92 replies to this topic

[ajnast4r]

Does it mean you support higher fat, lower carbs - but won't recommend it because I won't stick to it? (which is probably true, I tried atkins once and wasn't able to stick to it, too much things I didn't like and a lot of meat)

no.. i think the evidence point towards moderation with all macronutrients for the general population. i believe some people, probably due to genetics, function better on a lower carb/higher fat diet...but not the majority.

I think the best way for me would be little by little, add a bit of this, less from that, small steps

that is the best way for most people... small incremental changes tend to become ingrained easier. people who usually fail when trying to make dietary changes are usually people who take on so much change that it becomes a source of negativity/stress .

I also still can't find how to follow your advise of lowering my animal fat if I barely eat animal fat.

those were generalized recommendations.

Any other suggestions you could think of?

like you said your diet does suck in nutritional value... if you plan on living a long & disease free life it would be worth correcting.

i think you would do well to just eat a little more (correctly sourced) fat... your lipid profiles would probably improve if you a) added some good saturated (low sugar, milk free chocolate..coconut oil) in low-moderate amounts, monounsaturated (olive oil, avocado, almond) in moderate-higher amounts, and polyunsaturated (walnuts, fish) in low amounts b) replaced the refined carbs with whole complex carbs, ie: 100% whole grain breads instead of white/wholewheat... if you wanna get really crazy cut out wheat altogether
l

if youre only eating meat 5 times a month you need to get a good source of protein in your diet on a daily basis... drink more milk, eat more eggs, or find a good quality whey or egg protein shake.

[Luna]

Thanks for the reply again!
My bread is already the non-white type, but I need to check if it's wheat or grain I guess.
I am not afraid of the fat in the milk, I am afraid of the calories in the milk :D had a lot of weight problems before. I already drink milk pretty much every day with the cereals.
I can try increasing eggs and fish and fi the bread is whole wheat I can try find whole grain one.

It's a bit hard finding avocados, so I can try have more almonds (anything else? walnuts might be better? I seem to be able to eat them better than almonds) and does olive oil count if you used it for cooking or do I actually need to add it to foods, uncooked?

I am trying to think what I can add it to other than salad :X

Thanks

[Luna]

Ohh what about olives themselves?
I do eat quite a bit of olives, in salad or eggs and sandwiches.

Or just olive oil?

[meursault]

Does anyone consider sesame oil to be a healthy oil? How does it compare to coconut or olive?

[ajnast4r]

olives are great, one of the best foods you can eat imo...dont cook olive oil it goes rancid quickly. also get your viatmin d into the 50-60ng/ml range which will raise hdl among countless other health benefits. theres a post on heartscan blog about vitD and hdl increases today, check it out.

[ForeverYouthful]

also get your vitamin d into the 50-60ng/ml range

What is a good way to do this?

What do you all think about cod liver oil on this site? Or would some kind of multi-vitamin be better? (I'm looking into Ortho-Core because of reading this board)

[CobaltThoriumG]

also get your vitamin d into the 50-60ng/ml range

What is a good way to do this?

What do you all think about cod liver oil on this site? Or would some kind of multi-vitamin be better? (I'm looking into Ortho-Core because of reading this board)

Supplement with an oil-based D3. It's one of the cheapest supplements to buy. I use a D3 sourced from lanolin instead of fish oil. But they should be the same. You need to get tested to adjust the dosage and it may vary seasonally, with sun exposure.

[Skötkonung]

Why is no one acknowledging or refuting the information posted by ajnast4r?

because im the only one with a formal education in nutrition... too mainstream lol

Because one "source" is an About.com article. The other two use samples where both dietary fat and carbohydrate are high.

the article is a summary of the study, and the first sentence of the article refers to the journal in which the study was published. i didnt think it necessary to spend the time to look up the study... moderate to high carbohydrate is the way most people eat, and is the way she described her diet... she is clearly not too careful about her diet, so telling her to switch to a lowcarb/paleo style diet (which is not suited to everyone) would be a waste of time. so the studies and dietary advice i gave are accurate and in-line with the established science.

There is correlation between elevated triglyceride levels and heart disease, but correlation is not causation. No one knows if the triglycerides are the problem or are a marker for a different problem or just a coincidental finding. If there is anything that looks causal it's probably small LDL particle size. Since the elucidation of the LDL receptor garnered a Nobel, it stands to reason that an absolute for sure definitive answer to the lipid hypothesis would probably garner one as well.

