Fat

This article is about the type of nutrient in food. For fat in animals, see Adipose tissue. For chemistry of fats, see triglyceride. For other uses, see Fat (disambiguation).

Idealized representation of a molecule of a typical triglyceride, the main type of fat. Note the three fatty acid chains attached to the central glycerol portion of the molecule.

Composition of fats from various foods, as percentage of their total fat

In nutrition, biology, and chemistry, fat usually means any ester of fatty acids, or a mixture of such compounds, most commonly those that occur in living beings or in food.[1]

The term often refers specifically to triglycerides (triple esters of glycerol), that are the main components of vegetable oils and of fatty tissue in animals;[2] or, even more narrowly, to triglycerides that are solid or semisolid at room temperature, thus excluding oils. The term may also be used more broadly as a synonym of lipid—any substance of biological relevance, composed of carbon, hydrogen, or oxygen, that is insoluble in water but soluble in non-polar solvents.[1] In this sense, besides the triglycerides, the term would include several other types of compounds like mono- and diglycerides, phospholipids (such as lecithin), sterols (such as cholesterol), waxes (such as beeswax),[1] and free fatty acids, which are usually present in human diet in smaller amounts.[2]

Fats are one of the three main macronutrient groups in human diet, along with carbohydrates and proteins,[1][3] and the main components of common food products like milk, butter, tallow, lard, salt pork, and cooking oils. They are a major and dense source of food energy for many animals and play important structural and metabolic functions in most living beings, including energy storage, waterproofing, and thermal insulation.[4] The human body can produce the fat it requires from other food ingredients, except for a few essential fatty acids that must be included in the diet. Dietary fats are also the carriers of some flavor and aroma ingredients and vitamins that are not water-soluble.[2]

Biological importance

In humans and many animals, fats serve both as energy sources and as stores for energy in excess of what the body needs immediately. Each gram of fat when burned or metabolized releases about nine food calories (37 kJ = 8.8 kcal).[5]

Fats are also sources of essential fatty acids, an important dietary requirement. Vitamins A, D, E, and K are fat-soluble, meaning they can only be digested, absorbed, and transported in conjunction with fats.

Fats play a vital role in maintaining healthy skin and hair, insulating body organs against shock, maintaining body temperature, and promoting healthy cell function. Fat also serves as a useful buffer against a host of diseases. When a particular substance, whether chemical or biotic, reaches unsafe levels in the bloodstream, the body can effectively dilute—or at least maintain equilibrium of—the offending substances by storing it in new fat tissue.[6] This helps to protect vital organs, until such time as the offending substances can be metabolized or removed from the body by such means as excretion, urination, accidental or intentional bloodletting, sebum excretion, and hair growth.

Adipose tissue

The obese mouse on the left has large stores of adipose tissue. For comparison, a mouse with a normal amount of adipose tissue is shown on the right.

In animals, adipose tissue, or fatty tissue is the body's means of storing metabolic energy over extended periods of time. Adipocytes (fat cells) store fat derived from the diet and from liver metabolism. Under energy stress these cells may degrade their stored fat to supply fatty acids and also glycerol to the circulation. These metabolic activities are regulated by several hormones (e.g., insulin, glucagon and epinephrine). Adipose tissue also secretes the hormone leptin.[7]

Production and processing

A variety of chemical and physical techniques are used for the production and processing of fats, both industrially and in cottage or home settings. They include:

• Pressing to extract liquid fats from fruits, seeds, or algae, e.g. olive oil from olives
• Solvent extraction using solvents like hexane or supercritical carbon dioxide
• Rendering, the melting of fat in adipose tissue, e.g. to produce tallow, lard, fish oil, and whale oil
• Churning of milk to produce butter
• Hydrogenation to increase the degree of saturation of the fatty acids
• Interesterification, the rearrangement of fatty acids across different triglycerides
• Winterization to remove oil components with higher melting points
• Clarification of butter

Metabolism

See also: Fatty acid metabolism

Main article: Lipid metabolism

The pancreatic lipase acts at the ester bond, hydrolyzing the bond and "releasing" the fatty acid. In triglyceride form, lipids cannot be absorbed by the duodenum. Fatty acids, monoglycerides (one glycerol, one fatty acid), and some diglycerides are absorbed by the duodenum, once the triglycerides have been broken down.

In the intestine, following the secretion of lipases and bile, triglycerides are split into monoacylglycerol and free fatty acids in a process called lipolysis. They are subsequently moved to absorptive enterocyte cells lining the intestines. The triglycerides are rebuilt in the enterocytes from their fragments and packaged together with cholesterol and proteins to form chylomicrons. These are excreted from the cells and collected by the lymph system and transported to the large vessels near the heart before being mixed into the blood. Various tissues can capture the chylomicrons, releasing the triglycerides to be used as a source of energy. Liver cells can synthesize and store triglycerides. When the body requires fatty acids as an energy source, the hormone glucagon signals the breakdown of the triglycerides by hormone-sensitive lipase to release free fatty acids. As the brain cannot utilize fatty acids as an energy source (unless converted to a ketone),[8] the glycerol component of triglycerides can be converted into glucose, via gluconeogenesis by conversion into dihydroxyacetone phosphate and then into glyceraldehyde 3-phosphate, for brain fuel when it is broken down. Fat cells may also be broken down for that reason if the brain's needs ever outweigh the body's.

Triglycerides cannot pass through cell membranes freely. Special enzymes on the walls of blood vessels called lipoprotein lipases must break down triglycerides into free fatty acids and glycerol. Fatty acids can then be taken up by cells via fatty acid transport proteins (FATPs).

Triglycerides, as major components of very-low-density lipoprotein (VLDL) and chylomicrons, play an important role in metabolism as energy sources and transporters of dietary fat. They contain more than twice as much energy (approximately 9 kcal/g or 38 kJ/g) as carbohydrates (approximately 4 kcal/g or 17 kJ/g).[9]

Nutritional and health aspects

The most common type of fat, in human diet and most living beings, is a triglyceride, an ester of the triple alcohol glycerol H(–CHOH–)
₃H and three fatty acids. The molecule of a triglyceride can be described as resulting from a condensation reaction (specifically, esterification) between each of glycerol's –OH groups and the HO– part of the carboxyl group HO(O=)C− of each fatty acid, forming an ester bridge −O−(O=)C− with elimination of a water molecule H
₂O.

Other less common types of fats include diglycerides and monoglycerides, where the esterification is limited to two or just one of glycerol's –OH groups. Other alcohols, such as cetyl alcohol (predominant in spermaceti), may replace glycerol. In the phospholipids, one of the fatty acids is replaced by phosphoric acid or a monoester thereof. The benefits and risks of various amounts and types of dietary fats have been the object of much study, and are still highly controversial topics.[10][11][12][13]

Essential fatty acids

There are two essential fatty acids (EFAs) in human nutrition: alpha-Linolenic acid (an omega-3 fatty acid) and linoleic acid (an omega-6 fatty acid).[14][5] The adult body can synthesize other lipids that it needs from these two.

Dietary sources

Properties of vegetable oils[15][16]
The nutritional values are expressed as percent (%) by mass of total fat.

