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#81 |
Penultimate Amazing
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But the critical thing about Statins is that their advantage cones about via growth facotr, not LDL changes. As show by other drugs that lower LDL and do not benefit hearts.
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#82 |
Penultimate Amazing
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Probably the ASCOT study. Pubmed: [ASCOT-LLA] There was a follow up, [The Anglo-Scandinavian Cardiac Outcomes Trial: 11-year mortality follow-up of the lipid-lowering arm in the U.K.] |
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#83 |
Penultimate Amazing
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casebro's point is valid: we are at a stage for atorvastatin similar to where Jenner was when he confirmed vacaccination provided protection from smallpox. He didn't know exactly how it worked, but the studies show it did.
What Diamond's doing is what I call the French Philosopher's Disease: "Sure it works in the real world, but I don't understand how it works on paper, so I'm going to make a youtube video saying it doesn't actually work in the real world." |
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#84 |
Penultimate Amazing
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To put the numbers in context, if this was the ASCOT study, the timeframe was two years. If we extrapolate to lifetime benefits, let's say 30 years, the number of incidents would multiply by roughly 15, so instead of 3% placebo arm deaths we'd have 45%, the atorvastatin arm would be a third less at 30%. These numbers compare to the protection the population gets from not smoking vs smoking. It's potentially a big deal, but we don't have any studies performed this long to verify, my numbers are just back-of-the-envelope for illustrative purposes.
As mentioned in an above post, we're not sure how atorvastatin is protective. Diamond's hyperfocused on the lipid hypothesis (his rants seem to have originated from an outrage over health insurance pricing related to his cholesterol level, so he's on a mission to prove the lipid hypothesis wrong), and missing the other probable mechanisms, specifically there's a good case that the primary mechanism of protection is antiinflammatory. |
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#85 |
Agave Wine Connoisseur
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In which case, it would make more sense to address the cause of the inflammation..
Diet? |
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#86 |
Penultimate Amazing
Join Date: Jan 2006
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Age, for most of us. Genetics prevails. There are dietary suspects, but once the damage is done there's no known reversal.
(ref above, my undergrad is MBI, my primary focus was immune system, my masters was specifically research into how the immune system adapts/fails with exposure to HIV, but there is a lot of general knowledge; my second research project was lupus, which is an immune system glitch due to genetics) |
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#87 |
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#88 |
Penultimate Amazing
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I suspect that the data exists to tell which DNA variant is helped by Statins. Which will explain how Statins actually work. But don't expect Big Pharma to tell us that 60% of us shouldn't by their chemical.
Inflammation is a good candidate, via IRS-1 or another hormone receptor gene. Seems a known fact that statins lower insulin resistance, also raise IGF-1 levels. That, wah-lah, might be the answer. |
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#89 |
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#90 |
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Blutoski:
I would seriously be interested in an educated opinion of my post above... If you feel it would be inappropriate, I would be fine with that, also. |
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#91 |
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#92 |
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#93 |
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Does an educated opinion necessarily have to be advice?
Don't take this as contentious, but my question came from what I feel was " an argument from authority " on your part..
Quote:
" Your LDLc is higher than guidelines. We need to lower it. " MY PCP was oblivious to scientifically sound information that suggested I am not a good ( have nothing to gain, other than possible serious side effects ) candidate for statin therapy.. |
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#94 |
Penultimate Amazing
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Here's a bit of info re: the different functionality between Insulin, and Insulin like Growth Factor, IGF. Keep in mind that the IRS-1 ( Insulin Receptor Substrate) gene defect lowers the amount of IGF in your system- same substrate used for both the insulkin receptor and the growth hormone receptor, which kicks off the production of IGF.
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#95 |
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What do you mean by " high sugars "? High blood sugar?
A diet that is high in sugar will definitely drive all kinds of health issues. |
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#96 |
Penultimate Amazing
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We are talking diabetes and insulin resistance, so yeah, blood sugar levels.
