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How to improve my Cholesterol levels?


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#61 kismet

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Posted 06 October 2009 - 12:10 PM

oprimitivo, you are wasting too much time on this study. It's retrospective, it's worthless. It does not tell us a lot, or anything, about pathogenesis considering just how huge the time lag is + there are the mentioned biases. Let's get over it. I'd much prefer a summary of prospective studies, assessing LDL and cardiovascular mortality (not total cholesterol); something along the lines of your last link to total cholesterol & mortality, just for LDL/HDL ratios.

#62 Luna

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Posted 06 October 2009 - 11:50 PM

For the last few days I been making sure to eat salad every day and add olive oil ;)

Will try to eat more fish but this is harder :D my options are mostly canned tuna :X
Is that even good enough? any suggestions? how can I make canned tuna tastey :X

Usually I eat it either in sandwich (though I been having problems with that taste too!) or in tuna salad (eggs, tuna, a bit of mayonaise garlic and onions) which is much better tasting.

I really can't think of a good way to increase my fish intake with canned tuna as my best option.

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#63 oprimitivo

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Posted 07 October 2009 - 01:43 AM

Again, it only includes patient participating in the AHA's "Get With The Guidelines" program. Likely this includes patient who have a higher SES, more motivated and likely to improve their health, etc than the average patient. It also includes patient not there for acute causes but who can afford to be hospitalized for elective procedures, thus not being representative for those too poor for this. You really need a random sample, like all those seeking for MI.


Blue:
You insist that this sample is not representative of the typical patient hospitalized with heart disease but 75% of patients in the AHA study were diagnosed with STEMI/NSTEM, and these are acute causes. Also, I don't see why poor or rich, more or less motivated patients should have much different blood lipids when they are hospitalized. Do you truly believe LDL levels of poorer and less motivated people hospitalized with the same medical conditions would be any different? If we are so selective, no sample will ever be useful. Also, these studies are probably rare, as they say in the background section "lipid levels among contemporary patients hospitalized with coronary artery disease (CAD) have not been well studied". From my point of view, this is already a very good sample, it is at least a very large sample of blood lipids of real people hospitalized with heart disease.

The idea that "most CAD hospitalized patients don't present elevated LDL and/or TC values, on the contrary, they tend to show some cholesterol deficiency" is supported not only by the comparision of the two observational studies I quoted (1 and 2), with I don't think is worthless at all, but also supported by existing epidemiological data. When TC is higher than 210 mg/dl, TC levels are possibly positively associated with mortality from cardiovascular diseases. But when TC < 200 mg/dl, the case for most people in the world, lowered TC levels look clearly associated with higher (yes, higher!) mortality from cardiovascular disease. Since most patients (not taking statins) hospitalized with CAD present an average TC of 189 mg/dl, then it makes perfect sense, according to the epidemiological data, that msot of them present perfectly normal TC and LDL levels, or are even cholesterol defficient.

Does most of the population have bad lipids and that may explain why heart disease is so common? For the moment, I don't have an answer for that, I'll have to think about it.

kismet:
The problem is you can not conclude almost anything from intervention studies on LDL levels because the only way to significantly change LDL is using statins, as much as I know there are no clear lifestyle modifications that will for sure reduce LDL. And the problem with statins is that they not only lower LDL (which might be a negative effect, because it makes you cholesterol deficient and so puts you at higher risk of infections and parasitic diseases), but also have a series of other (positive) side effects unrelated to cholesterol lowering, for example reduced inflamation and anti-oxidant effects, and these might be the real beneficial effects of statins on reducing heart disease. Not necesarily the reduction of LDL by itself, you can't tell because the several effects can't be isolated. So, retrospective/observational studies, despite not being a tool to analyse causation/pathogenesis, are at least a valid tool to evaluate if a certain parameter is reliable or not as a risk maker. And I think this is not the case for LDL, by itself, without considering its subfractions.

Another issue: how do you know HDL/LDL is a good risk marker, or a better marker then HDL alone, for cardiovascular disease? If LDL is allways almost unchanged, on what concerns its average values, either you are healthy or if you are hospitalized with heart disease, and if supposing HDL is a truly powerful risk marker, then of course their ratio will also be an excellent marker for cardiovascular disease. But this happens only because LDL is a neutral factor in the whole process, almost a constant. Do people with cardiovascular disease necessarily show elevated LDL levels when they are hospitalized? Well, as we have already seen, at least rich and motivated people don't, many of them even tend to be cholesterol deficient. And even if HDL/LDL is an excelent marker for heart disease, just because of that, does it means LDL should be lowered by medication? Or that HLD should be increased by the same process? Or simply that you should change your lifestyle into something healthier?

Let me try to explain why I consider the analisys of TC vs detailed mortality quite important, or at least the easiest analysis.

First, we have on-line cholesterol and mortality data, for several countries in the world, easily accessible (in Excel format: BHF cholesterol + WHO mortality). And second because TC correlates well with several other blood lipids. It is actually quite easy to establish a relation between TC and HDL/LDL, not a strong relation but at least a clear relation, for example in the format HDL/LDL = a/TC^b, as long as you have access to some large blood lipids database. The great difficulty here, as you have seen in the total cholesterol vs detailed mortality chart, some of the observed variables present a U shaped format. Like cardiovascular diseases, which people assume are always positively associated with TC, but this only seams to be true when TC>210 mg/dl, not at the lower cholesterol levels. And since most countries in the world have their average TC around 180-220 mg/dl, they are exactly in the range where the U shaped curves change their derivative signals.

