Lab result explainedCholesterol and lipidsLast updated November 8, 2026

LDL cholesterol: what high and low LDL levels mean and how to lower it

LDL cholesterol (LDL-C) · Lipid panel · reported in mg/dL in the US; mmol/L elsewhere (1 mmol/L = 38.7 mg/dL; 100 mg/dL = 2.6 mmol/L)

LDL cholesterol is the cholesterol carried in low-density lipoprotein particles, the particles that deposit cholesterol in artery walls and drive atherosclerosis, which is why it is called the 'bad' cholesterol. An LDL under 100 mg/dL (2.6 mmol/L) is optimal, 100 to 129 is near optimal, 130 to 159 is borderline high, 160 to 189 is high, and 190 mg/dL or more is very high. These categories come from the US National Cholesterol Education Program and are retained in the 2018 American College of Cardiology and American Heart Association cholesterol guideline.

The two most common reasons LDL is high are diet and genetics, usually together: a diet rich in saturated and trans fats on top of the hundreds of common gene variants that each nudge LDL upward. An LDL of 190 or more in an adult, especially with a family history of early heart disease, raises the possibility of familial hypercholesterolemia, an inherited condition affecting about one in 250 people. Hypothyroidism, kidney disease, pregnancy, some medications and very-low-carbohydrate diets also raise it.

Unlike most lab markers, LDL is not read against a fixed normal range but against your overall cardiovascular risk. The same LDL of 140 mg/dL might need nothing but diet in a healthy 30-year-old and a statin in a 60-year-old with diabetes, because the benefit of lowering LDL is proportional to how high your risk is to start with. Decades of trials show that each 39 mg/dL (1 mmol/L) reduction in LDL lowers the risk of heart attack and stroke by about 22 percent, however it is achieved.

LDL-C at a glance

  • What it is: the amount of cholesterol carried in LDL particles, which deposit cholesterol in artery walls; the main lipid driver of heart attack and stroke.
  • Categories (mg/dL): under 100 optimal; 100–129 near optimal; 130–159 borderline high; 160–189 high; 190 or more very high. Multiply mmol/L by 38.7 to convert.
  • People with existing heart disease, stroke or diabetes are usually treated to under 70 mg/dL, and the highest-risk patients to under 55.
  • An LDL of 190 or more at any adult age warrants statin treatment and a check for familial hypercholesterolemia regardless of other risk factors.
  • Low LDL is not harmful; very low levels (under 40) on treatment are safe in trials, and untreated low LDL is usually genetic, or due to hyperthyroidism, illness or malnutrition.
  • Next step: your 10-year cardiovascular risk estimate decides treatment; diet changes lower LDL by 10 to 20 percent, statins by 30 to 55 percent. Recheck 4 to 12 weeks after any change.

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What LDL-C measures

Cholesterol does not dissolve in blood, so it travels packaged in lipoprotein particles. Low-density lipoproteins are the end product of the liver's fat-transport system: the liver releases triglyceride-rich VLDL particles, and as they unload triglyceride in tissues they shrink into cholesterol-rich LDL. Each LDL particle carries one apolipoprotein B molecule and is cleared from the blood when it binds to LDL receptors on liver cells. Anything that reduces the number or activity of those receptors, whether a gene defect, saturated fat, or hypothyroidism, leaves more LDL circulating. LDL particles that cross into the artery wall are oxidised, taken up by immune cells and form the fatty streaks that grow into plaques.

Most US labs do not measure LDL directly. They measure total cholesterol, HDL cholesterol and triglycerides and calculate LDL with the Friedewald equation: LDL = total cholesterol minus HDL minus triglycerides divided by 5 (in mg/dL). The formula underestimates LDL when triglycerides are high and is not valid above 400 mg/dL; many labs now use the Martin-Hopkins or Sampson equations, which are more accurate at high triglycerides and low LDL, or a direct LDL assay. Two labs can therefore give LDL values 5 to 15 mg/dL apart from the same sample.

Fasting is no longer required for a routine lipid panel: LDL changes by less than 10 mg/dL after a normal meal, and the 2018 guideline accepts non-fasting results for risk assessment, with a fasting repeat if triglycerides are over 400. LDL varies by 5 to 10 percent from week to week in the same person, falls sharply for 6 to 8 weeks after a heart attack, major surgery or serious infection, and rises 30 to 50 percent in late pregnancy, so treatment decisions rest on two measurements taken when you are well.

