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Re: Statins and training [Jimmy B.] [ In reply to ]
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Jimmy B. wrote:
Since being put on Atorvastatin (about 120 days) for high cholesterol, I have been having terrible numbness and pain in my feet during the bike and run). The statin has done a great job of lowering my bad cholesterol, but trying to train and race while on them isn't doable. As a test, I quit taking the statin meds for 4 days and the numbness and pain went away.

I have a clean diet, age 50, consistently train 14 or so hours per week (SBR and gym). High cholesterol likely genetic.

Is anyone using statins without this side-effect? If so, which one are you using?

Thanks in advance

To the OP:

I have heard countless stories about how statins affect patients. You need to talk with your MD about your specific side effect and what is to be done about it and what other choices there are. Dont' solicit advise from the internet...

In general, myalgia, or aching of the muscles occurs with a higher in incidence than reported, IMO. However, risks and benefits of why one is on the medicine needs to be seriously considered. Myopathy, is more rare. Both are less likely in third generations statins (atorva- and rosuva-/Lipitor and crestor). However, there is a track record with other meds being less likely to cause muscle aching-especially with prava- and pita- ((pravachol Livalo) and also fluva- but I almost never use this as it is a statin with less effect than many others. And even more importantly, guidelines changed recently for dosing and indications for being on statins.

*edited to add-and I see very little downside to trying coQ10-other than cost, so I usually do advise it --if aching in the muscles occurs while on any statin-even though it is not felt to be reliably useful-per studies

From Up to Date:

Statin muscle-related adverse events
Authors:Robert S Rosenson, MDSteven K Baker, MSc, MD Section Editor:Mason W Freeman, MD Deputy Editor:Gordon M Saperia, MD, FACC
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Apr 2018. | This topic last updated: Feb 07, 2018.
INTRODUCTION — Statins are the primary class of medication used to lower serum cholesterol concentration for both primary and secondary prevention of coronary disease. (See "Management of elevated low density lipoprotein-cholesterol (LDL-C) in primary prevention of cardiovascular disease" and "Management of low density lipoprotein cholesterol (LDL-C) in the secondary prevention of cardiovascular disease".)
Statins are both effective and generally safe. Although muscle toxicity remains a concern, severe myonecrosis leading to clinical rhabdomyolysis is unusual, affecting perhaps 0.1 percent of patients [1,2]. Muscle syndromes associated with statins, including myalgias, myopathy, myositis, and muscle injury (table 1) , are discussed here [3]. Other statin side effects are discussed separately. (See "Statins: Actions, side effects, and administration".)
PATHOGENESIS — The mechanism by which statins cause muscle toxicity is not well understood, but genetic studies have provided new insights [4]. They inhibit the conversion of HMG-CoA to mevalonic acid, which is an important early step in cholesterol synthesis.
Individual statins may have distinct effects on the synthesis of coenzyme Q10 (CoQ10, ubiquinone), which plays an important role in muscle cell energy production. It has been speculated that a reduction in ubiquinone in skeletal muscle may contribute to statin-induced muscle injury. Some studies have found that statins decrease skeletal muscle and plasma concentrations of ubiquinone [5-7]; however, other studies have not [8], and studies have come to different conclusions about whether statin treatment decreases levels of ubiquinone in skeletal muscle [7,9,10]. Long-term treatment with simvastatin (10 to 40 mg daily for >12 months) reduced ubiquinone content in skeletal muscles and decreased maximal mitochondrial oxidative phosphorylation capacity [11].
One study found increased levels of plant sterols in skeletal muscle in patients treated with high-dose statins [7]. Specifically, sitosterol was increased by approximately 50 percent. The authors of the study proposed that these increased cellular levels could contribute to the muscle toxicity of statins. Beta-sitosterol is an activator of AMP-activated protein kinase, which inhibits acetyl-CoA carboxylase. This results in reduced fat synthesis and increased beta-oxidation. Preliminary evidence suggests that statin-intolerant patients demonstrate increased fatty acid oxidation (FAO) in response to lovastatin, implicating an intrinsic FAO abnormality [12]. Statins increase the expression of mitochondrial carnitine acylcarnitine translocase and this effect may contribute to the alteration in FAO [13].
Atrogin-1, a muscle-specific ubiquitin protein ligase, may play an important role in statin toxicity. Lovastatin induces expression of atrogin-1 in humans with statin myopathy and in several in vitro models; in the models, myopathy could be prevented by knockdown of atrogin-1 [14]. These and other proposed mechanisms require further experimental confirmation.
Among patients experiencing statin-induced myalgia, skeletal muscle gene expression data show that persistent myalgia may result from cellular stress that results from mechanisms of post-inflammatory repair and end-organ susceptibility. The genetic basis for SAMS is supported by an increased frequency of single nucleotide polymorphisms that were increased in patients with statin myalgia (figure 1) [4].
DEFINITIONS — Terminology around statin-associated adverse muscle events is variable and has changed over time [15]. In this topic, where possible, we use the categories of events defined by the 2014 National Lipid Association Statin Muscle Safety Task Force [3]:
Myalgia – A symptom of muscle-discomfort, including muscle aches, soreness, stiffness, tenderness, or cramps with or soon after exercise, with a normal creatine kinase (CK) level. Myalgia symptoms can be described as similar to what would be experienced with a viral syndrome such as influenza.
Myopathy – Muscle weakness (not due to pain), with or without an elevation in CK level.
Myositis – Muscle inflammation.
Myonecrosis – Elevation in muscle enzymes compared with either baseline CK levels (while not on statin therapy) or the upper limit of normal that has been adjusted for age, race, and sex:
•Mild – Threefold to 10-fold elevation in CK.
•Moderate – 10-fold to 50-fold elevation in CK.
•Severe – 50-fold or greater elevation in CK.
Clinical rhabdomyolysis – Defined by the Task Force as myonecrosis with myoglobinuria or acute renal failure (an increase in serum creatinine of least 0.5 mg/dL [44 micromol/L]).
EPIDEMIOLOGY — Information about muscle injury and statins has come both from large clinical trials of statin therapy and from observational studies of statins in clinical use [16]. A meta-analysis of 42 randomized trials of statins found little or no excess risk of myalgias, creatine kinase elevations, rhabdomyolysis, or discontinuation of therapy versus placebo [17]. However, experience in clinical practice suggests that muscle side effects are relatively common, including side effects requiring discontinuation of statin therapy. The explanation for this difference is uncertain, but may relate to selection criteria in randomized trials that limit the ability to generalize their results to the side effect profiles seen in a broader population of patients [18].
Consistent with this, a six-month randomized trial in 420 healthy adults designed to examine the effects of statin therapy on muscle function found a higher incidence of myalgia in patients treated with atorvastatin 80 mg daily than with placebo (9.3 versus 4.6 percent) [19].
Clinically-significant myonecrosis, defined as a serum CK elevation more than 10 times normal in association with muscle symptoms, occurred in less than 0.5 percent of patients in large clinical trials [20-23]. A review of one year of records for 1014 patients taking statins in a primary care practice found that 0.9 percent of patients had CK elevations more than five times normal, and none of these appeared to be related to statin use [24]. Fourteen patients (2.1 percent) had elevations 2.5 to 5.0 times normal and, of these, two appeared to be potentially related to statin use.
In large clinical trials, massive rhabdomyolysis with acute renal failure was not seen in patients who did not have other risk factors. Rhabdomyolysis has primarily been seen when a statin is given concurrently with cyclosporine, gemfibrozil, or protease inhibitors (see 'Concurrent drug therapy' below) [25-27]. In addition, there have been case reports of rhabdomyolysis in patients taking statins in combination with niacin, macrolide antibiotics, digoxin, antifungal medications, and warfarin [28].
One study examined claims data from 11 managed care plans that included 252,460 patients treated with lipid lowering agents [2]. The average incidence of hospitalization for rhabdomyolysis was 0.44 per 10,000 patient-years (95% CI 0.20-0.84) for patients treated with atorvastatin, pravastatin, or simvastatin monotherapy. Although the study did not find a statistical difference in the incidence of rhabdomyolysis among these three statins, no cases of rhabdomyolysis were seen with pravastatin. The incidence was higher with cerivastatin monotherapy (5.34 per 10,000 patient-years).
Many individuals who are prescribed statins discontinue treatment due to perceived side effects. An internet-based survey that included 10,138 respondents (88 percent current statin users, 12 percent former users) found that the primary reason for discontinuation of statin therapy was side effects [29]. Muscle-related side effects were reported by 60 percent of former users and 25 percent of current users. However the study did not make it clear whether the temporal relation between symptoms and starting or stopping statin therapy was assessed, and it is uncertain whether the 25 percent of current users with muscle symptoms attributed those symptoms to their therapy. Concomitant use of medications that inhibit statin metabolism increased the risk for muscle symptoms and for discontinuation of statin therapy for such symptoms [30].