Just to finish my idea, I believe epidemiological data and its analysis should serve as a primary tool to establish the theoretical hypothesis, and then the intervention studies should be used to investigate and demonstrate causation. But trying to use only LDL intervention studies, that consider the lowering of LDL using statins, with all their know side effects, to defend the hypothesis that elevated LDL is a major cause for heart disease, not even some sub-fraction of LDL with a clear understandable physiological mechanism, when this hypothesis apparently has no support whatsoever by (strong? or only strong for the rich and motivated?) observational data, is probably not the most solid or scientific way to support that hypothesis. The so called Lipid Hypothesis!

Edited by oprimitivo, 07 October 2009 - 01:52 AM.


#64 Sillewater

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Posted 09 October 2009 - 06:26 AM

hear hear!

#65 Matt

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Posted 09 October 2009 - 01:03 PM

as much as I know there are no clear lifestyle modifications that will for sure reduce LDL


CR. My own LDL level is low from CR heres 3 different tests over the last few years. 1.7 (65mg/dl) , 1.5 (58mg/dl), 1.9 (74mg/dl) ref < 3.0

Edited by Matt, 09 October 2009 - 01:04 PM.


#66 Blue

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Posted 09 October 2009 - 04:52 PM

Again, it only includes patient participating in the AHA's "Get With The Guidelines" program. Likely this includes patient who have a higher SES, more motivated and likely to improve their health, etc than the average patient. It also includes patient not there for acute causes but who can afford to be hospitalized for elective procedures, thus not being representative for those too poor for this. You really need a random sample, like all those seeking for MI.


Blue:
You insist that this sample is not representative of the typical patient hospitalized with heart disease but 75% of patients in the AHA study were diagnosed with STEMI/NSTEM, and these are acute causes. Also, I don't see why poor or rich, more or less motivated patients should have much different blood lipids when they are hospitalized. Do you truly believe LDL levels of poorer and less motivated people hospitalized with the same medical conditions would be any different? If we are so selective, no sample will ever be useful. Also, these studies are probably rare, as they say in the background section "lipid levels among contemporary patients hospitalized with coronary artery disease (CAD) have not been well studied". From my point of view, this is already a very good sample, it is at least a very large sample of blood lipids of real people hospitalized with heart disease.

The idea that "most CAD hospitalized patients don't present elevated LDL and/or TC values, on the contrary, they tend to show some cholesterol deficiency" is supported not only by the comparision of the two observational studies I quoted (1 and 2), with I don't think is worthless at all, but also supported by existing epidemiological data. When TC is higher than 210 mg/dl, TC levels are possibly positively associated with mortality from cardiovascular diseases. But when TC < 200 mg/dl, the case for most people in the world, lowered TC levels look clearly associated with higher (yes, higher!) mortality from cardiovascular disease. Since most patients (not taking statins) hospitalized with CAD present an average TC of 189 mg/dl, then it makes perfect sense, according to the epidemiological data, that msot of them present perfectly normal TC and LDL levels, or are even cholesterol defficient.

Does most of the population have bad lipids and that may explain why heart disease is so common? For the moment, I don't have an answer for that, I'll have to think about it.

Still not a representative sample. Obivously richer, more educated, more interested patients who had had a previous episode of CVD (which many had, this was not a sample of first-timers) would be more likely to have taken steps to reduce their risk factors such as bad lipids. This is not not only medication, but also diet, exercise etc.

Total cholesterol is not very interesting these days when we can measure subtypes.

But lets look at other studies. Unfortunately we can not produce a perfect experimental study by simply changing LDL without changing anything else. But this is somewhat close:

"OBJECTIVES: To determine by how much statins reduce serum concentrations of low density lipoprotein (LDL) cholesterol and incidence of ischaemic heart disease (IHD) events and stroke, according to drug, dose, and duration of treatment. DESIGN: Three meta-analyses: 164 short term randomised placebo controlled trials of six statins and LDL cholesterol reduction; 58 randomised trials of cholesterol lowering by any means and IHD events; and nine cohort studies and the same 58 trials on stoke. MAIN OUTCOME MEASURES: Reductions in LDL cholesterol according to statin and dose; reduction in IHD events and stroke for a specified reduction in LDL cholesterol. RESULTS: Reductions in LDL cholesterol (in the 164 trials) were 2.8 mmol/l (60%) with rosuvastatin 80 mg/day, 2.6 mmol/l (55%) with atorvastatin 80 mg/day, 1.8 mmol/l (40%) with atorvastatin 10 mg/day, lovastatin 40 mg/day, simvastatin 40 mg/day, or rosuvastatin 5 mg/day, all from pretreatment concentrations of 4.8 mmol/l. Pravastatin and fluvastatin achieved smaller reductions. In the 58 trials, for an LDL cholesterol reduction of 1.0 mmol/l the risk of IHD events was reduced by 11% in the first year of treatment, 24% in the second year, 33% in years three to five, and by 36% thereafter (P < 0.001 for trend). IHD events were reduced by 20%, 31%, and 51% in trials grouped by LDL cholesterol reduction (means 0.5 mmol/l, 1.0 mmol/l, and 1.6 mmol/l) after results from first two years of treatment were excluded (P < 0.001 for trend). After several years a reduction of 1.8 mmol/l would reduce IHD events by an estimated 61%. Results from the same 58 trials, corroborated by results from the nine cohort studies, show that lowering LDL cholesterol decreases all stroke by 10% for a 1 mmol/l reduction and 17% for a 1.8 mmol/l reduction. Estimates allow for the fact that trials tended to recruit people with vascular disease, among whom the effect of LDL cholesterol reduction on stroke is greater because of their higher risk of thromboembolic stroke (rather than haemorrhagic stroke) compared with people in the general population. CONCLUSIONS: Statins can lower LDL cholesterol concentration by an average of 1.8 mmol/l which reduces the risk of IHD events by about 60% and stroke by 17%."
http://www.ncbi.nlm....pubmed/12829554

