Wellness Matters

12/08/2025

Shared!

Phosphatidylcholine is one of the quiet hero nutrients I rely on in many client protocols. It is not just a liver or brain supplement. It sits at the crossroads of methylation, choline metabolism, cell membrane integrity, pregnancy nutrition, inflammation, and detoxification. Certain SNPs make people much more dependent on this nutrient, which is why so many feel a profound shift when it is added strategically.

PEMT is one of the key genes I look at. This enzyme converts phosphatidylethanolamine into phosphatidylcholine in the liver, which is your backup system for making phosphatidylcholine when dietary choline is low. Common PEMT variants such as rs12325817 and rs7946 increase susceptibility to organ dysfunction and fatty liver when choline intake is inadequate. In a classic controlled feeding study, 78 percent of women carrying a PEMT risk allele developed fatty liver or muscle damage when placed on a choline deficient diet. People without these SNPs may tolerate low choline, but those with PEMT variants simply cannot.

Folate and methylation SNPs such as MTHFR, MTR, MTRR, and BHMT also increase choline needs. When methylation is impaired, the body diverts more dietary choline toward phosphatidylcholine production, which leaves less available for methyl donation, nervous system balance, and membrane repair. Clinically this looks like someone with an MTHFR PEMT combination who struggles with homocysteine, mood instability, liver congestion, or inflammation. These clients often feel more stable and grounded when we support choline and phosphatidylcholine rather than relying solely on methylated B vitamins.

Phosphatidylcholine also plays a major role in liver health. Without enough of it, the liver cannot package and export triglycerides in VLDL, leading to fatty liver. Both human and animal studies show that deficiency in choline or phosphatidylcholine rapidly induces hepatic fat accumulation and oxidative stress. Supplementation helps reverse steatosis, improves detoxification, and lowers inflammatory markers. In a randomized controlled trial, 2400 mg per day of phosphatidylcholine for 12 weeks improved liver fat and oxidative stress profiles in NAFLD patients. For clients with PEMT SNPs, elevated liver enzymes, poor bile flow, or stubborn metabolic symptoms, phosphatidylcholine is often a cornerstone.

In pregnancy and preconception it becomes even more essential. Choline, delivered largely as phosphatidylcholine, supports neural tube closure, brain development, memory formation, and lifelong cognitive resilience. Multiple studies show that higher maternal choline intake reduces the risk of neural tube defects and improves offspring attention and processing speed. DHA transport to the fetus also depends on phosphatidylcholine. Without enough of it, DHA cannot be efficiently delivered to the developing brain. Women with PEMT variants, low estrogen, or increased methylation demands often need more choline than standard prenatal guidelines suggest.

From a biochemical standpoint phosphatidylcholine is one of the largest consumers of SAMe in the body. When we supply preformed phosphatidylcholine, we spare methyl groups that can then be used for neurotransmitter balance, hormone metabolism, DNA methylation, fertility, and detoxification. This is why some clients who crash on methyl donors feel calmer and more regulated when phosphatidylcholine is introduced.

This is also why phosphatidylcholine shows up so often in my protocols. It supports the entire one carbon and phospholipid network. It helps the body build strong cell membranes, move fats efficiently, run methylation smoothly, and support the brain and nervous system without draining nutrient reserves. When genetics show PEMT, CHDH, or methylation related SNPs, when liver markers or gallbladder symptoms appear, or when a client is trying to conceive, phosphatidylcholine becomes one of the most targeted and effective tools we have.

12/07/2025

https://mara-labs.com/blogs/journal/can-a-turmeric-latte-improve-seasonal-depression

Discover why turmeric lattes deliver only a tiny fraction of curcumin needed for mood support this winter. Learn how research-backed curcumin supplements can reduce depression and anxiety symptoms, why bioavailability matters, and which formulations offer real benefits without toxicity. Perfect for....

12/05/2025

Endocannabinoid System & Depression

Compelling findings from a 2022 study in Frontiers in Cellular Neuroscience highlight the endocannabinoid system (ECS) as a dynamic, whole-body homeostatic and neuromodulatory system. It orchestrates stress responses, emotional behavior, motivation, metabolic balance, immune activity, gut integrity, circadian rhythms, and neuroplasticity, playing a key role in depressive symptoms linked to chronic stress, inflammation, and metabolic dysfunction.

