Category: Health News

In the evolving field of nutraceutical science, Magnolia officinalis continues to stand out — thanks to two key compounds: magnolol and honokiol.
These biphenolic molecules bridge neuroscience, inflammation, and metabolic regulation, offering a broad therapeutic spectrum that’s rare among botanical actives.

✅Neuroprotective & Cognitive Support

– Cross the blood–brain barrier
– Modulate GABA_A receptors → calm, focus, and sleep
– Reduce neuroinflammation & oxidative stress
– Support neuroprotection and healthy cognition

✅Cardiometabolic Support

– Activate AMPK → improved insulin sensitivity & lipid metabolism
– Reduce inflammatory cytokines
– Enhance endothelial and vascular function

✅Systemic Anti-Inflammatory & Antioxidant Effects

– Inhibit NF-κB and MAPK pathways
– Reduce oxidative and inflammatory stress across multiple systems

❇️Emerging Research Areas

– Oncology: Inhibits tumor growth & angiogenesis via PI3K/Akt and STAT3

– Gut & Liver: Supports microbiome balance and reduces endotoxemia

– Microbial Defense: Active against H. pylori and Candida albicans

As a product formulator, I find magnolol and honokiol particularly fascinating for their dual neuro-metabolic and anti-inflammatory synergy — bridging stress, inflammation, and metabolic imbalance, the underlying triad in many chronic conditions.

These compounds are now finding new relevance in precision nutraceutical and longevity formulations.

Key references:

Zhao et al., Frontiers in Pharmacology (2020)
Li et al., Phytomedicine (2018)
Fang et al., Biochem Pharmacol (2015)
Chen et al., J Ethnopharmacol (2020)


Rob Lamberton
Product Formulator | Consultant in Functional & Regenerative Health Innovation

Let’s connect if your company or clinic is exploring bioactive compounds and advanced nutraceutical formulations for brain, metabolic, or longevity applications.

#depression #anxiety #anxiolytic #health #healthcare #herbs #medicinalherbs #functionalmedicine #naturopathicmedicine #integrativemedicine #nutraceuticals #healthspan #lifespan #naturalmedicine #herbalmedicine #nutrition #naturalhealth

Ivermectin shown to have yet another significant potential benefit!

Content paraphrased from a Focus Points – Courageous Discourse Substack article by Nicolas Hulscher, MPH

Epidemiologist and Foundation Administrator, McCullough Foundation

https://mcculloughfnd.org

Landmark preclinical study shows intranasal ivermectin nanocapsules safely shrink glioblastoma in animal models at doses lower than the approved human antiparasitic dose.

Tumor Size Reduced by 70%

After just 10 days of treatment:

✅Control tumors averaged 254 mm³
✅IVM-NC tumors averaged only 79 mm³ — a 70% reduction in size, confirmed by histopathology
✅Non-encapsulated (free) ivermectin — given the same intranasal route — had no measurable effect

Zero Detectable Toxicity
At the same time, the nano-formulated ivermectin showed no adverse effects:

✳️No changes in body weight, liver, or kidney markers
✳️No lung inflammation, hemorrhage, or edema
✳️No cytotoxicity in normal fibroblast cell lines
✳️Even at repeated daily doses, the treatment remained completely well-tolerated.
✳️By contrast, the non-nano (free) ivermectin and silica nanoparticle formulations both caused tissue irritation and cell death at higher concentrations.

✅ These findings align with ivermectin’s 14 distinct anti-cancer mechanisms summarized by Yuwen et al., encompassing inhibition of oncogenic signaling (YAP1, Wnt–TCF, Akt/mTOR, EGFR/NF-κB, MAPK), mitochondrial and oxidative-stress induction, ion-channel modulation, and suppression of both cancer stem cells and the epithelial–mesenchymal transition (EMT).