"BACKGROUND: Results of previous randomised trials have shown that interventions that lower LDL cholesterol concentrations can significantly reduce the incidence of coronary heart disease (CHD) and other major vascular events in a wide range of individuals. But each separate trial has limited power to assess particular outcomes or particular categories of participant. METHODS: A prospective meta-analysis of data from 90,056 individuals in 14 randomised trials of statins was done. Weighted estimates were obtained of effects on different clinical outcomes per 1.0 mmol/L reduction in LDL cholesterol. FINDINGS: During a mean of 5 years, there were 8186 deaths, 14,348 individuals had major vascular events, and 5103 developed cancer. Mean LDL cholesterol differences at 1 year ranged from 0.35 mmol/L to 1.77 mmol/L (mean 1.09) in these trials. There was a 12% proportional reduction in all-cause mortality per mmol/L reduction in LDL cholesterol (rate ratio [RR] 0.88, 95% CI 0.84-0.91; p<0.0001). This reflected a 19% reduction in coronary mortality (0.81, 0.76-0.85; p<0.0001), and non-significant reductions in non-coronary vascular mortality (0.93, 0.83-1.03; p=0.2) and non-vascular mortality (0.95, 0.90-1.01; p=0.1). There were corresponding reductions in myocardial infarction or coronary death (0.77, 0.74-0.80; p<0.0001), in the need for coronary revascularisation (0.76, 0.73-0.80; p<0.0001), in fatal or non-fatal stroke (0.83, 0.78-0.88; p<0.0001), and, combining these, of 21% in any such major vascular event (0.79, 0.77-0.81; p<0.0001). The proportional reduction in major vascular events differed significantly (p<0.0001) according to the absolute reduction in LDL cholesterol achieved, but not otherwise. These benefits were significant within the first year, but were greater in subsequent years. Taking all years together, the overall reduction of about one fifth per mmol/L LDL cholesterol reduction translated into 48 (95% CI 39-57) fewer participants having major vascular events per 1000 among those with pre-existing CHD at baseline, compared with 25 (19-31) per 1000 among participants with no such history. There was no evidence that statins increased the incidence of cancer overall (1.00, 0.95-1.06; p=0.9) or at any particular site. INTERPRETATION: Statin therapy can safely reduce the 5-year incidence of major coronary events, coronary revascularisation, and stroke by about one fifth per mmol/L reduction in LDL cholesterol, largely irrespective of the initial lipid profile or other presenting characteristics. The absolute benefit relates chiefly to an individual's absolute risk of such events and to the absolute reduction in LDL cholesterol achieved. These findings reinforce the need to consider prolonged statin treatment with substantial LDL cholesterol reductions in all patients at high risk of any type of major vascular event."
http://www.ncbi.nlm....pubmed/16214597

#67 Blue

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Posted 09 October 2009 - 05:04 PM

Another meta-analysis regarding dietary fat.
"Objective: To assess the effect of reduction or modification of dietary fat intake on total and cardiovascular mortality and cardiovascular morbidity.
Design: Systematic review.
Data sources: Cochrane Library, Medline, Embase, CAB abstracts, SIGLE, CVRCT registry, and biographies were searched; trials known to experts were included.
Included studies: Randomised controlled trials stating intention to reduce or modify fat or cholesterol intake in healthy adult participants over at least six months. Inclusion decisions, validity, and data extraction were duplicated. Meta-analysis (random effects methodology), meta-regression, and funnel plots were performed.
Results: 27 studies (30 902 person years of observation) were included. Alteration of dietary fat intake had small effects on total mortality (rate ratio 0.98; 95% confidence interval 0.86 to 1.12). Cardiovascular mortality was reduced by 9% (0.91; 0.77 to 1.07) and cardiovascular events by 16% (0.84; 0.72 to 0.99), which was attenuated (0.86; 0.72 to 1.03) in a sensitivity analysis that excluded a trial using oily fish. Trials with at least two years' follow up provided stronger evidence of protection from cardiovascular events (0.76; 0.65 to 0.90).
Conclusions: There is a small but potentially important reduction in cardiovascular risk with reduction or modification of dietary fat intake, seen particularly in trials of longer duration."
http://www.bmj.com/c...ct/322/7289/757

#68 Blue

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Posted 09 October 2009 - 05:08 PM

Another review, saturated fat is bad
"The quality of dietary fat in relation to cardiovascular disease forms the basis of the diet-heart hypothesis. Current recommendations on dietary fat now emphasise quality rather than quantity. The focus of this review is to summarise the results from prospective cohort studies on dietary fat and cardiovascular disease outcomes. Relatively few prospective cohort studies have found an association between dietary fat quality and cardiovascular disease, partly because of limitations in estimating dietary intake. Saturated and trans fatty acids have increased cardiovascular risk in several studies. Both n-6 and n-3 polyunsaturated fatty acids have been associated with lower cardiovascular risk. Within the n-6 series, linoleic acid seems to decrease cardiovascular risk. Within the n-3 series the long-chain fatty acids (eicosapentaenoic and docosahexaenoic acids) are associated with decreased risk for especially fatal coronary outcomes, whereas the role of alpha-linolenic acid is less clear. Dietary fat quality also influences the activity of enzymes involved in the desaturation of fatty acids in the body. Serum desaturase indices have been consistently associated with adverse cardiovascular outcomes. Data from metabolic and clinical studies reinforce findings from observational studies supporting recommendations to replace saturated and trans fat with unsaturated fat in the prevention of cardiovascular disease."
http://www.ncbi.nlm....pubmed/18328267

