The Triglyceride/HDL Cholesterol Ratio

For years, measurements of blood cholesterol have been used to assess the risk of heart disease.

We have been intensively educated about the role of LDL-cholesterol (LDL-C), commonly nicknamed the bad cholesterol and HDL-cholesterol (HDL-C), often called the good cholesterol.

For many different reasons, lowering LDL-C has become a primary goal in cardiovascular prevention. There is substantial evidence available suggesting a relationship between LDL-C and the risk of coronary heart disease.

What Is Non-HDL Cholesterol?Medical professionals usually recommend lifestyle measures that lower LDL-C and statins (cholesterol-lowering drugs) are used by millions of people worldwide for the sole purpose of lowering LDL-C numbers.

However, to understand coronary heart disease and how plaques form in our arteries (atherosclerosis) we have to understand that focusing only on cholesterol is an oversimplification.

Because cholesterol is a fat substance, it can’t mix with water and can therefore not travel in blood on its own. The body’s solution to this problem is to bind fat molecules to lipoproteins that function as transport vehicles carrying different types of fats such as cholesterol, triglycerides (TG) and phospholipids.

It is important to understand that it is lipoproteins that interact with the arterial wall and initiate the development of atherosclerosis. Cholesterol is only one of many components of lipoproteins.


The Lipid Panel

A standard lipid panel includes total cholesterol, LDL-C, HDL-C, and TG. Although LDL-C usually gets the bulk of the attention, evidence suggests that other aspects of the lipid profile may not be less important. For example, non-HDL cholesterol is a strong marker of risk, maybe more important than LDL-C.

Relying on LDL-C alone can be misleading. For example, people with obesity, metabolic syndrome or diabetic lipid disorders often have raised TG, low HDL-C and normal or close to normal LDL-C. These individuals produce very low-density lipoproteins (VLDL) and intermediate density lipoproteins (IDL) which may increase the risk of atherosclerosis.

Many studies have found that the triglyceride/HDL cholesterol ratio (TG/HDL-C ratio) correlates strongly with the incidence and extent of coronary artery disease. This relationship is true both for men and women.

One study found that a TG/HDL-C ratio above 4 was the most powerful independent predictor of developing coronary artery disease.

With the increasing prevalence of overweight, obesity, and the metabolic syndrome this ratio may become even more important because high TG and low HDL-C is often associated with these disorders.

The Triglyceride/HDL Cholesterol Ratio. What Is Ideal?

The TG/HDL-C ratio can easily be calculated from the standard lipid profile. Just divide your TG by your HDL-C.

However, when looking at the ideal ratio, you have to check if your lipid values are provided in mg/dl like in the US or mmol/L like in Australia, Canada, and most European countries.

If lipid values are expressed as mg/dl (like in the US);

TG/HDL-C ratio less than 2 is ideal

TG/HDL-C ratio above 4 is too high

TG/HDL-C ratio above 6 is much too high

If you are using mmol/L (most countries except the U.S.) you have to multiply this ratio by 0.4366 to attain the correct reference values. You can also multiply your ratio by 2.3 and use the reference values above.

If lipid values are expressed as mmol/L (like in Australia, Canada, and Europe);

TG/HDL-C ratio less than 0.87 is ideal

TG/HDL-C ratio above 1.74 is too high

TG/HDL-C ratio above 2.62 is much too high

In this article, TG/HDL-C ratio is provided as in the US (mg/dl).

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Triglyceride/HDL Cholesterol Ratio and LDL Particles?

Recently, analyzing the number of LDL particles (LDL-P) and LDL particle size has become increasingly common. However, this method is not universally available, is expensive, and has not been widely applied in clinical practice.

High numbers of small, dense LDL particles are associated with increased risk for coronary heart disease in prospective epidemiologic studies. Subjects with small, dense particles (phenotype B) are at higher risk than those with larger, more buoyant LDL particles (phenotype A).

Interestingly, it has been found that the TG/HDL-C ratio can predict particle size. One study found that 79% of individuals with a ratio above 3.8 had a preponderance of small dense LDL particles, whereas 81% of those with a ratio below 3.8 had a preponderance of large buoyant particles.

