What are the obesity hypotheses, who are the proponents/authors and optionally what are their best works on the subject? Which hypothesis/hypotheses do you subscribe to?
Carbohydrate / Insulin Hypothesis - Gary Taubes
The Food Reward Hypothesis - Stephan Guyenet
Multipart series on his blog.
Hypothalamic Hypothesis of Obesity - Todd Becker
Obesity System Influence via the UK's Tackling Obesities project. Thank You Beth-WeightMaven for the below chart and info.
Calories in, Calories out - Colpo
Malnourishment - Paul Jaminet
Microbe theory of metabolic syndrome
http://flare8.net/health/doku.php/diseases#microbes1 (reference sources therein):
Excitotoxin theory of obesity likely traced to: Dr. Blaylock
asked byEric_12 (20378)
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on February 07, 2012
at 02:20 PM
on February 07, 2012
at 07:15 PM
Microbe theory of metabolic syndrome, via http://flare8.net/health/doku.php/diseases#microbes1 (reference sources therein):
Metabolic syndrome (MetS) has microbes:
17% of morbidly obese have small intestinal bacterial overgrowth syndrome 182) and circulating LPS (a type of endotoxin) is 76% higher in type 2 diabetics compared to controls 183). Herpes simplex 1 (a virus) concentrations correlate with percentage fat mass 184). HSV-2 is negatively associated with insulin sensitivity after controlling for BMI, age, and CRP 185). Genetically obese (leptin deficient) mice have enhanced intestinal permeability which leads to increased endotoxin levels 186). The microbiota of type 2 diabetic mice 187) and obese mice 188) and humans 189) 190) 191) are significantly different from their lean counterparts.
Inundation with microbes cause MetS:
Mice deficient in certain immune-fighting functions have altered gut flora and develop metabolic syndrome 192).
Transferring an obese mouse's gut flora to germ-free mice causes obesity in the colonized mice 193) 194).
Microbe actions can cause MetS:
In ob/ob mice, blocking or enhancing CB1 can cause an 88% decrease or 100% increase in plasma LPS, respectively, likely via modulation of gut barrier function. CB1 expression in mice can be decreased -25% by prebiotics, -60% by antibiotics, and increased 160% by a 'high fat' lab diet (but only by 60% if the HFD includes prebiotics) 195). Altering mice gut microbiotas via prebiotics and probiotics can significantly modulate intestinal permeability 196) 197).
- CB1 receptor knockout mice: protected from diet-induced obesity, despite similar caloric intakes as mice who do become obese 198) 199).
- CB1 blocker in diet-induced obese mice: -50% reduction in adiposity, correction of insulin resistance and lowered plasma leptin levels 200) 201).
- CB1 blocker in obese monkeys: -23% reduction in food intake, bodyfat by -39%, leptin by -34% (pair fed animals did not experience improvements) 202).
- CB1 blocker in humans: 4.7 kg greater weight loss over 1 year, compared to placebo 203).
The CB1 receptor can significantly modulate drug and palatable food seeking behavior in mice 204) 205) 206), including sugar 207) 208), chocolate 209), 'emotional behavior' 210), anxiety, stress and depressive-like behavior 211). CB1 blocking reduces reward seeking in rats 212) 213). CB1 receptors are densely expressed in neurons expressing dopamine D1 receptors 214).
Continuously injecting lipopolysaccharid (LPS) into mice, at levels that mimic the endotoxemia seen in metabolic-syndrome mice, causes glucose levels, insulin levels, and weight gain similar to 'high-fat' fed mice 215). Continuous LPS can cause insulin resistance in cats 216). A single LPS injection can cause a 100% increase in serum leptin levels and 44% increase in triglycerides 217).
Inflammation within adipose tissue occurs during obesity 218), and interrupting this inflammation prevents metabolic abnormalities 219). Continuously injecting humans with endotoxin can cause a 35% decline in insulin sensitivity, and increases adipose tissue inflammation 220) 221). Low doses of endotoxin in many ways dramatically increase inflammation in humans 222) 223) 224) 225).
"In conclusion???we found that metabolic concentrations of plasma LPS are a sufficient molecular mechanism for triggering the high-fat diet???induced metabolic diseases obesity/diabetes." 226)
Alleviating microbes ameliorates MetS:
Mice lacking LPS detectors resist both LPS and 'high-fat' diet-induced metabolic syndrome 227) 228) 229).
In two different mouse models of insulin resistance, antibiotic treatment caused a -36% decrease in plasma LPS and a significant -18% to -42% decrease in glucose levels 230), and effectively reverses metabolic syndrome in ob/ob and diet-induced obese mice, despite increased food intake 231) 232).
Germ free mice fed a 'high fat' lab diet are resistant to diet-induced obesity 233) 234) 235).
