70 replies to this topic

[DukeNukem]

LDL is not only associated with atherosclerosis, it is actually a causative factor for heart disease/atherosclerosis.

Wow, this myth still persists, I guess.

Here's some handy reading: It's the start of a long series, but it'll catch you up with modern science:
http://eatingacademy...lesterol-part-i

~~~~~

Ok, let's put that eggs-is-worse-than-cigarettes study in the coffin for good. It never made any sense to begin with, and it turns out to be just another case of poor science.

http://healthcorrela...-egg-study.html

http://www.zoeharcom...ue-bad-science/

[hivemind]

LDL is not only associated with atherosclerosis, it is actually a causative factor for heart disease/atherosclerosis.

Wow, this myth still persists, I guess.

No, not a myth. More like a law of nature at this point. Scientific evidence supporting it is just massive.

There are no real experts in the world who oppose the lipid hypothesis. Not one.

http://en.wikipedia....ipid_hypothesis

There is a scientific consensus.

Edited by hivemind, 20 August 2012 - 07:30 PM.

[hivemind]

LDL is not only associated with atherosclerosis, it is actually a causative factor for heart disease/atherosclerosis.

Here's some handy reading: It's the start of a long series, but it'll catch you up with modern science:
http://eatingacademy...lesterol-part-i

Wow, did Duke just link this article? This series of articles actually tells you what I already said: LDL is the cause of atherosclerosis AND it is a causative factor for heart disease

Now we can argue whether or not the LDL-P measurement is necessary. (many experts think it's not, except maybe for some special cases)
However, this argument has nothing to do with the fact that LDL is a cause of heart disease and NOT A MYTH.

Edited by hivemind, 20 August 2012 - 08:39 PM.

[James Cain]

Yeah, I was wondering why Duke thought that series of (very well reasoned, referenced, and presented, IMO) articles supported the "LDL doesn't matter" thinking.

[Godot]

Sorry to digress but does anyone have any tips on what to mix with avocado? Avocado really agrees with my body. I just struggle with the taste of it. It is creamy and there isn't anything wrong with that. It's the other taste it has which I can't really describe that makes it a chore to eat.

I tried mixing it with bacon as I thought the saltiness of the bacon would overpower the 'bleh' taste of avocado but unfortunately the avocado won the battle.

I might try it with a big chunky piece of gammon in a salad. Take that avocado?!

Why am I persisting with avocado? I think anything that is natural and improves my wellbeing and libido is worth keeping. Plus it's highly nutritious (decent mineral content), generally insulin friendly (in comparison to other fruits already mentioned such as mangos), has healthy fats and leaves me feeling centred, alkalized and full!

Any tips on improving its laborious taste?

Avocado is *delicious* when prepared with plenty of lemon juice, high quality sea salt (I like Malden), and fresh ground black pepper.

[TheFountain]

Fruit juices (aka sugar bombs) shut down your fat-burning metabolism for 3-4 hours. (A well-known fact for years.)

Orange juice limits postprandial fat oxidation after breakfast in normal-weight adolescents and adults.
Caloric beverages may promote weight gain by simultaneously increasing total energy intake and limiting fat oxidation.
http://www.ncbi.nlm....pubmed/22798004

Other sugar bombs: starchy vegetables like potatoes and carrots, grains of any type including rice, alcoholic drinks, sugary fruits like bananas. (Generally, if you must peel your fruit then it's not worth eating, because most beneficial nutrients are in the skin where they protect the fruit from the elements and bacteria -- the inside is where nature stores the energy in the form of sugars.)

If this hypothesis is true then I should have high body fat percentage from the 5-6 bananas I eat daily, the giant asiatic sweet potatoes I consume, all the lentils, all the oatmeal, all the other 'sugary' fruits. Right?

Here is a picture of my body that I took while on a fairly high fruit diet for several months straight. Yes I was also consuming berries during the course of this diet. But I was also consuming a lot of banana's as mentioned, plums, pears, grapes, sweet potatoes.

But get this, my dietary fat intake was on the low side! And in addition I was eating those nasty, icky seeds! Sunflower seeds, pumpkin seeds, you name it! If it was a SUGAR BOMB or a PUFA BOMB, I ATE IT! And guess what else? My A1C score was 4.6! OH........MY............GOD! I wonder how I pulled off a body fat percentage of about 10% on such a terrible diet?

