Loneliness Alters Genes Related to Immunity

[Hopeful]

and can cause increased inflamation: http://www.reuters.com/article/blogB...GPzEhlLZMlYJWk

Hopeful

[AlaskaAngel]

Were the genes measured before the loneliness? (Was the loneliness a result of the genetic makeup in the first place, or were the genes actually altered as they become lonely?)

[Hopeful]

followed by a link to the provisional pdf:

Background

Social environmental influences on human health are well established in the epidemiology literature, but their functional genomic mechanisms are unclear. The present study analyzed genome-wide transcriptional activity in people who chronically experienced high versus low levels of subjective social isolation (loneliness) to assess alterations in the activity of transcription control pathways that might contribute to increased adverse health outcomes in social isolates.
Results

DNA microarray analysis identified 209 genes that were differentially expressed in circulating leukocytes from 14 high- versus low-lonely individuals, including up-regulation of genes involved in immune activation, transcription control, and cell proliferation, and down-regulation of genes supporting mature B lymphocyte function and type I interferon response. Promoter-based bioinformatic analyses showed under-expression of genes bearing anti-inflammatory glucocorticoid response elements (GREs; p = 0.032) and over-expression of genes bearing response elements for pro-inflammatory NF-kB/Rel transcription factors (p = 0.011). This reciprocal shift in pro- and anti-inflammatory signaling was not attributable to differences in circulating cortisol levels, or to other demographic, psychological, or medical characteristics. Additional transcription control pathways showing differential activity in bioinformatic analyses included the CREB/ATF, JAK/STAT, IRF1, C/EBP, Oct, and GATA pathways.
Conclusions

These data provide the first indication that human genome-wide transcriptional activity is altered in association with a social epidemiological risk factor. Impaired transcription of glucocorticoid response genes and increased activity of pro-inflammatory transcription control pathways provide a functional genomic explanation for elevated risk of inflammatory disease in individuals who experience chronically high levels of subjective social isolation.

http://genomebiology.com/content/pdf...7-8-9-r189.pdf

Hopeful

[R.B.]

Food and environmental factors alter gene expression.

So you could be looking at other factors as well. Maybe people are more emotionally vulnerable because of dietary factors. {More likely than would appear to be the case at face value}

Then that is combined with a host of life indignities and realities in all their human complexity.

It is interesting and not unexpected that it emotion and behaviour link to the inflammatory pathways.

I have just downloaded the PDF - looks like it will be a fascinating read and of particular interest.

Many thanks for posting.


RB

[Sandy in Silicon Valley]

Hi,

I still think the CORRELATION of inflammatory & immunity characteristics linked with loneliness doesn't indicate whether they co-exist, or one follows the other.

For example, an alternative hypothesis could be that people with inflammatory tendencies might have more pain, and shun social contact more due to experiencing unpredictable pain that is socially-inhibiting. Similarly, someone whose immune system is compromised might, biologically, be more prone to stay away from closeness with other people, due to the risk of infection (whether the risk is conscious or more of a biological "fight or flight" reflex to having high vulnerability to infection/ disease.

Just some thoughts. If anyone can boil down the other articles that were cited, and explain how causality is determined by them, I'd appreciate the info!

(((hugs)))
Sandy in Silicon Valley

[Hopeful]

For anyone who wants to tackle the provisional pdf, the authors don't claim causality, just a relationship.

Hopeful