In rodents, ketogenic diets reduce reactive oxygen species in the brain34 and reduce central inflammation and reactive oxygen species in a model of multiple sclerosis.35 Two clinical papers have found that ketogenic diet feeding of 12 weeks to 6 months reduced signs of liver inflammation in obese patients with nonalcoholic fatty liver disease (in addition to improving various other physiological and biochemical variables).36, 37 Unfortunately, basic research into non-alcoholic fatty liver disease has been hampered by species differences between mice and humans in their hepatic reaction to ketogenic diets.
In rodents, ketogenic diets reduce reactive oxygen species
in the brain34 and reduce central inflammation and reactive oxygen species in a model of multiple sclerosis.35 Two clinical papers have found that ketogenic diet feeding of 12 weeks to 6 months reduced signs of liver inflammation in obese patients with nonalcoholic fatty liver disease (in addition to improving various other physiological and biochemical variables).36, 37 Unfortunately, basic research into non-alcoholic fatty liver disease has been hampered by species differences between mice and humans in their hepatic reaction to ketogenic diets.
in the brain34 and reduce central inflammation and reactive oxygen species
in a model of multiple sclerosis.35 Two clinical papers have found that ketogenic diet feeding of 12 weeks to 6 months reduced signs of liver inflammation in obese patients with nonalcoholic fatty liver disease (in addition to improving various other physiological and biochemical variables).36, 37 Unfortunately, basic research into non-alcoholic fatty liver disease has been hampered by species differences between mice and humans in their hepatic reaction to ketogenic diets.
in a
model of multiple sclerosis.35 Two clinical papers have found that ketogenic diet feeding of 12 weeks to 6 months reduced signs of liver inflammation
in obese patients with nonalcoholic fatty liver disease (in addition to improving various other physiological and biochemical variables).36, 37 Unfortunately, basic research into non-alcoholic fatty liver disease has been hampered by species differences between mice and humans in their hepatic reaction to ketogenic diets.
in obese patients with nonalcoholic fatty liver disease (
in addition to improving various other physiological and biochemical variables).36, 37 Unfortunately, basic research into non-alcoholic fatty liver disease has been hampered by species differences between mice and humans in their hepatic reaction to ketogenic diets.
in addition to improving various other physiological and biochemical variables).36, 37 Unfortunately, basic research into non-alcoholic fatty liver disease has been hampered by species differences between
mice and humans
in their hepatic reaction to ketogenic diets.
in their hepatic reaction to ketogenic diets.38