SCRIPT OF THE SHOW JULY 27 2013
Fighting Cancer with Fats
Ketogenic diet effective against metastatic cancer
Long-term effects of a ketogenic diet in obese patients
Morgellons-Biowarefare-with Nano Technolgy
The Global Threat of Persistent Organic Pollutants
Fighting Cancer with Fats
Barrow researcher explores innovative cancer treatment
For Barrow Researcher Adrienne C. Scheck, PhD, diets are far more than a health fad: Dr. Scheck is researching the potential of a therapy known as the ketogenic diet to complement traditional treatments for brain cancer such as radiation and chemotherapy.—Since the 1920s, the ketogenic diet has been used to control epilepsy, but its popularity has waxed and waned. It is now used almost exclusively in children whose seizures do not respond to conventional drug therapies. The highly regimented diet calls for nearly 80 percent of a patient’s calorie intake to come from fat and less than 1 percent from carbohydrates, with the remainder coming from protein.—-Researchers were spurred to investigate the ketogenic diet as a cancer therapy because cancer cells rely primarily on glucose to fuel their metabolism. The diet causes the body to enter a state called ketosis, where fat-derived chemicals called ketones are burned in response to the absence of carbohydrates. It has been theorized that because tumor cells cannot use ketones for energy, this metabolic change would starve tumor tissue, stunting its growth and improving survival rates for cancer patients.–While not ruling out the metabolic explanation, Dr. Scheck’s research has uncovered other ways that the diet acts on tumors.–Dr. Scheck and her team in the Barrow Neuro-Oncology Research Laboratory observed that live tumor models subjected to the ketogenic diet had fewer reactive oxygen species present in and around the cancerous tissue.–“Reactive oxygen species are created during normal cellular metabolism and are important in the control of many aspects of cell growth—too many or too few are bad for the cell,” says Dr. Scheck. “The metabolism of tumors is higher than that of normal tissue—a feature that may allow them to adapt to increases in reactive oxygen species and contribute to their resistance against chemotherapy.”—Dr. Scheck hypothesizes that by helping to reduce the number of reactive oxygen species tumor cells are accustomed to, the diet may enhance the effectiveness of chemotherapy.[F1] —The results of Dr. Scheck’s latest study also suggest that the diet affects gene expression in tumor cells. “We are seeing that the genetic profile of the tumor cells exposed to ketone bodies is shoved more toward the gene expression of normal cells,” says Dr. Scheck.—How the above mechanisms work together to slow cancer growth is not yet clearly defined, but the results of their combined action are reason to take notice. Dr. Scheck’s team reports that a ketogenic diet, combined with traditional therapies such as radiation and chemotherapy, has the potential to slow the growth of living cancer cells and significantly increase survival time.[F2] —Nonetheless, the ketogenic diet has its drawbacks. Dr. Scheck cautions that this treatment is very different from diets that people manage on their own. Rather, she says, it is a therapy that requires total compliance
Ketogenic diet effective against metastatic cancer
A research team from the Hyperbaric Biomedical Research Laboratory at the University of South Florida has finally found what the nutritional healing community has been crying hoarse about – that a ketogenic diet kills cancer cells. The study, “The Ketogenic Diet and Hyperbaric Oxygen Therapy Prolong Survival in Mice with Systemic Metastatic Cancer,” was published online on June 5, 2013 in PLOS ONE.—-In the study, mice with advanced metastatic cancer were fed either a standard high carbohydrate diet or carbohydrate-restricted ketogenic diet. Mice on both diets also received hyperbaric oxygen therapy, which uses a special chamber to increase the amount of oxygen in the tissues.—The ketogenic diet forces a physiological shift in substrate utilization from glucose to fatty acids and ketone bodies for energy. Normal healthy cells readily adapt to using ketone bodies for fuel, but cancer cells lack this metabolic flexibility, and thus become selectively vulnerable to reduced glucose availability. Solid tumors also have areas of low oxygen, which promotes tumor growth and metastatic spread. –Hyperbaric oxygen therapy involves breathing 100 percent oxygen at elevated barometric pressure, saturating the tumors with oxygen. When administered properly, both the ketogenic diet and hyperbaric oxygen therapy are non-toxic and even protect healthy tissues while simultaneously damaging cancer cells.–The research shows the effects of combining two nontoxic adjuvant cancer therapies, the ketogenic diet and hyperbaric oxygen therapy, in a mouse model of late-stage, metastatic cancer. While both therapies slowed disease progression independently, animals receiving the combined ketogenic diet and hyperbaric oxygen therapy lived 78 percent longer than mice fed a standard high-carbohydrate diet.—Metastasis, the spreading of cancer from the primary tumor to distant spots, is responsible for over 90 percent of cancer-related deaths in humans. A lack of available therapies effective against metastatic disease remains the largest obstacle in finding a cure for cancer.
How you can incorporate this into your lifestyle to not let cancer cells grow:
Restrict carbohydrates and replace them with healthy fats available in fish oil, nuts, seeds, extra virgin olive oil (raw) and healthy protein upasteurized milk, yogurt with fat ,kefir with fat,nuts, eggs, fish ghee-coconut oils-mct oils-tallow-lard. Concentrate on low glycemic index, high fibre carbohydrates in small quantities like apples-peaches-plums –pears-apricots.
When eating fruit, combine with spices-such as cinnamon-clove-cardamon-tumeric-galangal-ginger, as examples to avoid fructose related sugar spikes in the blood. The vitamins and minerals in fruits are anti-cancer hence fruits and fruit fibre are very important. Go for low GL foods like apple, papaya and fruits like pineapples with anti-inflammatory qualities. Consume raw, consume juices made from fresh veges home made and unpasteurized-if you use fruit juices then add the minerals zinc or chromium or manganese-or magnesium to them—or a full spectrum of minerals
To adapt hyperbaric oxygen therapy for prevention and to oxygenate your organs, practice deep breatheing techniques every day for 20-30 min. This will flush out the toxins from the blood and re-energise you while increasing oxygen in the blood flow, hence killing tumour cells in your body.
Remember, a strong immune system will fight cancer and tumour cells, and a ketogenic diet combined with oxygenating your body goes a long way in building immunity.
