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.