Is atherosclerosis caused by high cholesterol?
http://qjmed.oxfordj...t/full/95/6/397

I believe if you were to reference your nutrition textbooks, you'd see that enzymes in the GI tract break them down all carbohydrates (including low glycemic index foods) into simple sugars that are absorbed by the small intestine. One cup of complex carbohydrate goes into the blood as one cup of sugar, and since the body likes to keep about a teaspoon of sugar in the blood, this extra cup (or more) has to be dealt with metabolically by an enormous outpouring of insulin. All this insulin doesn't just lower the sugar level of the blood; it does a lot of other things such as driving fat into the fat cells, causing the kidney to retain sodium, and stimulating the production of VLDL in the liver. These triglycerides are the small, dense lipoproteins that get stuck in artery walls and induce dangerous inflammation.

Advising someone who already has a abnormal cholesterol levels to eat a high carbohydrate diet is irresponsible.

Fat, especially long-chain saturated fat digests very slowly, and doesn't reach the blood until much later than the two hour mark. While carbs go directly into the blood, fats take a different route. The process that breaks down dietary fat into its component fatty acids is a lengthy process as compared to the breakdown of carbohydrate. Once the fat has broken down, it has to combine with bile salts to make it into a form that is water soluble and can be taken up by the intestinal cells. Once taken up, unlike carbs, which are sent directly to the bloodstream, fats go into the lymphatic system, a much smaller and more static transport system than the vasculature. Once in the lymphatics, fats make their way to the thoracic duct, which empties into a large vein in the upper chest. The lymphatics are small vessels and take a long time to move their contents along since there is no heartbeat pushing them as there is with blood.

By the time dietary fat does make it to the bloodstream, it is not in a form that would induce inflammation and it is far lesser a quantity. It is well known that low-carbohydrate diets reduce LDL particle size and improve lipids:

http://www.jlr.org/c...tract/39/9/1799
"LDL particle type can independently predict changes in HDL cholesterol in men and accounts for 27% of the variance."
—Clifton, P. M., M. Noakes, and P. J. Nestel. LDL particle size and LDL and HDL cholesterol changes with dietary fat and cholesterol in healthy subjects"

Edited by Skotkonung, 05 October 2009 - 05:44 AM.

[oprimitivo]

In simplistic terms the lipid hypothesis is as follows:

Strawman. The lipid hypothesis deals with plasma cholesterol. And the lipid hypothesis is right; even someone from "your side" admited that the lipid "hypothesis" is correct (Stephan from whole health); it was merely refined in recent time without changing the concept (LDL vs HDL; modification and oxidation of LDL playing a key role, etc). The same happend with Darwin's theory of evolution by natural selection, but no one goes around crying that Darwin was wrong and refuted.

If the Lipid Hypothesis is so scientifically correct, and elevated LDL levels really promote heart disease, then we would expect, of course, that LDL levels of patients hospitalized with CAD would be truly high risk, most probably above 160 mg/dl and OF COURSE higher than the average LDL of the general population (127 mg/dl for people aged 60-69 years). BUT THEY ARE NOT! Actually In a very large cohort of 136,905 patients hospitalized with CAD, almost half have admission LDL levels <100 mg/dl. Also, these patients present LOWER total cholesterol than the average population. THEY ARE CHOLESTEROL DEFICIENT! So, the obvious conclusion is that most patients hospitalized with CAD are LDL deficient (104.9 mg/dl) and their average total cholesterol (174.4 mg/dl) is also usually well below normal levels (207 mg/dl for people aged 60-69 years). Obviously epidemiological evidence is not enough to demonstrate causality, but if an hypothesis totally fails to comply with evidence, if it simply doesn't matches reality, then that hypothesis is necessarily plain WRONG! One last note: most "scientific evidence" against saturated fats is based on this LDL dogma, enough to say that there is no evidence at all to prove that saturated fats are unhealthy. On the contrary, most prospective studies failed to establish a link between saturated fats and CHD. Also, most CHD dietary intevention trials, with lowered saturated fat intake, because THEY KNEW saturated fats would clog arteries, also failed miserably to reduce both CHD and total mortality, even though "unhealthy" high cholesterol levels were significantly reduced in those trials. You should read THE GREAT CHOLESTEROL CON, by Anthony Colpo, in order to understand that LDL, without considering its sub-fractions (sdLDL, oxLDL, Patterns A or B, etc.), is a complete waste of time, a useless parameter. Also, please notice that lowest mortality is observed when total cholesterol (t-C) is 200-240 mg/dl, low t-C is linked to more infectious and parasitic diseases and also low t-C maybe associated with higher CHD.


