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        New Message Board Archives >> Medications, Treatments, Therapies 2004 >> Lipitor
        
(Message started by: Giovanni on Aug 31^st, 2004, 11:41am)

Title: Lipitor
Post by Giovanni on Aug 31^st, 2004, 11:41am

Has anyone on cholesterol lowering drugs, Atorvastatin (Lipitor)(statin drugs), noticed an adverse effect with cluster headaches. In other words, does this make your headaches worse or more frequent?

Seems to me that it had an adverse effect with me. Floridian, I need your help here!!

John

Title: Re: Lipitor
Post by clavers on Aug 31^st, 2004, 12:05pm

I have been taking lipitor for a number of years, and before that zocor. I have not noticed any effect on my CH's from these, but who knows?

Title: Re: Lipitor
Post by Bob_Johnson on Aug 31^st, 2004, 3:45pm

Have been on Lipitor for several years and my clusters have declined to zero over the last 2-1/2 years. Have never seen this class of meds mentioned in relation to any type of headache in the med literature which I scan.

Title: Re: Lipitor
Post by echo on Aug 31^st, 2004, 4:04pm

Been on it for about two years. No change in frequency or severity of my CH.

Title: Re: Lipitor
Post by floridian on Aug 31^st, 2004, 4:19pm

A big 'don't know' and 'maybe' - nothing directly on your question, a few theoretical threads to suggest it could concievably make things worse for some people.

Not sure how relevant this first one is; not the same drug, but a smilar statin. Mevastatin increases nitric oxide in the blood vessels - more dilation, less contraction. It also makes the blood vessels less responsive to serotonin.

Quote:

Am J Physiol Regul Integr Comp Physiol. 2004 Aug;287(2):R342-8. Epub 2004 May 06.

Chronic mevastatin modulates receptor-dependent vascular contraction in eNOS-deficient mice.

Budzyn K, Marley PD, Sobey CG.

Department of Pharmacology, University of Melbourne, Parkville, Victoria 3010, Australia.

We tested the hypothesis that endothelial nitric oxide (NO) synthase (eNOS)-derived NO modulates rho-kinase-mediated vascular contraction. Because 3-hydroxy-3-methylglutaryl (HMG)-CoA-reductase inhibition can both upregulate eNOS expression and inhibit rhoA/rho-kinase function, a second hypothesis tested was that statin treatment modulates rho-kinase-mediated contraction and that this can occur independently of eNOS. Contractile responses to the receptor-dependent agonists serotonin and phenylephrine but not to the receptor-independent agent KCl were greater in aortic rings from eNOS-null (eNOS(-/-)) vs. wild-type (eNOS(+/+)) mice. Similarly enhanced responses were seen in eNOS(+/+) rings after acute NOS inhibition. The rho-kinase inhibitor Y-27632 abolished or profoundly attenuated responses to receptor agonists in both eNOS(+/+) and eNOS(-/-) rings, but responses in eNOS(+/+) were more sensitive to Y-27632. Mevastatin treatment (20 mg/kg sc per day, 14 days) reduced responses to serotonin and phenylephrine in female mice of both strains. KCl-induced contractions were slightly smaller in eNOS(+/+)-derived aortic rings only. Levels of plasma cholesterol, and aortic expression of rhoA and rho-kinase, did not differ between groups. Thus eNOS-derived NO suppresses rhoA/rho-kinase-mediated vascular contraction. Moreover, a similar suppressive effect on rho-kinase-mediated vasoconstriction by statin therapy occurs independently of effects on eNOS or plasma cholesterol.

The statins also may reduce serotonin and affect mental functioning:

Quote:

Arch Intern Med. 2004 Jan 26;164(2):153-62.

Conceptual foundations of the UCSD Statin Study: a randomized controlled trial assessing the impact of statins on cognition, behavior, and biochemistry.

Golomb BA, Criqui MH, White H, Dimsdale JE.

Department of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.

