Non-HDL Cholesterol (Non-HDL-C)

Recently, non-HDL cholesterol (non-HDL-C) has become a commonly used marker for a blood lipid pattern associated with increased risk of heart disease.

To calculate non-HDL-C, you only need to know the numbers for total cholesterol and high-density lipoprotein cholesterol (HDL-C).

But why is non-HDL-C such a useful measure of future risk?

Non-HDL Cholesterol (Non-HDL-C)Atherosclerosis is the most common underlying cause of cardiovascular disease. It is due by a complex interplay between lipoproteins, white blood cells (macrophages), the immune system and the natural elements of the arterial wall.

Lipoproteins are the particles that transport cholesterol and triglycerides in the blood stream.

Lipoproteins that are directly involved in atherosclerosis are termed atherogenic. Most of these lipoproteins carry cholesterol and other types of fats such as triglycerides.

A standard lipid profile measures total cholesterol, triglycerides, and HDL-C.

These numbers are then used to calculate low-density lipoprotein cholesterol (LDL-C), according to the so-called Friedwald equation. However, calculation of LDL-C has several limitations.

Limitations of LDL Cholesterol

For historical reasons, LDL-C has become a primary goal of therapy in cardiovascular prevention. Recommendations regarding diet and drug therapy to lower cholesterol are most often based on the LDL-C number.

However, LDL is not the only lipoprotein involved in atherosclerotic heart disease. Triglyceride-rich very low-density lipoprotein (VLDL) and the so-called remnant lipoproteins are also atherogenic.

Therefore, there is a need for a lipid parameter that better reflects the amount of cholesterol within all atherogenic particles. This is of particular importance when triglyceride levels are high which is quite common, for example among people with abdominal obesity or metabolic syndrome.

What Is Non-HDL Cholesterol and Why Is It Important?

HDL and LDL particles seem to play very different roles in the pathogenesis of atherosclerosis. Therefore, measuring the amount of cholesterol within these particles tells two different stories.

While high levels of LDL-C are associated with increased risk of heart disease, elevated levels of HDL-C are associated with lower risk. HDL particles appear to be involved in clearing and removing cholesterol from arteries and atherosclerotic plaques while LDL-particles seem to participate directly in the atherosclerotic process itself.

This is the reason the cholesterol carried by HDL particles (HDL-C) is often called “good cholesterol” and the cholesterol carried by LDL particles (LDL-C) is called “bad cholesterol.” Of course, it is the same cholesterol; the difference lies within the lipoproteins that carry it.

Measuring total cholesterol provides limited information about risk because the number includes both HDL-C and LDL-C.

If we, however, subtract HDL-C from the total cholesterol we will have a measure of the amount of cholesterol carried by all lipoproteins except HDL. Doing this simple math will give us the amount of cholesterol carried within all lipoproteins that are atherogenic. In other words; a measure of cholesterol carried within all the “bad” lipoproteins but not the “good” ones (which is only HDL). This measure is termed non-HDL cholesterol (non-HDL-C).

Relying on LDL-C alone may be misleading. For example, individuals with abdominal obesity, metabolic syndrome or diabetic lipid disorders often have elevated triglycerides, low HDL-C, and relatively normal calculated LDL-C. Despite their normal LDL-C, these patients produce highly atherogenic lipoproteins such as VLDL and IDL (intermediate density lipoprotein) as well as small dense LDL particles.

A patient with low LDL-C and high non-HDL-C is an example of a patient with increased risk who may slip through the cracks because we only look at LDL-C. These patients are also likely to have high LDL particle number (LDL-P) as well as high ApoB levels.

Recent evidence suggests that non-HDL-C shows a better correlation with small dense LDL particles than do other lipid parameters including LDL-C. Clinical studies strongly suggest that a predominance of small dense LDL-C is associated with increased risk of coronary heart disease.

Non-HDL-C has been shown to be a better marker of risk in both primary and secondary prevention studies. An analysis of data combined from 68 studies, non-HDL-C was the best risk predictor of all cholesterol measures, both for CAD events and for strokes.

How to Calculate Non-HDL Cholesterol

An advantage of using non-HDL-C is that you don’t need a fasting blood sample.