Trends in serum lipids and lipoproteins of adults, 1960-2002. (download pdf)
Carroll MD, Lacher DA, Sorlie PD, Cleeman JI, Gordon DJ, Wolz M, Grundy SM, Johnson CL.
National Center for Health Statistics, Centers for Disease Control and Prevention, Hyattsville, Md 20782, USA. mdc3@cdc.gov
CONTEXT: Serum total and low-density lipoprotein (LDL) cholesterol contribute significantly to atherosclerosis and its clinical sequelae. Previous analyses of data from the National Health and Nutrition Examination Surveys (NHANES) showed that mean levels of total cholesterol of US adults had declined from 1960-1962 to 1988-1994, and mean levels of LDL cholesterol (available beginning in 1976) had declined between 1976-1980 and 1988-1994. OBJECTIVE: To examine trends in serum lipid levels among US adults between 1960 and 2002, with a particular focus on changes since the 1988-1994 NHANES survey. DESIGN, SETTING, AND PARTICIPANTS: Blood lipid measurements taken from 6098 to 15 719 adults who were examined in 5 distinct cross-sectional surveys of the US population during 1960-1962, 1971-1974, 1976-1980, 1988-1994, and 1999-2002. MAIN OUTCOME MEASURES: Mean serum total cholesterol, LDL cholesterol, high-density lipoprotein (HDL) cholesterol, and geometric mean serum triglyceride levels, and the percentage of adults with a serum total cholesterol level of at least 240 mg/dL (> or =6.22 mmol/L). RESULTS: Between 1988-1994 and 1999-2002, total serum cholesterol level of adults aged 20 years or older decreased from 206 mg/dL (5.34 mmol/L) to 203 mg/dL (5.26 mmol/L) (P=.009) and LDL cholesterol levels decreased from 129 mg/dL (3.34 mmol/L) to 123 mg/dL (3.19 mmol/L) (P<.001). Greater and significant decreases were observed in men 60 years or older and in women 50 years or older. The percentage of adults with a total cholesterol level of at least 240 mg/dL (> or =6.22 mmol/L) decreased from 20% during 1988-1994 to 17% during 1999-2002 (P<.001). There was no change in mean HDL cholesterol levels and a nonsignificant increase in geometric mean serum triglyceride levels (P = .06). CONCLUSIONS: The decrease in total cholesterol level observed during 1960-1994 and LDL cholesterol level observed during 1976-1994 has continued during 1999-2002 in men 60 to 74 years and women 50 to 74 years. The target value of no more than 17% of US adults with a total cholesterol level of at least 240 mg/dL (> or =6.22 mmol/L), an objective of Healthy People 2010, has been attained. The increase in the proportion of adults using lipid-lowering medication, particularly in older age groups, likely contributed to the decreases in total and LDL cholesterol levels observed. The increased prevalence of obesity in the US population may have contributed to the increase in mean serum triglyceride levels.


Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines. (download pdf)
Sachdeva A, Cannon CP, Deedwania PC, Labresh KA, Smith SC Jr, Dai D, Hernandez A, Fonarow GC.
Department of Medicine, UCLA Medical Center, Los Angeles, CA90095-1679, USA.
BACKGROUND: Lipid levels among contemporary patients hospitalized with coronary artery disease (CAD) have not been well studied. This study aimed to analyze admission lipid levels in a broad contemporary population of patients hospitalized with CAD. METHODS: The Get With The Guidelines database was analyzed for CAD hospitalizations from 2000 to 2006 with documented lipid levels in the first 24 hours of admission. Patients were divided into low-density lipoprotein cholesterol (LDL), high-density lipoprotein cholesterol (HDL), and triglyceride categories. Factors associated with LDL and HDL levels were assessed along with temporal trends. RESULTS: Of 231,986 hospitalizations from 541 hospitals, admission lipid levels were documented in 136,905 (59.0%). Mean lipid levels were LDL 104.9 +/- 39.8, HDL 39.7 +/- 13.2, and triglyceride 161 +/- 128 mg/dL. Low-density lipoprotein cholesterol <70 mg/dL was observed in 17.6% and ideal levels (LDL <70 with HDL > or =60 mg/dL) in only 1.4%. High-density lipoprotein cholesterol was <40 mg/dL in 54.6% of patients. Before admission, only 28,944 (21.1%) patients were receiving lipid-lowering medications. Predictors for higher LDL included female gender, no diabetes, history of hyperlipidemia, no prior lipid-lowering medications, and presenting with acute coronary syndrome. Both LDL and HDL levels declined over time (P < .0001). CONCLUSIONS: In a large cohort of patients hospitalized with CAD, almost half have admission LDL levels <100 mg/dL. More than half the patients have admission HDL levels <40 mg/dL, whereas <10% have HDL > or =60 mg/dL. These findings may provide further support for recent guideline revisions with even lower LDL goals and for developing effective treatments to raise HDL.

