Wednesday, November 26, 2014

Trans fats have caused premature deaths in thousands of people since 1910

Biochemist Fred Kummerow, who turned 100 in October 2014, continues to conduct research on heart disease and trans fats. In 2009, he petitioned the US Food and Drug Administration (FDA) to ban trans fats in foods and followed up by filing a lawsuit in 2013. In November 2013, the FDA made a preliminary determination that partially hydrogenated vegetable oils (the primary source of industrially produced trans fats) are not generally recognized as safe in foods. Here is Kummerow’s latest commentary on the topic. 

  •  It took years to realize that all trans isomers did not have the same properties. Artificial trans fatty acids and ruminant trans fatty acids have entirely different properties in vivo as well as in vitro.
  • When the amount of artificial trans fat in margarines was lowered, the sudden cardiac death rate also showed a decrease.pho
  • When trans fats are out of the food supply, there will be 325,000 fewer sudden cardiac deaths per year, according to data from the US Centers for Disease Control.

In 1901, a German chemist named Wilhelm Normann showed that liquid oils could be hydrogenated, and patented the process in 1902. Production of partially hydrogenated oils (PHOs) commenced in 1909. The Procter & Gamble Co. acquired the US rights to the Normann patent and in 1911 it began marketing the first PHOs. The hydrogenated fat replaced lard and butter. PHOs had desirable culinary properties as they had melting points close to body temperatures and became liquid in the mouth like butter. In 1910, no one knew what effect PHOs would have on health.

The present mix of dietary fat in the marketplace results in less prostacyclin synthesis, which is an important factor in cardiovascular health (1). Prostacyclin is a dominant prostaglandin produced by endothelial cells in arteries and is a potent vasodilator and inhibitor of platelet aggregation and leukocyte adhesion. It limits the response to thromboxane, which is a powerful inducer of vasoconstriction and platelet adhesion on the arterial wall and is partially responsible for the interruption of blood flow. The rise of artificial trans fats in the diet correlates to the rate of age-adjusted heart disease-related deaths in the United States since 1910.

Composition of trans fats

It took nearly five decades before the biochemical structure of trans fatty acids was understood. The partial hydrogenation of soybean oil adds atoms of hydrogen to 50% of the bonds 9,12 in linoleic acid (n-6) and to 50% of the bonds 9,12,15 in linolenic acid (n-3), converting them to 50% stearic acid(2). Forty to fifty percent of the double bonds of fatty acids in n-6 and n-3 are shifted to different positions on the carbon chain, making nine different synthetic trans fatty acids and five different cis fatty acids. These are cis and trans isomers of octadecenoic and octadecadienoic acids that are not present in animal fats or plant oils.

Both the cis and trans isomers interfere with the action of two isoforms of constitutive COX-1 and an inducible COX-2 enzyme. COX-2 is the enzyme that recognizes the isomers produced during hydrogenation as a foreign substrate and reacts to them by causing inflammation and inhibition of prostacyclin. The 14 synthetic fatty acids are a source of energy but interfere with the conversion of n-6 to arachidonic acidand n-3 to eicosapentaenoic acid (2).

Several studies, in my laboratory, have called attention to the trans fatty acids (TFAs) present in margarines and shortenings. Samples of tissue obtained from human autopsies were shown to contain up to 14% TFAs(3). Samples of fat from human placental, maternal, fetal, and baby tissue were also examined for the presence of TFAs(4). While the maternal tissue contained considerable amounts of TFAs, these lipids were not found to any measurable extent in placental, fetal, or baby fat(5).

This was also shown in rats that were fed transfat. When the transfat was removed from the diet, their tissue metabolized the trans fat and no longer contained trans fat(6). The results of these studies indicated that the TFAs present in human tissue apparently arise solely from dietary fat, and they do not normally appear in the tissues unless a source of TFAs is included in the diet.

Difference between PHOs and ruminant fats

It was believed by the FDA that trans fat in partially hydrogenated soybean oil (PHO) had the same chemical structure and worked the same way in our bodies as natural vaccinic acid. However, these two trans fat sources have entirely different properties in vitro as well as in vivo ((1)). The elaidic acid in PHO has a double bond at position 9, while the vaccinic acid in ruminant fats is at position 11. The enzymes in the body recognize vaccinic acid (butterfat and beef fat) as the fatty acid that has been in the diet for untold generations(7).

