What do trans-fats do when in human body?

What do trans-fats do when in human body?

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Trans fats cause health problems, especially to the heart.

My guess is that all effects happen because trans-fats are inherently toxic as the body never evolved to process them. But then L-glucose has no harmful effects, even if it cannot be digested.

So how are trans-fats processed in the body differently, and where does all the harm happen?

In Ascherio & Willen (1997) it is mentioned that, and I quote:

[… ] Trans fatty acids increase plasma concentrations of low-density lipoprotein (LDL) cholesterol and reduce concentrations of high-density lipoprotein (HDL) cholesterol relative to the parent natural fat. [… ] [T]rans fatty acids increased the plasma ratio of total to HDL cholesterol nearly twofold compared with saturated fats. On the basis of these metabolic effects and the known relation of blood lipid concentrations to risk of coronary artery disease, we estimate conservatively that 30 000 premature deaths/y in the United States are attributable to consumption of trans fatty acids.

The US Heart Foundation explains in more layman's terms the same principles:

Trans fat is a type of unsaturated fat that behaves like a saturated fat because of its chemical structure. It increases our risk of heart disease by increasing the “bad” LDL cholesterol, while also lowering the “good” HDL cholesterol in our blood.

And from the Better Health Channel Australia we learn why LDL is 'bad':

Too much cholesterol circulating within LDL in our bloodstream leads to fatty deposits developing in the arteries. This causes the vessels to narrow and they can eventually become blocked. This can lead to heart disease and stroke.

Ascherio & Willen, Am J Clin Nutr 1997;66(suppl):1006S-lOS.

Unsaturated fats in plants eaten by ruminant animals undergo biohydrogenation via bacteria found in the rumen of the animal. 1 This process is natural and catalyzed by bacterial enzymes at normal body temperature and under normal body pressure. 1

In contrast, industrial trans fats are formed when liquid vegetable oil is converted into a solid through the chemical process of hydrogenation. This process is initiated by metal catalysts under enormous pressure at very high temperatures. Before they became widespread in the late 1940s, many of these trans fats had never before been encountered in nature or existed only in trace amounts. 2,3

Trans Fatty Acids: Definition, Usage, Harmful effects, and Key Facts

The Food Safety and Standards Authority of India (FSSAI) has reduced the levels of trans fatty acids (TFA) in oils and fats to 3% for 2021 and 2% by 2022 from the current permissible limit of 5%. It has been done through an amendment to the Food and Safety and Standards (Prohibition and Restriction on Sales) Regulations.

On 29 December, the country's food regulatory body notified the amendment more than a year after it issued a draft on the subject for consultation with stakeholders.

The Regulation deal is done with the prohibitions and restriction on sales of several food products, ingredients, and their admixtures.

Some key facts are as follows:

- The regulation that is applied to the edible refined oils, vanaspati which is partially hydrogenated oils, margarine, bakery, shortenings, and other mediums of cooking including vegetable fat spreads and mixed fat spreads.

- According to the World Health Organisation (WHO), approximately 5.4 lakh deaths take place every year worldwide due to the intake of industrially-produced trans-fatty acids. The WHO has also called for the global elimination of trans fats by 2023.

- At the time of the pandemic, FSSAI released a rule where the burden of non-communicable diseases (NCD) has risen. For cardiovascular diseases, trans-fat consumption is the main risk factor and accounts for most NCD deaths.

- In 2011, India first passes a regulation that set a TFA limit of 10% in oils and fats that was further reduced to 5% in 2015.

About Trans Fats

Trans fatty acids (TFA) or trans fats are a form of unsaturated fat and come in both natural and artificial forms.

Or we can say that two broad types of trans fats found in foods namely naturally-occurring and artificial trans fats.

Trans fats are the most harmful type of fats which can cause an adverse effect on a human body than any other dietary constituent.

Naturally-occurring trans fats are produced in the gut of some animals and foods made from these animals example milk and meat products. They may contain small quantities of these fats.

Artificial trans fats are generated through an industrial process that adds hydrogen to liquid vegetable oils to form them more solid. That is hydrogen is made to react with the oil to produce fats that resemble pure ghee or butter.

Let us tell you that the primary source for trans fats in processed food is "partially hydrogenated oils".

Trans Fat in Food

Partially hydrogenated oil is the manufactured form of trans fat that may be found in various variety of food products like

- Baked goods including cakes, cookies, and pies.

- Refrigerated dough like biscuits and rolls

- Fried Foods like french fries, doughnuts, and fried chicken

Therefore, we can say that trans fatty acid contains oils that can be preserved longer, food can be transformed into the desired shape and texture, and can easily substitute 'Pure Ghee'. Comparatively, they are lower in cost and thus add to profit or saving.

What are the harmful effects of Trans fatty acids?

TFA increases the risk of heart attacks, stroke, and type 2 diabetes. They also pose an unhealthy effect on cholesterol levels.

That is they not only increase total cholesterol levels but also reduce good cholesterol (HDL), which helps to protect against heart disease.

It also increases the risk of developing obesity, metabolic syndrome, insulin resistance, infertility, certain types of cancers and can also lead to compromised fetal development that can cause harm to the yet to be born baby.

There are two main types of cholesterol namely

Low-density lipoprotein (LDL) or "bad" cholesterol can build up in the walls of arteries and make them hard and narrow.

High-density lipoprotein (HDL) or "good" cholesterol that pics up excess cholesterol and takes it back to the liver.

Trans fat increases LDL cholesterol and decreases HDL cholesterol. Also, if inside the arteries trans fat deposits then it can tear or rupture them, a blood clot may form and block blood flow to a part of the heart which causes a heart attack or to a part of the brain causes a stroke.

Metabolic Syndrome like high blood pressure, high blood sugar, body fat increases around the waist, and abnormal cholesterol levels. The syndrome also increases the risk of heart attack and stroke in a person.

Do you know why some companies use trans fats?

Trans fats are easy to use, inexpensive to generate, and last for an extended time or long time. It provides food a desirable texture and taste. Several restaurants and fast-food outlets use trans fats to deep-fry foods because oils with trans fats can be used various times in commercial fryers. Various countries including Denmark, Switzerland, Canada, etc., and jurisdictions including California, New York City, Baltimore, etc. have reduced or restricted the utilization of trans fats in foodservice establishments.

How to avoid Trans fats?

It may be tricky to avoid trans fats. In the United States, manufacturers can label their products "trans-fat-free" as long as there are fewer than 0.5 grams of these fats per serving.

According to Ashim Sanyal, Chief Operating Officer of Consumer VOICE, "The FSSAI rule comes at the time of a pandemic where the burden of non-communicable diseases has risen. Cardiovascular diseases along with diabetes are proving fatal for COVID-19 patients.”

He added that the regulation must not be restricted to oils and fats, but must apply to all foods. “Hopefully, FSSAI will address this as well before January 2022 to eliminate chemical trans-fatty acids from the Indian platter.”

What are the efforts taken to reduce the intake of fatty acids?

A "Trans Fat Free" logo has been launched by the FSSAI for voluntary labeling to develop TFA-free products. The label is often used by bakeries, local food outlets, and shops for preparations containing TFA not exceeding 0.2 per 100 g.

A new mass media campaign is also launched by FSSAI named “Heart Attack Rewind” to eliminate industrially-produced trans fat in the food supply by the year 2022. It is a follow-up to an earlier campaign called “Eat Right”, which was launched in July 2018.

A pledge is also taken by edible oil industries to reduce the levels of salt, sugar, saturated fat, and trans fat content by 2% by 2022.

An initiative namely Swasth Bharat Yatra which was started under the "Eat Right" campaign is a Pan-India cyclothon to inform citizens regarding the issues of food safety, combating food adulteration, and healthy diets.

- India first passed a regulation in 2011 that set a TFA limit of 10% in oils and fats which was further reduced to 5% in 2015.

- In 2018, a REPLACE campaign was also launched by WHO for global-level elimination of trans-fats in industrially produced edible oils.


The most important elements in the chemical makeup of fats are the fatty acids. The molecule of a fatty acid consists of a carboxyl group HO(O=)C− connected to an unbranched alkyl group – (CH
x )
n H: namely, a chain of carbon atoms, joined by single, double, or (more rarely) triple bonds, with all remaining free bonds filled by hydrogen atoms [5]

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–)
3 H 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
2 O .

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 shape of fat and fatty acid molecules is usually not well-defined. Any two parts of a molecule that are connected by just one single bond are free to rotate about that bond. Thus a fatty acid molecule with n simple bonds can be deformed in n-1 independent ways (counting also rotation of the terminal methyl group).

Such rotation cannot happen across a double bond, except by breaking and then reforming it with one of the halves of the molecule rotated by 180 degrees, which requires crossing a significant energy barrier. Thus a fat or fatty acid molecule with double bonds (excluding at the very end of the chain) can have multiple cis–trans isomers with significantly different chemical and biological properties. Each double bond reduces the number of conformational degrees of freedom by one. Each triple bond forces the four nearest carbons to lie in a straight line, removing two degrees of freedom.

