Life Extension Magazine September 2003
|Treating High Cholesterol by Replacing Hormones Lost to Aging |
by Sergey A. Dzugan, Ph.D. & R. Arnold Smith, M.D.
Elevation of cholesterol is an excellent aging marker, which can be used to define the time when patients need to begin HT.
Our body is a very smart self-regulated system. These reasons are always for the elevation of cholesterol. It can be that the age-related decline in production of steroid hormones, pregnancy, or some problems with enzymes. But hypercholesterolemia is in most cases a consequence of some reason, not a reason in itself. That’s why it is not very important what method you are using for suppressing the production of cholesterol—drugs, diet or supplements. You can always correct a consequence (hypercholesteromia)! On the contrary, we attempt to eliminate the reason for total cholesterol elevation by restoring a youthful hormonal profile. The main difference between traditional medicine and our treatment policy is that traditional methods direct against normal physiology. During our therapy we try to model a normal, healthy physiology.
More research will be needed to determine the full clinical potential of such an approach to the management of hypercholesterolemia.
Some additional comments by Life Extension The purpose of this six-year study was to ascertain the effects of steroidal hormone restoration (HT) on cholesterol blood levels and to assess the effects of this therapy on the overall health of patients. This study showed that total and LDL cholesterol levels declined and all patients described a significant improvement in quality of life (even though they were aging during this period).
A “non-steroidal” hormone that also causes elevated cholesterol when deficient is thyroid. The authors of the study commented to Life Extension that some patients were already taking thyroid hormones before their program, but the level of total cholesterol and LDL remained high. They also mentioned that symptoms of hypofunction of thyroid hormones were improved after the start of their HT treatment. This can be explained by the restoration of sensitivity of cell membranes to the impulses of thyroid hormones.
This study showed that serum LDL decreased on average from 158.2 mg/dL before to 120.4 mg/dL after treatment. Optimal LDL levels, however, may be below 100 mg/dL. For those with chronically high LDL, the addition of thyroid restoration therapy (if tests reveal thyroid deficiency) could reduce LDL to optimal levels. The authors noted that complete HT was required to obtain these results. A deficiency in even one steroidal hormone could cause the liver to synthesize more cholesterol in a sometimes-futile attempt to naturally replenish the missing hormone in the body. The authors mentioned that pregnenolone was a hormone often found deficient. When pregnenolone was restored to normal levels, cholesterol reduction was observed. The significance of this is that pregnenolone is the natural precursor (mother hormone) of DHEA, testosterone, progesterone, the estrogens and other steroidal hormones. If one has healthy hormone transformation enzyme systems in place, it is theoretically possible that supplementation with pregnenolone by itself would maintain healthy levels of steroidal hormones (DHEA, progesterone, testosterone, estrogen, etc.) Unfortunately, aging people often suffer from defective hormone enzymatic transformation systems, meaning that pregnenolone does not cascade down into other critical steroidal hormones. This is why aging humans can derive so much benefit from natural DHEA, testosterone, progesterone and estrogen supplements and drugs.
The only downside to utilizing HT (hormonorestoration) in all aging people is that some have hormone sensitive cancers. Those with prostate, breast and certain reproductive cancers may not be able to enjoy the whole body benefits of HT and instead have to rely on drug therapy if their cholesterol levels are too high.
R. Arnold Smith, M.D. is a radiation oncologist who operates an integrative cancer practice in North Central Mississippi Regional Cancer Center in Greenwood, Mississippi. In addition to radiotherapy, Dr. Smith treats his cancer patients with multiple biological response modifiers that increase the percentage of cancer patients who experience long-term survival or complete response. Despite being located away from any convenient airport and doing no advertising, cancer victims who learn of Dr. Smith’s aggressive approaches to treating cancer travel from far distances to become patients. Dr. Smith has been a Life Extension advisor since 1983, and has provided enormous amounts of clinical data that The Life Extension Foundation has incorporated into its cancer treatment protocols. You may wonder how a busy radiation oncologist could find the time to do a study on the cholesterol-lowering effects of multi-hormone restorative therapy. One reason is that he has the assistance of a brilliant researcher named Sergey A. Dzugan, Ph.D. Dr. Smith has become so well known for his superior methods of treating cancer, that patients (and their families) insist that he treat other age-related diseases. As a result, Dr. Smith may be the only conventional oncologist to also practice anti-aging medicine.