Oh and did I mention that I was only exercising 2-3 times a week, and nothing extreme even?

Edited by TheFountain, 20 August 2012 - 09:52 PM.

[hivemind]

http://www.ncbi.nlm....pubmed/22818725

However, when within treatment group comparisons are made, consumption of 75 g dried apple (about two medium-sized apples) can significantly lower atherogenic cholesterol levels as early as 3 months. Furthermore, consumption of dried apple and dried plum are beneficial to human health in terms of anti-inflammatory and antioxidative properties.

http://www.ncbi.nlm....pubmed/22854401

In comparison with sucrose alone, ingestion of sucrose with whole berries resulted in reduced glucose and insulin concentrations during the first 30 min and a slower decline during the second hour and a significantly improved glycemic profile. Berries prevented the sucrose-induced late postprandial hypoglycemic response and the compensatory free fatty acid rebound. Nearly similar effects were observed when sucrose was consumed with berry nectars. The improved responses were evident despite the higher content of available carbohydrate in the berry and nectar meals, because of the natural sugars present in berries.

[hivemind]

Yeah, I was wondering why Duke thought that series of (very well reasoned, referenced, and presented, IMO) articles supported the "LDL doesn't matter" thinking.

Now I know why Duke linked that article series. It has some biased low carb propaganda in it.

But there is also some good stuff there. He definitely does not say that high LDL is good.

Edited by hivemind, 21 August 2012 - 12:22 AM.

[hivemind]

LDL is not only associated with atherosclerosis, it is actually a causative factor for heart disease/atherosclerosis.

Wow, this myth still persists, I guess.

Here's some handy reading: It's the start of a long series, but it'll catch you up with modern science:
http://eatingacademy...lesterol-part-i

http://www.lipid.org...Panel Paper.pdf

Better information. That blog you linked is not very accurate or unbiased information.

There are no studies to formally assess the incremental
risk prediction achieved by measurement of LDL subfractions
above and beyond traditional lipid measures
and nonlipid risk factors.
 There are no prospective studies to show that a treatment
strategy of changing LDL subfractions is superior to traditional
lipid-lowering therapy in terms of atherosclerosis
progression or CV morbidity and mortality.

Should LDL subfraction be a target of therapy?
If not, how should LDL subfractions affect
treatment decisions?
Several investigators have suggested that lifestyle
change and pharmacologic treatment can change LDL
particle distribution.208,209,224,225 However, such shifts are
always accompanied by changes in LDL-C concentration
and/or change in LDL-P, and often by changes in other lipoprotein
fractions (eg, HDL-C and triglyceride levels) or
nonlipid risk factors (eg, weight loss, improved insulin sensitivity,
improved blood pressure with lifestyle modification).
To date, there is no evidence that the shift in LDL
subfractions directly translates into change in disease progression
or improved outcome.

All lipoprotein particles in the LDL fraction are
atherogenic, independent of size.

LDL-P measurement is more for the unhealthy/sick people:

Individuals with elevated triglycerides or low
HDL-C manifest progressively greater elevations of
LDL-P concentrations at a given level of LDL-C.166,175
In observational studies of patients with type 2 diabetes
mellitus or metabolic syndrome and LDL-C ,100 mg/
dL (,20th percentile), discordantly elevated LDL-P levels
greater than the 20th percentile (.1000 nmol/L) occur in
75% of subjects.172,174 Similar results have also been
shown for patients with type 2 diabetes mellitus and
LDL-C ,70 mg/dL.172 In addition, discordance between
LDL-C and LDL-P levels frequently occurs in patients receiving
statin therapy because statins lower the LDL-C
concentration to a greater degree than the LDL-P
concentration

Low risk (,5% 10-year CHD event risk)
It is the consensus of the NLA Biomarkers Expert Panel
that treatment decisions are unlikely to be altered by use of
LDL-P among low risk patients. Hence, measurement of
LDL-P was ‘‘not recommended’’ for this patient group.

