The last 50 years in fat nutrition advice has centered entirely on the promotion of polyunsaturated fats at the expense of saturated fat. In this article, let us take a closer look at the evidence surrounding polyunsaturated fat consumption.
The Myth Of PUFA Essentiality
The first investigations into the essentiality of any fat was done close to a century ago in rats consuming a diet comprised of purified sucrose and casein amongst other things. The rats developed kidney damage, infertility and several overt symptoms of inflammation, eventually dying within 1 year [1,2]. It was later ascertained that this was a deficiency of essential fatty acids (EFAs).
Further experiments were done with rats fed butter and coconut oil which did not prove totally curative and with lard, corn oil, flax oil, liver and olive oil which all proved fully curative [1,2]. What did these fully curative foods and oils have in common? The presence of either linoleic (LA) or arachidonic acid (ARA), both being omega-6 (n-6) fatty acids. Indeed, it was shown that when LA or ARA are isolated in purified form, the requirement to cure deficiency is slightly over 2% of calories for the former and 0.7% of calories (lower amounts not tested) for the latter , a result that would be expected given that LA is a precursor to ARA. Thus, EFA deficiency is in fact a deficiency of ARA.
These requirements, however, may still be exaggerated. These experiments were done in rats consuming an extremely purified sucrose-casein chow. Refined sucrose has been show to increase the EFA intake requirement . Facilitating the conversion of LA to ARA are several vitamins and trace elements that modulate the EFA requirement. Vitamin B6 is so influential (desaturation of D6D) that later it would be shown to cure the deficiency when provided alone . Similarly, vitamin B7 also plays a key role in the elongation of the hydrocarbon chain in the conversion process . Oxidized vegetable oils , calcium deficiency  and zinc deficiency  also seem impair the conversion.
In a famous experiment in the late 30’s, an esteemed biochemist offered to subsist on a eucaloric diet incredibly low in fat for 6 months to study EFA deficiency. To the surprise of some, he did not develop any such deficiency, rather he experienced markedly improved health with his hypertension ameliorated, metabolic function improved, fatigue being greatly reduced and long history of migraines totally disappearing .
As a whole, even though EFA deficiency is able to be redressed with only a modest quantity of isolated LA or (particularly) ARA, it seems the requirement has still been greatly inflated by the failure to test lower amounts, the use of extremely purified and unnatural diets, inconsideration of numerous other dietary variables and experimentation on growing animals rather than weight-stable adults.
Hitherto only n-6 PUFA has been discussed. What of n-3? Just as LA is the mother of the n-6 family, alpha-linoleic acid (ALA) is the mother of the n-3 family of fatty acids. And it certainly seems that just as the n-6 ARA holds exclusive essentiality, it is only docosahexaenoic acid (DHA) that holds the same.
It is of interest to find that serum ARA and serum DHA are strongly correlated . The essentiality of DHA can be seen in its functional roles throughout the body. For example, the retina and cerebral cortex are comprised of predominantly DHA  and their levels are tightly maintained  providing strong evidence of its importance. In stark contrast, eicosepentaenoic acid (EPA) is not strictly regulated in any tissue.
There have been studies showing that supplementation with ALA has shown EPA to be the primary product, rather than DHA . The greater majority of these trials have shown minimal production of DHA with ALA doses ranging from around 50mg to 1g. However, these studies have suffered from the same incapacitating flaws as the first studies on n-6 essentiality did — a failure to consider other dietary variables that affect the conversion. Furthermore, the use of limited amounts of ALA with a huge amounts of LA would further suppress conversion through competition for enzymatic (D6D) activity  and by LA impairing D6D production .
Indeed, under conditions where LA is restricted to just over 0.5% of calories, lowering n-3 intake to a level as low as 0.05% of calories does not affect DHA levels . However, when LA is prescribed at 2% of calories and given as the only fat in the diet, DHA is depleted by around 90% [17,18]. These experiments suggest n-6 content of the diet is an important modulator of DHA rather than the n-3 of content of the diet per se.