BACKGROUND: Statin cholesterol-lowering drugs are among the most prescribed drugs in the United States. Their cardiac benefits are substantial and well supported. However, there has been persistent controversy regarding possible favorable or adverse effects of statins or of cholesterol reduction on cognition, mood, and behavior (including aggressive or violent behavior). METHODS: The literature pertaining to the relationship of cholesterol or statins to several noncardiac domains was reviewed, including the link between statins (or cholesterol) and cognition, aggression, and serotonin. RESULTS: There are reasons to think both favorable and adverse effects of statins and low cholesterol on cognition may pertain; the balance of these factors requires further elucidation. A substantial body of literature links low cholesterol level to aggressive behavior; statin randomized trials have not supported a connection, but they have not been designed to address this issue. A limited number of reports suggest a connection between reduced cholesterol level and reduced serotonin level, but more information is needed with serotonin measures that are practical for clinical use. Whether lipophilic and hydrophilic statins differ in their impact should be assessed. CONCLUSION: There is a strong need for randomized controlled trial data to more clearly establish the impact of hydrophilic and lipophilic statins on cognition, aggression, and serotonin, as well as on other measures relevant to risks and quality-of-life impact in noncardiac domains.

Title: Re: Lipitor
Post by crazy_mj on Aug 31^st, 2004, 5:20pm

I was only on it for about a month. It made me real dizzy and lightheaded.

Title: Re: Lipitor
Post by Rock_Lobster on Aug 31^st, 2004, 6:54pm

I have been on Lipitor for three years.

First episode on it was normal.

Second episode really sucked.

Title: Re: Lipitor
Post by Giovanni on Aug 31^st, 2004, 7:20pm

Thanks Floridian...............you came through again :)

I'm going to withdraw from this drug for a period of time and see what happens.

Thanks again,

John

Title: Re: Lipitor
Post by floridian on Aug 31^st, 2004, 9:13pm

Keep an eye on your cholesterol. Do the good diet / exercise thing and get more frequent blood tests. And talk to your doctor about this first.

Also, CoQ10 is depleted by the statins. Low levels of CoQ10 are associated with migraine, and long term use of CoQ10 reduces migraine frequency. The same thing may be true of clusters, although that hasn't been proven. Could be that an increase in CH is due to the depletion of Coq10, which could be remedied - again, just speculating.

Quote:

Treatmentupdate. 2001 Jun;13(2):4-7.

Extra co-enzyme Q10 for statin-users?

[No authors listed]

Co-enzyme Q10, or ubiquinone, is a nutrient that is produced in small amounts by the body and is also obtained from food. It plays a key role in helping the body convert food into energy. Co-enzyme Q10 is also an important antioxidant, the need for which appears to increase during HIV infection and in people who use certain lipid-lowering drugs called statins.

Quote:

Biofactors. 2003;18(1-4):101-11.

The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications.

Langsjoen PH, Langsjoen AM.

The depletion of the essential nutrient CoQ10 by the increasingly popular cholesterol lowering drugs, HMG CoA reductase inhibitors (statins), has grown from a level of concern to one of alarm. With ever higher statin potencies and dosages, and with a steadily shrinking target LDL cholesterol, the prevalence and severity of CoQ10 deficiency is increasing noticeably. An estimated 36 million Americans are now candidates for statin drug therapy. Statin-induced CoQ10 depletion is well documented in animal and human studies with detrimental cardiac consequences in both animal models and human trials. This drug-induced nutrient deficiency is dose related and more notable in settings of pre-existing CoQ10 deficiency such as in the elderly and in heart failure. Statin-induced CoQ10 deficiency is completely preventable with supplemental CoQ10 with no adverse impact on the cholesterol lowering or anti-inflammatory properties of the statin drugs. We are currently in the midst of a congestive heart failure epidemic in the United States, the cause or causes of which are unclear. As physicians, it is our duty to be absolutely certain that we are not inadvertently doing harm to our patients by creating a wide-spread deficiency of a nutrient critically important for normal heart function.

Quote:

Drug Metabol Drug Interact. 2003;19(3):151-60.

Reversal of statin toxicity to human lymphocytes in tissue culture.

Pettit FH, Harper RF, Vilaythong J, Chu T, Shive W.

Hydroxymethylglutaryl-CoA reductase inhibitors (statins) are widely used to inhibit biosynthesis of cholesterol in individuals with elevated serum levels of this risk factor for cardiovascular disease. We find that statins are toxic to human lymphocytes in cell culture at concentrations less than 0.1 microg/ml. Addition of their own plasma reverses this toxicity in some, but not all, individuals. Addition of coenzyme Q10 (CoQ10) with plasma is more effective than plasma alone in reversing toxicity in some individuals. Apparently, two factors are required to reverse the cellular toxicity of statins: CoQ10 and a plasma factor found in a subset of individuals. These observations may provide the basis for a method to assess individual susceptibility to statin toxicity and to predict which individuals may benefit from supplements of CoQ10.