Xenogamy and Current Obesity Pandemics
Author(s)
Sergey N. Rumyantsev
ABSTRACT
This article unites the results from an integrative reconsideration of actual data about obesity from the viewpoint of recent developments in general pathology, epidemiology, immunology, genetics, and evolution. The focus is on the origin of genetic diversity in obesity manifestations on different levels of the disease. In contrast to the current paradigm of nutritive origin of obesity, the revealed set of evidences shows that the origin of obesity is based on either hereditary or post-infectious incongruence between the regulators of fat metabolism and their receptors. The incongruence may be created either by the destruction of receptors during infection or by genome mutations, which by natural selection, lead both to life-saving incongruence between the infectious agent and its receptor, and simultaneously, in evolution to a life-threatening obesogenic incongruence in the regulator-receptor interaction. The pandemic spread of obesity is induced by xenogamous intercourse between constitutionally incongruent ethnoses, which regulator-receptor evolution has processed at different epidemic conditions. The achieved results have allowed a replenish model for the molecular pathogenesis of obesity to explain the genetics of both obesity and its pandemic spread. The formerly maladroit issues of obesity origin, genetic, pathogenesis, and pandemic spread are transformed in an entire replenished system.
This article unites the results from an integrative reconsideration of actual data about obesity from the viewpoint of recent developments in general pathology, epidemiology, immunology, genetics, and evolution. The focus is on the origin of genetic diversity in obesity manifestations on different levels of the disease. In contrast to the current paradigm of nutritive origin of obesity, the revealed set of evidences shows that the origin of obesity is based on either hereditary or post-infectious incongruence between the regulators of fat metabolism and their receptors. The incongruence may be created either by the destruction of receptors during infection or by genome mutations, which by natural selection, lead both to life-saving incongruence between the infectious agent and its receptor, and simultaneously, in evolution to a life-threatening obesogenic incongruence in the regulator-receptor interaction. The pandemic spread of obesity is induced by xenogamous intercourse between constitutionally incongruent ethnoses, which regulator-receptor evolution has processed at different epidemic conditions. The achieved results have allowed a replenish model for the molecular pathogenesis of obesity to explain the genetics of both obesity and its pandemic spread. The formerly maladroit issues of obesity origin, genetic, pathogenesis, and pandemic spread are transformed in an entire replenished system.
Cite this paper
nullRumyantsev, S. (2011) Xenogamy and Current Obesity Pandemics. Open Journal of Genetics, 1, 1-8. doi: 10.4236/ojgen.2011.11001.
nullRumyantsev, S. (2011) Xenogamy and Current Obesity Pandemics. Open Journal of Genetics, 1, 1-8. doi: 10.4236/ojgen.2011.11001.
References
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Rev sci tech Off int Epiz 1998; 17(1): 26-42. [40] So PW, Herlihy AH, Bell JD. Adiposity induced by adenovirus 5 inoculation. Int JObes (Lond) 2005; 29: 603- 606. [41] Stunkard AJ, Harris JR, Pedersen NL, et al. The body- mass index of twins who have been reared apart. N Engl J Med 1990; 322: 1483-1487. [42] The Australian and New Zealand Obesity Society. Prevalence of Obesity in Several Countries Worldwide. 2009. International Obesity Task Force. [43] Vangipuram SD, Sheel J, Atkinson RL, et al. A human adenovirus enhances preadipocyte differentiation. Obes Res 2004; 12: 770-777. [44] Vavilov NI. Immunity of plants to infectious diseases (In Russian). Moscow-Leningrad: Nauka, 1964. [45] Whigham LD, Israel BA, Atkinson RL. Adipogenic potential of multiple human adenoviruses in vivo and in vitro in animals. Am J Physiol Regul Integr Comp Physiol 2006; 290: R190-R194.
[1] [1] Obesity and overweight. Global Strategy on Diet, Physical Activity and Health. World Health Organization, 2010:http://www.who.int/dietphysicalactivity/publications/facts/obesity/en/. [2] Allison DB, Edlen-Nezin L, Clay-Williams G. Obesity among African American women: prevalence, conseque- nces, causes, and developing research Womans Health. Nature 1997; 33: 243-274. [3] Altrock BW, Arthur LO, Massei RJ, et al. Common surface receptors on both mouse and rat cells distinguish different classes of mouse mammary tumor viruses. Virology 1981; 109: 257-259. [4] Atkinson RL, Dhurandhar NV, Allison DB, et al. Human adenovirus-36 is associated with increased body weight and paradoxical reduction of serum lipids. Int J Obes (Lond) 2005; 29: 281-286. [5] Atkinson RL, Whigham LD, Kim C, et al. . Evaluation of human adenoviruses as an etiology of obesity in chickens. Int J Obes 2001; 25 (Suppl. 2): S12. [6] Boizard M, Le Liepvre X, Lemarchand P, et al. Obesity- related Overexpression of Fatty-acid Synthase Gene in Adipose Tissue Involves Sterol Regulatory Element- binding Protein Transcription Factors. J Biol Chem 1998; 273(44): 29164-71 [7] Carbone KM, Luftig RB, Buckley MR. Microbial Triggers of Chronic Human Illness. Washington, DC, USA: American Academy of Microbiology, 2005 [8] CDC. Overweight and Obesity. Centres for Diseases Control and Prevention, 2010. [9] Coop G, Pickrell JK, Novembre J, et al. The Role of Geography in Human Adaptation. PLoS Genet 2009; 5(6). [10] Enegren BJ, Burness ATH. Chemical structure of attachment sites for viruses on human erythrocytes. Nature 1977; 268: 536-537. [11] Farooqi IS. Partial leptin deficiency and human adiposity. Nature 2001; 414: 34-35. [12] Fernandez JR, Allison DB. Understanding racial differences in obesity and metabolic syndrome traits. Nutr Rev 61[9], 316-9. 2003. [13] Flegal KM, Carroll MD, Kuczmarski RJ, et al. Overweight and obesity in the United States: prevalence and trends, 1960-1994. Int J Obes Relat Metab Disord 1998; 22(1): 39-47. [14] Flier JS. Obesity wars: Molecular progress confronts an expanding epidemic. Cell 2004; 116(2): 337-350. [15] Friedman JM. Modern science versus the stigma of obesity. Nature Medicine 2004; 10(6): 563-569. [16] Friedman JM, Halaas JL. Leptin and the regulation of body weight in mammals. 396, 763-770. 1998. Nature 1998; 396: 763-770. [17] Gabbert C, Donohue M, Arnold J, et al. Adenovirus 36 and Obesity in Children and Adolescents. Pediatrics 2010; 126: 721-726. [18] Habbu A, Lakkis NM, Dokainish H. The obesity paradox: Fact or fiction?”. Am J Cardiol 2006; 98(7): 944-948. [19] Hamann A, Matthaei S. Regulation of energy balance by leptin. Exp Clin Endocrinol Diabetes 1996; 104(4): 293- 300. [20] Jondal M, Klein G, Oldstone MBA, et al. Association between complement and Epstein-Barr virus receptors on human lymphoid cells. Scand J Immunol 1976; 5: 401 -410. [21] Ledley FD, Mullin BR, Aloj SM, et al. Sequence similarity between cholera toxin and glycoprotein hormones: implications for structure activity relationship and mechanism of action. Biochem Biophys Res Commun 1976; 69: 852-9 [22] Lee G, Consiglio E, Habig W, et al. Structure:function studies of receptor for thyrotropin and tetanus toxin: Lipid modulation of effector binding to the glycoprotein receptor component. Biochem Biophys Res Commun 1978; 83: 313-20 [23] Lindback SM, Gabbert C, Johnson BL, et al. Pediatric nonalcoholic fatty liver disease: a comprehensive review. Adv Pediatr 2010; 57(1): 85-140 [24] Mokdad AH, Ford ES, VF, et al. . The continuing epidemics of obesity and diabetes in the United States. JAMA 2001; 286(10): 1195-200 [25] Montague CT, Farooqi IS, Whitehead JP, et al. Congenital leptin deficiency is associated with severe early-onset obesity in humans. Nature 1997; 387: 903-8 [26] Nagashima K, Zabriskie JB, Lyons MJ. Virus-induced obesity in mice: association with a hypothalamic lesion. J Neuropathol Exp Neurol 1992; 51: 101-9 [27] Novembre J, Stephens M. Interpreting principal component analyses of spatial population genetic variation. Nat Genet 2008; 40(5): 646-649. [28] Paxton W.A., Martin S.R., Tse D., et al. Relative resistance to HIV-1 infection of CD4 lymphocytes from persons who remain uninfected dispite multiple high-risk sexual exposure. Nat Med 1996; 2: 412-417. [29] Popovic M, Sarin PS, Robert-Gurroff M, et al. Isolation and transmission of human retrovirus (human T-cell leukemia virus). Science 1983; 219: 856-9 [30] Robson H.G., Vas S.I. Resistance of inbred mice to Salmonella typhimurium. J Infect Dis 1972; 126(4): 378- 386. [31] Rumyantsev S.N. Structural predestination of individual diversity in the course and severity of infectious diseases. TheScientificWorldJOURNAL 2002; 2: 205-216. [32] Rumyantsev SN. The intra-individual diversity in sene- scence. Biogerontology 2003; 4: 171-178. [33] Rumyantsev SN. Constitutional immunity and its molecular-ecological principles [in Russian]. Leningrad: Nauka, 1983. [34] Rumyantsev SN. The origin of individual differences in the course and severity of diseases. TheScientific World JOURNAL 2006; 6: 1674-1704. [35] Rumyantsev SN. Obesity: a reckoning both for genetic immunity to infection and xenogamy. Medical Hypothesis 2006; 66: 535-540 [36] Rumyantsev SN. Reasons of the strength and duration of post-infectious immunity. J Chin Clin Med 2007; 2(5): 273-281. [37] Rumyantsev SN. Hereditary Immunity: Fundamental Principles and Exploitation in Life Study and Health Care. New York: Nova Biomedical Books, 2008. [38] Rumyantsev SN, Gerasimov VK. The Origin and Functions of Biodiversity in Infectious and Non- Infectious Diseases. In: Schwartz J, ed. Focus on Biodi- versity Research. Nova Science Publishers, 2007: 199- 300 [39] Rumyantsev SN. Constitutional and non-specific immu- nity to infection. Rev sci tech Off int Epiz 1998; 17(1): 26-42. [40] So PW, Herlihy AH, Bell JD. Adiposity induced by adenovirus 5 inoculation. Int JObes (Lond) 2005; 29: 603- 606. [41] Stunkard AJ, Harris JR, Pedersen NL, et al. The body- mass index of twins who have been reared apart. N Engl J Med 1990; 322: 1483-1487. [42] The Australian and New Zealand Obesity Society. Prevalence of Obesity in Several Countries Worldwide. 2009. International Obesity Task Force. [43] Vangipuram SD, Sheel J, Atkinson RL, et al. A human adenovirus enhances preadipocyte differentiation. Obes Res 2004; 12: 770-777. [44] Vavilov NI. Immunity of plants to infectious diseases (In Russian). Moscow-Leningrad: Nauka, 1964. [45] Whigham LD, Israel BA, Atkinson RL. Adipogenic potential of multiple human adenoviruses in vivo and in vitro in animals. Am J Physiol Regul Integr Comp Physiol 2006; 290: R190-R194.