline and exercise-induced increases in cytokines such as IL-6 compared to women, which can make men more susceptible to exacerbation of subclinical myocarditis.
B. Myocarditis Prevalence
Men are more frequently diagnosed with myocarditis, potentially due to their more pronounced inflammatory response to physical stressors like exercise.
Exercise Intensity and Risk
Moderate Exercise
Moderate exercise tends to induce a balanced inflammatory response, with transient increases in cytokines and leukocytes returning to baseline relatively quickly.
Intense Exercise
High-intensity exercise results in significant and sustained increases in pro-inflammatory markers, potentially overwhelming the heart's capacity to manage inflammation in subclinical myocarditis.
This can lead to:
Myocarditis Exacerbation
Intensified inflammation can progress subclinical myocarditis to a more severe form, increasing the risk of complications.
6. Acute Cardiac Events
Elevated cytokine levels and WBC counts can precipitate arrhythmias or even myocardial infarction (heart attack).
7. Sudden Death
In severe cases, the acute inflammatory response combined with pre-existing myocardial inflammation can lead to catastrophic outcomes such as sudden cardiac death.
(extra data and sources):
Women's Immune Responses
Estrogen's Role: Estrogen enhances the production of anti-inflammatory cytokines like IL-10 and IL-1ra, while moderating the levels of pro-inflammatory cytokines like IL-1β and IL-6. This hormonal influence helps women to manage exercise-induced inflammation better, reducing the risk of myocarditis.
Cytokine Regulation
Women generally exhibit better regulation of IL-6 and IL-10 post-exercise, promoting an anti-inflammatory environment conducive to recovery and protection against myocarditis.
Men's Immune Responses
Higher Pro-inflammatory Tendency: Men tend to have higher baseline levels of pro-inflammatory cytokines and a less robust regulatory mechanism for anti-inflammatory cytokines like IL-10. This can lead to prolonged inflammation post-exercise, increasing the risk of myocarditis.
IL-1 and IL-6
Men may experience more pronounced and sustained increases in IL-1β and IL-6 post-exercise without the same level of counteracting IL-1ra and IL-10, leading to a higher risk of inflammation-related heart damage.
Cytokine Response to Exercise
IL-6: Exercise Response
Increases significantly post-exercise, with a greater increase observed in intense exercise (up to 26.79 times).
Myocarditis Implications: Elevated IL-6 is associated with inflammation and muscle damage, both of which are central to myocarditis pathology.
IL-8:Exercise Response
Rises after both moderate and intense exercise, peaking immediately and returning to baseline within hours.
Myocarditis Implications: Plays a role in neutrophil activation and migration, relevant in myocarditis where immune cell infiltration occurs.
IL-10:Exercise Response
Primarily increases after intense exercise, peaking within hours and returning to baseline within a day.
Myocarditis Implications: Acts as an anti-inflammatory cytokine, potentially modulating excessive inflammatory responses in myocarditis.
IL-1β:Exercise Response
Shows variable increases, more consistent in intense exercise.
Myocarditis Implications: A potent pro-inflammatory cytokine, contributing to the inflammatory milieu in myocarditis.
TNF-α:Exercise Response
Increases with intense, prolonged exercise.
Myocarditis Implications: Involved in systemic inflammation and has been implicated in the pathogenesis of myocarditis.
WBC: Increase
Observed immediately after intense exercise, including neutrophils, monocytes, and lymphocytes.
Duration: Levels generally return to baseline within 24 hours.
NK Cells Increase
Both number and activity increase with exercise intensity.
Impact: Enhanced immune surveillance transiently post-exercise.
Muscle Damage Indicators
CK:Increase
Seen in some studies after both moderate and intense exercise, with peaks varying (24 to 48 hours post-exercise).
Impact: Indicates muscle damage, though not consistently elevated across all studies.
Inflammatory Markers
CRP:Increase
Reported after both moderate and intense exercise, with peaks often observed 24 hours post-exercise.
Impact: Marker of inflammation, useful for assessing tissue injury and infection responses.
ncbi.nlm.nih.gov/pmc/articles/P…
frontiersin.org/journals/physi…
journals.physiology.org/doi/full/10.11…
ncbi.nlm.nih.gov/pmc/articles/P…
@drdrew
@DrJBhattacharya
@SenatorRennick
Gentlemen, I think this explains it
@DrJBhattacharya
@SenatorRennick
Gentlemen, I think this explains it
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