✅ By hitting multiple hallmarks of cancer simultaneously — proliferation, metabolism, invasion, and survival — ivermectin appears to function as a multi-targeted anti-tumor agent. In glioblastoma, these converging effects explain the 70% tumor-volume reduction observed with intranasal nano-ivermectin, achieved at doses below standard antiparasitic levels and without toxicity.

✅ Clinical translation in humans is urgently needed. Encouragingly, this effort may already be underway. On September 24, 2025, Governor Ron DeSantis and First Lady Casey DeSantis announced a $60 million funding opportunity through the Florida Cancer Innovation Fund, prioritizing translational cancer research, short-duration clinical trials, and the repurposing of safe, generic drugs such as ivermectin for cancer treatment.

As a nutritional supplement formulator and consultant, I’m always searching for ingredients that actively modulate the biological pathways of aging

One of the most impressive compounds I’ve worked with is L-Ergothioneine (ERG) — an amino acid found in mushrooms 🍄 that may be among the most powerful longevity molecules discovered so far

We actually have a dedicated transporter (OCTN1) to absorb and retain it — meaning it’s biologically essential for long-term cellular protection and repair

🧬 How L-Ergothioneine Impacts Longevity and Cellular Health

L-Ergothioneine can help increase both lifespan (in animal models) and healthspan, creating a foundation for cellular resilience and genomic integrity — the #1 predictor of longevity

💠 Genomic Stability & DNA Repair

• Protects and repairs both nuclear and mitochondrial DNA
• Prevents telomere shortening
• Repairs aging-dependent accumulation of point mutations in the mtDNA control region
• Eliminates DNA-damaging acids hypobromous and hypochlorous

💠 Mitochondrial & Metabolic Optimization

• Increases mitochondrial and metabolic activity
• Prevents mitochondrial dysfunction and supports efficient ATP production
• Increases cell viability by up to 45%

💠 Superior Antioxidant Power

• Eliminates all free radicals 3,435% more effectively than glutathione
• Inhibits cell membrane damage 270% better than CoQ10
• Neutralizes singlet oxygen up to 7,500% better than any known antioxidant
• Provides sustained antioxidant protection for up to 30 days

💠 Systemic Anti-Aging Benefits

• Supports cognition, cardiovascular health, and organ vitality
• Helps prevent sarcopenia and macular degeneration
• Reverses UV and sun damage by repairing and protecting skin DNA and mtDNA

ERG doesn’t simply slow aging — it addresses its root biological mechanisms, restoring cellular function from the inside out

⚗️ Formulation Insight

In advanced nutraceutical formulations, L-Ergothioneine pairs synergistically with:
🔹 Ingredients targeting mitochondrial biogenesis and energy metabolism
🔹 NAD+ Precursors → For NAD⁺ restoration and DNA repair
🔹 Compounds which activate NRF2 activation and cellular detox pathways

Together, these ingredients form the core of next-generation longevity formulations — designed to extend not just life, but quality of life

If your brand or clinic is exploring science-based formulation strategies for longevity, cognition, or metabolic vitality, reach out to me

Let’s connect to transform cutting-edge longevity science into real-world, market-ready innovation

Rob Lamberton, BSc, FNTP, FDN-P
🧪 Nutritional Supplement Formulator | Consultant | Integrative Health Strategist

Helping brands and practitioners develop evidence-based, biologically intelligent nutraceutical formulations

#longevity #nutraceuticals #healthyliving #formulationscience #healthspan #lifespan #formulationscience #ergothioneine #health #nutritionalsupplements #healthcare

Here are two resources I want share on this topic have provided me with some clarity:

– An article by Peter McCullough MD MPH

Peter is a highly respected cardiologist who has been quite vocal about the pandemic and it’s after effects ever since it started 

– A podcast by Peter Attia MD which reviews in depth some key studies on this topic – https://tinyurl.tools/e1b95f87

The Takeaway?

