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My variation of the diet is called "Cyclical Ketogenic Paleolithic" Some good references are: "Body Opus" by Dan Duchaine (for the athlete) "Neanderthin" by Ray Audette and the basic "Dr. Atkins New Diet Revolution" by Atkins :cool: TJ :cool:

CATEGORY: biology/metabolism TECHNICAL: ** SUMMARY: This document describes the main reason I tell people that low-carb diets are more effective that fasting, or low-cal (starvation type) diets. Everyone seems to think that by simply eating less they will lose weight.. That has simply never been true. In actuality, dieters should be striving to eat maintainance level calories and rely on activity to do the job. This keeps basal metabolism high instead of crashing it and placing you in "starvation mode". As you can see below, the net effect of low-cal diets is to decrease your thyroid output, and hence, your body's overall energy expenditure. (it gets greedy). This is the first document I've seen that's actually put a cut-off level on it. Their study showed that a 1000 cal/day deficit was enough for your body to turn off metabolism. Let's do the math.. 1000 kcal/day over 7 days is 7000 kcal/week. 7000 kcal is slightly less than 2 lbs. of fat. (one lb. of adipose is about 3550 kcal.). THEREFORE, according to this study, anyone who is losing 2 lbs. a week of weight cannot possibly be losing fat, and instead, it must be partly muscle that is being lost as well. (which is about right, as verified by other sources) So you see, why bother with killing yourself slowly with starvation diets? Try the low-carb approach and see if you, like many others, have a much easier time getting rid of that extra fat mass on your body. (aside from all of the health benefits of low carb diets too) ------------------------------------------------------------- Resting Metabolic Rate by Jeff Johnson, MS [ Jeff Johnson, MS of Performance Fitness & Nutrition is a strength & conditioning specialist and sports nutrition consultant, specializing in high performance and post-rehab conditioning. He is the exercise guide for The Mining Company at http://exercise.miningco.com ] In general, it appears that dieting decreases RMR, probably due to losses of muscle in fat-free mass. Some researchers believe that a permanently reduced metabolism is the reason that diets do not work and that weight is regained. Low calorie diets, in of themselves, as well as considerable energy expenditure (exercise) coincident with inadequate caloric intake have been found to have an effect on metabolism through reduced T3 hormone (triiodothyronine) production. This occurs almost immediately and long before any substantial loss in lean body mass occurs. This occurrence is sometimes referred to as the "starvation response". In a study on young women who exercise, it was found that T3 production was suppressed when "energy availability" fell below a 1,000 calorie-per-day level (Loucks 1994). "Energy availability" is the amount of energy available after subtracting caloric expenditure in exercise from daily caloric intake. The body is trying to conserve energy in a calorically restricted state. Thyroid hormone production and secretion decreases in an attempt to reduce basal metabolic rate and increase one's energy efficiency. Hypothyroidism often occurs coincident with diet-induced amenorrhea. Similarly, amenorrheic athletes frequently have depressed thyroid hormone concentrations compared to women with regular menstruation while training in a similar manner (Loucks 1992). Loucks AB, Laughlin GA, Mortola JF, Girton L, Nelson JC, Yen SS. Hypothalamic-pituitary-thyroidal function in eumenorrheic and amenorrheic athletes. Journal of Clinical Endocrinology and Metabolism 1992; 75(2):514-518. Loucks AB, Callister R. Induction and prevention of low-T3 syndrome in exercising women. American Journal of Physiology 1993; 264(5.2):R924-30. Loucks AB, Heath EM. Induction of low-T3 syndrome in exercising women occurs at a threshold of energy availability. American Journal of Physiology 1994; 350: R817-R823. Jeff Johnson, MS Performance Fitness & Nutrition :cool: TJ :cool:

CATEGORY: biology/cardiovascular_system TECHNICAL: ** SUMMARY: This document duscusses something caled "blood type conversion". This is a process where blood types A & B (and in the future AB) are converted into the mother blood type O. Many of you remember the discussion we had last year about the blood types and how they evolved. For those who were not on the list at that point, I'll provide a brief discussion of it here. At one point in the human evolutionary record, there was only one type of human blood. Type O. At some point (recently) in the genetic history of humans, 3 new "mutated" types appeared. These are type A, B, and AB. About a year ago, I did some research into what the cause of these mutations were. Mother nature doesn't make such a drastic change in evolution, unless there is a VERY significant change in the human condition. What I found was this: In essence, blood type A came about due to the shift of the human diet from hunter-gatherer to more a more *grain based* diet. As a result, type-A people can usually tolerate having grain in their diet better than most type-O individuals. (although this capacity diminishes with age..) Type B blood evolved in cultures that tended to consume more dairy. IE: people who had milk and cheese as a staple of their diets tended to produce later generations with B type blood. This document sort of clarifies that point by indicating galactose as one of the sugars that needs to be "clipped" from B blood. Galactose is a monosaccharide (simple sugar) found in dairy. Type AB blood is usually found in cultures with the longest exposure to both grain and dairy (which is a maximum of 20,000 years.. only a fraction of the human evolutionary period) Is it any wonder why I encourage people to stay away from grain and dairy? Those two, non-natural non-human, foods were behind what could be considered as a major shift in the evolution of human blood. Niether grain nor dairy is a good choice in a healthy human diet. As I have indicated before, no matter what blood type you are, the effects of these two foods on your body will end up harming you in the end. Not only are they the most allergenic substances known, but they are also the two most associated causes of cardio-vascular disease, diabetes, MS, and the rest of the degenerative diseases.. Once again, I emplore you: Eat like a caveman.. ------------------------------------------------------------- SCIENCE NEWS ONLINE January 11, 1997 Banking on Blood Conversion New technology may change the character of the U.S. blood supply By CORINNA WU Eager donors arrive at a local blood drive, ready to give the gift of life. But before their blood is allowed to flow into a plastic bag through needles plunged into their forearms, they must sit down with a pen and take a test. The questionnaire--along with biochemical tests on the blood itself--is part of a rigorous screening process that has made the U.S. blood supply one of the safest in the world. As a result of this vigilance, the risks of contracting AIDS or other infectious diseases from a blood transfusion have dropped substantially. Once that blood reaches the hospital, however, even the most careful initial screening efforts can't protect a patient from getting a fatal transfusion of the wrong blood type--a situation that occurs more often than most people think, says Harvey Klein, who is chief of transfusion medicine at the National Institutes of Health in Bethesda, Md. Sometimes, amid the chaos of an emergency room, or even in less hectic settings, a health care worker misreads a label or a chart and gives the wrong blood to a patient. If blood of type A or B is given to someone with type O blood, for example, the ensuing severe immune reaction can rapidly kill the person. Improving blood-handling procedures and worker training can forestall such deadly accidents. Some researchers, however, think they may have found a more foolproof solution by chemically converting types A and B red blood cells to the universal type O. That way, any unit of blood cells could be transfused into any patient, removing the need to match blood types. This innovation would have the added benefits of correcting imbalances in blood type inventories, reducing the amount of blood that gets outdated before it can be used, and cutting the costs of blood distribution. More than 15 years of research into this technique is reaching fruition; hospitals and blood centers may have blood conversion technology by next year. In any year, as many as 1 in 12,000 units of red blood cells meant for one person is mistakenly given to another, says Klein, but "most of the time, that won't cause any harm, just by luck." Type O blood can be given to anyone, and type A blood presents no problems for someone who happens to be A or AB. The real danger arises when, for example, a type O patient gets A or B blood or when a type A patient gets B blood. Unfamiliar molecules on the surface of the foreign blood cells trigger the immune system, which kicks into high gear and throws the patient into shock. The kidneys fail, and the depletion of blood-clotting factors causes bleeding "from the nose, ears--every orifice of the body," says Mark Popovsky, chief executive officer of the New England Region American Red Cross. About 1 in 100,000 people who receive a transfusion dies, including most people who get incompatible blood, Klein says. Although the risk of getting the wrong blood type is fairly low, it spells almost certain death when it happens. "It's sort of like a plane crash. One in 12,000, I've always thought, is a frightening statistic," he adds. Moreover, hospitals may underreport the problem. Some hospitals try to lessen the chance that a hurried doctor or nurse will make a fatal mistake by stocking only type O blood for emergency rooms and intensive care units, Klein says. This practice, however, can create a shortage of type O blood for the region. On the other hand, between 5 and 10 percent of A and B blood goes to waste, says Popovsky, simply because hospitals can't use those units within their 42-day shelf life. To minimize the waste of usable blood, hospitals sometimes ship their surplus to other institutions in the region that need more than they anticipated. Blood also travels between neighboring regional blood centers. "No one has good data on how frequently blood is moved around," Klein says, but "we know that there is a lot of movement." Conversion of all blood to type O can address these supply imbalances and reduce the amount of shipping necessary, says Jack Goldstein of the Kimball Research Institute at the New York Blood Center, who is one of the pioneers in the field. The idea explored by Goldstein and other researchers is to use an enzyme to alter the chemistry of the red cell surface. Chains of sugars, which cover the cell surfaces of the four human blood types--A, B, AB, and O--all have the same basic sequence, with fructose at the end and galactose next in line. The major distinction between types lies with the sugar that branches off from the galactose. On A cells, that sugar is N-acetylgalactosamine. On B cells, it's another galactose. O cells have no additional sugar at all, while AB blood cells bear a mix of A and B chains. In the United States, about 45 percent of the population has type O blood, 40 percent has type A, 11 percent has type B, and 4 percent has type AB. A and B cells cannot be transfused into people with O blood because the extra sugar branch stimulates the immune system's antibodies to attack the foreign cells. Clipping off that additional sugar branch from A and B cells transforms them into type O, averting the immune response. Goldstein found the right enzymes for the job in what might seem to be some unlikely places. He isolated the enzyme for B conversion, a-galactosidase, from coffee beans. "It's not so far-fetched," he says. Beans and seeds use the enzyme to break down large molecules into individual sugars, which provide energy. The enzyme for A conversion, a-N-acetylgalactosaminidase, came from chicken livers. These digestive enzymes, Goldstein says, are "ubiquitous in nature, but you have to use the right ones." In the beginning, he needed 50-pound batches of both coffee beans and chicken livers to get the necessary quantities of enzyme for experiments. "I think Mr. Perdue [the chicken magnate] was happy for a few years," Goldstein says. "We used a lot of chicken livers. [it was] so traumatic, I put them out of my mind." Researchers don't need to wallow in vats of chicken innards or mounds of coffee beans anymore. With the techniques of biotechnology, the enzymes have been cloned and are now synthesized in bulk. The large number of sugar chains and their different orientations on cell surfaces made finding the right conditions for conversion a real challenge, says Goldstein. Type B cells have over half a million sugar chains on their surface, while type A cells have twice that amount. Some are perpendicular to the surface; others lie parallel. "This is what fascinated me," says Goldstein, "to get enzymes and conditions where the enzymes would work." For example, the enzyme for B conversion works best at a high acidity, but blood cells do their job of carrying oxygen in neutral conditions. Goldstein had to strike a balance that allowed the enzyme to efficiently clip off the extra galactose without destroying the red cell's function. Eventually, he determined that the reaction could take place at 26oC, rather than the higher temperature the blood cells are accustomed to, and at a slightly acidic pH of 5.5 or 5.6. "When I started this work, no one had really treated red cells at such a low pH," he says. "It was thought that they would just become nonviable." That turned out not to be the case. Not every sugar chain on every cell gets changed, he says, but as long as enough are clipped, the body accepts the cells. A company called ZymeQuest in North Andover, Mass., is currently conducting clinical trials to determine whether converted B cells have the same medical utility as unconverted O cells. So far, studies have shown that converted B cells behave like normal O cells and don't trigger any immune reaction. ZymeQuest, which holds the license to develop Goldstein's technology, has designed an automated machine that performs the B-to-O conversion. Able to convert many units of blood with little human intervention, such machines could easily be incorporated into the daily routine of regional blood centers, says president Douglas Clibourn. He estimates that the company should have a salable product by the end of 1998, pending approval by the Food and Drug Administration. A similar technique could be used for A-to-O conversion, but that project is about a year behind. Effectively converting A cells is trickier than altering B cells, because about 75 percent of people with type A blood have two kinds of sugar chains on their cells. Out of the million or so structures on each A cell, about 50,000 have a second copy of the final three-sugar sequence, which includes an N-acetylgalactosamine. "It's not that far in, but it means that one has to use a different approach to remove it," Goldstein says. "We're very close to solving this problem." Starting experiments with type B blood turned out to be a good choice, he says. "If we had started with A, maybe I would have dropped this project earlier." Once conversion technology for A and B blood is established, altering the AB cells should be straightforward. "The cost of converting all the A, B, and AB blood to O," Clibourn says, "is less than the current cost of all of that blood shipping." Any technology that would convert blood to a true universal donor type must take another characteristic, Rh factor, into account. A cell surface protein first discovered in the blood of Rhesus monkeys, the Rh factor can provoke an immune reaction in people whose blood doesn't normally carry it. People who have the protein on their red blood cells are deemed Rh-positive; those who don't are Rh-negative. Rh incompatibility is less of a problem than ABO incompatibility, says Klein. A majority of people in the United States, about 84 percent, have Rh-positive blood. Moreover, an Rh-negative person can withstand one accidental transfusion of Rh-positive blood because the Rh-negative person doesn't develop anti-Rh antibodies until 3 or 4 months later, Klein says. "The second transfusion, after they already have that antibody they made as a result of the first transfusion, could be very serious." An Rh-negative woman who develops antibodies from bearing an Rh-positive child faces that risk if she conceives a second Rh-positive child or receives an Rh-positive blood transfusion. Several labs have cloned the Rh factor, Goldstein says, but no one fully understands its three-dimensional structure. Therefore, researchers are only beginning to explore techniques for Rh conversion. If researchers can identify which part of the protein stimulates the immune response, then perhaps they can alter that portion to make the blood cell effectively Rh-negative. Eventually they want to produce type O, Rh-negative blood--the kind any person can receive without fear. Despite the promise this technology holds, it doesn't produce a limitless supply of blood, Popovsky says. The key factor in maintaining the blood supply is still sufficient donation. "Today, the demand for blood is very great," Popovsky says. "We need healthy people to donate so that they support the blood system of this country. Without them, it would collapse." Although there is talk about artificial blood substitutes, he adds, humans still cannot chemically synthesize molecules that can do everything a red blood cell does. "The human red cell is a fantastic structure--there's nothing like it." copyright 1997 Science Service :cool: TJ :cool:

CATEGORY: biology/metabolism TECHNICAL: **** SUMMARY: This is a fairly technical document that describes the different types of fuel the body will use under variable exercise conditions. Some of you out there, with a background in medicine, will probably really enjoy the detail -- for others it's a pretty hard read. As a result, I'm going to summarize some of the more important (and interesting) points. * ATP is the body's only energy source, everything is converted into ATP at some point * the order of fuels used by the body under intense exercise conditions is: ATP first, CP second, muscle glycogen, blood glucose, and liver glycogen. (glucose and glycogen are the body's sugar reserves). If all of those resources are exhausted, amino acids (proteins) are then converted to glucose * "feeling the burn" in a particular muscle implies that the glucose or stored glycogen are being metabolized at a rate too fast for the amount of oxygen present. This leads to lactic acid (causing the burn) which can be carried back to the liver where it can be re-converted into glucose. (so it's sort of a self feeding cycle) * carbohydrate loading can, in general, double the amount of glycogen stored in the muscle and liver. (and hence improve your stamina and performance) * adrenaline and noradrenaline are mostly responsible for the release of stored glycogen from the liver, and stored free fatty acids from adipose. Hence, without these two, you won't be able to tap your body fat for fuel. Fortunately, exercise increases both of them. * the body stores fats inside active muscle cells too. This intra-muscular triglyceride can also be tapped as an energy source, but they are hit less and less as the intensity and duration of an exercise increases. * Proteins and ketones can be used as exercise substrate (fuel) as well, but they only account for a small percentage, and aren't very efficient at the task. * Fats and triglycerides compose a significantly larger percentage of your body's stored energy reserves. ATP/CP can only last for a few seconds, and glucose/glycogen reserves can be depeleted in only a few hours with the right kind of effort. ------------------------------------------------------------- Basic Exercise Fuel Metabolism (1,2,3) Introduction The energy to fuel exercise can be generated from many different sources. Which source provides the majority of energy during exercise is dependent on a host of factors (such as availability, intensity/duration of exercise, etc) all of which will be discussed in later sections. To provide adequate background for upcoming sections, it will be helpful to discuss the basics of energy generation first as well as the basic pathways of fuel utilization during exercise. ATP: the master chemical ATP is the only substrate which the body can use for the generation of energy. Hence, all energy generating pathways have as their ultimate goal the generation of ATP. When a muscle contracts, ATP provides energy by being broken down to Adenosine Diphosphate (ADP) in the following reaction with the help of an enzyme called an ATPase. ATPase ATP ------------> ADP + Pi + energy (Note: Pi represents an inorganic phosphate molecule) Within each muscle, there is about 6 seconds worth of ATP stored which can be used for immediate energy. So for activity to continue past 6 seconds, ATP must be generated through various other reactions. The first of these of these is through what is called the creatine phosphate (CP) system. The creatine phosphate system Also stored in the muscle is a substance called Creatine Phosphate (CP). This provides a phosphate molecule to ADP to regenerate ATP so that muscular activity can continue. CP donates it's high energy Phosphate molecule to ADP to regenerate ATP via an enzyme called creatine kinase in the following reaction. Creatine ADP + CP --------------> ATP + Creatine Kinase There is enough stored CP in a normal muscle to provide energy for approximately the first 15-20 seconds of muscular activity at which time intramuscular CP is depleted (this provides the physiological basis for creatine loading which will be discussed in depth in the supplement section). The CP system operates in the absence of oxygen (it is anaerobic) and can provide energy very quickly during exercise. However, as with ATP, it's overall capacity to produce energy is low due to the limited amounts available. Collectively, stored ATP and CP are known as the ATP-CP or Phosphagen system. However, the total energy yield from the ATP-CP system is low due to the small amount of ATP and CP available in the muscle. As exercise duration exceeds 10-15 seconds, the ability of the phosphagen system to provide energy decreases and the body must rely on other fuel sources to generate ATP. One of these is the breakdown of glucose or glycogen (known as glycolysis or glycogenolysis respectively although the term glycolysis will be used here generally to refer to the breakdown of bodily carbohydrate stores). Glycogen is a storage form of glucose which is present in muscle and the liver. Glucose circulates in the bloodstream freely and can be taken up into muscles as needed. Glycolysis In a normal individual following a mixed diet, total muscle glycogen stores may comprise 250-350 total grams of carbohydrate with an additional 15 grams of carbohydrate circulating in the blood. There is an additional 90-110 grams of glycogen in the liver but it will be discussed separately below. During prolonged exercise at 75% of VO2 max to exhaustion (30-60 minutes or so), muscle glycogen stores will be totally depleted. With depletion of carbohydrate stores (generally accomplished with either exhaustive exercise or a carbohydrate free diet or some combination of the two) followed by several days of a high carbohydrate diet, muscle glycogen stores can be doubled to 700 grams of glycogen or more. During exercise, glycogen or glucose is broken down to provide ATP in the following reaction: glycolytic enzymes (Aerobic) Glucose/Glycogen ---------------------------> ATP + Pyruvate --------> Krebs cycle, liver, etc (Anaerobic) | / Lactate The breakdown of glucose or glycogen always initially results in the formation of ATP and pyruvate. But depending on the availability of oxygen (which is a function of exercise intensity), the pyruvate generated has one of two major metabolic fates. If there is not adequate oxygen present (as with high intensity exercise), glycolysis only provides 2-3 ATP molecules and the resulting pyruvate is converted to lactate. Lactate is an acid, causing the burning sensation felt in the muscles during exercise by lowering pH inside the muscle. This lowering of muscle pH inhibits glycolysis and may be one cause of fatigue during high intensity exercise. In the past, lactate was thought of as only a waste product of glycolysis that caused fatigue. However, it is now recognized that lactate is another useful fuel substrate both during and after exercise. Lactate can be used for energy by slow twitch muscle fibers (Type I) as well as by the heart. Alternately, lactate can diffuse into the bloodstream, travel to the liver, and be converted to glucose or glycogen through the process of gluconeogenesis (literally "the making of new glucose"). Additionally, following exercise, lactate can be regenerated to muscle glycogen which may have implications for individuals following a strict ketogenic diet as glycogen availability is the limiting factor in many types of exercise. Post-workout glycogen resynthesis from lactate will be discussed in a later section. This pathway of glycogen and glucose breakdown is known as fast or anaerobic glycolysis. If there is adequate oxygen present, glyocolysis produces 38-39 molecules of ATP and the resulting pyruvate is oxidized in the mitochondria to produce more energy through what is known as the Krebs Cycle. Alternately, the pyruvate may be released into the bloodstream where it travels to the liver and is converted to glucose (to be released back into the bloodstream) through the process of gluconeogensis. This pathway of glucose or glycogen degradation is known as slow or aerobic glycolysis. Liver glycogen In addition to muscle glycogen and freely circulating blood glucose, liver glycogen can also play a role in energy production during exercise. The liver stores up 110 grams of glycogen under normal conditions and, as with muscle glycogen, this can be increased with carbohydrate loading. In general, the liver is a storage depot of sorts for the body. Normally, the liver has a slow output of glucose (from breakdown of liver glycogen) into the bloodstream. In response to the release of adrenaline and noradrenaline during exercise (see section on hormonal reponse to exercise), liver glycogen breakdown and release into the bloodstream is greatly increased to maintain blood sugar levels. Additionally, glucagon and cortisol levels (which are also affected by exercise) further influence liver glycogen release into the bloodstream. Total depletion of liver glycogen will occur with 24 hours of total fasting but this may only take several hours during prolonged exercise (or much less for high intensity exercise). When, liver glycogen is depleted, blood glucose will also drop and the resulting hypoglycemia may be one cause of fatigue. Additionally, as it pertains to ketogenic dieters, the depletion of liver glycogen (and subsequent drop in blood glucose) below a certain level is necessary for the intiation of ketogenesis. It should be noted that total bodily glycogen and glucose stores can only provide approximately 1500 calories of useful energy (this can be doubled with carbohydrate loading) or enough to run approximately 15 miles. As this is still fairly limited energy wise, the body has several other sources of fuel that it can utilize during exercise. Metabolism of free fatty acids (FFA) and intramuscular triglyceride (TG) The body has two major stores of fats which can be used during exercise to provide energy. An 70 kg male with 12% bodyfat has approximately 70,000 calories of useable energy stored in bodyfat and an additional 1500 calories stored as intramuscular triglyceride. Assuming you could use 100% fat for fuel, this would be sufficient to run 720 miles. Even the leanest athlete with only 3 lbs. of bodyfat (containing approximately 1000 calories worth of useable energy) could run 100 miles if they were able to use fat for fuel. The question of why humans are unable to utilize 100% fat for fuel during activity is one that many researchers have asked themselves and is a topic that will be discussed in more detail later. Adipose tissue triglyceride metabolism As stated, bodily stores of adipose tissue contain approximately 70,000 calories of useable energy stored in the form of triglyceride (TG) which is the combination of three free fatty acids (FFA) and a glycerol molecule. But, in order for these triglycerides to be used by the muscle for fuel, they must go through the following steps: 1. Mobilization: in response to specific hormonal signals during exercise, adipose tissue TG is broken down within the cell to free fatty acids (FFA's) and glycerol (which is then released into the bloodstream) via the enzyme Hormone Sensitive Lipase (HSL). HSL activity is the ultimate determinant of lipid mobilization during exercise. Adrenaline and noradrenaline (which increase during exercise) stimulates HSL to release FFA into the bloodstream while insulin (which decreases during exercise and increases in response to increases in blood glucose) inhibits HSL activity and release of FFA to be used for energy. Insulin and the catecholamines (adrenaline and noradrenaline) are the only two factors which regulate FFA release from the fat cell (refs). 2. Tranport: FFA's enter the bloodstream where they bind to a fatty acid binding protein (FABP) to travel through the bloodstream where they are picked up by the muscle. 3. Uptake: The FFA-FABP complex binds at the muscle and is carried into the mitochondria for oxidation via the enzyme carntine palmityl transferase (CPT). *Additionally, once ketogenesis is established in the liver, circulating free fatty acids will be taken up into the liver and converted to ketones. The issue of post-exercise ketosis will be discussed in a later section.* 4. Beta-oxidation: in the mitochondria, the FFA is oxidized yielding ATP and acetyl-Coa. This acetyl-CoA enters the Krebs cycle to produce more usable energy. As will be discussed in a later section, each of the above four steps has been implicated as the rate limiting factor for the utilization of FFA during exercise. The beta-oxidation of FFA requires oxygen to occur (it is sometimes referred to as aerobic lipolysis (refs)) On average, one molecule of FFA will yield 129 ATP or more depending on the length of the FFA that is burned. Thus, compared to even aerobic glycolysis, fats provide a much greater energy yield. However, it should be noted that the oxidation of FFA requires more oxygen than the oxidation of glycogen or glucose. As will be discussed later, this has implications for ketogenic dieters. Intramuscular triglyceride (TG) metabolism As an additional source of energy, there are droplets of intramuscular triglyceride stored within the muscle proper. Depending on a host of factors (to be discussed later), this intramuscular TG will be oxidized in the same manner as blood borne free fatty acids. As they exist directly within the muscle fiber, they may exist as a more immediate source of energy during exercise. In addition to the use of glycogen/glucose and adipose and intramuscular TG, the body can also use protein and ketones for fuel during activity. Protein Under normal circumstances, protein is not used to a great degree during exercise. Under most circumstances, it may provide 5% or less of the total energy yield during exercise. However, with glycogen depletion, protein in the muscle can be used for fuel either by conversion to glucose in the liver (again, via gluconeogenesis) or by direct utilization by the working muscle. Ketones The oxidation of ketones for fuel is similar to that of free fatty acids and intramuscular triglyceride. Under certain conditions, ketones can enter the muscle where they are converted to acetyl-Coa and enter the Krebs cycle to produce energy. However, even under conditions of heavy ketosis, ketones rarely provide more than 7-8% of the total energy yield which is a relatively insignificant amount. A chart summarizing the amount of energy available from each fuel source appears below. Substrate Total bodily stores Useable energy ---------------------------------------------------------------------- Aerobic/Anaerobic ATP N/A 1.8 kcal Anaerobic CP N/A 8.4 kcal Anaerobic Glyocgen (muscle) 250 grams 1025 calories Depends Glycogen (liver) 110 grams 451 calories Depends Blood Glucose 15 grams 62 calories Depends Adipose tissue 7,800 grams 71,000 calories Aerobic Intramuscular TG 161 grams 1,465 calories Aerobic Ketones (!) Varies Varies Aerobic Protein (#) Varies 24,000 Note: this assumes a 70kg man with 30kg of muscle and 12% bodyfat. (!) Ketones rarely provide more than 7-8% of total energy yield even in highly ketotic individuals (#) Protein only provides 5-10% of total energy yield and is generally not considered as a major source of energy during exercise. Summary The body can produce energy for exercise by the breakdown of many different substrates. Generally speaking, fuel utilization can be broken into two general categories: Anaerobic energy production direct breakdown of ATP and CP stored within the muscle, which predominates during the first 15-20 seconds of exercise anaerobic glycolysis of muscle glycogen or blood glucose which predominates during the first 30-70 seconds or so of exercise Aerobic energy production aerobic glycolysis of glycogen or blood glucose beta oxidation of free fatty acids and intramuscular triglycerides oxidation of amino acids: which generally provides very little of the total energy during exercise oxidation of ketone bodies: which generally provides very little of the total energy during exercise The determination of which substrate provides energy during exercise depends on a host of factors including availability, the intensity/duration of exercise, the individual's training status and gender all of which will be discussed in upcoming sections. References: 1. "Physiology of Sport and Exercise" Jack H. Wilmore and David L. Costill. Human Kinetics Publishers 1994. 2. "Endurance in Sport" Ed. R.J. Shephard & P.-O. Astrand. Blackwell Scientific Publishers 1992. 3. "Exercise Physiology: Human Bioenergetics and it's applications" George A Brooks, Thomas D. Fahey, and Timothy P. White. Mayfield Publishing Company, 1996. Lyle McDonald, CSCS Some chemistry humor: "If you're not part of the solution, you're part of the precipitate." -- anonymous :cool: TJ :cool:

Mmmmmmmmmmm *NOT* :shock: TJ :shock:

As far as healthy anti-oxidants go it is TONS (which is the original point of Niks post) This is misleading, because it looks like it's comparing a specific brand of "tea" against another specific brand of "green tea". I can see no other reason for such a big disparity. In essence, they're the same as "green tea" is "tea" (or black tea) that just hasn't been left out in the sun to dry (and turn black, and oxidize, etc..) http://www.cancer.org/docroot/ETO/content/...sp?sitearea=ETO Generally the "green" version of the tea has higher caffeine content because of less processing/drying/etc. (atleast according to my info) :cool: TJ :cool:

This is a pretty dry medical document that demonstrates a point I made in my last post. Many treatments used today to "treat" cancer actually are key contributors to it.. :cool: TJ :cool: ---------------------------------------------------------------------------- ---------------------------------------------------------------------------- Confirmation that Ionizing Radiation Can Induce Genomic Instability: What is Genomic Instability, and Why Is It So Important? John W. Gofman, M.D., Ph.D., and Egan O'Connor, Executive Director, CNR. Spring 1998. ---------------------------------------------------------------------------- ---------------------------------------------------------------------------- * Glossary + Genome + Genes and Chromosomes + The Code + The Mitochondrial DNA (mtDNA) * Part 1 -- A Deep Insight from 1914, Slowly Confirmed * Part 2 -- Ionizing Radiation as a Cause of Genomic Instability * Part 3 -- Implications: Curing vs. Preventing Cancer * Part 4 -- Five Key Facts and Three Restrained Comments * References * Genomic instability --- also called "genetic instability" and "chromosomal instability" --- refers to abnormally high rates (possibly accelerating rates) of genetic change occurring serially and spontaneously in cell-populations, as they descend from the same ancestral cell. By contrast, normal cells maintain genomic STABILITY by operation of elaborate systems which ensure accurate duplication and distribution of DNA to progeny-cells (Cheng 1993, p.124), and which prevent duplication of genetically abnormal cells. These systems ("metabolic pathways") involve an estimated 100 genes (Cheng 1993, p.142). * Why is genomic instability so important? Many (not all) cancer biologists now believe that genomic instability "not only initiates carcinogenesis, but also allows the tumor cell to become metastatic and evade drug toxicity" (Tlsty 1993, p.645), and "The loss of stability of the genome is becoming accepted as one of the most important aspects of carcinogenesis" (Morgan 1996, p.247), and "One of the hallmarks of the cancer cell is the inherent instability of its genome" (Morgan 1996, p.254). * Although these observations are far from new, they certainly did not receive the attention they merit until recently. ------------------------------------------------------------------ >>>>> GLOSSARY <<<<< * GENOME * GENES AND CHROMOSOMES * THE CODE * THE MITOCHONDRIAL DNA (mtDNA) * GENOME. A person's genome is one set of his (or her) genes. The human genes, which control a cell's structure, operation, and division, are located in the cell's nucleus. The full human genome (estimated at 50,000 to 100,000 genes) is present in every cell-nucleus, even though many genes are inactive in cells which have some specialized functions (the "differentiated" cells). * GENES AND CHROMOSOMES. Genes are composed of segments of DNA. In normal cell-nuclei, the DNA is distributed among 46 chromosomes (23 inherited at conception from a person's father, and 23 from the mother). Each chromosome consists of one very long strand of DNA and numerous proteins, which are required for successful management of the long DNA molecule. The longest chromosomes each "carry" thousands of genes. Every time a cell divides, the cell must duplicate the 46 chromosomes and must distribute one copy of each to the two resulting cells. * THE CODE. The DNA of each chromosome is composed of units --- "nucleotides" of four different types (A, T, G, C). These nucleotides are linked to each other in linear fashion. The sequence of the four types of nucleotides is critical, because the sequence produces the "code" which (a) determines the function of each particular gene, ( identifies the gene's start-point and stop-point along the DNA strand, and © permits certain regulatory functions. The code of the human genome consists of more than a billion nucleotides. * THE MITOCHONDRIAL DNA (mtDNA). Outside the nucleus, human cells also have some "foreign" DNA located in structures called the mitochondria. This small and separate set of DNA does not participate in the 46 human chromosomes, and is not part of "the genomic DNA." The mitochondria are inherited from the mother. ------------------------------------------------------------------ Part 1 * A Deep Insight from 1914, Slowly Confirmed * It was the year 1956 when the normal number of human chromosomes per cell was firmly established as 46. Soon thereafter, it became clear that cells of advanced cancers have often evolved an abnormal number of chromosomes ("aneuploidy"). * Such observations were consistent with the prediction of Theodor Boveri (Boveri 1914), a great German embryologist who postulated that malignancy is the result of inappropriate balance of instructions (genetic information) in the tumor cells. Such "imbalance" can result not only from numerical chromosome aberrations, but also from structural alterations within the 46 chromosomes. As a leading cause of structural chromosome aberrations (deletions, acentric fragments, translocations, inversions, dicentrics, etc.), ionizing radiation is well-established. * When my colleagues and I (JWG) initiated a research program in 1963 (at the Atomic Energy Commission's Livermore National Laboratory), to test Boveri's hypothesis, there was very little interest in the concept. Although the techniques for detecting structural chromosome aberrations were extremely crude then, compared with current techniques, we were making gradual progress (Minkler 1970, + Minkler 1971). However, the Atomic Energy Commission became angry with me after a paper I presented at an IEEE Symposium (Gofman 1969), and canceled our funding in the early 1970s (Seaborg 1993, Chapter 8, "Challenge from Within," + Terkel 1995, pp.406-408). * In October 1976, the journal Science published Peter C. Nowell's classic paper entitled, "The Clonal Evolution of Tumor Cell Populations" --- a paper almost always cited by today's analysts of genomic instability. Among other things, Nowell's 1976 paper discussed evidence, from various analysts, indicating that as tumor cells become increasingly aneuploid, the malignancy becomes increasingly aggressive (Nowell, p.25). Reasoning from the available evidence at that time, Nowell proposed the following model of multi-step carcinogenesis: * Tumor initiation occurs by an induced change in a single, previously normal cell, which makes the cell "neoplastic" (partially liberated from normal growth controls) and provides the cell with a selective growth advantage over adjacent normal cells (Nowell, p.23). * "From time to time, as a result of genetic instability in the expanding tumor population, mutant cells are produced ... Nearly all of these variants are eliminated, because of metabolic disadvantage or immunologic destruction ... but occasionally one has an additional selective advantage with respect to the original tumor cells as well as normal cells, and this mutant becomes the precursor of a new predominant subpopulation" (Nowell, p.23). And: * "Over time, there is sequential selection by an evolutionary process of sub-lines which are increasingly abnormal, both genetically and biologically ... Ultimately, the fully developed malignancy as it appears clinically has a unique, aneuploid karyotype associated with aberrant metabolic behavior and specific antigenic properties, and it also has the capability of continued variation as long as the tumor persists" (Nowell, p.23). And: * "The major contention of this article is that the biological events recognized in tumor progression represent (i) the effects of acquired genetic instability in the neoplastic cells, and (ii) the sequential selection of variant subpopulations produced as a result of that genetic instability" (Nowell, p.25). * The recent surge of interest in genomic instability reflects the recognition that the cancer process represents a trip (or set of trips) from the stable genome to the genome with diverse deviations. It has been a long wait for Boveri. ------------------------------------------------------------------ Part 2 * Ionizing Radiation as a Cause of Genomic Instability * Today, laboratory researchers are performing reality-checks on this logic: Genomic instability can be initiated and intensified by any type of genetic mutation (including chromosome aberrations), when such mutation alters some of the DNA which maintains genomic STABILITY. Of course, such DNA includes the numerous DNA segments which govern DNA synthesis, cell-division, and also the routine REPAIR of the genome --- the "repair genes" (Cheng 1993, p.131; Morgan 1996, p.248). * When a mutagen has induced genomic instability in a cell, some of the cell's descendants will experience new and unrepaired genetic abnormalities at an excessive rate, even though the descendants themselves received no exposure to the mutagen used in the experiment. This occurs because such cells have inherited a genome which was injured with respect to maintaining genomic STABILITY. * Very recently, a technique has been developed for efficiently detecting three of the types of chromosome aberrations which are very prominent in genomic instability: Aneuploidy (wrong number of chromosomes), deletions (permanent removal of DNA segments, long or short), and gene-amplifications (extra copies of specific DNA segments). This technique, called Comparative Genomic Hybridization, was first described by Kallioniemi (1992, in Science). However, such a technique does not detect many other kinds of mutations. * The nature of the genetic code is such that mutations need not be gross in order to have gross biological consequences. For instance, permanent removal of a single nucleotide (a micro-deletion) can totally garble much of a gene's code, by causing what is called a "frame-shift." Then this non-functional gene can be the phenomenon which wrecks part of the system which would otherwise maintain genetic STABILITY. * Amplification (instead of injury), of the crucial genes in the stability-system, also can permit a cell to escape the controls which otherwise prevent duplication of cells with injured genomes. Evidence is developing that gene amplification is associated with dicentric chromosomes and circular acentric fragments called "double minutes" (DiLeonardo 1993, p.656) --- very well-known products among the consequences of ionizing radiation. * The sequence, in which various mutations accumulate in tumor cells, may or may not matter. "For example, one or more pre-cancerous mutations might lie dormant until additional mutations create an environment in which the prior changes confer a selective advantage" (DiLeonardo 1993, p.655, citing Kemp 1993, + Fearon 1990, + Temin 1988). * The fact, that ionizing radiation is a mutagen capable of causing all known types of genetic mutation --- from micro to gross, at any DNA location along any chromosome --- made it utterly predictable that ionizing radiation would be a cause of genomic instability. Indeed, one of the last projects completed by our research group at the Livermore Lab, before the Atomic Energy Commission shut down our work, was a demonstration which showed that ionizing radiation can induce genomic instability. Our experiments used gamma rays and cultured human fibroblasts (Minkler 1971). * During recent years, multiple experiments have confirmed the fact that ionizing radiation can cause genomic instability. Such results have been observed after both low-LET radiation (such as xrays and gamma rays) and high-LET radiation (such as alpha particles). Among numerous papers, see, for instance: * Kadhim 1992; * Holmberg 1993 (who cites Minkler 1971); * Marder 1993 (especially p.6674); * Mendonca 1993; * Kadhim 1994; * Kronenberg 1994 (radiation dose-response, p.605); * Kadhim 1995; * Morgan 1996 (review). * In the mass media, some writers have expressed astonishment that radiation-induced genomic instability is not detected until several cell-divisions have occurred after the radiation exposure. They seem to imagine that the delay reflects a mysterious discontinuity between cause and effect. There is NO discontinuity, of course --- a point made explicitly in Kadhim 1992 (p.739). With current techniques, and with uncertainties about where to search closely among a billion nucleotides, it is just not possible to detect every intermediate step. ------------------------------------------------------------------ Part 3 * Implications: Curing vs. Preventing Cancer * The induction of genomic instability in a cell does not guarantee that it will become malignant. Genomic instability increases the RATE of mutation in that cell and its descendants, and with this higher rate, the cells each have a higher PROBABILITY that at least one of them will accumulate all the genetic powers of a killer-cancer. These powers include the ability to thrive BETTER than normal cells, to invade inappropriate tissue, to adapt to the new conditions there, to recruit a blood supply, to fool the immune system, and many other properties. * No one claims, yet, that genomic instability must precede every case of cancer. However, genomic instability helps to explain why cancer is sometimes called "at least a hundred different diseases." Indeed, genomic instability means that each case of cancer may develop a genome like no other case. Is it any wonder that individual tumors often differ in behavior from each other? * Nowell's 1976 paper was certainly not the last one to observe that cancers become increasingly deviant in their genomes, as they "advance." Tlsty 1993 (p.645) cites several more recent papers. Near the end of his paper, Nowell wrote (p.27): * "The fact that most human malignancies are aneuploid and individual in their cytogenetic alterations is somewhat discouraging with respect to therapeutic considerations ... With variants being continually produced, and even increasing in frequency with tumor progression, the neoplasm possesses a marked capacity for generating mutant sub-lines, resistant to whatever therapeutic modality the physician introduces ... The same capacity for variation and selection which permitted the evolution of a malignant population [of cells] from the original aberrant cell, also provides the opportunity for the tumor to adapt successfully to the inimical environment of therapy, to the detriment of the patient." And Some Lessons: ----------------- (A) * Genomic instability will probably keep cancer hard to cure. ( * The quickest path to less cancer-misery in the future would be a policy of reducing exposure to carcinogens. © * Ionizing radiation is almost certainly the most potent carcinogen to which vast numbers of people are actually exposed (see Part 4). ------------------------------------------------------------------ Part 4 * Five Key Facts and Three Restrained Comments (1) * Ionizing radiation is a mutagen having special properties which make some radiation-induced genetic injuries complex and impossible for a cell to repair correctly --- quite unlike the routine damage from endogenous free radicals (Ward 1988, + Gofman 1990, Chapter 18, Part 2, + Ward 1991, + Baverstock 1991, + Ward 1995, + Gofman 1997). (2) * Ionizing radiation is a mutagen which undeniably can cause every known kind of mutation, at any DNA location along any chromosome. The body does not always eliminate cells having harmful mutations. If it did, there would be no cancer or inherited afflictions. (3) * Ionizing radiation is a mutagen known to induce genomic instability (references provided in earlier sections). (4) * Ionizing radiation is a human carcinogen at every dose-level, not just at high doses; there is no threshold dose. A single photon or a single high-speed particle can cause unrepairable genetic damage. (See Gofman 1990, Chapters 18-21, + UNSCEAR 1993, Annex F, especially p.636 para.84, p.680 para.323, + NRPB 1995, especially pp.59-61, p.68, p.75, + Pierce 1996, p.9, + Gofman 1996, Chapter 45, + Riches 1997, p.519, + Hei 1997). (5) * Ionizing radiation is a mutagen observed to induce virtually every kind of human cancer (Gofman 1969, p.4, + BEIR 1980, Section 5, + UNSCEAR 1988, p.460 para.394). And the Comments: ----------------- (1) * In view of all the five facts above, it would be inappropriate to doubt the menace of low-dose ionizing radiation. (2) * And in view of all the five facts, it is strange --- in studies which attempt to explain a difference in cancer-rates between two groups --- that the question is so seldom asked: How do the radiation histories differ between the groups? In view of the five facts above, it should be the FIRST question. (3) * And in view of the five facts, it is sad that so many members of the medical profession give only lip-service to the need to reduce the unnecessarily high exposures to radiation administered by their own profession (UNSCEAR 1993, Annex C, + Gofman 1996, Chapter 48). Today, the two largest sources of voluntary radiation exposure are (i) pre-cancer medical procedures, including CT scans and fluoroscopy (NCRP 1987, p.59, + NCRP 1989, p.69) and (ii) cigarette-smoking --- which delivers appreciable alpha-particle radiation to the lungs (Martell 1974, 1975, 1983, + NCRP 1984, + BEIR 1990, p.19). As for involuntary exposures accumulated from nuclear pollution, they have been poorly ascertained --- to put it in a kindly fashion. ------------------------------------------------------------------ >>>>> Reference List <<<<< * Baverstock 1991 (Keith F.), "Comments on the Commentary by D. Billen," Radiation Research 126: 383-384 (letter). * BEIR 1980, Committee on the Biological Effects of Ionizing Radiation, "The Effects on Populations of Exposure to Low Levels of Ionizing Radiation." National Academy of Sciences, Washington DC. * BEIR 1990 (see BEIR 1980), "Health Effects of Exposure to Low Levels of Ionizing Radiation." 421 pages. ISBN 0-309-03995-9. National Academy of Sciences, Washington DC. * Boveri 1914 (Theodor), "The Origin of Malignant Tumors," first published as a book in German; English-language translation published in 1929 by Williams and Wilkins, Baltimore, Maryland, USA. * Cheng 1993 (Keith C.) + Lawrence A. Loeb, "Genomic Instability and Tumor Progression: Mechanistic Considerations," Advances in Cancer Research 60: 121-156. * DiLeonardo 1993 (A.) + S.P. Linke + Y. Yin + G.M. Wahl, "Cell Cycle Regulation of Gene Amplification," Cold Spring Harbor Symposia on Quantitative Biology 58: 655-667. * Fearon 1990 (E.R.) + Bert Vogelstein, "A Genetic Model for Colorectal Tumorigenesis," Cell 61: 759+. * Gofman 1969 (John W.) + Arthur R. Tamplin, "Low-Dose Radiation and Cancer," IEEE Transactions on Nuclear Science NS-17, Vol.1: 1-9. Presented October 29, 1969 at the 1969 Nuclear Science Symposium, Institute of Electrical and Electronic Engineering. Proceedings published February 1970 by the IEEE, New York City. * Gofman 1990 (John W.), "Radiation-Induced Cancer from Low-Dose Exposure: An Independent Analysis." 480 pages. ISBN 0-932682-89-8. Committee for Nuclear Responsibility Books, San Francisco. Also available on the Internet. * Gofman 1996 (John W.), "Preventing Breast Cancer: The Story of a Major, Proven, Preventable Cause of This Disease." 422 pages. ISBN 0-932682-96-0. Committee for Nuclear Responsibility Books, San Francisco. Also available on the Internet. * Gofman 1997 (John W.), "The Free-Radical Fallacy about Ionizing Radiation: Demonstration That a Popular Claim Is Senseless," Committee for Nuclear Responsibility, San Francisco. Also available on the Internet. * Hei 1997 (T.K.) + 4 co-workers, "Mutagenic Effects of a Single and an Exact Number of Alpha Particles in Mammalian Cells," Proceedings of the National Academy of Sciences USA 94: 3765-3770. * Holmberg 1993 (Kerstin) + Susann Falt + Annelie Johansson + Bo Lambert, "Clonal Chromosome Aberrations and Genomic Instability in X-Irradiated Human T-Lymphocyte Cultures," Mutation Research 286: 321-330. * Kadhim 1992 (Munira A.) + D.A. MacDonald + Dudley T. Goodhead + Sally A. Lorimore + 2 co-workers, "Transmission of Chromosomal Instability after Plutonium Alpha-Particle Irradiation," Nature 355: 738-740. * Kadhim 1994 (Munira A.) + Sally A. Lorimore + Mary D. Hepburn + Dudley T. Goodhead + 2 co-workers, "Alpha-Particle-Induced Chromosomal Instability in Human Bone-Marrow Cells," Lancet 344: 987-988. * Kadhim 1995 (Munira A.) + Sally A. Lorimore + K.M.S. Townsend + Dudley T. Goodhead + 2 co-workers, "Radiation-Induced Genomic Instability: Delayed Cytogenetic Aberrations and Apoptosis in Primary Human Bone-Marrow Cells," Internatl. Journal of Radiation Biology 67: 287-293. * Kallioniemi 1992 (Anne) + Olli-P. Kallioniemi + Damir Sudar + 4 co-workers, "Comparative Genomic Hybridization for Molecular Cytogenetic Analysis of Solid Tumors," Science 258: 818-821. * Kemp 1993 (C.J.) + L.A. Donehower + A. Bradley + A. Balmain, "Reduction of p53 Gene Dosage Does Not Increase Initiation or Promotion but Enhances Malignant Progression of Chemically Induced Skin Tumors," Cell 74: 813+. * Kronenberg 1994 (A.), "Radiation-Induced Genomic Instability," Internatl. Journal of Radiation Biology 66: 603-609. * Marder 1993 (Brad A.) + William F. Morgan, "Delayed Chromosomal Instability Induced by DNA Damage," Molecular and Cell Biology 13: 6667-6677. * Martell 1974 (Edward A.), "Radioactivity of Tobacco Trichomes and Insoluble Cigarette Smoke Particles," Nature 249: 215-217. * Martell 1975 (Edward A.), "Tobacco Radioactivity and Cancer in Smokers," American Scientist 63: 404-412. * Martell 1983 (Edward A.), "Bronchial Cancer Induction by Alpha Radiation: A New Hypothesis," paper C6-11 in Proceedings of the 7th International Congress of Radiation Research, edited by J.J. Broerse et al. Published by Martinus Nijhoff, Amsterdam, Netherlands. * Mendonca 1993 (Marc S.) + Ronald J. Antoniono + J. Leslie Redpath, "Delayed Heritable Damage and Epigenetics in Radiation-Induced Neoplastic Transformation of Human Hybrid Cells," Radiation Research 134: 209-216. * Minkler 1970 (Jason L.) + John W. Gofman + Robert K. Tandy, "A Specific Common Chromosomal Pathway for the Origin of Human Malignancy," British Journal of Cancer 24: 726-740. * Minkler 1971 (Jason L.) + Dolores Piluso + John W. Gofman + Robert K. Tandy, "A Long-Term Effect of Radiation on Chromosomes of Cultured Human Fibroblasts," Mutation Research 13: 67-75. * Morgan 1996 (William F.) + 4 co-workers, (review paper) "Genomic Instability Induced by Ionizing Radiation," Radiation Research 146: 247-258. * NCRP 1984, National Council on Radiation Protection (USA), "Evaluation of Occupational and Environmental Exposures to Radon and Radon Daughters in the United States." NCRP Report 78. Bethesda, Maryland. * NCRP 1987 (see NCRP 1984), "Ionizing Radiation Exposure of the Population of the United States." 87 pages. ISBN 0-913392-91-X. NCRP Report 93. Bethesda, Maryland. * NCRP 1989 (see NCRP 1984), "Exposure of the U.S. Population from Diagnostic Radiation." 105 pages. NCRP Report 100. Bethesda, Maryland. * Nowell 1976 (Peter C.), "The Clonal Evolution of Tumor Cell Populations," Science 194: 23-28. * NRPB 1995, National Radiological Protection Board (Britain), "Risk of Radiation-Induced Cancer at Low Doses and Low Dose-Rates for Radiation Protection Purposes." 77 pages. Volume 6, No.1 in "Documents of the NRPB." ISBN 0-85951-386-6. Sales agent in USA is Bernan Associates in Lanham, Maryland: Tel 1-800-274-4447. Internet: <www.bernan.com> * Pierce 1996 (Donald A.) + Yukiko Shimizu + Dale L. Preston + Michael Vaeth + Kiyohiko Mabuchi, "Studies of the Mortality of Atomic Bomb Survivors. Report 12, Part 1. Cancer: 1950-1990," Radiation Research 146: 1-27. * Riches 1997 (A.C.) + Z. Herceg + P.E. Bryant + D.L. Stevens, "Radiation-Induced Transformation of SV40-Immortalized Human Thyroid Epithelial Cells by Single Exposure to Plutonium Alpha-Particles in Vitro," Internatl. Journal of Radiation Biology 72: 515-521. (Experiment includes gamma radiation.) * Seaborg 1993 (Glenn T.) with Benjamin S. Loeb, "The Atomic Energy Commission under Nixon: Adjusting to Troubled Times." 268 pages. ISBN 0-312-07899-4. St. Martin's Press, New York City. * Temin 1988 (H.), "Evolution of Cancer Genes as a Mutation-Driven Process," Cancer Research 48: 1697+. * Terkel 1995 (Studs), "Coming of Age: The Story of Our Century by Those Who've Lived It." 468 pages. ISBN 1-56584-284-7. The New Press, New York City. * Tlsty 1993 (T.D.) + 10 co-workers, "Loss of Chromosomal Integrity in Neoplasia," Cold Spring Harbor Symposia on Quantitative Biology 58: 645-654. * UNSCEAR 1988, United Nations Scientific Committee on the Effects of Atomic Radiation, "Sources, Effects and Risks of Ionizing Radiation." ISBN 92-1-142143-8. United Nations sales number is E.88.IX.7. Sales agent in USA is Bernan Associates in Lanham, Maryland: Tel 1-800-274-4447. Internet: <www.bernan.com> * UNSCEAR 1993 (see UNSCEAR 1988), "Sources and Effects of Ionizing Radiation: Report to the General Assembly with Scientific Annexes." 922 pages (no index). ISBN 92-1-142200-0. United Nations sales number is E.94.IX.2 (see above). * Ward 1988 (John F.), "DNA Damage Produced by Ionizing Radiation in Mammalian Cells: Identities, Mechanisms of Formation, and Reparability," Progress in Nucleic Acid Research & Molecular Biology 35: 95-125. * Ward 1991 (John F.), "Response to Commentary by D. Billen," Radiation Research 126: 385-387 (letter). * Ward 1995 (John F.), "Radiation Mutagenesis: The Initial DNA Lesions Responsible," Radiation Research 142: 362-368 (commentary). Errata: Vol.143: 355. ---------------------------------------------------------------- Committee for Nuclear Responsibiity, Inc. (CNR) POB 421993, San Francisco, CA 94142, USA Internet http://www.ratical.com/radiation/CNR/ An educational group since 1971. Gifts are tax-deductible. ----------------------------------------------------------------

