Hydrogenated fats were introduced in the early 20th Century as a means to extend the shelf life of vegetable oils and to provide a saturated fat that melts at a higher temperature, making them beneficial products for baking. The resulting fat products (such as margarine and Crisco©) are more resistant to spoilage and have a decreased need for refrigeration.
Most commercial hydrogenated fat products made from vegetable oils go through a process of partial hydrogenation, which yields a more convenient product and produces side products called trans fatty acids (TFAs), or trans fats. The TFAs that result from partially hydrogenating vegetable oils may compose up to 40% of the final fat product and present a significant health hazard for people consuming these fats.
Trans fatty acids are present in many current U.S. food products, including margarines, baked goods, snack foods, fried foods, and many processed foods. Low levels are also found in dairy products, lamb and beef fat. Although TFAs occur naturally in such products as butter, the levels are much lower, usually at or below four percent.
Studies suggest that higher levels of meat irradiation may also increase the amount of TFA in ground beef and frankfurters. The processing of meats (i.e. in hydrogenated oils) may also increase the formation of TFAs due to oil absorption. Some evidence also suggests that diet may affect TFA composition of meat, although additional studies are needed.
It is estimated that TFAs make up about 2-3% of the total calories consumed daily among the U.S. population. TFAs have been found to be a bigger risk factor than saturated fats for coronary heart disease (CHD) by simultaneously lowering high-density lipoprotein (HDL, also known as "good" cholesterol), while raising low-density lipoprotein levels (LDL, also called "bad" cholesterol) in the blood.
Even very small amounts of TFAs in the diet (about 5 grams daily), are associated with a 25% increased risk of heart disease risk. Research suggests that these fatty acids are neither essential nor provide any known benefit to human health. According to an assessment by the National Academy of Science, dietary TFAs present a bigger risk factor for CHD than saturated fats. The U.S. Food and Drug Administration (FDA) requires the amount of TFA to be declared on the nutritional labels of all foods and beverages.
The current theory explaining the adverse effects of TFAs on CHD involve the human body's inability to properly digest and process these fatty acids. Consequently, it is thought that TFAs absorbed through the diet remain in circulation for longer periods of time in the bloodstream. By circulating for a longer time in the bloodstream, it is thought that these fatty acids are more prone to be deposited on vessel walls, thereby contributing to blockage. When this blockage happens in arteries that supply the heart with blood (coronary arteries), it is called CHD.
The use of partially hydrogenated fats accelerated in the 1960s, 1970s, and 1980s, as food processors responded to public health recommendations to move away from animal fats and tropical oils. Animal fats and tropical oils supply mainly saturated fats, which have been shown to be a dietary risk factor for coronary heart disease. At the time, the partially hydrogenated vegetable oils seemed a convenient alternative because of their stability, cost, and functionality. While partially hydrogenated oils do not contain as much saturated fat, the remaining fraction is made up of unsaturated fats that include TFAs. This fraction of TFAs may be as high as 45% of total fat in some products.
Denmark became the first country to strictly regulate the sale of foods containing TFAs in March 2003. This was the result of mounting data that have implicated TFAs in the development of CHD.
As of 2003, the FDA has required that manufacturers list trans fats on the labels of food products. This is usually listed under the total fat content, which is divided into the proportion of saturated and unsaturated fats, as well as TFA content. These proportions are usually listed in the total grams of each fat contained in the product. The current regulations allow products that have 0.5 grams or less of total fat contained as TFAs per serving to be officially labeled as "TFA-free."
Many of the efforts to ban TFAs were spearheaded in the United States by the organization BanTransFats.com, which launched a banning campaign by suing Kraft in 2003 over the TFA content in its cookies.
Since May 2005, a number of U.S. cities, including New York City, Philadelphia, and San Francisco, have issued bans on the use of TFAs in restaurants. Chicago has a partial ban. In January 2008, California became the first state to pass legislation banning the use of TFAs in restaurants. Packaged foods, however, are exempt from this ban. Much of the U.S. action followed the banning of TFAs in other countries, such as Denmark, which judged it prudent to restrict TFAs at the food production level so consumers would not have to monitor their intake.