- "four viruses have been reported to induce obesity (infectoobesity) in animal models (chickens, mice, sheep, goat, dogs, rats and hamsters)??? In a series of papers over the last ten years, however, the group of Prof. Dhurandhar (Pennington Biomedical Research Center, LA, USA) demonstrated that a human adenovirus, adenovirus-36 (Ad-36), is capable of inducing adiposity in experimentally infected chickens, mice and non-human primates (marmosets). Ad-36 is known to increase the replication, differentiation, lipid accumulation and insulin sensitivity in fat cells and reduces those cells' leptin secretion and expression. It also affects human primary preadipocytes. In rats increased adiposity was observed due to Ad-36 infection. Recent studies have shown that, in the USA, antibodies to Ad-36 were more prevalent in obese subjects (30%) than in non-obese subjects (11%)." 236)
- "This review discusses the 5 animal viruses and 3 human viruses that have been shown to cause obesity??? The first 4 viruses attack the central nervous system to produce obesity. SMAM-1, an avian adenovirus from India, acts directly on adipocytes and is the only animal virus that is associated with human obesity. The 3 human adenoviruses, adenovirus (Ad) 36, Ad-37, and Ad-5, that are associated with obesity also affect adipocytes directly. These viruses stimulate enzymes and transcription factors that cause accumulation of triglycerides and differentiation of preadipocytes into mature adipocytes. Ad-5 and Ad-37 have been shown to cause obesity in animals. Ad-36 has been studied the most and is the only human adenovirus to date that has been linked with human obesity. Ad-36 causes obesity in chickens, mice, rats, and monkeys and was present in 30% of obese humans and 11% of nonobese humans. In twins discordant for infection with Ad-36, the infected twins were heavier and fatter than their cotwins. The growing body of evidence demonstrating that viruses produce human obesity supports the concept that at least some of the worldwide epidemic of obesity in the past 25 years is due to viral infections." 237)
- "We previously reported that human adenovirus Ad-36 induces adiposity??? To evaluate the transmissibility of Ad-36 and Ad-36 induced adiposity using a chicken model??? As seen in experiment 1, Ad-36 infection can be transmitted horizontally from an infected chicken to another chicken sharing the cage. Additionally, experiment 2 demonstrated blood-borne transmission of Ad-36-induced adiposity in chickens. Transmissibility of Ad-36-induced adiposity in chicken model raises serious concerns about such a possibility in humans that needs further investigation." 238)
- "cross-sectional study of children 8 to 18 years??? A total of 124 children (median age: 13.6 years) were studied. Of those children, 46% were nonobese and 54% were obese. AD36 positivity was present in 19 children (15%). The majority of children found to be AD36-positive were obese (15 [78%] of 19 children). AD36 positivity was significantly (P<.05) more frequent in obese children (15 [22%] of 67 children) than nonobese children (4 [7%] of 57 children). Among the subset of children who were obese, those who were AD36-positive had significantly larger anthropometric measures, including weight, BMI, waist circumference, and waist/height ratio. " 239)
- "CDV was reported as the first obesity-promoting pathogen in 1982 when Lyons et al published the landmark article in Science, ???A virally induced obesity syndrome in mice??? that reported that CDV infection induced obesity in Swiss Albino mice. CDV-inoculated mice showed increased body weight as well as an increased number and size of fat cells. Anatomical damage and altered neurochemistry in the hypothalamus was subsequently demonstrated in CDV-infected mice[16-21]. The hypothalamus plays a well-documented role in appetite regulation, energy consumption and neuroendocrine function. CDV-infected mice showed down-regulated leptin receptors in the hypothalamic area of the brain, explaining their inability to generate a proper response to leptin in the brain. With lower number of leptin receptors, hunger may be induced despite high leptin plasma levels that signal satiety. RAV-7, an avian leukosis virus, was the second microbe reported to induce obesity. RAV-7 (avian leukosis virus subgroup C) is the most common poultry retrovirus associated with neoplastic disease. RAV-7 causes obesity in chickens combined with growth stunting, hypertriglycemia, hypercholesterolemia as well as enlarged fatty liver, anemia and immunosuppression" 240)
on February 09, 2012
at 09:08 AM
Dietary replacement... http://www.johnberardi.com/articles/nutrition/dietary_1.htm
on February 08, 2012
at 03:10 PM
Carb/insulin, calories in/calories out, AND food reward.
on February 08, 2012
at 03:54 AM
I include this, not because the researchers are leaders in obesity theory, but because there are so many working in this area:
Childhood inactivity is a direct cause of obesity. Once the problem is created it's hard to reverse.
on February 07, 2012
at 09:18 PM
I favor the excitotoxin theory of obesity, which I suppose would be traced back to Dr. Blaylock: http://www.rense.com/general79/obesity.htm
on February 07, 2012
at 06:45 PM
Malnourishment - Paul Jaminet http://perfecthealthdiet.com/?p=5387
on February 07, 2012
at 04:11 PM
Are there any theories that take into account Grehlin, Leptin, Insulin, Thyroid Hormones and Cortisol? I may be missing a few as well, but I think they all work in concert for fat storage. I have never heard of Todd Becker's theory, so I will have to check that out.