It follows that depictions of "saturated" fatty acids with no double bonds (like stearic) having a "straight zig-zag" shape, and those with one cis bond (like oleic) being bent in an "elbow" shape are somewhat misleading. While the latter are a little less flexible, both can be twisted to assume similar straight or elbow shapes. In fact, outside of some specific contexts like crystals or bilayer membranes, both are more likely to be found in randomly contorted configurations than in either of those two shapes.


Examples of 18-carbon fatty acids.
Stearic acid
Oleic acid
Elaidic acid
Vaccenic acid

Stearic acid is a saturated fatty acid (with only single bonds) found in animal fats, and is the intended product in full hydrogenation.

Oleic acid has a double bond (thus being "unsaturated") with cis geometry about midway in the chain it makes up 55–80% of olive oil.

Elaidic acid is its trans isomer it may be present in partially hydrogenated vegetable oils, and also occurs in the fat of the durian fruit (about 2%) and in milk fat (less than 0.1%).

Vaccenic acid is another trans acid that differs from elaidic only in the position of the double bond it also occurs in milk fat (about 1-2%).

Common fat names

Fats are usually named after their source (like olive oil, cod liver oil, shea butter, tail fat) or have traditional names of their own (like butter, lard, ghee, and margarine). Some of these names refer to products that contain substantial amounts of other components besides fats proper.

Chemical fatty acid names

In chemistry and biochemistry, dozens of saturated fatty acids and of hundreds of unsaturated ones have traditional scientific/technical names usually inspired by their source fats (butyric, caprylic, stearic, oleic, palmitic, and nervonic), but sometimes their discoverer (mead, osbond).

A triglyceride would then be named as an ester of those acids, such as "glyceryl 1,2-dioleate 3-palmitate". [6]


In the general chemical nomenclature developed by the International Union of Pure and Applied Chemistry (IUPAC), the recommended name of a fatty acid, derived from the name of the corresponding hydrocarbon, completely describes its structure, by specifying the number of carbons and the number and position of the double bonds. Thus, for example, oleic acid would be called "(9Z)-octadec-9-enoic acid", meaning that it has an 18 carbon chain ("octadec") with a carboxyl at one end ("oic") and a double bound at carbon 9 counting from the carboxyl ("9-en"), and that the configuration of the single bonds adjacent to that double bond is cis ("(9Z)") The IUPAC nomenclature can also handle branched chains and derivatives where hydrogen atoms are replaced by other chemical groups.

A triglyceride would then be named according to general ester rules as, for example, "propane-1,2,3-tryl 1,2-bis((9Z)-octadec-9-enoate) 3-(hexadecanoate)".

Fatty acid code

A notation specific for fatty acids with unbranched chain, that is as precise as the IUPAC one but easier to parse, is a code of the form ": cis- trans-", where is the number of carbons (including the carboxyl one), is the number of double bonds, is a list of the positions of the cis double bonds, and is a list of the positions of the trans bounds. Either list and the label is omitted if there are no bounds of that type.

Thus, for example, the codes for stearic, oleic, elaidic, and vaccenic acids would be "18:0", "18:1 cis-9", "18:1 trans-9", and "18:1 trans-11", respectively. The code for α-oleostearic acid, which is "(9E,11E,13Z)-octadeca-9,11,13-trienoic acid" in the IUPAC nomenclature, has the code "18:3 trans-9,11 cis-13"

By chain length

Fats can be classified according to the lengths of the carbon chains of their constituent fatty acids. Most chemical properties, such as melting point and acidity, vary gradually with this parameter, so there is no sharp division. Chemically, formic acid (1 carbon) and acetic acid (2 carbons) could be viewed as the shortest fatty acids then triformin would be the simplest triglyceride. However, the terms "fatty acid" and "fat" are usually reserved for compounds with substantially longer chains. [ citation needed ]

A division commonly made in biochemistry and nutrition is: [ citation needed ]

  • Short-chain fatty acid (SCFA) with less than six carbons (e. g. butyric acid).
  • Medium-chain fatty acid (MCFA) with 6 to 12 carbons (e.g. capric acid).
  • Long-chain fatty acids (LCFA) with 13 to 21 carbons (e.g. petroselinic acid).
  • Very long chain fatty acids (VLCFA) with 22 or more carbons (e. g. cerotic acid with 26)

A triglyceride molecule may have fatty acid elements of different lengths, and a fat product will often be a mix of various triglycerides. Most fats found in food, whether vegetable or animal, are made up of medium to long-chain fatty acids, usually of equal or nearly equal length.

Saturated and unsaturated fats

For human nutrition, an important classification of fats is based on the number and position of double bonds in the constituent fatty acids. Saturated fat has a predominance of saturated fatty acids, without any double bonds, while unsaturated fat has predominantly unsaturated acids with double bonds. (The names refer to the fact that each double bond means two fewer hydrogen atoms in the chemical formula. Thus, a saturated fatty acid, having no double bonds, has the maximum number of hydrogen atoms for a given number of carbon atoms — that is, it is "saturated" with hydrogen atoms.) [7] [8]

Unsaturated fatty acids are further classified into monounsaturated (MUFAs), with a single double bond, and polyunsaturated (PUFAs), with two or more. [7] [8] Natural fats usually contain several different saturated and unsaturated acids, even on the same molecule. For example, in most vegetable oils, the saturated palmitic (C16:0) and stearic (C18:0) acid residues are usually attached to positions 1 and 3 (sn1 and sn3) of the glycerol hub, whereas the middle position (sn2) is usually occupied by an unsaturated one, such as oleic (C18:1, ω–9) or linoleic (C18:2, ω–6). [9] )

While it is the nutritional aspects of polyunsaturated fatty acids that are generally of greatest interest, these materials also have non-food applications. They include the drying oils, such as linseed (flax seed), tung, poppy seed, perilla, and walnut oil, which polymerize on exposure to oxygen to form solid films, and are used to make paints and varnishes.

Saturated fats generally have a higher melting point than unsaturated ones with the same molecular weight, and thus are more likely to be solid at room temperature. For example, the animal fats tallow and lard are high in saturated fatty acid content and are solids. Olive and linseed oils on the other hand are unsaturated and liquid. Unsaturated fats are prone to oxidation by air, which causes them to become rancid and inedible.

The double bonds in unsaturated fats can be converted into single bonds by reaction with hydrogen effected by a catalyst. This process, called hydrogenation, is used to turn vegetable oils into solid or semisolid vegetable fats like margarine, which can substitute for tallow and butter and (unlike unsaturated fats) can be stored indefinitely without becoming rancid. However, partial hydrogenation also creates some unwanted trans acids from cis acids. [ citation needed ]

In cellular metabolism, unsaturated fat molecules yield slightly less energy (i.e., fewer calories) than an equivalent amount of saturated fat. The heats of combustion of saturated, mono-, di-, and tri-unsaturated 18-carbon fatty acid esters have been measured as 2859, 2828, 2794, and 2750 kcal/mol, respectively or, on a weight basis, 10.75, 10.71, 10.66, and 10.58 kcal/g — a decrease of about 0.6% for each additional double bond. [10]

The greater the degree of unsaturation in a fatty acid (i.e., the more double bonds in the fatty acid) the more vulnerable it is to lipid peroxidation (rancidity). Antioxidants can protect unsaturated fat from lipid peroxidation.

Cis and trans fats

Another important classification of unsaturated fatty acids considers the cistrans isomerism, the spatial arrangement of the C–C single bonds adjacent to the double bonds. Most unsaturated fatty acids that occur in nature have those bonds in the cis ("same side") configuration. Partial hydrogenation of cis fats can turn some of their fatty acids into trans ("opposite sides") variety.

Elaidic acid is the trans isomer of oleic acid, one of the most common fatty acids in human diet. The single change of configuration in one double bond causes them to have different chemical and physical properties. Elaidic acid has a much higher melting point than oleic acid, 45 °C instead of 13.4 °C. This difference is commonly attributed to the supposed ability of the trans molecules to pack more tightly, forming a solid that is more difficult to break apart. [11]

Omega number

Another classification considers the position of the double bonds relative to the end of the chain (opposite to the carboxyl group). The position is denoted by "ω−k" or "n−k", meaning that there is a double bond between carbons k and k+1 counted from 1 at that end. For example, alpha-Linolenic acid is a "ω−3" or "n−3" acid, meaning that there is a double bond between the third and fourth carbons, counted from that end that is, its structural formula ends with –CH=CH– CH
2 – CH
3 . [12]

Examples of saturated fatty acids

Some common examples of fatty acids:

    with 4 carbon atoms (contained in butter) with 12 carbon atoms (contained in coconut oil, palm kernel oil, and breast milk) with 14 carbon atoms (contained in cow's milk and dairy products) with 16 carbon atoms (contained in palm oil and meat) with 18 carbon atoms (also contained in meat and cocoa butter)

Examples of unsaturated fatty acids

    C14:1, ω−5, cis-9-tetradecenoic acid C16:1 ω−10, cis-6-Hexadecenoic acid C16:1, ω−7 , cis-9-hexadecenoic acid C18:1 ω−9, cis-9-octadecenoic acid C18:1 ω−12, cis-Octadec-6-enoic acid , C18:1 ω−7), cis-11-octadecenoic acid C18:1 ω−7, trans-11-octadecenoic acid 18:1 ω−9, trans-9-octadecenoic acid (trans-oleic acid) C20:1 ω−7, cis-13-eicosenoic acid C20:1 ω−11, cis-9-icosenoic acid 20:1 ω−9, cis-11-eicosenoic acid C22:1 ω−9, cis-15-tetracosenoic acid C22:1 ω−9, trans-15-tetracosenoic acid C24:1 ω−9, | cis-15-tetracosenoic acid