Switching statins — As discussed above, pravastatin, fluvastatin, and pitavastatin appear to have much less intrinsic muscle toxicity than other statins (see 'Statin characteristics' above). Thus, in patients who have developed statin myopathy (other than rhabdomyolysis) on a statin other than pravastatin or fluvastatin, an option is to switch to one of those two medications once symptoms have resolved off statin therapy [18].
Switching to fluvastatin was studied in a randomized trial in 199 patients with prior statin myopathy; 17 percent of patients treated with extended-release fluvastatin monotherapy developed recurrent muscle symptoms (versus 24 percent with ezetimibe and 14 percent with combination therapy) [153].
Alternate-day dosing — Daily dosing of statins is preferred whenever possible, since daily regimens are the ones that have been studied and proven to reduce clinical events. Clinical experience suggests that alternate-day dosing may improve the tolerability of statins in patients experiencing myalgias, and this strategy appears to have equal LDL-C lowering efficacy [149] and can reasonably be tried in patients unable to tolerate daily statin therapy. (See "Statins: Actions, side effects, and administration", section on 'Alternative dosing regimens'.)

Therapies of uncertain benefit
Coenzyme Q10 — We suggest not administering Coenzyme Q10 (CoQ10) to try to improve or prevent statin-associated muscle events.
As discussed above, CoQ10 depletion may play a role in statin myopathy (see 'Pathogenesis' above). However, there is little published evidence showing benefit of CoQ10 for the treatment of myopathy [3]:
●A small 30-day randomized trial that compared CoQ10 100 mg daily with vitamin E 400 IU daily in 32 patients with myopathic pain while receiving statins found a significant reduction in pain in patients treated with CoQ10, but not in patients treated with vitamin E; neither treatment affected plasma CK levels [154]. Short-term administration of CoQ10 would not be expected to substantially increase tissue levels of ubiquinone, and the findings from this trial need confirmation in a larger trial with a longer duration of CoQ10 therapy.
●A small randomized trial compared 12 weeks of CoQ10 200 mg daily with placebo in 44 patients with statin-induced myalgia [155]. Patients were off lipid-lowering therapy for two weeks prior to randomization and were then treated with escalating doses of simvastatin (10 to 40 mg daily as tolerated). CoQ10 supplementation increased plasma CoQ10 levels but reportedly did not increase the proportion of patients who tolerated simvastatin or decrease myalgia scores.
●A small randomized trial in patients with recent-onset myalgias after initiation or dose increase of statin therapy found no benefit of CoQ10 60 mg twice daily compared with placebo [156]. Patients with a CK level above 300 U/L were excluded from the trial.
●A small randomized trial with a complex design that included a crossover phase for some participants, found no benefit of CoQ10 600 mg daily in patients who had shown recurrence of myalgia with simvastatin during an earlier crossover phase of the study [157]. Patients were off simvastatin for four weeks and then received two weeks of either CoQ10 or placebo before simvastatin therapy resumed, and then were continued on CoQ10 or placebo during statin treatment.
A 2015 meta-analysis of randomized trials concluded that existing trials do not suggest any significant benefit of CoQ10 for statin myopathy, but that larger trials are needed to confirm this lack of benefit [158].
The evidence for CoQ10 for prevention of muscle events is even more limited. (See 'Use of coenzyme Q10' below.)
Red yeast rice — Red yeast rice (Monascus purpureus) is a nutraceutical that lowers LDL-C levels by 20 to 30 percent. The LDL-C lowering effect of red yeast rice is due to the presence of monacolin K, a compound similar to lovastatin. Although red yeast rice lowers LDL-C similar to a mild potency statin, and may be tolerated by some patients who have discontinued statin therapy for muscle side effects, this therapy is not recommended due to lack of clinical outcomes data, variable drug bioavailability, and possible toxic effects from contaminants. Red yeast rice may also induce muscle complaints because of its statin-like content [159,160]. (See "Lipid lowering with diet or dietary supplements", section on 'Red yeast rice'.)

