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monolith
climber
state of being
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It's curious that most people consider olive oil to be healthy. People want their oils and easily succumb to the olive oil is healthy' myth.
Same curious beliefs about red meat vs other meats. Most health conscious people believe red meat is bad(and they are right) and since they must have meat, assume non-red meat is healthy.
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fear
Ice climber
hartford, ct
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Funny thing is that whatever we eat... it eventually kills us.
Unless you've got some family history of major heart disease and early deaths from such disease I wouldn't be chasing numbers from a lab and gobbling down Big-Pharma's expensive tic-tacs.
We die when we'll die based largely on genetics (barring an unfastened harness or errant propane truck)
My family discovered some decades ago that some us inherited a genetic disorder called Hemochromatosis. It can cause elevated levels of iron in the blood along with a host of other problems. And thus began a decade of frenzied tests, changes to diets, and regular frequent blood-letting for those so "afflicted". Generations of women in my family have all lived healthy into their upper 90's and men well into their 70's prior to this sudden silent enemy being discovered on the mystical lab reports
Those who chose to be treated to get these elevated iron levels way down ended up far more screwed up and died sooner than those who did nothing.
I betcha sometimes high-cholesterol is just fine just like high levels of iron might be fine.
Moderation in all things, stay active, stay connected to people, stay away from ice climbing.
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monolith
climber
state of being
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Here's a guy that was highly fit, then needed a triple bypass. He got put on statins and other drugs, experienced similar problems described in this thread, then dumped all the drugs and reversed his condition by changing his diet. And not to some 'moderation' diet.
http://www.youtube.com/watch?v=hhEMtW2tYuc
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skcreidc
Social climber
SD, CA
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Monolith and I are definitely on the same page with this topic. McDougall, Greger, and Esselstyn are all medical doctors first, but then through observation and the scientific processes have arrived at a different outlook than what is currently accepted.
Mark, I did see those videos
Actually Healyje, my name is not Mark ;) it's Chris.
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Mark Force
Trad climber
Ashland, Oregon
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Yes, we eventually die regardless of what we eat...
Yep. I like you, Locker, you're always keepin' it real.
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Mark Force
Trad climber
Ashland, Oregon
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Here is a consideration for management -
Effects of a nutraceutical combination containing berberine (BRB), policosanol, and red yeast rice (RYR), on lipid profile in hypercholesterolemic patients: A meta-analysis of randomised controlled trials.
http://www.ncbi.nlm.nih.gov/pubmed/27131395
Note: Red yeast rice inhibits liver HMG-CoA reductase as do prescription statins. My clinical experience is that it is typically gentler and doesn't produce fatigue or myalgia as frequently nor does it make as much change on LDL levels as prescription statins. It may be an option for those who don't have to make a dramatic change in their lipid profile, is non-prescription and may be a cheaper. Never assume it would will - the effectiveness would have to be confirmed by lipid panel.
Relationship between insulin resistance and abnormal lipid profile in obese adolescents
http://www.ncbi.nlm.nih.gov/pubmed/7751990
This is an example of a body of studies that indicate an insulin resistance underlies abnormal lipid profile. Improving insulin sensitivity through diet and exercise alone consistently improves lipid profiles. There is certainly a subset High Total Cholesterol and high LDL demographic that is so strongly predisposed genetically to abnormal cholesterol profile that a prescription statin is indicated - it is small relative to the overall demographic. Taking statins does not improve insulin resistance and associated complications.
Doing the work to change to insulin sensitivity has the benefit of usually making a statin uneccessary and makes your body more sensitive to the anabolic effects of insulin - it has more overall effect on your anabolic balance than testosterone!
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Mark Force
Trad climber
Ashland, Oregon
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Insulin resistance is the overlooked elephant in the room in people who have abnormal lipid profile.
Here are the standards of diagnosis for insulin resistance from MedScape -
http://emedicine.medscape.com/article/122501-workup#c7
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.
Whoever wrote this did a great job. It certainly meets functional medicine standards for diagnosis!* Not included was fructosamine which can be used for shorter time frame metrics for response to diet and exercise.
*Note: Meeting a functional medicine standard requires to first determine the primary/conventional diagnosis and then determine the secondary functional diagnosis that includes the vector of causation for the primary diagnosis. Often the primary diagnosis is inclusive of the functional diagnosis (i.e. bacterial pneumonia), but this is not always the case (i.e. irritable bowel syndrome, migraine headache). Irritable Bowel Syndrome - the primary diagnosis - may be found to be seconday to insufficient small intestine bile as determined from exams and labs - the functional diagnosis. The secondary functional diagnosis is often the key to effective care that leads to objective changes on follow up exams and labs and resolution.
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slabbo
Trad climber
colo south
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Diabetes--- the terror
How many people aren't even diagnosed ?? 20%??? 40%???
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Mark Force
Trad climber
Ashland, Oregon
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A lot.
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. http://www.diabetes.org/diabetes-basics/statistics/
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Squesk
Gym climber
Perth, Western Australia
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Didnt read most of the replies.
