Kurt G. Harris MD

PāNu means paleonutrition. The "paleo" here signifies "old" and not necessarily paleolithic. The PāNu approach to nutrition is grounded on clinical medicine and basic sciences disciplined by knowledge of evolutionary biology and paleoanthropology. The best evidence from multiple disciplines supports eating a pastoral (animal-based) diet rather than a grain-based agricultural one, while avoiding what I call the neolithic agents of disease - wheat, excess fructose and excess linoleic acid.

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Main | Polyphenol Hormesis follow-up »

A cartoon view of lipoprotein (a)

Reader Kelly asks about Lp (a) in the comments.

Dr. Harris, I'm just loving the last two posts and how you relate it to Stephan G.'s recent series.  
Slightly off topic, can you  (or others) elaborate on why zero Lp(a) is worse than low Lp(a)? I've seen Peter mention this too but cannot find details anywhere.  (My Lp(a) was nondetectable when tested last year).  Is it possible to raise or is it a gene that I carry and permanent?   My doctor said I'll likely never have a heart attack because of it...

thanks, Kelly

The first thing to understand is that Lp (a) is not something you can do much about, other than if its high you can reduce it a bit with increased saturated fat intake. (Yeah, I know about niacin...)
This is my cartoon version of Lp (a) and atherosclerosis/ coronary events:

Lp(a) is genetically determined in that some have the increased kringle repeats and some don't. Lp(a) seems to function as a repair molecule - including vascular repair, and may relate to infection control as well.
There are two reasons you could have high Lp (a) levels, and one that you could have zero. 

1) You could have lots of vascular damage going on, and the high levels would reflect lots of repair activity being required. You are the United States, with lots of crappy asphalt highways that are falling apart, so Lp (a) is the repair crews, and seeing a lot of them reflects high levels of road repair. You have repair crews and as many of them as you can muster are out fixing things because the roads are crap.

2) You could be born with a very high level, and if there is not much vascular damage going on, the high levels just mean you have a lot of Lp(a) available.  You are Germany, where the roads are well-engineered high quality concrete, and the high German taxes have funded plenty of DOT repair crews - all hanging around and waiting for something to fix, just in case.
3) You could be born with very little or undetectable Lp (a). As long as little vascular damage occurs you might not need much. As long as you have good roads and keep the overweight 18-wheelers off them, you might not need a lot of road repair crews. But having some Lp (a) or some road repair crews is going to be better than none, no matter how good condition your arteries or roads start out in.

This little cartoon and road metaphor for Lp (a) fits pretty well with what the epidemiologic data tell us and with the known genetics and putative actions of it in humans and hedgehogs. In humans, it's that j-curve again. On a population basis, the lowest mortality is in people with low but nonzero Lp (a), the highest is in those with very high levels, most of whom are doing a lot of vascular damage and repair, but not all!

If you have Lp (a) that is 0, you are in category 3. The evidence I have so far is that I am in category 2. I have Lp(a) of 85 but my calcium score at age 49 is 0, my CIMT is the same as a typical 30 year old and ancestors who don't smoke (and even some with up to 50 pack years or more) typically live to the 9th decade with no coronary events. It's worth mentioning that all my relatives eat the SAD and no one has ever been diagnosed with diabetes at any age, either.

Lp(a) is a good model for how something can be a statistical risk factor for coronary events, but be relatively meaningless when applied to single individual. Of course, in my model, it is not "causing" heart attacks or anything else.


Reader Comments (10)

So in this model, using a drug to lower Lp(a) could actually be very very bad, as seemed to be the case with CETP inhibitors.

By the way, I am concerned about your family hstory. It seems you are genetically adapted the SAD diet. For you, meat and eggs may be paleolithic agents of disease!


Yes on the Lp (a) lowering drugs. I would expect that to be as "successful" (deadly) as torceptrapib.

