Element 7 Wellness

12/29/2025

12/03/2025

Fascial Counterstrain works on all of the systems mentioned below with the most specific physical medicine techniques on the planet.

https://www.facebook.com/share/p/1GqNeo42R1/?mibextid=wwXIfr th

The Neck–Trigeminal–Ocular–Vestibular Connection: Why Your Neck Can Change How You See, Balance, and Feel

The Functional Neurology Center – Minnetonka, MN

At The Functional Neurology Center (theFNC), we see every day how neck dysfunction can create dizziness, visual strain, headache, neural tension, jaw pain, sensory mismatch, autonomic symptoms, and even motion sensitivity.

This is not just “neck pain.”
This is a brain–stem–vestibular–trigeminal system problem.

Below is an easy-to-understand breakdown of why neck mechanics and proprioception directly influence your visual system, vestibular system, and cranial nerve function—and how we restore these connections during rehab.

1. The Cervical Spine Is a Sensory Organ for the Brain

The upper cervical spine (C0–C3) contains some of the densest proprioceptive receptors in the entire body. These receptors constantly tell the brain:
• Where your head is positioned
• How fast your head is moving
• How your eyes and inner ears should coordinate
• How to stabilize posture and balance

When these receptors become inaccurate due to injury, tight suboccipital muscles, whiplash, poor posture, or inflammation, the brain receives mismatched spatial information.

This is the foundation of cervicogenic dizziness, eye strain, motion sensitivity, and head pressure that so many patients experience before coming to theFNC.

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2. Neck Dysfunction Directly Activates the Trigeminal System

The trigeminal nerve (CN V) controls:
• Face and jaw sensation
• TMJ input
• Scalp and sinus sensation
• Eye pain/pressure
• Dural tension
• Autonomic responses

The upper cervical spine shares pathways with the trigeminal nucleus in the brainstem (the trigeminocervical complex).

When the neck is irritated or unstable, it can sensitize trigeminal pathways, creating symptoms such as:
• Facial tingling
• TMJ tension
• Eye pressure
• Headache
• Light sensitivity
• Migraine-like symptoms

This explains why neck injuries often show up as facial pain or TMJ issues—and why trigeminal maps light up in patients with chronic dizziness.

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3. The Eyes, Neck, and Vestibular System Must Agree on “Where You Are”

Your eyes, inner ears, and neck work as a three-part navigation system:

Eyes (Visual System)

Sense motion, horizon, environment, and spatial orientation.

Inner Ear (Vestibular System)

Detects head acceleration, tilt, and rotation.

Neck Proprioceptors

Confirm head position and fine-tune gaze stability.

If one system is off, the brain loses internal calibration and symptoms develop:
• Dizziness
• Motion intolerance
• Head pressure
• “Foggy eyes”
• Difficulty reading or scrolling
• Problems stabilizing gaze (VOR dysfunction)
• Anxiety in busy environments

This is the classic sensory mismatch we test and treat at theFNC.

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4. Why the Suboccipital Muscles Matter Most

The tiny muscles under the skull—including the re**us capitis posterior major/minor and obliquus capitis superior/inferior—contain extremely sensitive proprioceptors.

When they tighten or spasm from trauma or chronic stress, they pull on the dura mater, influence the trigeminal system, and alter:
• Eye tracking
• VOR gain
• Smooth pursuit
• Balance / posture
• Neck coordination
• Cranial blood flow

This is why so many patients feel relief when we restore proper motion and activation in these areas.

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5. How We Treat These Systems Together at theFNC

Our neuro-rehabilitation model is built to correct these pathways in the right order, using precise, brain-based interventions:

✓ Cervical Proprioceptive Training
• NeckCare sensors
• Joint-position-error training
• Light motor control re-patterning

✓ Trigeminal & TMJ Modulation
• Cranial mobilization
• Facial nerve stimulation
• Jaw mechanics and dural tension work

✓ Ocular Motor Rehabilitation
• Smooth pursuits, saccades
• Near–far vergence
• Gaze stabilization and VOR drills

✓ Vestibular Integration
• Head–eye reflex retraining
• Optokinetic stimulation
• Motion platforms (GyroStim / DOF Reality)

✓ Autonomic Regulation
• Breathing training
• HRV up-regulation
• Limbic calming techniques

✓ Multisensory Calibration

We reintegrate the three systems until the brain receives clear, accurate, synchronized signals again.