Intermediate risk (5–20% 10-year CHD event risk)
It is the consensus of the NLA Biomarkers Expert Panel
that there are a substantial number of patients for whom
LDL-C may not accurately reflect CVD risk. On the basis
of the data showing that discordantly elevated LDL-P is
more strongly associated with incident CVD risk than
LDL-C level,167,173 measurement of LDL-P is thought to be
‘‘reasonable for many patients.’’ When LDL-P is discordantly
elevated, consideration should be given to initiating
or intensifying LDL lowering therapy. Conversely, a more
conservative treatment approach could be considered for
patients with lower LDL-P values than predicted based on
their LDL-C (or non-HDL-C) concentrations. Populations
known to manifest increased prevalence of discordance (elevated
LDL-P for the level of LDL-C or non-HDL-C) include
patients with metabolic syndrome,171,174 as well as
those with low HDL-C and/or elevated triglycerides.

If you are a healthy person with healthy cholesterol levels, then standard lipid panel is fine. Don't get confused with all this stuff the low carb bloggers write about.

Edited by hivemind, 21 August 2012 - 01:06 PM.

[hivemind]

http://www.lipid.org...Panel Paper.pdf

[hivemind]

If you are a healthy person with healthy cholesterol levels, then standard lipid panel is fine. Don't get confused with all this stuff the low carb bloggers write about.

I'll add to this that if you have family history of heart disease, then it seems some of those additional tests are beneficial.

This panel accepted the ATP III definition of a premature
family history, namely of the presence of CHD before age
55 years in a male and before age 65 years in a female firstdegree
relative. Apo B received a ‘‘reasonable for many
patients’’ recommendation based, in part, on the fact that
FCH is the most common atherogenic dyslipoproteinemia
associated with premature CHD, far more common, in
fact, than familial hypercholesterolemia. Moreover, the clinical
risk associated with FCH is similar to the clinical risk
associated with heterozygous familial hypercholesterolemia.

Edited by hivemind, 21 August 2012 - 01:30 PM.

[DukeNukem]

Yeah, I was wondering why Duke thought that series of (very well reasoned, referenced, and presented, IMO) articles supported the "LDL doesn't matter" thinking.

The point of that article is that LDL, as a category, is NOT linked to heart disease. Only certain types of LDL are (in general, small particle LDL, the type created by eating too many carbs, and/or vegetable oils high in polyunsaturated fatty acids).

Calling LDL "bad cholesterol" betrays supreme ignorance of LDL, its absolutely essential role to health, and how it can be deformed (by a bad diet) into unhealthy versions.

Statins do not work, quite simply, because they only reduce the good type of LDL, not the heart disease causing small particle LDL. So, total LDL is reduced, and ignorant doctors think they've done something good. And yet, LDL count is not associated with CVD. In fact, if there's any association at all, it's that low LDL leads to heart disease.

Edited by DukeNukem, 22 August 2012 - 08:43 PM.

[James Cain]

The point of that article is that LDL, as a category, is NOT linked to heart disease. Only certain types of LDL are (in general, small particle LDL, the type created by eating too many carbs, and/or vegetable oils high in polyunsaturated fatty acids).

Calling LDL "bad cholesterol" betrays supreme ignorance of LDL, its absolutely essential role to health, and how it can be deformed (by a bad diet) into unhealthy versions.

Statins do not work, quite simply, because they only reduce the good type of LDL, not the heart disease causing small particle LDL. So, total LDL is reduced, and ignorant doctors think they've done something good. And yet, LDL count is not associated with CVD. In fact, if there's any association at all, it's that low LDL leads to heart disease.

Duke, I really respect you and I generally follow along with what you say, but this makes it apparent you didn't read the article series, or perhaps you're thinking of a different series. I will summarize so nobody gets the wrong idea.

The author says that LDL particles are associated with the development and progression of heart disease, and that the higher your LDL-P the worse off you are. He says that LDL-C is a surrogate marker to estimate LDL-P, but that this doesn't always work very well depending on the particle size. It can sometimes be assumed that larger LDL particle size for a given amount of LDL-C means each LDL particle has more cholesterol, and thus you have fewer particles, and thus a less atherogenic (less, not non-atherogenic) profile. However, as with using LDL-C to estimate LDL-P, particle size isn't always useful on it's own, and in general is only determined in tests that measure LDL-P anyway, which is the really useful number. He provides evidence that regardless of any other factor (meaning pretty much nothing else matters at all), LDL-P is the only direct measure of atherogenic potential. LDL is necessary for the development and progression of atherosclerosis, and the more particles the more this is possible. The author also goes on to discuss HDL and how to a large degree doesn't protect from elevated LDL-P.

