Dr. Arturo López Bastidas

Dr. Arturo López Bastidas Egresado de la Universidad Autónoma de Baja California. Posgraduado del Instituto Nacional de Psiquiatría. ENGLISH SPOKEN.

Certificado por el Consejo Mexicano de Psiquiatría y Miembro de la Asociación Psiquiátrica Mexicana.

05/05/2026

Cannabis use among teenagers is linked to delayed cognitive development and worse memory over time, the largest US study to date showed.

In an analysis of over 11,000 teenagers, cannabis use was associated with reduced improvement in memory, attention, language, and processing speed, compared to adolescents who did not use cannabis.

When researchers zeroed in on specific cannabis components, they found that those who used tetrahydrocannabinol (THC) showed worse memory as they grew older, compared to nonusers. https://mdsc.pe/42cOas4

Depresion. Una enfermedad sistemica
04/05/2026

Depresion. Una enfermedad sistemica

6-8 mil mayores de 60 8-10 mil menores de 60
28/04/2026

6-8 mil mayores de 60
8-10 mil menores de 60

Most people accept 10,000 steps a day as the benchmark for cardiovascular health. The number didn't come from a clinical trial. It came from a 1965 marketing campaign in Japan.

In 1965, the Yamasa Tokei company began selling a step counter called the Manpo-kei. The name translates literally to "10,000-step meter." The number was a brand identity, picked because the Japanese character for 10,000 resembled a person walking. There was no underlying mortality study. No randomized trial. The 10,000 target became a global health norm because the device was successful and the number was memorable.

The actual mortality data tells a different story.

Lee and colleagues (2019, JAMA Internal Medicine) measured step counts in 16,741 older women using accelerometers and tracked all-cause mortality over four years. Compared with the lowest step quartile (around 2,700 steps per day), women averaging 4,400 steps had significantly lower mortality. Risk continued declining with more steps. Then it leveled off. The plateau was around 7,500 steps per day. Beyond that, additional steps showed no further mortality benefit in this population.

Saint-Maurice and colleagues (2020, JAMA) measured 4,840 US adults aged 40 and older. Compared with 4,000 steps per day, taking 8,000 steps was associated with roughly half the all-cause mortality risk. Twelve thousand steps showed further benefit, though the marginal gain after 8,000 was smaller than the gain from 4,000 to 8,000.

Paluch and colleagues (2022, Lancet Public Health) pooled 15 international cohorts including 47,471 adults. They found the dose-response curve plateaued at 6,000-8,000 steps per day for adults 60 and older, and at 8,000-10,000 for adults under 60. The age-dependent plateau is the most replicable finding across the literature.

What this means in practice. If you are over 60, the data suggests most of the mortality benefit accrues by 7,000-8,000 steps per day. If you are under 60, that benefit window extends a bit further, into the 8,000-10,000 range. Going beyond your population's plateau is fine. It is just not adding measurable mortality benefit at the population level. The number to chase isn't 10,000. The number to clear is closer to 7,000 for most adults.

A few caveats. These are observational cohort studies, not randomized trials. Reverse causality is a concern at the low end, where people who walk less may walk less because they are already sick. The studies adjusted for known confounders but residual confounding likely remains. The data is also strongest for all-cause mortality. Step targets for specific outcomes like cardiovascular event reduction, weight management, or cognitive performance may differ. Stepping intensity, separately analyzed, did not predict mortality independently of total daily steps in any of these studies.

10,000 is a round number that came from a 1965 product name. It is not a research-derived target. The mortality data shows the curve flattens earlier than that for most adults, and the practical implication is that consistent walking at moderate volume captures most of the available benefit. The number on your wearable is not the goal.

Lee et al., JAMA Internal Medicine
2019 Saint-Maurice et al., JAMA, 2020
Paluch et al., Lancet Public Health, 2022