Long-term effects of a ketogenic diet in obese patients
Hussein M Dashti, MD PhD FICS FACS,1 Thazhumpal C Mathew, MSc PhD FRCPath,4 Talib Hussein, MB ChB,5 Sami K Asfar, MB ChB MD FRCSEd FACS,1 Abdulla Behbahani, MB ChB FRCS FACSI PhD FICS FACS,1 Mousa A Khoursheed, MB ChB FRCS FICS,1 Hilal M Al-Sayer, MD PhD FICS FACS,1 Yousef Y Bo-Abbas, MD FRCPC,2 and Naji S Al-Zaid, BSc PhD3
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Although various studies have examined the short-term effects of a ketogenic diet in reducing weight in obese patients, its long-term effects on various physical and biochemical parameters are not known.
To determine the effects of a 24-week ketogenic diet (consisting of 30 g carbohydrate, 1 g/kg body weight protein, 20% saturated fat, and 80% polyunsaturated and monounsaturated fat) in obese patients.
PATIENTS AND METHODS:
In the present study, 83 obese patients (39 men and 44 women) with a body mass index greater than 35 kg/m2, and high glucose and cholesterol levels were selected. The body weight, body mass index, total cholesterol, low density lipoprotein (LDL) cholesterol, high density lipoprotein (HDL) cholesterol, triglycerides, fasting blood sugar, urea and creatinine levels were determined before and after the administration of the ketogenic diet. Changes in these parameters were monitored after eight, 16 and 24 weeks of treatment.
The weight and body mass index of the patients decreased significantly (P<0.0001). The level of total cholesterol decreased from week 1 to week 24. HDL cholesterol levels significantly increased, whereas LDL cholesterol levels significantly decreased after treatment. The level of triglycerides decreased significantly following 24 weeks of treatment. The level of blood glucose significantly decreased. The changes in the level of urea and creatinine were not statistically significant. CONCLUSIONS:--The present study shows the beneficial effects of a long-term ketogenic diet. It significantly reduced the body weight and body mass index of the patients. Furthermore, it decreased the level of triglycerides, LDL cholesterol and blood glucose, and increased the level of HDL cholesterol. Administering a ketogenic diet for a relatively longer period of time did not produce any significant side effects in the patients. Therefore, the present study confirms that it is safe to use a ketogenic diet for a longer period of time than previously demonstrated. Keywords: Diet, Ketosis, Obesity Obesity has become a serious chronic disease in both developing and developed countries. Furthermore, it is associated with a variety of chronic diseases ( The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version. Therefore, the purpose of the present study was to investigate the long-term effects of a ketogenic diet on obesity and obesity-associated risk factors in a large population of obese patients. Go to: PATIENTS AND METHODS Patients and biochemical analysis The prospective study was carried out at the Academic Department of Surgery, Consultation and Training Centre, Faculty of Medicine, Kuwait University (Jabriya, Kuwait) in 83 obese subjects (39 men and 44 women). The body mass index (BMI) of men and women was 35.9±1.2 kg/m2 and 39.4±1.0 kg/m2, respectively. The mean age was 42.6±1.7 years and 40.6±1.6 years for men and women, respectively. The mean age, initial height, weight and BMI for all patients are given in Table 1. Fasting blood tests were carried out for all of the subjects. Initially, all patients were subjected to liver and renal function tests, and glucose and lipid profiles, using fasting blood samples, and a complete blood count. Thereafter, fasting blood samples were tested for total cholesterol, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, triglycerides, blood sugar, urea and creatinine levels at the eighth, 16th and 24th week. In addition, weight and height measurements, and blood pressure were monitored at each visit. TABLE 1 Patient data at baseline before treatment with the ketogenic diet Protocol for ketogenic diet-induced body weight reduction All 83 subjects received the ketogenic diet consisting of 20 g to 30 g of carbohydrate in the form of green vegetables and salad, and 80 g to 100 g of protein in the form of meat, fish, fowl, eggs, shellfish and cheese. Polyunsaturated and monounsaturated fats were also included in the diet. Twelve weeks later, an additional 20 g of carbohydrate were added to the meal of the patients to total 40 g to 50 g of carbohydrate. Micronutrients (vitamins and minerals) were given to each subject in the form of one capsule per day (Table 2). TABLE 2 Composition of the capsule* Statistical analysis ---Statistical differences between body weight, total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides, level of fasting blood sugar, and urea and creatinine levels before and after the administration of the ketogenic diet were analyzed using a paired Student’s t test using the Stat-view version 4.02 (Abacus Concepts Inc, USA). Weight, BMI and all biochemical parameters are expressed as mean ± SEM. Go to: RESULTS The mean initial weight of the subjects was 101.03±2.33 kg. The weight decreased significantly during all stages of the treatment period. The body weights at the eighth, 16th and 24th week were 91.10±2.76 kg, 89.39±3.4 kg and 86.67±3.70 kg, respectively (Figure 1). Similar to the loss in body weight, a significant decrease was observed in the BMI of the patients following the administration of the ketogenic diet. The initial BMI, and the BMI after the eighth, 16th and 24th week were 37.77±0.79 kg/m2, 33.90±0.83 kg/m2, 33.24±1.00 kg/m2 and 32.06±1.13 kg/m2, respectively The level of total cholesterol showed a significant decrease from week 1 to week 24 (Figure 3). The level of HDL cholesterol significantly increased (Figure 4), whereas LDL cholesterol levels significantly decreased with treatment (Figure 5). The level of triglycerides decreased significantly after 24 weeks of treatment. The initial level of triglycerides was 2.75±0.23 mmol/L, whereas at week 24, the level decreased to 1.09±0.08 mmol/L (Figure 6). The level of blood glucose significantly decreased at week 24. The initial blood glucose level and its level at the eighth, 16th and 24th week were 7.26±0.38 mmol/L, 5.86±0.27 mmol/L, 5.56±0.19 mmol/L and 5.62±0.18 mmol/L, respectively (Figure 7). The changes in the levels of urea (Figure 8) and creatinine (Figure 9) were not statistically significant. DISCUSSION Until recently, ketosis was viewed with apprehension in the medical world; however, current advances in nutritional research have discounted this apprehension and increased public awareness about its favourable effects. In humans, ketone bodies are the only additional source of brain energy after glucose ( The following popper user interface control may not be accessible. Tab to the next button to revert the control to an accessible version.- Thus, the use of ketone bodies by the brain could be a significant evolutionary development that occurred in parallel with brain development in humans. Hepatic generation of ketone bodies during fasting is essential to provide an alternate fuel to glucose. This is necessary to spare the destruction of muscle from glucose synthesis.