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Palmitic acid and palm oil

Palmitic acid and palm oil, rreview of the literature and implications on human health

Palm oil and fatty acid in it more present, palmitic acid, in recent years have been the subject of many studies by the scientific community, both epidemiological and laboratory models on in-vitro is in vivo, regarding their effect on human health.

Even the media have reported this topic in various newspapers in a more or less amplified and sometimes sensationalist way. With this brief review of the scientific literature of recent years, yes intends to offer an objective view of the topic.

Palmitic acid (16: 0, PA) is the most saturated fatty acid present in the human body. It can be di food origin or be synthesized endogenously by our cells (synthesis de novo). In phospholipids, important molecules constituting cell membranes and in triacylglycerols (TG) of adipose tissue, PA represents 20-30% of total fatty acids (FA)(Carta et al., 2017).

In foods, PA is found in meat and dairy products (50-60% total fat) and cocoa butter (26%) and olive oil (8-20%) and as the name suggests, PA is an important component of palm oil (44% of total fat). In addition, PA is 20-30% of total fat in breast milk (Innis et al., 1997). The synthesis de novo of FA in cells is borne by the enzymatic complex of fatty acid synthase, the final product of which is precisely PA having 16 carbon atoms and no double bond (16: 0).

Physiologically, the accumulation of PA is counteracted because normally a share is either modified into palmitoleic acid, inserting a double bond (16: 1) or elongated forming stearic acid (18: 0) and further unsaturated, forming oleic acid (OA , 18: 1) (Strable and Ntambi, 2010; Silbernagel et al., 2012).

The disruption of the balance of PA and its derivatives is often related to an uncontrolled endogenous biosynthesis, regardless of its dietary intake, which can lead to various pathophysiological conditions. In fact, it has been seen that in pathological conditions such as obesity, insulin resistance and non-alcoholic fatty liver disease, there is an increase in synthesis de novo which contributes heavily to fat deposition in the liver and changes in the fatty acid composition of phospholipids and TGs (Marques-Lopes et al., 2001).

This suggests that the desaturation of synthesized FA de novo it is necessary to modulate the biosynthesis of TG and prevent lipotoxic effects due to excessive accumulation of saturated fats (Collins et al., 2010) resulting in cellular dysfunction which can lead to a morbid condition, metabolic syndrome (Brookheart et al., 2009; Cnop et al., 2012). Therefore, the overproduction of synthetic PA de novo, Activated by pathophysiological conditions and chronic nutritional imbalance, leads to a systemic inflammatory response and metabolic dysregulation, resulting in dyslipidemia, insulin resistance and fat deposition and distribution (Donnelly et al., 2005). In the liver, for example, excess FA leads to an increase in TG exported, via the VLDL lipoproteins, into the plasma. Therefore, it can be hypothesized that control exists to maintain BP homeostasis and if there is an imbalance between saturated and unsaturated AF (FAs / FAi), this can induce transient hypertriglyceridemia and hypercholesterolemia and a moderate increase in deposition of TG in the liver. At the level of the phospholipids of cell membranes, maintaining the FAs / FAi balance is crucial for preserving the chemical-physical properties of the membrane and therefore cellular functionality (Abbott et al., 2012).

In different tissues, the composition of cell membranes in FAs remains rather constant even with very varied diets, suggesting that the concentration of FAs is poorly regulated by their dietary intake. (Abbott et al., 2012). Most of the studies conducted on fasting subjects show that the contribution of hepatic synthesis de novo to the total pool of FAs, it is modest in healthy subjects with a balanced diet. On the contrary, the content of ω-6 polyunsaturated fatty acids (PUFA) in the membranes is related to the ω-6 PUFA introduced with the dietetic diet, and this is more true for the ω-3 PUFA.

Instead, the plasma content of free fatty acids (NEFAs) released from adipose tissue reflects fat intake. In fact, the OA and the PA the most common FAs in the diet in plasma are about 31% and 27%.

In a recent work, Yuan et al., (2017) demonstrated that PA alters a cellular pathway that inhibits endothelial angiogenesis and therefore the authors suggest that excess PA could have implications for wound healing and diabetes, where an alteration of the functionality of the circulatory system is a frequent complication.

The association of circulating BP levels with the development of cancer is somewhat controversial. The association between blood fraction BP levels in relation to breast cancer risk was reported in a meta-analysis (Saadatian-Elahi et al., 2004) and a prospective study (Bassett et al., 2016), while another prospective study conducted in northern Italy found no association between saturated fatty acids and breast cancer risk (Pala et al., 2001).

