Statins, good or bad.

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Aardvark
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Statins, good or bad.

Post by Aardvark » June 24, 2009, 4:51 pm

http://www.westonaprice.org/moderndiseases/statin.html I have been on Lipitor for about six years and have suffered memory loss, libido loss, Muscle loss and a few other problems. Only yesterday was I shown some advice about taking Statins, which has frightened the fcuk out of me :yikes: What do you read into this, or what are your experiences. I want to know, cause as of yesterday I stopped taking this siht :shock:



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FrazeeDK
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Re: Statins, good or bad.

Post by FrazeeDK » June 24, 2009, 5:11 pm

I've been on Lipitor and previously other types of cholesterol lowering drugs for about 10 years.

Experiences:
- initially on 20mg of Lipitor a day with total cholesterol reductions for high 200's- low 300's to around 220.
- After over one year on 20mg a day I experienced creeping fatigue and muscle pain to the point where it was difficult to get up in the morning. Since I was getting older I attributed it to old age until it got so bad I just stopped taking any meds and in about a week all symptoms disappeared.
- In consultation with my Doc, I dropped my Liptior dosage to 10mg per day and the symptoms did not come back. total Cholesterol dropped to about 180, with LDL down commensurately and HDL up to around 50. The Doc was flummoxed over the symptoms saying Liptior perhaps could have caused it but shouldn't have.. Since the cessation of the symptoms happened when I stopped taking Lipitor I saw a definite cause-effect relationship.
- In retrospect, after reading the posted article, I have had memory issues over the last year or so, again which I attributed to "growing older".. Nothing serious but not as sharp as I used to be.. An inability to grab facts out of my head that previously were there crystal clear...

Lessons learned:
- don't ignore "creeeping" symptoms that get worse and attribute them to "old age". Listen to your body and take action.
- Do research such as the article in the string and make up your own mind as to the efficacy of drugs in concert with consulting your Doc..


conclusion:

- I'll stop my Liptior for a couple of weeks and see if my cognitive functions improve markedly..

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jingjai
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Re: Statins, good or bad.

Post by jingjai » June 24, 2009, 5:20 pm

Not saying this guy has all the answers...however he does offer some good advice:

http://www.drweil.com/drw/ecs/ask_dr_we ... tegory=395

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wazza
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Re: Statins, good or bad.

Post by wazza » June 24, 2009, 6:13 pm

Sorry for the long Copy and Paste - its from MIMS ( the Drug bible for GP's ) and it lists the Pharmocology in detail.

Remember that any medication taken is always subject to other pre exsisting illnesses or conditions as well a drug interactions, these 2 are the nightmares for GP's, particularly if patients see numerous medical practioners for other consitions etc......

See the adverse reactions, Suggest you refer your symptoms back to your GP / Consultant for a review.

hope this assists

MIMS Abbreviated Prescribing Information
Atorvastatin calcium
Pfizer
Section: 2(f) Hypolipidaemic agents - Cardiovascular System
Product Images: Lipitor 10 mg, Lipitor 20 mg, Lipitor 40 mg, Lipitor 80 mg
Pregnancy Category: C*

Permitted in sport

Use: HMG-CoA reductase inhibitor. Adjunctive therapy to diet in treatment of hypercholesterolaemia; hypertension with multiple CHD risks. See Section 2(f) headnote
Contraindications: Active hepatic disease; unexplained/ persistent elevated AST, ALT; pregnancy, lactation
Precautions: Hepatic dysfunction (monitor liver function); excessive alcohol intake; myopathy (monitor CK); risk factors for rhabdomyolysis eg severe acute infection, hypotension, major surgery, trauma, severe metabolic, endocrine, electrolyte disorders, uncontrolled seizures
Adverse Reactions: Rhabdomyolysis; myopathy; myalgia; GI upset; headache; rash; neuropathy; raised LFTs; others, see full PI
Interactions: Erythromycin, clarithromycin; protease inhibitors; colestipol; digoxin; OCs (norethindrone + ethinyloestradiol); antacids; fibric acid derivatives; niacin; CYP450 3A4 inhibitors incl grapefruit juice, cyclosporin, azole antifungals; amiodarone; steroid hormone lowering agents incl ketoconazole, spironolactone, cimetidine

Lipitor (Tablets) Rx (S4) CMI
Atorvastatin; lactose, white f-c; gluten free
Pack 10 mg [30] : Restricted - PBS/RPBS (Rp 5)
[Restricted benefit indication(s)]
PBS: $41.95
Pack 20 mg [30] : Restricted - PBS/RPBS (Rp 5)
[Restricted benefit indication(s)]
PBS: $59.65
Pack 40 mg [30] : Restricted - PBS/RPBS (Rp 5)
[Restricted benefit indication(s)]
PBS: $82.07
Pack 80 mg [30] : Restricted - PBS/RPBS (Rp 5)
[Restricted benefit indication(s)]
PBS: $115.31
Dose May be taken with or without food. Individualise dosage; 10-80 mg once daily; adjust dosage after 4 weeks if necessary

MIMS Full Prescribing Information
MIMS revision date: 1/12/2004
Composition Active. Atorvastatin calcium.
Inactive. Calcium carbonate, microcrystalline cellulose, lactose, croscarmellose sodium, polysorbate 80, hydroxypropylcellulose, magnesium stearate, Opadry White YS-1-7040, Simethicone Emulsion, candelilla wax (10, 20 and 40 mg tablets).


