The cat has long been out of the bag that eating fat doesn’t make you fat and saturated fat isn’t the diabolical dietary demon it had been made out to be for over sixty years. Thanks to bestselling books and articles in popular magazines with large readerships word is getting out that people can start eating butter again instead of vegetable oil spreads and that a nice fatty lamb chop is nothing to be afraid of. And it’s great that this message is getting the attention it deserves. But we can take things a step further.

People don’t need to put forth deliberate effort to avoid fat like the plague but might there be specific fatty acids people might want to be certain to get enough of? Of course there are EPA and DHA but what about any others? EPA and DHA aren’t the only omega-3s and even though the other essential fats—omega-6s—have a bit of a bad reputation they are also essential. (At least the “parent” omega-6 linoleic acid is.) One of these omega-6s—gamma-linolenic acid (GLA)—is one such fat that many people may not have adequate levels of and their health may be suffering as a result. 

GLA (18:3n-6) is derived from linoleic acid (18:2n-6) as the product of delta-6-desaturase adding a double bond to linoleic acid. Delta-6 desaturase (D6D) requires B6 as a cofactor so right off the bat anyone with inadequate B6 (plus zinc and magnesium) may be at risk for deficiencies of this special fatty acid as well as all others that come after it not to mention the longer chain omega-3 fats since the omega-3 pathway also uses D6D (in the conversion of alpha-linolenic acid to EPA and DHA). Others at risk for inadequate GLA synthesis include type 1 diabetics and type 2 diabetics with reduced beta cell function (insulin stimulates D6D) individuals with suboptimal thyroid function cancer patients and those with chronic viral infections. Consumption of trans fats also inhibits D6D activity. 

It’s important that the fatty acid conversion reactions happen effectively because most people do not regularly consume the primary sources of pre-formed GLA: evening primrose oil borage oil and black currant seed oil. (These can be taken as supplements of course.)

Health-conscious people “in the know” tend to avoid foods high in omega-6 (such as soybean corn and cottonseed oils) owing to the role of excess n-6 in driving inflammation. But the eicosanoid story isn’t quite that simple. Omega-6 fats are inflammatory and anti-inflammatory. GLA and the next fatty acid in the n-6 elongation pathway—dihomo-gamma-linolenic acid (20:3n-6) are building blocks for the anti-inflammatory prostaglandin PGE₁.

Owing to its anti-inflammatory effects GLA has been shown to improve signs and symptoms of rheumatoid arthritis. (Unfortunately the doses required may be off-putting to some especially if it must be administered solely through capsules as opposed to liquid form.) High intakes of GLA may help reduce the relative concentration of arachidonic acid in plasma lipids and in erythrocyte membranes which may be an additional anti-inflammatory mechanism aside from providing substrate for PGE₁ synthesis. 

GLA may be best known for ameliorating premenstrual discomfort. And while “n=1” experiments should not be dismissed and women who find relief from cramps and other discomfort should stick with what they feel is effective and works best for them the literature on the subject is somewhat disappointing. Some studies conclude any improvement from fatty acid supplementation on PMS symptoms is due to the placebo effect but nevertheless if a woman finds it effective she doesn’t need a PubMed reference to tell her she feels better.

Similar findings—basically that results vary and GLA may be effective for some people but not others—have been published regarding GLA for dry skin eczema and atopic dermatitis. A meta-analysis looking at borage oil and evening primrose oil for eczema concluded that these oils “lacked effect” and that symptom improvement was similar to that seen with placebos. A review examining borage oil for atopic dermatitis found that borage oil was “unlikely to have a major clinical effect but may be useful in some individual patients with less severe atopic dermatitis who are seeking an alternative treatment. Which patients are likely to respond cannot yet be identified.” That last part is key: some will respond and some won’t but there’s no surefire way to know which camp a particular patient will fall into except for giving it a try. Decades of clinical experience cannot be discounted and practitioners have sworn by GLA for decades for various skin ailments so “gold standard” RCTs or not the proof is in the pudding. 

Deficiencies of GLA and general fatty acid imbalances may play a role in the pathogenesis of diabetic neuropathy due in part to “functional and structural abnormalities of the axon the myelin and membrane-bound proteins…” Hyperglycemia and aberrations in insulin signaling may make things even worse and glycation is no doubt a factor in diabetic nerve damage but fatty acid imbalances may be setting the stage and making the consequences even worse. Supplementing with GLA may help preserve the structure and function of neurons and facilitate healthy microcirculation.

No eating fat won’t make you fat but we still need to pay attention to the kinds of fat we eat.