Statins for Gray Beards

If you really want to lower your cholesterol it requires a lifestyle change. Cut back or eliminate all animal products. No sweets, no deep fried foods, etc. It will drop and very quickly.

I've felt no discernable side-effects even though I'm cycling pretty darned hard.

Which countries ?

I don't think anyone has addressed my original question regarding their experiences with statins and muscle weakness.

One of the possible side effects of Statins is muscle weakness. I take statins and also work hard to be able to climb hard. Is it possible that, because of my statin use, it is more of an uphill battle to gain/maintain strength/endurance?

Muscle pain and damage
The most common statin side effect is muscle pain. You may feel this pain as a soreness, tiredness or weakness in your muscles. The pain can be a mild discomfort, or it can be severe enough to make your daily activities difficult. For example, you might find climbing stairs or walking to be uncomfortable or tiring.

Very rarely, statins can cause life-threatening muscle damage called rhabdomyolysis (rab-doe-mi-OL-ih-sis). Rhabdomyolysis can cause severe muscle pain, liver damage, kidney failure and death. Rhabdomyolysis can occur when you take statins in combination with certain drugs or if you take a high dose of statins.

I also take Co-Q10.

Functional medicine is not medicine, it's pseudo-scientific quackery fronting supplements businesses.

Would love to do the veggie alternative to statins, but I have kidney stones and that severely limits my options in that respect.

healyje, I like you, but that statement is total horseshit! There are crap physicians that practice conventional medicine and there are crap physicians that practice functional medicine.

Mark, I did see those videos

Yes, we eventually die regardless of what we eat...

Routine laboratory measurements in the evaluation of patients with insulin resistance syndrome include the following:

Plasma glucose level (fasting, random, and oral glucose tolerance test) - Diagnosis and monitoring of glucose intolerance (diabetes mellitus, impaired glucose tolerance [IGT], impaired fasting glucose [IFG])

Insulin resistance - May also be associated with hypoglycemia (autoimmune conditions)

Glycohemoglobin level – Used to assess chronic hyperglycemia

Fasting insulin level - A measure of the degree of insulin resistance in many patients with insulin resistance syndrome

Lipid profile (fasting total cholesterol, low-density lipoprotein [LDL], high-density lipoprotein [HDL], cholesterol, triglyceride) - Insulin resistance syndrome characterized by elevated LDL-B levels (small, dense, pattern B), high triglyceride levels, and reduced HDL-C levels

Combined use of insulin and lipid markers in atherosclerosis - Fasting insulin, apolipoprotein B, and small LDL levels are more biologically significant than are standard lipid tests. Elevations in the 3 markers increase the risk of coronary artery disease by nearly 20-fold.

Electrolyte levels (BUN [ blood urea nitrogen], creatinine, and uric acid levels) - Hyperuricemia is common and is often considered a component of the metabolic syndrome.

Urinalysis - Microalbuminuria is a marker of endothelial dysfunction.

Homocysteine (H[e]) - An elevated level is a risk factor for atherosclerosis, which predicts macrovascular disease. levels are regulated by insulin.

Plasminogen activator inhibitor (PAI)-1 - An elevated level is associated with insulin resistance syndrome and is correlated with obesity, waist-to-hip ratio, hypertension, fasting and postprandial insulin levels, proinsulin levels, fasting glucose levels, and elevated triglyceride and LDL levels. [45] An increased PAI-1 level signifies impaired fibrinolysis, thus indicating increased risk of atherosclerosis.
Other laboratory studies include measurement of fibrinogen levels and testing of endothelial function.

An increased fibrinogen level is a feature of insulin resistance syndrome. Endothelium plays an important role in insulin action, including in the regulation of tissue blood flow and in insulin delivery to interstitium. Endothelial dysfunction is an important component of insulin resistance syndrome and includes reduced capillary formation, reduced surface area, and abnormal reactivity of endothelium.[46]

Biochemical changes associated with endothelial dysfunction include (1) reduced nitric oxide and prostacyclin levels, (2) increased endothelin and angiotensin activity, and (3) increased local and systemic inflammation (increased C-reactive protein [CRP] levels).[11] Blood testing for CRP measurement is widely available. Smoking and abnormal lipids are major contributors to endothelial dysfunction.

An elderly population of athletes receiving HMA Co-A reductase inhibitors would appear to be ideally suited to experiencing the greatest benefit from coenzyme Q10 supplementation, given the high risk of mitochondrial dysfunction from coenzyme Q10 deficiencies in this group.

