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Robert Rowan, MD
The Toxic Impact of Heat on Food
Dr. Rowan is a well-known integrative medicine practitioner, author, and lecturer from Santa Rosa, California. He has been the editor-in-chief of Second Opinion, an international, monthly medical newsletter, for the last 12 years.1
Tracing his personal dietary history from carnivore/omnivore to a vegan/raw foods diet, he shared his exceptional personal improvements in physical fitness such as hiking Mount Whitney without injury as had befallen him on a previous attempt. Also improved were his blood parameters and blood pressure.
Were We Meant to Eat Meat?
Rowan noted that carnivore teeth are sharp for cutting. Herbivore: flattened for grinding. Human molars are for grinding. Carnivore jaws move vertically for tearing. Herbivores move horizontally for grinding. Human jaws grind. Carnivore intestines are short, three times torso length for eliminating the toxic byproducts of protein digestion quickly. Herbivore intestines are far longer, up to 30 feet. Carnivores cool by panting, herbivores cool through perspiration. Humans perspire. He concluded that there are many other parameters which prove the point that we should be vegetarian.
From 1932 to 1942, Francis M. Pottenger Jr., MD, of the famous Price-Pottenger Nutrition Foundation, studied experimental diets and physical characteristics of 900 unwanted cats. Their diets were identical in two groups except that one group was fed 2/3 raw meat with 1/3 raw milk and cod liver oil and the other was feed 2/3 cooked meat with 1/3 raw milk and cod liver oil. In every imaginable parameter, the raw-meat cats did much better through several generations of litters. Skull configuration, distinctive sex characteristics, tissue tone, quality of fur, bone makeup, resistance to infection from fleas and parasites, signs of allergy, and friendly, predictable, behavior were much better in the raw-food group. Miscarriages were rare and the litters averaged five kittens with the mother cat nursing her young without difficulty. In the cooked-food group there were great differences in size and skeletal patterns; even second and third generations of cats found many differences in dental and facial structure. In the third generation, some of the bones became soft and spongy or overly brittle. They had heart problems, nearsightedness and farsightedness, underactivity of the thyroid gland, infections of the kidney, liver, testes, ovaries, and bladder, with arthritis and inflammation of the joints, nervous system with paralysis, and meningitis. Abortions in females were rampant, running 25% in the first generation to as high as 70% in the second. The cooked-meat group had increased intestinal parasites, skin lesions, allergies, pneumonia, empyema, and diarrhea, leading to death. There was a high perinatal mortality of both mothers and kittens, with the kittens weighing 19 grams less than those in the raw-meat group. It required four generations for the deficient cats to regenerate to a state of normal health after the raw diet was reinstituted. A female cat subjected to a deficient diet for a period of 12 to 18 months caused her reproductive efficiency to be so reduced that she could never again bear normal kittens. An interesting rebuttal to the applicability of Pottenger's study to humans is "Lesson Of the Pottenger's Cats Experiment: Cats Are Not Humans" (http://www.beyondveg.com/tu-j-l/raw-cooked/raw-cooked-1h.shtml), especially as to cats' inability to synthesize taurine, which can be destroyed by heat and deficiency of which causes neurological damage.
Rowan thinks that Pottenger's experiment mirrors modern experiments on epigenetics (alterations in DNA expression) using nutrition deficiencies and environmental xenobiotics which may promote epidemics of autism, immune defects, cancer, allergy, suicide, violent behavior, and chronic disease.2
Maillard Reaction, AGES, Acrylomides, Pentosidine
The Maillard reaction imparts the unique taste and smell of cooked foods; however, it creates compounds not found in nature, such as acrylamides, now known to be carcinogens. The browning of meats, toasted bread, biscuits, malted barley or spirits, fried onions or any fried food, dried or condensed milk, and roasted coffee are all examples of the Maillard reaction. It also occurs in the human body. It is a step in the formation of advanced glycation end products (AGEs). This process can be tracked by measuring pentosidine. While studied in foods, it has shown a high correlation in different aging diseases, particularly degenerative eye diseases. AGEs accumulate on nucleic acids, proteins, and lipids. They can form from pathological oxidation reactions. AGEs are now correlated with a wide range of human degenerative conditions such as diabetes complications, pulmonary fibrosis, and neurodegeneration.
