For context, the relationship between LDL-cholesterol concentration and coronary heart disease risk appears linear across the entire physiological range
Little evidence that fasting [glucose] relates to risk of death in people without prediabetes or diabetes
4/10
Fasting glucose and morbidity risk?
Little evidence that fasting [glucose] relates to cardiovascular disease in people without prediabetes or diabetes
5/10
However, those whose [glucose] remains elevated above fasting, 2 h after 75 g oral glucose show higher mortality risk versus people whose [glucose] had returned to fasting.
Does this mean [glucose] matters?
6/10
Possibly but not necessarily.
The OGTT reflects many aspects of physiology
It could be that other aspects of physiology are the causal link to mortality, [glucose] is just a marker.
7/10
If glucose is causal, then it might be expected that free-living measures would also correlate with mortality or morbidity.
This is because the effect of physiology will be diluted by behaviour
So does HbA1c correlate with mortality?
8/10
Little evidence that HbA1c correlates with mortality in people without prediabetes or diabetes (or CVD)
So should people without prediabetes or diabetes care about their glucose under free-living conditions?
9/10
There may be some relevance of glucose within the non-diabetic range for some outcomes (e.g., physical activity, appetite etc.),
but its not yet clear that glucose in free-living conditions is important for hard outcomes of CVD or mortality
10/10
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If mice 🐁 are calorie restricted 🍽️ for a prolonged period of time (provided 30% fewer calories than they would choose to eat normally at baseline), what will happen to DNL?
2/8
The Q is a bit vague to have a clear A, as it depends if we are talking about DNL in liver, adipose tissue, or the whole body.
Before we delve into those areas, its worth noting that mice do lose weight when restricting calories by 30%