Low levels of Coenzyme Q10 were consistently associated with fatigue.

Of the 29.1 million (or 9.3% of the American population with diabetes in 2012), 21.0 million were diagnosed, and 8.1 million were undiagnosed.

In 2012, 86 million Americans age 20 and older had prediabetes (insulin resistance); this is up from 79 million in 2010.

It's true that you should modify your diet and exercise, but truthfully those only have on the order of a 10% effect on lowering LDL

...other than a long addiction to IBU..

Summary
1.HDL-C and HDL-P are not measuring the same thing, just as LDL-C and LDL-P are not.
2.Secondary to the total HDL-P, all things equal it seems smaller HDL particles are more protective than large ones.
3.As HDL-C levels rise, most often it is driven by a disproportionate rise in HDL size, not HDL-P.
4.In the trials which were designed to prove that a drug that raised HDL-C would provide a reduction in cardiovascular events, no benefit occurred: estrogen studies (HERS, WHI), fibrate studies (FIELD, ACCORD), niacin studies, and CETP inhibition studies (dalcetrapib and torcetrapib). But, this says nothing of what happens when you raise HDL-P.
5.Don’t believe the hype: HDL is important, and more HDL particles are better than few. But, raising HDL-C with a drug isn’t going to fix the problem. Making this even more complex is that HDL functionality is likely as important, or even more important, than HDL-P, but no such tests exist to “measure” this.

The action of 13 NSAIDs was compared in terms of their effect on cartilage GAG synthesis. 3 of these NSAIDs were also studied in terms of their effect on cartilage collagen synthesis. Consideration of the results in this study and from published material, led to the suggestion that NSAIDs may be divided into 3 categories in respect of their in vitro action on the extracellular matrix of human arthritic cartilages: 1. Those such as Aceclofenac, Tenidap and Tolmetin which can stimulate matrix synthesis 2. Those such as Piroxicam, Tiaprofenic Acid and Aspirin which appear to be without significant effect on matrix synthesis and, 3. Those like Naproxen, Ibuprofen, Indomethacin, Nimezulide which significantly inhibit matrix synthesis.

These experiments led to the suggestion that NSAIDs such as Aceclofenac would be appropriate for long-term treatment of arthritic conditions provided that one is prepared to extrapolate between in vitro experiments on human cartilage and what may be happening in vivo.

Curcumin combined with piperine introduced in the humans, resulted in 2000% increased bio-availability.

jgill: And that would be how? Please, no tumeric, etc.

Has anyone had experiences with muscle weakness while on Statins?

Exactly what statins are you people taking?

mynameismud

climber
backseat

Apr 13, 2016 - 08:23am PT
If you really want to lower your cholesterol it requires a lifestyle change.

very low rate of heart disease in India because they eat so much cumin and turmeric.

what statin are you taking?

very low rate of heart disease in India because they eat so much cumin and turmeric.

I’m suspicious

recent studies indicate that some of the cholesterol-independent or “pleiotropic” effects of statins involve improving endothelial function, enhancing the stability of atherosclerotic plaques, decreasing oxidative stress and inflammation, and inhibiting the thrombogenic response. Furthermore, statins have beneficial extrahepatic effects on the immune system, CNS, and bone. Many of these pleiotropic effects are mediated by inhibition of isoprenoids, which serve as lipid attachments for intracellular signaling molecules. In particular, inhibition of small GTP-binding proteins, Rho, Ras, and Rac, whose proper membrane localization and function are dependent on isoprenylation, may play an important role in mediating the pleiotropic effects of statins.

Protective properties of curcumin may influence HDL functionality; therefore, we reviewed the literature to determine whether curcumin can augment HDL function. In this review, we concluded that curcumin may modulate markers of HDL function, such as apo-AI, CETP, LCAT, PON1, MPO activities and levels. Curcumin may subsequently improve conditions in which HDL is dysfunctional and may have potential as a therapeutic drug in future. Further clinical trials with bioavailability-improved formulations of curcumin are warranted to examine its effects on lipid metabolism and HDL function.

I hope you’re predominantly suspicious of what you read here! YMMV

Curcumin quotes above are from NCBI

And Lorenzo had the same experience with calculator as I did.

Totally skewed for age.

may play an important role in mediating the pleiotropic effects of statins.

Further clinical trials with bioavailability-improved formulations of curcumin are warranted to examine its effects on lipid metabolism and HDL function.