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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.
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.
Atherogenic dyslipidemia is a clinical disorder characterized by high TG/HDL-C ratio, elevated levels of apolipoprotein B, and high concentration of small LDL particles.
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).
Triglyceride/HDL Cholesterol Ratio and LDL Particles?
Recently, analyzing the number of LDL particles (LDL-P) and LDL particle size has become more 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.
123 thoughts on “The Triglyceride/HDL Cholesterol Ratio”
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 says ‘get them checked in another 4 years!’)
Ir seems to me that my health has improved immeasurably and, at least for me, the TG/HDL seems to be a useful ratio.
the doctor who saw my numbers was freaking out…
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 :'(
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 statins. I figure if I die I die. I just can’t feel like hell on statins all the time. I am trying this supplement called syntrinol now. I doubt it will work, because nothing works. Good luck to you.
I have similar numbers to yours, not quite as good on the Trig/HDL ratio but at point I was at 7.65, now at 2.1 so much improved. Satans also made me very sick though it was insidious and took me 10 YEARS to realize that they were causing me problems. Have been off them for 3 years now and will never5 go on them again. High LDL may not be all that bad. Your comment is 6 years old as I write this and I hope you are still doing well.
Read Dr. Perlmutter “Grain Brain.” His low carb, high fat diet is the way to go.
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 insulin resistant with little hope, hypothyroid, finromyalgia, inflamed and you name it. A Gulf War veteran.
My TG/HDl ratio was way above 3. After 2 short months – it is 1.62!
My TC/HDL ratio was over 4-5 and is now: 2.7!
My LDL/HDL ratio was nearly 3 and is now 1.5!
My HDL has increased from 40 to 75 mg/dL.
My Tris have dropped from 139 to 122.
My LDL from 139 to 103 using the Friedewald formula.
I sleep much better knowing these changes are taking place because my father’s younger brother died as a child due to inflammation. My father died at 48 from CAD associated with cholesterol and inflammations.
Not to mention the 23 pounds lost and 3 inches from waist and hips.
I would recommend checking our Dr. Terry Wahl.
I do not think you will regret it.
Good health and prayers to ALL!
I live in Pakistan, how can I contact her.
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.
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! 🙂
LDL test normally is calculated using formula and can be way off. Ask your doctor to do actual LDL before getting concerned.
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.
According to my doctor if TG and HDL are almost the same and less than 100 we do not have to worry about the Total cholesterol. My TC is 300 ( kind of high) but the TG is almost the same as the HDL. My weight is ok and I exercise daily and eat well.
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.
what exactly is a health coach and what credentials are required to label yourself such?
I was on LCHF for a year.
LDL 222 raise shaply
TG 69 drop sharply
I think I eat too much.
The above lipid values are after LCHF diet or before?
Look up Dave Feldman channel on youtube and he will explain why some people see increased LDL on low carb diet. He also has a website https://cholesterolcode.com/
Try telling this to NICE in the UK. Think the target for intervention is approximately 3.2 LDL-C with statins, might be wrong.
What do you think of the waist-to-hip ratio as another indicator of the risk for heart disease?
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.
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 lots of non starchy veggies, especially greens, lean protein, avoiding sugar, even juice, too much fruit, having healthy fats and staying active (not just for your workout, but throughout the day) and managing stress levels will melt the belly fat. Don’t need special
pills or ab machines. Simply working your abdominal muscles, which lie UNDER the fat, will not melt belly fat. You need to eat cleanly and exercise large muscle groups to do this. Hope this is helpful to some.
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 ratio 4 when the measurements are in mg/dl.
I hope this is a valid question.
@ 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 remember), you can multiply your ratio by 2.3, e.g. 0.87 x 2.3 = 2.
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.
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 blood) and he majored his concern upon saturated fat.
Now, I can sense Keys reasoning that added dietary fats place a call for additional cholesterol to be supplied to the digestive track, and that additional cholesterol carrying lipoproteins would be passed over the gastrointestinal divide and find their way into the blood, but for the life of me I cannot see how saturated fats above all others would result in this supposed effect. Then, to complicate matters, lipoproteins fashioned in the GI track do not enter the blood directly. Instead they are called chylomicrons, despite they are still lipoproteins of a kind, and they enter the lymph system. Ergo, chylomicrons do not show up in blood test.
Besides, just as you indicate, the supply of glucose to, and the presence of insulin in, the blood have more bearing upon lipid profile counts, profiles, and ratios than do fats in the diet. The effects of a high fat diet upon cholesterol levels is actually counter intuitive to the Keys view and that promoted by the fat/cholesterol hypothesis.
Neither saturated fat or cholesterol are the major issue, while certain oxides of cholesterol and homocysteine are evidentially implicated in the business of atherogenicty that is the makings of CVD and thence promotes risk of cardiovascular events such as heart attack and stroke. The principle oxides of cholesterol to be concerned for are cholestane-3B,5a,6B-triol, 25-hyrdroxycholesterol, and perhaps 7-ketocholesterol. In all probability methyl deficiency permits the rise in oxidative stress that may result in conversion of numbers of cholesterol molecules to certain cholesterol oxides.
I would like you to be made aware that this post of yours, more than any other stimulus, proved the inspiration to write a concise and summary 2000 word review that suggests what’s wrong with the fat/cholesterol hypothesis and what is most likely most correct about its much needed successor. It just needs finalising and then I would hope to be able to share it with you one way or another.
Thank you for becoming a luminary casting light upon and advancing the truth on cholesterol and CVD.
“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.
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.”
“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 changes). The Work Group prioritized topics for evidence review and was unable to review the evidence on hard outcomes for dietary patterns and physical activity”
“The results of the Work Group systematic review are the 10 lifestyle recommendations (8 dietary and 2 physical activity recommendations)” – these are provided in a table. The recommendations are aimed at two risk factors, LDL-C and blood pressure.
These are the main points of the recommendations (table 5 in the paper):
Consume vegetables fruits, whole grains, low fat dairy products, poultry, fish, legumes, non-tropical vegetable oils and nuts; and limit intake of sweet, sugar sweetened beverages and red meats.
Aim for a dietary pattern that achieves 5-6 % of calories from saturated fat
Reduce percent of calories from saturated fat
Reduce percent of calories from trans fat
Achieve this pattern by following a plan such as the DASH dietary pattern, USDA food pattern, or the AHA diet.
Lower sodium intake
Consume no more than 2.400 mg/sodium/d.Further restriction to 1.500 mg/ day may further improve blood pressure.
In my mind this is a low fat approach. Basically the same thing that has been advocated fro 40-50 years.
Don’t misunderstand me though. I think this approach is appropriate in many situations. However, such guidelines have limited applications for the clinician. What I am highlighting in my writing is that we have to look further. People are different. There are other targets, other approaches that may be helpful. Look at all the people with the metabolic syndrome, type 2 diabetes for example. Of course I know the US guidelines were not supposed to cover these problems. But I doubt that an approach, focusing on two targets (LDL-C and hypertension) is of much help.
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!!! 🙁
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.
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 contributions to debate on cholesterol, upon diet, and upon CVD both here and elsewhere, especially upon the blog of Dr John Briffa. Hence I know Axel has been wrestling with the issues for a while, and I have some sense of how Axels opinions have trended. For what it’s worth, which is not much, his views are trending in the right direction.
The great problem with the fat/cholesterol hypothesis is that cholesterol is a hugely functional and ubiquitous molecule with a great dived in biology. Vertebrates have great need of cholesterol while plants have no need whatsoever. Cholesterol accounts for a great deal of difference between a vertebrate and a cabbage. Cholesterol holds the membranes of eukaryote cells together and provides for lipid rafts which can ferry important lipids across membranes.
The key thing to note is that cholesterol does not initiate the change in the behaviour of cells within the endothelial layer of the tissues of the artery that gives rise to the formation of atheromas, or ‘fatty plaques’. Also worth noting is that in the history of the formation of the hypothesis its founder, Dr Keys, never realised impurities in batch samples used in animal trials could have accounted for the results. Key impression of cholesterols capacity to cause atheromas was false. Certain oxides of cholesterol gave rise to the effect while neither the early trialists or Keys realised this was the case. More in the 70s and 80s it was establsihed that pure cholesterol is innocuous when tested in vivo and in vitro trials whereas certain oxides of cholesterol gave rise to atherogenesis. If you tried to suggest that my remarks were impertinent you could not be further from the truth.
Yes, Keys did amend his views over the years. It’s right he should.
In 1957 Yerushalmy and Hillboe exposed how Keys misused data to concoct his ‘six countries study’ alleging correlation between national consumption of saturated fat and heart related mortality. Keys 1953 study was sham science. Keys took data from the WHO, the data itself was second rate for having no standard method of collation, but the WHO had available data for 22 countries. Keys selected just six. The 22 proved no association, only the selected six did that.
Keys also coined the term Mediterranean diet and did much to promote the notion. Actually there are all manner of reasons why the Mediterranean lifestyle and environmental experience differs from that of the urbanised countries of more temperature latitudes. Keys did much to have the establishment convince almost everybody that diet is paramount. Diet is important up to a point, but there are other factors that are causally implicated in the etiology of CVD. Low fat high carbohydrate diets have been championed as representing diminished risks for CVD, yet this is actually the reverse of the truth.
