Statin OR Niacin?
swampwiz
diease, including 2 grandmothers who died of heart attacks at 43 and 63, and a
father that has had 5 carotid endoarterectomy and a bypass procedure and his
sister who had a stroke. My mother and her father seem to be immune to
cardiovascular problems. Her ratio is quite low ( ~ 2.5 .)
Up until I started with 10 mg Lipitor (I was 38 at the time, now 41), I had
cholesterol levels of about 120-130 LDL and 35 HDL (bad ratio, I know.) After
a year of Lipitor therapy, the LDL dropped to 85 (but the HDL also dropped, to
26.) I eat fairly normally (probably better than average, but not super
great.) My liver profiles since then seem to be normal.
About 10 years prior to starting the Lipitor, I did do a farily decent job of
a better diet, but the levels went down only about 10%. I am a former
weightlifter (no steroids), and exercise regularly. With Lipitor doing such a
great job, it seems that the effect of diet (short of the very difficult Dean
Ornish diet - I'm a carnivore) is noise compared to that of Lipitor.
OK, so when I visited a new health therapist, I was told that Niacin is a
better alternative to Lipitor. (She harped on how Lipitor is so bad for the
liver, which I know, but in my situation would rather have then cardio
problems.) I am open to new ideas, but Lipitor seems to be doing great for me
(although I would like the HDL to get boosted.) However, it seems that Niacin
has positive HDL effects, and this intrigues me.
I have never heard of Niacin being so good, and I wonder why it seems that
there has been little mention of this in the general culture. There must be a
reason, or else there never would have been a market for the statin drugs.
I'd like to get some good info on using Niacin. In fact, I would like to use
both Niacin and Lipitor.
Jim Chinnis
>I have never heard of Niacin being so good, and I wonder why it seems that
>there has been little mention of this in the general culture. There must be a
>reason, or else there never would have been a market for the statin drugs.
Niacin can't be patented, so it is the responsibility of the governments to
research it and spread the word. Basically, the governments have dropped the
ball. The corporations that developed and patented the statins have done
much better. There are many, many sudies showing that statins save lives and
none that I know of showing the same for niacin.
Call your congressman.
You can choose whether to take a drug (niacin) that boosts HDL but hasn't
been shown to save lives or a drug (statin) that doesn't do much for HDL but
saves lives for reasons unclear.
>I'd like to get some good info on using Niacin. In fact, I would like to use
>both Niacin and Lipitor.
Both are toxic to the liver.
I think it's a tough decision.
--
Jim Chinnis Warrenton, Virginia, USA
Pramesh Rutaji
Pramesh Rutaji
It is not the responsibility of the government to research niacin or any other
product. The free market can handle this all quite well if we let it work. The
drug companies on the other hand have legal monopolies and government sponsored
legal help to limit competition, restrict importation, and keep prices
artificially high and are allowed to be less than honest in their marketing
literature and published results.
As I recall, some longer term studies which showed significant benefits from
niacin, 5 years or more, were posted to the sci.life-extension group a while ago.
David Rind
There's essentially no evidence to suggest that niacin is good for
primary prevention. Whether someone whose only risk factors for CHD are
a family history and and a low HDL needs any medication for primary
prevention is a reasonable separate question, though. (Not clear from
the above whether it was the poster's father or grandfather who had the
CABG and CAEs.)
However, if a medication is needed for primary prevention, statins have
actually been shown to reduce mortality and cardiac events in this
setting (in at least some trials) and niacin has not.
In people with a low HDL who already have coronary disease, there is one
trial that suggests that adding niacin to a statin may decrease cardiac
events. It was a small trial, though, and because of bad effects on
mortality in other trials of lipid-lowering drugs, I worry that it
wasn't large enough to evaluate the effect on mortality.
It's unlikely that niacin adds much to statins for primary prevention,
since the rates of events are already so low with a statin alone.
