The effects of yoga on inflammation


This is interesting. It’s from Harvard, but they are also selling something on the page (a book about yoga). I’ll link to the original study below.

It seems to have involved a lot of yoga: 90 minutes per day, five days per week, for 12 weeks.

Chronic stress has been linked to accelerated biological aging, and increased chronic inflammation and oxidative stress, two processes that cause cellular and genetic damage. Scientists refer to chronic, low-grade inflammation in the body as “inflammaging.” Inflammaging has been associated with conditions like diabetes, heart disease, stress, depression, and a weakened immune system.

Several recent studies suggest that yoga could slow the harmful physical effects of stress and inflammaging. There are many different types of biomarkers in the blood that can be used to measure the level of chronic inflammation and stress in the body. Cortisol varies throughout the day based on the circadian rhythm, and a higher baseline level of cortisol is one indicator of high chronic stress. Cortisol becomes less variable throughout the day in people who are chronically stressed, signaling an overactive fight-or-flight or sympathetic nervous system.

In an exploratory study published in Oxidative Medicine and Cellular Longevity, researchers found that 12 weeks of yoga slowed cellular aging. The program consisted of 90 minutes of yoga that included physical postures, breathing, and meditation five days a week over 12 weeks. Researchers found indications of lower levels of inflammation and significantly decreased levels of cortisol. The study also found higher levels of BDNF after the yoga program, suggesting that yoga could have potential protective effects for the brain as well.

This study was designed to explore the impact of Yoga and Meditation based lifestyle intervention (YMLI) on cellular aging in apparently healthy individuals. During this 12-week prospective, open-label, single arm exploratory study, 96 apparently healthy individuals were enrolled to receive YMLI. The primary endpoints were assessment of the change in levels of cardinal biomarkers of cellular aging in blood from baseline to week 12, which included DNA damage marker 8-hydroxy-2′-deoxyguanosine (8-OH2dG), oxidative stress markers reactive oxygen species (ROS), and total antioxidant capacity (TAC), and telomere attrition markers telomere length and telomerase activity. The secondary endpoints were assessment of metabotrophic blood biomarkers associated with cellular aging, which included cortisol, β-endorphin, IL-6, BDNF, and sirtuin-1. After 12 weeks of YMLI, there were significant improvements in both the cardinal biomarkers of cellular aging and the metabotrophic biomarkers influencing cellular aging compared to baseline values. The mean levels of 8-OH2dG, ROS, cortisol, and IL-6 were significantly lower and mean levels of TAC, telomerase activity, β-endorphin, BDNF, and sirtuin-1 were significantly increased (all values p < 0.05) post-YMLI. The mean level of telomere length was increased but the finding was not significant (p = 0.069). YMLI significantly reduced the rate of cellular aging in apparently healthy population.