Eric Garza

Musings on food, energy and adaptation

Know Your Fats

Like most in my generation, I grew up in a fat-phobic household. We used margarine, not butter, and I remember my parents and even my grandparents goading me to cut every last shred of fat from pieces of meat they served me. Sometimes I’d sneak a bite anyway – it tasted so good! – but most of the time, like a good little boy who didn’t know any better, I did as I was told. Funny how we change as we get older.

I can’t come up with a precise date for when I started to look at my family’s fat-phobia with that first hint of skepticism. Perhaps it was when I entered college and learned how important a role the availability of animal fat played in our human lineage’s development of larger brains. Perhaps it was while chatting with a biochemistry instructor who was just infatuated with the metabolism of fatty acids in the human body. Perhaps it was just that lingering curiosity about why something that tasted so good, something that was so satiating, could be so bad for me. At any rate, perhaps 15 years back I started looking into the phenomenon of fat-phobia, and even back then my findings were downright fascinating.

Know Your FatsWhile it wasn’t the first book I read on fat, Mary Enig’s Know Your Fats has become my reference book of choice on the topic. Originally published in 2000 the book explored the incredibly important role that fats play in human health, both over an individual’s life as well as across generations. Know Your Fats is not a book of narrative, not a book filled with storytelling like those written by the likes of Michael Pollan or other notables in the emerging local food movement. It’s a dense, to-the-point, these-are-the-facts sort of reference book, the kind you read once to learn the book’s layout, then return to as needed to refresh your memory on specific topics. It’s a book that’s held a space on my personal bookshelf for years, although I’ll admit I’m on my third copy as I’ve twice made the mistake of lending it out to folks who found excuses not to return it.

The copies I’ve had over the years have proved their worth many times over, and do so even more frequently now that I’m offering more talks on ancestral health. I frequently turn to my current copy for pre-talk refreshers, and particularly find myself referring to chapter 4, which offers an in-depth look at the many sources of fat in our modern food supply and explains clearly the differences between so called ‘vegetable’ oils pressed from seeds like corn, soya and rape and more natural sources of animal fat. Admittedly the book’s age is starting to show, as a wealth of research has been done since Know Your Fats went to press over a decade ago, and some of that research fills important gaps or paves new ground such as studies researching advanced lipoxidation end products, but despite the book’s age it still holds its own.

Dr. Mary EnigWhile Mary Enig’s Know Your Fats is deserving of a review solely on its own merit, this review happens to be particularly timely. After a long, distinguished professional career and over a decade serving on the board of directors of the Weston A. Price Foundation, Mary Enig passed away earlier this September at the ripe age of 83. I never had a chance to meet her in person, but regardless she’s someone I’d come to deeply respect not only for her scientific acumen but also for her willingness to speak truth to power against those who continue to push fat phobia down people’s throats. In addition to Know Your Fats, Enig co-wrote Nourishing Traditions, a cookbook based loosely on the dietary ideals of dentist Weston A. Price, and the more recent book Eat Fat, Lose Fat, with Weston A. Price Foundation President Sally Fallon. Mary Enig’s passing will be grieved by many, even as her decades of thorough research are celebrated.

Advanced Glycation Endproducts

Earlier posts on heat-created toxins focused on heterocyclic amines, acrylamide and polycyclic aromatic hydrocarbons. While these are all worrisome – and to a large degree avoidable – compounds, I’ve saved the group of heat-generated toxins that concern me most for this post: advanced glycation end products. These compounds, often abbreviated as AGEs, are created when sugar molecules or their byproducts react with a molecule with a free amino group, such as proteins, lipids or nucleic acids, in the absence of enzymes [1]. While these compounds were first characterized in the 1950s, only since the 1980s has serious effort been invested to understand their role in human health, or more specifically their role in chronic, degenerative disease.