--
David Rind
dr...@caregroup.harvard.edu
Pramesh Rutaji
From the collection of large statin trials, all cause mortality is unchanged
from statin usage; while it is true that mortality from cardiovascular events
may be decreased, mortality from other causes are obviously increased from the
statins because all cause mortality remains unchanged, even after long term use.
Fish oil is more effective than statins in preventing cardiovascular events
without the long term mortality increases from other causes. Additionally,
there is a lot going for Niacin and the ignorant statement that there are no
studies for Niacin that show benefit is absolutely foolish. If you think that
lowering LDL, free fatty acids, and triglycerides, increasing HDL, creating more
protective HDL2 than HDL3, and increasing LDL particle sizes is meaningless,
then you have even begun to examine the medical literature.
1: Med Hypotheses. 2007 Jan 17; [Epub ahead of print]Click here to read Links
Anti-inflammatory effect is an important property of niacin on
atherosclerosis beyond its lipid-altering effects.
* Yu BL,
* Zhao SP.
Department of Cardiology, The Second Xiangya Hospital of Central South
University, Middle Ren-Min Road, No. 139, Changsha, Hunan 410011, PR China.
Niacin has been used for decades to lower the plasma concentrations of
cholesterol, free fatty acids, and triglycerides in humans, and in addition it
raises more than any other drug the levels of the protective high density
lipoprotein. These effects have been used to treat dyslipidemic states. Trials
have shown that treatment with niacin reduces progression of atherosclerosis,
and clinical events and mortality from coronary heart disease. The beneficial
clinical efficacy of niacin appropriately emphasizes the prominent role of its
lipid-altering effects; however, high expression of niacin receptor in a variety
of immune cell types, lowering of inflammatory markers, and beneficial impact on
adipokines expression could provide rational to the hypothesis that
anti-inflammatory effect is also an important property of niacin on
atherosclerosis beyond its lipid-altering effects.
PMID: 17239549 [PubMed - as supplied by publisher]
Pramesh Rutaji
1: Atherosclerosis. 2003 Nov;171(1):87-96.Click here to read Links
Antiatherothrombotic effects of nicotinic acid.
* Rosenson RS.
Preventive Cardiology Center, Northwestern University, The Feinberg School
of Medicine, 201 East Huron Street, Galter Pavilion 11-120, Chicago, IL 60612,
USA. r-ros...@northwestern.edu
Cardiovascular event reduction in hypercholesterolemic subjects
appropriately emphasizes the prominent role of statin therapy; however, niacin
(nicotinic acid) is also an effective lipid-altering agent that prevents
atherosclerosis and reduces cardiovascular events. Niacin has multifarious
lipoprotein and anti-atherothrombosis effects that improve endothelial function,
reduce inflammation, increase plaque stability, and diminish thrombosis. Niacin
reduces the atherogenicity of low-density lipoprotein (LDL) by changing the
distribution of small LDL to large LDL subclass, and the susceptibility of LDL
to oxidative modification. It is the most effective agent for increasing
high-density lipoprotein cholesterol. Moreover, it favorably alters high-density
lipoprotein composition, increasing apolipoprotein AI relative to apolipoprotein
AII. Niacin reduces blood viscosity through a variety of mechanisms, thus
improving blood flow and perfusion through stenotic segments of the vasculature.
Finally, niacin has cardioprotective effects that may limit ischemia-reperfusion
injury. By preserving glycolysis during periods of ischemia and improving
subendocardial blood flow during reperfusion, niacin can improve the functional
recovery of the myocardium.
PMID: 14642410 [PubMed - indexed for MEDLINE]
Jim Chinnis
>From the collection of large statin trials, all cause mortality is unchanged
>from statin usage; while it is true that mortality from cardiovascular events
>may be decreased, mortality from other causes are obviously increased from the
>statins because all cause mortality remains unchanged, even after long term use.
This is a very important observation, except that it is false.
