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HOSP6063 Food And Beverage Studies

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The study of lipids and their primary structural elements, fatty acids remains one of the most controversial research fields in nutrition and biology. As a component of the diet, fats provide essential fatty acids (FA) and help in the absorption of fat soluble vitamins plus essential nutrients. Fats found in the food also produce metabolic impacts which are complex effects of fat content (Fauzi et al., 2013). FAs are not only necessary for membrane synthesis, production of signalling compounds, construction of different structural elements in the cells and tissues, but also for solubility of non-polar and poorly soluble extracellular constituents.

 According to Fauzi et al.,(2013) a series of studies show that low fat (10%) high-carbs diet enriched in simple sugars raises fatty acid synthesis particularly palmitate and that difference between subjects in increased triacylglycerol concentrations vary significantly. However, it should be noted that the effects of saturated fatty acids on risk of diseases are complicated. Most reviews recommend a diet low in saturated fat and argue that it‘ll reduce the risks of cancer, coronary diseases and obesity to mention just a few. Also, other studies have advocated for finding the proportion of bad to good fat in the diet. This review will examine the three common saturated fatty acids  (stearic acid, myristic acid and palmitic acid ) their role in the body and the diseases associated with them such as cancer, obesity and inflammatory bowel disorder.

Stearic Acid

Stearic acid (SA) is an organic compound consisting of long chain carbon atoms without a double bond. Unlike other saturated fatty acids such as lauric and myristic that increase blood cholesterol levels, SA has proven to have no effect on blood total as well as low-density lipoprotein cholesterol levels (Hunter et al., 2010). This neutral effect on LDL cholesterol levels shows that stearic acid does not increase danger for coronary diseases.  According to the national health & nutrition examination, the average intake of SA is 5.7grams per day for females and 8.2 grams per day for males. For men and women aged 20 years and above, the dietary SA intake accounts for 25.7% of saturated fatty acid intake as well as 17. 9% of saturated fatty acids (Keys et al., 2012). However, the consumption of SA is preceded by palmitic acid that accounts for 54.2% of saturated fatty acids for women and 54.5% of SFA for men. The primary food sources of SA are milk and grain products and meat

Hunter et al. (2010) holds that the reason as to why SA does not raise blood cholesterol levels has been a subject of great debate, and multiple explanations have been proposed. Although early investigations pointed out that absorption of SA is less efficient compared to other SFAs such as lauric and myristic, other studies in humans have shown that the absorption rate of SA is slightly lower compared to other saturated fatty acids (Lee et al., 2001).  According to Lee et al., (2001), the reason as to why stearic acid does not raise cholesterol levels can be based on two things; first, the absorption of SA may be incomplete and second, the acid may be rapidly converted to oleic acid in the body.  However, a recent study has been done to eliminate the first possibility by examining the fatty acids composition of chylomicron fats after administration of a fatty meal where SA was one of the major components. According to Milanski et al., (2009), the composition of SA in chylomicron was the same as to that of dietary fat. However, if the uptake of SA has been much lower than that of other dietary SFA, the composition of stearic acid in chylomicron lipids would have lowered. But since this did not happen, it can be assumed that SA is absorbed approximately like other SFA. Hence the lack of cholesterol raising the action of SA can’t be attributed to lack of absorption. In the second possibility, where SA is swiftly converted to Oleic acid, a study in rats found out that SA was found to be quickly converted to oleic acid which palmitic acid was not (Milanski et al., 2009).

 Myristic Acid

Myristic acid is a long chain saturated hydrocarbon containing 14 carbon atoms. It occurs as vegetables and oils in plants and glycerol ester in animals. In animal fats like the shell fish and milk, the acid is present in small amounts of less than 1.5 grams per 100 grams of edible portion. However, the exception is shown in most dairy products including cheese and butter with an edible portion of 3.4 grams per 100grams and 8.3 grams per 100grams of edible portion respectively. Myristic acid usually raises the LDL cholesterol levels. Recent studies show that myristic acid increases the cholesterol levels to the same standard as palmitic acid (Rioux et al., 2007). Other reports show that show that Myristic acid is much of hypercholesterolemia compared to the PA.  If such hypothesis is correct, the myristic acid must contribute a lot to the hypercholesterolemia impact of butter fat as well as tropical oils, excluding palm oil. However, there have been no recent studies to test for the relative effects of MA on serum cholesterol levels in people. Moreover, no studies have been carried out to examine the effect of myristic acid on cholesterol levels directly. Ideally, such studies are of great importance since they are part of the systematic evaluation of the relative implications of every other saturated acid including stearic acid and palmitic acid (Simakova et al., 2009).