One of the ECS’s most influential functions is its continuous, bidirectional crosstalk with the gut microbiome—a mechanistic dialogue that shapes mood, stress resilience, and metabolic health. This gut–brain interaction provides a framework for understanding how lifestyle, diet, and microbial composition influence both mood and systemic homeostasis.

ECS–Microbiome Crosstalk in Stress & Mood

Within the gut epithelium, ECS signaling modulates motility, permeability, immune activity, and metabolic responses, while microbial metabolites and community composition, in turn, shape ECS tone. Bidirectional communication between the ECS and the gut microbiome is crucial for maintaining gut–brain homeostasis. Disruptions in this dialogue contribute to stress-induced alterations in the gut–brain axis, heightening inflammation, metabolic strain, and vulnerability to depressive symptoms.

Extensive evidence shows that chronic stress disrupts microbial composition, impairs gut barrier integrity, elevates inflammatory signaling, and alters intestinal and central endocannabinoid levels (AEA and 2-AG), collectively affecting HPA axis regulation, reward processing, and motivation.

ECS in Gut Integrity & Immunity

Evidence from multiple studies, including a 2021 review in Progress in Neuropsychopharmacology & Biological Psychiatry, highlights the ECS as a key regulator of intestinal homeostasis, linking gut barrier integrity to systemic inflammation and mood regulation. Reduced ECS activity is associated with inflammatory bowel disease, whereas increased activity correlates with obesity. When gut barrier function is impaired, bacterial metabolites such as LPS can translocate, acting as potent immune activators that drive systemic inflammation, metabolic dysfunction, and depressive symptoms.

A 2022 review in Cellular and Molecular Gastroenterology and Hepatology further demonstrates that ECS signaling dynamically regulates intestinal permeability, fluid secretion, and immune pathways while interacting with the gut microbiome in a reciprocal, adaptive manner. Together, these findings highlight the ECS–microbiome axis as a key regulatory pathway for intestinal and systemic homeostasis, demonstrating its dynamic variability across physiological and pathological states and supporting the potential for personalized microbial or ECS-targeted interventions

Diet, ECS Tone, & Metabolic–Mood Pathways

Diet is a rapid and potent modulator of both gut microbial communities and ECS signaling. An 8-week RCT found that adopting a Mediterranean diet lowered plasma AEA, increased beneficial OEA/PEA and OEA/AEA ratios, and increased gut levels of Akkermansia muciniphila independent of weight loss. These ECS shifts correlated with improvements in insulin resistance or inflammation depending on baseline ECS tone, highlighting how personalized ECS–microbiome signatures may predict metabolic and mood responses to dietary interventions.

Broader research on the ‘endocannabinoidome’—a network of more than 100 lipid mediators and around 50 proteins—demonstrates how the ECS interacts closely with the gut microbiome to help regulate energy balance, inflammation, and metabolic health. Because metabolic dysfunction, chronic inflammation, and depression frequently co-occur, these interconnected systems are highly relevant for understanding and addressing these conditions.

Microbial Diversity, ECS, & Motivation

A 2021 twin study of 786 adults examined how gut microbial diversity relates to anhedonia and amotivation via the ECS. Higher f***l levels of the ECS-related lipid PEA—reflecting greater excretion and potentially lower central availability—mediated the link between lower microbial diversity and reduced motivation. Serum PEA levels showed no effect, highlighting the role of the local gut–ECS pathway. These findings reveal a mechanistic connection between the microbiome and ECS signaling in shaping mood and motivation, supporting the ECS–microbiome axis in depressive symptoms.