As previously, mentioned, DHA plays essential roles most notably in the nervous tissue of the brain where levels are very tightly regulated. In the case of experimentally induced DHA deficiency, it seems the body goes to extreme lengths to maintain function by synthesizing a DHA replacement, docosapentaenoic acid (DPA) from ARA . In the absence of ARA (deficiency), the body then converts oleate (from carbohydrate, CHO) into an ARA replacement called mead acid (MA) . This rather laborious process of ensuring sufficient DHA or adequate substitutes indicates strongly that it is an EFA. No such process is observed for EPA.
In summation then, the idea that the n-6 LA and the n-3 EPA/DHA are essential is not entirely accurate. Evidence strongly suggests that ARA is the true essential n-6 PUFA and only DHA is the true essential n-3 PUFA. More importantly, the actual absolute requirement of these fatty acids to prevent deficiency in the diet is so infinitesimally small that eating a mixed, balanced diet containing nutrient-dense foods (such as animal fat) while ensuring a healthy intake of vitamins B6 and B7 and important trace elements such as magnesium, calcium and zinc while restricting if not totally eliminating refined sugar and vegetable oils will supply the EFAs abundantly. To reiterate, the cumulative impact of these factors present a compelling case that the true EFA requirement for weight-stable matured humans is so utterly miniscule that it is virtually unavoidable in all relevant contexts.
Are PUFAs Heart Healthy?
Much ado has been made about PUFAs and their ability to lower coronary heart disease (CHD) mortality due to their hypocholesterolemic (ability to lower serum cholesterol concentrations) effects. Assessing dietary PUFA as a whole is useless because the two dominant fatty acid families (n-6 and n-3) may have individual and disparate effects on CHD endpoints. The evidence that n-6 may be cardioprotective comes principally from controlled trials that have replaced saturated fat with LA rich vegetable oils and the evidence that n-3 may be cardioprotective derives mostly from fish-oil supplementation studies.
Concerning the former, there have been exactly 6 randomized controlled trials (RCTs) that have substituted saturated fat (SFA) for n-6 (vegetable oils). A meta-analysis of these trials found a nonsignificant increased risk of non-fatal myocardial infarction (heart attack, MI) and CHD mortality (RR = 1.13; 0.84-1.53) and an increased risk that closely approached statistical significance for all-cause mortality (RR = 1.16; 0.95 – 1.42) when n-6 PUFA substituted SFA . A meta-analysis in 2010 purportedly found beneficial effects  but the data used was patently biased and exposed elsewhere . Thus, the literature does not support a role for n-6 PUFA in the prevention of CHD or total mortality when substituted for SFA and there is evidence to suggest it is probably harmful.
As to the latter, fish oil supplementation has been experimented with widely in the past two decades after rising interest that n-3 may exert beneficial cardiovascular effects. In an extensive and critical review of studies, the Cochrane Group (reputed for their impartiality and and thoroughness) performed a meta-analysis of fish oil supplementation trials . They found paltry evidence that fish oil imparts any such beneficial effects on cardiovascular disease endpoints. Moreover, these have all been secondary-prevention trials making their results less applicable to a healthy population even if cardioprotective effects were consistently seen. To my knowledge, the only primary-prevention trial that exists is still in progress .
Together, the amassed evidence does not corroborate the currently pervasive notion that either n-6 or n-3 PUFA protect against diseases of the coronary system and in the case of the former, evidence points to a harmful effect instead.
The Forgotten Ones (Hundreds)
Before the turn of the 21st century, researchers everywhere were experimenting with the newly developed vegetable oils and PUFA diets. Most of the studies were performed on rodents and other animals which were easily reproducible and were quick to react to the intervention. Many of these studies were ignored as saturated fat became the target of public health policy. Regardless, these experiments and their implications have been largely forgotten but their results are just as relevant as they were 40 years ago.
