Because people can build up large stores of (essential) nutrients — enough to maintain proper physiological functioning for as long as years — diseases arising from dietary deficiencies should be expected to develop slowly and a long time after a deficient diet was imposed. But for the same reason, it’s extremely difficult to determine the essentiality of a particular nutrient, especially when the requirement for the nutrient is relatively low, as well as the fact that foods contain an array of nutrients in varying proportions.
However, two scientists, husband and wife, working in the Botany Department of the University of Minnesota, crafted a clever and sophisticated (but not full proof) way to test the idea as to whether certain fatty acids were “essential” or not.
Although the idea that the fat-soluble vitamins were essential to good health were proven beyond a doubt by the mid-1920s, when George and Mildred Burr suggested that certain fatty acids – in particular, linoleic acid – were not only merely fuel and vehicles for absorbing the fat-soluble vitamins, but also essential nutrients in themselves, they came up against skepticism from other scientists.
In a series of papers published by the Burrs – in particular the seminal 23-page paper published in 1929 – where the idea as to the essentiality of certain fatty acids was put forth, it was said that these “essential” fatty acids (EFAs) were cofactors for key metabolic processes. And when these EFAs were present in excess, they were burnt to fuel other metabolic processes.
The Burrs’ ideas were supported by their results: mere drops of flax oil or corn oil — both of which are rich in linoleic acid — daily for over 40 days reversed the characteristic signs and symptoms (like flaky feet, tails, and skin) brought on by the strict fat-free diets that were imposed on their rodent subjects. Lard worked, too. On the other hand, coconut oil — which contains only saturated and monounsaturated fatty acids — had no such effect. Because the addition of arachidonic acid, derived from linoleic acid, had a similar effect as linoleic acid, it was fair to suppose, which the Burrs did, that the beneficial effects of linoleic acid was due to its role as a precursor as well.
Since some of the defects resulting from the fat-free diets can be reversed by the addition of omega-3 fatty acids, and since mammals (likely) don’t have the wherewithal to convert omega-3 fatty acids to omega-6 fatty acids (and vice versa), it also wouldn’t be possible to rule out that some general physical and/or chemical property of the long-chain polyunsaturated fact acids are responsible for reversing the conditions brought about by a strict fat-free diet.[*]
Fatty acids are bound to various parts of cells and to various structures outside of cells, and changes in the kinds of fatty acids available changes the physical properties of the tissues to which they’re bound. Fatty acids come in many flavors, yes, but the variety isn’t infinite. But there are so many enzymes that act on many different fatty acids that the combination of the effects increase considerably. These effects typically take months or years to manifest.
As an example, consider for a second the molecule oleamide, which is essentially a molecule of oleic acid (omega-9), except that that -OH on the carboxylic acid group at the end of the molecule is replaced by an -NH2.
Oleamide induces sleep in animals. (Though, it’s unclear whether it’s the parent molecule itself or its cleavage products, ammonia and oleic acid.) However, when the diet is altered to the extent that EFAs displace the saturated and monounsaturated fatty acids in the brain, the same enzymes that make oleamide instead make similar molecules from EFAs. As to the consequences of this change — who knows?
It’s been said that the reversal of the symptoms seen upon the addition of the “EFAs” was due to the slowing of the rodents’ metabolic rates by the EFAs. As to the validity of that idea — I have my doubts. Most importantly, the symptoms didn’t just stop getting worse; they began to reverse quickly, eventually to the point of complete cure.
While keeping the metabolic rate up is good, especially when food is available, it’s not so good when food — particularly carbohydrate — is not available. If you’ve read any of the available literature on fasting, you’d know that there’s is an old observation, which has now become an accepted truth, that the desire for food goes away when a person is ill because food has to be withheld so that the body, through its vast wisdom, can activate its magical healing mechanisms.
The reality is simpler than that. When ill, the desire for food goes away to accelerate lipolysis so as to increase the supply of fatty acids to cells, namely to immune cells. As regular readers of this blog are well aware of, lipids in the blood are far more dangerous than lipids stored away in fat tissue. So this momentary drastic increase in lipolysis and increase in free fatty acids — especially polyunsaturated fatty acids — represents an emergency move that, while not without repercussions, allows us to fight off infections to live another day.[†] Apparently, small amounts of polyunsaturated fats are needed to manufacture immune cells at high rates.
But the Burrs’ rodents didn’t display the constellation of symptoms that would suggest a higher than normal metabolic rate, let alone hyperthyroidism. Nor was there a definitive way that the Burrs tested for it. It’s quite possible, and the Burrs say as much, that the exquisitely small amounts of fat simply improved the digestion and assimilation of the other nutrients eaten with it.
Suffice it to say here, the laboratory created fat-free diet is not a diet that can be recreated in the real world. The Burrs encapsulated the challenges in creating the purely fat-free diet in the following quotation: “In fact, it is impossible to conduct a fat-free experiment if corn-starch is used as a source of energy since it carries 0.6 per cent of fatty substance which is within the granule . . . the diets contained appreciable amounts of fat.”
Extremely extensive measures were taken to create the diets, which consisted of sugar, casein (highly purified to remove anything but casein [most importantly, fat]), B-complex vitamins (from dried yeast extract), and vitamins A and D (extracted from cod liver oil). The percentages of these ingredients were gradually changed to meet the changing nutritive demands as the rodents aged. The most important part of this step was that it allowed for even more of the “impurities”, i.e., fat, to be excluded, by replacing increasingly more of the casein with sugar.
The point is that it’s virtually impossible for a person to eat a diet that’s as deficient in fat, let alone polyunsaturated fat, as the Burrs’ diet. Many conditions have been linked to a polyunsaturated fatty acid or an EFA deficiency (most famously cystic fibrosis) yet these links are tentative or may have nothing to do with the conditions at all, and they may simply be indicative of a larger problem, like a generally poor diet or digestion. In the end, the argument as to whether these EFAs are, in fact, essential, is still moot, but it’s not an argument we need to entangle ourselves in — ever.
Of course, there are gradations in the effects of varying the amount and/or types of fats in the diet. Deliberately increasing the intake of polyunsaturated fats at the expense of saturated fats, for instance, reduces the useful activity of components of the immune system — especially natural killer cells and interleukin-2.[‡] In other words, PUFA, most strongly the omega-3s, decrease our resistance to (potentially lethal) infections.[§] But, this is a topic for a whole new post(s) . . . maybe.
References will be posted as soon as possible. (I encourage you to hate me for the delay.)
[*] This concept — the close relationship between the physical properties of a molecule with its structure and the ability to predict the physical properties of a molecule based on its structure — should be no surprise to the readers of this blog. And it should not be forgotten!
[†] However, as longs the fatty acids are taken up, stored, or burnt as fast as they’re released, the repercussions are minimized greatly.
[‡] To be more clear and precise, IL-2, a cytokine released from helper T cells, increases levels of natural killer cells and T cells.