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Dietary
fat has both suffered and enjoyed large swings in public and scientific
consensus over recent decades. The fat-reduction public education
initiatives of the 1980s and 1990s (Weinberg, 2004),
although credited with lower cardiovascular mortality, (Astrup,
2001) have also
been linked to over-consumption of dietary carbohydrate and the
obesity epidemic facing Western culture (Weinberg, 2004).
The escalating incidence of Syndrome X (central obesity, dislipidemia
and glucose intolerance) has helped bring a more "moderate"
approach to the Dietary Guidelines for Americans regarding
fat's percentage of total kcal (Gifford, 2002).
Additionally, an increased recognition of the types of dietary fat
has broadened scientific understanding beyond simply saturated and
unsaturated fatty acids. Further, researchers have referred to the
potency of various dietary lipids as pharmaceutical in nature (DeCaterina,
et al., 1996;
Fauconnot and Buist, 2001;
Watkins, et al., 2001).
For example, monounsaturated fatty acids, as common to the Mediterranean
diet, may reduce cardiovascular risks beyond any effects on plasma
lipids, such as via blood pressure normalized glucose tolerance
(Perez-Jimenez, et al., 2002;
Rasmussen, et al., 1995;
Thomsen, et al., 1995).
Highly unsaturated omega-3 fatty acids found in cold water fish
reduce inflammation (Browning, 2003;
Calder, 1997,
2001; Endres,
et al., 1989;
Endres, 1996;
Kremer, et al., 1987),
mediate psychiatric function (Logan, 2003;
Su, et al., 2003),
alter neuro-endocrine activity (Delarue, et al., 2003),
and decrease cardiac mortality (Richter, 2003).
A less common fatty acid found in dairy and beef, conjugated linoleic
acid (CLA), has the ability to dramatically alter body composition
in animal models (Belury and Koster, 2004).
This type of understanding is leading to changes in both dietary
recommendations (American Heart Association, 2002)
and a wide variety of dietary lipid supplements.
Athletes have special interests and needs regarding dietary fat.
Ironically, many are at risk of being hypocaloric (Burke, 2001;
Economos, et al., 1993;
Venkatraman, 2000),
yet they also seek glycogen sparing and fatigue prevention (Hargreaves,
et al., 2004).
These situations are aided by available, energy dense fat (9 kcal·g-1).
Athletes also commonly deal with joint, soft tissue, systemic and
even airway inflammation, which may also be affected by fat choices
(Browning, 2003;
Calder, 1997;
2001; Curtis,
et al., 2000;
Endres, et al., 1989;
Endres, 1996,
Mickleborough, et al., 2003).
Additionally, overtraining and staleness occur in roughly one-third
to one-half of athletes (Kentta, et al., 2001).
These disorders have established endocrine and psychiatric components
such as depressed testosterone or testosterone:cortisol ratio (Roberts,
et al., 1993;
Urhausen, et al., 1995),
increased epinephrine during intensity-type overtraining (Fry, et
al., 1994),
and even major depression (Armstrong and VanHeest, 2002;
Uutisalo, et al., 2004).
All of these maladies have been positively affected by various amounts
and types of dietary fat in various settings (Delarue, et al., 2003;
Dorgan, et al., 1996;
Hamlainen, et al., 1983;
Logan, 2003;
Reed, et al., 1987;
Su, et al., 2003).
It is also interesting to speculate that the effect of maintained
total fat intake on sex hormones (Dorgan, et al., 1996;
Hamlainen, et al., 1983,
Reed, et al., 1987)
and the reported protective effects of omega-3 fats against bone
catabolism (Albertazzi and Coupland, 2002;
Fernandes, et al., 2003;
Watkins et al., 2001),
may have future application to the "female athlete triad",
in which energy balance, sex hormones and bone mass are compromised.
As with all of the potential benefits resented in this review, either
directly applied or indirectly associated to athletes, further research
is needed.
This review will briefly address the general biochemistry and physiology
of dietary fat, dietary needs and food sources of various fats,
and potential benefits and risks of various dietary fat manipulations
to athletes.
