55 replies to this topic

[Michael]

All:

Despite the widespread cholesterol denialism that has become prevalent in the alternative health world, thanks to flawed arguments advanced by folks like Gary Taubes and Uffe Ravnskov, it's quite clear that LDL cholesterol is a strong risk factor for cardiovascular disease (just not as strong as HDL-to-total cholesterol). Less widely-discussed is the evidence from epidemiology showing reduced risk of age-related dementia and cognitive decline, including AD, from having a low-risk cholesterol profile. This has been found for various kinds of cholesterol patterns also associated with heart disease, including the full Framingham-type lipid panel (ie, total, HDL, and LDL cholesterol, plus triglycerides), metabolic syndrome (which includes low HDL and high triglycerides amongst other features) and, yes, high serum total cholesterol. This last was the subject of a systematic review(ie, a study that couldn't do a full-blown meta-analysis due to the heterogeneity of the study designs, but that used the same systematic, structured approach to selecting studies for includsion and for their evaluation): they found "Consistent associations between high midlife TC [total cholesterol] and increased risk of AD, and high midlife TC and increased risk of any dementia were found. There was no evidence supporting an association between late-life TC and AD, or between late-life TC and any dementia."

A recent study has tied the link down in a mechanistically-clear way, consistent with previous findings in experimental animals -- and provided evidence that the effect is not just due to confounding with the serum-cholesterol-raising (and also AD-related) APOE ε4 allele, or to effects on cardiovascular-mediated threats to cognitive integrity:

Curr Alzheimer Res. 2011 Jan 19. [Epub ahead of print]
Cholesterol and LDL Relate to Neuritic Plaques and to APOE4 Presence but Not to Neurofibrillary Tangles.
Lesser GT, Beeri MS, Schmeidler J, Purohit DP, Haroutunian V.


... we evaluated correlations of admission [total cholesterol (TC)], low-density (LDL) and high-density (HDL) cholesterol directly with the densities of Alzheimer hallmarks--neuritic plaques (NP) and neurofibrillary tangles (NFT)--in nursing home residents (n=281).

Results: Significant positive associations of TC and LDL with NP densities were found in both the neocortex (TC: r=0.151, p=0.013 and LDL: r=0.190, p=0.005) and the hippocampal/entorhinal (allocortical) region (TC: r=0.182, p=0.002 and LDL: r=0.203, p=0.003). Associations of HDL with NP were less strong but also significant. In contrast, after adjustment for confounders, no correlations of NFT with any lipid were significant.

When subjects with any non-AD neuropathology (largely vascular) were excluded, the TC-plaque and LDL-plaque associations for the remaining "Pure AD" subgroup were consistently stronger than for the full sample.

The TC- and LDL-plaque correlations were also stronger for the subgroup of 87 subjects with an APOE ε4 allele.

Conclusions: The findings indicate that serum TC and LDL levels clearly relate to densities of NP, but not to densities of NFT. The stronger associations found in the subgroup that excluded all subjects with non-AD neuropathology suggest that cerebrovascular involvement does not explain these lipid-plaque relationships. Since the associations of TC/LDL with NP were particularly stronger in ε4 carriers, varying prevalence of this allele may explain some discrepancies among prior studies.

PMID: 21244352

[Sillewater]

I'm glad I decided to abandon the views of Taubes and Ravsnkov and lower my cholesterol after doing high fat paleo.

[DukeNukem]

The high-cholesterol-is-bad myth remains strong in the medical and dietary professions. And the reason for this -- besides loads of outdated science -- is because the medical community makes no less than $25 billion from this ongoing myth, in terms of statin sales and other medical visits and procedures.

And yet...

Which Cholesterol Level Is Related to the Lowest Mortality in a Population with Low Mean Cholesterol Level: A 6.4-Year Follow-up Study of 482,472 Korean Men

To evaluate the relation between low cholesterol level and mortality, the authors followed 482,472 Korean men aged 30-65 years from 1990 to 1996 after a baseline health examination. The mean cholesterol level of the men was 189.1 mg/100 ml at the baseline measurement. There were 7,894 deaths during the follow-up period. A low cholesterol level (< 165 mg/100 ml) was associated with increased risk of total mortality, even after eliminating deaths that occurred in the first 5 years of follow-up. The risk of death from coronary heart disease increased significantly in men with the highest cholesterol level (£252 mg/100 ml). There were various relations between cholesterol level and cancer mortality by site. Mortality from liver and colon cancer was significantly associated with a very low cholesterol level (< 135 mg/100 ml) without any evidence of a preclinical cholesterol-lowering effect. With lengthening follow-up, the significant relation between a very low cholesterol level (< 135 mg/100 ml) and mortality from stomach and esophageal cancer disappeared. The cholesterol level related with the lowest mortality ranged from 211 to 251 mg/100 ml, which was higher than the mean cholesterol level of study subjects. Am J Epidemiol 2000; 151:739-47.
http://aje.oxfordjou.../8/739.full.pdf

LDL is likewise misrepresented by the vast majority of medical professionals -- in large part due to raw ignorance.

