Investigators at TPLH and the Mexican National Institute of Medical Sciences and Nutrition connect our body’s own steroids with aging.
Researchers disagree on whether our major stress hormone, cortisol, falls or rises as we age. This is a disagreement of some consequence. Both too much and too little cortisol, the major life-supporting steroid from our adrenal glands, can increase frailty and aging. Cortisol can also energize us under certain circumstances, which is why athletes take steroids to enhance their performance.
Cortisol has a great number of important actions in our bodies. Cortisol regulates our brains, fat deposition, appetite, bone strength, and our hearts and kidneys. It is important to understand how cortisol in the blood changes with aging and may act to regulate the speed of the aging process.
Timing of the age-related fall in corticosterone: In a recent publication in a leading aging journal, Age, we reported blood levels of corticosterone, the rat’s equivalent to human cortisol, right across the life-course, so as not to miss any early effects or late changes. No study of the total life-course has ever been conducted. Measurements right across the life-course are necessary to draw firm conclusions as to whether aging is accompanied by a rise or fall in cortisol. We measured corticosterone in rat blood at weaning, in young animals, mature adults, and through the aging phase to determine if there are significant changes in the second half of life. There was a clear fall in corticosterone in both males and females over the period equivalent to 50 to 72 years of human life.
The above graphs show blood corticosterone in control rats (open bars) at five ages (PND postnatal day). The ¥ sign indicates the first significant change when comparing each age with the one prior. Data are also presented for first generation offspring of obese mothers (closed bars). Data are mean ± SEM; group n=5–14. Further details are available in the full publication (AGE 2015;37:9774).
In conclusion, this study was the first to track the corticosterone across the majority of the life-course and demonstrate that a fall in corticosterone begins at least as early as the middle of life. This fall in corticosterone may be a consequence of aging, not necessarily a direct initiator of aging but may change its trajectory and determine the rate at which we age. We are exploring these two alternatives.
Aging-Developmental programming of aging. TPLH researchers and their colleagues throughout the world are studying how our early development before and immediately after birth affects how we age.
Our lives from womb to tomb: In humans, we know that offspring of obese mothers have shorter lifespans (BMJ 2013; 347:f4539). Our studies have shown that male and female offspring of fat rats have shorter lifespans than offspring of lean mothers. Male offspring of fat mothers live even shorter lives than females. This sex difference in lifespan is observed in humans. When we measured blood corticosterone in offspring of obese mothers, we found that the corticosterone levels are higher in females than males. However, the fall in corticosterone begins at a similar time to the fall that occurs in the offspring of normal weight mothers.
We conclude that the fall in corticosterone in the blood is a biomarker of aging. The earlier aging in offspring of fat mothers may be due to exposure of the tissues in offspring of fat mothers to higher levels of cortisol for longer periods of their lives, as the figure shows.
Full citation of Age paper discussed above:
Zambrano E, Reyes-Castro LA, Nathanielsz PW. Aging, glucocorticoids and developmental programming. Age (Dordr) 2015;37(3):9774. PMID:25953670.