Hydrogenated fats are created during a process called partial hydrogenation. During this process, metal catalysts (such as nickel) force extra hydrogen molecules into the oil. This results in a decrease in the amount of unsaturated carbon bonds. Some of the double bonds remain between carbon atoms, and the hydrogens shift position to become by-products called trans-unsaturated fatty acids. In general, hydrogenated fats produced by the process of partial hydrogenation may contain up to 45% of their total fat as TFAs in the final fat product.
The recommendations against the use of TFAs stem from guidelines developed by the National Academy of Sciences in 2002.
During the 1990s, multiple studies consistently showed negative effects of trans-fatty acids (TFAs) on blood lipoproteins, such as low-density lipoprotein (LDL) and high-density lipoprotein (HDL). LDL transports cholesterol to the body tissues, while HDL transports cholesterol to the liver. Higher LDL levels are associated with an increased risk of clogged arteries. Ideally, LDL levels should be kept lower than HDL levels. TFAs have been shown to have a negative effect on both lipoproteins at the same time, making TFAs more of a risk factor than that of saturated fats for coronary heart disease (CHD). TFA consumption has also been linked to other risk factors, such as high blood pressure, insulin resistance, and higher levels of markers for systemic inflammation (such as C-reactive protein, tumor necrosis factor-alpha, interleukin-6, and soluble intercellular adhesion molecule-1).
No safe limits of TFA consumption have been clearly established.
General: No safe limits of trans fatty acid (TFA) consumption have been clearly established.
In 2003, the World Health Organization (WHO) recommended that TFA intake be limited to less that one percent of overall caloric intake. Other recommendations include increasing intake of fruits, vegetables, and essential fatty acids (such as linoleic acid).
The American Heart Association (AHA) recommends balancing caloric intake with physical activity by consuming an overall healthy diet and aiming for a healthy body weight. The diet should be rich in fruits, vegetables, whole-grains, and fiber. Additionally, fish should be eaten at least twice a week. The AHA recommends that trans fats be limited to less than one percent of total energy intake.
It is generally recommended that in order to minimize intake of TFAs, consumers should avoid foods with the highest levels of TFAs, such as fried foods, processed snack foods, margarines, and baked goods.
Heart disease: The main health risk associated with TFAs is coronary heart disease (CHD), a disease where the vessels feeding blood to the heart gradually become blocked due to the build-up of fatty deposits on the walls. Even very small amounts of TFAs in the diet, around 5 grams daily, are associated with a 25% increase in heart disease risk over time.
In a meta-analysis of both animal and epidemiological studies, TFAs were found to increase this risk more than any other component of the diet on a per-calorie basis. This same study estimated that between 30,000 and 100,000 deaths from heart disease per year are attributed to the consumption of TFAs.
Intake of TFAs has been shown to increase the risk of heart disease by raising low-density lipoprotein (LDL) levels and lowering high-density lipoprotein (HDL) levels. LDL delivers cholesterol to the tissues, while HDL delivers cholesterol to the liver. Any rise in LDL levels means that there is a greater risk for depositing cholesterol to walls of blood vessels, which could eventually result in a blockage. When this occurs closer to the heart, it could result in a heart attack.
Saturated fats, which are a known risk factor for CHD, are fats that are solid at room temperature. These fats are mostly derived from animal sources and significantly raise blood cholesterol levels when consumed in high amounts in the diet. Unlike saturated fats, which only raise LDL levels, TFAs also lower HDL. Any lowering of HDL levels at the same time that LDL is raised means that TFAs have double the effect of saturated fats on blood cholesterol. This increase in circulating cholesterol increases the chances that it will be deposited into the walls of blood vessels.
Connections between TFA and elevated triglycerides levels are not clear at this time.