LDL on its own is near meaningless -- except for making statin pushers billions. Like I've described going back years ago, LDL is an umbrella of particle sizes/types. Generally, these various types/sizes are broken down into the pattern A (good, larger particle LDL) and pattern B (easily oxidized, small particle LDL).





Vegetable oils actually lower total LDL as advertised by the medical and nutritional communities, which is why they are considered "heart healthy." But in fact, while they do lower LDL, they change the balance to greatly favor pattern B LDL, which is entirely un-heart-healthy.

What raises HDL? Saturated fats, kiddo's. Saturated fats. That's how I and so many others in the paleo community keep our HDL sky-effing-high (near 100). I consider low HDL a sign of saturated fat deficiency. Sorry vegetarians. You were evolved to eat meat, just like cats and dogs. (Which, btw, are ALSO not designed to eat grains, which are highly inflammatory and fattening to nearly ALL mammals. Need to fatten pigs and cows? Don't feed 'em fat, just makes then skinnier. Nope, gotta feed 'em grains.

Bottom-line: Forget total cholesterol and total LDL. Instead, get a breakdown of your LDL, checking for Lp(a) and VLDL -- note that your typical doctor well question why you want these numbers (because, well, these number can't make them any money -- they can only save your life, a fact of secondary importance).

My total cholesterol is about 235. My HDL is near 100. Trigs at 50. My VLDL and Lp(a) are near zero. I'm right exactly where I want to be.

[1kgcoffee]

DukeNukem,
My question is, how much of a role do you think your supplement and hormonal regimen is playing in those numbers? I have no doubt that saturated fats are keeping your cholesterol numbers high, but maybe the combined effect of anti-inflmmatory, anti-oxidant and hormonal supplements deserve most of the credit. There are a few examples of people on this forum who follow that type of diet and have less than stellar numbers.

[DukeNukem]

Everything helps. I think diet helps the most.

Can't comment about people who follow a certain type of diet. There are numerous seemingly accepted versions of the paleo diet -- I think many of them are far less than optimal.

[APBT]

Duke

What role do you think genetics play in dietary selection, specifically fat consumption? This, from Berkeley Heart Labs, suggests APOE3/4 and 4/4 carriers should avoid fats, favoring a low fat diet.
Apo E Genotype�Metabolic Expression and Influence on Therapeutic Interventions

[DukeNukem]

APBT, it's impossible to give you an answer because I do not know what types of fats were used. Keep in mind, most researchers are still WAY behind-the-times believing plant oils are heart-healthy, and that animal fats are artery-clogging. So without know which oils/fats were used, the results of this study do not tell us much.

[mikeinnaples]

Duke, thoughts on Nicotinic Acid and the conversion process in the body being causitive of larger particle size?

[DukeNukem]

Duke, thoughts on Nicotinic Acid and the conversion process in the body being causitive of larger particle size?

I don't have much knowledge of niacin and I do not take any except what's in my 2 Vimmortal capsules I take daily. My cholesterol/lipid profile appears to be outstanding without the need to do additional niacin. But I do think it's can help. But overall, I think diet is by far the more significant factor.

[APBT]

APBT, it's impossible to give you an answer because I do not know what types of fats were used. Keep in mind, most researchers are still WAY behind-the-times believing plant oils are heart-healthy, and that animal fats are artery-clogging. So without know which oils/fats were used, the results of this study do not tell us much.

Fair enough, let me pose the question another way. Do you believe that genetic differences affect the way one processes and metabolizes fat? Or, do you believe that one-size-fits-all? That is, everyone would flourish (stellar lipid and inflammation profile) on your definition of a paleo diet.

As has been noted, there are myriad "versions" of the paleo diet. What is your definition of a paleo diet, or at least the diet you - successfully - follow; macro nutrient breakdown (percentages), types of fats, what is absolutely excluded and what is absolutely included?