Part
1. General Biochemistry and Physiology
Biochemistry
The preponderance of lipid in the human diet is in the form of triacylglycerols
(formerly "triglycerides"). These triacylglycerols are
composed of a glycerol "backbone" of three carbons with
three fatty acids attached. It is primarily these fatty acids, which
range widely in length up to approximately 22 carbons that are broken
down for energy. The sheer number of carbons in fatty acids, compared
to carbohydrate for example, is the reason for the fact that dietary
fats contain more than twice the energy (9 kcal) of carbohydrates
(4 kcal) in the body. That is, they contain comparatively long aliphatic
chains as opposed to a hexagonal or pentagonal-looking ring
structure (of six carbons). Proteins are not a primary source of
energy but do provide roughly the same amount of energy as carbohydrates
in the body (4 kcal). In order to be fully oxidized, or "burned",
fatty acids require a specific biochemical pathway called beta-oxidation
in the mitochondria of cells. Fatty acid oxidation will be addressed
in Part Four of this review. Exercise Metabolism.
Differences in fatty acid chain length, desaturation (the number
of carbon-carbon double bonds), and position of these double bonds
on the chain all contribute to a vast variety of biological effects
beyond simple provision of energy. For example, a lack of carbon-carbon
double bonds makes a saturated fatty acid, as is common to animal
fats. Even though not all saturated fats appear equally "unhealthy"
regarding heart disease risk and cell membrane effects (National
Cattlemen's Association, 2000),
these are generally considered less desirable. Arguably just as
detrimental are trans-fatty acids, which are simply common
"cis" fatty acids that have had the region about their
carbon-carbon double bonds altered via commercial hydrogenation.
This process improves commercial aspects such as reduced rancidity
but creates an "unnatural", straightened fatty acid that
has been linked to elevated heart disease risk, and inflammation
(Lichtenstein, 2000;
Popkin, et al., 2004).
Conversely, some fatty acids are pharmacologically beneficial and
even essential to health. That is, humans lack the enzymes to make
them, so in their absence symptoms develop. Linoleic acid is an
essential omega-6 (n-6) type of fatty acid that is perhaps too common
in the Western diet (Mann, et al., 1995;
Simopoulos, 2002)
but necessary for eicosanoid synthesis nonetheless. Linolenic acid
is another essential fatty acid, this time of the under-consumed
omega-3 (n-3) type (Simopoulos, 2002).
It has specific effects of its own (DeCaterina, et al., 1996)
but can also elongate and desaturate to have further biological
impact. EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid),
commonly referred to as "fish oils", are considered more
"potent" pharmacologically than linolenic acid in some
regards and are fellow omega-3 fatty acids (Ehringer, et al., 1990;
Su, et al., 1999). Omega-3 fats have been shown to have a number
of beneficial physiological effects in various settings; these include:
reduced cardiac arrhythmias and mortality,(Richter, 2003) improved
aspects of muscular recovery (Phillips, et al.,2003),
increased cell membrane fluidity (Ehringer, et al, 1990),
altered nerve chemistry and depression (Logan, 2003;
Su, et al., 2003),
reduced inflammation (Browning, 2003;
Endres, 1996;
Endres, et al., 1989;
Calder, 1997,
2001), and decreased
cartilaginous breakdown (Curtis, et al., 2000).
A portion of these effects stem from their ability to displace arachidonic
acid from cell membranes (Kelly, et al., 1999).
Interestingly, it appears that the ratio of n-6: n-3 fatty acids
in the diet, as opposed to gross amounts of either, is the determining
factor in many of the described effects (Boudreau, et al., 1991;
Simopoulos, 2002).
Toward this end, a ratio much lower than found in Western diets,
of approximately 5-10:1 has been recommended (Institute of Medicine,
2002).
Thus, the energy density and differing pharmacologic effects of
dietary fats makes them attractive to athletes from the perspectives
of health, performance, weight control and possibly even overtraining
and injury management. The body of dietary fat research relative
to exercise is necessarily expanding. Examples of common and oft-researched
dietary fats, their number of carbon atoms, dietary sources and
intake recommendations are provided in Table
1.
Fat Digestion and Absorption
Dietary fat digestion starts in the mouth. Lingual lipase is secreted
by the serous glands beneath the tongue and it is this enzyme that
accounts for the limited breakdown of triacylglycerol proximal to
the intestines (i.e. mouth and stomach). Upon reaching the stomach,
fats can slow gastric emptying, providing a high satiety value (Groff,
et al., 1995)
and tend to rise to the surface, "layering" gastric contents
(Edelbroek, et al., 1992;
Horowitz, et al., 1993).