Apparently, people with high TG/HDL-C ratio tend to have higher than average TG. Just like all other lipids, TGs have to be transported in the blood by lipoproteins; most are carried by chylomicrons and VLDL.

What happens under these circumstances is an interchange of lipids between lipoproteins. TGs are moved from VLDL into LDL and HDL in exchange for cholesteryl ester. The result is that LDL and HDL particles become cholesterol poor and rich in TG. Then, when TGs are removed from these particles, which usually is the case, the particles shrink and become smaller as they’re only transporting small amounts of cholesterol. This explains the relationship between high TG/HDL-C ratio and the number of small LDL particles.

However, the number of LDL particles present in the blood may be more important than particle size. Furthermore, particle number appears more important than how much cholesterol is carried within these particles. Blood levels of LDL-P and apolipoprotein B are strongly correlated with the risk of coronary heart disease. Both these measurements reflect the actual number of LDL-particles.

But, can the TG/HDL-C ratio reflect particle number? As a matter of fact, it can, to some extent. Take a look at the LDL-C, the amount of cholesterol carried in LDL-particles. A high TG/HDL-C ratio indicates that these particles are small. A small particle carries less cholesterol than a large particle. Therefore, a greater number of particles is needed to carry a certain amount of cholesterol if the particles are small than if they’re large. So, a high TG/HDL-C ratio likely reflects a large number of LDL-particles, unless LDL-C is very low.

Triglyceride/HDL Cholesterol Ratio and Insulin Resistance

Insulin resistance is a condition in which cells fail to respond to the normal actions of insulin. Most people with this condition have high levels of insulin in their blood. Insulin resistance appears to play a significant role in coronary heart disease and can predict mortality. The condition is common among individuals with abdominal obesity and the metabolic syndrome.

A study in which most of the participants were Caucasian and overweight identified TG/HDL-C ratio of 3 or greater as a reliable predictor of insulin resistance.

However, not all studies have found the TG/HDL-C ratio to be associated with insulin resistance. For example, in a relatively small study of 125 African American participants, neither fasting TG nor the TG/HDL-C ratio was shown to be a marker of insulin resistance.

Although confirmatory studies are needed, data suggests that an elevated TG/HDL-C ratio may be clinically useful for the prediction of insulin resistance.

How to Improve Your Triglyceride/HDL Cholesterol Ratio

Improving your TG/HDL ratio aims at lowering TG, raising HDL-C or preferably both.

If you are overweight, losing weight will probably lower your TG levels and so will reducing your intake of added sugar. Studies have found that high intake of fructose leads to high TG. High-fructose corn syrup is a major source of fructose.

Low-fat diets are usually not effective in lowering TG. In fact, low-fat, high-carbohydrate diets may raise TG. Adding omega-3 fatty acids, regular exercise and limiting alcohol may be helpful to reduce TG.

Similar methods may be useful for raising HDL-C. Losing weight, exercising and not smoking may help. In controlled trials, low-fat, high-carbohydrate diets decrease HDL-C, thereby raising theTG/HDL-C ratio.

In 1961, a group of investigators from the Rockefeller Institute, led by Pete Ahrens published a paper entitled “Carbohydrate-induced and fat-induced lipemia”.

The authors pointed out that fat-induced increase in TG following a meal is a postprandial phenomenon (we all have high TG for a few hours following a fatty meal) caused by chylomicrons is different from the carbohydrate-induced rise in TG (later found to be caused by an elevation of VLDL).

These findings have been confirmed in several more recent studies. Despite this, low fat, high carbohydrate diets are still being recommended as a primary option to reduce the risk of heart disease.

Although low-fat diets may help to lower LDL-C, low-carbohydrate diets are more effective in improving the TG/HDL-C ratio.

This suggests that solely selecting LDL-C as a target in cardiovascular prevention is an oversimplification, and may have led to wrong conclusions regarding the relationship between diet and heart disease.

