Eric Garza

Musings on food, energy and adaptation

To Cook or Not To Cook: The Question of 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.

To Cook or Not To Cook: The Question of 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.

To Cook or Not To Cook: The Question of Acrylamide

In 2002, Swedish researchers published a report noting their surprising discovery of the carcinogen acrylamide in several human foods, particularly starch-rich foods like fried potatoes [1]. The finding touched off a fierce, if brief, media frenzy that prompted outrage from citizens wondering what this horrible chemical was doing in their food. The frenzy spread throughout Europe and eventually to the United States, where in 2005 California Attorney General Bill Lockyer sued several snack and fast food producers to force the companies to add a warning label to their products noting the presence of acrylamide [2]. The case was settled out of court, the companies promised to reduce their products’ acrylamide levels, and media coverage of the issue has since waned.

French FriesAcrylamide is produced in food when the amino acid asparagine reacts with sugar, particularly glucose, when heated above 248 degrees Fahrenheit [3, 4]. This reaction is among those that produce the brown color on food due to heating, including the browning of toast, fried foods and barbecued meat. Unlike heterocyclic amines, which are typically found only in cooked meats, acrylamide will form in any cooked food that contains asparagine, including both plant and animal foods. Asparagine, you might note, is found in particular abundance in asparagus, and gives the urine of asparagus eaters that very particular, pungent scent. Depending on how a food item is prepared its total content of acrylamide can vary tremendously, with some researchers measuring up to parts per million levels in certain foods.

Given the relatively short amount of time that acrylamide’s dietary sources have been known, it shouldn’t surprise anyone that the overall risk posed by dietary consumption of the chemical remains controversial. Some epidemiological studies have documented a link between dietary intake of acrylamide and increased risks of endometrial and ovarian cancer [5, 6], which isn’t surprising given acrylamide’s capacity to interfere with sex hormones [7]. Links to most other forms of cancer seem absent. Given the capacity of acrylamide to interfere with sex hormones in women, it strikes me that the compound may be an endocrine disruptor, although I failed to find any references noting this.

It’s important to note that most all epidemiological studies attempting to link the consumption of dietary toxins – including acrylamide – to particular diseases are based on questionnaires asking participants to self-report their diets. These questionnaires can have inaccuracies. Even when accurate, food frequency questionnaires don’t provide data on actual toxin consumption, which must be inferred from data on common levels of toxins in particular consumed foods. The end result is a huge degree of uncertainty in actual acrylamide consumption among individuals who participate in most epidemiological studies, creating opportunities for both false-negatives and false-positives.

The amino acid asparagine, the necessary precursor to acrylamide, isn’t an essential amino acid; we can manufacture it in our bodies, and don’t need to consume it in our diets. Nonetheless it’s a very common one in foods we eat, and can be found in animal foods like meat, eggs and dairy products as well as vegetable foods like asparagus, potatoes and seeds of various sorts, including legumes, nuts and grains. It’s not necessary to avoid eating these foods, but if we want to minimize our dietary exposure to acrylamide we’d benefit from preparing them in ways that don’t require exposure to excessively high heats. Boiling and steaming seem to avoid acrylamide formation, and of course eating foods containing asparagine raw won’t result in toxin formation either.

Notes

  1. Analysis of acrylamide, a carcinogen formed in heated foodstuffs. E. Tareke, et alJournal of Agriculture and Food Chemistry, 2002, Vol. 50, Pgs. 4998-5006.
  2. Attourney General Lockyer Files Lawsuit to Require Consumer Warnings About Cancer-Causing Chemical in Potato Chips and French Fries. August 26, 2005. State of California Department of Justice, Office of the Attorney General.
  3. A review of mechanisms of acrylamide carcinogenicity. A. Besaratinia & G. Pfeifer, Carcinogenesis, 2007, Vol. 28, Pgs. 519-528.
  4. The acrylamide problem: a plant and agronomic science issue. N. Halford, et alJournal of Experimental Botany, 2012, Vol. 63, Pgs. 2841-2851.
  5. The plight of the potato: is dietary acrylamide a risk factor for human cancer? L. Mucci & H-O. Adami, Journal of the National Cancer Institute, 2009, Vol. 101, Pgs. 618-621.
  6. Mechanistic insights into the cytotoxicity and genotoxicity induced by glycidamide in human mammary cells. S. Bandarra, et alMutagenesis, 2013, Vol. 28, Pgs. 721-729.
  7. Associations between dietary acrylamide intake and plasma sex hormone levels. J. Hogervorst, et alCancer Epidemiology, Biomarkers and Prevention, 2013, Vol. 22, Pgs. 2024-2036.