Non-HDL cholesterol is your total cholesterol minus your HDL cholesterol

This is the formula:

Non-HDL Cholesterol = Total Cholesterol – HDL cholesterol

So if your Total Cholesterol is 220 mg/dL (5.7 mmol/L) and your HDL cholesterol is 50 mg/dL (1.3 mmol/L);

Non-HDL Cholesterol is 170 mg/dL (4.4 mmol/L)

If you know this simple formula, your knowledge outperforms 44 percent of providers in medical practice in the US. A survey showed that 44 percent of providers in practice could not calculate non-HDL-C when provided a standard lipid profile. Interestingly, cardiologists were just as likely as primary care physicians not to understand the calculation.

What Is a Desirable Level of Non-HDL Cholesterol?

The treatment goal for non-HDL-C is usually 30 mg/dL above the LDL-C treatment target. For example, if the LDL-C treatment goal is <70 mg/dL, the non-HDL-C treatment target would be <100 mg/dL.

Here you can see how non-HDL-C levels are looked at in terms of risk:

  • above 220 mg/dL (5.7 mmol/L) is considered very high
  • 190 – 219 mg/dL (4.9 – 5.6 mmol/L) is considered high
  • 160– 189 mg/dL (4.1 – 4.8 mmol/L) is considered borderline high
  • 130 – 159 mg/dL (3.4 – 4.0 mmol/L) is considered near ideal
  • below 130 mg/dL (below 3.4 mmol/L) is considered ideal for people at risk of heart disease
  • below 100 mg/dL (below 2.6 mmol/L) is considered ideal for people at very high risk of heart disease

How To Lower Non-HDL Cholesterol

Lowering non-HDL-C always begins with lifestyle therapy, usually aimed at lowering triglycerides. Traditionally, reduction in total calories, especially saturated and trans fatty acids, in combination with exercise is recommended. However, reducing sugar and carbohydrate consumption is often very effective in lowering triglycerides and non-HDL-C, particularly in patients with abdominal obesity or the metabolic syndrome

Foods that are high in omega-3 fatty acids may also be useful. Fatty fish such as salmon, sardines, mackerel, and herring is rich in omega-3. Omega-3 fatty acid-containing capsules or fish oils represent a reasonable alternative.

Moderate physical activity can help raise HDL-C and lower non-HDL-C.

Quitting smoking will improve your HDL-C and reduce non-HDL-C. Several studies have shown that male and female smokers have significantly lower HDL-C levels than non-smokers.

Successful reduction of elevated non-HDL-C may also be achieved with medical therapy. This would include the use of a statin drug to serve as the foundation for LDL-C lowering followed by a second treatment to bring non-HDL-C to within the target range. The three categories of drugs that would fall into this group include omega-3 fatty acid preparations, fibrates, and niacin.

However, there are very few clinical endpoint studies evaluating the potential benefit of combining each of these triglyceride lowering modalities with a statin as compared with a statin, making it very hard to recommend such a combination therapy.




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Henry
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Henry

These guidelines are out of date. Have you read up on the recent research in Cholesterol Clarity or Jimmy Bowden’s research on the Cholesterol Myth? Treat inflammation – not cholesterol is where the real focus should be. Thought?

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Henry. I’ve read Cholesterol Clarity and The Great Cholesterol Myth. Indeed I’ve written blog posts on both these books here and here. I still believe that understanding your lipid profile is important. I would guess Moore and Bowden also agree on that. That’s probably why they wrote their books. Understanding Non-HDL cholesterol may help us understand the lipid profile of people with the metabolic syndrome. It highlights the fact that looking only at LDL-C has several limitations. I have also recently written a blog post on Inflammation and Heart Disease. Although inflammation is important we can’t just ignore the role… Read more »

bhrdoc
Guest

Another excellent post Axel. In fact, as Cui showed in his article in the Archives of Internal Medicine (Cui, Y et al, Arch Int Med 2001;161:1413-19) LDL-C is the WEAKEST lipid predictor of CVD risk, with both elevated non-HDL-C and low HDL-C being far more predictive.

JanKnitz
Guest

Curious if the traditional lifestyle changes yielded the desired results, considering reduction of sat fat probably does not lower trigs, and people who reduce fat tend to eat more carbs which raise trigs?

Axel F Sigurdsson
Admin
Axel F Sigurdsson

In most circumstances avoiding sugar and refined carbs will be more helpful than avoiding animal or dairy fats when it comes to lowering triglycerides, and thereby non-HDL-C.

turtlefoot
Guest
turtlefoot

Have metabolic syndrome as well as a host of autoimmune disorders. But I also have somewhat enviable lab values and they are improving with a few strategic dietary tweaks: Triglyceride. 154 mg/dL(0 – 149) Cholesterol 203 mg/dL(112 – 199) HDL 76 mg/dL(>=40 – ) LDL Calculated 96 mg/dL Chol/HDL Ratio 2.7(0.0 – 4.5) Non HDL Chol 127 mg/dL So, yes, they are not ‘perfect’ but by focusing more on complex carbs and very little processed food, they’re getting better. I’ve actually acquired a distinct distaste for commercial baked goods (taste like chemicals to me) and prepared/canned food. Simple foods, well… Read more »

thehomeschoolingdoctor
Guest

Nice summary. Thank you.

Mike
Guest
Mike

Hi Doc, I recently discovered your blog and find it very helpful. In June, 2013, my physician wanted to put me on statins based on a standard blood test. I asked for the more detailed particle size NMR LipoProfile. I would rather continue to manage my health through improved diet and exercise. Your advice would be very appreciated. I am a 58 year old white male, 5’8″ tall. I am in good physical shape, exercise regularly, and have brought my weight down to 150 pounds. BP = 114/70. BMI = 23.36. Family history includes my (still going strong) 92 year… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Mike. According to the most recent US guidelines on cardiovascular prevention assessing total risk is more important than lipid numbers when deciding whether or not to treat with statins. Both LDL-C and LDL-P are elevated in your case. However, in the absence of strong family history of cardiovascular disease, high blood pressure, diabetes an smoking it would be hard for me to advocate statin therapy in your case.

Dayana Wiggins
Guest
Dayana Wiggins

We could calculate this 10 year ASCVD risk in order to make a decision. The risk estimator is available online so any clinician can use! here is the link
http://www.acc.org/tools-and-practice-support/mobile-resources/features/2013-prevention-guidelines-ascvd-risk-estimator

S.Babeanu
Guest
S.Babeanu

Hello Doctor. Interesting data. I would like to get from you an advice: I am female 75yrs old, ,BMI 30 Height 5″, exercise: walking 3-4 times a week 3km/day. Mild hypertension under Enalapril 20mg and Indapamide 1.5 mg is 130/84mmHg, with following blood tests:: TC 268, HDL-C 60,87, LDL-C 185,8, slightly increasing from the last to the present year TG 108, glycemia 86,59. Creatinine 1,25. I was advised to take statins at lower dose. Unfortunately the adverse effects were almost intolerable: muscular pain, important dizziness until vertigo irrespective of statin kind. I would highly appreciate if you could give me… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

With all those side effects you mention it’s obvious to me that taking statins will be very difficult for you. There’s no reason to believe that statin therapy will prolong your life more than improving your diet and lifestyle. So making your life miserable by statin treatment is not anything I would recommend. Try to look at other alternatives. You might want to improve your TG/HDL ratio and your non-HDL-cholesterol. Are you overweight? Do you exercise regularly. How about sugar? Can you cut down on refined sugars. If you’re overweight you might have insulin resistance. In that case losing weight… Read more »

SBabeanu
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SBabeanu

Thank you dr.Sigurdsson. The only thing I have to do is to lose weight. The rest I did except the exercise. I confess I am too lazy. Have a nice day

Ian Shaw
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Ian Shaw

My wife has had a recent lipogram which shows TC = 6.6 mmol/L, S-LDL 4.2 mmol/L, S-HDL 1.9 mmol/L, S-Non-HDL 4.6 mmol/L.
In the remote past, she took 10mg dosage of statins, but had no side effects. She is 55 yrs old, glucose 5 mmol/L,
BMI = 30 (obese), eats no sugar, exercises seldom,eats moderate amounts of meat and cheese, lots of vegetables, some fruit only low GI wholewheat rolls and uses only canola or olive oil for cooking.
Would you recommend statin (available is quiet cheap generic simvastatin) ?

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Assuming that family history is benign, she doesn’t smoke and blood pressure is normal, the only risk factor is a slightly elevated LDL-C. In that case my answer is no. I think there is very little to gain from statin treatment.

DR.NISHA LALWANI
Guest
DR.NISHA LALWANI

VERY INFORMATIVE,I MUST SAY.
IS THERE ANY WHO GUIDELINES AVAILABLE FOR NON HDL -C IN GENERAL LIPID PROFILE AND THERE REF.RANGE ? DOES DIRECTLY MEASURED LDL-C IS ALSO HAVING SAME SIGNIFICANCE AS CALCULATED ONE?IF D-LDL-C MEASURED STILL WE NEED TO CALCULATE NON HDL-C.PLEASE ELOBORATE.

Kjell Granelli
Guest

Elevated non-HDL-C might be the result of high levels of the “large, fluffy” LDL particles, which are generally considered benign and non-atherogenic. For example, ketogenic diets seem to easily produce a profile with high total cholesterol, high HDL, low TG and high calculated LDL. When you look at the numbers of small dense vs large fluffy (we call that “Apo ratio” in Sweden), almost invariably this confirms the benign nature of LDL. So is not looking at non-HDL-C potentially misleading, as a high value might reflect a high level of the benign LDL? (Maybe as benign as HDL itself!)

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Kjell.
I think you’re right. Non-HDL-C has its limitations although I believe it better reflects the concentration of atherogenic particles than does LDL-C. I agree with you that non HDL-C can’t differentiate between small and large particles. TG/HDL-C ratio on the other hand can to a certain degree reflect LDL-particle size and particle concentration. You can see a blog post I wrote on that here. I agree that Apo ratio provides additional information to the traditional lipid profile. Apo-B reflects particle number in a similar manner that LDL-P does.
Thanks for bringing this up.

Kjell Granelli
Guest

Axel,
Thanks for your reply. I have read that the TG/HDL ratio is a surrogate marker for oxidized LDL (which would be approximately the same as particle size) and insulin resistance. It would be very interesting to read the blog post you are referring to, but the link does not seem to work.

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Sorry Kjell, Here is the link.

Mie
Guest
Mie

Kjell,

“Elevated non-HDL-C might be the result of high levels of the “large, fluffy” LDL particles, which are generally considered benign and non-atherogenic.”

No matter how many times this is repeated, it’s simply not true. ALL LDL particle subtypes are atherogenic in large quantities (as they can all penetrate the arterial wall) and the “special” status of sdLDL is attenuated more or less totally when controlling for particle number. Studies as EPIC and MESA have shown this.

Kjell Granelli
Guest

Mie,
However, I believe the small dense are cleared less effectively by the liver than the large bouyant, so they remain much longer in the bloodstream, which would in itself make them more atherogenic. Of course, controlling for this time lapse as a confounder would then, as you point out, potentially make them more equally atherogenic – but it would seem incorrect to control for such an important factor which may decide whether there is an atherogenic effect at all. / Kjell Granelli

Mie
Guest
Mie

Kjell, “However, I believe the small dense are cleared less effectively by the liver than the large bouyant, so they remain much longer in the bloodstream, which would in itself make them more atherogenic.” SdLDL has somewhat lower affinity for LDL receptors which means lower hepatic clearance. These findings, however, are attenuated after adjusting for particle numbers (just like you yourself mentioned). And by no means does this mean that larger particles aren’t atherogenic! Every subclass can penerate the arterial wall, this has been demonstrated plenty of times. The final part of your message was odd. Did you really mean… Read more »

Kjell Granelli
Guest

Mie,
My final remark was not meant to suggest we do not measure the number of LDL particles. I simply suggest that if the larger LDL remain a shorter time in the bloodstream they are less atherogenic because of that. Therefore, a shift of LDL composition from more of the smaller to more of the larger would seem beneficial to lower CVD risk.
However, if the difference in rate of hepatic clearance is small, what I state above might be of small practical importance…. which is what I would like to understand 🙂

Mie
Guest
Mie

Ok. Although “less” is hardly a synonym for “non”, right? 🙂

Anyway, sdLDL (combined with high LDL-P) tends to be a problem for met.syndrome/DM2 patients and appears together with properly messed lipid etc. etc. values altogether. Shifts in particle size isn’t therefore a likely solution as such – lowering LDL (both C and P, perhaps especially the latter in population like this) is, as this can be accomplished via a variety of approaches. Particle size isn’t really an independent risk factor nor is there evidence that trying to modify it instead/in addition of e.g. LDL-P offers any benefits.

Claude M. McQuarrie III
Guest
Claude M. McQuarrie III

On whether combination therapy should be considered, you might want to re-read the ANCHOR trial results. There, Icosapent ethyl (IPE, also called EPA, brand name Vascepa) 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 increases EPA/AA ratio, reduces systemic inflammation, reduces oxidative stress and reverses endothelial dysfunction at the… Read more »

Kofi Akomeah
Guest
Kofi Akomeah

I am a 40 year old male with elevated blood pressure. I am currently taking losarten (100mg) and have been on it for almost 4 years. My reading are always around 123-116/82-75. I have been persuading my doctor to take me off the dose as i exercise very regularly and eat very well. I am 6 foot and weigh 172 pounds. Recently i had my annual physical and based on my results he wants to start me on cholestoral lowering drug based on my LDL (saying it needs to be below 75) since I am a high risk due to… Read more »

Mie
Guest
Mie

Claude,

“As you will remember, statins were prescribed for several years to reduce CVD risk before outcomes studies proved clinical efficacy. There is, today, greater evidence of clinical efficacy for lowering HTGs than there was when statins were first prescribed.”

You shouldn’t confuse the history of use of any given drug with proper criteria for clinical efficacy.

Jesse Lanou
Guest
Jesse Lanou

My TSH, HDL and LDL levels were’t too bad until I started taking anastrozole at the beginning of the year. Does anastrozole cause these levels to go up (especially my TSH that went from 1.81 to 5.92 in less than a year)? I have an appointment with my medical oncologist next week to talk about this, but his initial response is that he doesn’t think the anastrozole is to blame. Nothing else changed this year. I eat the same, take the same supplements, but switched from Tamoxifen to anastrozole in January. Thoughts?

George
Guest
George

MOST of you never need to be on statins … this will change your life – IF YOU DO IT:

https://www.dresselstyn.com/site/

kathleen Vaughn
Guest
kathleen Vaughn

hi
I just read your article and I feel much better about my lipid panel #s.( see below) I was shocked to see my #s art first because i eat pretty good. a usual day is Fruit and plain greek yogurt for breafast. kale salad and a sweet potato or tomato soup and 1 slice whole wheat bread with peanut butter(natural type) and dinner is usually fish or chicken with veggies. Apple as a snack and iced coffee with 1/2 & 1/2 and 1packet sugar.
my cholesterol non hdl is pretty good so I am hopeful.
thanks

CHOLESTEROL 221
TRIGLYCERIDE 50
HDL 74
LDL CALCULATED 137
CHOLESTEROL/HIGH DENSITY LIPOPROTEIN 3.0
CHOLESTEROL, NON-HDL 147

eniedorf
Guest

Do you know anything about Hypercholesterolemia? I have been on statins since I was 23. My father and brother have FH and both have had bypass this year. My father at 68, my brother at 44. I have recently found out both of my children, age 12 and 15 have total cholesterol levels around 300 and both are highly active in high cardio sports and we eat well, not perfect, but well. My total number is 310, with an HDL of 41, non-HDL of 269. I have been to the cardiologist and passed a stress test and show 6% calcification… Read more »

Maya
Guest
Maya

I have been a vegetarian for 35 years.I sparingly eat fish and seafood, mostly salmon and canned mackerel. For 16 months I have been fasting two days a week. My BMI is 21 and I exercise 2 or 3 times a week. My lunch is usually a veggie/fruit/protein shake with yogurt. My daily intake of food is small. Monthly junk food minimal. I do not drink sodas. Glucose level is normal and triglycerides are normal. However, my total cholesterol is now 314. Wow, I was amazed. Could this number be in any way related to my fasting for two days… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Maya. My first impression is that your high cholesterol is genetic. I don’t think it’s related to your fasting or your lifestyle. Is there a family history of high cholesterol or other lipid abnormalities?

Maya
Guest
Maya

Thank you very much for your response. My mother passed away in her early 90s and father in his late 80s. Mother was on Lipitor but don’t know about my father. I do remember that about 25 years ago my level was 170 and fast forward to 5 years ago it was 240. So with age, it seems to be going up despite the vegetarianism, exercise, fasting, etc. With a genetic predisposition, is this what happens or should I have had genetically high blood pressure many years ago? Thank you again.

Penny
Guest
Penny

Hi, I found this article very interesting. I researched it because I’m heading into my annual physical next week. I have a history (since at least 1985) of high total cholesterol, low TG, high HDL and high LDL. (I understand that these numbers “interact” with each other.) My recent lipid profile showed: Cholesterol 275 Triglycerides 69 HDL 101 LDL 163 Chol/HDL 2.7 LDL/HDL 1.6 TG/HDL .68 Last year my numbers were even higher (317, 118, 100, 198 respectively) so I had a test done for Particle concentration and size. HDL-P 44.4 SMALL LDL-P <90 LDL SIZE 22.2 LARGE VLDL-P 2.3… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Penny Despite your high total cholesterol there are a lots of positives regarding your risk profile. Of course I’m relying on that you don’t smoke. Firstly, the fact that your parents lived to be this old is a very good sign in terms of risk. The positive things about your lipid profile are the high HDL-C, the low TG’s, the low TG/HDL ratio, and the LDL-size (pattern A). The decision on when to give statins and when not to is always difficult. It has to be a shared decision making between you and your physician. It also has to take… Read more »

j
Guest
j

My family all have the cholesterol problem even with regular exercise and very low fat diet. I had post polio and I was told that cholesterol medications will weaken my muscle. My grandfather had stroke. My father has angina. Both my parents almost 80 and still live independently. My recent physical is total cholesterol :249 HDL: 50, Triglycerides:72, LDL-C:185, Non-HDL-C: 199, C/HDLC Ratio:5. Glu:92. Wt:124 Ht:5’2″. I exercise 3X/wk and 2 hrs each time. I eat 80% of vegetables and 20% meat. No rice. I have fish 3X/wk. I use grape seed oil or walnut oil for cooking. I use… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Hi J.
It appears that you are doing the best you can in terms of diet and exercise.
With a family history of high cholesterol you may have a hard time lowering your Non-HDL cholesterol further without taking medication (I´m not suggesting you should, that’s something you’ll have to discuss with our doctor).

Charlie G.
Guest
Charlie G.

Hello Dr., I have had chronic high lipids along with high Ferritin levels in the past and was wondering if you would suggest Prescription Medication for my scenario. I am 36, previously on low dose blood pressure medicine, chronic pain, several autoimmune issues, gout, and my grandfather had several heart issues: Cholesterol-292 LDL-183 HDL-58 Tri’s-256 Non HDL-234 Glucose-99 I’m admittedly 20-30lbs over my typical weight, currently 6’1 235. I have been able to correct the issues in the past to just slightly high levels with extremely strict diet and exercise and very limited alcohol use. This is a general life… Read more »

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Hi Charlie G.

Your LDL-C and Non HDL-C are both a bit high and Triglycerides are way up. You should trie to lose weight. Carbohydrate restriction might help you lower your triglycerides. Sometimes high ferritin levels may be caused by haemochromatois. Have your doctor go over these things with you.

Lowering TG/HDL ratio may be a target.

I’m sorry, but I can’t give any individual recommendations regarding prescription therapy etc. You’ll have to discuss these things with your doctor. I can only provide general information and advice as in the article above.

ch
Guest
ch

This will solve your problem. Take choleslo natural herbal supplement with no side effect. See how fast your level improve.I’m been using this product for a year now.

Clyde
Guest
Clyde

I’m 77 years old and had a heart attack in 1986. I’m scheduled for knee arthroscopy Jan 9. My numbers seem acceptable to me except for non-HDL cholesterol. It is so far out of line I don’t know what to think.
Cholesterol 114
Triglycerides 72
HDL cholesterol 63
Chol/HDL ratio 1.8
Non-HDL Chol 51

Your take on this situation?

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Hi Clyde
In fact your non-HDL cholesterol is ideal. Your total cholesterol and LDL cholesterol are both quite low as well. I assume your taking a statin drug. That could easily explain why your lipid profile looks this good.

Walter Rice
Guest
Walter Rice

Dr.,
I am a 66 year old male and had a lipid panel run a month ago. My PCP wants me to go on a statin drug. I currently take no prescription drugs, good blood pressure, about 20 pounds overweight.

My lipid panel:
Total Cholesterol 114
Triglycerides 106
HDL 35
LDL 58
VLDL 21
T Chol/HDL 3.3
Non-HDL 79

My cholesterol has ranged from 90-114 my entire life, but over the past 20 years my HDL has ranged from 29-40.

Your take? Am I truly a candidate for taking statin drugs?

Axel F Sigurdsson
Admin
Axel F Sigurdsson

Hi Walter
Your lipid panel looks fairly good. Total cholesterol is quite low and so is LDL-cholesterol (within target range). HDL-cholesterol is a bit low. In my opinion it’s unusual to approach a lipid profile like this with a statin drug. Remember however that there may be other reasons for treating with statins such as known cardiovascular disease or diabetes.

Walter Rice
Guest
Walter Rice

Dr,
Thanks. No diabetes or cardiovascular disease. Will diet changes (less dairy, sugar) and weight loss help raise HDL.? I am not a fan of taking statins or any prescription drug without justification.

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