Omega 6 Flashcards
Linoleic Acid (LA)
LA is an omega-6 fatty acid, 18:2 n 6.
• Food sources include vegetable oils safflower, sunflower, soybean, and corn oils . It is found in nuts, seeds and some vegetables
• Conversion of LA to GLA requires vitamin C, B3, B6, magnesium and zinc.
Gamma Linolenic Acid (GLA)
GLA is an omega-6 fatty acid, 18:3 n 6.
• Main food sources include evening primrose oil, blackcurrant seed oil, hemp and borage oils
Gamma Linolenic Acid (GLA): Therapeutic Uses
Rheumatoid arthritis
ADHD
Eczema
Gamma Linolenic Acid (GLA): Rheumatoid arthritis
• Lowers joint pain, swelling and morning stiffness in RA.
• GLA is converted to PG1, which has immune regulatory and anti inflammatory effects. This includes a reduction in NF- kB activity.
•Dosage : 1.4 g / d of borage seed oil.
Gamma Linolenic Acid (GLA): ADHD
• A combination of GLA and EPA shows improvements in attention and impulsivity.
Evening Primrose Oil (EPO)
EPO is abundant in LA, and contains GLA which is also present in borage, blackcurrant seed and hemp seed.
Evening Primrose Oil (EPO): Therapeutic Uses
Premenstrual syndrome (PMS)
Cyclical mastalgia (breast pain)
Female fertility
•GLA is a precursor to PG1, which
inhibits prolactin (↑ in women with
•Dosage: 1500 mg daily for three months.
•GLA forms PG1 which inhibits the synthesis of arachidonic acid metabolites (= anti inflammatory
•Dosage: 1000 mg 3 x daily for four to six months.
Evening Primrose Oil (EPO): Cyclical mastalgia (breast pain)
• GLA is a precursor to PG1, which inhibits prolactin (↑ in women with
• Dosage: 1500 mg daily for three months.
• GLA forms PG1 which inhibits the synthesis of arachidonic acid metabolites (= anti inflammatory
• Dosage: 1000 mg 3 x daily for four to six months.
Evening Primrose Oil (EPO): Female fertility
• GLA forms PG1 which inhibits the synthesis of arachidonic acid metabolites (= anti inflammatory
• Dosage: 1000 mg 3 x daily for four to six months.
Gamma Linolenic Acid (GLA): Drug interactions
Borage seed oil, and possibly other sources of GLA, should not be used during pregnancy.
• Dosages of greater than 3,000 mg / day may increase AA production.
Drug interactions:
• Ceftazidime it may increase the effectiveness of this antibiotic.
• Chemotherapy it may increase treatment effects.
• Cyclosporine it may increase the immunosuppressive effects.
• NSAIDs NSAIDs may counteract the effects of GLA.
• Phenothiazines they may increase the risk of seizures.
Arachidonic Acid (AA)
Arachidonic acid (AA) is an omega-6 fatty acid, 20:4 n-6.
• Arachidonic acid is primarily found in animal products such as meat, eggs and dairy, especially when those animals are intensively raised on grain.
• Dihomo gamma linolenic acid (DGLA) can be converted to AA using delta 5 desaturase.
However, this enzyme is used preferentially for the omega-3 pathway, so the majority of AA in the diet is from animal products.
Arachidonic Acid (AA): Inflammation
Arachidonic acid is often seen as inflammatory, but:
• Inflammation is a key part of the immune system’s response to injury and infection.
• AA is metabolised by COX-1 and COX-2 enzymes to the inflammatory prostaglandin series 2.
• This causes inflammatory effects including fever, vascular permeability and vasodilation, pain and oedema.
• However, to prevent excessive inflammation PG2 induces 15-LOX activity that leads to the formation of lipoxins (anti inflammatory).
Eicosanoids
Eicosanoids are made by the oxidation of omega-3 and 6 fats. They are locally acting hormone like signalling molecules.
• They have a short life span and are involved in:
– Inflammation.
– Blood vessel permeability and constriction.
– Blood coagulation.
