Comments on: Statin effects of low-carb diets

By: jeepifer

jeepifer — Mon, 08 Sep 2008 18:42:39 +0000

Okay, I'm confused. My LDL recently was 151, and my (Internal Med) doc wants to put me on a statin. I said no. I spoke to a cardiologist the other day, asking about the difference between the fluffy and dense LDL sizes, and why a statin? Her response was that the statin helps repair the endothelium, thus preventing the particles from adhering to the arterial walls, regardless of whether they're dense or fluffy. Can you comment on this? I'm now concerned as to whether the statin might help, after all. Also, she suggested I talk with an endocrinologist in regards to Metformin and increasing insulin sensitivity, which might have some success in helping Metabolic Syndrome pre-diabetics lose weight. Thoughts? First, you've got to understand that randomized, placebo-controlled studies (the only kind that really count) have shown no benefit in terms of longevity for women taking statins. Period. End of story. It didn't matter if the women were young or old or if they had already been diagnosed with heart disease or not, statins didn't make them live longer. Statins may or may not "repair endothelium," but it doesn't matter because the data show that the drugs don't make women live longer, which is the real issue. I suspect that the idea that these drugs repair the endothelium is an ad hoc hypothesis to somehow counter the idea that the drugs don't work in terms of increasing longevity. There is some evidence that Metformin does increase insulin sensitivity and that, consequently, it can help with weight loss. Metformin is one of the very few drugs that I use in my practice, but I try dietary changes first.

By: VAN

VAN — Fri, 23 May 2008 23:40:03 +0000

True or false: Most cholesterol under normal conditions is manufactured in extrahepatic tissues.
True

False

Explanation:
Most cholesterol under normal conditions is manufactured in extrahepatic tissues, and the principal and essential task is to move cholesterol to the liver for excretion as bile acids and unaltered cholesterol. The liver is the only organ that can excrete the cholesterol in these forms and in quantities necessary to maintain balance between excretion and the combined effects of dietary absorption and synthesis. It is believed that virtually all cells can synthesize sufficient cholesterol to meet the basic needs for normal function.

By: DavidC

DavidC — Fri, 18 Jan 2008 14:33:56 +0000

Would you kindly explain why BOTH the LDL receptors and HMG-CoA were down-regulated in the EGG (higher cholesterol) group. I�m guessing the cell�s needs remain constant�so do they just require less receptors to garner the same amount of cholesterol? Your insight is greatly appreciated, as always.

You’re correct. Because the cells have plenty of cholesterol available to them so they don’t have to make more or go out and drag it in. If the cells are deficient, they can get it two ways: they can make it and/or they can go out and pull it in with LDL receptors. If the cells contain plenty they don’t need to do either, and so they don’t activate the machinery to do so.

Cheers–

MRE

By: kayaman

kayaman — Wed, 16 Jan 2008 16:23:02 +0000

I’m a bit confused as to why BOTH the LDL receptors and HMG-CoA were down-regulated in the EGG group. I would have imagined an uptick in LDL-R concomitant with less being made inside the cell. Do cells just need less receptors to garner the same amount of cholesterol in this case? Any insight is greatly appreciated.

Because the cells have plenty of cholesterol available to them so they don’t have to make more or go out and drag it in. If the cells are deficient, they can get it two ways: they can make it and/or they can go out and pull it in with LDL receptors. If the cells contain plenty they don’t need to do either, and so they don’t activate the machinery to do so.

Cheers–

MRE

By: ec

ec — Sat, 12 Jan 2008 01:23:16 +0000

dr. mike! just catching up with all your posts – keep these statin posts coming!

building off another comment above, re: “rebound effect” when going off statins. are there any (good) studies you can point me to effects of quitting statins abruptly? more importantly, any studies linking this “rebound effect” and actual mortality (i.e., not just higher total cholesterol)?

finally, if someone is following LC – goes off statins – what is your expectation for the length of this rebound? could this be as short as 10 days (as you mentioned above – re: improvement time for lipids)?

Hi ec–

I don’t really know the answer to your question. Usually when I took patients off statins I didn’t recheck their bloodwork for six weeks, and by then the rebound effect was pretty much over. I would imagine the effect lasts for a week to 10 days, but I don’t know for sure.

