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Tests for Preventative Heart Health

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[edit] Tests for Preventative Heart Health

[edit] DIY test kits

[edit] EKG Stress tests and Nuk imaging

EKG Stress tests and Nuk imaging don't tell you ANYTHING about the amount of plaque in your arteries other than they are not extremely blocked - and most heart attacks are not caused by nearly blocked arteries!

[edit] Imaging Tests

Look for a heart scan (not a CT angiogram) but a Coronary Calcium Scoring heart scan. You won't get an accurate score number for arteries that have stents - but even if you have one left, it can help you see if your intervention works. Once a year if you are tracking plaque..

These test are rightfully criticized as a tool to get people into the cath lab prematurely, but it is the only way you will know the health of your coronary arteries and CAD (Coronary Artery Disease) is a leading killer. Used as preventative medicine, they can help one tailor diet, vitamins and medicines to control the progress of CAD.

[edit] lipoprotein(a) or Lp(a)

People with elevated lp(a) can have normal looking cholesterol tests and have aggressive CAD - There are ways to lower Lp(a) - I read one place that Lipitor can actually raise this level! You want this test in particle count (nmol/dl) not mass (mg/l) see NMR lp(a) test

6 months

Lp(a) is really an LDL cholesterol particle bound to an additional protein called apoprotein(a) (apo(a)). LDL cholesterol particles, just like VLDL and IDL, each contain one apoprotein B molecule (apo B). The apo(a) particle binds to the LDL particle via apo B, and they do so through two linked sulfur molecules, the so-called “disulfide linkage.”

Sirtori CR, Calabresi L, Ferrara S, Pazzucconi F, Bondioli A, Baldassarre D, Birreci A, Koverech A. L-carnitine reduces plasma lipoprotein(a) levels in patients with hyper Lp(a). Nutr Metab Cardiovasc Dis 2000;10:247-251.

ApoA-I production is decreased by Vitamin D - Wehmeier K, Beers A, Haas MJ, Wong NC, Steinmeyer A, Zugel U, Mooradian AD (2005). "Inhibition of apolipoprotein AI gene expression by 1, 25-dihydroxyvitamin D3". Biochim. Biophys. Acta 1737

[edit] NMR Cholesterol Tests

First, don't even look at your total cholesterol number, it fails to have much if any value. Basic Lipid targets of LDL 60 mg/dl, triglycerides 60 mg/dl or less, HDL 60 mg/dl or greater can be achieved. The problem here is that conventional lipid tests underestimate - often by 40-50% sometimes 100% the amount of LDL. There is a better NMR lipid test (You may have to find a lab that does not use labcorp which does not return all the numbers.) small vs large LDL - LDL-P Small-LDL-P (is this VLDL?) LDL-P is a very useful number that can be used to tweak treatment. This added detail is needed because not all LDL is terrible and not all HDLs are equally protective. The key number is not total LDL but the number of LDL particles. The standard test measures the wrong thing!

3 - 6 months

If you are stuck with only the 'standard' lipids tests and are eating low carb - consider the following link to correct the numbers:

[edit] HDLs

Increasing HDL can be accomplished with cheap Niacin and D3 - more effective than any statin. HDL may help to slightly reverse arterial plaque. NMR Lipid test cost $167 (2009)

  • NMR lipd test detects Apoprotein B

Standard lipid tests can under report LDL by large amounts - besides the test measures the wrong thing - you really need to know particle counts to see if you are reaching targets.

The problem is current medicine is using the obsolete lipid tests - and trusting them can get you into big trouble. Finding a doctor that will order and use these tests is the big hurdle.

[edit] ApoB-100 and Apo-A1

[edit] ApoE Genotype test

One time test - once you know it you can use the information to change interventions.

[edit] Thyroid Tests

Full panel - some evidence that taking T4 + T3 is best for CAD.

  • TYP Targets
    • TSH = < 1 0 - 1.5 shooting for 1 if tolerated.
    • Free T3 in upper half of 'normal' 350 and less than 420pg/dL (0.1 ng/dL is equivalent to 1 pg/mL or 100 pg/dL.)
    • Free T4 in upper half of 'normal' 1.2 - 1.9ng/dL

Test 6-8 weeks till corrected - then every 6 months.

Other Free T3 reference ranges: TYP 350 - 420 pg/dL Some lab -- 140 – 420 pg/dL NACB consensus statement 200 – 500 pg/dL Family Practice Notebook 230 – 619 pg/dL Quest Diagnostics 230-420 pg/dL (BTW Quest uses a premier endocrinology laboratory, the Nichols Institute in San Juan Capistrano, CA, as their reference laboratory)

It is clear that the TYP range is tighter and centered higher.

About Hypothyroidism

According to Ken Woliner, M.D., A.B.F.P :

... giving thyroid hormone to patients who are not truly hypothyroid does not cause these patients to lose weight. They wind up only getting the side effects (such as palpitations), but no benefits (there will be no weight loss if thyroid is not the true problem).

Hypothyroidism is associated with heart disease ( I have it) there may be something to treating with a combination T4 + T3 to help reduce Lp(a).