Description Chemical name: [R-(R*,R*)]-2-(4-fluorophenyl)- beta,delta-dihydroxy- 5-(1-methylethyl)- 3-phenyl- 4-[(phenylamino)carbonyl]- 1H-pyrrole- 1-heptanoic acid, calcium salt (2:1). Molecular formula: (C33H34FN2O5)2,Ca.3H2O. MW: 1,209.42. CAS: 134523-03-8.
Atorvastatin calcium is a white to off white crystalline powder that is practically insoluble in aqueous solutions of pH 4 and below. It is very slightly soluble in distilled water, pH 7.4 phosphate buffer and acetonitrile, slightly soluble in ethanol and freely soluble in methanol.
Actions Hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor.
Pharmacology. Mechanism of action. Atorvastatin is a synthetic lipid lowering agent. Atorvastatin is an inhibitor of HMG-CoA reductase, the rate limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor of sterols, including cholesterol. Triglycerides and cholesterol in the liver are incorporated into very low density lipoprotein (VLDL) and released into the plasma for delivery to peripheral tissues. Low density lipoprotein (LDL) is formed from VLDL and is catabolised primarily through the high affinity LDL receptor.
Atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the cell surface to enhance uptake and catabolism of LDL. Atorvastatin reduces LDL production and the number of LDL particles. Atorvastatin produces a marked and sustained increase in LDL receptor activity coupled with a beneficial change in the quality of circulating LDL particles.
A variety of clinical and pathological studies have demonstrated that elevated cholesterol and lipoprotein levels of total cholesterol, LDL cholesterol and apolipoprotein B (apo B) promote human atherosclerosis and are risk factors for developing cardiovascular disease. Similarly, decreased levels of HDL cholesterol are associated with the development of atherosclerosis. Epidemiological investigations have established that cardiovascular morbidity and mortality vary directly with the levels of total cholesterol and LDL cholesterol and inversely with the level of HDL cholesterol.
Atorvastatin reduces total cholesterol, LDL cholesterol and apo B in both normal volunteers and in patients with homozygous and heterozygous familial hypercholesterolaemia, nonfamilial forms of hypercholesterolaemia, and mixed dyslipidaemia. Atorvastatin also reduces VLDL cholesterol and triglycerides and produces variable increases in HDL cholesterol and apolipoprotein A-1. Atorvastatin reduces total cholesterol, LDL cholesterol, VLDL cholesterol, apo B and triglycerides, and increases HDL cholesterol in patients with isolated hypertriglyceridaemia. Atorvastatin reduces intermediate density lipoprotein cholesterol (IDL-C) in patients with dysbetalipoproteinaemia. In animal models, atorvastatin limits the development of lipid enriched atherosclerotic lesions and promotes the regression of pre-established atheroma.
Clinical trials. In a multicentre, placebo controlled, double blind dose response study in patients with hypercholesterolaemia, atorvastatin was given as a single daily dose over six weeks. Atorvastatin (10 to 80 mg) reduced total cholesterol (30 to 46%), LDL cholesterol (41 to 61%), apolipoprotein B (34 to 50%) and triglycerides (14 to 33%) while producing variable increases in HDL cholesterol and apolipoprotein A (see Table 1). A therapeutic response was seen within two weeks, and maximum response was achieved within four weeks.

In three further trials, 1,148 patients with either heterozygous familial hypercholesterolaemia, nonfamilial forms of hypercholesterolaemia or mixed dyslipidaemia were treated with atorvastatin for one year. The results were consistent with those of the dose response study and were maintained for the duration of therapy.
In patients with primary hypercholesterolaemia and mixed dyslipidaemia (Fredrickson types IIa and IIb), data pooled from 24 controlled trials demonstrated that the adjusted mean percent increases from baseline in HDL cholesterol for atorvastatin (10 to 80 mg) were 5.0 to 7.8% in a non-dose related manner.
Clinical studies demonstrate that the starting dose of atorvastatin 10 mg is more effective than simvastatin 10 mg and pravastatin 20 mg in reducing LDL cholesterol, total cholesterol, triglycerides and apo B. In several multicentre, double blind studies in patients with hypercholesterolaemia, atorvastatin was compared to other HMG-CoA reductase inhibitors. After randomisation, patients were treated with atorvastatin 10 mg/day or the recommended starting dose of the comparative agent. At week 16 a greater proportion of atorvastatin treated patients than those treated with simvastatin (46 versus 27%) or pravastatin (65 versus 19%) reached their target LDL cholesterol levels. Increasing the dosage of atorvastatin resulted in more patients reaching target LDL cholesterol goals.
Prevention of cardiovascular disease. In the lipid lowering arm of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT), the effect of Lipitor (atorvastatin calcium) on the composite endpoint of fatal coronary heart disease and nonfatal myocardial infarction was assessed in 10,305 hypertensive patients, 40 to 79 years of age, without a history of symptomatic coronary heart disease and with TC levels less than or equal to 6.5 mmol/L. Additionally patients were at moderate risk of coronary heart disease, having at least three of the predefined cardiovascular risk factors (male gender (81%), age greater than or equal to 55 years (84%), smoking (33%), noninsulin dependent diabetes mellitus (25%), history of CHD in a first degree relative (26%), plasma TC to HDL cholesterol ratio greater than or equal to 6 (14%), peripheral vascular disease (5%), left ventricular hypertrophy on echocardiography (14%), past history of cerebrovascular event (10%), specific ECG abnormality (14%), proteinuria/ albuminuria (62%)). Patients with a history of previous myocardial infarction or angina were excluded.
In this randomised, double blind, placebo controlled study patients were treated with antihypertensive therapy (goal BP < 140/90 mmHg for nondiabetic patients, < 130/80 mmHg for diabetic patients) and either Lipitor 10 mg daily (n = 5,168) or placebo (n = 5,137) and followed for a median duration of 3.3 years. At baseline, in the atorvastatin group, 38 patients (0.7%) had total-C levels less than 3.5 mmol/L; 2,340 patients (45.3%) had total-C greater than or equal to 3.5 mmol/L and less than 5.5 mmol/L; 2,304 patients (44.6%) had total-C levels greater than or equal to 5.5 mmol/L and less than 6.5 mmol/L; and 486 patients (9.4%) had total-C levels greater than or equal to 6.5 mmol/L. At baseline, 457 patients (9.8%) in the atorvastatin group had LDL-C levels less than or equal to 2.5 mmol/L; 1,731 patients (37%) had LDL-C greater than 2.5 mmol/L and less than 3.4 mmol/L; and 2,495 patients (53.3%) had LDL-C levels greater than or equal to 3.4 mmol/L. Median (25th and 75th percentile) changes from baseline after one year of atorvastatin treatment in total-C, LDL-C, TG and HDL-C were -1.40 mmol/L (-1.80, -0.90), -1.27 mmol/L (-1.66, -0.84), -0.20 mmol/L (-0.60, 0.10) and 0.00 mmol/L (-0.10, 0.10). Blood pressure control throughout the trial was similar in patients assigned to atorvastatin and placebo. See Table 2 for a summary of risk reductions in primary prevention patients.