It must be remembered that PA is an essential fatty acid as: a) it is an essential constituent of biological membranes; b) it is the main component of the pulmonary surfactant which is an essential substance for respiration. It is produced in the lungs by epithelial cells to reduce surface tension at the air / fluid interface of the pulmonary alveoli; c) it is the precursor of a particular endocannabinoid, PEA, a lipid mediator with neuroprotective, anti-neuroinflammatory and analgesic properties.

Palm oil, Yin e Yang

In recent decades, much has been debated on the possibility that a dietary intake of palm oil characterized by a high content in FAs, can increase the probability of suffering from cardiovascular diseases (CVD).

Palm oil is relatively rich in saturated fatty acids FAs, which account for about half of the total fat. Monounsaturated fatty acids (MUFAs) and PUFAs account for approximately 40% and 10%, respectively. In addition to the fatty acid content, palm oil native contains several phytocompounds such as tocotrienols and tocopherols (vitamin E) which have a beneficial action for human health, mainly due to their antioxidant activity (Loganathan et al., 2017). Red palm oil also contains α and β-carotene and Dong et al., (2017) in a meta-analysis they conclude that this oil is effective in the prevention of vitamin A avitamosis, indicating as the optimal dose ≤8 g / day as higher doses do not lead to further increases in serum retinol concentrations.

Below is the formula of TG present in palm oil, where in position snE-1 sn-3 glycerol is esterified while the PA is in place sn-2 instead there is the OA. When palm oil is taken in the intestine, pancreatic lipase cuts the bonds in snE-1 sn-3, but not in sn-2 where the oleic acid remains bound and the monoglyceride is absorbed by the cells. In the cell, enzymatic systems rebuild TG by inserting into snE-1 sn-3 preferably saturated fatty acids such as palmitic and stearic; finally, TG will form together with dietary cholesterol and some apoproteins, chylomicrons, a class of lipoproteins which will then be released into the circulatory system.

From Mancini et al., 2105 Molecules 2015, 20, 17339-17361; doi: 10.3390 / molecules200917339

Studies comparing the effects on lipoproteins following the intake of palm oil or soybean oil (a vegetable oil with more PUFA and less FAs than palm oil), have shown no substantial difference in the serum lipid profile, except for a increase of cholesterol HDL with palm oil (Zhang et al. 1997; Muller et al. 1998; Al-Shahib and Marshall 2003; Pedersen et al. 2005; Vega-Lopez et al. 2006; Utarwuthipong et al., 2009). Comparison with olive oil has shown, in some studies, either no effect or an increase in total and LDL cholesterol with palm oil (Ng et al. 1992; Choudhury et al. 1995; Truswell 2000).

A diet enriched in PA slightly increases LDL and HDL cholesterol levels but the HDL / LDL ratio, which is a valuable risk taker of cardiovascular disease, changes little.

There is currently no clear evidence of the negative role of PA for health and much less for palm oil native, which is a complex food matrix, in which the PA is only one of its components.

However, native palm oil undergoes various processes during the industrial production process. Oils, especially vegetable oils, are refined at high temperatures (about 200 ° C) where they undergo partial hydrolysis of TG with oxidation of glycerol, which leads to the formation of 3-monochloropropanediol (3-MCPD) and 2-mono-chloropropanediol (2-MCPD). The highest levels of these compounds have been observed during palm oil refining. In 2012, the Codex Alimentarius recommended the use of technological adjustments to reduce the levels of 3-MCPD in the finished product and in 2013, the International Agency for Research on Cancer (IARC) declared 3-MCPD as a possible human carcinogen (Group 2B ). EFSA recently updated the Tolerable Daily Intake of 2017-MCPD to 3 μg / kg body weight in 2.0 (EFSA 2018).

During the industrial processing the native palm oil like other vegetable oils also undergoes another chemical modification which is the inter-esterification or the randomization of the fatty acid which involves the positional redistribution of the FA chains inside the TG bringing to the formation of new molecular species. This process aims to modify the initial chemical-physical properties, making these oils more suitable for different applications in the food industry.

However, it has been seen that interesterification also has potential negative health effects due to the introduction into position sn-2 of chains of saturated fatty acids such as palmitic and stearic, which remain bound to glycerol, constituting the monoglyceride which is absorbed by intestinal cells. It would be precisely the absorption of palmitic acid in the monoglyceride related to the greater atherogenicity of palm oil (Kritchevsky 2000).

Hayes and Pronczuk (2010) in a meta-analysis they analyzed the studies that correlated the risk of cardiovascular disease with the intake of oils processed by inter-esterification. Some studies taken in examinations showed that a high intake of palmitic or stearic, esterified in sn-2, had negative biological effects on lipoproteins, blood sugar, insulin, immune function ed liver enzymes.