Sorry for the slow reply. I don't seem to get all of the notifications from "horsepower gain support group" posts.. Absolutely. In fact, I can demonstrate via my research and testimonials that chemo and radiation actually DECREASE your cancer survivability. Yeah, it might get one tumor, but it destroys your immune system leaving you open to many other kinds of cancer. There are so many references to it's success that you can find by just doing a web search it's practically obscene.. As far as "conspiracy theory" goes consider this: Most of the people in this group now realize that low carb/high fat is the healthiest way to go -- compare that to the popular literature, media, and govt. advice being handed out. Evidence enough of conspiracy? :cool: TJ :cool:

CATEGORY: diseases/cancer TECHNICAL: ** SUMMARY: This document details the "Budwig Diet", which is the anti-cancer diet I have spoken with some of you about. At first glance, many would consider the approach quackery. However, as many of you "long timers" to the list will recall, the diet actually works by boosting your immune response to mutagenic cells (IE: cancer and virus infected). It's actually quite a well based diet in the sense that it is loaded with Omega-3 oils, anti-oxidants, sulpher compounds, and proteins. All of these key ingredents help promote a healthy and active immune system, and that is the most important aspect of preventing or recovering from cancer. I won't go into the mechanisms here (like I did in the past), because they are too complicated for one single post. I will however, merge all of this (and the algae stuff) into one long post at a later time. Until then, if you know of anyone who is ailing from cancer, I encourage you to inform them of this diet. You should also buy the book. It's only $7, and it can literally save your life. It has certainly proven to be more effective than chemotherapy and radiation, which usually cuts the vicitims lifespan to only 5 years post therapy.. Low-carber's and paleo-dieters out there will also note that it's a low-sugar diet, and also emphasizes the consumption of as few man-made/processed products as possible. I've been investigating the option of substituting whey protein for the cottage cheese, because it has the same protein profile, but is much less allergenic than the cheese. ------------------------------------------------------------- OMEGA-3 OILS Omega-3 refers to a group of oils found in seafood and many cold-climate plants, but only very small amounts are contained in most vegetable oils. Unlike fish oils, which are high in EPA and DHA, flaxseed oil is the only source of large amounts of alpha linolenic acid, ALA (55-61%). From this, the body can manufacture its own EPA, which is important for helping regulate the production of prostaglandins (hormone-like substances) useful for good health ("The natural way to better health and longer life", Bullivant). THE BUDWIG FLAX OIL DIET The Flaxseed (Linseed) oil diet was originally proposed by Dr. Johanna Budwig, a german biochemist and expert on fats and oils, in 1951 and recently re-examined by Dr. Dan C. Roehm M.D. FACP (Oncologist and former cardiologist) in 1990. Dr. Roehm claims: "this diet is far and away the most successful anti-cancer diet in the world". Budwig claims that the diet is both a preventative and a curative. She says the absence of linol-acids [in the average western diet] is responsible for the production of oxydase, which induces cancer growth and is the cause of many other chronic disorders. The beneficial oxydase ferments are destroyed by heating or boiling oils in foods, and by nitrates used for preserving meat, etc. The theory is: the use of oxygen in the organism can be stimulated by protein compounds of sulphuric content, which make oils water-soluble and which is present in cheese, nuts, onion and leek vegetables such as leek, chive, onion and garlic, but especially cottage cheese. Ferments of cell respiration closely connected with the highly unsaturated fatty acids, are also needed for proper oxydation. It is essential to use only unrefined, cold-pressed oils with high linolic acid content, such as linseed, sunflower, soya, poppyseed, walnut, and corn oils. Such oil should be consumed together with foods containing the right proteins otherwise the oils will have the OPPOSITE EFFECT, causing more harm than good. The best combination is cottage cheese and linseed oil. The linseed should be freshly ground. Carbohydrates containing natural sugar, such as dates, figs, pears, apples and grapes, are also included in the diet. Honey is also beneficial. Most of the synthetic vitamin A preparations are bad because they contain oxidation products, but much carotine as provitamin A (from carrot) is consumed. Vitamin B from buttermilk, yoghurt, and natural yeast is beneficial. A person requires daily about 4 oz. of cottage cheese mixed well with 1.5 oz. of linseed oil and 1 oz. of milk. A blender or egg beater works fine. The mixture an be sweeten with honey or otherwise flavoured naturally. Fresh fruits can be added. Every morning 2 spoonfuls of freshly ground linseed oil should be taken in luke warm buttermilk or yoghurt. The diet is indicated for all kinds of chronic diseases, especially heart ailments (corony thrombosis), gall disorders, diabetes, arthritis, and malignancies. It improves failing hearing and sight. It is the ideal nutrient for children and infants. It is suggested that this diet be supplemented with lactic acid ferments (4). "What she (Dr. Johanna Budwig) has demonstrated to my initial disbelief but lately, to my complete satisfaction in my practice is: CANCER IS EASILY CURABLE, the treatment is dietary/lifestyle, the response is immediate; the cancer cell is weak and vulnerable; the precise biochemical breakdown point was identified by her in 1951 and is specifically correctable, in vitro (test-tube) as well as in vivo (real)... " (Roehm, "Townsend Letter for Doctors", July 1990) GENERAL RULES The patient has no nourishment on day #1 other than 250 ml (8.5 oz) of Flax Oil with honey plus freshly squeezed fruit juices (no sugar added!). In the case of a very ill person, champagne may be added on the first day in place of juice and is taken with the Flax Oil and honey. Champagne is easily absorbable and has a serious purpose here. 1) SUGAR IS ABSOLUTELY FORBIDDEN. Grape juice may be added to sweeten any other freshly squeezed juices. Honey is also allowed and is included in the recipes. Fortunately, honey, although sweet, is not detrimental like commercial white sugar. (unboiled Honey is best - available through Healthfood stores). 2) Other 'forbiddens' are: - All animal fats. - All Salad Oils (this included commercial mayonnaise) - All Meats (chemicals & hormones) - Butter - Margarine - Preserved Meats (the preservatives block metabolism even of Flax Oil) 3) Freshly squeezed vegetable juices are fine - carrot, celery, apple, and red beet. 4) Three times daily a warm tea is essential - peppermint, rose hips or grape tea - all sweetened as desired with honey. One cup of black tea before noon is fine. DAILY PLAN Before breakfast - a glass of Acidophilus milk or Sauerkraut juice is taken. Breakfast - Muesli (regular cereal) is overlaid with 2 tablespoons (30 ml) of Flax Oil and honey and fresh fruit according to season - berries, cherries, apricots, peaches, grated apple. Vary the flavour from day to day. Use any nuts except peanuts! Herbal teas as desired or black tea. A 4 oz (120 g) serving of THE SPREAD (directions below). This is fine to eat 'straight' like a custard, or add it to other foods taken in the day as you will see. Morning tea (10am) - A glass of fresh carrot juice, apple, celery, or beet-apple juice is taken. Lunch - Raw salad with yoghurt-Flax Oil Mayonnaise (directions below). In addition to 'greens' salads, use grated turnips, carrots, kohlrabi, radishes, sauerkraut or cauliflower. A fine powder of horseradish, chives or parsley may be added for flavour. Cooked Meal Course - Steamed vegetables, potatoes, or such grains as rice, buck-wheat or millet may be served. to these add either THE SPREAD or THE MAYO - for flavour and to up your intake of Flax Oil. Also mix THE SPREAD with potatoes for an especially hearty meal. Add caraway, chives, parsley or other herbs. Dessert - Mix fresh fruit other than those used for breakfast with THE SPREAD, this time (instead of honey), flavoured using cream of lemon, vanilla or berries. Afternoon Tea (4pm) - A small glass of natural wine (no preservatives) or champagne or fresh fruit juice with 1-2 tablespoons of honey-coated Fax Seeds. Supper - Have this early, at 6pm. Make a hot meal using buckwheat, oat or soy cakes. grits from buckwheat are the very best and can be placed in a vegetable soup, or in a more solid form of cakes with herbal sauce. Sweet sauces & soups can always be given far more healing energy by adding THE SPREAD. Only honey or grape juice can be used for sweeteners. NO white sugar (or brown!) Only freshly squeezed juices and NOT reconstituted juices (preservative danger) may be used. These must be completely natural. How to prepare 'THE SPREAD' Place 250 ml (8.5 oz) Flax Oil into a mixer bowl and add one pound (450 g) of 1% Cottage Cheese (ie low fat eg Quark) and add 4 tablespoons (60 ml) of Honey. Turn on the mixer and add just enough low fat milk or water to get the contents of the bowl to blend in together. In 5 minutes, a preparation of custard consistency results that has NO taste of the oil (and no oily 'ring' should be seen when you rinse out the bowl). Alternatively, you can use Yoghurt instead of Cottage Cheese in proportions of 1 oz (30 g) of Yoghurt to 1 tablespoon (15 ml) each of Flax Oil and of honey and blend as above. NOTE: When Flax Oil is blended like this, it does not cause diarrhoea even when given in large amounts. It reacts chemically with the (sulphur) proteins of the cottage cheese, yoghurt, etc. How to prepare 'THE MAYO' (Mayonnaise): Mix together 2 tablespoons (30 ml) Flax Oil, 2 tablespoons (30 ml) milk, and 2 tablespoons (30 ml) Yoghurt. Then add 2 tablespoons (30 ml) of Lemon juice (or Apple Cider Vinegar) and add 1 teaspoon (2.5g) Mustard plus some herbs such as marjoram or dill. Next add 2 or 3 slices of health food store pickles (no preservatives! - read label!) and a pinch of herbal salts. (The above mayonnaise plus lots of mustard and a few bananas is very tasty!) Concluding remarks by Dr. Roehm - "I only wish that all my patients had a PhD in Biochemistry and Quantum Physics to enable them to see how with such consummate skill this diet was put together. It is a wonder. The champagne vehicle IS easier to assimilate and get someone almost on their death-bed going again. A retention enema of 250 ml (8.5 oz) of oil is another route to get this precious life-furthering, ELECTRON-RICH oil into the body. It can also be applied to the skin for transdermal absorption. I'll answer your questions and give you "special orders" for you particular case. You will have to remain on this diet for a good 5 years, at which time your tumour may have disappeared. Persons who break the rules of this diet, Dr Budwig reports, (ie eating preserved meats, candy, etc) will sometimes grow rapidly worse and cannot be saved after they come back from their spree (bon-bons mean bye-bye). In 1967, Dr Budwig broadcast the following sentence during an interview over the South German Radio Network, describing her incoming patients with failed operations and x-ray therapy": "Even in these cases it is possible to restore health in a few months at most, I would truly say 90% of the time". "This has never been contradicted, but this knowledge has been a long time reaching this side of the ocean, hasn't it? Cancer treatment can be very simple and very successful once you know how. The cancer interests dont want you to know this. May those of you who have suffered from this disease (and I include your family and friends in this) forgive the miscreants who have kept this simple information from reaching you for so long". (signed) Dan C. Roehm, M.D. FACP ------- "The best, purest, most carefully prepared Flax Oil in America is, in my opinion", said Roehm, "is Omegaflo. Arrowhead mills label is most often seen in Florida (USA). Look for the Omegaflo". "FLAX (LINSEED) OIL is readily denatured by oxygen, heat, and light. That's why it is used in paint. Rancid oil is bad for health, so oil MUST be carefully produced, packed under nitrogen in light-proof containers, refrigerated until used, used as fresh as possible, and stabilised with protein (THE SPREAD, etc) promptly once the container is opened..." (In Australia: Stoney Creek Flaxseed oil is manufactured to these specifications - available through health food stores - Max) Flax Seeds may also be used. Seeds need only be cracked in a food blender, or they may be ground in a coffee grinder. One needs three times the amount of seed to get the oil equivalent. Seeds are high in calories, so one may gain weight. The seeds are also high in soluble fibre, so blending with liquid tends to produce ever-hardening "jellies". Fresh-cracked seed sprinkled on muesli & eaten promptly tastes great. ------- Ed McCabe (p85, "Oxygen Therapies") discusses his point of view on essential fatty acids: "The red blood cells in the lungs give up carbon dioxide and take on oxygen. They are then transported to the cell site via the blood vessels, where, they release their oxygen into the plasma. This released oxygen is "attracted" to the cells by the "resonance" of the pi-electron" oxidation-enhancing fatty acids. Otherwise, oxygen cannot work its way into the cell. "Electron rich fatty acids" play the decisive role in "respiratory enzymes, which are the basis of cell oxidation...". "Dont eat anything hydrogenated like (like margarine, or fried foods) as it defeats oxygenation. Avoid products that say "hydrogenated". "We should eat essential polyunsaturated fatty acids to enhance oxygenation. They can be found naturally in Carotene, Saffron, and Flaxseed oil." REFERENCES 1. "Promotion and Prevention of Tumour Growth Effects of Endotoxin, Inflamation, and Dietary Lipids", by Raymond Kearney, Ph.D, Department of Infectious Diseases, The University of Sydney, Sydney, N.S.W. 2006 Australia. International Clinical Nutrition Review, October, 1987 Vol. 7, No. 4. 2. Roehm, "Townsend Letter for Doctors", July 1990 3. Ed McCabe, "Oxygen Therapies" 4. "The natural way to better health and longer life", Bullivant. 5. Arlin J. Brown, "March of Truth On Cancer", (seventh edition). Summary of 79 nontoxic cancer treatments. Available from the Arlin J. Brown Information Centre Inc., P.O. Box 251, Fort Belvoir, Virginia, 22060. Ph: 1-703-752-9511. DISCLAIMER This information should not be construed as an attempt to encourage people to self-treat their disorders; nor does the information attempt to endorse any particular brand or product. Nor do the authors and/or compilers necessarily endorse any views presented in this document. Although, to the best of the compilers knowledge, this information is correct at the time of publishing, it should not be relied on as a substitute for the reader's own investigations. Except for any reproduction costs, this information is given freely and no responsibility or liability is accepted for the use of this information. Any person intending to treat themselves or their family is advised to first consult a sympathetic health-care professional who is familiar with the proposed mode of treatment. -END- :cool: TJ :cool:

CATEGORY: foods/manmade TECHNICAL: *** SUMMARY: This is the third and final part of the interview with Mary Enig on the subject of trans-fats and denatured oils. As I have previously indicated, this is one of the most telling documents on the topic. There are many important issues she addresses that ties together the whole concept of human evolution, health and denatured, man-made foods. Some key points to consider in this segment of the document are these: * We have let our natural diet be changed by processed food technology. * European has decided to limit TFAs to four percent of the energy source. * historically no people had a high intake of polyunsaturates in their diets. Mostly saturated animal fats.. * children are being encouraged to drink low-fat milk instead of whole milk. In addition to the fact that, there are a number of components in mothers milk that are anti-cancer (hence the budwig diet, and the new research on human milk fighting cancer) * properties and some of the fatty acids found in milk (and coconut oil) have anti-microbial properties. * the FDA is running with misinformation a lot of the time. But, if it suits their agenda, they will vigorously use it. ------------------------------------------------------------- PART III A Perspective on Fats and the Health Food Industry by Richard A. Passwater, Ph.D. In the two previous issues, Dr. Enig and I have been discussing how the trans fatty acids formed upon the partial hydrogenation of vegetable and marine oils are being shown to be more harmful than saturated fats. Margarine and other processed foods rich in Trans Fatty Acids (TFAs) were once touted to be healthy choices for good diets, but now many researchers are recognizing that TFAs are more harmful than the natural butter and animal or tropical fats they replaced. We discussed how the processed food industry tried to cover up this fact. As Rodney Leonard discusses in Nutrition Week, "The reputation that [hydrogenated] vegetable oil as the fat of choice in a healthy diet lies in ruins. And the real question is why the American health establishment did not act sooner to correct what may be the biggest scam ever perpetuated in nutrition and nutrition policy on the American public...These trans fatty acids were found to not only have more severe health consequences for persons at risks for heart disease, but also to increase the risk for individuals prone to certain types of cancer." [28] We have let our natural diet be changed by processed food technology. The European Community has decided to limit TFAs to four percent of the energy source. Unfortunately, as Dr. Enig has shown, the American diet is closer to 10 - 14 percent, with some individuals consuming as much as 60 grams of TFAs daily. Let's continue to look into the trumped-up reasons given to us by food processors as why we should switch to TFAs, and then see what the truth is. Passwater: Some "authorities" are implying that all saturated fats or animal fats greatly increase LDL cholesterol by shutting down LDL receptor production which consequently causes LDL cholesterol to build up in the blood, while they are also implying that all polyunsaturated fats or vegetable fats either lower LDL cholesterol or raise it only modestly. Would you share with us your perspective of what we can accept as fact about saturated fat, monounsaturated fats, polyunsaturated fats and TFAs with respect to blood cholesterol? Enig: This is a complex subject, that is difficult to explain in a few words, but I'll try to be brief. The current dogma on the effect of saturated fatty acids on LDL and LDL receptors is really an issue that is not satisfactorily clear-cut. It is not surprising that feeding different proportions of different fatty acids have different effects in different animals and different organ systems or tissues. Fatty acids are active components in regulating all sorts of homeostatic mechanisms in mammalian systems. But sometimes some of the basic research that identifies what is happening to one part of the cell does not really show what is going on in another part of the cell or in the whole person, and these reports have to be interpreted carefully. I am concerned about the inconsistencies in interpreting the research. One example of such inconsistency can be seen when you compare some of the research with recent reviews. In a section of a 1980 report that measured the effect of dietary fats on LDL- cholesterol in humans, i. e., the effect of saturated and polyunsaturated dietary fat on the composition of LDL, the total cholesterol in LDL from feeding saturated fat was 59.1% (balanced is phospholipid and triglyceride) and the total cholesterol in LDL from feeding polyunsaturated fat was 59.5%. Not very different and certainly not higher than from saturated fat! These data are from the research of Dr. Antonio M. Gotto's group at Baylor College of Medicine. [29] Given these findings, I have some real problems with the unreferenced or inappropriately-referenced statements in, for example, the recent chapter on regulation of LDL-cholesterol levels that appeared in the 1993 Annual Reviews of Nutrition. The statement was made that "... {fats} containing predominantly saturated fatty acids further increase the concentration of cholesterol carried in [the LDL] fraction ..." and that "... when fed at equal levels, saturated fatty acids are more active in increasing the LDL-C concentration than are unsaturated lipids in reducing the concentration." There was no reference given for the first part of the statement; the references for the latter part (a 1957 paper by Dr. Ancel Keys et al and a 1989 talk by Dr. Mark Hegsted) are really inappropriate in my opinion. Passwater: I see that you still tell it like it is. My next question won't be of interest to most of our readers, but I have to ask it because it will be important to other researchers. So readers please hang on for a brief moment while I get a tad technical, and then well get to the practical "take home" message. Dr. Enig, how about the LDL-receptor? Enig: Briefly, so much of the research on down regulation of the LDL-receptor appears to be done on cells like fibroblasts which are questionably appropriate. One report showed that down regulation of LDL-receptors by saturated fatty acids was considered a good phenomenon since the cell was a macrophage. In addition, any of the changes that are occurring in response to short-term feeding that are likely to be rearrangements of homeostatic mechanisms don't mean very much. I know that many feeding studies have been purposely cut off after a short term so that it would show something that would not show up in the long term. As I said, I think this very complex area probably needs a whole article that delves into the meaning of the inconsistencies. Many people have interpreted these reports as meaning that people should avoid saturated fatty acids and consume more polyunsaturated fatty acids. It is important to know that historically no people had a high intake of polyunsaturates in their diets. This is really a phenomenon of the present century, and the evidence against the excess intake of polyunsaturates is mounting. Passwater: Its ironical -- animal fats have been blamed for the damage caused by partially-hydrogenated oils -- which started out as wholesome vegetable oils -- that is, until they were chemically altered by man. I can't help but think about so many in the general public who are not scientifically trained and who have been brain-washed by the countless illegal commercials that promise that using margarine will protect them from heart disease. These people don't even read the newspaper accounts such as the report from Harvard that margarine actually is associated with increased heart disease and heart disease death. In the Harvard study of 85,000 nurses, after adjusting for all known possible confounding factors including total fat and total calorie intake, there was a fifty percent greater incidence of heart disease among those women with consuming the highest fifth of percentage of fats as TFAs compared to those in the lowest fifth. [3] Since all other factors, including total fat and total calories were compensated for, the researchers conservatively concluded, "these findings support the hypothesis that consumption of partially-hydrogenated vegetable oil may contribute to occurrence of coronary heart disease." Then there is the recent report in the American Journal of Clinical Nutrition that found that the risk of coronary heart disease increases as consumption of vegetable oil rises. [30] However, the years of newspaper, magazine and TV ads that falsely told them that margarine was good for the heart -- has made them think that it was true. Now we are learning that mothers are giving their children soda or skim milk with their meals so as to avoid the fat in milk. They want to protect their children against heart disease by giving them very low fat diets in their youth. What effect is the fear of saturated fat having on the health of our children? Enig: It is really unfortunate that children are being encouraged to drink low-fat milk instead of whole milk. In addition to the fact that milk is a good source of calories for growth (children actually need fat as an energy reserve so that the protein they are consuming can be well utilized for growth), there are a number of components in milk that are not widely appreciated. Milk fat globule membrane has anti-cancer properties and some of the fatty acids found in milk (and coconut oil) have anti-microbial properties. Passwater: I am seeing reports that there appears to be a link between TFAs and obesity? Dr. Lewis H. Kuller has made such comments in Lancet, and Drs. Edward Siguel and Robert Lerman have indicated such a possible link in the American Journal of Cardiology. [31,32] I have also read discussions where TFAs have been called "the obesity trigger." Enig: There was a report earlier this year at a major symposium on obesity that was held in New York, that the metabolic effect of increasing dietary TFAs changes characteristics of muscle cells that trigger the onset of diabetes and increasing obesity. I have not seen the actual research, but am looking forward to following it. Passwater: Dr Enig, many of our readers are hearing about trans fats for the first time. Others may not be sure of what your message is regarding red meat, animal fat and vegetable oil. Would you give us a "take home" perspective regarding your advice on dietary fats? Enig: The important thing to understand is that all fats are basically mixtures of saturated, monounsaturated and polyunsaturated fatty acids in different proportions. There isn't any real evidence that everyone needs to consume exactly the same balance of fatty acids, except that we do know that people need to take in at least 2-3% of their fat as the omega-6 fatty acids and at least 1-1.5% of their fat as omega-3 fatty acids. This means that smaller people expending fewer calories need fewer calories of each fatty acid and total fats than larger or more active people who consume more calories. The fats that humans have consumed for millennia, such as the fats they added to mixed dishes, were almost always more saturated than they were unsaturated. It was the easily extractable fat or oil. The fat came from the animal, or, in the case of areas such as the tropics, it was the oil that came from the coconut or the palm fruit that was used in cooking. Sometimes it was one of the very stable oils such as olive oil or sesame paste that contained lots of built-in antioxidants and weren't too polyunsaturated. People didn't really have the ability to extract oil from vegetables such as corn, or from many seeds as they do today. However, they got their essential polyunsaturated fatty acids from many of these plants when they were included in the foods they were eating. People used the intact leaf, root, nut, grain or seed along with all their antioxidants in the stews or the porridges that most people ate. This was the manner in which the polyunsaturates were historically consumed. The polyunsaturated fatty acids didn't have to be hydrogenated to protect their integrity and keep them from going rancid because they were consumed in a protected whole-food state. People on low-fat diets historically consumed adequate amounts of essential fatty acids from foods such as grains, vegetables and nuts; and then they made their own saturated fat for the necessary structural adipose (structural body fat) and energy storage. Those people with higher fat intakes in their diets still had about the same amount of essential fatty acids, and ultimately the same amount of saturated fat for storage or as the energy source. Regardless of whether they ate it or made it, the fat in the tissues of our ancestors was relatively saturated, and therefore, the fatty acid supply to the tissues was predictably saturated. Today, with the high levels of partially- hydrogenated vegetable and marine oils in the diets of many people, the tissues and organs are faced with a new situation. Many researchers have now concluded that the presence of the TFAs is causing shifts in favor of chronic disease. Not a good situation! The bottom line is to consume as many whole foods and whole food mixtures as possible. Since we live in a society where other people prepare most of the foods many of us eat, it is important to look for the least processed and the least likely to go rancid when it comes to fats and oils. There is nothing wrong with consuming your essential fatty acids from oils as long as those oils are safely extracted and carefully stored, but a good balance needs to be maintained with sources of the more saturated fats such as the animal tallows and/or dairy fats for those who are not vegetarians, or the more saturated fats such as palm or coconut oils for those who are vegetarians. Passwater: These facts will be hard to accept by those who have always heard just the opposite, and because of this constant repetition, they have come to believe the erroneous information. While we're on the subject of truth, let's shift gears for a moment. You attended the Waxman hearing in July. What comments do you have to offer about the FDA efforts to limit nutritional products and information? Enig: One major problem as I see it is that the members of congress and their staffs have only part of the information and almost none of the training to understand that the FDA is running with misinformation a lot of the time. But, if it suits their agenda, they will vigorously use it. The supplement industry needs to be sure of its facts, needs to spend the time and effort to document these facts. The science is on the side of whole foods and rational supplementation. There is one thing that bothers me; as an expert in lipids I notice mistakes in many books, magazines and newspapers being made by "spokespersons" about the effects of fats and oils in health. I immediately discount the reliability of source of the information and suspect anything else that is being said. Sometimes I make allowances and can salvage certain facts and separate the wheat from the chaff, but others not so inclined, might not be so lenient. Since the FDA has a very biased attitude towards the whole foods and supplement industry, any erroneous written material that is put out by that industry or on behalf of that industry is considered grist for the FDA's mill. I hate to see the good apples spoiled because of the presence of a few rotten ones. Passwater: There is so much that needs to be covered, and we didn't even get around to discussing omega-3 and omega-1 fatty acids. Perhaps you will be kind enough to chat with us again. I am sure that TFAs cause membrane abnormalities that can cause irregular heart beats and I want to pursue the research that suggests that TFAs trigger obesity. We are going to hear a lot more about TFAs in the future. It has taken 15 years, but I feel that the corner has now been turned and the momentum is building. The data can no longer be suppressed. Your pioneering studies will have a major impact on helping people select better diets in the future. Now the public will have to deal with the fact that most junk foods are high in trans fat -- and this is a deadly reality that can not be compensated for merely by juggling other food components. Changing the ratio of polyunsaturates or saturates does not alter or compensate for the accumulation of trans fats. People will no longer be able to rationalize junk food as "just" being devoid of nutrients which can be replaced with supplements. People will no longer be able to rationalize junk food as "just" being high in fat which can be held in check by keeping the total dietary fat to 30% or less of total calories by selecting low-fat high-sugar foods. The reality is that there are only two healthy choices -- either get the trans fats out of foods and pseudo foods such as margarine -- or don't eat them. At least we can control the latter. Dr. Enig, what are you looking into now? Enig: I have submitted a proposal for a research project that aims to evaluate a specific nutritional support approach that I think will be extremely useful for individuals with HIV/AIDS. I am currently waiting to hear about the funding. I am presently preparing some of the research done by our group at the University of Maryland for submission to the appropriate scientific journals. I am also writing articles and a book aimed at correcting a lot of the misinformation that has been written about fats and oils. The working title of the book is "Know Your Fats: The complete primer for understanding fats, oils and cholesterol." The book is meant to be a comprehensive primer that would accurately explain what I have realized most people involved in nutrition don't really understand. I am also teaching short courses and workshops on lipids and nutrient-drug interactions. I fell that there is a great need for people with my training to continue to teach and consult. Passwater: And, I am sure that you will continue to speak out for scientific truth. I can hardly wait for your book to be published. Thanks for taking the time to inform us about the dangers of trans fats in processed foods. I still admire your bravery in presenting the information in scientific forums, rather then taking the easy path of merely researching topics that are "politically" safe and don't risk losing funding or dirty tricks. I have always enjoyed our nutrition discussions through the years and look forward to more of your visits to the Solgar Nutritional Research Center. References 1. Enig MG, Munn RJ, Keeney M. Dietary Fat and Cancer Trends -- A critique. Federation Proceedings 1978; 37:2215-2220. 2. Passwater RA. The New Supernutrition. New York: Pocket Books, 1991: 3. Willett WC, Stampfer MJ, Manson JE, et al. Intake of trans fatty acids and risk of coronary heart disease among women. Lancet 1993; 341:581-585. 4. Sampugna J, Casterline J , Enig MG, Keeney M. Influence of a margarine containing diet on aryl hydrocarbon hydroxylase activity. J Amer Oil Chem Soc 1980; 57:Abstract # 178: 5. Enig MG. Modification of Membrane Lipid Composition and Mixed-function oxidases in mouse liver Microsomes by Dietary trans fatty acids. College Park, MD: Doctoral Dissertation, University of Maryland, 1984: 6a. Ostlund-Lindqvist AM, Albanus L, Croon LB. Effect of dietary trans fatty acids on microsomal enzymes and membranes. Lipids 1985; 20:620-624. 6b. Ponder DL, Green NR. Effects of dietary fats and butylated hydroxytoluene on mutagen activation in rats. Cancer Res 1985; 45:558-560. 6c. Hogan ML, Shamsuddin AM. Large intestinal carcinogenesis. I. Promotional effect of dietary fatty acid isomers in the rat model. J Natl Cancer Inst 1984; 73:1293-1296. 7. Barnard DE, Sampugna J, Berlin E, Bhathena SJ, Knapka JJ. Dietary trans fatty acids modulate erythrocyte membrane fatty acyl composition and insulin binding in monkeys. J Nutr Biochem 1990; 1:190-195. 8. Kuller LH. Trans fatty acids and dieting [letter]. Lancet 1993; 341:1093-1094. 9. Mantey S. The effect of trans fatty acids on some Murine T and B Cell functions. College Park, MD: Master's Thesis, University of Maryland, 1985: 10a. Koletzko B, Muller J. Cis- and trans-isomeric fatty acids in plasma lipids of newborn infants and their mothers. Biol Neonate 1990; 57:172-178. 10b. Koletzko B. [supply, metabolism and biological effects of trans-isomeric fatty acids in infants] Zufuhr, Stoffwechsel und biologische Wirkungen trans-isomerer Fettsauren bei Sauglingen. Nahrung 1991; 35:229-283. 10c. Koletzko B. Trans fatty acids may impair biosynthesis of long-chain polyunsaturates and growth in man. Acta Paediatr 1992; 81:302-306. 11a. Teter BB, Sampugna J, Keeney M. Milk fat depression in C57Bl/6J mice consuming partially hydrogenated fat. J Nutr 1990; 120:818-824. 11b. Teter BB. Alterations in milk fat percent and composition by isomeric fatty acids. College Park, MD: Doctoral Dissertation, University of Maryland, 1989: 12. Atal S. The effects of dietary trans fatty acids on adipose tissue composition and metabolism in male C57Bl/6J mice. College Park, MD: Doctoral Dissertation, University of Maryland, 1990: 13a. Holman RT. The importance of double bond position in the metabolism of unsaturated fatty acids. In: Emken EA, Dutton HJ, eds. Geometrical and Positional Fatty Acid Isomers. Champaign, IL: Amer. Oil Chem. Soc., 1979:283-302. 13b. Holman RT, Pusch F, Svingen B, Dutton HJ. Unusual isomeric polyunsaturated fatty acids in liver phospholipids of rats fed hydrogenated oil. Proc Natl Acad Sci U S A 1991; 88:4830-4834. 14. Pallansch LA. Metabolic Fate and Effect of Dietary Trans Fatty Acids. College Park, MD: Doctoral Dissertation, University of Maryland, 1983: 15. Anderson JT, Grande F, Keys A. Hydrogenated Fats in the Diet and Lipids of Man. J Nutr 1961; 75:388-394. 16. van den Reek MM, Craig-Schmidt MC, Clark AJ. Use of published analyses of food items to determine dietary trans octadecenoic acid. J Am Diet Assoc 1986; 86:1391-1394. 17. van den Reek MM, Craig-Schmidt MC, Weete JD, Clark AJ. Fat in the diets of adolescent girls with emphasis on isomeric fatty acids. Am J Clin Nutr 1986; 43:530-537. 18. Alam SQ, Ren YF, Alam BS. Effect of dietary trans fatty acids on some membrane-associated enzymes and receptors in rat heart. Lipids 1989; 24:39-44. 19. Watkins BA. Bioactive Lipids in Poultry. Washington, D.C.: FASEB Conference: Current Topics in Avian Lipid Met. Bio., 1990: 20. Wansil BJ, Herbein JH, Watkins BA. Effects of Dietary and Ruminally-Derived trans C18:1 Content. FASEB J 1991; 5:A1306, Abst. 5427: 21. Mensink RP, Zock PL, Katan MB, Hornstra G. Effect of dietary cis and trans fatty acids on serum lipoprotein[a] levels in humans. J Lipid Res 1992; 33:1493-1501. 22. Enig MG. Trans Fatty Acids in the Food Supply: A comprehensive report covering 60 years of research. Silver Spring, MD: Enig Assoc., 1993: 23. Passwater RA. Nutrient Interaction in Heart Disease: An interview with Dr. David Kritchevsky. Whole Foods 1993; (6):22-25,65. 24. Kritchevsky D. Diet and cholesteremia. Lipids 1977; 12:49-52. 25. Blackburn GL, Kater G, Mascioli EA, Kowalchuk M, Babayan VK, Bistrian BR. A Reevaluation of Coconut Oil's Effect on Serum Cholesterol and Atherogenesis. J Philippine Med Assoc 1989; 65:144-152. 26. Anonymous. McDonald's Should Revert to Old Fries, says CNI. Nutrition Week 1993; 23 (May 28):3 27. Woodhill JM, Palmer AJ, Leelarthaepin B, McGilchrist C, Blacket R . Low Fat, Low Cholesterol Diet in Secondary Prevention of Coronary Heart Disease. Adv Exptl Med Biol 1977; 109:317-330. 28. Leonard RE. Icons of American Diet Crash Into New Reality. Nutrition Week October 9,1992; 4-5. 29. Pownall HJ, Shepherd J, Mantulin WW, Sklar LA, Gotto AM, Tauton OD. Effect of saturated and polyunsaturated fat diets on the composition and structure of human low density lipoproteins. Atherosclerosis 1980; 36:299-314. 30. Hodgson J, Wahlqvist M, Boxall J, Balazs N. Can linoleic acid Contribute to Coronary Heart Disease? Amer. J. Clin. Nutr. 1993; 58:228-34. 31. Kuller LH; Trans Fatty Acids and Dieting. Lancet 1993; 341:1093-4. 32. Siguel EN, Lerman RH. Trans Fatty Acid Patterns in Patients with Angiographically Documented Coronary Heart Disease. Amer. J. Cardiology 1993; 71:916-20. All rights, including electronic and print media, to this article are copyrighted to Richard A. Passwater, Ph.D. and Whole Foods magazine (WFC Inc.). :cool: TJ :cool:

Enig Interview Part 2. CATEGORY: foods/manmade TECHNICAL: *** SUMMARY: This is the second part of the Mary Enig document on trans fats. As I said in the first part, this is truly one of the best works on identifying and detailing the problems with man-made trans-fatty acids which appear in almost all of our processed foods. There are several things to take note of in this segment. As you read through the document, consider some of these facts: * TFA's increase bad cholesterol and decrease good cholesterol. * TFA's have shown a statistical correlation with increased breast and prostate cancer. * Research showing that TFA's are harmful is consistently being surpressed by the food industry. * She also argues that antioxidant vitamins have a positive impact on cancer prevention. * The amount of TFA in ruminant meats and milk is significantly lower than in hydrogenated man-made oils. * The amount of hydrogenated oils in our diet is ever on the increase... (as high as 60g day!) * saturated fats have been blamed for heart disease, but can actually reduce the risk that is posed by TFA's when consumed in combination with TFA fats! * staurated fats are created by the body from excess carbohydrate and protein. * coconut and palm oils have actually demonstrated positive effects on blood cholesterol and health ------------------------------------------------------------- PART II Trans fats from partially-hydrogenated oils are the real culprits for which saturated fats have been blamed. by Richard A. Passwater, Ph.D. Last month we talked mostly about what trans fats (TFAs) were, how they interfere with "machinery" of our normal cell biology and that they are a recent and unnatural intrusion into our diets. In Part II, we will look into the health problems caused by TFAs, and in Part III, Dr. Enig will put the research on TFAs and other fats in perspective and give us her thoughts on the pluses and negatives of the Health Food Industry as seen from academia. Passwater: You mentioned the your research was stimulated by the early investigations of Drs. Fred Kummerow, George Mann and Edward Pinckney. What did you set out to investigate and what have others added to these findings? Enig: Much of the Trans-Fatty Acid (TFA) research that was accomplished at the University of Maryland from 1977 to today was done to answer some very basic questions. For example, we wanted to know how much TFAs people were being exposed to. So during some of the early research, we measured the amounts of TFAs in typical U. S. foods and then estimated the amounts in various diets and in the food supply. The next set of efforts was done to measure the effects that feeding diets containing physiologically relevant amounts of TFAs to laboratory animals had on some reproductive and lactation functions, on the alteration of membrane properties, and on the consequent alteration of enzyme functions that had physiological importance. These different efforts were measured by our research group, and many of our findings, e. g., that the enzyme functions were adversely affected, were repeated by various other research groups. It is hard to tell sometimes if we were repeating the findings of others or if others were repeating our findings. I think it is safe to say that the research was invariably reproducible as long as the same animal model and the same amount of TFAs were used. In other words, our findings were real and other researchers could easily find the same thing. A number of research groups were able to use some of our basic findings, and many of the researchers were using their own models and their research was providing information that was parallel and complementary to ours. In many instances, the other research teams had access to better funding and models that we did not have at the University of Maryland. One research group at Auburn University examined diets of adolescent girls and directly measured the TFAs in their diets by laboratory analytical methods. [16, 17] They found that approximately two-thirds of the TFAs in the diets of these adolescents could be predicted by the food composition data in our 1983 research paper for 220 foods. This is rather remarkable since their research was done in another part of the country. It does show the similarity of many of the same types of partially hydrogenated fats in diets across the US. A research group at Louisiana State University studied, among other things, the effects of TFAs on what is called "the second messenger," cyclic AMP and the digitalis receptor. [18] They found that TFAs affected both. Still another research group, this one at Virginia Polytechnic Institute, studied the effect of TFAs on bone development. [19, 20] Their research showed some very undesirable effects! AS far as I know, the latter two groups who were finding important effects have not been able to continue because of lack of funds for TFA research. Their efforts were done independent of our concerns and findings but parallel to our efforts. There have been a number of other research efforts that have been given widespread publicity. These include the published findings from Dr. Martijn Katan's lab in Holland that the TFAs lower the "good" High-Density Lipoprotein (HDL) and raise the "bad" lipoprotein [a] (Lpa) which is atherogenic. [21] Also, the published findings from Dr. Walter Willett's research at Harvard on 85,000 nurses, as well as other prospective studies, have showed that those people who consumed the most TFAs had the most heart disease. [3] Dr. Willett's group also has preliminary, as yet unpublished, data that those individuals who developed breast and prostate cancer had higher intakes of TFAs. These findings have been presented at scientific meetings by Dr. Willett and his staff. I have recently prepared a technical report which includes additional information that would normally not be found in typical scientific reviews. [22] This information is of special interest to many in the food industry and the regulatory agencies. The report identifies all of the different research groups that have been working on TFAs around the world over the past 60 years. Passwater: I remember how the processed food industry tried to suppress your early research. As Rodney Leonard, the editor of Nutrition Week noted, you fought tenaciously to bring out the truth and were "a burr under the saddle of the [processed food] industry and the government, persistently challenging the contention that the health threat of trans fatty acids is overplayed and that the current level of consumption poses no threat to public health." Most of those who were skeptical then have examined the steady stream of new data and now agree with you that TFAs are a major health threat. How were you able to keep on? What techniques were used against you and how did you overcome them? Where did you find moral and scientific support? Enig: As you know from some of our past conversations, we ran into some strong challenges from certain segments of the edible oil industry regarding our findings. In addition to writing several articles to "refute" our findings, and seeing to it that our major reports did not get properly referenced, those individuals who actively opposed our research were able to influence funding sources. Gradually though, other researchers started to realize that we were correct and appropriately conservative in our approach to research, and consequently, most of the "bad-mouthing" that we encountered has backfired. Passwater: Yes, I remember well how we were both encountering difficulties with "the establishment." I am happy to note, as you well know, that the same is happening regarding my findings regarding vitamin E and the prevention of heart disease, and of the antioxidant nutrients in the prevention of cancer. We never did get the funding needed to further pursue our research. Enig: You're right. At the University of Maryland we never did get the type of funding that you need to receive to continue the level of research that would have been desirable, but what funding we did receive was carefully managed and many of the people in our research group were dedicated to the research. I think we found moral support because we knew we were scientifically correct, and ultimately the scientific support came as other researchers started to evaluate the problems without having certain industry people set up their research protocol. AS you realize from your years of involvement in research, good research properly done is always reproducible, if all the variables are the same, but it is also possible for unscrupulous individuals to set up a research protocol designed to obfuscate, and if that gets published, it keeps other good researchers from continuing to work in the area. Frequently, those individuals who are coopted write their summary and abstract the way the industry wants them to, but they usually leave their data intact so that a knowledgeable researcher can recognize the inconsistency. However, it is a very time- consuming task to constantly challenge each piece of misinformation that you see. Passwater: Yes, it is a difficult task, but you and I give it our best shots. In the past we did a lot of challenging others to prove us wrong, and now we can smile a lot. Enig: Our work is not done yet! There is still much to do. Passwater: Right again! How big is the problem with TFAs? How extensive are trans fats in our modern diets, and how does this compare to ancient diets and other diets around the world. Enig: Today the levels of TFAs vary around the world from practically zero to levels much like those found in our foods in the U. S. It depends on how much partially hydrogenated vegetable fats or partially hydrogenated marine oils are present in the food supply. Without the commercial partial hydrogenation process, as would have been the case more than a hundred years ago, the levels of TFAs in diets would be relatively low. Only the ruminant fats would have supplied any, and the types of isomers that are found in the ruminant fats behave in a very different way from those found in the partially hydrogenated vegetable oils. Additionally, the research shows that the TFAs are more of a problem when the level of saturated fat is low. Diets that are higher in ruminant fats are also higher in saturated fats. Most ruminant fats have about 2-3% TFAs whereas the partially hydrogenated vegetable fats are commonly 30-40% and as high as 53% in foods in this country. After analyzing hundreds of food samples for TFAs, chemically analyzing food composites, and calculating dietary information, I am confident that there are many people in this country who consume 20% of the total fat in their diet as TFAs. On average though, 10.9% is the number we came up with when we looked at all of the published analyses. The typical french fried potatoes are around 40% TFAs, and many popular cookies and crackers range from 30 to 50% TFAs, and every donut I have analyzed has about 35 to 40% TFAs. Since these are all fairly high fat products, someone who eats a lot of these types of foods will get a large amount of TFAs. Several years ago, we documented nearly 60 grams of TFAs in someone's typical daily diet. Passwater: Wow! I hope that's no one I know. Dr. Enig, you mentioned that TFAs are atherogenic -- that is they cause atherosclerosis. Then you mention that TFAs are more of a problem when saturated fats are low. Yet most people fear saturated fats because they have been told that it is the saturated fats that cause heart disease. You are recognized as a leading expert on fats and oils, do saturated fats cause heart disease? Enig: The idea that saturated fats cause heart disease is completely wrong, but the statement has been "published" so many times over the last three or more decades that it is very difficult to convince people otherwise unless they are willing to take the time to read and learn what all the economic and political factors were that produced the anti-saturated fat agenda. Periodically, various reports have come out that show the inconsistencies in the theory. You have already discussed this with the well-known cholesterol and lipids researcher, Dr. David Kritchevsky of the Wistar Institute. [23] In 1977, Dr. Kritchevsky noted that it did not make any difference what kind of fat was added to the whole foods diets in animal studies -- only when the diets were very unnatural chemically could changes be brought about -- and from study to study these changes were inconsistent. [24] As you frequently report, the latest theories regarding heart disease point to oxidized fats and oxidized lipoproteins as culprits. This being the case, accusations against chemically- stable, basically non-oxidizable saturated fat don't make sense. Most people who find fault with saturated fats do not really understand that our cells are busy making saturated fatty acids all the time from carbohydrates and excess protein. Passwater: Do tropical oils cause heart disease? Enig: No they don't. Several studies have shown that there is no increase in heart disease in countries or communities where most of the fat is either coconut oil or palm oil. Palm oil that is not extensively refined has very high levels of antioxidants, and coconut oil has high levels of very useful medium chain fatty acids. There are many older research studies that showed that adding quite a bit of coconut oil to the diet of persons having high blood cholesterol reduced their level of cholesterol. Dr. George Blackburn from Harvard Medical School has written an extensive review on this topic. [25] It is unfortunate that this misinformation about these oils became so widespread because they are very stable oils that have unique functional properties and products made with them as the fat component usually have far less fat and therefore fewer calories. Needless to say, they would also have virtually no TFAs which are unquestionably atherogenic. When coconut oil was used in the manufacture of crackers, very little fat was added to each cracker, but the crackers did not become stale before they could be purchased. Now the fat-free crackers become very stale very quickly, and the crackers made with the more unsaturated oils are higher in fat and are greasy or they appear drier because they are made with the high-temperature melting partially hydrogenated oils. Deep fried foods made in these oils never absorb quite as much fat as they do when they are fried with the more unsaturated oils. Passwater: Speaking of deep fried french fries, I notice that the Community Nutrition Institute is pleading with McDonald's to go back to their old cooking oil, an animal tallow. CNI cited higher risks of coronary heart disease, coronary artery disease, and low birth-weight babies due to the partially hydrogenated vegetable oil that McDonald's has been using since 1990. [26] Enig: Yes, when I analyzed the oils, I found that the percentage of fat that was saturated fat in their french fries dropped from 49% to 24% when McDonald's switched from animal tallow to partially hydrogenated vegetable oil. But the percentage of fat that was TFAs rose from 5% to 42-48%. McDonald's own study showed that the total amount of fat in its fries rose from 17.6% to 27.9% Recently, McDonald's has again switched to an oil that has cut the TFAs in half. But, those who insist on eating french fries were better off when the beef tallow was used. Passwater: Why were earlier researchers misled about saturated fats and heart disease? Enig: The simplistic, abbreviated story of how some of the anti- saturated fat rhetoric got started and then took a strangle hold, is that when laboratory animals were fed semi-purified and artificially saturated (fat) diets, the animals actually became deficient in essential fatty acids. As a result, these animals developed lesions that were incorrectly defined as the equivalent of heart disease. This "research" was touted as showing an effect of "saturated" fat. Then when Dr. Ancel Keys of the University of Minnesota reported that hydrogenated fats were responsible for heart disease [15], the response from the threatened edible oil industry was to claim that it was only the saturated fats that were the culprits, and that the industry would get rid of the problem by only partially hydrogenating the oils. From that point on, the saturated fats stood "guilty as accused," even though study after study showed that there was no relationship between saturated fat intake and the development of heart disease. In fact, some of the studies showed that there was less progression of the disease process when the saturated component was higher. [27] Usually the proponents of the lipid hypothesis managed to squelch the effect of these reports. Of course the partially hydrogenated oils were really very little different in saturated fat level than the fats and oils that had been called "hydrogenated," but the public and the media and many of the naive researchers didn't know that. As time went on, the whole heart disease agenda became a multi-million dollar business that was benefiting the researchers funded by the part of the National Institutes of Health that deals with heart disease, the National Heart, Lung and Blood Institute. The only people not benefiting were and are the consumers who are continuing to get more and more heart disease at higher and higher costs. The consumer may not be dying from heart disease as often as they were 30 years ago, but they are undergoing more surgery such as by-pass and angioplasty, and they are swallowing more expensive cholesterol-lowering drugs. All in all, while the so-called mortality figures have decreased, the incidence has greatly increased. Of course, the ill-trained consumer activist groups have added to the problem by continuing to publish their own misinterpretations of the science, and this in turn, is further publicized in the media. Passwater: Well, I see that you haven't backed off and cow-towed to the consensus pseudo-scientists that form opinions without looking closely at the data. I would like you to explain the real facts and their proper interpretation for the benefit of our readers. So let's look at fats and cholesterol, TFAs and the obesity trigger, and your thoughts on helping the Health Food Industry in Part III. Health Risks from Processed Foods and Trans Fats: An interview with Mary Enig, Ph.D. :cool: TJ :cool:

ENIG Interview #1 ---------------------------------------------------------------- CATEGORY: foods/manmade TECHNICAL: *** SUMMARY: This document is one of the best works on the negative effects of hydrogenated oils. It's an interview with Mary Enig, who's a PhD. researcher of fats and oils. As you read through the document, you'll see just how much work she's done in that field. This is part one of a three part document. The major issue this article addresses is the fact that hydrogenated oils are far worse than natural non man-made oils. The question has come up on the list about whether the trans fats in natural dairy were safer than those found in margarines and shortenings. I think this passage sheds a little light on that question: "the misconception that processed margarine was better than natural butter. But the studies showed that not only was the amount much smaller (e.g., the fat in butter might be 2-3% of the ruminant trans), the effect on the "machinery" in the cell membranes was not different than without the trans. Yet all studies feeding the trans produced by partially hydrogenating the vegetable oils showed the adverse effect on the cell "machinery." Not only is it far less, but what is in the dairy affects the body alot less negatively. This does reinforce the point that humans were not designed to consume the dairy of other animals however.. This document is the one I also allude to when issues of trans fats contributing to heart disease and cancer come up. When you read through it, pay close attention to the number of times she mentions a statistically significant increase in cancer and CVD when discussing trans-fats and hydrogenated oils. My favorite passage for vegetarians is this one: "correlations between the increase in per capita dietary fat intake and total cancer mortality over a sixty-year period show significant positive correlations for total fat and vegetable fat, and negative correlation for animal fat." Many of ya'll have also heard me warn against eating deep fried foods. That was because deep frying denatures the foods far worse than any other preparation method. In fact, deep frying is akin to the hydrogenation process. Be sure to catch the section where she discusses the temperatures at which hydrogenation occurs, and remember that deep frying can reach temps. upwards of 440 deg. F. Consider how many toxins can be introduced in that kind of environment.. ------------------------------------------------------------- by Richard A. Passwater, Ph.D. Dr. Mary G. Enig, a nutritionist widely known for her research on the nutritional aspects of fats and oils, is a consultant, clinician, and the Director of the Nutritional Sciences Division of Enig Associates, Inc., Silver Spring, Maryland. She received her PhD in Nutritional Sciences from the University of Maryland, College Park in 1984, taught a graduate course in nutrient-drug interactions for the University's Graduate Program in Nutritional Sciences, and held a Faculty Research Associateship from 1984 through 1991 with the Lipids Research Group in the Department of Chemistry and Biochemistry. Dr. Enig is a Fellow of the American College of Nutrition, and a member of the American Institute of Nutrition. Her many years of experience as a "bench chemist" in the analysis of food fats and oils, provides a foundation for her active roles in food labeling and composition issues at the federal and state levels. Dr. Enig is a Consulting Editor to the "Journal of the American College of Nutrition" and formerly served as a Contributing Editor to "Clinical Nutrition." She has published 14 scientific papers on the subject of food fats and oils, several chapters on nutrition for books, and presented over 35 scientific papers on food and nutrition topics. She is the President of the Maryland Nutritionists Association, past President of the Coalition of Nutritionists of Maryland and was appointed by the Governor in 1986 to the Maryland State Advisory Council on Nutrition and served as the Chairman of the Health Subcommittee until the Council was disbanded in 1988. I first learned of Dr. Mary Enig's research from a 1978 report in the Federation Proceedings. [1] We met shortly after that, and since I had written about trans fats several times in Supernutrition, we had common concerns about the effect that these trans fats from processed foods were having. [2] We were both concerned particularly about the misconception that processed margarine was better than natural butter. In several visits by Dr. Mary Enig to the Solgar Nutritional Research Center I quickly learned that she was an exacting scientist who is not afraid to speak out and who supports good nutrition, not just going along with the establishment's party line. While studying for her Ph.D. at the University of Maryland, often she would first respond with the "correct" answer that was expected, and then she would explain why new research indicated "alternatives," such as optimal vitamin and mineral nourishment, provided a better answer. It is not easy be credentialed by the "system," while your own research shows other facts. In part I of my interview with Dr. Enig, we will discuss the harm caused by partially-hydrogenated fats that are present in processed foods. In Part II, we will discuss how partially-hydrogenated fats increase heart disease and cancer risks, and how the processed food industry tries to suppress this information. In her 1978 report, Dr. Enig challenged the speculation concerning the relationship of dietary fat and cancer causation. She concluded that correlations between the increase in per capita dietary fat intake and total cancer mortality over a sixty-year period show significant positive correlations for total fat and vegetable fat, and negative correlation for animal fat. That is the cancer rate is higher when the amount of vegetable fat or total fat is higher in the diet, but the cancer rate is lower when there there is more animal fat in the diet. These findings were unpopular then as they are today, but they are still correct. It is convenient to blame everything on red meat and animal fat, and believe that vegetable oil is the great dietary salvation -- even if it is partially hydrogenated. At least that is what the vegetable oil people would like everyone to believe. Now, we are not saying that lots of dietary fat is good for you and that vegetables are not good. Eating vegetables, fruits and other whole foods is very desirable. However, that is not the same as eating partially-hydrogenated vegetable oils. Americans eat too much fat (especially partially hydrogenated vegetable oils) and not enough fruits and vegetables. The problem is that the typical American is not eating enough whole foods, but instead, is eating too much partially-hydrogenated vegetable oil -- a fractionated food -- that has been made into "funny foods" such as margarine or added into baked goods. Such "funny foods" are far different than real whole foods. Hydrogenation ruins the nutritional value of vegetable oils! Why would anyone want to ruin the nutrition value of vegetable oils? The purpose of hydrogenation is to solidify an oil so that it can be made to resemble real foods such as butter. (see figure 1.) The hydrogenation process imparts desirable features such as spreadability, texture, "mouth feel," and increased shelf life to naturally liquid vegetable oils. In the hydrogenation process, vegetable oil is reacted under pressure with hydrogen gas at 250 - 400oF for several hours in the presence of a catalyst such as nickel or platinum. However, this industrial process cannot control where the hydrogen atoms are added to the "unsaturated" double bonds. Randomly adding hydrogen atoms to polyunsaturated fats converts natural food components into many compounds, some of which have never seen before by man until partially hydrogenated fats were manufactured. Some of the several dozens of altered compounds created in the manufacture of partially-hydrogenated fats are "trans" fatty acids. Fatty acids are the building blocks of fats, much like amino acids are the building blocks of proteins. Other new compounds accidentally synthesized include fatty acids having double bonds translocated to new and un-natural positions, and various molecular fragments. Many of these altered compounds are detrimental to health. Since "trans" fats are so detrimental to our health. permit me to briefly review the relevance of distinguishing between "trans" and "cis" fats before chatting with Dr. Enig. Recently, in the September issue, in the interview with Dr. Jim Clark and Mr. Lance Schilipalius, we discussed "trans" isomers of carotenoids. "Trans" means the same thing here. "Cis" and "trans" isomers refer to how identical atoms are added to double bonds. (See figure 2.) When the atoms are added to the same side of the double bond, the compound is called "cis" and the molecule is bent because of the crowding of the atoms on one side. When the atoms are added on opposite sides of the double bond, the compound is called "trans" and molecule is "space-balanced" and straightened. The shape of a molecule is important because enzymes and their substrates -- the molecules enzymes act upon -- must fit together like a key in a lock. Dr. Enig will discuss this during the interview, but the important thing to remember is that natural polyunsaturated fatty acids are "cis" compounds and are bent. Partial hydrogenation produces many un-natural "trans" fats which are straight and not intended for use in the human body. Figure 3 illustrates the differences between the shapes of "trans" and "cis" fatty acids You don't have to understand the difference between "trans" and "cis," but it is important that you know that there is a difference because, as Dr. Enig will explain, it can affect your health. Passwater: Dr. Enig, a lot of people are interested in "trans" fats now. You have been researching them since 1977. How are trans fats harmful to us? Enig: More than a decade of research at the University of Maryland, as well as research that was being done at other institutions, showed that consumption of trans fatty acids from partially hydrogenated (a process that adds hydrogen to solidify or harden) vegetable fats and oils had many adverse effects in health areas such as heart disease, cancer, diabetes, immunity, reproduction and lactation, and obesity. It is rather easy today to come up with a long list of these adverse effects from the published research done by many scientists around the world, as well as the researchers at the University of Maryland. The reason there is so much recent interest is that during the past three years there has been a number of major research reports published in prestigious medical journals that caught the attention of the press. These and earlier reports had shown, for example, that consumption of trans fatty acids lower the "good" HDL cholesterol in a dose response manner (the higher the trans fat level in the diet, the lower the HDL level in the blood) and raise the atherogenic lipoprotein(a) in humans as well as raising the "bad" LDL cholesterol and total blood cholesterol levels by 20-30 milligram-percent. These studies have usually been shown in independent non-industry studies. Perhaps the most significant event though was the report from researchers at Harvard University, who evaluated more than 85,000 women in a long-term prospective study and found that there was a significantly higher intake of trans fatty acids in those individuals who developed heart disease. [3] As regards to the question of cancer, trans fatty acids induce adverse alterations in the activities of the important enzyme system that metabolizes chemical carcinogens and drugs (medications), i. e., the mixed-function oxidase cytochromes P-448/450. The initial research in this area was done by the Maryland group in collaboration with the U. S. Food and Drug Administration, and was followed by the more extensive evaluation that I did for my Ph.D. dissertation; several groups around the country and the world also reported the same or similar results. [4-6] Several groups around the world reported a higher intake of partially hydrogenated fats in those individuals who have developed cancer. Both primate and human studies have shown inappropriate handling of blood sugar; trans fatty acids decrease the response of the red blood cell to insulin, thus having a potentially undesirable effect in diabetics. The primate research was initiated at Maryland in collaboration with the U. S. Department of Agriculture and the National Institutes of Health, and the human research is from the University of Pittsburgh and quite recent. [7,8] One major concern is that trans fatty acids adversely affect immune response by lowering efficiency of B cell response and increasing proliferation of T cells. This was shown in research done at Maryland using a mouse model and although there are reports from clinicians that there are problems of immune dysfunction in humans it still needs to be evaluated systematically in humans. [9] Recent research from outside the U. S. has indicated that trans fatty acids interfere with reproductive attributes and of concern is the finding that trans fatty acids lower the amount of cream (volume) in milk from lactating females in all species studies including humans, thus lowering the overall quality available to the infant. [10,11] The latter research was done at Maryland by my colleague Dr. Beverly Teter. Basically, trans fatty acids cause alterations to numerous physiological functions of biological membranes that are known to be critical for cell homeostasis, e.g., appropriate membrane transport and membrane fluidity, and these fatty acid isomers produce alterations in adipose cell size, cell number, lipid class and fatty acid composition. [12] Passwater: Now that trans fats are becoming of more interest, the term may still just be a buzz word to many of our readers. Would you explain just what are trans fats? Where do they come from? How are they formed? Enig: To understand what trans fatty acids are you have to understand what fatty acids are. Fatty acids are basically chains of carbon with a carboxyl group (COOH) at one end that can react (e.g., combine) with another molecule. When fatty acids are in fats or oils they are combined with glycerol in the proportions of three fatty acid molecules to one glycerol molecule and they form triacylglycerols or in common terminology, triglycerides. (See figure 4.) Fatty acids come in different chain lengths ranging from three carbons long (propionic acid) to 24 carbons long (lignoceric acid). These fatty acids are either "saturated" (with an adequate number of hydrogen atoms) and chemically stable, or they are "unsaturated" (missing adequate hydrogens) and chemically unstable. If a fatty acid is missing two hydrogens, it is called a monounsaturated fatty acid, and in place of the two hydrogens, the adjacent carbons "double" bond to each other. If the fatty acid is missing four or six or more hydrogens, it is called a polyunsaturated fatty acid, and it is even more unstable than the monounsaturated fatty acid. Because the double bonds in naturally occurring plant oil fatty acids are curved with a "cis" configuration, the fatty acids cannot pack into a crystal form at normal temperatures so their presence produces a liquid oil. Saturated fatty acids have a straight configuration and can pack into a solid crystal at normal temperatures. If the unsaturated fatty acids are altered by partial hydrogenation to straighten the chains so that they have some of the physical packing properties of saturated fatty acids they have had their "cis" double bond changed to a "trans" double bond and they turn a technically mostly unsaturated oil into a solid fat. The trans fatty acids are the same length and weight as the original "cis" fatty acid they were formed from, and although they have the same number of carbons, hydrogens, and oxygens they are shaped differently in space. The term that is used is that they are "isomers." The problem arises when a large number of the trans fatty acids are consumed from foods and they are deposited in those parts of the cell membranes that are supposed to have either saturated fatty acids or "cis" unsaturated fatty acids; under these circumstances the trans fatty acids essentially foul up the "machinery." Although the trans fatty acids are chemically "monounsaturated" or "polyunsaturated" they are considered so different from the "cis" monounsaturated or polyunsaturated fatty acids that they cannot be legally designated, e.g., monounsaturated for purposes of labeling. Most of the trans fatty acids produced by the partial hydrogenation process are chemically monounsaturates. There have always been small amounts of one kind of trans fatty acids in the human diet from the ruminant fats (dairy, sheep, goat, deer, buffalo, antelope, etc.) because the microorganisms in the rumen try to get rid of the polyunsaturated fatty acids that are found in the plant foods eaten by these animals. In the early days of trans fatty acid research, the researchers assumed that the trans fatty acids found in ruminant fats were no different than those produced by partial hydrogenation in the factory. But the studies showed that not only was the amount much smaller (e.g., the fat in butter might be 2-3% of the ruminant trans), the effect on the "machinery" in the cell membranes was not different than without the trans. Yet all studies feeding the trans produced by partially hydrogenating the vegetable oils showed the adverse effect on the cell "machinery." Passwater: Why are trans fats a problem? Enig: The various mechanisms through which the trans fatty acids disrupt function are related in part to the ability of trans fatty acids to inhibit the function of membrane related enzymes such as the delta-6 desaturase resulting in decreased conversion of e.g., linoleic acid to gamma-linolenic acid or arachidonic acid; interference with the necessary conversion of omega-3 fatty acids to their elongated tissue omega-3 fatty acids; and escalation of the adverse effects of essential fatty acid deficiency. This latter effect was shown especially by the work of Dr. Holman and his colleagues at the Hormel Institute at the University of Minnesota, the other effects have been shown by many researchers including the University of Maryland researchers. [13,14] Passwater: What were your early findings and what got you interested in this area of research? Enig: My initial published research in 1978 when I was at the University of Maryland showed that trans fatty acids, which were increasing in the food supply at the time and which had not been catalogued in any of the food data tables, were the very factors that explained the positive statistical relationship between the increase in cancer mortality and vegetable fat consumption in the U. S. [1] It was clear from the literature that once the trans fatty acids were identified as products of partial hydrogenation and studies were engaged in, there were a number of earlier researchers who questioned the biological safety of the trans fatty acids viz a viz their relationship to both cancer and heart disease. In fact, Dr. Ancel Keys had originally claimed that the partially hydrogenated vegetable oils with their trans fatty acids were the culprits in heart disease. [15] This was in 1958, and the edible oils industry was very swift in their squelching of that information; they shifted the emphasis to "saturated" fat and started the phoney attack on meat and dairy fats. Passwater: What have others added to your findings? Enig: As you have noted in some of your writings, we at the University of Maryland were not the first to raise the issue of trans fatty acids and adverse health effects; Dr. Fred Kummerow from the University of Illinois, Dr. George Mann from Vanderbilt University, and Dr. Edward Pinckney with the American Medical Association had sounded the alarm many years before my plunge into the foray. In fact, I had drawn heavily on the research findings of Dr. Kummerow and the informative writing of Dr. Mann when I first started to investigate what was known about health effects of trans fatty acids at the time. Our research findings have been duplicated by others, but more importantly other independent researchers have extended and explained many of our findings and concerns. Passwater: I remember how the processed food industry tried to suppress your early research. In Part II, let's discuss the techniques used against you and how you overcame them, and then we can more fully discuss the relationship of various fats to heart disease and cancer. :cool: TJ :cool:

CATEGORY: foods/tables TECHNICAL: * SUMMARY: This document is a short table that gives the caffeine content of a variety of popular beverages. One important fact that is missing from this analysis is the source of the caffeine. Keep in mind that 135mg of caffeine from natural brewed coffee has a much different effect than 130mg of synthetic caffeine from Excedrin. When caffeine is consumed, from a natural source, it is present with other xanthines (family of stimulant chemicals) which makes it much safer and better absorbed by the body. This is not the case with the synthetic caffeine in colas, stimulants like no-doz and vivarin. ------------------------------------------------------------- Typical doses: serving caffeine Coca-Cola 12 oz. 65 mg Mountain Dew 12 oz. 54 mg Jolt Cola 12 oz. 71 mg Drip coffee 6 oz 115-175 mg Espresso (1.5-2oz) 100 mg Brewed coffee 6 oz 80-135 mg Instant 65-100 mg Decaf 3-4 mg tea, iced (12 ozs.) 70 mg tea, brewed 6 oz 40-60 mg milk chocolate 1 oz. 1-15 mg dark chocolate 1 oz. 20 mg Anacin/Anacin-3 2 64 mg Excedrin 2 130 mg Midol 2 64 mg No-Doz 2 200 mg Vivarin 1 200 mg :cool: TJ :cool:

Eat a ton more fat and back off a little on the salads.. (throw down some nuts/seeds, pork skins, and fatty meats - ribs, sirloin, sausages, bacon, eggs, etc..) :cool: TJ :cool:

CATEGORY: biology/anabolism TECHNICAL: *** SUMMARY: This document talks about muscle growth, which by definition, is what anabolism means. As you read through this material, take note of a few of the facts. Specifically, that muscle cells can only hypertrophy (grow) and not hyperplasia (split into two). Also note the role of hGH, and IGF's. They are the key components of muscle anabolism, and will be discussed in greater detail in the future. "Muscle Memory" is one of the reasons I tell people to train. Because, no matter how out of shape you are (or how old), you'll be able to work yourself back to your best fitness level. You can even go beyond, if you work at it.. ------------------------------------------------------------- Date: Mon, 22 Jul 1996 12:47:15 -0400 Subject: Muscle Growth Muscle Growth Muscle growth is a specialized form of protein synthesis. As we saw above, a steroid hormone (testosterone) enters the muscle cell by diffusing directly across the cell membrane, combines with a receptor in the cell and then stimulates gene transcription and protein formation via the DNA -> mRNA -> tRNA -> protein pathway. Specific receptors and genes are involved. Muscle cells, as mentioned before, are long cells called myofibrils. They differ from most other cells in that when muscles grow, the individual cells simply become thicker and longer instead of dividing into entirely new cells. Muscle cells also differ from most other body cells in that muscle cells are multinucleated. A myofibril may increase in size up to 28 times its initial size. The interesting questions come in as we start looking at exactly how and when this process occurs. Human growth hormone (hGH) and insulin-like growth factors (IGFs) seem to play an important, though somewhat unclear, role. hGH is released from the anterior pituitary and travels through the blood. It acts on the liver to release IGFs. Both IGFs and hGH are peptide hormones; IGFs are structurally very similar to a large section of the insulin molecule - hence their name. What precisely happens at the muscle cell is not known, but we can make some fairly well-informed speculation. Since IGFs are similar to insulin, it makes sense to think that they would also have a similar function. So IGFs probably work to increase uptake of amino acids and glucose into muscle cells. It is not clear whether muscle cells have receptors for hGH, but if they do, then it could be that hGH increases nuclear division in muscle without triggering cellular division (mitosis). We have seen how DNA and RNA are critical to protein synthesis, so it is clear that having more nucleii within muscle would be very beneficial for more rapid protein synthesis (muscle growth). It turns out that each nucleus has a sort of effective "range". When the muscle grows, it can only grow as far as the nucleii will "reach". So the number of nucleii control the ultimate size of the muscle fiber. One of the major functions of hGH is to stimulate cell division. Now, if there are hGH receptors in muscle, but muscle cells lack the ability to divide, and hGH has an anabolic effect on muscle, it stands to reason that hGH is increasing the nuclear division process (and thus the total number of available nucleii in the muscle), but the cytoplasmic separation process never kicks in. Perhaps the mechanism for it that is found most cells has been lost over time in muscle as an evolutionary adaption. (There is no doubt that muscles are very important to survival!) It seems then that hGH and IGFs might have complementary functions in stimulating muscle growth. hGH could be instructing the muscle cells to "build more factories" for muscle while IGFs could be stimulating the cells to take in more "building blocks" for protein synthesis. Both hGH and IGFs may affect other important components in the process as well - such as increasing the production of hormone receptors or tRNA or activating enzymes that accelerate transcription. Multinucleation might explain the longstanding anecdotal phenomenon most bodybuilders call "muscle memory". Muscle memory is recognized when someone who has had a substantial muscular mass and then lost it due to injury or layoffs from training, returns to training and regains the majority of the mass in a much shorter time than was initially required to develop it. What could be happening is this: the specific muscle proteins in the muscle were cannibalized by the body for energy production during non-use. However, the muscle retains the higher than average number of nucleii that the previous exercise stress caused the body to create. When presented with exercise and proper nutrients, new protein synthesis can occur at an accelerated rate. :cool: TJ :cool:

CATEGORY: diseases/allergy TECHNICAL: ** SUMMARY: This document was one of the reasons I gave up most grain completely, and only consume rice and oats (whole grains) only once a week. Pay careful attention to some of the diseases being attributed to gluten intolerance (something all humans have to one degree or another). It's scary. I also liked the way this paper puts forth the paleo-neo-timeline so easily. I'll forward other documents in the future that detail the shift of humans from hunter-gatherer to agrarian. Also take note of the B8 gene - this mutation, along with blood type differences, can be attributed to agrarianism and grain consumption. The most important part of the document, though, is the part that discusses the genetic singularity in today's grain. Many people believe that older grains (like spelt) are better than wheat, but in fact, they are just as "man-made" (in the sense that man genetically altered them by cross breeding). The note even mentions lactose intolerance and the fact that, genetically, we are not well adept at consuming the milk of other animals. There really is so much info here. One thing I often tell people is that expectant mothers, and infants should avoid these foods as well too. Take a look below at the discussion of infant mortality rates and you'll probably agree. The note even briefly discusses the importance of breast feeding, but I have more complete info on this subject that I will send later. ------------------------------------------------------------- From the Neolithic Revolution to Gluten Intolerance _________________________________________________________________ Table Of Contents * Why So Many Intolerant To Gluten ? by Luigi Greco, D.C.H., M.Sc.(MCH), M.D., Department of Pediatrics, University of Naples 30.06.1995 + Hunters, Fishers and Gatherers + The Great Revolution: The First Farmers + The Expansion Of The Farmers + The Evolution Of Cereals + The Rise Of The Intolerance To Gluten + Hints On The Epidemiology Of Gluten Intolerance + Gluten Sensitive Versus Gluten Intolerant + References _________________________________________________________________ Why So Many Intolerant To Gluten ? We have recently reported on Lancet (1) a consistent cohort of patients affected by drug-resistant epilepsy with cerebral calcifications, half of which were cured by a gluten-free diet. All had an atrophic jejunal mucosa, which recovered on a gluten free diet. Gluten intolerance is now a recognized cause of brain calcifications and epilepsy, of dementia, of psychiatric disturbances: many researchers believe that, in genetically predisposed subjects, gluten is not healthy for the brain function (2). This is just too much. Having had over 25 years of variegated experience with gluten intolerance I find hard to imagine that the single most common food intolerance to the single most diffuse staple food in our environment might provoke such a complexity of severe adverse immunemediated reactions in any part of the human body and function. The list is endless, but malignancies, adverse pregnancy outcome and impaired brain function are indeed complications above the tolerable threshold of this food intolerance. On the other end today we know very well that the majority (as many as 9 to 1) of gluten intolerant subjects, identified by familial or population screening, do not manifest any complaint, although they do have a flat intestinal mucosa (3). In conclusion a sizable proportion of our population (from 0.3 to 1%) is gluten intolerant and reacts with a wide spectrum of symptoms from no apparent reaction to severe life-threatening diseases. This intolerance is strongly linked to specific genetic markers which have indeed required thousands years to develop and be selected: the 'population genetic' time is of this dimension, while the changes in the environment and in the food we eat, require centuries or less. Where did they come from? _________________________________________________________________ Hunters, Fishers and Gatherers Human beings have been on Earth for over 3 millions year, but Homo Sapiens Sapiens, our nearest parent, is only 100,000 years old. For ninety thousand years he conducted a nomadic life getting food by hunting, fishing and collecting fruits, seeds, herbs and vegetables from nature. Only quite recently (about 10.000 years ago) did some nomadic tribes start to have stable settlements because they developed the ability to gather enough food to be stored. The cultivation of wild seeds begun. Ten thousand years ago the last glaciation came to an end: a Neo-thermal period ensued which marked the passage from the Paleolithic to the Neolithic age. Ices melted gradually from the equator to the poles over several thousands years when new fertile and humid lands were uncovered in South East Asia all of Europe was still covered with ice and Northern Countries had to wait up to 4000 years more to get out from a frozen environment. _________________________________________________________________ The Great Revolution: The First Farmers The discovery in the Neolithic age of ways to produce and store food has been the greatest revolution mankind ever experienced. Passage from collection to production originates the first system in which human labor is transferred onto activities which produced income for long periods of time. The principle of property was consolidated and fortifications to protect the land and food stores were developed. Archeological findings suggest that this revolution was not initiated by the man hunter and warrior, but by the intelligent observations made by the woman. The woman carried the daily burden of collecting seeds, herbs, roots and tubers. Most probably she used a stick to excavate roots and tubers: during this activity she observed the fall of grain seeds on the ground and their penetration into the soil with rain. She may have been surprised to find new plants in the places which she herself dug with a stick, and made the final connection between fallen seeds and new 'cultivated' plants. She was, for thousands years, the sole leader of the farming practices and provided a more and more consistent integration to the scanty products of the man hunter (6). To our actual knowledge, the origin of farming practices should be located in the 'Fertile Crescent': the wide belt of South East Asia which includes Southern Turkey, Palestine, Lebanon and North Iraq. In the highlands of this area abundant rainfall was caused by the neo-thermal switch. In all of this area existed, and still exists, a wide variety of wild cereals, sometimes in natural extended fields, induced by the rainfalls. Triticum Dicoccoides (wheat) and Hordeum Spontaneum (barley) were common and routinely collected by the local dwellers. The wild cereals had very few seeds (2-4) which fell easily on the ground on maturation. The people from the Uadi el-Natuf Tell of South East Asia (7800 B.C.) provided the first traces of the gradual shift from hunters to grain cultivators. Their economy was based on the hunt of the gazelle, but their diet also included collected grain seeds. These gradually came to form a substantial proportion of their energy input, as cultivation practices ensued. There were no grinding stones or mills and it was most probable that gathering prevailed on cultivation. But during the Proto-Neolithic superior a cuneiform mortar appeared. 1000-2000 years later (5000 B.C.) wild animals, more rare due to incoming drought, formed only 5% of the daily diet, while cereals and farmed animals become a sizable part of it (4). Stable settlements were founded: the village of CatalHuyuk in Southern Turkey had a population of 5000 inhabitants 9000 years B.C. In that area a collection of sickles was found with inserted oxidian blades, smoothed by the routine contact with the siliceous stalk of cereals. The sickles indicate that it was possible to collect seeds not only by picking on the ground, but also by cutting stems of plants which were capable of retaining the seed in an ear (5). 'Mesopotamic' populations, originated in the first farmers, developed a great civilization with large cities and powerful armies to defend their land property and food stores. In Egypt a civilization based on farming practices developed in the 5th millennium: they became specialists in the cultivation of wheat, barley (to produce beer) and flax. _________________________________________________________________ The Expansion Of The Farmers While in South East Asia the progressive drought made hunting difficult and encouraged farming, in Europe the Paleolithic culture of hunters and gatherers persisted for 5000 years more, gradually transforming into the Mesolithic age. In the 'Fertile Crescent' the availability of food stores and the gradual development of animal farming stimulated an unprecedented demographic explosion. The nuclear family had had a small dimension for hundreds thousands of years: the birth rate had been limited by nomadic life. In transmigrations the mother had been able to carry one infant, while the others had been obliged to walk and move on their own. Small babies in between had less chances of surviving. Thus mankind remained of approximately the same size during entire ages. Farmers, on the contrary, were settlers, possessed food stores and most probably took advantages in the farming practices of more hands in the family. In this manner the family size exploded and, as a result, a progressive continuous need to gain more lands ensued. The farmer's expansion lasted from 9000 B.C. up to the 4000 B.C. when they reached Ireland, Denmark and Sweden covering most cultivable lands in Europe. The expansions followed the waterways of Mediterranean and of Danube across the time of Egyptians, Phoenicians, Greeks and Romans (7). The farmers' expansion was not limited to the diffusion of the agricultural practices, but was a 'demic' expansion: that is a substantial replacement of the local dwellers, the Mesolithic populations of Europe, by the Neolithic from South East Asia. More than 2/3 of our actual genetic inheritance originated in this new population, while the native genetic background has been progressively lost or confined to isolated geographical areas. The genetic replacement of the native European population is marked by the B8 specificity of the HLA system. Cavalli Sforza and coworkers showed that the migration of farmers is paralleled by the diffusion of B8. The frequency of B8 is inversely proportional to the time length of wheat cultivation. In practice B8 appears to be less frequent in populations which have lived on wheat for a longer time, as it is caused by a negative genetic selection in wheat cultivators (7). We are aware that in Ireland, where the wheat cultivation came only 3000 years B.C., a very high frequency of gluten intolerance has been reported. _________________________________________________________________ The Evolution Of Cereals The early wild cereals, of the Triticum (wheat) and Hordeum (barley) species were genetically diploid and carried few seeds, which usually fell on the ground at maturation, making any harvest very difficult. A chromosomes in ingle couples (diploidicity) allowed for a wide genetic and phenotypic heterogeneity with remarkable variations in the content of protein and starches. Poliploid plants occasionally originated in nature, but they had few chances to survive, without artificial (cultivation) practices and were usually lost (8). The beginning of farming, with the use of irrigation, allowed the survival, and the expansion, of poliploid grains. But the new poliploid grains had substantially reduced genetic variations (since each gene is represented in several copies) and more frequently autoimpollinate themselves, causing remarkable increase of the genetic uniformity. The first stable formation of poliploid grains is dated around 6000 years B.C.: the genetic uniformity caused a considerable rise in stability and yield, convincing the early farmer to nduce a progressive and rapid replacement of the wild species. Genetic variability of grains was essential in order to adapt the plant to the very different environmental conditions of different areas, but the yield was generally low (9). Triticum Turgide Dicoccoides was crossed with Triticum Fanschii to originate the Triticum Aestivum, which is the progenitor of all our actual wheat. The Aestivum is an esaploid wheat with 42 chromosomes, versus the 14 of the T. Monococcum. Such powerful grain replaced all existing varieties to the point where genetic variability nowadays is lost: over the world we have 20,000 cultivated species of the same unique T. Aestivum wheat. The Triticum Turgidum Dicoccoides, progenitor of the actual 'durum' wheat with which pasta is made, had just few seeds encapsulated into a pointed and twilled kernel: at maturation the seeds fell on the soil and penetrated into it with rain, eased by the arrow-shaped structure of the kernel. Ten thousand years ago it was difficult to pick them up: hence the attempt, made by the Neolithics, to select varieties which could retain the seed longer, in order to allow for an harvest. Genetic variability was already substantially reduced in Roman times: 'farrum', i.e. spelt, (T. Dicoccoides) and 'Siligo' (T. Vulgaris) were the common grains. Siligo was used for bread making and contained a certain amount of gluten, while spelt, used mainly for soups, was poorer in gluten content (10). But cultivation of wheat and barley was not started or diffused in the whole world: only a small geographic area (South East Asia) developed gluten-containing cereals. In Asia rice was the cultivated species, while in America maize prevailed and in Africa sorghum and millet. All these plants were present in nature and were gradually cultivated in the places of origin (7). In our part of the world grains had for centuries been selected in order to improve their homogeneity and productivity, but soon (Roman times or before?) another desirable quality was preferred: the ability to stick, to glue up a dough to improve bread making. Early bread making activities pushed towards grains that contained greater amounts of a structural protein which greatly facilitated the bread making: the gluten. Gluten was not chosen because of its, at the time unknown, nutritional value (which is not absolutely special, since it is a protein with relatively low nutritional value), but for its commercial qualities. Rice, maize, sorghum, millet do not contain gluten: no leavened bread was prepared with them: the majority of mankind never lived on bread, as we do know it. Over the last 200 years of our modern age active genetic selection, and actual genetic manipulation, have changed the aspect of the original Triticacee enormously: from few grains and little gluten to great wheat harvests very enriched in gluten (50% of the protein content), well adapted to cultivation practices and ready to be handled by monstrous machinery. _________________________________________________________________ The Rise Of The Intolerance To Gluten Did everybody adapt to such profound changes in the basic nutrition over such a short period of time? South Eastern populations, presumably well adapted to the new foods, grossly replaced the existing Mesolithic European dwellers who still lived on hunting and gathering. But a proportion of the local populations (or, rather, of their inheritance ) persisted beside the invaders. The feeding changes were not well tolerated by everybody. The best similar example is lactose intolerance: populations that have more recently adapted to milk consumption, still lack the genetic ability to digest lactose over the infancy period. Environment has changed centuries before any change in the inheritance may have been possible. Similarly a considerable proportion of the hunters and gatherers of the pre-Neolithic ages have not fully adapted to the great feed changes induced by the cultivation of wheat. These people could not recognize gluten as a 'tolerable' protein available for digestion and absorption: they may have not have any problem or complaint for centuries, since the content of gluten in the grains was very low, but when 'industrial' quantities of gluten were induced by selection of wheat in order to improve bread making, they were exposed to unbearable quantities of an 'intolerable' protein or peptide. This population, genetically identifiable today by their specific HLA pattern, did not recognized, through their HLA system, the gluten peptide as a tolerable item, but, because of the similarity of some sequences of gliadin peptides with several pathogenic viruses, they generate a complex defense mechanism (an immune response) which does not eventually find the pathogen to destroy, and most probably activate an auto-immune response which ultimately is the origin of the damage to their intestine and other organs. These fierce descendants of hunters and fishers, exposed to this subtle enemy, could not develop the defense of tolerance and, in the attempt to fight the unknown, they ultimately develop a disease due to excess defense. For centuries they underwent a negative selective pressure, with less chances to survive, and then to be manifest (11). In the last millennium gluten-intolerant children mostly had a harsh time behind them: after weaning, malabsorption and malnutrition were the underlying causes of poor defense to infections during infancy and early childhood. Acute infectious diarrhea was the main killer of infants up to 50 years ago in Europe and up to 15 babies every thousand died for this condition. In the suburbs of Naples, only 25 years ago, infectious diarrhea was the main killer (25% on an infant mortality rate of 100 per thousands live births) (12). The vast majority of gluten intolerance occurred among these poor infants. In my own clinical experience 25 years ago I observed several fatal gastrointestinal infections in babies with the 'celiac crisis', which has now disappeared from our wards. Few chances to survive, few intolerant children that reached the reproductive age, and become capable of transmitting the intolerance, few adult cases. Then gluten intolerance may have become extinct, as was in fact the case with several other pathogenic conditions? Not at all. The intolerance most probably had some selective advantage which counterbalanced the gluten intolerance: it is possible to suggest that it was their very effective HLA Class II system that gave them a selective advantage against infections, which compensated the disadvantage due to gluten intolerance. When, in the last 50 years, infantile infections greatly diminished, the descendants of the hunters and gatherers with very active immune-defense, 'over reacted' more frequently to the gluten than to their ordinary enemy. Hence the rise of the cohort that now appears to manifest, in different manners, a gluten intolerance. However, not all populations of the world were ever exposed to such a nasty protein: the vast majority of mankind, after the development of agriculture, lived on maize, rice, sorghum and millet, tubers: all gluten free. All of them did not underwent the selective pressure of gluten intolerance and they may in fact have been the reservoir of wild genes. Finally, breast feeding most probably played a major role in preserving some children from the fatal infection of infancy (13). The capacities of breast milk to protect against viral and bacterial attack, the protection given by maternal antibodies and the delaying effect on the manifestation of symptoms of gluten intolerance (in the predisposed subjects) may all have protected the hunters and gatherers, who in this manner avoided to develop fatal symptoms and managed to survive and transmit their genes to our population. _________________________________________________________________ Hints On The Epidemiology Of Gluten Intolerance The epidemiology of gluten intolerance, as we know it today, is the complex result of the apparition of the population of hunters and gatherers in our modern world. As the cohort of those born before the World War II had few chances to survive infancy, we nowadays have few adult cases and few long term complications. Where the intolerance is still manifested mainly in the classical way (infants and small children, malabsorption, diarrhea, often switched on by an infection) we do not frequent encounter 'atypical' presentations and adult cases or long term complications. In this case the epidemiological calculations on observed cases made by gastroenterologist may be in great contrast with those made by pediatricians. On the contrary the rarity of 'classical' cases, which has been used as the proof of the 'disappearance' of gluten intolerance, is counterbalanced by the presence of atypical and late diagnosis, where actively searched for. Finally nutritional attitudes have played a major role with regard to the chances for hunters to manifest themselves in different age groups: the example of Sweden as compared to the nearest Denmark or Finland is paradigmatic (14). As shown by Maki et al, the ability to identify atypical cases may completely change the observed epidemiological pattern in a given region. Hence the reason for the 'iceberg': most cases still to be discovered (15). Similarly, population-based screening programs uncover more 'silent' than overt cases (3). Nevertheless, the 'cohort effect', regional differences and so on, have up to now failed to overcome the limits of numbers: when local incidence rates are compared with other regions' rates, the 95% Confidence Intervals of the rates are very often so wide to contain the all lot of observed rates. No clear-cut statistical difference has really been shown in the incidence of gluten intolerance in Europe (16). Wherever extensive studies on symptomatic cases have been run an incidence of 1 case per each 1000 live births has been reached, but very often the incidence has been much lower: up to 1 cases every 250 live births. Population screening studies invariably come to an incidence rate of 1 every 250. This is very close to the rate predicted by age-adjusted incidence density studies (17). Recent reports indicate an incidence close to 1 case per every 100 live births, but this finding needs confirmation. _________________________________________________________________ Gluten Sensitive Versus Gluten Intolerant But the epidemiology of gluten intolerance, which entails the tracing of a group of our ancestors, may completely change once we consider the increasing knowledge about the 'gluten-sensitive' individuals. 6 to 10% of first degree relatives of known cases themselves are gluten intolerant and have a flat intestinal mucosa (these are silent cases), but up to 30% of sibs of cases, when challenged with a dose of gluten (or its digest) activates a specific mucosal immune-response (with increase in intraepithelial infiltration and activation of TCells), without having any sign of mucosal damage (potential cases?) (18). We may, in the near future, have a substantial group of individuals who do not activate, in presence of gluten, a 'pathogenic' immune response (auto-immunity), but who recognize gluten as a 'suspect' protein in the same way as their peers really intolerant. Finally gluten intolerance is indeed linked to a specific genetic predisposition: most probably at least two genetic loci are involved in running the risk of intolerance. How many possess these specific genetic risk at a 'carrier' state? Certainly more than 5% of the actual population. In conclusion we have a wide population of 'gluten-reactants' in Europe (EC): at least 1 million cases of total intolerance to gluten an estimated similar amount of 'gluten sensitive' people 10-15 times more 'carriers' of the risk of becoming gluten intolerant. So we have found our ancestral hunters and gatherers: they are a substantial proportion of our actual community and do deserve a 'gluten-free' alternative not only as a therapeutic mean, but as an option of our daily life. References 1. Gobbi G, Bouquet F, Greco L, Lambertini A, Tassinari CA, Ventura A, Zaniboni MG: "Coeliac Disease, epilepsy and cerebral calcifications" Lancet, 340, Nx 8817, 439-443, 1992 2. Epilepsy and other neurological disorders in Coeliac Disease. Republic of S. Marino Meeting, April 10-12 1995, G. Gobbi edt., Raven Press, in preparation. 3. Catassi C, Ratsch IM, Fabiani E, Rossini M, Bordicchia F, Candela F, Coppa GV, Giorgi PL: Coeliac Disease in the year 2000: exploring the iceberg. Lancet, 1994, 343: 200-203. 4. Furon R. Manuel de Prehistorie Generale., 1958, Payor, Paris. 5. Cambel H, Braidwood RJ. An old farmer's village in Turkey. Le Scienze, 1970, 22: 96-103. 6. Heichelheim F. An Ancient Economic History. A.W. Sijthoff edt., Leiden, 1970. 7. Cavalli-Sforza L. Chi Siamo (Who are we). 1993 Mondadori, Milano. 8. Raven PH, Evert RF, Eichorn S Biology of plants. 4th ed. Worth Publ. Inc, New York, 1986. 9. Feldman M, Sears ER The wild gene resources of wheat. Scientific American, 1981: 98-109. 10. Lucio Giunio Moderato Columella " Libri rei rusticae" Anni 60-65 dopo Cristo. Ed. Einaudi,1977. 11. Simoons FJ: Coeliac Disease as a Geographic Problem. Food, Nutrition and Evolution, 1982, 179-199. 12. Greco,L.: " Malnutrizione di classe a Napoli" Inchiesta, 24, 53-63, 1976. 13. Greco,L., Mayer,M., Grimaldi,M., Follo,D., De Ritis,G., Auric- chio,S.: "The effect of Early Feeding on the onset of Sympthoms in Coeliac Disease" J.Pediat. Gastroenterology Nutrition, 4:52-55, 1985. 14. Maki M, Holm K, Ascher H, Greco L.: Factors affecting clinical presentation of coeliac disease: role of type and amount of gluten containing cereals in the diet. In "Common Food Intolerances 1: Epidemiology of Coeliac Disease", Auricchio S, Visakorpi JK, editors, Karger, Basel, 1992, pp 76-83. 15. Maki M, Kallonen K, Landeaho ML, Visakorpi JK.:Changing pattern of childhood coeliac disease in Finland. Acta Paediatr Scand 1988; 77:408-412. 16. Greco L, Maki M, Di Donato F, Visakorpi JK. Epidemiology of Coeliac Disease in Europe and the Mediterranean area. A summary report on the Multicentric study by the European Society of Paediatric Gas- troenterology and Nutrition. In "Common Food Intolerances 1: Epidemiology of Coeliac Disease", Auricchio S, Visakorpi JK, editors, Karger, Basel, 1992, pp 14-24. 17. Magazzu, Bottaro G, Cataldo F, Iacono G, Di Donato F, Patane R, Cavataio F, Maltese I, Romano C, Arco A, Totolo N, Bragion E, Traverso G, and Greco L: "Increasing Incidence of childhood celiac disease in Sicily: results of a multicentric study" Acta Paediatr, 83:1065-1069, 1994. 18. Troncone R, Greco L, Mayer M, Mazzarella G, Maiuri L, Congia M, Frau F, De Virgiliis S, Auricchio S.: "In half of Siblings of Coeliac Chil- dren rectal gluten challenge reveals gluten sensitivity not restricted to coeliac HLA." :cool: TJ :cool:

I've heard about them, but never tried them. I'll see if I can find some locally and report my findings :grin: :cool: TJ :cool:

CATEGORY: foods/tables TECHNICAL: * SUMMARY: This document gives a table of common foods which contain the healthy omega-3 fatty acids. As you can see, a large number of these sources are nuts, seeds, and seafoods. In general, flax seed oil taken daily is the best way to go. But, if you can, it's a pretty good idea to supplement with other omega-3 sources. I personally am a big fan of pumpkin seeds, and walnuts. I also usually consume salmon, tuna or trout 2-3 times a week. ------------------------------------------------------------- Date: Fri, 25 Apr 1997 14:09:17 -0700 Subject: Re: LOWCARB omega oils Both this list & the last I posted are from _Beyond Pritikin_ by Ann Louise Gittleman. (She's big on EFAs.) Here's a list I have: Flaxseed 57% Chia Seed 30% Hemp Seed 30% Pumpkin Seed 15% Canola Oil 10% Soybean Oil 8% Walnut Oil 5% 3.5 oz of fish mg of Omega-3 Anchovy 747 Salmon, chinook 633 Herring 606 Mackerel 585 Tuna, albacore 337 Halibut, Pacific 194 Cod, Atlantic 93 Trout, rainbow 84 Haddock 72 Swordfish 30 Red Snapper 19 Sole 10 She also says the highest concentrations of O-3 is in north Atlantic sardine oil (at 18%, compared with 9% for salmon). :cool: TJ :cool:

YUP! :cool: TJ :cool:

CATEGORY: foods/manmade TECHNICAL: * SUMMARY: This document discusses one of the most harmful food products found in almost all of the diet (or lite) food products sold today in the US. That product, aspartame, is now becoming more and more prevalant across the globe. There are several places though, like Asia, Europe, and South America, where stevia is also taking a foothold. As you read through this document, you will see aspartame linked to multiple sclerosis, lupus, and other afflictions. I have seen other evidence that verifies this claim (with the exception of the statement that aspartame is causing seizures). I know that, I personally, noticed a drastic change in myself when I quit consuming aspartame. I decided to stop about 1.5 years ago after having been the type of person who drank 5-6 diet colas a day. For two weeks after quitting, I suffered from massive migraines (and I very *rarely* have headaches). After a month, all the headaches passed and I noticed (what I perceived) as my vision improving as well. The document also claims that aspartame is harmful for diabetics. I can say this much, aspartame has proven to stimulate insulin secretion, just like sugar, in diabetic patients. That adds further stress to their already overworked pancreas. Many of you have read the "MacDougall Cure" for Multiple Sclerosis.. It's up on the web page. He cured himself from MS by omitting all processed and man-made foods (like aspartame). Let me put it this way: What more proof do you need that food chemicals are not a healthy thing to consume? Money motivates all, and politicians have proven to be easily corruptable. Is it any wonder that there are collusion issues with the FDA and Monsanto? Once again I say: Eat like a caveman.. As funny as it sounds, it has a logic that is irrefutable! ------------------------------------------------------------- WORLD ENVIRONMENTAL CONFERENCE and the MULTIPLE SCLEROSIS FOUNDATION F.D.A. ISSUING FOR COLLUSION WITH MONSANTO Article written by Nancy Markle (11/20/97) I have spent several days lecturing at the WORLD ENVIRONMENTAL CONFERENCE on "ASPARTAME marketed as 'NutraSweet', 'Equal', and 'Spoonful"'. In the keynote address by the EPA, they announced that there was an epidemic of multiple sclerosis and systemic lupus, and they did not understand what toxin was causing this to be rampant across the United States. I explained that I was there to lecture on exactly that subject. When the temperature of Aspartame exceeds 86 degrees F, the wood alcohol in ASPARTAME coverts to formaldehyde and then to formic acid, which in turn causes metabolic acidosis. (Formic acid is the poison found in the sting of fire ants). The methanol toxicity mimics multiple sclerosis; thus people were being diagnosed with having multiple sclerosis in error. The multiple sclerosis is not a death sentence, where methanol toxicity is. In the case of systemic lupus, we are finding it has become almost as rampant as multiple sclerosis, especially Diet Coke and Diet Pepsi drinkers. Also, with methanol toxicity, the victims usually drink three to four 12 oz. Cans of them per day, some even more. In the cases of systemic lupus, which is triggered by ASPARTAME, the victim usually does not know that the aspartame is the culprit The victim continues its use aggravating the lupus to such a degree, that sometimes it becomes life threatening. When we get people off the aspartame, those with systemic lupus usually become asymptomatic. Unfortunately, we can not reverse this disease. On the other hand, in the case of those diagnosed with Multiple Sclerosis, (when in reality, the disease is methanol toxicity), most of the symptoms disappear. We have seen cases where their vision has returned and even their hearing has returned. This also applies to cases of tinnitus. During a lecture I said "If you are using ASPARTAME (NutraSweet, Equal, Spoonful, etc.) and you suffer from fibromyalgia symptoms, spasms, shooting pains, numbness in your legs, cramps, vertigo, dizziness, headaches, tinnitus, joint pain, depression, anxiety attacks, slurred speech, blurred vision, or memory loss-you probably have ASPARTAME DISEASE!" People were jumping up during the lecture saying, "I've got this, is it reversible?" It is rampant. Some of the speakers at my lecture even were suffering from these symptoms. In one lecture attended by the Ambassador of Uganda, he told us that their sugar industry is adding aspartame! He continued by saying that one of the industry leader's son could no longer walk - due in part by product usage! We have a very serious problem. Even a stranger came up to Dr. Espisto (one of my speakers) and myself and said, "Could you tell me why so many people seem to be coming down with MS?" During a visit to a hospice, a nurse said that six of her friends, who were heavy Diet Coke addicts, had all been diagnosed with MS. This is beyond coincidence. Here is the problem. There were Congressional Hearings when aspartame was included in 100 different products. Since this initial hearing, there have been two subsequent hearings, but to no avail. Nothing has been done. The drug and chemical lobbies have very deep pockets. Now there are over 5,000 products containing this chemical, and the PATENT HAS EXPIRED!!!!! At the time of this first hearing, people were going blind. The methanol in the aspartame converts to formaldehyde in the retina of the eye. Formaldehyde is grouped in the same class of drugs as cyanide and arsenic- DEADLY POISONS!!! Unfortunately, it just takes longer to quietly kill, but it is killing people and causing all kinds of neurological problems. Aspartame changes the brain's chemistry. It is the reason for severe seizures. This drug changes the dopamine level in the brain. Imagine what this drug does to patients suffering from Parkinson's Disease. This drug also causes Birth Defects. There is absolutely no reason to take this product. It is NOT A DIET PRODUCT!!! The Congressional record said, "It makes you crave carbohydrates and will make you FAT". Dr. Roberts stated that when he got patients off aspartame, their average weight loss was 19 pounds per person. The formaldehyde stores in the fat cells, particularly in the hips and thighs. Aspartame is especially deadly for diabetics. All physicians know what wood alcohol will do to a diabetic. We find that physicians believe that they have patients with retinopathy, when in fact, it is caused by the aspartame. The aspartame keeps the blood sugar level out of control, causing many patients to go into a coma. Unfortunately, many have died. People were telling us at the Conference of the American College of Physicians, that they had relatives that switched from saccharin to an aspartame product and how that relative had eventually gone into a coma. Their physicians could not get the blood sugar levels under control. Thus, the patients suffered acute memory loss and eventually coma and death. Memory loss is due to the fact that aspartic acid and phenylalanine are neurotoxic without the other amino acids found in protein. Thus it goes past the blood brain barrier and deteriorates the neurons of the brain. Dr. Russell Blaylock, neurosurgeon, said, "The ingredients stimulates the neurons of the brain to death, causing brain damage of varying degrees. Dr. Blaylock has written a book entitled "EXCITOTOXINS: THE TASTE THAT KILLS" (Health Press 1-800-643-2665). Dr. H.J. Roberts, diabetic specialist and world expert on aspartame poisoning, has also written a book entitled "DEFENSE AGAINST ALZHEIMER'S DISEASE" (1-800-814-9800). Dr. Roberts tells how aspartame poisoning is escalating Alzheimer's Disease, and indeed it is. As the hospice nurse told me, women are being admitted at 30 years of age with Alzheimer's Disease. Dr. Blaylock and Dr. Roberts will be writing a position paper with some case histories and will post it on the Internet. According to the Conference of the American College of Physicians, 'We are talking about a plague of neurological diseases caused by this deadly poison". Dr. Roberts realized what was happening when aspartame was first marketed. He said "his diabetic patients presented memory loss, confusion, and severe vision loss". At the Conference of the American College of Physicians, doctors admitted that they did not know. They had wondered why seizures were rampant (the phenylalanine in aspartame breaks down the seizure threshold and depletes serotonin, which causes manic depression, panic attacks, rage and violence). Just before the Conference, I received a FAX from Norway, asking for a possible antidote for this poison because they are experiencing so many problems in their country. This "poison" is now available in 90 PLUS countries worldwide. Fortunately, we had speakers and ambassadors at the Conference from different nations who have pledged their help. We ask that you help too. Print this article out and warn everyone you know. Take anything thatcontains aspartame back to the store. Take the "NO ASPARTAME TEST" and send us your case history. I assure you that MONSANTO, the creator of aspartame, knows how deadly it is. They fund the American Diabetes Association, American Dietetic Association, Congress, and the Conference of the American College of Physicians. The New York Times, on November 15, 1996, ran an article on how the American Dietetic Association takes money from the food industry to endorse their products. Therefore, they can not criticize any additives or tell about their link to MONSANTO. How bad is this? We told a mother who had a child on NutraSweet to get off the product. The child was having grand mal seizures every day. The mother called her physician, who called the ADA, who told the doctor not to take the child off the NutraSweet. We are still trying to convince the mother that the aspartame is causing the seizures. Every time we get someone off of aspartame, the seizures stop. If the baby dies, you know whose fault it is, and what we are up against. There are 92 documented symptoms of aspartame, from coma to death. The majority of them are all neurological, because the aspartame destroys the nervous system. Aspartame Disease is partially the cause to what is behind some of the mystery of the Desert Storm health problems. The burning tongue and other problems discussed in over 60 cases can be directly related to the consumption of an aspartame product. Several thousand pallets of diet drinks were shipped to the Desert Storm troops. (Remember heat can liberate the methanol from the aspartame at 86 degrees F). Diet drinks sat in the 120 degree F. Arabian sun for weeks at a time on pallets. The service men and women drank them all day long. All of their symptoms are identical to aspartame poisoning. Dr. Roberts says "consuming aspartame at the time of conception can cause birth defects". The phenylalanine concentrates in the placenta, causing mental retardation, according to Dr. Louis Elsas, Pediatrician Professor - Genetics, at Emory University in his testimony before Congress. In the original lab tests, animals developed brain tumors (phenylalanine breaks down into DXP, a brain tumor agent). When Dr. Espisto was lecturing on aspartame me, one physician in the audience, a neurosurgeon, said, "when they remove brain tumors, they have found high levels of aspartame in them". Stevia, a sweet food, NOT AN ADDITIVE, which helps in the metabolism of sugar, which would be ideal for diabetics, has now been approved as a dietary supplement by the F.D.A. For years, the F.D.A. has outlawed this sweet food because of their loyalty to MONSANTO. [You can obtain Stevia now in natural foods stores in either cut & sifted dried leaves or in powder form. I use it and it's great.] If it says "SUGAR FREE" on the label-DO NOT EVEN THINK ABOUT IT!!!!!l! Senator Howard Hetzenbaum wrote a bill that would have warned all infants, pregnant mothers and children of the dangers of aspartame. The bill would have also instituted independent studies on the problems existing in the population (seizures, changes in brain chemistry, changes in neurological and behavioral symptoms). It was killed by the powerful drug and chemical lobbies, letting loose the hounds of disease and death on an unsuspecting public. Since the Conference of the American College of Physicians, we hope to have the help of some world leaders. Again, please help us too. There are a lot of people out there who must be warned, *please* let them know this information. :cool: TJ :cool:

CATEGORY: drugs/vitamins TECHNICAL: * SUMMARY: This document is provided for those of you on the list doing "Atkin's like" diets. It is a table of the vitamin supplements recommended for his plan. Some of his suggested dosages are quite good. In fact, I recommend similar dosages for C, A, E, Calcium, Magnesium, Zinc, Iodine, and the complete B group. I'm not as familiar with some of the other substances like PABA, Choline, etc. I would advise against any iron supplementation though. ------------------------------------------------------------- I've been using Atkins for awhile. My books are probably a little old, but I follow the guidelines in Dr. Atkins "Super Energy Diet" and he lists this as a basic formula: Vitamin A 10,000 I.U. Vitamin D 400 I.U. Vitamin B-1 (Thiamine) 10 mg. Vitamin B-2 (Riboflavin) 75 mg. Vitamin C 1,500 mg. Niacin 50 mg. Niacinamide 100 mg. Calcium 600 mg. Vitamin B-6 200 mg. PABA 1,200 mg. Calcium Pantothenate 150 mg. Folic Acid 3.6 mg. Vitamin B-12 750 mcg. Vitamin E 200 I.U. Magnesium 300 mg. Manganese 6 mg. Zinc 45 mg. Choline 750 mg. Inositol 450 mg. Biotin 300 mcg. Rutin 45 mg. Bioflavenoids 300 mg. Iron (as ferrous fumarate) 18 mg. Iodine (as kelp) 225 mcg. What I do is take the ingredients of my multi-vitamin and subtract it from Atkins formula to see what else I need. With a high potency multi vitamin you probably only need to take Vit. C, folic acid, calcium, and a B-Complex. This works good for me. :cool: TJ :cool:

My Etrex Vista seems REALLY accurate.. :cool: TJ :cool:

Seems like the primary effect is octane enhancement.. As a result, I don't see how it would be that much more effective.. :cool: TJ :cool:

Yes, it's a charcoal product.. A "charcoal fuel broquet" TJ I think it's something sold by Kingsford