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Kevin O'Connell
Kevin O'Connell
5 years ago

4 years ago, I was eating HCLF and taking rosuvastatin (among other medications) with (US-type numbers): TC 171, HDL 66, LDL 63, TG 208 (TG/HDL 3.2). 3 years ago I switched to ‘Low-ishCHF’, stopped the statin (and other medications) and after 20 months like that (May 2013) had: TC 237, HDL 91, LDL 133, TG 64 (TG/HDL 0.7). Along the way (first 15 months) I dropped 36kg (ca. 30% body weight). Another year on, I have lost another 1-2kg and guess that my numbers remain about the same as last year, but see no reason to check them (my doctor… Read more »

Alfian Abdul Halin
5 years ago

the doctor who saw my numbers was freaking out…

TC 276
HDL 62
LDL 201
TG 68

But I’m freaking out too :'(
I think the LDL seems a bit high, although the ration of trig to hdl works out to 1.09…? Yes I know about what the article says. But can’t help noticing the higher LDL levels :'(

Lucy
Lucy
5 years ago

your numbers are very similar to mine. I have 250 cholesterol. 60 HDL and 62 triglycerides. My LDL is high. If I were going to fill my plate, I would put veggies on half the plate, a small piece of meat on the plate, a little fruit, and maybe some rice. I seriously eat like that. I don’t even like sugar and don’t even drink juice at all(no pop, no candy) whole grains. I think your case might be genetic like me. I tried statins and they made me sick! I have tried everything. There’s no way I am taking… Read more »

Amina98
Amina98
5 years ago

Read Dr. Perlmutter “Grain Brain.” His low carb, high fat diet is the way to go.

Dot Meindok, Esq.
5 years ago

Hi there. I just want to share with you all my story. I will skip the long background of destructive habits and eating and emotional trauma, etc…. I started seeing a fantastic doctor that began healing herself from progressive MS and went from near paraplegia to walking and back to teaching medicine! She did it all with food, nutrients and minerals. I was soooooooooooo skeptical at first. Really. But on my wits end decided I would give it try. I found I was sensitive to gluten (which I thought was a fad) and began eating differently. Almost Paleo. I was… Read more »

Fayyaz Rizvi
Fayyaz Rizvi
5 years ago

I live in Pakistan, how can I contact her.

Fhillsman
Fhillsman
5 years ago
Reply to  Fayyaz Rizvi

Dr. Wahl has a great book out called “The Wahl’s Protocol”. She offers three levels of nutrition plans. The one that worked for her was the Keto plan. I have been Keto for about 10 months now. Have lost weight and feel great. I highly recommend the Wahl’s book. I like a book called Keto Clarity too.

thePunkin8r
thePunkin8r
4 years ago
Reply to  Fayyaz Rizvi

Dr Terry Wahls is on Facebook, and yes, a ketogenic diet will even heal cancer, along with metabolic syndrome and diabetes. Internet search for Ketogenic diets, LCHF(LowCarbHighFat) diets and IF(IntermittentFasting-DrJasonFung – Intensive Dietary Management. Stay off starches i.e. all grains, sugars, potatoes etc. There is so much to learn on the internet! 🙂

Stef
Stef
4 years ago

LDL test normally is calculated using formula and can be way off. Ask your doctor to do actual LDL before getting concerned.

yaron
yaron
4 years ago

Yup.
As Stef mentioned, the LDL value was probably calculated using the Friedewald which isn’t that valid for high TG (>400) or low TG (<100). It is pretty complicated to calculate the real number of LDL particles (and their types – a or b), but in your case, it looks like the preferable way to go.

Giora
Giora
5 years ago

Lucy
I may have some information for you that can help you.Email me and I will forward to you a webinar that explain it and suggests what to do.
Giora Zeevy
Health Coach
[email protected]

Disqus11111
Disqus11111
4 years ago
Reply to  Giora

what exactly is a health coach and what credentials are required to label yourself such?

Tikamporn Keerati
Tikamporn Keerati
4 years ago

I was on LCHF for a year.
TC 283
HDL 47
LDL 222 raise shaply
TG 69 drop sharply
I think I eat too much.

Jugnu Shah
Jugnu Shah
3 years ago

The above lipid values are after LCHF diet or before?

Billuk
Billuk
5 years ago

Try telling this to NICE in the UK. Think the target for intervention is approximately 3.2 LDL-C with statins, might be wrong.

Kent Chapman
Kent Chapman
5 years ago

Great piece.

What do you think of the waist-to-hip ratio as another indicator of the risk for heart disease?