Type	Processing treatment[17]	Saturated fatty acids	Monounsaturated fatty acids		Polyunsaturated fatty acids				Smoke point
			Total[15]	Oleic acid (ω−9)	Total[15]	α-Linolenic acid (ω−3)	Linoleic acid (ω−6)	ω−6:3 ratio
Avocado[18]		11.6	70.6	52–66 [19]	13.5	1	12.5	12.5:1	250 °C (482 °F)[20]
Brazil nut[21]		24.8	32.7	31.3	42.0	0.1	41.9	419:1	208 °C (406 °F)[22]
Canola[23]		7.4	63.3	61.8	28.1	9.1	18.6	2:1	204 °C (400 °F)[24]
Coconut[25]		82.5	6.3	6	1.7	0.019	1.68	88:1	175 °C (347 °F)[22]
Corn[26]		12.9	27.6	27.3	54.7	1	58	58:1	232 °C (450 °F)[24]
Cottonseed[27]		25.9	17.8	19	51.9	1	54	54:1	216 °C (420 °F)[24]
Cottonseed[28]	hydrogenated	93.6	1.5		0.6	0.2	0.3	1.5:1
Flaxseed/linseed[29]		9.0	18.4	18	67.8	53	13	0.2:1	107 °C (225 °F)
Grape seed		10.4	14.8	14.3	74.9	0.15	74.7	very high	216 °C (421 °F)[30]
Hemp seed[31]		7.0	9.0	9.0	82.0	22.0	54.0	2.5:1	166 °C (330 °F)[32]
High-oleic safflower oil[33]		7.5	75.2	75.2	12.8	0	12.8	very high	212 °C (414 °F)[22]
Olive (extra virgin)[34]		13.8	73.0	71.3	10.5	0.7	9.8	14:1	193 °C (380 °F)[22]
Palm[35]		49.3	37.0	40	9.3	0.2	9.1	45.5:1	235 °C (455 °F)
Palm[36]	hydrogenated	88.2	5.7		0
Peanut[37]		16.2	57.1	55.4	19.9	0.318	19.6	61.6:1	232 °C (450 °F)[24]
Rice bran oil		25	38.4	38.4	36.6	2.2	34.4[38]	15.6:1	232 °C (450 °F)[39]
Sesame[40]		14.2	39.7	39.3	41.7	0.3	41.3	138:1
Soybean[41]		15.6	22.8	22.6	57.7	7	51	7.3:1	238 °C (460 °F)[24]
Soybean[42]	partially hydrogenated	14.9	43.0	42.5	37.6	2.6	34.9	13.4:1
Sunflower[43]		8.99	63.4	62.9	20.7	0.16	20.5	128:1	227 °C (440 °F)[24]
Walnut oil[44]	unrefined	9.1	22.8	22.2	63.3	10.4	52.9	5:1	160 °C (320 °F)[45]

Saturated vs. unsaturated fats

Different foods contain different amounts of fat with different proportions of saturated and unsaturated fatty acids. Some animal products, like beef and dairy products made with whole or reduced fat milk like yogurt, ice cream, cheese and butter have mostly saturated fatty acids (and some have significant contents of dietary cholesterol). Other animal products, like pork, poultry, eggs, and seafood have mostly unsaturated fats. Industrialized baked goods may use fats with high unsaturated fat contents as well, especially those containing partially hydrogenated oils, and processed foods that are deep-fried in hydrogenated oil are high in saturated fat content.[46][47][48]

Plants and fish oil generally contain a higher proportion of unsaturated acids, although there are exceptions such as coconut oil and palm kernel oil.[49][50] Foods containing unsaturated fats include avocado, nuts, olive oils, and vegetable oils such as canola.

Many scientific studies have found that replacing saturated fats with cis unsaturated fats in the diet reduces risk of cardiovascular diseases (CVDs),[51][52] diabetes, or death.[53] These studies prompted many medical organizations and public health departments, including the World Health Organization (WHO),[54][55] to officially issue that advice. Some countries with such recommendations include:

• United Kingdom[56][57][58][59][60]
• United States[53][61][62][63][64]
• India[65][66]
• Canada[67]
• Australia[68]
• Singapore[69]
• New Zealand[70]
• Hong Kong[71]

A 2004 review concluded that "no lower safe limit of specific saturated fatty acid intakes has been identified" and recommended that the influence of varying saturated fatty acid intakes against a background of different individual lifestyles and genetic backgrounds should be the focus in future studies.[72]

This advice is often oversimplified by labeling the two kinds of fats as bad fats and good fats, respectively. However, since the fats and oils in most natural and traditionally processed foods contain both unsaturated and saturated fatty acids,[73] the complete exclusion of saturated fat is unrealistic and possibly unwise. For instance, some foods rich in saturated fat, such as coconut and palm oil, are an important source of cheap dietary calories for a large fraction of the population in developing countries.[74]

Concerns were also expressed at a 2010 conference of the American Dietetic Association that a blanket recommendation to avoid saturated fats could drive people to also reduce the amount of polyunsaturated fats, which may have health benefits, and/or replace fats by refined carbohydrates — which carry a high risk of obesity and heart disease.[75]

For these reasons, the U.S. Food and Drug Administration, for example, recommends to consume less than 10% (7% for high-risk groups) of calories from saturated fat, with 15-30% of total calories from all fat.[76][74] A general 7% limit was recommended also by the American Heart Association (AHA) in 2006.[77][78]

The WHO/FAO report also recommended replacing fats so as to reduce the content of myristic and palmitic acids, specifically.[74]

The so-called Mediterranean diet, prevalent in many countries in the Mediterranean Sea area, includes more total fat than the diet of Northern European countries, but most of it is in the form of unsaturated fatty acids (specifically, monounsaturated and omega-3) from olive oil and fish, vegetables, and certain meats like lamb, while consumption of saturated fat is minimal in comparison. A 2017 review found evidence that a Mediterranean-style diet could reduce the risk of cardiovascular diseases, overall cancer incidence, neurodegenerative diseases, diabetes, and mortality rate.[79] A 2018 review showed that a Mediterranean-like diet may improve overall health status, such as reduced risk of non-communicable diseases. It also may reduce the social and economic costs of diet-related illnesses.[80]

A small number of contemporary reviews have challenged this negative view of saturated fats. For example, an evaluation of evidence from 1966 to 1973 of the observed health impact of replacing dietary saturated fat with linoleic acid found that it increased rates of death from all causes, coronary heart disease, and cardiovascular disease.[81] These studies have been disputed by many scientists,[82] and the consensus in the medical community is that saturated fat and cardiovascular disease are closely related.[83][84][85] Still, these discordant studies fueled debate over the merits of substituting polyunsaturated fats for saturated fats.[86]

Cardiovascular disease

Main article: Saturated fat and cardiovascular disease

The effect of saturated fat on cardiovascular disease has been extensively studied.[87] The general consensus is that there is evidence of moderate-quality of a strong, consistent, and graded relationship between saturated fat intake, blood cholesterol levels, and the incidence of cardiovascular disease.[53][87] The relationships are accepted as causal,[88][89] including by many government and medical organizations.[74][90][91][53][92][93][94][95]

A 2017 review by the AHA estimated that replacement of saturated fat with polyunsaturated fat in the American diet could reduce the risk of cardiovascular diseases by 30%.[53]

The consumption of saturated fat is generally considered a risk factor for dyslipidemia—abnormal blood lipid levels, including high total cholesterol, high levels of triglycerides, high levels of low-density lipoprotein (LDL, "bad" cholesterol) or low levels of high-density lipoprotein (HDL, "good" cholesterol). These parameters in turn are believed to be risk indicators for some types of cardiovascular disease.[96][97][98][99][100][92][101][102][103] These effects were observed in children too.[104]

Several meta-analyses (reviews and consolidations of multiple previously published experimental studies) have confirmed a significant relationship between saturated fat and high serum cholesterol levels,[53][105] which in turn have been claimed to have a causal relation with increased risk of cardiovascular disease (the so-called lipid hypothesis).[106][107] However, high cholesterol may be caused by many factors. Other indicators, such as high LDL/HDL ratio, have proved to be more predictive.[107] In a study of myocardial infarction in 52 countries, the ApoB/ApoA1 (related to LDL and HDL, respectively) ratio was the strongest predictor of CVD among all risk factors.[108] There are other pathways involving obesity, triglyceride levels, insulin sensitivity, endothelial function, and thrombogenicity, among others, that play a role in CVD, although it seems, in the absence of an adverse blood lipid profile, the other known risk factors have only a weak atherogenic effect.[109] Different saturated fatty acids have differing effects on various lipid levels.[110]

Cancer

The evidence for a relation between saturated fat intake and cancer is significantly weaker, and there does not seem to be a clear medical consensus about it.

• Several reviews of case–control studies have found that saturated fat intake is associated with increased breast cancer risk.[111][112][113]
• Another review found limited evidence for a positive relationship between consuming animal fat and incidence of colorectal cancer.[114]
• Other meta-analyses found evidence for increased risk of ovarian cancer by high consumption of saturated fat.[115]
• Some studies have indicated that serum myristic acid[116][117] and palmitic acid[117] and dietary myristic[118] and palmitic[118] saturated fatty acids and serum palmitic combined with alpha-tocopherol supplementation[116] are associated with increased risk of prostate cancer in a dose-dependent manner. These associations may, however, reflect differences in intake or metabolism of these fatty acids between the precancer cases and controls, rather than being an actual cause.[117]

Bones

Various animal studies have indicated that the intake of saturated fat has a negative effect on the mineral density of bones. One study suggested that men may be particularly vulnerable.[119]

Disposition and overall health

Studies have shown that substituting monounsaturated fatty acids for saturated ones is associated with increased daily physical activity and resting energy expenditure. More physical activity, less anger, and less irritability were associated with a higher-oleic acid diet than one of a palmitic acid diet.[120]

Amounts of fat types in selected foods

Monounsaturated vs. polyunsaturated fat

Schematic diagram of a triglyceride with a saturated fatty acid (top), a monounsaturated one (middle) and a polyunsaturated one (bottom).

