The importance of the fasting TG/HDL ratio

By George Henderson and Grant Schofield

If you have a standard lipid test done in New Zealand and most other parts of the world, it will usually give a couple of ratios at the bottom. One of these is the fasting triglyceride-to-HDL cholesterol ratio.

It can also be calculated from the other measurements using this online calculator.

Note that the reference range says that under 2 is ideal, 2-4 is “normal”, over 4 is high.
In our opinion TG/HDL ratios in the 2-4 range may be normal, but they are still likely to be unhealthy or predictive of future ill health. Why is this?

Fasting triglycerides (TG) are usually low (<1) in low carb, fat-adapted people. An exception can be during rapid weight loss.

If TG are high in the fasting state this indicates insulin resistance, and when triglycerides are too high their transfer to the HDL particles causes the HDL count to drop. Because the natural range of TG is fairly wide and context-dependent, the value of this single measurement is disputed, and HDL and the fasting TG/HDL ratio are taken as the more sensitive markers.

Another value is that these are cheap markers which are commonly tested. While there others that may be better, such as fasting insulin or 2-hour insulin, the TG/HDL ratio, especially considered in the context of other common measures including HbA1c and LDL cholesterol, often gives a valuable “look under the hood” at the state of metabolism and hormonal health.

We are constantly asked to comment on standard lipid panels. We think the TG/HDL ratio tells you a fair bit. So here’s our take.

First we will discuss evidence for HDL independently, then for the TG/HDL ratio.


This slide is from the SMART study group, and represents the risk for “all vascular events” in a lipid-lowering trial in 6,111 individuals with a previously diagnosed arterial disease.[1] The controls were a group taking a low-dose statin that didn’t significantly lower their LDL. As you can see, only the control arm in the highest quartile for HDL at baseline had a significant risk reduction. The mean baseline TG/HDL ratios by HDL quartile were 6.2, 3.6, 2.9, and 1.6.

What’s intriguing about this is that these are people with pre-existing arterial disease, often from years earlier (historical). The high HDL quartile has the lowest rates of diabetes and metabolic syndrome and the lowest BMI (25.1 vs 28.1) and waist circumference (92 vs 99.3 cm), so does this group include more historical cases, and represent to a greater extent these men and women who, after their event or diagnosis, managed to improve their hormonal metabolism in various ways? We don’t know, because this kind of evidence isn’t supplied, but an earlier study from the SMART study group showed this interesting correlation between HDL , LDL and new events in a population at high risk (with high cholesterol or high blood sugar). Highest HDL (≥1.50 mmol/l) is protective in people with high LDL (≥2.5 mmol/l), whereas for those with low LDL, a lower HDL is sufficient (≥1.26). Again this is with a TG/HDL ratio of 1.6 in the combined upper HDL quintile, and 2.7 in the 4th quintile.[2]


Some further evidence about TG and HDL comes from an older set of data, the Helsinki Heart Study. In this study a fibrate, Gemfibrozil, was used to lower cholesterol (fibrates lower triglycerides and small, dense LDL), and there was an untreated placebo arm (black bars). Here in this placebo arm we can clearly see the effect of triglycerides and HDL in reducing risk.[3]



In the placebo group (n = 2,045), the low density lipoprotein cholesterol (LDL-C)/high density lipoprotein cholesterol (HDL-C) ratio was the best single predictor of cardiac events. This ratio in combination with the serum triglyceride level revealed a high-risk subgroup: subjects with LDL-C/HDL-C ratio greater than 5 and triglycerides greater than 2.3 mmol/l had a RR of 3.8 (95% CI, 2.2-6.6) compared with those with LDL-C/HDL-C ratio less than or equal to 5 and triglyceride concentration less than or equal to 2.3 mmol/l. In subjects with triglyceride concentration greater than 2.3 mmol/l and LDL-C/HDL-C ratio less than or equal to 5, RR was close to unity (1.1), whereas in those with triglyceride level less than or equal to 2.3 mmol/l and LDL-C/HDL-C ratio greater than 5, RR was 1.2. The high-risk group with LDL-C/HDL-C ratio greater than 5 and triglyceride level greater than 2.3 mmol/l profited most from treatment with gemfibrozil, with a 71% lower incidence of coronary heart disease events than the corresponding placebo subgroup. In all other subgroups, the reduction in CHD incidence was substantially smaller.

