HDL Cholesterol – The “Good” Cholesterol Explained

Estimated reading time: 8 minutes

High-density lipoprotein cholesterol (HDL cholesterol) is commonly measured to assess the risk of heart disease.

If you’ve had a blood sample drawn for assessment of lipid panel you probably already know if your cholesterol level is acceptable or not. You might also recall something about good and bad cholesterol and the ratio between these two.

Of course, there is only one type of cholesterol. The “good” and “bad” has to do with the lipoproteins that carry cholesterol molecules in our blood stream.

HDL Cholesterol - The "Good" Cholesterol Explained

A standard lipid panel provides information about total cholesterol, triglycerideslow-density lipoprotein cholesterol (LDL cholesterol) and HDL cholesterol.

LDL cholesterol is often termed “the bad cholesterol” because high levels are associated with increased risk of heart disease.
On the other hand, HDL cholesterol is usually nicknamed “the good cholesterol” because high blood levels are associated with less risk of heart disease whereas low concentrations are correlated with increased risk.

In other words; there is an inverse relationship between HDL cholesterol and the risk of heart disease. It is believed that HDL’s act as scavengers, picking up excess cholesterol in the blood and transporting it to the liver where it’s broken down.

Atherosclerosis and Heart Disease

Atherosclerosis is the hallmark of coronary artery disease. It may be described as a chronic inflammation of the arterial wall.

Atherosclerosis leads to the formation of lesions or plaques that protrude into the lumen of the artery causing arterial narrowing, which can disturb blood flow. If this occurs in the coronary arteries, it may cause chest pain often termed angina pectoris.

The coronary arteries supply blood to the heart muscle. Acute heart attack (myocardial infarction) occurs when there is a sudden disruption of blood flow in a coronary artery. A sudden blockage is usually caused by a rupture of an atherosclerotic plaque in the vessel wall, with subsequent formation of a blood clot (thrombosis) at the rupture site. The sudden disruption of blood flow causes the death of heart muscle cells (infarction) and may impair the function of the heart muscle.

In 1961, the Framingham Study reported that high blood levels of cholesterol and high blood pressure were associated with increased risk of coronary artery disease and acute heart attack. This lead to the term “coronary risk factors” being defined.

Cigarette smoking, various fractions of cholesterol, insulin resistance, diabetes, obesity, physical activity, mental stress and depression are all examples of modifiable risk factors which, if present increase the risk of heart attack. However, although many risk factors have been identified, coronary heart disease remains a common disorder. Despite extensive research, our understanding of the mechanisms behind this disease is incomplete.

Lipids and Lipoproteins

Lipids, like cholesterol and triglycerides, are essential substances for the human body. They are used by cells for energy utilization, hormone production, bile acid formation and much more.

Because lipids are insoluble in blood, they are carried by lipoproteins that transport them to various tissues and organs. Lipoproteins consist of cholesterol, triglycerides, phospholipids and protein. The lipoproteins act as carriers transporting essential fat substances to the organs of the body.

There are five major types of lipoproteins; chylomicrons, very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density lipoprotein (HDL).

HDL and LDL lipoprotein particles have very different roles. Therefore, measuring the amount of cholesterol within these particles tells two different stories.

Elevated levels of LDL cholesterol are associated with increased risk of heart disease, but high levels of HDL cholesterol are associated with low risk. HDL particles seem to be involved in clearing and removing cholesterol from arteries and atherosclerotic plaques while LDL particles appear directly involved in the atherosclerotic process.

HDL Particles

It is important to understand that measurements of HDL cholesterol only provide information about the amount of cholesterol carried by HDL particles. HDL particles differ in size and function, and there are many types, both small and large.

HDL particle number can be measured by NMR (Nuclear Magnetic Resonance). Studies have shown that such measurements are more strongly associated with atherosclerosis than measurements of HDL cholesterol.

Recent studies have shown that simple measurements of HDL cholesterol may not always reflect HDL function. Thus, there is growing evidence that HDL function may sometimes be impaired although measurements of HDL cholesterol are normal. Therefore, measuring HDL cholesterol may not be the best method to assess HDL function.

Although incomplete, HDL cholesterol is still the most widely used measurement to assess HDL.