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6. What Patients Usually Notice First

As these pathways normalize, patients often report:
• Clearer vision
• Reduced dizziness
• Less facial/eye pressure
• More stable balance
• Improved neck mobility
• Better posture and spatial awareness
• Reduced headaches and jaw tension
• More confidence moving through the world

This happens because the eyes, ears, and neck finally agree again.

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When patients come to theFNC with dizziness, visual strain, head pressure, TMJ issues, or neck pain, the underlying problem is often the cervical–trigeminal–ocular–vestibular network.
This interconnected system determines how you see, balance, sense motion, and feel.

When we rehabilitate it holistically—with precision and sequencing—the results are life-changing.

12/02/2025

Among published studies involving older adults without cognitive impairment, plasma p-tau217 was shown to reliably differentiate amyloid-positive from amyloid-negative individuals, with a large effect size and high diagnostic accuracy.

These data support the clinical utility of plasma p-tau217 as a minimally invasive, scalable tool for detecting preclinical Alzheimer disease (AD) pathology.

https://ja.ma/4omxDue

11/22/2025

PCSK9 is one of the more fascinating examples of how human biology carries the fingerprints of our ancestral environment and how modern medicine can selectively “turn down” traits that once helped us survive, but now work against us.

PCSK9 was first discovered in the early 2000s in families with extremely high cholesterol and premature heart disease. Researchers found that these individuals carried gain-of-function mutations in a gene that increases the destruction of LDL receptors on liver cells. Fewer receptors mean fewer LDL particles cleared from the blood and therefore higher lifetime exposure to apoB, the protein backbone of LDL and other atherogenic lipoproteins.

But the story becomes more interesting when you flip it around. Some people instead have loss-of-function mutations in PCSK9, meaning the gene is naturally “dialed down.” These individuals have LDL levels 20–40% lower their entire lives and, unsurprisingly (unless you subscribe to internet LDL-deniers), dramatically lower rates of cardiovascular disease. Most importantly to note, this also comes without any apparent downside.

This was one of the great clues that led to the development of PCSK9 inhibitors.

From an evolutionary perspective, the reason for the occurrence of PCSK9 fits well into the broader “thrifty gene” framework: humans evolved in an environment of periodic scarcity, where conserving energy and maintaining adequate cholesterol synthesis (in all cells) for hormone production, cell membranes, and immune function would be essential.

So genes that favored keeping LDL particles in the blood stream during trying times by reducing removal via fewer LDL receptors, could have provided a survival edge in famine conditions.

However in a modern environment of chronic caloric abundance, longer lifespans, and very different causes of mortality, this same mechanism that gave an advantage thousands of years ago becomes maladaptive and harmful. So the high LDL-apoB exposure that once helped keep people alive long enough to procreate, now over a longer lifespan is a driver of atherosclerosis, not a benefit.

This is where PCSK9 inhibiting therapies fit in. These drugs essentially recreate the biology of people with natural loss-of-function variants: they block PCSK9, preserve LDL receptors on the liver, and increase clearance of apoB-containing particles. In other words, they reduce the activity of a gene function that most of us simply no longer need operating at full strength in the modern world.

It’s a rare example of precision medicine aligned almost perfectly with evolutionary logic, taking advantage of what nature already proved to be both safe and protective, and applying it to millions of people at risk today.

Cool stuff for people who really need it.

11/12/2025

11/04/2025

In this powerful episode of The Alternative Flight Plan Podcast, host Dr. Kristin Barnes welcomes Dr. Holly Christy—naturopathic doctor, acupuncturist, and founder of The Bridge Back Project—for a fascinating look into the world of fascial counterstrain, an emerging hands-on therapy changing how we understand chronic pain, trauma, and healing.

Dr. Christy shares insights from her recently published study in the Military Medicine journal, which examined the impact of counterstrain therapy on veterans and first responders living with chronic pain and PTSD. Together, she and Dr. Barnes explore how this precise, physiology-based approach can help reset the body’s nervous system—offering relief where traditional medicine often falls short.

From life-altering patient stories to groundbreaking clinical results, this conversation sheds light on the future of integrative care. Dr. Christy also discusses her vision for expanding access through The Bridge Back Project, which funds treatments and research for trauma recovery and supports practitioners dedicated to this work.

If you’ve ever wondered how the body holds—and can release—pain and trauma, this episode is a must-listen.

