Is saturated fat bad for your health?

The fatty you eat ( and the fat you store in your body ) is made up of unlike types of fatso acids, each with a long chain of carbon atoms bonded in concert. Saturated fatso acids ( SFAs ) have no double bonds, whereas mono unsaturated fatso acids ( MUFAs ) have one and poly unsaturated fatty acids ( PUFAs ) have two or more. The “ kinks ” those bonds form in fatty acidic chains prevent the fatso acids from packing near together, which is why unsaturated fats are liquid at room temperature, whereas saturated fats normally aren ’ thymine ( they ’ rhenium 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 impregnation does not predict how they are handled by the body. [ 1 ] Based on the duration of its fag end ( the number of carbons in its chain ), a impregnate fatness belongs to one of four independent subcategories, each with its own biological effects .
Different forms of saturated fats tied within each subcategory, the versatile fatso acids have different health effects .
For example, although palmitic acerb and stearic acerb are both long-chain impregnate fats, the former causes a greater increase in rake cholesterol levels. [ 2 ] similarly, although caprylic acid and capric acid are both medium-chain saturated fats, the early results in a larger blood ketone response. [ 3 ]

Those variations greatly limit our ability to discuss saturated fat in general. good 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 saturate fatty 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 consumption as a food supplement. traditionally, they ’ ve served to mimic a ketogenic diet ( a identical restrictive, very-low-carbohydrate diet ) in children with epilepsy. [ 4 ] Today, MCTs are besides advertised as helping with fatness loss, practice performance, and brain health, though the attest is limited .
The richest natural reservoir of MCTs, coconut oil, is ≈14 % MCTs by weight, [ 5 ] so you ’ five hundred need to eat 100 grams of adipose tissue ( 900 kcal ) from coconut petroleum to consume 14 grams ( 1 tablespoon ) of MCTs. For that reason, people concern in MCTs normally 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 promptly history lesson on why people think saturated fat is unhealthy .
Since the 1950s, many studies have linked the pulmonary tuberculosis of saturated fat with increases in rake cholesterol levels. [ 6 ] Those studies, combined with experimental research on the association between diet and kernel disease, [ 7 ] led Dr. Ancel Keys to propose the diet-heart guess, which suggests that saturated fat raises blood cholesterol levels and frankincense increases the risk of center disease. [ 8 ] [ 9 ] A brief history of the diet-heart hypothesis Despite some researchers arguing that there were meaning flaws in the datum Keys used to support his claims, [ 10 ] 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 termination 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 consumption, it makes feel to address heart disease first base .

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 assimilation of some nutrients but not others. In our lineage, one of the “ nutrients ” that penetrates the endothelium is low-density lipoprotein ( LDL ), whose primary coil problem is to transport cholesterol throughout the body .
The key event for the formation of plaques in arteries is the memory of LDL particles in the distance beneath the endothelium ( called the intima ). [ 11 ] once there, LDL is more susceptible to becoming oxidized, which signals the immune system to attack because oxidise LDL is seen as harmful to the body. This incendiary response involves certain ashen blood cells called macrophages that literally “ corrode ” the oxidize LDL particles. The LDL-engulfing process turns macrophages into foam cells, which can ’ metric ton function properly and accumulate into the fatty build-up we call plaque .
General overview of atherosclerosis 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, fleshiness, smoke, lack of exert, and infection. [ 12 ] Any process that affects LDL retentiveness and oxidation or excitement is going to influence plaque formation and the risk of suffering from kernel disease. consequently, 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 ’ sulfur effects on blood lipids were thoroughly investigated in a systematic inspection and meta-analysis published by the World Health Organization ( WHO ) in 2016. [ 13 ] This meta-analysis included 84 randomized controlled trials ( RCTs ) involving a sum of 2,353 healthy adults ; it evaluated the effects of replacing 1 % of thermal consumption from carbohydrates or unsaturated fats with 1 % of thermal consumption from saturated fatty .
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 exercise, 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 .
Effects of replacing 1% of caloric intake from carbohydrates or unsaturated fats with 1% of caloric intake from saturated fat Eating saturated fat alternatively of unsaturated fatten or carbohydrates systematically increased lipid and lipoprotein concentrations in the lineage. The one exception was a decrease in triglycerides when saturated fatten was consumed alternatively of carbohydrates. importantly, these effects were found to be consistent between sexes and across a wide-eyed stove of baseline blood-lipid values and saturated-fat intakes ( 1.6–24.4 % of calories ). They were besides reproducible between studies, whatever the year of issue .
An important limitation of this meta-analysis is that it could not differentiate between the assorted food sources of the nutrients, which is an authoritative retainer we shall discuss by and by. furthermore, studies investigating hydrogenated oils, fish petroleum mho, 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.