The most common fatty acids in human diet are unsaturated or mono-unsaturated. Monounsaturated fats are found in animal flesh such as red meat, whole milk products, nuts, and high fat fruits such as olives and avocados. Olive oil is about 75% monounsaturated fat.[121] The high oleic variety sunflower oil contains at least 70% monounsaturated fat.[122] Canola oil and cashews are both about 58% monounsaturated fat.[123] Tallow (beef fat) is about 50% monounsaturated fat,[124] and lard is about 40% monounsaturated fat.[125] Other sources include hazelnut, avocado oil, macadamia nut oil, grapeseed oil, groundnut oil (peanut oil), sesame oil, corn oil, popcorn, whole grain wheat, cereal, oatmeal, almond oil, hemp oil, and tea-oil camellia.[126]

Polyunsaturated fatty acids can be found mostly in nuts, seeds, fish, seed oils, and oysters.[127]

Food sources of polyunsaturated fats include:[127][128]

Food source (100g)	Polyunsaturated fat (g)
Walnuts	47
Canola oil	34
Sunflower seeds	33
Sesame seeds	26
Chia seeds	23.7
Unsalted peanuts	16
Peanut butter	14.2
Avocado oil	13.5[129]
Olive oil	11
Safflower oil	12.82[130]
Seaweed	11
Sardines	5
Soybeans	7
Tuna	14
Wild salmon	17.3
Whole grain wheat	9.7

Insulin resistance and sensitivity

MUFAs (especially oleic acid) have been found to lower the incidence of insulin resistance; PUFAs (especially large amounts of arachidonic acid) and SFAs (such as arachidic acid) increased it. These ratios can be indexed in the phospholipids of human skeletal muscle and in other tissues as well. This relationship between dietary fats and insulin resistance is presumed secondary to the relationship between insulin resistance and inflammation, which is partially modulated by dietary fat ratios (omega−3/6/9) with both omega−3 and −9 thought to be anti-inflammatory, and omega−6 pro-inflammatory (as well as by numerous other dietary components, particularly polyphenols and exercise, with both of these anti-inflammatory). Although both pro- and anti-inflammatory types of fat are biologically necessary, fat dietary ratios in most US diets are skewed towards omega−6, with subsequent disinhibition of inflammation and potentiation of insulin resistance.[73] This is contrary to the suggestion that polyunsaturated fats are shown to be protective against insulin resistance.^[citation needed]

The large scale KANWU study found that increasing MUFA and decreasing SFA intake could improve insulin sensitivity, but only when the overall fat intake of the diet was low.[131] However, some MUFAs may promote insulin resistance (like the SFAs), whereas PUFAs may protect against it.[132][133]^[clarification needed]

Cancer

Levels of oleic acid along with other MUFAs in red blood cell membranes were positively associated with breast cancer risk. The saturation index (SI) of the same membranes was inversely associated with breast cancer risk. MUFAs and low SI in erythrocyte membranes are predictors of postmenopausal breast cancer. Both of these variables depend on the activity of the enzyme delta-9 desaturase (Δ9-d).[134]

Results from observational clinical trials on PUFA intake and cancer have been inconsistent and vary by numerous factors of cancer incidence, including gender and genetic risk.[135] Some studies have shown associations between higher intakes and/or blood levels of omega-3 PUFAs and a decreased risk of certain cancers, including breast and colorectal cancer, while other studies found no associations with cancer risk.[135][136]

Pregnancy disorders

Polyunsaturated fat supplementation was found to have no effect on the incidence of pregnancy-related disorders, such as hypertension or preeclampsia, but may increase the length of gestation slightly and decreased the incidence of early premature births.[127]

Expert panels in the United States and Europe recommend that pregnant and lactating women consume higher amounts of polyunsaturated fats than the general population to enhance the DHA status of the fetus and newborn.[127]

"Cis fat" vs. "trans fat"

Main article: Trans fat

In nature, unsaturated fatty acids generally have double bonds in cis configuration (with the adjacent C–C bonds on the same side) as opposed to trans.[137] Nevertheless, trans fatty acids (TFAs) occur in small amounts in meat and milk of ruminants (such as cattle and sheep),[138][139] typically 2–5% of total fat.[140] Natural TFAs, which include conjugated linoleic acid (CLA) and vaccenic acid, originate in the rumen of these animals. CLA has two double bonds, one in the cis configuration and one in trans, which makes it simultaneously a cis- and a trans-fatty acid.[141]

Trans fat contents in various natural and traditionally processed foods, in g per 100 g [142]

Food type	Trans fat content
butter	2 to 7 g
whole milk	0.07 to 0.1 g
animal fat	0 to 5 g[140]
ground beef	1 g

The processing of fats by hydrogenation can convert some unsaturated fats into trans fat]]s. The presence of trans fats in various processed foods has received much attention.

Margarine, a common product that can contain trans fats

Cover of original Crisco cookbook, 1912. Crisco was made by hydrogenating cottonseed oil. The formula was revised in the 2000s and now has only a small amount of trans fat.

Omega-three and omega-six fatty acids

Main articles: Omega-3 fatty acid and Omega-6 fatty acid

The ω−3 fatty acids have received substantial attention. Among omega-3 fatty acids, neither long-chain nor short-chain forms were consistently associated with breast cancer risk. High levels of docosahexaenoic acid (DHA), however, the most abundant omega-3 polyunsaturated fatty acid in erythrocyte (red blood cell) membranes, were associated with a reduced risk of breast cancer.[134] The DHA obtained through the consumption of polyunsaturated fatty acids is positively associated with cognitive and behavioral performance.[143] In addition, DHA is vital for the grey matter structure of the human brain, as well as retinal stimulation and neurotransmission.[127]

Interesterification

Some studies have investigated the health effects of interesterified (IE) fats, by comparing diets with IE and non-IE fats with the same overall fatty acid composition.[144]

Several experimental studies in humans found no statistical difference on fasting blood lipids between a diet with large amounts of IE fat, having 25-40% C16:0 or C18:0 on the 2-position, and a similar diet with non-IE fat, having only 3-9% C16:0 or C18:0 on the 2-position.[145][146][147] A negative result was obtained also in a study that compared the effects on blood cholesterol levels of an IE fat product mimicking cocoa butter and the real non-IE product.[148][149][150][151][152][153][154]

A 2007 study funded by the Malaysian Palm Oil Board[155] claimed that replacing natural palm oil by other interesterified or partially hydrogenated fats caused adverse health effects, such as higher LDL/HDL ratio and plasma glucose levels. However, these effects could be attributed to the higher percentage of saturated acids in the IE and partially hydrogenated fats, rather than to the IE process itself.[156][157]

Rancification

Main article: Rancidification

Unsaturated fats undergo auto-oxidation, which involves replacement of a C-H bond with C-OH unit. The process requires oxygen (air) and is accelerated by the presence of traces of metals, which serve as catalysts. Doubly unsaturated fatty acids are particularly prone to this reaction. Vegetable oils resist this process to a small degree because they contain antioxidants, such as tocopherol. Fats and oils often are treated with chelating agents such as citric acid to remove the metal catalysts.

Role in disease

Main article: Hypertriglyceridemia

In the human body, high levels of triglycerides in the bloodstream have been linked to atherosclerosis, heart disease[158] and stroke.[9] However, the relative negative impact of raised levels of triglycerides compared to that of LDL:HDL ratios is as yet unknown. The risk can be partly accounted for by a strong inverse relationship between triglyceride level and HDL-cholesterol level. But the risk is also due to high triglyceride levels increasing the quantity of small, dense LDL particles.[159]

Guidelines

The National Cholesterol Education Program has set guidelines for triglyceride levels:[160][161]

Level		Interpretation
(mg/dL)	(mmol/L)
< 150	< 1.70	Normal range – low risk
150–199	1.70–2.25	Slightly above normal
200–499	2.26–5.65	Some risk
500 or higher	> 5.65	Very high – high risk

These levels are tested after fasting 8 to 12 hours. Triglyceride levels remain temporarily higher for a period after eating.