The key to understanding the real cause of heart disease is to appreciate that oxidative stress is the big driver of risk of atherogenicity. Oxidative stress is not an easy concept to grasp but levels of oxidative stress are always present within the body. Levels of oxidative stress can rise above that which is merely basal, and stress is a big driver of this, so too is methyl deficiency.
Methyl deficiency arises when not enough antioxidants of the right kind are available to donate methyl groups (CH3) to reactive oxygen species to ‘zap’ them and detoxify them. being stressed raises competition for methyl groups and so can determine there are not enough donors to match demand. When this happens level;s of a substance called homocysteine rise and homocyteine may convey oxidative stress the way of cholesterol resulting that some cholesterol molecules are converted to certain oxides of cholesterol. This then has bearing for the behaviour of cells and degeneration of tissues of the artery sets in.
Mie, you may think you are contributing to the discussion but your remarks read like you are scoffing at comments passed by people who have given matters more contemplation than you have. If you are malcontent it is better and healthier for you to address the cause. And do not get me wrong, there is much about our world to be malcontent about.
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 no idea. Needless to say I am now on the B vits in an attempt to lower the Homocysteine. Any advice welcome
“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 same things. This
“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.”
implies that you’re mixing them up on purpose. Of course diet has a role in CVD prevention- this has been established – and the development of atherosclerosis but it cannot be reduced the SAFA as such. Nope, it’s a lot more complicated. However, lipid levels in BLOOD are what counts and improving them isn’t just about the diet alone, let alone the fat content in one’s diet. And yes, lipid levels (such as increased levels of e.g. LDL) have been proven to be a risk factor (you do know what a “risk factor” is, don’t you?). To suggest anything else is to utter a religious statement.
Now, this doesn’t mean that they’re the ONLY thing that matters in the development of atherosclerosis and/or that we know every little detail there is to know. Nonetheless, the amount of the irrelevant Internet mumbo-jumbo, including the fraudulent “Keys-faked-data” claim, you chose to spam at the end of your message doesn’t contribute to this nor does it change anything. It’s just crap that people who sell popular books and rule the low carb/paleo forums spew out. I’ve seen it thousands of times. No new information, no facts, no nothing except a virulent meme.
“Mie, you may think you are contributing to the discussion but your remarks read like you are scoffing at comments passed by people who have given matters more contemplation than you have.”
You’re probably the last person who should complain that I’m not “contributing”. Stating that nonsense is nonsense is contribution too. Science advances by sorting out disinfo from info. Axel brought out information concerning TG/HDL ratio and its role in predicting CVD risk. You chose to spam his blog with religious dogma. Unfortunately so.
“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
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. But bear in mind that particularly hypertension management (by diet) is a major issue nowadays. And guidelines are by no means there to limit the clinician’s practical work in cases where the problem is e.g. low HDL and high TG etc.
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 low in sweets, sugar-sweetened beverages, and red meats. The DASH dietary pattern is low in saturated fat, total fat, and cholesterol“.
So, I guess it’s a matter of definition (or opinion for that matter), whether the AHA/ACC approach is low-fat or not.
By the way, because you mention hypertension it is worth pointing out that a systematic review and meta-analysis has shown a very positive effect of low carbohydrate diets on both systolic and diastolic blood pressure.
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 lipid profile test account for qualitative variation amongst lipoproteins?
How did we get so hung up on those ‘cholesterol numbers’ in the first instance?
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.
“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 has shown a very positiev effect of low carbohydrate diets on both systolic and diastolic blood pressure”
Care to provide a reference? A variety of higher quality diets (that is, diets that aren’t the standard Western diet) improve blood pressure. E.g. vegetarian:
And Med (not a review but from a recent RCT):
I have no doubt that low carb diets can show similar benefits. But are they better than the abovementioned alternatives?
Well, let’s see the paper you mentioned. 🙂
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.
@ 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.
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 that the heart can pump in and out through the ventricles.
I experienced an MI in 1988 at age 38.
Since then, I have changed diet radically, got educated with this c**t of a disease, and survive on medication and supplements.
Care to share what sup’s and meds you are on please ?
I repleid to your question.
It did noy get through….sorry, but i won’t re-produce the post. I did not save it.
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 balances in the zone may take place highly likely. Cells can have an embryonic phase. In this phase they lack differentiation of function seen in mature tissues. They are cells that haven’t adopted specialised function.
5) All cells maintain electrical potential. The potential inside a cell differs with space around it. This is called resting potential. There is a pd even across the bilayer of the cells membrane. This means there are gradients of electrical potential across interfaces that delineate the cell, its structure, and the medium beyond. These potentials govern what and how stuff may pass in and out. Some metabolites and signalling molecules are ions, and some are zwitterions. Zwitterions are shifty, They have polar charge, but the charge they display is responsive to aspects of the medium around. That an alteration to resting potential displayed by a cell can influence the the greeting it signals to ions and zwitterions especially is implied.
6) De-differentiation and re-differentiation has been achieved under study and while details may be sketchy the mechanism may be that alterations to potential and the flow of weak currents has bearing for DNA. The current reorganises the methyl switches that flag a gene as being turned on or off. The first phase of healing then is to recode epigenetic tags (switches) so that cells can revert to basic type, then as healing advances the epigenome (switching layer attached to genes) is recoded so cells begin to form alternate ‘species’ and take on specialised function.
7) Heat is generated when energy meets with resistance. When medics mention ‘inflammation’ the term doesn’t mean much beyond saying heat is present. The heat arises because current is flowing, as ions perhaps, and is meeting with resistance. Inflammation is evidence of an immune or healing response in which the flow of ions or electricity signals something to cells.
8) Oxides of cholesterol get interesting. They seem to signal something to cells, adjusting or interfering with the way cells behave. Some cholesterol oxides seem to have legitimate physiological function, some can interfere with enzymic expression, some interfere with HMG-Co reductase and inhibit it, and some seem just plain toxic to cells.
9) LDL, nor any other lipoprotein, can become oxidised. However reactive oxygen species, antioxidants, and oxidised lipids may be present in lipoproteins. In other words liporteins can harbour oxidised agents.
10) LDL may convey oxidised lipids to the LDL receptors in the region but it is not the LDL that does the harm, it is aspects of its constituents that are present. That lipoproteins, including LDL, can convey oxidised cholesterol molecules alongside ‘healthy’ cholesterol ought not be in doubt.
11) The study of cholesterol oxides has resulted some have been identified as being cytotoxic and/or atherogenic. Prominent atherogens in the family of cholesterol oxides are cholestane-3beta,5alpha,6beta-triol and 25-hydroxycholesterol. Another potent atherogen is homocysteine which is a potent oxidising agent and notable zwitterion.
12) If it were established beyond doubt that homcysteine may oxidise cholesterol to form atherogenic oxides of cholesterol then that would be the breakthrough needed. The question then would follow on, where does this contact arise? Is it in liporproteins, in the liver where cholesterol is reprocessed and manufactured, or does it arise in the cell where cholesterol is a vital feature of the cell and a structural component of its membrane?
13) Homocysteine levels can rise for alternate reasons. In otherwise healthy people elevated levels of homocysteine arise due to stress or to a deficiency of methyl donating antioxidants. Stress raises the demand for methyl donations. If supply cannot match overall demand methyl deficiency occurs with a corresponding rise in homocysteine. Methyl deficiency permits levels of oxidation and oxidative stress to rise above that which could be considered merely basal and normal.
14) Much the same body of work that identified cholesterol oxides, and that then identified which may act as potent atherogens, has also established cholesterol is not the atherogen the fat/cholesterol hypothesis makes it out to be.
15) A lot of confusion has arisen amongst medical professionals. Few leave med school with a real understanding of the difference between lipoproteins and cholesterol.Unless studied at length, and from first base, the terminology, discussion, and nomenclature is designed to confuse. The notion of good cholesterol / bad cholesterol is completely misleading as is the branding of HDL-c and LDL-c. LDL-cholesterol has no real meaning. And another gripe and insult to a science is that the term ‘triglyceride’ has been granted alternate meaning. Its original and pure meaning, which refers to three fatty acids linked with a molecule of glycerol, has been de-emphasised, while its new meaning is applied to a summing of certain lipoprotein factions.
16) The issue of plaque formation (atherogenicity) is one matter, while the contrast between stable and unstable plaques that rupture is another, and as you direct the rupture of the plaque has consequence.
Mie, has accused me of spamming and posting off-topic. I cannot think why. The concept of dyslipidemia is firmly rooted in the will to apply the fat.cholesterol hypothesis – to test for dyslipdemia. The notion began with a weird notion of surplus cholesterol doing harm. Cholesterol only does good. It does no harm. Any harm associating with cholesterol arises only under the conditions under cholesterol molecules may be oxidised to form certian of a large family of cholesterol oxides. Testing for ‘cholesterol’ is dishonest. Testing for cholesterol is impractical so they test for lipoproteins instead. This ‘lipid profile test’ is next to meaningless. Lipoproteins resemble snowflakes for being infinitely variable one to next, not just in terns of size or density but in detailed variation in composition. The branding of terms like HDL, LDL IDL, VlDL is a disserviuce to their sophistication and diversity. As Axel suggests above lipoproteins overcome a significant natural challenge in the biology of vertebrates.