Eric Wertheim
Eric Wertheim
5 years ago
Reply to  Kent Chapman

I first heard about the ‘apple-ass’ versus the ‘pear-ass’ theory of determining health-risk around 1990 but not much since. More recently I have read some articles about fat build-up above the hips being dangerous. I think there is a meaningful relationship between the two concepts. If true, this would be an extremely helpful way of determining one’s state of risk. I suppose the unscientific basis seems frivolous to many people (and doctors?) so research was not continued. However, I think it merits further study.

Surfdancer
Surfdancer
4 years ago
Reply to  Eric Wertheim

Eric, there’s lots of research on abdominal circumference being linked to many diseases, not just heart disease. Larger abdominal circumferences (more than half your height in inches, measured right across the belly button), will increase your risk of diabetes, heart disease, stroke, cancer and many other diseases. Belly fat is unlike other fat in the body, in that it is METABOLICALLY ACTIVE. It doesnt just sit there for cusion and warmth- it sends hormones out which interfere with the heart’s actions, especially the rhythm of beating. Stress, sugar, alcohol, processed foods, being sedentary, all contribute to greater belly fat. Eating… Read more »

Ken McMurtrie
5 years ago

A question please, Dr Sigurdsson, Regarding the units of the measurements of respective levels of the individual componenets, which can be mmol/L, or mg/dl. I can understand that to create a ratio number, in this case between TG and HDL-C the same units of measurement need to be used for each item. I don’t understand why a change of units, providing the same unit is used for both components, can need any further conversion when comparing ratios and assessing ‘safe’ ratio levels. In other words, a ratio of say 4 for TG/HDL-C measured in mmol/L should be equivalent to the… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Ken McMurtrie

@ Ken. When Triglycerides and HDL are converted from mg/ml to mmol/L, different constants are used causing the ratio to be different. Let’s take an example. Person A has TG 80 mg/dl and HDL-C 40 mg/dl. His TG/HDL-C ratio is 80/40 = 2. If we convert (you can use the convertor here) his numbers to mmol/l: TG 0.90 and HDL-C: 1.03. The TG/HDL ratio will be 0.87. You would have had the same result if you multiplied by 0.4366. 0.4366 x 2 = 0.87 If you are using mmol/L but want to use the US reference (which is easier to… Read more »

John
John
5 years ago

To further clarify, the reason is because when converting from mg to mmol, each substance’s mass is divided by its own molecular weight (which are not the same). The ratio of the molecular weights of TG and HDL is 0.4366, which is how that number is getting introduced, so you have to mathematically “undo” this by multiplying by 0.4366.

Christopher Palmer
Christopher Palmer
5 years ago

Axel, thank you so much for such an inspiring post. I do so agree with the way your opinions and posts appear to be trending. The father of the fat/cholesterol hypothesis thought work by Anitschkow and Chalotov (1913) proved cholesterol to be an atheorgen. But their result was really artefact and confounding error. Cholesterol impurities produced the results. Neither they nor Keys knew this and it was not until 1976 the error was properly illuminated. Keys needed a reason to explain his perceived phenomenon of hypercholesterolemia. He sensed fat in the diet might promote hyopercholesterolemia (high levels of cholesterol in… Read more »

Mie
Mie
5 years ago

Axel,

“However, low fat diets are still being recommended as a primary option to reduce the risk of heart disease.”

Err, no, they aren’t. Unless you’re referring to Ornish et co.

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Mie

@ Mie You commented on the following conclusion in my article “However, low fat diets are still being recommended as a primary option to reduce the risk of heart disease.” by writing “Err, no, they aren’t. Unless you’re referring to Ornish et co” I have to disagree with you. The authors of the 2013 AHA/ACC Guidelines on Lifestyle Management to Reduce Cardiovascular Risk point out that “randomized clinical trials examining the examining the effects on hard outcomes (MI, stroke, heart failure and CVD-related death) are difficult if not impossible to conduct for several reasons (e.g. long term adherence to dietary… Read more »

GoianiaHeights
GoianiaHeights
4 years ago

not too sure what mie is trying to say. altho some awareness has been raised, esp in the US, I would say institutions and industry are not rejecting low-fat and keys. i also want to remind you that the developing world takes only the simplified information from the US. here in brazil, low-fat is still gospel amongst the majority of professionals and the media!!! 🙁

Mie
Mie
5 years ago

Christopher,

isn’t it high tine to move on from the 50s/60s? The medical community has, but for some people it seems impossible to let go off Keys – despite the fact that his initial ideas (mind you, later on he disgarded the idea of total fat being the problem and focused on fat type AND especially of the ENTIRE dietary pattern) have nothing to do with Axel’s post.