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 9 food calories (37 kJ = 8.8 kcal). [13]

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. [ citation needed ] 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

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. [14]

The location of the tissue determines its metabolic profile: visceral fat is located within the abdominal wall (i.e., beneath the wall of abdominal muscle) whereas subcutaneous fat is located beneath the skin (and includes fat that is located in the abdominal area beneath the skin but above the abdominal muscle wall). Visceral fat was recently discovered to be a significant producer of signaling chemicals (i.e., hormones), among which several are involved in inflammatory tissue responses. One of these is resistin which has been linked to obesity, insulin resistance, and Type 2 diabetes. This latter result is currently controversial, and there have been reputable studies supporting all sides on the issue. [ citation needed ]

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:

    to extract liquid fats from fruits, seeds, or algae, e.g. olive oil from olives using solvents like hexane or supercritical carbon dioxide. , the melting of fat in adipose tissue, e.g. to produce tallow, lard, fish oil, and whale oil. of milk to produce butter. to reduce the degree of unsaturation of the fatty acids. , the rearrangement of fatty acids across different triglycerides. to remove oil components with higher melting points. of butter.

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. [15] [16] [17] [18]

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). [19] [13] Other lipids needed by the body can be synthesized from these and other fats.

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. [20] [21] [22]

Plants and fish oil generally contain a higher proportion of unsaturated acids, although there are exceptions such as coconut oil and palm kernel oil. [23] [24] Foods containing unsaturated fats include avocado, nuts, olive oils, and vegetable oils such as canola.

Saturated esterified fatty acids as percentage of total fat [25]
Food Lauric acid Myristic acid Palmitic acid Stearic acid
Coconut oil 47% 18% 9% 3%
Palm kernel oil 48% 1% 44% 5%
Butter 3% 11% 29% 13%
Ground beef 0% 4% 26% 15%
Salmon 0% 1% 29% 3%
Egg yolks 0% 0.3% 27% 10%
Cashews 2% 1% 10% 7%
Soybean oil 0% 0% 11% 4%

Many careful studies have found that replacing saturated fats with cis unsaturated fats in the diet reduces risk of risks of cardiovascular diseases, [26] [27] diabetes, or death. [28] These studies prompted many medical organizations and public health departments, including the World Health Organization, [29] [30] to officially issue that advice. Some countries with such recommendations include:

  • United Kingdom [31][32][33][34][35]
  • United States [28][36][37][38][39]
  • India [40][41]
  • Canada [42]
  • Australia [43]
  • Singapore [44]
  • New Zealand [45]
  • Hong Kong [46]

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. [47]

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, [48] 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. [49]

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. [50]

For these reasons, the United States Food and Drug Administration (FDA), for example, does not advise the complete elimination of saturated fat, but only recommends that it does not exceed 30% of one's daily caloric intake. [ citation needed ] A 2003 report by the World Health Organization and the Food and Agriculture Organization (FAO) recommends limiting the saturated fatty acids to less than 10% of daily energy intake and less than 7% for high-risk groups. [49] A general 7% limit was recommended also by the American Heart Association in 2006. [51] [52]

The WHO/FAO report also recommended replacing fats so as to reduce the content of myristic and palmitic acids, specifically. [49]

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. [53] 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. [54]

A small number of contemporary reviews have challenged this negative view of saturated fats. For example, an evaluation of evidence from 1966-1973 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. [55] These studies have been disputed by many scientists, [56] and the consensus in the medical community is that saturated fat and cardiovascular disease are closely related. [57] [58] [59] Still, these discordant studies fueled debate over the merits of substituting polyunsaturated fats for saturated fats. [60]

Cardiovascular disease

The effect of saturated fat on cardiovascular disease has been extensively studied. [61] 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. [28] [61] The relationships are accepted as causal, [62] [63] including by many government and medical organizations. [49] [64] [65] [28] [66] [67] [68] [69]

A 2017 review by the American Heart Association estimated that replacement of saturated fat with polyunsaturated fat in the American diet could reduce the risk of cardiovascular diseases by 30%. [28]

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. [70] [71] [72] [73] [74] [66] [75] [76] [77] These effects were observed in children too. [78]

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, [28] [79] which in turn have been claimed to have a causal relation with increased risk of cardiovascular disease (the so-called lipid hypothesis). [80] [81] However, high cholesterol may be caused by many factors. Other indicators, such as high LDL/HDL ratio, have proved to be more predictive. [81] 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. [82] 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. [83] Different saturated fatty acids have differing effects on various lipid levels. [84]


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.

  • A meta-analysis published in 2003 found a epidemiology and etiology of breast cancer#Specific dietary fatty acidssignificant positive relationship between saturated fat and breast cancer. [85] However two subsequent reviews have found weak or insignificant relation, [86][87] and noted the prevalence of confounding factors. [86][88]
  • Another review found limited evidence for a positive relationship between consuming animal fat and incidence of colorectal cancer. [89]
  • Other meta-analyses found evidence for increased risk of ovarian cancer by high consumption of saturated fat. [90]
  • Some studies have indicated that serum myristic acid[91][92] and palmitic acid[92] and dietary myristic [93] and palmitic [93] saturated fatty acids and serum palmitic combined with alpha-tocopherol supplementation [91] 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. [92]


Various animal studies have indicated that the intake of saturated fat has a negative effect on effects on the mineral density of bones. One study suggested that men may be particularly vulnerable. [94]

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. [95]

Monounsaturated vs. polyunsaturated fat

Assuming given that unsaturated fatty acids (UFAs) are generally healthier than saturated ones (SFAs), another question that has gained attention in recent decades is the risks and benefits of monounsaturated fatty acids (MUFAs, with a single double bond) versus polyunsaturated fatty acids (PUFAs, with two or more double bonds).

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. Algal oil is about 92% monounsaturated fat. [96] Olive oil is about 75% monounsaturated fat. [97] The high oleic variety sunflower oil contains at least 70% monounsaturated fat. [98] Canola oil and cashews are both about 58% monounsaturated fat. [ citation needed ] Tallow (beef fat) is about 50% monounsaturated fat. [99] and lard is about 40% monounsaturated fat. [ citation needed ] 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, sunflower oil, hemp oil, and tea-oil Camellia. [100]

Polyunsaturated fatty acids can be found mostly in nuts, seeds, fish, seed oils, and oysters. [7]

Food sources of polyunsaturated fats include: [7] [101]

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 [102]
Olive Oil 11
Safflower Oil 12.82 [103]
Seaweed 11
Sardines 5
Soybeans 7
Tuna 14
Wild Salmon 17.3
Whole Grain Wheat 9.7

Cardiovascular disease

Studies have given conflicting indications about the effect of MUFA/PUFA intake and cardiovascular disease. Although PUFAs seem to protect against cardiac arrhythmias, a study concluded that PUFA intake is positively associated with coronary atherosclerosis progression in a group of post-menopauseal women, whereas MUFA intake is not. [104] This probably is an indication of the greater vulnerability of polyunsaturated fats to lipid peroxidation, against which vitamin E has been shown to be protective. [105]

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. [48] But this is contrary to the suggestion of more recent studies, in which polyunsaturated fats are shown as protective against insulin resistance.

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. [106] However, some MUFAs may promote insulin resistance (like the SFAs), whereas PUFAs may protect against it. [107] [108] [ clarification needed ]


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). [109]

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. [110] 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. [110] [111]

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. [7]

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. [7]

"Cis fat" vs. "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. [112] Nevertheless, trans fatty acids (TFAs) occur in small amounts in meat and milk of ruminants (such as cattle and sheep), [113] typically 2–5% of total fat. [114] 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. [115]

Trans fat contents in various natural and traditionally processed foods, in g per 100 g [116]
Food type Trans fat content
butter 2g to 7 g
whole milk 0.07g to 0.1 g
animal fat 0g to 5 g [114]
ground beef 1 g

Concerns about trans fatty acids in human diet were raised when they were found to be an unintentional byproduct of the partial hydrogenation of vegetable and fish oils. While these trans fatty acids (popularly called "trans fats") are edible, they have been implicated in many health problems. [117]

The hydrogenation process, invented and patented by Wilhelm Normann in 1902, made it possible to turn relatively cheap liquid fats such as whale or fish oil into more solid fats and to extend their shelf-life by preventing rancidification. (The source fat and the process were initially kept secret to avoid consumer distaste. [118] ) This process was widely adopted by the food industry already in the early 1900s first for the production of margarine, a replacement for butter and shortening, [119] and eventually for various other fats used in snack food, packaged baked goods, and deep fried products. [120] [121]

Full hydrogenation of a fat or oil produces a fully saturated fat. However, hydrogenation generally was interrupted before completion, to yield a fat product with specific melting point, hardness, and other properties. Unfortunately, partial hydrogenation turns some of the cis double bonds into trans bonds by an isomerization reaction. [120] [121] [122] The trans configuration is favored [ citation needed ] because it is the lower energy form.