Actually, what I said about the SAD should be modified. Always plenty of meat, real butter and eggs and whole milk but also some wheat and sugar and veggie oils in restaurant food. I think if you add lots of animal products to the SAD, you get something healthier even if the NAD are still there.

March 2, 2011 | Unregistered CommenterJohn

Dr Harris:
I think the second to last paragraph may be most meaningful as it alludes to the importance of genetics. All relatives on SAD diet,some smokers, and living to 9th decade. Genetics may not be determinative with regard to health outcomes-heart disease,cancer, etc, but they are still pretty damn important. So, were there a history of heart disease an elevated Lp(a) might take on greater importance.


See the previous comment re: the heavy reliance on animal products. We never, ever bought into the diet-heart hypothesis, so it was not really the year 2000 version of the SAD, with huge amounts of low fat garbage and margarine - more like the 1950 version. Cookies were usually made with Crisco, though.

But yes, resistance to the SAD is heavily influenced by genetics. And I never said there were no DOCs, just no diabetes or coronary events. My paternal grandmother died at 67 of a presumed stroke but was a lifelong heavy smoker. My grandfather's sister died at about 65 of a stroke - also a long-time smoker. My Dad's sister died at 76 of lung cancer from smoking. The ones who quit smoking before age 50 tend to live to around 90. My grandfather had 12 siblings and I think 8 lived to be 90. Perhaps the smokers would last longer with a better diet. Who knows? So yes, both sides of my family tree are somewhat SAD resistant, but life is trying to kill us, so why not try to be even healthier?

March 2, 2011 | Unregistered Commentersteve

Great analogies- thanks! Heart disease is rare in my family history too, thank goodness. Mom and her side never went for the margarines and frankenfoods either, so it wasn't in our home growing up (grandma was Belgian).

March 2, 2011 | Unregistered CommenterKelly A.

An interesting post. Do you know of any data that shows to which degree Lp(a) concentrations can vary in a given individual (by comparison to the genetically-determined baseline) in response to either acute cardiovascular crises or, maybe, to a suppression therapy, e.g. with mega-doses of niacin?

Any studies showing what's happening to Lp(a) as people age and their vascular repair needs presumably go up?


March 2, 2011 | Unregistered CommenterKaa

Very interesting article, and something I'd been wondering about since my doctor was just talking to me about my Lp(a) level. I'm curious though, because my level just increased a bit and my doctor told me I'm now on the upper limit of a "good" Lp(a) level.

Last year my Lp(a) was 5. I just had a follow up VAP and it went up to 10. The only changes I made in the last six months were supplementing 6k units of Vitamin D3 - which raised my D level from 31 to 75 - and supplementing 200mg of Magnesium Glycinate nightly (I can't do 400mg, it knocks me out - it's like I took a NyQuil).

Could those two supplements have caused the increase, or is this just a sign that I had a bit more "road repair" required. Is that jump from 5 to 10 even something to worry about?


KGH: Those are both low values. I am suspicious of supplementing to D levels that high. 30 ng/dl is probably plenty. Vit D from sunshine is far preferable to pills.

March 2, 2011 | Unregistered CommenterMark B

Dr Harris:

My family history is oriented towards CAD. Paternal grandfather died of heart attack in 50's(smoker), father had heart attack in 60's, but still alive having had bypass and stents at 83, and brother(non smoker) had heart attack at age 52. I am 60 and have diagnosed CAD via IMT and calcium score of 220. I have never smoked, weight not an issue(nor was it for relatives who had events) When i had an NMR i was shocked to see a LDL particle count of 1795 and all small! For the last several years due to your blog and some others, i elimiated neolithic agents,etc, but without the assistance of hated statins could not get the number below 1100 to 1300 with predominance of small particles. No grains or starch in the diet at the time. Now have added some "safe starches" Metabolically, something is not right, because even when on SAD type diet, trigs were never more than 75. Now, they are around 28-32. So, perhaps even with best diet, genetics may still play a predominant role. I listened to Loren Cordain on Jimmy Moore who talked about plaque accumulation still happening to those on the Paleo diet, but with no occurrence of events so i will continue to keep N-3 agents out of diet and hopefully see the 9th decade event free!