Of course you could have a large amount of LDL floating around with no impetus for it to enter the endothelium, but I'd suggest that this is basically impossible. This isn't to say that low-carb, high-fat, Paleo, etc. diets can't be beneficial in many ways, or even be an improvement for avoiding heart disease, but these diets and their principles in no way invalidate the lipid hypothesis. If you have any evidence that LDL particles don't contribute to heart disease otherwise, please share.

[hivemind]

Yeah, I was wondering why Duke thought that series of (very well reasoned, referenced, and presented, IMO) articles supported the "LDL doesn't matter" thinking.

The point of that article is that LDL, as a category, is NOT linked to heart disease. Only certain types of LDL are (in general, small particle LDL, the type created by eating too many carbs, and/or vegetable oils high in polyunsaturated fatty acids).

Calling LDL "bad cholesterol" betrays supreme ignorance of LDL, its absolutely essential role to health, and how it can be deformed (by a bad diet) into unhealthy versions.

Statins do not work, quite simply, because they only reduce the good type of LDL, not the heart disease causing small particle LDL. So, total LDL is reduced, and ignorant doctors think they've done something good. And yet, LDL count is not associated with CVD. In fact, if there's any association at all, it's that low LDL leads to heart disease.

All lipoprotein particles except HDL are atherosclerotic. LDL particles are the most atherosclerotic particles. All LDL subfractions cause atherosclerosis.
As you can see from that chart I posted: the LDL subfraction analysis is not recommended for anybody.
LDL is essenial to health of course. The problem is that people have too much of it.

Statins do work:




Your last sentences are just pure ignorance. I can't believe somebody still thinks like that. The lipid hypothesis has been proven beyond any reasonabe doubt. The amount of evidence is huge. I recommend you read this book:

Edited by hivemind, 23 August 2012 - 01:52 AM.

[Hebbeh]

LDL is essenial to health of course. The problem is that people have too much of it.

How much is too much? I eat 2 eggs every single day and my cholestrol is never over 140. Actually, the last test was 141 and that was the highest it's been. Before eating eggs, my choloestrol had been tested as low as 105 and I feel much much better now.

edit: and I can post results.

Edited by Hebbeh, 23 August 2012 - 02:28 AM.

[Hebbeh]

LDL is essenial to health of course. The problem is that people have too much of it.

How much is too much? I eat 2 eggs every single day and my cholestrol is never over 140. Actually, the last test was 141 and that was the highest it's been. Before eating eggs, my choloestrol had been tested as low as 105 and I feel much much better now.

edit: and I can post results.

Attached Files

•  Hebbeh Cholesterol.jpeg   44.15KB   31 downloads

[TheFountain]

Hey guys, the last time I had my cholesterol checked this is what it came out to.

Triglycerides-57

HDL-80

LDL-90


Thoughts?

[James Cain]

All lipoprotein particles except HDL are atherosclerotic.

HDL can also contribute to atherosclerosis through a number of mechanisms. Apo A-I, and other functional protein on the HDL particle, can become oxidized or modified by an inflammatory environment just as LDL can, and this not only impairs HDL's reverse cholesterol transport function, but it can actually make the particle pathogenic. Here are some good summaries:




http://www.ncbi.nlm....pubmed/21304474

HDL and cardiovascular disease: atherogenic and atheroprotective mechanisms.

Nat Rev Cardiol. 2011 Apr;8(4):222-32. Epub 2011 Feb 8.
Navab M, Reddy ST, Van Lenten BJ, Fogelman AM.