#69 Blue

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Posted 09 October 2009 - 05:10 PM

Saturated fats are bad again:
"BACKGROUND: Some previous prospective studies showed that dietary intake of omega3 polyunsaturated fatty acids was associated with lower risk of heart failure (HF), but no study has examined the association between plasma fatty acids and HF. METHODS: We included 3,592 white participants from the Minneapolis field center of the Atherosclerosis Risk in Communities (ARIC) Study, aged 45 to 64 at baseline (1987-1989), initially free of coronary heart disease, stroke, and HF and who had cholesterol ester and phospholipid plasma fatty acids measured. Participants were followed through 2003, and incident HF was defined by a hospital discharge or death including a HF International Classification of Diseases code. RESULTS: During the 14.3-year follow-up, we identified 197 cases of HF (110 for men and 87 for women). After adjustment for age and other confounders, higher saturated fatty acids, especially myristic (14:0) acid, were associated positively with incident HF in both men and women. Higher arachidonic (20:3,omega6) and long-chain omega3 polyunsaturated fatty acids, especially docosahexaenoic (22:6,omega3) acid, were associated inversely with HF in women but not in men. Neither plasma alpha-linolenic nor eicosapentaenoic acid was associated with incident HF. CONCLUSIONS: In both men and women, greater levels of saturated fatty acids may increase risk of HF. In women, arachidonic acid and long-chain omega3 polyunsaturated fatty acids may decrease risk of HF."
http://www.ncbi.nlm....pubmed/19061714

#70 kismet

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Posted 09 October 2009 - 05:23 PM

Also, I don't see why poor or rich, more or less motivated patients should have much different blood lipids when they are hospitalized. Do you truly believe LDL levels of poorer and less motivated people hospitalized with the same medical conditions would be any different?
...

Do people with cardiovascular disease necessarily show elevated LDL levels when they are hospitalized? Well, as we have already seen, at least rich and motivated people don't, many of them even tend to be cholesterol deficient.

What part of this is a cross-sectional trial don't you understand? Why should they have elevated chol. levels? The only explanation would be if their doctor failed miserably and did not make the patient take appropriate meassures (life style interventions, statins & other drugs).
And think about athoergenesis and tell me again that we don't need prospective trials.

But when TC < 200 mg/dl, the case for most people in the world, lowered TC levels look clearly associated with higher (yes, higher!) mortality from cardiovascular disease.

Hailing high triglyceridse as healthy is a new one. I don't even see paleo adherents do it. Honestly, I don't know if I should laugh or cry. You're climbing the evidence ladder down, not up. Cross-sectional studies are bad enough, but, wow, (unadjusted?!) ecological studies are even worse.

There may be a reason why starving peoples of Africa have low blood lipids, high rates of infectious and parastic disease and high mortality. Why could that be? And why the opposite picture for affluent nations? ...

Edited by kismet, 09 October 2009 - 05:26 PM.


#71 Blue

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Posted 09 October 2009 - 05:24 PM

Fats and and saturated fats bad yet again
"Aims/hypothesis The aim of this study was to investigate the association of dietary macronutrient composition and energy density with the change in body weight and waist circumference and diabetes incidence in the Finnish Diabetes Prevention Study.Subjects and methods Overweight, middle-aged men (n=172) and women (n=350) with impaired glucose tolerance were randomised to receive either ‘standard care’ (control) or intensive dietary and exercise counselling. Baseline and annual examinations included assessment of dietary intake with 3-day food records and diabetes status by repeated 75-g OGTTs. For these analyses the treatment groups were combined and only subjects with follow-up data (n=500) were included.<a name="ASec3">Results Individuals with low fat (<median) and high fibre (>median) intakes lost more weight compared with those consuming a high-fat (>median), low-fibre (<median) diet (3.1 vs 0.7 kg after 3 years). In separate models, hazard ratios for diabetes incidence during a mean follow-up of 4.1 years were (highest compared with lowest quartile) 0.38 (95% CI 0.19–0.77) for fibre intake, 2.14 (95% CI 1.16–3.92) for fat intake, and 1.73 (95% CI 0.89–3.38) for saturated-fat intake, after adjustment for sex, intervention assignment, weight and weight change, physical activity, baseline 2-h plasma glucose and intake of the nutrient being investigated. Compared with the low-fat/high-fibre category, hazard ratios were 1.98 (95% CI 0.98–4.02), 2.68 (95% CI 1.40–5.10), and 1.89 (95% CI 1.09–3.30) for low-fat/low-fibre, high-fat/high-fibre, and high-fat/low-fibre, respectively.Conclusions/interpretation Dietary fat and fibre intake are significant predictors of sustained weight reduction and progression to type 2 diabetes in high-risk subjects, even after adjustment for other risk factors."
http://www.springerlink.com/content/87670082865607x6/


#72 Blue

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Posted 09 October 2009 - 05:44 PM

Some general points regarding the evidence paleos and ketogenics like to cite. 1. There are several short-term studies showing that high-protein, high-fat diets can cause greater weight reduction than high-carbohydrate diets. Weight reduction will generally improve many other metabolic variables in the obese so short-term these diets appear more successful. 2. The second type of study is those showing an change by high fat, high protein diets in specific subtypes of LDL and HDL cholesterol which are argued to be beneficial as compared to carbohydrates.

The problem with these studies is that they are short term and does not directly measure what is really relevant, namely morbidity and mortality. In long-term studies measuring real disease outcomes high-fat and saturated fat diets fare poorly as demonstrated.