In vitro and in vivo study

An in vitro study showed that the fatty acids in partially hydrogenated fat had different properties than fatty acids in animal fat or vegetable oil. Trans acids increased the incorporation of 45Ca2+ into the cells, whereas cisacids did not incorporate 45Ca2+ into the coronary artery cells(8). An in vivo study showed that the TFAs inhibited the synthesis of arachidonic acid, a polyunsaturated fatty acid, in the phospholipid membrane of arterial cells (8). It was concluded that dietary trans fat perturbed essential fatty acid metabolism, which led to changes in the phospholipid fatty acid composition in the arterial wall, the target tissue of atherogenesis. Partially hydrogenated fat is a risk factor in the development of coronary heart disease because arachidonic acid is needed to synthesize prostacyclin.

Data from the CDC

Data obtained from the Centers for Disease Control (CDC) show the rate of death from heart disease started increasing in 1910 and continued until 1968, at which time the industry lowered the percentage of trans fat in shortenings and edible oils from 44% to 27% and increased the amount of linoleic acid from 8% to 25% (Table 1) (1).

Table 1. Average composition of shortening and mar

In 1968, the age-adjusted rate of heart disease-related deaths began to decrease. Data from the CDC state that almost 600,000 Americans died of heart disease in 2011, with 325,000 of those from sudden cardiac death. The other 275,000 deaths were due to calcification of the coronary arteries to 100% occlusion( (1)).

Tentative determination to ban PHOs

On November 7, 2013, FDA released a tentative determination regarding PHOs (9). It stated that PHOs, which are a primary source of industrially produced TFAs, are not generally recognized as safe (GRAS) for any use in food. The FDA requested comments of scientific data and information on this determination giving 60 days for responses. Before the 60 days were over, the agency extended the comment period by another 60 days until March 8, 2014. When the determination is finalized, it will mean that food manufacturers would no longer be permitted to sell PHOs without prior FDA approval.

The FDA released this information in the Federal Register on November 8, 2013 (9): “Trans fats are an integral component of PHOs and are purposely produced in these oils to affect the properties of the oil and the characteristics of the food to which they are added.” At zero percent of trans fat content in the body, the prostacyclin release from vascular endothelial cells is 38.7 ng/mg of cell protein (1).

Data released in the Federal Register states that in 2012 the average American consumed 2.1 grams of trans fats per day, with the 90% percentile consuming 4.2 grams per day (9). While consuming 2.1 grams of trans fat per day, the arterial cells will release 25 ng/mg cell protein, which is a significant drop from 38.7 ng/mg at zero percent. Consuming 4.2 grams/day of trans fat the cells will only release 15.5 ng/mg cell protein (1). As more grams per day of transfat are consumed, prostacyclin release from vascular endothelial cells to cell protein will decrease, proving an inverse relationship between the two processes.


The partial hydrogenation of vegetable oils has been shown to have an adverse effect on  health. The FDA believed that artificial trans fats had the same chemical structure and worked the same way in the human body as natural trans fats. It has been shown that this is not true. The sooner the FDA finalizes its decision to make artificial trans fat non-GRAS, the sooner more lives will be saved.
I believe that heart disease is not a disease but a somatic response to a simple error involving the effect of trans fat in partially hydrogenated oil on prostacyclin synthesis. Therefore, the present mix of dietary fat in the marketplace results in less prostacyclin synthesis and more sudden cardiac death.

Fred A. Kummerow is an adjunct professor in comparative biosciences at the University of Illinois Urbana-Champaign. He can be contacted at

  1. Kummerow, F.A., Two lipids in the diet, rather than cholesterol, are responsible for heart failure and stroke, Clin. Lipidol. 9:189–204, 2014.
  2. Kummerow, F.A., The negative effects of hydrogenated trans fats and what to do about them, Atherosclerosis 205:458–465, 2009.
  3. Johnston PV, Johnson OC, Kummerow FA. Occurrence of trans fatty acids in human tissue. Science. 1957;126:698-699.
  4. Johnston PV, Johnson OC, Kummerow FA. Non-transfer of trans fatty acids from mother to young. Proc Soc Exp Biol Med 1957;96:760-762.
  5. Johnston PV, Kummerow FA, Walton CH. Origin of the trans fatty acids in human tissue. Proc Soc  Biol Med. 1958;99:735-736.
  6. Johnston PV, Johnson OC, Kummerow FA. Deposition in tissues and fecal excretion of trans fatty acids in the rat. J Nutr. 1958;65:13-23.
  7. Kummerow FA. Improving hydrogenated fat for the world population. CVD Prevention and Control. 2005;1:157-164.
  8. Kummerow, F.A., Q. Zhou, M.M. Mahfouz, et al, Trans fatty acids in the phospholipid of arterial cells, Life Sci. 74:2707-2723, 2004.
  9. Tentative Determination Regarding Partially Hydrogenated Oils; Request for Comments and for Scientific Data and Information, Federal Register 78:67169–67175, 2013. Access online.

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