Evidence indicates that TFAs may raise the concentration of lipoprotein (a) Lp(a), a genetic variant of LDL and an independent risk factor for CHD. Although Lp(a) shares some characteristics with LDL, it is an independent risk factor because of an additional risk trait. Its chemical structure has the property of preventing the action of a chemical (plasminogen) to dissolve blood clots. As Lp(a) accumulates in fatty plaque, it promotes the formation of clots that are more difficult to dissolve.
In a follow-up, researchers tracked the diets and health of women for 14 years. The authors reported that TFAs were associated with an increased risk of CHD, especially among young women.
While data from long-term cohort studies are not as strong as that from metabolic studies and meta-analyses, the overall evidence is still strong enough to warrant recommendations for a reduction in dietary TFA intake. One of the limitations of cohort studies has been estimating dietary intake of TFAs, which until recently, has been a problem due to lack of information on food labels.
Diabetes: TFAs may increase risk of developing type 2 diabetes, although the data from studies are not clear. Limited but growing evidence links consumption of TFAs with the development of insulin resistance and visceral adiposity (the accumulation of fat in the abdomen), a major risk factor contributing to the development of type 2 diabetes. In human study of more than 84,000 women aged 34-59 over a 14-year period with validated dietary questionnaires, a significant relationship was found between TFA intake and increased risk for the development of type 2 diabetes.
This link is not as clear in men at this time, and there may be gender differences involved.
To further reduce risk for type 2 diabetes, it is also recommended to incorporate exercise into daily regimens. Endurance exercise has been shown to improve skeletal muscle insulin sensitivity, thereby possibly reducing the impact of TFAs in the diet.
Studies in animals indicate that dietary fats affect the composition of fatty acids in cell membranes. TFAs may negatively affect cell membrane lipid composition so that there is a decrease in insulin sensitivity.
Inflammation: Intake of TFAs has been shown to increase general (systemic) inflammation in healthy people. Systemic inflammation is an independent risk factor for heart disease. The development of CHD has been shown to involve an inflammatory response that contributes to the formation and growth of arterial plaque, which if unchecked, may result in blocked arteries.
Although markers for inflammation, such as C-reactive protein, tend to be higher in patients with CHD, TFAs may worsen inflammation in patients who already have heart problems. Steps for preventing a second heart attack typically include reducing the amount of fat in the diet and quitting smoking. Dietary changes, such as avoiding TFAs and maximizing fruit and vegetable intake, may enhance current therapies, such as the use of drugs and surgery, by reducing inflammation. Fruits and vegetables contain antioxidants, such as carotenoids and anthocyanins, which also act to decrease inflammation in the body.
Obesity: Growing evidence suggests a link between inflammation and obesity. By contributing to higher levels of circulating inflammatory mediators (chemicals that can increase the amount of inflammation), TFAs may promote obesity. Because of changes in dietary fat composition associated with the typical American diet, infants are exposed to higher saturated fats and TFAs, while getting less of the omega-3 fatty acids that decrease many of the adverse metabolic changes associated with obesity. The omega-3 fatty acids are the fatty acids, such as those from fish oils, whose higher intake in the diet are associated with less inflammation in the body, as well as possibly being beneficial against CHD. Other sources for these fatty acids include plant seed oils and leafy vegetables, to a lesser extent. Because children are eating higher levels of TFAs in the diet and less beneficial fats, such as the omega-3 fatty acids, they are more predisposed to developing underlying conditions that lead to obesity.
Brain function: Some evidence suggests that diets high in saturated fats and TFAs may play a role in cognitive decline in adults. In a study of adults (65 years of age and older), cognitive function and dietary habits were assessed over a six-year period. These cognitive tests measured such things as immediate and delayed recall and mental state. A connection was found between high TFA intake and cognitive decline. Although mechanisms are still being examined, some probable causes include the brain's sensitivity to insulin decreasing, as well as inflammation in the central nervous system.
