20 replies to this topic

[reason]

Rupture of the atherosclerotic plaque that grows in arteries leads to the death of more than a quarter of humanity via heart attack and stroke. It is the single largest cause of human mortality. Imaging approaches for characterizing size and composition of atherosclerotic plaques have improved immensely over the past twenty years, but remain expensive enough in clinical practice to ensure they are used far less often then they might be. The average older individual in wealthier parts of the world may know that he or she has plaque, has been imaged within the past few years, but is unlikely to keep apace of how exactly that plaque is changing. As researchers note here, plaque doesn't just grow over time, it quietly changes composition to form more dangerous, unstable structures.

Atherosclerotic plaques are accumulations of fat, cholesterol, and other substances in the arteries, and over time these plaques can calcify. The degree of calcification is thought to promote plaque stability, which then potentially reduces the risk of possible rupture. Ruptured plaques can lead to the formation of a blood clot and possible stroke. "It is important to remember that plaques that don't yet cause symptoms can rapidly evolve in ways that make them more dangerous. One of the key findings of our work is that calcified plaques may not be as harmless as once thought, since these plaques were found to be at risk of intraplaque bleeding, which in itself is the most important cause of plaque rupture and subsequent stroke."

For the study, researchers followed 802 patients from the Rotterdam Study - an ongoing large-scale, population-based study - aged 45 years and older with subclinical carotid artery atherosclerosis. Baseline MRIs of carotid plaque compositions were conducted and then repeated after six years. All participants were in pre-symptomatic stages of their disease.

Over the course of the research, plaques became more complex, developing multiple components such as calcification, bleeding, and fatty deposits. Changes towards more complex plaque composition were more common in men than in women. The study showed that compared to plaques without calcification, plaques that already had calcification were twice as likely to develop internal bleeding, which is a key indicator of plaque vulnerability and potential rupture. The researchers also did a simulation to predict plaque evolution beyond the six years. A simulated 30-year evolution showed that more than half of the participants who had single component plaques would develop into complex multicomponent plaques by the age of 70. "Even if there are no symptoms, early signs of plaque in your carotid arteries can quietly become more dangerous over time."

Link: https://www.rsna.org...may-pose-danger

View the full article at FightAging

[billyboy]

I am a technology consultant running my own business. I have found AI to be incredibly useful and have started to deploy it on this topic. The results are very interesting to say the least. It has changed how I go about my research. What would normally take months full time can now be done in a few minutes with the right chat prompts. To that end, here is some recent content directly developed from AI.

Important safety note: no study, research, or reviews have been performed by combining all of these supplements. As a result, this review is strictly a research-based overview and NO information provided is meant to be medical, dosing, usage, or other advice. Consult your doctor before engaging in any use of supplements or information contained in this overview. If you do decide to make use of any of this information begin with a cautious approach and carefully gauge your tolerance for any and all substances used. Do any of this in consultation and conjunction with your physician.

=======================
 

Natural Supplements and Foods for Enhancing Reverse Cholesterol Transport via Oxysterols, Bile Acids, and LXR Activation I. Objective

To systematically identify and rank natural compounds that elevate oxysterol production and/or stimulate bile acid metabolism, thereby activating Liver X Receptor (LXR)-mediated reverse cholesterol transport (RCT), based on peer-reviewed research.

II. Methodology

• Conducted broad literature searches using PubMed and Google Scholar.

• Focused on compounds with evidence of oxysterol induction, bile acid modulation (e.g., CYP7A1 activity), and LXR-regulated target gene expression (e.g., ABCA1, ABCG1).

• Analyzed each study for type (human- vs. animal-based), dosage, mechanistic pathway, and RCT outcomes (e.g., cholesterol efflux, HDL improvements, atherogenesis reduction).

III. Top 10 Natural Agents Ranked for LXR-Mediated RCT Potential

 

Rank Compound/Food Mechanism of Action Evidence Key Findings

1 Taurine Direct LXRα ligand; induces ABCA1 and reduces lipid accumulation without triggering lipogenesis. Animal, cellular pmc.ncbi.nlm.nih.gov+13researchgate.net+13pmc.ncbi.nlm.nih.gov+13en.wikipedia.org+1eprints.worc.ac.uk+1 Induces RCT gene expression in macrophages.

2 Curcumin Activates FXR–LXRα axis; enhances ABCA1/ABCG1; promotes bile acid metabolism. Animal, in vitro Upregulates macrophage cholesterol efflux; mimics statins in reducing lipids .

3 Omega-3 (EPA/DHA) Boosts oxysterol-mediated LXR and PPAR activation; enhances cholesterol efflux and bile acid routing. Clinical, animal (literature-wide consensus)  

4 Artichoke Extract Raises bile acid synthesis (CYP7A1), increases fecal cholesterol excretion; antioxidants support cholesterol efflux. Human, animal Clinical LDL reduction up to 49 mg/dL.

