1. Brian was appointed adjunct professor in the College of Pharmacy and Health Sciences at Texas Southern University (1998-1999). The former President of the University (Dr. James Douglas) stated, “…His nutritional discoveries and practical applications through Life-Systems Engineering [Science] are unprecedented.” Dr. Habib is board certified in both pediatrics and pediatric endocrinology, a fellow in the American Academy of Pediatrics and the American College of Endocrinology. He was one of the first 200 board-certified graduates in pediatric endocrinology. Dr. Habib is committed to bringing the highest degree of science into the medical arts. Cancer as cause of death was easily determined in 1900. That is why the National Center for Health Statistics and the American Cancer Society gave 3% as the number of people dying from cancer in 1900. Brian was appointed adjunct professor in the College of Pharmacy and Health Sciences at Texas Southern University (1998-1999). The former President of the University (Dr. James Douglas) stated, “…His nutritional discoveries and practical applications through Life-Systems Engineering [Science] are unprecedented.” Dr. Habib is board certified in both pediatrics and pediatric endocrinology, a fellow in the American Academy of Pediatrics and the American College of Endocrinology. He was one of the first 200 board-certified graduates in pediatric endocrinology. Dr. Habib is committed to bringing the highest degree of science into the medical arts.
2. Cancer as cause of death was easily determined in 1900. That is why the National Center for Health Statistics and the American Cancer
Society gave 3% as the number of people dying from cancer in 1900.
3. “Age Distribution of Cancer: The Incidence Turnover at Old Age,” by Francesco Pompei and Richard Wilson, Human and Ecological Risk Assessment: Vol. 7, No. 6, pp. 1619-1650, 2001. “Cancer reaches a maximum cumulative probability of affliction with any cancer of about 70% for men and 53% for women in the US…”
4. Racing to The Beginning of The Road: The Search For The Origin Of Cancer, Robert A. Weinberg, Harmony Books, New York, NY, 1996.
5. “On the Origin of Cancer Cells,” Otto Warburg, Science, February 1956, Volume 123, Number 3191.
6. One Renegade Cell: How Cancer Begins, by Robert A. Weinberg, Ph.D. (New York: Basic Books, 1998), pp. 67, 90, 95, 153.
7. “Cancer: Looking Beyond Mutations,” by Eric Berger, Houston Chronicle, June 27, 2005, page 1.
8. Journal of American Medical Association, 285:769-776, 799-801: “Further analysis for consumption of green leafy vegetables and fruits … showed a similar lack of association with breast cancer risk.”
9. Lancet, October 14, 2000; 356:1286-1287, 1300-1306 and New England Journal of Medicine, Jan. 21, 1999, Vol. 340, No 3.
10. International Journal of Health Services, Vol. 31, No. 3, 2001, pp. 605-615.
11 . “Omega-3 Polyunsaturated Fatty Acids, Inflammation and Immunity,” by Philip C. Calder, Institute of Human Nutrition, University of Southampton, Bassett Crescent End, Southampton, UK.
12. “Controlled Trial of Fish Oil for Regression of Human Coronary Atherosclerosis,” Frank M. Sacks, et al., Journal of the American College of Cardiology Vol. 25, No. 7, June 1995:1492-8, “Effect of dietary supplementation with omega-3 fatty acids on progression of atherosclerosis [plaque buildup in interior of arteries] in carotid [heart to brain] arteries,”Angerer, P., et al., Cardiovascular Research; 54:183-190, 2002, Clemens von Schacky, et al., “The Effect of Dietary Omega-3 Fatty Acids on Coronary Atherosclerosis: A Randomized, Double-Blind, Placebo-Controlled Trial,” Annals of Internal Medicine;130:554-562, 1999.
13. Burr et al., “Lack of benefit of dietary advice to men with angina: results of a controlled trial,” Eur J Clin Nutr 2003, 57:193-200.
14. Cancer ranks first as Japan’s leading cause of death since 1981. In 2002 cancer accounted for over 30% of the total number of deaths. Heart disease and cerebrovascular disease is next. Ref.: Vital Statistics of Japan, Statistics and Information Department, Minister’s Secretariat, Minister of Health, Labour and Welfare. In 2002 Japan had 241/100,000 population cancer deaths and America had 194/100,000 population—Japan has a whopping 24%[(241-194)/194 ]/100,000 worse death rate due to cancer than America.