[rwac]

Here's what Dr. Davis has to say on the subject:

But there’s one group of people who can experience unexpected effects with this diet: The 25% of people with apoprotein E4.
...
I hate apo E4. I hate apo E4 because it means I’ve got to dust off the nonsense I used to tell patients about cutting their fat, cutting their saturated fat. But that’s what apo E4 people have to do. But it doesn’t end there.

The exception to low-carb

[APBT]

Here's what Dr. Davis has to say on the subject:

But there’s one group of people who can experience unexpected effects with this diet: The 25% of people with apoprotein E4.
...
I hate apo E4. I hate apo E4 because it means I’ve got to dust off the nonsense I used to tell patients about cutting their fat, cutting their saturated fat. But that’s what apo E4 people have to do. But it doesn’t end there.

The exception to low-carb

Thanks for the link rwac.

Ah, so then if ~25% of the (genetically unfortunate) population were to follow a high (saturated) fat diet, they'd essentially be accelerating atherogenesis. Their lab numbers would be antithetical to Duke's stellar numbers.

Furthermore, ~25% of the US population is ~75 million folks, not a small number. It seems the responsible thing to do when dispensing dietary advise would be to provide the disclaimer that if one is APOE3/4 or 4/4, a high fat diet would be contraindicated. Of course without some sort of genetic testing (23andme or the like), one wouldn't have a clue. It seems that one-size-does NOT-fit-all, when it concerns diet. I find it refreshing that Dr. Davis acknowledges this.

[DukeNukem]

Here's what Dr. Davis has to say on the subject:

But there’s one group of people who can experience unexpected effects with this diet: The 25% of people with apoprotein E4.
...
I hate apo E4. I hate apo E4 because it means I’ve got to dust off the nonsense I used to tell patients about cutting their fat, cutting their saturated fat. But that’s what apo E4 people have to do. But it doesn’t end there.

The exception to low-carb

Thanks for the link rwac.

Ah, so then if ~25% of the (genetically unfortunate) population were to follow a high (saturated) fat diet, they'd essentially be accelerating atherogenesis. Their lab numbers would be antithetical to Duke's stellar numbers.

Furthermore, ~25% of the US population is ~75 million folks, not a small number. It seems the responsible thing to do when dispensing dietary advise would be to provide the disclaimer that if one is APOE3/4 or 4/4, a high fat diet would be contraindicated. Of course without some sort of genetic testing (23andme or the like), one wouldn't have a clue. It seems that one-size-does NOT-fit-all, when it concerns diet. I find it refreshing that Dr. Davis acknowledges this.

I've yet to encounter anyone who doesn't see dramatic blood test improvement by following the diet I talk about. Which is primarily: avoid fructose, gluten and processed vegetable oils. I definitely recommend that most fats should come from non-plant sources, with a few well-known exceptions (olive oil, coconut oil, macadamia nut oil, and a few others).

[rwac]

I've yet to encounter anyone who doesn't see dramatic blood test improvement by following the diet I talk about. Which is primarily: avoid fructose, gluten and processed vegetable oils. I definitely recommend that most fats should come from non-plant sources, with a few well-known exceptions (olive oil, coconut oil, macadamia nut oil, and a few others).

Maybe the difference is that Dr. Davis sees mostly sick people and you mainly give advice to mostly healthy people.

[steampoweredgod]

her serum cholesterol was 750 mg/dl (milligrams/deciliter)—normal is anything below 200 and her triglycerides (another blood fat usually measured in the 100-to-250- mg/dl range) were a whopping 3,000 mg/dl!...
So it’s no surprise that her doctor—following standard medical protocol—completely bypassed Step One and immediately started her on the National Cholesterol Awareness Program Step-Two Diet and two potent cholesterol-lowering medications...

Jayne faithfully followed her doctor’s orders for six months, although not without difficulty. The medications nauseated her, and the diet kept her constantly hungry...she had improved some, but not nearly enough. Her cholesterol had dropped from 750 mg/dl to 475 mg/dl and her triglycerides from 3,000 mg/dl to 2,000 mg/dl—an improvement to be sure, but still cause for great concern to both Jayne and her physician.

We instructed Jayne to stop taking both of her cholesterol-lowering medications and to change her diet drastically...new nutritional regimen...