In my first post I wanted to be circumspect and avoid offending Axels feelings. If oxidative stress is the cause of CVD then the lipid profile test informs very little indeed. No amount of ad-hoc interprtation and reinterpretation of results will really inform much, not in the sense of conventional wisdom upon these matters.
The alteration to lipid counts and profiles seems to vary for reasons that are several. Its counter intuitive. Keys assumed additional fat in the diet would raise the count of lipoproteins and cholesterol, and he that saturated fat would have the strongest effect. It was outright speculation on Keys part. As you suggest, Michael, and as is intimated in Axels post, hyperglyceamia may bear upon lipoprotein counts and profiles. So lipid profile counts may rise or alter under conditions of a high carbohydrate diet and not a high fat diet as has always been promoted and remains the case. Conventional wisdom then has this wrong and backwards roads about. When they insist you cut back on dietary fat to reduce your cholesterol they’re actually recommending the opposite of what is needed.
To be plain then discussion of HDL/triglyceride ratios doesn’t impress me much. They do not inform much about how epiphysiological risk factors result in atherogenicity. On the other hand come at this from an endocrinological perspective and there is a strong indication that hormonal alterations that accompany stress increased demand for methyl groups and could result in methyl deficiency and a rise in oxidative stress. And while this last statement may still rest upon conjectural basis there is a lot about the statement that is in accord accord with evidence that has been established but ignored by the mainstream who remain insistent that cholesterol and dyslipidemia cause heart disease, which is contrary to the evidence on cholesterol and cholesterol oxides entirely.
Peng and Morin, ‘Biological effects of cholesterol oxides’ (book) is a good source doubters could visit.
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, 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. No one’s claiming that cholesterol per se is the problem, understand? And as for oxidative stress and lipoprotein oxidation in atherosclerosis … Well, it’s been TEXTBOOK material for decades. As well as the roles of different types of fat and lipid levels (FYI, saturated fat does indeed increase both LDL and HDL levels in blood). Etc. etc.
Therefore, nothing you’ve brought into the discussion is new nor does it benefit the discussion of the topic itself (predictive and/or therapeutic value of TG/HDL ratio). Judging by your messages, you’re a case in point of an Internet-era “expert”: a person who doesn’t have a clue of basic calculus but who nonetheless goes on repeating a few catch phrases from the field of theoretical physics he’s picked up on a random website.
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 concise does not do great service to the processes at work, so peoples preference for simple and concise is the reason they fall victim to poor information or outright cons.
The professionals sitting on panels that guide NICE ought to be able to grasp explanations that are a step above the merely simple, concise and dogmatic. They should approach curiosity from more cause centric approaches simply because all chronic disease has a cause. Unfortunately they do not and this inadequate level of curiosity that prevails within medicine is blighting standards of delivery and hindering real progress in the development of much improved hypotheses. Even professionals seem to like to go about their business wearing blinkers simply because it eases the work and cognitive loads.
If cardiologists are afflicted that is lamentable.
After so many millions of years of evolution the inner workings of the human species defy simple and concise explanation. Simple and concise can only lead to misunderstandings.
“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.
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 have climbed from the high 20’s to a current mid-70s level.
Besides changing my diet dramatically, I added a very moderate exercise (cardio and weights) plan to my lifestyle. At least 5 days per week, I do my exercise plan.
As a result of these major changes, both my weight and blood pressure have dropped to attractive levels. And all my inflammation markers are now in the healthy zones too.
The only negatives, per my past doctors, are higher total cholesterol and LDL-C levels. And my LDL-P still is at an abnormally high level, but it has been cut in half with the new diet/exercise lifestyle.
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.
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@example.com
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 rabbit (fed high cholesterol/SFA fare) was switched into another rabbit on a typical rabbit diet. It was shown that CHD was caused by elevated blood cholesterol not by by diet per se. SFA/cholesterol was only a vehicle to elevate blood cholesterol.
I wonder if you can show me an experimental model in which atherosclerosis was reversed by modulating HDL-C and/or triglycerides with high SFA diet, at the presence of elevated LDL. I emphasize the wording “at the presence of elevated LDL” since this is what low carbers are left with.
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 model you mentioned I can only say that I’m not going to “chase rabbits” at your demand. It’s out of my scope.
“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 somewhere.
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?
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 from cholesterol lowering from those who don’t?
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 but only LDL lowering can result in regression of atherosclerotic process within the wall. This is basic stuff.
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 1973 someone finally realized that seed oils need to be protected from oxidation, so they utilized vitamin E. Excerpt: “Weekly veterinary evaluation of the appearance and health of the calves revealed no abnormalities associated with the dietary treatments. The calves were examined for condition of coat, abnormalities of stance or gait, stiffness and evidence of muscular dystrophy, excitability or nervousness, and respiratory infections or abnormality. This result contrasts with the reports of others (Adams et al., 1959a,b; Gullickson, Fountaine and Fitch, 1942) who experienced poor weight gains, bad health, and considerable mortality of calves on rations high in unsaturated vegetable fat. All the calves in our study, whether fed milk containing high or normal amounts of polyunsaturated fatty acids, received supplemental vitamin E. The presence of this vitamin E during these early growth stages may be the explanation for the very satisfactory growth and weight gains during the milk feeding period, which contrasts with the growth deficiencies and health problems encountered by Adams et al.” https://www.journalofanimalscience.org/content/37/6/1419.full.pdf
In that same article the researchers said, “The possibility exists that food products containing high levels of polyunsaturated fatty acids may be useful in dietary prevention and alleviation of atherosclerosis. If clinicians prove an associative effect of dietary fatty acid saturation with incidence of cardiovascular disease, it will become desirable for dairy and beef producers to develop methods of increasing the degree of polyunsaturation in milk and meat fat.”
One wonders how levels of polyunsaturated fat intake that destroy the health of veal calves could possibly prevent heart disease in humans, especially without vitamin E supplementation.
“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 question?
“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 from cholesterol lowering from those who don’t?”
Same here. Don’t know about Icelandic treatment guidelines, but e.g. in Finland the risk is assessed as a WHOLE, not just based on LDL. Just because the current evidence in risk management and/or disease prevention shows this to be the best approach.
In addition, the fundamental nature of PREVENTATIVE medicine is such that we’re not dealing with absolute certainties, especially not in the case of an individual. Should that prevent us from treating the patient?
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.
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.
btw, did you see Blackburn's response to Big Fat Lie Book. Good stuff.
“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 to see the error of my ways rather than a “not-talking-to-you”. Nor was I deliberately twisting your words – I’m sorry if that’s how it seemed. I respect your opinions and enjoyed this blog post (and agree with the basic idea that there are patients in whom the risk can be substantial although common markers don’t show this) but couldn’t really understand how else I should’ve interpreted e.g. the abovementioned ” How can we tell when high cholesterol is important and when it’s not?” part.
So please, do explain a bit further.
I’ve read Blackburn’s response. Good show, although bloggers like Seth at “Science of Nutrition” and our Finnish colleague, Jussi Riekki, have essentially covered the same topic earlier. And I – once again – wish you’d give ecological data a rest.
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.
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.
And Richard chose to forsake civilized conversation, once again. If you want to force someone to do something, then force yourself to gain some reason and manners instead of going nuts over a blog post. Go drool someplace else.
People, people don’t waste my time with useless nothingness. I read all the comments and realise that someone has totally wasted my time.
I respect all theories, experiences and solid science regarding the topic at hand…..in this case Triglyceride/HDL Ratio, that Axel has opened.
I have a vested interest in CHD/CVD…I have lived with this disease for over 30 years and rely on medication ( tolerating side effect), nutrition control and supplements. I basically have no interest, need or amusement with people trashing this informative site with dysfunctional minds.
For those that post with nothing but their ‘dick in their hands’ wishing to piss on others….don’t spoil and waste other peoples time. Some are so ignorant and biased,they think they no best..well! You don’t.
On a brighter note and relating to the topic…my numbers:
In mmol/L (fasting)
Trigs=0.7 (were better when taking niacin…but after the last 2 trials, thrive, ceased using)
LDL/HDL ratio =1.3
Chol/Hdl ratio =2.5
Homocyteine=12.6 (can be reduced with B12-B6-folate)
Apo B=0.48 g/l
Lp (a)=0.02 gl
BNP=28.8 (this is high because I continue to smoke and drink at least 1 litre red wine daily) had a MI 27 years ago and currently running on one coranary artery).
Basically the lab work would be considered excellent, as far as lipids are concerned.