  • IMHO until they prove that for all the effects of thyroid (including long term ones) (and thyroid effects almost everything) that there is no difference between T4 vs T4+SRT3, we should take the conservative road of mimicking our bodies own production of both T4+SRT3 as best as we can.
  • I replace T4 with 1 part T3 for 4 parts T4 - normal bodies make 20% as T3


  • Slow release T3 compounders:
Knowles Apothecary
10400 Connecticut Ave, Suite 100
Kensington, MD 20895
301-942-7979 301-942-5544 (fax)
$35 60 of 5uG
  • Medaus Pharmacy
800 526 9183 info@medaus,com
800 526 9184 FAX
$49.20 60 of 5uG

[edit] 25HydroxyD-3 (Vit d)

D3 can raise HLD (the good cholesterol) - some studies report reduction of CAD Target for D3 is either 50-60 ng/ml or 125-150 nmol/l (Others say 60-80 ng/ml is optimal)

Test 2-3 months until stable - then 6 months - February and August

No substitute for blood testing - response to supplements varies greatly.. Test every 3mo until stable - then once/ year.

You do NOT test via !>> 25(OH)D2 or 1.25(OH)2D <<!!

[edit] Oxidized LDL assay

A quote from Stephan Guyenet Ph.D: "GRAS [Global Risk Factor Assessment Score] was able to correctly differentiate a healthy person from a person with coronary artery disease 49% of the time, while oxLDL was correct 82% of the time. Thus, oxLDL by itself was far more accurate than a whole battery of traditional cholesterol and cardiac markers. Coronary patients had more than twice the level of circulating oxLDL than the healthy comparison group."'


That PUFA seems to increase Oxy-LDL is clear - but just like 'fats" PUFAs are not one thing - there are both O-6 and 0-3 PUFAs and several kinds of PUFAs I think it would be rather easy to clear this up. It seems that the tool of Oxidized LDL assays should help us optimize our diet strategy.

[edit] Providers

[edit] Homocysteine Level

(Stress > homocysteine > plaque but may be indicator not cause?? Deplin L-Methylfolate?) It appears that B-vitamins lower homocysteine - but don't reduce CAD - side effect of high cortical levels? Methylfolate seems to CAUSE Restenosis according to this quality study (biggest shortcoming was it was only 60-month long)

There seems to be a lack of conclusion if lowering homocysteine is of any benefit.

N-acetylcysteine (NAC) and TMG also reduce homocysteine - they are all methyl donors - will they also induce Restenosis?

There are still some practical lessons to learn from homocysteine, even if you choose to not treat it: --It can indicate B12 and/or folate deficiency. B12 deficiency first detected by increased homocysteine is reasonably common. --There may be benefit in people with Lp(a), since homocysteine may enhance Lp(a) assembly --It can suggest or support the diagnosis of hypothyroidism. In fact, some have suggested that high homocysteine can be used as a surrogate for hypothyroidism. Beyond that, we sure need clarification on this question.

we could have the case that if homocysteine is high - slightly upping T4 may bring it down and might be a very useful treatment parameter?

One more reason we really need to be using computer 'expert systems' - homocysteine alone may not mean much - but combine it with somewhat elevated Lp(a) and/or subclinical hypothyroid results of TSH and Free T3 -- and the intervention becomes clear. I don't think the average doctor is going to see these patterns - we need to start using data mining now!

[edit] DHEAS

DHEA is precursive to several hormones. DHEA has also been shown to reduce the amount of atherosclerotic plaque in rabbits fed a high-cholesterol diet.

[edit] High sensitivity C-Reactive Protein (aka "Hs-CRP" or just "CRP")

Inflammation is related to CAD

We want CRP to be below 1mg/l

Test quarterly

[edit] PSA (prostate specific antigen)

Not a specific cardiac marker, but can indicate systemic inflammation specific to the prostate in men

[edit] Lp-PLA2 (the "PLAC" test)


[edit] Blood pressure

Target less than 115/70

[edit] Magnesium

[edit] Phosphate

Phosphate levels are consistently linked with cardiac calcification

[edit] Gluten Sensitivity

Creates chronic inflammation and other problems.

[edit] Fibrogen

[edit] CRP

CRP is an inflammatory mediator released by the liver. It prevents cholesterol from exiting macrophages in cell culture.

[edit] Testosterone / esterogen

[edit] Blood Sugar

Run a real glucose tolerance test

Buy a meter and a case of glucola

Fasting level every 3 months

[edit] Platlets

???

[edit] Other tests

  • Creatine Kinase Activity, Serum
  • Creatine Kinase MB Total
  • CK-MB, CK-MM, CK-BB (as a % of total CK)
  • Fibrinogen Activity
  • Fibrinogen Antigen
  • Troponin I
  • Il-1B
  • Interleukin-6 (IL-6) - most connected to CAD of the ILs
  • IL-8
  • ox-LDL
  • ICAM-1
  • Urotensin-II (U-II)
  • IL-1RA
  • TNF
  • HPT, Hemoglobin-binding Protein, Hp Formal name: Haptoglobin
  • possible stress to CAD axis tests AChE, BChE and PON
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