#82

The cost would be lower than a full body MRI since you’re only scanning a specific part and for shorter.

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#83

On this note, because dutasteride can make it harder to find prostate cancer, my husband is now getting a yearly MRI at Stanford to monitor.

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#85

Expanding the List of Adverse Experiences

I interviewed 29 formerly incarcerated youth offenders about their childhoods for my recently published book, Before Their Crimes: What We’re Misunderstanding About Childhood Trauma, Youth Crime, and the Path to Healing. I asked many questions about home life, parents, school, and never asked specifically about problematic experiences, yet the open-ended recounting of childhood memories revealed the ACE scores of the people I spoke with as clearly as if they had checked the boxes on an ACE screen.

Their descriptions of childhood convinced me that the ten ACEs did not capture the difficulties that impinged powerfully on their developing selves. The memories they shared led me to create another list, first among which was the death of a parent. In my small sample, nearly 30% had lost a parent when they were under the age of 15, and in every case, a cascade of other risks and ACEs followed.

I added ten more, each of which can and often does put children at increased risk of negative outcomes. I included having parents who were teenagers themselves; experiencing foster care; multiple home moves; school moves during elementary, middle, and high school; being bullied; school suspensions and expulsions; having a relative who is a gang member; being introduced to crime by a family member; and witnessing gun violence. Even this list does not exhaust derailing experiences that can occur.

Read the Full story: The List of ACEs Should Be Longer | Psychology Today

References

Bay Area Research Consortium on Toxic Stress and Health (2018) Pediatric ACEs and Related Life Events Screener (PEARLS). https://globalprojects.ucsf.edu/project/bay-area-research-consortium-toxic-stress-and-health

Felitti, V., Anda, R., Nordenberg, D., Williamson, D., Spitz, A., Edwards, V., Koss, M., & Marks, J. (1998) Relationship of childhood abuse and household dysfunction to many of the leading causes of death in adults: The adverse childhood experiences (ACE) study. Amer J of Preventive Medicine, 14(4).

#86

Childhood Stress Echoes: New Review Links Early Adversity to Accelerated Brain Aging and Neurodegenerative Risk

Date: December 3, 2025 Source: International Journal of Molecular Sciences

A comprehensive narrative review published in the International Journal of Molecular Sciences synthesizes evidence linking Adverse Childhood Experiences (ACEs) to the pathogenesis of neurodegenerative diseases (NDs) like Alzheimer’s (AD), Parkinson’s (PD), and Multiple Sclerosis (MS). The authors argue that “toxic stress” experienced early in life does not merely vanish but undergoes “biological embedding,” manifesting decades later as accelerated cognitive decline and structural brain atrophy.

The central thesis posits that chronic dysregulation of the Hypothalamic–Pituitary–Adrenal (HPA) axis serves as the primary transducer of psychosocial trauma into cellular pathology. This “allostatic load” disrupts glucocorticoid signaling, leading to a cascade of systemic inflammation and mitochondrial dysfunction. Specifically, the review highlights that persistent elevation of cortisol downregulates hippocampal glucocorticoid receptors (GR) via FKBP5 methylation, impairing feedback loops and leaving the brain vulnerable to excitotoxicity.

Crucially, the authors map these stress pathways to specific neurodegenerative mechanisms. Chronic activation of the NF-κB pathway drives the release of pro-inflammatory cytokines (IL-6, TNF-α), causing microglial priming—a state where brain immune cells overreact to future insults. This neuroinflammation exacerbates oxidative stress, evidenced by mitochondrial DNA (mtDNA) depletion and telomere shortening. Ultimately, this cellular exhaustion compromises proteostasis, facilitating the aggregation of misfolded proteins such as amyloid-beta, tau, and alpha-synuclein, the hallmarks of AD and PD. The paper proposes that monitoring stress-associated biomarkers could provide a “preventive window” decades before clinical symptoms arise.