Department of Medicine, David Geffen School of Medicine, UCLA, 10833 Le Conte Avenue, Los Angeles, CA 90095-1679, USA. mnavab@mednet.ucla.edu

Abstract
The lipoprotein HDL has two important roles: first, it promotes reverse cholesterol transport, and second, it modulates inflammation. Epidemiological studies show that HDL-cholesterol levels are inversely correlated with the risk of cardiovascular events. However, many patients who experience a clinical event have normal, or even high, levels of HDL cholesterol. Measuring HDL-cholesterol levels provides information about the size of the HDL pool, but does not predict HDL composition or function. The main component of HDL, apolipoprotein A-I (apo A-I), is largely responsible for reverse cholesterol transport through the macrophage ATP-binding cassette transporter ABCA1. Apo A-I can be damaged by oxidative mechanisms, which render the protein less able to promote cholesterol efflux. HDL also contains a number of other proteins that are affected by the oxidative environment of the acute-phase response. Modification of the protein components of HDL can convert it from an anti-inflammatory to a proinflammatory particle. Small peptides that mimic some of the properties of apo A-I have been shown in preclinical models to improve HDL function and reduce atherosclerosis without altering HDL-cholesterol levels. Robust assays to evaluate the function of HDL are needed to supplement the measurement of HDL-cholesterol levels in the clinic.

PMID: 21304474

http://www.ncbi.nlm....pubmed/14638544

Inflammatory/antiinflammatory properties of high-density lipoprotein distinguish patients from control subjects better than high-density lipoprotein cholesterol levels and are favorably affected by simvastatin treatment.


Circulation. 2003 Dec 2;108(22):2751-6. Epub 2003 Nov 24.
Ansell BJ, Navab M, Hama S, Kamranpour N, Fonarow G, Hough G, Rahmani S, Mottahedeh R, Dave R, Reddy ST, Fogelman AM.
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, Calif 90095-1679, USA.

Abstract
BACKGROUND:
The inflammatory/antiinflammatory properties of HDL were compared with HDL cholesterol in 2 groups of patients and in age- and sex-matched control subjects.

METHODS AND RESULTS:
Group 1 consisted of 26 patients not yet taking a statin who presented with coronary heart disease (CHD) or CHD equivalents by National Cholesterol Education Program Adult Treatment Panel III criteria studied before and 6 weeks after 40 mg/d of simvastatin. Group 2 consisted of 20 patients with documented CHD and HDL cholesterol > or =84 mg/dL. The inflammatory/antiinflammatory properties of HDL were determined by the ability of the subject's HDL to alter LDL-induced monocyte chemotactic activity (MCA) in a human artery wall coculture. Induction of MCA by a control LDL was determined in the absence or presence of the subject's HDL. Values in the absence of HDL were normalized to 1.0. Values >1.0 after the addition of HDL indicated proinflammatory HDL; values <1.0 indicated antiinflammatory HDL. Group 1 values before simvastatin were LDL cholesterol, 118+/-24 mg/dL; HDL cholesterol, 57+/-13 mg/dL; triglycerides, 125+/-64 mg/dL; and high-sensitivity C-reactive protein (hs-CRP), 1.7+/-1.9 mg/L; and MCA values were 1.38+/-0.91, compared with 0.38+/-0.14 for control subjects (P=1.5x10(-5)). After simvastatin, values were LDL cholesterol, 73+/-24 mg/dL; HDL cholesterol, 61+/-14 mg/dL; triglycerides, 99+/-52 mg/dL; and hs-CRP, 1.3+/-1.3 mg/L; and MCA values were 1.08+/-0.71. In group 2, values were LDL cholesterol, 108+/-34 mg/dL; HDL cholesterol, 95+/-14 mg/dL; triglycerides, 89+/-44 mg/dL; and hs-CRP, 0.8+/-0.7 mg/L; and MCA values were 1.28+/-0.29, compared with 0.35+/-0.11 for control subjects (P=1.7x10(-14)). Similar results were obtained with the cell-free assay.

CONCLUSIONS:
The inflammatory/antiinflammatory properties of HDL distinguished patients from control subjects better than HDL cholesterol and were improved with simvastatin.

PMID: 14638544

[hivemind]

Hey guys, the last time I had my cholesterol checked this is what it came out to.

Triglycerides-57

HDL-80

LDL-90


Thoughts?

High LDL which is good. LDL is good too, but could maybe be even lower (50-70). Triglyserides are good.