In experimental trials, a group of 344 rats was split into a control diet and a thermolyzed diet with short exposure of 122 ºC for 30 minutes in an atmosphere devoid of oxygen. Hence oxygen could not be the culprit in findings, but heat. The experimental group became thiamine deficient measured by transketolase with increased oxidative stress measured by reduced GSH. The experimental group had increased markers of Maillard reactions measured by the presence of a-oxoaldehydes (glyoxals and methyl glyoxals). The protein adducts of these carbonyls and protein oxidation levels were increased. The experimental diet also increased oxidative stress biomarkers in livers and colons and increased macrophage infiltration into colons by 4-fold. This infiltration was believed to be caused by AGEs interacting with cell surface receptors. AGEs were believed to be signaling inflammatory cytokines such as TNF alpha. Nitrotyrosine is formed by the reaction of tyrosine and peroxynitrite (formed by NO reacting with superoxide). Nitrotyrosine adducts were increased in the plasma, liver, and colon of the experiment group with the highest concentration (3.6x) found in the colon. The same research group previously found that a thermolyzed diet leads to non-beriberi thiamine depletion, which increases oxidative stress and aberrant crypt foci (ACF), a forerunner of colon cancer.3
What about Heated Fats?
Heating oils creates an alphabet soup of damaged, oxidized, and carcinogenic byproducts that are implicated and proven to disrupt cell membranes and create disease. Nonesterified fatty acids are an independent risk factor of sudden death in middle-aged males, as well as PVCs and ventricular tachyarrhthmias.4 Dr. Rowan gave in-depth documentation of the nomenclature of all the adducts of thousands of individual new compounds and explained the poor information on the cell membranes and intracellular membranes that causes extremely toxic reactions for our body economy.
Metabolic Rate, Membrane Composition, and Lifespan
Membrane damage via vulnerable fatty acids means that saturated and monounsaturated fatty acyl chains (SF and MUFA, respectively) are essentially resistant to peroxidation while polyunsaturated fatty acids (PUFAs) are damaged. Furthermore, the greater the degree of polyunsaturation of PUFA, the more prone it is to peroxidative damage. Holman empirically determined (by measurement of oxygen consumption) the relative susceptibilities of the different acyl chains.5 Docosahexaenoic acid (DHA), the highly polyunsaturated omega-3 PUFA with 6 double bonds, is extremely susceptible to peroxidative attack and 8 times more prone to peroxidation than linoleic acid (LA), which has only 2 double bonds. DHA is 320 times more susceptible to peroxidation than the monounsaturated oleic acid (OA). Thus lipid peroxidation should not be perceived solely in a "damage to lipids" scenario, but also considered a significant endogenous source of damage to other cellular macromolecules, such as proteins and DNA (including mutations). In this way, variation in membrane fatty acid composition, by influencing lipid peroxidation, can have significant effects on oxidative damage to many and varied cellular macromolecules. For example, peroxidized cardiolipin in the mitochondrial membrane can inactivate cytochrome oxidase by a mechanism similar to hydrogen peroxide. Because the PUFAs are more vulnerable to free radical attack, they experience greater lipid oxidative damage, and lipid peroxidation products have been shown to contribute significantly to membrane rigidity. Lipid peroxidation products and peroxidized lipids are likely dominant factors in creating age-related membrane rigidity.
Experimental mammals of similar size show differences in longevity related to the content of DHA in their cell membranes, with the high-DHA animals being shorter lived. The relationship between human longevity, membrane composition, and dietary DHA in humans may be complex and is still to be fully elucidated. For example, humans with severe coronary atherosclerosis have erythrocyte membranes with more PUFAs and particularly more DHA.
Cholesterol Oxidation Products (COPs - Oxysterols)
COPs (damaged cholesterol) occur from nonenzymatic conversion (via reactive pro-oxidants such as metals) or enzymatic catalysis as well as heating.6 The toxicity of COPs has been well studied and may induce apoptosis and necrogenic effect on vascular cells, and is pro-inflammatory and highly atherogenic, while cholesterol itself is not. Oxidized lipids form easily in heated food, occur spontaneously in vivo (membrane peroxidation), and result in cleavage of the cholesterol molecule, creating ketones and aldehydes (highly teratogenic) and polymerization of molecules akin to boiled linseed oil.