Acetaminophen may have a minor/negligible impact on the development of ASD – Autism Spectrum Disorder – or even none 

Following is the article by Peter McCullough

Confounded Association Between Prenatal Tylenol and Childhood Neuropsychiatric Disorders

Large, Conclusive Swedish Study Finds Relationship, Demonstrates Lack of Independence

PETER A. MCCULLOUGH, MD, MPH

Before the recent HHS press briefing on autism, there was little or no discussion on mainstream, social, or Substack media on acetaminophen use during pregnancy. Many did not know Tylenol is one of many drugs implicated.

An AI search found at least thirty drugs used during pregnancy “linked” to neuropsychiatric problems later on in the child.

There are numerous prenatal drugs and substances that have been associated with increased risk of childhood neuropsychiatric or neurodevelopmental disorders (such as autism spectrum disorder, ADHD, intellectual disability, anxiety, depression, behavioral problems, or cognitive deficits) in the scientific literature. Based on a synthesis of peer-reviewed sources (including systematic reviews, cohort studies, and meta-analyses from PubMed, JAMA, BMJ, and other databases), at least 30 specific drugs have been associated with these risks to varying degrees. Citations are rendered inline where direct sources are available.

Anticonvulsants/Antiseizure Medications (5+ drugs) These are commonly linked to neurodevelopmental risks, especially autism and intellectual disability, due to interference with brain development.

  • Valproic acid/valproate: Strongly associated with ASD (up to 7-fold increased risk), lower IQ, and behavioral disorders.jamanetwork.com +3
  • Carbamazepine: Neural tube defects and potential cognitive delays.womensmentalhealth.org
  • Phenytoin: Linked to developmental delays and cognitive deficits (though evidence is weaker than for valproate).pmc.ncbi.nlm.nih.gov
  • Topiramate: Increased risk of ASD and intellectual disability.med.stanford.edu
  • Lamotrigine: Mixed evidence; some studies show weak links to oral clefts or learning difficulties, but often considered lower-risk.aafp.org +1

Antidepressants (15+ drugs) Prenatal exposure, especially in the first trimester, has been linked to ASD, ADHD, altered brain development, and behavioral issues, though evidence is conflicting and often tied to underlying maternal depression.

  • SSRIs (selective serotonin reuptake inhibitors) as a class: Increased ASD risk (up to 2-fold) and altered pain response or stress axis function.womensmentalhealth.org
    • Fluoxetine: Autism-like behaviors, lifelong behavioral abnormalities, altered serotonin function.
    • Paroxetine: Attention problems, aggression, hyperactivity.
    • Sertraline: Cognitive and behavioral changes.
    • Citalopram: Neonatal distress with potential long-term behavioral effects.
    • Escitalopram: Musculoskeletal defects and psychomotor delays.
  • TCAs (tricyclic antidepressants) as a class: Neonatal syndrome, long-term behavioral changes (e.g., altered social interaction, cognition).
    • Amitriptyline: Developmental delays, central nervous system effects.
    • Clomipramine: Autism-like responses, reduced anxiety in models.
    • Desipramine: Altered behavioral responsiveness.
    • Imipramine: Behavioral changes, altered brain histology.
    • Nortriptyline: Decreased body weight and potential developmental effects (animal models).
    • Trimipramine: Major abnormalities (animal models).
  • SNRIs (serotonin-norepinephrine reuptake inhibitors): Similar to SSRIs; disrupted behaviors.
    • Venlafaxine: Decreased exploratory/social behaviors.
  • Atypical antidepressants: Anxiety-like behaviors.
    • Bupropion: Increased anxiety, stress vulnerability, substance sensitivity.
    • Trazodone: Decreased exploratory/social behaviors.
  • MAOIs (monoamine oxidase inhibitors): Limited data, but linked to ASD.
    • Selegiline: Increased ASD risk.

Antipsychotics (7+ drugs) Associated with neurodevelopmental disorders and learning difficulties, though evidence is emerging and often for neonatal withdrawal rather than long-term effects.