Best–

MRE

By: Leonard Rosenkrans

Leonard Rosenkrans — Tue, 08 Jan 2008 21:54:31 +0000

Is there a study that shows a correlation between LC and changes in cholesterol levels? From what I’ve heard anecdotally on the LC websites, it seems that at least the gross levels of total cholesterol and LDL don’t tend to respond uniformly. At least not like triglycerides which seem to really decrease dramatically in the majority of people. I’ve heard of many instances where ratios seemed to improve even though total cholesterol remained elevated or even increased a bit. Just wondering if there is any consensus yet on what blood lipid effects you might expect. I’m sure it is going to depend on body fat and rate of fat loss. You would think it was common sense that when fat stores are being broken down and mobilized, there might be some transient increase. Though it would seem that triglyceride catabolism more than keeps up with this as those levels decrease early in the process of doing LC.

There are numerous studies showing decreases in total and LDL-cholesterol levels with low-carb diets. But the data in most of these studies shows that there is not a uniform response in these numbers across all subjects whereas a lowering of triglycerides is a uniform finding. What does seem to be a uniform finding is that even when LDL-cholesterol levels don’t decrease (or even increase) the particle size either doesn’t change or gets larger. With low-fat diets the opposite holds. Uniformly LDL falls to some extent, but particle size always gets smaller.

Cheers–

MRE

By: David

David — Sat, 05 Jan 2008 04:25:40 +0000

So low-carb breaks the cholesterol-synthesis chain, and it does it at the same place as statins.
Then does low-carb potentially have some of the same side effects as do statins? In particular, if they both equally shut down synthesis of mevanolate, then aren’t they both equally shutting down production of CoQ10 (ubiquitin)? If not, why not?

I’ve been low-carbing for 4+ years. Should I then be taking a CoQ10 supplement?

David

Hi David–

No, it doesn’t have the same effect that statins do. Statins reduce the level of the enzyme all the time, whereas the insulin and glucagon in the diet do it whenever appropriate.

Cheers–

MRE

By: Alex

Alex — Fri, 04 Jan 2008 16:17:15 +0000

As always thank you for these very interesting posts, doc.

While browsing another blog, I came across this link on the comments:

http://www.opinions3.com/how_it_really_works.htm

It’s an article by Liz Pavek. It’s well written but I think it may have some misinformation regarding cholesterol medications.

“then they take cholesterol-lowering drugs that force the body to make its own cholesterol by preventing the body from utilizing any from dietary sources. ”

There are some cholesterol-lowering drugs that may work that way, but not statins. The way I understand it, statins block the production of the body’s cholesterol, and the body is forced to get it from the blood via the LDL-receptors.

Off topic, I found a picture of “modern-day David” and pasted the original next to it for added effect. I’m not sure the image tag will work, but if it doesn’t here’s a direct link.
[IMG]http://i66.photobucket.com/albums/h267/mtflight/health/david.jpg[/IMG]

http://i66.photobucket.com/albums/h267/mtflight/health/david.jpg

Hey Alex–

You’re on the money with your analysis of how statins and non-statins work. Statins do work by inhibiting HMG-CoA reductase.

Thanks for the image of David. It’s terrific. I’ve got to figure out how to use it to great effect.

Cheers–

MRE

By: Joyce

Joyce — Fri, 04 Jan 2008 05:41:16 +0000

If that same study would have been done with the subjects eating 30-40% carbs, what would you expect the rise in cholesterol to be in the group eating eggs compared to the group eating egg substitute?

Can you think of any type of person who really needs more than about 15% carbs or more than about 80grams daily? Maybe a young extremely active person? I think you wrote before that most people can get all the benefits of a low carb diet with about 60g daily (Groves and Lutz also recommend something around that number).

Thanks

Yep, I would expect an increase with a higher carb diet. That’s what most of the studies have shown.

I can’t think of anyone who would physiologically benefit from more than 15% carbs: hedonistically, however, is another situation.

Cheers–

MRE

By: Chris H

Chris H — Fri, 04 Jan 2008 03:05:39 +0000

Thanks for this Doc. From what I’ve read though I don’t worry too much about cholesterol anyway.

by the way, interesting study I just read that a low fat intake was associated with more injuries in runners. I’ve written about it here:

http://conditioningresearch.blogspot.com/2008/01/eating-more-fat-protects-runners-from.html

Hey Chris–

Thanks for the link. I remember back in the old days when NFL players didn’t get hurt all that often, then some started following low-fat diets to keep their weight down, and the injuries ran rampant.

Cheers–

MRE