BaconAdvanced glycation end products form on their own in the human body, most commonly on long-lived tissues like the collagen fibers that compose our connective tissue and the myelin that forms the protective membranes surrounding our nerves. This is problematic because AGEs cause cross-linking in these tissues, reducing their flexibility and making them challenging to heal or rebuild. In addition to their native creation within the human body, AGEs are also formed in foods through cooking – particularly in grilling, frying and baking – and when ingested they add to the AGE burden of the body [2].

Excessive AGE levels in the body have been linked with the progression of many chronic, degenerative diseases, largely because the compounds and the cross-links they cause are inflammatory [2-4]. Because so many chronic degenerative diseases are linked to chronic inflammation, dietary AGE exposure and native AGE production within the body should be something health conscious people pay attention to. Diabetics, because of their inability to control their blood sugar, often have elevated levels of AGEs in their tissues that lead to a range of health complications, and additional intake of dietary AGEs doesn’t help [5, 6]. With heart disease, AGE-caused cross-links in the walls of blood vessels trap lipids like cholesterol, initiating and promoting the formation of the arteriosclerotic plaques that characterize this condition [2, 7].

Owing to the fact that dietary sources of AGEs are known to have health impacts, reducing our dietary intake of these compounds can have therapeutic value [8]. Data is available on the AGE content of different foods prepared different ways, and, in general, dairy products, cooked meats, and foods containing processed, cooked grains contain the most AGEs, with fried meats – particularly bacon – containing the highest levels [9]. Raw meats contain far lower levels of AGEs than cooked meats, although even raw meats have higher AGE contents than raw fruits and vegetables.

AGE contents of foods

As with the previously listed heat-created toxins, I see value in reducing my exposure to AGEs. In fact, given AGEs’ role in inflammation and these compounds’ links to chronic degenerative diseases such as arteriosclerosis and diabetes, I find myself inspired to be even more conscientious about reducing my dietary intakes than of other heat-created toxins. It’s quite convenient that the very processes that yield high levels of AGEs in foods also yield high concentrations of other heat-created toxins, making my task of avoidance quite a bit easier.

Notes

  1. Advanced glycoxidation and lipoxidation end products (AGEs and ALEs): an overview of their mechanisms of formation. G. Vistoli et alFree Radical Research, 2013, Vol. 47, Pgs. 3-27.
  2. Diet-derived advanced glycation end products are major contributors to the body’s AGE pool and induce inflammation in healthy subjects. J. Uribarri et alAnnals of the New York Academy of Science, 2005, Vol. 1043, Pgs. 461-466.
  3. Advanced glycoxidation end products in chronic diseases – clinical chemistry and genetic background. M. Kalousová et alMutation Research, 2005, Vol. 579, Pgs. 37-46.
  4. Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation. R. Ramasamy et alGlycobiology, 2005, Vol. 15, Pgs. 16R-28R.
  5. Advanced glycation end products: a review. R. Singh et alDiabetologia, 2001, Vol. 44, Pgs. 129-146.
  6. Advanced glycation endproducts – role in pathology of diabetic complications. N. Ahmed, Diabetes Research and Clinical Practice, 2005, Vol. 67, Pgs. 3-21.
  7. Glycoxidation and lipoxidation in atherogenesis. J. Baynes & S. Thorpe, Free Radical Biology & Medicine, 2000, Vol. 28, Pgs. 1708-1716.
  8. Food-derived advanced glycation end products (AGEs): a novel therapeutic target for various disorders. S. Yamagishi et alCurrent Pharmaceutical Design, 2007, Vol. 13, Pgs. 2832-2836.
  9. Advanced glycation end products in foods and a practical guide to their reduction in diet. J. Uribarri et alJournal of the American Dietetics Association, 2010, Vol. 110, Pgs. 911-916.