The primary endpoint examined in ASCOT was the rate of fatal coronary heart disease or nonfatal myocardial infarction over 3.3 years. These coronary events occurred in 1.9% of atorvastatin treated patients compared to 3% of placebo treated patients, a relative risk reduction of 36% (p = 0.0005) (Table 2). Although this difference was statistically significant for the whole trial population, this difference was not statistically significant in specified subgroups such as diabetes, patients with left ventricular hypertrophy (LVH), previous vascular disease or metabolic syndrome.
There was no statistically significant reduction in the rate of total mortality, cardiovascular mortality or heart failure in the atorvastatin treated group compared to placebo.
Noninsulin dependent diabetes mellitus (NIDDM). A 26 week randomised, double blind, comparator study in NIDDM subjects showed that atorvastatin is effective in dyslipidaemic patients with NIDDM. A dose of atorvastatin 10 mg produced a 34% reduction in LDL cholesterol, 27% reduction in total cholesterol, a 24% reduction in triglycerides and a 12% rise in HDL cholesterol.
Homozygous familial hypercholesterolaemia. Lipitor has also been shown to reduce LDL cholesterol in patients with homozygous familial hypercholesterolaemia, a population that has not usually responded to other lipid lowering medication. In an uncontrolled compassionate use study, 29 patients aged 6 to 37 years with homozygous familial hypercholesterolaemia received maximum daily doses of atorvastatin 20 to 80 mg. The mean LDL reduction in this study was 18%. 25 patients with a reduction in LDL cholesterol had a mean response of 20% (range 7 to 53%, median 24%). Five of the 29 patients had absent LDL receptor function, three of whom responded to atorvastatin with a mean LDL cholesterol reduction of 22%. Experience in paediatric patients has been limited to patients with homozygous familial hypercholesterolaemia.
Hypertriglyceridaemia. In patients with hypertriglyceridaemia (baseline triglycerides greater than or equal to 2.26 mmol/L and LDL cholesterol < 4.14 mmol/L) Lipitor (10 to 80 mg) reduced serum triglycerides by 31 to 40%.
In patients with severe hypertriglyceridaemia (baseline triglycerides > 5.7 mmol/L), Lipitor (10 to 80 mg) reduced serum triglycerides by 30 to 56%.
In a randomised, placebo controlled, double blind, multicentre study in patients with hypertriglyceridaemia (triglycerides greater than or equal to 3.95 mmol/L, LDL cholesterol less than or equal to 4.1 mmol/L), Lipitor 20 mg/day and 80 mg/day produced significantly greater reductions in triglyceride levels than placebo (see Table 3).

Dysbetalipoproteinaemia. In patients with dysbetalipoproteinaemia, Lipitor (10 to 80 mg) reduced intermediate density lipoprotein cholesterol (IDL-C) (range 28 to 52%) and IDL cholesterol + VLDL cholesterol (range 34 to 58%).
In an open label, randomised, crossover study in patients with dysbetalipoproteinaemia, treatment with Lipitor 80 mg/day resulted in significantly greater mean percent decreases in IDL cholesterol + VLDL cholesterol, IDL cholesterol, total cholesterol, VLDL cholesterol and apo B than either simvastatin 40 mg/day or gemfibrozil 1,200 mg/day and significantly greater mean percent decreases in triglycerides than simvastatin 40 mg/day (see Table 4).