Sergey A. Dzugan, M.D., Ph.D., joined Dr. Smith’s practice in July 1, 1996. One of Dr. Dzugan’s jobs is to search the peer-reviewed published literature in order to identify better methods for treating cancer and slowing aging. Dr. Dzugan participates in conducting studies and writing articles that are later published in scientific journals. Sergey A. Dzugan was formerly a heart surgeon and Chief of Cardiovascular Surgery at the Donetsk Regional Medical Center in Donetsk, Ukraine. His Ph.D. in cardiovascular surgery was received in 1990 and pertained to heart rhythm disorder. He was the Associate Professor of Medical University in Donetsk, Ukraine. Dr. Dzugan’s current primary interest is in anti-aging and biological therapy of cancer and he participates in patient care research in Greenwood, Mississippi. Dr. Dzugan has worked with the Cancer Center for more than six years and is the author of 113 publications in medical journals and these publications include surgical, oncological, academic and anti-aging topics. While Sergey Dzugan is an accredited medical doctor, he is not currently licensed to practice in the United States.
Cancer patients who want to inquire about Dr. Arnold Smith’s state-of-the art treatment modalities may call 1-800-720-8933 for specific information.
1. Starfield B. Is U.S. health really the best in the world? JAMA 2000;284(4):483-5.
2. Smith D. Cardiovascular disease: a historic perspective. Jpn J Vet Res 2000;48(2-3):147-66.
3. Jacobson TA. Clinical context: current concepts of coronary heart disease management. Am J Med 2001;110 Suppl 6A:3S-11S.
4. Seman LJ, DeLuca C, Jenner JL, et al. Lipoprotein(a)-cholesterol and coronary heart disease in the Framingham Heart Study. Clin Chem 1999;45(7):1039-46.
5. Samanek M, Urbanova Z. Cholesterol and triglyceride levels and their development from 2 to 17 years of age. Cas Lek Cesk 1997;136(12):380-5.
6. Yang YH, Kao SM, Chan KW. A retrospective drug utilization evaluation of antihyperlipidaemic agents in a medical centre in Taiwan. J Clin Pharm Ther 1997;22(4):291-9.
7. Okada T, Murata M, Yamauchi K, et al. New criteria of normal serum lipid levels in Japanese children: The nationwide study. Pediatr Int 2002;44(6):596-601.
8. Suthutvoravut U, Charoenkiatkul S, Chitchumroonchokchai C, et al. Elevated serum cholesterol levels in Bangkok children and adolescents. J Med Assoc Thai 1999;82 Suppl 1:S117-21.
9. Gaist D, Jeppesen U, Andersen M, et al. Statins and risk of polyneuropathy: a case-control study. Neurology 2002;58(9):1333-7.
10. Schuff-Werner P, Kohlschein P. Current therapy of hypercholesterolemia. How much statin does your patient need? MMW Fortschr Med 2002;144(31-32):24-6.
11. Papassotiropoulos A, Hawellek B, Frahnert C, et al. The risk of acute suicidality in psychiatric inpatients increases with low plasma cholesterol. Pharmacopsychiatry 1999;32(1):1-4.
12. Gould AL, Rossouw JE, Santanello NC, et al. Cholesterol reduction yields clinical benefit. A new look at old data. Circulation 1995;91(8):2274-82.
13. Geurian KL. The cholesterol controversy. Ann Pharmacother 1996;30(5):495-500.
14. Bzduch V, Behulova D, Kajaba I. A new approach to cholesterol. Cas Lek Cesk 2001;140(22):685-7.
15. Chung N, Cho SY, Choi DH, et al. STATT: a titrate-to-goal study of simvastatin in Asian patients with coronary heart disease. Simvastatin Treats Asians to Target. Clin Ther 2001;23(6):858-70.
16. Scheen AJ. Fatal rhabdomyolysis caused by cerivastatin. Rev Med Liege 2001;56(8):592-4.
17. Muldoon MF, Manuck SB, Matthews KA. Lowering cholesterol concentrations and mortality: a quantitative review of primary prevention trials. BMJ 1990;301(6747):309-14.
18. Law MR, Thompson SG, Wald NJ. Assessing possible hazards of reducing serum cholesterol. BMJ 1994;308(6925):373-9.
19. Law MR, Wald NJ, Thompson SG. By how much and how quickly does reduction in serum cholesterol concentration lower risk of ischaemic heart disease? BMJ 1994;308(6925):367-72.
20. Hawthon K, Cowen P, Owens D, et al. Low serum cholesterol and suicide. Br J Psychiatry 1993;162:818-25.
21. Banga JD. Myotoxicity and rhabdomyolisis due to statins. Ned Tijdschr Geneeskd 2001;145(49):2371-6.
22. Scheen AJ. Fatal rhabdomyolysis caused by cerivastatin. Rev Med Liege 2001;56(8):592-4.
23. Kromhout D. Diet and cardiovascular disease. J Nutr Health Aging 2001;5(3):144-9.
24. Bissonnette F, Lussier-Cacan S, Fugere P, et al. Metabolic effect of two hormonal preparations in postmenopausal women. Maturitas 1997;27(3):275-84.
25. van Vlijmen BJ, van ’t Hof HB, Mol MJ, et al. Modulation of very low density lipoprotein production and clearance contributes to age- and gender- dependent hyperlipoproteinemia in apolipoprotein E3-Leiden transgenic mice. J Clin Invest 1996;97(5):1184-92.
26. Binder EF, Williams DB, Schechtman KB, et al. Effects of hormone replacement therapy on serum lipids in elderly women, a randomized, placebo-controlled trial. Ann Intern Med 2001;134(9 Pt 1):754-60.
27. Regelson W, Loria R, Kalimi M. Hormonal intervention: “buffer hormones” or “state dependency”. The role of dehydroepiandrosterone (DHEA), thyroid hormone, estrogen and hypophysectomy in aging. Ann NY Acad Sci 1988;521:260-73.
28. Ozata M, Yildirimkaya M, Bulur M, et al. Effects of gonadotropin and testosterone treatments on Lipoprotein(a), high density lipoprotein particles, and other lipoprotein levels in male hypogonadism. J Clin Endocrinol Metab 1996;81(9):3372-8.
29. Morales AJ, Nolan JJ, Nelson JC, et al. Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age. J Clin Endocrinol Metab 1994;78(6):1360-7.
30. Gaspard UJ. Evaluation of the cardiovascular impact of hormonal replacement therapy in menopausal women. J Gynecol Obstet Biol Reprod (Paris) 1996;25(7):671-6.
31. Brochier ML, Arwidson P. Coronary heart disease risk factors in women. Eur Heart J 1998;19 Suppl A:A45-52.
32. Blakely JA. The heart and estrogen/progestin replacement study revisited: hormone replacement therapy produced net harm, consistent with the observational data. Arch Intern Med 2000;160(19):2897-900.
33. Erberich LC, Alcantara VM, Picheth G, et al. Hormone replacement therapy in postmenopausal women and its effects on plasma lipid levels. Clin Chem Lab Med 2002;40(5):446-51.
34. Grady D, Herrington D, Bittner V, et al. Cardiovascular disease outcomes during 6.8 years of hormone therapy: Heart and Estrogen/progestin Replacement Study follow-up (HERS II). JAMA 2002;288(1):49-57.
35. Dzugan, S.A., Smith, R.A. Broad spectrum restoration in natural steroid hormones as possible treatment for hypercholesterolemia. Bull Urg Rec Med 2002;3(2):278-84.
36. Dzugan, S.A., Smith, R.A. Hypercholesterolemia treatment: a new hypothesis or just an accident. Med Hypothesis 2002;59(6):751-6.
37. Parini P, Angelin B, Rudling M. Cholesterol and lipoprotein metabolism in aging: reversal of hypercholesterolemia by growth hormone treatment in old rats. Arterioscler Thromb Vasc Biol 1999;19(4):832-9.
38. Lee M-LT, Rosner BA, Weiss ST, et al. Predictors of Cardiovascular Death: The Normative Aging Study – 1963-1998. Clinical Geriatrics 1999;7(9): (www.mmhc.com/cg/articles/CG9909/lee.html).
39. Dzugan, S.A., Smith, R.A. Hypercholesterolemia treatment: a new hypothesis or just an accident. In: Conference of Anti-Aging Therapeutics for the Office-Based Physician & Health Practitioner. Fort Lauderdale, FL USA 2003:139-55.
40. Erkkola R, Viikari J, Irjala K, et al. One-year follow-up of lipoprotein metabolism after pregnancy. Biol Res Pregnancy Perinatol 1986;7(2):47-51.
41. Martin U, Davies C, Hayavi S, et al. Is normal pregnancy atherogenic? Clin Sci (Lond) 1999;96(4):421-5.
42. Loke DF, Viegas OA, Kek LP, et al. Lipid profiles during and after normal pregnancy. Gynecol Obstet Invest 1991;32(3):144-7.
43. Smolarczyk R, Romejko E, Wojcicka-Jagodzinska J, et al. Lipid metabolism in women with threatened abortion. Ginekol Pol 1996;67(10):481-7.
44. Atmaca M, Kuloglu M, Tezcan E, et al. Serum leptin and cholesterol levels in patients with bipolar disorder. Neuropsychobiology 2002;46(4):176-9.
45. Umeki S. Decreases in serum cholesterol levels in advanced lung cancer. Respiration 1993;60(3):178-81.
46. Cassidy F, Carroll BJ. Hypocholesterolemia during mixed manic episodes. Eur Arch Psychiatry Clin Neurosci 2002;252(3):110-4.
47. Boston PF, Dursun SM, Reveley MA. Cholesterol and mental disorder. Br J Psychiatry 1996;169(6):682-9.
48. New AS, Sevin EM, Mitropoulou V, et al. Serum cholesterol and impulsivity in personality disorders. Psychiatry Res 1999;85(2):145-50.
49. Capurso A. Lipid metabolism and cardiovascular risk: should hypercholesterolemia be treated in the elderly? J Hypertens Suppl 1992;10(2):S65-8.
50. Newman TB, Hulley SB. Carcinogenicity of lipid-lowering drugs. JAMA 1996;275(1):55-60.
51. Black DM, Bakker-Arkema RG, Nawrocki JW. An overview of the climical safety profile of atorvastatin (lipitor), a new HMG-CoA reductase inhibitor. Arch Intern Med 1998;158(6):577-84.
52. Wysowski DK, Gross TP. Deaths due to accidents and violence in two recent trials of cholesterol-lowering drugs. Arch Intern Med 1990;150(10):2169-72.
53. Bratus’ VV, Talaieva TV, Lomakovs’kyi OM, et al. Modified lipoproteins--their types and role in atherogenesis. Fiziol Zh 2000;46(2):73-81.
54. Ladeia AM, Guimaraes AC, Lima JC. The lipid profile and coronary artery disease. Arq Bras Cardiol 1994;63(2):101-6.