After an encounter with bile (stimulated by cholecystokinin) and
continued shearing forces in the duodenum, the partially hydrolyzed,
fine lipid droplets are increasingly emulsified. At this time, they
are also exposed to pancreatic lipases, which function in the higher
pH environment supplied by pancreatic bicarbonate secretion into
the duodenum. Pancreatic lipase activation is complex, requiring
other duodenal contents including colipase, calcium ions, and bile
salts. Diacylglycerols (DAG), monoacylglycerols (MAG) and free fatty
acids (FFA) reach the mid-intestine (ileum) in micellar form
- small enough to pass into the intramicrovillus spaces of enterocytes.
During contact with the brush border, or unstirred layer
DAG, MAG and FFA move down a concentration gradient into the enterocyte.
Inside, they are re-esterified back into triacylglycerol. These
newly reassembled triacylglycerols then enter the lymphatic system
on the "other side" of the intestinal cell in a chylomicron
package. Ultimately, the lymphatic circulation carrying these chylomicrons
enters the thoracic duct and then empties into the left subclavian
vein of the bloodstream. Peak lipid concentrations in the plasma
occur from one to three hours post-meal and return to normal within
six hours (Groff, et al., 1995).
It is only after circulation in the bloodstream that triacylglycerol-containing
chylomicrons can reach tissues that possess lipoprotein lipase (LPL)
along their capillary beds and release their DAG and FFA for cellular
fuel. Within muscle cells, the hormone sensitive lipase (HSL) finally
hydrolyzes remaining DAG and any existing triacylglycerols into
free fatty acids (and residual glycerol, which can serve as a gluconeogenic
precursor). These free fatty acids can then be activated by coenzyme
A and transported via carnitine into the mitochondria for (beta-)
oxidation. The result of beta-oxidation and subsequent tricarboxylic
cycle/electron transport system processing is nine kilocalories
per gram of triacylglycerol.
In the adipocytes, conversely, the DAG and FFA released by passing
chylomicrons are generally re-esterified into triacylglycerols for
storage. These can later be hydrolyzed via HSL into FFA and glycerol
for release directly back into the blood - where FFA bind to albumin
and glycerol can enter the liver for formation of nascent glucose.
Hydrolysis of stored triacylglycerol occurs during periods of fasting
and exercise when insulin concentrations are low and catecholamines,
growth hormone and cortisol are increased.
Animation 1 illustrates this
process. It begins with activation of triacylglycerol breakdown
via catecholamines in an adipocyte. After a pause, the animation
then illustrates how cortisol and growth hormone also induce triacylglycerol
hydrolysis. After another pause, the animation finally shows caffeine
as a negative controller (inhibitor) of phosphodiesterase (PDE)
- which facilitates triacylglycerol breakdown - and insulin as a
positive controller of PDE, which suppresses triacylglycerol breakdown
(Also see Resting and Exercise Metabolism sections
of this review).
Part 2. Dietary Needs and Food Sources
Dietary fats are generally recommended to comprise a "moderate"
20-35 percent of energy in the diet (Gifford, 2002;
Institute of Medicine, 2002).
Although dietary fat proportions have been manipulated many times
in attempts to improve performance, there presently appears to be
little need to deviate from this 30 percent recommendation for health
or ergogenic purposes. The composition of individual fatty acid
types within that 35 percent "ceiling", however, has received
recent attention. Based upon literature that the Western diet is
too high in omega-6 fatty acids (mostly linoleic acid) and too low
in omega-3 fatty acids (Boudreau, et al., 1991;
Simopoulos, 2002),
the Institute of Medicine published Dietary Reference Intakes for
Fatty Acids in September, 2002
suggesting that an omega-6:omega-3 ratio of 5-10 to one. This equates
to 12 to 17 g per day of linoleic acid and 1.2 to 1.6 g per day
of alpha-linolenic acid (women and men, respectively). Similarly,
a safe intake of 3 g of fish oil daily has been suggested by the
United States Department of Agriculture (Morcos and Camilo, 2001).
Food sources of various fatty acids are shown in Table
1.