ECS in Depression & Stress Regulation

Research shows ECS dysregulation is central to depressive symptoms. ECS components—including CB1 receptors, endocannabinoid ligands, and degrading enzymes—regulate motivation, cognition, emotion, and stress responses, with deficits observed in both depressed patients and animal models. The ECS directly influences neurotransmission (particularly via CB1), neuroendocrine signaling, and neuroimmune pathways, all disrupted in depression. CB1 agonists and inhibitors of anandamide degradation produce antidepressant-like effects in preclinical models. The ECS is also implicated in cardiovascular, metabolic, and neurodegenerative processes, underscoring its broad systemic relevance as a homeostatic regulator in depression.

Clinical Relevance: ECS–Microbiome Interactions in Depression

Across studies, a consistent picture emerges:

The ECS maintains homeostasis across metabolic, immune, neuroendocrine, and emotional systems.
The gut microbiome continuously shapes—and is shaped by—ECS tone, influencing barrier integrity, inflammation, metabolic function, and stress resilience.
Dysregulation of this axis may underlie co-occurring depression, anxiety, inflammation, metabolic imbalance, gastrointestinal symptoms, and altered stress response
Recognizing these interactions can guide integrated approaches that address metabolic, immune, nutritional, and neuropsychiatric factors in mood disorders.

Supporting the ECS–Microbiome Axis

Nutrition: Mediterranean-style diets, fiber-rich foods, polyphenols, and probiotics support microbial diversity and beneficial ECS signaling (including shifts in AEA/OEA balance).
Exercise: Physical activity increases ECS ligand availability and promotes a microbial profile associated with metabolic and stress resilience.
Sleep: Consistent, high-quality sleep supports circadian regulation of ECS signaling and microbial composition.
Sunlight & Nature Exposure: Natural light entrains circadian rhythms and may modulate ECS activity, while nature exposure enhances microbial diversity.
Stress Reduction: Mind-body practices such as meditation and yoga can boost endocannabinoids—including anandamide (AEA) and 2-AG—and BDNF, improving mood, focus, and well-being. Conversely, chronic stress may increase FAAH activity, lowering endocannabinoid signaling and impairing mood regulation. These findings suggest that stress management can support ECS–microbiome balance and reduce inflammation.
Together, these lifestyle strategies reinforce the ECS–microbiome axis, highlighting the dynamic, bidirectional mechanisms through which these factors shape mood, metabolic health, and systemic resilience.

Related Biotics Research Products:

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Biodolph 7 plus

12/04/2025

The Holiday Melatonin Myth — Busted (Just in Time for December)

‘Tis the season for sugar comas, airport lighting, and Netflix jet lag.
And once again, the refrain: “Melatonin makes me groggy in the morning.”

Here’s the reality — it’s not melatonin’s fault.

Melatonin acts as the starter pistol, not the marathon. It signals the body to begin sleep, but doesn’t sustain it. Without sufficient GABAergic tone, the “off switch” in the nervous system doesn’t engage, leading to that all-too-familiar fragmented sleep and morning haze.

Here’s why that matters:
Most oral GABA supplements don’t work. GABA is too large to cross the blood-brain barrier. You need molecules that modulate or mimic GABA — like Agarin and Dihydrohonokiol-β, both shown to activate GABA-A receptors.
That’s the secret behind Tro+ Somna. This practitioner-strength sleep troche combines GABAergic modulators with optional low-dose melatonin in a buccal delivery system — bypassing first-pass metabolism for faster, more reliable onset.
Oblipair™ synergy = GABA + circadian alignment. By pairing GABA-A receptor modulators with melatonin, Tro+ Somna smooths the landing into restorative, stage-4 sleep — without next-day sedation.
And during the holidays, when stress, travel, and blue-light exposure throw circadian rhythms into chaos, this combination becomes a clinical lifesaver.

Clinician Quick Take:
Melatonin alone ≠ deep sleep. It signals initiation but doesn’t maintain depth.
GABA + melatonin = smooth descent. GABAergic modulation helps maintain natural sleep-stage progression.
Timing is everything. Administer 30–60 minutes before bed. Too early shifts the circadian phase; too late extends into the morning.
Ritual reinforces physiology. Dim lights, limit screens, and maintain consistent timing to strengthen endogenous cues.
In Practice - This December, help your patients restore rest:
✅ DO: Combine low-dose melatonin with effective GABAergic support and a stable bedtime ritual (Tro+ Somna).