Christopher Palmer
Christopher Palmer
5 years ago

I regret Mie I cannot discern if you are agreeing/complementing my comment or challenging/disagreeing with it. I challenge your point that the medical community has moved on from the 50s/60s. It has but only in the sense that it is commonplace to adopt the fat/cholesterol hypothesis as virtuous and true. It isn’t. That dietary fat (with specific emphasis on saturated fat) might raise cholesterol and that raised cholesterol causes heart disease has been the consistent mantra within general practice, primary prevention, and cardiology for six decades and shows only marginal signs of giving way. I have been witness to Axels… Read more »

smartersig
5 years ago

My cholesterol ratios are OK but it took me 20 months of personal research to reveal that my Homocysteine levels are quite high at 22. During the 20 months since I had a heart attack coming off one of my customary runs I have never been given a Homocysteine check. When I asked my doctor about getting one he said we do not offer it, not even if you are willing to pay. Here in the UK we are hopelessly behind in practice and thinking. I had to explain to my GP what an LDL particle size was, he had… Read more »

Mie
Mie
5 years ago

Christopher, “I regret Mie I cannot discern if you are agreeing/complementing my comment or challenging/disagreeing with it.” I thought it was obvious? I couldn’t understand the reason to bring Keys into the discussion here. Notice the past tense “couldn’t” – your latest message clarified the reason why you did this. I’ll address it later. “I challenge your point that the medical community has moved on from the 50s/60s. It has but only in the sense that it is commonplace to adopt the fat/cholesterol hypothesis as virtuous and true. It isn’t.” First of all, lipid hypothesis and diet/heart hypothesis aren’t the… Read more »

Mie
Mie
5 years ago

Axel, “In my mind this is a low fat approach. Basically the same thing that has been advocated fro 40-50 years.” You’re somewhat cutting corners here. There’s NO mention of how many percent of total E should come from fat (or the other macronutrients for that matter). And DASH, which is low on total fat, isn’t the only dietary pattern mentioned. The same goes for ESC guidelines https://www.escardio.org/guidelines-surveys/esc-guidelines/GuidelinesDocuments/guidelines-CVD-prevention.pdf Nothing about total fat. Nada. “But I doubt that an approach, focusing on two targets (LDL-C and hypertension) is of much help.” Well not to those who have no problems with these.… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Mie

@ Mie In fact there is mention of percent fat in the AHA/ACC Guidelines. The two diet patterns recommended are a Mediterranean (MED) type diet and DASH. According to the paper, “The MED patterns examined tended to be moderate in total fat (32% to 35% of total calories), relatively low in saturated fat (9% to 10% of total calories), high in fiber (27 to 37 g/day), and high in polyunsaturated fatty acids (particularly omega–3s)”. The guideline’s authors own words on DASH: “The DASH dietary pattern is high in vegetables, fruits, low-fat dairy products, whole grains, poultry, fish, and nuts; and… Read more »

Christopher Palmer
Christopher Palmer
5 years ago

Mie, If I asked you to give a brief account of your take on the business of atherogenicity how might you describe the process? If I asked you to name the most potent f the established atherogens which biochemicals would you name? If I invited you to discuss the issue of ‘convergence’ that must apply to risk factors and the pathophysiology of the proliferation of atheromas how might you go about this? If I invited you to discuss the difference between stable plaques and unstable ones that rupture what ’cause’ might you identify to account for the ‘effect’? Does the… Read more »

Mie
Mie
5 years ago

How about this: instead of trying to hide the fact that you offered a dose of nonsense (incoherent blabbering about Keys, fat etc. etc. you posted earlier) by asking a bunch of questions NOT related to the topic of Axel’s post, comment on the issue at hand.