– Immune cell behaviour.
– Lipid accumulation.
– Central nervous system signalling
• Eicosanoids include prostaglandins, leukotrienes, thromboxanes, resolvins and protectins
Eicosanoids: Formation
Fatty acids are released from the membrane phospholipids by the enzyme phospholipase A2.
• These are converted to eicosanoids by cyclooxygenase (COX) and lipoxygenase (LOX) this is dependent on the starting fatty acid and an outside stimulus.
• Eicosanoids can be made from arachidonic acid (AA), eicosapentaenoic acid (EPA) and dihomo y linolenic acid (DGLA).
• They can have both pro and anti inflammatory effects.
Eicosanoids: Prostoglandins
Prostaglandins fall into three families or series, depending on which fatty acid they are made from:
Series 1 Prostaglandins (PG1) made from DGLA
Series 2 Prostaglandins (PG2) made from AA
Series 3 Prostaglandins (PG3) made from EPA
Eicosanoids: Series 1 Prostaglandins (PG1) made from DGLA
Keep blood platelets from sticking together.
Remove excess sodium and water from the body.
Relax blood vessels promoting circulation.
ANTI- INFLAMMATORY
Eicosanoids: Series 2 Prostaglandins (PG1) made from AA
Mostly promote platelet aggregation.
Promote sodium and water retention (↑ BP)
Oppose functions of series 1 prostaglandins.
PRO-INFLAMMATORY
Eicosanoids: Series 3 Prostaglandins (PG1) made from EPA
Some have weak platelet aggregating properties.
Prevent the release of AA from cell membranes.
EPA is the most important factor limiting PG2 production.
ANTI-INFLAMMATORY
Eicosanoids: Inflammatory Cycle
Eicosanoids made from arachidonic acid produce initial inflammation. This is ‘shut off’ by the introduction of eicosanoids made from DGLA and EPA.
EFA Metabolism
Cell membrane fatty acid composition determines which prostaglandins will predominate; e.g. a diet rich in arachidonic acid leads to the formation of more pro-inflammatory PG2.
• The more abundant fatty acids will occupy the enzyme active sites, which highlights the importance of omega 3 and 6 balance.
• A high consumption of EPA and DHA from omega 3 means that a higher proportion of fatty acids resides in the cell membrane at the expense of AA.
• This can result in immune suppression. Hence, it is all about balance.
EFA Metabolism: Genetic variability
Genetic variability affects the synthesis of EPA and DHA. Polymorphisms are common in the genes coding for delta-6 and delta-5 desaturase.
• Other omega 6 and omega 3 fatty acids can be synthesised from ALA and LA respectively.
• By desaturation addition of a double bond between two carbon atoms and / or elongation addition of two carbon atoms.
• Both LA and ALA compete for the same desaturase and elongase enzymes.
• Only 1-20% of ALA is converted to EPA.
• Women of reproductive age convert ALA 2.5 times better than men
EFA Metabolism Map
Inhibitors of EFA Metabolism: Delta-6 Desaturase
Magnesium, B6, zinc deficiency
Insulin resistance
Viruses
Refined sugars
Alcohol
Stress hormones, e.g. cortisol
High intake of EPA
DHA
Excess trans fats and cholesterol
Inhibitors of EFA Metabolism: Delta-5 Desaturase
Insulin resistance
Zinc deficiency
Alcohol
Excess trans fats and cholesterol
Stress hormones, e.g. cortisol
High intake of EPA / DHA
Omega Testing
EFA testing includes:
• Omega 3 index a marker for cardiovascular risk.
• Omega 6:3 ratio a marker for chronic illness.
• AA:EPA ratio a marker of ‘silent’ inflammation.
Maintaining the balance of omega 3 and omega 6 can be addressed by supplementing EPA / DHA, along with addressing any co factor deficiencies needed for interconversion.
• Fatty acid profile testing options:
– Genova essential and metabolic fatty acids test (blood test).
– Wiley’s Finest omega 3 index test (blood spot).
– Igennus Opti O-3 (blood spot).