Summary so far: From both the SMART study and Helsinki we see that the TG/HDL ratio is especially important when LDL cholesterol is high. Why is this?

In this graph from a paper by Boizel et al you see that the TG/HDL ratio predicts LDL particle size. The proportion of small, dense atherogenic LDL particles rises sharply, and the proportion of intermediate and large particles falls, as the TG/HDL ratio increases in these patients (n=60 with type 2 diabetes and HDL ≥ 1 mmol/l).[4]


The typical dyslipoproteinemia of type 2 diabetes is characterized by elevated VLDL, small (dense) LDL particles, and decreased HDL (4). The percentage of individuals having small LDL is increased by at least twofold in type 2 diabetes (5).
The prevalence of this qualitative abnormality of LDL has been reported to be surprisingly high, even in the absence of the characteristic diabetic dyslipidemia. Thus, up to 45% of patients with low triglyceride (TG) levels and an even higher percentage of patients with borderline hypertriglyceridemia have small LDL, in comparison with 30% in nondiabetic men and 10% in nondiabetic women (5–8).
Three prospective studies have established that small dense LDL is the best predictor
of future coronary artery disease (CAD) in nondiabetic subjects, even after adjustment for confounding by TG, LDL cholesterol, and HDL cholesterol levels (9).

These authors propose a TG/HDL ratio cut-off of 1.5 to diagnose atherogenic LDL particle size in people with type 2 diabetes.

The fasting TG/HDL ratio is highly correlated with 2-hour insulin (insulin levels 2 hours after consuming glucose) and, with a higher cut off, is also predictive of fasting hyperinsulinaemia.[5] Insulin activates the same HMG-CoA reductase (HMGR) pathway that statins inhibit.[6, 7, 8] This explains why the protective effects of HDL and of statins are not at all additive, and why in SMART and Helsinki, as well as the JUPITER trial, lipid lowering treatments made little or no difference to high HDL and/or low TG groups, who were already at lower risk.

This evidence also predicts that drugs such as statins may be more effective than the large studies say they are when patients are carefully chosen on the basis of individual diagnostic markers, including the fasting TG/HDL ratio; bearing in mind, however, that this is an easy marker to change with a low carb healthy fat diet, which, if it changes the TG/HDL ratio, will also change LDL particle size and insulin levels for the better, amongst other things. There will be less chance of harmful side effects on the LCHF diet compared to drug interventions.

Take homes:

  1. LCHF will have an important and postive effect on the fasting TG/HDL ratio
  2. Fasting is critical. There has been a tendency in NZ, to go with non-fasted. We imagine this is just easier because of compliance issues.  But it totally ruins the ratio as TG change rapidly when you eat. They are very prone to a rapid rise with carb intake because insulin fluxes carb-derived TG out of the liver.
  3. Fasted TG and HDL measures will  mean your estimate of LDL (which is never directly measured) will be more accurate. So our advice is to do the blood lipid tests fasted for a more accurate and meaningful result.


Lowering of 2-hour post-prandial insulin response by a 20% carbohydrate diet vs 40% carbohydrate, from Gannon and Nuttall 2009.[9]

[1] van de Woestijne AP, van der Graaf Y, Liem A, Cramer MM, Westerink J, Visseren FJ. Low High-Density Lipoprotein Cholesterol Is Not a Risk Factor for Recurrent Vascular Events in Patients With Vascular Disease on Intensive Lipid-Lowering Medication. J Am Coll Cardiol.2013;62(20):1834-1841.

[2] Hajer GR, van der Graaf Y, Bots ML, Algra A, Visseren FL; SMART Study Group.
Low plasma HDL-c, a vascular risk factor in high risk patients independent of LDL-c.
Eur J Clin Invest. 2009 Aug;39(8):680-8. doi: 10.1111/j.1365-2362.2009.02155.x. Epub 2009 May 12.

[3] Manninen V, Tenkanen L, Koskinen P, et al.
Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment. 
[4] Boizel R, Benhamou PY, Lardy B, Laporte F, Foulon T, Halimi S. Ratio of triglycerides to HDL cholesterol is an indicator of LDL particle size in patients with type 2 diabetes and normal HDL cholesterol levels. Diabetes Care. 2000 Nov;23(11):1679-85.

[5] Li C, Ford ES, Meng YX, Mokdad AH, Reaven GM.Does the association of the triglyceride to high-density lipoprotein cholesterol ratio with fasting serum insulin differ by race/ethnicity?
Cardiovasc Diabetol. 2008;28;7:4.

