All About Cooking & Carcinogens
We know that cooking food has some benefits:
- It can make food safer
- It can concentrate tastes and flavors
- It can reduce spoilage
- It can soften tough foods
- It increases the amount of energy our bodies can get from food
- It breaks starch molecules into more digestible fragments
- It denatures protein molecules
But before we get too excited about cooking, the modern diet can be overwhelmingly heat-processed. Higher cooking temperatures can create chemical reactions among amino acids, creatines, and sugars — reactions that may produce dangerous carcinogens and mutagens (compounds that can damage our DNA).
Now suddenly we have “unhealthy” compounds created in otherwise “healthy” foods — stuff like potatoes, fish, whole grains, etc.
Don’t freak out and throw your barbecue grill off the balcony just yet. Let’s start by learning more about what these compounds are, and how they work.
Cooking creates chemical compounds
Heat plus food molecules can create several products in the process of chemical conversion known as cooking. (And you thought you were just slapping a burger on the grill! Now you can say “I am chemically converting proteins!” Fancy.)
Some of the most notable end products include:
- Heterocyclic amines and polycyclic aromatic hydrocarbons
- Advanced glycation end products
Let’s look at each of these in more depth.
Heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs)
What are they and where do they come from?
HCAs are made when creatines and amino acids (both found in meats) react together with heat. PAHs include over 100 different compounds formed by the incomplete burning of organic matter (e.g., oil, gas, coal, food, etc.) at temperatures in excess of 392 degrees F (200 C).
Thus, raw foods don’t have HCAs nor PAHs. Indeed, more than 90% of our exposure to HCAs and PAHs comes from cooked food.
Protection against loss of innate defenses in adulthood by low advanced glycation end products (AGE) intake: role of the antiinflammatory AGE receptor-1.
Increased oxidant stress and inflammation (OS/infl) are linked to both aging-related diseases and advanced glycation end products (AGEs). Whereas AGE receptor-1 (AGER1) reduces OS/infl in animals, this has not been assessed in normal humans.
The objectives of the study were to determine whether AGER1 correlates with AGEs and OS/infl and a reduction of dietary AGEs (dAGEs) lowers OS/infl in healthy adults and chronic kidney disease (CKD-3) patients.
This study was cross-sectional with 2-yr follow-up studies of healthy adults and CKD-3 patients, a subset of which received a reduced AGE or regular diet.
The study was conducted at general community and renal clinics.
Participants included 325 healthy adults (18-45 and >60 yr old) and 66 CKD-3 patients.
An isocaloric low-AGE (30-50% reduction) or regular diet was given to 40 healthy subjects for 4 months and to nine CKD-3 patients for 4 wk.
Relationships between age, dAGEs, serum AGEs, peripheral mononuclear cell AGE-receptors, and OS/Infl before and after reduction of dAGE intake were measured.
AGEs, oxidant stress, receptor for AGE, and TNFalpha were reduced in normal and CKD-3 patients after the low-AGE diet, independently of age. AGER1 levels in CKD-3 patients on the low-AGE diet resembled 18- to 45-yr-old normal subjects. Dietary, serum, and urine AGEs correlated positively with peripheral mononuclear cell AGER1 levels in healthy participants. AGER1 was suppressed in CKD-3 subjects, whereas receptor for AGE and TNFalpha were increased.
Reduction of AGEs in normal diets may lower oxidant stress/inflammation and restore levels of AGER1, an antioxidant, in healthy and aging subjects and CKD-3 patients. AGE intake has implications for health outcomes and costs and warrants further testing.