Inspired Wellness, PLLC

12/07/2025

12/02/2025

Most people take omega-3s for heart health… but they also change your muscle tissue.

Not just inflammation.
Not just triglycerides.
Actual muscle biology.

This diagram breaks down what happens to omega-3 fats (EPA + DHA) once they enter your system, and why they influence insulin sensitivity, energy use, fat storage, and even protein synthesis.

1. It starts in the gut.

Omega-3s come in through the diet → absorbed in the small intestine → packaged into chylomicrons and VLDLs.

2. They move through the bloodstream.

From here, EPA and DHA end up in HDL particles, plasma, and eventually… the muscle membranes themselves.

3. Once omega-3s enter muscle, everything changes.

They modify the fatty acids sitting in the surface of muscle cells, leading to:

• Better insulin sensitivity
• Better glycogen use
• Less fat stored inside muscle
• Higher metabolic flexibility

This is one of the reasons omega-3 intake improves glucose control, even without changing calories.

4. Omega-3s activate a whole network of enzymes (phospholipases).

These enzymes shift the “internal messaging” inside muscle cells:

Lipase D → boosts long-chain omega-3 phospholipids

Lipase C → influences IP3/DAG signaling tied to protein synthesis

Lipase A2 → drives eicosanoid pathways tied to new sarcomere formation

In simple terms:
Omega-3s don’t just sit in the membrane — they signal the muscle to build, repair, and use energy differently.

5. The end result?

Muscle that’s richer in long-chain omega-3s shows:

• Better insulin response
• Less intramuscular fat
• Less energy wasted on fat synthesis
• Potential improvements in protein synthesis
• Better metabolic function overall

This is why omega-3s keep showing up in studies on athletic recovery, lean mass retention, aging, and metabolic health.

Your muscles aren’t just passive tissue — they’re listening to everything you eat.

And omega-3s speak their language.

doi:10.1051/ocl/2024011

12/02/2025

Join us for a special WINTER SOLSTICE Breathwork + Sound Bath experience at the North Whidbey Center for Wellbeing.

12/01/2025

After hundreds (maybe thousands) of bottles prescribed, I have yet to see this in clinical practice. Have you?

That said, it’s worth knowing about. Recent reports are describing cases of acute liver injury linked to turmeric or curcumin supplementation, and many (over 70%) involve individuals carrying the HLA B*35:01 allele, suggesting a genetic predisposition in a small subset of people.

So what does this mean?
👉 Periodic chemistry screens with liver function testing (LFTs) are just smart medicine.
👉 And yes, sometimes, we may need to consider that our beloved turmeric could be the cause.
Most people recover fully after discontinuing turmeric, though rare severe cases, including liver failure and even death, have been reported.

Here’s a quick summary of what the literature shows:
✅ Turmeric and curcumin have long been considered low-risk for liver injury.
⚠️ However, rare reports describe hepatocellular injury (elevated ALT/AST) developing over weeks to months.
💊 Most cases involve enhanced bioavailability formulations — often those combined with piperine or lipid carriers.
🧬 A strong HLA-B*35:01 genetic association has been noted, suggesting an immune-mediated or idiosyncratic mechanism.
🚫 Rechallenge (restarting turmeric after suspected injury) is strongly discouraged due to recurrence risk.
To be clear, these cases are very rare, estimated between 1 in 10,000 and 1 in 100,000 exposures.

But “rare” doesn’t mean “never,” and it reminds us why functional medicine should always include:
✨ A personalized approach
✨ Ongoing monitoring
✨ A willingness to question even our most trusted tools

Have you seen hepatotoxicity from turmeric in your practice?
👇 I’d love to hear your experience.

Source: https://www.ncbi.nlm.nih.gov/books/NBK548561/

12/01/2025

When a muscle contracts, it releases signaling molecules that travel through the bloodstream and directly influence brain function. This chart maps out that communication in real time.