The AHA recommends an optimal triglyceride level of 100 mg/dL (1.1 mmol/L) or lower to improve heart health.[162]

Reducing triglyceride levels

This section is an excerpt from Hypertriglyceridemia § Treatment.[edit]

Lifestyle changes including weight loss, exercise and dietary modification may improve hypertriglyceridemia.[163][164][165][166] This may include dietary changes such as restriction of fat and carbohydrates (specifically fructose[165][167] and sugar-sweetened beverages[164]) and increased consumption of omega-3 fatty acids from algae, nuts, and seeds.[168][169]

The decision to treat hypertriglyceridemia with medication depends on the levels and on the presence of other risk factors for cardiovascular disease. Very high levels that would increase the risk of pancreatitis is treated with a drug from the fibrate class. Niacin and omega-3 fatty acids as well as drugs from the statin class may be used in conjunction, with statins being the main drug treatment for moderate hypertriglyceridemia where reduction of cardiovascular risk is required.[164] Medications are recommended in those with high levels of triglycerides that are not corrected with lifestyle modifications, with fibrates being recommended first.[164][170][171] Epanova (omega-3-carboxylic acids) is another prescription drug used to treat very high levels of blood triglycerides.[172]

See also

• Animal fat
• Monounsaturated fat
• Diet and heart disease
• Fatty acid synthesis
• Food composition data
• Western pattern diet
• Oil
• Lipid