Other metrics that are currently being tested include HDL particle number, average HDL size, specific HDL subclasses, and HDL functional properties.

HDL Cholesterol and Heart Disease

An inverse relationship exists between HDL cholesterol and the development of coronary artery disease. In other words, high levels are associated with low risk of heart disease, and low levels are linked to high risk.

Based on data from the Framingham Heart Study the risk of heart attack increases about 25 percent for every 5 mg/dl (0.13 mmol/L) decrement in blood levels of HDL cholesterol. However, whether HDL cholesterol is a causal risk factor or merely a marker of risk is still intensely debated.

The most widely accepted hypothesis regarding the protective properties of HDL when it comes to atherosclerosis is that it promotes the uptake of cholesterol from tissues, including the vascular wall, and returns the cholesterol to the liver from where it is excreted. This process is often termed “reverse cholesterol transport.”

It has also been postulated that HDL’s may promote normal function of the endothelium, the innermost layer of the arteries. Furthermore, HDL’s may reduce inflammation, protect against oxidation of LDL, and positively affect blood clotting (thrombosis).

HDL Cholesterol Range

The table below shows the reference values;

HDL cholesterol (mg/dL)
(U.S. and some other countries)
HDL cholesterol (mmol/L
(Canada and most of Europe)
Below 40 mg/dL (men)
Below 50 mg/dL (women)
Below 1.0 mmol/L (men)
Below 1.3 mmol/L (women)
Too Low
40-49 mg/dL (men)
50-59 mg/dL (women)
1-1.3 mmol/L (men)
1.3-1.5 mmol/L (women)
60 mg/dL and above1.6 mmol/L and aboveVery good


Levels above 60 mg/dl (1.6 mmol/L) are associated with low risk of coronary heart disease. This is more likely to be seen among women than men.

HDL cholesterol below 40 mg/dL (1.0 mmol/L) is considered too low and appears to be an independent risk factor for coronary artery disease. Furthermore, the definition of metabolic syndrome includes low HDL cholesterol as one of the five criteria for classification. Low HDL cholesterol is one of the most common phenotypes seen in persons with premature heart disease.

HDL cholesterol in the range of 20-40 (0.5-1.0 mmol/L) may appear in isolation but is often associated with high triglyceride concentration, insulin resistance and increased risk of type 2 diabetes. Furthermore, some drugs, such as beta-blockers may lower HDL cholesterol. Anabolic steroids can markedly reduce HDL cholesterol and should be suspected particularly in healthy young men with unexpectedly low HDL cholesterol levels.

Levels of less than 20 mg/dL (0.5 mmol/L) are uncommon and can sometimes be attributed to very high triglycerides. It may also be due to rare genetic mutations, such as Tangier disease and fish-eye disease.

Individuals with high HDL cholesterol often have large LDL particles. They are also likely to have low LDL particle number (LDL-P). LDL-P is a reliable marker of risk for coronary artery disease.

Measuring apolipoprotein B or LDL-P may help to estimate risk among individuals with high levels of both LDL-and HDL cholesterol. Calculating non-HDL cholesterol may also be useful to assess risk under these circumstances. Determining the triglyceride/HDL cholesterol ratio may provide further information.

How Can HDL Cholesterol Be Influenced?

HDL cholesterol can be influenced by lifestyle modification.

Smoking reduces HDL cholesterol, and smoking cessation is associated with moderately increased levels.

Regular aerobic exercise can modestly increase HDL cholesterol. This increase is related to the frequency and intensity of physical activity, with greatest increases occurring with frequent, low-intensity exercise, such as five 30-minute sessions per week.

Obesity is associated with low HDL cholesterol levels and high triglyceride levels. A negative correlation exists between HDL cholesterol and body mass index (BMI), meaning that HDL cholesterol tends to be lower with increasing BMI. Weight loss usually raises HDL cholesterol.

Dietary choices affect HDL cholesterol. If the intake of fat is reduced, levels of LDL- and HDL cholesterol both decline. In one study comparing calorically balanced diets, those who consumed a low-fat diet had lower HDL-cholesterol than those who were fed a high-fat diet.

Intake of saturated fats usually increases both LDL- and HDL cholesterol. Substituting monounsaturated fat for saturated fatty acids may improve the ratio between these two subfractions of cholesterol.

