Lipids
LDL, HDL, and Triglycerides: your cardiovascular risk markers.
The LDL/HDL ratio tells you how your LDL cholesterol relates to your HDL cholesterol: one number divided by the other. In women that number naturally runs low, and that is less reassuring than it looks. Oestrogen keeps HDL higher, so the denominator is larger, and the result stays low even when your LDL is already high. Around menopause the picture reverses: LDL climbs while HDL slips, so numerator and denominator move against you at the same moment and the ratio rises faster than either value on its own. Never read this number apart from your LDL, and do not compare it with a man's.
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No established reference range
There is no generally accepted Dutch reference value for the LDL/HDL ratio. The NVKC does publish a cholesterol ratio - total cholesterol divided by HDL (below 5, ideally below 3.5) - but no LDL/HDL ratio. The NHG-Standaard CVRM (2024) no longer uses a cholesterol ratio for risk assessment, looking instead at LDL- and non-HDL-cholesterol themselves. For the LDL/HDL ratio specifically there is therefore no Dutch standard we can show; we would rather state no number than one without a source. Discuss your cholesterol with your doctor, looking at your LDL, your non-HDL and, if useful, the cholesterol ratio (total/HDL).
Unit: ratio
Reference ranges may vary between laboratories. When you order a test, a BIG-registered doctor assesses your personal results in context. For treatment decisions, discuss your results with your GP.
The numerator of this number is your LDL cholesterol, the cholesterol that can accumulate in the artery wall; the denominator is your HDL cholesterol, the cholesterol carried back to the liver. No separate tube of blood is drawn for it: the laboratory divides two values that were already on your report and prints the outcome as a single figure without a unit. What makes the ratio distinctive in women sits in the denominator.
Oestrogen stimulates the production of HDL particles. Women in their reproductive years therefore carry a markedly higher HDL on average than men of the same age, and a larger denominator makes every fraction smaller. At an identical LDL your outcome lands lower than your partner's, without anything having been said about your artery wall. Work it through: an LDL of 3.6 mmol/l alongside an HDL of 1.8 mmol/l gives 2.0, while the very same LDL alongside an HDL of 1.1 mmol/l lands at 3.3. One numerator, two entirely different conclusions.
That numerator is meanwhile the most fragile part of the sum. In most laboratories your LDL is not measured but estimated: total cholesterol, reduced by the HDL and by a fixed share of the triglycerides. The estimate assumes triglycerides stay modest. Take an oestrogen preparation by mouth and they climb instead, so the estimated LDL drops away when it should not. The cholesterol/HDL ratio does not carry that flaw, because both of its values are determined directly.
Do not confuse the two either. The cholesterol/HDL ratio puts total cholesterol above the line, and for that one the NVKC publishes a limit of 5, preferably below 3.5. For the LDL/HDL ratio the NVKC publishes no limit; the 3 that is often quoted is an international rule of thumb without a Dutch source, and that is why this page shows no reference value.
A single rule of thumb for both sexes sounds even-handed, but it lands unevenly. Because women's HDL sits higher on average, the often quoted limit of 3 is in practice a far gentler test for you than for a man. You can sit comfortably below 3 with an LDL your own doctor would want to raise with you. That is the heart of the objection to this number in women: it reassures at exactly the moment there is something to discuss.
On top of that comes the arithmetic blindness of any fraction. Take two women who both land on 3.0. The first has 3.0 mmol/l LDL alongside 1.0 mmol/l HDL. The second has 4.5 mmol/l LDL alongside 1.5 mmol/l HDL. Their figure is identical, yet the second carries half as much harmful cholesterol again. It is that absolute quantity which settles into the artery wall across decades.
Then the transition. In the years around menopause you lose the oestrogenic protection from two sides at once: LDL climbs while HDL often slips a little. With almost any other cause only one half of the fraction moves; here they move together. The consequence is that the ratio rises more steeply than the LDL or the HDL on their own, and a woman used to years of favourable results can see a very different number within a few years. That is no personal failure and certainly no diagnosis; it is a hormonal shift becoming visible in your lipids.