Watch the full episode here: https://youtu.be/dgVEeVONee0

10/18/2025

10/18/2025

Astrocytes, Not Neurons, Hold the Key to Emotional Memory

A groundbreaking study shows that emotional memories depend on astrocytes—glial cells once thought to simply support neurons.

After intense experiences, certain astrocytes become “tagged” to respond during future recall, helping to preserve the memory over time.

Disrupting their activity weakens memory retention, while overstimulating them amplifies fear responses.

This discovery may transform how we understand memory persistence and open new routes for treating trauma and anxiety disorders.

10/09/2025

Atherosclerosis (AS), a progressive inflammatory disease of coronary arteries, the aorta, and the internal carotid artery, is considered one of the main contributors to cardiovascular disorders. Blood flow is restricted by accumulating lipid-rich macrophages (foam cells), calcium, fibrin, and cellul...

10/09/2025

🧠 Scientists reverse Alzheimer’s symptoms using nanoparticles that clear brain plaque and restore memory

In an astonishing breakthrough, researchers from Spain and China have developed nanoparticles that not only remove toxic Alzheimer’s plaques from the brain — but also repair the brain’s natural defense system.

The study, published in Signal Transduction and Targeted Therapy, showed that just three injections of these “supramolecular drugs” cleared up to 60 % of amyloid-beta buildup in only one hour in mice. Even more remarkably, within six months, animals suffering from severe memory loss began behaving normally again — effectively reversing half a year of cognitive decline.

What makes this discovery stand out is its focus on the blood–brain barrier (BBB) — the brain’s gatekeeper that becomes leaky and dysfunctional in Alzheimer’s. Instead of just dissolving plaque, the nanoparticles reactivate a key waste-clearing protein called LRP1, restoring the brain’s ability to flush out harmful material naturally. This dual action improves blood flow, reduces inflammation, and helps the brain reboot its self-healing processes.

Though still in early-stage animal testing, this research offers a bold new direction: tackling neurodegenerative diseases by repairing the body’s cleanup system — not just treating the symptoms. If these results translate to humans, they could mark a turning point in the fight against Alzheimer’s.

📖 Source:
Battaglia G., Tian X. et al. (2025). Signal Transduction and Targeted Therapy. Institute for Bioengineering of Catalonia & West China Hospital, Sichuan University.

10/03/2025

IMPORTANT NUANCE SOME MAY NOT BE AWARE OF:

Vascular calcification, vitamin K2, calcium supplementation, and their relationship to atherosclerosis and cardiovascular risk:

Types and Mechanisms of Vascular Calcification:

Vascular calcification occurs as calcium phosphate deposits in arterial walls, primarily in two layers:

Intimal calcification:
Occurs within atherosclerotic plaques in the intima, associated with lipid accumulation, inflammation, and plaque development. It plays a role in plaque stability or rupture and is directly linked to atheroma formation and cardiovascular events like heart attacks.

Medial calcification (Mönckeberg’s sclerosis): Occurs in the medial layer of arteries, independent of lipid plaques. It results from vascular smooth muscle cell (VSMC) transformation into bone-like cells triggered by mineral imbalances like excess calcium, phosphate, or insufficient inhibitors such as vitamin K2. This calcification stiffens arteries, raising cardiovascular risk **via increased blood pressure and ventricular strain**, but does not cause plaque rupture [1][2][3].

Calcium Supplementation and Vascular Calcification:
Excess calcium intake may elevate serum calcium transiently, stimulating VSMCs to mineralize the arterial media, leading to medial calcification.
This process does not require pre-existing atherosclerotic plaque and can occur in conditions of mineral imbalance, chronic kidney disease, or vitamin K2 deficiency.

Calcium supplementation may accelerate vascular calcification primarily by this medial mechanism rather than promoting plaque formation [7][8][1].

Vitamin K2 and Calcification:
Vitamin K2 activates matrix Gla protein (MGP), a natural inhibitor preventing calcium deposition in soft tissues and vessels.

Supplementing vitamin K2 can reduce the progression of vascular calcification caused by mineral imbalance and support maintaining arterial flexibility.

However, there is currently no consistent evidence that vitamin K2 can regress or remove existing calcification associated with atherosclerotic plaques.

Clinical anecdotes of K2 reducing "vascular calcification" may primarily reflect effects on non-atherosclerotic, mineral-induced calcification, which cannot be distinguished from plaque calcification on CT or X-ray imaging [9][10][11][12].