Compared to carbohydrates and unsaturated fats, saturated fat raises the levels of lipoproteins and most lineage lipids. These changes have well-researched implications for the gamble of developing kernel disease .
The greater the numeral of LDL particles in the blood ( LDL-P ), the more likely some will pass into artery walls, become oxidise, and kickstart brass formation. [ 11 ] Therefore, to predict heart disease, LDL-P matters more than LDL-C, [ 14 ] [ 15 ] which is merely a measure of the come of cholesterol being carried by LDL particles .
If two people have the like LDL-C but one has cholesterol-rich LDL ( large, “ downy ” 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 gamble of heart disease .
The WHO meta-analysis didn ’ deoxythymidine monophosphate cover LDL-P. [ 13 ] however, it did report the levels of apolipoprotein B ( apoB ), the protein component of LDL. Since each LDL particle has one atom of apoB, apoB concentrations provide a good estimate of LDL-P concentrations and are a strong predictor of affection disease hazard. [ 16 ] [ 17 ]

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. [ 18 ] HDL basically does the diametric of LDL. While calling HDL-C “ good cholesterol ” and LDL-C “ bad cholesterol ” is simplistic, studies do show that a higher proportion of LDL-C to HDL-C ( and of full cholesterol to HDL-C ) leads to a higher risk of center disease. Those ratios matter more than your absolute numbers for LDL-C, HDL-C, and even full cholesterol. [ 19 ] The WHO meta-analysis reported that eating more impregnate fatty increased HDL-C, but the addition was one-tenth that of LDL-C. Therefore, the proportion of LDL-C to HDL-C ( and of entire cholesterol to HDL-C ) increased, [ 13 ] and with it the risk of heart disease .
A like model was seen with apoA1, the major protein component of HDL particles, akin to apoB for LDL particles. Although replacing unsaturated fatten by saturated fat led to increases in apoA1, the increase was merely 30–60 % that in apoB. [ 13 ] The proportion of apoB to apoA1 is considered a better forecaster of heart-disease risk than other blood lipid biomarkers and their ratios. [ 20 ] [ 21 ] If apoB increases more than apoA1, then the apoB-to-apoA1 ratio increases, and with it the gamble 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.

last, the triglyceride to HDL-C proportion represents a potent, independent predictor of heart disease when LDL-C levels are below 160 mg/dL, [ 22 ] and has similar predictive ability as LDL-C for determining the extent of atherosclerosis in at-risk patients. [ 23 ] Having a triglyceride-to-HDL-C ratio above 3.8 is associated with having more modest, dense LDL particles, which are specially susceptible to oxidation. [ 24 ] The WHO meta-analysis reported that eating more polyunsaturated fat reduced the proportion, whereas eating more carbohydrates increased it, when saturated-fat inhalation was reduced. [ 13 ] however, the changes were very little and not of clinical meaning. A 10 % reduction in calories from saturated fat would increase the triglyceride-to-HDL-C proportion by a mere 0.16 if more carbohydrates were eaten, and decrease it by only 0.04 if more polyunsaturated fatty 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. consequently, reducing systemic inflammation could help fight atherosclerosis, and in this manner decrease the risk of heart disease. [ 25 ] [ 26 ] Saturated fat may worsen systemic inflammation by increasing the absorption of lipopolysaccharides ( LPS ), [ 27 ] which are bacterial endotoxins that strongly stimulate our immune system. [ 28 ] [ 29 ] even very minor serum concentrations of LPS, on a picogram scale, have the potential to elicit in humans an incendiary reply with a clear dose-response kinship. [ 30 ] however, a taxonomic inspection found no reproducible associations between consumption of saturated fat and a diverseness of inflammatory biomarkers, including cytokines, adipokines, acute-phase reactants, and cell adhesion molecules. [ 31 ] Clearly, the role of saturated fatty on ignition is not square .
still, one RCT reported that, compared to a diet high in SFAs, a diet high in MUFAs decreased LDL oxidation, a diet high gear in omega-6 fatty acid ( n-6 ) PUFAs increased it, and a diet high in omega-3 fatty acid ( n-3 ) PUFAs did not affect it. [ 32 ] The study authors attributed those differences to the fatty-acid typography of the LDL particles ( i, to whether they contained largely 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 bespeak, we have reviewed the effects of impregnate fat on heart-disease risk factors preferably than on heart disease itself .
The step between the two should be a belittled one, but that ’ s where things turn wyrd : despite a logical theoretical framework connecting diets high in saturated fat to atherosclerosis, meta-analyses of observational studies have reported no significant associations between saturated fat intake and risk of coronary heart disease, stroke, or cardiovascular disease in general. [ 33 ] [ 34 ] even long-run RTCs that assessed hard endpoints of heart disease ( such as suffering a heart attack, or dying from one ) reported discrepant links with saturated-fat consumption. For example, one meta-analysis reported that every 5 % reduction in calories from SFAs ( replaced by PUFAs ) reduced the risk of affection disease by ≈10 %, [ 35 ] 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. [ 36 ] One reason for the discrepancies is the bankruptcy of many studies to isolate the effects of altering saturated-fat intake. For model, some studies gave dietary advice to only one of the interposition 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. [ 37 ] When looking only at trials that minimized confounding factors, we see that replacing SFAs with primarily n-6 PUFAs has no consequence on the hazard of developing heart disease or dying from it. [ 37 ]