And what I am saying is that high BS may not be the driver of morbidity that we have been taught. Hyperinsilinemia and low IGF are the drivers of much of the Diabetic morbidity. IGF injections have been used to treat the hyperinsulinemia. I may try some to treat my leg muscles that have been bad since childhood. (Insulin resistance is life long, the diabetes symptom starts later) My endogenous IGF level is only tenth percentile. To get the IGF, I think I can go to the muscle man gym, and hang put in the locker room, wait for some one to ask if I want to speed up the body building process. The steroids they use are IGF. Try it a couple weeks, see if my legs are capable of tap dancing- and want to. |
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#97 |
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The fact remains, in most cases, a low carb diet will reverse type 2 diabetes..
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#98 |
Penultimate Amazing
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Let me say this slowly: DIABETES IS ONLY THE SUGARS.
The patient still has the insulin resistance, the cause of so many of the side effects that get blamed on the sugars. You are not believing me, do your own search <pseudo acromegaly> But here is a partial list of my symptoms, things I have heard the docs say "we see a lot of that among diabetics" : Trigger finger Carpal tunnel tendonitis ruptured discs skin tags colon polyps clogged arteries calcifications lucent lesions (bones) Mayalgia Scalloped cervical bones pseudo foramen (looks like I drilled a hole in my thumb bone) Peripheral neuropathy. ad on nearly infinitum, I had a list of 45. ALL are listed as possible symptoms of Acromegaly, in spite of patients having normal sugars. Acromegaly, a messed up hormone system- like hyper insulinism, is caused by too much IGF. Too much insulin acts like-.... too much IGF. And some of my symptoms have been since childhood, I didn't turn obese and diabetic until my 20s. I know, diet and exercise will push diabetes into remission, but I still won't be able to snap my fingers or do the cub scout salute. Or feel my fingers and toes. (nerve sheath overgrowth, like artery lining overgrowth, cuts down circulation) eta: In fact, being a diabetic, studies show that it's OK to allow sugars to run twice as high as normals. Because? trying for normal doesn't do much at all for preventing the side effects. Not even enough to pay for the extra drugs. Look up UKPDS, United Kingdom Prospective Diabetes Study. |
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#99 |
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0h, I believe you.
I am talking mainly about type 2... lots of sugar creates the insulin resistance, and things like fatty liver disease.. Surprise! It's not dietary fat that does that. Most of the items in your list can be attributed to nutritional deficiencies and/or excesses.. |
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#100 |
Penultimate Amazing
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Are you assuming I am T1? Nope, it's my T2 that is tied inextricably to insulin resistance.
T1 is an auto-immune problem- your immune system attacks the insulin making beta cells in the pancreas. So you don't make insulin. It's only about 5% of diabetics. But guess what- the IRS gene defects are so common, T1 folks get all them disease symptoms too. Which adds to the confugalty of whether it's the high sugars or the high insulin that causes all those symptoms. |
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#101 |
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No, but on this forum, there's been an informal practice to not give opinions about specific cases when it's about a real person's medical diagnosis or prescription. There's no rule, and many members are happy to dispense medical advice all day, for example, the members in MLMs selling dietary supplements, but I personally prefer to fall on the side of caution.
It was, and that's not necessarily a bad thing, despite what pseudoskeptics hide behind. The fallacy is 'argument from invalid authority' (eg: we should listen to her opinions on vaccines because she's a famous actress). In contrast ("This is a heart disease topic, we should listen to the expert in heart disease") is not an example of argument from invalid authority fallacy, it is in fact a good argument. The answer depends on the guidelines communicated to MDs by their respective College in their region. As mentioned above, the drugs have long been demonstrated to work independently of their cholesterol reducing capacity, so many regions want GPs to consider multiple risk factors such as family history, current BMI, age, &c. |
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#102 |
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I just got back form my diabetes nurse/educator. She doen't even want to test some lipids nowadays. Though they are included in the risk calculations, along with age, sex,race, smoker, some more items. My risk score for a heart attack in the next ten years is 33%. I'm a 65yo diabetic, I didn't think 33% is half bad.
eta:, Hmmm, life expectancy of 75, ten years from now, 40% of us die of heart attacks, looks to me that I am beating the numbers. But that just means that I'll die of cancer, ;like all of my brothers (2). |
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#103 |
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It's not the glucose level (diabetes), nor the obesity, it's the insulin resistance
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#104 |
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SG's personal inventory included having had smoked in the past, which according to Health Canada's website is actually up there as a risk factor with high lipid scores, obesity, and sedentary lifestyle. Lower than current smoker, but the risk seems to stay pretty high even after quitting. However, that's Health Canada's calculator. US regions may estimate risk differently and ask their GPs to act accordingly.