  • Typical antipsychotics as a class: Potential congenital malformations.
    • Haloperidol: Teratogenic risks low, but neonatal effects.
    • Perphenazine: Malformations (low-potency agents).
    • Trifluoperazine: Similar to above.
  • Atypical antipsychotics as a class: Risk of specific neurodevelopmental disorders; neonatal extrapyramidal signs or withdrawal.sciencedirect.com
    • Olanzapine: No major malformations, but neonatal complications.
    • Risperidone: Similar neonatal risks.
    • Quetiapine: Obstetrical/neonatal complications.
    • Clozapine: Limited data; potential malformations.
    • Aripiprazole: Limited data.

Opioids (4+ drugs)Linked to lower cognitive/motor skills, ADHD, and behavioral disorders, though not always substantial increases.  bmj.com +4

  • Methadone: Lower mental development, neurodev impairment.
  • Morphine: Altered stress responses, anxiety-like behaviors.
  • Oxycodone: Similar to morphine; long-term morbidity.
  • Buprenorphine: Neonatal withdrawal, behavioral changes.

Other Medications (3+ drugs)

  • Acetaminophen: Increased risk of NDDs (e.g., autism, ADHD) and other neuropsychiatric disorders.ehjournal.biomedcentral.com +1
  • Benzodiazepines (class): Possible increased risk of learning/neuropsychiatric disorders, cleft lip/palate (weak long-term data).womensmentalhealth.org
  • Synthetic glucocorticoids (e.g., dexamethasone, betamethasone): Attention problems, executive dysfunction, cortical thinning.pmc.ncbi.nlm.nih.gov

As an epidemiologist and a long-standing journal editor, I have become skilled at determining and examining the best and most conclusive sources of evidence among many publications on a topic. The reported link between prenatal acetaminophen use and the development of neuropsychiatric disorders several years later in the child is best evaluated by Ahlqvist et al, JAMA 2024

By Rob Lamberton, BSc, FNTP, FDN-P
Functional Medicine Practitioner & Product Formulator


Most people already know that soda isn’t exactly a wellness beverage. But far fewer understand that one particular ingredient — phosphoric acid — may be doing far more harm than the sugar itself.

Used in many cola drinks for its sharp, tangy flavor and as a preservative to inhibit bacterial growth, phosphoric acid has been linked to a range of negative effects on bone, kidney, heart, and dental health.

Let’s look at what the science reveals — and why reducing your exposure could support long-term health and vitality.


🦴 1. Bone Health: The Silent Calcium Drain

Phosphoric acid increases urinary calcium loss, creating a calcium deficit that your body compensates for by drawing calcium from the bones.

Over time, this can lead to bone demineralization, lower bone density, and an elevated risk of osteopenia and osteoporosis — particularly in women.

👉 In the Framingham Osteoporosis Study, women who consumed cola beverages daily had significantly lower bone mineral density compared to non-cola drinkers — even when calcium and vitamin D intake were adequate.

Tucker KL et al., Am J Clin Nutr. 2006;84(4):936–942.


💧 2. Kidney Health: Acid Load and Stone Formation

Phosphoric acid contributes to urine acidification, which can promote the formation of uric acid and phosphate-based kidney stones.

Excess dietary phosphate may also cause renal tubular injury and accelerate renal aging and fibrosis, even in those without existing kidney disease.

Sullivan CM et al., Clin J Am Soc Nephrol. 2017;12(12):2034–2043.

For individuals with reduced kidney function or metabolic issues, this acid load can further compromise the body’s ability to regulate phosphate balance.


❤️ 3. Cardiovascular Impact: Accelerated Vascular Aging

Elevated serum phosphate levels have been associated with vascular calcification, arterial stiffness, and endothelial dysfunction — all precursors to cardiovascular disease.

Even modest increases in phosphate within the high-normal range are linked to greater all-cause and cardiovascular mortality.

Ellam TJ, Chico TJ. Clin Sci (Lond). 2012;122(10):397–407.

Essentially, excessive phosphate may “age” the arteries from the inside out, contributing to premature cardiovascular decline.


😬 4. Dental Health: Erosion Without Sugar

Sugar isn’t the only dental villain. Phosphoric acid is highly erosive to tooth enamel, stripping away minerals that protect against decay.

Even sugar-free sodas can degrade enamel due to their acidity. Over time, this leads to tooth sensitivity, cavities, and enamel thinning.

Barbosa CS et al., J Clin Pediatr Dent. 2020;44(1):22–26.


⚖️ 5. Acid-Base Imbalance and Mineral Depletion

Your body works hard to maintain a stable pH balance. Regular consumption of acidic beverages like soda can lead to low-grade metabolic acidosis, prompting the body to buffer acid by drawing alkaline minerals such as calcium and magnesium from bones and muscles.

This process can contribute to mineral depletion, fatigue, and musculoskeletal discomfort over time.

Bushinsky DA, J Nephrol. 2017;30(2):215–221.


🍭 6. Nutrient Displacement and Metabolic Stress

Every can of soda replaces a more nourishing beverage such as water, mineral water, or herbal tea. The result is reduced intake of key nutrients — and an increase in sugar, caffeine, and phosphate, which together amplify insulin resistance, metabolic syndrome, and weight gain.

Vartanian LR et al., Am J Public Health. 2007;97(4):667–675.


💡 The Takeaway

Phosphoric acid isn’t just a flavor enhancer — it’s a biochemically active compound with real physiological effects.

Even diet sodas, though free from sugar, can still:
✅ Weaken bones
✅ Stress kidneys
✅ Promote vascular calcification
✅ Erode dental enamel

Over time, these effects add up, contributing to premature aging of multiple organ systems.

If you’re looking to protect your long-term health and longevity, start by replacing soda with health-promoting alternatives:

💧 Mineral-rich sparkling water
🍋 Water with lemon or trace minerals
🌿 Herbal infusions or adaptogenic teas

Your bones, kidneys, teeth, and heart will thank you.


📚 References

  1. Tucker KL, et al. Colas, but not other carbonated beverages, are associated with low bone mineral density in older women. Am J Clin Nutr. 2006;84(4):936–942.
  2. Sullivan CM, et al. Phosphate toxicity in chronic kidney disease: new insights. Clin J Am Soc Nephrol. 2017;12(12):2034–2043.
  3. Ellam TJ, Chico TJ. Phosphate: the silent killer? Clin Sci (Lond). 2012;122(10):397–407.
  4. Barbosa CS, et al. Dental enamel erosion by acidic soft drinks: an in vitro study. J Clin Pediatr Dent. 2020;44(1):22–26.
  5. Bushinsky DA. Acid-base imbalance and bone disease. J Nephrol. 2017;30(2):215–221.
  6. Vartanian LR, et al. Effects of soft drink consumption on nutrition and health: a systematic review and meta-analysis. Am J Public Health. 2007;97(4):667–675.

✳️ About Rob Lamberton

Rob Lamberton, BSc, FNTP, FDN-P, is a Functional Medicine Practitioner, Health Consultant, and Product Formulator specializing in longevity and regenerative health solutions.
Through his work, Rob helps individuals and health companies develop science-based strategies that optimize human performance and healthspan.

👉 Learn more at www.roblamberton.com

Psychedelics – in particular psilocybin are gaining a lot of attention as a therapeutic modality for the treatment of emotional/psychological issues such as anxiety, depression, PTSD, and the emotional stress of terminal illnesses.

Now a new study suggests that it may also act as a potent anti-aging molecule.  

Following is an article from Rhonda Patrick PhD on this topic. 

Rhonda hosts a very popular podcast and puts out a newsletter which is well worth checking out.

Here is a link to her website.