This side reaction accounts for most of the trans fatty acids consumed today, by far. [123] [124] An analysis of some industrialized foods in 2006 found up to 30% "trans fats" in artificial shortening, 10% in breads and cake products, 8% in cookies and crackers, 4% in salty snacks, 7% in cake frostings and sweets, and 26% in margarine and other processed spreads. [116] Another 2010 analysis however found only 0.2% of trans fats in margarine and other processed spreads. [125] Up to 45% of the total fat in those foods containing man-made trans fats formed by partially hydrogenating plant fats may be trans fat. [114] Baking shortenings, unless reformulated, contain around 30% trans fats compared to their total fats. High-fat dairy products such as butter contain about 4%. Margarines not reformulated to reduce trans fats may contain up to 15% trans fat by weight, [126] but some reformulated ones are less than 1% trans fat.

High levels of TFAs have been recorded in popular "fast food" meals. [124] An analysis of samples of McDonald's French fries collected in 2004 and 2005 found that fries served in New York City contained twice as much trans fat as in Hungary, and 28 times as much as in Denmark, where trans fats are restricted. For Kentucky Fried Chicken products, the pattern was reversed: the Hungarian product containing twice the trans fat of the New York product. Even within the United States, there was variation, with fries in New York containing 30% more trans fat than those from Atlanta. [127]

Cardiovascular disease

Numerous studies have found that consumption of TFAs increases risk of cardiovascular disease. [19] [13] The Harvard School of Public Health advises that replacing TFAs and saturated fats with cis monounsaturated and polyunsaturated fats is beneficial for health. [128]

Consuming trans fats has been shown to increase the risk of coronary artery disease in part by raising levels of low-density lipoprotein (LDL, often termed "bad cholesterol"), lowering levels of high-density lipoprotein (HDL, often termed "good cholesterol"), increasing triglycerides in the bloodstream and promoting systemic inflammation. [129] [130] [131]

The primary health risk identified for trans fat consumption is an elevated risk of coronary artery disease (CAD). [132] A 1994 study estimated that over 30,000 cardiac deaths per year in the United States are attributable to the consumption of trans fats. [133] By 2006 upper estimates of 100,000 deaths were suggested. [134] A comprehensive review of studies of trans fats published in 2006 in the New England Journal of Medicine reports a strong and reliable connection between trans fat consumption and CAD, concluding that "On a per-calorie basis, trans fats appear to increase the risk of CAD more than any other macronutrient, conferring a substantially increased risk at low levels of consumption (1 to 3% of total energy intake)". [135]

The major evidence for the effect of trans fat on CAD comes from the Nurses' Health Study – a cohort study that has been following 120,000 female nurses since its inception in 1976. In this study, Hu and colleagues analyzed data from 900 coronary events from the study's population during 14 years of followup. He determined that a nurse's CAD risk roughly doubled (relative risk of 1.93, CI: 1.43 to 2.61) for each 2% increase in trans fat calories consumed (instead of carbohydrate calories). By contrast, for each 5% increase in saturated fat calories (instead of carbohydrate calories) there was a 17% increase in risk (relative risk of 1.17, CI: 0.97 to 1.41). "The replacement of saturated fat or trans unsaturated fat by cis (unhydrogenated) unsaturated fats was associated with larger reductions in risk than an isocaloric replacement by carbohydrates." [136] Hu also reports on the benefits of reducing trans fat consumption. Replacing 2% of food energy from trans fat with non-trans unsaturated fats more than halves the risk of CAD (53%). By comparison, replacing a larger 5% of food energy from saturated fat with non-trans unsaturated fats reduces the risk of CAD by 43%. [136]

Another study considered deaths due to CAD, with consumption of trans fats being linked to an increase in mortality, and consumption of polyunsaturated fats being linked to a decrease in mortality. [132] [137]

Trans fat has been found to act like saturated in raising the blood level of LDL ("bad cholesterol") but, unlike saturated fat, it also decreases levels of HDL ("good cholesterol"). The net increase in LDL/HDL ratio with trans fat, a widely accepted indicator of risk for coronary artery, is approximately double that due to saturated fat. [138] [139] [140] One randomized crossover study published in 2003 comparing the effect of eating a meal on blood lipids of (relatively) cis and trans-fat-rich meals showed that cholesteryl ester transfer (CET) was 28% higher after the trans meal than after the cis meal and that lipoprotein concentrations were enriched in apolipoprotein(a) after the trans meals. [141]

The citokyne test is a potentially more reliable indicator of CAD risk, although is still being studied. [132] A study of over 700 nurses showed that those in the highest quartile of trans fat consumption had blood levels of C-reactive protein (CRP) that were 73% higher than those in the lowest quartile. [142]

Breast feeding

It has been established that trans fats in human breast milk fluctuate with maternal consumption of trans fat, and that the amount of trans fats in the bloodstream of breastfed infants fluctuates with the amounts found in their milk. In 1999, reported percentages of trans fats (compared to total fats) in human milk ranged from 1% in Spain, 2% in France, 4% in Germany, and 7% in Canada and the United States. [143]

Other health risks

There are suggestions that the negative consequences of trans fat consumption go beyond the cardiovascular risk. In general, there is much less scientific consensus asserting that eating trans fat specifically increases the risk of other chronic health problems:

    : A study published in Archives of Neurology in February 2003 suggested that the intake of both trans fats and saturated fats promote the development of Alzheimer disease, [144] although not confirmed in an animal model. [145] It has been found that trans fats impaired memory and learning in middle-age rats. The trans-fat eating rats' brains had fewer proteins critical to healthy neurological function. Inflammation in and around the hippocampus, the part of the brain responsible for learning and memory. These are the exact types of changes normally seen at the onset of Alzheimer's, but seen after six weeks, even though the rats were still young. [146] : There is no scientific consensus that consuming trans fats significantly increases cancer risks across the board. [132] The American Cancer Society states that a relationship between trans fats and cancer "has not been determined." [147] One study has found a positive connection between trans fat and prostate cancer. [148] However, a larger study found a correlation between trans fats and a significant decrease in high-grade prostate cancer. [149] An increased intake of trans fatty acids may raise the risk of breast cancer by 75%, suggest the results from the French part of the European Prospective Investigation into Cancer and Nutrition. [150][151] : There is a growing concern that the risk of type 2 diabetes increases with trans fat consumption. [132][152] However, consensus has not been reached. [135] For example, one study found that risk is higher for those in the highest quartile of trans fat consumption. [153] Another study has found no diabetes risk once other factors such as total fat intake and BMI were accounted for. [154] : Research indicates that trans fat may increase weight gain and abdominal fat, despite a similar caloric intake. [155] A 6-year experiment revealed that monkeys fed a trans fat diet gained 7.2% of their body weight, as compared to 1.8% for monkeys on a mono-unsaturated fat diet. [156][157] Although obesity is frequently linked to trans fat in the popular media, [158] this is generally in the context of eating too many calories there is not a strong scientific consensus connecting trans fat and obesity, although the 6-year experiment did find such a link, concluding that "under controlled feeding conditions, long-term TFA consumption was an independent factor in weight gain. TFAs enhanced intra-abdominal deposition of fat, even in the absence of caloric excess, and were associated with insulin resistance, with evidence that there is impaired post-insulin receptor binding signal transduction." [157] : One 2007 study found, "Each 2% increase in the intake of energy from trans unsaturated fats, as opposed to that from carbohydrates, was associated with a 73% greater risk of ovulatory infertility. ". [159] : Spanish researchers analysed the diets of 12,059 people over six years and found that those who ate the most trans fats had a 48 per cent higher risk of depression than those who did not eat trans fats. [160] One mechanism may be trans-fats' substitution for docosahexaenoic acid (DHA) levels in the orbitofrontal cortex (OFC). Very high intake of trans-fatty acids (43% of total fat) in mice from 2 to 16 months of age was associated with lowered DHA levels in the brain (p=0.001). [145] When the brains of 15 major depressive subjects who had committed suicide were examined post-mortem and compared against 27 age-matched controls, the suicidal brains were found to have 16% less (male average) to 32% less (female average) DHA in the OFC. The OFC controls reward, reward expectation, and empathy (all of which are reduced in depressive mood disorders) and regulates the limbic system. [161]
  • Behavioral irritability and aggression: a 2012 observational analysis of subjects of an earlier study found a strong relation between dietary trans fat acids and self-reported behavioral aggression and irritability, suggesting but not establishing causality. [162]
  • Diminished memory: In a 2015 article, researchers re-analyzing results from the 1999-2005 UCSD Statin Study argue that "greater dietary trans fatty acid consumption is linked to worse word memory in adults during years of high productivity, adults age <45". [163] : According to a 2015 study, trans fats are one of several components of Western pattern diets which promote acne, along with carbohydrates with high glycemic load such as refined sugars or refined starches, milk and dairy products, and saturated fats, while omega-3 fatty acids, which reduce acne, are deficient in Western pattern diets. [164]

Biochemical mechanisms

The exact biochemical process by which trans fats produce specific health problems are a topic of continuing research. Intake of dietary trans fat perturbs the body's ability to metabolize essential fatty acids (EFAs, including Omega-3) leading to changes in the phospholipid fatty acid composition of the arterial walls, thereby raising risk of coronary artery disease. [165]

Trans double bonds are claimed to induce a linear conformation to the molecule, favoring its rigid packing as in plaque formation. The geometry of the cis double bond, in contrast, is claimed to create a bend in the molecule, thereby precluding rigid formations. [ citation needed ] .

