Scientists have known for a long time that cholesterol like other basic food components forms an essential component in a healthy human body. It forms the cell membrane architecture (or the cell wall), helps produce the sex hormones, and assists in the formation of bile that helps in the digestion of food. The dietary guidelines recommend an intake of 200-300mg of cholesterol daily. It is important to understand that your own body produces cholesterol in the liver, in addition to what is consumed in your diet. Plants, on the other hand cannot produce cholesterol, and therefore dietary sources of cholesterol remain meat and diary.
Cholesterol is carried around the bloodstream attached to low-density lipoprotein (LDL) “bad cholesterol” and high-density lipoprotein (HDL) “good cholesterol”. Your doctor has probably requested this on a number of occasions as a blood test to evaluate your cardiovascular risk. Recently, another biomarker Apolipoprotein B (ApoB) has come to the forefront as being a better representation of the number of cholesterol-laden particles circulating in the blood stream.
In MS higher total cholesterol and LDL-cholesterol levels have been linked to worsening disability, with greater ApoB levels at disease onset being linked to increased number of lesions on MRI brain scans over a 2 year period. Whether, there may be link with the underlying neurodegeneration is unknown, and forms the focus of the study presented below.
Murali et al. in Buffalo, New York, studied the longitudinal changes of cholesterol biomarkers (total cholesterol, HDL-C, LDL-C, Apo profiles and their genotyping) over a 5 year period in healthy subjects and MS, and their relationship with brain lesions and volume loss. The study involved 41 healthy controls (HC), 76 relapsing-remitting MS (RR-MS), and 37 progressive MS (P-MS) subjects.
They found that, whilst a rise in LDL-C was associated with the development of new MS lesions, HDL-C and ApoA-I (a component of HDL-C) were associated with less grey matter and cortical volume loss (area of the brain where the neuronal cell bodies sit). The highest quartiles of LDL-C were linked to the greatest number of new MS lesions (see Figure 1 below). The opposite was true for HDL-C with the lowest quartile of HDL-C change being associated with more gray matter and cortical volume loss. Both imply, that extremes in change are somehow very harmful; that is to to high LDL-C levels or to low HDL-C levels.
Moreover they observed something interesting in the who did and did not progress (of the 76 RRMS, 11 converted to SPMS; these numbers are small and any interpretation of the findings should be noted with caution). Although, the converted and non-converted did not differ by total cholesterol levels, the percentage rise in HDL-C was much greater in the non-converted group (data not shown here). However, there were no differences noted in the percentage ApoB change.
The important question then becomes, how much weight should we place on good versus bad cholestrol in our body compositions? And, one also wanders whether these findings are bystander changes, more reflective of the association between cholesterol and inflammation, rather than a direct effect of cholesterol levels on disease activity and progression.
Cholesterol and Neurodegeneration: Longitudinal Changes in Serum Cholesterol Biomarkers Are Associated with New Lesions and Gray Matter Atrophy in Multiple Sclerosis Over 5-years Follow-up.
Cholesterol is an important structural component of myelin and essential for brain homeostasis.
To investigate whether longitudinal changes in cholesterol biomarkers are associated with neurodegeneration in multiple sclerosis (MS).
This prospective, longitudinal study (n = 154) included 41 healthy controls (HC), 76 relapsing-remitting MS (RR-MS), and 37 progressive MS (P-MS) subjects. Neurological examination, brain MRI and blood samples were obtained at baseline and at 5-year follow-up visits. Cholesterol biomarkers measured included plasma total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and the apolipoproteins (Apo), ApoA-I, Apo-II, ApoB, ApoC-II and ApoE. Key cholesterol pathway single nucleotide polymorphisms were genotyped.
Greater percent increases in HDL-C and ApoA-I levels were associated with a lower rate of gray matter and cortical volume loss. Greater percent increases in LDL-C were associated with increases in new T2 lesions. The percent increases in HDL-C (p = 0.032) and ApoA-I (p = 0.007) were smaller in the patients RR-MS at baseline who converted to secondary progressive MS during the 5-year follow-up period. Changes in HDL-C and ApoA-I were associated with lipoprotein lipase rs328 genotype status.
Increases in HDL-C and ApoA-I have protective associations with MRI measures of neurodegeneration in MS. This article is protected by copyright. All rights reserved.