If not, answer your own questions instead.

Mie
Mie
5 years ago

Axel, “In fact there is mention of percent fat in the AHA/ACC Guidelines. The two diet patterns recommended are a Mediterranean (MED) type diet and DASH.” Yes, there’s a mention of fat (as in “the amount of fat of total E”) in the case of these two dietary patterns. However, nowhere is it stated that these two are the ONLY alternatives. And there’s no convincing indication that total fat, unless you go super-low or super-high, has a role in decreasing/increasing CVD risk. “By the way, because you mention hypertension it is worth pointing out that a systematic review and meta-analysis… Read more »

Mie
Mie
5 years ago

Ah, for some reason the link to the review didn’t appear in your post when I read it first? Ok, thanks for the reference. Yes, it seems that I was right on the money: in short-term trials, low carb works in lowering blood pressure – as do a number of other dietary patterns, too.

Ken McMurtrie
5 years ago

@ Axel, re unit conversions.
ok, thanks for your reply.
A millimole (mmol) is apparently not a measure of mass, but of “an amount of substance”, obviously not simply mass.
So we are not, as I was thinking, converting from one mass/volume figure to another mass/volume figure.
Appreciate your forbearance.

michael goroncy
michael goroncy
5 years ago

It is my understanding/novel research that CHD/CVD is precipitated by inflammation. (1) Hyperglycaemia oxidises LDL (2) This oxidised LDL works it’s way under the endothelium and forms plaque. (3) The plaque will gradually build up and eventually rupture causing an infarct. So! a Heart attack will primarily occur with (a) Electrical current causing V Fib. Causing the heart to go spasmodically s**thouse and end in cardiac arrest (low survival rate) (b) Heart attack (infarct) where heart muscle dies, leaving a % of the heart depleted. This % of damage is expressed as a ‘Ejection Fraction’ which determines the blood flow… Read more »

smartersig
5 years ago

Care to share what sup’s and meds you are on please ?

michael goroncy
michael goroncy
5 years ago
Reply to  smartersig

Yo! smartersig
I repleid to your question.
It did noy get through….sorry, but i won’t re-produce the post. I did not save it.

Christopher Palmer
Christopher Palmer
5 years ago

Michael, Hi. I think what you say is broadly correct. 1) It is oxidative stress that delivers atherogenic agents to the site where the atheroma will form. 2) The atherogenic agents interfere with the behaviour of cells destabilising them, making them less viable and killing some. Results have been obtained in vivo and vitro. 3) When cells are destabilised and, say, smooth muscle cells in the area begin dying other cells are triggered into response. The response in part is to invoke healing mode. 4) That de-differentiation of cells may take place is a possibility, and that alteration to electrical… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago

@ Christopher
Thanks for your comments. I appreciate your input. However, please avoid such lengthy posts with so much off topic discussion. I usually reject such comments because I don’t think people read them and they take up a lot of space. The purpose of the discussion is to debate around the subject presented in the blog article.

Mie
Mie
5 years ago

“Mie, has accused me of spamming and posting off-topic. I cannot think why.” Perhaps the fact that you try to “educate” people here by uttering oh-so-goddamn-obvious claims as “good and bad cholesterol are misleading terms” etc. etc. and the fact that you – evidently without ANY regard for integrity and honesty – spread out the same lies as n other internet spam bots might have something to do with it? And e.g. here “The notion began with a weird notion of surplus cholesterol doing harm. Cholesterol only does good. It does no harm.” you provide further evidence for the matter.… Read more »

Christopher Palmer
Christopher Palmer
5 years ago

Thanks Axel, you make a good point. People appreciate explanations that are simple and concise, and that is understandable. Even the people advising NICE are much the same. They think the case for lipid modification through prescription of pharmacological agents makes for good policy, and they asses the patients risk factors through the QRISK2 calculation tool, whose computation relies heavily upon the results of the lipid profile test. the case for lipid modification is based more upon absence of evidence than upon evidence, and a lot of the distraction stems from this obsession with those ‘cholesterol’ numbers. Unfortunately simple and… Read more »

Mie
Mie
5 years ago

Christopher wrote:

“Even the people advising NICE are much the same. They think the case for lipid modification through prescription of pharmacological agents makes for good policy, and they asses the patients risk factors through the QRISK2 calculation tool, whose computation relies heavily upon the results of the lipid profile test.”

