This is a follow up to my last question regarding why APS sufferers feel better when our INR goes higher. It was established in the answers to my question that our blood is, indeed, "sticky" when our INRs dip too low. This causes all our symptoms and can lead to truly life-threatening outcomes such as strokes, heart attacks, etc.
So it would seem important, then, to know if our blood, in the absence of anticoagulation therapy, is ALWAYS sticky or just SOMETIMES sticky.
I am no immunologist, but what I understand of immune responses is that they are reactions to the presence of a specific pathogen. For example, you get this year's flu shot. Should you be exposed to the flu virus, the antibodies you've created tag the virus and it is then destroyed. In the absence of exposure to the flu, those antibodies play no role -- they just hang out in the blood stream or go wherever antibodies go when they aren't needed.
If we apply the same logic to APS, sufferers should have persistent, chronic sticky blood in the absence of anticoagulation therapy. Why? Because the "pathogens" are always present -- i.e. phospholipids. Our phospholipids are ALWAYS present, they don't go on vacation. Therefore, the antibodies we have created against phospholipids should ALWAYS be attacking.
Where things seem to get interesting, is when we consider that APS, at least anecdotally speaking, tends to "flare." We have bouts with this disease that are sometimes worse than others. And for those who experienced these bouts BEFORE diagnosis and the start of anticoagulation therapy, it would seem that they were not consistently feeling unwell or consistently throwing clots (I assume). And in terms of onset of the disease, we read that a person may have headaches/migraines in their teens that go away in their 20s and return in their 30s.
This on-again/off-again behavior of the disease, does not make sense to me from an immunological perspective. Phospholipids were present in our bodies in our teens, 20s, 30s, 40s, etc. So why the disappearance of a symptom or a lack or absence of DVTs??
And if they disease is episodic and not always chronic and persistent, then that means there are OTHER confounding and underlying triggers that can and should be identified and addressed. In fact, it might actually mean that a cure is more plausible than previously thought.
Because if there is an additional trigger(s) that MUST be present in order for the anti-bodies to spring into action and cause us all these problems, then it would be possible to treat that trigger(s).
I know I'm just an amateur, but does any of this make sense to anyone?