Vitamina D
18/04/2026

Vitamina D

Vitamin D is not just a bone nutrient. It has a nuclear receptor physically present inside the dopamine-producing neurons of the human substantia nigra. When activated, it controls three gene targets that determine how much dopamine those neurons produce and how long they survive.
Cui et al. (2013, Neuroscience) confirmed this directly using immunohistochemistry in both human and rat brain tissue. The vitamin D receptor (VDR) is located in the nucleus of tyrosine hydroxylase-positive neurons, the cells that synthesize dopamine, in the substantia nigra. This is the brain region that degenerates in Parkinson's disease. In the developing rat brain, VDR expression emerges between embryonic day 12 and 15, the exact window when the majority of midbrain dopamine neurons are born.
What happens when vitamin D activates VDR in these neurons has been mapped across multiple studies. In SH-SY5Y neuroblastoma cells overexpressing VDR, Cui et al. (2015, Neuroscience) showed that 1,25-dihydroxyvitamin D3 significantly increased tyrosine hydroxylase expression, the rate-limiting enzyme in dopamine synthesis. TH-positive cell count more than doubled compared to controls. The effect was dose- and time-dependent. Dopamine production increased. The immature neuronal marker NEUROG2 decreased, indicating the cells were being pushed toward a mature dopaminergic phenotype rather than remaining undifferentiated.
Pertile et al. (2023, J Neurochem) extended this work, showing that vitamin D increased neurite outgrowth, neurite branching, and the number and distribution of presynaptic protein puncta in dopaminergic cells. They also demonstrated increased functional dopamine release. The neurons were not just producing more dopamine. They were building longer processes, forming more synaptic connections, and redistributing their release machinery outward along those processes.
The survival pathway is equally significant. Vitamin D upregulates glial-derived neurotrophic factor (GDNF), which is the primary survival signal for dopamine neurons. Pertile et al. (2018, FASEB J) showed that VDR directly binds the promoter of C-Ret, the GDNF receptor, using chromatin immunoprecipitation. This is not indirect signaling. It is direct genomic regulation of the receptor that keeps dopamine neurons alive. When GDNF synthesis is chemically blocked, vitamin D's effect on dopamine neuron number disappears, confirming that the GDNF pathway is essential to the mechanism.
In rodent models, developmental vitamin D deficiency reduces expression of dopamine specification factors Nurr1 and p57kip2 in the mesencephalon, decreases TH expression in the embryonic brain, reduces dopamine turnover, and alters dopamine transporter density and binding affinity in the adult brain. These changes persist into adulthood even after vitamin D status is corrected postnatally.
The Parkinson's disease connection is observational but consistent. Vitamin D deficiency prevalence is significantly higher in Parkinson's cohorts. In 6-OHDA lesioned rats (a standard Parkinson's model), vitamin D administration partially restores TH expression and TH-immunoreactive fibers in the substantia nigra and striatum while increasing GDNF protein.
The honest gap: this is almost entirely preclinical evidence. VDR presence in human dopamine neurons is confirmed. The downstream gene regulation, the dopamine production increases, the survival signaling, all of this is from cell culture and rodent models. No human randomized controlled trial has tested whether correcting vitamin D deficiency improves dopamine function, Parkinson's outcomes, or any dopamine-related clinical endpoint. The mechanism is well-characterized. The translation to human clinical outcomes has not been done.
Cui et al., Neuroscience, 2013
Cui et al., Neuroscience, 2015
Pertile et al., FASEB J, 2018
Pertile et al., J Neurochem, 2023

09/04/2026

Scientists are certain that ma*****na doesn’t ease anxiety.

Two comprehensive new analyses published in Lancet Psychiatry and JAMA have debunked the long-held belief that ma*****na serves as an effective treatment for mental health. Despite being frequently prescribed for anxiety, depression, and PTSD, researchers found "no evidence" that any form of cannabis, including CBD and THC, provides clinical benefits for these conditions.

Lead researcher Jack Wilson noted that most studies used controlled oral formulations, meaning real-world smoked cannabis likely has even less proven efficacy. This creates a concerning gap between medical practice and scientific reality, as nearly half of medical ma*****na users specifically use the drug to manage their psychological well-being.

Beyond the lack of benefits, experts warn that the soaring potency of modern ma*****na—which can reach THC concentrations of 80% in concentrates—poses serious health risks.

Frequent use of high-potency products is linked to cannabis use disorder and an increased risk of developing psychotic disorders like schizophrenia, particularly in young adults.

Rather than relying on unproven cannabis treatments, medical professionals recommend turning to gold-standard interventions such as Selective Serotonin Reuptake Inhibitors (SSRIs) and Cognitive Behavioral Therapy (CBT).

These evidence-based methods remain the most reliable path for individuals seeking relief from mental health challenges without the risks of addiction or long-term cognitive harm.

source: LaMotte, S. (2026). Scientists say ma*****na doesn’t ease anxiety or other mental health conditions. CNN Health.

** Full , original studies are uploaded to our Addiction Actually Membership Subscribers Group. Joining button on our main page. **

Disclaimer: This content is for informational and educational purposes only. via Quantam Science

04/04/2026

I’m just going to leave this right here for your consideration. The Lancet, Volume 407, 2026

27/03/2026

El Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz conmemora este 27 de marzo el XX aniversario luctuoso del Dr. Ramón de la Fuente Muñiz, ocurrido el 31 de marzo.

En el marco del XXII Coloquio de Neurohumanidades, se llevará a cabo un homenaje luctuoso en su honor

27/03/2026
11/03/2026

For patients with unresponsive to initial antipsychotic therapy, clozapine improved symptom response rates and reduced discontinuation due to insufficient efficacy vs olanzapine or amisulpride.

https://ja.ma/3MWL2wt

08/03/2026

Join us at the 26th World Congress of Psychiatry (WCP 2026), which will take place from 23-26 September 2026, in Stockholm, Sweden.

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