Several extrahepatic causes of asymptomatic elevations of liver transaminase levels can be pursued based on the clinical scenario. It is not clear how thyroid disorders elevate liver transaminase levels, but measurement of serum thyroid-stimulating hormone can help rule out this potential cause. Celiac disease has also been implicated in asymptomatic liver transaminase elevations; tissue transglutaminase antibody testing can have a role in this diagnosis. 5 Hemolysis and strenuous exercise also may be potential causes. Muscle disorders such as rhabdomyolysis or polymyositis are unlikely in asymptomatic patients, but measurement of creatine kinase and aldolase may be reasonable in the appropriate clinical setting.
A small but revealing study suggests that even mildly stressful intellectual challenges change our emotional states and behaviors, even if they do not profoundly alter brain metabolism. Fourteen female Canadian college students either sat around, summarized a passage of text or completed a series of computerized attention and memory tests for 45 minutes before feasting on a buffet lunch. Students who exercised their brains helped themselves to around 200 more calories than students who relaxed. Their blood glucose levels also fluctuated more than those of students who just sat there, but not in any consistent way. Levels of the stress hormone cortisol, however, were significantly higher in students whose brains were busy, as were their heart rates, blood pressure and self-reported anxiety. In all likelihood, these students did not eat more because their haggard brains desperately needed more fuel; rather, they were stress eating.
Messier has related explanation for everyday mental weariness: "My general hypothesis is that the brain is a lazy bum," he says. "The brain has a hard time staying focused on just one thing for too long. It's possible that sustained concentration creates some changes in the brain that promote avoidance of that state. It could be like a timer that says, 'Okay you're done now.' Maybe the brain just doesn't like to work so hard for so long."
I’m not sure if anyone else has pointed this out yet. But in the paper looking at different genotypes for the snp rs2287019 that you got all the graphs from is not at all applicable to a ketogenic diet. If you look at the methods section for the paper and the macro-nutrient breakdown, you’ll see that there is no way any of the subjects were in ketosis. There were two “Low Fat” diets. The first was, (20% fat, 15% protein, and 65% carbs). The second “Low Fat” diet consisted of (20% fat, 25% protein, and 55% carbs). The “High Fat” diets consisted of (40% fat, 15% protein and 45% carbs) for the first and (40% fat, 25% protein, and 35% carbs) for the second. All four diets were caloric restriction diets which explains the weight loss. If you want to compare a “Low Fat” diet to a true ketogenic diet it needs to be “High fat, low carb” with carbohydrate composition of around 10% or less.