References

1. Entry for "fat" Archived 2020-07-25 at the Wayback Machine in the online Merriam-Webster disctionary, sense 3.2. Accessed on 2020-08-09
2. Thomas A. B. Sanders (2016): "The Role of Fats in Human Diet". Pages 1-20 of Functional Dietary Lipids. Woodhead/Elsevier, 332 pages. ISBN 978-1-78242-247-1doi:10.1016/B978-1-78242-247-1.00001-6
3. "Macronutrients: the Importance of Carbohydrate, Protein, and Fat". McKinley Health Center. University of Illinois at Urbana–Champaign. Archived from the original on 21 September 2014. Retrieved 20 September 2014.
4. "Introduction to Energy Storage". Khan Academy.
5. Government of the United Kingdom (1996): "Schedule 7: Nutrition labelling Archived 2013-03-17 at the Wayback Machine". In Food Labelling Regulations 1996 Archived 2013-09-21 at the Wayback Machine. Accessed on 2020-08-09.
6. Wu, Yang; Zhang, Aijun; Hamilton, Dale J.; Deng, Tuo (2017). "Epicardial Fat in the Maintenance of Cardiovascular Health". Methodist DeBakey Cardiovascular Journal. 13 (1): 20–24. doi:10.14797/mdcj-13-1-20. ISSN 1947-6094. PMC 5385790. PMID 28413578.
7. "The human proteome in adipose - The Human Protein Atlas". www.proteinatlas.org. Retrieved 2017-09-12.
8. White, Hayden; Venkatesh, Balasubramanian (2011). "Clinical review: Ketones and brain injury". Critical Care. 15 (2): 219. doi:10.1186/cc10020. PMC 3219306. PMID 21489321.
9. Drummond, K. E.; Brefere, L. M. (2014). Nutrition for Foodservice and Culinary Professionals (8th ed.). John Wiley & Sons. ISBN 978-0-470-05242-6.
10. Rebecca J. Donatelle (2005): Health, the Basics, 6th edition. Pearson Education, San Francisco; ISBN 978-0-13-120687-8
11. Frank B. Hu, JoAnn E. Manson, and Walter C. Willett (2001): "Types of dietary fat and risk of coronary heart disease: A critical review". Journal of the American College of Nutrition, volume 20, issue 1, pages 5-19. doi:10.1080/07315724.2001.10719008
12. Lee Hooper, Carolyn D. Summerbell, Julian P. T. Higgins, Rachel L. Thompson, Nigel E. Capps, George Davey Smith, Rudolph A. Riemersma, and Shah Ebrahim (2001): "Dietary fat intake and prevention of cardiovascular disease: systematic review". The BMJ, volume 322, pages 757-. doi:10.1136/bmj.322.7289.757
13. George A. Bray, Sahasporn Paeratakul, Barry M. Popkin (2004): "Dietary fat and obesity: a review of animal, clinical and epidemiological studies". Physiology & Behavior, volume 83, issue 4, pages 549-555. doi:10.1016/j.physbeh.2004.08.039
14. Dariush Mozaffarian, Martijn B. Katan, Alberto Ascherio, Meir J. Stampfer, and Walter C. Willett (2006): "Trans fatty acids and cardiovascular disease". New England Journal of Medicine, volume 354, issue 15, pages 1601–1613. doi:10.1056/NEJMra054035 PMID 16611951
15. "US National Nutrient Database, Release 28". United States Department of Agriculture. May 2016. All values in this table are from this database unless otherwise cited or when italicized as the simple arithmetic sum of other component columns.
16. "Fats and fatty acids contents per 100 g of Avocado oil". Nutritiondata.com, Conde Nast from the USDA National Nutrient Database, Standard Release 21. 2014. Archived from the original on 31 August 2014. Retrieved 13 January 2025. Values from Nutritiondata.com (SR 21) may need to be reconciled with most recent release from the USDA SR 28 as of Sept 2017.
17. "USDA Specifications for Vegetable Oil Margarine Effective August 28, 1996" (PDF).
18. "Avocado oil, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
19. Ozdemir, Feramuz; Topuz, Ayhan (June 2004). "Changes in dry matter, oil content and fatty acids composition of avocado during harvesting time and post-harvesting ripening period". Food Chemistry. 86 (1): 79–83. doi:10.1016/j.foodchem.2003.08.012.
20. Wong M, Requejo-Jackman C, Woolf A (April 2010). "What is unrefined, extra virgin cold-pressed avocado oil?". Aocs.org. The American Oil Chemists' Society. Retrieved 26 December 2019.
21. "Brazil nut oil, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
22. Katragadda, Harinageswara Rao; Fullana, Andrés; Sidhu, Sukh; Carbonell-Barrachina, Ángel A. (May 2010). "Emissions of volatile aldehydes from heated cooking oils". Food Chemistry. 120 (1): 59–65. doi:10.1016/j.foodchem.2009.09.070.
23. "Canola oil, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
24. Wolke RL (May 16, 2007). "Where There's Smoke, There's a Fryer". The Washington Post. Retrieved March 5, 2011.
25. "Coconut oil, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
26. "Corn oil, industrial and retail, all purpose salad or cooking, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
27. "Cottonseed oil, salad or cooking, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
28. "Cottonseed oil, industrial, fully hydrogenated, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
29. "Linseed/Flaxseed oil, cold pressed, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
30. Garavaglia J, Markoski MM, Oliveira A, Marcadenti A (2016). "Grape Seed Oil Compounds: Biological and Chemical Actions for Health". Nutrition and Metabolic Insights. 9: 59–64. doi:10.4137/NMI.S32910. PMC 4988453. PMID 27559299.
31. Callaway, James; Schwab, Ursula; Harvima, Ilkka; Halonen, Pirjo; Mykkänen, Otto; Hyvönen, Pekka; Järvinen, Tomi (April 2005). "Efficacy of dietary hempseed oil in patients with atopic dermatitis". Journal of Dermatological Treatment. 16 (2): 87–94. doi:10.1080/09546630510035832. PMID 16019622.
32. Melina V. "Smoke points of oils" (PDF). veghealth.com. The Vegetarian Health Institute.
33. "Safflower oil, salad or cooking, high oleic, primary commerce, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
34. "Olive oil, salad or cooking, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
35. "Palm oil, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
36. "Palm oil, industrial, fully hydrogenated, filling fat, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
37. "Oil, peanut". FoodData Central. usda.gov.
38. Orthoefer, Frank T. (2020). "Rice Bran Oil". Bailey's Industrial Oil and Fat Products. pp. 1–25. doi:10.1002/047167849X.bio015.pub2. ISBN 978-0-471-38460-1.
39. "Rice bran oil". RITO Partnership. Retrieved 22 January 2021.
40. "Oil, sesame, salad or cooking". FoodData Central. fdc.nal.usda.gov. 1 April 2019.
41. "Soybean oil, salad or cooking, fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
42. "Soybean oil, salad or cooking, (partially hydrogenated), fat composition, 100 g". US National Nutrient Database, Release 28, United States Department of Agriculture. May 2016. Retrieved 6 September 2017.
43. "FoodData Central". fdc.nal.usda.gov.
44. "Walnut oil, fat composition, 100 g". US National Nutrient Database, United States Department of Agriculture.
45. "Smoke Point of Oils". Baseline of Health. Jonbarron.org.
46. "Saturated fats". American Heart Association. 2014. Retrieved 1 March 2014.
47. "Top food sources of saturated fat in the US". Harvard University School of Public Health. 2014. Retrieved 1 March 2014.
48. "Saturated, Unsaturated, and Trans Fats". choosemyplate.gov. 2020. Archived from the original on 2020-10-15. Retrieved 2020-08-30.
49. Reece, Jane; Campbell, Neil (2002). Biology. San Francisco: Benjamin Cummings. pp. 69–70. ISBN 978-0-8053-6624-2.
50. "What are "oils"?". ChooseMyPlate.gov, US Department of Agriculture. 2015. Archived from the original on 9 June 2015. Retrieved 13 June 2015.
51. Hooper L, Martin N, Abdelhamid A, Davey Smith G (June 2015). "Reduction in saturated fat intake for cardiovascular disease". The Cochrane Database of Systematic Reviews. 6 (6): CD011737. doi:10.1002/14651858.CD011737. PMID 26068959.
52. Hooper, L; Martin, N; Jimoh, OF; Kirk, C; Foster, E; Abdelhamid, AS (21 August 2020). "Reduction in saturated fat intake for cardiovascular disease". The Cochrane Database of Systematic Reviews. 2020 (8): CD011737. doi:10.1002/14651858.CD011737.pub3. PMC 8092457. PMID 32827219.
53. Sacks FM, Lichtenstein AH, Wu JH, Appel LJ, Creager MA, Kris-Etherton PM, Miller M, Rimm EB, Rudel LL, Robinson JG, Stone NJ, Van Horn LV (July 2017). "Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association". Circulation. 136 (3): e1 – e23. doi:10.1161/CIR.0000000000000510. PMID 28620111. S2CID 367602.
54. "Healthy diet Fact sheet N°394". May 2015. Retrieved 12 August 2015.
55. World Health Organization: Food pyramid (nutrition)
56. "Fats explained" (PDF). HEART UK – The Cholesterol Charity. Archived (PDF) from the original on 2019-02-21. Retrieved 20 February 2019.
57. "Live Well, Eat well, Fat: the facts". NHS. 27 April 2018. Retrieved 20 February 2019.
58. "Fat: the facts". United Kingdom's National Health Service. 2018-04-27. Retrieved 2019-09-24.
