The Sabbath, Chronic Stress, and the Hippocampus

Jesus says this while defending hungry disciples who were picking grain on the Sabbath (Mark 2:23-28). His point is not that rest is optional. It is that the Sabbath is a gift fitted to human need, not a burden laid on top of it. Neuroscience has a lot to say about what happens when that need goes unmet.

Allostatic load. Bruce McEwen of Rockefeller University and Eliot Stellar introduced the term allostatic load (McEwen & Stellar, 1993), and McEwen (1998) made it widely known. The idea is simple. Your body’s stress systems are built to switch on in a crisis and then switch off. When they switch on too often, or fail to switch off, the cumulative cost is wear and tear on the body.

The main hormonal stress system is the HPA axis, short for hypothalamic-pituitary-adrenal. It is a three-step relay. The hypothalamus at the base of the brain signals the pituitary gland, the pituitary signals the adrenal glands above the kidneys, and the adrenals release cortisol, the main stress hormone. Working alongside it is the fast-acting sympathetic (“fight or flight”) nervous system. The cardiovascular, metabolic, and immune systems all respond to these signals, so they carry the cost when the signals never stop. In McEwen’s framework, acute stress responses are protective. Chronic activation without recovery is what does the damage.

Why the hippocampus? The hippocampus is a seahorse-shaped structure deep in each temporal lobe. It is essential for forming new memories, and it is also one of the brain’s main brakes on the HPA axis. It is packed with both types of cortisol receptor. When cortisol rises, the hippocampus senses it and helps signal the hypothalamus to turn the system back down. It is not the only brake. In animals, removing the hippocampus weakens this feedback without abolishing it (Jacobson & Sapolsky, 1991). But its high density of receptors makes it unusually exposed to cortisol, which helps explain why stress can impair memory.

In rats, repeated stress makes the branching dendrites of neurons in the hippocampal CA3 region retract, and it suppresses the birth of new neurons in the dentate gyrus. These changes are largely reversible when the stress ends (McEwen, 1999). One worry follows naturally. If chronic stress weakens the hippocampus, the hippocampus brakes the stress response less well, and stress runs longer. That is a hypothesized vicious cycle, not an established human fact.

What the human evidence actually shows. The clearest human data come from Cushing’s disease, where a tumor drives cortisol far above normal for years. In 12 such patients, hippocampal volume was negatively correlated with cortisol levels (r = -0.73), and smaller volume went with poorer verbal memory (Starkman, Gebarski, Berent, & Schteingart, 1992). After surgery lowered cortisol in 22 patients, hippocampal volume increased by up to 10% (mean 3.2%), and the size of the gain tracked the size of the cortisol drop (Starkman et al., 1999). That is encouraging: the change is at least partly reversible. In a small group of older adults whose cortisol rose over several years, those with the highest levels had smaller hippocampi and poorer memory (Lupien et al., 1998). Lupien, McEwen, Gunnar, and Heim (2009) review how the timing and duration of stress-hormone exposure shape the brain across the lifespan.

Ordinary stress is a different matter. The largest PTSD imaging study, 1,868 people from 16 cohorts, found smaller hippocampi in current PTSD, but the average difference was small (Cohen’s d = -0.17; Logue et al., 2018). A study of identical twins suggests that some of the difference was there before the trauma and may be a risk factor rather than damage (Gilbertson et al., 2002). A study of 30 people with long-term occupational stress and 68 controls found no hippocampal difference at all. The reductions it did find were in prefrontal and striatal regions involved in attention and self-regulation (Blix, Perski, Berglund, & Savic, 2013). All of these studies are correlational. So we should not assume that a stressful season is shrinking anyone’s hippocampus. The stronger, safer claim is the general one: stress systems are built to cycle, and recovery is part of the design.

Recovery is something you do. Occupational research supplies the human, behavioral side. Sonnentag and Fritz (2015) reviewed cross-sectional, longitudinal, and daily-diary studies showing that psychological detachment, mentally switching off from work during off-hours, is a key route to recovery. Heavy workloads erode detachment, and low detachment predicts strain and burnout. A meta-analysis of 91 samples (about 38,000 employees) found that detachment goes with less exhaustion, better sleep, and greater well-being (Wendsche & Lohmann-Haislah, 2017). The effects were small to medium. Two honest limits: the data are mostly self-report, and detachment was not significantly related to physiological stress markers such as cortisol.

Rhythm matters as much as quantity. A meta-analysis of vacation studies found that vacations improve health and well-being (d = 0.43) but that the benefit fades soon after people return to work (d = -0.38; de Bloom et al., 2009). A once-a-year break cannot do the work of a weekly one. Sleep is part of this too. When 11 young men were restricted to 4 hours in bed for six nights, their evening cortisol rose and their sympathetic nervous system activity increased (Spiegel, Leproult, & Van Cauter, 1999). Rest that cuts into sleep is not rest.