Limiting intake of simple carbohydrates is usually helpful, in particular, if triglycerides are elevated. This is often the case in obese people and those with metabolic syndrome.

A diet rich in n–3 polyunsaturated fatty acids (omega-3) – sources include oils (olive, canola, soy, flaxseed), nuts (almonds, peanuts, walnuts, pecans), cold-water fish (salmon, mackerel), and shellfish — with limited carbohydrates, such as those found in ready-to-eat cereals, potatoes, white bread, and snack foods, is often recommended.

Moderate alcohol consumption raises HDL cholesterol but is usually not recommended for that purpose.

Several classes of medications increase HDL cholesterol levels; these include niacin and fibrates, and, to a lesser degree, statins. With the exception of statins, drug therapy that elevates HDL cholesterol has not been shown to improve outcome or reduce the risk of coronary events.

The 2013 American College of Cardiology/American Heart Association Guidelines for the Treatment of Blood Cholesterol to Reduce Cardiovascular Risk do not make a recommendation to add therapy to raise low HDL cholesterol in patients who are on maximal statin therapy.

31 thoughts on “HDL Cholesterol – The “Good” Cholesterol Explained”

  1. Axel, you claimed that

    “With the exception of statins, drug therapy that elevates HDL cholesterol has not been shown to improve outcome or reduce the risk of coronary events.”

    This is the case only when statin therapy is the point of comparison. See e.g. this meta-analysis of niacin trials done before the “statin age” – niacin reduces the risk of coronary events:


    And fibrates reduce the risk of non-fatal MI


  2. As you know Mie
    ‘Thrive” and another trial put the ‘Cross’ on Niacin (nicotinic acid,B3) due to the effectiveness of Statins.
    However if the patient cannot be treated to goal with statins…Niacin is an excellent add-on,
    elevating HDL and lowering ApoB.

  3. Doc,

    what about the people who are born with very low HDL levels which persist throughout the lives of these people? Are these people at higher risk of developing CHD compared to people who have genetically elevated HDL since birth? What about the lean and fit rural Japanese of the 1950s who smoked more than the Americans did at the time and certainly had much lower HDL cholesterol than the Americans and Eastern Finns did, did these Japanese have more CHD compared to Americans? Care to elaborate?

    BTW, the people at UT Southwest Medical Center in Dallas Texas do not believe that atherosclerosis is a disease of inflammation. This is the school that harbors Brown & Goldstein and the people who did the preliminary work on PCSKY9-inhibitors. In animal models inflammation does not persist when LDL is lowered.

    The chief editor of American Journal of Cardiology stated:

    “..In contrast to feeding cholesterol and/or saturated fat, it is not possible to produce atherosclerotic plaques in herbivores by raising the blood pressure chronically, by blowing cigarette smoke in their faces for their entire lifetimes, or by somehow raising the blood glucose levels without simultaneously feeding them an atherogenenic diet. Presently, it is commonly stated that “atherosclerosis is an inflammatory disease.” Inflammatory cells, however, are infrequent in plaques of coronary arteries studied at necropsy or in endarterectomy specimens. When present, the few mononuclear cells—even giant cells—appear to be present due to a reaction to the deposits of lipid (pultaceous debris) present in the plaque.“ Inflammation” appears to be a surrogate for elevation of serum C-reactive protein or various cytokines (interleukins 1 and 6, tumor necrosis factor, etc), not for inflammatory cells in plaques. Thus, it is a definition situation, and the morphologic definition of inflammation is not applicable”.


    Prevention of heart disease: is LDL reduction the outcome of choice? Absolutely yes

    “There is only one well-established relationship between blood cholesterol lipid fractions and coronary artery disease (CAD) that meets all the Heiss and Tyroler criteria of causality. While there are a number of blood lipid fractions, only LDL cholesterol satisfies these criteria”


  4. My diet and lipid results are both usual, so I would like your opinion. I am 67 years old, body fat about 10% (5’11” 155 pounds). Last spring I developed peripheral neuropathy with an A1C of 5.7, despite being lean and eating a low carb diet. Since June I have eaten a very low carb, very high fat paleo diet. I feel very good on this diet, work full time and also exercise (running, cycling, kayaking, hiking and weight lifting) about 12 hours per week. I eat a lot of saturated, monunsaturated and omega-3 fatty acids, but try to avoid oils rich in omega 6 fatty acids. I eat a lot of nonstarchy vegetables, but almost no grains or potatoes.

