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Lp(a)

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  • Lp(a) is formed by the "binding" of Apo B100 to apo(a).
  • Lp(a) "recruits" inflammatory cells for intrusion into the artery wall.
  • Lp(a) "adheres" and intrudes into the artery wall upon artery wall injury.

Contents

[edit] Testing and isoforms

LP(a) appears with different isoforms of apolipoprotein - 40% of the variation in Lp(a) levels when measured in mg/dl can be attributed to different isoforms. Combine that with the lighter Lp(a) being more disease causing and a test in mg/dl is not useful.

  • Lipoprotein (a) Cholesterol, Serum Recently a high correlation was demonstrated between Lp(a) and oxidized LDL, suggesting that the atherogenicity of Lp(a) lipoprotein may be mediated in part by associated proinflammatory oxidized phospholipids.

[edit] Reducing Lp(a)

[edit] Reduce Stearic acid intake?

[edit] Niacin

a combination with a fibrate (clofibrate) may work better than Niacin alone

Niacin essentially constitutes the nicotinamide ring, the reactive site of the NADP and NADPH molecule. Ascorbate reduces the NADP molecule to NADPH and thereby "recharges" the molecule for metabolic reactions. Niacin and ascorbate have also been shown to be effective in lowering elevated plasma levels of low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL). Thus NADPH may also be involved in the regulation of other potentially atherogenic lipoproteins. Further confirmation of this therapeutic mechanism will establish the value of dietary niacin and ascorbate supplementation in reducing elevated plasma levels of atherogenic lipoproteins.

Should we be using IR Niacin? Not clear

[edit] Niceritrol (Pentaerythritol tetranicotinate)

[edit] Estrogen

  • estrogen is known to lower Lp(a) American Association of Clinical Endocrinologists Medical Guidelines for Clinical Practice for the Diagnosis and Treatment of Dyslipidemia from 2000

[edit] Testosterone

  • According to this article one might lower Lp(a) with testosterone (T) ? (Seems to say it won't work and latter it works?)
Additionally, T administered even in combination with an aromatase inhibitor suppresses lipoprotein-a levels. (aromatase inhibitors block the production of estrogen)
  • via DHEA?

[edit] IGF-1

Perhaps IGF-1( insulin-like growth factor–I) may reduce lipoprotein(a) levels.

Contrasting Effects of Growth Hormone and Insulin-Like Growth Factor–I}

According to Wikipiedia

IGF-1 in the circulation include an individual's genetic make-up, the time of day, his or her age, gender, exercise status, stress levels, nutrition level and body mass index (BMI), disease state, race, estrogen status and xenobiotic intake

More at:

There do appear to be some drugs that increase IGF-1 according to the Wiki article..

This might be why thyroid optimization is important in CAD

[edit] CQ10

CQ10? 60mg BID

[edit] Apheresis

Apheresis is the most effective way of reducing lipoprotein a levels. Apheresis involves separating the blood externally to the body, so that the lipoprotein(a) may be effectively 'filtered out', and the blood is then returned back to the patient. This treatment is very expensive and generally only available to very high risk patients.

[edit] Half-life of Lp(a)

  • After creation, Lp(a) particles last for about 6 days in the blood before being eliminated by the kidneys.

[edit] oxLDL oxLp(a)


I also found more than one article that shows that Human grow hormone may INCREASE Lp(a) while improving the overall lipid profile. Makes me question DHEA?






  1. Park YM, Febbraio M, Silverstein RL. CD36 modulates migration of mouse and human macrophages in response to oxidized LDL and may contribute to macrophage trapping in the arterial intima. J Clin Invest 2009;119:136-45
  2. ^ Curtiss LK, Clinical Implications of Basic Research: Reversing Atherosclerosis? N Engl J Med 2009;360:1114-1116

From Wiki

NADPH oxidase is a major cause of atherosclerosis, and NADPH oxidase inhibitors may reverse atherosclerosis. Atherosclerosis is caused by the accumulation of macrophages containing cholesterol (foam cells) in artery walls (in the intima). NADPH oxidase produces ROSs. These ROSs activate an enzyme that makes the macrophages adhere to the artery wall (by polymerizing actin fibers). This process is counterbalanced by NADPH oxidase inhibitors, and by antioxidants. An inbalance in favor of ROS produces atherosclerosis. In vitro studies have found that the NADPH oxidase inhibitors apocynin and diphenyleneiodonium, along with the antioxidants N-acetyl-cystine and resveratrol, depolymerized the actin, broke the adhesions and allowed foam cells to migrate out of the intima


This suggests that vit C will reduce Lp(a) and L-lysine and L-proline may protect the arteries.:

It may be that Vit C helps because it converta proline to hydroxyproline.. The latest reference in this paper was 1992..

www.pubmedcentral.nih.gov/picrender.fcgi Evidence that the Fibrinogen Binding Domain of Apo(a) Is Outside the Lysine Binding Site of Kringle IV-10 A Study Involving Naturally Occurring Lysine Binding Defective Lipoprotein(a) Phenotypes

EACA decreased the binding of Lp(a) to PM-fibrinogen

Core of the Proteoglycan Decorin ]

So:

What dosage of L-lysine and L-proline would make sense?

What about apocynin ?


It appears that actone and Homocysteine thiolactone are related in some way.. and Homocysteine is related to Osteoporosis. Vitamin D, estrogen, actone, HGH, and testosterone all increase bone density and might reduce Lp(a). This seems somehow linked to reducing Lp(a).

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