While the mechanisms through which trans fatty acids contribute to coronary artery disease are fairly well understood, the mechanism for their effects on diabetes is still under investigation. They may impair the metabolism of long-chain polyunsaturated fatty acids (LCPUFAs). [166] However, maternal pregnancy trans fatty acid intake has been inversely associated with LCPUFAs levels in infants at birth thought to underlie the positive association between breastfeeding and intelligence. [167]

Trans fats are processed by the liver differently than other fats. They may cause liver dysfunction by interfering with delta 6 desaturase, an enzyme involved in converting essential fatty acids to arachidonic acid and prostaglandins, both of which are important to the functioning of cells. [168]

Natural "trans fats" in dairy products

Some trans fatty acids occur in natural fats and traditionally processed foods. Vaccenic acid occurs in breast milk, and some isomers of conjugated linoleic acid (CLA) are found in meat and dairy products from ruminants. Butter, for example, contains about 3% trans fat. [169]

The US National Dairy Council has asserted that the trans fats present in animal foods are of a different type than those in partially hydrogenated oils, and do not appear to exhibit the same negative effects. [170] While a recent scientific review agrees with the conclusion (stating that "the sum of the current evidence suggests that the Public health implications of consuming trans fats from ruminant products are relatively limited"), it cautions that this may be due to the low consumption of trans fats from animal sources compared to artificial ones. [135]

More recent inquiry (independent of the dairy industry) has found in a 2008 Dutch meta-analysis that all trans fats, regardless of natural or artificial origin equally raise LDL and lower HDL levels. [171] Other studies though have shown different results when it comes to animal-based trans fats like conjugated linoleic acid (CLA). Although CLA is known for its anticancer properties, researchers have also found that the cis-9, trans-11 form of CLA can reduce the risk for cardiovascular disease and help fight inflammation. [172] [173]

Two Canadian studies have shown that vaccenic acid, a TFA that naturally occurs in dairy products, could be beneficial compared to hydrogenated vegetable shortening, or a mixture of pork lard and soy fat, by lowering total LDL and triglyceride levels. [174] [175] [176] A study by the US Department of Agriculture showed that vaccenic acid raises both HDL and LDL cholesterol, whereas industrial trans fats only raise LDL with no beneficial effect on HDL. [177]

Official recommendations

In light of recognized evidence and scientific agreement, nutritional authorities consider all trans fats equally harmful for health and recommend that their consumption be reduced to trace amounts. [178] [179] [180] [181] [182] The World Health Organization recommended that trans fats make up no more than 0.9% of a person's diet in 2003 [114] and, in 2018, introduced a 6-step guide to eliminate industrially-produced trans-fatty acids from the global food supply. [183]

The National Academy of Sciences (NAS) advises the United States and Canadian governments on nutritional science for use in public policy and product labeling programs. Their 2002 Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids [184] contains their findings and recommendations regarding consumption of trans fat (summary).

Their recommendations are based on two key facts. First, "trans fatty acids are not essential and provide no known benefit to human health", [129] whether of animal or plant origin. [185] Second, given their documented effects on the LDL/HDL ratio, [130] the NAS concluded "that dietary trans fatty acids are more deleterious with respect to coronary artery disease than saturated fatty acids". A 2006 review published in the New England Journal of Medicine (NEJM) that states "from a nutritional standpoint, the consumption of trans fatty acids results in considerable potential harm but no apparent benefit." [135]

Because of these facts and concerns, the NAS has concluded there is no safe level of trans fat consumption. There is no adequate level, recommended daily amount or tolerable upper limit for trans fats. This is because any incremental increase in trans fat intake increases the risk of coronary artery disease. [130]

Despite this concern, the NAS dietary recommendations have not included eliminating trans fat from the diet. This is because trans fat is naturally present in many animal foods in trace quantities, and thus its removal from ordinary diets might introduce undesirable side effects and nutritional imbalances. The NAS has, thus, "recommended that trans fatty acid consumption be as low as possible while consuming a nutritionally adequate diet". [186] Like the NAS, the World Health Organization has tried to balance public health goals with a practical level of trans fat consumption, recommending in 2003 that trans fats be limited to less than 1% of overall energy intake. [114]

Regulatory action

In the last few decades, there has been substantial amount of regulation in many countries, limiting trans fat contents of industrialized and commercial food products.

Alternatives to hydrogenation

In recent years, the negative public image and strict regulations have driven many fat processing industries to replace partial hydrogenation by fat interesterification, a process that chemically scrambles the fatty acids among a mix of triglycerides. When applied to a suitable bend of oils and saturated fats, possibly followed by separation of unwanted solid or liquid triglycerides, this process can achieve results similar to those of partial hydrogenation without affecting the fatty acids themselves in particular, without creating any new "trans fat".

Researchers at the United States Department of Agriculture have investigated whether hydrogenation can be achieved without the side effect of trans fat production. They varied the pressure under which the chemical reaction was conducted – applying 1400 kPa (200 psi) of pressure to soybean oil in a 2-liter vessel while heating it to between 140 °C and 170 °C. The standard 140 kPa (20 psi) process of hydrogenation produces a product of about 40% trans fatty acid by weight, compared to about 17% using the high-pressure method. Blended with unhydrogenated liquid soybean oil, the high-pressure-processed oil produced margarine containing 5 to 6% trans fat. Based on current U.S. labeling requirements (see below), the manufacturer could claim the product was free of trans fat. [187] The level of trans fat may also be altered by modification of the temperature and the length of time during hydrogenation.

A University of Guelph research group has found a way to mix oils (such as olive, soybean, and canola), water, monoglycerides, and fatty acids to form a "cooking fat" that acts the same way as trans and saturated fats. [188] [189]

Omega-three and omega-six fatty acids

The ω−3 fatty acids have received substantial atterntion in recent years.

In preliminary research, omega-3 fatty acids in algal oil, fish oil, fish and seafood have been shown to lower the risk of heart attacks. [110] Other preliminary research indicates that omega-6 fatty acids in sunflower oil and safflower oil may also reduce the risk of cardiovascular disease. [190]

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. [109] The DHA obtained through the consumption of polyunsaturated fatty acids is positively associated with cognitive and behavioral performance. [191] In addition DHA is vital for the grey matter structure of the human brain, as well as retinal stimulation and neurotransmission. [7]


Some studies have investigated the health effects of insteresterified (IE) fats, by comparing diets with IE and non-IE fats with the same overall fatty acid composition. [192]

Several experimental studies in humans found no statistical difference on fasting blood lipids between a 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. [193] [194] [195] 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. [196] [197] [198] [199] [200] [201] [202]

A 2007 study funded by the Malaysian Palm Oil Board [203] claimed that replacing natural palm oil by other interesterified or partial 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. [204] [205]

Fats are broken down in the healthy body to release their constituents, glycerol and fatty acids. Glycerol itself can be converted to glucose by the liver and so become a source of energy. Fats and other lipids are broken down in the body by enzymes called lipases produced in the pancreas.

Many cell types can use either glucose or fatty acids as a source of energy for metabolism. In particular, heart and skeletal muscle prefer fatty acids. [ citation needed ] Despite long-standing assertions to the contrary, fatty acids can also be used as a source of fuel for brain cells through mitochondrial oxidation. [206]

Trans Fat in Your Body

Your body processes trans fat slightly differently than it does other fats. According to naturopath Dr. Stephen Gangemi, it takes your body longer to metabolize trans fat than it does other fats. That means that there may still be trans fat in your body.

Unfortunately, there's no way to speed up your body's natural processing and detoxification systems. And a so-called "detoxification diet" won't work either. A healthy adult's body does a perfectly good job of getting rid of toxins, and there's no scientific research to support the claim that detox diets are effective, according to the National Center for Complementary and Integrative Health.

The Scientific Case for Banning Trans Fats

Last month the U.S. Food and Drug Administration made the welcome, belated determination that partially hydrogenated oils&mdashthe primary source of trans fats&mdashcould no longer be considered &ldquogenerally regarded as safe&rdquo (GRAS). Although the ruling is preliminary, it is expected to become permanent. If it does, it will virtually eliminate industrially produced trans fat in the U.S, saving thousands of lives each year with minimal cost to industry.

Artificial trans fats, or trans unsaturated fatty acids, have been around for a little more than a century. In 1901 the German chemist Wilhelm Normann discovered the process of partial hydrogenation, which converts inexpensive liquid vegetable oils into shortenings and margarines and creates trans fats as a by-product. Because these cheaper, longer-lasting products mimicked the traditional cooking fats of European and North American cuisines, many countries quickly incorporated them into their food supplies. World War II&ndashera food shortages and economic stresses greatly expanded the presence of trans fats in the U.S. diet. But because fat was primarily considered a metabolic fuel, no one paid much attention to its potential health effects. In fact, in 1912 the inventors of partial hydrogenation received the Nobel Prize.

