"It is in your DNA!". When people talk like this the impression is given that if it is in your DNA then that is it, end of discussion, this is a characteristic that is predetermined. You are going to be fat or thin, have a dodgy heart or whatever.
This is not really how it is. The world is not like that. Theologically I am not a Calvinist - I cannot take the determinism. Scientifically it is the same. Just because you have these genes, it doesn't mean that they will all be "turned on". You can influence these things.
This is the idea of gene expression, which wikipedia defines as
You activity levels, exercise, diet, environment etc can all influence which genes are turned on, how gene expression happens. Art DeVany had a couple of good posts on this a while ago. (another one here)
This article I've just seen is another element to the mix. It notes how another element can influecen gene expression - social factors. being fit and healthy is not just about diet and exercise....you need to have your social life in a healthy state too. As the Bible says
Loneliness can be bad for your immune system.
The researchers said
“In this study, changes in immune cell gene expression were specifically linked to the subjective experience of social distance,” said Dr. Cole. “The differences we observed were independent of other known risk factors for inflammation, such as health status, age, weight, and medication use. The changes were even independent of the objective size of a person’s social network. What counts, at the level of gene expression, is not how many people you know, it’s how many you feel really close to over time.”
So in all your exercising and dietary control, do not forget your friends and family if you want to be really well.
Anyway, for the article, a pdf of which is available here:
Social regulation of gene expression in human leukocytes
Abstract (provisional)
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
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.
This is not really how it is. The world is not like that. Theologically I am not a Calvinist - I cannot take the determinism. Scientifically it is the same. Just because you have these genes, it doesn't mean that they will all be "turned on". You can influence these things.
This is the idea of gene expression, which wikipedia defines as
the process by which the inheritable information which comprises a gene, such as the DNA sequence, is made manifest as a physical and biologically functional gene product, such as protein or RNA.
You activity levels, exercise, diet, environment etc can all influence which genes are turned on, how gene expression happens. Art DeVany had a couple of good posts on this a while ago. (another one here)
This article I've just seen is another element to the mix. It notes how another element can influecen gene expression - social factors. being fit and healthy is not just about diet and exercise....you need to have your social life in a healthy state too. As the Bible says
And the LORD God said, [It is] not good that the man should be alone; Genesis 2:18
Loneliness can be bad for your immune system.
The researchers said
“In this study, changes in immune cell gene expression were specifically linked to the subjective experience of social distance,” said Dr. Cole. “The differences we observed were independent of other known risk factors for inflammation, such as health status, age, weight, and medication use. The changes were even independent of the objective size of a person’s social network. What counts, at the level of gene expression, is not how many people you know, it’s how many you feel really close to over time.”
So in all your exercising and dietary control, do not forget your friends and family if you want to be really well.
Anyway, for the article, a pdf of which is available here:
Social regulation of gene expression in human leukocytes
Abstract (provisional)
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.
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.
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