We told her to call in three weeks to check in and to come back to have her blood checked in six weeks...
The results of her blood work astounded her. Jayne’s cholesterol level had fallen to 186 mg/dl and her triglycerides to 86 mg/dl...- Protein Power

Dr. Michael Eades seems to've been able to effectively lower cholesterol, even stratospherically above recommended limit statin+diet resistant individuals into healthy range with his nutritional methods. If it is true that even strastospheric statin + diet resistant cholesterol can be brought drastically down with nutritional methods, it would make the statins nothing more than very expensive unecessary poisons for the majority of people(there may still be special cases needing'em).

The blockbusters for six months showing paltry pathetic results, while raising multiple risks for side effects, yet a simple nutritional approach drastically beat the blockbusters into submission in a mere 6 weeks.

researchers developed a strain of mice that produced human LDL receptors in their livers at a rate about have times that of the mouse LDL receptors in the livers of the normal mice used as experimental controls.

scientists fed both groups of animals a diet high in saturated fat and cholesterol.As anticipated, the levels of LDL in the blood of the normal mice zoomed upward, while there was no increase in the level of LDL in the blood of the experimental mice. In the words of the authors of in the blood of the experimental mice. In the words of the authors of the study, “… increasing LDL receptor expression above its normal level in the mouse can prevent hypercholesterolemia
...
can we increase the production of LDL receptors in our cells? Yes, we can.
...
if we could somehow slow down the rate at which our cells make cholesterol internally, they would have to increase the number of LDL receptors they send to the surface to pull more LDL from the blood. Again, this is exactly what happens; in fact the most potent cholesterol-lowering drug available today—lovastatin (Mevacor)—works on this principle.

Raising LDL receptors, the method of the most powerful cholesterol drug, and also a method that seems to make mice resistant to the effects of dietary fat on blood ldl cholesterol profiles.

Wouldn’t it be great if there were a way to get the same cholesterol-lowering results without having to resort to drug therapy? There is.

...

Our nutritional plan relies on food to balance insulin and glucagon and reduces blood cholesterol levels in exactly the same way that lovastatin does, but without the unpleasant side effects and hefty expense. And that’s not the end of the story.

As the data on diet and cholesterol continue to accumulate, the evidence indicates that the high-complex-carbohydrate, low-fat diet doesn’t live up to its billing as a cholesterol solution. Most studies show that although these diets lower total and LDL cholesterol somewhat, they lower HDL cholesterol by a greater percentage, leading to a worsening of the ratios that are more important than the individual measurements by themselves.
...
the ideal cholesterol level is in the area where the Ushaped curve bottoms out, in the 180 mg/dl-to-200 mg/dl range. Avoid
trying to get it lower; don’t trade one serious health problem for another...- protein power

the lowest rates of all cause mortality are for cholesterol readings of 200<TC<240 mg/dl...

In 1987, in the Journal of the American Medical Association Framingham Study investigators reported these two important findings: 1) Over age 50 there is no increased overall mortality with either high or low serum cholesterol levels, and 2) In people with a falling cholesterol level (over the first 14 years of the study), for each 1% mg/dl drop in cholesterol there was an 11 percent increase in all-cause mortality over the next 18 years. -LarryAJ, lowcarber.org

Within that range all cause mortality is lowest, lower or higher and mortality seems to rise for average individuals. Though I would say if one has optimal ratios and has it higher, or if one has optimal ratios and has it lower the effects would need to be checked. For example CR puts mean around 160mg/dl,

Alter the insuling glucagon axis favorably and it is said you will directly influence the rate limiting enzyme involved in cholesterol synthesis, vastly increasing ldl receptor and protecting from dietary fat while moving towards ideal blood profiles...

Even ingesting 5000mg of cholesterol daily and 50g of saturated fat(25 eggs) seemingly won't take your cholesterol out of the optimal range.

Daily
5000mg cholesterol consumption
total
cholesterol, 200 mg/dl; LDL, 142 mg/dl, and HDL, 45 mg/dl; his
LDL/HDL ratio was 3.16.
-protein power

Daily 175g fat(50g saturated fat)

If the recommendations of Dr. Eades bear fruit, as they seem to do, it seems like a powerful approach to dealing with cholesterol issues.

Edited by steampoweredgod, 09 December 2011 - 01:47 AM.

[albedo]

I do have high LDL and tried several "natural" ways including (moderate) increased niacin (100mg), policosanol (20mg), RYR (600mg), guggulipid (1000mg) with only very limited results. I am trying Zoning for some time already and recently adopted CRONOMETER (where i do seem taking fats more than target). Moderately exercising too. I am 56, APO E3 e3/e3 genotype. High homocysteine too: 13 (<15 umol/l)

Do you think I need to start considering a statin at least for a short period of time? My Calcium Score is very low (3) and did not change over 5 years though.