David Rind
> From the collection of large statin trials, all cause mortality is
> unchanged from statin usage; while it is true that mortality from
> cardiovascular events may be decreased, mortality from other causes are
> obviously increased from the statins because all cause mortality remains
> unchanged, even after long term use.
That's actually a pretty good description of what has been seen in many
of the trials that used medications other than statins for lipid
lowering, but is not accurate with regard to statins. Most trials of
statins showed similar reductions in cardiac events, cardiac mortality,
and all-cause mortality.
> Fish oil is more effective than
> statins in preventing cardiovascular events without the long term
> mortality increases from other causes.
It's funny that you should mention fish oil after the above comments.
Take a look at the rates of cardiac mortality and all-cause mortality in
the enormous JELIS trial published last month in Lancet.
> Additionally, there is a lot
> going for Niacin and the ignorant statement that there are no studies
> for Niacin that show benefit is absolutely foolish. If you think that
> lowering LDL, free fatty acids, and triglycerides, increasing HDL,
> creating more protective HDL2 than HDL3, and increasing LDL particle
> sizes is meaningless, then you have even begun to examine the medical
> literature.
I'm pretty sure I've examined the medical literature somewhere along the
way. I'm not impressed by biochemical evidence of "benefit" with
medications -- no one should ultimately care what effect a medication
has on their lipid profile. They should care whether the medication
makes it more or less likely that they will have a cardiac event, a side
effect, or die.
And in terms of clinical benefits, there is essentially no evidence to
suggest that niacin is good for primary prevention. The CETP inhibitor
torcetrapib seems to have great effects on the lipid profile, lowering
LDL and dramatically raising HDL. Unfortunately, as studies found this
past December, it also seems to kill people.
--
David Rind
dr...@caregroup.harvard.edu
David Rind
> x-no-archive: yes
>
> David Rind wrote:
>
>> I'm pretty sure I've examined the medical literature somewhere along
>> the way. I'm not impressed by biochemical evidence of "benefit" with
>> medications -- no one should ultimately care what effect a medication
>> has on their lipid profile. They should care whether the medication
>> makes it more or less likely that they will have a cardiac event, a
>> side effect, or die.
>
>
> I think those are researcher's chosen end points, and not necessarily
> the primary ones for patients.
>
> First comes quality of life. If the drug causes fatigue, lethargy,
> aching muscles, cognitive losses, that has to be factored into the
> overall benefit/risk equation.
>
> Susan
Umm, I was counting all those in "side effect". People are typically
willing to make minor quality of life sacrifices to live longer, but not
major quality of life sacrifices. However individuals need to make there
own decisions on where these things balance out.
--
David Rind
dr...@caregroup.harvard.edu
Jim Chinnis
>I'm pretty sure I've examined the medical literature somewhere along the
>way. I'm not impressed by biochemical evidence of "benefit" with
>medications -- no one should ultimately care what effect a medication
>has on their lipid profile. They should care whether the medication
>makes it more or less likely that they will have a cardiac event, a side
>effect, or die.
This is what's known as the "bottom line." And if our theories about risks
and biological processes were very good, we would have had cures for every
cancer at least a decade ago. But we didn't.
Every time I've bought a little stock in a drug company that had great
test-tube results or even real-life improvements to known markers and risk
factors, I've lost.
Even when I've treated myself based on biochemical evidence--such as taking
folic acid, B6, and B12 for homocysteine reduction--I've lost.
Jim Chinnis
>I take it you haven't suffered those chronic ills? I have, and the last
>thing I'd call them is minor.
He didn't say they are minor.
David Rind
> x-no-archive: yes
>
> Susan
You might try rereading (in context) what I wrote without preconceived
notions, and you'll likely conclude that Jim Chinnis is correct.
