Blood lipids and disease activity are they related?

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The headline is “How Lipid Level Tests Can Help People with Multiple Sclerosis”

 
We have been striving to understand how statins can work in MS.
These are cholesterol-lowering drugs.
 
Altered lipid metabolism is a feature of chronic inflammatory disorders. Increased plasma lipids and lipoproteins have been associated with multiple sclerosis (MS) disease activity. Our objective was to characterise the specific lipids and associated plasma lipoproteins increased in MS and to test for an association with disability. Plasma samples were collected from 27 RRMS patients (median EDSS, 1.5, range 1–7) and 31 healthy controls. Concentrations of lipids within lipoprotein sub-classes were determined. Plasma cytokines were measured. Differences between the patient and volunteer groups were found for lipids within very low density lipoprotein (VLDL) and  high density lipids (HDL) lipoprotein sub-fractions (p < 0.05). Multivariate regression demonstrated a high correlation between lipids within VLDL sub-classes and the Expanded Disability Status Scale (EDSS) (p < 0.05). An optimal model for EDSS included free cholesterol carried by VLDL-2, gender and age (R2 = 0.38, p < 0.05). Free cholesterol carried by VLDL-2 was highly correlated with plasma cytokines CCL-17 and IL-7 (R2 = 0.78, p < 0.0001). These results highlight relationships between disability, inflammatory responses and systemic lipid metabolism in RRMS. Altered lipid metabolism with systemic inflammation may contribute to immune activation.
 
You can read the abstract but sorry to break the bubble, as an R2=0.38  is not a high correlation. 
 
 

R2 is the coefficient of determination and pronounced “R squared”, is the proportion of the variance in the dependent variable that is predictable from the independent variable(s).

 
Time and time again we see correlations but the problem is that whilst VLDL may correlate with movement problems (is this cause or perhaps effect), there is no real predictive value for the individual and so will having a test tell you anything for the that you don’t know already. It cannot tell you your future accureately Maybe Ari will do a “Guest post” and you can get it from the horse’s mouth.

The VLDL (carries triglycerides, a type of fat, to your tissues also known as Bad Cholesterol) are associated with the detection of CCL17 a chemokine (a protein that your cells migrate towards) expressed notably on dendritic cells and interleukin 7 (IL-7) a T cell cytokine which is implicated in MS Susceptibility which is also produced by dendritic cells. 
 
Did you know that  oxidised low density lipid promotes dendritic cell formation form monocytes?. No neither did I until I read this. Apparently these dendritic cells produce IL-12 (cytokine)…Oh no…does this mean it promotes pro-inflammatory Th1 cells? VLDL receptor can influence dendritic cells function too…Is this the link? I’ve no idea its not my project.

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MouseDoctor

3 comments

    • When Th2 was all the rage this was the mechanism but now Tregs are the bees knees.

      In our experiments in animals, you give the drug and there is no disease you stop the drug and within 48h 100 percent of the animals relapse how is this an effect on Th2 or Treg?..

      Next up the in vitro data is meaningless as they use up to 5-20micromolar, the steady state plasma cell level in humans is about 10nM (https://www.ncbi.nlm.nih.gov/pubmed/19810580).

      Atorvastarin was using in relapsing MS it failed, its use is potentially in progressive MS you need a different mechansism than the same old same old. It is formulatic research. 🙂

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