Element 7 Wellness

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

08/28/2025

A scientist is helping uncover the role of the immune system in endometriosis—while managing the disease herself.

Learn more: https://scim.ag/4lIfl5e

08/27/2025

Thank you to all who have supported us in these past 8 years! We did it!

AbstractIntroduction. Posttraumatic stress disorder (PTSD) is associated with hyperactivity of the sympathetic nervous system (SNS) and elevated levels of