--
David Rind
dr...@caregroup.harvard.edu
bigvince
bigvince
>
> Susan
No I thought david did. Thanks Vince
David Rind
I wrote the paragraph about "side effects" (with the their/there typo),
but not that subsequent sentence. With headers it looks like Susan wrote
that sentence, but I don't recall seeing such a post from her, and she
points out that she did not write it. I'm assuming Vince wrote that
sentence, but that's not actually clear from the posting.
In any case, I agree with the first half of the sentence -- there are
not a lot of studies that show a great reduction in all cause mortality
when statins are used for primary prevention. There are really only a
couple of such studies that were large enough (and early enough, before
everyone was already taking statins), and the absolute reductions in
all-cause mortality are small. WOSCOPS was the first such study and
all-cause mortality was reduced by 22%.
I completely disagree with the second half. We have overwhelming
evidence that statins reduce cardiovascular events (as well as all-cause
mortality) in patients with known CHD. The ads that give a disclaimer
like the one mentioned are typically for a statin that has not been used
in outcomes studies (mostly Crestor), or for a nonstatin drug like Zetia.
--
David Rind
dr...@caregroup.harvard.edu
bigvince
>
> - Show quoted text -
I did wright that sentance; perhaps not clearly.Let me try again.
There are not a lot of studies that show a large reduction in all
cause mortality when statins are used in primary prevention. And the
evidence that they prevent cardiovascular events again when used in
primary prevention is also not that strong. Never was I talking about
people with know CHD where the evidence is much stronger. Also it is
important that each statin be looked at individualy ;as the effects
they show may be specific to each; and may differ even with comparible
effects on lipids. Thanks Vince
David Rind
> I did wright that sentance; perhaps not clearly.Let me try again.
> There are not a lot of studies that show a large reduction in all
> cause mortality when statins are used in primary prevention. And the
> evidence that they prevent cardiovascular events again when used in
> primary prevention is also not that strong. Never was I talking about
> people with know CHD where the evidence is much stronger. Also it is
> important that each statin be looked at individualy ;as the effects
> they show may be specific to each; and may differ even with comparible
> effects on lipids. Thanks Vince
For the most part, I think the effects of statins appear to be class
effects such that one statin is similar to another in terms of benefits.
There do seem to be some differences in side effects between the
lipophilic and hydrophilic statins, though this difference probably
isn't large.
The beneficial clinical effects are similar enough, and the drugs are
similar enough, that I don't think every new statin needs to prove its
clinical benefits, but I do think all need to be studied for side
effects and lipid lowering effects. This is in contrast to my feelings
about nonstatin lipid-lowering medications that absolutely need to prove
clinical benefit.
The one area where I think individual statins may show distinct benefits
(rather than benefits as a class) is in acute coronary syndromes, and
perhaps other situations soon after the medication is started. The
results of the two large trials in ACS suggest that atorvastatin has
early benefits and simvastatin does not. I would only use atorvastatin
in ACS until other statins show similar clinical benefits.
--
David Rind
dr...@caregroup.harvard.edu
bigvince
The permise that all statins as a class show the same benefits has
never been proven . It is based on the belief that statins work
directly by their effect on lipids. If that is true than any drug
that has a similar effect on lipids should show a comparible reduction
in coronary events. When non statin drugs changed lipid profiles the
results where not the same. As statins have many and sometimes serious
side effects it is important that the basic premise be carefully
proven. If statins do not work directly thur there influence on lipids
how else might they work. Statins have a antiinflamatory effect ; it
is possible that this is the mode by which they act. We know different
statins have different side effects profiles :if their side effects
vary by individual drug then their benefit may also. In medicine it is
very important that these thing be proven. I think the use of statins
in primary prevention does not have a well proven risk benefit ratio.
Also there should be enough data showing they may not have the same
profile that I do not think it prudent to treat them as equivalents.
The evidence for their use in primary prevention is weak based of all
cause mortality datas . To use them as interchangable drugs is
probably not prudent either as if they actually work thur other
mechanisms than lipid reduction. They could have large difference in
outcome even in treating people with CHD. A point that your
observation about ACS tend to make . If two statins show comparable
effects on lipids but different clinical results then then they must
be working by adifferent mode. Thanks Vince
David Rind
> The permise that all statins as a class show the same benefits has
> never been proven .
