Posts Tagged ‘Immune system’

Have you ever seen the list “100 Benefits of Meditation“?  Of course, many of these benefits are psychological. You know, things like: helps control own thoughts (#39) and helps with focus & concentration (#40).  But many of the 100 benefits are rather physical, bodily, physiological, immunological and even biochemical benefits (such as #16- reduction of free radicals, less tissue damage).

These are awesome claims, and I’ve certainly found that mediation helps me feel more emotionally balanced and physically relaxed,  but I’m wondering – from a hard science point of view – how legit some of these claims might be.  For example, “#12 Enhances the immune system – REALLY?  How might yoga and mediation enhance my immune system?

In a previous post on the amazing vagus nerve – the only nerve in your body that, like the ancient Kundalini serpent, rises from the root of your gut to the brain – AND – a nerve that is a key to the cure of treatment resistant depression – it was suggested that much of the alleviation of suffering that comes from yoga comes from the stimulation of this amazing nerve during postures and breathing.

Somehow, the ancient yogis really got it right when they came up with the notion of Kundalini serpent – so strange, but so cool!

I happened to stumble on a paper that explored the possibility that the vagus nerve might also play a role in mediating communication of the immune system and the brain – and thus provide a mechanism for “#12- Enhances the immune system” Here’s a quote from the article entitled, “Neural concomitants of immunity—Focus on the vagus nerve” [doi:10.1016/j.neuroimage.2009.05.058] by Drs. Julian F. Thayer and Esther M. Sternberg (Ohio State University and National Institute of Mental Health).

By the nature of its “wandering” route through the body the vagus nerve may be uniquely structured to provide an effective early warning system for the detection of pathogens as well as a source of negative feedback to the immune system after the pathogens have been cleared. … Taken together these parasympathetic pathways form what has been termed “the cholinergic anti-inflammatory pathway

The scientists then investigate the evidence and possible mechanisms by which the vagus nerve sends immunological signals from the body to the brain and also back out to the immune system.  Its not a topic that is well understood, but the article describes several lines of evidence implicating the vagus nerve in immunological health.

So bend, twist, inhale and exhale deeply.  Stimulate your vagus nerve and, as cold and flu season arrives, awaken the serpent within!

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Antigen presentation stimulates T cells to bec...
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Its not often that Nature magazine publishes a triple-back-to-back-to-back, so take note if you’re interested in the genetics of mental illness. The 3 papers – [doi:10.1038/nature08185] involving 3,322 individuals with schizophrenia and 3,587 controls, [doi:10.1038/nature08186] 4,999 cases and 15,555 controls and [doi:10.1038/nature08192] 8,008 cases and 19,077 controls – are as massive and powerful as any genome-wide effort to-date.  The results?  Overall a common result showing linkage to the major histocompatibility complex or so-called ‘MHC genes’ located on chromosome 6.  What to these genes do? and what’s the relevence to mental illness?

Here’s a quickie immunology primer on the biological function of the major histocompatibility genes.  They encode proteins whose molecular function is display short peptides on the surface of aptly named antigen presenting cells in the immune system (think of your hand as an MHC protein holding onto an apple (the short peptide) and holding it out or presenting it to someone (an Helper T-Cell).  This act of “presentation” is done so that the Helper T-Cells can determine whether such peptides are “self” or “non-self”.  If such displayed peptides are non-self (such as a virus, endotoxin or bacterium), then the helper T-Cells will sound the alarm and initiate a T- or B-Cell based immune response aimed specifically at the offending invader.  The movies below show the MHC proteins in their place displaying antigen peptides on the cell surface for binding with a helper T-Cell.

So, what does this have to do with mental illness? Although there are other non-immunological genes interspersed among the MHC genes, there is good reason to begin to explore the role of external infection and early development.  The authors of one paper note that,  “Schizophrenia patients are more likely, compared to the general population, to have been born in the winter or the spring. Although infections such as influenza and measles have been proposed as a possible mechanism for this distortion, a clear association between infectious agents and schizophrenia has not been demonstrated.”

The more we know, the more we don’t know.  Hopefully more early environment data will be analyzed.

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Schematic representation of MHC class I molecu...
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To me, phylogenetics is one of the coolest ways to use human sequence diversity. I’m not an expert, but roughly speaking, the method involves looking at sequences among ancestral populations and comparisons to sequences in groups that have migrated out over space and time. In these out groups, recombination and mutation have caused genetic sequences to diverge – in some cases new alleles have been naturally selected for, and in most cases, new alleles thrived or crashed due the size and mating structure of a population. The genome carries the historical record of this change – the ultimate history book !

I recently had my Y-chromosome analyzed by the Genographic Project and was intrigued to discover a southwest asian heritage. More recently, Kenneth Kidd and colleagues report a detailed analysis of sequences in the KIR receptor gene complex on chromosome 19q13 and variation in the human leukocyte antigen (HLA) class I gene complex on chromosome 6p23. It has long been known that these regions are hypervariable, which is a good thing since our immune system exploits this diversity to counter ever-changing pathogen invasions – but how do two parts of the immune system continue to work together (KIR receptors bind to HLA antigens) when the separate, unlinked genomic regions show hypervariability ? Worse yet, if the KIR-HLA interaction is too weak, we are susceptible to infection, but, if too strong, we are susceptible to autoimmune attack. Quite a tight-wire to walk, amidst a deluge of pathogen invasions ! Kidd and colleagues use the ALFRED database to reveal some clues to the historical record of this. Apparently, the co-evolution is selective, where activating receptor (19q13) -ligand (6p23) complexes were strongly negatively selected for but not inhibitory receptor-ligand pairs.

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