And then this: no guideline sets a target for this fraction. The European ESC/EAS guideline steers on the LDL itself, with non-HDL cholesterol and ApoB as secondary goals; the Dutch NHG CVRM standard steers on LDL and non-HDL. If either of those appears on your report, let it weigh more heavily than any fraction. Non-HDL also counts the VLDL and remnant particles that are entirely absent from this ratio, and ApoB counts the number of harmful particles rather than their cargo. Both tell you something this division cannot.
You do not order this ratio separately; it arrives automatically as soon as a lipid panel has determined the LDL and the HDL. So the question is when such a panel yields anything meaningful, and in women that depends more on life stage than on age.
Your cycle is not a serious obstacle here: cholesterol values drift slightly with it, but not enough to overturn a result. Hormone use counts for far more. Starting or stopping the pill, switching to another preparation, or beginning hormone therapy around menopause changes your profile within a few months. So do not test in the first weeks afterwards, and record with every result which preparation you were using at the time.
Fasting weighs more heavily here than for the individual cholesterol values, because your LDL is derived from the triglycerides. Above roughly 4.5 mmol/l that derivation is no longer valid and the outcome says nothing. Pregnancy also lifts the whole lipid profile substantially; a panel belongs some months after delivery. Wait a few weeks after an infection or surgery as well, and when comparing two results allow for the natural noise of five to ten percent on the LDL.
A newly unfavourable profile deserves an explanation before your diet takes the blame. An underactive thyroid raises LDL and occurs considerably more often in women than in men, so have a TSH included in the first round. Poorly controlled diabetes, kidney and liver disease, heavy alcohol use and a range of medicines can equally explain the picture.
Each life stage moves the ratio in its own direction. In the reproductive years without a hormone preparation, LDL is on average lower than in men of the same age and oestrogen keeps HDL higher, so the ratio runs structurally low, even with an LDL that deserves attention. On a combined pill with oral oestrogen, HDL usually rises, although some progestogens push it down, and triglycerides rise alongside, which makes the calculated LDL less reliable. Hormone therapy taken as tablets lowers LDL and raises HDL, because the oestrogen passes through the liver first, while the higher triglycerides distort the numerator; by patch or gel the profile barely changes, because the skin route bypasses the liver. In perimenopause LDL begins to rise and HDL may slip slightly, so the ratio climbs faster than the LDL alone. After menopause LDL sits structurally higher and HDL on average slightly lower, and the ratio shifts towards the male level.
Always have your result assessed by a doctor, together with your individual values and your full risk profile.
You cannot feel a low LDL/HDL ratio. Cholesterol gives no signal, whatever proportion it circulates in, so there are no complaints that belong to a low value, and in itself a low outcome is perfectly fine.
The risk lies in the reassurance. In women a low ratio is the normal state: your HDL sits naturally higher, so the fraction comes out small by itself. An outcome of 2.2 therefore says far less than the same figure in a man. On top of that come the distortions. Oral oestrogen, whether from the pill or from hormone tablets, raises HDL and triglycerides at once: the first shrinks the fraction and the second artificially depresses the calculated LDL. Alcohol likewise raises HDL and improves nothing at all. And after an infection or surgery cholesterol falls temporarily of its own accord.
A good-looking ratio is therefore no proof of a favourable profile. Always place your LDL beside it and have the whole picture assessed by a doctor.
A raised LDL/HDL ratio causes no complaints either. Atherosclerosis proceeds noiselessly for years, and there is no fatigue, no hot flush and no other signal by which you could recognise an unfavourable cholesterol balance. What you do notice belongs to the cause underneath.
