Prolonged Stabilization of Amyotrophic Lateral Sclerosis (ALS) with a Specially Fermented Soy Product (FSWW08): Case Report and Discussion

Authors

  • Kimberley Goslin Providence Portland Medical Center
  • Adolf E. Schindler Institute for Medical Research and Education
  • Uwe D. Rohr The Vienna Stress Relief Clinic

DOI:

https://doi.org/10.6000/1929-5634.2013.02.01.2

Keywords:

Amyotrophic lateral sclerosis, neuro-degeneration, motor neuron disease, genetics, FSWW08, dyslipidemia, triglyceride, cholesterol

Abstract

Abstract: Amyotrophic lateral sclerosis (ALS) is typically characterized by adult-onset degeneration of the upper and lower motor neurons in mostly male patients, and is usually fatal within 2 to 5 years and is by definition a progressive disease. Only one drug, riluzole, has been approved to treat ALS, which typically provides only a gain of survival of a few months. The exact etiology of ALS isn't known. However most researchers suggest, that ALS increases inflammation and increases cellular stress so that arriving stem cells and local stem cells cannot differentiate into functional nerve cells: ALS shares on a genetic level many similarities with cancer resistance and supports the view that tissue repair and cancer are related. Deteriorating general immunity in nerve cells causes dementia, mental stress, and anxiety. A fermented soy formulation (FSWW08) has been shown to improve local and general immunity in cancer patients and reduces stress on the molecular as well as a clinical level: FSWW08 improved on the genetic molecular level MAP-kinase, c-Jun, and NF-kB, which are impaired in ALS patients. A 50 year old man diagnosed two years ago with ALS in the neck was given one month later over a two year period standard therapy, standard physical care, riluzole anti-inflammatory drugs, oxybutynin for urge incontinence, and additionally FSWW08. Three month before being diagnosed with ALS; the patient suffered from severe mood swings (anxiety disorders but not depression), which were treated by a psychiatrist. The patient complained about severe sleeping disorders at that time. Improvement of mental and physical well-being of FSWW08 was documented by two questionnaires specifically developed for ALS (Amyotrophic Lateral Sclerosis-Frontotemporal Dementia-Questionnaire [ALS-FTD-Q]) and a quality of life questionnaire from the ESQR questionnaires. The progress of local muscle impairment in the neck, which caused the disease, was stopped after 2 month of consumption of FSWW08, as well as breathing being stabilized at a low, but stable levels above the defined level for obstructive disease. Strong on/off fluctuations of ALS symptoms were observed and documented with the consumption of FSWW08, standard medication was continued and had no effect on on/off motor functions of ALS. When the consumption of the FSWW08 was stopped motor dysfunctions of the arms reappeared within two weeks and the patient lost his ability to speak. When consumption of FSWW08 was resumed the disturbances disappeared within 7 days. Additionally it was observed that immune disturbances, hay fever and usual infections during winter, were completely eliminated. Under FSWW08, mental stress and anxiety was reduced, accompanied by a normal sleeping pattern at night and increased energy levels, which caused increased physical activity. Patient reported improved breathing, documented by stable FVW. The patient exhibited a normalization of blood pressure (from pre diagnosed ALS and no consumption of FSWW08, similarly in the off phase, when FSWW08 was not taken) from 170/100 mm HG to 120/80 mm HG under FSWW08 consumption) within seven days, blood lipids were normalized (cholesterol, triglycerides, HDL, LDL). It is reported in the literature that unfavorable blood lipids are related to severity of ALS in Japanese and Western patients. This is the first time stabilization of ALS has been observed accompanied by improvements in blood lipids in patients. This single report corroborates studies conducted with FSWW08 in other diseases including cancer, severe mental diseases (PTSD and Schizophrenia) and severe virus infections. The FDA has granted a general unspecific Health Claim that soy improves blood lipids like cholesterol and triglycerides. This is the first time a fermented soy formulation, FSWW08, has prevent progression of ALS over a two years period and normalized blood lipids. The special fermentation of FSWW08 causes an increase in immunity, cellular stress reduction and blood lipids. Larger clinical trials in ALS patients with FSWW08 are now warranted to investigating whether these results can be confirmed, and whether FSWW08 increases survival, as well as whether blood lipids are a prognostic marker of ALS.

References

[1] Amyotrophic lateral sclerosis. Wikipedia.http://en.wikipedia. org/wiki/Amyotrophic_lateral_sclerosis
[2] Pratt AJ, Getzoff ED, Perry JJ. Amyotrophic lateral sclerosis: update and new developments. Degener Neurol Neuromuscul Dis 2012; 2012(2): 1-14.
[3] Martin LJ, Price AC, Kaiser A, Shaikh AY, Liu Z. Mechanisms for neuronal degeneration in amyotrophic lateral sclerosis and in models of motor neuron death (Review). Int J Mol Med 2000; 5(1): 3-13.
[4] Siddique T, Hu P, Hentati A, Deng G, Hung WY, McInnis MG, et al. A molecular genetic approach to amyotrophic lateral sclerosis. Int J Neurol 1991-1992; 25-26: 60-9.
[5] Wijesekera LC, Leigh PN. Amyotrophic lateral sclerosis. Orphanet J Rare Dis 2009; 4: 3.
http://dx.doi.org/10.1186/1750-1172-4-3
[6] Ince PG, Tomkins J, Slade JY, Thatcher NM, Shaw PJ. Amyotrophic lateral sclerosis associated with genetic abnormalities in the gene encoding Cu/Zn superoxide dismutase: molecular pathology of five new cases, and comparison with previous reports and 73 sporadic cases of ALS. J Neuropathol Exp Neurol 1998; 57(10): 895-904.
http://dx.doi.org/10.1097/00005072-199810000-00002
[7] Ferraiuolo L, Kirby J, Grierson AJ, Sendtner M, Shaw PJ. Molecular pathways of motor neuron injury in amyotrophic lateral sclerosis. Nat Rev Neurol 2011; 7(11): 616-30.
http://dx.doi.org/10.1038/nrneurol.2011.152
[8] Sta M, Sylva-Steenland RM, Casula M, de Jong JM, Troost D, Aronica E, Baas F. Innate and adaptive immunity in amyotrophic lateral sclerosis: evidence of complement activation. Neurobiol Dis 2011; 42(3): 211-20.
http://dx.doi.org/10.1016/j.nbd.2011.01.002
[9] Khandelwal PJ, Herman AM, Moussa CE. Inflammation in the early stages of neurodegenerative pathology. J Neuroimmunol 2011; 238(1-2): 1-11.
http://dx.doi.org/10.1016/j.jneuroim.2011.07.002
[10] Moviglia GA, Varela G, Gaeta CA, Brizuela JA, Bastos F, Saslavsky J. Autoreactive T cells induce in vitro BM mesenchymal stem cell transdifferentiation to neural stem cells. Cytotherapy 2006; 8(3): 196-201.
http://dx.doi.org/10.1080/14653240600735958
[11] Finkelstein A, Kunis G, Seksenyan A, Ronen A, Berkutzki T, Azoulay D, et al. Abnormal changes in NKT cells, the IGF-1 axis, and liver pathology in an animal model of ALS. PLoS One 2011; 6(8): e22374.
http://dx.doi.org/10.1371/journal.pone.0022374
[12] Akhvlediani T, Kvirkvelia N, Shakarishvili R, Tsertsvadze T. Als-like syndrome in the patient with chronic hepatitis C. Georgian Med News 2009; (172-173): 70-2.
[13] Miana-Mena FJ, González-Mingot C, Larrodé P, Muñoz MJ, Oliván S, Fuentes-Broto L, et al. Monitoring systemic oxidative stress in an animal model of amyotrophic lateral sclerosis. J Neurol 2011; 258(5): 762-9.
http://dx.doi.org/10.1007/s00415-010-5825-8
[14] Galan L, Gomez-Pinedo U, Vela-Souto A, Guerrero-Sola A, Barcia JA, Gutierrez AR, et al. Subventricular zone in motor neuron disease with frontotemporal dementia. Neurosci Lett 2011; 499(1): 9-13.
http://dx.doi.org/10.1016/j.neulet.2011.05.019
[15] O'Reilly EJ, Wang H, Weisskopf MG, Fitzgerald KC, Falcone G, McCullough ML, et al. Premorbid body mass index and risk of amyotrophic lateral sclerosis. Amyotroph Lateral Scler Frontotemporal Degener 2012 Oct 29. [Epub ahead of print].
[16] Turner MR, Wotton C, Talbot K, Goldacre MJ. Cardiovascular fitness as a risk factor for amyotrophic lateral sclerosis: indirect evidence from record linkage study. J Neurol Neurosurg Psychiatry 2012; 83(4): 395-8.
http://dx.doi.org/10.1136/jnnp-2011-301161
[17] Moreau C, Brunaud-Danel V, Dallongeville J, Duhamel A, Laurier-Grymonprez L, de Reuck J, et al. Modifying effect of arterial hypertension on amyotrophic lateral sclerosis. Amyotroph Lateral Scler 2012; 13(2): 194-201.
http://dx.doi.org/10.3109/17482968.2011.610110
[18] Ikeda K, Hirayama T, Takazawa T, Kawabe K, Iwasaki Y. Intern Med. Relationships between disease progression and serum levels of lipid, urate, creatinine and ferritin in Japanese patients with amyotrophic lateral sclerosis: a cross-sectional study 2012; 51(12): 1501-8.
[19] Bungener C. Emotions and amyotrophic lateral sclerosis: a psychopathological perspective. Geriatr Psychol Neuropsychiatr Vieil 2012; 10(1): 57-64.
[20] Praline J, Vourc'h P, Guennoc AM, Veyrat-Durebex C, Corcia P. Co-occurrence of progressive anarthria with an S393L TARDBP mutation and ALS within a family. Amyotroph Lateral Scler 2012; 13(1): 155-7.
http://dx.doi.org/10.3109/17482968.2011.598168
[21] Fang F, Chen H, Wirdefeldt K, Ronnevi LO, Al-Chalabi A, Peters TL, et al. Infection of the central nervous system, sepsis and amyotrophic lateral sclerosis. PLoS One 2011; 6(12): e29749. PLoS One 2011; 6(12): e29749.
http://dx.doi.org/10.1371/journal.pone.0029749
[22] Kim DS, Kim JY, Han Y. Curcuminoids in neurodegenerative diseases. Recent Pat CNS Drug Discov 2012; 7(3): 184-204.
http://dx.doi.org/10.2174/157488912803252032
[23] Kastenholz B, Garfin DE. Medicinal plants: a natural chaperones source for treating neurological disorders. Protein Pept Lett 2009; 16(2): 116-20.
http://dx.doi.org/10.2174/092986609787316234
[24] Rohr UD, Li WW, Ziqiang H, Wainright W, Schindler AE. The effect of fermented soy (FSWW08) on blood hematology and cachexia in cancer patients. Horm Mol Biol Clin Invest 2012.
http://dx.doi.org/10.1515/hmbci-2012-0028
[25] Jacob U, Gocan A, Bachg D, Rohr UD. Applikation von fermentierter Soja bei Krebspatienten zur Verminderung von Kachexieund Erhöhung der Apoptose – eine prospektive Pilotstudie. J Gynecol Endokrinol 2009; 19: 18-28.
[26] Gocan AG, Bachg D, Schindler AE, Rohr UD. Managing immunity in resistant cancer patients correlates to survival: resultsand discussion of a pilot study. Horm Mol Biol Clin Invest 2011; 8: 455-69.
[27] Rohr UD, Gocan AG, Bachg D, Schindler AE. Cancer protection ofsoy resembles cancer protection duringpregnancy. Horm Mol Biol Clin Invest 2010; 3: 391-409.
[28] Gocan AG, Bachg D, Schindler AE, Rohr UD. Balancing steroidal hormone cascade in treatment-resistant veteran soldiers with PTSD using a fermented soy product (FSWW08): a pilot study. Horm Mol Biol Clin Invest 2012; 10: 301-14.
[29] Roozendaal B, Kim S, Wolf OT, Kim MS, Sung KK, Lee S. The cortisol awakening response in amyotrophic lateral sclerosis is blunted and correlates with clinical status and depressive mood. Psychoneuroendocrinology 2012; 37(1): 20-6.
http://dx.doi.org/10.1016/j.psyneuen.2011.04.013
[30] Ikeda K, Hirayama T, Takazawa T, Kawabe K, Iwasaki Y. Relationships between disease progression and serum levels of lipid, urate, creatinine and ferritin in Japanese patients with amyotrophic lateral sclerosis: a cross-sectional study. Intern Med 2012; 51(12): 1501-8.
http://dx.doi.org/10.2169/internalmedicine.51.7465
[31] Zoccolella S, Simone IL, Capozzo R, et al. An exploratory study of serum urate levels in patients with amyotrophic lateral sclerosis. J Neurol 2011; 258: 238-43.
http://dx.doi.org/10.1007/s00415-010-5735-9
[32] Qureshi M, Brown RH Jr, Rogers JT, Cudkowicz ME. Serum ferritin and metal levels as risk factors for amyotrophic lateral sclerosis. Open Neurol J 2008; 2: 51-54.
[33] Goodall EF, Haque MS, Morrison KE. Increased serum ferritin levels in amyotrophic lateral sclerosis (ALS) patients. J Neurol 2008; 255: 1652-56.
http://dx.doi.org/10.1007/s00415-008-0945-0
[34] Qureshi M, Cudkowicz ME, Schoenfeld D, et al. Elevated serum ferritin levels correlate with faster disease course in ALS. Neurology 2009; 72(Suppl. 3): A418.
[35] Mitchell RM, Simmons Z, Beard JL, Stephens H, Connor JR. Plasma biomarkers associated with ALS and their relationship toiron homeostasis. Muscle Nerve 2010; 42: 95-103.
http://dx.doi.org/10.1002/mus.21625
[36] Paganoni S, Deng J, Jaffa M, Cudkowicz ME, Wills AM. Body mass index, not dyslipidemia, is an independent predictor of survival in amyotrophic lateral sclerosis. Muscle Nerve 2011; 44: 20-24.
http://dx.doi.org/10.1002/mus.22114
[37] Brooks BR, Miller RG, Swash M, Munsat TL. World federation of neurology research group on motor neuron diseases. El Escorial revisited: revised criteria for the diagnosis of amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord 2000; 1: 293-99.
http://dx.doi.org/10.1080/146608200300079536
[38] Jackson IMD. Effect of prolonged starvation on blood lipid levels of obese subjects. Metabolism 1969; 18: 13-17.
http://dx.doi.org/10.1016/0026-0495(69)90128-0
[39] Suzuki H, Matsuoka M. The JNK/c-Jun signaling axis contributes to the TDP-43-induced cell death. Mol Cell Biochem 2012; [Epub ahead of print].
[40] Ikenaka K, Katsuno M, Kawai K, Ishigaki S, Tanaka F, Sobue G. Disruption of axonal transport in motor neuron diseases. Int J Mol Sci 2012; 13(1): 1225-38.
http://dx.doi.org/10.3390/ijms13011225
[41] Meyerowitz J, Parker SJ, Vella LJ, Ng DCh, Price KA, Liddell JR, et al. C-Jun N-terminal kinase controls TDP-43 accumulation in stress granules induced by oxidative stress. Mol Neurodegener 2011; 6: 57.
http://dx.doi.org/10.1186/1750-1326-6-57
[42] Hossaini M, Cardona Cano S, van Dis V, Haasdijk ED, Hoogenraad CC, Holstege JC, et al. Spinal inhibitory interneuron pathology follows motor neuron degeneration independent of glial mutant superoxide dismutase 1 expression in SOD1-ALS mice. J Neuropathol Exp Neurol 2011; 70(8): 662-77.
http://dx.doi.org/10.1097/NEN.0b013e31822581ac
[43] Seldeen KL, McDonald CB, Deegan BJ, Bhat V, Farooq A. Dissecting the role of leucine zippers in the binding of bZIP domains of Jun transcription factor to DNA. Biochem Biophys Res Commun 2010; 394(4): 1030-5.
http://dx.doi.org/10.1016/j.bbrc.2010.03.116
[44] Kim EK, Choi EJ. Pathological roles of MAPK signaling pathways in human diseases. Biochim Biophys Acta 2010; 1802(4): 396-405.
http://dx.doi.org/10.1016/j.bbadis.2009.12.009
[45] Klein A, He X, Roche M, Mallett A, Duska L, Supko JG, et al. Prolonged stabilization of platinum-resistant ovarian cancer in a single patient consuming a fermented soy therapy. Gynecol Oncol 2006; 100(1): 205-9.
http://dx.doi.org/10.1016/j.ygyno.2005.08.006
[46] Rudrabhatla P, Albers W, Pant HC. Peptidyl-prolyl isomerase 1 regulates protein phosphatase 2A-mediated topographic phosphorylation of neurofilament proteins. J Neurosci 2009; 29(47): 14869-80.
http://dx.doi.org/10.1523/JNEUROSCI.4469-09.2009
[47] Wojda I. MAP kinase pathways--their evolution and role in some neurodegenerative diseases. Postepy Biochem 2012; 58(1): 79-90.
[48] Freedman DM, Curtis RE, Daugherty SE, Goedert JJ, Kuncl RW, Tucker MA. The association between cancer and amyotrophic lateral sclerosis. Cancer Causes Control 2013; 24(1): 55-60.
http://dx.doi.org/10.1007/s10552-012-0089-5
[49] Tanaka F, Niwa J, Ishigaki S, Katsuno M, Waza M, Yamamoto M, et al. Gene expression profiling toward understanding of ALS pathogenesis. Ann NY Acad Sci 2006; 1086: 1-10.
http://dx.doi.org/10.1196/annals.1377.011
[50] Kudo LC, Parfenova L, Vi N, Lau K, Pomakian J, Valdmanis P, et al. Integrative gene-tissue microarray-based approach for identification of human disease biomarkers: application to amyotrophic lateral sclerosis. Hum Mol Genet 2010; 19(16): 3233-53.
http://dx.doi.org/10.1093/hmg/ddq232
[51] Ringer C, Weihe E, Schütz B. Calcitonin gene-related peptide expression levels predict motor neuron vulnerability in the superoxide dismutase 1-G93A mouse model of amyotrophic lateral sclerosis. Neurobiol Dis 2012; 45(1): 547-54.
http://dx.doi.org/10.1016/j.nbd.2011.09.011
[52] Cedarbaum JM, Stambler N, Malta E, Fuller C, Hilt D, Thurmond B, et al. The ALSFRS-R: a revised ALS functional rating scale that incorporates assessments of respiratory

function. BDNF ALS Study Group (Phase III). J Neurol Sci 1999; 169(1-2): 13-21.
http://dx.doi.org/10.1016/S0022-510X(99)00210-5
[53] Raaphorst J, Beeldman E, Schmand B, Berkhout J, Linssen WH, van den Berg LH, et al. The ALS-FTD-Q: a new screening tool for behavioral disturbances in ALS. Neurology 2012; 79(13): 1377-83.
http://dx.doi.org/10.1212/WNL.0b013e31826c1aa1
[54] Ravasco P, Monteiro-Grillo I, Marques Vidal P, Camilo ME. Impact of nutrition on outcome: a prospective randomized controlled trial in patients with head and neck cancer undergoing radiotherapy. Head Neck 2005; 27(8): 659-68.
http://dx.doi.org/10.1002/hed.20221
[55] Swanney MP, Ruppel G, Enright PL. Using the lower limit of normal for the FEV1/FVC ratio reduces the misclassification of airway obstruction. Thorax 2008; 63(12): 1046-51.
http://dx.doi.org/10.1136/thx.2008.098483
[56] Sahebjami H, Gartside PS. Pulmonary function in obese subjects with a normal FEV1/FVC ratio. Chest 1996; 110(6): 1425-9.
http://dx.doi.org/10.1378/chest.110.6.1425
[57] Mac Sweeney R, McAuley DF, Matthay MA. Acute lung failure. Semin Respir Crit Care Med 2011; 32(5): 607-25.
http://dx.doi.org/10.1055/s-0031-1287870
[58] Militello A, Vitello G, Lunetta C, Toscano A, Maiorana G, Piccoli T, et al. The serum level of free testosterone is reduced in amyotrophic lateral sclerosis. J Neurol Sci 2002; 195(1): 67-70.
http://dx.doi.org/10.1016/S0022-510X(01)00688-8
[59] Fowler B. Homocystein--an independent risk factor for cardiovascular and thrombotic diseases. Ther Umsch 2005; 62(9): 641-6.
http://dx.doi.org/10.1024/0040-5930.62.9.641
[60] Klack K, Bonfa E, Borba Neto EF. Diet and nutritional aspects in systemic lupus erythematosus. Rev Bras Reumatol 2012; 52(3): 384-408.
[61] Ceprnja M, Derek L, Uni? A, Blazev M, Fistoni? M, Kozari?-Kovaci? D, et al. Oxidative stress markers in patients with post-traumatic stress disorder. Coll Antropol 2011; 35(4): 1155-60.
[62] Yang Y, Mauldin PD, Ebeling M, Hulsey TC, Liu B, Thomas MB, et al. Effect of metabolic syndrome and its components on recurrence and survival in colon cancer patients. Cancer 2012.
http://dx.doi.org/10.1002/cncr.27923
[63] Albert SM. Dyslipidemia in ALS: good, bad, or unclear? Neurology 2008; 70(13): 988-9.
http://dx.doi.org/10.1212/01.wnl.0000306636.61882.42
[64] Lisch HJ, Bolzano K, Herbst M, Sailer S, Sandhofer F, Braunsteiner H. Effect of body weight changes on plasma lipids in patients with primary hyperlipoproteinemia. Atherosclerosis 1974; 19(3): 477-84.
http://dx.doi.org/10.1016/S0021-9150(74)80013-4
[65] Dattilo AM, Kris-Etherton PM. Effect of body weight changes on plasma lipids-A metaanalysis. Am J Clin Nutr 1992; 56: 308-14.
[66] Loria RM. Immune up-regulation and tumor apoptosis by androstene steroids. Steroids 2002; 67(12): 953-66.
http://dx.doi.org/10.1016/S0039-128X(02)00043-0
[67] Xiao CW. Health effects of soy protein and isoflavones in humans. J Nutr 2008; 138(6): 1244S-9S.
[68] Ma L, Grann K, Li M, Jiang Z. A pilot study to evaluate the effect of soy isolate protein on the serum lipid profile and other potential cardiovascular risk markers in moderately hypercholesterolemic Chinese adults. Ecol Food Nutr 2011; 50(6): 473-85.
http://dx.doi.org/10.1080/03670244.2011.620875
[69] Cubeddu LX, Hoffmann IS. Metabolic syndrome: an all or none or a continuum load of risk? Metab Syndr Relat Disord 2012; 10(1): 14-9.
http://dx.doi.org/10.1089/met.2011.0058
[70] Weinstock-Guttman B, Zivadinov R, Mahfooz N, Carl E, Drake A, Schneider J, et al. Serum lipid profiles are associated with disability and MRI outcomes in multiple sclerosis. J Neuroinflammation 2011; 8: 127.
http://dx.doi.org/10.1186/1742-2094-8-127
[71] Klack K, Bonfa E, Borba Neto EF. Diet and nutritional aspects in systemic lupus erythematosus. Rev Bras Reumatol 2012; 52(3): 384-408.
[72] Von Känel R, Kraemer B, Saner H, Schmid JP, Abbas CC, Begré S. Posttraumatic stress disorder and dyslipidemia: previous research and novel findings from patients with PTSD caused by myocardial infarction. World J Biol Psychiatry 2010; 11(2): 141-7.
http://dx.doi.org/10.3109/15622970903449846
[73] Soreca I, Wallace ML, Frank E, Hasler BP, Levenson JC, Kupfer DJ. Sleep duration is associated with dyslipidemia in patients with bipolar disorder in clinical remission. J Affect Disord 2012; 141(2-3): 484-7.
http://dx.doi.org/10.1016/j.jad.2012.01.046
[74] Watanabe J, Suzuki Y, Someya T. Lipid effects of psychiatric medications. Curr Atheroscler Rep 2013; 15(1): 292.
http://dx.doi.org/10.1007/s11883-012-0292-6
[75] P?str?igu? C, Ancu?a C, Miu S, Ancu?a E, Chirieac R. Knee osteoarthritis, dyslipidemia syndrome and exercise. Rev Med Chir Soc Med Nat Iasi 2012; 116(2): 481-6.
[76] Wainright WH. Not all soy products are created equal: interpretation of research results diffi cult. Townsend Lett 2008; 16: 487-96.
[77] Saijo K, Collier JG, Li AC, Katzenellenbogen JA, Glass CK. An ADIOL-ER?-CtBP transrepression pathway negatively regulates microglia-mediated inflammation. Cell 2011; 145: 584-95.
http://dx.doi.org/10.1016/j.cell.2011.03.050
[78] Norata GB, Cattaneo P, Poletti A, Catapano AL. The androgen derivative 5alpha-androstane-3beta,17-diol inhibits tumor necrosis factor alpha and lipopolysaccharide induced inflammatory response in human endothelial cells and in mice aorta. Artheriosclerosis 2010; 212: 100-106.
[79] Esposito K, Chiodinin P, Capuano A, Belasstella G, Majorino MI, Paretta E, et al. Effect of metabolic syndrome and its components on prostate cancer risk: Meta-analysis. Endocrinol Invest 2013; 36: 132-9.
[80] Yang Y, Mauldin PD, Ebeling M, Hulsey TC, Liu B, Thomas MB, et al. Effect of metabolic syndrome and its components on recurrence and survival in colon cancer patients. Cancer 2012.
http://dx.doi.org/10.1002/cncr.27923

Downloads

Published

2013-03-31

Issue

Section

Articles