Leaving Your Job Due to Mandate

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For those of you who have recognized your employer can terminate you for not taking the COVID vaccine and have decided on or are considering employment elsewhere please share your experiences here. How do you feel about having to make that choice? 

The purpose of this thread is not to condemn those making this decision or debate whether they should vaccinate or not. 

Specializes in CRNA, Finally retired.
8 hours ago, 10GaugeNeedles said:

Well I'm still wading through it but, what it showed me is, this is no "ordinary" virus. It seems to cause a much bigger inflammatory response through triggering an auto immune response itself. 

"We found that there are several similar processes of immune dysregulation in patients with COVID-19 and in those with lupus, with several other alterations seen in other pathological states"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8189735/#!po=50.3968

"The above mention findings regarding autoantibodies production in SARS-CoV-2 infected patients (Table 1 ), strengthen our belief on the possibility that there could be potentially additional autoantibodies present in similar patients, and these autoantibodies might have a pivotal role in the pathophysiology of severe and life-threating manifestations in COVID-19 patients."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7598743/#!po=15.4762

-It seems possible that, while there may be some auto immune response with a covid vaccine (my main concern), it appears to be short lived in most people. D dimer "micro studies" run by PCPs I've heard about but no wide spread report of long lasting platelet activation... This is just my assumption that those positive clot labs suggest auto immune response....I haven't found anything specific.

In the interim, I've heard allot of talk about vit d. This study was holy cr#p fascinating:

"ACE2is also the receptor on host cell surface and the major entry point into cells for some coronaviruses such as HCoV‐NL63, SARS‐CoV which causes SARS and SARS‐CoV‐2 which causes COVID‐19...

...Induction of type 1a Ang II receptor (AGTR1A) enhances pulmonary vascular permeability, thereby causing lung injury and pneumonia; this possibly explains the lung damage following decreasing ACE2 expression....

...Immune cells are not only targets for active vitamin D, but are also local producers of vitamin D and are able to activate this hormone in a local fashion, thereby arguing for an autocrine or paracrine function for this vitamin within the immune system. 42 From this view, inadequate vitamin D levels can be linked to the immune anomalies, such as higher infection rates and autoimmunity. 42 According to the recent review, vitamin D is capable in lowering the risk of COVID‐19 infections and deaths through different mechanisms including maintenance of cell junctions, strengthening cellular immunity by reducing the cytokine storm with impacts on tumor necrosis factor α (TNF‐α) and interferon γ (IFN‐γ), 43 and modulating adaptive immunity by suppressing T helper cell type 1 responses and promoting T regulatory cells induction...

...Persistent deficiency in vitamin D level may activate the RAS [renin-angiotensin system], thereby leading to chronic CVD and decreased lung function as well as inducing RAS activation lung fibrosis. 58 Patients with these comorbidities account for a higher proportion of critically ill cases in COVID‐19. 58 The COVID‐19 infection becomes more severe especially in elderly, hypertensive, diabetic and obese patients and smokers. 59 Particularly in the presence of diabetes mellitus and accompanying comorbid conditions such as hypertension, obesity, old age and smoking, cytosolic pH is low, thus the virus easily may enter the cell by attaching to ACE2."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7362103/#!po=50.0000

-angiotensin 2 is a big driver in lung inflammation and it's regulated partly by vitD. A dysregulated ACE/renin system seems to be a primary causative factor behind the severe symptoms of covid not to mention it's infectivity given that the spike protein binding site is the ACE2 receptor. Low Vit D seems to be a very key component in this disease.

so here's what I'm thinking. I wonder if supplementing with vit d (which most of us are deficient in, I know I am), getting my levels up before taking a vaccine would help protect from any auto immune response from the vaccine. The paper suggests "Although it is more likely that any protective effect of vitamin D against COVID‐19 is related to suppression of cytokine response and reduced severity/risk for ARDS, there is also evidence from a meta‐analysis that regular oral vitamin D2/D3 intake (in doses up to 2000 IU/day) is safe and protective against acute respiratory tract infection, especially in subjects with vitamin D deficiency."..." To reduce the risk of infection, it is recommended that individuals at risk of COVID‐19 take 10 000 IU/day of vitamin D3 for a few weeks to rapidly increase 25(OH)D levels above 40‐60 ng/mL, followed by 5000 IU/day." 