Edited by oprimitivo, 05 October 2009 - 11:52 AM.

[JLL]

Why is no one acknowledging or refuting the information posted by ajnast4r?

Because one "source" is an About.com article. The other two use samples where both dietary fat and carbohydrate are high.

My understanding was that the suggestion there was that saturated animal fat was bad, not saturated fats from non-animal sources.

The body doesn't know where the saturated comes from. If saturated fat from animal sources is somehow worse than saturated fat from plant sources (which doesn't make much sense from an evolutionary perspective), we should be able to identify which saturated fatty acids are responsible for this.

[Luna]

Wasn't vitamin D related to breast cancer?
Or was it related to reduced breast cancer..

[health_nutty]

Why is no one acknowledging or refuting the information posted by ajnast4r?

Because one "source" is an About.com article. The other two use samples where both dietary fat and carbohydrate are high.

My understanding was that the suggestion there was that saturated animal fat was bad, not saturated fats from non-animal sources.

The body doesn't know where the saturated comes from. If saturated fat from animal sources is somehow worse than saturated fat from plant sources (which doesn't make much sense from an evolutionary perspective), we should be able to identify which saturated fatty acids are responsible for this.

The fatty acid profile is different.

[kismet]

From your link:
One of the most well known early modern proponents that saturated fats and cholesterol in the blood are the cause of heart disease was Ancel Keys, whose first paper on the topic was published in 1953^[6], and whose book Eat Well and Stay Well^[7] helped the issue gain popular awareness.^[8]

Ancel Keys chose to study only those countries where both saturated fats consumption and heart disease were high. He ignored other countries that ate similar diet but had low rates of heart disease...

But cholesterol in the blood does cause heart disease, so where's the issue? I already said that just because a theory is refined (let's say for simplicity's sake that sat. fat has no influence on atherogenesis, even though, IIRC even Stephan admits that at least in certain contexts sat. fat may play a role), doesn't mean the theory is completely wrong.

I stand by my descrption. You created a strawmen ("sat. fact causes heart disease") even though it's a. not sure that sat. fat is innocent and b. more importantly not the only or even the most important part of the lipid "hypothesis". Please just adopt Stephan's more precise and less biased terminology: "The Diet[ary sat. fat and cholesterol]-Heart Hypothesis"; not lipid hypothesis.

oprimitivo, I won't even address your red herring. Just one thing which is blatant: obviously CAD patients have low LDL, because they are treated with statins. For god's sake you posted a cross-sectional trial, do you think we're that stupid?

Edited by kismet, 05 October 2009 - 05:22 PM.

[Blue]

The paleos are everywhere!

Regarding one claim, that small-ldl is particularly harmful while large-ldl is not so the paleos do not have to worry regarding their high ldls. This is likely incorrect according to this study.