---A ketogenic diet is clinically and experimentally effective in antiepileptic and antiobesity treatments; however, the molecular mechanisms of its action remain to be elucidated. In some cases, a ketogenic diet is far better than modern anticonvulsants Recently, it has been shown that a ketogenic diet is a safe potential alternative to other existing therapies for infantile spasms It was further shown that a ketogenic diet could act as a mood stabilizer in bipolar illness --Beneficial changes in the brain energy profile have been observed in subjects who are on a ketogenic diet ( This is a significant observation because cerebral hypometabolism is a characteristic feature of those who suffer from depression or mania It has also been found that a ketogenic diet affects signal transduction in neurons by inducing changes in the basal status of protein phosphorylation. In another study (it was shown that a ketogenic diet induced gene expression in the brain. These studies provide evidence to explain the actions of a ketogenic diet in the brain. --One of the mechanisms of a ketogenic diet in epilepsy may be related to increased availability of beta-hydroxybutyrate, a ketone body readily transported through the blood-brain barrier. In support of this hypothesis, it was found that a ketogenic diet was the treatment of choice for glucose transporter protein syndrome and pyruvate dehydrogenase deficiency, which are both associated with cerebral energy failure and seizures. One argument against the consumption of a high fat diet is that it causes obesity. The major concern in this regard is whether a high percentage of dietary fat promotes weight gain more than a low percentage of fat intake. Because fat has a higher caloric density than carbohydrate, it is thought that the consumption of a high fat diet will be accompanied by a higher energy -On the contrary, recent studies from our laboratory and many other laboratories of various chronic diseases of the body. A recent showed that sugar can accelerate aging. Several recent studies have pointed to the fact that a diet with a high glycemic load is independently associated with the development of cardiovascular diseases, type II diabetes and certain forms of cancer. Glycemic load refers to a diet of different foods that have a high glycemic index. Glycemic index is a measure of the elevation of glucose levels following the ingestion of a carbohydrate. The classification of a carbohydrate based on its glycemic index provided a better predictor of risk for coronary artery diseases than the traditional method of classification of carbohydrate into simple or complex forms In other studies it was shown that the risk of dietary glycemic load from refined carbohydrates was independent of other known risk factors for coronary diseases. It is now evident that high carbohydrate diets increase fasting plasma triglyceride concentrations and decrease HDL cholesterol concentrations These changes are associated with enhanced atherogenesis However, it has been shown that short-term ketogenic diets improve the lipid disorders that are characteristic of atherogenic It has also been found that sugary drinks decreased blood levels of vitamin E, thus reducing the amount of antioxidants in the body. It has been proven, beyond a doubt, that disrupting the oxidant-antioxidant status of the cell will lead to various diseases of the body - The relation between a high fat diet and cancer is not conclusive. Recent epidemiological studies could not explain a specific causal relationship between dietary fat and cancer. It has been found that altered energy metabolism and substrate requirements of tumour cells provide a target for selective antineoplastic therapy. The supply of substrates for tumour energy metabolism can be reduced by dietary manipulation (eg, ketogenic diet) or by pharmacological means at the cellular level (eg, inhibitors of glycolysis or oxidative phosphorylation). Both of these techniques are nontoxic methods for controlling tumour growth in vivo . Sugar consumption is positively associated with cancer in humans and test animals This observation is quite logical because tumours are known to be enormous sugar absorbers. It has also been found that the risk of breast cancer decreases with increases in total fat intake Further studies on the role of a ketogenic diet in antineoplastic therapy are in progress in our laboratory.- A link between low fat diets and osteoporosis has been suggested. Very low fat diets are considered to be low in calcium content. Women on low fat diets excrete most of the calcium they consume; therefore, they are more prone to osteoporosis. However, a high fat diet can rectify this situation In the present study, a control population on a low fat diet was not included due to the difficulties in recruiting subjects for a control group. However, several studies with appropriate control groups that compared the effect of a low fat diet with a low carbohydrate ketogenic diet have recently been published. In this regard, these two recent studies are comparable with the present study. Brehm et al showed that obese women on a low carbohydrate ketogenic diet lost 8.5 kg over six months compared with 4.2 kg lost by those in the low fat diet group (P<0.001). Twenty-two subjects from the low carbohydrate ketogenic diet and 20 subjects from the low fat diet completed the study, with both groups reducing their energy intake by approximately 450 kcal from the baseline level. In another study performed in 132 severely obese subjects for six months there was greater weight loss in the low carbohydrate ketogenic diet group than in the low fat diet group (5.8 kg versus 1.9 kg, P=0.002). Both of these studies support the findings presented in the present paper. CONCLUSIONS The data presented in the present study showed that a ketogenic diet acted as a natural therapy for weight reduction in obese patients. This is a unique study monitoring the effect of a ketogenic diet for 24 weeks. There was a significant decrease in the level of triglycerides, total cholesterol, LDL cholesterol and glucose, and a significant increase in the level of HDL cholesterol in the patients. The side effects of drugs commonly used for the reduction of body weight in such patients were not observed in patients who were on the ketogenic diet. Therefore, these results indicate that the administration of a ketogenic diet for a relatively long period of time is safe. Further studies elucidating the molecular mechanisms of a ketogenic diet are in progress in our laboratory. These studies will open new avenues into the potential therapeutic uses of a ketogenic diet and ketone bodies. REFERENCES 1. Bray GA. Medical consequences of obesity. J Clin Endocrinol Metab. 2004;89:2583–9. [PubMed] 2. Grundy SM, Barnett JP. Metabolic and health complications of obesity. Dis Mon. 1990;36:641–731. [PubMed] 3. Pi-Sunyer FX. Medical hazards of obesity. Ann Intern Med. 1993;119:655–60. [PubMed] 4. Simopoulos AP, Van Itallie TB. Body weight, health, and longevity. Ann Intern Med. 1984;100:285–95. [PubMed] 5. McGinnis JM, Foege WH. Actual causes of death in the United States. JAMA. 1993;270:2207–12. [PubMed] 6. Thomas PR, editor. Washington: National Academy Press; 1995. Weighing the Options: Criteria for Evaluating Weight-Management Programs. 