I attach the latest VAP profile (have a 6 years historic but with a different lab, hence need to extrapolate results, only another full VAP profile 5 years ago which only shows a better Total/HDL ratio and better TGs).

Attached Files

•  Lipid Panel Nov 11.doc   241.5KB   11 downloads

Edited by albedo, 28 January 2012 - 02:30 PM.

[albedo]

Just wish to add to my previous post (cannot edit it) ...

I have the luck of my wife being a clinical dietitian as background, loving to cook every day. I thinks I am eating a pretty healthy diet with fats coming mainly from extra virgin olive oil and will know better using the Cronometer. I cannot really understand my dyslipidemia (which I think in Rakel is called "primary" vs "familial" (LDL>130 HDL>40 TG<150, Familial: LDL>200, Primary: LDL 130-199 (linked to nutrition, obesity, behavior and genetic))

Btw, my apologies, this is not a reply to the original post but decided to put my concerns here trying to pick some of the expert brains in this thread ...

[niner]

I do have high LDL and tried several "natural" ways including (moderate) increased niacin (100mg), policosanol (20mg), RYR (600mg), guggulipid (1000mg) with only very limited results. I am trying Zoning for some time already and recently adopted CRONOMETER (where i do seem taking fats more than target). Moderately exercising too. I am 56, APO E3 e3/e3 genotype. High homocysteine too: 13 (<15 umol/l)

Do you think I need to start considering a statin at least for a short period of time? My Calcium Score is very low (3) and did not change over 5 years though.

Aside from LDL, your VAP profile is mostly good. LP(a) and IDL are both within target, and they are more atherogenic than LDL, according to Atherotech. They've assigned your LDL particle size distribution as the healthier "A" pattern, which is more biased toward the large buoyant variety. Your triglycerides are pretty good; between those and your LDL size distribution, it looks like you are doing a decent job of keeping the carbs under control. A low calcium score is also great to see. I don't know if you need a statin, but they aren't the worst drugs in the world. A lot of doctors would tell you to use a statin. I wonder what Bill Davis, the cardiologist who runs the Track Your Plaque blog, would have to say about it? He'd tell you to stop eating wheat, take a ton of vitamin D, and also some iodine. Also Fish oil. Are you taking any of those?

[albedo]

I do have high LDL and tried several "natural" ways including (moderate) increased niacin (100mg), policosanol (20mg), RYR (600mg), guggulipid (1000mg) with only very limited results. I am trying Zoning for some time already and recently adopted CRONOMETER (where i do seem taking fats more than target). Moderately exercising too. I am 56, APO E3 e3/e3 genotype. High homocysteine too: 13 (<15 umol/l)

Do you think I need to start considering a statin at least for a short period of time? My Calcium Score is very low (3) and did not change over 5 years though.

Aside from LDL, your VAP profile is mostly good. LP(a) and IDL are both within target, and they are more atherogenic than LDL, according to Atherotech. They've assigned your LDL particle size distribution as the healthier "A" pattern, which is more biased toward the large buoyant variety. Your triglycerides are pretty good; between those and your LDL size distribution, it looks like you are doing a decent job of keeping the carbs under control. A low calcium score is also great to see. I don't know if you need a statin, but they aren't the worst drugs in the world. A lot of doctors would tell you to use a statin. I wonder what Bill Davis, the cardiologist who runs the Track Your Plaque blog, would have to say about it? He'd tell you to stop eating wheat, take a ton of vitamin D, and also some iodine. Also Fish oil. Are you taking any of those?

Thank for your reply Niner.

From time to time I check William Davis's blog. I am intrigued by his claim you can actually reverse plaque with aggressive actions. However, I am not yet buying into some of those as the massive Vitamin D you need to reach the 25OH 60-70ng/ml range. First, I am pretty happy of staying in my 30-40 ng/ml range as this seems the optimum in the overall mortality risk curve (e.g. see here) and second because, being genetically at higher risk of athrial fibrillation, excesses should be avoided (e.g. see here , I am not saying he is advocating those excesses though!). I keep my range with 1000-1500IU supplementation. I also avoid massive fish oil doses as supplements as I eat oily fishes regularly and, when I don't, use a 1000mg capsule. Much concerned here with rancidity and oxidation. From my supplements I have about 32 mg of iodine.