Finally, a review of the literature (Hooper et al., 2012) who examined studies on modification of the type of dietary fat and cardiovascular prevention concluded that reducing and modifying dietary FAs can reduce cardiovascular risk while maintaining the same total fat consumption but replacing a part with FAi, especially PUFA, but not with carbohydrates. The PREDIMED study, a randomized clinical trial on a high-risk Mediterranean population, reached the same conclusion. Zock et al., (2016), conclude that diets high in refined carbohydrates and sugars but low in fat are not effective at reducing CVD. The restriction of high FAs content animal fats, replacing them with high MUFA and / or PUFA vegetable oils found in fatty fish, has multiple metabolic benefits and is associated with lower risk of CVD and fatal stroke. Currently it has been shown that only fatty acids tranny are associated with an increased risk of CVD.

This protective effect of FAi is due to the fact that PA and OA contribute differently to insulin resistance. Studies on subjects who reduced their FA intake by increasing MUFA intake showed a significant improvement in insulin sensitivity (Vessby et al., 2001). Three main mechanisms have been reported in PA-mediated insulin resistance: (i) increased synthesis of deleterious complex lipids; (ii) impaired function of cell organelles; and (iii) inflammation mediated by receptors. In adipocytes of non-obese people, PA increases the expression of tumor necrosis factor (TNF-α), pro-inflammatory cytokines and IL-6 and decreases the mRNA levels of the anti-inflammatory cytokine IL-10 and adiponectin. Conversely, OA decreases the expression of pro-inflammatory cytokines and causes an increase in the expression of IL-10 and adiponectin.

OA has an anti-inflammatory action, has the ability to inhibit endoplasmic reticulum stress, prevent the attenuation of the insulin signaling pathway and improve the survival of the beta cells of the pancreas, which produce it. In conclusion, the cellular / metabolic effect of PA and OA are the opposite of each other.

Finally, in a recent meta-analysis, Ismail et al., (2018) whereas in the light of current data it is difficult to establish clear evidence for or against palm oil consumption related to CVD risk and specific cardiovascular disease mortality. Further studies are needed to establish the association of palm oil with CVD.

However, palm oil has possible health effects if abused, depending on the high concentration of FAs; its consumption, is not related to risk factors for cardiovascular disease in young people with a normal weight and cholesterol, if its intake is counted within 10% of saturated fatty acids that the nutritional recommendations indicate as the maximum daily value for this category of fatty acids. Conversely, the elderly and individuals with dyslipidemia or previous cardiovascular events or hypertension are at increased risk (DiGenoa et al., 2018).

Palm oil and children

It must be remembered that the monoglyceride with the PA in sn-2 (also called beta-palmitate), is a natural component of breast milk. When added to formulas it plays favorable metabolic and functional roles, with immunomodulatory and anti-inflammatory effects. In infant formulas, the percentage of PA in sn-2 it can be increased by using mixtures of interesterified triglycerides from different vegetable oils (Delplanque et al., 2015). The position of PA in sn-2 it makes it easier to absorb which promotes rapid growth in the first months of life (Listenberger, et al., 2003; Ertunc and Hotamisligil, 2016). In human milk, there are also optimal percentages of essential fatty acids (α-linolenic and linoleic), prevalent compared to saturated fatty acids, but above all the stereospecific distribution of the different fatty acids in the triglycerides guarantees advantageous absorption.

Important point not to forget that with weaning the caloric contribution of lipids decreases from 50 to 35-40% at 3 years and with a maximum of 10% in sFA, due to the concomitant increase in the quantity of carbohydrates. The percentage of fat in the diet will be further decreased to 30% in adulthood.

Conclusions

After an evaluation of the recent literature it is possible state the following.

  1. To date, there is no evidence that palm oil is a risk to human health (Marangoni et al., 2017). The important thing is to consume it with moderatetion, counting it together with animal fats in the 10% of saturated fatty acids that the nutritional advice indicates as maximum value daily (LARN, 2014).

  2. It is true that The only Native palm oil is a source of phytocompounds such as tocotrienols and tocopherols (vitamin E) and vitamin A.

  3. It is true that processed palm oil may contain toxic substances such as 2-MCPD and 3-MCPD, but in recent years the transformation processes used have significantly lowered the likelihood of formation. Based on scientific research, EFSA has revised the maximum daily limit of the 3-MCPD alone to 2.0 μg / kg body weight.

  4. It is true that the inter-esterification process, which leads to an increase in esterification in sn-2 of the PA, can have negative biological effects on lipoproteins, blood sugar, insulin, immune function and liver enzymes.

  5. It is incorrect to say that palm oil is not suitable for children. Palmitic acid is essential in childhood.

Paola Palestini

Professor of Biochemistry, UMilan-Bicocca University

Coordinator of the II level master in Nutrition and Applied Dietetics master ADA

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