59. "How to eat less saturated fat - NHS". nhs.uk. April 27, 2018.
60. "Fats explained". British Heart Foundation.
61. "Key Recommendations: Components of Healthy Eating Patterns". Dietary Guidelines 2015-2020. Retrieved 20 February 2019.
62. "Cut Down on Saturated Fats" (PDF). United States Department of Health and Human Services. Retrieved 2019-09-24.
63. "Trends in Intake of Energy, Protein, Carbohydrate, Fat, and Saturated Fat — United States, 1971–2000". Centers for Disease Control. 2004. Archived from the original on 2008-12-01.
64. "Dietary Guidelines for Americans" (PDF). United States Department of Agriculture. 2005.
65. "Dietary Guidelines for Indians - A Manual" (PDF). Indian Council of Medical Research, National Institute of Nutrition. Archived from the original (PDF) on 2018-12-22. Retrieved 2019-02-20.
66. "Health Diet". India's Ministry of Health and Family Welfare. Archived from the original on 2016-08-06. Retrieved 2019-09-24.
67. "Choosing foods with healthy fats". Health Canada. 2018-10-10. Retrieved 2019-09-24.
68. "Fat". Australia's National Health and Medical Research Council and Department of Health and Ageing. 2012-09-24. Archived from the original on 2013-02-23. Retrieved 2019-09-24.
69. "Getting the Fats Right!". Singapore's Ministry of Health. Retrieved 2019-09-24.
70. "Eating and Activity Guidelines for New Zealand Adults" (PDF). New Zealand's Ministry of Health. Retrieved 2019-09-24.
71. "Know More about Fat". Hong Kong's Department of Health. Retrieved 2019-09-24.
72. German JB, Dillard CJ (September 2004). "Saturated fats: what dietary intake?". American Journal of Clinical Nutrition. 80 (3): 550–559. doi:10.1093/ajcn/80.3.550. PMID 15321792.
73. Storlien LH, Baur LA, Kriketos AD, Pan DA, Cooney GJ, Jenkins AB, et al. (June 1996). "Dietary fats and insulin action". Diabetologia. 39 (6): 621–31. doi:10.1007/BF00418533. PMID 8781757. S2CID 33171616.
74. Joint WHO/FAO Expert Consultation (2003). Diet, Nutrition and the Prevention of Chronic Diseases (WHO technical report series 916) (PDF). World Health Organization. pp. 81–94. ISBN 978-92-4-120916-8. Archived (PDF) from the original on 2013-04-21. Retrieved 2016-04-04.
75. Zelman K (2011). "The Great Fat Debate: A Closer Look at the Controversy—Questioning the Validity of Age-Old Dietary Guidance". Journal of the American Dietetic Association. 111 (5): 655–658. doi:10.1016/j.jada.2011.03.026. PMID 21515106.
76. Nutrition, Center for Food Safety and Applied (2022-03-07). "Health Claim Notification for Saturated Fat, Cholesterol, and Trans Fat, and Reduced Risk of Heart Disease". FDA.
77. Lichtenstein AH, Appel LJ, Brands M, Carnethon M, Daniels S, Franch HA, Franklin B, Kris-Etherton P, Harris WS, Howard B, Karanja N, Lefevre M, Rudel L, Sacks F, Van Horn L, Winston M, Wylie-Rosett J (July 2006). "Diet and lifestyle recommendations revision 2006: a scientific statement from the American Heart Association Nutrition Committee". Circulation. 114 (1): 82–96. doi:10.1161/CIRCULATIONAHA.106.176158. PMID 16785338. S2CID 647269.
78. Smith SC, Jackson R, Pearson TA, Fuster V, Yusuf S, Faergeman O, Wood DA, Alderman M, Horgan J, Home P, Hunn M, Grundy SM (June 2004). "Principles for national and regional guidelines on cardiovascular disease prevention: a scientific statement from the World Heart and Stroke Forum" (PDF). Circulation. 109 (25): 3112–21. doi:10.1161/01.CIR.0000133427.35111.67. PMID 15226228.
79. Dinu M, Pagliai G, Casini A, Sofi F (January 2018). "Mediterranean diet and multiple health outcomes: an umbrella review of meta-analyses of observational studies and randomised trials". European Journal of Clinical Nutrition. 72 (1): 30–43. doi:10.1038/ejcn.2017.58. hdl:2158/1081996. PMID 28488692. S2CID 7702206.
80. Martinez-Lacoba R, Pardo-Garcia I, Amo-Saus E, Escribano-Sotos F (October 2018). "Mediterranean diet and health outcomes: a systematic meta-review". European Journal of Public Health. 28 (5): 955–961. doi:10.1093/eurpub/cky113. PMID 29992229.
81. Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, Ringel A, Davis JM, Hibbeln JR (February 2013). "Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis". BMJ. 346: e8707. doi:10.1136/bmj.e8707. PMC 4688426. PMID 23386268.
82. Interview: Walter Willett (2017). "Research Review: Old data on dietary fats in context with current recommendations: Comments on Ramsden et al. in the British Medical Journal". TH Chan School of Public Health, Harvard University, Boston. Retrieved 24 May 2017.
83. de Souza RJ, Mente A, Maroleanu A, Cozma AI, Ha V, Kishibe T, Uleryk E, Budylowski P, Schünemann H, Beyene J, Anand SS (August 2015). "Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies". BMJ. 351 (Aug 11): h3978. doi:10.1136/bmj.h3978. PMC 4532752. PMID 26268692.
84. Ramsden CE, Zamora D, Leelarthaepin B, Majchrzak-Hong SF, Faurot KR, Suchindran CM, et al. (February 2013). "Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis". BMJ. 346: e8707. doi:10.1136/bmj.e8707. PMC 4688426. PMID 23386268.
85. Ramsden CE, Zamora D, Majchrzak-Hong S, Faurot KR, Broste SK, Frantz RP, Davis JM, Ringel A, Suchindran CM, Hibbeln JR (April 2016). "Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73)". BMJ. 353: i1246. doi:10.1136/bmj.i1246. PMC 4836695. PMID 27071971.
86. Weylandt KH, Serini S, Chen YQ, Su HM, Lim K, Cittadini A, Calviello G (2015). "Omega-3 Polyunsaturated Fatty Acids: The Way Forward in Times of Mixed Evidence". BioMed Research International. 2015: 143109. doi:10.1155/2015/143109. PMC 4537707. PMID 26301240.
87. Hooper L, Martin N, Jimoh OF, Kirk C, Foster E, Abdelhamid AS (2020). "Reduction in saturated fat intake for cardiovascular disease". Cochrane Database of Systematic Reviews (Systematic review). 5 (5): CD011737. doi:10.1002/14651858.CD011737.pub2. ISSN 1465-1858. PMC 7388853. PMID 32428300.
88. Graham I, Atar D, Borch-Johnsen K, Boysen G, Burell G, Cifkova R, et al. (2007). "European guidelines on cardiovascular disease prevention in clinical practice: executive summary". European Heart Journal. 28 (19): 2375–2414. doi:10.1093/eurheartj/ehm316. PMID 17726041.
89. Labarthe D (2011). "Chapter 17 What Causes Cardiovascular Diseases?". Epidemiology and prevention of cardiovascular disease: a global challenge (2nd ed.). Jones and Bartlett Publishers. ISBN 978-0-7637-4689-6.
90. Kris-Etherton PM, Innis S (September 2007). "Position of the American Dietetic Association and Dietitians of Canada: Dietary Fatty Acids". Journal of the American Dietetic Association. 107 (9): 1599–1611 [1603]. doi:10.1016/j.jada.2007.07.024. PMID 17936958.
91. "Food Fact Sheet - Cholesterol" (PDF). British Dietetic Association. Archived (PDF) from the original on 2010-11-22. Retrieved 3 May 2012.
92. "Cardiovascular Disease Risk Factors". World Heart Federation. 30 May 2017. Archived from the original on 2012-05-10. Retrieved 2012-05-03.
93. "Lower your cholesterol". National Health Service. Archived from the original on 2009-09-02. Retrieved 2012-05-03.
94. "Nutrition Facts at a Glance - Nutrients: Saturated Fat". Food and Drug Administration. 2009-12-22. Retrieved 2012-05-03.
95. "Scientific Opinion on Dietary Reference Values for fats, including saturated fatty acids, polyunsaturated fatty acids, monounsaturated fatty acids, trans fatty acids, and cholesterol". European Food Safety Authority. 2010-03-25. Retrieved 3 May 2012.
96. Faculty of Public Health of the Royal Colleges of Physicians of the United Kingdom. "Position Statement on Fat" (PDF). Retrieved 2011-01-25.
97. Report of a Joint WHO/FAO Expert Consultation (2003). "Diet, Nutrition and the Prevention of Chronic Diseases" (PDF). World Health Organization. Archived from the original (PDF) on April 4, 2003. Retrieved 2011-03-11.
98. "Cholesterol". Irish Heart Foundation. Retrieved 2011-02-28.
99. U.S. Department of Agriculture and U.S. Department of Health and Human Services (December 2010). Dietary Guidelines for Americans, 2010 (PDF) (7th ed.). Washington, DC: U.S. Government Printing Office.
100. Cannon C, O'Gara P (2007). Critical Pathways in Cardiovascular Medicine (2nd ed.). Lippincott Williams & Wilkins. p. 243.
101. Catapano AL, Reiner Z, De Backer G, Graham I, Taskinen MR, Wiklund O, et al. (July 2011). "ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS)". Atherosclerosis. 217 Suppl 1 (14): S1-44. doi:10.1016/j.atherosclerosis.2011.06.012. hdl:10138/307445. PMID 21723445.
102. "Monounsaturated Fat". American Heart Association. Archived from the original on 2018-03-07. Retrieved 2018-04-19.
103. "You Can Control Your Cholesterol: A Guide to Low-Cholesterol Living". MerckSource. Archived from the original on 2009-03-03. Retrieved 2018-01-02.