In women a few causes stand out. The hormonal transition raises LDL and lowers HDL, so the outcome can shift within a few years without anything having changed in your habits. An underactive thyroid raises LDL and occurs far more often in women than in men. Reduced insulin sensitivity, as commonly accompanies polycystic ovary syndrome, goes together with high triglycerides and a lower HDL. Smoking lowers HDL directly, and pregnancy lifts the entire lipid profile temporarily.
A high ratio is no diagnosis and no proof of cardiovascular disease. It is a reason to pull up the individual values, to have an underlying cause ruled out and to discuss the whole picture with a doctor.
Start with what you should not do: treat this number as a goal. A fraction can be improved in two ways, and the easier of them, pushing HDL upwards, changes nothing about the amount of cholesterol that can accumulate in your artery wall. In large trials of medicines that specifically raise HDL, the HDL duly went up while the number of cardiovascular events stayed the same. So steer by your LDL, and by non-HDL cholesterol or ApoB where your report carries them.
What genuinely lowers LDL has long been established: replace saturated and trans fat with unsaturated sources, eat more fibre from pulses, oats, vegetables and fruit, keep a healthy weight and move regularly. Stopping smoking also raises HDL, and that is one of the few steps where this number and your health move in the same direction. Strength training and adequate protein belong on the list around menopause in any case, though more for your bones and muscle mass than for your lipids.
Leave alcohol out of that list. It raises HDL and so flatters the outcome, while simultaneously driving triglycerides up and making the calculated LDL less reliable.
If your profile shifts around the transition, do not hold it against yourself; that is a hormonal change. Never start, stop or alter hormone therapy or a cholesterol-lowering medicine on your own initiative on the basis of a self-ordered result, and do not switch from tablet to patch by yourself either. That conversation belongs with your doctor, who weighs your full risk profile.
Because oestrogen keeps your HDL higher on average, and the HDL sits below the line. A larger denominator makes the outcome smaller by itself, even when your LDL is exactly equal to his. The difference therefore says something about your hormones and nothing about which of you carries more harmful cholesterol. Compare your own LDL with your previous LDL instead.
Both halves move against you at once: LDL rises as oestrogen production winds down, and HDL often slips slightly with it. Because the numerator grows while the denominator shrinks, the outcome climbs more steeply than either value on its own. A woman used to years of favourable results can therefore see a clearly higher number within a few years.
Usually yes, and not in one direction. The oestrogen in a combined pill raises HDL, which lowers the outcome, but also raises triglycerides, which makes the calculated LDL unreliable. Some progestogens push HDL down instead. The net effect therefore differs per preparation. Record with every result which pill you were taking, or you will compare two measurements that are not comparable.
For this number it does. Oestrogen you swallow passes through the liver first and changes the lipid profile clearly: LDL falls, HDL rises and triglycerides climb. A patch or gel bypasses that liver passage and leaves the profile largely untouched. Your ratio can therefore change through the route of administration alone. The choice between them is a conversation with your doctor.
For this ratio that is no strict requirement. Cholesterol values drift slightly with the cycle, but the effect stays smaller than the ordinary variation of the measurement itself. Fasting matters more, because your LDL is derived from the triglycerides. If you follow your values across years, always test under the same conditions and at the same laboratory; that gains you more than counting cycle days.
Because your doctor looks at your LDL and at your whole risk profile. The 3 is an international rule of thumb without a Dutch source and applies to both sexes, while your higher HDL pulls the outcome structurally downwards; you can therefore sit well below it with an LDL that is too high for your age and risk profile. The guideline sets no goal for this ratio, but it does for the LDL.
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This marker is included in the following test panels.
LDL, HDL, and Triglycerides: your cardiovascular risk markers.
Key health markers: CBC, lipids, and Vitamin D.
Our broadest panel: CBC, thyroid, vitamins, lipids, liver, kidney, and HbA1c.
Medical reviewer
Dr. Naimi oversees the medical standards behind our content and assessments.
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Every result includes a professional assessment from a BIG-registered doctor. For treatment decisions, discuss your results with your GP.
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