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Low-carb LDL hyper-responders

Eating a low-carb diet has been shown to improve weight loss, blood sugar control, and insulin sensitivity, among other benefits.​​1

However, the effect low-carb diets may have on low-density lipoprotein (LDL) cholesterol remains a significant concern for many clinicians, preventing some of them from recommending these potentially beneficial diets.

Scientific studies support that low-carb and ketogenic diets do not significantly increase LDL cholesterol for the average person with type 2 diabetes or obesity.2 Instead, people following low-carb diets usually see an increase in high-density lipoprotein (HDL) cholesterol with a decrease in triglycerides, triglyceride-rich remnant cholesterol, and small LDL particles.3 One study even demonstrated an overall reduction of LDL particles.4

However, these results represent an average of study participants. Some individuals may see a dramatic rise in their LDL by over 50% and be considered an LDL hyper-responder.5

Specific populations, like lean athletes, may be even more likely to develop elevated LDL levels.6

Low-carb-LDL-hyper-responders-
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What is an LDL hyper-responder?

Understanding the risks posed to low-carb LDL hyper-responders is tricky, as these individuals fall into an emerging area of study where little clear evidence exists. However, Dave Feldman, an engineer and popular low-carb “citizen-scientist,” has partnered with a prominent physician-researcher to start a scientific study on the subject. They have proposed a definition for enrollment in the study for a specific subset of hyper-responders termed “lean mass hyper-responders” as having the following:

  • An increase of 50% or more in LDL cholesterol to at least 190 mg/dL (5 mmol/L) since adopting a low-carb diet
  • HDL cholesterol at 60 mg/dL (1.5 mmol/L) or above
  • Triglycerides at 80 mg/dL (0.9 mmol/L) or below 

For practical purposes, we prefer a simpler definition for all low-carb hyper-responders that focuses exclusively on LDL:

  • An increase of 50% or more in LDL cholesterol, to a level considered elevated by a clinical provider, since adopting a low-carb diet

Other cardiovascular risk markers such as HDL, triglycerides, insulin resistance calculations, blood pressure, lipoprotein(a), and coronary calcium scores may further clarify the potential risk imparted by elevated LDL and should likely be evaluated.

When considering whether you are a low-carb LDL hyper-responder, it’s also important to confirm that you don’t have familial hypercholesterolemia (FH). Familial hypercholesterolemia is a genetic condition in which LDL receptors aren’t able to clear LDL from the circulation. This condition results in markedly elevated LDL levels from birth and likely carries a different prognosis than isolated high LDL after a dietary change.7


Why does LDL go up on a low-carb diet?

Since the inquiry into the cardiovascular health of LDL hyper-responders is relatively new, no mechanistic studies prove why LDL increases in low-carb hyper-responders. But several theories exist:

  • Energy delivery model
    Engineer and “citizen-scientist” Dave Feldman from cholesterolcode.com first popularized the energy delivery model. This model states that people eating a low-carb diet depend on triglycerides (fat) more than glucose for energy. Therefore, the liver produces more triglyceride-rich, very low-density lipoprotein (VLDL) particles. These particles go into circulation and deliver the triglycerides to tissues — such as muscles — that need them for energy.
    When a VLDL particle releases triglycerides, it eventually transforms into an LDL particle. Therefore, this hypothesis suggests the increased LDL is the downstream result of an individual requiring more energy delivery from triglycerides.
  • Increased substrate model
    This model suggests that the body’s process of creating ketones also increases the production of the molecule acetyl CoA. One fate of acetyl CoA is that our bodies eventually convert it into cholesterol. Therefore, this hypothesis suggests more acetyl CoA leads to more LDL cholesterol.8
  • Increased cholesterol and saturated fat intake
    This model suggests that eating more fat and dietary cholesterol increases the amount of cholesterol delivered to the liver, ultimately resulting in a downregulation of liver LDL receptors.9Having fewer LDL receptors on the liver results in less cholesterol being cleared from the circulation; this leads to an increased number of LDL particles and LDL cholesterol in the blood.
  • Lower insulin levels
    Similar to increasing dietary saturated fat, lower insulin levels may downregulate LDL receptors as well, thereby decreasing the clearance of LDL particles and increasing their overall numbers.10
  • Genetic predisposition
    Some maintain that LDL elevations above 190 mg/dL (5 mmol/L) represent occult familial hypercholesterolemia, and are therefore genetically predetermined. However, an observational study of self-reported hyper-responders makes this unlikely as the magnitude of rise in LDL showed a clear inverse correlation with BMI and TG:HDL ratio – features that are not related to familial hypercholesterolemia. In addition, those with a dramatic LDL elevation had a nearly identical baseline LDL (135 mg/dL or 3.5 mmol/L) as those who saw a smaller rise.11

We don’t know which of these hypotheses, if any, is correct. They may all play a role, or there may be a completely different explanation for why LDL increases in some people — but not others — upon starting a low-carb diet.

Regardless of the mechanism, the keys are evaluating whether or not the increased LDL creates a net harm for the individual, and if so, if there are ways to safely and effectively lower the value.


Is elevated LDL harmful for low-carb hyper-responders?

Multiple lines of scientific evidence report that higher LDL levels are associated with higher rates of heart disease in the general population.12 In addition, lower LDL levels — either through inborn genetic mutations or treatment with statins — correlate with a lower risk of heart disease.13

However, the magnitude of risk posed by elevated LDL in the general population is often lower than many people expect.14 You can read more about the specifics in our guide, Is LDL cholesterol harmful?

Most influential medical societies believe the balance of evidence is sufficiently strong to support the stance that elevated LDL increases the risk of cardiovascular disease, and that lowering LDL is beneficial.15

The main unanswered question is whether increased LDL in low-carb hyper-responders has a more benign prognosis than the same elevation in those eating a standard diet. 

To answer that, we need to look at other situations where LDL has been shown to not correlate with increased cardiovascular risk.

For example, some research suggests that elevated LDL, in the presence of high HDL and low triglycerides, carries little or no increased cardiovascular risk.16 However, more research is needed to confirm these findings and determine if the very-high values of LDL seen in LDL hyper-responders confer the same risk as in the general population.17

Because clinical data are only suggestive — not conclusive — that there can be situations where high LDL isn’t harmful, we need to assess the strength of mechanistic arguments as to why this could be the case.

One such mechanism is that people eating low-carb diets reduce their more harmful small LDL particles and shift to larger particles.18 Although there is debate about whether larger particles contribute to atherosclerosis, it seems clear that — at a minimum — large LDL particles contribute less than smaller particles.19

In addition, some researchers speculate that low-carb diets may lead to a reduction in oxidized LDL cholesterol. Since elevated oxidized LDL particles have a very strong association with heart disease, a lifestyle that lowers oxidized LDL is presumed to have a beneficial cardiovascular effect.20

In addition, LDL is clearly involved in the process of forming vascular plaque. But LDL by itself likely isn’t sufficient to initiate and cause vascular injury and the entire plaque-forming cascade.21 Since other factors are required — like high blood pressure, vascular inflammation, high blood sugar, etc.— another hypothesis is that in the absence of those factors, elevated LDL doesn’t carry the same increased risk.

While there isn’t clear evidence that elevated LDL in a low-carb hyper-responder imparts less risk than in the general population, reasonable hypotheses exist as to why it might, and they deserve further investigation.

We also need to wonder if there is a threshold effect beyond which LDL elevations signify significant risk. Most medical guidelines consider an LDL level of 190 mg/dL (5 mmol/L) as an absolute dangerous level. However, would this threshold level be higher — like 220 or 250 mg/dL (5.8 or 6.6 mmol/L) — in metabolically healthy low-carb eaters without evidence of familial hypercholesterolemia?

We don’t have the answer to that question.


How can hyper-responders lower LDL on a low-carb diet?

fibre-foods-low-carb

If you have elevated LDL while eating a low-carb diet and want to lower it, we have some tips that may be helpful. You can read more details in our evidence-based guide on lowering LDL while on a low-carb diet, but here’s a summary of the main recommendations:22

  • Increase your carb intake
    Either cycling more carbs or continuously eating more carbs will frequently lower LDL.23 Evaluating your carb target and why you set it at that limit is a good place to start, as it may be time to reevaluate your goals. Note that increasing carbs may not be an appropriate option if you are eating a strict low-carb diet to treat a medical condition such as diabetes or epilepsy.
  • Increase your fiber intake
    Studies show that higher fiber intake can lower LDL.24 While none of the studies were done on low-carb diets, clinical experience suggests fiber may also lower LDL on low-carb diets. Since fiber found in whole foods doesn’t contribute to your net carb count, this is a good first step for those who want to maintain a strict low-carb diet.
  • Decrease your saturated fat intake
    Although many low-carb and keto diets don’t significantly increase saturated fat, reducing it may still help reduce LDL. Good places to start are the “extra” sources of saturated fat like butter or cream in your coffee, adding cream to your recipes, or adding extra servings of fatty sauces. Switching to more monounsaturated fat, by eating more nuts, olive oil, and avocado, may help you remain low carb and reduce your LDL.25 26

When to consider medications 

Elevated LDL is not a marker to casually dismiss. There may be reasons to be concerned, and in some cases, add medication to reduce your risks.

You and your clinician may want to consider the following questions when deciding whether to  add an LDL-lowering medication:

  • Do you want to follow the cardiology guidelines because that gives you peace of mind?
  • Do you have other significant cardiac risk factors such as:
    • high blood pressure, prediabetes, hyperinsulinemia, or elevated lipoprotein(a)?
    • a strong family history of premature heart disease?
  • Do you have an elevated coronary calcium score or other evidence of significant vascular plaque?
  • Do you feel that lowering LDL is important but believe you’re experiencing other benefits from a low-carb lifestyle — so much so that you’re not interested in changing your diet?

If you answer “yes” to one or more of these questions, medication may be a good option.

This list is not meant to be comprehensive, as there may be other reasons to consider medication. Please consult with your healthcare provider.

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Action items if you are a LDL hyper-responder

The first thing to do is make sure you are genuinely a hyper-responder. That usually means ruling out familial hypercholesterolemia and checking that your LDL is considerably elevated (at least 50% above your baseline), while HDL and triglyceride levels are normal. 

Next, understand that we don’t have definitive evidence for this population. Current cardiology guidelines recommend a low-fat diet and medical treatment to lower LDL. However, you may want to individualize your approach and weigh the risks and benefits of continuing a low-carb diet, given the unclear implication of elevated LDL in hyper-responders.

Consider working with a clinician familiar with low-carb nutrition and LDL hyper-responders who can assess your overall cardiac risk. You can find many of them listed on our Find a doctor map. Your clinician may recommend some of the other diagnostic tests described in this guide.

Know that there are dietary changes you can make to try to lower your LDL while remaining on a low-carb diet. 

And finally, if you are a low-carb LDL hyper-responder, you can help advance the science. Enroll in an ongoing clinical trial to contribute to better evidence in this emerging area of study. At the time of this guide’s publication in 2021, we know of one that you can learn more about at citizensciencefoundation.org.


  1. Reviews in Endocrinology and Metabolic Disorders 2020:
    Efficacy and safety of very low calorie ketogenic diet (VLCKD) in patients with overweight and obesity: A systematic review and meta-analysis
    [systematic review of randomized trials; strong evidence]

    BMJ 2021: Efficacy and safety of low and very low carbohydrate diets for type 2 diabetes remission: systematic review and meta-analysis of published and unpublished randomized trial data [systematic review of randomized trials; strong evidence]

    JCI Insight 2019: Dietary carbohydrate restriction improves metabolic syndrome independent of weight loss [randomized trial; moderate evidence]

  2. Nutrition Reviews 2019: Effects of carbohydrate-restricted diets on low-density lipoprotein cholesterol levels in overweight and obese adults: a systematic review and meta-analysis
    [systematic review of randomized trials; strong evidence]

  3. Cardiovascular Diabetology 2018: Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study. [non-randomized trial; weak evidence]

    Nutrition in Clinical Practice 2011: Low-carbohydrate diet review: shifting the paradigm [review article; ungraded]

    British Journal of Nutrition 2016: Effects of low-carbohydrate diets v. low-fat diets on body weight and cardiovascular risk factors: a meta-analysis of randomised controlled trials [strong evidence]

  4. American Journal of Clinical Nutrition 2021: Effect of carbohydrate-restricted dietary interventions on LDL particle size and number in adults in the context of weight loss or weight maintenance: a systematic review and meta-analysis
    [systematic review of randomized trials; strong evidence]

  5. This is based on the consistent clinical experience of practitioners familiar with low-carb nutrition. [weak evidence]

  6. BMJ Open Sport and Exercise Medicine 2018: Paradox of hypercholesterolaemia in highly trained, keto-adapted athletes
    [non-controlled study; weak evidence]

  7. There are no studies comparing clinical outcomes for someone with FH and someone who is a low-carb LDL hyper-responder, but many experts in the field of low-carb nutrition believe their prognosis would be different.

    A diagnosis of FH is usually made using scoring tools such as the Simon Broome or Dutch criteria, which may include a genetic test for FH. While discussing the diagnosis of FH is beyond the scope of this guide, suffice it to say that the diagnosis should not be made based solely on one’s LDL level. History of heart disease, physical exam findings of high cholesterol, family history of high cholesterol or heart disease, and genetic testing should all be considered in the course of making a diagnosis.

  8. Dr. Nadir Ali, a cardiologist experienced with low-carb nutrition, has promoted this hypothesis in some of his online talks.

  9. Journal of Nutrition 1998: Dietary fatty acids and the regulation of plasma low density lipoprotein cholesterol concentrations [overview article; ungraded]

  10. The following paper supports the concept that lower insulin levels result in a downregulation of LDL receptors. However, this has primarily been studied in the setting of insulin deficiency (type 1 diabetes) and insulin resistance plus insulin deficiency (type 2 diabetes). We don’t know if the concept holds for an LDL hyper-responder — whose pancreas functions normally, but who tends to have lower insulin levels due to increased insulin sensitivity and decreased dietary carbohydrate intake.

    Trends in Endocrinology and Metabolism 2013: The regulation of ApoB metabolism by insulin [overview article; ungraded]

  11. One important diagnostic criterion for familial hypercholesterolemia is what a person’s LDL has been throughout their life and how early in life their LDL was elevated. This study of hyper-responders showed that the magnitude of LDL-rise was higher with both lower BMI and lower TG:HDL ratio but had no association with age.

    Current Developments in Nutrition 2021 Elevated LDL-Cholesterol with a Carbohydrate-Restricted Diet: Evidence for a ‘Lean Mass Hyper-Responder’ Phenotype [non-randomized study with self-reported data, very weak evidence]

  12. Circulation 1998: Prediction of coronary heart disease using risk factor categories
    [nutritional epidemiology study with HR<2, very weak evidence]

  13. JAMA 2016: Association between lowering LDL-C and cardiovascular risk reduction among different therapeutic interventions: A systematic review and meta-analysis
    [systematic review of randomized trials; strong evidence]

    Journal of Clinical Lipidology 2016: A review of low-density lipoprotein cholesterol, treatment strategies, and its impact on cardiovascular disease morbidity and mortality
    [overview article; ungraded]

    Athersclerosis, Thrombosis, and Vascular Biology 2010: Genetic variants influencing circulating lipid levels and risk of coronary artery disease
    [overview article; ungraded]

  14. Studies suggest that an elevated LDL could increase cardiac risk five-fold over 35 years. But what does this mean? A five-fold increase is a relative increase, so if the baseline risk is very low, like 0.25%, then a 5-fold risk is still small in an absolute sense – in this case 1.25%. With higher baseline risk, such as 5%, then a five-fold increase is much more significant — 25% in this case.

    Journal of the American Heart Association 2019: Trajectories of blood lipid concentrations over the adult life course and risk of cardiovascular disease and all-cause mortality: Observations from the Framingham study over 35 years
    [non-controlled study; weak evidence]

  15. Journal of the American College of Cardiology 2019: 2019 ACC/AHA guideline on the primary prevention of cardiovascular disease: A report of the American College of Cardiology/American Heart Association task force on clinical practice guidelines
    [overview article; ungraded]

    European Heart Journal 2020: 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk
    [overview article; ungraded]

  16. Circulation 2001: Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S
    [non-controlled study; weak evidence]

    Canadian Journal of Cardiology 1998: Cholesterol and lipids in the risk of coronary artery disease — the Framingham Heart Study
    [nutritional epidemiology study with HR<2, very weak evidence]

    Metabolic Syndrome and Related Idsorders 2003:
    Triglycerides, high-density lipoprotein cholesterol, and risk of ischemic heart disease: a view from the Copenhagen Male Study
    [non-controlled study; weak evidence]

  17. Some hyper-responders have LDL elevations to 220 mg/dL, while others may see values as high as 400 mg/dL or more. The conventional wisdom in the mainstream cardiology community is that the absolute level directly correlates with risk, whereas many in the low-carb medical community question if that is true.

    Although we suspect — but don’t know for certain — that elevated LDL in hyper-responders may represent a very different mechanism and clinical course than in familial hypercholesterolemia, most studies looking at very high LDL have been done in people with FH. We have, therefore, included some of these data below, as we examine other risk factors that might correlate more strongly with risk than LDL.

    One study reported that for individuals with heterozygous FH, factors such as hypertension, smoking, and diabetes increased heart attack risk more than absolute elevation of LDL.

    Atherosclerosis 2014: Severe heterozygous familial hypercholesterolemia and risk for cardiovascular disease: a study of a cohort of 14,000 mutation carriers
    [nutritional epidemiology study with HR<2, very weak evidence]

    And another study reported that VLDL and HDL were more predictive of cardiac risk than absolute level of LDL.

    Circulation 1995: Coronary artery disease in heterozygous familial hypercholesterolemia patients with the same LDL receptor gene mutation
    [nutritional epidemiology study with HR<2, very weak evidence]

    However, in the absence of well-designed trials, the majority of evidence still supports the hypothesis that extreme elevations of LDL may significantly increase cardiac risk.

  18. American Journal of Clinical Nutrition 2021” Effect of carbohydrate-restricted dietary interventions on LDL particle size and number in adults in the context of weight loss or weight maintenance: a systematic review and meta-analysis [systematic review of randomized trials; strong evidence]

  19. Circulation 2004: Atherogenic lipoprotein particles in atherosclerosis
    [overview article; ungraded]

    Athersclerosis, Thrombosis, and Vascular Biology 2005: Low-density lipoprotein subfractions and the long-term risk of ischemic heart disease in men: 13-year follow-up data from the Québec Cardiovascular Study [non-controlled study; weak evidence]

    Athersclerosis 2014: Comparison of four methods of analysis of lipoprotein particle subfractions for their association with angiographic progression of coronary artery disease [non-controlled study; weak evidence]

  20. Circulation 2005: Plasma oxidized low-density lipoprotein, a strong predictor for acute coronary heart disease events in apparently healthy, middle-aged men from the general population
    [observational study with HR>2; weak evidence]

    Although data are lacking, Dr. Volek and others published a paper suggesting that, because low-carb diets reduce systemic inflammatory markers, it is likely that they would also lower oxidized LDL.

    Journal of Nutrition 2005: Modification of Lipoproteins by Very Low-Carbohydrate Diets[overview article; ungraded]

    And since oxidized LDL is associated with metabolic syndrome, a diet that improves metabolic syndrome may help reduce oxidized LDL. The following study demonstrates the association between oxidized LDL and metabolic syndrome. However, the assumption that treating metabolic syndrome with a low-carb diet will reduce oxidized LDL is an unproven hypothesis.

    Diabetes 2017: Oxidized LDL Is Associated With Metabolic Syndrome Traits Independently of Central Obesity and Insulin Resistance
    [non-controlled study; weak evidence]

  21. American Journal of Pathology 2012: Plaque attack: one hundred years of atherosclerosis in The American Journal of Pathology [overview article; ungraded]

  22. These recommendations are based on clinical experience, as studies regarding LDL reduction through dietary means for hyper-responders are lacking.

  23. An observational study including five case studies of low-carb LDL hyper-responders reported that increasing carbohydrate intake from less than 25 grams per day to between 50 and 100 grams per day led to an LDL decrease between 100 mg/dL (2.6 mmol/L) and 480 mg/dL (12.6 mmol/L). These case reports were extreme examples but they highlight that modestly adding back carbs seems to have a profound LDL-lowering effect in those who have a significant rise upon starting a very low-carbohydrate diet.

    Current Developments in Nutrition 2021 Elevated LDL-Cholesterol with a Carbohydrate-Restricted Diet: Evidence for a Lean Mass Hyper-Responder Phenotype [nonrandomized study with self-reported data, very weak evidence]

  24. American Journal of Clinical Nutrition 2000: Long-term cholesterol-lowering effects of psyllium as an adjunct to diet therapy in the treatment of hypercholesterolemia [randomized trial; moderate evidence]

  25. Journal of Clinical Lipidology 2016: Impact of avocado-enriched diets on plasma lipoproteins: A meta-analysis [systematic review of randomized controlled trials; strong evidence]

    Archives of Internal Medicine 2010: Nut consumption and blood lipid levels: a pooled analysis of 25 intervention trials. [strong evidence]

  26. Reducing saturated fat may also unintentionally reduce protein. Therefore, you may want to consider increasing your lean protein intake to ensure you continue to get metabolic benefit from a low-carb diet. You can read more about the benefits of high-protein diets in our evidence-based guide.