Wednesday, April 21, 2010

proclus : Michael L. Love: parsley and triglycerides

proclus : Michael L. Love: parsley and triglycerides

Michael L. Love: proclus molecules blog

Welcome to Michael L. Love on Vitacost!Probably my most recognizable feature is that I don't own a car, and I bicycle for exercise twice most days.

Michael L. Love: parsley and triglycerides
How might apigenin chloride channel blockade decrease serum triglycerides?  In other words, could one reduce serum triglycerides by eating parsley?  What follows is abit speculative, and I will admit that I have not yet researched the topic fully in the literature.  More will follow.  If you are comfortable with the fact the following may contain inaccurate extrapolations, the proceed.The first thing to observe is that a decrease in serum triglycerides would be a paradoxical effect.  The channel blockade agents that are being considered here are also COX inhibitors and COX expression inhibitors, so that at low dose they can be expected to raise serum triglycerides, as observed.
At high dose, the agents would tend to raise the hydrostatic pressure of the cell, by blocking one of the primary means of reducing that pressure, the CFTR chloride channels.  The physical model indicates, that increased hydrostatic pressure may lead to increased inward vesicular transport, and reduce serum triglycerides.  The mechanism is unknown to me at this time.
Some things about the pathway and mechanism are known to me, for example, COX inhibitors would tend to raise serum triglycerides, because the product of the COX reaction, prostaglandins, binds to PPAR alpha and activates inward vesicular transport, probably by some genetic mechanism.  It should be noted that prostaglandin production is the direct result of the activity of phospholipase, which provides the COX reagents.
One could hypothesize that a cellular response to CFTR blockade combined with COX inhibition would be the release of agents which activate phospholipase activity, such as histamine and norepinephrine.  By doing this, the cell would be attempting to make more COX reagents, so that the inward vesicular transport can be turned on, perhaps in order to avoid hydrostatic rupture.
Hydrostatic rupture is probably an over-statement, and what we are discussing are more like tendencies, rather than requirements.  One observation in support of this argument would be that cAMP-activated CFTR chloride permeabiltiy is able to overcome the blockade to varying degrees.  The blockade is unlikely to be complete under cAMP-activated conditions.  In fact, in cells which express cAMP coupled receptors, such as the beta-adenergic receptors, extra-cellular ligands to these receptors can be expected to alleviate hydrostatic pressure, without recourse to vesicular transport.  Moreover, the cell likely has other means of releasing solutes to draw out water.  For example, there is another important chloride channel, which may play a key role.  More on that later.
Two of the ligands which can activate both phospholipase and cAMP production are histamine and adenergics, such as epinephrine and norepinephrine, and cellular secretion of these products would be expected to help relieve hydrostatic pressure, by activating both CFTR, and inward vesicular transport, even during CFTR blockade which tends to be partial.  This cellular response may take time to come to full fruition, perhaps days or weeks.
It should be noted that alpha-1 and H1 activation leading to phospholipase activity is the very stress response that we are trying to avoid.  Phospholipase activity is associated with many problems, being implicated in cancer for example, and one infers that phospholipase activators would have the same association.
My experience is consistent with adenergic activation resulting from CFTR blockade, but I will need another week or so to eliminate some extraneous factors.  Such activation would also be consistent with some of the puzzling and unexpectedly elevated blood pressure readings that I have had transiently in recent days.
Are blockading levels of resveratrol or flavonoids beneficial in the overall sense?  My parsley experience clearly rings a cautionary note, but the animal experiments are indicating that a higher dose is consistent with deeper CR memesis, and that it is more healthfully beneficial than a lower dose.  Perhaps the explanation for this observation resides in the intestine, resulting from CFTR blockade, but it may also result from a greater increase in triglyceride transport, especially inward transport.  I am anxiously awaiting my next blood triglyceride assay.  I would also add that increasing water intake is recommended for the parsley regimen in order to compensate for the diminished mucous secretion, among other things.  
Published Friday, January 29, 2010 01:23 PM by proclus
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