For completeness, I am also looking at my thyroid function which looks normal but I am constantly (very) deficient on DHEA-S, though this supplementation is not recommended at my age with mild symptoms of BPH. I might have seen a better ratio TC/HDL when supplementing with a physiological 25 mg dose of DHEA though.

So a statin seems to me still an option (agree with you while disagreeing with one of my doctor friend saying they are harmless even when taken for life!) at least for short time with an appropriate liver function monitoring and protection. Too early to say but some even think statins can be helpful with BPH, even if I am perfectly conscious this might be driven by the need to open other "markets" though this is not bad per se.

[niner]

From time to time I check William Davis's blog. I am intrigued by his claim you can actually reverse plaque with aggressive actions. However, I am not yet buying into some of those as the massive Vitamin D you need to reach the 25OH 60-70ng/ml range. First, I am pretty happy of staying in my 30-40 ng/ml range as this seems the optimum in the overall mortality risk curve (e.g. see here) and second because, being genetically at higher risk of athrial fibrillation, excesses should be avoided (e.g. see here , I am not saying he is advocating those excesses though!). I keep my range with 1000-1500IU supplementation. I also avoid massive fish oil doses as supplements as I eat oily fishes regularly and, when I don't, use a 1000mg capsule. Much concerned here with rancidity and oxidation. From my supplements I have about 32 mg of iodine.

For completeness, I am also looking at my thyroid function which looks normal but I am constantly (very) deficient on DHEA-S, though this supplementation is not recommended at my age with mild symptoms of BPH. I might have seen a better ratio TC/HDL when supplementing with a physiological 25 mg dose of DHEA though.

So a statin seems to me still an option (agree with you while disagreeing with one of my doctor friend saying they are harmless even when taken for life!) at least for short time with an appropriate liver function monitoring and protection. Too early to say but some even think statins can be helpful with BPH, even if I am perfectly conscious this might be driven by the need to open other "markets" though this is not bad per se.

The associations with 25-OH-D3 levels and various bad outcomes are a bit noisy. The optima are quite broad, and if you wanted to go higher you could probably get away with it safely. The paper linking A-fib risk to D only had an effect at a very high (100ng/ml) level, without showing a dose response. I'm concerned about risks of excess D also, so I don't think it's at all crazy to be cautious. The benefit of fish oil is substantial here, and the risk from rancidity is quite low. I've been taking capped fish oil for years, and I've never had a problem with observable rancidity whenever I've bit into a capsule. I would raise your level to 2 or even 3 grams/day. Note the response to fish oil shown in the chart here for ApoE 3 genotypes. That's a lot of iodine! 32 milligrams? I'm taking 225 micrograms. Statins can help BPH? Wow, that's interesting. I'll have to look into that.

[niner]

Statins can help BPH? Wow, that's interesting. I'll have to look into that.

Not so much, it appears.

Eur Urol. 2007 Aug;52(2):503-9. Epub 2007 Feb 20.
Atorvastatin treatment for men with lower urinary tract symptoms and benign prostatic enlargement.
Mills IW, Crossland A, Patel A, Ramonas H.

Pfizer Global Research and Development, Sandwich, UK. ian.w.mills@pfizer.com

OBJECTIVE:

To evaluate the effects of atorvastatin in men with lower urinary tract symptoms (LUTS) and prostatic enlargement due to presumed BPH.
METHODS:

This was a phase 2, double-blind, randomised, placebo-controlled clinical study. Eligible patients were aged > or =50 yr, with International Prostate Symptom Score (IPSS) > or = 13, total prostate volume (TPV) > or = 30 ml, and maximum urinary flow rate 5-15 ml/s. All patients had serum low-density lipoprotein (LDL) 100-190 mg/dl at baseline. Patients received either atorvastatin 80 mg daily (n=176) or placebo (n=174) for 26 wk. End points included IPSS, TPV, transition zone volume (TZV), maximum urinary flow rate (Q(max)), serum PSA, and lipids.
RESULTS:

There was no difference between the effects of atorvastatin and placebo on the primary end point of mean change from baseline in IPSS after 26 wk of double-blind treatment (-4.5 vs. -4.3; p=0.263). Similarly, no effect was seen on the lower urinary tract secondary end points including TPV (-1.6 vs. -1.9 ml; p=0.654), TZV (-0.0 vs. -0.8 ml; p=0.421), Q(max) (+1.1 vs. +0.7 ml/s; p=0.612), and PSA (-0.24 vs. -0.14 ng/ml; p=0.235). Atorvastatin had a significant effect on serum lipid levels compared with placebo (eg, LDL: -75.6 vs. -6.1 mg/dl; p<0.001).
CONCLUSIONS:

Atorvastatin is not effective over 6 mo in the treatment of men with LUTS and prostatic enlargement due to presumed BPH who have serum LDL in the range 100-190 mg/dl.
Comment in Eur Urol. 2007 Aug;52(2):316-7.

