It has been proposed that diets high in fat are have the potential of modulating endocannabinoids levels irrespective of their FA composition [14–16]. Regarding the dietary intake as one of the important factors in determining of the endocannabinoids tones, it appears that complete investigation to identify dietary patterns can be helpful in understanding the association of diet and AEA, 2-AG levels. To the best of our knowledge, this study was the first study which has evaluated the association of dietary patterns with endocannabinoids levels in overweight/obese women.
In the current study, three major dietary patterns were identified in in overweight/obese women: the "western", the "healthy", and traditional dietary patterns. Our results were in line with those of Esmaillzadeh and colleagues who identified three major dietary patterns among 486 obese women: healthy, western, and Iranian dietary pattern [17]. Also, in nurses with premenstrual syndrome and female with metabolic syndrome three major dietary patterns including "western", "healthy", and "traditional" patterns were extracted [18, 19]. Additionally, in a rather large sample size (1433 Iranian adults), western, semi healthy and healthy fat patterns were identified [20]. However, in a study by Hu et al. among men aged 40–75 years two major patterns: the “western” pattern (high intakes of processed meat, red meat, French fries, high-fat dairy products, refined grains, sweets, and dessert) and the “prudent” pattern (high intakes of whole grains, legumes, vegetables, fruit, fish, and poultry) were reported [21]. Agodi et al., derived two major dietary patterns, the first one named western which was high in hot-dog, hamburger, processed meat, fries, white bread, and salty snacks. On the contrary, the other dietary pattern named prudent was specified by high intake of nuts, cereals, cooked and raw vegetables, fruit, fish, jam and honey [22]. Compared to previous studies, the observed differences in our findings might stem from the different types of the diseases, the number of food items in used FFQ and differences in geographic areas of conducted studies.
In present study, high adherence to western dietary pattern resulted in significantly higher levels of AEA and 2-AG compared to the high adherence to healthy dietary pattern. The positive association between the western pattern and endocannabinoids levels could be due to the food groups components found on this dietary pattern. In this pattern organ meat, processed meat, pizza, French fries, soft drinks were dominant. There is notable shift to western dietary pattern consumption greatly loaded in red meats, fast foods, and soft drinks in developing countries such as Iran [20]. Moreover, the prevalence of high fat diets (~ 40% of energy) is rising globally due to their palatability and also the fats low cost [23, 24]. ECS are lipid mediators and their biosynthesis can be modified directly by dietary fat intake.
In animals, diets high in fat prompt binge eating behaviors [25] and lead in significantly elevated levels of AEA and 2-AG [26, 27] and intestinal motility [28] which in turn can increase the stimulation of cannabinoid receptor. Also, high fat diets cause an increase in FA synthesis which is partially triggered by chronic CB1 activation and subsequent induction of expression of the lipogenic transcription factor sterol regulatory element-binding protein-1c (SREBP-1c), and greater production of acetyl coenzyme-A carboxylase-1 and fatty acid synthase production [27]. As a result, the fatty acid biosynthetic pathway might indicate a common molecular target for the central appetitive and peripheral metabolic effects of endocannabinoids. Also, a decrease in MGL and FAAH activity and an increase in NAPE-PLD action have been found to cause an elevation in AEA and 2-AG levels in response to high fat diets in animals [29].
Additionally, since de novo synthesis of ω-6 and ω-3 fatty acids is not possible, the dietary intake of these fatty acids is reflected in the tissues fatty acid composition [30]. A high dietary intake of linoleic acid (ω-6) can raise the arachidonic acid synthesis triggering EC production [31]. Elevated levels of 2-AG in the whole brain and plasma of adults and developing animals was observed in rats deficient in ω-3; whereas, supplementation with ω-3 seems to decrease AEA levels [32, 33]. Furthermore, Alvheim et al., showed that in a diet with 60% of energy from lipids rising energy from linoleic acid from 1–8% led to an elevation in AA in the red blood cells and liver and a subsequent 3-fold increase in both AEA and 2-AG [34].
Researchers have largely focused on the macronutrient portions rather than particular FA intakes. We evaluated the association of dietary patterns with AEA and 2-AG levels which can be regarded as the main strength point of present study.
In light of some limitations the presented findings should be interpreted: the cross-sectional design, which makes it impossible to demonstrate the causality of the interactions. A FFQ with standard portion sizes was applied to estimate the food intakes in which the measurement error might not be precluded and may contain inaccuracies.