Pharmacokinetics. Absorption. Atorvastatin is rapidly absorbed after oral administration; maximum plasma concentrations occur within one to two hours. A constant proportion of atorvastatin is absorbed intact. The absolute bioavailability is 14%. The low systemic availability is attributed to presystemic clearance in gastrointestinal mucosa and/or hepatic first-pass metabolism. Although food decreases the rate and extent of drug absorption by approximately 25 and 9% respectively as assessed by Cmax and area under the plasma concentration time curve (AUC), LDL cholesterol reduction is similar whether atorvastatin is given with or without food. Plasma atorvastatin concentrations are lower (approximately 30% for Cmax and AUC) following evening drug administration compared with morning. However, LDL cholesterol reduction is the same regardless of the time of day of drug administration (see Dosage and Administration).
Distribution. The mean volume of distribution of atorvastatin is about 400 L. Atorvastatin is greater than or equal to 98% bound to plasma proteins. A red blood cell plasma ratio of approximately 0.25 indicates poor drug penetration into red blood cells. Based on observations in rats, atorvastatin is likely to be secreted in human milk (see Precautions, Use in lactation).
Metabolism. In humans, atorvastatin is extensively metabolised to o- and p-hydroxylated derivatives. In vitro inhibition of HMG-CoA reductase by o- and p-hydroxylated metabolites is equivalent to that of atorvastatin. Approximately 70% of circulating inhibitory activity for HMG-CoA reductase is attributed to active metabolites. In vitro studies suggest the importance of atorvastatin metabolism by cytochrome P450 3A4, consistent with increased plasma concentrations of atorvastatin in humans following coadministration with erythromycin, a known inhibitor of this isozyme (see Interactions). In animals, the o-hydroxy metabolite undergoes further glucuronidation.
Excretion. Atorvastatin is eliminated primarily in bile following hepatic and/or extrahepatic metabolism. However, the drug does not appear to undergo enterohepatic recirculation. Mean plasma elimination half-life of atorvastatin in humans is approximately 14 hours, but the half-life of inhibitory activity for HMG-CoA reductase is 20 to 30 hours due to the contribution of active metabolites. Less than 2% of a dose of atorvastatin is recovered in urine following oral administration.
Pharmacodynamics. Atorvastatin and its metabolites are responsible for pharmacological activity in humans. The liver is its primary site of action and the principal site of cholesterol synthesis and LDL clearance. Drug dose rather than systemic drug concentration correlates better with LDL cholesterol reduction. Individualisation of drug dose should be based on therapeutic response (see Dosage and Administration).
Special populations. Elderly. Plasma concentrations of atorvastatin are higher (approximately 40% for Cmax and 30% for AUC) in healthy elderly subjects (greater than or equal to 65 years) than in young adults. Lipid effects are comparable to that seen in younger patient populations given equal doses of atorvastatin.
Children. Pharmacokinetic studies have not been conducted in the paediatric population.
Gender. Plasma concentrations of atorvastatin in women differ (approximately 20% higher for Cmax and 10% lower for AUC) from those in men; however, there is no clinically significant difference in lipid effects with atorvastatin between men and women.
Renal insufficiency. Renal disease has no influence on the plasma concentrations or lipid effects of atorvastatin; thus, dose adjustment in patients with renal dysfunction is not necessary (see Dosage and Administration).
Haemodialysis. While studies have not been conducted in patients with endstage renal disease, haemodialysis is not expected to significantly enhance clearance of atorvastatin since the drug is extensively bound to plasma proteins.
Hepatic insufficiency. Plasma concentrations of atorvastatin are markedly increased (approximately 16-fold in Cmax and elevenfold in AUC) in patients with chronic alcoholic liver disease (Childs-Pugh B) (see Dosage and Administration, Precautions and Contraindications).
Indications An adjunct to diet for the treatment of patients with hypercholesterolaemia. Prior to initiating therapy with atorvastatin, secondary causes of hypercholesterolaemia (e.g. poorly controlled diabetes mellitus, hypothyroidism, nephrotic syndrome, dysproteinaemias, obstructive liver disease, other drug therapy and alcoholism) should be identified and treated.
Hypertensive patients with multiple risk factors for coronary heart disease (CHD) which may include diabetes, history of stroke or other cerebrovascular disease, peripheral vascular disease or existing asymptomatic CHD (see Actions, Clinical trials) to reduce the risk of nonfatal myocardial infarction and nonfatal stroke.
These effects do not replace the need to independently control known causes of cardiovascular mortality and morbidity such as hypertension, diabetes and smoking.
Contraindications Hypersensitivity to any component of this medication.
Active liver disease or unexplained persistent elevations of serum transaminases (see Precautions).
Pregnancy and lactation. Women of childbearing potential, unless on an effective contraceptive and highly unlikely to conceive (see Precautions).
Precautions Liver dysfunction. As with other lipid lowering agents of the same class, moderate (greater than three times upper limit of normal (ULN)) elevations of serum transaminases have been reported following therapy with atorvastatin.
Persistent increases in serum transaminases greater than three times ULN occurred in 0.7% of patients who received atorvastatin in clinical trials. The incidence of these abnormalities was 0.2, 0.2, 0.6 and 2.3% for 10, 20, 40 and 80 mg, respectively. Increases were generally not associated with jaundice or other clinical signs or symptoms. When the dosage of atorvastatin was reduced, or drug treatment interrupted or discontinued, transaminase levels returned to pretreatment levels. Most patients continued treatment on a reduced dose of Lipitor without sequelae.
Liver function tests should be performed before the initiation of treatment and periodically thereafter. Patients who develop increased transaminase levels should be monitored until the abnormalities resolve. Should an increase in ALT or AST of greater than three times ULN persist, reduction of dose or withdrawal of Lipitor is recommended.
Lipitor should be used with caution in patients who consume substantial quantities of alcohol and/or have a history of liver disease. Active liver disease or unexplained persistent transaminase elevations are contraindications to the use of atorvastatin (see also Contraindications).
Skeletal muscle. Uncomplicated myalgia has been reported in atorvastatin treated patients (see Adverse Reactions). Myopathy, defined as muscle aching or muscle weakness in conjunction with increases in creatine kinase (CK) values > 10 x upper limit of normal (ULN), should be considered in any patient with diffuse myalgias, muscle tenderness or weakness and/or marked elevation of CK. Patients should be advised to report promptly unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. Lipitor therapy should be discontinued if markedly elevated CK levels occur or myopathy is diagnosed or suspected.
The risk of myopathy during treatment with other drugs in this class is increased with concurrent administration of cyclosporin, fibric acid derivatives, erythromycin, niacin or azole antifungals. Doctors considering combined therapy with Lipitor and fibric acid derivatives, erythromycin, immunosuppressive drugs, azole antifungals or lipid lowering doses of niacin should carefully weigh the potential benefits and risks and should carefully monitor patients for any signs and symptoms of muscle pain, tenderness or weakness, particularly during the initial months of therapy and during any periods of upward dosage titration of either drug. Periodic creatine kinase (CK) determinations may be considered in such situations, although there is no assurance that such monitoring will prevent the occurrence of severe myopathy.
As with other drugs in this class, rhabdomyolysis with acute renal failure has been reported. Lipitor therapy should be temporarily withheld or discontinued in any patient with an acute, serious condition suggestive of a myopathy or having a risk factor predisposing to the development of renal failure secondary to rhabdomyolysis (e.g. severe acute infection, hypotension, major surgery, trauma, severe metabolic, endocrine and electrolyte disorders and uncontrolled seizures).
Endocrine function. HMG-CoA reductase inhibitors interfere with cholesterol synthesis and theoretically may blunt adrenal and/or gonadal steroid production. Clinical studies have shown that atorvastatin does not reduce basal plasma cortisol concentration nor impair adrenal reserve. The effects of HMG-CoA reductase inhibitors on male fertility have not been studied in adequate numbers of patients. The effects, if any, on the pituitary gonadal axis in premenopausal women are unknown. Caution should be exercised if an HMG-CoA reductase inhibitor is administered concomitantly with other drugs that may decrease the levels or activity of endogenous steroid hormones such as ketoconazole, spironolactone and cimetidine.
Effect on ubiquinone levels (CoQ10). Significant decreases in circulating ubiquinone levels in patients treated with atorvastatin and other statins have been observed. The clinical significance of a potential long-term, statin induced deficiency of ubiquinone has not been established.
Effect on lipoprotein (a). Like other HMG-CoA reductase inhibitors, atorvastatin has variable effects on lipoprotein (a). It is unclear whether the beneficial effects of lowering LDL cholesterol and total cholesterol in some patients may be blunted by raised lipoprotein (a) levels.
Use in the elderly. Treatment experience in adults greater than or equal to 70 years with doses of atorvastatin up to 80 mg/day has been evaluated in 221 patients. The safety and efficacy of atorvastatin in this population were similar to those of patients < 70 years of age.
Carcinogenesis, mutagenesis, impairment of fertility. In a two year study in rats given 10, 30 or 100 mg/kg/day, the incidence of hepatocellular adenoma was marginally, although not significantly, increased in females at 100 mg/kg/day. The maximum dose used was eleven times higher than the highest human dose (80 mg/kg) based on AUC (0 to 24) values. In a two year study in mice given 100, 200 or 400 mg/kg, incidences of hepatocellular adenoma in males and hepatocellular carcinoma in females were increased at 400 mg/kg. The maximum dose used was 14 times higher than the highest human dose (80 mg/kg) based on AUC (0 to 24) values. Other HMG-CoA reductase inhibitors have been reported to induce hepatocellular tumours in mice and rats.
Atorvastatin did not demonstrate mutagenic or clastogenic potential in an appropriate battery of assays. It was negative in the Ames test with Salmonella typhimurium and Escherichia coli, and in the in vitro hypoxanthine guanine phosphoribosyl transferase (HGPRT) forward mutation assay in Chinese hamster lung cells. Atorvastatin did not produce significant increases in chromosomal aberrations in the in vitro Chinese hamster lung cell assay and was negative in the in vivo mouse micronucleus test.
The effects of atorvastatin on spermatogenesis and human fertility have not been investigated in clinical studies. Dietary administration of atorvastatin 100 mg/kg/day to rats caused a decrease in spermatid concentration in the testes, a decrease in sperm motility and an increase in sperm abnormalities. Similar effects, however, were not observed in male rats dosed by gavage to 175 mg/kg/day (plasma AUC for HMG-CoA reductase inhibitory activity 14 times higher than in humans dosed at 80 mg/day) and male fertility was not affected in either study. No adverse effects on fertility or reproduction were observed in female rats given doses up to 225 mg/kg/day (plasma AUC for enzyme inhibitory activity 56 times higher than in humans dosed at 80 mg/day). Atorvastatin caused no adverse effects on sperm or semen parameters, or on reproductive organ histopathology in dogs given doses of 10, 40 or 120 mg/kg for two years (plasma AUC for enzyme inhibitory activity 13 times higher than in humans).
Use in pregnancy. (Category C)
Atorvastatin is contraindicated in pregnancy.
Atherosclerosis is a chronic process and discontinuation of lipid lowering drugs during pregnancy should have little impact on the outcome of long-term therapy of primary hypercholesterolaemia. Cholesterol and other products of cholesterol biosynthesis are essential components for fetal development (including synthesis of steroids and cell membranes). Since HMG-CoA reductase inhibitors decrease cholesterol synthesis and possibly the synthesis of other biologically active substances derived from cholesterol, they may cause fetal harm when administered to pregnant women. Lipitor should be administered to women of childbearing age only when such patients are highly unlikely to conceive and have been informed of the potential. If the patient becomes pregnant while taking this drug, therapy should be discontinued and the patient apprised of the potential hazard to the fetus (see Contraindications).
Atorvastatin crosses the rat placenta and reaches a level in fetal liver equivalent to that in maternal plasma. Animal reproduction studies showed no evidence of teratogenic activity in rats or rabbits at oral doses up to 300 mg/kg/day and 100 mg/kg/day, respectively. Increased postimplantation loss, decreased fetal weight and increased skeletal variations were observed in rats dosed at 100 to 300 mg/kg/day and rabbits dosed at 50 to 100 mg/kg/day. In a perinatal/ postnatal study, rats dosed at 225 mg/kg/day showed an increased incidence of stillbirths, decreases in birthweight, an increased incidence of dilated renal pelvis, increased postnatal mortality, suppression of pup growth, retardation of physical development and abnormal behavioural development. Some of these effects were also observed at the nonmaternotoxic dose of 100 mg/kg/day; the plasma AUC for HMG-CoA reductase inhibitory activity at the no effect dose level of 20 mg/kg/day was similar to that in humans dosed at 80 mg/day.
Use in lactation. It is not known whether this drug is excreted in human milk. In rats, plasma concentrations of atorvastatin are similar to those in milk. Because of the potential for adverse reactions in breastfeeding infants, women taking Lipitor should not breastfeed (see Contraindications and Precautions).
Use in children. Treatment experience in a paediatric population is limited to doses of atorvastatin up to 80 mg/day for one year in eight patients with homozygous familial hypercholesterolaemia. No clinical or biochemical abnormalities were reported in these patients.
Interactions Atorvastatin is metabolised by cytochrome P450 3A4.
Based on experience with other HMG-CoA reductase inhibitors caution should be exercised when Lipitor is administered with inhibitors of cytochrome P450 3A4 (e.g. cyclosporin, macrolide antibiotics including erythromycin and azole antifungals including itraconazole). The risk of myopathy during treatment with other HMG-CoA reductase inhibitors is increased with concurrent administration of cyclosporin, fibric acid derivatives, erythromycin, azole antifungals or niacin (see Precautions). Grapefruit juice has also been shown to inhibit cytochrome P450 3A4. There may be a potential for increased plasma concentrations of HMG-CoA reductase inhibitors upon coadministration with grapefruit juice and other compounds which affect this enzyme system.
The effect of inducers of cytochrome P450 3A4 (e.g. rifampicin or phenytoin) on Lipitor is unknown. The possible interaction with other substrates of this isozyme is unknown but should be considered for other drugs with a narrow therapeutic index, for example, antiarrhythmic agents class III including amiodarone.
Drugs that affect Lipitor. The following drugs have been shown to have an effect on the pharmacokinetics or pharmacodynamics of Lipitor.
Antacids. Coadministration of an oral antacid suspension containing magnesium and aluminium hydroxides with atorvastatin decreased atorvastatin plasma concentrations approximately 35%. However, LDL cholesterol reduction was not altered.
Colestipol. Plasma concentrations of atorvastatin were lower (approximately 25%) when colestipol and atorvastatin were coadministered. However, LDL cholesterol reduction was greater when atorvastatin and colestipol were coadministered than when either drug was given alone.
Erythromycin, clarithromycin. In healthy individuals, coadministration of atorvastatin (10 mg once daily) and erythromycin (500 mg four times daily), or clarithromycin (500 mg twice daily), known inhibitors of cytochrome P450 3A4, was associated with higher plasma concentrations of atorvastatin (see Precautions).
Protease inhibitors. Coadministration of atorvastatin and protease inhibitors, known inhibitors of cytochrome P450 3A4, was associated with increased plasma concentrations of atorvastatin.
Drugs that are affected by Lipitor. The following drugs have been shown to have their pharmacokinetics or pharmacodynamics affected by Lipitor.
Digoxin. When multiple doses of digoxin (0.25 mg once daily) and atorvastatin 10 mg were coadministered, steady-state plasma digoxin concentrations were unaffected. However, steady-state plasma digoxin concentrations increased by approximately 20% following administration of digoxin with atorvastatin 80 mg daily. Patients taking digoxin should be monitored appropriately.
Oral contraceptives. Coadministration with an oral contraceptive containing norethindrone and ethinyloestradiol increased AUC values for norethindrone and ethinyloestradiol by approximately 30 and 20%. These increases should be considered when selecting an oral contraceptive for a woman taking atorvastatin.
Drugs shown not to interact with Lipitor. Cimetidine. Atorvastatin plasma concentrations and LDL cholesterol reduction were not altered by coadministration of cimetidine.
Warfarin. Atorvastatin had no clinically significant effect on prothrombin time when administered to patients receiving chronic warfarin treatment.
Terfenadine. Coadministration of atorvastatin (80 mg once daily) and terfenadine (single dose of 120 mg) did not produce a clinically significant effect on the pharmacokinetics of terfenadine.
Amlodipine. Atorvastatin pharmacokinetics were not altered by the coadministration of atorvastatin 80 mg daily and amlodipine 10 mg daily at steady state.
Azithromycin. Coadministration of atorvastatin 10 mg daily and azithromycin (500 mg once times daily) did not alter the plasma concentrations of atorvastatin.
Other concomitant therapy. In clinical studies, atorvastatin was used concomitantly with antihypertensive agents and oestrogen replacement therapy without evidence of clinically significant adverse interactions. Interaction studies with all specific agents have not been conducted.
Laboratory tests. Lipitor can cause elevations in ALT/AST, alkaline phosphatase, gamma-glutamyl transpeptidase (GGT), bilirubin and creatine kinase.
Adverse Reactions Lipitor is generally well tolerated. Adverse reactions have usually been mild and transient. Less than 2% of patients were discontinued from clinical trials due to side effects attributed to atorvastatin. The most frequent (greater than or equal to 1%) adverse effects associated with Lipitor therapy, in patients participating in controlled clinical studies were as follows.
Body as a whole. Headache, asthenia, abdominal pain.
Digestive system. Dyspepsia, nausea, flatulence, constipation, diarrhoea.
Nervous system. Insomnia.
Musculoskeletal system. Myalgia.
Clinical adverse experiences. Adverse experiences reported in greater than or equal to 2% of patients in placebo controlled clinical studies of atorvastatin, regardless of causality assessment, are shown in Table 5.