PMID 17343981

[albedo]

...From my supplements I have about 32 mg of iodine....

...That's a lot of iodine! 32 milligrams? I'm taking 225 micrograms..

oops ... sorry ... I meant mcgs!

[albedo]

Statins can help BPH? Wow, that's interesting. I'll have to look into that.

Not so much, it appears.

Eur Urol. 2007 Aug;52(2):503-9. Epub 2007 Feb 20.
Atorvastatin treatment for men with lower urinary tract symptoms and benign prostatic enlargement.
Mills IW, Crossland A, Patel A, Ramonas H.
Pfizer Global Research and Development, Sandwich, UK. ian.w.mills@pfizer.com
...... Atorvastatin is not effective over 6 mo in the treatment of men with LUTS and prostatic enlargement due to presumed BPH who have serum LDL in the range 100-190 mg/dl....

Agree. There is only a limited evidence in vitro. E.g. ".... It is unlikely that lovastatin, per se, will be an effective treatment for BPH in vivo, but it does provide a means for inducing apoptosis in vitro. Understanding the apoptotic process in BPH stromal cells ultimately may lead to new therapeutic strategies for BPH..." http://jcem.endojour.../82/5/1434.long

[hivemind]

The high-cholesterol-is-bad myth remains strong in the medical and dietary professions. And the reason for this -- besides loads of outdated science -- is because the medical community makes no less than $25 billion from this ongoing myth, in terms of statin sales and other medical visits and procedures.

And yet...

Which Cholesterol Level Is Related to the Lowest Mortality in a Population with Low Mean Cholesterol Level: A 6.4-Year Follow-up Study of 482,472 Korean Men

To evaluate the relation between low cholesterol level and mortality, the authors followed 482,472 Korean men aged 30-65 years from 1990 to 1996 after a baseline health examination. The mean cholesterol level of the men was 189.1 mg/100 ml at the baseline measurement. There were 7,894 deaths during the follow-up period. A low cholesterol level (< 165 mg/100 ml) was associated with increased risk of total mortality, even after eliminating deaths that occurred in the first 5 years of follow-up. The risk of death from coronary heart disease increased significantly in men with the highest cholesterol level (£252 mg/100 ml). There were various relations between cholesterol level and cancer mortality by site. Mortality from liver and colon cancer was significantly associated with a very low cholesterol level (< 135 mg/100 ml) without any evidence of a preclinical cholesterol-lowering effect. With lengthening follow-up, the significant relation between a very low cholesterol level (< 135 mg/100 ml) and mortality from stomach and esophageal cancer disappeared. The cholesterol level related with the lowest mortality ranged from 211 to 251 mg/100 ml, which was higher than the mean cholesterol level of study subjects. Am J Epidemiol 2000; 151:739-47.
http://aje.oxfordjou.../8/739.full.pdf

LDL is likewise misrepresented by the vast majority of medical professionals -- in large part due to raw ignorance.

LDL on its own is near meaningless -- except for making statin pushers billions. Like I've described going back years ago, LDL is an umbrella of particle sizes/types. Generally, these various types/sizes are broken down into the pattern A (good, larger particle LDL) and pattern B (easily oxidized, small particle LDL).





Vegetable oils actually lower total LDL as advertised by the medical and nutritional communities, which is why they are considered "heart healthy." But in fact, while they do lower LDL, they change the balance to greatly favor pattern B LDL, which is entirely un-heart-healthy.

What raises HDL? Saturated fats, kiddo's. Saturated fats. That's how I and so many others in the paleo community keep our HDL sky-effing-high (near 100). I consider low HDL a sign of saturated fat deficiency. Sorry vegetarians. You were evolved to eat meat, just like cats and dogs. (Which, btw, are ALSO not designed to eat grains, which are highly inflammatory and fattening to nearly ALL mammals. Need to fatten pigs and cows? Don't feed 'em fat, just makes then skinnier. Nope, gotta feed 'em grains.