​❌ DON’T: Rely on high-dose melatonin or (of course) ignore light exposure, meal timing, and evening stimulants as best as we can council!

Pro tip: Tro+ Somna supports both short-term sleep rescue (jet lag, acute stress) and longer-term circadian recalibration — without dependence, withdrawal, or rebound insomnia.

Watch Dr. Scott’s clinical deep dive on Tro+ Somna for dosing insights, combination strategies, and practical applications for optimizing sleep and reducing next-day sedation.

-Dr. Scott and the Troscriptions Team

Smurf mode: Optional. Here’s how to get the boost without the blue aftermouth (no, that’s not a typo). 💙You CAN enjoy methylene blue without turning your mo...

12/03/2025

https://pendulumlife.com/blogs/news/your-gut-healthy-holiday-guide

Written by: Katie Chennault The holidays are almost here — and with them come delicious treats, festive drinks, late nights and a break from your usual routine. While it’s a season of joy, it can also be tough on your gut. Fact: Your gut microbiome plays a key role in your immune system, energy ...

12/02/2025

https://www.aninconvenientstudy.com/

An Inconvenient Study: This could change everything. An ICAN Production.

12/02/2025

The Aorta: The First Organ to Age

Summary written by Chief Medical Herbalist, Lee Carroll

This recent paper highlights that the aorta is the first organ in the human body to age, and once it becomes senescent, it begins releasing “senokines”, inflammatory aging signals that can accelerate decline throughout the whole body.

If vascular aging is the trigger upstream of everything else, it suddenly makes a lot more sense why so many traditional longevity medicines focus on circulation and vessel integrity.

This is where fungi and mushrooms become especially interesting:

• Reishi has always been called the “mushroom of immortality” and has significant effects on cardiovascular tone and endothelial health.

• Ergothioneine accumulates in stressed vascular tissue and protects it from oxidative stress.

So perhaps longevity really does begin with the aorta, and Reishi + ergothioneine may be one of the most elegant synergistic strategies to defend it.

A 50-year multi-tissue proteomic atlas reveals transcriptome-proteome decoupling, proteostasis decline with amyloid accumulation, and asynchronous aging clocks, identifying circulating senoproteins contributing to vascular and systemic aging.

12/02/2025

Progress is progress. Now let’s all watch an Inconvenient Study….

11/30/2025

https://youtu.be/Tns-g2bfe0Q?si=1q0a0Qi0En1RII6y

Methylene blue might look like a simple blue dye—but in *clinical practice*, it’s become one of the most powerful tools for energy, focus, and cellular repai...

11/29/2025

Nicotinamide & Skin Health

Nicotinamide
JAMA Dermatology has recently published the results of a retrospective cohort study evaluating the efficacy of supplementation with nicotinamide, vitamin B3, for the prevention of skin cancer. This study included data from nearly 34,000 patients in the Veterans Affairs Corporate Data Warehouse over a 25-year period, with analyses conducted both for the general population and a subset of recipients of solid organ transplants. Patients were considered exposed to nicotinamide if they had taken it at a dose of 500mg twice per day for at least 30 days, with the main outcome being time to the next skin cancer after baseline.

Overall, they report a significant 14% reduction in skin cancer risk with nicotinamide use, though if nicotinamide was initiated after the first skin cancer, the risk reduction was as high as 54%. The benefit declined when initiated after subsequent skin cancers, suggesting that supplementation after the initial skin cancer may have the largest preventative effect. A risk reduction was observed for skin cancers overall, basal cell carcinoma, and especially cutaneous squamous cell carcinoma.

While this was not a randomized trial, its large patient population does buttress a previously published phase 3 randomized and controlled trial, which found a 23% reduction in the risk for new non-melanoma skin cancers when supplemented at 500mg twice per day by people with a history of at least two non-melanoma skin cancers within the last 5 years. This study also reported a 13% lower incidence of actinic keratoses by the end of the 12-month study, with no difference in adverse events between groups over the course of the study.

11/28/2025

It’s time!!!