Fertility: TFAs may affect fertility. Decreases in insulin sensitivity have been shown to contribute to some types of infertility. In women with polycystic ovary syndrome (PCOS), certain pharmaceuticals that enhance insulin sensitivity also improve reproductive metabolic profiles and ovary function. Because TFAs have the opposite effect on insulin, they have been associated with an increased risk of infertility in women. Animal studies have shown irregularities in the estrous cycles and gestation periods of female rats and abnormal sperm production in male rats that ate diets rich in hydrogenated oil.
FUTURE RESEARCH OR APPLICATIONS
Although the National Academy of Sciences (NAS) has not recommended an absolute ban on trans fatty acids (TFAs), many countries are following the example of Denmark and instituting restrictions on the use of TFAs in the food industry. The main reason that the NAS has not issued an absolute ban of TFAs is because very small levels occur naturally in animal products. The NAS argues that an absolute ban would not be in line with normal diets because of these naturally occurring versions of TFAs.
The U.S. Food and Drug Administration (FDA) regulations implemented in 2006 require manufacturers to indicate the amounts of trans fatty acids (TFAs) on their product labels, allowing consumers to make educated decisions about their food intake. However, if there is 0.5 grams of TFAs or less per serving, products are officially labeled as "trans-fat free."
Alternatives to hydrogenated fats (which have trans fatty acids as a by-product) are being developed for use in baking and cooking commercial products.
This information has been edited and peer-reviewed by contributors to the Natural Standard Research Collaboration (www.naturalstandard.com).
- Astrup A. The trans fatty acid story in Denmark. Atheroscler Suppl. 2006 May;7(2):43-6. Epub 2006 May 24. View abstract
- Astrup A, Dyerberg J, Selleck M et al. Nutrition transition and its relationship to the development of obesity and related chronic diseases. Obes Rev 2008 Mar;9 Suppl 1:48-52. View abstract
- Booker CS, Mann JI. Trans fatty acids and cardiovascular health: Translation of the evidence base. Nutr Metab Cardiovasc Dis 2008 Jul:18(6):448-56. View abstract
- Chardigny JM, Destaillats F, Malpuech-Brugere C, et al. Do trans fatty acids from industrially produced sources and from natural sources have the same effect on cardiovascular disease risk factors in healthy subjects? Results of the trans Fatty Acids Collaboration (TRANSFACT) study. Am J Clin Nutr 2008 - 87:558-566. View abstract
- Chavarro J, Rich-Edwards J, Rosner B, et al. Dietary fatty acid intakes and the risk of ovulatory infertility. Am J Clin Nutr 2007;85:231-7. View abstract
- Corcoran M, Lamon-Fava S, Fielding R. Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty acids and exercise. Am J Clin Nutr 2007; 85:662-77. View abstract
- Dalainas I, Ioannou HP. The role of trans fatty acids in atherosclerosis, cardiovascular disease and infant development. Int Angiol. 2008 Apr;27(2):146-56. View abstract
- Dietary guidelines for Americans 2005, Department of Health and Human Services, Department of Agriculture. www.healthierus.gov. Accessed December 9, 2008.
- Discepolo W, Wun T, Berglund L. Lipoprotein(a) and thrombocytes: potential mechanisms underlying cardiovascular risk. Pathophysiol Haemost Thromb. 2006;35(3-4):314-21. View abstract
- Eckel RH, Borra S, Lichetenstein AH, et al. Understanding the complexity of trans fatty acid reduction in the American diet: American Heart Association Trans Fat conference 2006 Report Circulation 2007 Apr 24;115(16):2231-2246. View abstract
- Esmaillzadeh A, Azadbakht L. Home use of vegetable oils, markers of systemic inflammation, and endothelial dysfunction among women. Am J Clin Nutr. 2008 Oct;88(4):913-21. View abstract
- Innis SM. Dietary lipids in early development: relevance to obesity, immune and inflammatory disorders. Curr Opin Endocrinol Diabetes Obes. 2007 Oct;14(5):359-64. View abstract
- Mozaffarian D, Katan MB, Ascherio A, et al. Trans fatty acids and cardiovascular disease. N Engl J Med. 2006 Apr 13;354(15):1601-13. View abstract
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