[6] Ness GC, Zhao Z, Wiggins L.
Insulin and glucagon modulate hepatic 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity by affecting immunoreactive protein levels.
J Biol Chem. 1994 Nov 18;269(46):29168-72.
[7] Vincent TS, Wülfert E, Merler E.
Inhibition of growth factor signaling pathways by lovastatin. Biochem Biophys Res Commun. 1991 Nov 14;180(3):1284-9.

[8] Chen H, Ikeda U, Shimpo M, Shimada K.
Direct effects of statins on cells primarily involved in atherosclerosis.
Hypertens Res. 2000 Mar;23(2):187-92.

[9] Gannon MC, Nuttall FQ.
Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition.
Nutrition & Metabolism2006;3:16


  1. Regarding the way LDL is calculated from the 3 other values (total cholesterol, HDL, and TG) this calculator is invaluable

    The “Iranian” calculation here gives more accurate results than the “Friedwald”, which is the formula always used in NZ (and I would think anywhere else), when TG is low. The references for the 2 different formulas are in the links.

    You can see by playing with the calculator on the test formula that non-fasted TG (which will be higher) will give you LDL that’s a bit lower by Friedwald, and much higher by Iranian, than it should be.
    The difference that fasting TG plus the Iranian formula makes to the LDL calculation when fasting TGs are under 100 mg.dL (1.13 mmol/l) is significant in terms of risk calculations.

    “Statistical analysis showed that when triglyceride is <100 mg/dL, calculated low- density lipoprotein cholesterol is significantly overestimated (average :12.17 mg/dL or 0.31 mmol/L), whereas when triglyceride is between 150 and 300 mg/dL no significant difference between calculated and measured low-density lipoprotein cholesterol is observed. In patients with low serum triglyceride and undesirably high total cholesterol levels, Friedewald equation may overestimate low-density lipoprotein cholesterol concentration and it should be either directly assayed or be calculated by a modified Friedewald equation. Using linear regression modeling, we propose a modified equation."

    Even the Iranian formula may not be accurate if total cholesterol isn't high – it was designed for people with total cholesterol above 250 mg/dL (6.46 mmol/L) – but it's the best we have to date for people with low fasting TGs.

  2. Interestingly the lab my current GP used to use measured LDL as it came out neatly between the Friedwald and Iranian calculated numbers. I used to have high LDL, very high trigs and low HDL, for the last twelve years I have good HDL, slightly high LDL and trigs generally around or below 1.

    Sadly the lab she now uses does Friedwald, as did the labs used by previous doctors. Even more sadly, increasing numbers of patients no longer have their trigs tested – or reported.

    1. that is interesting, do you mean directly measured LDL? in this study that appeared today (a must-read for anyone interested in the effect of saturated fat ) the LDL also seems to be different from both Friedwald and Iranian.
      It doesn’t specify in the methods, but LDL was probably calculated directly by NMR.

      1. Yes I believe so, once when she rang through my results I was all set to tell her what they *actually* were using the Iranian Equation then I noticed they were off from the Friedwald values anyway. Dunno what sort of lab equipment they used to use. Currently they quite closely correspond to the Iranian Equation and the variance from Friedwald reduces with my trigs.

  3. Thanks for this great article George and Grant. I am guessing you might have already seen this study but just in case…

    1. Thanks Nelly – here’s a follow-up poster

      What’s interesting here is that all cases were treated with statins and that should have nullified the protective association with HDL, yet the TG/HDL ratio still retains some predictive power.

      Looking for more on that study lead me to this one;

      An A to Z type diet trial looking at HDL size.

  4. Based on a multiethnic sample, we identified TG/HDL-C cut-off values of 1.62 in men and 1.18 in women that were best able to discriminate between men and women with and without MetSY.

    Our results indicate that TG/HDL-C is a superior marker to identify men and women with MetSy compared to TC/HDL-C, LDL-C/HDL-C, and nonHDL-C/HDL-C.

