“I’ll have the egg white omelet, please.”
Since the 1950’s, we’ve been told that eating fat makes you fat and that avoiding traditional fats (i.e. butter, animal meats, lard, eggs) in lieu of industrialized, man-made fat substitutes is highly recommended. Why did we agree to disavow several millennia of instinctive eating in favor of a high carb and sugar diet, deficient in this staple? It started with a misinterpretation of a manipulated study. In 1958, Ancel Keys set out to “prove” a correlation between the consumption of saturated fat (rendered synonymous with animal fat which is typically high in poly- and monounsaturated fats) and heart disease. He tabulated the incidence of this multidimensional, chronic medical problem in 22 nations, but must have been disappointed by the scattered dots on his graph, so he obscured a couple of them until he found a linear relationship between 6 of those surveyed. This study seemed to be the green light that corporate food execs needed to get to work making and distributing hydrogenated butter-like substances and processed vegetable oils. In the wake of this tremendous shift in nutrition paradigm, we have enjoyed ever-escalating rates of chronic inflammatory diseases like diabetes and the very heart disease we were aiming to prevent. But what beyond an over-worked pancreas and an irritated vascular system do we have to worry about in this low-fat world?
Here I would recommend that women struggling with hormonal imbalance and mood symptoms listen up, because it turns out that cholesterol is a vital nutrient for brain health, a fact that has gotten lost amidst all the fat-hating. Have you noticed, on your lab results, that there is an upper limit, but no lower limit, for normal total cholesterol? This may be related to a gross lack of appreciation for the risks associated with hypocholesterolemia. Cholesterol performs many vital functions, but we’ll focus on three specifically: cell membrane structure and support, hormone synthesis, and vitamin D production.
As my patient’s results come in, I often note that those with fertility, premenstrual, and postpartum (> 3 months) mood symptoms invariably present with a fasting cholesterol below 160. Their internists may be impressed and pleased with their low fat diets, but I’m not. Rather than experiencing reassurance that waxy goo is not clogging up their pipes, I envision floppy, decrepit cell membranes adrift in a hormone-less wasteland. The cell membrane is an 8 nanometer thick magical pearly gate where information, nutrients, and cellular messengers are trafficked through protein gates supported of phospholipids and their polyunsaturated fatty acids. Cholesterol and saturated fat provide essential rigidity in balance with other membrane components. Without them, the membrane becomes a porous, dysfunctional swinging gate. In a self-preservational effort, cholesterol supports production of bile acids, integral to the breakdown and absorption of consumed essential dietary fats.
This very same lipid is also recruited to produce pregnenolone, the sex hormone precursor without which reproductive function goes very awry. Think libido, harmonious menstrual cycle, clear skin, balanced metabolism, cognition. Additionally, vitamin D, a steroid-like wonder hormone is produced from cholesterol precursors and its deficiency appears to be correlated with maladies too numerous to mention.
Perhaps related to these vital functions, perhaps to others yet undiscovered, low cholesterol has also been linked to suicide and depression. (Kunugi et al, Biol Psych, 1997) (Modai at al, J Clin Psych, 1994) ( Lindberg et al, BMJ, 1992) In patients hospitalized for affective episodes, significantly more patients than controls were noted to have low plasma cholesterol. (Gluek et al, Am J of the Med Sci, 1994). A Duke University study assessed the correlation between depressive and anxious personality traits and low cholesterol. Another looking at the Melbourne Women’s Midlife Health Project suggested that improved performance on memory testing was achieved with increased total cholesterol in women longitudinally monitored.
But the medical industrial complex would have you believe that cholesterol-lowering medications equate to preventive medicine. This is one area we really should have held out on a bit. First we need to better understand some of the putative mechanisms of heart disease, and why there are exceptions to the “high cholesterol = mortality” theory that seriously beg our attention. Where there are numerous exceptions, there’s a flawed theory, and we are watching the error of our ways unfold before us in the form of transient global amnesia, neuropathy, heart failure, pancreatitis, and cognitive impairment. There is also speculation that the potential positive effects of cholesterol lowering are secondary to anti-inflammatory (blocking mevalonate) effects, and that lowering of cholesterol may be an unnecessary and potentially harmful byproduct of a therapeutic action. The ripple effects of our creative scientific interventions may not be felt until decades after they are widely implemented, but these ripple effects are germane to targeted medication treatment.
With an eye toward minimizing sources of inflammation such as sugar and sugar-like foods, maximizing nutrient dense whole foods, and running from commercial concoctions, we can help support our innate bodily processes and the myriad interrelated connections that a linear model fails to encompass.