Studies of Sabbath-keeping itself. These are few and correlational, and none measures the brain or hormones. In a survey of 5,411 North American Seventh-day Adventists, Sabbath-keeping was associated with better self-reported health. The link was partly explained by religious coping, religious support, diet, and exercise (Superville, Pargament, & Lee, 2014). In 1,316 United Methodist clergy, keeping more Sabbath days went with higher spiritual well-being and quality of life. After adjusting for other factors, though, it was not significantly related to depression, anxiety, or physical health (Hough et al., 2019). In a 9-month follow-up of 167 clergy after Sabbath workshops, those whose Sabbath-keeping declined reported more anxiety and were less likely to be flourishing. Increases in Sabbath-keeping were linked to only one modest benefit. That study had no control group, and the authors note that most findings would not survive a correction for multiple comparisons (Proeschold-Bell et al., 2022). Adventists’ well-documented longevity (Fraser & Shavlik, 2001) is usually traced to diet, exercise, and not smoking. It cannot be credited to the Sabbath alone.

So I am not aware of any neuroimaging or cortisol study of Sabbath-keeping, and I will not pretend otherwise. The convergence is at the level of design principle: a body built with a stress system that must cycle between activation and recovery, and a Creator who built a rhythm of work and rest into the week.

Practice

Living it out

Five practices drawn from this passage. Each says how strong the research behind it is. What the labels mean.

1. 1

   Keep a weekly day, not just an annual vacation

   Pick a recurring 24-hour block and guard it the way you would guard a meeting with your boss. Vacation benefits fade within weeks of returning to work (de Bloom et al., 2009), and a weekly rhythm keeps renewing them. That is closer to the creation pattern than an annual break.

   ModerateModerate for “recovery helps and fades” (a meta-analysis of 7 studies); the Sabbath-specific benefit is only weak and correlational.
2. 2

   Detach on purpose: close the laptop, silence the work email

   Detachment means not thinking about work, not just not doing it. Put the phone’s work apps in a folder you do not open on the Sabbath, and write tomorrow’s to-do list Saturday night so your mind can let go of it. This is the best-supported element: detachment is consistently linked to less exhaustion and better sleep (Sonnentag & Fritz, 2015; Wendsche & Lohmann-Haislah, 2017).

   ModerateModerate to strong for self-reported well-being; not shown to change cortisol.
3. 3

   Protect sleep as part of the Sabbath

   Do not trade the Sabbath for a late night of catching up. Six nights of short sleep raised evening cortisol and sympathetic activity in young men (Spiegel et al., 1999). A Sabbath that begins with a full night’s sleep starts the reset.

   StrongStrong experimental evidence that sleep loss raises stress physiology, though in a small lab sample.
4. 4

   Make it worship and fellowship, not just time off

   In the Adventist data, the Sabbath’s link with health ran partly through religious coping and religious support (Superville et al., 2014). Among clergy, social support was the factor most consistently tied to health (Hough et al., 2019). Spend part of the day in worship, at a shared meal, or walking with your wife or a brother from the group.

   CorrelationalCorrelational and self-report only; plausible, but not proven.
5. 5

   Watch for the slide, and get back on track

   In the clergy follow-up, losing the Sabbath was more clearly tied to anxiety than gaining it was to benefit (Proeschold-Bell et al., 2022). Ask a man in the group to check in with you weekly (“Did you keep your day?”), and treat a missed week as a signal, not a failure.

   EarlyWeak (uncontrolled, 167 participants, findings fragile after multiple-comparison correction), but it fits the broader recovery literature.