This is where I frustrate the risk analyzers: my parents both died in their 20s from situations that had nothing to do with chronic illness, so my risk level is unknown, and many calculators don't have the ability to incorporate that. |
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#105 |
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If my lungs and arteries are all clear, what is the likelihood that my having last smoked over thirty years ago, actually a risk factor for me now?
Also as I mentioned above, my Cardiac CT calcium score is zero.. This indicates a risk of CVD at less than 5%.. My PCP is apparently using a risk calculator that does not include either of these factors.. The best calculator would include her own judgement which she seems to be reluctant to use.. |
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#106 |
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#107 |
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Quote:
It's the IR that kills us. |
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#108 |
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Nuther one:
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#109 |
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#110 |
Penultimate Amazing
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Building on my previous reading, I see that the IRS-1 gene (insulin resistance gene) also directly causes hypertension by interfering with a PPAR enzyme in the PI3 system. And guess what- Statins are PPAR ummm ligands or substrates or inhibitors, whatever... So it looks like the actual benefits of Statins are probably NOT from lowering cholesterol, but from boosting endogenous output of NOx in the endothelial cell lining the arteires, which relaxes arteries and lowers blood pressure.
Google points to papers looking into it circa 2004-2013, and a Cochrane review, but I couldn't find the Cochrane report. eta: here's one https://www.ncbi.nlm.nih.gov/pubmed/20129921 " Does peroxisome proliferator-activated receptor-gamma (PPAR gamma) protect from hypertension directly through effects in the vasculature? " |
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#111 |
Penultimate Amazing
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A little closer to the OP subject:
And another data-bit today, sorry no link, was a Cochrane review looking at the efficacy of Statins: For every 1,000 people treated for 5 years, 18 heart attacks are postponed. They used the word "prevented" but I think it really means 'postponed beyond the five year mark'. Ok. done with my flurry for today. ![]() |
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#112 |
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WTF? That could mean 982 people out of a thousand had heart attacks!
Do you have a link to the study? |
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#113 |
Penultimate Amazing
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Time to re-open this thread, Iwas atmy dibetes nurse/educator to day. She recommended I start Zetia to lower my cholesterol.
Quote:
Numbers were mentioned in other cites/sites. The 34.7 vs 32.7 works out to the 18/1000 mentioned somewhere upthread. Or, 1.8 per hundred, or 2% OVER SIX YEARS. Or, I guess I'll not bother taking it. No improvement in total end points. But that 2% was in strokes? So it must have raised some other endpoints? (end points include not only deaths, but also hospitalizations for artery disease, bypasses, stents...) And she mentioned my risk of having a heart attack has gone up from 33% in ten years to 44%. I asked wahh? She said because I got a year older. Hmm, I wonder how to prevent THAT? But I will be doubling up on one of the 6 BP meds I take. Stroke, kidney disease prevention. But I do want to find a graph of Pressure vs "End points", I'm sure it's a curve, though they act like it's a spike at 130. |
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#114 |
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Big surprise, the longer you live with heart disease, the more likely you are to die from it sometime in the future. However, this has nothing to do with statin therapy reducing the risk of heart disease. Ask the Dr how much the statin therapy will drive down that 44% risk.
It will be ' 0 ', because the risk formula doesn't include statin therapy. Why not? There are many studies that show that lowering cholesterol is of little benefit for CVD, but causes increased risk for dementia, T2D and Rhabdomyolysis to name a few.. Here is one study: Statins: No benefit as primary prevention in elderly
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