104. Sanchez-Bayle M, Gonzalez-Requejo A, Pelaez MJ, Morales MT, Asensio-Anton J, Anton-Pacheco E (February 2008). "A cross-sectional study of dietary habits and lipid profiles. The Rivas-Vaciamadrid study". European Journal of Pediatrics. 167 (2): 149–54. doi:10.1007/s00431-007-0439-6. PMID 17333272. S2CID 8798248.
105. Clarke R, Frost C, Collins R, Appleby P, Peto R (1997). "Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies". BMJ (Clinical Research Ed.). 314 (7074): 112–7. doi:10.1136/bmj.314.7074.112. PMC 2125600. PMID 9006469.
106. Bucher HC, Griffith LE, Guyatt GH (February 1999). "Systematic review on the risk and benefit of different cholesterol-lowering interventions". Arteriosclerosis, Thrombosis, and Vascular Biology. 19 (2): 187–195. doi:10.1161/01.atv.19.2.187. PMID 9974397.
107. Lewington S, Whitlock G, Clarke R, Sherliker P, Emberson J, Halsey J, Qizilbash N, Peto R, Collins R (December 2007). "Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths". Lancet. 370 (9602): 1829–39. doi:10.1016/S0140-6736(07)61778-4. PMID 18061058. S2CID 54293528.
108. Labarthe D (2011). "Chapter 11 Adverse Blood Lipid Profile". Epidemiology and prevention of cardiovascular disease: a global challenge (2 ed.). Jones and Bartlett Publishers. p. 290. ISBN 978-0-7637-4689-6.
109. Labarthe D (2011). "Chapter 11 Adverse Blood Lipid Profile". Epidemiology and prevention of cardiovascular disease: a global challenge (2nd ed.). Jones and Bartlett Publishers. p. 277. ISBN 978-0-7637-4689-6.
110. Thijssen MA, Mensink RP (2005). "Fatty acids and atherosclerotic risk". Atherosclerosis: Diet and Drugs. Handbook of Experimental Pharmacology. Vol. 170. Springer. pp. 165–94. doi:10.1007/3-540-27661-0_5. ISBN 978-3-540-22569-0. PMID 16596799.
111. Dandamudi A, Tommie J, Nommsen-Rivers L, Couch S (2018). "Dietary Patterns and Breast Cancer Risk: A Systematic Review". Anticancer Research. 38 (6): 3209–3222. doi:10.21873/anticanres.12586. PMID 29848668. S2CID 44149964.
112. Xia H, Ma S, Wang S, Sun G (2015). "Meta-Analysis of Saturated Fatty Acid Intake and Breast Cancer Risk". Medicine. 94 (52): e2391. doi:10.1097/MD.0000000000002391. PMC 5291630. PMID 26717389.
113. Brennan SF, Woodside JV, Lunny PM, Cardwell CR, Cantwell MM (2017). "Dietary fat and breast cancer mortality: A systematic review and meta-analysis". Critical Reviews in Food Science and Nutrition. 57 (10): 1999–2008. doi:10.1080/10408398.2012.724481. PMID 25692500. S2CID 34098509.
114. Lin OS (2009). "Acquired risk factors for colorectal cancer". Cancer Epidemiology. Methods in Molecular Biology. Vol. 472. pp. 361–72. doi:10.1007/978-1-60327-492-0_16. ISBN 978-1-60327-491-3. PMID 19107442.
115. Huncharek M, Kupelnick B (2001). "Dietary fat intake and risk of epithelial ovarian cancer: a meta-analysis of 6,689 subjects from 8 observational studies". Nutrition and Cancer. 40 (2): 87–91. doi:10.1207/S15327914NC402_2. PMID 11962260. S2CID 24890525.
116. Männistö S, Pietinen P, Virtanen MJ, Salminen I, Albanes D, Giovannucci E, Virtamo J (December 2003). "Fatty acids and risk of prostate cancer in a nested case-control study in male smokers". Cancer Epidemiology, Biomarkers & Prevention. 12 (12): 1422–8. PMID 14693732.
117. Crowe FL, Allen NE, Appleby PN, Overvad K, Aardestrup IV, Johnsen NF, Tjønneland A, Linseisen J, Kaaks R, Boeing H, Kröger J, Trichopoulou A, Zavitsanou A, Trichopoulos D, Sacerdote C, Palli D, Tumino R, Agnoli C, Kiemeney LA, Bueno-de-Mesquita HB, Chirlaque MD, Ardanaz E, Larrañaga N, Quirós JR, Sánchez MJ, González CA, Stattin P, Hallmans G, Bingham S, Khaw KT, Rinaldi S, Slimani N, Jenab M, Riboli E, Key TJ (November 2008). "Fatty acid composition of plasma phospholipids and risk of prostate cancer in a case-control analysis nested within the European Prospective Investigation into Cancer and Nutrition". The American Journal of Clinical Nutrition. 88 (5): 1353–63. doi:10.3945/ajcn.2008.26369. PMID 18996872.
118. Kurahashi N, Inoue M, Iwasaki M, Sasazuki S, Tsugane AS (April 2008). "Dairy product, saturated fatty acid, and calcium intake and prostate cancer in a prospective cohort of Japanese men". Cancer Epidemiology, Biomarkers & Prevention. 17 (4): 930–7. doi:10.1158/1055-9965.EPI-07-2681. PMID 18398033. S2CID 551427.
119. Corwin RL, Hartman TJ, Maczuga SA, Graubard BI (2006). "Dietary saturated fat intake is inversely associated with bone density in humans: Analysis of NHANES III". The Journal of Nutrition. 136 (1): 159–165. doi:10.1093/jn/136.1.159. PMID 16365076. S2CID 4443420.
120. Kien CL, Bunn JY, Tompkins CL, Dumas JA, Crain KI, Ebenstein DB, Koves TR, Muoio DM (April 2013). "Substituting dietary monounsaturated fat for saturated fat is associated with increased daily physical activity and resting energy expenditure and with changes in mood". The American Journal of Clinical Nutrition. 97 (4): 689–97. doi:10.3945/ajcn.112.051730. PMC 3607650. PMID 23446891.
121. Abdullah MM, Jew S, Jones PJ (February 2017). "Health benefits and evaluation of healthcare cost savings if oils rich in monounsaturated fatty acids were substituted for conventional dietary oils in the United States". Nutrition Reviews. 75 (3): 163–174. doi:10.1093/nutrit/nuw062. PMC 5914363. PMID 28158733.
122. Huth PJ, Fulgoni VL, Larson BT (November 2015). "A systematic review of high-oleic vegetable oil substitutions for other fats and oils on cardiovascular disease risk factors: implications for novel high-oleic soybean oils". Advances in Nutrition. 6 (6): 674–93. doi:10.3945/an.115.008979. PMC 4642420. PMID 26567193.
123. Shute, Nancy (2012-05-02). "Lard Is Back In The Larder, But Hold The Health Claims". NPR. Retrieved 2022-06-29.
124. National Research Council (US) Board on Agriculture and Renewable Resources (1976). Fat content and composition of animal products: proceedings of a symposium, Washington, D.C., December 12-13, 1974. Washington: National Academy of Sciences. ISBN 978-0-309-02440-2. PMID 25032409.
125. "Ask the Expert: Concerns about canola oil". The Nutrition Source. 2015-04-13. Retrieved 2022-06-29.
126. Aizpurua-Olaizola O, Ormazabal M, Vallejo A, Olivares M, Navarro P, Etxebarria N, Usobiaga A (January 2015). "Optimization of supercritical fluid consecutive extractions of fatty acids and polyphenols from Vitis vinifera grape wastes". Journal of Food Science. 80 (1): E101-7. doi:10.1111/1750-3841.12715. PMID 25471637.
127. "Essential Fatty Acids". Micronutrient Information Center, Oregon State University, Corvallis, OR. May 2014. Retrieved 24 May 2017.
128. "National nutrient database for standard reference, release 23". United States Department of Agriculture, Agricultural Research Service. 2011. Archived from the original on 2015-03-03. Retrieved 2009-02-22.
129. "Vegetable oil, avocado Nutrition Facts & Calories". nutritiondata.self.com.
130. "United States Department of Agriculture – National Nutrient Database". 8 September 2015. Archived from the original on March 12, 2016.
131. Vessby B, Uusitupa M, Hermansen K, Riccardi G, Rivellese AA, Tapsell LC, Nälsén C, Berglund L, Louheranta A, Rasmussen BM, Calvert GD, Maffetone A, Pedersen E, Gustafsson IB, Storlien LH (March 2001). "Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study". Diabetologia. 44 (3): 312–9. doi:10.1007/s001250051620. PMID 11317662.
132. Lovejoy JC (October 2002). "The influence of dietary fat on insulin resistance". Current Diabetes Reports. 2 (5): 435–40. doi:10.1007/s11892-002-0098-y. PMID 12643169. S2CID 31329463.
133. Fukuchi S, Hamaguchi K, Seike M, Himeno K, Sakata T, Yoshimatsu H (June 2004). "Role of fatty acid composition in the development of metabolic disorders in sucrose-induced obese rats". Experimental Biology and Medicine. 229 (6): 486–93. doi:10.1177/153537020422900606. PMID 15169967. S2CID 20966659.
134. Pala V, Krogh V, Muti P, Chajès V, Riboli E, Micheli A, Saadatian M, Sieri S, Berrino F (July 2001). "Erythrocyte membrane fatty acids and subsequent breast cancer: a prospective Italian study". Journal of the National Cancer Institute. 93 (14): 1088–95. doi:10.1093/jnci/93.14.1088. PMID 11459870.
135. "Omega-3 Fatty Acids and Health: Fact Sheet for Health Professionals". US National Institutes of Health, Office of Dietary Supplements. 2 November 2016. Retrieved 5 April 2017.
136. Patterson RE, Flatt SW, Newman VA, Natarajan L, Rock CL, Thomson CA, Caan BJ, Parker BA, Pierce JP (February 2011). "Marine fatty acid intake is associated with breast cancer prognosis". The Journal of Nutrition. 141 (2): 201–6. doi:10.3945/jn.110.128777. PMC 3021439. PMID 21178081.
137. Martin CA, Milinsk MC, Visentainer JV, Matsushita M, de-Souza NE (June 2007). "Trans fatty acid-forming processes in foods: a review". Anais da Academia Brasileira de Ciências. 79 (2): 343–50. doi:10.1590/S0001-37652007000200015. PMID 17625687.
