Food and Behaviour Research

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Dietary Fat and the Human Brain: Redefining Food for Thought

by David Katz

That what we eat, in general, affects brain function should come as no surprise to anyone. Food is the fuel that runs the human machine in all of its remarkable capacities, and that pertains as fully above the neck as below.

This is crucial throughout our lifespan, as we are continuously burning through, and replacing, the parts of our parts. Enzymes and neurotransmitters are depleted and replaced in countless numbers daily. Hormones and other chemical messengers are, in essence, Kamikazes -- fulfilling their physiologic mission only at the cost of their own molecular suicide. These, too, must be replaced daily. There is as well a daily turnover of hundreds of millions of our cells. We are, to some extent, a bit like rivers -- renewed by the flow and flux of ourselves, and never entirely the same.

Compelling as all that may be, it pales in comparison to the reliance on food as a basic construction material in the first place -- for in childhood, it is exactly that. The adult human body is being renewed, but is no longer being manufactured from scratch. The embryonic and then infant version of us is subject to just that phenomenon. But, of course, matter cannot be constructed from nothing; it must come from the conversion of energy, or from other matter.

The growth of human children is a product of both, with food supplying both the energy and the construction material. I have noted before that once we acknowledge food as the one and only source of construction material for the bodies of children we love, "junk food" rather loses its sheen of harmless fun. There is nothing harmless in the construction of something we hope to thrive through decades out of junk.

In all matters of human construction, and refurbishment, the distribution of materials on hand is obviously germane. Just as the construction of a well-made house depends on the right materials in the right proportions, so too the manufacture and maintenance of the human body, and brain.

One very well characterized illustration of this is the relationship between omega-6 and omega-3 fats. These are both families of polyunsaturated fats, and both described as "essential fatty acids," because our bodies need them and cannot manufacture them without dietary intake.

These fats have opposing effects, which may be simplistically described as "pro" and "anti" inflammatory. They enter into the same biochemical pathways, but then travel down different branch points. As a result, they can compete with one another both in their effects, and in their use of the available assembly lines. Too much dietary omega-6 fat, for instance, relative to omega-3 fat, will co-opt the machinery required to make long-chain omega-3s, and use it to crank out long-chain omega-6 fats instead, notably arachidonic acid.

The right way to think of all this is not in terms of good and bad, but rather in terms of balance. Omega-6 and omega-3 fats are Yin and Yang to our metabolism. We need them both, and we need them in proportion, to achieve the right balance between the pro-inflammatory molecules that help us fight off microbes and cancer cells; and the anti-inflammatory molecules that defend us against allergy, autoimmune disease, and chronic degenerative diseases as well.

In addition to this role, essential fatty acids are of structural importance to our cells, contributing to the composition of cell membranes. This proves to be of singular importance to brain development, and function. The human brain is, apart from adipose tissue itself, the fattiest organ in the body, and it preferentially soaks up docosahexaenoic acid (DHA), a long-chain omega-3 fat. Numerous studies suggest functional, developmental, and cognitive liabilities from a deficiency of this crucial, structurally important molecule. Humans get this nutrient from one of two sources. We can consume it, from breast milk as infants -- which is among the reasons for the many established benefits of breast milk over all alternatives -- and later from foods such as fatty fish. Or, we can make it from a precursor, a shorter-chain omega-3 called alpha linolenic acid (ALA), found in a variety of plant foods, notably walnuts, flaxseeds, algae, hemp and chia seeds.

This is where the riveting, and directly relevant dialogue with colleagues last week picks up. My friend and colleague, Dr. Tom Brenna, a nutritional biochemist at Cornell, described research showing that when malnourished children are given a therapeutic food with a relative excess of omega-6 fat (particularly, linoleic acid), they wind up with a relative deficiency of DHA in their blood -- and thus, their brains. This is because the surplus omega-6 fat blocks the pathway that would allow the body to make DHA from ALA. The concerning implication of this, then, is that supplemental ALA would not fix the problem, and the research findings indicate exactly that.

Dr. Brenna discussed the evidence that in the presence of excessive omega-6 fat, supplemental ALA will boost levels of one long-chain omega-3, called eicosapentaenoicacid (EPA), but not DHA. Another colleague at the meeting, Dr. David Nieman of Appalachian State University, described intervention research with adult athletes, corroborating exactly this result. When athletes were fed high concentrations of ALA, their levels of ALA and EPA rose; but in the context of high, habitual intake of omega-6 fat, their DHA levels did not budge.

These findings pertain directly to a massive, population-level dietary trend. Over recent decades, more and more of the oil in the typical American diet has come first from corn, and then from soybeans. In both cases, that oil is an unusually concentrated source of omega-6, linoleic acid. The direct metabolic implication of this is immediately clear: the production of DHA is being inhibited at an enormous scale.

The public health ramifications are less clear, but clearly worrisome. Is widespread interference with the production, and brain uptake of DHA, a contributing factor to trends in autism, ADD, and other disorders of behavior and cognition? Proof of causality is an elusive standard, but the proposition is every bit as plausible as it is disturbing.