15. The Journal of the American Medical Association, Vol. 295, No. 4, January 25, 2006.
16. Hooper, Lee, et al., “Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review.” Prepublication reference: BMJ, doi:10.1136/bmj.38755.366331.2F (published 24 March 2006).
17. Thomas H. Shepard, et al., 262 (22), June 2, 1960, pages 1099-1103.
18. http://www.cfsan.fda.gov/~djw/pltx.cgi?QUERY=soy.
19. New Trends Publishing, Inc., Washington, DC, 2005, ISBN 0-9670897-5-1, pg. 31.
20. J Am Coll Nutr 1990, Apr; 9(2): 164-167.
21. Canadian Journal of Biochemistry, 1975 Dec;53(12):1337-41.
22. Otto Warburg: Cell Physiologist, Biochemist, and Eccentric, by Hans Krebs (in collaboration with Roswitha Schmid), trans. Hans Krebs and Anne Martin (New York: Clarendon Press-Oxford University Press, 1981).
23. Biography of Otto Warburg, Nobel e-Museum, “Medicine”: www.nobel.se/medicine/laureates/1931/warburg-bio.html.
24. Otto Warburg: Cell Physiologist, Biochemist, and Eccentric, by Hans Krebs (in collaboration with Roswitha Schmid), trans. Hans Krebs and Anne Martin (New York: Clarendon Press-Oxford University Press, 1981).
25. Otto Warburg: Cell Physiologist, Biochemist, and Eccentric, by Hans Krebs (in collaboration with Roswitha Schmid), trans. Hans Krebs and Anne Martin (New York: Clarendon Press-Oxford University Press, 1981), page 4.
26. Biography of Otto Warburg, Nobel e-Museum, “Medicine”: www.nobel.se/medicine/laureates/1931/ warburg-bio.html.
27. Volume 23, pages 1079-1088 in 1959 and Volume 38, pages 839-863 in 1967.
28. Otto Warburg, “On the Origin of Cancer Cells,” Science, February 1956, Volume 123, Number 3191.
29. ibid.
30. Radiotherapy and Oncology 1993, Jan;26(1):45-50, makes Dr. Warburg’s #1 fact clear. “Intratumoral pO2 [partial pressure of oxygen] predicts survival in advanced cancer of the uterine cervix,” by Knoop, Hockel, et al., Radiotherapy and Oncology 53 (1999) 113 -11 7, makes Dr. Warburg’s Number #1 fact clear again in the article titled, “Oxygenation of head and neck cancer: changes during radiotherapy and impact on treatment outcome,” by David Brizel, et al.
31. In science, any new theory must allow for more out of it than you put into it. The theory must have predictive value. If I input one thing, the theory must lead to the explanation of many things, and the cancer explanation based on Dr. Warburg’s research uniquely meets this criteria.