It took decades for scientists to realize how deadly trans fats could be. When coronary heart disease (CHD) first emerged as a national epidemic in the U.S., physicians quickly came to suspect that saturated fat and dietary cholesterol, delivered mainly in butter and lard, were important causes. But they did not make a connection to trans fats. On the contrary, because margarines and vegetable shortenings were low in saturated fat and free of cholesterol, they were widely promoted as healthy alternatives to butter and lard beginning in the 1960s.

Then in the mid 1970s a few scientists began suggesting that trans fats should be given a closer look. Fred Kummerow of the University of Illinois at Urbana&ndashChampaign reported that trans fats had adverse effects on arteries in his studies of pigs. Mary Enig of the University of Maryland, College Park, described the correlation over time between increases in trans fat intake and higher rates of coronary heart disease. I was particularly concerned about the process of partial hydrogenation itself: the vegetable oils being processed are primarily composed of linoleic acid and alpha-linolenic acid, precursors of molecules with many critical biological functions in the human body. But the process of partial hydrogenation changes the shape of those molecules, which almost certainly alters their function in unpredictable ways.

Despite the mounting questions, the food industry and the cardiovascular prevention community both dismissed these concerns.

In 1980 my colleagues and I set out to examine in greater detail the relation between intake of trans fat and risk of CHD. We included trans fat in a comprehensive assessment of diet in the Nurses&rsquo Health Study cohort of over 100,000 women and developed a regularly updated database of the trans fat content of foods. After eight years of follow-up, and after accounting for known risk factors for heart disease, we found that women with the highest intake of trans fat had a 50 percent greater risk of hospitalization or death due to coronary heart disease. Margarine, the primary source of trans fat in 1980, was also associated with greater risk.

We were not the only ones subjecting trans fat to greater scrutiny. Around the same time, the Dutch researcher Martijn Katan and colleagues were investigating the metabolic effects of trans fats among healthy volunteers, doing carefully controlled feeding studies lasting several weeks. They found that trans fat and saturated fat increased &ldquobad&rdquo LDL cholesterol to a similar degree&mdashbut unlike any other type of fat, trans fat also reduced &ldquogood&rdquo HDL cholesterol. Other researchers confirmed these findings and documented additional adverse metabolic effects, including increases in blood concentrations of triglycerides and inflammatory factors. Calculations suggested that eliminating industrially produced trans fats would prevent approximately 20 percent of avoidable CHD deaths in the U.S.

By 2003, the FDA found the evidence compelling enough to require that trans fat be included on food labels. Most manufacturers responded by eliminating trans fat entirely. Soon thereafter New York City banned the use of trans fats in restaurants, and other cities nationwide followed. By 2012, approximately 75 percent of the trans fat had been removed from the U.S. food supply. Blood cholesterol levels responded nationally, just as expected.

The U.S. Centers for Disease Control has estimated that the 25 percent of trans fats still coursing through the American food supply account for approximately 7,000 premature deaths per year. The FDA&rsquos most recent action would prevent those deaths. The food industry is likely to take the new ruling in stride. It has already phased out the large majority of trans fat, and in Denmark trans fats have already been banned for a decade, proving that full elimination is feasible.

The FDA&rsquos action is cause for a bit of celebration. It means that the efforts of many scientists from many disciplines will soon lead to the elimination of a major cause of premature death. Because of the FDA&rsquos global leadership role, the ruling is even likely to stimulate similar changes worldwide. But we should not get too carried away with the celebration. It is sobering that it has taken more than a century for this moment to arrive. The case of trans fats should provoke us to consider how future risks might be prevented, detected or eliminated more quickly.

A Prelude to Disease

If left unchecked, improper dietary fat consumption can lead down a path to severe health problems. An increased level of lipids, triglycerides, and cholesterol in the blood is called hyperlipidemia. Hyperlipidemia is inclusive of several conditions but more commonly refers to high cholesterol and triglyceride levels. When blood lipid levels are high, any number of adverse health problems may ensue. Consider the following:

  • Cardiovascular disease. According to the AHA, cardiovascular disease encompasses a variety of problems, many of which are related to the process of atherosclerosis. Over time the arteries thicken and harden with plaque buildup, causing restricted or at times low or no blood flow to selected areas of the body.
  • Heart attack. A heart attack happens when blood flow to a section of the heart is cut off due to a blood clot. Many have survived heart attacks and go on to return to their lives and enjoy many more years of life on this earth. However, dietary and lifestyle changes must be implemented to prevent further attacks.
  • Ischemic stroke. The most common type of stroke in the United States, ischemic stroke, occurs when a blood vessel in the brain or leading to the brain becomes blocked, again usually from a blood clot. If part of the brain suffers lack of blood flow and/or oxygen for three minutes or longer, brain cells will start to die.
  • Congestive heart failure. Sometimes referred to as heart failure, this condition indicates that the heart is not pumping blood as well as it should. The heart is still working but it is not meeting the body’s demand for blood and oxygen. If left unchecked, it can progress to further levels of malfunction.
  • Arrhythmia. This is an abnormal rhythm of the heart. The heart may beat above one hundred beats per minute (known as tachycardia) or below sixty beats per minute (known as bradycardia), or the beats are not regular. The heart may not be able to pump enough volume of blood to meet the body’s needs.
  • Heart valve problems. Stenosis is a condition wherein the heart valves become compromised in their ability to open wide enough to allow proper blood flow. When the heart valves do not close tightly and blood begins to leak between chambers, this is called regurgitation. When valves bulge or prolapse back into the upper chamber, this condition is called mitral valve prolapse.
  • Obesity. Obesity is defined as the excessive accumulation of body fat. According to US Surgeon General Richard Carmona, obesity is the fastest growing cause of death in America. The HHS reports that the number of adolescents who are overweight has tripled since 1980 and the prevalence of the disease among younger children has doubled [2] .
  • Obesity has been linked to increased risks of developing diabetes and heart disease. To help combat this problem important dietary changes are necessary. Reducing the type and amount of carbohydrates and sugar consumed daily is critical. Limiting the intake of saturated fats and trans fats, increasing physical activity, and eating fewer calories are all equally important in this fight against obesity.


Lipoproteins are divided into 5 subgroups, by density/size (an inverse relationship), which also correlates with function and incidence of cardiovascular events. Unlike the larger lipoprotein particles, which deliver fat molecules to cells, HDL particles remove fat molecules from cells. The lipids carried include cholesterol, phospholipids, and triglycerides, amounts of each are variable. [2]

Increasing concentrations of HDL particles are associated with decreasing accumulation of atherosclerosis within the walls of arteries, [2] reducing the risk of sudden plaque ruptures, cardiovascular disease, stroke and other vascular diseases. [2] HDL particles are commonly referred to as "good cholesterol", because they transport fat molecules out of artery walls, reduce macrophage accumulation, and thus help prevent or even regress atherosclerosis. [3]

Because of the high cost of directly measuring HDL and LDL (low-density lipoprotein) protein particles, blood tests are commonly performed for the surrogate value, HDL-C, i.e. the cholesterol associated with ApoA-1/HDL particles. In healthy individuals, about 30% of blood cholesterol, along with other fats, is carried by HDL. [3] This is often contrasted with the amount of cholesterol estimated to be carried within low-density lipoprotein particles, LDL, and called LDL-C. HDL particles remove fats and cholesterol from cells, including within artery wall atheroma, and transport it back to the liver for excretion or re-utilization thus the cholesterol carried within HDL particles (HDL-C) is sometimes called "good cholesterol" (despite being the same as cholesterol in LDL particles). Those with higher levels of HDL-C tend to have fewer problems with cardiovascular diseases, while those with low HDL-C cholesterol levels (especially less than 40 mg/dL or about 1 mmol/L) have increased rates for heart disease. [4] Higher native HDL levels are correlated with lowered risk of cardiovascular disease in healthy people. [5]

The remainder of the serum cholesterol after subtracting the HDL is the non-HDL cholesterol. The concentration of these other components, which may cause atheroma, is known as the non-HDL-C. This is now preferred to LDL-C as a secondary marker as it has been shown to be a better predictor and it is more easily calculated. [6]

With a size ranging from 5 to 17 nm, HDL is the smallest of the lipoprotein particles. [2] It is the densest because it contains the highest proportion of protein to lipids. [2] Its most abundant apolipoproteins are apo A-I and apo A-II. A rare genetic variant, ApoA-1 Milano, has been documented to be far more effective in both protecting against and regressing arterial disease atherosclerosis.