Skeletal muscle behaves like an endocrine organ. The molecules it releases, collectively called myokines, reach the brain and help regulate learning, memory, blood flow, metabolism, and inflammatory balance.

signals shown in the diagram:

📌 BDNF
Increases with aerobic exercise. Supports synaptic plasticity, memory formation, and neurogenesis.

📌 IGF-1
Elevated with resistance training. Promotes neuronal survival, repair, and long-term brain plasticity.

📌 Irisin
Produced when the FNDC5 protein is cleaved during muscle contraction. Influences brain metabolism and inflammatory pathways.

📌 IL-6
Released in large amounts during sustained exercise. Regulates energy availability and exerts anti-inflammatory effects post-exercise.

📌 VEGF
Stimulated by endurance work. Supports angiogenesis, improving cerebral blood flow and oxygen delivery.

Different training types shift the myokine profile:

• Aerobic exercise → stronger signals for neuroplasticity and vascular adaptation
• Resistance training → stronger signals for repair, growth, and metabolic regulation
• Interval or combined training → blended signaling with broad cognitive and metabolic benefits

Across studies, regular physical activity maintains this muscle–brain communication as we age. Declines in myokine release are linked to reduced cognitive resilience, while consistent training helps preserve mitochondrial function, vascular health, and anti-inflammatory signaling in the brain.

Movement isn’t just mechanical effort. It’s biochemical communication that supports the nervous system with every contraction.

PMID: 38008091

11/26/2025

To me, food isn’t just nourishment: it’s a form of spiritual practice. The colors, the cycles, the way plants grow in community and not isolation… each meal is a reminder of how nature teaches unity, diversity, and purpose. When we eat in connection with the earth, we’re not just feeding the body, we’re feeding the part of us that remembers where we came from. The wholeness of nature shows us our wholeness. ✨🌈

11/18/2025

Sometimes detox isn’t about doing more, it’s about noticing more. Over the years, I’ve learned that cleansing happens on many levels, not just in the liver or the gut. It’s in the way we think, feel, move, choose, and even how we hold light and awareness in our lives.

When something feels “stuck,” it’s often not physical at all: it might be emotional residue, old patterns, a boundary that needs strengthening, or a microbiome that’s asking for more color and diversity. This is the Whole Detox spectrum I return to whenever I feel out of alignment. It reminds me that detox is not an event but a way of living with more clarity, honesty, and vibrancy.

Which part of the spectrum is calling you today?

11/18/2025

After teaching on environmental health for three days, I came across this article in my PubMed alerts this morning. They provided a fantastic illustration of how environmental inputs have a ripple effect on the body and how we physiologically alter cells and systems as a result. This is a keeper!

Image credit: PubMedKulcsárová, K., Piel, J.H.A. & Schaeffer, E. Environmental toxins in neurodegeneration - a narrative review. Neurol. Res. Pract. 7, 93 (2025). https://doi.org/10.1186/s42466-025-00452-6.

11/12/2025

11/12/2025

Where neurotransmitters and micronutrients team up in your body

Neurotransmitters are chemicals that help your brain and nerves communicate, and they rely on micronutrients to be made. This chart shows how amino acids like L-phenylalanine and L-tryptophan turn into key neurotransmitters with the right vitamins and minerals.

1️⃣ Dopamine, Norepinephrine, Epinephrine (from L-phenylalanine) These "feel-good" and stress-response chemicals start with L-phenylalanine, turning into L-tyrosine, then L-DOPA, and finally dopamine. Iron, niacin, and vitamins C and B6 help this process. Dopamine becomes norepinephrine with copper and niacin, and epinephrine with SAMe and magnesium.
🟢 Example: Low vitamin C might slow dopamine production, affecting mood.
🟢 Example: Magnesium helps turn norepinephrine into epinephrine for energy during stress.

2️⃣ Serotonin and Melatonin (from L-tryptophan) L-tryptophan turns into 5-HTP, then serotonin, a mood and sleep regulator, with vitamins B6, C, and minerals like zinc. Serotonin becomes N-acetylserotonin with folate and SAMe, then melatonin with SAMe, aiding sleep.
🟢 Example: Low B6 can reduce serotonin, making you feel down.
🟢 Example: More tryptophan at night supports melatonin for better sleep.