Studies cited on this page19

1. ↗ Blix, E., Perski, A., Berglund, H., & Savic, I. (2013). Long-term occupational stress is associated with regional reductions in brain tissue volumes. PLoS ONE, 8(6), e64065. https://doi.org/10.1371/journal.pone.0064065
2. ↗ de Bloom, J., Kompier, M., Geurts, S., de Weerth, C., Taris, T., & Sonnentag, S. (2009). Do we recover from vacation? Meta-analysis of vacation effects on health and well-being. Journal of Occupational Health, 51(1), 13–25. https://doi.org/10.1539/joh.k8004
3. ↗ Fraser, G. E., & Shavlik, D. J. (2001). Ten years of life: Is it a matter of choice? Archives of Internal Medicine, 161(13), 1645–1652. https://doi.org/10.1001/archinte.161.13.1645
4. ↗ Gilbertson, M. W., Shenton, M. E., Ciszewski, A., Kasai, K., Lasko, N. B., Orr, S. P., & Pitman, R. K. (2002). Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nature Neuroscience, 5(11), 1242–1247. https://doi.org/10.1038/nn958
5. ↗ Hough, H., Proeschold-Bell, R. J., Liu, X., Weisner, C., Turner, E. L., & Yao, J. (2019). Relationships between Sabbath observance and mental, physical, and spiritual health in clergy. Pastoral Psychology, 68(2), 171–193. https://doi.org/10.1007/s11089-018-0838-9
6. ↗ Jacobson, L., & Sapolsky, R. (1991). The role of the hippocampus in feedback regulation of the hypothalamic-pituitary-adrenocortical axis. Endocrine Reviews, 12(2), 118–134. https://doi.org/10.1210/edrv-12-2-118
7. ↗ Logue, M. W., van Rooij, S. J. H., Dennis, E. L., Davis, S. L., Hayes, J. P., Stevens, J. S., Densmore, M., Haswell, C. C., Ipser, J., Koch, S. B. J., Korgaonkar, M., Lebois, L. A. M., Peverill, M., Baker, J. T., Boedhoe, P. S. W., Frijling, J. L., Gruber, S. A., Harpaz-Rotem, I., Jahanshad, N., … Morey, R. A. (2018). Smaller hippocampal volume in posttraumatic stress disorder: A multisite ENIGMA-PGC study: Subcortical volumetry results from posttraumatic stress disorder consortia. Biological Psychiatry, 83(3), 244–253. https://doi.org/10.1016/j.biopsych.2017.09.006
8. ↗ Lupien, S. J., de Leon, M., de Santi, S., Convit, A., Tarshish, C., Nair, N. P., Thakur, M., McEwen, B. S., Hauger, R. L., & Meaney, M. J. (1998). Cortisol levels during human aging predict hippocampal atrophy and memory deficits. Nature Neuroscience, 1(1), 69–73. https://doi.org/10.1038/271
9. ↗ Lupien, S. J., McEwen, B. S., Gunnar, M. R., & Heim, C. (2009). Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience, 10(6), 434–445. https://doi.org/10.1038/nrn2639
10. ↗ McEwen, B. S. (1998). Protective and damaging effects of stress mediators. New England Journal of Medicine, 338(3), 171–179. https://doi.org/10.1056/NEJM199801153380307
11. ↗ McEwen, B. S. (1999). Stress and hippocampal plasticity. Annual Review of Neuroscience, 22, 105–122. https://doi.org/10.1146/annurev.neuro.22.1.105
12. ↗ McEwen, B. S., & Stellar, E. (1993). Stress and the individual: Mechanisms leading to disease. Archives of Internal Medicine, 153(18), 2093–2101.
13. ↗ Proeschold-Bell, R. J., Stringfield, B., Yao, J., Choi, J., Eagle, D., Hybels, C. F., Parnell, H., Keefe, K., & Shilling, S. (2022). Changes in Sabbath-keeping and mental health over time: Evaluation findings from the Sabbath Living study. Journal of Psychology and Theology, 50(2), 123–138. https://doi.org/10.1177/00916471211046227
14. ↗ Sonnentag, S., & Fritz, C. (2015). Recovery from job stress: The stressor-detachment model as an integrative framework. Journal of Organizational Behavior, 36(S1), S72–S103. https://doi.org/10.1002/job.1924
15. ↗ Spiegel, K., Leproult, R., & Van Cauter, E. (1999). Impact of sleep debt on metabolic and endocrine function. The Lancet, 354(9188), 1435–1439. https://doi.org/10.1016/S0140-6736(99)01376-8
16. ↗ Starkman, M. N., Gebarski, S. S., Berent, S., & Schteingart, D. E. (1992). Hippocampal formation volume, memory dysfunction, and cortisol levels in patients with Cushing’s syndrome. Biological Psychiatry, 32(9), 756–765. https://doi.org/10.1016/0006-3223(92)90079-f
17. ↗ Starkman, M. N., Giordani, B., Gebarski, S. S., Berent, S., Schork, M. A., & Schteingart, D. E. (1999). Decrease in cortisol reverses human hippocampal atrophy following treatment of Cushing’s disease. Biological Psychiatry, 46(12), 1595–1602. https://doi.org/10.1016/s0006-3223(99)00203-6
18. ↗ Superville, D. J., Pargament, K. I., & Lee, J. W. (2014). Sabbath keeping and its relationships to health and well-being: A mediational analysis. The International Journal for the Psychology of Religion, 24(3), 241–256. https://doi.org/10.1080/10508619.2013.837655
19. ↗ Wendsche, J., & Lohmann-Haislah, A. (2017). A meta-analysis on antecedents and outcomes of detachment from work. Frontiers in Psychology, 7, 2072. https://doi.org/10.3389/fpsyg.2016.02072