The following additional adverse effects have been reported in clinical trials of atorvastatin.
Body as a whole. Angioneurotic oedema.
Digestive system. Vomiting, anorexia, hepatitis, pancreatitis, cholestatic jaundice.
Nervous system. Paraesthesia, peripheral neuropathy.
Musculoskeletal system. Muscle cramps, myositis, myopathy.
Skin and appendages. Pruritus, alopecia.
Urogenital system. Impotence.
Metabolic and nutritional disorders. Hypoglycaemia, hyperglycaemia.
Not all effects listed have been causally associated with Lipitor therapy. Gynaecomastia has been reported with another HMG-CoA reductase inhibitor and thus cannot be ruled out with atorvastatin.
In ASCOT (see Actions, Clinical trials) involving 10,305 participants treated with Lipitor 10 mg daily (n = 5,168) or placebo (n = 5,137), the safety and tolerability profile of the group treated with Lipitor was comparable to that of the group treated with placebo during a median of 3.3 years of follow-up.
Postmarketing experience. Rare adverse events that have been reported postmarketing (which are not listed above), regardless of causality, include the following.
Body as a whole. Allergic reactions (including anaphylaxis), chest pain, malaise.
Musculoskeletal system. Rhabdomyolysis.
Nervous system. Hypoaesthesia, dizziness, amnesia.
Ear and labyrinth disorders. Tinnitus.
Skin and appendages. Bullous rashes (including erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis), urticaria.
Metabolic and nutritional disorders. Peripheral oedema, weight gain.
Haemic and lymphatic system. Thrombocytopenia.
Dosage and Administration Lipitor can be administered within the dosage range of 10 to 80 mg/day as a single daily dose. Lipitor can be taken at any time of the day, with or without food. Therapy should be individualised according to the target lipid levels, the recommended goal of therapy and the patient's response. After initiation and/or upon titration of Lipitor, lipid levels should be reanalysed within four weeks and dosage adjusted according to the patient's response.
Primary hypercholesterolaemia and mixed dyslipidaemia. The majority of patients are controlled with Lipitor 10 mg once a day. A therapeutic response is evident within two weeks, and the maximum response is usually achieved within four weeks. The response is maintained during chronic therapy.
Homozygous familial hypercholesterolaemia. Adults. In the compassionate use study of patients with homozygous familial hypercholesterolaemia, most patients responded to Lipitor 80 mg with a greater than 15% reduction in LDL cholesterol (18 to 42%).
Children. Treatment experience in a paediatric population (with doses of Lipitor up to 80 mg/day) is limited.
Dosage in patients with renal insufficiency. Renal disease has no influence on the plasma concentrations or on the LDL cholesterol reduction of atorvastatin; thus, no adjustment of the dose is required (see Actions, Pharmacology).
Dosage in patients with hepatic insufficiency. Plasma concentrations of atorvastatin are markedly increased in patients with chronic alcoholic liver disease (Childs-Pugh B). The benefits of therapy should be weighed against the risks when atorvastatin is to be given to patients with hepatic insufficiency (see Actions, Pharmacology).
Overdosage There is no specific treatment for Lipitor overdosage. Should an overdose occur, the patient should be treated symptomatically, and supportive measures instituted as required. Due to extensive drug binding to plasma proteins, haemodialysis is not expected to significantly enhance atorvastatin clearance.
Presentation Tablets, 10 mg (white, elliptical, film coated, marked 10 mg, PD 155 on reverse): 30's; 20 mg (white, elliptical, film coated, marked 20 mg, PD 156 on reverse): 30's; 40 mg (white, elliptical, film coated, marked 40 mg, PD 157 on reverse): 30's; 80 mg (white, elliptical, film coated, marked 80 mg, PD 158 on reverse): 30's.
See Product Identification Guide. Lipitor 10 mg; Lipitor 20 mg; Lipitor 40 mg; Lipitor 80 mg.
Storage Store below 25 deg. C.
Poison Schedule S4.
Date of TGA approval or last amendment 07/07/2004
Please refer to disclaimer
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Aardvark
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Re: Statins, good or bad.

Post by Aardvark » June 25, 2009, 12:54 pm

Thanks very much for the input guys, it is much appreciated. Frazee, I hear where your coming from and I intend to lay off these drugs for a while and see how things pan out. When and if I have suitable ammunition I will confront my Doctor with the facts and see what she has to say. It's not Rocket Science, if my symptoms change for the better I will do without the drugs and take my chances with the higher Cholesterol it's as simple as that, cheers Aard.

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Re: Statins, good or bad.

Post by Farang1 » June 25, 2009, 2:18 pm

I understand apple cider vinegar will help in keeping the arteries cleaned out. A tablespoon in an 8oz glass of water. 1 in morning and 1 in evening.

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Re: Statins, good or bad.

Post by rjj04 » July 21, 2018, 6:40 am

I know this is an old thread, but I really think an update about these supposed cardio-protective drugs is extremely important. Anybody taking any of these medicines ought to check out this video from Dr. Greger about the efficacy of drugs vs diet....

https://nutritionfacts.org/video/the-ac ... -vs-drugs/

In the words of Ricky Ricardo... Medical industry, you gotta lotta splainin to do.

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Re: Statins, good or bad.

Post by DuiDui49 » July 21, 2018, 7:59 am

In my eyes it spells L A Z YN E S S,plain and simple.

We humans tend to overeat,no exercise,smoking,drinking and more.And then we wounder why we have to eat all these Med's..go figure.Have a saying:

The more i learn about the human beeing,the more i love my dog.Yeah,sometime i think animals are far smarter then we give the credit for,and at the same time,humans,you and me,are so stupid/lazy so we just continue whith these negatives..and it gives us what..We have to belive in the Magic Pill intead of taking time to change our behavior.Not easy maybe,but i think that's the way to go.
Not saying that i'm 100% healthy,but my take is this:

The better i eat and drink (water)..eat like you're an diabetic person,eat something every 3-4 hours,not huge meals..but something to keep an even bloodsugar level most of the time,not eating sweets..okey.Drink 4-6 600ml of water every day,sounds alot,i know..it's a learning process but your never going to suufer from headaches due to dehydration..and contipation..forget it.
Alittlebit goes a long way,take baysteps to change your life,maybe even get of these pills that your on..Try it and you might like your new style of your body and mind.