Palmitic Acid

Palmitic acid is one of the most common saturated fatty Acid found in plants and animals. It has 16 carbon chains with no double bonds. Compared to carbohydrates and unsaturated fats, the acid raises the levels of LDL cholesterol and total cholesterol without even affecting the levels of high-density lipoprotein cholesterol (Fauzi et al., 2013). A comparison between impacts of dietary laureate Myristate as well as the palmitic acid in humans shows that palmitic acid reduces serum cholesterol. However, the substitution of dietary laureate Myristate with palmitate-oleate has a significant impact on the relative index of thrombogenesis that is the ratio of thromboxane to prostacy in the plasma. The mechanisms by which saturated fatty acids do not activate the innate are not fully known, but the palmitic acid is known to induce the myocardial inflammatory injury via the toll like receptor accessory protein MD2 in louse as well as cell structure experimental models. According to Fauzi et al., (2013), the MD2 knockout mice are usually protected against palmitic acids and high-fat diet induced myocardial injury. According to Wei et al., (2006), studies on the cell free proteins, cell surface binding plus molecular docking simulations show that palmitic acid directly binds to the MD2, supporting the mechanism by which palmitic acid activates the toll like receptor 4 plus downstream inflammatory responses. Therefore, it can be concluded that palmitic acid is a significant contributor to obesity associated myocardial injury that is controlled through its binding to the MD2.

Diseases Associated With Saturated Fatty Acids

Increased uptake of a diet rich in saturated fatty acids has increased the number of diseases which have a detrimental effect on the health of a person. Consuming too much of saturated fat raises the bad cholesterol as well as increases the risks of coronary diseases. Wu et al., (2011) holds that bad cholesterol plays a significant role in the body, but its particles can build up and attach themselves to the wall of the arteries thus forming blockages that may result in heart attacks and other severe health threats.  Saturated fat found in meat and other high fat dietary dairy products have also shown to increase inflammation as well as weight gain leading to obesity (Wei et al., 2006). However, the impact of certain SFAs on inflammation could be the main view to how food fats affect health.  According to studies, evidence on the SFAs inflammation interactions can be described when the SFAs induce inflammation in part by imitating the actions of lipopolysaccharides translocation. All in all, it should be well understood that loosing extra weight helps reduce the risks of developing cancer as well as other chronic diseases such as the coronary diseases. According to Rioux et al., (2007), lowering the consumption of saturated fat would help to tackle the issue of diseases associated with SFAs.


Fats play a crucial role in the body of a person. Apart from maintaining healthy skin, fats play a significant role in promoting good eyesight as well as brain development in infants and teenagers. But for all good it does, fat is usually considered as the culprit in the battle for many human diseases. This is because excess saturated fats pack more calories of protein as well as carbohydrates thus leading to weight gain and risks of developing cardiovascular diseases. It should be noted that diet rich in saturated fat raises blood cholesterol concentrations, thus leading to clogged arteries that may stop the flow of oxygenated blood to the brain and the heart. However, low-fat diets might not reduce the artery blocking compounds in the bloodstream to every other person, so when it comes to dietary fats, quantity and quality plays a critical role

In summary, it should be noted that there is no dietary requirement for saturated fatty acids since our bodies are made to produce all that it needs. On the same note, there is also no need to shun from food rich in saturated fats in the name of good health. What needs to be is to ensure that the saturated fats should be kept below 10% in all the fat consumed.

Reference List

Fauzi, H., Metselaar, H.S., Mahlia, T.M.I., Silakhori, M. and Nur, H., 2013. Phase change material: optimizing the thermal properties and thermal conductivity of myristic acid/palmitic acid eutectic mixture with acid-based surfactants. Applied Thermal Engineering, 60(1), pp.261-265.

Hunter, J.E., Zhang, J. and Kris-Etherton, P.M., 2010. Cardiovascular disease risk of dietary stearic acid compared with trans, other saturated, and unsaturated fatty acids: a systematic review. The American journal of clinical nutrition, 91(1), pp.46-63.

Keys, A., Anderson, J.T. and Grande, F., 1965. Serum cholesterol response to changes in the diet: IV. Particular saturated fatty acids in the diet. Metabolism, 14(7), pp.776-787.

Lee, J.Y., Sohn, K.H., Rhee, S.H. and Hwang, D., 2001. Saturated fatty acids, but not unsaturated fatty acids, induce the expression of cyclooxygenase-2 mediated through Toll-like receptor 4. Journal of Biological Chemistry, 276(20), pp.16683-16689.

Milanski, M., Degasperi, G., Coope, A., Morari, J., Denis, R., Cintra, D.E., Tsukumo, D.M., Anhe, G., Amaral, M.E., Takahashi, H.K. and Curi, R., 2009. Saturated fatty acids produce an inflammatory response predominantly through the activation of TLR4 signaling in hypothalamus: implications for the pathogenesis of obesity. Journal of Neuroscience, 29(2), pp.359-370.

Rioux, V., Catheline, D. and Legrand, P., 2007. In rat hepatocytes, myristic acid occurs through lipogenesis, palmitic acid shortening and lauric acid elongation. Animal, 1(6), pp.820-826.

Simakova, I., Simakova, O., Mäki-Arvela, P., Simakov, A., Estrada, M. and Murzin, D.Y., 2009. Deoxygenation of palmitic and stearic acid over supported Pd catalysts: effect of metal dispersion. Applied Catalysis A: General, 355(1), pp.100-108.

Wei, Y., Wang, D., Topczewski, F. and Pagliassotti, M.J., 2006. Saturated fatty acids induce endoplasmic reticulum stress and apoptosis independently of ceramide in liver cells. American Journal of Physiology-Endocrinology and Metabolism, 291(2), pp.E275-E281.

Wu, S. and Fang, G., 2011. Dynamic performances of solar heat storage system with packed bed using myristic acid as phase change material. Energy and Buildings, 43(5), pp.1091-1096.

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