In a new study, psilocybin showed exciting potential as an anti-aging molecule. Human cells treated with psilocin (the active form of psilocybin) lived up to 57% longer, experienced less DNA damage, had lower stress at the cellular level, and maintained healthier telomeres—the protective caps on our DNA associated with longevity.
 Older mice given monthly psilocybin doses lived significantly longer (80% survival vs. 50% in untreated mice) and looked visibly younger, with fuller, healthier fur and less gray hair.

 No matter your stance on psychedelics, including the fact that they’re a Schedule I substance, these findings provide tantalizing new evidence that may open a path toward ‘psychedelic-assisted senotherapeutics’ for healthy aging

Psilocybin as a Longevity Molecule

Should we expand our thinking about psychedelics as more than just tools for mental health? It’s true that psilocybin has primarily been investigated for mental health conditions, including depression and anxiety, and even for neurodegenerative diseases like Alzheimer’s, where clinical evidence supports robust improvements in outcomes for as long as 5 years after just a single high dose.

Through its active metabolite psilocin, psilocybin exerts profound effects on the brain and mental health by acting as a serotonin 2A receptor agonist, triggering downstream glutamate release and enhancing neuroplasticity.

This leads to reduced activity in the default mode network (DMN), a brain region linked to rumination and depression, fostering a shift toward present-moment awareness and reduced self-referential thinking, akin to effects seen in long-term meditation. 

In controlled settings, psilocybin induces mystical-type experiences characterized by interconnectedness, sacredness, and authenticity, which result in rapid, sustained reductions in anxiety and depression. These experiences also increase the personality trait of openness, suggesting lasting neuroplastic changes that may disrupt maladaptive neural patterns, with emerging evidence even indicating potential neurogenesis in the hippocampus.

 What if these improvements in mental health, reductions in chronic stress, and fewer negative emotional states indirectly mitigate physiological aging processes? That’s exactly what this new study suggests. It might be time to think about psilocybin as a longevity molecule.   Psilocin and Psilocybin

Extend Lifespan in Cells and Mice

The study involved in vitro and in vivo components—investigating psilocybin’s effects in isolated cells and in mice.

 For the in vitro study, human lung and skin cells were exposed to psilocin—the metabolite that’s produced after psilocybin is ingested and metabolized by the body. Other cells were exposed to a control treatment, and both treatments continued until the cells reached replicative senescence—a state where cells become “old,” stop dividing, and enter a permanent growth arrest. It occurs after a finite number of cell divisions, often due to the progressive shortening of telomeres (protective DNA caps at chromosome ends) with each division. Senescence is a well-recognized “hallmark of aging.”

 Psilocin extended the lifespan of cells by 29%, effectively slowed the exhaustion of their replicative capacity, increased the number of cell doublings, and reduced the cells’ doubling time. Cellular lifespan extension was enhanced even more when a higher dose (10x the initial dose) was used, with a 57% increase observed compared to untreated cells. Psilocin also delayed cellular senescence.

 Even more remarkable was the impact of psilocin on the “hallmarks of aging” and age-related cellular changes. For one, psilocin reduced the activity of β-gal and markers of cell cycle arrest and increased the activity of markers of cell proliferation and DNA replication. Psilocin also elevated sirtuins (i.e., SIRT1) and reduced markers of DNA damage and oxidative stress in a dose-dependent manner.

Lastly, psilocin reduced one of the most well-established markers of cellular aging—telomere shortening. While the telomeres of the untreated cells were naturally shortened during cell senescence (as occurs in human aging), the telomeres of the psilocin-treated cells were preserved. ­

For the in vivo study, 19-month-old female mice (which corresponds to about age 60–65 in humans) were given a monthly dose of psilocybin for 10 months: 5 mg/kg for the first month and then 15 mg/kg thereafter.
 During the treatment period, 80% of mice who were given psilocybin survived while only 50% of the non-treated mice survived—a meaningful difference in survival rate between the two groups. Furthermore, psilocybin enhanced some physical features of the mice, including improvements in fur quality, hair growth, and less white hair and hair greying. So not only did they live longer, but they looked younger too (and who doesn’t want that?)

