Why should we demonize palm oil?

For a number of years now a defamatory campaign has been taking place against palm oil, or better, palm fat, considering its physical state at room temperature. During the first stages of this campaign, palm oil and its major component, palmitic acid, were accused of causing child obesity, one of the most alarming pathologies emerging in industrialized countries. Sweet snacks, and their creamy fillings, were considered the main cause of this epidemic, and not the fact that children were left for hours on end in front of the TV with a load of junk food at their disposal. A sedentary lifestyle and an excessive consumption of these snacks, which because of their calorie content are more suitable for very active children, are in fact the real causes of obesity.

At a second stage, fingers were pointed at the environmental impact of these crops: the accusation, often backed up by dramatically exaggerated documentaries, was of destroying lush natural environments in favour of squalid plantations of palm trees. Whatever the actual impact may be, one should take into account that palm oil has also turned out to be a cheap, bio-fuel, hence an alternative to the more polluting fossil fuels, and this is why its demand has increased so remarkably.

These claims, stirred up by mass media ravenously seeking scoops more than concrete facts, are provoking an emotional response that is reminiscent of the GMOs case: producers are now modifying their recipes so that their snacks can bear the claim “Palm-oil free”.

Investigations focusing on the relationship between the fatty acid profile of platelet membranes and pathologies such as mood disorders and ischemic heart disease have revealed that there is a close, complex relationship between fatty acids and membrane viscosity, but only the most advanced statistical models such as Artificial Neural Networks can shed light on the exact responses [1].

It is easy to lay all the blame on one fatty acid alone, but before demonizing it, one should consider that the network of relationships between all the various fatty acids is so complex that standard deviation and significance lose much of their importance. Indeed, in the case of depression and ischemic heart disease [2-6], most fatty acids were observed to be statistically significant, but more complex mathematical models only selected a few, and did not take these two parameters into account.

As Aseem Malhotra states [7], saturated fat is not the major issue and correlation does not mean cause.
Many are the mistakes that have been made throughout the years with respect to fatty acids. In children, for instance, platelet membranes have high levels of saturated fats, which reduce the risk of their aggregation [7-14]. It is worth mentioning that the innate aversion that many children have for fruit and vegetables may be a consequence of this condition. Children do not need large amounts of antioxidants because the fatty acids composition of their membranes does not require them.

Researchers have recently re-analyzed all the results of previous experiment investigations focusing on the interaction between ingested fats and human health. Many seemingly reliable data that had affected the consumption of certain foods have been debunked [7-8], and we now know that:

1. There is no correlation between the amount of fatty compounds ingested, if not overly excessive, and colorectal cancer.

2. The consumption of moderate amounts of saturated fatty acids is not linked to an increased risk of cardiovascular diseases, but the elderly are still advised to consume less of them.

3. On the other hand, compounds full of polyunsaturated fatty acids, such as the famous “omega-3 and omega-6” and present in high levels in all seed-derived oils, should be consumed in more limited amounts, since they are more sensitive to oxidation. The advised daily intake levels are of about 140 milligrams omega-3 – equal to 20 grams of olive oil (roughly two tablespoonfuls), which contains about 0.7% of this compound.

4. Palmitic acid is also present in extra virgin olive oil, as well as many other types of food. It is found at high levels in every cell of our body and plays a key role in preserving the integrity of cell membranes.
Higher levels of polyunsaturated oils could cause a variety of problems, because of the oxidation processes that they would trigger.

There is a reason for all these half-truths and/or lies on this topic. In 1977, a series of articles was published focusing on the typical American diet, where meat and dairy products, containing high levels of saturated fats, play a prominent role. That year the US Government issued its first dietary recommendation. By “demonizing” saturated fatty acids it hoped to reduce the consumption of fat-rich foods and therefore the health problems linked to high-calorie diets (obesity and weight-related pathologies). The rest of the world, trusting the nutritional guidelines issued by the US, immediately accepted and endorsed them, without adapting them to their traditional eating habits, which were often quite different from the American ones.
Moreover, as could be expected, many companies immediately took the opportunity to promote the consumption of alternative fats (such as seed oils and margarines) in place of the more traditional ones (such as butter and olive oil).

