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Originally posted by thedoctorswife
One question, are you a parent, if you are then i concede.
Originally posted by thedeadtruth
reply to post by intrepid
Humans have been raising kids for a pretty long time.
But widespread obesity is only a new problem.
Explain to me again how being a parent makes you fat ?
Deny ignorance indeed.
Originally posted by BlackOps719
reply to post by David_Reale
I have a theory to that extent as well, even though Im not sure it is correct.
I believe that the harder one's ancestors had to work to eat and struggle to survive, the more likely it is that obesity is prevelant in the gene pool.
Some people just gain weight and their body holds on to every pound like it will be its last, where as some metabolize calories quickly. I think part of it stems from that working poor starving man syndrome, that chromosome in our bodies that can still remember going without food for days on end in harsh conditions.
Also it explains how some can be sedentary and gain weight quickly, because their recent lineage has been that of hard physical work and physical struggle. Since we arent out chasing animals, moving rocks or plowing fields with our bare hands any longer, those calories stick to us and turn to fat, where as before they would have been easily burned in day to day struggles.
Ever notice how certain ethnic groups seem to gain weight and are just larger in general than many others.
I blame my bastardized Scotish / Viking heritage. We are big people in my family. Not necessarily fat, just large framed, tall, sturdy people.
Some cultures I attribute it to poor diet and high carb eating habits, like hispanic culture for example. Everything made of beans and rice and flower, hence the tendency for obesity. Same with white southern culture, same with black culture, lots of fried foods, rich butter based sauces, too much fat and sugar.
But I do believe genetics plays a big part.
Originally posted by Liamoville
The funny thing about this is, i'm English and i spent 4 months over in the States this summer and i actually didn't see that many fat people. Occasionally i would see some HUGELY obese person but i wouldn't see it regularly.
Both obesity and heart disease are epidemic in the USA, causing widespread stroke and early death. A virus may cause obesity says one study; another links obesity to heart disease. Different research links heart disease to pollution. Earlier studies show chronic infections play a role in heart disease and stroke - and the EPA links obesity to genetic mutations caused by exposure to environmental chemicals during pregnancy. It's all true, says the new science paradigm. Going well beyond old-science assumptions of simple cause-and-effect, the new paradigm says modern diseases are interconnected, and result from the interaction of multiple factors like infections, pollution and new genetic mutations caused by both.
Links between obesity and prion-related diseases like Mad Cow were made some time ago. Prion diseases are known to make fat cells or "lipids" mutate, but no one quite understands how it all works. Research presented at the recent Biochemical Society Symposium helps unravel the mystery.
A key molecular event in prion diseases is the conversion of PrP (prion protein) from its normal cellular form (PrP(c)) into the disease-specific form (PrP(Sc)). The transition from PrP(c) to PrP(Sc) involves a major conformational change, resulting in amorphous aggregates and/or fibrillar amyloid deposits. Here, we review several lines of evidence implicating membranes in the conversion of PrP, and summarize recent results from our own work on the role of lipid membranes in conformational transitions of prion proteins. By establishing new correlations between in vivo biological findings with in vitro biophysical results, we propose a role for lipid rafts in prion conversion, which takes into account the structural heterogeneity of PrP in different lipid environments.
Biochem Soc Symp. 2005;(72):211-22. Lipids, Rafts and Traffic: Chapter 20 - Aggregation and fibrillization of prions in lipid membranes. Kazlauskaite J, Pinheiro TJ. Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, U.K. PMID: 15649144
Hyperinsuline mia induced by canine distemper virus infection of mice and its correlation with the appearance of obesity. Comp Biochem Physiol B. 1988;91(4):691-6. Bernard A, Zwingelstein G, Meister R, Wild TF. Unite de Virologie Fondamentale et Appliquee, INSERM U.51, CNRS UA 613 Lyon, France.
1. Weanling Swiss mice surviving an acute infection with canine distemper virus were persistently infected. Among these mice, up to 30% had hyperinsulinemia and this was followed by an obesity syndrome. 2. Analysis of the lipid composition of various organs revealed that compared to control animals, the obese had an accumulation of triglycerides in both liver and adipose tissue. 3. Studies on the lipid metabolism using a number of radioactive lipid precursors showed a specific accumulation of the triglycerides of the obese animals. 4. A decrease of lipogenesis was observed in white adipose tissue of obese mice. Glycogenesis and serum glucose levels were unaffected during obesity. 5. The model of canine distemper virus-induced obesity is compared with other experimental models.
Distribution of Borna disease virus in the brain of rats infected with an obesity-inducing virus strain. Brain Pathol. 2000 Jan;10(1):39-48. Herden C, Herzog S, Richt JA, Nesseler A, Christ M, Failing K, Frese K. Institut fur Virologie, Justus-Liebig-Universitat Giessen, Germany.
Experimental infection of Lewis rats with Borna disease virus (BDV), a nonsegmented, single-stranded RNA virus, usually causes an immune-mediated biphasic neurobehavioral disorder. Such animals develop a persistent infection of the CNS with viral antigen expression in all brain regions and a disseminated nonpurulent meningoencephalitis. Interestingly, intracerebral infection of Lewis rats with a BDV-variant (BDV-ob) causes a rapid increase of body weight with the development of an obesity syndrome without obvious neurological signs. The obese phenotype is correlated with a characteristic distribution of inflammatory lesions and BDV-antigen in the rat brain. Infiltration with mononuclear immune cells and viral antigen expression are restricted to the septum, hippocampus, amygdala and ventromedian tuberal hypothalamus. Therefore, infection with the obesity-inducing BDV-ob results most likely in neuroendocrine dysregulations leading to the development of an obesity syndrome. This might be due to the restriction of viral antigen expression and inflammatory lesions to brain areas which are involved in the regulation of body weight and food intake. The BDV-induced obesity syndrome represents a model for the study of immune-mediated neuroendocrine disorders caused by viral infections of the CNS.
Infectobesi ty: obesity of infectious origin. J Nutr. 2001 Oct;131(10):2794S-2797S. Dhurandhar NV. The Department of Nutrition and Food Science and the Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 48202, USA. email@example.com
In the U.S., the prevalence of obesity increased by 30% from 1980 to 1990, and this increase appears to be continuing. Although obesity has multiple etiologies, an overlooked possibility is obesity of an infectious origin. Six pathogens are reported to cause obesity in animals. Canine distemper virus was the first virus reported to cause obesity in mice, followed by Rous-associated virus-7, an avian retrovirus, which has been shown to cause stunting, obesity and hyperlipidemia in chickens. Next, the obesity-promoting effect of Borna disease virus was demonstrated in rats. Scrapie agents were reported to induce obesity in mice and hamsters. The final two reports were of SMAM-1, an avian adenovirus, and Ad-36, a human adenovirus that caused obesity in animals. Additionally, an association with human obesity is the unique feature of SMAM-1 and Ad-36. Although the exact mechanism of pathogen-induced obesity is unclear, infection attributable to certain organisms should be included in the long list of potential etiological factors for obesity. In addition, the involvement of some pathogens in etiology of obesity suggests the possibility of a similar role for additional pathogens.
Alteration of the leptin network in late morbid obesity induced in mice by brain infection with canine distemper virus. J Virol. 1999 Sep;73(9):7317-27. Bernard A, Cohen R, Khuth ST, Vedrine B, Verlaeten O, Akaoka H, Giraudon P, Belin MF. INSERM U433, Neurobiologie Experimentale et Physiopathologie, Faculte de Medecine RTH Laennec, 69372 Lyon Cedex 08, France. firstname.lastname@example.org
Viruses can induce progressive neurologic disorders associated with diverse pathological manifestations, and therefore, viral infection of the brain can impair differentiated neural functions, depending on the initial viral tropism. We have previously reported that canine distemper virus (CDV) targets certain mouse brain structures, including the hypothalamus, early and selectively. Infected mice exhibit acute encephalitis, with late disease, characterized by motor impairment or obesity syndrome, appearing in some of the surviving mice several months after the initial viral replication. In the present study, we show viral persistence in the hypothalami of obese mice, as demonstrated by low, but still significant, levels of CDV nucleoprotein transcripts, associated with a dramatic decrease in F gene mRNAs. Given the pivotal role of the hypothalamus in obesity (eating behavior, energy consumption, and neuroendocrine function) and that of leptin, the adipose tissue-derived satiety factor acting through hypothalamic receptors, we analyzed the leptin networks in both obese and nonobese mice. The discrepancy found between the chronic and dramatic increase in blood leptin levels and the occurrence of obesity may be due to leptin resistance in the brain. In fact, expression of the long leptin receptor isoform, representing the functional leptin receptor, was specifically downregulated in the hypothalami of obese mice, explaining their inability to generate an adequate response to leptin in the brain. Intriguingly, during the acute phase of infection, its expression was increased in CDV-targeted structures in all infected mice and remained high in obese mice in all CDV-targeted structures, except for the hypothalamus. The biphasic change in hypothalamic leptin receptor expression seen during the progression of CDV-induced obesity provides a new paradigm for understanding mechanisms of neuroendocrinological, virus-induced abnormalities.
Also worth looking for:
Virus-induced obesity. Am J Physiol Regul Integr Comp Physiol. 2006 Jan;290(1):R188-9. Greenway F. PMID: 16352860 (No Abstract)