Tuesday, February 02, 2010

Lipoprotein(a) genetics press release

Richard over at Free the Animal discussed this press release, relating to this paper, delivered a day early from the NEJM, by Santa, to cardiologists all over the world.

The paper itself is a piece of trivia (next post) but it is useful personally as it has me back to thinking about Lp(a), arteriosclerosis and genetics. Before I start talking about the abstract there are a couple of laughs/cries to be had from the press release itself.

First is Eric Topol. When you read a technical paper and you see the word "Atkins™" in the discussion, you know you are sitting on a garbage heap. When you see Eric "rent a quote" Topol in a press release you know you are in for a laugh too. Just how funny Eric is requires that you read Malcolm Kendrick's superb essay on Treating to New Targets, the TNT study, which obviously went like a bomb. Or bombed.

You really must read the original essay if you haven't already, but always remember the statistical significance and the biological significance of being dead are two quite different things, unless you sell a statin of course. Eric is owned by statin pushers.

Now, for another giggle, down at the end of the press release there is the section which is as predictable as the musings from dear Eric. This time Kathiresan gets the idiot award:

"Finally," adds Kathiresan, "the genetic data suggest the hypothesis that lowering the plasma Lp(a) lipoprotein level by pharmacologic means will lower the risk of coronary disease."

That sounds perfectly reasonable, if you have Kathiresan's outlook, until you get to the follow on, added by the pharmaceutical company which owns Heartwire's tame author, Lisa Nainggolan:

"Another group of drugs in development that lower Lp(a) are the cholesteryl-ester transfer protein (CETP) inhibitors (such as anacetrapib), which also raises HDL..."

Now if anyone out there thinks that anacetrapib is going to turn out to be remotely different from torcetrapib or the genetic defects giving low CETP activity in Japanese or non-Japanese USA citizens, all of which raise HDL while killing people of heart disease, well you must be on a statin.

Equally, if you think a pure Lp(a) reducing pharmaceutical agent is going to stop heart disease, you're probably wrong. As Dr BG says, Lp(a) has some seriously good effects but you shouldn't run with scissors...

Now, reducing the need for the body to make Lp(a), that's a different approach to lowering it pharmacologically!



Ross said...

I don't see "Atkins" anywhere in the discussion. Did you mean "Watkins"?

Dr. B G said...

Great posts!! I enjoy ALL of your stat analyses...

Boy. These press releases are so FUNNY.


I think they're running around with scissors *haa*

WHY is it such a bloody media 'secret' what works...?!
--egg yolks
--saturated fat (animal, marine, coconut/almond, etc)
--high omega-3
--low carb
--ketosis (which mimics NIACIN)

...what does NOT work for Lp(a)?
--high carb
--low saturated fat
--kidney failure

Dr. B G said...

Whoops. Forgot statins (and zetia) -- these don't work either. They both raise Lp(a). Perhaps this is why these drugs fail to reverse coronary calcification (and CIMT, respectively).

I think most cardiologists are pretty dumb to this, dunno why...

Peter said...

Sorry Ross, the Atkins allusion was a back reference to the paper I got bogged down on for the last six or seven posts!


Salik said...

Lp(a) in some individuals is provoked by a diet high in cereals like wheat. It is a survival mechanism in conditions where cereals are not available but fat is. The opposite of APOE4, where a tiny bit of fat goes a long way.
Without knowing the genetic make up of populations,advising high or vey low fat is futile.
Coronary artery disease is multifactorial, prolonged sugar and fat circulation times have to be considered.