Because of them, we hate margarines and industrial sweets that contain them. Indeed, trans fatty acids are harmful, but we have been ingesting them for a long time from meat and milk. There are different scientific opinions as to whether the benefits and harms of natural and industrial trans fatty acids differ. In the divergence of these two opinions, we fell in love with conjugated linoleic acid (CLA) because of weight loss and pomegranate oil in cosmetics.
Sources of trans and conjugated fatty acids in the diet
In the chemistry of fatty acids, it has already been said that there are multiple sources of trans and conjugated fatty acids in food. There are two dominant sources: ruminant meat and milk (rTFA), and industrial trans fatty acids (iTFA) obtained by hydrogenation of vegetable oils (margarines).
According to a large TRANSFAIR study by Aro et al., Conducted in 14 European countries, the total amount of rTFA depends on the species from which milk and meat are obtained.
|Source||% of trans acids from total fatty acids|
|Cow's milk and dairy products||3,2-6,2|
|Goat/sheep milk and dairy products||2,7-7,1|
The authors, logically, found that there are numerous seasonal variations, but also variations depending on the diet of domestic animals.
So they found that milk in summer contains 57% more trans fatty acids. It reminded me of an unusual, thousand-year-old claim from Hildegard of Bingen that milk is less healthy in summer than in winter. The dominant fatty acid is vaccenic acid.
After limiting the use of industrial trans fatty acids in the diet, primarily margarines, there was an improvement in the ratio of natural rTFA to iTFA. Kuhnt et al. investigated TFA sources in German diet and concluded that there is a higher proportion of rTFA intake compared to iTFA, except in some products (potatoes fried in oil, some sweets). According to the already cited TRANSFAIR study, rTFA intake varies from 28-79% of total TFA, while in the Mediterranean diet this ratio is usually higher than 50%.
Effects of trans and conjugated fatty acids
Mechanism of harmful action of trans acids
The very name of trans fatty acids has become quite infamous, primarily due to industrial margarines. Legal restrictions on these fatty acids in food have developed people’s awareness, so that today some large food chains and margarine producers even boast in marketing campaigns that their products do not contain trans fatty acids. And that is to be commended. However, the question arose – are all trans fatty acids harmful? It has already been described how rTFA and iTFA differ in chemistry, so it is obvious that they also differ in action. Several groups of authors have tried to decipher whether there are clear epidemiological differences, based on the mechanism of action, between natural, rTFA, and synthetic iTFA.
The mechanism of adverse action of iTFA is only partially elucidated. A very large number of studies agree on one thing: TFAs raise the level of harmful cholesterol (LDL) in the blood and reduce the level of “good” cholesterol (HDL). Thus, the risk of cardiovascular diseases increases. The mechanism of this harmful inversion is somewhat unclear. Attia-Skhiri et al. in their review consider several proposed models:
- increased production of ApoB100 protein involved in the formation of LDL lipoprotein particles. High levels of ApoB100 are a negative prognostic marker for cardiovascular disease. However, an elevated level of ApoB100 production alone would not be sufficient to increase LDL cholesterol, but it has been observed that increased TFA intake reduces the breakdown of LDL particles.
- increased activity of CETP (cholesterol ester transfer protein) and PLTP (phospholipid transfer protein) which reduce the proportion of HDL cholesterol. However, several studies have not confirmed an increase in CETP activity in the presence of TFA.
Of course, these are just some of the proposed mechanisms of action. Chen et al. believe that there is an increased risk of developing atherosclerosis caused by TFA, based on reducing the response of vascular endothelium to TGF-β (transforming growth factor beta), which increases the risk of deposition and inflammatory process in atherosclerosis.
Whatever the mechanism, the consequences are relatively clear. An increase in LDL cholesterol leads to an increased vascular disease risk, and other immune mechanisms, such as action on TGF-β, also contribute to increase this risk. Due to such data, there has been a restriction of industrial trans fatty acids in food.
Natural (rTFA) versus industrial (iTFA) fatty acids
It took a lot of effort to “separate” the effects of rTFA and iTFA on humans. It is a demanding job in epidemiological terms, as most of the population ingests food from both groups of TFA. The mechanism itself is a little easier to “dissect” in animal and human studies.
Gebauer et al. compare seventeen epidemiological studies on the impact of rTFA on the body, more specifically on the cardiovascular system and the risk of tumours. These studies did not agree – some showed an increase in risk, some did not show a statistically significant increase in risk, and some showed an inverse correlation (decrease in risk). The meta-analysis, i.e. the analysis of all studies, shows that rTFA does not contribute to risk, while iTFA does. This was a very important observation in assessing the impact of these two TFA groups. In ten clinical studies of the effects of rTFA, three studies found an increase in LDL cholesterol, one showed a decrease, and the others found that there was no statistically significant effect of rTFA on LDL cholesterol levels. These varied results indicate that other dietary factors that cannot be ruled out in the study affect the action of rTFA. The authors analyse a total of 35 animal studies. Although the results of these studies are not unequivocal, the general conclusion is that rTFAs show more beneficial than adverse effects. This is a very important conclusion. Although rTFA like vaccenic acid cannot be viewed as a possible therapeutic intervention, we can conclude that their presence in food is less harmful than iTFA.
Brouwer et al. publish a different conclusion. Based on 39 clinical studies, they determine that dietary TFA intake should generally be reduced regardless of whether rTFA and iTFA are involved.
Therefore, the official position of medicine is still unclear and it will take time to reach a final judgment. These opinions speak in favour of modern trends in nutrition, which emphasize the need to reduce the intake of dairy foods and limit the consumption of red meat to a reasonable extent. In these measures, the complete elimination or drastic reduction of iTFA is entirely justified. However, the risk of TFA itself, based on the application of HDL and LDL cholesterol levels, is always associated with other factors- diet and lifestyle.
Conjugated linoleic acid (CLA)
Conjugated linoleic acid is found, along with vaccenic acid, in ruminant milk and meat. Its content is relatively low, so for commercial use it must be isolated in order to be used as a raw material for the production of food supplements. It is isolated not from meat and dairy products, but from safflower oil (Carthamus tinctorius). There are 28 described isomers of CLA, but in ruminants meat and milk the largest share has cis-9, trans-11 CLA (rumenic acid). Safflower oil also contains high levels of trans-10, cis-12 CLA. This is important information for later discussion about the effect of the CLA.
Conjugated linoleic acid is also produced in the human intestine. Devillard et al. publish how the genus Bifidobacterium , present in the human microbiome (flora), metabolizes linoleic acid to vaccenic and rumenic acid. Based on the fact that CLA is isolated from the linoleic chemotype of safflower oil, it has encouraged some people to use this oil instead of CLA supplements. That is not justified. Namely, safflower oil contains too low a level of CLA. As early as 1998, Herbel et al. published how safflower oil consumption does not raise CLA levels in blood.
The history of CLA research begins by observing the effect on tumour development. Ha et al. compared the effects of CLA and linoleic acid, and found that CLA, unlike linoleic acid, reduces the incidence of chemically induced tumours in mice. However, this work would be forgotten as many others investigating the effect of natural substances on tumours. The situation changed when Park et al. proved that CLA in mice reduces adipose tissue by 57- 60% which was a spectacular result even for an animal model. Other groups of authors set out to investigate these effects in humans as well. But despite a very large number of smaller clinical studies, the results were very different. Kennedy et al., Silveira et al. and Benjamin et al. publish a relatively similar conclusion: based on all studies, we cannot conclude the efficacy of CLA in obesity. Indeed, several studies have shown an increase in total body weight. Interestingly, Gaullier et al. observed that CLA affects adipose tissue of precisely defined parts of the human body- legs and abdomen. Furthermore, it seems that CLA can have a more beneficial effect only if the weight loss regimen is accompanied by exercise. Michishita et al., comparing the effect of an amino acid supplement without CLA, show that CLA is superior in reducing the ratio of abdominal to hip diameter in the exercise regimen. Interestingly, this is exactly how CLA is advertised, as a dietary supplement for weight loss with exercise. This explains the result of other studies where this factor was not taken into account. Macaluso et al. analysed the results of seven studies on physical performance in exercise. Although the results of these studies are diverse, the authors conclude that there is a clear indication that CLA supplementation has a beneficial effect on the ratio of adipose to muscle tissue, especially in doses above 3g per day and over a longer period of time. Because of all of the above, CLA is popular today primarily among people who exercise.
As always with dietary supplements, the question was whether they were harmful. In 2007, Iwata et al. examined unwanted side effects of 3,4 and 6,8g of CLA daily for 12 weeks. They found that during this time the use of 3,4 grams was safe, but that a dose of 6,8g increased the level of liver enzymes which is not a desirable effect. It was this study that set the dose at 3-3,4 grams of CLA per day, but the scientific community has previously been interested in the mechanism of harmfulness. Larsen et al. already warned of the possible harmful effects of one of CLA components in commercial preparations- trans-10, cis-12 CLA. Namely, this isomer of CLA inhibits stearoyl-coenzyme-A, an enzyme that produces unsaturated fatty acids from saturated fatty acids. This leads to an unwanted increase in saturated fatty acids. Furthermore, in cows and rats CLA reduces milk production. Although this effect has not been well studied in humans, it is wise to avoid CLA supplements during breastfeeding. The U.S. Agriculture Agency conducted a study in which they proved the redistribution of other unsaturated fatty acids, DHA (docosahexaenoic acid) in organs- CLA reduces DHA in the heart and increases it in the spleen. In the aforementioned study, Benjamin et al. present other possible risk effects, such as a paradoxical effect on fat gain, insulin resistance, and inflammatory markers. Most of these phenomena were related to the trans-10, cis-12 isomer. Therefore, a study that would prove the safety of using CLA was definitely needed. The need to accurately define the ratios of trans-10, cis-12 and cis-9 trans-11 isomers was emphasized. In a two-year study Gaullier et al. examined the impact of 3,4 g CLA daily with ratios of the above isomers 1:1. They found that this dose was safe, and thus “saved” CLA as a dietary supplement. But this is a reminder to take good care that the isomer ratio is at least 1:1 in favour of cis-12 and cis-9, trans-11 isomers in the products.
Kennedy et al. analysed possible mechanisms of action in their work. It seems that the beneficial effect is shown due to the reduction of calorie intake, more favourable energy consumption in the body and the formation of adipose tissue (adipogenesis).
Pomegranate seeds oil is extremely rich in punicic acid, another well-known conjugated fatty acid. Today, its use is mostly limited to cosmetics as an “anti-age” ingredient, and some more expensive commercial cosmetic lines use this ingredient in products.
It is less known that this acid shows other beneficial effects on the human body. Mirmiran et al. used 2x400mg pomegranate seed oil in a clinical study as a dietary supplement and demonstrated a beneficial effect on triglyceride levels in patients with elevated blood triglycerides. This is an interesting study because a relatively small number of natural substances affect triglyceride levels. Interestingly, this oil did not act to lower cholesterol and blood glucose, suggesting a specific and still unclear mechanism of action. Asghari et al. tried to prove whether this effect is achieved by reducing proinflammatory cytokines in patients with elevated blood lipid levels, but have failed to demonstrate such a mechanism of action. Several preclinical studies have found a beneficial effect in models of osteoporosis, inflammatory bowel disease, obesity and tumour, but this application has yet to possibly gain its application in clinical practice. A clinical study of pomegranate seed oil did not show a beneficial effect on menopausal symptoms, therefore oils rich in γ-linolenic acid (GLA) still remain the first choice in the treatment of these ailments.