Choice of statin — As discussed above, pravastatin, fluvastatin, and pitavastatin appear to have much less intrinsic muscle toxicity than other statins (see 'Statin characteristics' above). Both these agents are relatively lower potency statins; however, whenever they are adequate for the clinical situation, we suggest treating with one or the other to reduce the risk of statin myopathy.
As discussed below, the choice of statin is also important in dealing with potential drug interactions. (See 'Drug interactions' below.)
Drug interactions — Certain drug interactions are discussed below. Additional detail about specific statin interactions and management suggestions for avoiding increased myopathy risk is available by using the Lexi-Interact program included with UpToDate.
CYP3A4 drugs — As discussed above, the risk of muscle injury is substantially increased when taking the combination of statins extensively metabolized by cytochrome P450 3A4 (lovastatin, simvastatin, atorvastatin) and drugs that inhibit CYP3A4 (table 2) (see 'Concurrent drug therapy' above). Pravastatin, fluvastatin, and pitavastatin are preferred when concurrent therapy with a strong inhibitor of CYP3A4 cannot be avoided.
The importance of using a statin that is not extensively metabolized by CYP3A4 when administering a CYP3A4 inhibitor is illustrated by the moderate CYP3A4 inhibitor cyclosporine. Regular-dose lovastatin (40 to 80 mg/day) and simvastatin (20 mg/day) are associated with an appreciable risk of myositis (as high as 13 to 30 percent) in cyclosporine-treated patients [20,76,77]. Lovastatin levels much higher than the therapeutic range have been noted in patients with rhabdomyolysis who were treated with cyclosporine [20]. Although the data are limited, myositis has also been described when cyclosporine is given with atorvastatin, which is metabolized by CYP3A4 [78,79]. In contrast, pravastatin and fluvastatin, which are not extensively metabolized by CYP3A4, do not appear to increase the risk of myopathy when given concurrently with cyclosporine [77,161-163].
The safety of pravastatin in such patients was illustrated in an open-label study that compared pravastatin (40 mg/day) with simvastatin (20 mg/day) in 87 cardiac transplant recipients [77]. Rhabdomyolysis or myositis occurred only with simvastatin therapy (13.3 percent). A similar lack of muscle toxicity was noted in a placebo-controlled trial in which none of 50 cardiac transplant recipients treated with pravastatin (40 mg/day) developed myalgia or myositis during one year of therapy [161].
The safety of fluvastatin (20 and 40 mg/day) taken with cyclosporine in hypercholesterolemic renal transplant patients has been demonstrated in several small trials; mean serum trough levels of cyclosporine were not significantly altered [96,164,165].
Although pitavastatin and rosuvastatin are not significantly metabolized by CYP3A4, manufacturers' pharmacokinetic data show they can interact with cyclosporine, apparently by a non-CYP mechanism [89,95]. Hepatic uptake of pitavastatin and rosuvastatin is regulated by hepatocyte membrane transporters, known as organic anion transport proteins (OATPs), whose effects can be inhibited by certain drugs (ie, cyclosporine, erythromycin, clarithromycin) causing increased levels of pitavastatin or rosuvastatin [166,167]; there is some evidence that clarithromycin can increase the risk of rhabdomyolysis even in patients taking statins that are not metabolized by CYP3A4 [168].
Fibrates — Gemfibrozil can increase plasma levels of statins and thus the risk for muscle toxicity. Options include choosing pravastatin or fluvastatin when treating with gemfibrozil or treating with fenofibrate rather than gemfibrozil; fenofibrate is the preferred fibrate in patients who require combined therapy with a statin and fibrate due to minimal increases in statin levels [169]. Combination therapy with gemfibrozil and even pravastatin or fluvastatin should be used cautiously and only if the benefit is likely to outweigh the low risk of muscle toxicity [170].