  5. Diane Soffe · · Reply

    Good morning, try as I may, my briain is just not scinetific enough to follow your very detailed information! I do know that I now need to fast prior to a blood test. This is my previous test, and as you can imagine, the dr wants a repeat. As far as I can tell, the TRI/LDL is really good so I think I should be right, but is this your take on it? I follow very much the LCHF lifestyle.
    Total Cholesterol 10.60
    LDL 8.01
    HDL 2.13
    Triglyceride 1.00
    Total Cholesterol/HDL 4.98
    HDL/LDL 0.266
    Tri/HDL 1.075

    1. Hi Diane,

      (this is NOT medical advice as we know very little about you, but just general discussion of these numbers!)

      if you use the Iranian calculation, designed for cases like yours (high cholesterol, low TG) the LDL is 7.23.

      This makes the ratios a bit better, but I’m not going to lie, while high cholesterol may be OK, these levels are very high. Whether this is risky or not depends on many factors such as sex (female is good), age (more is better), blood pressure, HbA1c and so on, but the lower the TG/HDL ratio the better, so a fasting test is definitely called for. This may well have some effect on the total and calculated LDL.

      If someone has started the diet recently and is losing weight the high cholesterol may reflect this and come down somewhat eventually, though it is likely to remain in the “high” category (you don’t say whether it has always been high overall).

      In cases of persistently high cholesterol it may be worth having thyroid function checked as hypothyroidism is a fairly common cause of high cholesterol (including HDL), and thyroid dysfunction can be an effect of autoimmunity, including intolerance to a grain-based diet, that leads some people to try the LCHF and Paleo diets in the first place.

      1. Little remembered fact – before IR/metabolic syndrome became so prevalent I understand doctors would always check thyroid when they saw high LDL. They did mine and in the past TSH always came in around 1 but my LDL was high, HDL low and trigs through the roof. They told me to eat less fat, naturally.

        Little known fact, because it’s rarer – hypERthyroid drops LDL, in my case exactly as much as the statin I no longer take. Then it shot up again when I was overtreated (TSH went from 0.001something to 12) and there’s no point looking at my lipids again until this is back in range. There’s actually little point in looking anyway with HDL at 1.4 or above and trigs at 1 or less, but you know doctors . . .

  6. Diane Soffe · · Reply

    Thank you very much for the prompt reply. I’m 60 years old, fit and healthy. I’m not over weight (53kg), I excercise regularly. I haven’t had many cholestrol tests, but the last one, several years ago, and before LDHF was about 8. My mother has always had high cholesterol (8.6) and has been asked to take statins. I took up the LCHF for the long term health benefits, and to try to stop the slow, steady upward weight gain that’s often associated with ageing! Thanks again for all the interesting, scientific information you offer. I’l certainly look at having the thyroid test done too.

  7. Merry christmas and happy new year 2017, Grant and George.


  9. Hi George and Grant,

    Good explanation of the significance of a TG/HDL ratio.

    Back a few years in 2014 when I started a low carb high fat diet, I tested my blood after 4 months.

    TG/HDL = 70.88/69.66 = 1.05

    My wife started at the same time as me, took the test too and got

    TG/HDL = 70.74/69.66 = 1.15

    These are pretty much perfect figures.

  10. I was recently diagnosed with FH by a well-respected lipidologist at a local teaching hospital in Oregon. He based my diagnosis on lipid numbers and family history of early heart disease (my sister had an MI at 49 yrs old), using the “Dutch method.” No other physical symptoms other than slight amount of corneal arcus. I have an appointment with a geneticist next week for test to confirm FH diagnosis.

    Not surprisingly, the doctor wants me to go on statin (atorvastin) therapy because I am at “high risk”. I am very reluctant for a number of reasons.

    I’m not looking for medical advice, but have been doing tons of my own research trying to make sense of things. I respect your opinion and am trying to find a little perspective here. I have no science background, so bear with me. 😉

    I am a 56 year old woman who was diagnosed at 38 (18 years ago) with PCOS and insulin resistance by a reproductive endocrinologist. I had been overweight/obese since childhood. For reference, my BMI was 44 and this was my lipid panel at the time:

    TC 245
    HDL 46
    LDL 182
    TG 187

    Prior to beginning a keto diet 3 years ago, I had maintained (more or less) a weight loss of 65 lbs in the intervening years (average BMI around 35-40) and these were my numbers (not much different):

    TC 277
    HDL 55
    LDL 190
    TG 160

    I’ve since lost an additional 75 lbs (now BMI 23.3) and have maintained that loss for nearly two years. My overall health has improved dramatically, and many chronic issues have been resolved (including high blood pressure). My most recent lipid panel:

    TC 367
    HDL 82
    LDL 266
    TG 93
    ApoB 192 mg/dL (range 55-125)
    Lp(a) <10 mg/dL (range <30)

