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Expedted levels for lipoprotein(a)?

cardiovascular apolipoprotein apo lipoprotein lipoprotein(a)

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#1 panhedonic

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Posted 20 October 2016 - 09:29 PM


Hi there. 47yo male, normal weight here. 

 

I just received what I think is a pretty bad lipid panel

 

Total  254

HDL 54

LDL 183 (yikes!)

TG  86

 

Also had an APO panel:

 

Apolipoprotein A-I 145

Apolipoprotein B  154

Lipoprotein(a)    67 

 

(All values in mg/dl)

 

I know there are some complexities in APO, like LP A-I is protective, and LP(a) increases risk steeply after certain levels, but what are those levels? What's the lipoprotein(a) reference like? I couldn't find that in the googles. 

 

Additionally, if you know of a supp regimen that can make me live longer given this panel, I will be thankful for all those added years ^_^

 

Thanks!



#2 panhedonic

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Posted 20 October 2016 - 09:33 PM

Excuse the typo in the topic name



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#3 pamojja

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Posted 20 October 2016 - 10:15 PM

Note that 'normal' reference ranges vary from lab to lab, since they are usually calculated by taking out the lowest and highest 2.5% of all tested, that means 95% of tests are arbitrary considered 'normal':

 

Apolipoprotein A-I = 90 - 170 mg/dl

Apolipoprotein B = 40 - 115 mg/dl

Lipoprotein(a) mass = 0 - 30 mg/dl

Quotient: ApoB / ApoA1 = 0.45 - 1.25

 

Some therefore go after more 'optimal' levels, like:

 

Apolipoprotein A-I = 60 - 200 mg/dl

Apolipoprotein B = ≤ 70 mg/dl

Lipoprotein(a) mass = < 20 mg/dl

Quotient: ApoB / ApoA1 = ≤ 0.4

 

There is also a differing Lipoprotein(a) particle test with a normal range of <10, if I remember it right.

 

LDL 183 (yikes!)

TG  86

 

 

LDL comes in different variants too. More dangerous small dense, or larger fluffy. Hence a more dangerous high LDL-P number, or less so. Usually with trigs about 150 mg/dl all LDL is of the dangerous kind, at about 50 mg/dl much less so. The most straight forward way to keep trigs low is eating lower in carbs. At least avoid anything with sugar.

 



#4 pamojja

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Posted 20 October 2016 - 10:27 PM

Here what was recommended in a TYP special report behind a pay-wall (already superseded by updated recommendations, therefore I don't believe giving this excerpt could be minded).

The main recommendation nowadays against high Lp(a) there is high-dose fish oil, with a combined EPA/DHA content of 6 grams/daily, which has shown significant reductions in about 60% of those who tried it after 1-2 years. Not it me though.

 

Lipoprotein(a) is reduced by:

* Niacin is the most effective direct treatment for Lp(a). However, higher doses may be required than for other abnormalities like low HDL or small LDL. The niacin preparations we favor are prescription Niaspan® (Kos Pharmaceuticals) or over-the-counter Slo-Niacin® (Upsher-Smith). Both are better tolerated than over-the-counter “immediate-release” niacin, which tends to cause intolerable hot flushing. However, immediate-release niacin is otherwise safe but should not be taken more frequently than twice a day. All three preparations are very safe, with little risk of liver toxicity if taken properly. Total daily niacin doses of >500 mg should be taken with the supervision of a physician.
* Estrogen in females may lower Lp(a) around 25%, though estrogen, of course, has other considerations that need to be fully discussed with your doctor. Testosterone can be helpful for men and reduces Lp(a) by 25%. We use testosterone cream with great success. (A common dose for men >50 years old is 50 mg twice per day of a topical cream; dosing is best based on blood levels and must be prescribed). For any hormonal preparation, we advise bio-identical human preparations, i.e, preparations that are identical to the human form, not Premarin® or other non-human forms.
* L-carnitine can be a useful nutritional supplement; 2000–4000 mg per day (e.g., 1000 mg twice a day) can reduce Lp(a) 7–8%, and occasionally will reduce it up to 20%. The only drawback is cost; it can be pretty pricey. L-carnitine is not powerful enough to be used as sole treatment, however. It’s better as an adjunct with either niacin and/or hormones.
* Ground flaxseed (2–3 Tbsp/day) exerts a modest effect of no more than 7% Lp(a) reduction, but it’s healthy effects on reducing LDL and perhaps small LDL make it a useful adjunct. Use it as a hot cereal or added to yogurt or other foods. The seeds must be ground (e.g., purchased ground or ground in your coffee grinder).
* Almonds—Preferably raw or dry roasted (with no added ingredients like hydrogenated oils), ¼–1/2 cup/day, are our favorite, as they not only reduce Lp(a) but also reduce LDL and partly counteract the small LDL particle abnormality.
* Vitamin C—1000–3000 mg/day, with reported reductions of approximately 7%.

Track Your Plaque target: If measured in nmol/l, <75 nmol/l is desirable. In mg/dl, <30 mg/dl is desirable. (However, because of the lack of standardization, “normal” values in your laboratory may vary, depending on the means of measurement; discuss with your doctor.)

Copyright 2006, Track Your Plaque.

 

 

In my own case Lp(a) only came down substantially when my serum DHEAs normalized.



#5 panhedonic

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Posted 21 October 2016 - 04:20 PM

Found thisd study on lipoprotein(a), which in a way renders the whole thing irrelevant for men. Or am I misunderstanding it? 

 

 

(excerpt from "results") 
Association Between Cardiovascular Disease and Risk Factors

On multivariate analysis, age, diabetes, hypertension, total cholesterol, and triglycerides were significantly associated with increased risk of CAD and CVD in women (Table 3). The same risk factors were associated with CAD in men except for triglycerides (Table 4). Only age, hypertension, and diabetes were independent risk factors for CVD in men. HDL semiquantitative determinations on electrophoresis were not significantly associated with CAD or CVD risk. Smoking status was not entered into the analysis because it was not available in all subjects.

 

From <http://circ.ahajourn...ntent/96/5/1390



#6 pamojja

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Posted 22 October 2016 - 12:27 PM

Found thisd study on lipoprotein(a), which in a way renders the whole thing irrelevant for men. Or am I misunderstanding it? 

 

(excerpt from "results") 
Only age, hypertension, and diabetes were independent risk factors for CVD in men.

 

From <http://circ.ahajourn...ntent/96/5/1390

 

Independent risk factor means if you only had high Lp(a). But none of the other mutually dependent risk factors. You do have others, and are in the process of aging..


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#7 panhedonic

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Posted 24 October 2016 - 12:52 AM

pamojja, thanks for explaining. Sorry to not understand this. I don't have high BP or diabetes. So this still means that lp(a) without diabetes and high BP is a reliable predictor for risk of CVD?



#8 pamojja

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Posted 24 October 2016 - 08:38 AM

pamojja, thanks for explaining. Sorry to not understand this. I don't have high BP or diabetes. So this still means that lp(a) without diabetes and high BP is a reliable predictor for risk of CVD?

 

From what I've read (sorry for not having sources at hand), Lp(a) becomes more risky especially with high LDL. In Standard of care Lp(a) therefore isn't chased down, but instead aggressive lowering of LDL pursued. Usually < 70 mg/dl with Statins.


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#9 niner

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Posted 24 October 2016 - 09:32 PM

My understanding of lp(a) is that it is a problem in itself, but because doctors think there is no way to lower it (because Big Pharma doesn't have a drug for it), they push on all the other factors as a way of reducing CVD risk.   Recently I heard that one of the new hyper-expensive CETP inhibitors also reduces lp(a).  Here's a paper on it.



#10 RWhigham

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Posted 27 October 2016 - 06:22 AM

 Lp(a) is just regular LDL with an added lipoprotein-a molecule. The lipoprotein-a molecule comes in 3 genetically determined lengths with a short, medium, or long sticky section.

 

Lp(a) is made by the liver in response to cells signaling the presence of oxPhos in their cell walls. Lp(a) collects oxPhos from cell membranes, and is eliminated by the kidneys taking the collected oxPhos with it. (In contrast, regular LDL is eliminated primarily by the liver).

 

High Lp(a) is an indicator of too much poly-unsaturated fats in your cell membranes which is oxidizing easily. If you have the short version of lipoprotein-a your liver will have to make much more Lp(a) to handle a given oxPhos load. Reduce your oxPhos in your cell membranes and your liver will normally make less Lp(a). 

 

Doctors misguidedly recommend high dietary poly-unsaturated fat in place of dietary saturated fat to reduce LDL and hence total cholesterol. High dietary poly-unsaturated fat results in the liver destroying a lot of oxLDL (containing oxPhos lipids) instead of releasing it. Then a lot more LDL oxidizes after being released.

 

Your body hates oxPhos and is not happy with high poly-unsaturated fat. The ratio of fats in heavy cream which evolution has likely optimized for young mammals is approximately 62% saturated, 29% mono-unsaturated, 2% poly-unsaturated omega 6, and 1% poly-unsaturated omega 3.

 

Macrophages consume oxLDL which leads to the formation of plaque (It's still an open question if LDL gets oxidized mostly after getting trapped in the artery wall, or if it gets trapped because its oxidized). I want my LDL as hard to oxidize as possible while still allowing for adequate membrane permeability.

 

High lp(a) is bad because the oxidation of lipids is bad. Many restaurants in the US are frying everything in poly-unsaturated oil. (Others are still using cheap trans-fats which are worse and not banned in the US until 2018). I personally will not eat anything fried in a restaurant.

 
 

Edited by RWhigham, 27 October 2016 - 07:08 AM.

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#11 TheFountain

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Posted 13 February 2020 - 09:51 PM

Old post but, 

 

Isn't  high LP (A) considered an independent risk factor that could be higher than average regardless of how healthy you eat, regardless of how good your cholesterol panels look, regardless of how fit you are, because it is considered entirely genetic?

 

When fitness instructor Bob Harper had his event it was attributed to higher than average LP (A) which is probably because a first degree relative also had it. Such as Mother, father or sibling. 

 

At least this is my understanding. 



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#12 panhedonic

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Posted 19 June 2021 - 04:28 AM

so what's the latest recommended for us high LP(a)? I heard of pcsk9, >4g EPA's, Niacine and Fibrates (podcast by Peter Attia, lipidologist)







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