Mechanistic Interpretation for Longevity

  • HPA-Mitochondrial Axis: Chronic cortisol acts as a metabolic uncoupler. By altering FKBP5 expression, early stress induces glucocorticoid resistance, preventing the “off-switch” for inflammation. This forces mitochondria into a chronic high-output state, increasing Reactive Oxygen Species (ROS) generation and depleting NAD+, likely suppressing Sirtuin activity and AMPK signaling.
  • Inflammaging & Autophagy: The study details how elevated IL-6 and TNF-α impair autophagy, the cellular cleanup process. This failure allows protein aggregates (tau, a-synuclein) to accumulate. The activation of cGAS-STING pathways by leaked mtDNA (from damaged mitochondria) is a probable downstream effector, further amplifying neuroinflammation.
  • Vascular & Glial Involvement: Elevated GFAP (glial fibrillary acidic protein) levels highlight astrocyte reactivity, suggesting that the blood-brain barrier (BBB) is compromised early in this stress cascade, allowing systemic inflammatory factors to penetrate the brain parenchyma.

Novelty

The paper’s primary novelty lies in its temporal integration: it reframes neurodegeneration not as a disease of old age, but as a lifespan process initiated by pediatric “biological scars.” It specifically correlates non-biological triggers (ACEs) with specific molecular biomarkers (NfL, GFAP, FKBP5 methylation), validating the “biological embedding” theory with hard biochemical targets. It also formally introduces Benevolent Childhood Experiences (BCEs) as a quantifiable biological buffer that can neutralize these risks.

Actionable Insights for the “Biohacker Parent”

  • The “BCE” Protocol (Benevolent Childhood Experiences): The paper explicitly identifies positive experiences not merely as “nice to have,” but as biological counter-weights that can neutralize the effects of stress.
    • Action: Audit your child’s BCE score just as you would their grades. Ensure the presence of at least 1–2 consistent, non-parental supportive adult figures (mentors/coaches) and predictable family routines (e.g., fixed dinner times).
    • Mechanism: BCEs function as “epigenetic buffers,” preventing the methylation of FKBP5 and keeping the HPA axis responsive rather than reactive.
  • HPA Axis Calibration via Sleep:
    • Action: Prioritize circadian entrainment over social/academic flexibility. Enforce darkness at night and morning sunlight exposure.
    • Rationale: Disrupted sleep in childhood doesn’t just cause fatigue; it flattens the Cortisol Awakening Response (CAR). A robust CAR is essential for appropriate immune regulation and synaptic pruning.
  • Nutritional “Allostatic” Reduction:
    • Action: Eliminate ultra-processed foods and added sugars to the greatest extent possible.
    • Mechanism: The study highlights that oxidative stress and mitochondrial dysfunction drive neurodegeneration. A high-sugar diet creates “metabolic stress” that stacks with “psychological stress,” accelerating the threshold for mitochondrial exhaustion and microglial priming.
  • Distinguish “Positive” vs. “Toxic” Stress:
    • Insight: Not all stress is damaging. “Positive stress” (e.g., a difficult exam, a sports match) with supportive buffering builds resilience. “Toxic stress” is adversity without support.
    • Action: Do not aim to remove all stressors (snowplow parenting). Instead, focus on “scaffolding”—providing the emotional recovery period immediately after a stressor to ensure cortisol returns to baseline. This trains the GR feedback loop to shut off efficiently.
  • Environmental Toxin Audit:
    • Action: Reduce exposure to endocrine disruptors (plastics/phthalates) and air pollution.
    • Rationale: While the paper focuses on psychosocial stress, the biological pathway (oxidative stress/inflammation) is shared. Chemical stressors add to the “Allostatic Load,” making the child’s system more vulnerable to psychological insults.

Feasibility & Limitations for Parents:

  • Biomarkers: It is generally not recommended to track serum biomarkers (NfL, IL-6) in healthy children due to invasiveness and lack of pediatric reference ranges.
  • Observation over Data: Instead of blood tests, monitor behavioral biomarkers of HPA dysregulation: sleep regression, digestive issues (gut-brain axis), or persistent anxiety. These are the visible proxies for the internal cortisol state.

Study Parameters

  • Institution: School of Medicine and Health Sciences, Tecnológico de Monterrey
  • Country: Mexico
  • Journal: International Journal of Molecular Sciences
  • Rank: Q1 (Biochemistry & Molecular Biology); Impact Factor ~4.9–5.6
  • Study Type: Narrative Review (Synthesis of existing in vivo and human cohort data)

Source paper (open access) From Early Adversity to Neurodegeneration: Stress Biomarkers as Predictive Signals for Lifespan Brain Health

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#87