http://www.tcolincam...Hash=4d17bdc0d0

LDL cholesterol: According to the NCEP, LDL cholesterol levels below 100mg/dL are considered ideal. A range of 100 to 129 mg/dL is near optimal. Borderline is 130 to 159 mg/dL. High is 160 to 189 mg/dL. However, increasing evidence supports stricter standards. Many researchers and clinicians believe that 100 mg/dL should be the upper limit for everyone, and some recommend reductions below 70 mg/dL for high-risk individuals.

Studies of hunter-gatherer populations and normal newborn babies have modified the concept of normal cholesterol levels. Normal human LDL cholesterol concentration may be as low as 50 to 70 mg/dL. Coronary heart disease risk decreases as LDL cholesterol concentration decreases, and may reach its lowest level at approximately 40 mg/dL.

Edited by hivemind, 23 August 2012 - 12:29 PM.

[niner]

As you can see from that chart I posted: the LDL subfraction analysis is not recommended for anybody.

I would prefer to have at least one inexpensive VAP test rather than waiting for the first heart attack or stroke.

Edited by niner, 23 August 2012 - 03:02 PM.

[hivemind]

As you can see from that chart I posted: the LDL subfraction analysis is not recommended for anybody.

I would prefer to have at least one inexpensive VAP test rather than waiting for the first heart attack or stroke.

If you have total cholesterol under 150 your whole life and no family history of CVD you are not going to get that first heart attack.

If you want to avoid stroke you should be measuring your blood pressure instead of LDL subfractions..

Edited by hivemind, 23 August 2012 - 07:15 PM.

[TheFountain]

Hey guys, the last time I had my cholesterol checked this is what it came out to.

Triglycerides-57

HDL-80

LDL-90


Thoughts?

High LDL which is good. LDL is good too, but could maybe be even lower (50-70). Triglyserides are good.

http://www.tcolincam...Hash=4d17bdc0d0

LDL cholesterol: According to the NCEP, LDL cholesterol levels below 100mg/dL are considered ideal. A range of 100 to 129 mg/dL is near optimal. Borderline is 130 to 159 mg/dL. High is 160 to 189 mg/dL. However, increasing evidence supports stricter standards. Many researchers and clinicians believe that 100 mg/dL should be the upper limit for everyone, and some recommend reductions below 70 mg/dL for high-risk individuals.

Studies of hunter-gatherer populations and normal newborn babies have modified the concept of normal cholesterol levels. Normal human LDL cholesterol concentration may be as low as 50 to 70 mg/dL. Coronary heart disease risk decreases as LDL cholesterol concentration decreases, and may reach its lowest level at approximately 40 mg/dL.

Who are "high risk" individuals? And is 90 really high for these individuals? You saw my physical condition a few posts up, I don't know.

If you have total cholesterol under 150 your whole life

Really? 150? Regardless of how much of it is LDL vs HDL?

What is your current diet and regimen and what is your total number?

[Hebbeh]

And is 90 really high for these individuals? You saw my physical condition a few posts up, I don't know.

In reality, you're just a kid....so you better be at your peak condition...because it doesn't get any better...you only get older. And you're vegan too, aren't you? Check back in 30 years when you're 55 and see how it's working for you. I'm 55 and my numbers are still better....so you must be doing something wrong. And as far as physical condition?.....you look like a kid...what more is there to say?

[niner]

As you can see from that chart I posted: the LDL subfraction analysis is not recommended for anybody.

I would prefer to have at least one inexpensive VAP test rather than waiting for the first heart attack or stroke.

If you have total cholesterol under 150 your whole life and no family history of CVD you are not going to get that first heart attack.

If you want to avoid stroke you should be measuring your blood pressure instead of LDL subfractions..

Are you sure about that? Isn't total cholesterol a poor predictor of heart attack? I discovered from a VAP test that I have high lp(a). I'd rather know that than be in the dark about it.

[hivemind]

Who are "high risk" individuals? And is 90 really high for these individuals? You saw my physical condition a few posts up, I don't know.

If you have total cholesterol under 150 your whole life

Really? 150? Regardless of how much of it is LDL vs HDL?

What is your current diet and regimen and what is your total number?

I think your risk is very low with those numbers. Your HDL is very high. It might be unnecessary for you to lower your LDL.
Yes, with 150 I don't think one has worry that much about LDL vs. HDL.