By the way,did i mention that i love cokkies/sweets alot,BUT my way of thinking/doing is the BETTER i eat/exercise the more i can indulge in my Brownies..whitout getting fat.I also do maybe once a week were i eat moore soups or food that goes thrue the sytem quickly,and then i have days that i indulges in both burgers and fries/pizzas..When i have had those "sloppy"eating days i then give myself days for the body to "recup"by eating food that digest more easy..like soups.

I'm 60 now,and i hate hospitals like a plage.I'm not on ANY med's at all.I do a yearly check up,2600Bath full blood check at UdonLab,well worth the money me think.

Remember,it's never to late to make a change in life,never.

Have a awsome day all,and thanks for reading..:-)..not spellchecked ;-)
Best regards
//DuiDui
"Exercise is individual and nutrition is queen: together, you have a kingdom."

“Gratitude is not only the greatest of virtues but the parent of all others.” 

"To grow and mature demands time and willingness to learn from your own misstakes"

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Re: Statins, good or bad.

Post by kakariki » July 22, 2018, 2:10 am

I've been taking APO-Atorvastatin 80mg for about 12 months now, it has reduced my cholesterol, and I've had no other side effects, but I guess drugs effect different people in different ways.

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Re: Statins, good or bad.

Post by rjj04 » July 22, 2018, 7:31 am

Firstly, I am obviously not a doctor, and their are people on this website, who I am sure know infinitely more than I do about these things, but I'll say my two bits anyway :) ...

kakariki, did you watch the video? I think the question isn't, whether or not a statin can lower your cholesterol, it is whether or not you will significantly lower your risk of death. That is the goal after all. From the below video you will see that a recent study shows that ALL, yes, ALL people who take a statin suffer muscle damage, despite being asymptomatic. Albeit, slight muscle damage. So, perhaps the statins are lowering cholesterol, but at the same time offsetting that good result by weakening heart muscle tissue?

https://nutritionfacts.org/video/statin ... -toxicity/

Anyway, I posted this just to give people more information. If somebody is not willing to change their lifestyle to change their health the whole point is moot and they probably ought to stay on their prescribed medicine. Discussing these things with your Doctor might be worthwhile though.

Hell, even I, can't stay away from a lovely McD's sausage egg mcmuffin once a month or so when I get into Udon... life's a b..ch ain't it \:D/

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Re: Statins, good or bad.

Post by kopkei » July 22, 2018, 8:26 am

for some people the op question is irrelevant ,i have normally always problem cholesterol (hereditary in the family) ,i only knew this after an urgent 5 bypass ,i was not far from eating porridge upstairs....,so now for 4 years i must take 40mg statin , first it was lipitor (atorvastatin ) but i changed it to the cheaper simvastatin (bestatin/berlin) ,@ 300 baht/100 box, and they are doing the job too , because last blood check my cholesterol levels were ok , i am sure all these alternatives will not be enough ,until now (after 4 years)i do not have any side effects and i am still alive ...
a friend of mine has to take all his life already 80 mg , if not he would drop dead also , i do not believe taking 2 spoons of apple cider vinegar will do the same job for us , and taking apple cider vinegar every day has also his side effects ..
bottom line , i do not like to take medicine too ,but in this case it is necessary, as i do not want to go eat some rice porridge upstairs...so only answer here for me ...good ... ;)

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Re: Statins, good or bad.

Post by pf-flyer » July 22, 2018, 9:09 am

Quote " McD's sausage egg mcmuffin once a month or so."
I feel the same way.
Not to stray away from the subject on this thread. I just wanted to add that I have been on Satins for Cholesterol also and ACE Inhibitors for Blood Pressure for about 18 years. ACE Inhibitors have a side effect that affects short term memory. The doctors told me that the benefits out weight the side effects. However get regular checkups that include blood work to keep tabs on how well your body is responding the prescriptions that you are taking and the doctors will determine if any adjustments need to be made. I recommend that you find a doctor that you are comfortable with and have confidence in and work with Him or Her. There are Health issues such as High Blood Pressure that are silent until you have an unfortunate event.
"Life is like a tube of toothpaste. Outward pressure brings out the inward contents."

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Re: Statins, good or bad.

Post by rjj04 » July 22, 2018, 9:13 am

kopkei, did you actually watch the video(s)? I mean, no where in the videos cited does it discuss apple cider vinegar. People can't fix a lifetime of bashing their bodies into bits by forcing down a tablespoon or two of vinegar a day, and nobody is suggesting that - straw-man. You might want to watch Dr. Greger's introductory video below, that discusses why he wanted to become a doctor... his grandma was written off as good as gone by her doctors after having a few heart surgeries and she was sent home to die... she went on a specific plant-based diet and lived another +30 plus years (if I recall right)*

https://nutritionfacts.org/video/the-st ... facts-org/

The EVIDENCE is clear, from peer-reviewed studies...
cardio protective drugs - can reduce a patients probability of having a heart attack by less than 5%
a plant-based diet - can reduce a patients probability of having a heart attack by approx. 60%

note - the second method also reduces the probability, massively in some cases, of diabetes, cancer, and most of the top 15 killers of most western people (different countries have a different list of top killers, obviously).

That is the data, at the moment. It is not theory or conjecture.

*Anecdotal evidence, is not the same as peer-reviewed evidence.

When talking to people about diet, people really do seem to get defensive. I'm just desirous of an open discussion about why patients on these drugs think they are getting massive help from them, when the evidence is overwhelmingly against that supposition. Less than 5% is not much help on an individual basis, of course societally it is in the tens or hundreds of thousands of people helped. On the other hand, switching people over to a more plant-based diet though would save millions from death. Unless of course those millions think life without cheese pizza isn't worth living... I have to say here, that is a tough call for me too :lol: Ah those caso"morphin"s
Last edited by rjj04 on July 22, 2018, 9:43 am, edited 3 times in total.

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Re: Statins, good or bad.

Post by rjj04 » July 22, 2018, 9:15 am

Apparently the statins have an effect on the memory as well, and also increase the risk of diabetes 2
Just something to be aware of.

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Re: Statins, good or bad.

Post by rjj04 » July 22, 2018, 10:08 am

kopkei wrote:
July 22, 2018, 8:26 am
for some people the op question is irrelevant ,i have normally always problem cholesterol (hereditary in the family)
Once again, I'm not an expert here but, could it be that none of your ancestors were vegetarians? If one of your ancestors was a vegan, for more than a few years, and yet they still had high cholesterol, then one might assume that there could be some genetic predisposition involved. On the other hand, if all your ancestors were also meat, poultry, and dairy eaters, then I'm not sure how one could determine whether or not there is a genetic issue involved. Did a medical doctor actually inform you that he analysed your DNA and found some gene that would raise your cholesterol? Also of course, gene expression is involved, that is, even if you have gene XYZ, after leaving the womb, that gene would need to be expressed by some environmental stimuli, or no? Did you try a strict vegan diet for a few months and find that, indeed your cholesterol did not drop? That also might be an indication of some sort of genetic issue, I'd assume. At least this is my extremely limited knowledge, I could be full of BS, for what it is worth :) Anyway, I'd be interested in understanding this high cholesterol due to genes issue.

