”we evaluated the full spectrum of nutrient intake and identified a significant positive correlation between ImP [imidazole propionate] and saturated fat intake (driven by high cheese intake)”

Perhaps this depends on the type of cheese consumed.

Of course, it’s a correlation; ImP could be modulating eating habits and making people prefer eating cheese.

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fcpk 5 days ago | parent [-]

This is much more likely related to gut microbia metabolism than it is to histidine. Unlike the dogma wants it to be believed, high protein and fat intake does not necessarily lead to cardiovascular issues. It does when combined with other lifestyle(sedentary, low intensity), metabolic(diabetes/prediabetes, inflammation), nutritional(highly refined carbohydrates, nitrated compounds, oxalate/other anti nutrients and refined seed oils) and dysbiosis issues.

There is an enormous scandal to come behind the vilification of cholesterol and the simplification of its level's interpretation to come, which led to the current epidemic of obesity and metabolic/inflammatory/autoimmune diseases. Cholesterol levels vary hugely based on the genetics, epigenetics and lifestyle of an individual, and there is a very large amount of individuals that are within normal range with much higher ldl levels. For example, the cholesterol levels of centennials are usually extremely high.

Things to look out for: - high very small LDL(you need a proper analysis of your LDL levels with a histogram of the size distribution, which is very rarely done and more expensive) - high Triglyceride/HDL ratio(in US units, anything above 2 is not a very good sign) - high hbA1C (metabolic issues) - high lp(a) and/or lp(b) - high hs-CRP (general inflammation, but can be caused by infection if you are sick)

Usually those are all related and high when affecting a normally healthy individual).

	▲	cluckindan 5 days ago \| parent [-]
		”This is much more likely related to gut microbia metabolism than it is to histidine” Yes and no: the study linked to in the El Pais article suggests that certain bacteria are converting histidine to imidazole proprionate. More histidine -> more food for those bacteria -> bacterial overgrowth, dysbiosis and increased ImP levels -> eventually atherosclerosis. There are probably some microbe(s) capable of outcompeting the ImP-producing ones even in the presence of increased histidine, which would serve as a mitigating factor.