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
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).
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).
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.
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.
Dietary replacement... http://www.johnberardi.com/articles/nutrition/dietary_1.htm