7. Andersen T, Stokholm KH, Backer OG, Quaade F. Long-term (5-year) results after either horizontal gastroplasty or very-low-calorie diet for morbid obesity. Int J Obes. 1988;12:277–84. [PubMed] 8. Kramer FM, Jeffery RW, Forster JL, Snell MK. Long-term follow-up of behavioral treatment for obesity: Patterns of regain among men and women. Int J Obes. 1989;13:123–36. [PubMed] 9. Peni MG. Improving maintenance of weight loss following treatment by diet and lifestyle modification. In: Wadden TA, Van Itallie TB, editors. Treatment of the Seriously Obese Patient. New York: Guilford; 1992. pp. 456–77. 10. Sondike SB, Copperman N, Jacobson MS. Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factors in overweight adolescents. J Pediatr. 2003;142:253–8. [PubMed] 11. Yancy WS, Jr, Guyton JR, Bakst RP, Westman EC. A randomized, controlled trial of a low-carbohydrate ketogenic diet versus a low-fat diet for obesity and hyperlipidemia. Am J Clin Nutr. 2002;72:343S. 12. Dashti HM, Bo-Abbas YY, Asfar SK, et al. Ketogenic diet modifies the risk factors of heart disease in obese patients. Nutrition. 2003;19:901–2. [PubMed] 13. Wilder RM. The effect of ketonemia on the course of epilepsy. Mayo Clin Proc. 1921;2:307–8. 14. Pilkington TR, Rosenoer VM, Gainsborough H, Carey M. Diet and weight-reduction in the obese. Lancet. 1960;i:856–8. [PubMed] 15. Howard BV, Wylie-Rosett J. Sugar and cardiovascular disease: A statement for healthcare professionals from the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2002;106:523–7. Erratum in 2003;107:2166. [PubMed] 16. Franceschi S, Favero A, Decarli A, et al. Intake of macronutrients and risk of breast cancer. Lancet. 1996;347:1351–6. [PubMed] 17. Liu S, Manson JE, Stantpfer MJ, et al. Dietary glycemic load assessed by food-frequency questionnaire in relation to plasma high-density-lipoprotein cholesterol and fasting plasma triacylglycerols in postmenopausal women. Am J Clin. 2001;73:560–6. [PubMed] 18. Gaziano JM, Hennekens CH, O’Donnell CJ, Breslow JL, Buring JE. Fasting triglycerides, high-density lipoprotein and risk of myocardial infarction. Circulation. 1997;96:2520–5. [PubMed] 19. Kreitzman SN. Factors influencing body composition during very-low-caloric diets. Am J Clin Nutr. 1992;56(l Suppl):217S–23S. [PubMed] 20. Mitchell GA, Kassovska-Bratinova S, Boukaftane Y, et al. Medical aspects of ketone body metabolism. Clin Invest Med. 1995;18:193–216. [PubMed] 21. Koeslag JH. Post-exercise ketosis and the hormone response to exercise: A review. Med Sci Sports Exerc. 1982;14:327–34. [PubMed] 22. Winder WW, Baldwin KM, Holloszy JO. Exercise-induced increase in the capacity of rat skeletal muscle to oxidize ketones. Can J Physiol Pharmacol. 1975;53:86–91. [PubMed] 23. Yehuda S, Rabinovitz S, Mostofsky DI. Essential fatty acids are mediators of brain biochemistry and cognitive functions. J Neurosci Res. 1999;56:565–70. [PubMed] 24. Amiel SA. Organ fuel selection: Brain. Proc Nutr Soc. 1995;54:151–5. [PubMed] 25. Singhi PD. Newer antiepileptic drugs and non surgical approaches in epilepsy. Indian J Pediatr. 2000;67:S92–8. [PubMed] 26. Janigro D. Blood-brain barrier, ion homeostatis and epilepsy: Possible implications towards the understanding of ketogenic diet mechanisms. Epilepsy Res. 1999;37:223–32. [PubMed] 27. Kossoff EH, Pyzik PL, McGrogan JR, Vining EP, Freeman JM. Efficacy of the ketogenic diet for infantile spasms. Pediatrics. 2002;109:780–3. [PubMed] 28. El-Mallakh RS, Paskitti ME. The ketogenic diet may have mood-stabilizing properties. Med Hypotheses. 2001;57:724–6. [PubMed] 29. Ziegler DR, Araujo E, Rotta LN, Perry ML, Goncalves CA. A ketogenic diet increases protein phosphorylation in brain slices of rats. J Nutr. 2002;132:483–7. [PubMed] 30. Cullingford TE, Eagles DA, Sato H. The ketogenic diet upregulates expression of the gene encoding the key ketogenic enzyme mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase in rat brain. Epilepsy Res. 2002;49:99–107. [PubMed] 31. Prentice AM. Manipulation of dietary fat and energy density and subsequent effects on substrate flux and food intake. Am J Clin Nutr. 1998;67(3 Suppl):535S–41S. [PubMed] 32. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med. 2003;348:2082–90. [PubMed] 33. He K, Merchant A, Rimm EB, et al. Dietary fat intake and risk of stroke in male US healthcare professionals: 14 year prospective cohort study. BMJ. 2003;327:777–82. [PMC free article] [PubMed] 34. Westman EC, Mavropoulos J, Yancy WS, Volek JS. A review of low-carbohydrate ketogenic diets. Curr Atheroscler Rep. 2003;5:476–83. [PubMed] 35. Petersen KF, Befroy D, Dufour S, et al. Mitochondrial dysfunction in the elderly: Possible role in insulin resistance. Science. 2003;300:1140–2. [PMC free article] [PubMed] 36. Foster-Powell K, Holt SH, Brand-Miller JC. International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr. 2002;76:5–56. [PubMed] 37. Leeds AR. Glycemic index and heart disease. Am J Clin Nutr. 2002;76:286S–9S. [PubMed] 38. Liu S, Willett WC, Stampfer MJ, et al. A prospective study of dietary glycaemic load, carbohydrate intake, and risk of coronary heart disease in US women. Am J Clin Nutr. 2000;71:1455–61. [PubMed] 39. Sims EA, Danford E, Jr, Horton ES, Bray GA, Glennon JA, Salans LB. Endocrine and metabolic effects of experimental obesity in man. Recent Prog Horm Res. 1973;29:457–96. [PubMed] 40. Golay A, DeFronzo RA, Ferrannini E, et al. Oxidative and non-oxidative glucose metabolism in non-obese type 2 (non-insulin dependent) diabetic patients. Diabetologia. 1988;31:585–91. [PubMed] 41. Defronzo RA, Simonson D, Ferrannini E. Hepatic and peripheral insulin resistance: A common feature of type 2 (non-insulin-dependent) and type 1 (insulin-dependent) diabetes mellitus. Diabetologia. 1982;23:313–9. [PubMed] 42. Defronzo RA, Diebert D, Hendler R, Felig P. Insulin sensitivity and insulin binding in maturity onset diabetes. J Clin Invest. 1979;63:939–46. [PMC free article] [PubMed] 43. Hollenbeck B, Y-Di Chen, Reaven GM. A comparison of the relative effects of obesity and non-insulin dependent diabetes mellitus on in vivo insulin-stimulated glucose utilization. Diabetes. 1984;33:622–6. [PubMed] 44. Kolterman OG, Gray RS, Griffin J, et al. Receptor and postreceptor defects contribute to the insulin resistance in noninsulin-dependent diabetes mellitus. J Clin Invest. 1981;68:957–69. [PMC free article] [PubMed] 45. Gresl TA, Colman RJ, Roecker EB, et al. Dietary restriction and glucose regulation in aging rhesus monkeys: A follow-up report at 8.5 yr. Am J Physiol Endocrinol Metab. 2001;281:E757–65. [PubMed] 46. Hansen BC, Bodkin NL. Primary prevention of diabetes mellitus by prevention of obesity in monkeys. Diabetes. 1993;42:1809–14. [PubMed] 47. Coulston AM, Liu GC, Reaven GM. Plasma glucose, insulin and lipid responses to high-carbohydrate low-fat diets in normal humans. Metabolism. 1983;32:52–6. [PubMed] 48. Chen YDI, Swami S, Skowronski R, Coulston AM, Reaven GM. Effects of variations in dietary fat and carbohydrate intake on postprandial lipemia in patients with non-insulin dependent diabetes mellitus. J Clin Endocrinol Metab. 1993;76:347–51. [PubMed] 49. Chen YD, Hollenbeck CB, Reaven GM, Coulston AM, Zhou MY. Why do low-fat high-carbohydrate diets accentuate postprandial lipemia in patients with NIDDM? Diabetes Care. 1995;18:10–6. [PubMed] 50. Gardner CD, Kraemer HC. Monosaturated versus polyunsaturated dietary fat and serum lipids and lipoproteins. Arterioscler Thromb Vasc Biol. 1995;15:1917–25. [PubMed] 51. Jeppesen J, Schaaf P, Jones C, Zhoue MY, Chen YD, Reaven GM. Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in post-menopausal women. Am J Clin Nutr. 1997;65:1027–33. [PubMed] 52. Mensink RP, Katan MN. Effect of dietary fatty acids on serum lipids and lipoproteins. Arterioscler Thromb. 1992;12:911–9. [PubMed] 53. Groot PH, Van Stiphout WA, Krauss XH, et al. Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease. Arterioscler Thromb. 1991;11:653–62. [PubMed] 54. Patsch JR, Miesenbock G, Hopferweiser T, et al. Relation of triglyceride metabolism and coronary artery disease studies in the postprandial state. Arterioscler Thromb. 1992;12:1336–45. [PubMed] 55. Abbasi F, McLaughlin T, Lamendola C, et al. High carbohydrate diets, triglyceride-rich lipoproteins and coronary heart disease risk. Am J Cardiol. 2000;85:45–8. [PubMed] 56. Sharman MJ, Kraemer WJ, Love DM, et al. A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. J Nutr. 2002;132:1879–85. [PubMed] 57. Mohanty P, Hamouda W, Garg R, Aljada A, Ghanim H, Dandona P. Glucose challenge stimulates reactive oxygen species (ROS) generation by leucocytes. J Clin Endocrinol Metab. 2000;85:2970–3. [PubMed] 58. Kaaks R. Nutrition and colorectal cancer risk: The role of insulin and insulin-like growth factor-1. European Conference on Nutrition and Cancer. International Agency for Research on Cancer and Europe Against Cancer Programme of the European Commission; Lyon, France. June 21 to 21; 2001. A0.14. (Abst) 59. Berrino F, Bellati C, Oldani S, et al. DIANA trial on diet and endogenous hormones. European Conference on Nutrition and Cancer. International Agency for Research on Cancer and Europe Against Cancer Programme of the European Commission; Lyon, France. June 21 to 24; 2001. A0.27. (Abst) 60. Willett WC. Cancer prevention: Diet and risk reduction: Fat. In: DeVita V, Hellman S, Rosenberg S, editors. Cancer: Principles and Practice of Oncology. 5th edn. New York: Lippincott-Raven; 1997. pp. 559–66. 61. Fearon KC. Nutritional pharmacology in the treatment of neoplastic disease. Baillieres Clin Gastroenterol. 1988;2:941–9. [PubMed] 62. Wolf RL, Cauley JA, Baker CE, et al. Factors associated with calcium absorption efficiency in pre- and perimenopausal women. Am J Clin Nutr. 2000;72:466–71. [PubMed] 63. Brehm BJ, Seeley RI, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab. 2003;88:1617–23. [PubMed] 64. Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med. 2003;348:2074–81. [PubMed] ************************************************************************* Morgellons-Biowarefare-with Nano Technolgy In 1999 the world completely changed. The money trust , the law (commerical code/contract law , applicability of public/statutory presumptions, etc.), technology (nano-tech), and the general direction of the planet completely changed. In order to even remotely grasp what is happening you must disconnect your mind from the last century's way of thinking. Failure to change the way you think will preclude you from seeing reality accurately. There is no money anymore, taxes are a thing of the past and no written law applies to you. So what we now have is a real brave new world. The purpose of this site is to simply show the extent at which they have leveraged nano-technology directly on you, how they control everyone on demand with it, and end the confusion around the subject of chemtrails and how they fit into the larger picture while showing how the media and movies are conditioning the mind of the general public. This web site is my account of the entire last decade. I'm sure I'm missing something here or there, but this is 98% accurate and applies to every single person on the planet today in one way (typically via phase 1) or another. The Reason for Everything Let's just get right to it. Forget everything you know. Here it is, the epitome of reality. This video is the best example that summarizes what's happening or has happened in your body already. This is the most prevalent secret in the whole world because it has been forced onto everyone unknowingly. What you see here is a nano-bot encapsulating a neuron or synapse (for example your purkinje neurons) or other nerve ending/bridge. It's only a simulation, but accurately summaries everything that has happened in the past decade. This allows complete control of the host (your body) remotely as demonstrated repeatedly in the movies (for example Metropia (2009), Ultrasonic (2012)). A more sophisticated set of nano-bots would and very well has subsequently allowed for a complete and full BioAPI to be installed without the host (you) even knowing it. If you want to get technical your neurons have been encapsulated, your synapses have been bridged. The basic idea consists of a set of nano-wires tethered to electronics in the main catheter such that they will spread out in a "bouquet" arrangement into a particular portion of the brain's vascular system. Such arrangement could support a very large number of probes (in the millions). Each n-wire would be used to record, very securely, electrical activity of a single or small group of neurons without invading the brain parenchyma. What is the Purpose of Chemtrails Chemtrails are a huge logistical operation. Larger than the hoover damn, trans-alaska pipeline or moon landing. It's large. And expensive. The biggest mistake one can make is assuming there is only one reason for chemtrails. There are about five or six reasons and possibly more. The top six are listed below with a brief summary. This web site is concerned with the last. A visual overview may help by reviewing a flowchart here. · Blocking the Sun: This is the standard reason given to fools in the government. We need to secretly stop global warming, so keep it a secret that we're spraying. Global warming is the catch all con for everyone in the government. If you're smarter than this they'll give you a better reason. · Blocking the Sun (Again): A reduction in sun light across the planet works well to decrease or manipulate crop yields slightly. This is part of the requirement to engineer a food crisis and bring in a famine. You can dismiss this. · Superheating the Atmosphere: In order to create earthquakes and steer hurricanes (for example hurricane Katrina in New Orleans) the atmosphere needs to be more conductive for electricity so installations such as HAARP (HAARP is just what they want you to see, HAARP has nothing to do with anything) can work their magic. So the chemtrails spray barium and aluminum among other things to create a more conductive upper atmosphere. · Health Erosion: As a side effect everyone's health and immune systems become slightly compromised. This is usually not an issue for most healthy people. Older people on average will now die sooner and any health complication is slightly more likely to be fatal. This is both a side effect of spraying and intentional. · Climate Modification: To help or hurt crops, keep skies clear for a major event (like the Olympics), cause a typhoon, steer super storms, etc. · Nano-fiber Propagation: To universally install a BioAPI in everyone they need to spray nano-fibers. These fibers cannot be put into the food supply or given in some other way, the uptake