I wouldn't claim to suggest vitD is itself protective against covid infection like a vaccine is. But. It seems it has protective effects against the immune response responsible for most of the symptoms. I wonder if it can also limit any possible vaccine injury as well. Couldn't hurt. 

We've known about the Vit. D connection pretty much from the beginning but it is still tenuous.  But a small dose of Vit. D is good for us in a multiple of ways.  If you are interested, you can have your levels measured.  But if you live in a northern climate or wear sunscreen all over, you will probably need a supplement; almost half of the country is deficient.  It does act as an anti-inflammatory and has cardio-protective effects.  Perhaps that is why it is used for Covid patients.  Check it out.

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Specializes in Neurosciences, stepdown, acute rehab, LTC.
27 minutes ago, londonflo said:

The best advice in the world! Go for it!

 

I didn't say the quote you responded to. I must have quoted someone who did? Anyway, I agree friend! 

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Specializes in Acute Dialysis.

I think I have the pieces I've needed to help allay my concerns. As I've said, my main concern is vaccine injury long term from auto immune processes. I'm still concerned about that. My biggest concern is the denial game. Pro vax people seem to be desperate to get us to stop acknowledging things we here about, which degrades confidence (not to mention the hostile attitude).

Anyway. Before getting on this forum, I didn't really know what questions to ask. At this point I've whittled it down to 3 things: 1) what is the proposed physiological mechanism behind a possible,(as yet unacknowledged and denied by official sources) link to an auto immune response from the virus and or vaccine? 2) is there steps I can take to minimize this theoretical risk of a vaccine injury? 3) does the vaccine mrna persist in making spike protein (ie, can I take steps from 2 as a prophylactic, temporary measure or should I worry about needing long term protection from vaccine injury)? 

1) I've been able to see a number of very excellent studies outlining a very real auto immune connection from the virus. Sensory loss after both vaccination and infection widely reported specifically suggests blood brain barrier crossing, and the very unpredictable symptom group suggests to me multiple mechanisms of pathology makes sense if auto immune processes is a primary mechanism of pathology. The reported cases of vaccine injury I've seen are relatively consistent: female. It's proposed the x chromosome and undiagnosed but previously present autoimmune disorders are the primary group at risk of any vaccine injury. Thus it doesn't seem universal (that is good). So, IMO, the risk is there, but possibly doesn't include me. 

2) low vitamin d seem to predispose people to the auto immune effects (see below). So I could raise my vitamin d levels over a month before getting the vaccine. Thus at least I won't be able to say I didn't do everything I could to mitigate a potential injury.

3) I'm convinced now that the vaccine is not long lasting. First, once the mrna particles are destroyed intra cellularly, there's no continued spike protein production (at least as far as I've read).  Thus if there is an injury to cells (which I still believe does happen) it should not continue long term since, if there's no instruction to make spike protein, none gets produced. And that makes sense. 

So, I think I'll spend the next month getting my vit d levels up, then get vaccinated after that. 

 

This is what I found, posted earlier:

"what it showed me is, this is no "ordinary" virus. It seems to cause a much bigger inflammatory response through triggering an auto immune response itself. 

 

"We found that there are several similar processes of immune dysregulation in patients with COVID-19 and in those with lupus, with several other alterations seen in other pathological states"

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8189735/#!po=50.3968

 

"The above mention findings regarding autoantibodies production in SARS-CoV-2 infected patients (Table 1 ), strengthen our belief on the possibility that there could be potentially additional autoantibodies present in similar patients, and these autoantibodies might have a pivotal role in the pathophysiology of severe and life-threating manifestations in COVID-19 patients."