#73 oprimitivo

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Posted 09 October 2009 - 10:13 PM

First paper (please see abstract below): It ilustrates the predominant importance of inflammation over lipid levels on the survival of patients with severe CAD. Notice that most of these patients, either they were taking or not taking statins, were cholesterol deficient, as their average TC (181 mg/dl) was LOWER than the average values of the general population (207 mg/dl). Also their average LDL level (120 mg/dl) was almost EQUAL (actually a bit lower) to the LDL of the general population (127 mg/dl). Another thing to notice is their average HDL level is very small, only 34 mg/dl (not good at all). If they have severe CAD then they are high risk cardiovascular patients and so, according to the "bad LDL theory", they should present "high risk" LDL levels. But they don't, their LDL levels are notably normal, why? They also found that "lipid levels, including levels of TC, LDL, HDL and the TC:HDL ratio, did not predict mortality after angiographic CAD diagnosis in this population." Very interesting, so lipids might be useless cardiovascular markers for severe CAD patients? On the other hand, C-reactive protein, a general inflammatory marker, was found to be a strong predictor of mortality in patients with CAD. Despite of these results, the authors insist that "although lipid levels did not predict mortality in this or other secondary prevention studies, this does not contradict the wealth of data supporting cholesterol as a risk factor for primary development of CAD". They seam to be ON DENIAL, just like the authors of this second study.

Second paper: These authors also KNOW that "hypercholesterolemia is a risk factor for coronary artery disease". Yet, they also have to admit that "[hypercholesterolemia] is also associated with lower risk of adverse outcomes in patients with acute coronary syndromes (ACS)." How can this be? Hypercholesterolemia could be good and bad at the same time? Well, when your "a priori" ideas don't match reality, and you really don't want to discard them, just call them "a paradox". Like the French Paradox and many other paradoxes. These authors recognize "once a patient has developed ACS, a history of hypercholesterolemia appears to be protective". How is this possible then? Is there any chance that maybe high cholesterol can be protective against heart disease? Epidemiological data actually supports this idea. But we KNOW hypercholesterolemia has to be a risk factor for CAD. No problem, let's just call it a PARADOX and the problem is solved!

Statins: LDL lowering studies tell nothing about the "advantages" of lowering LDL because, as already referred, statins have huge effects beyond just lowering LDL. It would be nice if statin papers reported their successful results not only as absolute values but also the corresponding NNT values. Figures wouldn't be so fantastic, woulnd't they?

kismet: "Hailing high triglyceridse as healthy is a new one." I must totaly agree with you, high TG is bad. Where did you get that idea? Are you assuming that people with higher cholesterol levels necessarily have higher TG? Please forget about Friedewald formula. Did you know that TC is almost independent of TG? Yes, BELIEVE ME, there are even more powerful prediciton formulas for TC, than the old Friedewald formula, that rely only on LDL and HDL. Just because a parameter is used to explain a variable, it doesn't mean it can't be discarded and yet the new formula provide a better explanation. When TC increases, HDL also has a tendency to some increase. Is this enough to compensate for LDL increase? And is LDL bad at all, or is it totally irrrelevant? I don't think so! Increasing TC at the expenses of only TG increase is truly bad and high risk. But this is probably not the case in real populations (I have data to support this idea). I believe TG/HDL ratio is perhaps one of the best risk markers for CAD. TC doesn't tell you much and, most probably, LDL doesn't tell you nothing (but LDL sub-fractions tell a lot!). I would like to present more data here, some new formulas I have.


Statin therapy, lipid levels, C-reactive protein and the survival of patients with angiographically severe coronary artery disease. (download pdf)
Horne BD, Muhlestein JB, Carlquist JF, Bair TL, Madsen TE, Hart NI, Anderson JL.

Cardiovascular Department, LDS Hospital and University of Utah, Salt Lake City 84143, USA.

OBJECTIVES: The joint predictive value of lipid and C-reactive protein (CRP) levels, as well as a possible interaction between statin therapy and CRP, were evaluated for survival after angiographic diagnosis of coronary artery disease (CAD). BACKGROUND: Hyperlipidemia increases risk of CAD and myocardial infarction. For first myocardial infarction, the combination of lipid and CRP levels may be prognostically more powerful. Although lipid levels are often measured at angiography to guide therapy, their prognostic value is unclear. METHODS: Blood samples were collected from a prospective cohort of 985 patients diagnosed angiographically with severe CAD (stenosis > or =70%) and tested for total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and CRP levels. Key risk factors, including initiation of statin therapy, were recorded, and subjects were followed for an average of 3.0 years (range: 1.8 to 4.3 years) to assess survival. RESULTS: Mortality was confirmed for 109 subjects (11%). In multiple variable Cox regression, levels of TC, LDL, HDL and the TC:HDL ratio did not predict survival, but statin therapy was protective (adjusted hazard ratio   = 0.49, p = 0.04). C-reactive protein levels, age, left ventricular ejection fraction and diabetes were also independently predictive. Statins primarily benefited subjects with elevated CRP by eliminating the increased mortality across increasing CRP tertiles (statins: HR = 0.97 per tertile, p-trend = 0.94; no statins: HR = 1.8 per tertile, p-trend < 0.0001). CONCLUSIONS: Lipid levels drawn at angiography were not predictive of survival in this population, but initiation of statin therapy was associated with improved survival regardless of the lipid levels. The benefit of statin therapy occurred primarily in patients with elevated CRP.


Hypercholesterolemia paradox in relation to mortality in acute coronary syndrome. (download pdf)
Wang TY, Newby LK, Chen AY, Mulgund J, Roe MT, Sonel AF, Bhatt DL, DeLong ER, Ohman EM, Gibler WB, Peterson ED.