Normal range for LDL-C

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

GroupTypical range (mg/dL in the US; mmol/L elsewhere (1 mmol/L = 38.7 mg/dL; 100 mg/dL = 2.6 mmol/L))Notes
OptimalUnder 100 mg/dL (2.6 mmol/L)NCEP ATP III categories, used in the 2018 ACC/AHA guideline. Average US adult LDL is about 110 mg/dL.
Near optimal / above optimal100–129 mg/dL (2.6–3.3 mmol/L)Fine for most people at low cardiovascular risk; above target for people with heart disease or diabetes.
Borderline high130–159 mg/dL (3.4–4.1 mmol/L)Diet and lifestyle change for most; a statin is considered when 10-year risk is 7.5 percent or more, or 5 to 7.5 percent with risk enhancers.
High160–189 mg/dL (4.1–4.9 mmol/L)Persistently 160 or more is itself a risk enhancer in the 2018 guideline; a statin is usually discussed.
Very high190 mg/dL (4.9 mmol/L) or higherHigh-intensity statin recommended at any age 20 to 75 regardless of other factors; evaluate for familial hypercholesterolemia and screen first-degree relatives.
Treatment threshold, established heart disease or strokeUnder 70 mg/dL (1.8 mmol/L); under 55 (1.4) for very high riskIf LDL stays at 70 or more on a maximal statin, ezetimibe and then a PCSK9 inhibitor are added. European guidelines set under 55 for very-high-risk patients.
Children and adolescentsUnder 110 acceptable; 110–129 borderline; 130 or more highUniversal screening is recommended once at age 9 to 11 and again at 17 to 21. An LDL of 160 or more in a child suggests familial hypercholesterolemia.
PregnancyRises 30 to 50 percent by the third trimesterExpected; not treated and not used for risk assessment. Remeasure 3 months after delivery or after breastfeeding ends.

High LDL cholesterol

A high LDL means more cholesterol-carrying particles are circulating than your liver is clearing, and the excess slowly accumulates in artery walls. The damage is cumulative, a product of how high LDL is and for how long, which is why an LDL of 160 at 25 matters more than the same value at 65 and why guidelines increasingly talk about lifetime exposure. Genetic studies of people born with lifelong low LDL show that each 39 mg/dL (1 mmol/L) lower LDL from birth cuts coronary risk by about half, roughly three times the benefit of achieving the same reduction with a statin started in middle age.

What a given value means for you depends on everything else. The 2018 ACC/AHA guideline uses a 10-year risk calculator (age, sex, blood pressure, smoking, diabetes, total and HDL cholesterol) rather than LDL alone. An LDL of 130 to 189 with a 10-year risk under 5 percent is managed with diet and lifestyle; at 7.5 percent or more a moderate-intensity statin is recommended; and between 5 and 7.5 percent the decision is tipped by 'risk enhancers' such as a family history of early heart disease, persistent LDL of 160 or more, metabolic syndrome, chronic kidney disease, inflammatory disease, South Asian ancestry, lipoprotein(a) of 50 mg/dL or more, apolipoprotein B of 130 or more, or a coronary artery calcium scan showing plaque.

An LDL of 190 mg/dL or more is treated differently: statin therapy is recommended regardless of calculated risk, because about one in four people at this level has familial hypercholesterolemia (FH), a dominant gene defect in the LDL receptor pathway that causes LDL to run at 190 to 400 from childhood. Untreated, about half of men with FH have a heart attack by 50 and about a third of women by 60. Clues are tendon xanthomas (cholesterol lumps on the Achilles or knuckle tendons), a corneal arcus before age 45 and a parent or sibling with a heart attack before 55 (men) or 65 (women). First-degree relatives are tested because each has a 50 percent chance of carrying the gene.

Common causes

  1. Diet high in saturated and trans fat

    Saturated fat (fatty meat, butter, cheese, coconut and palm oil) reduces LDL receptor activity; each 1 percent of calories switched from saturated to polyunsaturated fat lowers LDL by about 2 mg/dL. Industrial trans fats raise LDL and lower HDL; they are now largely removed from the US food supply. Dietary cholesterol itself has a smaller effect in most people.

  2. Polygenic (common) high cholesterol

    Hundreds of common gene variants each shift LDL by a fraction of a mg/dL; people who inherit many of them run LDL of 130 to 190 on an ordinary diet. This is the usual explanation for high LDL that runs in a family without the very high values or tendon xanthomas of FH.

  3. Familial hypercholesterolemia

    Mutations in the LDL receptor, apolipoprotein B or PCSK9 genes; about 1 in 250 people. LDL is typically 190 to 400 mg/dL from birth in the heterozygous form and over 400 to 1,000 in the rare homozygous form, which causes heart disease in childhood. Most people with FH are undiagnosed.

  4. Hypothyroidism

    Thyroid hormone drives LDL receptor expression, so an underactive thyroid raises LDL by 20 to 50 mg/dL or more; it falls back once thyroid hormone is replaced. TSH is checked in anyone with a new or unexplained rise in LDL.

  5. Kidney disease with protein loss (nephrotic syndrome) and cholestatic liver disease

    Heavy protein loss in the urine triggers the liver to overproduce lipoproteins, pushing LDL above 200. Blocked bile flow (primary biliary cholangitis, obstruction) raises total and LDL cholesterol through an abnormal particle called lipoprotein X.

  6. Medications

    Thiazide diuretics, some beta-blockers, anabolic steroids, progestin-dominant contraceptives, corticosteroids, cyclosporine, isotretinoin, some HIV protease inhibitors, amiodarone and some antipsychotics each raise LDL by roughly 5 to 20 percent.

  7. Very-low-carbohydrate and ketogenic diets

    In a subset of people, particularly lean, active individuals, a ketogenic diet raises LDL dramatically, sometimes above 200 to 300 mg/dL, through increased lipoprotein production and reduced clearance when carbohydrate is very low. The rise reverses within weeks of reintroducing carbohydrate.

  8. Menopause and ageing

    LDL rises about 10 percent across the menopause transition as estrogen falls, and increases gradually with age in both sexes until about 60 to 65, after which it tends to plateau or decline.

  9. Obesity, insulin resistance and type 2 diabetes

    These raise triglycerides and lower HDL more than they raise LDL, but they shift LDL toward small, dense particles that are more atherogenic, so LDL particle number and apolipoprotein B are often high even when LDL cholesterol looks only moderately raised.

  10. Anorexia nervosa

    Paradoxically, severe calorie restriction can raise LDL to 150 to 250 mg/dL through reduced thyroid hormone and slowed cholesterol clearance; it normalises with refeeding.

Symptoms that can go with it

  • None; high LDL itself causes no symptoms, which is why it is found on screening
  • Yellowish deposits on the eyelids (xanthelasma) or firm lumps on the Achilles or hand tendons (xanthomas) with very high or inherited levels
  • A grey or white ring around the edge of the cornea before age 45 (corneal arcus)
  • Chest pressure or breathlessness on exertion (angina), the first sign that plaque has narrowed a coronary artery
  • Calf, thigh or buttock pain when walking that eases with rest (peripheral artery disease)
  • Sudden one-sided weakness, facial droop or speech difficulty (stroke or mini-stroke), consequences of long-standing high LDL

Low LDL cholesterol

There is no lower limit of normal for LDL in clinical use, and a low value in someone who feels well is good news for their arteries. People with inherited loss-of-function variants in PCSK9 or apolipoprotein B live with LDL of 30 to 70 mg/dL from birth and have 50 to 90 percent less coronary heart disease than average, with no consistent downside. On treatment, the FOURIER and ODYSSEY trials took LDL below 30 mg/dL in thousands of patients for several years, with the same rates of cancer, cognitive problems, cataracts and diabetes as in the comparison groups, and the benefit continued to grow as LDL fell.

A low LDL that appears without treatment and without a family history of low cholesterol is a different matter and sometimes a clue to illness. Hyperthyroidism speeds LDL clearance; malabsorption, malnutrition and advanced liver disease reduce cholesterol production; and serious acute illness, chronic inflammation and some cancers suppress it. The level itself is not harmful; the question is why it fell, particularly if it dropped from a previously higher baseline or came with weight loss, diarrhoea or fatigue.

Two specific associations deserve a mention. Observational studies link LDL under about 70 mg/dL with a slightly higher rate of haemorrhagic (bleeding) stroke, although this is far outweighed by the reduction in ischaemic stroke and heart attack in statin trials. And the rare inherited condition abetalipoproteinemia, with LDL near zero, causes fat malabsorption and vitamin E deficiency with nerve and eye damage, but it presents in childhood.

Common causes

  1. Statins, ezetimibe, PCSK9 inhibitors and other cholesterol-lowering drugs

    The intended effect. High-intensity statins lower LDL by 50 percent or more; adding ezetimibe another 20 to 25 percent; PCSK9 inhibitors a further 50 to 60 percent, often to 20 to 40 mg/dL. There is no evidence that any of these levels is too low.

  2. Inherited low LDL (familial hypobetalipoproteinemia, PCSK9 loss of function)

    Affects roughly 1 in 1,000 to 3,000 people; LDL is typically 20 to 70 mg/dL lifelong and cardiovascular risk is markedly reduced. Some variants raise the risk of fatty liver because the liver cannot export fat as efficiently.

  3. Hyperthyroidism

    Excess thyroid hormone increases LDL receptor activity and cholesterol turnover, lowering LDL by 20 to 40 percent; it returns to the person's baseline with treatment.

  4. Malnutrition, malabsorption and chronic illness

    Celiac disease, pancreatic insufficiency, inflammatory bowel disease, chronic infections such as HIV and tuberculosis, advanced COPD and heart failure all reduce LDL through reduced intake, absorption or synthesis.

  5. Advanced liver disease

    The liver makes most of the body's cholesterol, so cirrhosis and acute liver failure lower LDL and total cholesterol; a falling cholesterol in known liver disease signals declining synthetic function.

  6. Acute illness, surgery and inflammation

    LDL falls by 20 to 40 percent within a day or two of a heart attack, sepsis or major surgery and stays low for 6 to 8 weeks, which is why a lipid panel during a hospital stay underestimates the usual level.

  7. Cancer and blood disorders

    Some leukaemias, myeloma and advanced solid tumours lower LDL by increased uptake or reduced production; a new unexplained fall is one of several reasons for a fuller work-up.

Symptoms that can go with it

  • None; low LDL does not cause symptoms
  • Weight loss, heat intolerance, tremor or palpitations if hyperthyroidism is the cause
  • Diarrhoea, bloating, greasy stools or fatigue if malabsorption is the cause
  • Jaundice, abdominal swelling or easy bruising if advanced liver disease is the cause
  • Fever, night sweats or unexplained weight loss, which point to infection, inflammation or cancer rather than to the cholesterol level
  • Bruising, bleeding or neurological symptoms are not caused by low LDL and need their own explanation

Read it alongside

  • Total cholesterol, HDL cholesterol and triglycerides — the rest of the lipid panel; LDL is usually calculated from them, so a high triglyceride makes the LDL figure less reliable.
  • Non-HDL cholesterol (total minus HDL) — captures all atherogenic particles including VLDL and remnants; it is a better guide than LDL when triglycerides are over 150.
  • Apolipoprotein B — one molecule per atherogenic particle, so it counts particles directly; useful when LDL and triglycerides disagree or LDL seems only mildly high in someone with diabetes or metabolic syndrome.
  • Lipoprotein(a) — an inherited particle measured once in a lifetime; a level of 50 mg/dL (125 nmol/L) or more is a risk enhancer and explains some early heart disease despite normal LDL.
  • TSH — hypothyroidism is a common, reversible cause of high LDL and should be excluded before long-term treatment.
  • Fasting glucose and A1C — diabetes changes the treatment threshold: adults 40 to 75 with diabetes are offered a statin whatever their LDL.
  • ALT and creatinine kinase — checked before and sometimes during statin therapy, since both liver disease and muscle problems affect treatment choices.
  • hs-CRP and coronary artery calcium score — used to refine the decision when risk is borderline; a calcium score of zero can justify holding off a statin, a score over 100 favours one.

What usually happens next

  1. Ask what your estimated 10-year cardiovascular risk is (the ACC/AHA Pooled Cohort Equations or PREVENT calculator); the LDL number is interpreted through it, not in isolation.
  2. If your LDL is 190 or more, or 160 or more with a family history of early heart disease or high cholesterol, ask about familial hypercholesterolemia; genetic testing is available and relatives, including children, should be screened.
  3. Check for secondary causes before starting lifelong treatment: TSH, fasting glucose, kidney function, liver tests and a urine protein check, plus a review of medications and recent diet changes.
  4. Give lifestyle changes a fair trial: 3 to 6 months of reduced saturated fat, more soluble fibre, nuts and plant sterols typically lowers LDL by 10 to 20 percent. Recheck 4 to 12 weeks after any change in diet or medication.
  5. If a statin is recommended, moderate intensity lowers LDL by 30 to 49 percent and high intensity by 50 percent or more; muscle aches occur in 5 to 10 percent of people in practice but are often reproducible with placebo, and a different statin or dose usually solves it.
  6. If LDL stays above target on a maximal statin and your risk is high, ezetimibe, bempedoic acid, PCSK9 inhibitors and inclisiran are the next steps; a lipid clinic referral is reasonable for LDL that will not come down.

Diet, lifestyle and natural levers with evidence

What can move LDL-C once the cause is known. Nothing here replaces finding the cause.

Soluble fibre, particularly psyllium and oat beta-glucan

Strong evidence

A meta-analysis of 28 randomised trials found psyllium at a median 10 g a day lowered LDL by 13 mg/dL (0.33 mmol/L), about 7 percent, with similar falls in non-HDL cholesterol and apolipoprotein B, and it works on top of a statin. Oats and barley providing 3 g a day of beta-glucan lower LDL by 9 to 10 mg/dL (about 5 to 7 percent). Each gram of soluble fibre from any source lowers LDL by roughly 2 mg/dL by binding bile acids in the gut and forcing the liver to pull cholesterol from the blood to make more.

Take psyllium with a full glass of water and separate it by 2 hours from medications, whose absorption it can delay; start low to limit bloating. Rare allergic reactions in people exposed to psyllium dust.

Plant sterols and stanols

Strong evidence

Plant sterols and stanols block cholesterol absorption in the gut. A meta-analysis of 124 trials found 2 g a day (the amount in fortified spreads, yoghurt drinks or supplements) lowers LDL by 8 to 10 percent, about 12 to 15 mg/dL, within 2 to 3 weeks, with the effect levelling off above 3 g. The reduction is additive to both diet and statins. No trial has been large enough to show a change in heart attacks, so the endorsement rests on the LDL effect.

Avoid in the rare inherited condition sitosterolemia. Reduces absorption of beta-carotene and other carotenoids by 10 to 20 percent, so eat vegetables alongside. Not studied in pregnancy or children under 5.

Nuts and soy protein

Strong evidence

A meta-analysis of 61 trials found about one serving (28 g) of tree nuts a day lowered LDL by 4.8 mg/dL and total cholesterol by 4.7, with a dose-response and no weight gain; walnuts, almonds and pistachios have the most data. A separate meta-analysis of 46 trials reviewed by the FDA found 25 g a day of soy protein (tofu, soy milk, edamame) lowered LDL by 4.8 mg/dL, about 3 to 4 percent. Both work partly by displacing meat and dairy fat and partly through plant protein and unsaturated fat.

Nuts are calorie-dense (about 170 kcal per 28 g); swap them for other snacks rather than adding them. Soy is safe for people with a history of breast cancer according to current evidence, but check with your oncologist if you have been told otherwise.

Portfolio diet and cutting saturated fat

Strong evidence

The Portfolio diet combines the levers above: 2 g plant sterols, 10 to 25 g viscous fibre, 50 g soy protein and 45 g nuts a day within a plant-based pattern low in saturated fat. In the original 4-week metabolic-ward trial it lowered LDL by 29 percent, the same as 20 mg of lovastatin (31 percent); in a 6-month real-world trial with dietary advice only, the fall was 13 percent, and a 2018 meta-analysis puts the average at about 17 percent (0.73 mmol/L). Replacing saturated fat with unsaturated fat alone lowers LDL by about 2 mg/dL per 1 percent of calories swapped, and a Cochrane review of 15 trials found that reducing saturated fat cut cardiovascular events by 17 percent.

Red yeast rice

Moderate evidence

Red yeast rice contains monacolin K, which is chemically identical to the statin lovastatin. A meta-analysis of 20 trials found it lowered LDL by 39 mg/dL (1.02 mmol/L) compared with placebo, equivalent to a low-dose statin, and a large Chinese trial of a standardised extract (Xuezhikang) in 4,870 heart attack survivors cut coronary events by 45 percent over 4.5 years. The evidence that it lowers LDL is solid; the problem is the product.

The FDA has ruled that red yeast rice products containing more than trace monacolin K are unapproved drugs, so US supplements are either low in the active ingredient or technically illegal, and an analysis of 12 US products found monacolin K ranging from 0.3 to 11 mg per capsule, with four contaminated by the kidney toxin citrinin. Expect statin side effects (muscle pain, liver enzyme rise) and statin interactions (grapefruit, some antibiotics and antifungals, cyclosporine); do not combine with a prescribed statin; avoid in pregnancy, breastfeeding and liver disease. If you want a known dose of lovastatin, a prescription is the safer route.

Berberine

Moderate evidence

Berberine increases LDL receptor numbers on liver cells by a different route from statins (stabilising receptor mRNA and lowering PCSK9). Meta-analyses of randomised trials, mostly 8 to 12 weeks at 500 mg two or three times a day, found LDL falls of about 25 mg/dL (0.65 mmol/L) and total cholesterol of 24 mg/dL, with triglycerides down about 40 mg/dL. Trials are small and mostly from China, and there are no cardiovascular outcome data, so it is a reasonable adjunct, not a replacement for proven therapy.

Constipation, diarrhoea and stomach upset are common; it inhibits CYP3A4, CYP2D6 and P-glycoprotein, raising levels of cyclosporine, some statins, and potentially warfarin and other drugs; lowers blood glucose additively with diabetes medication; avoid in pregnancy, breastfeeding and infants. Product quality varies widely.

When to see a clinician promptly

  • Chest pressure, pain spreading to the arm, jaw or back, breathlessness or sudden sweating, particularly with known high cholesterol: possible heart attack, call emergency services.
  • Sudden weakness or numbness on one side, facial droop, slurred speech, loss of vision or severe sudden headache: possible stroke, call emergency services even if it passes.
  • An LDL of 190 mg/dL or more at any age, or 160 or more with a parent or sibling who had a heart attack or stroke before 55 (men) or 65 (women): needs assessment for familial hypercholesterolemia and family screening.
  • A child or teenager with an LDL of 160 or more, or lumps over the Achilles tendons or knuckles: refer to a lipid specialist.
  • Unexplained muscle pain, weakness or dark urine after starting a statin or red yeast rice: possible myopathy, which needs a creatine kinase test, promptly if severe.
  • An LDL that has fallen sharply without treatment, especially with weight loss, diarrhoea, night sweats or jaundice: the cause, not the number, needs investigating.

Frequently asked questions

What is a normal LDL level?

Under 100 mg/dL (2.6 mmol/L) is optimal, 100 to 129 near optimal, 130 to 159 borderline high, 160 to 189 high and 190 or more very high. There is no single 'normal' because the right target depends on your risk: for a healthy person with no other risk factors an LDL under 130 is acceptable, while someone with heart disease or diabetes is usually treated to under 70. The average LDL among US adults is about 110 mg/dL.

Is an LDL of 130 high?

An LDL of 130 mg/dL is at the bottom of the 'borderline high' band (130 to 159). For a younger adult with normal blood pressure who does not smoke and has no diabetes or family history, it is usually managed with diet and lifestyle and rechecked in a year or so. For someone over 50 with high blood pressure, diabetes or a 10-year cardiovascular risk of 7.5 percent or more, the same value would prompt a conversation about a statin. The number only makes sense alongside your overall risk.

Is an LDL of 160 or 190 dangerous?

An LDL of 160 to 189 is high and roughly doubles coronary risk compared with under 100 over the long term; it is a 'risk enhancer' in US guidelines and most people at this level are offered a statin if lifestyle change does not bring it down. An LDL of 190 or more is very high: statin treatment is recommended regardless of other risk factors, because sustained exposure at this level causes heart attacks in middle age, and about one in four people with it has familial hypercholesterolemia, so relatives should be tested.

How can I lower LDL without medication?

The measures with the best evidence are: replacing saturated fat (fatty meat, butter, cheese, coconut oil) with unsaturated fats (olive and rapeseed oil, nuts, oily fish), which lowers LDL by about 2 mg/dL per 1 percent of calories swapped; 10 g a day of psyllium or 3 g of oat beta-glucan (LDL down 7 to 10 percent); 2 g a day of plant sterols (8 to 10 percent); a handful of nuts (about 5 mg/dL) and 25 g of soy protein (3 to 4 percent). Combined, as in the Portfolio diet, these lower LDL by 15 to 30 percent, which is comparable to a low-dose statin. Weight loss and exercise help more with triglycerides and HDL than with LDL.

What LDL level requires a statin?

US guidelines recommend a statin for anyone with existing heart disease or stroke, anyone 20 to 75 with LDL of 190 or more, adults 40 to 75 with diabetes, and adults 40 to 75 with LDL of 70 to 189 whose 10-year cardiovascular risk is 7.5 percent or more (and consider it at 5 to 7.5 percent with risk enhancers). So there is no single LDL cut-off below 190; a 45-year-old with an LDL of 150 and no other risk factors may not need one, while a 65-year-old with diabetes and an LDL of 90 does.

Can LDL cholesterol be too low?

Not as far as trials can tell. People born with genetically low LDL (30 to 70 mg/dL) are healthy and have much less heart disease, and trials that lowered LDL below 30 mg/dL with statins plus PCSK9 inhibitors for several years found no increase in cancer, memory problems, diabetes or cataracts. Cholesterol needed for cell membranes and hormones is made inside cells, not taken from LDL in the blood. An LDL that falls unexpectedly without treatment should be explained (thyroid, liver, absorption, illness), but the low value itself is not the danger.

Why is my LDL high on a keto or low-carb diet?

A minority of people, often lean and physically active, see LDL climb steeply, sometimes above 200 or 300 mg/dL, within weeks of cutting carbohydrate below about 50 g a day. The liver appears to export more cholesterol-rich particles and clear them more slowly when carbohydrate is scarce and saturated fat intake is high. Whether this LDL is as harmful as the same level from other causes is unsettled, but there is no evidence that it is harmless, and most lipid specialists advise bringing it down by reintroducing some carbohydrate and replacing saturated with unsaturated fat.

Do I need to fast for an LDL test?

Usually not. LDL changes by less than 10 mg/dL after an ordinary meal, and the 2018 US guideline accepts non-fasting lipid panels for screening and risk assessment. Fasting for 9 to 12 hours is still asked for when triglycerides were over 400 mg/dL on a previous test (because calculated LDL becomes unreliable), when a precise LDL is needed to judge treatment in someone with very high risk, or when the panel is drawn alongside a fasting glucose.

References

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  3. Ference BA, Ginsberg HN, Graham I, et al.. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. European Heart Journal (2017)
  4. Cholesterol Treatment Trialists' (CTT) Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet (2010)
  5. Jovanovski E, Yashpal S, Komishon A, et al.. Effect of psyllium (Plantago ovata) fiber on LDL cholesterol and alternative lipid targets, non-HDL cholesterol and apolipoprotein B: a systematic review and meta-analysis of randomized controlled trials. American Journal of Clinical Nutrition (2018)
  6. Ras RT, Geleijnse JM, Trautwein EA. LDL-cholesterol-lowering effect of plant sterols and stanols across different dose ranges: a meta-analysis of randomised controlled studies. British Journal of Nutrition (2014)
  7. Del Gobbo LC, Falk MC, Feldman R, Lewis K, Mozaffarian D. Effects of tree nuts on blood lipids, apolipoproteins, and blood pressure: systematic review, meta-analysis, and dose-response of 61 controlled intervention trials. American Journal of Clinical Nutrition (2015)
  8. Blanco Mejia S, Messina M, Li SS, et al.. A meta-analysis of 46 studies identified by the FDA demonstrates that soy protein decreases circulating LDL and total cholesterol concentrations in adults. Journal of Nutrition (2019)
  9. Jenkins DJ, Kendall CW, Marchie A, et al.. Effects of a dietary portfolio of cholesterol-lowering foods vs lovastatin on serum lipids and C-reactive protein. JAMA (2003)
  10. Gerards MC, Terlou RJ, Yu H, Koks CH, Gerdes VE. Traditional Chinese lipid-lowering agent red yeast rice results in significant LDL reduction but safety is uncertain: a systematic review and meta-analysis. Atherosclerosis (2015)
  11. Gordon RY, Cooperman T, Obermeyer W, Becker DJ. Marked variability of monacolin levels in commercial red yeast rice products: buyer beware!. Archives of Internal Medicine (2010)
  12. Lan J, Zhao Y, Dong F, et al.. Meta-analysis of the effect and safety of berberine in the treatment of type 2 diabetes mellitus, hyperlipemia and hypertension. Journal of Ethnopharmacology (2015)

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.