across the population would take forever and not propagate very effectively. It's much easier just to spray everyone like an insect; and because it's happening to everyone the universal herd mentality of the unwashed masses then justifies it. Nano-fiber Basics Nano-fibers specifically are a transport mechanism. Nothing more. They hold a payload for delivery. A payload that would otherwise be compromised by the sun or atmosphere or not make it to its destination (your body). Such as viral RNA code, metals such as aluminum, nano-components, etc. The fibers are (surprisingly) quite harmless as everyone has them. Examples of these fibers can be found all over the internet or in the physical examples section of this site. The fibers must be independently sprayed, if they we're added to the jet fuel the extreme heat would destroy the payload. So it's not the fiber that is critical, it's the payload. Why? This is a complicated question. The people creating and doing this are trying to force biblical principles onto the populace (including themselves) through technology. For example the seven deadly sins. They take a basic human requirement (food, sex, a specific emotion) and quantify it (within the BioAPI). If the result is to extreme (for example you eat too much) or you do something not approved of then they decide that you're not worthy of life or judge you accordingly. In the alternative your are added to a program. There is a good or beneficial angle to it as mentioned on the chemtrails flowcart page or even in this partially out of context clip for the The Simpsons. ----Note the possibilities for the BioAPI or nano-tech in general is endless. Therefore you should not focus on any one reason as being the end all purpose. It's too dynamic. It's to complex. As I mentioned on the top of page 5 of the media references - 'the BioAPI is the greatest revelation in human history'. For example see the last paragraph of the description for Vexille (2007), specifically the trailer for H+ mentioned in it. ---Also see question #9 of the frequently asked questions for a brief explanation on how this (and chemtrails) are (mostly) lawful. Who? The same group of people that brought humanity HIV in the late 1970's. BioAPI Phases There are essentially two phases involved with the installation of the BioAPI. I categorize it as phase 1 and phase 2. If you can imagine a new laptop computer, all it has is the operating system like Windows, so it's kind of useless. This would be the equivalent to phase 1. So a new computer can be remotely controlled (aka phase 1, see Surrogates (2009)) by your IT tech support guy, but that is all. There are no programs installed (provided by phase 2) to do much else with it. These names of a phase 1 and 2 are not necessarily just random nonsense I made up, see the clip and movie for Control Factor (2003) in which they use these exact names in the exact same context; because they are telling you everything. · Phase 1: Everyone on the planet is affected and involved in this phase. Everyone to some extent has the nano-fibers within their body cavity, and therefore wired ['I'm wired too.' - Michael Hall, Gamer (2009)]. Side effects include a clicking sound from within the skull and basic annoying body complications like aching joints. This phase provides complete remote control of your speech and thought patterns through suggestion (partially subconsciously). I guess about 99% of the populace of the entire planet has this phase complete. Phase 1 could be construed as positive and beneficial to you, at least in the future. See John Hodgman (2012) for more information. You should also see question 9 of the FAQs. · Phase 2: This phase must be triggered (by nano-trigger-bots) and is extreme. It completely compromises your health and can do anything from kill you to simply monitor you. This phase cannot be forced onto you like phase 1 (technically it can but they don't do that yet). This involves multiple nano-sensors from ocular to heart and everything in between. I figure about 2% of the population has gone through this phase. If this phase is triggered in you they consider you evil as shown within the media examples page of this site. You must do something to trigger this phase, including eating cheap red meat, kissing specific people, using specific corporate health care/beauty products, etc. The objective they are (partially) reaching for here is to connect each event with a deadly sin of some sort. For example morgellons would be connected with vanity because your skin goes to hell. Ultimately this phase provides complete remote control of your body and mind, including the monitoring of your emotions, thoughts, body functions and everything in between. Phase 2 then can be considered a nano-tech disease (as clearly shown in the Family Guy clip) in which the contagious aspect can be switched on and off. For example I have phase 2, but I am not contagious, but I can be if they decide to make me contagious in some way - typically kissing. This allows them to completely control the transmission/vector or spreading of the nano-disease. If you want to get specific, the nano-tech or nano-implants that compose phase 2 of the BioAPI is actually just the vehicle they use to monitor, torment, test and hurt people. The disease itself is actually one of dishonor. The more dishonor you demonstrate, the more they hate you, the worse things get for you. They do not want people to figure that out. See Meeting Evil (2012) for clear details. Phase 2 can or is definitely detrimental to your life. That is the point of it. Thoughts on a cure can be found in the review for Rise of the Zombies (2012). Nano-fiber and BioAPI Side Effects Of course with something as extreme as nanotech being installed within people's body's you would assume there would be health implications and side effects. This is correct and covered on this site. The approach to handle these side effects has been one of "embrace and extend" it's called. There are several examples in the media section that show how the specific side effects listed below are recognized and then associated with something ridiculous or stupid which then discounts the authenticity in the mind of the viewer. In effect convincing the viewer to dismiss a real side effect as being something that's too crazy to be real. Each side effect is dealt with in a media example. Additional technical possibilities are also talked about in the BioAPI details section. · Phase 1 & 2 - Cranium Clicking/Screeching: A phase 1 side effect goes back as early as 2001. Exactly what is happening is not completely known but involves some sort of nano-chip being installed/operated in the cranium (your head) of the host. This is probably the equivalent of a CPU of some sort. The actual clicking/screeching sound observed is usually at night on average once a month and only lasts for a few seconds. Completely painless and easily ignored or passed off by the person. The entire purpose of the movie Shutter Island (2010) is to discount this. The nano-implant that is specifically and clearly responsible for this side effect is symbolically referenced in the second clip for Surrogates (2009). I suspect over time they have improved this side effect. · Phase 1 & 2 - Aching Joints, Headaches, Fatigue, etc.: The saturation of nano-fibers