3️⃣ Micronutrient Support Vitamins (like B6, C) and minerals (like iron, magnesium) act as helpers, ensuring each step works. Without them, your brain can’t produce enough neurotransmitters.
🟢 Example: Iron deficiency might stall dopamine, leading to fatigue.
🟢 Example: Calcium and folate keep serotonin and melatonin on track.

Your brain uses these nutrients to build neurotransmitters, starting with amino acids from food. The process happens in nerve cells, with vitamins and minerals acting like tools to keep mood, energy, and sleep balanced.

11/11/2025

3 types of hunger explained "simply"

Hunger isn’t just about an empty stomach. Your brain receives signals from body composition, hormones, emotions, and even gut microbes. Here’s how the three major types work:

1️⃣ Homeostatic Hunger (Energy Balance Hunger)
This is your body’s “fuel gauge.” It rises and falls based on energy needs and metabolic signals.
What drives it: Ghrelin from the stomach stimulates hunger; leptin from fat cells and incretin hormones (GLP-1, PYY, CCK) reduce it.

What it does: Ensures your intake matches your energy needs for exercise, growth, and tissue repair.

🟢 Example: After a long run, homeostatic hunger pushes you to replace calories and glycogen.

2️⃣ Hedonic Hunger (Reward-Driven Hunger)
This is your “food pleasure” system. It’s triggered by sight, smell, habits, and emotions, not by actual energy needs.
What drives it: Brain reward circuits activated by highly palatable foods (sugar, fat, salt).

What it does: Encourages eating even when you’re not truly hungry. Weak satiety signals make it harder to stop.

🟢 Example: Craving dessert after dinner even though you’re full.

3️⃣ Microbiota-Driven Hunger (Gut Microbe Hunger)
Your gut bacteria also shape hunger signals by producing metabolites that influence hormones and the brain.

What drives it: Microbes generate compounds that mimic hunger or satiety signals, affect insulin, and modulate ghrelin, GLP-1, and PYY.

What it does: Links gut health to appetite regulation and metabolic control.

🟢 Example: Certain bacterial imbalances may increase cravings or weaken satiety, nudging overeating.

Fasano, A. (2025). The physiology of hunger. The New England Journal of Medicine, 392(4), 372–381.

11/11/2025

The way your muscles are built determines how your body handles energy; lean muscle uses it, while obese muscle is prone to storing it.

What you’re seeing

This image compares skeletal muscle from lean and obese individuals, revealing how changes in fiber type, mitochondria, and lipid content shift muscle from an energy-burning organ to an energy-storing one.

🟡 Lean muscle has more type I oxidative fibers, which are dense with mitochondria and glucose transporters. These fibers efficiently oxidize fat and glucose, maintaining insulin sensitivity and steady energy output.

🟡 Obese muscle contains fewer oxidative fibers and more type II glycolytic fibers, which tire quickly and accumulate fat droplets within the tissue. Mitochondrial content is lower, GLUT4 expression declines, and overall fuel utilization becomes inefficient.

🟡 This imbalance creates a ripple effect; less glucose uptake, impaired fat oxidation, reduced insulin sensitivity, and higher risk of metabolic and cardiovascular disease.

The bigger picture:
Skeletal muscle is one of the body’s most powerful metabolic regulators. Its cellular composition reflects lifestyle, nutrition, and physical activity. Exercise reverses these changes by increasing oxidative fiber content and mitochondrial density, transforming muscle back into a metabolic engine that supports long-term health.

Citation:
Serrano, N., Hyatt, J. P. K., Houmard, J. A., Murgia, M., & Katsanos, C. S. (2023). Muscle fiber phenotype: a culprit of abnormal metabolism and function in skeletal muscle of humans with obesity. American Journal of Physiology – Endocrinology and Metabolism, 325(6), E545–E556.