An increased risk of muscle toxicity, as high as 1 to 5 percent, has been described with the administration of some statins (eg, lovastatin and atorvastatin) with gemfibrozil [20,27,97,98]. Pravastatin and fluvastatin appear to have little muscle toxicity when used in combination with gemfibrozil [171-174], despite the observation that gemfibrozil increases plasma concentrations of pravastatin twofold [175].
The potential importance of the type of statin was evaluated in a study that examined claims data from 11 managed care plans, which included 252,460 patients treated with lipid lowering agents [2]. The average incidence of hospitalization for rhabdomyolysis was 5.98 per 10,000 patient-years (95% CI 0.72-216.0) for patients treated with atorvastatin, pravastatin, or simvastatin in combination with a fibrate. The incidence of hospitalization was approximately 10-fold higher with combination fibrates and statins than with statin monotherapy. Although the study did not find a statistical difference in the incidence of rhabdomyolysis among these three statins, no cases of rhabdomyolysis were seen with pravastatin.
Toxicity can also be minimized by using other statins in relatively low doses [173,176,177]. This was illustrated in a trial of 389 patients with refractory familial combined hyperlipidemia who were randomly assigned to pravastatin (20 mg/day) plus gemfibrozil or simvastatin (20 mg/day) plus either gemfibrozil or ciprofibrate [173]. After a mean follow-up of 29 months, no patient developed myopathy or rhabdomyolysis.
Fenofibrate appears to be safer than gemfibrozil when used with statins. Glucuronidation, which is an important pathway for renal excretion of lipophilic statins, appears to be significantly inhibited by gemfibrozil but not fenofibrate [178,179]. In clinical studies, serum levels of statins increase 1.9- to 5.7-fold in gemfibrozil-treated subjects but are unchanged in fenofibrate-treated subjects.
In the randomized, placebo-controlled FIELD trial of fenofibrate in almost 10,000 patients with type 2 diabetes, there was a low incidence of myopathy (less than 1 percent) that was not different from placebo, whether or not patients were also taking a statin [180]. Meta-analyses of randomized trials have found no increase in muscle-related adverse events in patients taking fenofibrate plus a statin compared with a statin alone [181,182].
Niacin — Although the absolute increase in risk appears to be small, niacin seems to increase the risk of myopathy in patients receiving simvastatin, and perhaps other statins (see 'Concurrent drug therapy' above). This increased risk may be a particular concern in patients from China (see 'Patient characteristics' above), and we suggest avoiding the combination of simvastatin and niacin in Chinese patients and only using niacin with caution in patients receiving other statins.
Dose limitations — Manufacturer recommendations for simvastatin, and also for lovastatin, state that the medications are contraindicated in patients treated with most strong CYP3A4 inhibitors (table 2) and that there are dose limitations or recommendations to avoid these statins when used in conjunction with a number of other medications, including limiting simvastatin to 20 mg daily when taken with amlodipine [63,86].
Given high rates of myopathy with simvastatin 80 mg daily [183], and the availability of rosuvastatin and generic atorvastatin, we suggest not treating patients with doses of simvastatin above 40 mg/day. Additionally, clinicians should strongly consider switching even patients who are currently tolerating simvastatin 80 mg/day to one of these other statin options. (See "Statins: Actions, side effects, and administration", section on 'Potency'.)
For more detailed information about dose limitations, refer to the individual Lexicomp drug monographs included with UpToDate.
Use of coenzyme Q10 — Some clinicians recommend that patients taking statins take CoQ10 to try to prevent myopathy. Although there is anecdotal evidence for benefit, there are no published controlled trials or even moderate-size case series. A few case reports have noted benefit with doses of 30 to 250 mg daily [184]. There is currently inadequate evidence to recommend CoQ10 supplementation for prevention of statin-induced muscle toxicity [185].