has different effects on different people. The sheer numbers involved results is a random combination of health implications. Most people will not notice anything, or pass any slight symptom off as getting older. Other people who have more of a reaction will go to the doctor and get diagnosed with fibromyalgia. Fibromyalgia is a catch all disease that was created about a decade ago to give doctors something to tell the patient when they complained. The doctors can't accurate diagnose or understand what or why a patient is feeling a certain way, so the corrupt medical establishment gives them this nonsense to spew. These side effects are primarily phase 1 but are a constant problem across the board. Notice the root word of fibromyalgia is fib[e]r, it's not a coincidence. This Family Guy clip indirectly references Fibromyalgia. · Phase 2 - Itching: For whatever reason they may force harsh itching on you when they do not agree with what you are doing or how you are behaving. You probably will have no idea it is phase 2 at the beginning. This is shown in Flash of Genius (2008) when they show her typing and zoom in on her hand (@ 44:50 in the movie) when she itches it. She's presumed to be a bad wife for leaving her husband (no clip is provided; screenshot here ; you'll have to read this whole site to understand this). The exact same concept is shown in Lay the Favorite (2012) where Bruce Willis itches his forearm clearly and intentionally after referencing it a few seconds earlier (screenshot here ). Why? Why would they put that in? I mean millions of dollars are spent on these scripts and production thereto. This happens in real life to countless people around the world all day long, he's being warned. Why? Because in the movie he's thinking about cheating on his wife with the hot blonde that just walked in. In people with phase 2, the BioAPI is monitoring thought and emotional patterns which if conflict triggers an itch; it's automated. For example lust + guilt (because he's married) do not go together. Think Pontypool (2008). So they are judging you (or more accurately people with phase 2 who are pre-targeted). Itching is also shown in Fast Zombies with Guns (2011), as they turn into zombies [contract phase 2 in real life] they itch a lot . Again, why show this? Because it's real. Most targeted individuals will understand the extremely itchy forearm . So itching is not a side effect in the common sense of the term; it is instead intentionally inflected via the BioAPI as reflected in the aforementioned references as well as loosely shown in A Scanner Darkly (2006) @ 0:44 in the clip/trailer. · Phase 2 - Burning Smell: Phase 2 encapsulates the person's ability to smell, so they can read/write scents. It's used to help warp the reality of someone they have specifically targeted (aka Black Limousine (2010)). When inhaling or specifically exhaling quickly its often a burning/smoke smell that is noticed. This is an unwanted side effect - or more accurately to encapsulate any neuron in the body involved in sensing (for example, smell, taste, etc.) there ends up being be some minor side effect. Interestingly when I cry the smell is amplified and it smells like buttered popcorn of all things. An example of how the media discounts this is demonstrated in the movie Bandits (2001). · Phase 2 - The Left Eye: One of the concepts they push in the movies is the left eye is evil for some reason. Or to a lesser extent use the eye as a gateway to demonstrate functionality such as with Technotise (2009) or Gamer (2009). In phase 2 an actual nano-camera will be installed in the left eye. People with this might comment on how they feel like there's a small bump in their eye under slightly drier conditions such as when going to sleep at night. This is documented in the physical example page. Note if you figure out you have a camera in the left eye they will probably install something in the right eye too. Clips referencing this concept are now available here, here and here and now also Doomsday Book (2012). · Phase 2 - Permanent Metallic Taste: Some people will comment on a metallic taste in the mouth. Typically when going to sleep it becomes prevalent. This is mostly a direct response to be monitored. The more they monitor you or your BioAPI the more of a metallic taste you'll receive. It is not a side effect of medication, that's the typical response a doctor will give you. If you are not on medication and otherwise completely healthy and all of a sudden have a permanent metallic taste in your mouth, you are being recorded (but not watched) 24/7 as per the trailer for A Scanner Darkly (2006). · Phase 2 - Morgellons: Morgellon's can strike anyone. It's a direct problem from the nano-fibers, whether intentional or accidental. The body's immune system can't see or recognize the fibers at all. So when the body can't accept the fibers anymore it beings to push them out through the skin. But the skin is a barrier because the fibers are too large. So the skin breaks up which is why people get lesions. Note that technically everyone has morgellons (nano-fibers), the actual mogellon's symptoms are when the person's body tries to get rid of them the only way possible. Some more conclusions can be seen here and examples within media references including this. Chemtrail Nano-fiber Examples & Evidence Ultimately you need some proof. This is very difficult, as we all don't exactly have nano-tech labs in our basements. The only thing possible at this point in time is to put out the physical evidence that is known and back it up with media/movie supporting clips. A complete list of unbelievable things this technology can do is listed here, also make sure you see the real life body & mind control examples in Media References. ********************************************************************** The Global Threat of Persistent Organic Pollutants There is a connection between pesticides, both general and POPs (Persistent Organic Pollutants), to a myriad of adverse health effects such as cancer and neurological disorders, particularly Parkinson’s Disease. For these reasons alone, it is important to look at the standards currently set for such chemicals by the international standard-setting organization known as Codex Alimentarius.----As mentioned in the first article in this series, There will be a comparison between two different types of pesticides for the sole purpose of the topic of discussing Codex Alimentarius guidelines – general pesticides and POPs. General pesticides should be recognized as, quite simply, those pesticides not considered a Persistent Organic Pollutant by the Stockholm Convention. General pesticides are those which are most widely used since the Stockholm Convention actually banned the use of POPs altogether. Nevertheless, it is important to make the distinction for the purpose of clearly understanding Codex guidelines in this regard.