 Collectively, these results reveal something novel and exciting about psilocybin—it appears to be having direct effects on mechanisms of cellular aging that are independent of its psychedelic properties. 
 However, the mind-altering nature of psilocybin might also indirectly impact how we age. ­  

Tying Psilocybin’s Anti-Aging Effects to Depression and Mental Health

When we talk about aging and its causes, the focus is typically on intrinsic biological processes, the role of physical inactivity, and the effects of diet and other lifestyle factors. Of course, each of these plays a profound role in how quickly (or how slowly) we age and therefore, our healthspan and lifespan.

 But mental health is also crucial for healthy aging. Indeed, depression and anxiety have been linked to shorter telomeres, a greater risk of chronic diseases, and even mortality. This indicates that psychological (dis)tress likely accelerates biological aging at the cellular level. On the other hand, positive psychological states are associated with telomere lengthening and lower rates of disease.

 This is where psilocybin enters the picture as a potential longevity molecule.

 The Psilocybin-Telomere Hypothesis posits that psilocybin may have a measurable, beneficial effect on biological aging by lengthening telomeres. The hypothesis is based on two well-established premises. The first is that depression and chronic stress are associated with shortened telomeres, and shorter telomeres are linked with age-related diseases and mortality.

Second, psilocybin has clinically documented antidepressant and stress-reducing effects. Therefore, if psilocybin reduces depression, and depression shortens telomeres, then psilocybin may help preserve or even lengthen telomeres. By inducing positively valenced, and sometimes even life-altering, psychological experiences, psilocybin may leave “quantifiable marks at the molecular genetic [and] epigenetic level.”

 Though it’s just a hypothesis, several lines of evidence support the idea that psilocybin exerts biological anti-aging effects, with pathways including:  Reduced rumination and depression, both of which are linked to telomere shortening. Downregulation of the default mode network (DMN), which is overactive in depression. Increased neurogenesis and neuroplasticity, particularly in the hippocampus.

Elevated levels of BDNF to support neuron survival and greater telomerase activity. Reduced inflammation and oxidative stress, which are implicated in telomere erosion. Modulation of the serotonin system (the 5-HT2A receptor and serotonin transporter gene SLC6A4), which is linked to depression and stress resilience.

 Lending further support to this hypothesis is research on meditation—an intervention that induces similar states of consciousness to psilocybin therapy—which also prevents telomere attrition and even lengthens telomeres in some cases.

The late Dr. Roland Griffiths refers to psilocybin-assisted therapy as a “crash course in meditation,” abruptly shifting consciousness to reveal alternative ways of perceiving reality. Dr. Elizabeth Epel and others propose that “some forms of meditation may have salutary effects on telomere length by reducing cognitive stress and stress arousal and increasing positive states of mind and hormonal factors that may promote telomere maintenance.”

 While psilocybin and meditation aren’t identical in their therapeutic effects, it’s clear that our psychological state influences our biology, and therefore our speed of aging. If you’re interested in learning more about psilocybin and other psychedelic therapies, check out my interview with the late Dr. Roland Griffiths.  

Final thoughts

Regardless of your stance on psychedelics, this study is a tantalizing glimpse into new frontiers for healthy aging. It suggests psilocybin could be a novel tool in combating age-related decline.
 
However, it’s critical to note that psilocybin remains a Schedule I controlled substance in many jurisdictions, including the United States, where it is illegal outside of approved research settings due to its psychedelic properties. While the science is exciting, any exploration of psilocybin’s therapeutic potential will have to await further studies and regulatory changes.
 
The interconnectedness of mind and body when it comes to health is indisputable, and that’s perhaps what makes psilocybin and other psychedelic-assisted therapies so intriguing as longevity interventions, even though we might not think of them as such. 
 
Whether it’s psychedelics or meditation, our subjective experiences are intimately tied to biological aging. When you “change your mind,” you also change your cells.