How could this ever be proven for any class of drugs, since new drugs
are always being developed? That is, describe a study that would prove
that a class of drugs all have the same clinical benefit.
(Assuming you cannot come up with such a study, do you disbelieve in
class effects for all medications or just for statins?)
>It is based on the belief that statins work
> directly by their effect on lipids.
Your asserting this does not make it true. I believe statins have a
class effect because multiple different statin drugs have produced
similar relative risk reductions in a whole bunch of different placebo
controlled trials. It doesn't require any assumption about how statins
work to notice that, as a class, they have similar effects on clinical
outcomes.
>If that is true than any drug
> that has a similar effect on lipids should show a comparible reduction
> in coronary events.
No, not at all. This is an assumption and extrapolation you are making.
ACE inhibitors lower blood pressure and appear to exhibit class effects
on kidney disease, stroke, and heart failure. Alpha blockers also lower
blood pressure, but do not seem to have the same effects on clinical events.
The whole notion of class effects is that very similar drugs typically
produce similar clinical outcomes when equipotent doses are used, but
that drugs across classes cannot be counted on to produce similar
clinical outcomes even when they have similar effects on some surrogate
endpoint like LDL or blood pressure.
--
David Rind
dr...@caregroup.harvard.edu
bigvince
The premise that all statins as a class show the same benefits has
> > never been proven .
>
> How could this ever be proven for any class of drugs, since new drugs
> are always being developed? That is, describe a study that would prove
> that a class of drugs all have the same clinical benefit.
These drugs have all been approved on the basis of their effect
on lipids, They are marketed as preventing CVD on the basis of their
effect on lipids and as that is the clinical benefit they showed to
get FDA approval as a matter of fact as a class they have similar
clinical benefit they all lowering lipids.They are used
interchangeably on that basis. There are in fact very few studies that
show much benefit in primary prevention for all cause mortality from
these drugs. The premise that these drugs are interchangeable is based
on exactly the premise that lowering lipids in itself reduces the risk
of death however that premise at least in primary prevention has never
been proven. > How could this ever be proven for any class of
drugs, since new drugs
> are always being developed? That is, describe a study that would prove
> that a class of drugs all have the same clinical benefit.
>
I think all statins where approved as a class on the clinical effect
that they lower lipids. I also believe a better target would be their
effect on end results such as all cause mortality
Vince said > >It is based on the belief that statins
work
> > directly by their effect on lipids.
>
> Your asserting this does not make it true. I believe statins have a
> class effect because multiple different statin drugs have produced
> similar relative risk reductions in a whole bunch of different placebo
> controlled trials. Please just cite me a few studies where a few different statins caused similar reduction of any none lipid end point ;particulaily all cause mortality as I can find very few. And again this is in primary prevention > ACE inhibitors lower blood pressure and appear to exhibit class effects
> on kidney disease, stroke, and heart failure. Alpha blockers also lower
> blood pressure, but do not seem to have the same effects on clinical events.
>
As ace inhibitors and Alpha blockers are different classes of
drug ;the fact that they show different profiles is not
surprising David says..... The
whole notion of class effects is that very similar drugs typically
> produce similar clinical outcomes when equipotent doses are used, but
> that drugs across classes cannot be counted on to produce similar
> clinical outcomes even when they have similar effects on some surrogate
> endpoint like LDL or blood pressure.
Even within classes significant differences can occur When the
original premise is flawed Atenolol the most widely used beta blocker
has recently been shown to increase mortality rates in several meta-
analysis while another beta blocker does not. Statin drugs likewise
need to be shown to be interchangeable .If there effect is not from
lipid reduction. They should be required to show the ability to
decrease mortality or some other real world event. I think that
evidence is far from certain. Thanks Vince