Non-invasive quantification
of disease. The program uses serial EBCT to assess the segmental extent of disease
and effectiveness of supplements in the treatment CAD. Symptomatic patients on
cardiovascular or lipid medication are placed on supplements as an adjunct therapy.
Because of the low variability of EBCT (< 10% CAS & < 8%
CA) and the high predicted relative progression of CAD (mean 51%; 32% median in
symptomatic pts), EBCT is used as an accurate assessment of outcome.
In identifying the cause
of CAD, eg hyperhomocysteinemia, ALP’s and treating the cause with nutritional
supplements, many patients have documented regression and reversal of CAD.
The premise of the nutritional
treatment is two fold; first to improve cardiovascular and endothelial function
by providing therapeutic amounts of vitamins, minerals, trace elements, EFA’s
that are known to be essential to cardiovascular cellular function. Second, is
to treat identified genetic or probable cause of CAD with specific add-on supplements
in therapeutic amounts, ie-individualized therapy.
The following are examples
of science based treatment of certain aspects of coronary artery disease:
Hyperhomocysteinemia:
vitamins B6, folic acid, B12 and Betaine reduce homocysteine in a dose-related
response to improvement in the methylation cycle. A few patients require N-acetylcysteine
to reduce the homocysteine level below the therapeutic goal of 8.5 Umol/L. Below
8.5 minimal damage occurs to the endothelium. Some patients with a normal fasting
homocysteine may have a decreased clearing of Hcy and are identified with a methionine-loading
test.
C-Reactive Protein:
aspirin in amounts of 81 to 325 mg a day are used to reduce CRP.
Oxidation of LDL:
antioxidants vitamin A, C, E, & Beta-carotene are provided initially in empirical
therapeutic amounts and subsequent dosing is based on intracellular oxidation
studies by a lymphocyte proliferation test. Dosing is increased until the oxidative
potential is above the 75th percentile. Obtaining optimal oxidation
status is a critical aspect of the therapy, as patients currently taking other
supplements should stop these products to avoid the pro-oxidant effects of excess
antioxidants.
Platelet function:
in addition to aspirin, 300 mg of omega-3 oil a day provides as 120 mg docosahexaenoic
acid and 180 mg as eicosapentaenoic acid. There are many positive functional reasons
but in cardiac patients the main purpose is to decrease the platelet synthesis
of thromboxane A2, ie decrease platelet aggregation.
Endothelial function:
can be grossly assessed with brachial artery studies but is initially treated
with calcium, magnesium and occasionally with arginine HCL.
Hyperfibrinogenemia:
is treated with NAC and all of the above to reduce fibrinogen levels and blood
viscosity.
ALP’s: Atherogenic
Lipid Profile (pattern, B, type B hyperlipidemia) is treated with 1.2 - 1.6 gm/day
of no-flush niacin (inositol hexa-niacinate) or Niaspan by prescription at 2 to
3.5 gm/day. Berkeley LDL-GGE blood test is used to monitor therapeutic effectiveness.
Lp (a): hyperlipoproteinemia
with Lp(a) is treated initially primarily with NAC but generally resolves as dyslipidemia
is corrected.
Hyperinsulinemia:
(syndrome X) is treated best with omega-3, weight loss and although provided in
the supplements only a few patients will respond to 400 mcg of chromium or the
addition of 10 mg of vanadium sulfate and 200 mg alpha-lipoic acid per day.
Occasionally patients with
syndrome X will require insulin sensitizers’, ie prescription drugs such as thiazolidinediones
(Avandia and Actos) and possibly a sulfonylurea or biquanide type drug. These
patients need diet instruction and diabetic teaching.
Although there numerous
other concomitant metabolic disorders, eg hypertriglyceridemia and selected intracellular
deficiencies, therapy should be individualized.
David Martin, Pharm.D.,
FACN CNS