Neither observational studies nor RCTs support the notion that eating a diet high in saturated fat 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

indeed, what gives ? We have attest that eating more saturated fatness ( alternatively of unsaturated fat ) increases known risk factors for heart disease, such as blood lipids, but studies looking at the large video do not find a connection between saturated fat and heart disease. How can this be ?
The childlike answer is that fatten inhalation is but a single firearm of the heart-disease puzzle. Eating more saturated fat may increase your risk of developing kernel disease, but that doesn ’ deoxythymidine monophosphate mean you will develop kernel disease. conversely, banning all saturated fat from your diet does not make your heart attack proof .
In early words, quite than singling out any food or nutrient, we need to consider a person ’ second overall diet and life style .
Let us use dairy as an example.
Dairy fat is ≈70 % saturated fat, [ 38 ] making it a prime target for nutritional interventions. however, results from experimental and experimental studies on the effects of dairy products on blood lipid levels are not conclusive, [ 39 ] [ 40 ] and can even appear confounding. For case, there is RCT evidence that diets high in saturated fat from butter increase LDL-C, but that diets evenly high in impregnate fatness from tall mallow might not. [ 39 ] Different dairy products, such as butter and cheese, have different food matrices ( structures in which the food compounds are arranged ), and frankincense different metabolic effects. [ 41 ] similarly, one meta-analysis reported a miss of significant associations between heart disease mortality and high intakes of kernel or dairy products ( including milk and cheese ). [ 42 ] however, high intakes of action meat did increase the risk of kernel disease. It is well established that processed meats contain several carcinogenic compounds, which can influence affection disease gamble. [ 43 ] 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 exercise, replacing saturated fat by carbohydrates from hale grains is associated with a reduce gamble of kernel disease, whereas replacing saturated fatten by carbohydrates from refined grains fails to confer the lapp benefit. [ 44 ] similarly, replacing SFAs by plant-based MUFAs is associated with a reduce gamble of center disease, whereas replacing SFAs by animal-based MUFAs is not. [ 45 ]

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 quiz tubes by and large support the placement 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 damaging effects on brain development and cognitive affair. [ 46 ] [ 47 ] 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 anoint ) increased self-reported anger ( 4.7 vs. 2.2 out of 5 points ) and overall temper disturbances ( 13 vs. 7 out of 20 points ) compared to eating a diet high in MUFAs ( from hazelnut vegetable oil ). [ 48 ] other studies have reported that eating SFAs alters mind activation during cognitive tests and at rest, although the implications of these findings are not known. [ 49 ] [ 50 ]

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


Weight derive or personnel casualty depends greatly on thermal intake. According to a review of 24 studies, different types of fatten affect subjective appetite similarly, at least in the short-run ( for example, single-meal assessments ), in cattiness of repletion hormones being affected more by saturated than unsaturated fat. [ 51 ] however, differences in study protocols and participants make it unmanageable 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.


Compared to meals eminent in unsaturated adipose tissue, meals high in saturated fat tend to result in lower levels of post-meal energy outgo and fatty-acid oxidation. [ 52 ] Studies using isotope tracers indicate that the body would quite use unsaturated than saturated fats as an energy source. [ 53 ] [ 54 ] however, long-run studies are inconsistent. [ 52 ]

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


Eating more monounsaturated fat in plaza of saturated fatten appears to spontaneously increase physical natural process levels. [ 48 ]

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

Saturated fat and your hormones


respective 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 gear 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 ’ metric ton 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 little 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 affect on your health than your total testosterone .
Two studies with big sample sizes, controlled diets, and direct measurement of release testosterone reported that, compared to high-fat diets ( 33–40 % of calories ), low-fat diets ( 14–19 % of calories ) reduced entire testosterone levels in goodly men, but did not interpolate levels of exempt or bioavailable testosterone. [ 55 ] [ 56 ] Two other studies with smaller sample distribution sizes, less accurate measurement methods, and less dietary control reported reductions in both total and free testosterone levels. [ 57 ] [ 58 ]

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

There is not enough evidence to directly link saturated fat with positive or negative effects on heart health. 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.

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