CATEGORY: foods/healthy TECHNICAL: ** SUMMARY: This document provides an in-depth discussion of stevia rebaudiana. As many of you know, I try to use stevia as a sweetener exclusively. As this note shows, it is completely natural, and has been put through a variety of saftey tests. In fact, as you read, you will see that the substance has actually demonstrated medicinal value. Even having benefical affects in regard to diabetes, the cardio-vascular system, and the digestive tract. I encourage all of you (who are interested) to choose it over aspartame, saccharine, and common table sugar. After all, 1500 years of safe use is a pretty hard track record to beat. ------------------------------------------------------------- Life With Stevia: How Sweet It Is! Nutritional and Medicinal Uses Daniel Mowrey, Ph.D. "Life with Stevia: How Sweet It Is!" was reprinted with permission of the publisher. Copyright 1992 by Daniel B. Mowry Life with Stevia: How Sweet It Is! is not intended as medical advice. Its intention is solely educational. Please consult a medical or health professsional for medical advice. When one first observes the plant, nothing particular about it summons the attention, but when even a small piece of the leaf is placed in the mouth, one is amazed by its sweetness. A mere fragment of leaf is enough to sweeten the mouth for an hour. 1 Those few simple words, issued in 1899, opened one of the more remarkable chapters in the history of botanical science, and introduced the world at large to a unique and potentially revolutionary plant from Paraguay known as stevia, or "honey leaf." In South America it is primarily known as yerba dulce, but among the Guarani Indians of Paraguay, who have used the plant for centuries, it has a variety of interesting names: Caa-ehe, Azuca-caa, Kaa-he-e and Ca-a-yupe; most of these names, in one way or another, draw attention to the sweet, nectar-like flavor of the leaf. Many Guarani medicinal and nutritional plactices incorporate stevia in one way or another. The remarkable Guarni possess one of the most advanced native cultures, in terms of philosophy, nutrition and medicine, of any similar group in the world. Yet their ways are still only vaguely understood by other people. A case in point is their use of stevia. Despite centuries of use by the Indians, it wasn't until 1899 that the plant was discovered by "civilized" man. M.S. Bertoni (quoted above) observed that the natives used the plant to sweeten their bitter drinks. Eventually, Bertoni was to be credited with the discovery of a new species; in his honor, stevia is now known as Stevia rebaudiana Bertoni.2-3 It is amazing to contemplate that most of the important herbs and spices of the world have been known, described, catalogued and used by diverse populations for several centuries; yet here is one of the most wonderful plants of world that went undeteected until the turn of this century. Experts estimate that South America is the source of dozens, perhaps hundreds, of plants with properties as momentous as stevia that yet remain unused and unrecognized by anyone but the native populations. The Guarani are in possession of a good portion of these, some of which are becoming ever more important: yerba mate and lapacho. Others, like stevia, are less known. Stevia as a Flavor Enhancer There are three distinct traditions of stevia use. The first is for flavor enhancement; the second is as an herbal tea. The third is medicinal. The primary impetus for the development of stevia science was the discovery by Bertoni that the herb possessed an extraordinary sweetness. A good quality leaf is estimated to be 30 times sweeter than cane sugar, or sucrose. The active constituents of stevia are considered by the world's leading food scientists as the "sweeteners of the future." Therefore, every new development in the area of stevia research is anxiously awaited and thoroughly analyzed when it appears. Countries in which the currently used artificial sweetners are on the brink of being banned are desperately trying to find new, safe, non-caloric sweeteners. And in other countries, firms that hold exclusive rights to currently used sweeteners are extremely fearful of the advent of new, safer sweeteners, over which they will have no control. For these firms, the emergence of a totally natural, non-patentable sweetener is the ultimate horror. Stevia, whether these firms like it or not, will one day have a dramatic impact on all countries of the world. The necessary forces simply need to be properly aligned, the raging fury of mega-monstrous companies firmly bridled by caring governments, and the supply of stevia raised to meet the enormous demand. Steviosides and rebaudiosides are the principal constituents of diterpene glucosides with differing sugar molecules attached, as found in the leaves of the stevia plant. Extracted, they are currently being used as sweetening agents in several countries, including Japan, China, Korea, Taiwan, Israel, Uraguay, Brazil, and Paraguay. In Japan, commercialization of stevia was very rapid, beginning with the ban of artificial sweeteners during the 1960's. In 1970 the Japanese National Institute of Health began importing stevia for investigation, and by 1980 it was being used in hundreds of food products throughout the country.4 This is remarkable progress, considering that as recently as 1921 scientists were just getting around to naming the main constituent (stevioside), and the molecule wasn't even accurately described until 1931, when scientists reported it to be a white, crystalline, hygroscopic powder, approximately 300 times sweeter than cane sugar.5 And it wasn't until 1955 that the earlier work was replicated and extended.6 By 1963, the complete chemical structures of the active molecules of stevia were finally worked out.7 To jump from there to the status of a major food sweetener by the mid-1970's was a truly astounding feat, one that would have simply been impossible in the United States or Europe. Today, the Japanese, who cultivate stevia extensively in their own country, are anxious that other countries adopt the use of the plant so that they might export it. The ironic thing is that the Japanese are not as encumbered with weight problems as the rest of us; they are not, therefore, adverse to using copious amounts of plain old sugar. Yet they have access, in the form of stevia, to one of the best sugar substitutes. While most of the attention focuses on the steviosides, research has shown that the rebaudiosides are actually much better tasting; there are just fewer of them. One rebaudioside in particular, Rebaudioside A, appears to be far superior. Its sweetening power is estimated to be 30% higher than that of stevioside. Efforts to genetically select for this constituent are underway in Japan. However, according to some sources, the plantations maintained by the Guarani in Paraguay contain perhaps the best tasting natural whole-leaf stevia available. Efforts to remove stevia from its native habitat and cultivate it in foreign soils may be primarily responsible for the off taste that characterizes non-Paraguayan stevia. The best stevia may indeed still be obtainable only from parts of Paraguay under native cultivation. Interestingly, a recent report showed that none of the stevia used in Japan is imported from Paraguay. Of the 1000 tons used in Japan in 1982, 300 were produced in Japan, 450 came from Continental China, 150 from Taiwan, 100 from Thailand and 50 from Korea, Brazil and Malaysia. It is said that the Paraguayans will not sell to Japan. Much, if not most, of the stevia sold in the U.S. is imported from China and other non-Paraguayan sources. "The sweetness of (stevia) satisfies my craving for sweets; also it helps keep the blood sugar balance." "When I'm drinking 2 or 3 cups of stevia tea a day, I don't experience my usual mood swings." Along these same lines, it may be that the use of whole leaf is an easier way to obtain better taste than through efforts aimed at trying to improve the taste of certain specific constituents. It is surprising, therefore, to see how much research has gone into attempting to improve the taste of individual steviosides or rebaudiosides. Since the white crystaline powder exhibits a quite persistent bitter and astringent aftertaste, cites use as a commercial sweetener often backfires. Thus, most manufacturers who use the isolated constituents of stevia usually have to combine it with other kinds of typical sugars! Since rebaudiosides taste better, methods are constantly being sought to synthetically convert steviosides to rebaudiosides. But even the rabaudiosides must be combined with other kinds of sugars to obtain necessary sweetness. Finally , in the ultimate irony, there are processes currently under development for improving the taste of stevioside by combining it in various ways with other substances obtained directly from stevia!8-9 It is the opinion of this author that most, if not all, of these convoluted attempts to improve the taste of single constituents could be satisfactorily avoided simply by using WHOLE LEAF, or whole leaf EXTRACT, the way nature intended stevia to be used. In the final analysis, pure stevioside is attractive to manufacturers mainly because of the higher profits to be achieved from using a purified, therefore patentable, material. In this country, where use of whole leaf is the only possible mode of administration, consumers have developed some rather sophisticated applications, especially in the medicinal area (see next section). In the area of combining with other foods, one can also find some useful aplications. Stevia is appropriate for use in conjunction with a variety of other herbal teas. One can mimic the South American practice of combining stevia with yerba mate, lapacho, and other native herbs, or one can experiment with stevia in altering the taste parameters of any number of traditional teas. "We are intrigued by the honeyleaf sweetener . . . and started to use it in our breadmaking to test it for our diabetic customers. We were so pleased with the results and the improvement in the texture and softness, that we have continued to use it on a regular basis in our bread and so have all of our customers, diabetic or not." Stevia is available in bulk, in tea bags, or as a liquid extract. Combine one tea bag of stevia with other herbal tea bags. Try straight stevia tea. Search for commercial products that contain stevia. You may find that some of these are too sweet for your taste. Others may be just right. If you purchase stevia in bulk, individual leaves and pieces of leaf can be added to beverages, sprinkled over salads or cooking vegetables and substituted for sugar in recipes without creating a problem due to the presence of the leaf itself. A little bit goes a long way. While there is no question that stevia is sweet, many users will admit that they have also experienced a bitter aftertaste from some brands. In fact, one of the problems with stevia products currently available from health food retailers is that many of them just plain do not taste good. They often have a distinct grassy taste, with varying degrees of bitterness associated with the sweet. These differences in quality may partly be a result of using non-Paraguayan stevia, partly due to poor extraction and processing techniques and partly the result of ignorance on the part of manufactureres concerning the real nature of the stevia plant. One knowledgeable producer of stevia products is attempting to set up industry standards for grading stevia leaves according to their quality. Grade A stevia would be the highest quality, an extremely sweet grade, with little bitter aftertaste and a concentrated degree of sweetness. This grade is very difficult to obtain due to climatic conditions that prevent harvesting at just the right time. Grade B would be a little less sweet with some minor deterioration of the leaf. Most of the best stevia arriving in the United States from Paraguay is Grade B. The vast majority of stevia sold in the United States would be classified as Grade C, a poor grade with a good deal of grassy, bitter flavor. Extracts of Grade C are particularly unpalatable, possessing far too much bitterness. Manufacturers often try to dress them up with other flavoring agents, but such attempts seldom work. Once you have tasted a premium stevia, you will never be satisfied by lesser products. The bitter principles are actually found in the veins of the leaf, while the leafy material between the veins contains the sweet components. Great care must be taken during production of stevia extract to avoid contaminating the sweet with the bitter. This pertains as much to extraction as it does to milling. Due to FDA regulations, pure stevioside or rebaudioside is not allowed in the United States. Even the leaf is suspect if it is labeled as a sweetener. Producers must exercise great caution in their labeling practices to avoid FDA involvement. Stevia and stevia extract are considered foods. Sweeteners are not foods, but food additives. Therefore, stevia cannot be called a sweetener. This, of course, restricts a manufacturer's ability to "get the word out" on stevia's use as a sweetening agent for teas or whatever. In practice, as long as the stevia industry poses no significant threat to the U.S. sugar or sugar substitute industries, the FDA will probably not be pressured to concern itself with what goes on with stevia labelling or use. Any perceived threat at all, however, could tip the scales the opposite way, and all forms of stevia could be banned. To keep things low-key, remember that the sweetening effect is simply a pleasant by-product. The primary reason that stevia is combined with the other herbs is to enhance the nutritive value of the other herbs! Stevia is, after all, nutrient-rich, containing substantial amounts of protein, calcium, phosphorous and other important nutrients.10-11 Medicinal Uses Carrying the above thought a step further, there are many very ligitimate reasons for using stevia as a medicinal food. In spite of the prominence stevia has obtained as a flavor enhancer, it contains a variety of constituents besides the steviosides and rebaudiosides, including the nutrients specified above and a good deal of sterols, triterpenes, flavonoids, tannins, and an extremely rich volatile oil comprising rich proportions of aromatics, aldehyde, monoterpenes and sesquiterpenes.12 These and other, as yet unidentified constituents, probably have some impact on human physiology and may help explain some of the reported therapeutic uses of stevia. Hypoglycemic action. It is probably the presence of the steviosides themselves that has produced dozens of empirical and semi-controlled reports of hypoglycemic action. Paraguayans say that stevia is helpful for hypoglycemia and diabetes because it nourishes the pancreas and thereby helps to restore normal pancreatic function13 In semi-controlled clinical reports one also encounters this action. Oviedo, et. al., reported a 35.2% fall in normal blood sugar levels 6-8 hours following the ingestion of a stevia leaf extract.14 Similar trends have been reported in humans and experimental animals by other workers.15-16 These kind of results have led physicians in Paraguay to prescribe stevia leaf tea in the treatment of diabetes;13 similarly, in Brazil, stevia tea and stevia capsules are officiallly approved for sale for the treatment of diabetes.12 However, it is important to note that stevia does not lower blood glucose levels in normal subjects. In one study, rats were fed crude extracts of stevia leaves for 56 days at a rate of 0.5 to 1.0 gram extract per day. These procedures were replicated by another team of scientists.17-18 Neither group observed a hypoglycemic action. Similar negative results have been obtained by other observers.19 Then there is research in which the findings show trends toward hypoglycemic action, but are inconclusive.20-21 In at least one of these studies, alloxan-diabetic rabbits were used. The authors felt the results supported an anti-diabetic action, but the results were transient at best. To date, the experimental research on the effects of stevia on blood sugar levels in human patients with either diabetes or hypoglycemia is sparse. The general feeling in the scientific community is that the mild acting nature of the plant and its total lack of toxic side effects argues against the need for extensive and expensive research programs. However, many of the anecdotes reporting a definite and significant blood sugar lowering action in diabetics, and a pronounced exhilarating effect in hypoglycemics, are sound enough to justify considerable experimental work in the area. Perhaps , when this missing piece to the puzzle is supplied, we will then have a better understanding of how stevia works - why, for example, many diabetic humans experience a profound lowering of blood sugar levels following the ingestion of several cups of stevia tea (24-32 oz.) during the course of a 24 hour period. Cardiovascular Action. A good deal of experimental work has been done on the effects of stevia and stevioside on cardiovascular functioning in man and animals. Some of this work was simply looking for possible toxicity, while some was investigating possible therapeutic astion. In neither case have significant properties been found. When any action at all is observed, it is almost always a slight lowering of arterial blood pressure at low and normal doses, changing to a slight rise in arterial pressure at very high doses.22 The most curious finding is a dose dependent action on heart beat, with a slight increase appearing at lower doses, changing to a mild decrease at higher doses. In neither instance is the result remarkable, and it is extremely doubtful that humans would experience any effect at normal doses.23 The long term use of stevia would probably have a cardiotonic action, that is, would produce a mild strengthening of the heart and vascular system. Antimicrobial Action The ability of stevia to inhibit the growth and reproduction of bacteria and other infectious organisms is important in at least two respects. First, it may help explain why users of stevia-enhanced products report a lower incidence of colds and flus, and second, it has fostered the invention of a number of mouthwash and tooth paste products. Research clearly shows that Streptococcus mutans, Pseudomonas aeruginos, Proteus vulgaris and other microbes do not thrive in the presence of the non-nutritive stevia constituents.24 This fact, combined with the naturally sweet flavor of the herb, makes it a suitable ingredient for mouth washes and for tooth pastes.25 The patent literature contains many applications for these kinds of stevia-based products. Stevia has even been shown to lower the incidence of dental caries. Digestive Tonic Action. In the literature of Brazil, stevia ranks high among the list of plants used for centuries by the "gauchos" of the southern plains to flavor the bitter medicinal preparations used by that nomadic culture. For example, it was widely used in their "mate." Through much experimentation, these people learned that stevia made a significant contribution to improved digestion, and that it improved overall gastrointestinal function.26 Likewise, since its introduction in China, stevia tea, made from either hot or cold water, is used as a low calorie, sweet-tasting tea, as an appetite stimulant, as a digestive aid, as an aid to weight management, and even for staying young.46 Effects on the Skin. One of the properties of a liquid extract of stevia that has not yet been investigated experimentally is its apparent ability to help clear up skin problems. The Guarani and other people who have become familiar with stevia report that it is effective when applied to acne, seborrhea, dermatitis, eczema, etc. Placed directly in cuts and wounds, more rapid healing, without scarring, is observed. (This treatment may sting for a few seconds, but this is followed by a significant lowering of pain.) Smoother skin, softer to the touch is claimed to result from the frequent appllication of stevia poultices and extracts. Current FDA labelling regulations are forcing U.S. suppliers to label their stevia as something other than a sweetener; an appeal to its soothing action on the skin has been the most frequent alternative. Effects on Reproduction. An interesting pseudo-phenomenon arose at one time, and, sadly, still receives attention from time to time, in the popular press and even by serious scientists. It is sad because the whole thing is a hoax; if not that, it is at least a case of very badly mistaken identity. It seems that in 1968 a paper appeared that claimed that certain tribes of Indians in Paraguay (the Matto Grosso) used stevia tea as a contraceptive, with apparently very good results27 In subsequent experimental work, utilizing rats, these researchers found that the treatment was supposedly good for periods up to 2 months. Subsequent work has repeatedly failed to replicate the 1968 study.28-31 Furthermore, at least one attempt to locate tribes in northeastern Paraguay that used stevia to control fertility failed to confirm the story. One effect on reproductive physiology that appears to be valid, but which is in need of further study before definitive conclusions can be drawn, is a healing effect on the processes underlying prostate disease.32 Just how important this finding is must await further research. Safety Information One of the most obvious indications of the safety of stevia is that there have never been any reports of ill effects in over 1500 years of continuous use by Paraguayans. A similar indication of safety is the observaion that despite over ten years of widespread use of stevioside as a sweetening agent in Japan, years in which literally scores of tons of stevioside were ingested, not a single report of side effects of any kind has been reported. Compare that record to the track record of aspartame, which is the number one source of consumer food complaints made to the FDA. In spite of the record of safety, however the official laboratory tests must take place. The first official investigation of possible toxicity from stevia was performed in 1931 by Pomaret and coworkers in South America. Their tests were negative.33 They observed that stevioside passes through the human alimentary canal without being altered by digestive processes. That is, it goes out in exactly the same form that it goes in. In the decades since that observation there has raged a minor debate over this issue, but so far nobody has been able to prove Pomaret wrong. The issue is important because some of the metabolites of stevioside, as opposed to whole leaf, have been shown to be toxic (see below), and researchers have cautioned against the use of stevioside for human consumption until it is known for certain that stevioside is not metabolized in the human body. A typical statement is this from a report published in 1974:" . . . the long-term effects of ingestion of stevioside would have to be investigated carefully before it could be considered for human use as a sweetener in the United States . . . It remains to be proved that stevioside does not split to form any steviol in the human digestive tract." (italics theirs).34 This challenge is, of course, tantamount to proving a negative. Perhaps that is why the United States resists all efforts to seriously explore the possible use of stevia as a sweetener. No further progress on the issue has been made since 1974. It appears that Pomaret's observations still hold. More elaborate safety tests were performed by the Japanese during their evaluations of stevia as a possible sweetening agent. Few substances have ever yielded such consistently negative results in toxicity trials as has stevia. Almost every toxicity test imaginable has been performed on stevia extract or stevioside at one time or another The results are always negative. No abnormalities in weight change, food intake, cell or membrane characteristics, enzyme and substrate utilization, or chromosome characteristics. No cancer,no birth defects, no acute and no chronic untoward effects. Nothing.35-39 The only related effect ever observed was the inhibition cell respiration (oxidative phosphorylation) in certain isolated cell components, but never in whole cells. The only observable result of this action, even after prolonged observation, was a reduction in toxicity due to a substance known as atractylignin, a poison that attacks cells of the liver. This result suggests that stevia could be used as an antidote to rare cases of poisoning by that chemical. The overall result of this action of stevia, then, turns out to be positive.40 An example of a good toxicology trial was one performed in 1985 by Yamada and coworkers. They administered stevioside and rebaudioside A to rats for two years at the rate of 0.3 - 1% of their diet. The animals were then sacrificed, and the researchers conducted bio-chemical, anatomic, pathological and carcinogenic tests on 41 organs following autopsy. In addition they performed ongoing hematologic and urine tests on the same animals. Each of the animals was matched to a control animal that experienced exactly the same treatment except for the stevia. In the end, the symptoms and alterations noted by the research staff did not vary at all between the groups, and no dose-response effects were noted, even at the highest dose (1%), which is equivalent to 125 times the average daily dose of sweeteners that a normal human would require.41 Similar batteries of tests carried out by the National Ministry of Health and Welfare in Japan also failed to find any form of toxicity whatsoever.42 But there is a fly in the ointment, so to speak. As mentioned earlier, there has been a fear that metabolites of stevioside and rebaudioside A might be doing serious harm to the body. As one author put it: "In spite of the fact that acute oral administration of large doses of stevioside and/or Stevia rebaudiana extracts and long-term studies with feeding either of these materials to laboratory animals have shown them to be virtually devoid of toxic effects, one must consider the limited data available on metabolites (italics mine) of the major sweet principles of this plant."43 Now this comment was made in full knowledge of the fact that stevioside and the other glycosides of stevia are remarkable for their chemical stability; that is, due to their peculiar chemical or molecular shape, stevia glycosides are extremely resistant to acid and enzymatic degradation. They simply cannot be broken down into their metabolites under normal gastric conditions. Gastric acids and enzymes, as found in humans, are incapable of degrading these extremely stable molecules. This is in line with Pomaret's study that found that steviosides passed unchanged through the human gastrointestinal tract. Apparently the situation is different in the rat. In 1980 R.E. Wingard and associates reported that stevioside and rebaudioside A were both degraded to steviol by rat intestinal microflora in a test tube.44 Steviol is one of the nasty metabolites that could, maybe, perhaps, do humans serious harm. Wingard incubated the stevioside for 2-4 days in a specially prepared solution containing the contents of the rat cecum. Under these conditions, conversion was almost 100%. However, as Kinghorn and Soejarto have pointed out, there are just two things wrong with extrapolating these results to humans.45 First, humans do not have a cecum, as does the rat; therefore, a critical step in the conversion process has no equivalent physical location in which to occur. And second, there is no good reason to believe that the microflora of the human intestinal tract contains the same microorganisms as does the rat cecum. One would think, in light of the seriousness of the theoretical charge posed by Wingard, that scientists would be clamoring to settle the issue through appropriate experimental measures. Not so. It's as if no one really takes the threat seriously. After all, it is unlikely that some kind of observable consequence of steviol (the metabolite) intoxication would not have been reported during decades of stevia use if, in fact, a real problem existed. Since no reports have been forthcoming, we can daringly conclude (apparently along with the rest of the scientific community) that humans are different from rats. Conclusions from Safety Data. One might reasonably ask, based on these toxicological data, why efforts to make stevia the sugar substitute of choice in the United States and Europe have failed so miserably, and why, in fact, individuals who have attempted to produce high quality stevia liquid extracts in the United States have been threatened with prosecution. Here we have a plant, totally innocuous, posing no threat to human life and health, holding out in fact great hope for the production of a non-caloric sweetener with health benefits, that is being systematically suppressed. Perhaps, in view of the numerous health benefits discussed in this booklet (and the dozens of anecdotal uses not discussed, such as the ability to reduce the craving for sweets and fatty foods, and as a stop-smoking and/or stop drinking aide, the time has arrived for consumers to begin insisting on their right to freely use this fine, delectable plant from Paraguay. This author is certainly growing impatient with ongoing regulatory actions that appear to be deliberately designed to keep stevia out of his diet--a sad fate for a wonderful food like stevia. "The Symfre tea is the only natural decongestant that we have found that works. It's a good feeling to have a natural product that we can give to the whole family, including the baby, that clears congestion without drugs." From The Jungles To You Imagine that you live off the land in the lush tropical forests of South America, surrounded by an almost unimaginable array of trees, bushes, flowers, exposed to thousands of types of roots and berries and leaves. You are appointed medicine man (or woman) and your job is to keep yourself and the rest of the tribe healthy and to cure what ails them. What would you do? How would you go about devising techniques that work? Certainly you summon the help of whatever Gods and Spirits you believe in, and make the most out of whatever hype you could come up with. In that regard you would bear a close resemblance to the modern medical establishment. But then you would probably start looking for agents in nature that would serve your medicinal needs. Would you find anything? You bet you would. For the tropical forests of South America are the earth's richest storehouse of medicinal agents. You would probably jealously guard your secrets as you learned them, and eventually you might even try to make yourself into some kind of God. At some point you would select an heir to your knowledge, and over the centuries your knowledge would be enlarged upon by succeeding generations. "My son came home from college with the flu and had to go work that night. I got him on Symfre all day and he was fine (flu gone) by the time he went to work. Everyone else had it for 5 days." This hypothetical situation is a fairly accurate account of what could have happened to you, had you been a member of the Guarani Indian tribes of Paraguay. These people first came to the attention of Europeans sometime in the 1600's and were the subject of an intense missionary effort in the early 1700's. They were found to be a beautiful, ethical, highly skilled, very intelligent and gifted culture. Today, pure-blooded Guarani are declining in number, but much of their civilization has been preserved in one form or another. Thus it is that every once in a while, some one will be lucky enough to learn one or two of the secrets of the Guarani; even more rarely, such a lucky person will share it with the rest of us. As a result, we are just barely beginning to see some of the Guarani medical remedies reach the shores of North America. "I am having the best allergy season I ever had since I was seven years old back in 1938 !!! I've been in the hospital in oxygen tents more times than I can remember . . . I make 8 cups of Symfre and yerbamate mixed. And 5 cups of lapacho, I then mix 2 1/2 cups of lapacho with the yerbamate and Symfre and take a large bottle with me to work and sip it all day . . . . I have had no sign of any infection or bronchitis or asthma; and best of all I can get up in the morning and not sneeze 75 times before I get to work. I am thrilled!!!" One of the most promising of Guarani medicinal substances is, of course, stevia. It is known as "sweet leaf," or "honey leaf." This suggests the primary use of the plant in folklore use. Long before the country was colonized by the Spaniards in the sixteenth century, stevia was being employed to make food and drink palatable. Medicinally, the plant was used to treat diabetic and hypoglycemic conditions, and externally for keeping skin and hair youthful and healthy. Today, in homes and some clinics in rural Paraguay, stevia in high doses is given in tea form as a remedy for high blood sugar levels. The tonic, stomach-soothing, digestive, hypotensive and immune-stimulating actions of stevia are well known. It is interesting to see where stevia occurs in the traditional folk remedies of the native Guarani. Numerous are the folk medicines that contain stevia, either as a flavor enhancer or for its own medicinal properties. Most of these remedies are unknown beyond the edges of the fields and jungles. Natural Remedy for the Flu and Common Cold One example of a Guarani remedy (O'HO'MGUARA, meaning "It must go.") that has recently become available in the United States is a combination of stevia with a combination of two other plants: Piper dilatatum L. Rich, known colloquially as Yaguarundi, and Cecropia prachystachya Trecul, known as Amba-y. These latter two herbs have been re-designated in English as licorice pepper and Azteca, respectively. Very little is known about these plants beyond the edge of the villages. Yet it was one Peace Corps worker's good luck to be treated by this combination when he fell ill while working in Paraguay. Equally fortunate was the man's ability to persuade the Guarani indians to share the formula with him. But perhaps most important for those of us who use the comercial version of this compound, was the occasion upon which the Peace Corps worker shared his knowledge of O'HO'MGUARA with a friend in the United States. This herbal neophyte, at first highly skeptical of his friend's prepostrous claim that an obscure group of South American Indians had a cure for the common cold, was soon to become the world's leading advocate of this treatment. During subsequent trips to Paraguay, as he retells his experience, he personally witnessed the verification (in others and in himself!) of Indian claims that colds and flu could be cleared up in a day, and that sore throats could be cured in a matter of hours, as a result of the proper application of O'HO'MGUARA. Since that time, this American has shared the tea with thousands of others,, and has successfully brought the tea to the marketplace for all to enjoy. The difficult-to-pronounce Indian name was changed to the trade name Symfre, pronounced sym-free, as in sympton-free. Now, even some of the Paraguayan people refer to their native tea by that trade name. In Guarani lore, licorice pepper was used by itself for colds, flus, allergies, sore throat, coughs, and sinus congestion. Azteca was also used for the common cold, flu, coughs, allergies and sinus and lung congestion. It is also considered to be especially helpful for bronchial and pulmonary problems. Used together, the effect was said to be several orders of magnitude more dramatic and effective. Stevia was used to flavor the product and add stomach-soothing and digestive properties. "Having tried several of the herbal teas, to wit: lapacho, yerbamate and Symfre, I am very impressed! One of the most noticeable results has been . . . weight loss. Another has been fewer and less severe headaches. Also, some improvement regarding asthma, food allergies, and digestion . . . Generally, I've been feeling ever so much better, with vim and vigor. These herbal beverages. . . have been the best thing to come my way in years!" Another popular use for stevia in South America is to improve the taste of yerbamate. Many North Americans go to South America and become intrigued by mate only to be put off by the taste. Often they will resort to using large amounts of sugar in the tea to mask the flavor. Little do they realize that the ideal solution to the problem could be obtained simply by observing native practices. The addition of stevia to yerbamate markedly improves the taste for most of us. There are some people who seem to enjoy the natural flavor of mate, and feel the addition of sweetening agents of any kind makes the beverage too sweet. The majority of people, however, like it sweet. Stevia is the perfect answer to the question of how one sweetens the tea without adding calories and/or questionably safe artificial sweeteners. "Since I've been drinking this herbal tea (stevia and yerbamate), I have found energy I didn't know I had . . . I was sluggish, had headaches daily and basically was rundown . . . The tea has relieved all my problems, and most of all, I feel better knowing that it is completely natural, no harsh drugs or stimulants. I really enjoy the sweet taste with the benefit of no calories." These are just a couple of examples of the medicinal treasures hidden away in the lore of Paraguay and other South American countries. "I had a series of colds and sore throats. Very unusual for me. I ordered the yerba mate and Symfre and began drinking the tea. It broke up the infections, and I shared it several times with others, who also were relieved from cold symptoms." Slowly, these marvels are being uncovered and brought to the attention of the world. Let us hope that the day will soon come when simple, time-honored, health traditions with extraordinary potential for improving the lot of mankind, can be freely and openly offered to the world without interference from self-serving individuals, agencies, organizations and corporations which profit from the suppression of such fabulous, compelling and ultimately superior natural remedies. How to Use SYMFRE A. For symptomatic relief of colds, flu, coughs, allergies, sinus congestion: Drink 8 cups (2 quarts) of tea in the course of one day, about 1 cup every 2-3 hours. Use 1 tablespoon per 8 oz. of water. B. For relief of sore throat: Follow above directions but expect reslts in 4-5 hours. C. For maintenance purposes: Drink tea made from 1 teaspoon per 8 oz. water, as desired. NOTE 1: For an even more dramatic and health promoting action, combine equal amounts of Symfre and yerbamate in 12-14 oz. hot water. Consume this every 3 hours throughout the day, with 1 or 2 cups the next morning. NOTE 2: Follow the native practice of combining Symfre with both yerbamate and lapacho. This is especially suggested in case of a deficiency in immune system functioning. "I have been using (a combination of yerbamate and stevia) for about two years. For 25 years, 365 days of each year, I had a sinus problem! Since I started using (the tea), the only time I have a problem is when I don't drink 3-4 eight ounce cups of tea each day. I am also a diabetic and I use about 10 drops of the (stevia extract) in each cup of tea. As long as I eat properly and exercise, I get a negative reading on my test. Two years ago my doctor wanted to put me on insulin, but now I no longer have to take any medication for my condition." Note on the Text The material appearing in large italic print with quotation marks around it, throughout this pamphlet, was taken from actual letters in my files. Where necessary, the generic terms, such as 'lapacho' and 'yerbamate' were used in place of brand names. The brand name Symfre has passed into colloquial usage, even in Paraguay, and is therefore used here in place of the generic Paraguayan designation O'HO'MGUARA for convenience of pronounciation. References 1. Bertoni, M.S. "El Caa-ehe (Eupatorium rebaudianum, species nova)". Rev. Agr., Ascunion 1: 35-37, 1899. 2. Bertoni, M.S. "Le Kaa He-e. Sa nature et ses properietes." Ancient. Paraguayos, 1(5), 1-14, 1905. 3. Bertoni, M.S. "Caa-hee (stevia rebaudiana Bertoni)." Bol. Est. Agr. Puerto Bertoni Paraguay, V(2), 54, 1911. 4. Fujita, H. & Edahiro, T. "Safety and utilization of stevia sweetener." The Food Industry. 22(22), 1-8, 1979. 5. Bridel, M. & Lavielle, R. "Sur le principe sucre des feuilles de kaa-he-e (stevia rebaundiana ." Compt. Rend., Acad. Sci., Parts 192, 1123-1125, 1931. 6. Wood, Jr., H.B., et. al., "Stevioside. I. The structure of the glucose moieties." J. Org. Chem. Washington, 20, 875-883, 1955. 7. Mosettig, E., et.al., "The absolute configuration of steviol and isosteviol." J. Am. Chem. Soc., 85(15), 2305-2309, 1963. 8. Morita, T., MOrita, E. & Fujita, I. Jpn Kokai Tokkyo Koho, 77,57,366; Chem Abstr., 87, 132564t, 1977. 9. Morita, T., Fujita, M. & Morita, E. Jpn. Kokai Tokkyo Koho, 77,105,260; thru Chem Abstr. 88, 49255t, 1978. 10. Viana, A.M. & Metivier, J. "Changes in the levels of total soluble proteins and sugars during leaf ontogeny in stevia rebaudiana Bert." Annals of Botany, 45, 469-474, 1980. 11. "Hierbas Medicinales, Caa Jhee." Bulletin, Centro de Promocion de las Exportaciones, Ministerio de Industria Y Comercio, Paraguay. 12. Reviewed by Kinghorn, A.D. & Soejarto, D.D. "Current status of stevioside as a sweetening agent for human use." Economic and Medicinal Plant Research, Volume 1, Wagner, H., Hikino, H. and Farnsworth, N.R. (eds.) Academic Press, New York, 1985, pp. 1-51. 13. Soejarto, D.D., et.al., Econ. Bot., 37, 74, 1983. 14. Oviedo, C.A., et.al., "Accion hipoglicemiante de la stevia rebaudiana Bertoni (Kaa-he-e)." Excerpta Medica, 208, 92-93, 1971. (International Congress Series). 15. Alvares, M., et.al., Abstract Pap., Semin. Bras. Stevia Rebaudiana Bertoni 1st, 1981, p. XIII.I. 16. Suzuki, H., et.al., "Influence of oral administration of stevioside on levels of blood glucose and liver glycogen of intact rats." Nippon Nopei Kagaku Kaishi, Tokyo, 51(3), 171-173, 1977. 17. Akashi, H. & Yokoyama, Y. "Dried-leaf extracts of stevia. Toxicological test." Shokihin Kokyo, Tokyo, 18(20), 34-43, 1975. 18. Lee, C.K., et.al., Hanguk, Sikp'um Kwahakhoe Chi, 11, 224-6, 1979. 19. Usami, M., et.al., Horm. Metab. Res., 12,705, 1980. 20. Piheiro, C.E. & Gasparini, O.T. Abstr. Pap., Semin. Bras. Stevia rebaudiana, 1st, 1981, pp. XV.I-XV.IV. 21. Boeckh, E.M.A., "Stevia rebaudiana (Bert.) Bertoni: clinical evaluation of its acute action on cardio-circulatory, metabolic and electrolitic parameters in 60 healthy individuals." Third Brazilian Seminar on Stevia Rebaudiana (Bert.) Bertoni, (Summaries), Angelucci, E. (Coordinator), July, 1986, pp. 22-23. 22. Machado, E., Chagas, A.M. & Reis, D.S. "Stevia rebaudiana (Bert.) Bertoni in the arterial presure of the dog." Third Brazilian Seminar on Stevia Rebaudiana (Bert.) Bertoni, (Summaries), Angelucci, E. (Coordinator), July 1986, p. 11. 23. Boeckh, E.M.A. op.cit. 24. Yabu, M., et.al., "Studies on stevioside, natural, sweetener." Hiroshima Daigaku Shigaku Tasshi, 9(1), 12-17, 1977. 25. Berry, C.W. & Henry, C.A. J. Dental Res., 690,430,1981. 26. Alvarez, M. "Stevia rebaudiana (Bert.) Bertoni: Toxicological aspects." Third Brazilian Seminar on Stevia Rebaudiana (Bert.) Bertoni, (Summaries), Angelucci, E. (Coordinator), July 1986, p. 4-7. 27. Planas, G.M. & Kuc,J. "Contraceptive properties of stevia rebaudiana." Science, Washington, 162, 1007, 1968. 28. Farnsworth, N.R. "Current status of sugar substitutes." Am. Perfum. Cosmet., 88(7), 27-35. 1973. 29. Akashi and Yokoyama, 1975, op.cit. 30. Fujita and Edahiro, 1979, op.cit. 31. Silva, A.R., Saldanha, C.M., Boelter, R. & Chagas, A.M. "Fertility of rats: Aqueous extract of stevia rebaudiana (Bert.) Bertoni and stevioside, " Third Brazilian Seminar on Stevia Rebaudiana (Bert.) Bertoni, (Summaries), Angelucci, E. (Coordinator), July 1986, p. 19. 32. Oliveira-Filho, R.M. Valle, L.B.S. Minetti, C.A.S.A. & Uchara, O.A. "Evaluation of the effects of raw stevia rebaudiana extract in the endocrinous sphere; study on rats." Third Brazilian Seminar on Stevia Rebaudiana (Bert.) Bertoni, (Summaries), Angelucci, E. (Coordinator), July 1986, p. 20. 33. Pomaret, M. Lavieille, R. "Le principe & saveur sucree du Kaa-he-e (stevia rebaundiana bertoni), IV. Quelques proprietes physiologiques du stevioside." Bull, Soc. Chim, Biol., 13, 1248-1252, 1931. 34. Hodge, J.e. & Inglett, G.E. "Structural aspects of glycosidic sweeteners containing (1'2)-linked disaccharides." In Inglett, G.E. (ed.) Symposium Sweeteners. The Avi Publishing Company, Inc. Conn., 1974, pp. 216-234. 35. Mitsuhashi, H., et.al., Yakugaku Zasshi, 95, 127; and 95, 1501. 36. Akashi, H. & Yokoyama, Y. "Dried leaf extracts of stevia. Toxicological test." Shokuhin Kogyo, 18(20), 34-43, 1975. 37. Fujita, H. & Edahiro, T. Shokuhin Kogyo, 22(20), 66, 1979, 22 (22), 65, 1979. 39. Medon, P.J., et.al., Fed. Proc., Fed. Am. Soc. Exp. Biol., 41, 1568, 1982. 40. Ishit,p. 9. E.I. & Bracht, A. "Stevioside inhibits the toxic action of actractiloside on the liver,," Third Brazilian Seminar on Stevia Rebaudiana (Bert.) Bertoni, (Summaries), Angelucci, E. (Coordinator), July 1986, 41. Yamada, et.al., Shokuhin Eisegaku Zasshi, 26(2), 169-183, 1985. 42. Food Chemistry Division, Environmental Health Bureau, Ministry of Health and Welfare. "Toxicological effect of a sugar alternative, stevia products." January 1981. 43. Kinghorn & Soejarto, 1985, op.cit. 45. Wingard, R.E. (reviewed in Kinghorn (Sejarto, 1985) 46. Kinghorn,, D.a. & Soejarto, D.D. "Stevioside," in Economic and Medical Plant Research, Vol. 7, Academic Press, 1991, pp. 157-171. ABOUT THE AUTHOR Dr. Mowry is known primarily for his efforts to bring scientific data about herbal medicine to the attention of the American public. Toward this end he has published the books entitled the Scientific Validation of Herbal Medicine, and Guaranteed Potency Herbs: Next Generation Herbal Medicine, which have become standard texts in the field. Dr. Mowry is Director of the Mountainwest Institute of Herbal Sciences, in Salt Lake City, Utah. :cool: TJ :cool: