Answer: Try meditating.
This is a big breakthrough. Click the link below to read the scientific paper:
Relaxation response induces temporal transcriptome changes in energy metabolism, insulin secretion and inflammatory pathways.
Benson-Henry Institute for Mind Body Medicine at Massachusetts General Hospital, Boston, Massachusetts, United States of America.
Abstract
The relaxation response (RR) is the counterpart of the stress response. Millennia-old practices evoking the RR include meditation, yoga and repetitive prayer. Although RR elicitation is an effective therapeutic intervention that counteracts the adverse clinical effects of stress in disorders including hypertension, anxiety, insomnia and aging, the underlying molecular mechanisms that explain these clinical benefits remain undetermined.
To assess rapid time-dependent (temporal) genomic changes during one session of RR practice among healthy practitioners with years of RR practice and also in novices before and after 8 weeks of RR training, we measured the transcriptome in peripheral blood prior to, immediately after, and 15 minutes after listening to an RR-eliciting or a health education CD.
Both short-term and long-term practitioners evoked significant temporal gene expression changes with greater significance in the latter as compared to novices. RR practice enhanced expression of genes associated with energy metabolism, mitochondrial function, insulin secretion and telomere maintenance, and reduced expression of genes linked to inflammatory response and stress-related pathways. Interactive network analyses of RR-affected pathways identified mitochondrial ATP synthase and insulin (INS) as top upregulated critical molecules (focus hubs) and NF-κB pathway genes as top downregulated focus hubs.
Our results for the first time indicate that RR elicitation, particularly after long-term practice, may evoke its downstream health benefits by improving mitochondrial energy production and utilization and thus promoting mitochondrial resiliency through upregulation of ATPase and insulin function. Mitochondrial resiliency might also be promoted by RR-induced downregulation of NF-κB-associated upstream and downstream targets that mitigates stress.
Here is a key paragraph from the discussion:
In summary, we conducted the first study to employ advanced genomic analysis methodology and systems biology analysis to examine temporal transcriptional changes during one session of RR practice and found that RR practice induced upregulation of ATPase and insulin function. This suggests that RR elicitation may enhance mitochondrial energy production and utilization. At the same time RR induced downregulation of NF-κB-dependent pathways, with effects on upstream and downstream targets that may mitigate oxidative stress. These findings, while preliminary, suggest that RR practice, by promoting what might be called mitochondrial resiliency, may be important at the cellular level for the downstream health benefits associated with reducing psychosocial stress [68]. Mitochondria have evolved the capacity to modulate specific anabolic and catabolic circuitries that control programmed cell death and autophagocytosis. They also confer an ability to sense the intracellular environment and help the cell adapt to a variety of stressors [69].
The RR significantly affects multiple pathways through mitochondrial signaling that may promote cellular and systemic adaptive plasticity responses. In essence these adaptive responses become markers of what might be called mitochondrial resiliency or mitochondrial reserve capacity. The gene expression data indicate the RR specifically upregulates energy production of ATP through the ATP synthase electron transport complex. This might result in an enhanced mitochondrial reserve providing the capacity to meet the metabolic energy demands required to buffer against oxidative stress that emerges in many stress related diseases. Depending on variables such as genetic endowment and epigenetic interactions with micro- and macro-environmental circumstances, different mitochondria will have variable capacities to dampen the pathogenic effects of oxidative stress, and this has sometimes been referred to as differential mitochondrial reserve capacity [70]. When cells experience severe oxidative stress through increased cellular metabolic demands, there is a loss of mitochondrial reserve capacity contributing to a fall in mitochondrial resiliency, which may be a major contributor in disease vulnerability.
An earlier paper by the same group reporting supporting findings:
Click on this link to read the paper: Genomic counter-stress changes induced by the relaxation response.
Genomic counter-stress changes induced by the relaxation response.
Source
Benson-Henry Institute for Mind Body Medicine at Massachusetts General Hospital, Chestnut Hill, Massachusetts, United States of America.
Abstract
BACKGROUND:
Mind-body practices that elicit the relaxation response (RR) have been used worldwide for millennia to prevent and treat disease. The RR is characterized by decreased oxygen consumption, increased exhaled nitric oxide, and reduced psychological distress. It is believed to be the counterpart of the stress response that exhibits a distinct pattern of physiology and transcriptional profile. We hypothesized that RR elicitation results in characteristic gene expression changes that can be used to measure physiological responses elicited by the RR in an unbiased fashion.
METHODS/PRINCIPAL FINDINGS:
We assessed whole blood transcriptional profiles in 19 healthy, long-term practitioners of daily RR practice (group M), 19 healthy controls (group N(1)), and 20 N(1) individuals who completed 8 weeks of RR training (group N(2)).
2209 genes were differentially expressed in group M relative to group N(1) (p<0.05) and 1561 genes in group N(2) compared to group N(1) (p<0.05). Importantly, 433 (p<10(-10)) of 2209 and 1561 differentially expressed genes were shared among long-term (M) and short-term practitioners (N(2)). Gene ontology and gene set enrichment analyses revealed significant alterations in cellular metabolism, oxidative phosphorylation, generation of reactive oxygen species and response to oxidative stress in long-term and short-term practitioners of daily RR practice that may counteract cellular damage related to chronic psychological stress. A significant number of genes and pathways were confirmed in an independent validation set containing 5 N(1) controls, 5 N(2) short-term and 6 M long-term practitioners.
CONCLUSIONS/SIGNIFICANCE:
This study provides the first compelling evidence that the RR elicits specific gene expression changes in short-term and long-term practitioners. Our results suggest consistent and constitutive changes in gene expression resulting from RR may relate to long term physiological effects. Our study may stimulate new investigations into applying transcriptional profiling for accurately measuring RR and stress related responses in multiple disease settings.
