Main findings:

• Persistent stress is associated with markers of accelerated aging, notably shorter telomeres (the protective end caps on chromosomes) and other cellular aging signs.
• A central mechanism is oxidative stress: chronic stress increases production of reactive oxygen species (ROS), which damage deoxyribonucleic acid (DNA), proteins and lipids — ROS are largely produced in mitochondria, so mitochondrial health is a key node linking stress → damage → aging.
• Mitochondrial dysfunction and defective mitophagy (the process that clears damaged mitochondria) amplify reactive oxygen species and inflammation; that feeds into a cycle of cellular damage and senescence (cells that stop dividing but secrete inflammatory factors). The review emphasizes mitochondria and mitophagy as crucial.
• Inflammation (sometimes called “inflammaging”) and immune cell changes — especially macrophage activation and altered cytokine profiles seen in conditions like post-traumatic stress disorder (PTSD) and chronic stress — are described as mechanisms that accelerate tissue aging and raise risk for age-related diseases (for example, atherosclerosis, diabetes, and neurodegeneration).
• The authors summarize potential interventions suggested by the biology: boosting mitophagy, promoting mitochondrial uncoupling (to reduce reactive oxygen species production), activating telomerase expression, and using antioxidants — all proposed as strategies that might reduce stress-related oxidative damage and slow aging signals. These ideas are mostly theoretical or experimental rather than proven clinical cures.

Ok, But, what does this actually mean?

• Most human data are associational: people under long-term stress tend to have biological signs consistent with “older” cells/tissues, but proving cause over effect is still difficult. Studies vary in methods and populations.
• Measuring aging is tricky: telomere length is useful but imperfect (blood telomere measures reflect averages, can be transient, and may not capture the shortest telomeres that trigger senescence). Tissue specificity and laboratory methods vary, so results can differ across studies.

This works like this:

1. Stress → more chemical sparks.
   When you’re constantly stressed your body makes more reactive oxygen species (ROS) — imagine tiny sparks or rust particles. Those sparks damage DNA, proteins, and fats inside cells.
2. The cell batteries get sick.
   Mitochondria (the cell’s batteries that make energy) get damaged by those sparks. If broken mitochondria aren’t cleared away, they make even more sparks. Mitophagy (the cell’s garbage-pickup for mitochondria) is the process that should remove damaged batteries — if that system fails, the mess grows.
3. Cells go grumpy and loud.
   Damaged cells can stop dividing but start releasing inflammatory signals (this is called cellular senescence). That chronic low-level inflammation (sometimes called “inflammaging”) is like neighbors yelling all the time — it wears down your tissues and speeds up aging.

Limitations

• The review points out gaps: we need more longitudinal, tissue-specific human studies and standardized biomarker methods to establish causality and to test whether the proposed interventions actually change clinical aging outcomes.

Give It To Me Straight...

Chronic psychological stress is strongly linked to biological signs of accelerated aging through reactive oxygen species/mitochondrial damage, inflammation, telomere attrition and cellular senescence — the review maps plausible molecular routes and highlights mitophagy, telomerase modulation and antioxidant strategies as promising (but largely experimental) ways to counteract those effects.

The understandable version of that is that chronic stress accelerates aging by creating cellular “sparks” that damage mitochondria and DNA, triggering inflammation and cellular dysfunction — but lifestyle changes that reduce stress, improve sleep, exercise, and eat nutrient-dense foods can help slow that process.

How Do I 'Slow' This Process?

(These are ideas scientists are exploring — not proven cures.)

• Boost mitophagy = help the cell’s cleanup crew remove broken batteries. Could slow the spark cycle.
• Mitochondrial uncoupling = slightly change how mitochondria run so they produce fewer sparks (a technical, experimental idea).
• Activate telomerase = try to slow or reverse shortening of telomeres (very early-stage research).
• Antioxidants = substances that neutralize sparks — some are dietary and helpful, while others are still being tested.

What this actually means for a real person — practical takeaways

You can’t flip a switch and “stop aging,” but you can reduce the processes the review flags. These things have the best evidence for lowering biological wear-and-tear:

• Reduce chronic stress: proven approaches include therapy (for example, cognitive behavioral therapy), regular meditation/mindfulness, or structured stress-management programs.
• Prioritize sleep: consistent, good-quality sleep helps repair cells and lowers stress hormones.
• Move regularly: aerobic exercise + resistance (strength) training improve mitochondrial health and lower inflammation.
• Eat a mostly whole-food diet: lots of vegetables, fruit, fiber, and sources of omega-3 fats — these support antioxidant defenses and reduce inflammation.
• Avoid big harms: smoking, excess alcohol, and very poor sleep drive oxidative stress and inflammation.
• Social connection & purpose: strong relationships and meaningful activity are reliably protective against chronic stress.
• Be cautious with supplements & “anti-aging” treatments: some things (like generic antioxidants) are fine as food; others (telomerase activators, experimental drugs) are not proven and need medical supervision.