Essential fatty acids (EFAs) are important nutrients, both for those following a low-calorie diet and for those simply wishing to ensure optimal nutrition. However, the proportions of the omega-6 to omega-3 EFAs in the daily intake are nearly as important as the absolute amounts consumed, since the balance of eicosanoids generated from the dietary intake is the deciding factor in homeostasis and for many metabolic processes. Since both omega-6 and omega-3 EFAs share the same metabolic pathways leading to the eicosanoids, an imbalance in intake can readily lead to an imbalance in the eicosanoids ultimately produced in the body. Much reference is made in this section of the website to Bari-EFA®, since as far as we can ascertain, this is the only product that has been developed specifically with maintenance of a correct balance in mind. The figure which follows illustrates the metabolic pathways leading from the parent EFAs to the three families of eicosanoids, and should serve to reinforce the need for “balance”!
Except under extreme circumstances, the essential fatty acids (EFAs) have no therapeutic applications, but there is a considerable body of evidence that a deficiency of EFAs, whether due to a direct dietary lack or to the presence of interfering substances (such as trans fatty acids in the diet), can cause a very wide range of metabolic and pathologic disorders, one of which is a decrease in thermogenesis (the increase in metabolic rate which occurs in response to food containing, particularly, protein or on consumption of thermogenic herbs).
There is also considerable evidence that an imbalance in the dietary intake of specific EFAs (of omega-6 and omega-3 families) can likewise cause a variety of disorders, including thrombosis, a predisposition to some types of cancer, and gallstones.
With respect to both interfering substances or imbalances, the composition of stored body fat (which broadly reflects the composition of dietary fat consumed) may under certain circumstances play a large role.
This section summarizes the consequences of EFA deficiencies and imbalances, and indicates how these may be eliminated or ameliorated by the use of a correctly formulated and balanced product, such as Bari-EFA®. The Structure/Function statement for Bari-EFA® summarizes the roles of the EFAs in human physiology and metabolism:
The gamma-linolenic acid (GLA) present in borage seed oil (Borago officinalis), and the eicosapentaenoic and docosahexaenoic acids (EPA and DHA) present in many marine oils, are respectively members of the omega-6 and omega-3 families of essential fatty acids. Because they have already undergone some degree of metabolic transformation in the species from which they are obtained, they are more efficient precursors for eicosanoids (prostaglandins) than are the parent essential fatty acids from these families, linoleic acid (omega-6) and a-linolenic acid (omega-3). Eicosanoids are required for the optimal function of many physiological and metabolic systems in the human body. This statement has not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
- 1 The classical situation. The body uses EFAs to make small amounts of substances which are called eicosanoids, though they are better known under the name of prostaglandins. The prostaglandins belong to three families, and they must be in balance to maintain homeostasis, because prostaglandins from the different families often have opposing effects. Prostaglandins regulate nearly every biochemical reaction at cellular level, and their presence at suboptimal levels is characterized by a variety of disorders, some serious. Since EFAs play such a basic role in the function of the body, it is to be expected that their deficiency could result in a wide variety of disorders, some subtle and detectable only by refined testing procedures, others not so subtle, though the relationship to dietary intake of EFAs, or lack thereof, may not always be obvious. It is precisely the protean and variable nature of EFA deficiency states that renders their recognition and acknowledgement so difficult. Siguel and Schaefer (1988), for example, state:
- 2 EFA deficiency and thermogenesis.
- 3 EFA metabolism.
- 4 Storage of fatty acids in the body.
- 5 Release of stored fat.
- 6 EFA requirements.
The classical situation.
The body uses EFAs to make small amounts of substances which are called eicosanoids, though they are better known under the name of prostaglandins. The prostaglandins belong to three families, and they must be in balance to maintain homeostasis, because prostaglandins from the different families often have opposing effects. Prostaglandins regulate nearly every biochemical reaction at cellular level, and their presence at suboptimal levels is characterized by a variety of disorders, some serious. Since EFAs play such a basic role in the function of the body, it is to be expected that their deficiency could result in a wide variety of disorders, some subtle and detectable only by refined testing procedures, others not so subtle, though the relationship to dietary intake of EFAs, or lack thereof, may not always be obvious. It is precisely the protean and variable nature of EFA deficiency states that renders their recognition and acknowledgement so difficult. Siguel and Schaefer (1988), for example, state:
In general, a deficiency of essential fatty acids will lead to histological changes in all body organs and, therefore, it is difficult to diagnose a specific fatty acid deficiency from clinical symptoms.
These Authors review EFA deficiency syndromes in depth, and provide evidence that relative essential fatty acid deficiency may play a causative role in many of our “diseases of civilization”, including:
Heart disease, hyperlipidaemia, hypertension, diabetes mellitus, rheumatoid disorders, brain dysfunction, visual disorders, skin diseases.
It is particularly of interest that these Authors indicate that the obese may have higher EFA requirements, and they further note “supplements may allow . . . . especially overweight individuals to meet the nutritional requirements for EFA . . “.
In further studies, it has been demonstrated that EFA deficiency is indeed associated with coronary artery disease (Siguel and Lerman, 1993, 1994), neuropathy and impaired immune function (Holman, 1998), that it occurs in patients with chronic gastrointestinal disorders (Siguel and Lerman, 1996), that it is found in pregnancy and lactation (Holman et al., 1991), that it is associated with anorexia nervosa (Holman et al., 1995) and that EFA “insufficiency” (subclinical EFA deficiency) is relatively widespread in North America (Siguel and Lerner, 1994).
A report by the FAO/WHO (FAO/WHO, 1980) exemplifies the point of variability of the symptoms of EFA deficiency:
The severe clinical manifestations of EFA deficiency in humans . . . . . include eczematous lesions, refractive impetigo, dry scaly skin, coarse and sparse hair, frequent stools, perianal irritation, oozing in the intertriginous folds, and generalized erythema. These symptoms are variable, and not useful for quantified estimates of EFA status.
Possibly because they approach the topic from the point of view of total parenteral nutrition (TPN), which in the early days (before clinicians realized the importance of EFAs) was rather an extreme situation, Goodwin and Wilmore (1988) are quite dramatic in describing the consequences of EFA deficiency:
When lipids are omitted from the diet for periods exceeding 1 – 2 weeks, unsaturated fatty acid deficits occur and cause a characteristic syndrome. This essential fatty acid deficiency presents with dermatitis, hemolytic anemia, thrombocytopenia, impaired wound healing, loss of hair, and early death.
EFA deficiency and thermogenesis.
It has been known for some time that rates of weight loss can be increased if intake of essential fatty acids is adequate; EFAs of the omega-6 and omega-3 families have been shown to increase thermogenesis.
It is not known whether this is an intrinsic consequence of their mechanisms of action (as precursors for eicosanoids and as membrane constituents), or whether it merely represents the rectification of a pre-existent but unsuspected EFA deficiency.
Goubern et al. (1990), for example, showed that brown adipose tissue cells recovered from EFA-deficient rats responded poorly to noradrenaline (the direct initiator of thermogenesis), but that rectifying the deficiency normalized the response. Alam et al. (1995) also presented evidence that cyclic adenosine monophosphate (cAMP) production can be impaired in EFA deficiency, which would manifest as decreased sensitivity to catecholamines, with subsequent reduced thermogenesis. Clandinin et al. (1992) similarly showed that linoleic acid increased the binding of insulin to adipose tissue cells (and thus improved their metabolic responses). These researchers also reported that omega-3 EFAs increased the responsiveness of muscles to insulin, and significantly increased the rate of glucose uptake by the muscle. Takada et al. (1994) showed that a dietary intake of gammalinolenic acid increased the ability of the liver to oxidize fats.
At an empirical level, Bucci (1994) cites studies which have shown that supplementation with long chain omega-3 EFAs (from fish oil) improves aerobic metabolism, while some research groups (Cunnane et al., 1986; Jones and Schoeller, 1988) have shown that increases in EFA intake improve rates of weight loss by a presumed thermogenic mechanism and also improve the efficiency of energy-generating metabolic processes in the body.
The parent omega-6 and omega-3 EFAs are linoleic acid (18:2n6) and alpha-linolenic acid (18:3n3). Under normal circumstances these are the predominant EFAs found in the diet, but those who eat red meat also obtain arachidonic acid (20:4n6) in the diet (Jones, 1993a, 1993b). The parent EFAs share the same enzymes for their further transformation into eicosanoids (prostaglandins), of which the most important are the delta-6-desaturase which desaturates both 18:2n6 and 18:3n3 to gammalinolenic acid (GLA; 18:3n6) and stearidonic acid (18:4n3) respectively (Sprecher, 1977), and the various enzymes, including cycloxygenase, which convert the three 20-carbon EFAs, dihomogammalinolenic acid (20:3n6), arachidonic acid (20:4n6) and eicosapentaenoic acid (20:5n3) into eicosanoids of the PG1, PG2 and PG3 families.
The delta-6-desaturase is important because it is inhibited by trans fatty acids; dietary trans fatty acids thus effectively cause an EFA deficiency (Hill et al., 1982).
The various enzymes that convert the 20-carbon EFAs into eicosanoids are important, since they are subjected to complex competitive inhibition (all three EFAs compete for the same enzymes), and thus the “mix” of EFAs available to these enzyme systems will govern the balance of the eicosanoid families produced.
This is important because eicosanoids of the PG2 family (derived from arachidonic acid) are those which, for example, mediate inflammation and cause platelet aggregation (the first stage of thrombosis), and in this they are opposed by eicosanoids of the PG1 and PG3 families, particularly those of the PG3 family derived from eicosapentaenoic acid (EPA). In brief, an imbalance in favour of arachidonic acid predisposes to inflammation and thrombosis (as well as other serious disorders, including cancer and gallstones; vide infra).
Storage of fatty acids in the body.
The fatty acid composition of the stored fat reflects the composition of fat eaten. If the diet contains trans fatty acids, they can be found in quite high levels in adipose tissue (Chen et al., 1995). Arachidonic acid (much from red meat; Phinney, 1996) is also stored in adipose tissue (London et al., 1991); vegetarians have lower levels of stored arachidonic acid (Phinney et al., 1990b).
Release of stored fat.
Under conditions of an energy deficit (for example, when dieting), or when energy reserves are called upon (for example, prolonged exercise, such as jogging), both trans fatty acids and arachidonic acid can be released to give high levels in the blood (Rossner et al., 1989; Wilson et al., 1989; Phinney et al., 1991). At such times, a trans fatty acid-induced EFA deficiency may develop, or an imbalance in eicosanoid families, favouring PG2 eicosanoids, may occur.
An EFA deficiency, even when caused by endogenous release of trans fatty acids previously stored, may cause one or more of the conditions classically associated with EFA deficiencies (FAO/WHO, 1980; Siguel and Schaefer, 1988; Goodwin and Wilmore, 1988), as well as general impairment of metabolic efficiency and specific impairment of thermogenesis (Jones, 2000, in press). An imbalance in favour of arachidonic acid may result in thrombosis (Jones, 1993a, 1993b; Zhang et al., 1997), inflammatory disorders or gallstones (Marks et al., 1991, 1992, 1997), and possibly other serious conditions, including cancer (Phinney, 1996).
Based on the guidelines issued originally by FAO/WHO (FAO/WHO, 1980), adopted by many countries, the omega-6 intake as linoleic acid (18:2n6) should be 3% of calories, which corresponds to about 9 grams per day. A further requirement that the intake of alpha-linolenic acid should be 0.5% of calories has been adopted by some Governments, and with upper and lower limits of 10:1 and 4:1 for the ratio of linoleic to alpha-linolenic acids. The FAO (FAO, 1995) has now also stated that the ratio of linoleic to alpha-linolenic acids should be in the range of 5:1 to 10:1. To achieve these requirements on a normal diet requires a minimum fat intake of 22% of calories, based on carefully selected edible oils (Jones, 1994).
HOWEVER (and this is important), this minimum is based on an intake of fat that is approximately 1/3rd saturated, 1/3rd mono-unsaturated and 1/3 polyunsaturated, AND DOES NOT CONTAIN SYNTHETIC TRANS FATTY ACIDS (the unnatural fatty acids that are found in partially hydrogenated domestic oils) or red meat. If more saturated fatty acids are consumed, or if red meat is a significant part of the diet, then an increased amount of poly-unsaturated fatty acids must also be consumed, to ensure that EFA deficiencies do not develop, so the minimum goes up!
Saturated fats therefore increase EFA requirements, but provided that the amount of EFA in the diet is adequate, the saturated fats do no harm. The original studies that showed bad effects of saturated fats on blood lipids were mostly flawed (Grundy, 1991), since they did not allow for EFA status or the presence of trans fatty acids in the diet.