    Other relevant information:

    A1C 5.0% (from a high of 5.7%, never officially 'prediabetic')
    hs-CRP 1.44 mg/dL (range <0.7)
    TSH 3.245, up from 2.064 (waiting for referral to address this)
    Vit D3 34.5 (down from 88; resumed 10,000 IU/day of D3)
    CAC (Agaston) score: 2.3 (last month); up from 1.0 (2.5 years ago)
    ApoE: e3/e3
    Started HRT 2 months ago
    Major surgery (5-hour) 12 months ago
    Current macros: net carbs <25 g, protein 95-105 grams, fat 130-135 g

    From much of the research I have been doing about CAD, FH, and statins, these are my questions:

    Within the context of FH, while there is an increase overall in CAD, there doesn't appear to be a direct correlation between LDL and CAD, and those with otherwise good metabolic markers (low insulin) seem far less affected. Also, while mortality from CAD is higher, total mortality is less so (protective aspects?), with mortality risk being about even with general population by age 60. What's your opinion?

    With my LDL/HDL ratio being 3.2 and my TG/HDL ratio being 1.1, my overall risk of a CAD event appears to be relatively low based on what you've discussed here. Do you think this lower risk carries over to those of us with FH and otherwise good metabolic markers?

    For primary prevention for women, statins seem to have little benefit in terms of preventing CAD events and virtually none for improving overall mortality. The risks to multiple systems of the body are concerning (particularly blood glucose, muscles, cognition, etc.). My lipidiolgist refers to those as “perceived risks,” by the way, as if they are not valid concerns.

    Beyond statins, there are some experts (Zoe Harcombe, for instance), who seem to think that trying to lower LDL (within the context of FH) could even be dangerous in that it appears that the cells are already not uptaking LDL the way they should and to force lowering of LDL would starve them further. Based on this, should I even be concerned with my saturated fat intake and addressing lowering LDL with supplements, much less prescription meds?

    While my CAC score is more than 0 and has increased slightly from 1.0 to 2.3 over the past two and a half years, it is still quite low. How does this factor into my overall risk?

    My lipidologist seems to think that all of my “good” markers don't make up for the high LDL, ApoB, and the CAD evidenced on the CAC (which he points out has grown). While he didn't challenge my keto diet directly, he did mention that “ketogenic diets are often not beneficial for people with FH,” before sending me off to meet with his dietician. To his credit, he did say that I should not take the statins (or any course of treatment) if I did not feel comfortable with it. He did point out that, even if I embraced every non-pharmaceutical approach (extra-low sat fat diet, supplements, etc.), it would probably not be “enough.”

    I know that this is a lot of information, and let me reiterate that I am not looking for advice. I would be grateful, however, if you could share your perspective with me and perhaps point me in the right direction.

    Thanks in advance! Laura

    1. Hi Laura,

      from what I can tell the TG/HDL ratio is critically important in FH.

      the CAC score has grown little (what is the margin of error for a change from 1-2.3?), and you did have other things going on. You can lower TG/HDL without being strictly keto, of course, but it seems as if keto agrees with you, apart from the rise in LDL and ApoB. The vitamin D3 will help, because the higher LDL and lower LDL-R means that fat soluble vitamins are not transported into arterial cells efficiently; this applies to vitamin E too and this is potentially important for CHD risk.

      If your LDL (and ApoB?) was lower before keto, then there may well be a way of reducing it again while keeping the improved TG/HDL ratio, and this would surely reduce risk (calculated risk, anyway).

      I hope this helps, Grant will surely have more to say as well.

    2. I’d certainly see if you can get your thyroid addressed, T4 and T3 would be useful tests if available. That TSH would be not be considered for treatment in the UK, you might be more fortunate and getting it back nearer to 1 might improve symptoms you didn’t realise you had yet. It would reduce LDL but not sure by how much. Overtreating it would not be a good way of lowering the LDL though, personal experience is that when my thyroid goes high my leg arteries get mashed up and improve when I get it back around normal despite the LDL going down. An interesting observation about the causality of “cholesterol”.

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s

Richard David Feinman

Richard Feinman, the Other

The Science of Human Potential

Understanding how to be the best you can be. Professor Grant Schofield.


A topnotch site

LCHF, Diet & Health


Eat real food. Enjoy real health.

%d bloggers like this: