Different types of cardiovascular disease (CVD) may benefit most from different amounts, types, or doses of exercise, and major guidelines don’t provide such tailored advice. In 2018, a team of experts created a system called the EXercise Prescription in Everyday practice & Rehabilitative Training (EXPERT) tool to help clinicians give their patients tailored exercise advice based on their needs.

The team released a consensus statement that provides specific exercise recommendations for several cardiovascular risk states based on the evidence they considered.^[12] Some of the team’s recommendations are summarized below.

Each recommendation is accompanied by a grade denoting the level of the recommendation.

“A” indicates the recommendation is supported by high-quality systematic reviews or randomized controlled trials that are directly relevant for the population at hand.

“B” indicates high-quality observational evidence or inference from randomized trials supports the recommendation.

“C” indicates the recommendation is supported by well-conducted case-control or cohort studies with overall consistent results that could be applicable to the target population.

“D” indicates the recommendation is supported by poorer-quality observational evidence, inference from higher-quality observational evidence, or expert opinion.

Exercise recommendations by CVD risk factors

Reference: Hansen et al. Sports Med. 2018.^[12]

In healthy adults, caffeine intake of up to 400 mg per day has not been linked to increases in cardiovascular disease risk.^[9][10] However, the evidence is uncertain regarding the long-term effects of regular caffeine intake for people with high blood pressure or pre-existing heart conditions.^[9][11] This also applies to people for whom stimulants in general are not recommended. Low to moderate intake may be generally safe, but this must be assessed on a case-by-case basis in consultation with a physician.

The fat you eat (and the fat you store in your body) is made up of different types of fatty acids, each with a long chain of carbon atoms bonded together. Saturated fatty acids (SFAs) have no double bonds, whereas monounsaturated fatty acids (MUFAs) have one and polyunsaturated fatty acids (PUFAs) have two or more. The “kinks” those bonds form in fatty acid chains prevent the fatty acids from packing close together, which is why unsaturated fats are liquid at room temperature, whereas saturated fats usually aren’t (they’re packed solid).

Saturated fats are fatty acids with no double bonds, which is why they are usually solid at room temperature.

However, classifying fatty acids by degree of saturation does not predict how they are handled by the body.^[13] Based on the length of its tail (the number of carbons in its chain), a saturated fat belongs to one of four main subcategories, each with its own biological effects.

Even within each subcategory, the various fatty acids have different health effects.

For example, although palmitic acid and stearic acid are both long-chain saturated fats, the former causes a greater increase in blood cholesterol levels.^[14] Similarly, although caprylic acid and capric acid are both medium-chain saturated fats, the former results in a larger blood ketone response.^[15]

Those variations greatly limit our ability to discuss saturated fat in general. Just as it would be inappropriate to generalize the effects of poisonous mushrooms to all mushrooms, it is inappropriate to generalize the effects of one kind of saturated fat to all kinds of saturated fat.

Saturated fats differ by their length (as indicated by the number of carbons in the fatty acid chain) and can each have unique biological effects.

Medium-chain triglycerides, aka MCTs

Medium-chain triglycerides (MCTs) are saturated fats containing 6–10 carbons. Long-chain triglycerides (LCTs) are saturated fats containing 12–18 carbons.

The ketogenic nature of MCTs has led to a growing interest in their use as a food supplement. Traditionally, they’ve served to mimic a ketogenic diet (a very restrictive, very-low-carbohydrate diet) in children with epilepsy.^[16] Today, MCTs are also advertised as helping with fat loss, exercise performance, and brain health, though the evidence is limited.

The richest natural source of MCTs, coconut oil, is ≈14% MCTs by weight,^[17] so you’d need to eat 100 grams of fat (900 kcal) from coconut oil to consume 14 grams (1 tablespoon) of MCTs. For that reason, people interested in MCTs usually turn to concentrated MCT oils.

Medium-chain triglycerides (MCTs) and long-chain triglycerides (LCTs) are two groups of saturated fats. Your body metabolizes MCTs and LCTs very differently. Unlike LCTs, MCTs are not easily obtained in large quantities from whole foods (the best source is coconut oil, but you would need to eat 7 tablespoons to obtain 1 tablespoonful of MCTs), so they won’t be considered throughout this article.

Why do people think saturated fat is so unhealthy?

A quick history lesson on why people think saturated fat is unhealthy.

Since the 1950s, many studies have linked the consumption of saturated fat with increases in blood cholesterol levels.^[18] Those studies, combined with observational research on the association between diet and heart disease,^[19] led Dr. Ancel Keys to propose the diet-heart hypothesis, which suggests that saturated fat raises blood cholesterol levels and thus increases the risk of heart disease.^[20][21]

Despite some researchers arguing that there were significant flaws in the data Keys used to support his claims,^[22] the diet-heart hypothesis persisted and resulted in the belief that a heart-healthy diet should limit saturated fat. Within the academic and medical communities, this conclusion was widely accepted as fact, and it influences official dietary guidelines even today.

Research conducted throughout the later half of the 1900s led Dr. Ancel Keys to propose the diet-heart hypothesis, which posits that dietary saturated fat raises blood cholesterol levels and thus increases the risk of heart disease.

Saturated fat and your heart

Since the diet-heart hypothesis led to official recommendations against saturated-fat intake, it makes sense to address heart disease first.

How does arterial plaque form?

Our arteries are lined with a layer of cells called the endothelium, which functions as a selectively permeable barrier between our blood and the rest of our body. This is akin to our intestinal tract, which allows for the absorption of some nutrients but not others. In our blood, one of the “nutrients” that penetrates the endothelium is low-density lipoprotein (LDL), whose primary job is to transport cholesterol throughout the body.

The key event for the formation of plaques in arteries is the retention of LDL particles in the space beneath the endothelium (called the intima).^[23] Once there, LDL is more susceptible to becoming oxidized, which signals the immune system to attack because oxidized LDL is seen as harmful to the body. This inflammatory response involves certain white blood cells called macrophages that literally “eat” the oxidized LDL particles. The LDL-engulfing process turns macrophages into foam cells, which can’t function properly and accumulate into the fatty build-up we call plaque.

As you can see, several events need to occur for heart disease to develop. This helps explain why heart disease has numerous environmental and genetic risk factors such as diabetes, obesity, smoking, lack of exercise, and infection.^[24]

Any process that affects LDL retention and oxidation or inflammation is going to influence plaque formation and the risk of suffering from heart disease. Therefore, it makes sense to look at how saturated fat affects each of these processes.

Heart disease is most commonly the result of atherosclerosis (the buildup of plaque in arteries). Atherosclerosis happens when LDL particles penetrate arterial walls, become oxidized, and are attacked by white blood cells.

Effects of saturated fat on blood lipids

Saturated fat’s effects on blood lipids were thoroughly investigated in a systematic review and meta-analysis published by the World Health Organization (WHO) in 2016.^[25] This meta-analysis included 84 randomized controlled trials (RCTs) involving a total of 2,353 healthy adults; it evaluated the effects of replacing 1% of caloric intake from carbohydrates or unsaturated fats with 1% of caloric intake from saturated fat.

To be included in the analysis, all studies were required to meet stringent criteria, so as to best isolate the effects of dietary substitution. For example, all food was provided to the participants, calories and protein were matched between diets, and all interventions lasted at least two weeks. The results are summarized in the table below.

Eating saturated fat instead of unsaturated fat or carbohydrates consistently increased lipid and lipoprotein concentrations in the blood. The one exception was a reduction in triglycerides when saturated fat was consumed instead of carbohydrates. Importantly, these effects were found to be consistent between sexes and across a wide range of baseline blood-lipid values and saturated-fat intakes (1.6–24.4% of calories). They were also consistent between studies, whatever the year of publication.

An important limitation of this meta-analysis is that it could not differentiate between the various food sources of the nutrients, which is an important consideration we shall discuss later. Moreover, studies investigating hydrogenated oils, fish oils, and medium-chain triglycerides were excluded.

Saturated fat increases lipid and lipoprotein concentrations in the blood when compared to carbohydrates, monounsaturated fat, and polyunsaturated fat.

LDL and HDL

Compared to carbohydrates and unsaturated fats, saturated fat raises the levels of lipoproteins and most blood lipids. These changes have well-researched implications for the risk of developing heart disease.

The greater the number of LDL particles in the blood (LDL-P), the more likely some will pass into artery walls, become oxidized, and kickstart plaque formation.^[23] Therefore, to predict heart disease, LDL-P matters more than LDL-C,^[26][27] which is simply a measure of the amount of cholesterol being carried by LDL particles.

If two people have the same LDL-C but one has cholesterol-rich LDL (large, “fluffy” particles) and the other cholesterol-poor LDL (smaller, denser particles), the second will have a greater LDL-P (more LDL particles total) and be at greater risk of heart disease.

The WHO meta-analysis didn’t cover LDL-P.^[25] However, it did report the levels of apolipoprotein B (apoB), the protein component of LDL. Since each LDL particle has one molecule of apoB, apoB concentrations provide a good estimate of LDL-P concentrations and are a strong predictor of heart disease risk.^[28][29]

To predict heart disease, LDL-P (the number of LDL particles) matters more than LDL-C (the amount of cholesterol those particles carry). There is one molecule of apolipoprotein B (apoB) in each LDL particle, so apoB is a good estimate of LDL-P. Consuming saturated fat (instead of unsaturated fat) increases apoB concentrations — and therefore your heart-disease risk.

High-density lipoprotein (HDL) removes cholesterol from arteries and plaques, protects the endothelium from damage, and inhibits LDL oxidation.^[30]

HDL basically does the opposite of LDL. While calling HDL-C “good cholesterol” and LDL-C “bad cholesterol” is simplistic, studies do show that a higher ratio of LDL-C to HDL-C (and of total cholesterol to HDL-C) leads to a higher risk of heart disease. Those ratios matter more than your absolute numbers for LDL-C, HDL-C, and even total cholesterol.^[31]

The WHO meta-analysis reported that eating more saturated fat increased HDL-C, but the increase was one-tenth that of LDL-C. Therefore, the ratio of LDL-C to HDL-C (and of total cholesterol to HDL-C) increased,^[25] and with it the risk of heart disease.

A similar pattern was seen with apoA1, the major protein component of HDL particles, akin to apoB for LDL particles. Although replacing unsaturated fat by saturated fat led to increases in apoA1, the increase was only 30–60% that in apoB.^[25] The ratio of apoB to apoA1 is considered a better predictor of heart-disease risk than other blood lipid biomarkers and their ratios.^[32][33] If apoB increases more than apoA1, then the apoB-to-apoA1 ratio increases, and with it the risk of heart disease.

The HDL-C and apoA1 numbers reflect the amount of HDL in the blood. HDL has cardioprotective effects, but while eating saturated fat (instead of unsaturated fat) increases both HDL-C and apoA1, it increases LDL-C and apoB even more.

Finally, the triglyceride to HDL-C ratio represents a strong, independent predictor of heart disease when LDL-C levels are below 160 mg/dL,^[34] and has similar predictive ability as LDL-C for determining the extent of atherosclerosis in at-risk patients.^[35] Having a triglyceride-to-HDL-C ratio above 3.8 is associated with having more small, dense LDL particles, which are especially susceptible to oxidation.^[36]

The WHO meta-analysis reported that eating more polyunsaturated fat reduced the ratio, whereas eating more carbohydrates increased it, when saturated-fat intake was reduced.^[25] However, the changes were very small and not of clinical significance. A 10% reduction in calories from saturated fat would increase the triglyceride-to-HDL-C ratio by a mere 0.16 if more carbohydrates were eaten, and decrease it by only 0.04 if more polyunsaturated fat were eaten.

The triglyceride-to-HDL-C ratio correlates with the number of small, dense LDL particles and represents a strong risk factor for heart disease. However, changes in saturated-fat intake have little effect on this ratio.

Effects of saturated fat on inflammation

Plaque development requires that the immune system attack oxidized LDL particles within the arteries. Therefore, reducing systemic inflammation could help fight atherosclerosis, and in this manner decrease the risk of heart disease.^[37][38]

Saturated fat may worsen systemic inflammation by increasing the absorption of lipopolysaccharides (LPS),^[39] which are bacterial endotoxins that strongly stimulate our immune system.^[40][41] Even very small serum concentrations of LPS, on a picogram scale, have the potential to elicit in humans an inflammatory response with a clear dose-response relationship.^[42]

However, a systematic review found no consistent associations between consumption of saturated fat and a variety of inflammatory biomarkers, including cytokines, adipokines, acute-phase reactants, and cell adhesion molecules.^[43] Clearly, the role of saturated fat on inflammation is not straightforward.

Still, one RCT reported that, compared to a diet high in SFAs, a diet high in MUFAs decreased LDL oxidation, a diet high in omega-6 (n-6) PUFAs increased it, and a diet high in omega-3 (n-3) PUFAs did not affect it.^[44] The study authors attributed those differences to the fatty-acid composition of the LDL particles (i.e., to whether they contained mostly SFAs, MUFAs, or either kind of PUFAs).

Saturated fat may raise endotoxin levels to a greater extent than unsaturated fat, but it does not appear to affect systemic inflammation. Omega-6 polyunsaturated fat appears to increase LDL oxidation more than saturated fat (which is bad), whereas monounsaturated fat significantly reduces it (which is good).

Effects of saturated fat on heart disease

Up to this point, we have reviewed the effects of saturated fat on heart-disease risk factors rather than on heart disease itself.

The step between the two should be a small one, but that’s where things turn weird: despite a logical theoretical framework connecting diets high in saturated fat to atherosclerosis, meta-analyses of observational studies haven't reported consistently strong associations between saturated fat intake and risk of coronary heart disease, stroke, or cardiovascular disease in general.^[45][46]

Even long-term RTCs that assessed hard endpoints of heart disease (such as suffering a heart attack, or dying from one) reported inconsistent links with saturated-fat intake. For instance, one meta-analysis reported that every 5% reduction in calories from SFAs (replaced by PUFAs) reduced the risk of heart disease by ≈10%,^[47] but another reported that replacing SFAs by PUFAs was protective only when the PUFAs included both n-3 and n-6 fatty acids — replacing SFAs by only n-6 PUFAs tended to increase the risk of heart disease.^[48]

One reason for the discrepancies is the failure of many studies to isolate the effects of altering saturated-fat intake. For example, some studies gave dietary advice to only one of the intervention groups — advice such as eating more plant-based foods; eating more n-3 PUFAs from fish and seafood; eating less sugar; and eating less trans-fat from margarines, shortenings, and partially hydrogenated oils.^[49] When looking only at trials that minimized confounding factors, we see that replacing SFAs with primarily n-6 PUFAs has no effect on the risk of developing heart disease or dying from it.^[49]

Neither observational studies nor RCTs support the notion that eating a diet high in saturated fat strongly increases the risk of developing heart disease or dying from it.

Understanding the difference between heart-disease risk factors and actual rates of heart disease

So, what gives? We have evidence that eating more saturated fat (instead of unsaturated fat) increases known risk factors for heart disease, such as blood lipids, but studies looking at the big picture do not find a link between saturated fat and heart disease. How can this be?

The simple answer is that fat intake is but a single piece of the heart-disease puzzle. Eating more saturated fat may increase your risk of developing heart disease, but that doesn’t mean you will develop heart disease. Conversely, banning all saturated fat from your diet does not make your heart attack proof.

In other words, rather than singling out any food or nutrient, we need to consider a person’s overall diet and lifestyle.

Let us use dairy as an example.

Dairy fat is ≈70% saturated fat,^[50] making it a prime target for nutritional interventions. However, results from observational and experimental studies on the effects of dairy products on blood lipid levels are not conclusive,^[51][52] and can even appear contradictory. For instance, there is RCT evidence that diets high in saturated fat from butter increase LDL-C, but that diets equally high in saturated fat from cheese might not.^[51] Different dairy products, such as butter and cheese, have different food matrices (structures in which the food compounds are arranged), and thus different metabolic effects.^[53]

Similarly, one meta-analysis reported a lack of significant associations between heart disease mortality and high intakes of meat or dairy products (including milk and cheese). ^[54] However, high intakes of processed meat did increase the risk of heart disease. It is well established that processed meats contain several carcinogenic compounds, which can influence heart disease risk.^[55]

Whether saturated fat is good or bad for your heart may depend on what it is replacing — or being replaced by — in your diet. For example, replacing saturated fat by carbohydrates from whole grains is associated with a reduced risk of heart disease, whereas replacing saturated fat by carbohydrates from refined grains fails to confer the same benefit.^[56] Similarly, replacing SFAs by plant-based MUFAs is associated with a reduced risk of heart disease, whereas replacing SFAs by animal-based MUFAs is not.^[57]

If you care about your heart, you can’t just focus on saturated fat — or on any other nutrient. You need to look at the foods that provide it, and beyond that, at your overall diet and lifestyle. Doing otherwise means missing the forest for the trees.

Saturated fat and your brain

Studies in animal models and test tubes generally support the position that, compared to diets high in MUFAs or n-3 PUFAs, diets high in SFAs (and, to a lesser extent, diets high in n-6 PUFAs) have detrimental effects on brain development and cognitive function.^[58][59] However, whether results in animals can be applied to humans is questionable.

Unfortunately, human studies are scarce. One study reported that eating a diet high in SFAs (from palm oil) increased self-reported anger (4.7 vs. 2.2 out of 5 points) and overall mood disturbances (13 vs. 7 out of 20 points) compared to eating a diet high in MUFAs (from hazelnut oil).^[60] Other studies have reported that eating SFAs alters brain activation during cognitive tests and at rest, although the implications of these findings are not known.^[61][62]

Studies in animals suggest that diets high in saturated fat may impair cognitive function and brain development. However, studies in humans are few and inconclusive.

Saturated fat and your weight

Appetite

Weight gain or loss depends greatly on caloric intake. According to a review of 24 studies, different types of fat affect subjective appetite similarly, at least in the short-term (e.g., single-meal assessments), in spite of satiety hormones being affected more by saturated than unsaturated fat.^[63] However, differences in study protocols and participants make it difficult to draw overarching conclusions.

The effects of fat type on appetite regulation are not clear, but compared to monounsaturated and polyunsaturated fats, saturated fat appears to be either equally filling or slightly less filling.

Thermogenesis

Compared to meals high in unsaturated fat, meals high in saturated fat tend to result in lower levels of post-meal energy expenditure and fatty-acid oxidation.^[64] Studies using isotope tracers indicate that the body would rather use unsaturated than saturated fats as an energy source.^[65][66] However, long-term studies are inconsistent.^[64]

Compared to unsaturated fat, saturated fat reduces energy expenditure and fat oxidation, but the long-term implications are not clear.

Activity

Eating more monounsaturated fat in place of saturated fat appears to spontaneously increase physical activity levels.^[60]

Compared to unsaturated fat, saturated fat might reduce energy expenditure via reductions in physical activity.

Saturated fat and your hormones

Testosterone

Several RCTs have been conducted to evaluate the effects of dietary fat (amount and type) on men’s testosterone levels. To best understand these studies, we must first briefly discuss what they measured.

• Tightly bound testosterone. About two-thirds of the testosterone in your blood is bound to sex-hormone-binding globulin (SHBG). Your body can’t use it.
• Loosely bound testosterone. About a third of the testosterone in your blood is bound to albumin. Your body can use it, with some effort.
• Free testosterone. A small percentage of the testosterone in your blood (1–4%, as a rule) just floats around freely. Your body can readily use it.

Together, your loosely bound testosterone and your free testosterone compose your bioavailable testosterone, which has a greater impact on your health than your total testosterone.

Two studies with large sample sizes, controlled diets, and direct measurement of free testosterone reported that, compared to high-fat diets (33–40% of calories), low-fat diets (14–19% of calories) reduced total testosterone levels in healthy men, but did not alter levels of free or bioavailable testosterone.^[67][68] Two other studies with smaller sample sizes, less accurate measurement methods, and less dietary control reported reductions in both total and free testosterone levels.^[69][70]

Compared to diets high in fat (30–40% of calories), diets low in fat (14–19% of calories) appear to reduce total testosterone levels, but not necessarily free testosterone levels. In all cases, the reductions are fairly small and not clinically significant.

The big picture

Compared to monounsaturated fat (MUFAs) and omega-6 polyunsaturated fat (n-6 PUFAs), saturated fat (SFAs) does increase several risk factors for heart disease. However, compared to n-6 PUFAs only, SFAs also reduce some risk factors. In other words, eating more MUFAs appears to have the most favorable effect on risk factors for heart disease overall, whereas SFAs and n-6 PUFAs are on relatively equal footing.

There is some evidence that, compared to monounsaturated fat, saturated fat might have a negative effect on cognition, appetite, and energy expenditure; but further research is required.