Conclusions
All fatty acids are useful, in certain amounts and contribute to preserving cell membrane homeostasis. They adapt to the changing temperatures by modulating enzyme activity in charge of determining the length and saturation levels of fatty acids. Palmitic acid in particular is extremely important, for it is the precursor from which stearic acid first, and oleic acid later, are produced. The mechanisms regulating these processes require the consumption of adequate and balanced amounts of fatty compounds such as palmitic acid, present in most food. Avoiding all excesses is the only important rule in human nutrition, and this is true for every type of food. There is absolutely no need or reason to demonize any nutrient.

The authors

Giovanni Lercker: Dipartimento di Scienze e Tecnologie Agro-Alimentari (DISTAL), Alma Mater Studiorum-Università di Bologna

Massimo Cocchi: “Paolo Sotgiu” Institute for research in Quantitative & Quantum Psychiatry & Cardiology
L.U.de.S University, Lugano, Switzerland; Dipartmento di Scienze Mediche Veterinarie (DIMEVET), Alma Mater Studiorum-Università di Bologna

Bibliography

[1] Benedetti S., Bucciarelli S., Canestrari F., Catalani S., Mandolini S., Marconi V., Mastrogiacomo A., Silvestri R., Tagliamonte M., Venanzini R., Caramia G., Gabrielli F., Tonello L., Cocchi M. (2014) Platelet’s Fatty Acids and Differential Diagnosis of Major Depression and Bipolar Disorder through the Use of an Unsupervised Competitive-Learning Network Algorithm (SOM). Open Journal of Depression, 3, 52-73.

[2] Cocchi M., Tonello L., Bosi S., Cremonesi A., Castriota F., Puri B., Tsaluchidu S. (2004) Platelet oleic acid as Ischemic Cardiovascular disease marker. BMJ, 329:1447.

[3] Cocchi M., Gabrielli F., Tonello L. (2013) Platelet’s Fatty Acids Secrets in Coronary Artery Disease (CAD), Letter to the Editor, BMJ, October 28th.

[4] Cocchi M., Tonello L., Lercker G. (2010) Fatty acids, membrane viscosity, serotonin and ischemic heart disease. Lipids in Health and Disease, 9:97.

[5] Cocchi M., Tonello L., Martínez Álvarez J.R. (2009) Nutritional considerations on platelet fatty acids in Major Depression and Ischemic Cardiovascular Disease. Nutr. clín. diet. hosp.; 29(2):46-54.

[6] Cocchi M., Tonello L. (2007) “Platelets, Fatty Acids, Depression and Cardiovascular Ischemic Pathology”, Progress in Nutrition., Vol.9 (2), 94-104.

[7] Malhotra A. (2013) Saturated fat is not the major issue. BMJ;347:f6340)

[8] Ascherio A., Rimm E.B., Giovannucci E.L., Spiegelman D., Stampfer M., Willett W.C. (1996) Dietary fat and risk of coronary heart disease in men: cohort follow up study in the United States. BMJ; 13;313(7049):84-90.

[9] Linder M.E. (2000) Reversible modification of proteins with thioester-linked fatty acids. Protein Lipidation, F. Tamanoi and D.S. Sigman, Eds., pp. 215-40 (San Diego, CA: Academic Press).

[10] Rocks O., Peyker A., Kahms M., Verveer P.J., Koerner C., Lumbierres M., Kuhlmann J., Waldmann H., Wittinghofer A., Bastiaens P.I. (2005) An acylation cycle regulates localization and activity of palmitoylated Ras isoforms. Science 307 (5716): 1746–1752.

[11] Basu, J. ( 2004) Protein palmitoylation and dynamic modulation of protein function. Current Science, Vol. 87, No. 2, pp. 212-217.

[12] Brigidi G.S., Sun Y., Beccano-Kelly D., Pitman K., Jobasser M., Borgland S.L., Milnerwood A J, Bamji S.X. (2014) Palmitoylation of [delta]-catenin by DHHC5 mediates activity-induced synapse plasticity. Nature Neuroscience 17: 522–532).

[13] Cocchi M., Tonello L., Lercker G. (2009) Platelet Stearic Acid in different population groups: biochemical and functional hypothesis. Nutr. Clin. Diet, hosp., 29(1), 34-45. ISSN: 02116057

[14] Lercker G., Cocchi M. (2010) Il grasso del latte: membrane, composizione e struttura. Progress in Nutrition, 12(2), 183-194. ISBN 9788890709500

Massimo Cocchi