Gee, wonder why? Perhaps due to the fact that both are soundly founded on existing evidence on CVD risk factors and disease management/prevention?

Cholesterol denialism is a zombie that just won’t die, now matter what.

JamesK
JamesK
5 years ago

Recently, I had to fire both my primary physician and cardiologist. Despite my moving the Trig/HDL ratio into very favorable territory (1.1 – mg/dl), they both kept insisting that I needed statins due to higher than normal LDL-C (my particle size is phenotype A). Both doctors demanded I switch my diet back to the high carb, low fat diet that I had abandoned two years ago. Prior to my changing to a moderately low carb/high fat diet, my Trig/HDL ratio was consistently in the danger zone – as high as 9.3! My trigs are well below 100 now and HDLs… Read more »

Mark Kiser
Mark Kiser
3 years ago
Reply to  JamesK

James ~ If you don’t mind, I would like to know more about how you got your TG/HDL ratio down from 9:3 Mine is currently at 8 and I need to make some major changes. I’ve already had a mild heart attack at 43 and had a stint implanted. I have changed over to a low car/ high fat diet and taking supplements. Please email me at: [email protected]

LDL Richard
LDL Richard
5 years ago

Axel, a critic to your text would say that risk-predictor is not a synonym with a causal factor. Low carb results in better trig/hdl ratio, so? Does this translate to a) regression of CHD within the artery wall and/or b) less risk of developing clinical cardiadic event? The early experimental scholars induced severe atherosclerosis in rabbits and mices by feeding them cholesterol and saturated fats….standard textbook material. The early critics pointed out that rabbits were vegeterians and thus the result might not have relevance to humans. The experimental scholars responded by designing an experiment in which the serum of a… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  LDL Richard

Richard. This figure from The Framingham study clearly show that cholesterol levels are associated with risk of CAD (coronary artert disease). However, there is a lot of overlap. High cholesterol is present among many individuals with no CAD and low cholesterol is present among many with CAD. It all comes down to the fact that people are different. For some people cholesterol levels certainly appear important when it comes to assessing risk and target treatment. For other people cholesterol appaears less important and other aspects of the lipid profile or inflammatory markers (hs-CRP) may become more important. Regarding the experimental… Read more »

Ben
Ben
5 years ago

“I have yet to locate doctors in my area of the U.S. who have moved away from the antiquated, conventional low fat, low cholesterol paradigm. It’s unfortunate, but my impression from personal experience is that the old model of heart disease still rules at the ground level of medical practice.” JamesK is living prof that medicine is now so sophisticated there are barely any healthy people left. Even people who take initiatives to improve markers and profiles for health and achieve results still feel pressured to succumb to the diagnosis and prescription that stems from ‘counting cholesterol’. Something is amiss… Read more »

Mie
Mie
5 years ago

Richard, everything doesn’t evolve around mere LDL count as there are people in whom it isn’t enough as a risk predictor nor can CAD prevention on population level be reduced to examining mechanisms in the formation of atheroma – problems understanding that?

And Axel, surely we all do realize that on a population level risk factors don’t mean that everyone with one is going to get CAD? Why point out the obvious?

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Mie

Mie. It, I don’t think its obvious at all, although it may to you. If cholesterol is an important causative factor, why doesn’t everyone with high levels get atherosclerosis?. Well I would guess it’s because other factors come into play, and because cholesterol’s role as a causative factor is minimal. Isn’t cholesterol merely a passenger that happens to be there?. This also highlights another question. How can we tell when high cholesterol is important and when it’s not? Many people reach high age with extremely high cholesterol levels, without ever taking statins. How can we differentiate those who may benefit… Read more »

LDL Richard
LDL Richard
5 years ago

Doc, cigarette’s CAUSE lung cancer, yet most smokers don’t get lugn cancer. Many of them do, though. Moreover, we need to seperate atherosclerosis as a a) process within the artery wall and b) atherosclerosis as a clinical manifestation, cardiadic events. This is the root of confusion. All Western people have atherosclerotic arteries at old age due to cumulative exposure to high LDL but not all of us have cardiadic event during our lifetime. Cardiadic events can reduced even though atherosclerotic process within the artery is progressing. Evidence based meditation protocol, lowering blood pressure, loosing weight, smoking cessation etc all helps… Read more »