Division of Cardiology, Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina 27705, USA. wang0085@mc.duke.edu

BACKGROUND: Hypercholesterolemia is a risk factor for coronary artery disease, yet is associated with lower risk of adverse outcomes in patients with acute coronary syndromes (ACS). HYPOTHESIS: We explored this paradox in 84,429 patients with non-ST-segment elevation ACS in the Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the American College of Cardiology/American Heart Association Guidelines registry. METHODS: We examined the association between a history of hypercholesterolemia and in-hospital mortality after adjusting for clinical covariates. After excluding patients with previously diagnosed hypercholesterolemia, we repeated the analysis, examining the association between newly diagnosed hypercholesterolemia (in-hospital low-density lipoprotein cholesterol [LDL-C] > or = 100 mg/dL) and mortality. RESULTS: A history of hypercholesterolemia was associated with lower in-hospital mortality (unadjusted odds ratio [OR]: 0.58; 95% confidence interval [CI]: 0.55, 0.62). This protective association persisted after adjusting for baseline characteristics (OR: 0.71; 95% CI: 0.66, 0.76) and prior statin use (OR: 0.74; 95% CI: 0.68, 0.80). Among 22,711 patients with no history of hypercholesterolemia, 12,809 had a new in-hospital diagnosis of hypercholesterolemia. Unadjusted mortality in these patients was lower than among those with normal LDL levels (OR: 0.58; 95% CI: 0.50, 0.67); however, this difference was not significant after multivariable adjustment (OR: 0.86; 95% CI: 0.73, 1.01). CONCLUSIONS: The association of hypercholesterolemia with better outcomes highlights a major challenge in observational analyses. Our results suggest this paradox may result from confounding due to other clinical characteristics, impact of statin treatment, and perhaps most importantly, the fact that previously diagnosed hypercholesterolemia is a marker for patients with more prior medical contact. Copyright 2009 Wiley Periodicals, Inc.

Edited by oprimitivo, 09 October 2009 - 10:26 PM.


#74 Blue

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Posted 09 October 2009 - 10:50 PM

Regarding your first paper, lets see what the researchers say themselves:
"Although lipid levels did not predict mortality in this or
other secondary prevention studies (19,20), this does not
contradict the wealth of data supporting cholesterol as a risk
factor for primary development of CAD. Several possible
explanations exist. First, our results may suggest that high
cholesterol levels do not increase the risk of death once
CAD has developed. Death after the establishment of
disease may involve different (acute phase) mechanisms that
do not depend heavily on processes influenced by lipid
levels. Second, once a patient has developed CAD, the lack
of association for lipids may indicate that the lipid levels are
too high for that particular patient, regardless of whether
the absolute lipid levels are above what might be considered
a typical at-risk level. If so, lipid-lowering treatment may be
warranted. Finally, statins may work through mechanisms
unrelated or only indirectly dependent on lowering of
plasma lipid levels (i.e., anti-inflammatory effects, lowering
of plaque oxidized-LDL, etc.)."

Again, this was not a study of first-timers (it was patients undergoing coronary arteriography which is often used for follow-up and treatments) and the study explicitly states that prior statin use was unknown. But in such a groupone would expect that advise had been given regarding diet, exercise, and lipid lowering medications given. Again, you can say that just because average lipids are similar to population average that this is healthy. Even if this had been virgin first-timers regarding CVD the population average lipids are unhealthy.

Regarding the second study and what the authors are meaning, I suggest you check up the difference between primary, secondary, and tertiary prevention. Or I may make it easier. One possibility is that lipids are not important once you have already developed advanced disease. Does not mean that that they are not important before this.

Edited by Blue, 09 October 2009 - 10:53 PM.


#75 ajnast4r

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Posted 09 October 2009 - 11:43 PM

this is what an imminst thread should look like...cheers


tangent: we need to stop exploring week predictors of cvd like cholesterol and its carriers and focus on finding the yet unknown markers for chronic subclinical inflammation that are the REAL cause of cvd and many other chronic diseases

Edited by ajnast4r, 09 October 2009 - 11:49 PM.


#76 Blue

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Posted 10 October 2009 - 01:25 AM

this is what an imminst thread should look like...cheers


tangent: we need to stop exploring week predictors of cvd like cholesterol and its carriers and focus on finding the yet unknown markers for chronic subclinical inflammation that are the REAL cause of cvd and many other chronic diseases

Weak? See this graph for primary prevention of CVD (that is, for people without CVD at the time of the study):
http://www.lipidsonl...1...study&dpg=3

#77 ajnast4r

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Posted 10 October 2009 - 02:37 AM

this is what an imminst thread should look like...cheers


tangent: we need to stop exploring week predictors of cvd like cholesterol and its carriers and focus on finding the yet unknown markers for chronic subclinical inflammation that are the REAL cause of cvd and many other chronic diseases

Weak? See this graph for primary prevention of CVD (that is, for people without CVD at the time of the study):
http://www.lipidsonl...1...study&dpg=3




dont worry i'm on your side on this one :|w

#78 Blue

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Posted 10 October 2009 - 06:55 AM

Regarding the question of this thread, ldl is likely easier to fix than hdl, with statins if nothing else. Hdl is much more difficult. I find this blog post by a physician treating lipid disorders fascinating:
http://www.wellspher...d-and-hdl/35300
http://www.wellspher...itamin-d/239875

Fascinating enough there does not seem to be a single study of how high dose vitamin D affects HDL. I guess they will be coming soon.

(Notice also that the advice to skip the carbohydrates and wheat and exercise and reduce weight does not do much good.)

#79 Luna

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Posted 11 October 2009 - 05:57 PM

I am not sure if I should be seeing effects so soon after.. probably not.