On the subject of triglyceride lowering, there is a drug, Icosapent ethyl (IPE, also called EPA, brand name Vascepa), that does it with virtually no side effects. In ANCHOR, it was given with statins to patients with persistently high TGs (200-499 mg/dL) vs. statin plus placebo. IPE 4g/day lowered TG by 21.5%, non-HDL by 13.6%, LDL by 6.2%, VLDL by 24.4%, hs-CRP by 22%, Apo B by 9.3%, and Apo-C III by 19.2% (among others). The only side effect was arthralgia in about 1.5%. (All figures placebo adjusted.)
EPA also increases EPA/AA ratio, reduces systemic inflammation, reduces oxidative stress and reverses endothelial dysfunction at the cellular level, significantly increases coronary fibroatheroma cap thickness (increasing plaque stability), all with essentially no side effects.
EPA does not raise LDL-C as does its cousin, Lovaza (which contains DHA). In some trials, it has raised HDL slightly.
Whether to wait for an outcomes trial result to prove EPA’s clinical efficacy before adopting its use is becoming more problematic for several reasons:
1. HTG subgroup analyses in 6/6 TG-lowering CVD outcome studies (JELIS, FIELD, ACCORD, AIM-HIGH, BIP, VA-HIT) involving varied populations and 3 different classes of medications all showed CVE reduction.
2. Meta-analytical data from 61 studies; 17,018 CVD deaths in 726,030 subjects; 58,419 all-cause deaths in 330,566 subjects showed “Elevated blood triglycerides were dose-dependently associated with greater risk of both CVD and all-cause mortality … [and] suggest that controlling triglycerides can help to prevent CVD and other causes of death … [with] each 1 mmol/L increase in triglycerides was associated with 13% increase in CVD mortality and 12% increase in all-cause mortality.” Liu, et al; Lipids Health Dis 2013; 12:159.
3. Genetic data is accumulating to suggest a causal relationship between elevated TGs and CVD. Do, et al; Nat Genet 2013 Oct 6; Eur Heart J 2013; 34: 1826-1833.
4. Very recently, two groups (one, Kathiresan, et al, the other from Denmark) independently concluded that ApoC-III mutations resulted in lowered ApoC-III, 40% lower TGs and about 40% fewer CVD events, again suggesting the possibility that HTG may play a causal role in CVD. NEJM, June 18, 2014 (e-pub).
The Japanese have been studying EPA for many years; we are just now starting to catch up. We have much to learn from them.
In a few years (2017) the REDUCE-IT trial results (using a western population) will be published, and there is an excellent chance in my opinion that once analyzed and digested, using EPA adjunct to statins will become common. Watch for the CHERRY trial results in 2015. They will inform somewhat what we should expect to see in REDUCE-IT.
Your claims regarding IPE seem to be exagerated in relation to improving multi lipid markers.Perhaps usefull in rare Trig. elevation.
“The US Food and Drug Administration (FDA) has approved omega-3 carboxylic acids (Epanova , AstraZeneca) for use as an adjunct to diet to reduce triglyceride levels in adults with severe hypertriglyceridemia (triglyceride levels >500 mg/dL), a condition that affects around 4 million Americans.
The approval was based on data from the phase 3 Epanova for Lowering Very High Triglycerides (EVOLVE) trial, which examined the efficacy of the product in lowering triglycerides and other key lipid parameters in patients with very high triglycerides.
Epanova will be the third prescription formulation of an omega-3 polyunsaturated fatty-acid (PUFA) product approved in the United States for the treatment of hypertriglyceridemia.
It is the first FDA-approved prescription omega-3 in free fatty-acid form, the company notes. The approved dose is 2 g (2 capsules) or 4 g (4 capsules), making it the first prescription omega-3 product to have a dosing option as few as 2 capsules, once a day, which can be taken with or without food.
Amarin’s synthetic ethyl eicosapentaenoic acid (EPA), icosapent ethyl (Vascepa), was given the FDA nod 2 years ago, andLovaza (GlaxoSmithKline), which contains a combination of ethyl esters of omega 3 fatty acids, principally EPA and docosahexaenoic acid (DHA), has been available for the same indication for a number of years.
AstraZeneca says it plans to file for regulatory approval of Epanova for severe hypertriglyceridemia in other markets.
Race to Gain Approval in Conjunction With Statins
AstraZeneca is also hoping to succeed where others have failed in gaining approval of Epanova in conjunction with use of statins for the much wider indication of mixed dyslipidemia; a study in this patient population, called Statin Residual Risk Reduction With Epanova in High Cardiovascular Risk Patients With Hypertriglyceridemia (STRENGTH), is planned in around 13,000 patients, and the company says it will pursue development of a fixed-dose combination of Epanova with a statin .
Last year, the FDA rejected Amarin’s application for expanded approval of Vascepa based on the results of the ANCHOR trial in the same patient population.
Amarin is now examining Vascepa combined with statin therapy in a larger trial, in around 8000 patients, called Reduction of Cardiovascular Events With EPA—Intervention Trial (REDUCE-IT).”
My statements regarding IPE/EPA are not at all exaggerated, and your source is incorrect.
The FDA did NOT “reject” Amarin’s application to expand the Vascepa label from its existing 500 mg/dL and higher TG (MARINE) marketing approval. Instead, despite the ANCHOR (TG = 200-499 mg/dL) trial having met all primary and secondary endpoints, FDA decided to rescind the previously agreed SPA with Amarin, believing, incorrectly, that the ACCORD, AIM-HIGH and HPS2-THRIVE CVD outcome trial results make unlikely that IPE+statins in the persistently HTG population would result in any clinical benefit.
Since then, the ANCHOR sNDA has been put on hold while Amarin is appealing the FDA’s rescission of the SPA (that appeal is still under consideration). Once the appeal from the SPA rescission is resolved, FDA will decide the ANCHOR sNDA.
Meanwhile, Congress has become involved, most recently requiring FDA to explain why and on what basis the rescission occurred.
As well, there has been a public outcry, as the FDA’s logic in rescinding the SPA is weak, at best. For example, the three TG-lowering outcome studies FDA used to justify its position used niacin and fibrates, not EPA; as well, they used populations whose median TG levels were normal or borderline, but not high (not 200-499 mg/dL). Moreover, HTG subgroup analyses in two of the three studies actually showed a CVD benefit (the third, HPS2-THRIVE, has not yet published HTG subgroup analysis).
The lipid parameter improvements I listed (with one exception) are from the peer-reviewed article in which ANCHOR was reported and can be found at Am J Cardiol. 2012; 110 (7): 984-992. The exception is the ANCHOR ApoC-III data, which was first presented in a poster presentation at the May 2014 NLA conference and also make public in a press release by Amarin (and which can be found on Amarin’s website).
If you go to the peer-reviewed journal articles cited in my previous comment, you will find that there is substantial, recent, genetic meta-analytical data strongly suggesting that HTGs play a causal role in atherogenesis and CVD. As well, the June 18, 2014 NEJM articles regarding the effect of ApoC-III mutation on TG levels and CVD rate reduction is striking.
EPA was found in a pilot study (presented at AHA in a poster session, Abstract 8893 ) to reduce coronary plaque volume by 21.9% (in addition to its cap thickening effect). The CHERRY trial (ongoing, fully enrolled, I think) is measuring that in a larger study (both Japanese). I believe CHERRY will inform us somewhat regarding what to expect in the REDUCE-IT outcome trial (which is about 80% enrolled, I believe).
Also at the May 2014 NLA conference was presented data from two Harvard researchers (Mason, et al) showing that EPA+statins reverses endothelial dysfunction, corroborating findings by Toyama et al published at Cardiovasc Drugs Ther (2014) 28:53-59. Mason’s work will soon be published in a peer-reviewed journal.
Your skepticism results from much of this knowledge having not yet become widely known.
Claude M. McQuarrie III
July 24, 2014
On the subject of triglyceride lowering, there is a drug, Icosapent ethyl (IPE, also called EPA, brand name Vascepa), that does it with virtually no side effects. In ANCHOR, it was given with statins to patients with persistently high TGs (200-499 mg/dL) vs. statin plus placebo. IPE 4g/day lowered TG by 21.5%, non-HDL by 13.6%, LDL by 6.2%, VLDL by 24.4%, hs-CRP by 22%, Apo B by 9.3%, and Apo-C III by 19.2% (among others). The only side effect was arthralgia in about 1.5%. (All figures placebo adjusted.) ‘
I Don’t think so! Claude.
Drug companies are not in the bussiness of providing a public service. They all lie,cheat and hide negative data.
They don’t even bother adding COQ10 to Statins..which would be a public service.
Albeit, drugs can be lifesaving and life prolonging. But the above claims are a nonsence and the Bigpharma are trying to obtain a patent for Fish/Krill oil that can be obtained natuarally and cheaper.
Below is an example:
michael goroncy 15 June 2013 at 3:01 am #
Confessions of a lab rat
In 2005 I joined several thousand others in Pfizer’s CEPT Illuninate study.
Within a short time 2 things happened!
(a) my HDL tripled (marvellous) this is what the trial depended on.
(b) my BP sky-rocketed (mystery) because the side effects were predicted to be marginal and no need for concern)
Up until then, my BP was ‘bobbing along’ nicely in the 110-120/ 70-80..Although having severe CHD, my BP was excellent and never an issue.