Polycyclic Aromatic Hydrocarbons

Polycyclic aromatic hydrocarbons, often abbreviated as PAHs, are a group of compounds that, in addition to their natural occurrence in crude oil and coal deposits and their common release from automobile exhaust pipes and factory smokestacks, are readily created by different cooking processes. As with other heat-created toxins, PAHs are most readily formed when foods are cooked at high heat – by grilling or frying – or when foods are exposed to direct flame or smoke [1-3]. While grilled, fried and smoked meats are commonly recognized as being contaminated by PAHs, other foods, among them breads, can also be contaminated by PAHs when toasted or baked such that they’re exposed to smoke or flame, as when loaves of bread are baked in wood-fired ovens [4, 5].

Smoked meatMost, but not all, polycyclic aromatic hydrocarbons are toxic. Their primary mode of action appears to be the formation of highly reactive metabolites created by activation via our native P450 enzymes, the enzyme dihydrodiol dehydrogenase, or free radicals [3, 6]. Once so activated, PAHs can form adducts that bind to and damage DNA. The overall impacts of this DNA damage will depend on where it happens in the body, and which genes are affected.

Several PAHs are classified as probable carcinogens by the United States Environmental Protection Agency, owing to their demonstrated capacity to cause DNA damage that impedes the capacity of cells to properly regulate cell growth [7]. One PAH, benzo(a)pyrene, carries the distinction of being the first chemical to be identified as having carcinogenic properties. DNA damage in developing germ cells (sperm in men, eggs in women) can also possibly lead to birth defects or other developmental problems.

Beyond their mutagenic effects, PAHs have also been demonstrated to promote the formation of arteriosclerotic plaque in arterial walls [8]. As with their role in causing DNA damage, this process begins with the metabolic activation of PAHs, although beyond this point the precise mode of action remains unclear; PAHs may induce arteriosclerosis via their normal DNA damaging pathways, epigenetics may play a role, or perhaps they contribute via promotion of chronic inflammation. Regardless, the link between PAH exposure and arteriosclerosis seems fairly strong.

While there are many routes of exposure to PAHs, dietary ingestion is known to be among the most important for most people [3]. Given that our eating habits play a substantive role in determining our exposure to these compounds, I’ve chosen to make adjustments in my own eating patterns to lessen by exposure and thus reduce my risk of PAH-mediated health impacts. Avoiding foods that are cooked at high temperatures or exposed while cooking to flames and/or smoke seems easy enough, at least to me.

Notes

  1. Toxic Substances Portal – Polycyclic Aromatic Hydrocarbons (PAHs). Agency for Toxic Substances and Disease Registry, United States Center for Disease Control and Transmission.
  2. Concentrations of polybrominated diphenyl ethers, hexachlorobenzene and polycyclic aromatic hydrocarbons in various foodstuffs before and after cooking. G. Perelló, et alFood and Chemical Toxicology, 2009, Vol. 47, Pgs. 709-715.
  3. Bioavailability and risk assessment of orally ingested polycyclic aromatic hydrocarbons. A. Ramesh, et alInternational Journal of Toxicology, 2004, Vol. 23, Pgs. 301-333.
  4. Effects of toasting procedures on the levels of polycyclic aromatic hydrocarbons in toasted bread. L. Rey-Salgueiro, et alFood Chemistry, 2008, Vol. 108, Pgs. 607-615.
  5. Levels, fingerprint and daily intake of polycyclic aromatic hydrocarbons (PAHs) in baked bread using wood as fuel. S. Orecchio & V. Papuzza, Journal of Hazardous Materials, 2009, Vol. 164, Pgs. 876-883.
  6. Metabolic activation of polycyclic and heterocyclic aromatic hydrocarbons and DNA damage: a review. W. Xue & D. Warshawsky, Toxicology and Applied Pharmacology, 2005, Vol. 206, Pgs. 73-93.
  7. The Carcinogenic Effects of Polycyclic Aromatic Hydrocarbons, Ed. A. Luch, World Scientific, 2005, 516 Pgs.
  8. Bioactivation of polycyclic aromatic hydrocarbon carcinogens within the vascular wall: implications for human atherogenesis. K. Ramos & B. Moorthy, Drug Metabolism Reviews, 2005, Vol. 37, Pgs. 595-610.