"BACKGROUND: Previous studies showing that smaller low-density lipoprotein (LDL) size is associated with greater atherosclerotic risk did not adequately control for small and large LDL particle correlation. METHODS AND RESULTS: We studied the association of lipoproteins measured by proton nuclear magnetic resonance spectroscopy with carotid intima-media thickness (IMT) in apparently healthy individuals (N = 5538, 38% White, 28% African American, 22% Hispanic, 12% Chinese). Small and large LDL particle concentrations (LDL-p) were inversely correlated (r = /-0.63, P < 0.0001). Controlling for risk factors but not for LDL subclass correlation, LDL size and small LDL-p separately were associated with IMT (-20.9 and 31.7 microm change in IMT per 1-S.D., respectively, both P < 0.001), but large LDL-p was not (4.9 microm, P = 0.27). When LDL subclasses were included in the same model, large and small LDL-p were both associated with IMT (36.6 and 52.2 microm higher IMT per 1-S.D., respectively, both P < 0.001; 17.7 and 11.6 microm per 100 nmol/L, respectively). LDL size was not significant after accounting for LDL subclasses and risk factors (P = 0.10). CONCLUSION: Both LDL subclasses were significantly associated with subclinical atherosclerosis, with small LDL confounding the association of large LDL with atherosclerosis. Future studies of LDL size should account for the strong inverse correlation of LDL subclasses."
BACKGROUND: Previous studies showing that smaller low-density lipoprotein (LDL) size is associated with greater atherosclerotic risk did not adequately control for small and large LDL particle correlation. METHODS AND RESULTS: We studied the association of lipoproteins measured by proton nuclear magnetic resonance spectroscopy with carotid intima-media thickness (IMT) in apparently healthy individuals (N = 5538, 38% White, 28% African American, 22% Hispanic, 12% Chinese). Small and large LDL particle concentrations (LDL-p) were inversely correlated (r = /-0.63, P < 0.0001). Controlling for risk factors but not for LDL subclass correlation, LDL size and small LDL-p separately were associated with IMT (-20.9 and 31.7 microm change in IMT per 1-S.D., respectively, both P < 0.001), but large LDL-p was not (4.9 microm, P = 0.27). When LDL subclasses were included in the same model, large and small LDL-p were both associated with IMT (36.6 and 52.2 microm higher IMT per 1-S.D., respectively, both P < 0.001; 17.7 and 11.6 microm per 100 nmol/L, respectively). LDL size was not significant after accounting for LDL subclasses and risk factors (P = 0.10). CONCLUSION: Both LDL subclasses were significantly associated with subclinical atherosclerosis, with small LDL confounding the association of large LDL with atherosclerosis. Future studies of LDL size should account for the strong inverse correlation of LDL subclasses.
http://www.ncbi.nlm....pubmed/16765964

Edited by Blue, 05 October 2009 - 04:48 PM.

[Luna]

Google seems to find vitamin D is good to prevent breast cancer.. so I guess it's even a better idea

[ajnast4r]

Wasn't vitamin D related to breast cancer?
Or was it related to reduced breast cancer..

vitamin d reduced breast cancer incidence...along with most other cancers and most other common diseases. see the attached chart... adequate vitamin D levels are, imo, the #1 thing you can do for health & longevity.

http://www.grassroot...hart_101608.pdf
http://www.uctv.tv/s...px?showID=16940

also get your vitamin d into the 50-60ng/ml range

What is a good way to do this?

What do you all think about cod liver oil on this site? Or would some kind of multi-vitamin be better? (I'm looking into Ortho-Core because of reading this board)

an oil based d3 is best... get your levels tested, then add 1000iu to increase your blood levels by 10ng/ml. iherb carries good d3 supplement for cheap by jarrow and now. you can get your levels check for 40$ from http://www.grassrootshealth.net/

But cholesterol in the blood does cause heart disease, so where's the issue? I already said that just because a theory is refined (let's say for simplicity's sake that sat. fat has no influence on atherogenesis, even though, IIRC even Stephan admits that at least in certain contexts sat. fat may play a role), doesn't mean the theory is completely wrong.

I stand by my descrption. You created a strawmen ("sat. fact causes heart disease") even though it's a. not sure that sat. fat is innocent and b. more importantly not the only or even the most important part of the lipid "hypothesis". Please just adopt Stephan's more precise and less biased terminology: "The Diet[ary sat. fat and cholesterol]-Heart Hypothesis"; not lipid hypothesis.

pay this man

Regarding one claim, that small-ldl is particularly harmful while large-ldl is not so the paleos do not have to worry regarding their high ldls. This is likely incorrect according to this study.

pay this man

Attached Files

•  disease_incidence_prev_chart_101608.pdf   563.95KB   51 downloads

[gregandbeaker]

How variable day to day are lipid panels in normal adults? If I checked my lipid panel every day for a month how much variation would I see assuming my diet was pretty regular and consistent during that time?

[oprimitivo]

oprimitivo, I won't even address your red herring. Just one thing which is blatant: obviously CAD patients have low LDL, because they are treated with statins. For god's sake you posted a cross-sectional trial, do you think we're that stupid?

According to the American Heart Association study, "before admission, only 28,944 (21.1%) patients were receiving lipid-lowering medications". Notice these are lipid levels in the first 24 hours of admission. So, there were 78.9% patients not taking statins, and 21.1% on statins (for each 10 patients, only 2 were on lipid-lowering medications). Let do some elementary math here, considering lipid values of people aged 60-69 years, which are at higher risk of CAD (the average age of patients in the AHA study was 65 years):

average LDL_patients = 0.789*average LDL_patients(no_statins) + 0.211*average LDL_patients(statins)
What is the maximum average LDL lowering power of a statin? Well, it can't be much lower that 60 mg/dl (and the LDL oficial ATP3 goal is only 100 mg/dl), so let's be conservative and consider LDL_patients(statins) = 60 mg/dl
Then: 104.9 mg/dl = 0.789*average LDL_patients(no_statins) + 0.211*60 mg/dl
This is equivalent to average LDL_patients(no_statins) = 116.9 mg/dl

What's the average LDL value of the general population (60-69 years)? 127 mg/dl > 116.9 mg/dl (CAD patients & no statins, conservative value; should be a bit lower)
So, most CAD patients that are not taking statins do present some LDL deficiency when they are admitted to hospital.

Let's now do the same calculation for total cholesterol (TC):

average TC_patients = 0.789*average TC_patients(no_statins) + 0.211*average TC_patients(statins)
Minimum average TC on statins? I'm not sure but let be very conservative: TC_patients(statins) = 120 mg/dl?
if so, then: 174.4 mg/dl = 0.789*average TC_patients(no_statins) + 0.211*120
And then, average TC_patients(no_statins) = 189 mg/dl

What's the average TC of the general population (60-69 years)? 207 mg/dl > 189 mg/dl (CAD patients & no statins)
So, most CAD patients that are not taking statins also do present TC deficiency when they are admited to hospital.

You may notice that I was comparing average values here, and not maximum LDL or TC values, those that, according to the Lipid Hypothesis, are the cause of heart disease. This is not a problem because, from the statistical point of view, the population mean predicts the number of deviant individuals.

Main conclusion: most CAD hospitalized patients that are not taking statins DON'T present elevated LDL and/or TC values. On the contrary, they tend to show some CHOLESTEROL DEFICIENCY, because their average LDL and TC values are usually below the average values of the general population.

What's the problem with quoting a cross-sectional trial? Could you please be more specific?

Here is some good information from some "random blogs" (not from "well established medical institutions") regarding these cholesterol issues:

http://www.thincs.org
http://www.ravnskov.nu/cholesterol.htm
http://www.cholesterol-and-health.com
http://www.drbganima...rm.blogspot.com
http://high-fat-nutrition.blogspot.com
http://www.spacedoc.net

Edited by oprimitivo, 05 October 2009 - 07:05 PM.

[Blue]

Regarding the CAD hospital admission study, the study was certainly not a random sample. 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. You really need a random sample, like all those seeking for MI.

Their BMI was not very high compared to the US population at 28.9. Are you therefore arguing that obesity is not a risk factor?

[oprimitivo]

Regarding the CAD hospital admission study, the study was certainly not a random sample. 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. You really need a random sample, like all those seeking for MI.

Their BMI was not very high compared to the US population at 28.9. Are you therefore arguing that obesity is not a risk factor?

Hi Blue. I don't see why the factors you refer to should be considered limiting factors. Maybe I'm missing something, I'm not a specialist in these subjects.

Regarding IMC, I would first quote this NEMJ study: Overweight, Obesity, and Mortality in a Large Prospective Cohort of Persons 50 to 71 Years Old. It's conclusion, as we would expect, is that "excess body weight during midlife, including overweight, is associated with an increased risk of death." But if you look at the graphs on page 769, you will notice that, if your IMC is in the range 24-30 kg/m2, the relative risk of death doesn't vary much, but, anyway, it increases when IMC is higher that 27. This is what concerns total mortality, so as long as your IMC is not too extreme (outside the range 24-29 kg/m2), being slightly overweight perhaps should not be a major risk factor for your overall health.

Now, specifically about heart disease, let's see this study: Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies. If you see Figure 3 on page 17, IMC doesn't seem to be a major risk factor for stroke but it certainly is for IHD. So being overweight is for sure a risk factor for (or already a symptom of?) ischaemic heart disease.

About the AHA study, the 28.9 kg/m2 average IMC value means that most individuals hospitalized with CAD are overweight or even obese. What's the average IMC value of the general population? Well, from page 765, table 1, of the first study (older people, aged 50-71 years, who have higher CAD risk), I estimated an average value of 27.3 kg/m2. So, it's lower that the 28.9 value of the AHA study, meaning being overweight should also be a risk factor for CAD. Is it a major risk factor? I don't know, but I suspect there are other much more serious risk factors: hypertension, smoking, high carb/sugar/fructose diet, sedentary lifestyle, low vitamin D, stress / worrying too much about cholesterol, etc.

Edited by oprimitivo, 05 October 2009 - 09:11 PM.

[Blue]

Hm, so what you are not very clear regarding your opinion. Is being very obese like say having a BMI>40 a risk factor for heart disease in your opinion?

[oprimitivo]

Regarding the CAD hospital admission study, the study was certainly not a random sample. 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. You really need a random sample, like all those seeking for MI.

Their BMI was not very high compared to the US population at 28.9. Are you therefore arguing that obesity is not a risk factor?

Blue, one last thought: as much as I understand, the conclusion of the AHA study was that "These findings may provide further support for recent guideline revisions with even lower LDL goals and for developing effective treatments to raise HDL". Since these guidelines are for the general population, we may conclude that the AHA considers this study ("Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines.") representative enough, of the general population at risk for heart disease, in order to make general recommendations. So, if there were the "random sample problems" or any of the other problems you refer to, certainly they couldn't make their conclusions applicable for the general population, isn't' it? The same way, we can consider that this study is representative of the population hospitalized with CAD, and we can compare their blood lipid profiles with those of the general population, in order to evaluate if a certain parameter is raised or not, or if it should be considered a risk factor or not. Please anyone correct me if I'm wrong.

[oprimitivo]

Hm, so what you are not very clear regarding your opinion. Is being very obese like say having a BMI>40 a risk factor for heart disease in your opinion?

Being extremely overweight (BMI above 40 kg/m2) is a risk factor for most diseases of civilization, including heart disease!
At BMI 40, heart disease mortality is raised perhaps by a factor of 3 or even more.

Edited by oprimitivo, 05 October 2009 - 11:13 PM.

[Blue]

Regarding the CAD hospital admission study, the study was certainly not a random sample. 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. You really need a random sample, like all those seeking for MI.

Their BMI was not very high compared to the US population at 28.9. Are you therefore arguing that obesity is not a risk factor?

Blue, one last thought: as much as I understand, the conclusion of the AHA study was that "These findings may provide further support for recent guideline revisions with even lower LDL goals and for developing effective treatments to raise HDL". Since these guidelines are for the general population, we may conclude that the AHA considers this study ("Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines.") representative enough, of the general population at risk for heart disease, in order to make general recommendations. So, if there were the "random sample problems" or any of the other problems you refer to, certainly they couldn't make their conclusions applicable for the general population, isn't' it? The same way, we can consider that this study is representative of the population hospitalized with CAD, and we can compare their blood lipid profiles with those of the general population, in order to evaluate if a certain parameter is raised or not, or if it should be considered a risk factor or not. Please anyone correct me if I'm wrong.

Wrong interpretation and selective citation. Immediately before this they stated: "Ideal lipid levels (LDL
<70 mg/dL with HDL ≥60 mg/dL) are seen in only 1.4% of patients hospitalized with CAD." So obviously there were much room for improvement. They certainly never that that this a representative sample.

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.

Edited by Blue, 05 October 2009 - 11:20 PM.

[Blue]

Hm, so what you are not very clear regarding your opinion. Is being very obese like say having a BMI>40 a risk factor for heart disease in your opinion?

Being extremely overweight (BMI above 40 kg/m2) is a risk factor for most diseases of civilization, including heart disease!
At BMI 40, heart disease mortality is raised perhaps by a factor of 3 or even more.

But how can this be??? According to your own logic regarding lipids, since the patients in the study only had lipids similar to the population average, then lipids cannot be dangerous. By the same logic, since the patients had BMI similar to the population average, then BMI cannot be dangerous!!!

Edited by Blue, 05 October 2009 - 11:16 PM.

[oprimitivo]

Hm, so what you are not very clear regarding your opinion. Is being very obese like say having a BMI>40 a risk factor for heart disease in your opinion?

Being extremely overweight (BMI above 40 kg/m2) is a risk factor for most diseases of civilization, including heart disease!
At BMI 40, heart disease mortality is raised perhaps by a factor of 3 or even more.

But how can this be??? According to your own logic regarding lipids, since the patients in the study only had lipids similar to the population average, then lipids cannot be dangerous. By the same logic, since the patients had BMI similar to the population average, then BMI cannot be dangerous!!!

Of course it doesn't means lipids can't be dangerous if they are at abnormal levels (by analogy, BMI at 40 kg/m2 is extremely high and at these levels it becomes a major risk factor by itself). What I was saying is that since most people hospitalized with CAD don't present LDL higher than the LDL of the average population, this means LDL should not be considered the main reason for heart disease. Hypertension and diabetes are certainly more serious risk factors than elevated LDL, and are real diseases.

[Blue]

Hm, so what you are not very clear regarding your opinion. Is being very obese like say having a BMI>40 a risk factor for heart disease in your opinion?

Being extremely overweight (BMI above 40 kg/m2) is a risk factor for most diseases of civilization, including heart disease!
At BMI 40, heart disease mortality is raised perhaps by a factor of 3 or even more.

But how can this be??? According to your own logic regarding lipids, since the patients in the study only had lipids similar to the population average, then lipids cannot be dangerous. By the same logic, since the patients had BMI similar to the population average, then BMI cannot be dangerous!!!

Of course it doesn't means lipids can't be dangerous if they are at abnormal levels (by analogy, BMI at 40 kg/m2 is extremely high and at these levels it becomes a major risk factor by itself). What I was saying is that since most people hospitalized with CAD don't present LDL higher than the LDL of the average population, this means LDL should not be considered the main reason for heart disease. Hypertension and diabetes are certainly more serious risk factors than elevated LDL, and are real diseases.

Have you considered that most of the population may have bad lipids which may explain why heart disease is so common?

Again, this is not a representative sample of all people developing CAD. It is most likely a richer, better educated, more interested group than the average CAD patient. As such this study says little regarding the average CAD patient.

Furthermore, this is not a study of patients having their first symptom of CAD but a mix of various forms of patients with CAD many not hospitalized for acute reasons but elective procedures. Maybe these patients when they had their first clinical symptom, then they reduced their weight and improved their diet which improved their lipids. Again, the study says little regarding if lipids cause cause CAD.

[Cyberbrain]

My cholesterol improved so much after I increased my level of extra virgin olive oil, fish oil, I also ate dark chocolate.... I avoided animal fats as much as a I could. My HDL went from 39 to 59mg/dl

Total : 3.7 (144mg/dl).
HDL: 1.5 (59mg/dl)
LDL: 1.9 (74mg/dl,
Triglycerides: 0.6 (53mg/dl) - this for me can go as low as 35mg/dl.
Total Cholesterol : HDL Ratio 2.5

but i'm also on CR as you probably know...


Luna, you have plenty of time to experiment with which way will work for you. not like you're gonna get a heart attack anytime soon

Hey Matt! thank you for the reply
How do you increase those weird oils? :O

should I throw anything from my diet?

I think I am on CR.. usually :D
What else can I do?

I also like Matt's advice.

Since we're still young, imo we don't have to have a radical change in our lifestyles like some say. We don't need drugs or a a lot of supplements, and we don't need to stop eating our favorite foods.

What I do is simply eat a lot of fish, take omega 3 supps (about 1g a day), eat as many diverse and organic raw vegetables, use extra virgin olive oil, and of course exercise (though I'm not the best at this lol). Everything else you eat should simply be in moderation.

Cheers!

[dubcomesaveme]

 Cholesterol problems? Niacin. Check how much niacin you are consuming from your diet. Add niacin rich food like FRESH salmon. Niacin is one of the quickest ways to increase your HDL, exercising is another.

[CerebralCortex]

Eat a LOT more fat, especially saturated fat (from animals and virgin coconut oil). Saturated fat is the best fat to both improve your HDL, and you large LDL (the desirable kind of LDL). Avoid processed oils, especially any oil higher that 10% polyunsaturated fatty acids -- note that olive oil is okay, while canola oil should be avoided. Common modern oils like corn, soy, flax, and peanut oils should be avoided completely, processed or not.

What's wrong with peanut oils? I eat a lot of peanut butter.