Now! For the ‘Circus’ part and it’s management.
My BP shot up to 160-180/ 90/130…not exactly a marginal increase.
I mentioned this to the Cardiac Research Team who were monitoring Lipids, BP and ECG periodically.
I told them I know with absolute certainty that I am in the Trial Arm and not the Control Group…They responded with “You don’t know that”.
Then I dragged my GP (PCP) into the picture and explained this remarkable change in HDL and BP. He was a good, caring GP….and do you know! We spent over a year, adding different Hypertensive drugs and adjusting dosage with no success.
Meanwhile, I am keeping track of Torcetrapib on the net, and can only hear the ‘crowing’ and excitement of this ‘wonder drug’. The closest I could get to any negative..was that the HDL might in fact be a ‘false reading’ (even though the numbers go up- incidence remains the same).
As you all know…Pfizer pulled the plug with extreme haste…when only days before, they could ‘smell the money rolling in’. To me, their noble excuse (a pitiful increase in death with the Combo takers) didn’t equate to flushing hundreds of millions down the toilet. And abandoned their search for the holly grail…and never likely to return down that road. And, even though Steven(rent a quote)Nissen came in to deliver an eloquent eulogy…I have some simple questions to put to Pfizer.
What numbers were they seeing with BP and other markers?
They ‘shat themselves’ for some reason, and I don’t think we will ever know.
The ANCHOR trial results came from very well-respected investigators across the country, were peer-reviewed before publication, and were thoroughly vetted by FDA. Nobody, including FDA, questions their authenticity.
Your reluctance to accept the ANCHOR data on the basis of your belief that drug companies “all lie, cheat and hide negative data” is illogical and unsupported. Again, the ANCHOR data come from outside investigators, are peer-reviewed, and (here) were thoroughly vetted by the FDA.
As additional data regarding IPE/EPA are published, the drug’s utility in reducing the incidence of cardiovascular disease will become more widely appreciated.
It ain’t so! Claude
I am not a ‘Conspiratory Theorist’ or against ‘Big Pharma’..as a matter of fact, it’s drugs that keep me alive.
Your delusion that the ‘Anchor Data’ proves multi improvements in so many markers is nonsense and plain wrong.
You appear to have a vested financial interest, and disclosure on your part would be appropriate.
Triglycerides-HDL-Inflamatory markers can all be significantly improved with Nutrition.
I am basically ‘Low..carbish/Moderate high fat’ ….Ghee,coconut oil,butter, clean eggs.
Looked into bread/gluten 12 years ago. From late teens up til then was always steady at 100kg. Being a bread/pasta lover and only adding tiny amounts of protein for taste. I eliminated bread/gluten and within a short time (5 months), 2 remarkable things happened. My lipid markers went from sub-standard to excellent and my weight dropped to 79-82kg and has remained in that range up to the present, even though my (good) fat consumption has quadrupled.
“Your delusion that the ‘Anchor Data’ proves multi improvements in so many markers is nonsense and plain wrong.”
So that you don’t have to take my word for it, here’s the abstract:
American Journal of Cardiology
Volume 110, Issue 7 , Pages 984-992, 1 October 2012
Efficacy and Safety of Eicosapentaenoic Acid Ethyl Ester (AMR101) Therapy in Statin-Treated Patients With Persistent High Triglycerides (from the ANCHOR Study)
Christie M. Ballantyne, MD
Corresponding Author Information
, Harold E. Bays, MD
, John J. Kastelein, MD, PhD
, Evan Stein, MD, PhD
, Jonathan L. Isaacsohn, MD
, Rene A. Braeckman, PhD
, Paresh N. Soni, MD, PhD
Received 2 March 2012; received in revised form 23 May 2012; accepted 23 May 2012. published online 23 July 2012.
AMR101 is an ω-3 fatty acid agent containing ≥96% pure icosapent-ethyl, the ethyl ester of eicosapentaenoic acid. The efficacy and safety of AMR101 were evaluated in this phase 3, multicenter, placebo-controlled, randomized, double-blinded, 12-week clinical trial (ANCHOR) in high-risk statin-treated patients with residually high triglyceride (TG) levels (≥200 and <500 mg/dl) despite low-density lipoprotein (LDL) cholesterol control (≥40 and <100 mg/dl). Patients (n = 702) on a stable diet were randomized to AMR101 4 or 2 g/day or placebo. The primary end point was median percent change in TG levels from baseline versus placebo at 12 weeks. AMR101 4 and 2 g/day significantly decreased TG levels by 21.5% (p <0.0001) and 10.1% (p = 0.0005), respectively, and non-high-density lipoprotein (non-HDL) cholesterol by 13.6% (p <0.0001) and 5.5% (p = 0.0054), respectively. AMR101 4 g/day produced greater TG and non-HDL cholesterol decreases in patients with higher-efficacy statin regimens and greater TG decreases in patients with higher baseline TG levels. AMR101 4 g/day decreased LDL cholesterol by 6.2% (p = 0.0067) and decreased apolipoprotein B (9.3%), total cholesterol (12.0%), very-low-density lipoprotein cholesterol (24.4%), lipoprotein-associated phospholipase A2 (19.0%), and high-sensitivity C-reactive protein (22.0%) versus placebo (p <0.001 for all comparisons). AMR101 was generally well tolerated, with safety profiles similar to placebo. In conclusion, AMR101 4 g/day significantly decreased median placebo-adjusted TG, non-HDL cholesterol, LDL cholesterol, apolipoprotein B, total cholesterol, very-low-density lipoprotein cholesterol, lipoprotein-associated phospholipase A2, and high-sensitivity C-reactive protein in statin-treated patients with residual TG elevations.
As I noted, the ApoC-III data were just recently released. Here is an excerpt from the company's press release:
May 2, 2014
Amarin Announces Presentation of New MARINE and ANCHOR Post-Hoc Analyses at National Lipid Association Annual Scientific Sessions Showing Vascepa(R) Significantly Reduced Apolipoprotein C-III Levels
Analyses Extend Finding of Potentially Beneficial Lipid Effects of Vascepa in Patients With Elevated TG Levels, Including Effects on Top of Statin Therapy
BEDMINSTER, N.J., and DUBLIN, Ireland, May 2, 2014 (GLOBE NEWSWIRE) — Amarin Corporation plc (Nasdaq:AMRN), a biopharmaceutical company focused on the commercialization and development of therapeutics to improve cardiovascular health, announced today the presentation at the National Lipid Association Annual Scientific Sessions, of new post-hoc analyses of the MARINE and ANCHOR studies that showed the use of Vascepa® (icosapent ethyl) capsules significantly reduced apolipoprotein C-III (ApoC-III) levels. ApoC-III is a small protein that resides on various lipoproteins, and is an important regulator of lipoprotein and triglyceride (TG) metabolism.i This research is being presented today by Christie M. Ballantyne, M.D. from Baylor College of Medicine as part of a peer-reviewed poster session at the National Lipid Association Annual Scientific Sessions in Orlando, Florida.
"The significantly reduced Apo C-III levels with Vascepa in the MARINE and ANCHOR trials add to previously reported TG- and ApoB-lowering effects in patients from these studies," said Steven B. Ketchum, Ph.D., President of Research and Development, Senior Vice President, Amarin Corporation. "We are pleased to continue to analyze and share data from these trials that support the clinical value of Vascepa as an adjunct to diet to reduce triglyceride (TG) levels in adult patients with severe (≥ 500 mg/dL) hypertriglyceridemia."
MARINE and ANCHOR were 12-week, phase 3, double-blind studies that randomized patients to Vascepa 4 g/day, 2 g/day, or placebo. MARINE randomized 229 patients with TG ≥ 500 and ≤ 2000 mg/dL while ANCHOR randomized 702 patients at high risk for cardiovascular disease with TG ≥ 200 and < 500 mg/dL despite low-density lipoprotein cholesterol (LDL-C) control while on statin therapy. In the MARINE study, stable statin therapy was permitted but not required. In the ANCHOR study, patients were required to be at high risk for cardiovascular disease as defined by the NCEP ATP III guidelines and on stable statin dose (atorvastatin, rosuvastatin, or simvastatin).
This post-hoc analysis assessed the median percent change from baseline to study end in ApoC-III levels compared with placebo. ApoC-III levels were measured post hoc and lipid levels were measured as previously reported. Total ApoC-III levels were assessed in 148 and 612 patients in MARINE and ANCHOR, respectively. In MARINE, Vascepa 4 g/day and 2 g/day statistically significantly reduced ApoC-III levels by 25.1% (P < 0.0001) and 14.3% (P=0.0154) versus placebo, respectively. In ANCHOR, Vascepa 4 g/day and 2 g/day statistically significantly reduced ApoC-III levels by 19.2% (P < 0.0001) and 8.5% (P=0.0008) versus placebo, respectively. In the MARINE and ANCHOR studies Vascepa significantly reduced TG, Apo B- and ApoC-III levels without increasing LDL-C levels in patients at the dose of 4 g/day.
