Discussion
We examined the effects of flaxseed consumption on anthropometric indices, serum leptin, lipids and adiponectin in overweight or obese women. Our findings indicated that the flaxseed group had significant reduction in weight and anthropometric indices such as waist and hip circumference and WHR. However, flaxseed consumption did not result in statistically significant effect on lipid profile compared to placebo.
Our data suggesting that flaxseed may have additional benefits on central adiposity compared with controls is in line with previous studies (16). Park et al. (34), found that flaxseed lignan (primarily secoisolariciresinol diglucoside) [SDG] might provide beneficial effects on obesity via reducing weight and fat accumulation. Wu et al. (35) showed that flaxseed supplementation (30 g/d) for 12 weeks reduced central obesity, weight and waist circumference when combined with healthy lifestyle counseling. Conversely, Pindea et al. (36), reported no significant change in weight, BMI, and waist circumference following supplementation with 30 g/d flaxseed for 8 weeks. We assume that the duration of the study (less than 12 weeks) might be the reason why no significant anthropometric effects were observed (37).
The exact mechanisms by which flaxseed can ameliorate abdominal obesity remain unclear. Some studies have suggested that a diet rich in PUFAs may result in reduction of abdominal obesity (35), because increasing PUFAs in the diet might act as an important modulator for body fat deposition, Also according to previous studies, the high content of SDG can reduce or prevent obesity through increased fat oxidation (3, 38).
Very few randomized clinical trials have examined the effect of flaxseed supplementation on blood adiponectin and leptin concentration in people who are healthy (31, 39, 40). Some of experimental studies reported remarkable effects of flaxseed on leptin and adiponectin (3,7) and also altered circulating level of these hormone following supplementation with flaxseed (7, 23).
In the present study, the serum concentration of adiponectin increased significantly in the flaxseed group compared to control group. Cassani et al. (41) also showed that weight loss diet with 60 g/d flaxseed supplementation in men with cardiovascular risk factors could improve adiponectin levels. Contrary to present study findings , Hutchins et al. (42), found no significant change in adiponectin levels with flaxseed supplementation in obese men and women with pre-diabetes. This contradictory finding might be due to the association of adiponectin with insulin resistance. According to other studies, response of adiponectin to an intervention might be quite different in an insulin-resistant population than in insulin-sensitive individuals (43-45). Furthermore, Nelson et al. (31) found a decrease in adiponectin levels of healthy overweight adults that were treated by flaxseed oil for 8 weeks which is consistent with our findings. The present study demonstrated that this effect might be attributed to a reduced demand for adiponectin’s anti-inflammatory actions in face of high omega-3 fatty acids. In fact, in the case of adiponectin, the dosage of flaxseed given in different studies is critical, because the insulin-sensitizing and anti-inflammatory effects of ALA (the main component of flaxseed products) might deactivate the effects of adiponectin and result in a decreased demand for adiponectin (46). On the other hand, some researchers did not find significant correlation between PUFAs and circulating levels of adiponectin (47). So, they suggested ALA as an activator of peroxysomal proliferator activated receptor gamma (PPARγ) in adipocytes.
The adiponectin inducing effect of flaxseed might be because of its rich content of ALA. It seems that ALA is involved in increasing adiponectin secretion through stimulating transcription factors PPARγ (39). PPARγ is one of the key transcription factors which regulates adipogenesis and it can also control expressions of adiponectin, leptin and glucose transporter type 4 (GLUT4) (48). Moreover, SDG in flaxseeds could act as a PPARγ agonist and regulate adiponectin through an increase in PPARγ DNA binding activity in adipocytes (3). So, Flaxseed could probably be an effective component which can alter the metabolic process in adipose tissues in favor of lower visceral fat accumulation.
It should be noted that different outcome from flaxseed intervention may be related to inter-individual differences involved in the metabolic processes, resulting in altered adiponectin levels in circulation (15).
Previously high concentration of leptin in obese individuals has been reported in several studies (10, 49). We found reduction in serum leptin of both groups. However, this reduction was only significant in the flaxseed group. McCullough et al. (7) have found that leptin expression correlated positively to ALA content of flaxseed, so its effects on obesity related diseases might be due to a change in leptin expression, but in a study by Taylor et al. (37) which investigated the effect of dietary milled flaxseed and flaxseed oil on patients with type2 diabetes, leptin concentration did not change. Zhou et al (50) have suggested that insulin resistance might be correlated to depressed desaturase enzyme activity, so these patients are not able to transform ALA to Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA). This reason could probably why Taylor study could not show beneficial effect of omega-3 PUFAs from flaxseed on leptin levels.
Our findings that flaxseed consumption did not have a significant effect on lipid profile is consistent with that reported by Kaul et al., which showed that among apparently healthy adults, intake of 2 g/day flaxseed oil for 12 weeks had no significant effect on the lipid parameters in blood (51). In contrast, several clinical trials conducted in individuals with elevated levels of blood lipids, reported the beneficial effect of flaxseed supplementation on decreasing serum lipids (22, 52-55). Torkan et al. showed that consumption of 30 g/d of flaxseed powder in hyperlipidemic patients for 40 days caused a significant decrease in TG, TC, and LDL-C compared to the placebo (54). Moreover, another clinical trial conducted in postmenopausal women with hypercholesterolemia showed a significant reduction in TC and LDL-C compared to the placebo following the flaxseed supplementation at the dosage of 30 g/day for 12 weeks (53). In the present study, the mean serum concentrations of lipids in both study groups were within the normal ranges, which could be the reason for disagreement of our results with previous studies. Not all of the clinical trials that were conducted on patients with hyperlipidemia, resulted in significant effects of flaxseed on blood lipids outcomes. Paschos et al. for example, found that the intake of 15 ml of flaxseed oil for 12 weeks had no significant effect on lipid parameters in patients with dyslipidemia (56). Also, in a study among 62 individuals with baseline values of LDL-C between 130 and 200 mg/dl, intake of 40g/day of flaxseed-containing baked products for 10 weeks did not significantly change LDL-C and even caused a significant decrease in HDL-C in men, but not in women (57). Besides the initial serum lipids, it should be noted that some methodological differences such as small sample size, short duration of follow-up, type of the flaxseed product, the dosage of supplementation, and the degree of adherence to the intervention may be the possible reasons for the discrepancy between the studies.
Several mechanisms have been suggested for the beneficial effect of flaxseed on blood lipids. Flaxseed has a high content of ALA, an omega-3 fatty acid found in plants, as well as its highest amount of lignin among the plant foods (58). It has been shown that these compounds could reduce TC and LDL-C by reducing the gene expression of Sterol Regulatory Element-Binding Protein 1-C (SREBP-1c), which is involved in synthesis of fatty acids, and increasing the mRNA expression of Peroxisome Proliferator-Activated Receptor-α (PPAR-α), which stimulates β-oxidation of fatty acids (22, 24, 59). In addition, flaxseed is a rich source of dietary fibers, both soluble and insoluble. Dietary fiber is proposed to reduce blood cholesterol mainly through increasing bile acid excretion, synthesis of short-chain fatty acids, and insulin sensitivity (60).
This study has some important strengths including the use of an appropriate placebo for flaxseed. In addition, we used whole grain flaxseed instead of flaxseed oil or lignan. Nonetheless, our findings should be considered in light of several limitations. In particular, our sample size was small. Also, the present study cannot distinguish if the effects are due directly to ALA or lignin in flaxseeds. Moreover, whilst some studies found significant effect of flaxseed on lipid profiles, ours found no such effect. The possible reasons for non-significant results following the whole flaxseed products may be due to the differences in the quality of the test product, the amount of bioactive components and their bioavailability in the presence of some compounds such as glycosides and phytic acid (57) in the flaxseed products.