Imaging Limitations:
Both intimal and medial calcification appear as calcium deposits on imaging modalities such as coronary artery calcium (CAC) scoring via CT.
Imaging cannot reliably differentiate whether calcification is from plaque formation or mineral imbalance.

This lack of distinction complicates interpretation of calcification changes in response to interventions like vitamin K2 supplementation [12][13][14].

Cardiovascular Risk Implications:
While vascular calcification from excess calcium/phosphate or low vitamin K2 is not directly related to atherosclerosis or plaque rupture, it raises cardiovascular risk through arterial stiffening.

Atherosclerotic plaque calcification carries direct risk of plaque rupture and acute coronary events.
Both types of calcification are indicators of underlying cardiovascular pathology and merit risk management, but their pathophysiology and clinical consequences differ [15][16][17][1].

Summary:
Vascular calcification has distinct pathogenic forms- one linked to atherosclerosis and plaque formation (intimal calcification), and another linked to mineral disturbance (medial calcification) such as from excess calcium or low vitamin K2. Both increase cardiovascular risk but through different mechanisms. Vitamin K2 reduces vascular calcification caused by mineral imbalance and supports inhibition of new deposits but has limited evidence for removing atherosclerotic plaque calcification. On CT/X-ray, these calcifications look the same, making clinical differentiation challenging. Thus, anecdotal calcification improvement with high dose K2 likely comes from reducing non-atherosclerotic calcification, not regression of plaque calcium.

References are drawn from comprehensive review articles and recent clinical studies on vascular calcification, vitamin K2 biology, mineral metabolism, and imaging limitations [1][2][3][9][10][8][12][15][16].

Sources
[1] Vascular Calcification: Pathophysiology and Risk Factors - PMC https://pmc.ncbi.nlm.nih.gov/articles/PMC3959826/
[2] Vascular Calcification: an Update on Mechanisms and Challenges ... https://pmc.ncbi.nlm.nih.gov/articles/PMC3714357/
[3] Vascular calcification: types and mechanisms - Nefrología https://www.revistanefrologia.com/en-vascular-calcification-types-mechanisms-articulo-X2013251411051719
[4] Calcium Deposits (Calcification): Types, Causes & Risks https://my.clevelandclinic.org/health/diseases/23117-calcium-deposits
[5] Coronary Calcification: Types, Morphology and Distribution https://www.icrjournal.com/articles/coronary-calcification-types-morphology-and-distribution?language_content_entity=en
[6] Calcification: Types, Causes, and Diagnosis - Healthline https://www.healthline.com/health/calcification
[7] The Bone—Vasculature Axis: Calcium Supplementation and the ... https://pmc.ncbi.nlm.nih.gov/articles/PMC6370658/
[8] [PDF] Effects of Calcium Supplementation on Cardiovascular Disease in ... https://touroscholar.touro.edu/cgi/viewcontent.cgi?article=1163&context=sjlcas
[9] Vitamin K Dependent Proteins and the Role of Vitamin K2 in the ... https://pmc.ncbi.nlm.nih.gov/articles/PMC4052396/
[10] Vitamin K2—a neglected player in cardiovascular health - Open Heart https://openheart.bmj.com/content/8/2/e001715
[11] Vitamin K supplementation and vascular calcification: a systematic ... https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2023.1115069/full
[12] Lower limb arterial calcification and its clinical relevance ... - Frontiers https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2023.1271100/full
[13] Beyond the Basics: Unraveling the Complexity of Coronary Artery ... https://pmc.ncbi.nlm.nih.gov/articles/PMC10742130/
[14] Medial Arterial Calcification: JACC State-of-the-Art Review https://www.sciencedirect.com/science/article/pii/S0735109721056977
[15] Coronary Artery Calcification and Risk of Cardiovascular Disease ... https://pmc.ncbi.nlm.nih.gov/articles/PMC5798875/
[16] Vascular calcifications as a marker of increased cardiovascular risk https://pmc.ncbi.nlm.nih.gov/articles/PMC2672434/
[17] How Coronary Artery Calcification Predicts Heart Health - 4DMedical https://4dmedical.com/how-coronary-artery-calcification-predicts-heart-health/

Coronary artery calcification is a strong indicator of heart health and potential heart attack risk. The calcification aspect refers to the collection of calcium in your heart’s two main arteries (the coronary arteries). These arteries are responsible for pumping blood to the rest of the body. A w...

09/16/2025