138. Kuhnt K, Baehr M, Rohrer C, Jahreis G (October 2011). "Trans fatty acid isomers and the trans-9/trans-11 index in fat containing foods". European Journal of Lipid Science and Technology. 113 (10): 1281–1292. doi:10.1002/ejlt.201100037. PMC 3229980. PMID 22164125.
139. Kummerow, Fred August; Kummerow, Jean M. (2008). Cholesterol Won't Kill You, But Trans Fat Could. Trafford. ISBN 978-1-4251-3808-0.
140. Trans Fat Task Force (June 2006). TRANSforming the Food Supply. Trans Fat Task Force. ISBN 0-662-43689-X. Retrieved 7 January 2007.
141. "DIETA DETOX ✅ QUÉ ES Y SUS 13 PODEROSOS BENEFICIOS". October 24, 2019.
142. Tarrago-Trani MT, Phillips KM, Lemar LE, Holden JM (June 2006). "New and existing oils and fats used in products with reduced trans-fatty acid content". Journal of the American Dietetic Association. 106 (6): 867–80. doi:10.1016/j.jada.2006.03.010. PMID 16720128.
143. van de Rest O, Geleijnse JM, Kok FJ, van Staveren WA, Dullemeijer C, Olderikkert MG, Beekman AT, de Groot CP (August 2008). "Effect of fish oil on cognitive performance in older subjects: a randomized, controlled trial". Neurology. 71 (6): 430–8. doi:10.1212/01.wnl.0000324268.45138.86. PMID 18678826. S2CID 45576671.
144. Mensink, Ronald P.; Sanders, Thomas A.; Baer, David J.; Hayes, K. C.; Howles, Philip N.; Marangoni, Alejandro (2016-07-01). "The Increasing Use of Interesterified Lipids in the Food Supply and Their Effects on Health Parameters". Advances in Nutrition. 7 (4): 719–729. doi:10.3945/an.115.009662. ISSN 2161-8313. PMC 4942855. PMID 27422506.
145. Zock PJ, de Vries JH, de Fouw NJ, Katan MB (1995), "Positional distribution of fatty acids in dietary triglycerides: effects on fasting blood lipoprotein concentrations in humans." (PDF), Am J Clin Nutr, vol. 61, no. 1, pp. 48–551, doi:10.1093/ajcn/61.1.48, hdl:1871/11621, PMID 7825538, archived (PDF) from the original on 2016-03-03
146. Nestel PJ, Noakes M, Belling GB, et al. (1995), "Effect on plasma lipids of interesterifying a mix of edible oils." (PDF), Am J Clin Nutr, vol. 62, no. 5, pp. 950–55, doi:10.1093/ajcn/62.5.950, PMID 7572740, archived (PDF) from the original on 2016-03-03
147. Meijer GW, Weststrate JA (1997), "Interesterification of fats in margarine: effect on blood lipids, blood enzymes and hemostasis parameters.", Eur J Clin Nutr, vol. 51, no. 8, pp. 527–34, doi:10.1038/sj.ejcn.1600437, PMID 11248878
148. Grande F, Anderson JT, Keys A (1970), "Comparison of effects of palmitic and stearic acids in the diet on serum cholesterol in man." (PDF), Am J Clin Nutr, vol. 23, no. 9, pp. 1184–93, doi:10.1093/ajcn/23.9.1184, PMID 5450836, archived (PDF) from the original on 2016-03-03
149. Berry SE, Miller GJ, Sanders TA (2007), "The solid fat content of stearic acid-rich fats determines their postprandial effects." (PDF), Am J Clin Nutr, vol. 85, no. 6, pp. 1486–94, doi:10.1093/ajcn/85.6.1486, PMID 17556683, archived (PDF) from the original on 2016-03-03
150. Zampelas A, Williams CM, Morgan LM, et al. (1994), "The effect of triacylglycerol fatty acids positional distribution on postprandial plasma metabolite and hormone responses in normal adult men.", Br J Nutr, vol. 71, no. 3, pp. 401–10, doi:10.1079/bjn19940147, PMID 8172869
151. Yli-Jokipii K, Kallio H, Schwab U, et al. (2001), "Effects of palm oil and transesterified palm oil on chylomicron and VLDL triacylglycerol structures and postprandial lipid response." (PDF), J Lipid Res, vol. 42, no. 10, pp. 1618–25, PMID 11590218, archived (PDF) from the original on 2020-01-04
152. Berry SE, Woodward R, Yeoh C, Miller GJ, Sanders TA (2007), "Effect of interesterification of palmitic-acid rich tryacylglycerol on postprandial lipid and factor VII response", Lipids, 42 (4): 315–323, doi:10.1007/s11745-007-3024-x, PMID 17406926, S2CID 3986807
153. Summers LK, Fielding BA, Herd SL, et al. (1999), "Use of structured triacylglycerols containing predominantly stearic and oleic acids to probe early events in metabolic processing of dietary fat" (PDF), J Lipid Res, vol. 40, no. 10, pp. 1890–98, PMID 10508209, archived (PDF) from the original on 2020-01-04
154. Christophe AB, De Greyt WF, Delanghe JR, Huyghebaert AD (2000), "Substituting enzymically interesterified butter for native butter has no effect on lipemia or lipoproteinemia in man", Annals of Nutrition and Metabolism, 44 (2): 61–67, doi:10.1159/000012822, PMID 10970994, S2CID 22276158
155. Sundram K, Karupaiah T, Hayes K (2007). "Stearic acid-rich interesterified fat and trans-rich fat raise the LDL/HDL ratio and plasma glucose relative to palm olein in humans" (PDF). Nutr Metab. 4: 3. doi:10.1186/1743-7075-4-3. PMC 1783656. PMID 17224066. Archived (PDF) from the original on 2007-01-28. Retrieved 2007-01-19.
156. Destaillats F, Moulin J, Bezelgues JB (2007), "Letter to the editor: healthy alternatives to trans fats", Nutr Metab, vol. 4, p. 10, doi:10.1186/1743-7075-4-10, PMC 1867814, PMID 17462099
157. Mensink RP, Zock PL, Kester AD, Katan MB (2003), "Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials." (PDF), Am J Clin Nutr, vol. 77, no. 5, pp. 1146–1155, doi:10.1093/ajcn/77.5.1146, PMID 12716665, archived (PDF) from the original on 2004-02-14
158. "Boston scientists say triglycerides play key role in heart health". The Boston Globe. Retrieved 2014-06-18.
159. Ivanova EA, Myasoedova VA, Melnichenko AA, Grechko AV, Orekhov AN (2017). "Small Dense Low-Density Lipoprotein as Biomarker for Atherosclerotic Diseases". Oxidative Medicine and Cellular Longevity. 2017: 1273042. doi:10.1155/2017/1273042. PMC 5441126. PMID 28572872.
160. "Triglycerides". MedlinePlus. Archived from the original on 28 February 2014. Retrieved 2015-04-23.
161. Crawford, H., Micheal. Current Diagnosis & Treatment Cardiology. 3rd ed. McGraw-Hill Medical, 2009. p19
162. "What's considered normal?". Triglycerides: Why do they matter?. Mayo Clinic. 28 September 2012.
163. Koneru SC (2022-03-01). "Fellow's voice: Hypertriglyceridemia: Understanding the current guideline". American Journal of Preventive Cardiology. 9: 100322. doi:10.1016/j.ajpc.2022.100322. ISSN 2666-6677. PMC 8885448. PMID 35243465.
164. Berglund L, Brunzell JD, Goldberg AC, Goldberg IJ, Sacks F, Murad MH, Stalenhoef AF (September 2012). "Evaluation and treatment of hypertriglyceridemia: an Endocrine Society clinical practice guideline". The Journal of Clinical Endocrinology and Metabolism. 97 (9): 2969–2989. doi:10.1210/jc.2011-3213. PMC 3431581. PMID 22962670.
165. Nordestgaard BG, Varbo A (August 2014). "Triglycerides and cardiovascular disease". Lancet. 384 (9943): 626–635. doi:10.1016/S0140-6736(14)61177-6. PMID 25131982. S2CID 33149001.
166. Gill JM, Herd SL, Tsetsonis NV, Hardman AE (February 2002). "Are the reductions in triacylglycerol and insulin levels after exercise related?". Clinical Science. 102 (2): 223–231. doi:10.1042/cs20010204. PMID 11834142.
167. European Association for Cardiovascular Prevention & Rehabilitation; Reiner, Zeljko; Catapano, Alberico L.; De Backer, Guy; Graham, Ian; Taskinen, Marja-Riitta; Wiklund, Olov; Agewall, Stefan; Alegria, Eduardo; Chapman, M. John; Durrington, Paul; Erdine, Serap; Halcox, Julian; Hobbs, Richard; Kjekshus, John (July 2011). "ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS)". European Heart Journal. 32 (14): 1769–1818. doi:10.1093/eurheartj/ehr158. ISSN 1522-9645. PMID 21712404.
168. Davidson MH, Cannon CP, Armani AM (28 January 2008). "Pharmacological Therapy for Cardiovascular Disease". In Davidson MH, Toth PP, Maki KC (eds.). Therapeutic Lipidology. Contemporary Cardiology. Totowa, New Jersey: Humana Press, Inc. pp. 141–142. ISBN 978-1-58829-551-4.
169. Anagnostis P, Paschou SA, Goulis DG, Athyros VG, Karagiannis A (February 2018). "Dietary management of dyslipidaemias. Is there any evidence for cardiovascular benefit?". Maturitas. 108: 45–52. doi:10.1016/j.maturitas.2017.11.011. PMID 29290214.
170. Abourbih S, Filion KB, Joseph L, Schiffrin EL, Rinfret S, Poirier P, et al. (October 2009). "Effect of fibrates on lipid profiles and cardiovascular outcomes: a systematic review". The American Journal of Medicine. 122 (10): 962.e1–962.e8. doi:10.1016/j.amjmed.2009.03.030. PMID 19698935.
171. Jun M, Foote C, Lv J, Neal B, Patel A, Nicholls SJ, et al. (May 2010). "Effects of fibrates on cardiovascular outcomes: a systematic review and meta-analysis". Lancet. 375 (9729): 1875–1884. doi:10.1016/S0140-6736(10)60656-3. PMID 20462635. S2CID 15570639.
172. Blair HA, Dhillon S (October 2014). "Omega-3 carboxylic acids (Epanova): a review of its use in patients with severe hypertriglyceridemia". American Journal of Cardiovascular Drugs. 14 (5): 393–400. doi:10.1007/s40256-014-0090-3. PMID 25234378. S2CID 23706094.