David Brown
5 years ago

Christopher Palmer wrote, ” If oxidative stress is the cause of CVD then the lipid profile test informs very little indeed.” Good point. There’s frequent mention of oxidative stress in relation to arterial damage but the role of omega-6s is rarely mentioned. It’s interesting that calves cannot tolerate soybean oils unless their ration of skim milk and soybean oil also contains sufficient vitamin E to prevent oxidative stress. For decades, researchers testing alternatives to butter fat on veal calves, found that polyunsaturated seed oils made calves sick ultimately killing many of them. Beef tallow and lard caused no problems. In… Read more »

Mie
Mie
5 years ago

Axel, “Mie. It, I don’t think its obvious at all, although it may to you. If cholesterol is an important causative factor, why doesn’t everyone with high levels get atherosclerosis?. Well I would guess it’s because other factors come into play, and because cholesterol’s role as a causative factor is minimal. Isn’t cholesterol merely a passenger that happens to be there?” Oh please. Do you really need to be explained the etiology of CAD vs the pathophysiology of atheroma? Risk factors vs mechanism? (Richard already mentioned this, although simplified it somewhat). You know this all. Then why ask such a… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago
Reply to  Mie

Mie.
It’s not a simple as that. Sometimes treatment decisions are based solely on LDL-C. The AHA/ACC guidelines recommend statins to all individuals with LDL-C above 190 mg/dl (4.9 mmol/L).

In fact it seems that you’re totally missing my point here and deliberately trying to twist my words. I’ll let our discussion rest here. Furthermore, remember that I usually reject comments that are impolite and disrespectful.

RichardLDL
RichardLDL
5 years ago

Doc, you can perceive cholsterol as ionizing radition (stochastic risk).More ionizing radiation, more cancer in a given population, but not all individuals exposed to radiation get cancer. Some individuals are protected from cancer. When cholesterol levels are a high in a given population very many suffer cardiadic event, even when food additives, excess weight gain, McDonald’s, Coca-Cola etc are entirely absent in this population (f.ex see Finnish baseline cohort data at the 7CS). However, when cholesterol levels in a given population are <3,7mmol/l atherosclerotic CHD is basically non-existent. There's a hefty ecologic data to back this assertion. Mie, btw, did… Read more »

Mie
Mie
5 years ago

Axel, “Sometimes treatment decisions are based solely on LDL-C. The AHA/ACC guidelines recommend statins to all individuals with LDL-C above 190 mg/dl (4.9 mmol/L).” Sometimes, yes. You’re right. I mentioned Finnish guidelines which don’t recommend treating mere elevated LDL unless it’s very high, 6 mmol/l. “In fact it seems that you’re totally missing my point here and deliberately trying to twist my words. I’ll let our discussion rest here. Furthermore, remember that I usually reject comments that are impolite and disrespectful.” If you feel I missed something, please don’t let it rest. If I was mistaken, I’d prefer an explanation… Read more »

RichardOrnishForLife
RichardOrnishForLife
5 years ago

Doc,

the upcoming president of your professional body, American Collage of Cardiology, shares his ideas about a healthy diet. This is the stuff I’ve been trying to tell your for what…years, now. But you choose to bang your head in the wall. You exemplify the fact that in the future we need to force doctors to adopt new treatment protocols. We cannot rely on their own judgement since stubborn cranks like you, who get it 180-degree wrong are always present among us.
https://www.medpagetoday.com/Cardiology/Prevention/46860

Axel F Sigurdsson
Admin
Axel F Sigurdsson
5 years ago

@ Richard.
I’ve never said anything negative on my blog about vegan diets. I may have said that they’re hard to stick with. Otherwise I think people do very well on vegan diets in terms of cardiovascular risk.
So I’m not sure there is so much disagreement between us, apart from the fact that I don’t prefer using words like “stubborn cranks” when communicating with other people. I’m letting this one pass, but generally I reject comments that are impolite and disrespectful. You should know that by now.

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