Cholesterol and
low-carb diets

Cholesterol is an essential component of our bodies and, although there are clear data showing an association between having high blood cholesterol levels and increased cardiovascular risk, it is not clear that cholesterol always equates with increased cardiovascular risk for everyone.1
Read on to learn what cholesterol is, how your body uses it, why low-carb and keto diets may lead to a change in blood cholesterol levels, and whether you should be concerned if your cholesterol increases with a keto or low-carb lifestyle.

Disclaimer: The negative effects of high serum cholesterol levels on human health are well established in the medical literature, but are controversial for populations not represented by these studies, such as in the context of a low-carb diet.

This guide is our attempt at summarizing what is known. It is written for adults who are concerned about cholesterol and health, especially when eating a low-carb diet. Discuss any lifestyle changes with your doctor. Full disclaimer

For even more details and relevant research on connected topics, see our guides to healthy fats, vegetable oils and saturated fats. Also see our list of core scientific studies related to heart disease, cholesterol and saturated fats.


The basics: What is cholesterol?

Cholesterol is a waxy substance that is essential for the life of all animals, including humans.2 Cholesterol is found in virtually every cell of your body and is necessary for many bodily functions, including:

  • Cell integrity: As an integral part of every cell membrane in the body, cholesterol is required for maintaining cell structure and fluidity.
  • Hormone synthesis: Cholesterol is needed to make steroid hormones such as estrogen, testosterone, cortisol, and other related hormones, such as vitamin D3.
  • Creation of bile acids: Your liver converts cholesterol into bile acids, which help you absorb fats and the essential fat-soluble vitamins A, D, E and K.
  • Myelin formation: The myelin sheath that surrounds and protects nerve cells contains plenty of cholesterol.3

Your body makes most of the cholesterol that is found in your bloodstream. It’s primarily produced in the liver.

Dietary cholesterol – found in animal foods like eggs, shellfish, cheese, and organ meat – makes up a smaller portion of your blood cholesterol pool.

Unlike fat, which contains nine calories per gram, cholesterol has no calories. Because it’s present in foods in very small amounts, it’s measured in milligrams instead of grams. Most fatty meats and whole-milk dairy products contain just a little cholesterol, whereas some shellfish and organ meats are high in cholesterol, yet low in fat.

After years of advice to toss the egg yolks and eat only the whites, we’ve learned that eating cholesterol-rich foods doesn’t impact blood cholesterol levels very much. In fact, when people take in more cholesterol from food, the liver usually produces less, resulting in stable blood cholesterol.4


How is cholesterol transported in your body?

Cholesterol is absorbed from your digestive tract or produced by your liver and circulated throughout your bloodstream, where it can be used by cells as needed. The remaining cholesterol then returns to the liver to be converted into bile acids or used for other purposes.

Importantly, cholesterol doesn’t travel around your bloodstream on its own. As a hydrophobic (water-repelling) substance, it must be packaged within lipoproteins to move around the bloodstream.

Think of lipoproteins as boats needed to safely carry cholesterol through the bloodstream. When we talk about blood cholesterol levels, we’re referring to the amount of cholesterol contained in different lipoprotein particles (sort of like the number of passengers on the boats).

In addition to cholesterol, these lipoprotein particles also contain special proteins called apolipoproteins, triglycerides, and other compounds.

  • Cholesterol packaged in lipoproteins that contain apolipoprotein B100 (usually called Apo B) is referred to as LDL (low-density lipoprotein) cholesterol, or LDL-C (referred to by the more common term LDL for the rest of this guide).5
  • Cholesterol packaged in lipoproteins that contain apolipoprotein A is referred to as HDL (high-density lipoprotein) cholesterol, or HDL-C (referred to by the more common term HDL for the rest of this guide).

Despite what we’ve all heard, there’s actually no such thing as “good” or “bad” cholesterol; there is only one type of cholesterol. Your LDL and HDL values refer to how much cholesterol is carried in your HDL and LDL lipoprotein particles. In fact, the same cholesterol is continuously transferred among these and other types of lipoproteins as they make their way through the bloodstream.

LDL is often referred to as “bad” cholesterol because high levels have been linked to increased heart disease risk. By contrast, HDL is frequently called “good” cholesterol because low levels of HDL have been associated with increased heart risk. In addition, one of HDL’s main functions is to carry cholesterol back to the liver to be used as needed or excreted through bile.

However, this is an overly simplistic view of LDL and HDL, and it ignores the fact that LDL likely has important beneficial functions. For instance, studies suggest LDL has a role in immune function and injury response, among other roles.6

In addition, this simplistic thinking assumes all LDL is the same, which we would argue is not be the case.7 This is especially true when we consider metabolic disease and its influence on LDL, as well as the role of oxidized LDL.8

So LDL is not inherently “bad” just as HDL is not inherently “good.” But they can play good and bad roles in our bodies, depending on the specific situation.


What are “normal” cholesterol levels?

The recommended targets for cholesterol vary slightly among different countries and health agencies. The US National Institutes of Health website lists the following optimal cholesterol and triglyceride values for people at low risk for heart disease, measured after a fast of 9-12 hours:

  • Total cholesterol: < 200 mg/dL (5.2 mmol/L)
  • LDL cholesterol: < 100 mg/dL (2.6 mmol/L)
  • HDL cholesterol: > 40 mg/dL (1.0 mmol/L) for men, > 50 mg/dL (1.3 mmol/L) for women
  • Triglycerides: < 150 mg/dL (1.7 mmol/L)

LDL levels >160 mg/dL (4.1 mmol/L) are considered high, and levels 190 mg/dL (4.9 mmol/L) and above are considered very high.

Many factors can affect your blood cholesterol, including genetics, hormonal changes, injury, and certain health conditions. For instance, people with untreated hypothyroidism often have elevated cholesterol.

A person’s diet can also influence cholesterol levels – sometimes significantly.9

Some would argue that since these cut-off points are based on epidemiologic studies, they likely do not apply the same to all individuals regardless of their baseline metabolic health and overall health. For instance, there are data that show people with low LDL levels can have heart attacks and people with high LDL can live long lives.10

The point is that LDL levels should be regarded as one of many variables for evaluating cardiovascular risk, using an individual’s metabolic status and other risk factors to adjust that risk assessment up or down.


How does keto or low-carb eating affect your cholesterol?

In some people who follow keto or low-carb diets, blood total cholesterol goes up little, if at all. Some even experience a drop in LDL cholesterol after starting low carb. However, others experience an increase in both LDL and HDL cholesterol levels.11 Or, there is an increase only in HDL cholesterol resulting in an improved LDL/HDL ratio.12

One meta-analysis of randomized trials reported that people eating a low-carb diet, on average, experience a reduction in both total LDL and small LDL particles, as well as an increase in the peak LDL size.13

A rise in cholesterol during keto or low-carb eating may be related to losing weight. Although cholesterol levels often drop during the first 2-3 months of losing large amounts of weight, there can be a later rise in cholesterol that persists until weight stabilizes. Once weight loss ceases, cholesterol levels tend to come back down.14

Therefore, it could make sense to wait until someone’s weight has been stable for a few months before assessing cholesterol levels.

For an estimated 5 to 25% of people – whether weight loss occurs or not – LDL cholesterol goes up significantly in response to very-low-carb diets, sometimes by 200% or more. Many of these folks seem to belong to a group that Dave Feldman at Cholesterol Code refers to as lean mass hyper-responders (LMHRs).15 These often healthy people are sometimes shocked to discover that their LDL cholesterol has soared above 200 mg/dL (5.2 mmol/L) after going keto.

We realize that quoting data from a blog does not conform to the highest scientific standard. Unfortunately, the medical literature in this field is lacking, so we’ve decided to present the data that exists. We recognize that Dave’s work has not been held up to the same degree of scientific community scrutiny as the papers published in medical journals.

Feldman’s theory about lean mass hyper-responders is based on experiments he’s conducted on himself and from data he has gathered from hundreds of other low-carbers doing similar self-experiments.

He states that the higher energy demands, lower body fat stores, and lower glycogen stores in these LMHRs trigger the liver to increase production of lipoprotein particles so that triglycerides (fat) can be transported to cells for use as fuel. Since cholesterol travels along with the triglycerides, blood cholesterol levels might rise as the liver pumps out more lipoproteins to keep up with the body’s energy demands.

To date, the lipidology community has not endorsed Dave’s theory, or any other theory on hyperresponders for that matter. However, other potential explanations exist.

Another theory is that higher saturated fat intake increases cholesterol absorption while a low insulin state decreases LDL receptor activity. The reduced receptor activity thereby decreases the amount of LDL being pulled out of circulation and excreted through bile. When combined, these factors could significantly increase circulating LDL concentration.16

Cholesterol synthesis and absorption are complex mechanisms that are influenced by nutrition, genes, and other factors. Therefore, it isn’t surprising that a minority of low-carb dieters experience significant changes in their blood LDL cholesterol levels, and that may be why the exact mechanism remains elusive.

In general, no major concerning serum-lipid changes occur when consuming a ketogenic diet. Typical findings are stable LDL cholesterol levels, a decrease in triglycerides, and an increased HDL cholesterol.17



Should you be concerned if your cholesterol increases with low-carb eating?

This is an emerging area of research that is currently the focus of a great deal of debate and uncertainty.

Traditional experts in the field of lipids and heart disease view elevated LDL cholesterol with concern because it typically reflects a high concentration of LDL particles (LDL-P) circulating in the bloodstream.

Excessive amounts of LDL particles have been found to be associated with the development of atherosclerosis, the underlying cause of heart disease. In atherosclerosis, LDL particles are known to end up in damaged artery walls, and connected to an inflammatory response. Over time, cholesterol, calcium, white blood cells and other substances accumulate at the site to form a plaque. Many – if not most – heart attacks and strokes are caused when a plaque ruptures and forms a clot that blocks arterial blood flow.

The length of time that arteries are exposed to high levels of LDL particles is believed to play a significant role in the development of atherosclerosis. Smaller LDL particles typically spend more time in the bloodstream than larger particles do, making them easier targets for oxidation and incorporation into plaque.18 Moreover, people who have a lot of small LDL particles tend to have low HDL cholesterol and elevated triglycerides – all of which are markers of insulin resistance and reflect increased cardiovascular disease risk.

Even though small LDL particles may be especially problematic, some large studies have also found an association between high concentrations of large LDL particles and heart disease (although these did not control for metabolic health or insulin resistance).19

Despite these associations between high concentrations of LDL particles and heart disease, research has consistently shown that keto diets help reduce many heart disease risk factors in people with diabetes and other insulin-resistant conditions.20 Granted, these are not outcome trials, showing an actual reduction in heart attacks, but those trials don’t yet exist. But the demonstrated improvement in risk factors suggests that we may eventually see such beneficial results.

For example, a 2009 randomized study comparing a low-fat diet to a very-low-carb diet in people with metabolic syndrome found that the very-low-carb diet was more effective at improving many cardiovascular health markers, including the following:21


  • Decrease in body fat and abdominal fat
  • Decrease in triglycerides
  • Increase in HDL cholesterol
  • Decrease in small LDL particles
  • Lower blood glucose levels
  • Lower insulin levels
  • Increase in insulin sensitivity

Similarly, a nonrandomized trial showed a ketogenic diet reduced the percentage of smaller LDL and increased the larger LDL. This trial also showed no significant increase in atherosclerosis or lipid accumulation in the carotid artery at two-years, even in the hyperresponders.22

The fact that so many risk factors remain stable or improve with carb restriction – even if LDL cholesterol levels increase – demonstrates the importance of not viewing any one value in isolation. Instead, it may be better to look at the body as a whole system.

Prominent lipidologist and vocal lipid educator Dr. Thomas Dayspring, however, urges caution. In his paper “Lipidaholics Anonymous Case 291: Can losing weight worsen lipids?” he states:

“The advocates of low-carb diets say there is no study showing harm of elevated LDL-P and LDL-C in patients who have eliminated or drastically reduced their insulin resistance and inflammatory markers by low carbing. That is true, but what they want to ignore is that there is no data anywhere that shows they are an exception.”

Many low-carb proponents, however, counter that none of the studies showing a connection between elevated LDL and heart disease were conducted in people eating keto or low-carb diets.

Dave Feldman is trying to gather as much data as possible about people who have had this experience, and over time, it may very well provide valuable information. If you are a hyper-responder and would like to be part of his ongoing data collection, please get in touch with him by commenting on one of his posts at

At this time, because there aren’t any formal studies that have looked at this response, we don’t have the ability to predict what will happen long term with people who get very high LDL cholesterol on a low-carb diet.


Five ways to lower your LDL on a keto or low-carb lifestyle

Has your cholesterol increased on a low-carb diet? Do you fear that you may need to abandon this way of eating and its potential benefits?

Here are five ways you can reduce your total and LDL cholesterol levels while maintaining a keto or low-carb lifestyle. Consider trying them in this order.

1. Avoid Bulletproof coffee

Bulletproof coffee refers to adding butter, coconut fat or MCT oil in coffee. Avoid drinking significant amounts of fat at all when you’re not hungry. This alone can sometimes normalize elevated cholesterol levels.23

2. Eat only when hungry

Only eat when hungry and consider adding intermittent fasting. This may reduce cholesterol levels. Although most research on intermittent fasting and LDL reduction come from low-quality observational studies during Ramadan, a recent pilot study of time restricted eating showed a significant reduction in LDL.24 While we need more data, this remains a promising intervention.

3. Eat foods higher in unsaturated fats instead of saturated fats

Foods higher in unsaturated fats include fats like olive oil, fatty fish and avocados. Replacing sources of saturated fat with these foods may be enough to lower LDL cholesterol.

However, remember that many unsaturated oils are highly processed. As with food, we recommend focusing on the least processed oils like olive oil, macadamia oil, and avocado oil.

4. Eat LDL-lowering keto-friendly foods

These low-carb plant foods may help lower cholesterol levels somewhat:

Starch structureStarch structureStarch structureStarch structure

  • Avocado: An analysis of 10 studies found that eating avocados on a regular basis led to a significant decrease in LDL cholesterol.25
  • Green vegetables: Dark leafy greens and cruciferous vegetables bind to bile acids, which are excreted as waste rather than reabsorbed in the gut, ultimately resulting in slightly lower blood cholesterol. To maximize this effect, you may want to steam your greens rather than eating them raw.26
  • Cocoa and dark chocolate: In addition to lowering LDL cholesterol, cocoa and dark chocolate might help protect LDL from becoming oxidized or damaged.27 To avoid unnecessary sugar intake, you may want to choose chocolate that contains at least 85% cocoa.
  • Nuts and seeds: Nuts and seeds are rich in fiber and monounsaturated fats, which can help lower cholesterol. One analysis of 25 studies found that eating two servings of nuts per day reduced LDL cholesterol by an average of 7%.28

5. Eat more carbs

Finally, if steps 1-4 are not enough: Consider whether you really need to be on a strict keto diet for health reasons.

If a more moderate or liberal low-carb diet (e.g. 50–100 grams of carbs per day) can still work for you, it may also lower your cholesterol. Just remember to choose unprocessed carb sources (e.g., not wheat flour or refined sugar).

Bonus: K2

This is still speculative and no high-quality evidence exists yet. But eating enough foods containing vitamin K2 might help reduce the risk of atherosclerosis.

Vitamin K exists in two forms: K1 and K2. Vitamin K1 is found in plants and is involved in blood clotting. By contrast, vitamin K2 is found mainly in animal products.

There is still no definite proof, but eating enough vitamin K2 might help protect heart health by keeping calcium in your bones and out of your arteries.29The best sources of vitamin K2 include liver, eggs, grass-fed dairy products and chicken.


Advanced testing

As mentioned above, sometimes a rise in LDL cholesterol is temporary, especially during weight loss. However, if yours remains very high and especially if you have additional risk factors (family history of heart disease, certain genetic markers, diabetes, or if you are a smoker), you may want to look into having some advanced testing performed. This may give a clearer indication of your risk profile and state of health, compared to conventional blood cholesterol levels alone:

  • NMR spectroscopy (Nuclear Magnetic Resonance): provides detailed information about your LDL and HDL particle sizes and counts, along with an insulin resistance score that reflects your risk of developing diabetes.
  • CAC scan (Coronary Artery Calcium): measures calcium accumulation in your coronary arteries by computed tomography in order to identify early signs of heart disease.
  • CIMT test (Carotid intima-media thickness): measures the thickness of the inner layer of your carotid artery in order to identify atherosclerosis and lipid deposits.


Recommended viewing and reading


Dave Feldman: The cholesterol network system
Dr. Andrew Mente: Dietary fat and cardiovascular disease
Sarah Hallberg: LDL on LCHF
Dr. Peter Attia: The straight dope on cholesterol


Dr. Peter Attia: The straight dope on cholesterol (part 1 of 9)

Dr. Thomas Dayspring: Understanding the entire lipid profile

Cholesterol Code: Are you a lean mass hyper-responder?

/ Franziska Spritzler, RD


  1. The medical community generally accepts that elevated cholesterol is associated with increased cardiovascular risk. Examples of observational studies showing this include the Framingham study

    Annals of Internal Medicine 1971: Serum cholesterol, lipoproteins, and the risk of coronary heart disease. The Framingham Study [observational study, weak evidence]

    While we do not question the validity of that data, we do question if they are applicable to all groups in the same fashion. There are a number of studies questioning the link between high cholesterol and cardiovascular risk, although these studies do not specifically examine those following a low-carb lifestyle. At Diet Doctor, we endeavor to understand if this risk is applicable to people eating low-carb:

    BMJ Open 2016: Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review [meta-analysis of observational studies; weak evidence]

    In addition, this trial showed no correlation between coronary calcification and cholesterol level in women

    Journal of the American College of Cardiology 2001: Electron beam tomography and national cholesterol education program guidelines in asymptomatic women [observational study, weak evidence]

    And another study of patients with low LDL-cholesterol who had been hospitalized with heart attacks showed they had a higher chance of dying within 3 years.

    Cardiology Journal 2009: Low admission LDL-cholesterol is associated with increased 3-year all-cause mortality in patients with non ST segment elevation myocardial infarction [observational study, weak evidence]

  2. Huff, Jialal 2019: Physiology, Cholesterol
    [textbook; ungraded]

  3. Hindawi 2012: Cholesterol: Its regulation and role in central nervous system disorders [overview article; ungraded]

    Nature Neuroscience 2005: High cholesterol level is essential for myelin membrane growth [mouse study; very weak evidence]

  4. Arteriosclerosis, Thrombosis, and Vascular Biology 1996: Dietary cholesterol feeding suppresses human cholesterol synthesis measured by deuterium incorporation and urinary mevalonic acid levels. [randomized trial; moderate evidence]

  5. VLDL (very low density lipoprotein) and IDL (intermediate density lipoprotein) particles also contain apolipoprotein B and are precursors to LDL particles.

  6. Microbiology and Immunology 2010: Plasma lipoproteins are important components of the immune system [overview article; ungraded]

    Infection and Immunity 1995: Role for circulating liopoproteins in protection from endotoxin toxicity [rat study; very weak evidence]

  7. Many physicians would agree with the statement that not all LDL is the same, yet risk calculators and guidelines focus mostly on LDL and don’t encourage the measurement of small or oxidized LDL particles.

  8. Current Vascular Pharmacology: Insulin resistance, small LDL particles, and risk for atherosclerotic disease [overview article; ungraded evidence]

    Diabetes 2017: Oxidized LDL Is Associated With Metabolic Syndrome Traits Independently of Central Obesity and Insulin Resistance [observational study with HR>2, weak evidence]

  9. Dave Feldman of has run numerous personal experiments where he shows simply changing his diet can alter his cholesterol level by more than 100 points. His website and Facebook group have hundreds of examples of others who have done the same. While this is far from a scientific study, it suggests that diet can affect cholesterol levels much more than commonly believed by most physicians.

  10. American Heart Journal 2009: Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines [observational study; weak evidence]

    BMJ Open 2016: Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review [meta analysis of observational studies; weak evidence]

  11. 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]

    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]

    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]

  12. In a randomized trial of patients with type 2 diabetes who either were given information to eat moderate LCHF (with an increased relative intake of saturated fat) or a low-fat diet, there was no change in LDL cholesterol while HDL cholesterol increased on LCHF. Furthermore, the patients randomized to LCHF achieved better glycemic control and decreased low-grade inflammation while also reporting better health-related quality of life than those on the low-fat diet.

    Diabetologia 2012:
    In type 2 diabetes, randomisation to advice to follow a low-carbohydrate diet transiently improves glycaemic control compared with advice to follow a low-fat diet producing a similar weight loss
    [randomized trial; moderate evidence]

    Annals of Medicine 2014: Advice to follow a low-carbohydrate diet has a favourable impact on low-grade inflammation in type 2 diabetes compared with advice to follow a low-fat diet[randomized trial; moderate evidence]

    Diabetes Reserach and Clinical Practice 2014: Randomization to a low-carbohydrate diet advice improves health related quality of life compared with a low-fat diet at similar weight-loss in Type 2 diabetes mellitus[randomized trial; moderate evidence]

  13. 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 [strong evidence]

  14. The American Journal of Clinical Nutrition 1991: The transient hypercholesterolemia of major weight loss. [non-randomized trial; weak evidence]

    Journal of the American College of Nutrition 1983: Effect of weight reduction on circulating lipids: An integration of possible mechanisms [observational study, weak evidence]

    Journal of Nutrition 1960: Serum cholesterol in acute starvation: A report of 20 cases [nonrandomized study, weak evidence]

  15. Although Dave is not a physician or scientist, he is an engineer with a knack for self-experimentation. Through his self-experimentation, he has shown how he can dramatically change his LDL cholesterol level over the course of days to weeks just by altering his diet.

  16. To be clear, these are hypothetical theories at this point with no convincing data to prove either is “correct.”

  17. European Journal of Clinical Nutrition 2013:
    Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets
    [overview article; ungraded]

    Journal of Nutrition 2002:
    A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men
    [nonrandomized study, weak evidence]

  18. Current vascular pharmacology 2014: Insulin resistance, small LDL particles, and risk for atherosclerotic disease [overview article; ungraded evidence]

  19. Atherosclerosis 2007: LDL particle subclasses, LDL particle size, and carotid atherosclerosis inthe Multi-Ethnic Study of Atherosclerosis (MESA) [observational study with HR < 2; very weak evidence]

    European Heart Journal 2015: Low-density lipoprotein particle diameter and mortality: the Ludwigshafen Risk and Cardiovascular Health Study [observational study with HR < 2; very weak evidence]

  20. 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]

    Nutrition Reviews 2018: Effects of carbohydrate-restricted diets on low-density lipoprotein cholesterol levels in overweight and obese adults: a systematic review and meta-analysis [strong evidence]

  21. Lipids 2009: Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet [randomized trial; moderate evidence]

    Progress in Lipid Research 2008: Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome[overview article; ungraded]

  22. Cardiovascular Diabetology 2020: Impact of a 2-year trial of nutritional ketosis on indices of cardiovascular disease risk in patients with type 2 diabetes
    [nonrandomized study, weak evidence]

  23. Based on clinical experience and anecdotal reports. [weak evidence]

  24. The following studies suggest that periodic fasting can improve cholesterol levels even when there is active weight loss.

    Clinical Nutrition ESPEN 2018: Impact of intermittent fasting on the lipid profile: Assessment associated with diet and weight loss. [overview article; ungraded]

    Cell Metabolism 2019: Ten-hour time-restricted eating reduces weight, blood pressure, and atherogenic lipids in patients with metabolic syndrome [non-controlled study; weak 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]

  26. Nutrition research (New York, N.Y.) 2008: Steam cooking significantly improves in vitro bile acid binding of collard greens, kale, mustard greens, broccoli, green bell pepper, and cabbage [mechanistic study; ungraded evidence]

  27. American Institute of Nutrition 2007: Plasma LDL and HDL cholesterol and oxidized LDL concentrations are altered in normo- and hypercholesterolemic humans after intake of different levels of cocoa powder [randomized controlled trial; moderate evidence]

    British Journal of Nutrition 2015: Cocoa flavanol intake improves endothelial function and Framingham Risk Score in healthy men and women: a randomised, controlled, double-masked trial: the Flaviola Health Study [moderate evidence]

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

  29. Athersclerosis 2009: High dietary menaquinone intake is associated with reduced coronary calcification [nutritional epidemiology study with HR<2; very weak evidence]

    Nutrition, Metabolism, and Cardiovascular Disease 2009: A high menaquinone intake reduces the incidence of coronary heart disease [nutritional epidemiology study with HR<2; very weak evidence]

    Journal of Nutrition 2004: Dietary intake of menaquinone is associated with a reduced risk of coronary heart disease: the Rotterdam Study [nutritional epidemiology study with HR<2; very weak evidence]