32. For example, in 1947, Dr. F. Windesch of Germany demonstrated that by intermittent withholding of oxygen, normal body cells could be changed into cancer cells. Dr. H.A. Schweigart, another German, also found that cancerous tissue is always deficient in oxygen. However, the first notable long-term experimental induction of cancer by oxygen deficiency was described in 1953 by an American physician, Dr. Goldblatt (Journal of Experimental Medicine, Vol. 97, 1953, pages 525-552). Dr. Warburg references this important finding in his On the Origin of Cancer Cells publication: “…[Goldblatt, an M.D. and Cameron] exposed heart fibroblasts in tissue culture to intermittent oxygen deficiency for long periods and finally obtained transplantable cancer cells. In the control cultures that they maintained without any oxygen deficiency, no cancer cells resulted.” This experiment was conducted over a 2½-year timeframe. The results were meticulously tabulated, and the conclusions rock solid. Dr. Warburg’s work was extensively referenced in their paper (Warburg’s findings were very well-known at that time). Goldblatt and Cameron also verified Dr. Warburg’s finding (published in 1925) that a “respiration-impacted,” destined-to-become cancerous cell could be STOPPED if it was oxygenated early enough. On page 527 of Goldblatt and Cameron’s journal paper, they reported: “…The length and frequency of exposure of the different [normal] cultures to nitrogen [cutting off oxygen] were varied greatly at first, in order to determine the periods that would prove definitely injurious in greater or less degree, but from which most of the cultures RECOVERED readily after the return to aerobic [oxygenated] conditions were 15 minutes of nitrogen twice in 24 hours, for 3 successive days with an interval of 11 ¾ hours between successive exposures. It was found that even after exposure to nitrogen for ½ hour, 3 times in every 24 hours, for 7 consecutive days, with an interval of 7 ½ hours between successive exposures, recovery could still occur, although the injury was great; but recovery was slower and less certain after such long periods of anaerobiosis [oxygen deprivation]; and some of the cultures did NOT recover.” They also noted, on page 535 of their publication that once damage is too great to the cell, then no amount of oxygen will return the cell’s respiration back to normal—it is forever doomed to a cancerous life. This is why prevention is the ultimate solution to never contracting cancer. In 1955, two American scientists and physicians, R.A. Malmgren and C.C. Flanigan, again confirmed these findings, publishing them in the medical journal, Cancer Research. (“Localization of the vegetative form of clostridium-tetani in mouse tumors following intravenous spore administration,” Vol. 15(7), 1955, pages 473-478). An especially clever and convincing experiment added to the long list of experiments clearly demonstrating that oxygen deficiency is always present when cancer develops. These physicians referenced Dr. Warburg’s work on page 478 of their publication. This is how Dr. Warburg explained their accomplishments in his 1966 Prime Cause and Prevention of Cancer lecture: “…However, if one injects tetanus spores into the blood of tumor-bearing mice, the mice sicken with tetanus, because the oxygen pressure in the tumors can be so low that the spores can germinate. These experiments demonstrate in a unique way the anaerobiosis [low oxygen] of cancer cells and the non-anaerobiosis [normal oxygen] of normal cells, in particular the non-anaerobiosis of growing embryos.” Note: Rats and mice have much shorter lives than humans, so results, both good and bad, occur much faster, making them very useful in medical experiments.
33. “The Metabolism of Carcinoma Cells,” The Journal of Cancer Research, Vol. 9, 1925, pages 148-163; in particular pages 152, 154, 159, and 163. Dr. Warburg’s paper makes it quite clear: “Thus the quantitative difference between malignant and benign tumors becomes a qualitative one, when we pass from benign tumors to normal growth. The respiration of normally growing tissues suffices to bring about the disappearance of the glycolysis-products, whereas in tumors the respiration is too small [low] for this. This, then, is the difference between ordered [intelligent] and disordered growth.” , “…From the embryonal type of metabolism there has again arisen the tumor type benign or malignant, depending on the duration of the oxygen deficit.” , “In this manner [adding higher degrees of cyanide to curtail respiration] we obtain from the embryonic type of metabolism the tumor type—the benign tumor type when the concentration of cyanide is low [less impacted respiration]; the malignant type, when it is high [highly impacted cellular respiration]…. [T]here has again arisen the tumor type—benign or malignant, depending upon the duration of the oxygen deficit.”
34. Wiesenhof, August 1966 Otto Warburg, “The Prime Cause and Prevention of Cancer” (Revised Lindau Lecture).
35. “Metabolism of essential fatty acids by human epidermal enzyme preparations: evidence of chain elongation,” R.S. Chapkin, et. al, Journal of Lipid Research, Volume 27, pages 945-954, 1986.
36. Agneta Anderson, et al., “Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men,” American Journal of Endocrinological Metabolism, 279: E744-E751, 2000.
37. “Prevention of coronary heart disease: the role of essential fatty acids,” Postgrad Med J 1980 Aug;56(658):579-84S; Bunting, S. Moncada, and J.R. Vane, “Prostacyclin—Thromboxane A2Balance: Pathophysiological and Therapeutic Implications,” British Medical Journal, (1983) Vol. 39, No. 3, pages 271-276; Smart Fats, Michael A. Schmidt, Ph.D., pgs. 27-30; “Pathophysiological and Therapeutic Implications,” British Medical Journal, (1983) Vol. 39, No. 3, pages 271-276; Crawford, M.A., “Commentary on the workshop statement. Essentiality of and recommended dietary intakes for Omega-6 and Omega-3 fatty acids,” Prostaglandins Leukot Essent Fatty Acids 2000 Sep; 63(3):131-4; Fu, Z. and Sinclair, A.J., “Increased alpha-linolenic acid intake increases tissue alpha-linolenic content….” Lipids 2000 Apr; 35(4):395-400; “Fatty acid Composition of Serum Lipids Predicts Myocardial Infarction [Heart Attack],” British Medical Journal, Oct. 9, 1982, 285:993; and from PUFA Newsletter, (www.fatsoflife.com): “Alpha-Linolenic Acid Conversion Revisited,” by Norman Salem, et al., are a sample of those physicians and scientists that understand the details.
38. Grass-fed beef is best because this is the food nature intended the cattle to eat—not the grains they are forced to consume. Their EFA structure is drastically unbalanced with grain and much more balanced with grass. However, if you choose a nutritional supplement, you can counteract this effect and eat all the grain-fed beef you desire.
39. Dr. Rowen is affectionately known as the “Father of Medical Freedom” for pioneering America’s first statutory protection for alternative medicine. He was appointed for a term on the Alaska State Medical Board and is internationally recognized for his work in alternative and integrative medicine. He is currently editor-in-chief of Second Opinion Newsletter. It’s a newsletter devoted to informing the public about innovative breakthroughs and natural means to maintain and regain health, in contrast to chemical symptom suppression often found in orthodox medicine. He is a “Living Foods” advocate and has most impressive laboratory numbers on himself that confirms his message.
40. “Essential fatty acids [EFAs] are found in the structural lipids of the cell… and are concerned with the structural integrity of the mitochondrial membrane [respiratory-based energy producing].” Harper’s Illustrated Biochemistry, 26th edition, page 191.
41. “Linoleic acid [parent omega 6] comprises about 55 per cent [the majority] of the fatty acids in cholesterol esters of LDL and HDL, and about 20% of the free fatty acids in the phospholipids in each class…” , “…It must also be remembered that all tissues need EFA which must come from the diet and for most tissues through the plasma where they are almost entirely transported in lipoproteins, mainly in their cholesterol esters and phospholipids,” “Essential Fatty Acids in Perspective,” Sinclair, H.M., Human Nutrition: Clinical Nutrition, (1984) 38C, pages 245-260.
42. Willett, W. C. et al., “Dietary fat and the risk of breast cancer,” New England Journal of Medicine, 1987; 316:No.1, 22-28.
43. “Effect of Modification of Plasma Membrane Fatty Acid Composition of Fluidity and Methotrexate Transport in L1210 Murine Leukemia Cells,” Burns, C. Patrick, et al., Cancer Research 39, 1726-1732, May 1979: “The plasma membrane lipid composition in L1210 was dependent upon the type of fat [EFAs and hydrogenated/ transfats, etc.] fed to the host animal.
44. “Quantitative Effects of Dietary Polyunsaturated Fats [EFAs] on the Composition of Fatty Acids in Rat Tissues,” Department of Biological Chemistry, University of Illinois at Chicago, published in the medical journal Lipids, Vol. 25, No. 9, 1990, pages, 505-516, make it very clear: “…The tissues maintained a linear relationship [proportional] between the amount of 18-carbon polyunsaturated fatty acids [EFAs] in the diet and in the tissue ….” , “….With higher amounts of 18:2n-6 [parent omega-6] in the diet, the rat tissues maintained progressively higher levels of 18:2n-6 [parent omega-6] in triglycerides. The linear trend was similar for plasma, liver, and adipose ….”
45. “…This decrease (of inhibited lymphocyte proliferation and natural killer cell activity) causes increased cellular bacteria [infection] and impaired tumor cell killing.”
46. Angerer, P., et al., Cardiovascular Research; 54:183-190, 2002. The medical journal’s quote: “In this group of selected patients with documented coronary artery disease, omega-3 PUFA [polyunsaturated fatty acids] given for 2 years did not demonstrate an effect on slowing progression of atherosclerosis in carotid arteries as measured by ultrasound.”
47. Frank M. Sacks, et al., Journal of the American College of Cardiology Vol. 25, No. 7, June 1995: 1492-8.
48. “Introducing The Body of Evidence,” Reliant Pharmaceuticals, Inc. (September 2005), page 17. © 2005
49. One Renegade Cell: How Cancer Begins, Robert A. Weinberg, Basic Books, New York, 1998, p. 146.
50. Health and Survival in the 21st Century, Ross Horn, Chapter 13, 1997, HarperCollins Publishers, Pty Ltd., Australia, page 6 of Internet edition at www.soilandhealth.org.
51. Crawford, M.A., “Commentary on the workshop statement. Essentiality of and recommended dietary intakes for Omega-6 and Omega-3 fatty acids,” Prostaglandins Leukot Essent Fatty Acids 2000 Sep; 63(3):131-4.
52. Cancer ranks first as Japan’s leading cause of death since 1981
53. Houston Chronicle, Page 1, July 20, 2004, (Source: New York Times, by Andrew Pollack).
54. Mary Duenwald, New York Times, June 2003, “Daily Pill Proposed to Fight Cardiovascular Disease.”
55. “Eicosanoids [made from EFAs], other fatty acid metabolites and the vascular system: Are the present antithrombotic approaches rational?,” Prostaglandins in the Cardiovascular System, pages 273-281, 1992.
56. British Medical Journal, October 9, 1982, 285:993.
57. “Dietary polyunsaturated fatty acids and compositions of human aortic plaque,” Felton, CV, et al., Lancet; 344:1195-1196, 1994.
58. Waddington, E., et al., “Identification and quantification of unique fatty acid and oxidative products in human atherosclerotic plaque using high-performance lipid chromatography,” Annals of Biochemistry; 292:234-244, 2001; Kuhn, H., et al., “Structure elucidation of oxygenated lipids in human atherosclerotic lesions,” Eicosanoids; 5:17-22, 1992.
59. “Postprandial Lipid Oxidation and Cardiovascular Disease Risk,” Bowen, Phyllis, et al., Current Atherosclerosis Reports; 6:477- 484, 2004.
60. “Essential Fatty Acids in Perspective,” Sinclair, H.M., Human Nutrition: Clinical Nutrition, (1984) 38C, pages 245-260.
61. Journal of American Physicians and Surgeons, Vol 10, No. 3, Fall 2005, by Anthony Colpo. “…However, there was no association between oxidized LDL concentrations and total LDL levels [in Japanese patients undergoing surgery to remove plaque].” The cholesterol “number” meant nothing – it is all about the cholesterol structure. Too much parent omega-6 gets oxidized and the simple solution is to keep adding enough unadulterated parent omega-6 daily.
62. Life-Systems Engineering Science terms cholesterol a dependent variable. Recall from high school algebra that if you have three variables in an equation, you can select or change two of them, but the third variable is entirely determined by the other two. Cholesterol acts in exactly the same fashion. Cholesterol varies so that other more important factors can be rigidly maintained.
63. Textbook of Medical Physiology, page 87.
64. New England Journal of Medicine, 337:1491-149.
65. Kelsey, F.E., Longenecker, H.E., J. Biol. Chem., 1941, Vol. 139, page 727.
66. H.M. Sinclair, “Deficiency of Essential Fatty Acids and Atherosclerosis, Etcetera,” Lancet, April 7, 1956.
67. Burns CP, Spector AA: “Effects of Lipids on Cancer Therapy, Nutrition Reviews,” 48, No.6, 233-240, 1990 pages 381-383.
68. Campbell IM, Crozier DN, Caton RB: Abnormal fatty acid composition and impaired oxygen supply in cystic fibrosis patients. Pediatrics 57, 480-486, 1976.
69. Ibid.
70. “Drugs to Lower Cholesterol May Cause Cancer, Study Says,” David Perlman, San Francisco Chronicle, 1995; pre-pub. Ref., JAMA, vol.275, pages 55-60, 1996.
71. Lands WEM, Morris A, and Libelt B: “Quantitative effects of dietary polyunsaturated fats on the composition of fatty acids in rat tissues,” Lipids 25, 505-516, 1990.