    My total cholesterol, HDL and LDL were all high (268, 94 and 164 mg/dL, respectively and my triclycerides was low 48 on a test two weeks ago. Two months ago, the values were total 250, HDL 106 and LDL 140 with TG 43.

    I take extra Na in my diet to hydrate well befor exercise, getting my BP up to about 130/80 in the morning. By bedtime my BP is typically 110/65.

    I am assuming that my lipids are good, since my ratio of TG/HDL is about 0.50 (mg/dl units). In any case, I would prefer to have high LDL than to have nerve damage in my feet. What do you think? I have been an athelete all my life and can race at a high level in my age group.


    P.S. In my view, the idea that saturated fat is a risk is false as long as one doesn’t combine high fat with high carbs.

    • Bill.
      I think you’re doing fine. Don’t worry too much about the numbers. As you said TG/HDL ratio is good and Non HDL-C is only borderline high. Although many experts would like to see LDL-C a bit lower, the low TG may indicate a pattern of predominantly large particles.

      In my opinion the important thing is to choose a healthy diet rich in fresh foods and avoid refined carbs and sugar. A food that makes you feel well. I also do believe exercise is a key feature of a healthy lifestyle. So, I guess the only thing I can say is “keep up the good work”.

  5. hello my name rajesh bhardwaj my TRIGLYCERIDES level is 110.0mg AndHDL level is 99.0 mg And LDL level is164.0 VLDL level is 22.0 mg BUT CHOLESTEROL level is 285.o can there is any risk of heart deased. THank

  6. I had a blood test recently;
    My results were:
    Triglycerides 1.2 mmol/L
    Cholesterol 3.1 mmol/L
    HDL Cholesterol 1.1 mmol/L
    LDL Cholesterol 1.5 mmol/L

    Non- HDL Cholesterol 2.0 mmol/L

    I am 55 male, 184 lbs and 5ft 7in
    Is this normal?

  7. Dear Doctor Sigurdsson, Just had a concern about my very high HDL Levels. I am a 47 year old male, of South Asian heritage, no chronic illnesses, no medications for anything, on a paleo/LCHF diet, supplements that I use are fish oil, magnesium, vitamin d, vitamin k2, vitamin c and a probiotic. My Cholesterol profile is-(all mg/dl) TC 248, LDL 123 (measured directly) HDL 120, Trigs 67 and VLDL 5. My BP is about 115 over 70. CT Heart Scan score of 0 (3 years ago) and a fasting glucose of about 80-85 mg/dl. HBA1C 5.1 My HDL keeps rising every year and is worrying me. People keep telling me that there can be too much of a good thing. Please give me your feedback. Thanks.

    • Hi James
      I don’t think there’s a reason for you to worry. High HDL cholesterol isassociated with low risk in almost all studies. There’s now evidence suggesting that “too much” HDL-choletserol is a problem. Besides, a calcium score of zero confirms low risk.

  8. Sorry Doctor Sigurdsson, I forgot to mention I’m 5ft 8 inches tall, 134 lbs and I exercise moderately. I don’t drink excessively and do not smoke. Thanks.

  9. Dear Dr Sigurdsson
    I have just recently had my bloods done and TC is high 7.8 mmol/l, triglycerides 0.9, HDL 3.5mmol/l, LDL 3.9mmol/l, ratio CHOL/HDL 2.2mmol/l. I am a 56 year old female, 5’3″ 63 kgs, eat a very healthy diet of fruits, vegetables, fish, lean meats etc physically active, cardio, weights training five days a week 2 hours plus per day. I also run a couple of half marathons per year. What are my risks of heart desease or do I already have this as my GP is pushing statin therapy, and scaring me with the threats of heart attacks and coronary complications in the near future if I dont start these medication immediately . I have requested a coronary CT scan, before any medication therapy.
    Your thoughts and feedback would be much appreciated .
    Regards Ann

  10. What are my risks of heart desease or do I already have this as my GP is pushing statin therapy, and scaring me with the threats of heart attacks and coronary complications in the near future if I dont start these medication immediately

    Don’t take a statin!!!! At least until your GP acknowledges potential serious adverse effects. Check on line for how much your risk of CVD would be reduced. Minuscule amount, even if only looking at LDL level. If you did a bit further, even less risk, I’m guessing.

    I ran and trekked and did tai chi until I got statins shoved on me. Look at this, and if you want to know more reginaofthesun@yahoo.com


    • Hi Howfussiner

      Thanks for your reply yes that makes for an interesting read. So far everything I have read about statins scares the hell out of me, with the damage and side effect. Then when you ask your doctor thepros and cons the benefits far out weigh the damage they do is all I have ever heard.
      I personally think I will take my chances without statin therapy.


  11. Hello Ann, Your numbers are similar to mine, but interestingly, I got mine following a Low Carb High Fat Diet. My numbers are TC 6.41, HDL 3.1, LDL 3.19 Trigs 0.8 and my ratio is 2.1

    I am no expert like Dr. Sidgurdsson, but I am almost sure that you do not need statins, so you were probably right to refuse it. Your TC is high because your HDL is super high, so there is no way round a high total.

    One thing is that I am not so sure about the benefits or safety of such a high HDL (I am also slightly concerned about mine). The jury is still out on this one. I would recommend the heart scan (my score 4 years ago was zero) and a NMR LipoProfile test just to put you at ease. My bet is your score will be zero on the heart scan and your NMR LipoProfile test will be stellar. Hope this helps.

  12. Hi James
    Thank you for your reply, I know my TC count is high because of the HDL levels, my GP is ignoring the HDL levels and quoting hook line and sinker on the TC count and the LDL count. I personally don’t think the LDL count in it self is overly high and from the reading I have been doing have thoughts a long the line that the HDL cancels out the LDL as LDL travels through the blood system to the various cells arteries etc and the HDL travels and picks the deposits of LDL and takes it back to the liver to be recycled.
    Do they do the calcium score when the do the CT scan?

    On the Blood test results it says:
    *Total chol: 7.8 mmol/l <5.5 – high because of high HDL
    Triglycerides 0.9 <1.8 – low side of normal
    HDL 3.5 1.1 – 3.5 -I read this as within normal limits
    CHOL/HDL ratio 2.2 <3.5 -low side of normal
    *LDL Chol 3.9 <3.5 -I read this as .05 above normal limit
    All other blood tests came back perfect.
    Your thoughts

    • Hi Ann

      I agree the high HDL-cholesterol makes your lipid profile much more benign. Non-HDL cholesterol is an important marker, maybe more important than LDL-C. Calcium score will be performed when you do the CT scan.

      You seem to be doing great things with regards to your lifestyle. Keep up the good work 🙂

    • Hi Ann,

      Thomas Dayspring (google him) says HDL can become dysfunctional (therefore atherogenic), and higher is not always better. The NMR LipoProfile can tell you a lot if such is high HDL is healthy or not. I have a similar HDL and I am concerned about what I am reading. LDL is not overly high, but do the NMR LipoProfile test and all will be clear. Triglycerides can never be too low, HDL is within so called within normal limits but all physicians I have ever seen say mine is the highest they have ever seen, that in itself should be slightly scary. Chol/HDL should be as low as possible. Yours is very good. Check out a book by Jimmy Moore called Cholesterol Clarity, its very informative and not expensive.

  13. Hi Ann
    My name is actually David. Although a statin drug wrecked my life, and although I know that statins are massively over-prescribed, I’m not categorically saying that no-one should take a statin.

    When I got poisoned, they gave me the statin to lower my LDLs. The cardiologist said it should be in the water supply and was the reason people now live longer. Nonsense. It’s sad to say that you can’t just trust your doctor on statins. The research, sales, advertising, expert panels—all bloated with money from Big Pharma..

    In my case the only reason the doctors pushed (and pushed and pushed) a statin on my was “high” LDLs. The possible benefit was tiny. Your case may be different. But the odds are, it’s like mine. Most people who get statined are in good health, as I used to be.

  14. Dr Sigurdsson
    Thank you for the quick response. After the CT scan and the results are back is there any other tests that you would suggest if my GP is still trying to push the statins.
    From what I have read when they do standard fasting blood cholestrol tests they don’t actually test for LDL they get this number from total cholestrol -HDL-Triglycerides, so seems to me to be an inaccurate LDL reading, a guess at best.
    Kind regards

    • Dear Ann, There is a method to test direct LDL cholesterol (not calculated) but it is not very common. Once you get your heartscan and NMR LipoProfile results and if your doctor is proven to be dead wrong, then I suggest you drop him.

  15. Dr Sigurdsson
    Just following up with my Heart Risk scan…coronery artery CT calcium score. Indications show a total coronary calcium score of 1074 it goes on to say this is a very high score. It indicates the presence of likely extensive atherosclerotic plaque within the coronary vessels at the present time. This would carry a high risk of myocardial infarction and cardiac events if not adequately treated.
    A calcium score of this degree carries a high chance of having at least one severe obstruction within the major coronary vessels and further noninvasive testing eg exercise stress test, stress echocardiogram or myocardial perfusion scan may be indecated for further assessment in this regard.BP 120/80, the twelve lead electrocardiogram was within normal limits.
    Provided noninvasivetesting satisfactorily excluded severe obstructive disease then the management would consist of very agressive attention to all treatable cardiac risk factors including consideration of statin therapy and prophylactic low dose asprin.
    Calcified atherosclerotic plaque is present in the right coronary artery (agatston 382) the left anterior descending coronary artery (agatston 529) and the left circumflex artery (agatston 163)
    Comment. Extensive coronary atherosclerotic plaque. High likelyhood of at least one significant coronary narrowing.
    Calcium plaque burden, volumn 887 – calcium score (agatston) 1074. All other arteries score 0
    Where to from here as no doubt im expecting a call from my GP when he receives and reads these results. Can you suggest further tests?
    I am quite concerned with these results considering my healthy lifestyle and diet.
    Kind regards

    • Hi Ann, just wondering if the changes in lifestyle/diet have yielded positive results that you can share. I have recently done the calcium score test and debating whether to go on the statin therapy plus aspirin, as recommended by the GP. Thank you!

      • To be honest I went to see my GP, we went through the results, told him I had been doing some study on statins, cholesterol numbers, hdl, ldl, total chol & Triglycerides etc he was so rude and told me I shouldn’t believe everything I read in magazines….excuse me I don’t read magazines, my information is from studies & trials conducted overseas Mayo clinic,etc… He went to write a script for statins, told him not to bother and walked out the door, never to return, let say I haven’t been near a GP since that day approximately 20 months ago. I am at present sticking to a healthy diet that I have followed for years, plus plenty of daily exercise, walking, running , gym, weights. I have also been researching Vit K2 MK7 & D3 and its effects on the cardiovascular system, calcium deposits. I added this supplement to my daily routine approximately 6 months ago. DN with regards yourself and whether you take statin therapy or not, this is entirely up to you as I am not a GP, I cannot tell you what you should or should not do, that is your decision. I wish you all the best

      • Update
        Early March I began to suffer some dizzy spells, after 6 weeks of these dizzy spells I went to my GP to investigate the cause and seek a solution. His first thoughts were its probably just age progression, Pardon! He did a few tests and decided it wasn’t and sent me off for a few tests. The first was a complete set of bloods, the second was a CT Coronary Angiogram.

        Clinical History: Hyperlipidemia. Total Cholesterol 7.5. Right ICA aneurysm
        Calcium Score 1357 (99th Percentile)
        Dominance The circulation is right dominant< normal origin, course and termination of the coronary arteries

        Left main Coronary Artery Normal origin from the left coronary cusp. Normal length with distal bifurcation into the LAD andLCx. No stenosis.

        Left Anterior Descending Mild 25-49% proximal LAD stenosis. The mild and distal are widely patent. The first large calibre diagonal branch demonstrates a large calcified plaque proximally which obscures the lumen. Obstructivedisease cannot be excluded in this segment.

        Left Curcumflex There is minimal luminal encroachment of the proximal left circumflex artery by calcified plaques. The distal left circumflex terminates an OM distribution with minimal luminal encroachmentOM 1 is widely patent.