Note i was not suggesting you stay on a SAD diet; just was finding it interesting that your family members thankfully had no adverse consequences,(genetics) The Nick Lane book you recommended looks tremendous and will be ordering it via this site. Thank you!

March 2, 2011 | Unregistered Commentersteve

Thank you for this information. I received what I considered perfect blood panel results, but my Dr. said I need to come back to address my 'higher than normal' Lp(a) levels. I had a 16. Not a word about how my other results were so good. And then when I researched Lp(a) I could hardly find any information that didn't say it is not a # that you can easily change because it is most likely genetic. I am trying to reverse my MS with nutrition and having great success. I do eat dark chocolate uncontrollably (which I know I have to get that under control, but it is my last frontier), and I saw that in my a1c level (5.3). I was so proud of my blood work, but felt profoundly deflated when all the Dr. could say was that I need to get my cholesterol under control because of the lp(a) #. I got this link from the Healthy Skeptic and I can't wait to read every word of your blog. Thanks again for this post.

March 2, 2011 | Unregistered CommenterWhitney Ross

well diabetes, obesity and heart disease run rampant on my dad's side of the family and cancer on my moms... guess im doomed for failure but they way i see most things...do i really want to or need to know everything about how my body is working? if i feel healthy, act healthy and live accordingly i surely dont want some doctor tellin me in 5 years im going to die of a heart attack b/c i am better off not knowing. i dunno, maybe it is just me

March 2, 2011 | Unregistered CommenterMallory

While strictly anecdotal, with 2 gms/day of Niaspan (plus 40 mg per day of Crestor, plus fish oil, as a matter of full disclosure), I have reduced my Lipoprotein A from 180 to 30 over the course of 2 years (slow, continuous reduction). {Bad family hx of CAD: father died at 39 of MI, brother at 47 of MI, another brother with 5 stents. My current age: 54 years.}

My cardiologist and I have reduced my Lipitor to 20 and Niaspan to 1 gm: total cholesterol 66 (sic), HDL 45, triglycerides 70, CPK up only a little.

More on full disclosure: I govern my dietary intake with Weight Watchers online and, while I avoid many foods with high glycemic index, I eats fruits freely and bread & pasta in moderation.

In any case, while only an anecdote - from my perspective - niacin is worthy of more than just a parenthetical comment, given Lipoprotein-A's role as an "evil-doer"

Mike Leavell

KGH: There is no evidence whatever that lowering your LP (a) with any drug will do anything at all for your coronary risk. If you have a reference for a trial showing such an effect with Lp (a) lowering, let us know, but I've not seen it, and once you get familiar with the literature, you'll understand what I've said, even if your cardiologist doesn't.

A weight-watchers diet with bread and pasta would not be my first choice for a "non-atherogenic" diet, but as Peter might say if he were American "You pays your money and you takes your chances".

Maybe I was not clear enough. I don't think it is is an "evildoer" - I think it is a repair kit.

Hello Dr. Harris,

I am curious to hear your thoughts on the Pauling/Rath theory of atherosclerosis- that Lp(a) deposits cholesterol on the arterial walls as a temporary fix until vitamin C would actually repair the damage. It seems they view(ed) atherosclerosis as a disease of vitamin-C-deficiency.

A detailed overview here: www.orthomolecular.org/library/jom/1992/pdf/1992-v07n01-p005.pdf

I love your blog and always tell people to check it out- it is seriously the "red pill" of the American nutritional matrix.

KGH: Thanks for the compliment. I can't say I've read of a Pauling/Rath theory before so can't comment. "Orthomolecular?" Hmmmm......

March 3, 2011 | Unregistered CommenterDaniel

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