Questionnaire-based studies like this are of low scientific quality and do not actually control for response biases (Including Hawthorne effect) due to impossibility of blinding. It is quite possible the effect is just a change in questionnaire answering behaviour and not an actual reduction in guilt.

A more robust methodology would to objectively measure effect of guilt on real world behaviours.

You seem mistaken on the role of cortisol in the body. I realise there is a lot of confusing information out there that can lead to such a misunderstanding.

Cortisol does not "cause stress".

Cortisol is a metabolic hormone, it's primary function is to increase blood sugar through gluconeogenesis in the liver. The increase in cortisol while doing exercise is quite healthy and beneficial as it means the individual won't suddenly have to stop due to low blood sugar.

The reason cortisol is sometimes referred to a stress-hormone is that it is also a feed-forward hormone - in two ways. The first is that there is a daily cycle - it is low while we sleep and spikes in the morning to give us a boost, to deal with the spike of activity in the morning when we get up. Secondly the level of cortisol in circulation will increase when an individual anticipates a need for higher activity levels (and thus metabolic demand) in the near future. If the individual actually needed that spike in blood sugar due to increased activity then this is quite beneficial (at least in the short term).

However, this increased cortisol can sometimes lead to problems (including weight gain and risk of type 2 diabetes) if an individual constantly anticipates or experiences problems ("stress") over long periods of time without cessation.

Can neutrophils decide to be autoimmune?

No, because they don't have adaptive receptors targeted towards self antigens.

It is important not to confuse autoinflammitory with autoimmunity. Autoimmunity is based on either T-cells or B-cells (or plasma cells which are derived from B-cells) having their characteristic adaptive receptor (B cell receptor or T cell receptor) strongly bind to specific self antigens.

Note that T-cell autoimmune diseases are still hypothetical.

(More specifically, no one has characterised the T-cell receptor repertoire and demonstrated close to 100% sensitivity or specificity for a T-cell receptor subset for any disease - anyone claiming I am wrong is going to have trouble citing proof). T-cells undergo a strong selection process in the thymus to prevent autoimmunity, whereas no such process occurs for B-cells. B-cell autoimmunity doesn't necessarily need T-cell autoimmunity either.

Whereas all currently well-characterised autoimmune diseases are either B-cell diseases (associated with autoantibodies) or are in fact autoinflammatory, rather than autoimmune diseases. For example the Arthropathies do involve self-reactive T-cells but this self reactivity isn't primary driven due to self-reactive T-cell receptors, but rather they are causing inflammation regardless of what the T-cell receptor codes for.

There are parenoplastic diseases (T-cell cancers) that can rarely be autoreactive but these are extremely rare and the primary disease is the cancer.

All of these measures need to be tied to something a little more concrete. I can imagine something along the lines of operationalising Max Neef's conception of human needs and satisfiers/unsatisfiers.

From the conclusion:

>Although the reporting rate of GBS after COVID-19 vaccination was not
statistically different than that of the general population, the
increased reporting of GBS within the first 6 weeks after COVID-19
vaccination, more so than with other vaccinations, suggests that some
cases of GBS are temporally associated with COVID-19 vaccination.
However, there is a reduction in the reporting rate of GBS after other
vaccines, compared to reporting rates pre-COVID-19, highlighting
limitations inherent in any passive surveillance system. These findings
warrant continuous analysis of GBS after COVID-19 vaccination.