In a recent study, Chien et al. studied the kinetics of cholesterol oxidation during heating of cholesterol at 150 ºC for up to 30 minutes.7 The COPs concentration was found to increase with increasing heating time. Routine cooking of meat (beef, veal, and pork) was done in an electric skillet (135 ºC) for 10 minutes each side and compared with raw. The COPs levels of cooked beef, veal, and pork increased by 1.7-, 2.3-, and 2.5-fold respectively. When beef, pork, and veal were oven-cooked at 220 ºC for 60, 80, and 90 minutes, respectively, the COPs levels increased by 3.5-, 5.4-, and 4.2-fold.
The three-dimensional structure of protein is destroyed by heating. Rowan likens this process to the effect of a tornado on a city. All the components of the homes are still present - but three-dimensional structure is gone.
He lists typical nutrient losses from heating and concludes by stating his "Rowan Theory."8 Cooked foods are adding molecular compounds to human biological systems never before seen in our evolution. Is it possible that these "foreign" and unmetablolizable compounds are gumming up our cell membranes and cellular machinery? He postulates that this is so, and is at least in part responsible for cellular damage and adverse epigenetic effects in our modern population, compounded by toxic chemical excess and nutritional deficiencies.
Julia Ross, MA, MFT, NNTS
21st-Century Sugar Addiction: Defeating the Greatest Dietary Crisis of All Time
Julia Ross is executive director of Recovery Systems, Mill Valley, California. She directs an outpatient program that treats eating disorders and addictions, as well as mood problems more generally, with therapeutic nutritional protocols along with counseling, education, and holistic medical care. She has received many honors, awards, and appointments and has authored several publications, including her very successful books The Diet Cure and The Mood Cure.9,10
After demonstrating the differences in average dietary composition before and after 1970, she shows the pictures of the new malnutrition from fast food and vastly increased sugar consumption. She cites the recent publication by Robert Lustig, MD, pediatric endocrinologist at UCSF School of Medicine, who delineates the metabolic pathway of sugar and especially fructose in causing liver damage and obesity, particularly childhood obesity.11
Recent annual worldwide deaths due to tobacco use were calculated at 5.3 million and deaths due to sugar consumption at 35 million. Another study revealed that 15 million US binge eaters and many more overeaters comprise our 60% overweight population. Subjects in the study who were provided unlimited sweets one hour/day became binge eaters in 2 weeks, consuming 4 times more food than controls.
A University of Bordeaux study in 2007 found that sugar and sugar substitutes are 4 times more addictive than cocaine. She asserts that sugar is an addictive drug. The definitions of addiction: loss of control, continued use despite adverse consequences, withdrawal symptoms, and relapse.
Addiction and Neurotransmitter Deficits
Ross focuses on the deficient neurotransmitters of serotonin, GABA, catecholamines (norephinephrine and dopamine), and endorphin as causes of sugar addiction. Richard Wurtman from MIT and other researchers have documented sugar dependency via insulin-mediated serotonin activation since the 1980s. Multiple studies from1982-2012 document that sweets addict via endorphin (opiate) pathways. Hypoglycemia creates well-documented cravings for sugar to relieve the danger to the brain caused by glucose crashes.12 Like cocaine, sugar can "reward" by stimulating dopamine activity.13
Ross lists addictive foods as sucrose (glucose and fructose), high-fructose corn syrup (HFCS; glucose and fructose), refined starch, chocolate, gluten, and casein (cow's milk protein). Fructose in HFCS is twice as sweet as glucose and generates equal amounts of triglycerides lasting 12 times longer in the blood and is equal in liver damage to alcohol. HFCS has increased in soda intake by 135% since 1970, and powerful satiety factors are specifically dysregulated by fructose: insulin, leptin, ghrelin, as well as glucose. Our modern diets that skip meals, with low protein, low good fats, caffeine, diet foods, sodas, appetite suppressants, and artificial sweeteners can cause overeating and bulimia. Voluntary starvation can cause drops in blood sugar, serotonin, and thyroid levels within 8 hours and creates rebound cravings, overeating, negative moods, weight gain, eating disorders, and health decline.
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