I take 40mg per day, one thing that was not told to me by my doc was that effects the CoQ enzyme. so taking CoQ is recommended.
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zBrown
Ice climber
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This is a very complex subject.
One and two dimensional approaches seem extremely limiting. That being said, if you throw in a few "other things being equal" or controlled for and/or randomized perhaps some true and verifiable relationships be established.
So what can be said of the combination of n-acetyl cysteine and alpha lipoic acid in the battle against thryoid disease and cataracts (and others)?
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Mark Force
Trad climber
Ashland, Oregon
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zB,
Now you're getting into some complex biochemistry that makes the statin-CoQ10 issue pale by comparison. The discussion probably isn't suited to this forum, especially with your question being so open-ended.
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emilines
Trad climber
Mountain View, CA
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I'm a physician and this is something that many folks ask about. There is a potential adverse of effect of statins called "statin myopathy" which is characterized as muscle weakness and soreness, typically occurring within weeks to months of initiation of the drug as a result of muscle cell inflammation or breakdown. On the most severe end of the spectrum, patients can have rhabdomyolysis, but this is particularly rare (90% of patients, the myopathy resolves in 2 months with discontinuation of the drug.
In other words, I see this as more of an acute event and less of something that would affect you in the way you've described - decreasing exercise tolerance or impairing muscle growth but without the occurrence of a discrete statin myopathy. I was only able to find one peer reviewed article on this (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4450764/); which showed in a RCT that there was no decrease in exercise tolerance.
On the other hand, statins (and their effect in long term cardiovascular and neurovascular health) are super well studied and there's a great body of evidence to say that these things reduce the risk of heart attacks and stroke. 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, whereas statins have an effect on the order of 30-60% (depending on dose and drug).
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skcreidc
Social climber
SD, CA
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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
This is a very interesting discussion, but I have to comment on this one part. With all due respect to all your years of training and your skill as a physician emilines, this is the same nonsense my personal physician told me. And frankly, it's just wrong for many people (I'm not saying for everyone). Diet is another option. My brother in law, a recently retired physician who lives near your neck of the woods, told me this past Christmas that he saw amazing improvement in his patients in his last year of practice. The patients who took to the dietary path vs perscriptions saw much improvement in cardiovascular health over patients on perscriptions alone. This is including large improvements in the LDL after years of being on statins. He told me he wished he'd figured this out years earlier.
In my case, I had total cholesterol of 232 (I don't remember the LDL, but my doc said it was bad) and was told to get on Lipitor asap (I also had mild hypertension). I took the diet and exercise path and got total cholesterol down to 180 with a great ratio (according to my doc). My physician then proceeded to give me props on my genes, and I had to remind him of the "only 10% effect" of diet and exercise he told me about and what I did. "Most people could not do what you did", was his reply. So basically I was not given the option, as it was written off for me. This was almost 10 years ago and my blood chemistry is holding up well, according to my personal physician. One thing I do have going for me is support. My wife is eating the same (whole foods plant based) and her total dropped from 190 to 137 with great LDL numbers. Oh, and my hypertension? Gone.
I'm going to turn 60 this year, and I'm still holding off the pills. I figure at a minimum, it at least gives me more options later. But it still kind of pisses me off I had to figure this out on my own; that my own physician could not give me the all the options. Basically I like him as a doctor too. Frankly, I think it has more to do with what physicians are taught and the system they are "brought up" in. But I am guessing on that point.
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slabbo
Trad climber
colo south
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Interesting indeed,,my Ch was around 145,,yet heart failure and a few MI's (4) made a statin a choice for these issues. Q-10, magnesium and other meds have stabilisec things pretty well.
other than a long addiction to IBU,,,what caused this ?
Went climbing yesterday and didn't die..I guess experience helps
I saved the easy climbs for now
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Mark Force
Trad climber
Ashland, Oregon
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...other than a long addiction to IBU..
International Beer Units?
Ibuprofen and other NSAID anti-inflammatory drugs trigger the leukotriene cascade as a side effect that ultimately has the nasty outcome of degrading collagen - connective tissue, ligaments, tendons, cartilage - when used chronically (consistently over long periods of time). "Vitamin I" is OK as short-term management of pain, but is a bad idea as a regular thing for chronic pain that is best handled differently.
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zBrown
Ice climber
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Righto Mark Force.
I'm doing the reading myself, but I'm taking the NAC - alpha lipoic acid combo and will monitor the few variables I can get access to regarding myself.
I introduce it as a public service since there are some strong claims for the benefits.
I find it interesting that there is some indication that it is possible to "dissolve" catatacts, though the only claim about the combo is that it may delay or retard their development.
I was diagnosed as hypothyroid in 2000 and have gone through a progression of hypo, subclinical hyper, hypo, outright hyper and am now back in the hypo group trying to get my labs back in range.
I'm told I have an "unusual" pattern.
Eye Drops Could Clear Up Cataracts Using Newly Identified Chemical
Here's a "dissolve" link for anyone who is interested.
http://www.ucsf.edu/news/2015/11/176886/eye-drops-could-clear-cataracts-using-newly-identified-chemical
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