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Re: Statins, good or bad.

Post by rjj04 » July 22, 2018, 10:30 am

https://ghr.nlm.nih.gov/condition/hyper ... emia#genes

Familial hypercholesterolemia?

Apparently 1 in 400 Americans might be affected? 1:200-250? Genetic abnormalities involved. That NIH site says there are genetic tests that can check for FH.

" FH likely accounts for 2%-3% of myocardial infarctions in individuals younger than age 60 years."
- from the NIH site.

Looks like some people who have been fighting high LDL levels from a young age ought to test for this FH.
The HDL and triglyceride’s are at normal levels, yet LDL is high?

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Re: Statins, good or bad.

Post by rjj04 » July 22, 2018, 10:59 am

Interesting story in the link below of a woman on a vegan diet for 12 years, who still had high cholesterol numbers... she got tested for this FH, and found she had that. So, then she went whole hog and cut cooking oils out of her diet and dropped her cholesterol numbers way down. It seems, that even with FH, and not taking statins, one can keep FH under control... but it takes massive will power. Yikes!

http://www.vegsource.com/sarah-taylor/v ... terol.html

For the rest of us, without this FH, >99%, it is not an issue thank goodness.

I'm probably annoying a few people with all these posts, so I'll go about my biz now.
Cheers!!

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Re: Statins, good or bad.

Post by yartims » July 23, 2018, 11:20 pm

mixed messages on statins all i know is its a billion dollar business for those yanks

from the dailymail article

Are statins really the wonder-drug that everyone says they are?

Last updated at 22:06 23 January 2007

Two experts give the arguments for and against statins...

Yes says Dr Jane Armitage, Reader in Clinical Epidemiology at Oxford University

There is a huge amount of evidence that taking statins saves lives and reduces heart attacks and the need for bypass surgery and similar types of operation.

We are all at risk of heart disease and there is a lot of evidence that more people should be taking statins rather than fewer.

Most sensible people accept there is a link between the risk of heart disease and somebody's cholesterol level.

We have been involved in a very large trial involving 20,000 UK volunteers who took a statin for five years.

We saw fewer deaths and strokes and few significant side effects in the group takng statins than those who did not.

Our findings were that the more you lower your cholesterol the better the benefit you get. There were no significant side effects at all.

A wider study, of 90,000 people from different parts of the world backs up the view that statins are safe.

In our Western diet, which most of us live on it is hard to make big changes to our cholesterol level, although some people manage to lower their cholesterol level on a low fat diet, but it's very hard to comply with over a lifetime.

Whereas if you take a statin tablet you will get a big change in your cholesterol.

When drugs are as well tolerated as statins are - and you only have to take a single pill each night - people can generally improve their life expectancy.

Heart disease is the biggest killer in the

country. Last year around 100,000 people died from the disease - a great deal more than breast cancer, which kills 2,300.

Each year about 1.3 million people have a heart attack and about two million people suffer from angina.

Statins have been incredibly successful in treating heart disease. Much of the fall in death rates since 2000 from heart disease can be put down to a tripling in the prescription of statins.

Statins saved 9,700 lives in 2005 compared with 2,900 lives saved in 2000 according to Department of Health statistics.

If people stop taking statins that will be a public health disaster and indirectly will lead to people dying, and that's sad and tragic.

No says Dr Malcolm Kendrick, a GP who works with the European Society of Cardiology

Statins are hailed as wonder-drugs. The reality is that, for a few people, they are beneficial.

For the majority they provide no benefits, cost a huge amount of money and create a series of unpleasant side-effects.

For a man diagnosed with heart disease, it is probably a good idea take a statin to reduce the risk of further heart disease.

However, a man without heart disease will not live one day longer by taking a statin.

And for a woman, with or without heart disease, taking a statin is a waste of time.

Yet doctors are urging all men and women with a cholesterol level greater than five to take statins.

This is the vast majority of the adult population - as 80 per cent of adults in the UK have a cholesterol greater than five.

By the age of 50 this figure is nearly 90 per cent. Statins have many effects - one of which is lowering cholesterol.

But it is becoming increasingly clear that as lowering cholesterol does not prevent heart disease, targeting people with high cholesterol will have no effect.

The over-prescription of statins is already having massive financial implications to the NHS. The cost of prescribing statins is set to reach £1 billion a year shortly.

And this figure does not include cholesterol tests, and consultations with doctors and nurses.

Add these costs in and we could well be looking at £2 billion a year, and this figure is set to go ever higher.

This would not be such a big issue if it were not for the fact that statins have some pretty unpleasant side-effects up to, and including, death.

Statins have been directly implicated in several hundred deaths in the US. Apart from killing people, statins create many other, lesser, side-effects.

The commonest is muscle pain. Although the text-books say this is rare, the reality is that up to 40 per cent of people will suffer some degree of pain and weakness.

An Austrian study on athletes showed that only 20 per cent of them could tolerate statins.

It is becoming increasingly clear that statins also have major effects on brain function. Side-effects here include depression, memory loss, confusion, irritability and aggression.

And statins also increase the risk of polyneuropathy - which leads to numbness, tingling and nerve pain - by over two thousand per cent.

Recently some disturbing new evidence has emerged that statins may cause Parkinson's and a Japanese study suggested a strong link to cancer.

888888888888888888888888888888888888888888888
i stopped taking them as my figures are not high AND THE SIDE EFFECTS WERE TOO BAD ..brain fog was bad and general feeling of malaise was bad ..so i use an aspirin of 37
the only good Tory is a lavatory

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Re: Statins, good or bad.

Post by kopkei » July 24, 2018, 8:17 am

well , as info , everyone whom has problem high cholesterol hereditary like me ,will have to take something ,as diet only will not be enough ..so regular blood checks are needed to know if what ever you are taking is working ...
an easy one.
as to prevent heart attack many people take an aspirin daily , in my case it is 80mg , gastric juice resistant coated,as a regular aspirin on daily base would not be healthy for your stomach and intestines ...
another medicine i need to take is bisoprolol,(to lower my heartbeat)buy them 5mg , but need only half/day ....
so taking these 3 medicines is to me a necessary evil ,as i also do not enjoy taking medicine, and as to the side effects? ,which i not yet have a problem after only 4 years , i will have to accept them too ,always better than dropping dead .... ;)

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Re: Statins, good or bad.

Post by Mex » July 25, 2018, 6:09 pm

CoQ10 does eliminate one side effect of taking statins.
If it looks good..and smells good..go for it..

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