View of cardiovascular system, a vein with blood cells


QUESTION: Can you speak regarding the effectiveness of IV therapy in CV disease?

ANSWER: You have to think about the total treatment and the underlying disease as well as the combination of therapies. Many therapies historically used for CV or other diseases in IV therapy have very good reasons for use, but have a lot of folklore around them regarding why they actually work, and even more misunderstanding regarding their actual mechanisms of action. This leads to a lot of curious clinical uses that are well intended but useless.

HCl: A very good cytokine stimulant shown in many older and one newer clinical trials with infectious diseases especially bacterial. If (IF) used appropriately and frequently enough (appropriate is as a push only, frequency in most studies is more than once weekly in acute infections) it can be a great adjunct. When people put HCl into an IV Bag it is a useless addition as it loses it’s cytokine stimulation ability and simply barely adjusts the pH of the bag. MANY people teach and propagate this practice meaning well, but if one considers why HCl works the way it does it is not useful to do. (Unless adding H and Cl ions to an IV bag magically does something, but that would be totally different than an HCl push).

Heparin: Many with CV dz have hyper coagulable blood and heparin is used at particular doses for this. If one looks at Pouiseuille’s Equation: less coagulation = less vessel friction, which = less intrinsic clotting cascade activation. This leads to less internal thrombi formation. Experts debate the uses of lower dose anticoagulant Tx but, in general, it can be helpful in a larger Tx context. In the OLDEN days we used Heparin in all our EDTA formulas – which is not a bad idea but unlikely at that dose and frequency to do much long term. It was originally added to help with inter-IV clotting, but that didn’t turn out to be a big problem. That said it isn’t a bad addition, and the TACT trial formula used it (largely for historical purposes).

Myer’s Coctail: Aside from the one IV Push formula that Dr. Alan Gaby published (of Dr. Myers) in Alt Med Rev long ago, there is no real Myers Coctail recipe (it is a euphemism for a vitamin mineral IV which could have two million possible ingredient combinations). That said vitamin IV have a different role in CV Dz. On one hand people receiving IV chelation must have IV remineralization between IV chelation sessions (we now say this after a couple of MI’s caused during chelation and one cardiogenic death during chelation). In that we teach specific IV Vit-Min formulas to replete an IV chelation patient. This both rebalances the good minerals depleted by chelation as well as providing nutrient support to antioxidant balance (see below).

EDTA: Long ago we ascribed the CV benefits of EDTA to calcium chelation– and of course were dead wrong about the MOA but still did notice benefit. People who claim the CV benefit from EDTA is due to calcium manipulation are old like me and learned incomplete MOA theory – not totally inaccurate, just very incomplete. EDTA in ANY form has positive CV benefits on multiple biochemically logical and pharmacologically valid bases. These include, but are not limited to:

  • Antioxidant – it removes transition metals, lowering oxidative state.
  • Direct Nitric Oxide augmentation – NO is known to be inhibited directly by many heavy metals and the NOS systems especially in the vessel and liver are directly chelated by the EDTA, hence the common decrease in angina and BP after chelation.
  • Hepatoprotectant / antioxidant – EDTA generally lowers LFT’s; initially, however,it can raise and then lower them.
  • Non Nitric Oxide enzyme augmentation – Other enzymes that cause coagulation, vessel spasm, and other direct CV effects are also affected by metals, and EDTA can lower those interfering effectors as well.
  • Calcium manipulation – When one calculates the total Ca++ removed during a Na2EDTA chelation, it is small, and the idea of bulk movement cleaning the arteries of calcium is really a misnomer. That said, the movement of Ca++ via either Na2EDTA or CaNa2EDTA is a strong manipulator of many of the above effects as well as one below – so while not as simple as advertised, a small movement of Ca++ can make changes in the biology which affects the CV system.
  • PTH stimulation – EDTA is known to have a temporary pulse effect on calcium which has a temporary pulse effect on PTH causing more appropriate bone turnover IF the levels of Vit-D and Ca / Mg / PO4 are adequate.
  • Also EDTA is used in research as the main agent for Biofilm manipulation (in non-human science as well as in IV catheter biofilm formation for example). Biofilm formation leads in some cases to additional plaquing and vessel inflammation which is obviously better if diminished or removed.

The TACT trial mentioned had best results in the most oxidized folks (diabetics) which would follow along with all the MOA above as patients with DM have one of each problem in higher levels. The above really just scratches the surface of our knowledge and understanding of these agents. We do go into some of this in the Detox and Chelation IV courses as well as others.

Official TACT Q&A

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