        Right Coronary Artery Normal origin from the Right Coronary cusp Minimal <25% luminal narrowing throughout the RCA due to calcified plaques. Dual PDA patent Tiny PLB

        Non Coronary Cardiac Findings
        Normal cardiac chamber size and wall thickness. No intracardiac filling defect. No pericardial effusion. Tricuspid aortic valve Aorta and MPA calibre are within normal limits. Conventional systemic and pulmonary venous drainage.

        Extracardiac Findings
        No significant findings

        1. High absolute and relative calcified coronary artery plaque burden
        2. CACS 1357 (99th percentile)
        3. No obstructive coronary artery disease in the evaluable segments
        4. Obstructive disease not excluded a large calibre D1 due to calcified plaque burden.

        The GP also sent me for a Carartoid Artery Scan
        which showed a small right ICA intracavernous aneurysm measuring 2mm in maximal diameter

        The GP told me to cease all gym workouts, no running, to avoid heavy lifting, told me I was not to fly, and the in the future, once I had been assessed by a Cardiologist and treatment commenced that I would be told by the cardiologist what I could do in the future regards gym, weight, ect and that I could forget about running ever again.

        I was then referred to a Cardiologist for assessment, who at the appointment was quite surprised that I presented in front of him with (from the GPs laymans description) 3 blocked arteries, the first being 29% blocked, the second being 49% blocked and the third being 100% blocked, calcium score 1357, an aneurysm on the brain and another in the carartoid artery in the neck. These finding did not match my bloods workout, cholesterol score.

        Cholesterol 7.5
        Tryglcerides 1.0
        HDL 2.7
        Coronary risk Ratio 2.8
        LDL 4.3
        Non HDL Chol 4.8
        The Cardiologist said that my overall results to my cholesterol readings were really good, that he had not seen prior to me a HDL that was that high, that the LDL wasn't that high and that the HDL cancelled the LDL out.

        He sent me for another and a CT, I do not at this stage have the written results, however I was booked in last Thursday for another Angiagram, plus a cardiac catheterisation and possible stents.

        Arrive at the hospital, last patient of the day, taken to the OR, left arm IV llight sedation, right wrist catheter inserserted, 20 minutes later the Cardiologist says its all finished, he said you don't need stents, there are no blockages, there is a slight narrowing in a couple of the the arteries, but at present of no concern, the Calcium score is nothing like what was reported in the CT scan in fact he said the two MRIs and the two CT scan that I had had were as far as he was concerned false positives. He said that I could return to the gym, return to my running, keep up the good work and to check in with him in a months time.

        He tried to peddle the statins and I said thank but No thanks.

        I believe that the Vit K2 MK7 & Vit D3 mixture I take along with CoQ10 300mg and other vitamins has helped along with exercise and a healthy diet.

        Last but not least, the dizzy spells finally subsided a few weeks later!


  16. Axel, great website. Went off statins six months ago after being on for ten years. Started having muscle soreness problems. HDLc actually went up to 63 from 47. Tryglicerides stayed the same at 125. But LDL went from 139 to 239. LDLp is a skyhigh according to my physician 2891 (dont have previous readings) and small LDLp is 960. New doc wants me on low dose new statin, but my Try/HDL ratio seems ok with no family history. I am 50 yrs old.

  17. Hi Doctor Sigurdsson,

    I am a medicine student and am glad to have found your magnificent website with so many interesting writings. I really enjoyed reading them.

    Can the following dietary ingredients prevent HDL from dysfunction? Can you please share some ideas which food can prevent HDL from dysfunction?

    1). taking 3 teaspoons of Extra Virgin Olive Oil per day?

    2). drinking 50 ml of pomegranate juice per day?

    3). taking Ubiquinol supplements ?

    4). at what levels of HDL (in mmol/L) would indicate dysfunctional HDL?

    Many thanks for your ideas.

    • These are difficult issues Quin.
      HDL-function is complicated and still not completely understood.
      I’m sorry, but I don’t have the knowledge to provide answers to your questions.

  18. My total colestrol is 264. My HDL IS 54 even though my total is 264. Is the 54 a good reading. Do I have anything to worry about?


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