What matters is clinical benefit in hard endpoints, that is in reducing CVD events and/or deaths. No drug should be taken into clinical use on the basis of risk marker data alone.
Hi male age 45 on the noakes for about 6 months diet, TC 8.3 HDL 1 TG 1.79 LDL 6.55 GLUCOSE 5.7 This is Mmol Can you tell me what is good or bad. Regards Colin
Your total cholesterol and LDL-cholesterol are quite high. This is fairly common on a low carb high fat diet. TG/HDL ratio is 1.74 which is a bit too high as well. Glucose is fine. Would be interesting to know how and whether your numbers have changed on the current diet.
I like how you demonstrated that there are two ways to increase TG. One through a fatty meal and the other through carbohydrate. I remember one of my professors in medical school commenting how your blood would appear pink after a large fatty meal due to the huge load of chylomicrons entering the venous circulation. Clearly the greatest source would be eating processed, carb rich foods and drinking pop.
I did want to clarify for your readers that fish oil is remarkably good at lowering TG. I am in the process of publishing a book (inflaNATION.com) where I demonstrate to my readers how I cured my heart disease. I had a massive heart attack at age 40 (I’m now 56) which left me with chronic angina that was so bad I couldn’t walk up two flights of stairs without chest pain and shortness of breath. Within 72 hours of high-dose, pharmaceutical grade fish oil I could already feel relief of my angina. It wasn’t complete relief but it was nothing short of miraculous for me that I got any relief at all. In about a year the angina completely disappeared.
My most recent labs and heart scan confirm that I have reversed atherosclerosis doing several key things beyond fish oil. Heart disease has perhaps 30 separate risk factor or what I like to call Irritating Agents (IA). LDL cholesterol is only one player and only when it is OXIDIZED. The best way to prevent and reverse this disease then has to do with keeping your oxidation state low, not by decreasing cholesterol.
Long story short, I was able to reverse this disease with a low carb Mediterranean diet of my making. An anti-inflammatory diet in essence which also eliminates omega 6 fats since they are a cause of heart disease. Fish oil was and still is a key component. The important point is that I never took a statin or any other drug to reverse this disease. Had I stayed in the system I believe I would be very sick by now since the AHA dietary approach makes your CAD worse over time because it promotes high TG, low HDL and pattern B sdLDL which is not good. Then there’s the effects of high glucose levels and high insulin levels both of which produce inflammation, and both are higher in the high carb diets like the AHA’s. Most patients will need to stay at or near a 20% safe carb limit.
Three studies in the last two years have also shown that statins accelerate atherosclerosis. (see Confirm Registry) I’m not surprised since statins are mycotoxins and cellular poisons. Put a stain in a petri dish with some cells and the cells die within 48 hours. Read Stephane Seneff or MIT for an interesting take on statins. Or the new book by Dr Yoseph. How Statin Drugs Really Lower Cholesterol and kill you one cell at a time.
In your article you suggest that fish oil “might” be helpful in lowering TG. I would add that fish oil is probably the most potent, reliable, and healthy way to lower TG along with diet. There are other drugs that work but why on earth would anyone take a drug when we have fish oil?
It lowers TG in a dose dependent fashion. But it is so much more since it helps to heal your endothelium-ground zero for CAD and CVD.
Lastly, I wish people to know that there is an easier and better way to cure your CAD that has nothing to do with the Commercial Sick Care System and its myopic view on cholesterol and heart disease. Thanks much for pointing out that TG levels are far better at predicting CAD risk and how this serves as indirect proof that CAD/CVD is a disease of excessive carbohydrate consumption (which Yudkin pointed out nearly 5 decades earlier but lost out to the diet-heart hypothesis of Keyes) NOT fat and cholesterol.
Very nice article……useful for all
I started eating a vegan diet five months ago. I recently did blood work. Here are the results compared to earlier blood work. I am a bit perplexed with the comparisons.
gluc – 116
chol – 154
trig’s – 293
hdl – 32
ldl – 63.4
pH – 5.0
A1c – 5.2
gluc – 111
chol – 132
trig’s – 359
hdl – 26
ldl – 34.2
pH – 6.5
A1c – 5.2
cm… from what I’ve learnt from the ATOZ study by Dr Chris Gardner, if ure one a high carb (altho vegan) diet, it can cause ure HDL to go down, and LDL as well. And if ure diabetic (it seems that ure pre from ure fasting glucose?), it might not improve ure condition if u are very2 insulin resistant (However, some might disagree, such as those following Dr McDougall or Dr Barnard’s reccomendations). It seems that ure trigs have gone up quite a bit….
I am not preaching low carb high fat… but after going on low carb and high fat (not vegetarian tho, as I eat meat) my HDL increased and LDL also went up (but from the ration, it seems I have the bigger fluffier types). Blood sugar tremendously improved (from a 246 to mostly 90s-100 now [these are fasting numbers]). If you wanna give it a go, and if ure vegetarian, there is a way to do it. But not sure myself how. Someone in my FB group does low carb high fat vegetarian style, and her numbers are great! 😀
I just turned 40. My TC was 309 over a year ago and I was placed on a statin. My body didn’t react well with it so I quit amidst all the articles I read about how bad statins are for the body. Since then, I’ve lost 20 pounds, exercise almost daily, and completely changed my diet to high (healthy) fats, no grains, no gluten, no processed foods, etc. At my check up this week, my doctor commented on my improved condition, weight loss, etc. and ordered an updated blood test. My cholesterol is still right at 309. NO CHANGE. He is now wanting to put me on 10mg of Zetia (states that it is for those with statin sensitivity) to lower it. My wife has no clue, nor done any research about the benefits of cholesterol and how statins are not the cure. She just wants me on the med thinking I’m not going to see the age of 50. I’m at a loss. I have to keep the peace at home.
Sounds like a difficult situation. Curious though about the rest of your lipid profile, TG, HDL-C and LDL-C. This is usually taken into account when deciding on lipid lowering therapy as well as history of high blood pressure, smoking and family history of heart disease.
See my post below. Has your doctor looked at your Vitamin D levels? My genetics, I suspect, are similar to yours.
I am in great shape, low BP (typically 110/70), good CT scan 2.5 years ago. but the elevated LDL, small particle size and high numbers is disconcerting because that can be troublesome at some point, also indicates possible insulin resistance, etc
My blood vitamin D levels were low. I am not one for quack cures, and there is hard study-supported evidence that D supplementation will mitigate statin side effects (myalgia), among other positive things. So I am taking 5000 iu a day.
My myalgia from statins has about disappeared. I feel much better now taking Lipitor once a week.
I apologize for not giving the details.
I have a family history of high cholesterol, stroke, high blood pressure, etc.
I am a non smoker, always have been, and eat properly. Hope this helps.
I am 32 yrs male , my blood numbers are
Cholesterol 220 , Tryc is 370 , LDL 76 and hld is 30 . I am currently 80 kg and height 5.5 . Should I start medication for sure or can I try diet to reduce .. My blood numbers are typically same for past 10 years ( b4 that never checked) . Both my parents are type 2 diabetic.
I suggest you discuss the high TG with your doctor. Is there some underlying cause? Furthermore, it may be difficult to calculate LDL-C when TG are this high. Also, be sure it’s a fasting blood sample. That’s important when measuring TG.
The general rule is to try lifestyle modification before drugs are prescribed. Your BMI suggests you’re overweight. Losing weight and limiting sugar, starches and refined carbs may help.
Thanks , Yes its fasting Blood counts,i was told by my new trainer to start Paleo Diet for weight loss, which looks similar to your article about eating good fats to reduce weight , but wanted to check with my condition of high TG, is that appropriate?
I think you should be fine with Paleo. Have your lipids tested again though in a few weeks or months. People respond differently to different diets. Best of luck 🙂
I have a genetic predisposition to dyslipidemia. Typically, without medication, my total cholesterol will be 250-275, TG 200-300, HDL 50-65, small LDL particles, high numbers.
All that said, I had a calcium CT scan in 2012 and zero blockage of any kind or presence of calcium. So maybe genetics dealt me a good deal there. I am also a fitness buff, eat well, don’t smoke or drink.
But, my numbers aren’t good, regardless . . . So I have gone back and forth with my doctor (who is excellent) on medication.
I also have a difficult time tolerating statins, have been on and off Lipitor and lovastatin. I get abdominal bloating (likely from an enlarged liver) and pretty bad muscle and joint pain, especially in my hands and sides (trunk). I also can’t tolerate niacin.
I have cut back Lipitor to 20mg once a week. Not surprisingly, the muscle ache side effects are worse a day or two after I take it. But I have also been taking the following:
EPA/DHA supplement (fairly high ratio of EPA to DHA)
Vitamin D3 (5000iu daily)
I have also increased my cardiovascular/aerobic conditioning work. More grass-fed meat, fruit and vegetables, less grains. And I am confident this regimen will get my numbers much more in line with where they should be.