A diet low in fat (14–19% of calories) might reduce total testosterone levels by 10–15% in otherwise healthy men. Total testosterone remains within normal range, however, and the biologically active free testosterone appears unaffected. Clinical significance is not known.

Vitamin K is poorly understood, both by the general public and among health professionals. It has a wide range of potential benefits, but their nature and extent are still uncertain.

Why is that?

Some vitamins are more popular than others. In the past, a lot of research went into vitamin C, which became a popular supplement. Nowadays, a lot of research goes into vitamin D, whose popularity as a supplement is steadily growing.

By contrast, research on vitamin K is still scarce, having slowly developed over the past two decades. Further, it is scattered, because there exist several forms of vitamin K. Some of those forms are present only in a few foods. Others exist in various foods, but only in minute amounts. Few have been the subject of human trials.

The human trials that do exist, however, are overall promising. In order to understand their value and limitations, first you need to know a few basic facts. So let’s begin:

What is vitamin K?

Of the four fat-soluble vitamins (A, D, E, and K), vitamin K was discovered last. In 1929, Danish scientist Henrik Dam discovered a compound that played a role in coagulation (blood clotting).^[71] When he first published his findings, in a German journal, he called this compound Koagulationsvitamin, which became known as vitamin K.

Today, we know that vitamin K participates in some very important biological processes, notably the carboxylation of calcium-binding proteins (including osteocalcin and matrix GLA protein).^[72] In other words, vitamin K helps modify proteins so they can bind calcium ions (Ca²⁺). Through this mechanism, vitamin K partakes in blood clotting, as Henrik Dam discovered, but also of calcium regulation: it helps ensure that more calcium gets deposited in bones and less in soft tissues, thus strengthening bones and reducing arterial stiffness.

What complicates matters is that each vitamin has different forms, called vitamers, each of which may affect you differently. Vitamin K has natural vitamers, K₁ (phylloquinone) and K₂ (menaquinone), and synthetic vitamers, the best-known of which is K₃ (menadione).

Vitamin K1

K₁ is produced in plants, where it is involved in photosynthesis: the greener the plant, the greater its chlorophyll content; the greater its chlorophyll content, the greater its K₁ content. When it comes to foods, K₁ is especially abundant in green leafy vegetables.

K₁ makes for 75–90% of the vitamin K in the Western diet.^[73] Unfortunately, K₁ is tightly bound to chloroplasts (organelles that contain chlorophyll and conduct photosynthesis), so you could be absorbing very little of what you eat^[74] — maybe less than 10%.^[75] Since vitamin K is a fat-soluble vitamin, however, its absorption can be enhanced by the co-ingestion of fat: adding fat to cooked spinach can raise K₁ bioavailability from 5% to 13%.^[76]

Vitamin K2

Things become more complicated here, because just as there are several forms of vitamin K, there are several forms of vitamin K2. To be more precise, the side chain of K₁ always has four isoprenoid units (five-carbon structures), so there is only one form of K₁, but the side chain of K₂ has n isoprenoid units, so there are n forms of K₂, called MK-n.^[77][78]

Whereas the side chain of K₁ has four saturated isoprenoid units, the side chain of K₂ MK-4 has four unsaturated isoprenoid units. Although K₁ is directly active in your system, your body can also convert it to MK-4.^[79][80][81] How much gets converted depends notably on your genetic heritage.^[73]

MK-4 is present in animal products (meat, eggs, and dairy), though only in small quantities. Because those foods usually contain fat, dietary MK-4 should be better absorbed than dietary K₁,^[82] but future studies will need to confirm this hypothesis.

Other than MK-4, all forms of K₂ are produced by bacteria. Your microbiota was once thought to produce three-fourths of the vitamin K you absorb.^[83] Vitamin K, however, is mostly produced in the colon, where there are no bile salts to facilitate its absorption, so the actual ratio is probably much lower.^[82][84]

Bacteria-produced K₂ can be found in fermented foods, such as cheese and curds, but also in liver meat.^[85] The richest dietary source of K₂ is natto (fermented soybeans), which contains mostly MK-7.^[86][87] As it stands, MK-7 is the only form of K₂ that can be consumed in supplemental doses through food (i.e., natto). For that reason, MK-7 is the most-studied form of K₂, together with MK-4.

K₁ and MK-4 both have a side chain composed of four isoprenoid units; their half-life in your blood is 60–90 minutes. MK-7 has a side chain composed of seven isoprenoid units; it remains in your blood for several days. Due to their different side-chain lengths, the various forms tend to be transported on different lipoproteins, which are taken up at different rates by various tissues.^{[88][89][90][91][92]} K₁ and MK-4 are used quickly (K₁ in the liver, MK-4 in other specific tissues), whereas MK-7 has more time to travel and be used throughout the body (which makes it, in theory, the best option for bone health).

Vitamin K₃

K₁ and K₂ are the only natural forms of vitamin K, but there exist several synthetic forms, the best known of which is K₃. However, whereas the natural forms of vitamin K are safe, even in high doses, K₃ can interfere with glutathione, your body’s main antioxidant. K₃ was once used to treat vitamin K deficiency in infants, but it caused liver toxicity, jaundice, and hemolytic anemia. Nowadays, it is used only in animal feed, in small doses. In the animals, vitamin K₃ gets converted into K₂ MK-4,^[93] which you can consume safely.

Vitamin K is a family of fat-soluble vitamins. K₁ and K₂, the natural forms, are safe even in high doses. There is only one type of K₁; it is found in plants, notably green leafy vegetables; your body can use it directly or convert it to K₂ MK-4. Aside from MK-4, all other types of K₂ are produced by bacteria, including the bacteria populating your gut. MK-4 is present in animal products (meat, eggs, dairy), whereas other types of K₂ can be found in fermented foods and liver meat.

Vitamin K and your health

As far as we know, vitamin K mainly affects bloodclotting, cardiovascular health, and bone health. Epidemiological studies have mostly focused on K₁; cardiovascular trials, on K₁ and MK-7 (the main type present in natto, the richest dietary source of K₂); bone trials, on MK-4 (the type of K₂ your body can make out of K₁).

Blood clotting

Vitamin K deficiency impairs blood clotting, causing excessive bleeding and bruising. It is rare in adults, but more common in newborns (more than 4 cases per 100,000 births in the UK^[94]), where it can result in life-threatening bleeding within the skull. For that reason, the American Academy of Pediatrics recommends that newborns receive K₁ shortly after birth (intramuscular injections have shown greater efficacy than oral administration).^[95]

If you suffer from hypercoagulation (if your blood clots too easily), you might be prescribed a vitamin K antagonist (VKA), such as warfarin, a medication that hinders the recycling of vitamin K. Some doctors recommend that VKA users shun vitamin K entirely, but preliminary evidence suggests that, under professional supervision, vitamin K supplements might help stabilize the effects of VKAs.^[85]

Which form should be supplemented, though, and in what amount, is still uncertain. There is some evidence that K₁ enhances coagulation more than does MK-4^[96][97] but less than does MK-7.^[90] With regard to daily supplementation, 100 μg of K₁ is considered safe, but in some people 10 μg of MK-7 is enough to significantly impair VKA therapy.^[98]

Remember that natto is rich in MK-7. A single serving of natto can increase blood clotting for up to four days,^[99] so it is one food VKA users should avoid. Other foods should be safe to eat. Please note that in people who do not suffer from hypercoagulation, and thus do not need to medicate with VKA, high intakes of natto have never been correlated to excessive blood clotting. Similarly, human studies saw no increase in blood-clot risk even from 45 mg (45,000 μg) of MK-4 taken once^[100] or even thrice^[101] daily.

Cardiovascular health

As we saw, vitamin K partakes in calcium regulation: it helps ensure that more calcium gets deposited in bones and less in soft tissues, thus reducing arterial stiffness. This is why people who take vitamin K antagonists, such as warfarin, are more likely to suffer from vascular calcification.^[102][103]

Epidemiological studies^{[104][105][106]} and mechanistic evidence^[107] suggest that dietary K₂ benefits cardiovascular health more than an equal dose of dietary K₁.

Clinical trials on supplemental vitamin K have focused on K₁^[108][109] and MK-7.^{[110][111][112]} Often, those trials used a combination of vitamin D and other nutrients, but with vitamin K being the key difference between the intervention group and the control groups. Both of these forms of vitamin K seem to cause a consistent reduction in arterial stiffness (with better evidence for MK-7), and less consistent reductions in coronary calcification and carotid intima-media thickness. Judging from those trials and the epidemiological evidence, MK-7 seems the better choice.

Bone health

As we have just seen again, vitamin K partakes in calcium regulation: it helps ensure that less calcium gets deposited in soft tissues and more in bones, thus strengthening the latter. This is why people who take vitamin K antagonists, such as warfarin, might be more at risk of bone fractures,^[113][114] though not all studies agree they are.^[115]

Current evidence suggests that supplementing with vitamin K — or, at least, with certain forms of vitamin K — can benefit bone health, especially in the elderly (who have lower levels of circulating K₂).^[116] This potential should be explored, since, as the world population grows (and grows older), so does the number of osteoporotic fractures.^{[117] [118][119]}

MK-7 appears to support the carboxylation of osteocalcin (a major calcium-binding protein in bones) more efficiently than K₁.^[90] Clinical trials suggest that, for the purpose of increasing bone density, MK-4 and MK-7 work more reliably than K₁.^[120]

More significantly, a meta-analysis of MK-4 trials found an overall decrease in fracture risk.^[121] The effect of K₁ or MK-7 supplementation on fracture risk is less clear. Only one K₁ trial looked at fracture risk; it reported a decrease, but without a concomitant increase in bone mineral density.^[122] Of the two MK-7 trials, one reported no difference in the number of fractures between the placebo group and the MK-7 group,^[123] whereas the other reported fewer fractures in the MK-7 group;^[124] there were, however, no statistical analyses for either study.

More research on vitamin K and fracture risk will be needed to clarify the effects of the different forms at different dosages. Currently, if you wish to supplement for bone health, a very high dose of MK-4 (45,000 μg) is the option best supported by human studies.^[121] Those studies, all in Japanese people, focused on the prevention of bone fractures, and yes, much smaller dosages can probably help support bone health; but how much smaller?

In a 12-month study, 20 patients suffering from a chronic kidney disorder were given a daily glucocorticoid (a corticosteroid that has for side effect to decrease bone formation and increase bone resorption). In addition, half the patients received 15 mg of MK-4 daily, while the other half received a placebo. The placebo group experienced bone-density loss (BDL) in the lumbar spine, while the MK-4 group did not.^[125]

More recently, a 12-month study in 48 postmenopausal Japanese women gave 1.5 mg of MK-4 daily to half of them and found a significant reduction in forearm BDL, but not in hip BDL, and it didn’t evaluate fractures.^[126]

So there is some evidence for dosages lower than 45 mg/day. It is, however, a lot weaker.

In healthy people, vitamin K supplementation does not increase the risk of blood clots. Judging from limited evidence, MK-7 seems to be the best form of vitamin K for cardiovascular health, and MK-4 the best form of vitamin K for bone health.

How much vitamin K do you need?

Since vitamin K is crucial to your health, why is it the subject of relatively few studies? One of the reasons is simply that vitamin K deficiency is very rare in healthy, well-fed adults. It is mostly a concern in newborns, in people who have been prescribed a vitamin K antagonist, in people who suffer from severe liver damage, and in people who have problems absorbing fat.^{[127][128][129]}

Vitamin K is abundant in a balanced diet, and the bacteria in your colon can also produce some. Moreover, your body can recycle it many times, and this vitamin K-epoxide cycle more than makes up for the limited ability your body shows for storing vitamin K.

Still, you can recycle vitamin K many times, but not forever, and so you still need to consume some regularly. But how much, exactly?

No one knows. There is, as yet, not enough evidence to set a Recommended Dietary Allowance (RDA) for vitamin K, so an Adequate Intake (AI) has been established at a level assumed to prevent excessive bleeding. In the United States, the AI for vitamin K is 120 μg/day for men and 90 μg/day for women. In Europe, the AI for vitamin K is 70 μg/day for men and women. More recent research, however, suggests that those numbers should be increased.^[89]

Since 100 g of collards contain, on average, 360 μg of vitamin K,^[130][77] getting enough vitamin K looks easy. But can’t you just as easily get too much?

Fortunately, no. Though allergic reactions have occurred with vitamin K injections,^{[131][132][133]} no incidence of actual toxicity has ever been reported in people taking natural vitamin K, even in high supplemental doses.^[134] For that reason, neither the FDA nor the EFSA has set a Tolerable Upper Intake Level (UL) for vitamin K. One should note, however, that we lack long-term, high-dose studies on vitamin K safety.

Sources of vitamin K

K₁ can be found in plant products, notably green leafy vegetables. K₂ MK-4 can be found in animal products (meat, eggs, and dairy). The other types of K₂ can be found in fermented foods and liver meat.

Table references: ^{[135][136][77][137][138][92][130][139][140]}

Meats’ vitamin K content correlates positively but non-linearly with their fat content and will vary according to the animal’s diet (and thus country of origin). Forms of K₂ other than MK-4 and MK-7 have not been well studied but are likely to have some benefit — cheeses and beef liver are notable sources of others forms of K₂^[136][140] and cheese consumption is associated with a reduced risk of cardiovascular disease.^[141]

While well-conducted controlled trials provide the most reliable evidence, most such trials used amounts of vitamin K2 that far exceed what could be obtained through foods, save for natto. This leaves us wondering if dietary K₂ has any effect.

Fortunately, it seems to be the case: a high dietary intake of K₂ (≥33 μg/day seems optimal) may reduce the risk of coronary heart disease — an effect a high dietary intake of K₁ doesn’t appear to have.^{[104][106][105][142]} It doesn’t mean, of course, that foods rich in K₁ are valueless: dietary K₁ intake will protect you from excessive bleeding and is inversely associated with risk of bone fractures.^[143]

Observational studies, however, are less reliable than controlled trials, so we know less about the effects of dietary intake than about the effects of supplemental intake. If you wish to supplement with vitamin K, here are the dosages supported by the current evidence:

Summary

Although much more research needs to be performed, there is early evidence that vitamin K, whether in food or in supplemental form, can benefit cardiovascular health and bone health.

Cardiovascular diseases (CVDs) are the #1 cause of death globally. But a mix of the right foods and complementary supplements can help decrease your risk factors.

February is National Heart Month. Although heart disease is the leading cause of death for men and women worldwide, it’s largely preventable. That makes heart-health supplements a big business, which means a lot of hype and marketing fluff by various supplement companies.

So we’ve taken it upon ourselves to analyze five supplements that have actual evidence behind their benefits. As always, remember to always consult with your physician before taking anything — some supplements have medication interactions.

Nitrates

Nitrates are one of the reasons why vegetables are so good for you. Nitrates break down into nitrites, which circulate in the body and are turned into nitric oxide (NO). Nitrates, found abundantly in beetroot and a variety of leafy greens (arugula, collards, etc.), are a reliable and effective way to increase nitric oxide synthesis in the body. Elevated NO levels are associated with better circulation and lower blood pressure.^[144]

Eating a diet with a good amount of nitrate-containing vegetables decreases your risk for hypertension^[144] and can improve endothelial cell function (the cells that line the inside of your blood vessels).^[145] As an added bonus, increasing your overall vegetable (and fruit!) intake can reduce the risk of cardiovascular disease, cancer, and premature death.^[146]

Although you can find nitrates in processed meats, it’s not quite the same as getting them through vegetables. It is thought that various compounds in the meat interact with the nitrates during cooking and processing to form potentially pro-carcinogenic elements like nitrosamines. You can read up on this process and how it may affect your health here: Scientists found that red meat causes cancer ... or did they?

Garlic

While garlic can also enhance NO signaling in the body, its blood pressure lowering effects are mostly due to another compound: hydrogen sulfide (H₂S). Whether part of your diet or supplemented, garlic is a cheap and potent way to increase hydrogen sulfide signaling in the body — which in turn relaxes blood vessels and lowers blood pressure.^[147]

In those with elevated cholesterol (>200 mg/dL, >5.5 mmol/L), consistently consuming garlic for two months or more can moderately reduce total as well as low-density lipoprotein (LDL) cholesterol and can slightly bump up high-density lipoprotein (HDL).^[148] Because it can improve several cardiovascular parameters, garlic makes a good heart-health supplement.

Vitamin K2

A healthy artery is a flexible one. During arterial calcification, calcium adheres to the artery wall, increasing its stiffness. Arterial stiffness and flexibility are very reliable biomarkers of mortality from cardiovascular diseases. Vitamin K2, found in egg yolks and some fermented foods, is one of the few dietary supplements that may be able to reduce arterial calcification^[107] and stiffness.^[111]

Vitamin K can roughly be broken up into 3 groups: K₁, K₂, and K₃. K₁ plays a large role in blood clotting, while K₂ is responsible for calcium regulation. K₃ is a synthetic provitamin not used in human food fortification or supplementation, as it can harm your health.^[134]

While most can get adequate K₁ from eating green leafy vegetables, K₂ supplementation may be necessary to reap some of K₂ cardiovascular benefits.

Bonus: Vitamin K2 provides benefits for bone health too!^[121] It’s especially useful if you take vitamin D and calcium.

Berberine

Insulin resistance can worsen cardiovascular health over time, since chronically elevated blood sugars can cause tissue damage and increased blood pressure.^[149][150]

Berberine is an AMP-Activated Protein Kinase (AMPK) activator — which means it can help draw glucose and lipids into a cell, allowing them to be used as energy.

With blood sugar reduction comparable to the diabetes drug Metformin, berberine is a very potent blood glucose-lowering agent that can be beneficial for people with impaired glucose regulation. When paired with lifestyle interventions, berberine can greatly improve glucose levels (HbA1c) and help bring down high cholesterol in those with type 2 diabetes.^[151]

Taurine

Taurine (L-taurine) is a conditionally essential amino acid found abundantly in the body — particularly in heart tissues where it helps maintain a regular heartbeat.^[152] Under healthy conditions, our bodies can produce taurine from the amino acids methionine and cysteine and from vitamin B6.

In patients with heart failure, short-term taurine supplementation (~2 weeks) yielded improvements in cardiovascular function surrounding a bout of exercise.^{[153][154][155]} Studies have also suggested that taurine may have some beneficial effects on blood pressure in those with pre-hypertension or hypertension.^[156][157]

Better heart health through food and supplementation

Adding more garlic, leafy greens, and beets to your diet is an easy first step to protect your heart and February is the perfect time to get started!

Remember — supplementation is complimentary to good nutrition, not a replacement for it (and make sure you’re getting high-quality sleep and a fair amount of exercise). It’s not sexy and it’s not a magic pill, but that’s what the evidence points towards.

If you want more specific details on when to take these supplements, how much to take, and step-by-step directions, check out our Heart & Circulation Supplement Guide, a thorough guide on the latest evidence for heart health supplements.

Historically, nutrition guidelines for reducing the risk of cardiovascular disease (CVD) have included recommendations to limit dietary cholesterol. However, the 2015–2020 Dietary Guidelines for Americans did not issue explicit guidance for dietary cholesterol intake due to inconsistencies in the evidence base. Does this mean eggs can be on the breakfast menu every day without raising CVD risk?

Eggs are a relatively inexpensive and nutrient-dense food. They are a high-quality source of protein and rich in choline, vitamin B2, and the carotenoids lutein and zeaxanthin.^[158] They also contain a notable amount of cholesterol: about 186 mg per large egg.

Evidence from randomized controlled trials (RCTs) demonstrates that foods high in cholesterol increase low-density lipoprotein cholesterol (LDL-C),^[159] which increases the risk of CVD.^[160] More specifically, it’s reported that the consumption of more than 1 egg per day increases LDL-C by about 7.7 mg/dL (0.2 mmol/L), with similar effects in healthy people and people with dyslipidemia.^[161]

Nonetheless, studies report the average response and the individual response to dietary cholesterol is highly variable. It appears that the majority of people are able to roughly maintain LDL-C in response to an increase in dietary cholesterol intake.^{[162][163][164]} This lack of response is due to a combination of suppression in endogenous cholesterol synthesis, a reduction in dietary cholesterol absorption, and an increase in biliary excretion of cholesterol.^[165]

On the other hand, there is a notable subset of individuals who, partly due to genetic differences, lack these feedback control mechanisms and experience a significant increase in LDL-C in response to increases in dietary cholesterol intake (i.e., hyper-responders).^[166] In this population, it may be particularly worthwhile to limit egg consumption to prevent LDL-C from rising to an unhealthy level.

For many people, moderate egg consumption is permissible and possibly even beneficial as part of an otherwise healthy diet. However, hyper-responders and people with high cholesterol or dyslipidemia may benefit from limiting their egg consumption or removing eggs from the diet altogether, as this can lead to a clinically meaningful decrease in LDL-C.^[6]