I started to eat more vegetables every day and add extra extra olive oil..

I was scheduled a blood test anyways, unrelated..

Old results:
CHOLESTEROL: 135 - mg/dL
TRIGLYCERIDES: 60 - mg/dL
CHOLESTEROL- HDL: 32 (way too low according to my chart!!!) - mg/dL
CHOLESTEROL-LDL calc: 91 - mg%
CHOLESTEROL/ HDL: 4 - Not stated
NON-HDL_CHOLESTEROL: 103 - mg/dL


New results:
CHOLESTEROL: 131- mg/dL
TRIGLYCERIDES: 55- mg/dL
CHOLESTEROL- HDL: 33 - mg/dL
CHOLESTEROL-LDL calc: 87- mg%
CHOLESTEROL/ HDL: 4 - Not stated
NON-HDL_CHOLESTEROL: 98- mg/dL

I guess that's some improvement .. O_o

The weird thing is that my results for glucose showed 67 (instead of the usual 71).. I always find my glucose weird to be so low with all the sweets I eat, and the day before the test I had quite a bit of cakes (holidays!).. I feel my metabolism is weird :X

Edit:
Apparently my HB, HCT, RBC levels also dropped, a bit below the miniumum too.. 12.1 g/dl, 35.5%, 4.11 *10^6/ul

My iron is 120 ug/dl.. so I think I am not anemic...

I asked them to do vitamin d test too but they seem to have forgot..

Edited by Luna, 11 October 2009 - 06:26 PM.


#80 six

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Posted 14 October 2009 - 03:00 AM

wow...what an interesting thread. olive oil? I had no idea... I thought oatmeal was the way to lower cholesterol?? I'm certainly switching to dark chocolate! :-D

#81 yoyo

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Posted 14 October 2009 - 08:28 AM

Ok first off noone mentioned drinking alcohol. have a drink, it helps cholesterol and inflammation. and drink some tea the rest of the day.

Well the smell of canned tuna is a horror i remember from childhood and will never subject myself to again. but if i had to, i'd nuke with hot sauce, curry powder, lemon juice, etc until the taste was drowned out. thats sort of my approach for vegetables.

perhaps try breaking out of the 'sandwich' paradigm, where a meal automatically starts with bread. some nuts with a fruit; some vegetables with hummus; or some soup. lots of ways to make a meal. not that bread is poison, but not the best thing either.

ldl being calculated from the other measured values (which is the usual way that the score you get is determined) means you don't really know what it is.

as far as increasing HDL: could add saturated fat, particularly lauric (coconut oil/milk). see this review for effects of various satu;rated fats http://www.ajcn.org/.../full/77/5/1146 (though it confuses various polyunsaturates). not saturated fat from cows.

still, most studies i've seen seem to indicate all saturates increase inflamation, which is intimately related to cholesterol in chronic disease.

reducing ldl is easier than increasing hdl.

here's a pretty thorough review for hdl http://jama.ama-assn.../jama;298/7/786

generally i think fruit>legumes>barley/oats>wheat. i think of carbs as mostly determined by how much you are active. if you are running/lifting/whatever for 2 hours a day, a big bowl of rice is ok. if you mostly sit around, just a few fruits and a small serving of beans. do you get some exercise most days?

#82 TheFountain

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Posted 14 October 2009 - 09:01 AM

still, most studies i've seen seem to indicate all saturates increase inflamation

Can you show me some of those studies please?

#83 yoyo

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Posted 15 October 2009 - 02:16 AM

still, most studies i've seen seem to indicate all saturates increase inflamation

Can you show me some of those studies please?


i'd love to.

Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study fulltext-> http://www.direct-ms.....ds inflam.pdf

Relation of dietary fat and fiber to elevation of C-reactive protein☆
Dana E King, MDaCorresponding Author Informationemail address, Brent M Egan, MDb, Mark E Geesey, MSa
Received 6 June 2003; received in revised form 11 August 2003; accepted 11 August 2003.
Abstract

We examined the relation of dietary fiber, fat, and other dietary factors to levels of highly sensitive C-reactive protein (CRP) in 4,900 adult participants in the 1999 to 2000 National Health and Nutrition Examination Survey (NHANES 99-00), which was a cross-sectional study of a nationally representative sample of noninstitutionalized United States residents. After controlling for demographic factors, body mass index, smoking, alcohol consumption, exercise, and total caloric intake, subjects in the third and fourth highest quartiles of fiber consumption had a lower risk of elevated CRP (odds ratio [OR] 0.64, 95% confidence interval [CI] 0.43 to 0.96; OR 0.58, 95% CI 0.38 to 0.88, respectively) compared with the lowest quartile. Saturated fat consumption was modestly associated with elevated CRP (third quartile: OR 1.58, 95% CI 1.02 to 2.44; fourth quartile 1.44, 95% CI 0.80 to 2.58). The findings suggest that inflammation may link dietary fiber and fat to cardiovascular disease.
http://www.ajconline...1193-7/abstract


Dietary fat intake and proinflammatory cytokine levels in patients with heart failure.
Lennie TA, Chung ML, Habash DL, Moser DK.

College of Nursing, University of Kentucky, Lexington, USA.

