Brownsfan and bromley,
I am also a bit puzzled why Dr. Swank's observations of benefit of low-fat diets have not gotten a closer look. The problem with dietary studies is they can't be blinded for a clinical trial. Studies with supplements can be blinded and placebo-controlled, but the participant is always aware of changing diet unless the study gives participants mystery pre-packaged foods - and no one is going to want to spend years, even months, eating like that. I think changing my diet in some manners similar to Dr. Swank's recommendations has helped my overall health and symptoms possibly relating to MS. But of course I'm biased on that point! One possibility for studying diet influences is to use the parameters measured in cardiovascular studies, and see if diet changes improve lipid profiles (or other clinical chemistry), and if that objective measure has any influence on MS symptoms. Such a study could be a two-for-one, with both MS and cardio information generated.
The recent additional inspiration for my own diet change was some cardiovascular blood work I had done, which showed I had a genetic risk factor for cardiovascular disease (apoproteinE 4 allele; the "normal" allele is designated ApoE 3). Having this allele and its association with MS has been investigated already, because it is more common in people of northern European descent compared to southern Europeans and that got some researchers excited enough to look at MS associations. (ApoE4 is also more common in some aboriginal populations outside Europe, and there is interesting anthropology-related studies suggesting the ApoE 4 is the original "wild-type" allele from pre-agricultural days. That is a whole other post!) Researchers have shown having an ApoE 4 doesn't make it more likely to get MS, but some studies have shown having it makes the MS progression worse, which wasn't cheerful news. My blood lipid profile was actually not that bad given the genetic propensity for it, probably because I had already modified my diet for a year prior to the blood work. It gave me incentive to try a low-dose statin plus sustained release niacin to improve my LDL:HDL ratios. The jury is still out, but I find that I'm suddenly feeling much better and mentally sharper. I'm not sure if it is the statin, the pharmacological-dose niacin doing something else (that tryptophan tie-in) or just coincidence. I'll get more cardio blood work done in March or April to follow up. Changes in blood chemistry are objective measurements and it will be interesting to see if anything correlates with subjective ones. In the meantime, I will look into both lipids and tryptophan and start new posts.
Here's an interesting abstract from PubMed, published in Nature October of this year. It shows one of the tie-ins between lipid metabolism (potentially diet-influenced) and immunological function. How it relates exactly to MS I don't know but something tells me it might be important on both diet and infection angles:
Apolipoprotein-mediated pathways of lipid antigen presentation.
van den Elzen P, Garg S, Leon L, Brigl M, Leadbetter EA, Gumperz JE, Dascher CC, Cheng TY, Sacks FM, Illarionov PA, Besra GS, Kent SC, Moody DB, Brenner MB.
Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Peptide antigens are presented to T cells by major histocompatibility complex (MHC) molecules, with endogenous peptides presented by MHC class I and exogenous peptides presented by MHC class II. In contrast to the MHC system, CD1 molecules bind lipid antigens that are presented at the antigen-presenting cell (APC) surface to lipid antigen-reactive T cells. Because CD1 molecules survey endocytic compartments, it is self-evident that they encounter antigens from extracellular sources. However, the mechanisms of exogenous lipid antigen delivery to CD1-antigen-loading compartments are not known. Serum apolipoproteins are mediators of extracellular lipid transport for metabolic needs. Here we define the pathways mediating markedly efficient exogenous lipid antigen delivery by apolipoproteins to achieve T-cell activation. Apolipoprotein E binds lipid antigens and delivers them by receptor-mediated uptake into endosomal compartments containing CD1 in APCs. Apolipoprotein E mediates the presentation of serum-borne lipid antigens and can be secreted by APCs as a mechanism to survey the local environment to capture antigens or to transfer microbial lipids from infected cells to bystander APCs. Thus, the immune system has co-opted a component of lipid metabolism to develop immunological responses to lipid antigens.
PMID: 16208376 [PubMed - indexed for MEDLINE
Ian, I'm interested in the infectious angle too, particularly why it seems people with MS, or at least some people with MS, seem to have evidence of persisting infections or associations with certain infections. Why is that??? What is the susceptibility factor? I have gotten interested in weird inherited metabolic diseases in which (usually) infants with the disease have not only severe myelin disorders but also persistent infections they can't clear. What if some people with MS are heterozygous (carriers) for some of these rare recessive diseases, such that evidence of a partial enzyme disorder doesn't show up until much later in life?
The oncology paper you cited was interesting in discussing associations with cancer and viral infections in susceptible people. Years ago when I was in grad school it was known that certain viruses could induce cancers in lab animals, but there was no "human evidence" that viruses cause cancer in humans. That thinking has certainly changed. And there is some epi evidence that like the cancer clusters, MS seemingly "spreads" - not that MS itself is infectious, but that a relatively common infection moving through a population will cause some people to develop MS. I'll see if I can find that abstract again, I think it was a Swedish study.