-- The term Persistent Organic Pollutant applies to specific types of pesticides and chemicals. These substances have been used mostly in pest control, “disease control,” agriculture, and other different industries. The EPA distinguishes between two different types of POPs in terms of their production – intentional and unintentional. Intentionally produced POPs are those which are produced for the purpose of being used in manufacturing, agriculture, pest/disease control, or other industrial uses. To put it quite simply, intentionally produced POPs are those that are produced intentionally. Unintentionally produced POPs are those that are essentially byproducts of industrial processes or combustion (like the incineration of waste) etc. The chemical in question has to meet fairly stringent requirements in order to obtain the status of POP, however. Additionally, the label “organic” means the chemicals must be carbon-based (organic) substances. According the website of the Stockholm Convention on Persistent Organic Pollutants, they must also meet the following requirements. They possess a particular combination of physical and chemical properties such that, once released into the environment, they: Remain intact for exceptionally long periods of time (many years); Become widely distributed throughout the environment as a result of natural processes involving soil, water and, most notably, air; Accumulate in the fatty tissue of living organisms including humans, and are found at higher concentrations at higher levels in the food chain; and Are toxic to both humans and animals.  Initially, the Stockholm Convention, the United Nations treaty that requires nations to cease or reduce the production, application, and release of POPs, distinguished 12 substances as those that should be eliminated. This treaty places the POPs into 3 different categories: pesticides, industrial chemicals, and by-products. POPs and their categories are listed below: Pesticides: Aldrin; Chlordane; Dichlorodiphenyl tricholoreothane (DDT); Dieldrin; Endrin; Heptachlor; Hexachlorobenzene; Mirex; Toxaphene; Industrial Chemicals: Hexachlorobenzene; Polychlorinated biphenyls (PCBs) By-Products: Hexachlorobenzene; Polychlorinated dibenzo-p-dioxins; Polychlorinated Dibenzofurans; PCBs In May 2009, the Conference of the Parties to the Stockholm Convention agreed to add 9 new chemicals to the list of POPs. They are as follows: Pesticides: Chlordecone; Alpha Hexcholorocyclohexane; Beta Hexachlorocyclohexane; Lindane; Pentachlorobenzene; Industrial Chemicals: Hexabromobiphenyl; Hexabromodiphenyl ether/Heptabromodiphenyl ether; Pentachlorobenzene; Pefluorooctane Sulfonic Acid, its salts, and Perfluorooctane Sulfonyl Fluoride; Tetrabromodiphenyl ether, Pentabromodiphenyl ether By-Products: Alpha Hexachlorocyclohexane; Beta Hexachlorohexane; Pentachlorobenzene;  The major difference between general pesticides and POPs is not necessarily in their level of danger but the fact that they meet the guidelines listed above and that they remain intact for long periods of time, become widely distributed, and accumulate in fatty tissue. The accumulation of POPs in fatty tissue is at the heart of the problem with these chemicals due to the fact that they can pose an even more serious threat to predators at the top of the food chain than those at the bottom. This is due to the process known as biomagnification, where POPs accumulate in the fatty tissue of organisms and become more and more concentrated as they move from one organism to the other. As they work their way through the food chain, becoming more and more contaminated as they move along, those organisms at the very top of the food chain will be ingesting the largest amounts of the chemicals. It is for this reason that even small releases of POPs can be disastrous, especially for localized ecosystems that dine on local game/fish. An example cited on the EPA’s website reflects on a study conducted by the Arctic Monitoring and Assessment Programme, where it was found that caribou in the Northwest Territories of Canada had as much as 10 times the amounts of PCBs as the lichen that they ate. Not only that, but the wolves that dined on the caribou contained 60 times the amount of PCBs as the lichen. The adverse effects of POPs on wildlife are very similar to those on humans. Studies conducted on wildlife communities showed “reproductive, developmental, endocrine, immunologic, and carcinogenic effects.” Other studies have shown further connections between thyroid and estrogen disorders. Marine animals warrant a particular concern due to the fact that POPs have low water solubility and therefore bond easily with particulate matter in sediment. This gives them the ability to lay dormant for a long time in the water supply, becoming active again when disturbed years later. Not only that, but the fact that POPs do not have to be directly applied to an area or species to be present or have an effect on these organisms creates a pollution problem that knows no boundaries[F3] . The discovery of POPs in the Alaskan Arctic, thousands of miles away from any known source, is a prime example of this. It is well-known that POP compounds can attach themselves not only to aquatic sediment material, but also to airborne particles. Along with the ability of most POPs to exist as gases, this allows them to have increased ability to travel long distances and potentially pollute the entire globe.[F4] Some of these chemicals are able to evaporate from land and water sources into the air, and return to the earth in rain, snow, and mist. Add to this the transportability of the POPs by airborne and aquatic means, as well as by the very human and animal organisms being contaminated by them, and one can easily see the problem posed here. However, it should be noted that although only 21 of these substances are listed as POPs, the potential for any of the thousands more combinations of chemicals to do the same is still very real. Notes:  “Persistant Organic Pollutants: A Global Issue, A Global Response.” Environmental Protection Agency. December 17, 2009.http://www.epa.gov/international/toxics/pop.htm  “What are POPs?” Stockholm Convention on persistant organic pollutants. Accessed March 23, 2010. http://chm.pops.int/Convention/ThePOPs/tabid/673/language/en-US/Default.aspx  “What are POPs?” Stockholm Convention on persistant organic pollutants. http://chm.pops.int/Convention/ThePOPs/tabid/673/language/en-US/Default.aspx Accessed March 23, 2010.  Ibid.  Ibid.  “Persistant Organic Pollutants: A Global Issue, A Global Response.” Environmental Protection Agency. December 17, 2009.http://www.epa.gov/international/toxics/pop.htm  Abelsohn, Alan., Gibson, Brian L., Sanborn, Margaret D., Weir, Erica. “Identifying and managing adverse environmental health effects:5. Persistant Organic Pollutants.” Canadian Medical Association Journal. June 11, 2002. 166 (12). http://www.cmaj.ca/cgi/content/full/166/12/1549 Accessed May 24, 2010.  Ibid.  Ibid. TOP C -------------------------------------------------------------------------------- [F1]In this case the chemo preferred would be herbals and botanicals and foods using chemistry that id by design to assist people in restoration and renewal [F2]So By incorporating a ketone type diet and the use of supplements –herbs and foods we should see a improvement [F3]Consider the GMO’s and there by products how much have they spread in 40 years and with the increased levels of these organisms being planted and the reduction of the traditional foods and the added chemicals and mixes ---how long will they lay dormant?? And how much as people eating the foods fed the gmos ho much more are we getting?? [F4]With harp this is more then likely