|Posted on Monday, February 20, 2006 - 6:14 pm: || |
This was on our local news tonight-the theory that obesity can be caused by a virus. Why, oh why, if 'they' can research and believe this, can't 'they' understand about MSG?
I know that is a rhetorical question.
|Posted on Tuesday, February 21, 2006 - 1:57 am: || |
The theory that obesity is caused by a virus has advantages over the theory that obesity is caused by MSG:
1. The theory that MSG causes obesity would be bad for the MSG industry and the restaurant industry. They would prefer the virus theory.
2. The theory that MSG causes obesity would be bad for the medical industry. If people avoided MSG (and thereby a whole bunch of health problems), doctors would lose business.
3. The virus theory would be better for the vaccine/medical industry. They would make more money peddling vaccines. (BTW, vaccines, in addition to the fact that they don't work, tend to contain MSG and mercury and aluminum and all kinds of bleep and this increases business.)
Obviously the virus theory is better than the MSG theory. Scientists, being rational people, prefer the virus theory. And besides, that's what they are paid to prove.
|Posted on Tuesday, July 25, 2006 - 5:09 pm: || |
Effect of cholecystokinin on feeding is attenuated in monosodium glutamate obese mice.Maletinska L, Toma RS, Pirnik Z, Kiss A, Slaninova J, Haluzik M, Zelezna B.
Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, Flemingovo nam. 2, 166 10 Praha 6, Czech Republic.
Extract: Treatment of newborn mice with monosodium glutamate (MSG) is neurotoxic for hypothalamic arcuate nucleus (ARC) and causes obesity. In the MSG-treated 16-week-old NMRI mice, we detected specific ablation of ARC neuronal cells, 8 times higher fat to body mass ratio but unchanged body mass compared to controls, advanced hyperglycemia and hyperinsulinemia - both more pronounced in males, and hyperleptinemia - more severe in females. After fasting, the MSG-treated mice showed attenuated food intake compared to controls. Cholecystokinin octapeptide, which decreased food intake in a dose-dependent manner in 24 h fasted controls, did not significantly affect food intake in the MSG-treated animals. We propose that the obesity-related changes in the feeding behavior of the MSG-treated obese mice were the result of missing leptin and insulin receptors in ARC and consequent altered neuropeptide signaling. This makes the MSG model suitable for clarifying generally the central control of food intake.