●Terminology around statin-associated adverse muscle events is variable and has changed over time. In this topic, we use the categories of events defined by the 2014 National Lipid Association Statin Muscle Safety Task Force. (See 'Definitions' above.)
●Statin muscle-related adverse events are relatively uncommon. Myalgias and myopathy occur with a frequency of 2 to 11 percent. However, severe myonecrosis and clinical rhabdomyolysis are much rarer (0.5 percent and less than 0.1 percent, respectively). Patients can experience statin-induced myalgias without an elevation in serum creatine kinase (CK) concentration. (See 'Epidemiology' above.)
●The risk of muscle injury is substantially higher when taking a statin that is extensively metabolized by cytochrome P450 3A4 (lovastatin, simvastatin, atorvastatin) together with a drug that interferes with CYP3A4 (table 2). Pravastatin, fluvastatin, rosuvastatin, and pitavastatin are preferred when given to a patient receiving another drug that is a strong inhibitor of CYP3A4. (See 'CYP3A4 drugs' above.)
●Grapefruit juice inhibits CYP3A4; however, daily consumption of eight ounces or less of grapefruit juice or one-half of a grapefruit or less is unlikely to increase the risk of an adverse interaction or muscle injury. (See 'Concurrent drug therapy' above.)
●In patients being treated with gemfibrozil who require statin therapy, we suggest pravastatin or fluvastatin (Grade 2B). However, in patients who require combined therapy with a statin (including pravastatin or fluvastatin) and a fibrate, we suggest fenofibrate rather than gemfibrozil (Grade 2B). (See 'Fibrates' above.)
●Enhanced susceptibility to statin-associated myopathy occurs in patients with acute or chronic renal failure, obstructive liver disease, and hypothyroidism. (See 'Patient characteristics' above.)
●Muscle symptoms and/or signs usually begin within weeks to months after starting statins. Myalgias, weakness, and serum CK concentrations usually return to normal over days to weeks after drug discontinuation. (See 'Time course of muscle events' above.)
●The diagnosis of symptomatic statin myopathy with laboratory abnormalities (ie, increased serum CK) is typically straightforward and based on a temporal association for both onset with initiation of statin therapy and resolution with statin withdrawal. However, some patients can have muscle symptoms from statin therapy without an elevation in serum CK, and it can then be difficult to be certain whether muscle symptoms are due to statin therapy. (See 'Diagnosis' above.)
●Clinical judgment is necessary in interpreting increased CK levels in patients on statins. CK elevations can be related to hypothyroidism or muscle injury during sports (eg, running, diving for a volleyball, hockey), and patients who engage in high-impact sports should be advised to have a CK measured before engaging in exercise that day. (See 'Diagnosis' above.)
●We suggest not routinely monitoring serum CK levels in patients on statin therapy (Grade 2C). It is useful to obtain a baseline CK level for reference purposes prior to starting statin therapy. Patients treated with statins should be alerted to report the new onset of myalgias or weakness. (See 'Monitoring' above.)
●In patients who develop evidence of muscle toxicity while on statin therapy, we assess for drug interactions, and, if none are noted, we check a vitamin D level and thyroid function (algorithm 1). (See 'Concurrent drug therapy' above and 'Hypothyroidism, hypovitaminosis D, and other disorders' above and 'Vitamin D' above.)
Pravastatin and fluvastatin appear to have much less associated muscle toxicity than other statins. Thus, in patients who have developed statin myopathy (other than rhabdomyolysis) on a statin other than pravastatin or fluvastatin, we suggest switching to one of those two medications once symptoms have resolved off statin therapy (Grade 2B). (See 'Switching statins' above.)
●In patients who are unable to tolerate daily dosing of pravastatin or fluvastatin, we suggest a trial of alternate-day or less frequent dosing (one to two times weekly) of statin therapy (Grade 2C). (See 'Alternate-day dosing' above.)
●We suggest not administering Coenzyme Q10 (CoQ10) for treatment or prevention of statin myopathy (Grade 2C). (See 'Coenzyme Q10' above and 'Use of coenzyme Q10' above.)
Last edited by: dtoce: May 29, 18 14:24
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Re: Statins and training [dtoce] [ In reply to ]
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What he's describing isn't myalgia or any type of myopathy. Up To Date is a good tool if you use it correctly.
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Re: Statins and training [hubcaps] [ In reply to ]
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hubcaps wrote:
What he's describing isn't myalgia or any type of myopathy. Up To Date is a good tool if you use it correctly.

Hubcaps, your history and physical exam skills online exceed brilliance.

To be sure, neither you nor I have no real idea what his specific symptoms are from. I never said that he had Statin associated myalgia or myopathy I simply pointed out what it actually is, Using ‘up to date’ for the description.

He needs to discuss his symptoms with his doctor and hopefully find out what the cause of pain/numbness and tingling are in his feet.

I can tell you that I certainly have seen myalgia present as pain/numbness and tingling in the feet in patients on statins rx. And in a lot if other ways...

We have no idea if the OP is diabetic or not and has associated peripheral neuropathy or other inflammatory issues. We don’t know ANY medical information and the internet should not be used for real medical issues/concerns. A lot of misinformation appear all too frequently.

I do know that I don’t need to be told how to use “up to date”.
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Re: Statins and training [dtoce] [ In reply to ]
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You are so right. I took care of a family with severe familial hypercholesterolemia. There were relatives who were having MIs in their mid to late twenties. One kid had cholesterol so severe they were centrifuging it out of his blood weekly. The OP has a chol of >400 I would imagine NNT is quite low to prevent premature MI.

They constantly try to escape from the darkness outside and within
Dreaming of systems so perfect that no one will need to be good T.S. Eliot

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