Intakes of PUFA have been shown to increase lipid peroxidizability and/or oxidative stress [26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46]. The mechanism behind this action is should be apparent to anyone with a decent grasp in biochemistry. A PUFA fatty acid contains two or more double-bonds between carbon atoms. These double-bonds are extremely susceptible to oxidation (free-radical degradation of electrons). The oxidized double-bonds attract oxygen which binds to it and turns the fatty acid into a peroxyl radical, wreaking havoc on cellular membranes, proteins and even DNA.
Higher intakes of PUFA have also been shown to induce and accelerate cancer [47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63] being confirmed in humans , increase the activity of free radicals when PUFA is heated [65, 66, 67, 68, 69, 70, 71, 72] and correlated with atherosclerosis development or CHD [73, 74, 75, 76, 77, 78, 79, 80, 81]. Moreover, plaques in arterial blood vessels mostly contain PUFA  and have been shown to positively correlate with serum levels . Those plaques containing more PUFA are more likely to rupture and cause heart attacks .
PUFAs have been shown to be immunosuppressive [85, 86 ,87, 88, 89, 90, 91, 92, 93, 94], involved in protein degradation [95,96], diabetes and insulin resistance [97, 98], pulmonary dysfunction , cardiopathogenic effects , liver damage [101, 102, 103], CNS function [104, 105], cerebral damage [106, 107, 108, 109] and cytotoxicity [110, 111, 112, 113, 114, 115, 116, 117, 118, 119, 120, 121].
It cannot be said with adequate confidence that the literature cited here is exhaustive. Indeed, the research on PUFAs and their ill-effects span close to a century with much of the substantive matter emerging from the 60s, 70’s and 80’s. It is crucial to remember that the consideration and interpretation of each study by their strength and design is absolutely necessary. However, together, this literature shows without question that there exists substantial evidence contradicting recommendations to increase PUFA intake.
The Living Exemplars
Primitive populations around the world yet untouched by modern industrialization have been observed to enjoy freedom from diseases of civilization eating their traditional diets. Some people have taken this to mean that the imitation of their diets will necessarily yield the same health benefits. This approach is fundamentally flawed, unscientific and requires willful ignorance of the established literature . Nevertheless, it remains that these populations at least present a starting point or a hypothesis. Therefore, they should be considered as observational evidence and treated as such. The macronutrient composition of some primitive populations and their implications for PUFA intake are briefly discussed.
Three notable populations have been observed to be free from CHD and generally all modern degenerative maladies. The Kitavans , Pukapukan’s  and Tokelauan’s  all live in the Polynesian atolls and consume only around 2% of their total calories as PUFA. These observations should warrant pause and raise questions regarding the current recommendations to increase PUFA to at least 10% of calories, with further increases encouraged .
Putting It All Together
At this point, many people reading this would probably be experiencing a severe bout of cognitive dissonance. For the last 5 to 6 decades we have been told that saturated fat is ‘bad’ – even though there no serious evidence exists to support this  – and PUFA in large amounts is healthful. Others may now be wondering about the role of nuts, fresh fish or fish-oil capsules in the diet. The message of this article is simple and should not be misconstrued: PUFAs in large amounts, or more specifically, in quantities above 5% of calories may begin to have untoward health effects while an even higher intake (10%+ of calories) is most probably damaging.
Numerous lines of multidisciplinary evidence are discordant with the prevailing notion that polyunsaturated fatty acids should be consumed in large quantities. The idea that LA is essential is derived from a greatly exaggerated interpretation of the founding investigations. If EFAs exist at all, the minimum requirement is so miniscule as to render the word ‘essential’ literally meaningless in the context of an overarching dietary regimen.
The benefits of n-6 and n-3 for heart health have also been overstated and clinical demonstration of their effectiveness has been limited. Various studies have shown excess PUFAs to be generally damaging to total health status via a number of mechanisms. And finally, the recommendation to limit total PUFAs to at least under 5% of calories is consistent with living primitive populations who have been observed to be free from diseases of civilization consuming less than half that. Enjoy a diet that includes an expansive menu of both nutrient-dense plant and animal foods and is devoid of processed foods such as vegetable oils and soda beverages. That is the start to good health.