But, interestingly, and this is for others who have struggled with muscle/joint side effects from statins. There is a study out that indicates that even once weekly statin dosing can be effective. AND, there are more studies that indicate that vitamin D3 supplementation, which is good for you on numerous levels, can mitigate these painful statin side effects—and they appear to be doing that for me. Most of my post-statn dosing side effects have disappeared since I started taking the D3.
Hi! Maybe you can offer an opinion regarding last year’s blood lipid analysis and this year’s numbers. I’m worried that the numbers may have dropped too much.
Last year: Total Cholesterol = 280; Trig = 126; HDL = 65; LDL = 190; Glucose = 83
This year: Total Cholesterol = 166; Trig = 142; HDL = 56; LDL = 82; Glucose = 75
This has happened without the use of Statin Drugs.
I’m wondering if these numbers are good now.
My brief history is this: 98% blocked carotid artery, then surgery to clean out; I worked hard to lose weight (lost 40 lbs) via strength-training and lots of exercise routines indoors and out; changed from a S.A.D. dietary habit to one of organic whole foods (including animal products when of grass-fed / free-range / wild caught origins).
Thanks for your opinion, in advance.
Hi I am Australian, 70 years old, in good health with good blood pressure, excellent blood sugar and homocystine levels. I have never been in hospital apart from childbirth, never had a general anaesthetic or any major illness, yet I have a familial cholesterol problem. Currently my total cholesterol is 10.8, my HDL chol 2.2, LDL 8.2, Triglceride 0.8. The LDL/HDL ratio is 3.7 and the Chol/HDL ratio is 4.9. My doctor would like me to go on medication, which I am loathe to do since all other health indicators are good. My query is: Are my ratios okay and should I take more notice of those rather than the total cholesterol figure and the LDL cholesterol figure (the bad cholesterol)?
I have also read that the homocystine level is a better indication of heart health than cholesterol.
There seems to be confusion or at least vast differences amongst professionals on the whole cholesterol issue.
These numbers are similar to mine.
Your TG/HDL ratio is 0.363, so indicating large, safe and non-oxidzing particles.
My doctor wants me to take statins (I did try them once before I knew their destructive nature), I refuse. They kill you one cell at a time, as they don’t allow cell division, and by the same pathway they stop the production of the CQ10 enzyme that is heart healthy.
I gather that eating saturated fats makes particles larger and polyunsaturates, when digested, cause inflammaion.
Everyone should do their own research, as doctors have no clue.
Hello, I am almost 59 and my most recent blood test results came in Total cholesterol is 107, Triglyceride level is 132, LDL is 50, and HDL is only 31. I started going to the gym in December 2014 and have worked up to a five-day workout schedule. I have made big changes for the better with my diet, get 7-8 hours sleep a night and drink over 64 oz. water a day. When might I see the HDL numbers go up? By the way, my weight has gone from 199 in September 2014 to 225 in February 2015. Not sure what I am doing wrong. Josh
ComponentStandard RangeYour ValueCHOLESTEROL<=200 mg/dL169240 HighTRIGLYCERIDE FASTING0-149 mg/dL251HDL>=40 mg/dL26LDL CALCULATED 93189 Very HighNON-HDL CHOLESTEROL 143CHOL/HDL RATIO 7
I have a very low HDL/Tri ratio 1700. I follow a paleo diet (semi strict) and have not been exercising regularly for a year, but am still relatively fit and slim. How much do I need to worry about my LDL P #?
Read this book: https://www.amazon.com/Prevent-Reverse-Heart-Disease-Nutrition-Based/dp/1583333002
HCLF WHOLE FOODS PLANT BASED DIET.
Hi Doc. I really hope you can help me out with a question that I can’t find answers to with any of my searches. I emailed you one year ago and partially based on what you told me, I decided to go with a keto diet to see if it would help. My LDL-P number was alarmingly high. After eating this way for one year, please see my attached comparison of results. Yes, my numbers improved, but the LDL-P number has not improved ENOUGH. I can’t find anything online about a combination of low triglycerides and high LDL-P, or a TG/HDL ratio of less than 2 paired with high LDL-P. Everything I read says that low TG is a reflection of low LDL-P (large, fluffy particles that are desirable). Have you heard of my combination, and if so, what does it mean? Should I continue on eating this way (LCHF)? I have to say that my test results were not so motivating after one year of practically no carbs! I know that once again when I go to my annual check-up, I will be getting pressure to start a statin. Thanks in advance.
Your numbers are a LOT like mine, same issue with high LDL-P and otherwise ok to good numbers, although your TG is marginally better than mine. My last numbers were:
And I take 20mg Lipitor once a week.
(Typically, my HDL is higher and I actually think the statin might be adversely affecting that, though not sure).
What is interesting is I am 54—had a calcium CT angiogram a couple of years ago, with zero blockage or plaque evident and therefore zero risk of cardiac event over the next 5 years. My BP is typically 100-110/70. Blood glucose within normal ranges. So by those metrics, I am fine. Low inflammation? My exercise regimen (heavy weights/cardio/crossfit)? Luck? Dunno.
But the LDL-P is troubling.
So rather than up the dose or frequency of the statin (which gives me nasty side effects), I started supplementing that with low dose niacin every day (500mg or less) and a glass or two of orange juice, snacking on almonds, to try to support a higher HDL level, without affecting total or LDL-P levels (actually studies show niacin will reduce LDL-P as well). I am also increasing my cardiovascular exercise as well.
Ultimately, I have a lot of faith in the TG/HDL ratio. My HDL has always been high, regardless of my other numbers, typically 50-65, until my last panel. And my health sort of speaks for itself. So my goal really is to get my HDL high, without a corresponding rise in LDL or LDL-P, and my TG lower. My ratio right now is just under 4/1. I want it more like 2/1. I suspect, achieving that, a lot of the other numbers like LDL-P should fall in line.
Seems to me, lipids, LDL-P, etc., only tell part of the story. A test that shows you what’s actually going on (or not) in your arteries, not to mention something that reflects on your level of inflammation, ADDS to the picture.
Good luck. Curious what your diet/exercise/supplementation is like—your numbers are really very similar to mine.
Thanks Shannon for commenting and sharing your lipid numbers.
It’s interesting to see how much your Trig’s, HDL-C and TG/JDL ratio have improved.That’s certainly positive. Your LDL-C has dropped by approximately 15% and your LDL-P by approximately 10%. The number of small particles has dropped significantly as well. So far so good.
I understand that you would want to see lower LDL-P numbers.
In fact, LDL-C and LDL-P don’t always go down on an LCHF diet. They can even go up significantly on a ketogenic diet.
I assume you’re eating a lot of fat being on LCHF. If your aim is to lower LDL-P further, you will probably see results by reducing your intake of saturated fat (dairy fat, coconut oil etc) and replacing them with other types of fat (mono- and polyunsaturated fats).
Dietitian Franziska Spritzer wrote an interesting article on her blog explaining how her lipids, in particular LDL-C and LDL-P reacted to a LCHF/ketogenic diet https://www.lowcarbdietitian.com/blog/lipid-changes-on-a-very-low-carb-ketogenic-diet-my-own-experience
All the best..
Thank you so much for your reply!
Great one – you can calculate also the ratio of your cholesterol here
My best panel in the last 7 years was
I have a question. I have familial hypercholesterolemia. Cholesterol has been high since I was a child. Untreated, my total cholesterol is 328. LDL is 276, HDL is 40, but triglycerides are 57. So my numbers are generally awful, but my HDL/Tri ratio is fantastic. Is this good or bad? I’ve taken statins since I was 26 and am now 42, but stopped statins last year due to terrible side effects.
Great, easy to understand article. Kaiser (health Ins) focuses too much on LDL, especially since the AMA guidelines are now at 100 for LDL! (I and other professionals suspect it’s due to pharmaceutical driven studies). Anyway, I have a ratio of 2.97 and an LDL reading of 135. Don’t focus solely on your LDL but all readings.
A year ago my cholesterol was the following.
TC-274, HDL-67, NON HDL-207, LDL-198, TG-47, TG/HDL 0.7
I do not drink or smoke, my blood pressure is normal, weight normal (120lbs), I walk 4 miles every day. My doctor still recommended a low fat diet and statins which I declined.
After doing research, I cut out all sugar from my diet and went on the ketogenic diet.
A year later my choleserol is the following
TC-388, HDL-60, NON HDL-328, LDL-312, TG-81, TG/HDL 1.35
I asked for the LPP and Doc says results of that test wont matter because my cholesterol is so high. I wonder if that’s true. My TG/HDL ratio is good.
I live in the UK where doctors haven’t heard of the Try/HDL ratio.
So I have an important query about the conversion factor mentioned above required for those in Canada & Europe
Whether both numbers are in m.mol/L (as in Europe), or, in mg/dL (as in US) it is a RATIO!
A ratio of two (mass-per-unit-volume) density-units is surely the same (across measurement systems) as long as the two are consistent with each other within their own system???
Please can someone clarify, I speak to the doc. tomorrow.
Dr. Peter Attia has a great 10 part series on cholesterol called ” The straight dope on cholesterol.” He discusses this very thing about LDL-P concentration as being the premier marker for heart disease.