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7598743/#!po=15.4762

 

-It seems possible that, while there may be some auto immune response with a covid vaccine (my main concern), it appears to be short lived in most people. D dimer "micro studies" run by PCPs I've heard about but no wide spread report of long lasting platelet activation... This is just my assumption that those positive clot labs suggest auto immune response....I haven't found anything specific.

 

In the interim, I've heard allot of talk about vit d. This study was holy cr#p fascinating:

 

"ACE2is also the receptor on host cell surface and the major entry point into cells for some coronaviruses such as HCoV‐NL63, SARS‐CoV which causes SARS and SARS‐CoV‐2 which causes COVID‐19...

 

...Induction of type 1a Ang II receptor (AGTR1A) enhances pulmonary vascular permeability, thereby causing lung injury and pneumonia; this possibly explains the lung damage following decreasing ACE2 expression....

 

...Immune cells are not only targets for active vitamin D, but are also local producers of vitamin D and are able to activate this hormone in a local fashion, thereby arguing for an autocrine or paracrine function for this vitamin within the immune system. 42 From this view, inadequate vitamin D levels can be linked to the immune anomalies, such as higher infection rates and autoimmunity. 42 According to the recent review, vitamin D is capable in lowering the risk of COVID‐19 infections and deaths through different mechanisms including maintenance of cell junctions, strengthening cellular immunity by reducing the cytokine storm with impacts on tumor necrosis factor α (TNF‐α) and interferon γ (IFN‐γ), 43 and modulating adaptive immunity by suppressing T helper cell type 1 responses and promoting T regulatory cells induction...

 

...Persistent deficiency in vitamin D level may activate the RAS [renin-angiotensin system], thereby leading to chronic CVD and decreased lung function as well as inducing RAS activation lung fibrosis. 58 Patients with these comorbidities account for a higher proportion of critically ill cases in COVID‐19. 58 The COVID‐19 infection becomes more severe especially in elderly, hypertensive, diabetic and obese patients and smokers. 59 Particularly in the presence of diabetes mellitus and accompanying comorbid conditions such as hypertension, obesity, old age and smoking, cytosolic pH is low, thus the virus easily may enter the cell by attaching to ACE2."

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7362103/#!po=50.0000

 

-angiotensin 2 is a big driver in lung inflammation and it's regulated partly by vitD. A dysregulated ACE/renin system seems to be a primary causative factor behind the severe symptoms of covid not to mention it's infectivity given that the spike protein binding site is the ACE2 receptor. Low Vit D seems to be a very key component in this disease.

 

so here's what I'm thinking. I wonder if supplementing with vit d (which most of us are deficient in, I know I am), getting my levels up before taking a vaccine would help protect from any auto immune response from the vaccine. The paper suggests "Although it is more likely that any protective effect of vitamin D against COVID‐19 is related to suppression of cytokine response and reduced severity/risk for ARDS, there is also evidence from a meta‐analysis that regular oral vitamin D2/D3 intake (in doses up to 2000 IU/day) is safe and protective against acute respiratory tract infection, especially in subjects with vitamin D deficiency."..." To reduce the risk of infection, it is recommended that individuals at risk of COVID‐19 take 10 000 IU/day of vitamin D3 for a few weeks to rapidly increase 25(OH)D levels above 40‐60 ng/mL, followed by 5000 IU/day." 

 

I wouldn't claim to suggest vitD is itself protective against covid infection like a vaccine is. But. It seems it has protective effects against the immune response responsible for most of the symptoms. I wonder if it can also limit any possible vaccine injury as well. Couldn't hurt."

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To be fair and square, how about if employees who've had the COVID-19 infection be directed to check their titer before being forced to take the vaccine? Just like any other virus, e.g. hepatitis B, MMR, etc, the doctor usually tells you to get the vaccine if your titer is below protective level. And then recheck the level again some time after vaccination, to compare. Just a thought.

