Yes, I guess lower stress and early treatment of the repercussions…
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I just hope for the sake of my kids (growing up with a severely delusional psychotic mother (also a source of chronic stress for me unfortunately)) that knowing about the potential issues later in life will either stop it from happening or allow them to recognise it early so they can quickly do something about it.
I do try to give them as many positive experiences as possible so hopefully that mitigates as the second article suggests.
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Related to this issue, I’ve read that plenty of Omega 3 fatty acids for children during childhood can help prevent psychosis… see these studies:
A new study, the largest of its kind, published in Biological Psychiatry today [12 June], tracked the blood test results of over 3,500 participants for a span of 17 years to explore a possible link between diet and mental health.
Led by Queen’s University Belfast, the longitudinal study, using data from the University of Bristol’s Children of the 90s, examined how blood levels of omega-6 and omega-3 fatty acids, as well as a specific omega-3 fatty acid called docosahexaenoic acid (DHA), changed over time.
Working in collaboration with researchers from the University of Cambridge and RCSI University of Medicine and Health Sciences, the aim was to identify if, and how, these variations were related to the development of symptoms of psychosis in young adults aged 24.
Researchers tracked the participants, who are part of the Avon Longitudinal Study of Parents and Children (ALSPAC), also known as ‘Children of the 90s’, from childhood into adulthood.
The fatty acid levels were measured in the blood tests collected from the participants throughout their lives, at the specific ages of 7, 15, 17 and 24 years old.
The findings reveal that those with persistently higher levels of omega-6 compared to omega-3 fatty acids in their blood, as well as consistently low DHA levels, had more psychotic experiences at age 24 compared to people whose levels remained average over this time period. Psychotic experiences include thoughts of paranoia or hearing sounds others cannot.
In addition, these participants also showed greater negative symptoms of psychosis. Negative symptoms include experiencing a loss of interest in activities, flattening of emotions and social withdrawal.
Adequate intake of omega-3 fatty acids is recommended for general health, and the balance of omega-6 to omega-3s is thought to be important for various physical and mental health benefits.
Foods high in omega-3 include certain fish and seafood, some vegetable oils, nuts, and high fat plant foods such as chia seeds, flaxseeds, brussels sprouts and more. Omega-6 fatty acids can be found in sunflower, safflower, soy, sesame, and corn oils.
Commenting on the significance of the findings, Dr David Mongan, Academic Clinical Lecturer at Queen’s University, said: “This inaugural study is important because the results suggest that optimising fatty acid status during crucial stages of development, whether through diet or supplementation, warrants further investigation in relation to reducing psychotic symptoms in early adulthood.”
Omega-3s May Have Ability to Delay or Prevent Psychosis
Therefore, the omega-3 fatty acids can “reduce the risk of progression to psychotic disorder and may offer a safe and efficacious strategy for indicated prevention in young people with subthreshold psychotic states,” Amminger and his team concluded.
“I think this is a very important paper,” Scott Woods, M.D., a Yale University professor of psychiatry and one of the scientists trying to keep prodromal schizophrenia from developing into full-blown illness, told Psychiatric News. “Omega-3s are safe, and it would be terrific if they could really prevent psychosis.”
https://psychiatryonline.org/doi/10.1176/pn.45.6.psychnews_45_6_024
Nature Open Access Paper:
Longer-term outcome in the prevention of psychotic disorders by the Vienna omega-3 study
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This is the reason all the children in my extended family take Omega 3s.
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It isn’t a genetic issue so they should be fine in that respect, but thanks for thinking about that possibility.
Key Insights and Implications
One of the study’s most striking findings involves cortisol, a steroid hormone commonly associated with stress. The researchers found that when cortisol levels doubled, biological age increased by approximately 1.5 times. This suggests that chronic stress could accelerate aging at a biochemical level, reinforcing the importance of stress management in maintaining long-term health.
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I think this jives with the common epigenetic aging factors. Students have a higher epigenetic age before a test and lower after. Mothers have a higher epigenetic age before giving birth and an even higher one after. 
Childhood Stress Rewires the Brain: Study Reveals Widespread White Matter Disruption
A study by Mass General Brigham involving over 9,000 participants found that early life adversity is linked to weaker white matter connections in the brain, which can raise the risk of cognitive challenges. However, supportive relationships may help buffer against these effects.
Researchers at Mass General Brigham have found that adverse experiences in early childhood are linked to reduced development of white matter, the brain’s communication pathways, during adolescence. This diminished connectivity is also associated with poorer performance on cognitive tasks. However, certain protective social factors, such as strong neighborhood cohesion and supportive parenting, may help buffer these effects. The findings are published in the Proceedings of the National Academy of Sciences.
White matter serves as the brain’s communication network, enabling different regions to work together to support thinking and behavior.
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I swear, every time I start to lose patience and let things start getting to me, @RapAdmin links another article relating stress and longevity and it reminds me to just breathe and take things a little slower. 
One of my all-time favorite papers is also relevant to this thread:
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I wonder if these drugs, or other anxiety or anti-depressant drugs might increase lifespan in people who live stressful lives (or are going through very stressful periods in their lives). Seems like something some good animal studies might reveal:
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Generally I think everyone that ages will get every aging disease suiting their sex, but in different orders and generally people die before getting all of them. That is because the balance of mitochondrial quality and burden of senescence varies.
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Epigenetic biomarkers of mortality risk in mice under chronic social stress
A strong association exists between exposure to life stressors and accelerated aging in humans and animal models. However, the molecular mechanisms that underlie the adverse effect of stress on aging remain poorly characterized, and there is a paucity of prognostic predictors of stress-induced disease outcomes and life expectancy. To address this gap, we developed mathematical models to predict remaining lifespan based on healthspan data across two independent cohorts which were part of a large study (350 + mice) on social stress and aging in mice. We then relate remaining lifespan to changes in DNA methylation, due to its strong association with age as well as environmental factors such as stress exposure. Multivariate multiple regression identified blood glucose as a major trait associated with DNA methylation. An independent neural network analysis also identified blood glucose among the traits most associated with mortality risk. Finally, elastic net regression identified several DNA methylation sites, including Ptp4a3, Lrrc3b, Adgrb1, Mron5, and Gm6549, which represent possible targets at the intersection of glucose, stress and survival. Overall, the main finding of our analysis is that epigenetic biomarkers of mortality risk reveal an association with blood glucose levels, informing on individual life trajectories shaped by the impact of chronic social stress.
Open Access Paper:
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For example, in one 2024 study of male mice, Bartolomucci’s team demonstrated that social stress during a relatively brief period in early life led to an increase in levels of a key marker of cellular senescence, called p16, in the brain, fat tissue and immune cells7.
See: How your brain controls ageing — and why zombie cells could be key (Nature)
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