Since 2012 I have been regularly fasting, and mostly eating a raw food diet. However, in the last 6-7 weeks I have switched to a LCHF Ketogenic diet. My blood tests this week were:
I am very happy with these result. My blood sugar also fell substantially.
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Trying to make sense of this whole topic, being an ex nurse doesn’t really help here- my total chol is deemed very high- 280 mg, my hdl good at 64, trig ok at 106. using just these figures a Dr would no doubt put me on statins (being a post menopausal female age 60) albeit borderline normotensive and BMI-fairly active and generally ‘well’ . But if we are to use tg/hdl ratio as a marker of risk- mine is 0.72 which would indicate low risk, also I do know my cardiac calcium score is zero. I have heard that HDL over the optimum level of 60 can act as LDL? but I think the jury is out on much of this presently. Any comments?
Despite the high total chol and LDL chol there are at least two signs suggesting that your risk is low. One is the low TG/HDL-C ratio and the other is a calcium score of zero. The latter is associated with a very low risk of cardiovascular events.
According to recent data from the Biolmage study those with a calcium score of zero sholud probably not be treated with statins due to low risk. https://www.docsopinion.com/2016/10/17/targeting-statin-treatment-biolmage/
thank you ! much appreciated and as I thought . Apologies – I used US mg/dl for all but the TG/HDL ratio where I reverted back to UK mmol/L of 0.72 which should have read 1.65. just thought I’d add that for clarity-not sure who else might read the thread. thank you again
Hi there, I was wondering if I could get some input on my recent numbers. I started LCHF at the end of August and have dropped 25lbs…. Still losing. I had blood work done at the Dr’s and my cholesterol showed really high so my Dr. had me go back because he thought the lab might have messed up. I want to stay off statins!
TC – 362
TG – 103
HDL – 51
LDL – 290
TC – 332
TG – 82
HDL – 46
LDL – 270
What I personally feel is you have to be moderate in everything….and especially diet when it comes to ingestion of macronutrients (carbs, protein, fat) or micronutrients (vitamins, minerals) for that matter. High fat is also not good as in yr case it increased total cholesterol and even LDL. I am very much aware that LCHF followers say it doesn’t matter…what matter is TG and HDL…for insulin resistance…but there are some hyper responders to this kind of diet and their bodies would react negatively to low carb high fat diet. Take a middle approach of moderate carbs i.e atleast around 100-120 g carbs in a day..to avoid constipation and headache and optimal metabolism. High fat should be taken only in form of good fat like nuts and seeds…if you take high amount of butter, cheese may not be good. I think about 50-60 g of fat in a day would be ok…and do not take protein more than 70 g in a day….otherwise it may give you kidney problems as I saw in some cases following LCHF taking high protein for replacement of carbs. This comes to 100 g carbs + 70 g protein = 170 g x 4 calories so almost 700 calories…and if you take 60 g fat it would be 60 x 9 calories= 540 calories so you should not take more than 1200-1300 calories in a day. However, you can increase your carb content to about 150 g in a day if you are highly active and doing exercise daily…say for every 10 g of carbs you eat over 100g, you need to walk about 1 km a day. Depends on your energy requirement. Protein has to be taken in amount of 1 g per kg. of body weight.
There is an excellent article written by Dr. Gregory Pokrywka that explains why cholesterol (more specifically the LDL/ApoB) levels increase in some people doing the LCHF diet. It has something to do with the conversion of excess ketones driving the increased synthesis of cholesterol. He also provided some useful advice how to go about it.
You can find the article here: https://www.lipid.org/sites/default/files/lipidspin/2016_sela_lipid_spin_final_0.pdf (page 10)
@Dr. Axel – thank you for this article. I’ve always been a big fan of your concise and yet exquisite explanations.
I appreciate the knowledge share. It takes a lot of researching (reading technical studies) to parse this information. You do a good job of distilling dense ideas into simple statements. Per my extensive reading, the biggest indicator for ACD, as you stated, is number of LDL particles (and not LDL-C!). But it’s nice to see you correlate this ratio to LDL-P.
“It is in vain to speak of cures, or think of remedies, until such time as we have considered of the causes . . . cures must be imperfect, lame, and to no purpose, wherein the causes have not first been searched.”
—Robert Burton, The Anatomy of Melancholy, 1621
Dr. My HDL-C is 111 and my Triglycerides are 55 if I’m doing the math right that puts my ratio at .44 which is terrible. I eat a very healthy well rounded diet and exercise daily crossfit and or lifting plus walking daily. My LDL-P is 1175 and LDL-C is 123. I take fish oil and niacin daily. I would really appreciate your advice on how to improve. Thank you!
Your TG/HDL ratio is 0.5 (55/111) which is ideal.
A year ago I went Keto and soon morphed to a virtual zero-carb version known as carnivore (animal based products only…meats, fish, eggs, 0-carb cheese). My total cholesterol is up to 350 now, but my HDL has more than doubled to 81 and triglycerides have fallen from over 200 to 84. Doing the math stated herewith, my TG/HDL Ratio is a very desirable 1.04. Incidentally, while I was not overweight at the start, I’m now consuming 3000+ calories per day with zero weight gain. Plus I feel great.
Just wondering if all the talk about cholesterol is really a defining factor in assessing risk. I have CAD, but my numbers are the only thing that seem to be bad. I had two stents ten years ago but several heart caths since that showed no blockages. Just got blood tests back and the usual 330 cholesterol, which has been that way for 15 years. TG:HDL = 13 and LD:/HDL is 8. Presently, no heart pain or any other symptoms. Thanks.
The units used are irrelevant when calculating the ratios as long as both of the numbers used, use the same units. The units cancel out. It would appear that maths are not the forte of the authors.
This is incorrect.
The maths may indeed be the forte of the authors.
Triglycerides and cholesterol have different molecular weights so the units don’t cancel out.
Let’s take an example: TG is 88.6 mg/dl and HDL-C is 38.7 mg/dl. The TG/HDL-C ratio is 2.3.
TG of 88.6 equals 1.0 mmol/L and HDL-C of 38.7 equals 1.0 mmol/L. Hence, the TG/HDL-C ratio is 1.0.
So, a TG/HDL-C ratio of 1 if mmol/L is used equals a ratio of 2.3 if mg/dl are used.
“In this study of 108 243 individuals from a contemporary ongoing general population cohort, we found a U shaped association between levels of LDL-C and the risk of all cause mortality, with low and high levels associated with an increased risk. The concentration of LDL-C with the lowest risk of all cause mortality was 3.6 mmol/L (140 mg/dL), well above the generally considered optimal concentration. These new results are likely to have implications for the interpretation of levels of LDL-C in clinical practice.” https://www.bmj.com/content/371/bmj.m4266
This observation runs in the face of the prevailing treatment strategy of reducing at all cost the LDL-C level in a patient. What good is it if the patient ends up dying of cancer or another cause instead of cardiovascular disease?
This may be a better alternative, using myself as an illustration. My calculated LDL-C is 150, which turns out to be reasonably close to the “optimal” 140 level observed in the aforesaid study. My TG/HDL-C ratio is 1.0. Why should I use a stain, with all of its baggage, to lower my LDL-C?
If my TG/HDL-C ratio were higher, say 2.5, then what I should do is, again, not to try to lower my LDL-C, but rather to try to improve my ratio by lowering TG and/or raising HDL-C. An effective way to achieving this is adopting a low carb diet.
I practice LCHF, coupled with intermittent fasting. My TG/HDL-C ratio 20 months ago was 1.6, now 1.0.
My current Triglyceride/HDL ratio is 0.42. 50/120. I eat 75% fat [mostly saturated, the healthiest kind] and 25% protein. Zero carbs functionally. I do eat beets, sauerkraut, bell peppers and strawberries on an occasional basis. And there are carbs in Greek yogurt and bacon and beef and eggs. But if you average out my carb intake over a month it’s lower than 50g a day. And on the rare occasion when it goes over 50g in a day, it’s all low glycemic carbs. Controlling the amount of insulin is key and carbs are a freight train for insulin and fat storage. Insulin will turn brown fat into white fat and you lose a natural mechanism for dumping unwanted energy as heat [keeping you toasty on cold days], thus storing everything as fat.
I switched my aging Great Pyrenees to one meal a day of some kibble and 4 oz of chicken thigh with a copious amount of bacon fat poured over it. She’s lost weight and about 3 years of age [which for a dog is 21 yrs].
Research and personal experience shows that the brain functions many times better on fatty acids rather than glucose. It’s been years since I had any brain fog. Even if my dog gets me up at 2am. I’m alert. It’s wonderful.
So much of what our culture believes about lipids, heart health, metabolic disorders, nutrition and food is just pure BS. From Harvard Medical to your local GP, the ignorance in these matters is enormous. From pushing carbohydrates and demonizing saturated fat, to pushing statins and cardiac surgery as attempts to deal with the disastrous effects of the massive push to consume carbohydrates and vegetable oils, the industry is corrupt to its core.
Since Ansel Keys in the 1950’s they have been lying and manipulating data: Truly a stain on science and medicine.