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Because no one knows how long those antibodies last, not a helpful lab test. Again it is always your choice to work where it is not mandated.

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You are not a victim if you chose not to get vaccinated and get hospitalized or worse. Why wouldn’t the world blame humans that choose not to be vaccinated for this crisis, my patients and family and staff were begging for a vaccine before it was authorized. Also to comment on the poor guy earlier, I broke my femur and went to the OR from the ER when I was 19, the delta surge has lowered the access to care in low vaccination areas because why? Rhetorical.  And our for profit health care system is mediocre in my opinion for the volume of funds swirling around ie ER charging $75 for “IV stick” and $10 for s 4x4. And who doesn’t think Medicare is socialized medicine. That’s for another very important thread, sorry. 

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Specializes in Public Health, TB.
25 minutes ago, nikeasnetty said:

To be fair and square, how about if employees who've had the COVID-19 infection be directed to check their titer before being forced to take the vaccine? Just like any other virus, e.g. hepatitis B, MMR, etc, the doctor usually tells you to get the vaccine if your titer is below protective level. And then recheck the level again some time after vaccination, to compare. Just a thought.

Various illnesses evoke different immune responses, thus different titers are used. Varicella titer is different from Hep B, etc.  For some, there are no reliable titers. For instance TB. 

I don't believe there is an accurate titer or measure of immunity for SarsCov2, but I could be wrong. 

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How about the data on how long the antibody last from COVID-19 vaccination? Only a few months? Because now the are giving booster to people who got the vaccination 6-8 months ago. That means the protection levels are dropping significantly for them to need booster. So, we all know that everything about COVID-19 continues to need more studies to be conducted on making better vaccines, on their safety and efficacies, following up closely on those developing adverse events, and including checking the titers some time after natural infection and after vaccination and to compare them. Just keep an open mind, is what I am trying to do. Keep ourselves up to date on the science behind it all.

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Specializes in Public Health, TB.
Just now, nikeasnetty said:

How about the data on how long the antibody last from COVID-19 vaccination? Only a few months? Because now the are giving booster to people who got the vaccination 6-8 months ago. That means the protection levels are dropping significantly for them to need booster. So, we all know that everything about COVID-19 continues to need more studies to be conducted on making better vaccines, on their safety and efficacies, following up closely on those developing adverse events, and including checking the titers some time after natural infection and after vaccination and to compare them. Just keep an open mind, is what I am trying to do. Keep ourselves up to date on the science behind it all.

I could be wrong, but I think the waning immunity data is based on reinfection rates from Israel, not on measurements antibodies .

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Specializes in Acute Dialysis.
4 minutes ago, nursej22 said:

Various illnesses evoke different immune responses, thus different titers are used. Varicella titer is different from Hep B, etc.  For some, there are no reliable titers. For instance TB. 

I don't believe there is an accurate titer or measure of immunity for SarsCov2, but I could be wrong. 

I thought PPD and quantiferon tested for exposure rather than immunity (exposure bad, non exposure good). So probably don't want an immune response in the case of tb. Not sure TB is a good counter example to tests for immunity. Am I misunderstand?

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Thank you Nikeasnetty but with all due respect if we keep an open mind and up to date on the science we would not be having this conversation. 

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Specializes in Public Health, TB.
Just now, 10GaugeNeedles said:

I thought PPD and quantiferon tested for exposure rather than immunity (exposure bad, non exposure good). So probably don't want an immune response in the case of tb. Not sure TB is a good counter example to tests for immunity. Am I misunderstand?

PPD and IGRA (Quantiferon and T Spot) test for an immune response to TB. A person successfully treated for LTBI and active disease may still show a positive immunity response. And a person can have a negative test and be positive for TB. I used TB as an example to show not all infections evoke the same sort of immune response. 

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