The liver synthesizes these lipoproteins as complexes of apolipoproteins and phospholipid, which resemble cholesterol-free flattened spherical lipoprotein particles, [2] whose NMR structure was recently published [7] the complexes are capable of picking up cholesterol, carried internally, from cells by interaction with the ATP-binding cassette transporter A1 (ABCA1). [8] A plasma enzyme called lecithin-cholesterol acyltransferase (LCAT) converts the free cholesterol into cholesteryl ester (a more hydrophobic form of cholesterol), which is then sequestered into the core of the lipoprotein particle, eventually causing the newly synthesized HDL to assume a spherical shape. HDL particles increase in size as they circulate through the blood and incorporate more cholesterol and phospholipid molecules from cells and other lipoproteins, such as by interaction with the ABCG1 transporter and the phospholipid transport protein (PLTP). [2]

HDL transports cholesterol mostly to the liver or steroidogenic organs such as adrenals, ovary, and testes by both direct and indirect pathways. HDL is removed by HDL receptors such as scavenger receptor BI (SR-BI), which mediate the selective uptake of cholesterol from HDL. In humans, probably the most relevant pathway is the indirect one, which is mediated by cholesteryl ester transfer protein (CETP). [2] This protein exchanges triglycerides of VLDL against cholesteryl esters of HDL. As the result, VLDLs are processed to LDL, which are removed from the circulation by the LDL receptor pathway. The triglycerides are not stable in HDL, but are degraded by hepatic lipase so that, finally, small HDL particles are left, which restart the uptake of cholesterol from cells. [2]

The cholesterol delivered to the liver is excreted into the bile and, hence, intestine either directly or indirectly after conversion into bile acids. Delivery of HDL cholesterol to adrenals, ovaries, and testes is important for the synthesis of steroid hormones. [2]

Several steps in the metabolism of HDL can participate in the transport of cholesterol from lipid-laden macrophages of atherosclerotic arteries, termed foam cells, to the liver for secretion into the bile. This pathway has been termed reverse cholesterol transport and is considered as the classical protective function of HDL toward atherosclerosis.

HDL carries many lipid and protein species, several of which have very low concentrations but are biologically very active. For example, HDL and its protein and lipid constituents help to inhibit oxidation, inflammation, activation of the endothelium, coagulation, and platelet aggregation. All these properties may contribute to the ability of HDL to protect from atherosclerosis, and it is not yet known which are the most important. In addition, a small subfraction of HDL lends protection against the protozoan parasite Trypanosoma brucei brucei. This HDL subfraction, termed trypanosome lytic factor (TLF), contains specialized proteins that, while very active, are unique to the TLF molecule. [9]

In the stress response, serum amyloid A, which is one of the acute-phase proteins and an apolipoprotein, is under the stimulation of cytokines (interleukin 1, interleukin 6), and cortisol produced in the adrenal cortex and carried to the damaged tissue incorporated into HDL particles. At the inflammation site, it attracts and activates leukocytes. In chronic inflammations, its deposition in the tissues manifests itself as amyloidosis.

It has been postulated that the concentration of large HDL particles more accurately reflects protective action, as opposed to the concentration of total HDL particles. [10] This ratio of large HDL to total HDL particles varies widely and is measured only by more sophisticated lipoprotein assays using either electrophoresis (the original method developed in the 1970s) or newer NMR spectroscopy methods (See also nuclear magnetic resonance and spectroscopy), developed in the 1990s.

Subfractions Edit

Five subfractions of HDL have been identified. From largest (and most effective in cholesterol removal) to smallest (and least effective), the types are 2a, 2b, 3a, 3b, and 3c. [11]

Major lipids in the human body Edit

Lipids are a heterogeneous group of compounds which are relatively insoluble in water and soluble in non-polar solvents. Triglycerides (TGs), cholesterol, and phospholipids are the major lipids in the body. They are transported as complexes of lipid and proteins known as lipoproteins.

TGs (triglycerides): TGs are formed by combining glycerol with three molecules of fatty acid. TGs, as major components of VLDL and chylomicrons, play an important role in metabolism. When the body requires fatty acids as an energy source, the hormone glucagon signals the breakdown of the TGs by lipase to release free fatty acids. TGs are water-insoluble, non-polar neutral fats. These are not the structural components of biological membranes. TGs synthesis and storage mostly occurs in liver and adipose tissue. Free fatty acids and glycerol must be activated prior to the synthesis of TGs into acyl-coA and glycerol-3-phosphate respectively.

Cholesterol: The name cholesterol originates from the Greek chole (bile) and stereos (solid), and the chemical suffix -ol for an alcohol. It is an essential structural component of cell membrane, where it is required to establish proper membrane permeability and fluidity. In addition, cholesterol is an important component for the manufacture of bile acids, steroid hormones, and vitamin D. Although cholesterol is an important and necessary molecule, a high level of serum cholesterol is an indicator for diseases such as heart disease. About 20–25% of total daily cholesterol production occurs in the liver.

Phospholipids: Phospholipids are TGs that are covalently bonded to a phosphate group by an ester linkage. Phospholipids perform important functions including regulating membrane permeability and in maintaining electron transport chain in mitochondria. They participate in the reverse cholesterol transport and thus help in the removal of cholesterol from the body. They are involved in signal transmission across membranes and they act as detergents and help in solubilization of cholesterol.

Lipoprotein: These consist of a central core of a hydrophobic lipid (including TGs and cholesteryl esters) encased in a hydrophilic coat of polar phospholipid, free cholesterol and apolipoprotein. There are six main classes of lipoprotein, differing in the relative proportion of the core lipids and in the type of apoprotein.

  • Chylomicrons
  • VLDL-C particles
  • IDL-C particles
  • LDL-C particles
  • HDL-C particle
  • Lipoprotein (a) [LP(a)]

Men tend to have noticeably lower HDL levels, with smaller size and lower cholesterol content, than women. Men also have an increased incidence of atherosclerotic heart disease. Alcohol consumption tends to raise HDL levels, [12] and moderate alcohol consumption is associated with lower cardiovascular and all-cause mortality. Recent studies confirm the fact that HDL has a buffering role in balancing the effects of the hypercoagulable state in type 2 diabetics and decreases the high risk of cardiovascular complications in these patients. Also, the results obtained in this study revealed that there was a significant negative correlation between HDL and activated partial thromboplastin time (APTT). [ citation needed ]

Epidemiological studies have shown that high concentrations of HDL (over 60 mg/dL) have protective value against cardiovascular diseases such as ischemic stroke and myocardial infarction. Low concentrations of HDL (below 40 mg/dL for men, below 50 mg/dL for women) increase the risk for atherosclerotic diseases.

Data from the landmark Framingham Heart Study showed that, for a given level of LDL, the risk of heart disease increases 10-fold as the HDL varies from high to low. On the converse, however, for a fixed level of HDL, the risk increases 3-fold as LDL varies from low to high. [13] [14]

Even people with very low LDL levels are exposed to increased risk if their HDL levels are not high enough. [15]

Clinical laboratories formerly measured HDL cholesterol by separating other lipoprotein fractions using either ultracentrifugation or chemical precipitation with divalent ions such as Mg 2+ , then coupling the products of a cholesterol oxidase reaction to an indicator reaction. The reference method still uses a combination of these techniques. [16] Most laboratories now use automated homogeneous analytical methods in which lipoproteins containing apo B are blocked using antibodies to apo B, then a colorimetric enzyme reaction measures cholesterol in the non-blocked HDL particles. [17] HPLC can also be used. [18] Subfractions (HDL-2C, HDL-3C) can be measured, [19] but clinical significance of these subfractions has not been determined. [20] The measurement of apo-A reactive capacity can be used to measure HDL cholesterol but is thought to be less accurate. [ citation needed ]

Recommended ranges Edit

The American Heart Association, NIH and NCEP provide a set of guidelines for fasting HDL levels and risk for heart disease. [21] [22] [23]

Level mg/dL Level mmol/L Interpretation
<40/50 men/women <1.03 Low HDL cholesterol, heightened risk considered correlated for heart disease
40–59 1.03–1.55 Medium HDL level
>59 >1.55 High HDL level, optimal condition considered correlated against heart disease

High LDL with low HDL level is an additional risk factor for cardiovascular disease. [24]

As technology has reduced costs and clinical trials have continued to demonstrate the importance of HDL, methods for directly measuring HDL concentrations and size (which indicates function) at lower costs have become more widely available and increasingly regarded as important for assessing individual risk for progressive arterial disease and treatment methods.

Electrophoresis measurements Edit

Since the HDL particles have a net negative charge and vary by density & size, ultracentrifugation combined with electrophoresis have been utilized since before 1950 to enumerate the concentration of HDL particles and sort them by size with a specific volume of blood plasma. Larger HDL particles are carrying more cholesterol.

NMR measurements Edit

Concentration and sizes of lipoprotein particles can be estimated using nuclear magnetic resonance fingerprinting. [25]

Optimal total and large HDL concentrations Edit

The HDL particle concentrations are typically categorized by event rate percentiles based on the people participating and being tracked in the MESA [26] trial, a medical research study sponsored by the United States National Heart, Lung, and Blood Institute.