Bottom-line: Forget total cholesterol and total LDL. Instead, get a breakdown of your LDL, checking for Lp(a) and VLDL -- note that your typical doctor well question why you want these numbers (because, well, these number can't make them any money -- they can only save your life, a fact of secondary importance).

My total cholesterol is about 235. My HDL is near 100. Trigs at 50. My VLDL and Lp(a) are near zero. I'm right exactly where I want to be.

LDL causes atherosclerosis and vascular disease. Total cholesterol should be kept under 150.

That U-curve thing is nonsense. Many sick people have low cholesterol because they are sick or on statin drugs. Healthy people with low cholesterol live the longest lives.

HDL is controversial and complex. Raising your HDL might not be very beneficial. Sorry paleo community, but humans have evolved with low cholesterol levels. Primitive people have cholesterol levels under 150.

LDL is meaningless? LDL is the main cause of atherosclerosis. LDL-particles have most of the atherogenic apoB-proteins. Lipitor patent has already expired. These drugs save lives, but you can achieve the same with a good diet without the side effects.

Bottom-line: Standard lipid panel is good. Keep your total and LDL-cholesterol low. If your HDL is high, then that is good too, but do not try to raise your HDL with saturated fat. Also, it is not a good idea to eat a lot of those vegetable oils. You should prefer whole foods. Whole grains are good.


http://www.youtube.com/watch?v=6bSdnQ1MKGo

http://www.youtube.com/watch?v=qGt97ojn5zs

http://www.youtube.com/watch?v=SD48EGuP0QY

Edited by hivemind, 05 August 2012 - 10:19 AM.

[hivemind]

[Turnbuckle]

LDL causes atherosclerosis and vascular disease. Total cholesterol should be kept under 150.

Reading this thread, my world was crumbling. Everything I knew was wrong! But now this brings it all back to me. I feel okay again. Now I have the programing to ignore the following--

Conclusions: Low cholesterol was related to high mortality even after excluding deaths due to liver disease from
the analysis. High cholesterol was not a risk factor for mortality.

https://www.jstage.j...JE20100065/_pdf

[hivemind]

LDL causes atherosclerosis and vascular disease. Total cholesterol should be kept under 150.

Reading this thread, my world was crumbling. Everything I knew was wrong! But now this brings it all back to me. I feel okay again. Now I have the programing to ignore the following--

Conclusions: Low cholesterol was related to high mortality even after excluding deaths due to liver disease from
the analysis. High cholesterol was not a risk factor for mortality.

https://www.jstage.j...JE20100065/_pdf

This is nonsense. In a higher cholesterol population low cholesterol is a result of a disease NOT THE OTHER WAY AROUND. Those low cholesterol people include people on statin drugs and other sick/old people with low cholesterol.

The healthiest people have low cholesterol through their whole life.

Edited by hivemind, 05 August 2012 - 11:14 AM.

[Turnbuckle]

The healthiest people have low cholesterol through their whole life.

Well, that's not saying much for statins, is it? Or any sort of treatment at all. Though it sounds right. Do you have a study that shows that it is?

Edited by Turnbuckle, 05 August 2012 - 11:39 AM.

[hivemind]

The healthiest people have low cholesterol through their whole life.

Well, that's not saying much for statins, is it? Or any sort of treatment at all. And it even sounds right. But do you have a study that shows that it is?

There are many studies that confirm high cholesterol as the cause of atherosclerosis. It is very hard (or even impossible) to get atherosclerosis if the cholesterol level is low enough. Statins save lives. That has been shown beoynd any doubt.

[Turnbuckle]

The healthiest people have low cholesterol through their whole life.

Well, that's not saying much for statins, is it? Or any sort of treatment at all. And it even sounds right. But do you have a study that shows that it is?

There are many studies that confirm high cholesterol as the cause of atherosclerosis. It is very hard (or even impossible) to get atherosclerosis if the cholesterol level is low enough. Statins save lives. That has been shown beoynd any doubt.

You said that the healthiest people have low cholesterol their entire lives, but there doesn't seem to be any data to back that up. For those with the very highest cholesterol, perhaps there is some advantage to lowering it with statins. But what is the level where there is a net benefit rather than harm? I can tell you I found statins to be an insidious poison, and I'll bet half those on it are suffering to a lesser degree but haven't made the connection.

Edited by Turnbuckle, 05 August 2012 - 12:01 PM.