BACKGROUND: Dietary fat intake affects proinflammatory cytokine levels of healthy adults. Whether dietary fats have similar effects in patients with heart failure (HF) is unknown. The purposes of this study were to determine (1) effect of dietary fat on interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, and soluble receptors sTNF-R1 and sTNF-R2 levels in patients with HF and (2) subsequent impact of these levels on event-free survival. METHODS AND RESULTS: Forty-two patients provided 4-day food diaries and blood for cytokines. Event-free survival curves were calculated by Kaplan-Meier method and groups compared using log-rank test. IL-6 was not related to fat intake. TNF-alpha levels were elevated in patients with diets higher versus lower in saturated (6.9 +/- 5 versus 4.2 +/- 2 pg/mL) and trans fats (6.8 +/- 4.5 versus 4.5 +/- 2.8 pg/mL). Patients consuming diets higher in polyunsaturated fats had lower sTNF-R1 (2391 +/- 1010 versus 3373 +/- 2098 pg/mL) and sTNF-R2 (3803 +/- 1187 versus 5974 +/- 3275 pg/mL) levels. Higher omega-3 intake produced similar results: sTNF-R1 (2323 +/- 1304 versus 3307 +/- 1973) and sTNF-R2 (4117 +/- 2646 versus 5409 +/- 2801). Event-free survival was decreased in patients with higher TNF-alpha and sTNF-R1 levels. CONCLUSION: Dietary fat intake may affect proinflammatory cytokine levels in patients with HF. Research to determine whether changing composition of dietary fat can alter proinflammatory cytokine activity of HF patients is warranted.
http://www.ncbi.nlm....pubmed/16230265



#84 stephen_b

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Posted 15 October 2009 - 05:18 PM

There are issues with both of those studies. The first is epidemiological and so cannot determine causation. It doesn't seem to say whether the "modest" association of higher saturated fat was still present when adjusting for factors like carbohydrate intake.

Here's a study about a high saturated fat diet that was also starch free, Effect of a High Saturated Fat and No-Starch Diet on Serum Lipid Subfractions in Patients With Documented Atherosclerotic Cardiovascular Disease (full text available, PMID 14601690).

In patients with atherosclerotic cardiovascular disease, mean ± SD total body weight (TBW) decreased 5.2%±2.5% (P<.001) as did body fat percentage (P=.02). Nuclear magnetic resonance spectroscopic analysis of lipids showed decreases in total triglycerides (P<.001), very low-density lipoprotein (VLDL) triglycerides (P<.001), VLDL size (P<.001), large VLDL concentration (P<.001), and medium VLDL concentration (P<.001). High-density lipoprotein (HDL) and LDL concentrations were unchanged, but HDL size (P=.01) and LDL size (P=.02) increased. Patients with polycystic ovary syndrome lost 14.3%±20.3% of TBW (P=.008) and patients with reactive hypoglycemia lost 19.9%±8.7% of TBW (P<.001) at 24 and 52 weeks, respectively, without adverse effects on serum lipids.

Everything improved.

StephenB

Edited by stephen_b, 15 October 2009 - 05:18 PM.


#85 yoyo

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Posted 16 October 2009 - 09:36 AM

well i posted three studies, not two. look at the first one i linked to, it is a controlled intervention, not epidemiological.


and your study involved putting people on a weight loss diet. weight loss or gain will trump any macronutrient effect because being fat really is that unhealthy. eating a hypocaloric diet of potato chips and alcopop would improve things too. and a keto diet is going to be a monkey wrench too, and not something most people are going to want to do, so whatever the hypothesized benefits its sort of irrelevant.

Edited by yoyo, 16 October 2009 - 09:38 AM.


#86 Blue

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Posted 16 October 2009 - 09:44 AM

There are issues with both of those studies. The first is epidemiological and so cannot determine causation. It doesn't seem to say whether the "modest" association of higher saturated fat was still present when adjusting for factors like carbohydrate intake.

Here's a study about a high saturated fat diet that was also starch free, Effect of a High Saturated Fat and No-Starch Diet on Serum Lipid Subfractions in Patients With Documented Atherosclerotic Cardiovascular Disease (full text available, PMID 14601690).

In patients with atherosclerotic cardiovascular disease, mean ± SD total body weight (TBW) decreased 5.2%±2.5% (P<.001) as did body fat percentage (P=.02). Nuclear magnetic resonance spectroscopic analysis of lipids showed decreases in total triglycerides (P<.001), very low-density lipoprotein (VLDL) triglycerides (P<.001), VLDL size (P<.001), large VLDL concentration (P<.001), and medium VLDL concentration (P<.001). High-density lipoprotein (HDL) and LDL concentrations were unchanged, but HDL size (P=.01) and LDL size (P=.02) increased. Patients with polycystic ovary syndrome lost 14.3%±20.3% of TBW (P=.008) and patients with reactive hypoglycemia lost 19.9%±8.7% of TBW (P<.001) at 24 and 52 weeks, respectively, without adverse effects on serum lipids.

Everything improved.

StephenB

Of course everything will improve with a weight loss diet.

#87 Luna

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Posted 02 November 2009 - 06:50 PM

So I test vitamin d!
Result 17 ng/ml, normal is 20-58 @@..

#88 Blue

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Posted 02 November 2009 - 08:23 PM

Somewhat strange since Israel should be sunny and it is not winter yet.

#89 stephen_b

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Posted 02 November 2009 - 10:51 PM

Somewhat strange since Israel should be sunny and it is not winter yet.

Lots of people work indoors though.

#90 niner

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Posted 03 November 2009 - 03:10 AM

So I test vitamin d!
Result 17 ng/ml, normal is 20-58 @@..

Oh man, Luna. Time to start supplementing! Get the gelcap (oil-based) formulation; the dry formulation is not well absorbed. You should probably take about 3000 IU/day, and retest in a couple months. Try to hit 40-50ng/ml. I'm surprised to see them call 20-58 "normal". I would call 20ng/ml "frank deficiency". Doesn't the usual definition of normal start at 30ng/ml? Maybe this lab always reads low?




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