What this study implies is quite astounding, imo...
Fat mice and fat people have different gut bacterial flora than lean mice and lean people. The "fat" flora in both can better metabolize carbohydrates (for fat mice and people...and diabetics...that is precisely what we don't want). The digestive floral community that exists in our digestive tract is dictated by what our immune system will allow.
The implications of obviously far reaching: By controlling gut bacteria, we can control metabolism...what gets processed vs.what goes undigested and simply passes through as waste...
In other words, using antibiotics to reduce or eliminate metabolic syndrome, ie. no moreinsulin resistance.
Some will argue this explains the strong genetic disposition of diabetes. Others will argue that eating bad food and insufficient exercise compromises our immune system.
Others may argue that the starches involved in the processed food that are eaten by individuals causes a growth of the new bacteria, this leads to a fat gain, yet the inability to process the glucose in the system leads to hunger even though full. This leads to greater eating and more of the same. The big question is like the chicken and the egg?
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