Flaxseed oil contains several types of fatty acids (FAs). It contains a high concentration of alpha-linolenic acid (ALA), ranging from 40% to 60%, and is the most concentrated plant source of omega-3 FA identified to date.
FSO also contains unsaturated FAs, such as linolenic, linolenic acid, linoleic acid and oleic acid. Linoleic acid (LA or C18:2n-6) and oleic acid each contribute 15% to the total FA content of the oil. Due to the range of FA present, it contains precursors for the omega-3, -6 and -9 families. FSO may also contain varying amounts of the lignan, secoisolariciresinol diglycoside (SDG), which is a precursor to enterodiol and enterolactone.
Flax seeds contain 41 % fat, 28% dietary fibre, 21% protein and significantly higher amounts of lignans, which behave as phytoestrogens (Morris 2001). However, this review focuses on FSO.
Clinical note — Is FSO equivalent to the fish oils?
Flaxseed oil has been commercially promoted as the vegetarian or vegan alternative to fish oils, with many of the health benefits ascribed to fish oils also being attributed to the oil. A review of the literature suggests that FSO is unlikely to be equipotent with fish oils in the treatment of a variety of conditions.
The ALA present in FSO can theoretically undergo desaturation and elongation to synthesise eicosapentanoic acid (EPA) and docosahexaenoic (DHA), which are found in fish oil; however, most studies using oral FSO intake demonstrate only moderate increases in EPA and DHA remains unchanged (Allman et al 1995, Kelley et al 1993, Mantzioris et al 1994, Nestel et al 1997). Although results from one early study suggest that increases in DHA levels may be achieved with long-term supplementation (Cunnane et al 1993), more recent studies fail to confirm this result (Harper et al 2006, Hussein et al 2005).
Conversion rates of ALA to EPA and docosapentaenoic acid (DPA) are reported to be < 10% (Harris et al 1997) and approximately 8%, respectively, whereas the DHA yield ranges from 0% to 0.5%. One explanation for this is that DHA synthesis is under separate regulatory control, a hypothesis supported by enzymatic studies (Burdge 2004). This means a 20 mL serve of FSO, providing 11.1 g of ALA, would result in a maximum of 880 mg DPA and 5 mg of DHA.
Adding to this puzzle is a wide range of other variables that can inhibit the conversion of ALA into its metabolites. For instance, high dietary intake of linoleic
acid (LA), common in Western cultures, inhibits both the uptake of ALA and its conversion to long-chain metabolites. An interesting study conducted in 1998, which used radioactively labelled ALA, showed that a diet high in omega-6 fats reduced conversion by 40-50% (Gerster 1998). This adds weight to the argument that the ratios of FAs may have the primary influence on their resultant health benefits. The authors of this study suggest that the ratio of omega-6:omega-3 should not exceed 4.
Other studies have reported abnormal or compromised activity of the delta-6 and delta-5 desaturase enzymes in the elderly, diabetics and patients with a variety of metabolic disorders, as well as those individuals with increased dietary intake of saturated fats, trans-fatty acids and alcohol (David & Kris-Etherton 2003). Studies using radioisotopes of ALA have revealed significant gender differences in conversion capability, with women demonstrating higher levels of FA metabolites. It is believed this is due to their higher oestrogen levels, a theory supported by the increased conversion capacity evident in women taking synthetic oestrogens and speculated as representing a physiological adaptation that ensures adequate EFA delivery to the foetus in pregnancy (Burdge 2004).
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