I have not taken the test recently. I am taking it soon, that's why I have been studying this stuff recently.
My diet is plant based, low in cholesterol and saturated fat, relatively low in fat and animal products.
About 1.2 grams of protein per kg of body weight, about 20-25% fat(mostly unsaturated) and a lot of starch and fresh vegetables and berries plus fruit also.

Edited by hivemind, 24 August 2012 - 01:56 AM.

[Hebbeh]

Who are "high risk" individuals? And is 90 really high for these individuals? You saw my physical condition a few posts up, I don't know.

If you have total cholesterol under 150 your whole life

Really? 150? Regardless of how much of it is LDL vs HDL?

What is your current diet and regimen and what is your total number?

I think your risk is very low with those numbers. Your HDL is very high. It might be unnecessary for you to lower your LDL.
Yes, with 150 I don't think one has worry that much about LDL vs. HDL.
I have not taken the test recently. I am taking it soon, that's why I have been studying this stuff recently.
My diet is plant based, relatively low in fat and animal products.

You're changing your tune now....his total C has to be approaching 200....so what is it?

And you never answered me... in spite of eating 2 eggs every day and being 55...I have numbers you claim are unachievable for an egg eater....explain.

Attached Files

•  Hebbeh Cholesterol.jpeg   44.15KB   10 downloads

[hivemind]

You're changing your tune now....his total C has to be approaching 200....so what is it?

And you never answered me... in spite of eating 2 eggs every day and being 55...I have numbers you claim are unachievable for an egg eater....explain.

I'm not changing my tune. I am shooting for LDL between 50-70 and total under 150. But he has a huge HDL level. His risk is probably pretty low even with that LDL of 90, but of course even he would probably lower his risk by lowering his LDL. It just depends on how strict you want to be and what is a significant risk reduction. If you use the Framingham risk calculator, you can see that such a high HDL gives a massive risk reduction. The thing is, that even if HDL might not be a causative factor, it is associated with something that has a powerful protective effect.

I am not saying they are unachievable for an egg eater. I know a guy who eats much more eggs than 2 per day and has a TC value considerably under 150.

edit: even your HDL of 60 is so high that you will probably not die with a little bit more relaxed LDL number.

Edited by hivemind, 24 August 2012 - 02:21 AM.

[hivemind]

Are you sure about that? Isn't total cholesterol a poor predictor of heart attack? I discovered from a VAP test that I have high lp(a). I'd rather know that than be in the dark about it.

http://www.lipid.org...Panel Paper.pdf

Yes, lp(a) is more useful it seems than the LDL subfractions. You are probably right that lp(a) is useful, but it is not recommended for standard measurement for low risk people without a family history of CVD by that expert panel. I would want to know my lp(a) too.

Edited by hivemind, 24 August 2012 - 02:45 AM.

[algae]

Grains, Vegetarians, Vegans and Nutritional Density
This article seems to claim to encompass all vegans, but compares eating grains and fruit to omnivores; completely ridiculous. There are some other big holes in that article, most notably admitting there are successful vegetarian societies but not vegan societies. This is true, but you can't actually believe dairy is necessary? Vegan foods are far more nutritionally dense than animal products, and you won't be able to show me any nutrients I need that I can't get from a vegan diet. Could you please point me to the secret nutrient I can't get in a more nutritionally dense form from vegan foods?

I'll give you some examples:
Spirulina is 65% complete protein, higher than any animal source
Moringa leaf has many times the calcium of milk, potassium of bananas, and more

But let me also say, I'm not completely vegan because I love the taste of dairy cheese. However, I feel much better eating completely vegan, and for me, that's the biggest indicator that it's good for me. I am aware that active forms of B12 aren't found in plants, and that probiotics only create inactive forms of B12. I'm not convinced people need active forms of B12, maybe the inactive forms are somehow OK. I'm assuming your opinion on this is that we need meat for B12, and that Indians shouldn't be alive?

[rwac]

I'm not convinced people need active forms of B12, maybe the inactive forms are somehow OK. I'm assuming your opinion on this is that we need meat for B12, and that Indians shouldn't be alive?

Indians drink milk and eat plenty of milk products, mainly yogurt and cheese. Not even remotely vegan.