Part 3. Resting Metabolism
Under resting fasting conditions, stored triacylglycerol is the
primary source of human energy. The respiratory exchange ratio (RER),
a ratio of carbon dioxide on the breath to oxygen consumed, is approximately
0.8, signifying that approximately 60-66% of the fuel being used
by the body is from fat and perhaps 33% is from carbohydrate (Brooks,
1997; Wilmore
and Costill, 1999).
The RER is much less than 1.0 due to the large relative amount of
inspired oxygen needed to "burn" fatty acids (See Part
4: Exercise Metabolism.).
As with exercise, resting metabolism is under energetic and hormonal
control. In the relative absence of insulin and the presence of
growth hormone, cortisol, sympathetic catecholamines and glucagon,
hormone-sensitive lipase (HSL) is stimulated via cyclic-AMP and
non-esterified fatty acids (NEFA) are either immediately oxidized
(e.g. muscle) or released by adipose tissue into the blood for energy.
A brief summary of the process is illustrated in Animation
1.
Body composition and weight control are important to many sports
in addition to skill-related fitness. According to Burke (2001),
"Many athletes are over-focused on reducing body mass and body
fat below levels that are consistent with long-term health and performance."
Hence, athletes periodize training goals throughout the year. Toward
this end, dietary tactics may be undertaken to maximize fat loss
and to build or preserve skeletal muscle. Although energy (kcal)
balance is a widely accepted determinant of body mass, macronutrient
manipulations allow for further management.
The choice of whether to principally restrict dietary fat or carbohydrate
for weight control is an ongoing debate. Dietary fat reduction makes
an energy deficit easier (Horvath, et al., 2000)
but dietary carbohydrate reduction reduces insulin concentrations
(Sharman, et al., 2002;
Volek, et al., 2002),
facilitating lipolysis. Additionally, a higher dietary fat content
appears to induce superior nitrogen sparing (McCargar, et al., 1989).
Both approaches appear to reduce body fat mass (Astrup, 2001;
Hayes, et al., 2004;
Stern, et al., 2004;
Volek et al., 2002)
but both types of restriction carry risks. Very low fat diets have
been shown to reduce sex hormone concentrations (Dorgan, et al.,
1996; Hamalainen,
et al., 1983;
Reed, et al., 1987)
and may suppress intake or absorption of fat-soluble vitamins and
essential fatty acids. Very low carbohydrate intake retards glycogen
resynthesis after exercise (Roy & Tarnopolsky, 1998),
appears to increase protein breakdown in the body (Lemon & Mullin,
1980), and may
reduce dietary fiber consumption (Kappagoda, et al., 2004).
Ketosis during low-carbohydrate diets, however, appears to be of
less concern in non-diabetics due in part to basal concentrations
of circulating insulin.
Performance, rather than body composition, however, is of primary
interest to the competitive athlete (aside from bodybuilders), and
thus weight control approaches must not unduly interfere. Ergogenesis
is addressed in Part 4 of this review.
Part 4. Exercise Metabolism
The large, almost limitless fat stores of the body (e.g. 9 kcal·g-1
x 12 kg fat mass = 108 000 kcal) in relation to available carbohydrate
stores (e.g. 4 kcal·g-1 x 450 g glycogen = 1 800 kcal)
make it an attractive focus for extending endurance exercise. That
is, increasing hydrolysis of stored triacylglycerol and subsequent
oxidation of free fatty acids should spare limited glycogen stores,
which have an impact on fatigue in moderately high intensity settings
(e.g. a runner "hitting the wall" during a marathon).
Hence, various attempts to manipulate the diet, and subsequently
the body's substrate oxidation, are discussed later in this section.
Exercise affects fat metabolism greatly, not simply increasing it
at a constant rate but rather controlling it in reciprocal proportion
to carbohydrate. Both the intensity and the duration of a bout of
exercise have an impact.
Intensity:
The "Crossover Concept"
During the course of aerobic exercise, that is, physical activity
utilizing the cardiorespiratory system and primarily large muscle
groups for sustained periods of time (American College of Sports
Medicine, 2000),
multiple fuel sources (carbohydrate, fat, and to a small extent
protein) are used depending on the intensity and duration of the
activity. The point of intensity at which the body starts to rely
more on carbohydrate than fat as a fuel is the "crossover".
The metabolic control of this process is still under investigation.
The process of hydrolyzing free fatty acids form stored triacylglycerol
in adipose tissue, transporting them in the blood and oxidizing
them within the muscle mitochondria appears to be too slow to keep
pace with metabolic demand. It is also plausible that some aspect
of rapid carbohydrate oxidation within the working muscle itself
interferes with long-chain fatty acid transport into the mitochondria
(Sidossis, et al., 1997).
Fuel usage is commonly measured by the respiratory exchange ratio
(RER) and the respiratory quotient (RQ); the RER measures metabolism
at the mouth (carbon dioxide produced vs. oxygen consumed as seen
in air breathed) and the RQ looks at metabolism at the cellular
level (e.g., in muscle tissue) (Houston, 2001;
Wilmore and Costill, 1999).
During light intensity exercise (RER ~8.5), fat still supplies nearly
half of the energy needed in the body (Wilmore and Costill, 1999;
Klein, et al., 1994).
With increasing intensity and oxygen consumption (VO2),
the body shifts toward carbohydrate as a primary fuel (mostly from
glycogen but also from blood glucose; RER reaching 1.0), since it
is most readily available for breakdown (Brooks, 1997).
Duration: The "Fat Shift"
Unlike the inverse relationship between exercise intensity and fat
oxidation (that is, higher intensity = lower fat usage), is the
"fat shift" that occurs with increasing duration of exercise.
This direct relationship between the time spent at a given (moderate)
intensity of aerobic exercise and the amount of stored fatty acids
used as fuel is well documented (Brooks, 1997;
Sidossis, et al., 1997).
It is measurable via both a reduced RER (oxidation) and a gradually
increasing appearance of glycerol in the circulation (lipolysis).
After a prolonged period of exercising at a sustained moderate intensity,
for example, jogging for more than 20 minutes (out to several hours),
fat becomes increasingly available for use as an energy source.
This is due in part to the fact that oxygen is now more accessible
and able to be used to oxidize fat molecules (Abernethy, et al.,
1990).
Hence, long duration, low intensity exercise may appear to be superior
for body fat reduction. It is in fact most effective for direct
fat usage. Yet one must keep in mind the absolute kcal expended
during a bout. An individual can workout for less time and at a
higher intensity and expend the same amount of kcal as if
he had exercised for a longer amount of time, at a lower intensity.
Based solely on energetics, the impact on body fat stores should
be virtually the same, since the absolute number of kcal has been
expended. This is possible due to indirect metabolic processes beyond
direct, mid-exercise fat oxidation, such as continued elevated metabolism
and interactions among stored substrates.
Part 5. Dietary Fat, Ergogenesis and Athletic
Recovery
The human body becomes better at mobilizing, transporting and oxidizing
fat as an endurance training adaptation. Similarly, increased ingestion
of fat as a proportion of total kcal enhances the body's ability
to use it as fuel, in part due to fatty acid availability (Hawley,
et al., 2000;
Schiffelers, et al., 2001;
Stepto, 2002;
Zderic, et al., 2004).
In an effort to maximize both effects and spare glycogen, thus enhancing
energy delivery to working muscles, attempts have been made to increase
dietary fat during various periods prior to exercise. The results
from these potential ergogenic manipulations are equivocal to date,
however. In some studies, an increase in dietary fat resulted in
elevated maximal aerobic capacity (VO2max) and increased
time-to-exhaustion (Venkatraman, et al., 1997;
2000: 2001)
but in others the result was either no effect, decreased performance
and/ or increased rate of perceived exertion (Fleming, et al., 2003;
Hargreaves, et al., 2004;
Stepto, 2002).
Regarding fatty acid types and athletic recovery, there are mixed
reports in the scientific literature. Although at least one study
reported no effects on delayed-onset muscle soreness, hanging arm
angle, creatine kinase (CK), cortisol or IL-6 after 30 days of 1.8
g fish oil daily, (Lenn, et al., 2002),
others have shown a fish oil-containing supplement to decrease eccentric
exercise-induced IL-6 and C-reactive protein (Phillips, et al.,
2003). Dose
and co-consumed nutrients may be a factor. Specific to the CK variable,
the increased membrane fluidity induced by omega-3 fatty acids (Ehringer,
et al., 1990)
may be a factor in studies resulting in increased release in older
humans (Cannon, et al., 1995)
and rabbits (Chen, et al., 1999).
This elevation was considered beneficial in the human research,
as it restored post-exercise CK in older adults to concentrations
like those of young participants (Cannon, et al, 1995).
Regarding more chronic recovery issues, data from Venkatraman (1997,
2000) suggests
that higher total fat intakes are immunosupportive in aerobic athletes.
Further, data on immune-challenged (ultra-violet radiation) mice
supports the benefits of EPA on immunocompetence as well (Moison
and Beijersbergen Van Henegouwen, 2001).
Collectively, data on dietary fat amounts and types suggest an immuno-modulatory,
rather than immuno-stimulating effect, as certain parameters of
the acute phase response to stress and injury are reduced
while other immune system aspects remain intact or enhanced.
Finally, it is also notable that the natural adaptations to exercise
itself, without purposeful omega-3 ingestion or supplementation,
increases oleic acid, DHA and total omega-3 fatty acids human muscle
tissue of humans (Andersson, et al., 2000;
Helge, et al., 2001).
Part 6. Dietary Fat Supplements
Throughout this review, evidence from dietary supplements and whole
food manipulations has helped clarify the biological need for and
pharmaceutical possibilities of dietary fats. But in addition to
efficacy, one must consider safety. A wide variety of dietary supplements
have been investigated. Each of the following fats could constitute
a review in itself; hence, they will be only briefly described here.
Fish oil (EPA and DHA)
Pollution affects fish (oil) quality. Polychlorinated biphenyls
(PCBs) contaminate various species of fish and affect cognitive
function in both children and adults (McCook, 2001).
The risk of heavy metal (e.g. mercury) contamination is real with
regards to fish consumption, particularly larger predatory fish
like swordfish, which consume smaller fish, accumulating toxins
in their flesh (Mendez, et al., 2001).
The controversy over whether ingested mercury negates the benefits
of accompanying fish fats for humans is not settled, however (Guallar,
E., et al., 2002;
Yoshizawa, K., et al., 2002).
In either case, dietary supplements may be a way to avoid the effects
of such pollution. Over recent decades, a number of investigations
screening fish oil products have resulted in negligible or absent
mercury contamination (Bugdahl, 1975;
ConsumerLab, 2001;
Foran, et al., 2003;
Koller, et al., 1989).
At least one review has revealed a lack of "key ingredient"
in fish oil products, however (ConsumerLab, 2001).
A comprehensive screening of all available fish oil supplements
for mercury contamination or even EPA and DHA content is not likely,
however. Hence risks remain.
EPA and DHA themselves have been investigated for toxicity. Concerns
over excessive clot inhibition, oxidative stress, red cell deformation
and enlarged liver have been noted (Rabbani, et al., 2001).
Most of these effects are seen with extremely high doses - doses
as high as 15ml·kg-1 per day in rat studies. At least
one human study has involved administration of 18 grams daily for
six weeks and another up to 27 grams daily for one month without
problems, however (Barber, and Fearon, 2001;
Endres, et al. 1989).
Caution is nonetheless necessary. Any toxicity surrounding these
fatty acids would likely be an extended situation, if any was found,
as wash out periods for fish oil effects persist 10-18 weeks (Endres,
et al. 1989;
Kremer, et al., 1987).
Peroxidative effects and physiological benefits appear to be improved
by co-consumption of vitamin E (Hsu, 2001;
Tidow-Kebritchi and Mobarhan, 2001).
In consideration of all available factors, the USDA has recommended
a chronic intake of no more than three grams per day of EPA and
DHA from all dietary sources (Morcos & Camilo, 2001).
Conjugated linoleic acid (CLA)
Conjugated linoleic acid (cis-9, trans-11 or trans-10, cis-12 octadecadieneoic
acid) is actually an entire group of trans fatty acids that ironically
appear to possess healthful aspects. The isomers, in singular or
combined amounts, have dramatically reduced body fat in animal models
(Belury and Koster, 2004,
Pariza, et al., 2001;
Mougios, et al., 2001)
but human studies have been more modest and mixed in this regard
(Belury and Koster, 2004).
Similarly, investigations into muscle and strength gain have been
mixed, perhaps confounded by methodological differences (Belury
and Koster, 2004;
Krieder, et al., 2002;
Lowery, et al. 1998.)
Clearly, the hypo-responsive and/ or hard-to-control nature of humans
compared to animals warrants further investigation. Species and
dose appear to influence effects. As with fish oil, toxicity appears
generally low, with human studies generally involving 3.0-7.2 grams
daily for 6-12 weeks (Belury & Koster, 2004;
Blankson, et al., 2000;
Mougios, 2001),
yet no upper limit of safety has been established.
Primrose, Borage, Black Cuurant oil (GLA)
As sources of gamma-linolenic acid (all cis-6,9,12 octadecatrieneoic
acid), primrose, borage and black currant oils may have the capacity
to reduce arthritic inflammation and improve aspects of diabetes
(Belch and Hill, 2000;
Salway, 1994).
Situations in which the human delta-6 desaturase is relatively inactive,
such as diabetes, alcoholism and advancing age, appear to be a particular
target for GLA intervention (Horrobin, 1981;
Salway, 1994).
Dietary supplementation with GLA acts similar to EPA in that is
proportionately enhances the less inflammatory Series 1 and Series
3 prostaglandins, in effect displacing the pro-inflammatory effects
of the 2 Series (Salway, 1994).
As with other types of fat, toxicity appears low (Belch & Hill,
2000; Yang-Yi
and Chapkin, 1998).
Olive,
Canola oil (Monounsaturates)
By no means the only source of monounsaturated fatty acids (MUFA),
olive and canola oils do offer a plentiful source of omega-9 oleic
acid (C18:1) in proportion to other fatty acids in their makeup.
The benefits of MUFA on blood pressure, serum lipids, and glucose
metabolism (Perez-Jimenez, et al., 2002;
Rasmussen, et al., 1995;
Thomsen, et al., 1995)
as well as antioxidant status (Sola, et al., 1997),
coupled with minimal toxicity, generally acceptable taste and heavy
consumption in long-lived cultures, has made it an attractive replacement
for a portion of carbohydrate in the diet. There is no need to purchase
MUFA in supplement form; they are plentiful in the noted common
oils.
Diacylglycerols
A diacylglycerol (DAG) has just two fatty acids attached to its
glycerol "backbone". Recent reports suggest increased
oxidation as opposed to storage and a potential for reduced body
weight gain (Flickinger & Matsuo, 2003;
Murase, et al., 2002).
An absence of any fatty acid at the middle, sn-2 position of the
glycerol molecule reportedly alters DAG metabolism, eliciting these
effects (Flickinger & Matsuo, 2003;
Murase, et al., 2002).
Further research is necessary to determine the anti-obesity efficacy
of DAG in free living humans. Widely available in Japan since 1999,
DAG oils are now sold commercially in some U.S. cities (Flickinger
& Matsuo, 2003)
and are likely to garner future research interest.
Structured
Triacylglycerols
Using technology similar to DAG, structured triacylglycerols strategically
place fatty acids onto a host glycerol molecule. Further, a fatty
acid of interest can be esterified directly onto the middle sn-2
position for optimal biological delivery (Bell, et al., 1997).
Structured triacylglycerols appear to have superior effects to simple
physical mixtures of fats, such as nitrogen retention in burn patients
(Babyan, 1986).
Medium
Chain Triacylglycerols
The shorter length (6-12 carbons) of medium chain triacylglycerols
(MCTs) results in biological usage more similar to carbohydrate
than longer fatty acids. Being less hydrophobic, MCTs enter the
blood stream directly at the portal vein as opposed to taking an
initial circulation and are more readily oxidized than longer fatty
acids (Berning, 1996;
Delany, et al., 2000;
Jeukendrup, et al., 1998).
Although these factors have led to speculation over ergogenic properties
and glycogen sparing due to rapid energy delivery, research is generally
negative (Berning, 1996)
and gastric distress has been reported due to the small amounts
that are tolerable (Jeukendrup, et al., 1998).
Nutrient-nutrient
and Nutrient-Drug Interactions
Due to the thrombolytic effects of omega-3 lipids, other substances
that reduce clotting such as vitamin E, ginkgo biloba, aspirin,
and garlic) could conceivably result in hemorrhage. Despite this,
at least one investigation has demonstrated safety during co-administration
of fish oil and garlic (Morcos and Camilo, 2001).
More research is needed to explore the existence and severity of
such interactivity.
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