Total HDL particle Table
MESA Percentile Total HDL particles μmol/L Interpretation
>75% >34.9 Those with highest (Optimal) total HDL particle concentrations & lowest rates of cardiovascular disease events
50–75% 30.5–34.5 Those with moderately high total HDL particle concentrations & moderate rates of cardiovascular disease events
25–50% 26.7–30.5 Those with lower total HDL particle concentrations & Borderline-High rates of cardiovascular disease
0–25% <26.7 Those with lowest total HDL particle concentrations & Highest rates of cardiovascular disease events
Large (protective) HDL particle Table
MESA Percentile Large HDL particles μmol/L Interpretation
>75% >7.3 Those with highest (Optimal) Large HDL particle concentrations & lowest rates of cardiovascular disease events
50–75% 4.8–7.3 Those with moderately high Large HDL particle concentrations & moderate rates of cardiovascular disease events
25–50% 3.1–4.8 Those with lower Large HDL particle concentrations & Borderline-High rates of cardiovascular disease
0–25% <3.1 Those with lowest Large HDL particle concentrations & Highest rates of cardiovascular disease events

The lowest incidence of atherosclerotic events over time occurs within those with both the highest concentrations of total HDL particles (the top quarter, >75%) and the highest concentrations of large HDL particles. Multiple additional measures, including LDL particle concentrations, small LDL particle concentrations, VLDL concentrations, estimations of insulin resistance and standard cholesterol lipid measurements (for comparison of the plasma data with the estimation methods discussed above) are routinely provided in clinical testing.

Fasting serum lipids have been associated with short term verbal memory. In a large sample of middle aged adults, low HDL cholesterol was associated with poor memory and decreasing levels over a five-year follow-up period were associated with decline in memory. [27]

While higher HDL levels are correlated with lower risk of cardiovascular diseases, no medication used to increase HDL has been proven to improve health. [2] [28] Numerous lifestyle changes and drugs are under study to increase HDL levels, as of 2017. [2]

HDL lipoprotein particles that bear apolipoprotein C3 are associated with increased, rather than decreased, risk for coronary heart disease. [29]

Diet and exercise Edit

Certain changes in diet and exercise may have a positive impact on raising HDL levels: [30]

  • Decreased intake of simple carbohydrates. [31][32][33][34][35][36] consumption [37] supplements raise HDL-C. [38]
  • Addition of soluble fiber to diet [39]
  • Consumption of omega-3 fatty acids such as fish oil [40] or flax oil[41]
  • Consumption of pistachio nuts. [42]
  • Increased intake of unsaturated fats[43]
  • Consumption of medium-chain triglycerides (MCTs).
  • Removal of trans fatty acids from the diet [44]

Most saturated fats increase HDL cholesterol to varying degrees but also raise total and LDL cholesterol. [45] A high-fat, adequate-protein, low-carbohydrate ketogenic diet may have similar response to taking niacin (vitamin B3) as described below (lowered LDL and increased HDL) through beta-hydroxybutyrate coupling the Niacin receptor 1. [46]

Recreational drugs Edit

HDL levels can be increased by smoking cessation, [36] or mild to moderate alcohol intake. [47] [48] [49] [50] [51] [52]

Cannabis in unadjusted analyses, past and current cannabis use was not associated with higher HDL-C levels. [53] A study performed in 4635 patients demonstrated no effect on the HDL-C levels (P=0.78) [the mean (standard error) HDL-C values in control subjects (never used), past users and current users were 53.4 (0.4), 53.9 (0.6) and 53.9 (0.7) mg/dL, respectively]. [53]

Pharmaceutical drugs and niacin Edit

Pharmacological therapy to increase the level of HDL cholesterol includes use of fibrates and niacin. Fibrates have not been proven to have an effect on overall deaths from all causes, despite their effects on lipids. [54]

Niacin (vitamin B3) increases HDL by selectively inhibiting hepatic diacylglycerol acyltransferase 2, reducing triglyceride synthesis and VLDL secretion through a receptor HM74 [55] otherwise known as niacin receptor 2 and HM74A / GPR109A, [46] niacin receptor 1.

Pharmacologic (1- to 3-gram/day) niacin doses increase HDL levels by 10–30%, [56] making it the most powerful agent to increase HDL-cholesterol. [57] [58] A randomized clinical trial demonstrated that treatment with niacin can significantly reduce atherosclerosis progression and cardiovascular events. [59] Niacin products sold as "no-flush", i.e. not having side-effects such as "niacin flush", do not, however, contain free nicotinic acid and are therefore ineffective at raising HDL, while products sold as "sustained-release" may contain free nicotinic acid, but "some brands are hepatotoxic" therefore the recommended form of niacin for raising HDL is the cheapest, immediate-release preparation. [60] Both fibrates and niacin increase artery toxic homocysteine, an effect that can be counteracted by also consuming a multivitamin with relatively high amounts of the B-vitamins, but multiple European trials of the most popular B-vitamin cocktails, trial showing 30% average reduction in homocysteine, while not showing problems have also not shown any benefit in reducing cardiovascular event rates. A 2011 niacin study was halted early because patients adding niacin to their statin treatment showed no increase in heart health, but did experience an increase in the risk of stroke. [61]

In contrast, while the use of statins is effective against high levels of LDL cholesterol, most have little or no effect in raising HDL cholesterol. [57] Rosuvastatin and pitavastatin, however, have been demonstrated to significantly raise HDL levels. [62]

Lovaza has been shown to increase HDL-C. [63] However, the best evidence to date suggests it has no benefit for primary or secondary prevention of cardiovascular disease.

Though it has not yet been FDA-approved, the PPAR modulator (sometimes referred to as a SARM) GW501516, currently a research chemical (not for human consumption), has shown a positive effect on HDL-C [64] and an antiatherogenic where LDL is an issue. [65]

Types of Fat

Fat is organized into two subgroups: saturated fat, and unsaturated fat. Unsaturated fat is further classified as monounsaturated fat, polyunsaturated fat, and trans-fat. These different classifications determine the effects of these fats on an organism, and the roles that they have in metabolism.

Saturated Fat

Unsaturated Fat

Unsaturated fat, or vegetable fat, is composed of a glycerol backbone with three fatty acid chains where there is at least one sp 2 hybridized carbon. This forms a double bond somewhere in the chain. Monounsaturated fats have one double bond in the chain, while polyunsaturated fats have two or more.

Naturally occurring unsaturated fats, since they are produced by enzymes, have specific stereochemistry. Natural fats always show the cis conformation, which has a higher solubility in water, and is easily broken down by the metabolic machinery. Artificially produced fats, since they are produced using organic synthesis techniques, contain a racemic mixture of trans and cis bonds. Trans fats are less soluble – like saturated fats. However, they are not readily metabolized by cellular machinery.

Types of Unsaturation:
The unsaturated fats are classified by the position of the unsaturation. This designation is denoted by the ω symbol, then the number of carbon with the unsaturation. For example, ω-3 fats have an unsaturation at the third carbon position. Ω-3,7 polyunsaturated fats have an unsaturation at the third and seventh carbon position. The position of the unsaturation determines the metabolic pathway that the fat will follow.

Lowering triglycerides

If you've had your triglycerides tested and are worried about high levels, you can take actions to lower them. Most actions involve improving your diet and exercise habits. Wright provided the following advice for lowering your triglyceride levels:

  • Lose weight. If you're overweight, losing 5 to 10 pounds can help lower your triglycerides.
  • Avoid sugary and refined foods. Simple carbohydrates, such as sugar, can increase triglycerides.
  • Choose healthier fats. Trade saturated fat found in meats for healthier monounsaturated fat found in plants, such as olive, peanut and canola oils. Substitute fish high in omega-3 fatty acids, such as mackerel and salmon, for red meat.
  • Limit how much alcohol you drink. Alcohol is high in calories and sugar and has been shown to raise triglyceride levels.

If making healthy lifestyle changes doesn't sufficiently lower your triglyceride levels, your doctor may prescribe medicines to take in conjunction with a good diet and exercise regime. The following medicines are often prescribed, according to the Mayo Clinic:

Niacin is also known as vitamin B3 and nicotinic acid. It is a water-soluble vitamin important for a healthy body, and is normally acquired through foods like milk, eggs, rice, fish, lean meats and legumes, according to the NIH. For people with high triglyceride levels or high LDL cholesterol, a very high dose of niacin may be prescribed. It is important not to take prescription-strength niacin without a prescription because in large, unregulated doses it can be toxic. It can also interact with other medications to your detriment.

Niacin is usually only prescribed to people with triglyceride levels over 500 mg/dL (5.7 mmol/L). According to the Mayo Clinic, niacin can raise HDL (good) cholesterol levels by more than 30 percent. It has also been linked to slowing atherosclerosis, heart attack and stroke when paired with statins or colestipol (other cholesterol-lowering medications), according to the University of Maryland Medical Center.

Statins are well known for their cholesterol-lowering abilities. These drugs include atorvastatin (Lipitor) and simvastatin (Zocor). Statins interfere with the liver's production of LDL cholesterol and raise HDL cholesterol levels. They are typically prescribed for people with high LDL cholesterol levels or histories of clogged arteries or diabetes. While they are relatively safe for most people, muscle pain is a common side effect.

Omega-3 fatty acids

Found in fish oil, these healthy fatty acids are an important part of any good diet. In high doses, they can help lower triglyceride levels. Scientists theorize that omega-3 fatty acids' ability to lower inflammation could be related to its triglyceride-lowering capabilities, according to an article in Biochimica et Biophysica Acta. Because high doses of fish oil can add a great deal of calories, interfere with blood clotting and cause nausea and diarrhea, prescription-strength omega-3 fatty acid supplements are only given to people with triglyceride levels higher than500 mg/dL (5.7 mmol/L). Some names of prescription-strength fish oil are Epanova, Lovaza and Vascepa. Fish oil does not lower cholesterol.