72. Textbook of Medical Physiology, page 1023.
73. Brian Scott Peskin, Amid Habib, The Hidden Story of Cancer, Pinnacle Press, Houston, Texas (USA), 2006.
References for The 5 Step Program to Minimize Your Risk of Contracting Cancer
1. “Who’s Afraid of N-6 Polyunsaturated Fatty Acids?” by E.M. Berry, Nutr Metab Cardiovasc Dis. 3 (11 June 2001) : 181-188. This article stated, “N-6 Fatty Acids [omega-6] are essential for normal growth…. and it is therefore wrong to condemn only n-6 fatty acids in their etiology.”
2. (Voet’s) Biochemistry, page 790, in the chapter titled “Adipose Tissue.” ”: “Following the ingestion of a high protein meal, the gut and liver utilize most of the absorbed amino acids…. The liver takes up 60-70% of the amino acids in the portal vein….”
3. “The Insulin Connection,” by Brenda Goodman in U.S. News & World Report, September 5, 2005, pages 60-62.
References for Why You Need Alternative Medicine Even With Chemotherapy and Radiation
1. “PET/CT Brings New Hope TO Patients With Deadly Form of Breast Cancer,” Medical News Today, Nov. 28, 2007.
2. Matsumoto, S., et al., “Low-field paramagnetic resonance imaging of tumor oxygenation and glycolytic activity in mice,” J Clin Invest. 2008 May 1; 118(5): 1965–1973.
3. Samuni, A., et al., “Effects of Hypoxia on Radiation-Responsive Stress-Activated Protein Kinase, p53, and Caspase 3 Signals in TK6 Human Lymphoblastoid Cells,” Cancer Res 2005; 65(2): 579-86.
4. Brown, J., “Tumor microenvironment and the response to anticancer therapy,” Cancer Biol Ther; 2002;1:453–8.
5. Hockel, M., et al., “Association between tumor hypoxia and malignant progression in advanced cancer of the uterine cervix,” Cancer Res 1996;56:4509–15.
6. Eric, E., “The oxygen effect and reoxygenation.” In: Radiobiology for the radiologist. Philadelphia: JB Lippincott Co.; 1994. p. 133–52
7. Coleman, C., “Modulating the Radiation Response,” The Oncologist 1996;1:227-231.
8. Cairns, R., et al., “Metabolic targeting of hypoxia and HIF1 in solid tumors can enhance cytotoxic chemotherapy,” Proceedings of the National Academy of Science, May 29, 2007; vol. 104, no. 22: 9445–9450.
9. Harrison, L., Blackwell, K., “Hypoxia and Anemia: Factors in Decreased Sensitivity to Radiation Therapy and Chemotherapy?,” The Oncologist 2004;9(suppl5):31-40.
10. Ibid
11. Ibid.
12. Teicher, B, “Physiologic mechanisms of therapeutic resistance. Blood flow and hypoxia,” Hematol Oncol Clin North Am 1995;9:475-506.
13. Teicher B, et al., “Classification of antineoplastic agents by their selective toxicities toward oxygenated and hypoxic tumor cells,” Cancer Res 1981;41:73-81.
14. Teicher B, et al., “Classification of antineoplastic treatments by their differential toxicity toward putative oxygenated and hypoxic tumor subpopulations in vivo in the FSaIIC murine fibrosarcoma,” Cancer Res 1990;50:3339-3344.
15. Teicher B., “Hypoxia and drug resistance,” Cancer Metastasis Rev 1994;13:139-168.
16. One Renegade Cell: How Cancer Begins, Robert A. Weinberg, Basic Books, New York, 1998, p. 146.
17. Health and Survival in the 21st Century, Ross Horn, Chapter 13, 1997, HarperCollins Publishers, Pty Ltd., Australia, page 6 of Internet edition at www.soilandhealth.org.
18. Crawford, M.A., “Commentary on the workshop statement. Essentiality of and recommended dietary intakes for Omega-6 and Omega-3 fatty acids,” Prostaglandins Leukot Essent Fatty Acids 2000 Sep; 63(3):131-4.
19. “The Insulin Connection,” by Brenda Goodman in U.S. News & World Report, September 5, 2005, pages 60-62.
