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decrease the HDL


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6 minutes ago, Strange said:

Looks like it. Apparently, infection and inflammation cause a reduction in HDL and LDL levels (eg https://www.ncbi.nlm.nih.gov/books/NBK326741/)

I was just talking to a cardiologist about cholesterol and Gram-positive bacteria, and the connections being made. This morning, in fact. Interesting coincidence.

As to the question from the OP, I don't think we have enough information to even guess. Patients vary, infections vary, diets vary. 

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49 minutes ago, Phi for All said:

High-density lipoproteins?

That's what I guessed but didn't know any association with infection, so I had a doubt.

52 minutes ago, Strange said:

Looks like it. Apparently, infection and inflammation cause a reduction in HDL and increase in LDL levels (eg https://www.ncbi.nlm.nih.gov/books/NBK326741/)

 

FTFY. HDL is the good stuff and LDL is not. HDL moves fat out of cells and LDL moves it into them.

From your link:

Quote

The most common changes are decreases in serum HDL and increases in triglycerides. The increase in serum triglycerides is due to both an increase in hepatic VLDL production and secretion and a decrease in the clearance of triglyceride rich lipoproteins. The mechanisms by which inflammation and infection decrease HDL levels are uncertain.

 

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37 minutes ago, StringJunky said:

FTFY. HDL is the good stuff and LDL is not. HDL moves fat out of cells and LDL moves it into them.

Thank you! But it looks like LDL is more complicated because it also says 

Quote

LDL levels are frequently decreased

 

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20 minutes ago, Strange said:

Thank you! But it looks like LDL is more complicated because it also says 

 

I don't  understand that bit.LDL levels are decreased by what? Maybe @CharonY does and can clarify. Here's the part from the abstract:

Quote

 LDL levels are frequently decreased but the prevalence of small dense LDL is increased due to cholesterol ester transfer protein (CETP) mediated exchange of triglycerides from triglyceride rich lipoproteins to LDL followed by triglyceride hydrolysis.

EDit: Scrap that, I understand now. I should have prefaced that post with "generally".

Edited by StringJunky
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HDL-LDL relationship is complex and the literature is shifting if you even take your eyes off it for a minute. While medically recommendations are being made, the actual mechanisms are uncertain and some statistical associations are less stable than one might hope for. There is a decent chance that e.g. increased LDL is an indicator of certain cardiovascular events rather than the cause, for example. Or that certain ratios are more relevant than absolute level. Or dozens of other things. One connection with HDL is its role to reduce the activity of LDL-derived oxidized phospholipids for example, and is therefore considered to be anti-inflammatory (in this context). However, in animal models under certain conditions HDL can actually promote inflammation. Perhaps another aspect that sometimes causes confusion: LDL and HDL refer to lipoproteins, which are actually a class of diverse proteins that carry cholesterol and are not cholesterol per se (but the complex is often referred to as LDL/HDL cholesterol).

That is is just the pre-emptive caveat to state that there is a lot of uncertainty in play with regard to lipid metabolism/transport and associated disease. Similarly, the connection to infections as well as inflammation. The issue with post-infection levels is (among others) the close connection with the inflammatory response, which may persist even after clearance. Though most commonly HDL are reduced allowing higher levels of LDL oxidation (due to the dimished anti-inflammatory effects mentioned before). Changes in LDL depend a lot on the type of infection or inflammatory response. During acute infections general HDL and LDL levels often decrease, with some LDL-species being elevated.  I am not sure whether the mechanisms for that is known.

Since there is also a disruption in triglyceride transport, it will depend on numerous factors on when levels will return to baseline (i.e. before infection).

 

Edit: I should add that the complex knowledge situation is not due to the fact that researchers are silly bastards and just make up things (well mostly not because of that) but because the role of LDL/HDL in disease is explored from various angles and methodologies. Much of the effects on overall health and coronary disease are based on cohort studies, which tells us something about association, but not the functional relationship. On the other end of the spectrum we got molecular mechanism, often in animal models, but they provide an incomplete view how diseases develop and ultimately affect health.

Edited by CharonY
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