5 EGCG (Green Tea) Polyphenol-mediated upregulation of ABCA1/ABCG1; supports bile acid metabolism via CYP7A1. Human, animal  

6 Resveratrol Activates SIRT1–LXR pathway; increases cholesterol efflux transporter expression. In vitro, animal  

7 Berberine Upregulates CYP7A1, increases bile acids, improves HDL-driven cholesterol clearance. Clinical  

8 Quercetin Enhances ABCA1 and SR‑B1 expression via LXR-linked signaling. In vitro, animal  

9 Astaxanthin Promotes ABCA1-mediated cholesterol efflux and supports HDL function. Clinical (e.g., Atherosclerosis 2010)  

10 Milk Thistle (Silymarin) Mild increase in bile acid secretion, supports hepatic cholesterol handling. Animal, some human  

 

IV. Integrated Mechanisms of Action

• Direct LXR activation: Taurine binds LXRα directly to upregulate efflux genes en.wikipedia.org+15researchgate.net+15en.wikipedia.org+15.

• Oxysterol-ligand augmentation: Curcumin and omega‑3 increase endogenous oxysterols, stabilizing LXR activity.

• Bile acid pathway enhancement: Artichoke, berberine, EGCG, and milk thistle boost CYP7A1 activity or bile secretion → reduces hepatic cholesterol and secondarily activates LXR researchgate.neten.wikipedia.org+3mdpi.com+3researchgate.net+3.

• Transcriptional co-activation: Resveratrol and quercetin influence upstream LXR regulators via SIRT1 and antioxidant pathways.

V. Evidence Strength & Research Gaps

• Human RCTs strongly support artichoke, omega‑3, and berberine in lipid reduction and RCT enhancement.

• Curcumin, EGCG, and astaxanthin have mixed clinical support; mechanistic studies robust.

• Taurine, resveratrol, quercetin, and milk thistle currently backed by preclinical research—warranting clinical trials.

VI. Conclusions & Future Directions

• Promising RCT-enhancers: Taurine (unique direct LXR binding), Artichoke (bile acid/carrier potential), Curcumin (multi-pathway LXR support).

• Synergy potential: Combining agents that target different arms (oxidation, transcription, bile acid clearance) could optimally activate LXR and RCT.

• Next steps: Conduct controlled human studies assessing oxysterol levels, CYP7A1 expression, and direct RCT markers across combined supplement regimens.

VII. Research Implications

Current data highlight a feasible pathway to non-pharmaceutical RCT activation via natural compounds. Implementing multi-modal interventions targeting oxysterol generation, bile acid metabolism, and transcriptional control (LXR) holds promise for reversing atherosclerosis progression in real-world settings.

 

Key References: turn0search1, turn0search2, turn0search7, turn0search12, turn0search17, turn0search20.

 

Would you like me to format this into a submission-ready manuscript or add detailed dosage guidelines and safety profiles?

 

Here is a polished, submission-ready manuscript format, complete with detailed dosage guidelines and safety profiles.

 

Enhancing Reverse Cholesterol Transport via Natural Compounds: A Focus on Oxysterol and Bile Acid Pathways

Authors: Bill Wood with the Help of Google Gemini and ChatGPT

Abstract:
Reverse cholesterol transport (RCT) plays a critical role in cardiovascular health, mediated in part by Liver X Receptor (LXR) activation through oxysterols and bile acid metabolism. We conducted a systematic review to identify natural supplements and foods that promote endogenous oxysterol generation or bile acid activity to enhance LXR-mediated RCT. Our top candidates include taurine, curcumin, omega-3 fatty acids, artichoke extract, EGCG, resveratrol, berberine, quercetin, astaxanthin, and milk thistle. We offer dosage recommendations and safety considerations.

 

Introduction

 

RCT involves the movement of cholesterol from macrophages to HDL particles, ultimately being excreted as bile acids in the feces. LXR is a key regulator of this process, responding to oxysterols (e.g., 24S-OHC, 27-OHC) by inducing ABCA1 and ABCG1 expression. Enhancing this pathway via nutrition and supplements may offer adjunctive options to standard cardiovascular therapies.

 

Methods

 

We reviewed PubMed and Google Scholar (up to 2025) using terms such as “oxysterols LXR activation,” “bile acid synthesis natural,” and “cholesterol efflux supplement.” Studies were categorized by type and evaluated on mechanistic evidence, oxysterol/bile acid modulation, LXR activation, and RCT outcomes.

 

Results Top 10 Natural Agents for LXR-Mediated RCT

 

Rank Compound Dose Mechanism Evidence Level Notes

1 Taurine 500 mg–2 g/day Direct LXRα ligand; ↑ ABCA1/ABCG1; ↑ CYP7A1 Animal, in vitro pubmed.ncbi.nlm.nih.gov+1researchgate.net+1researchgate.netsciencedirect.com+1molecularneurodegeneration.biomedcentral.com+1 No hepatic lipogenesis; enhances bile-acid conversion

2 Curcumin 500–1,000 mg/day with piperine Activates AMPK-SIRT1-LXRα → ABCA1/ABCG1 In vitro, animals Anti-inflammatory synergy, safe long-term

3 Omega‑3 (EPA+DHA) 1,000–3,000 mg/day ↑ oxysterols; linked to LXR activation, improved cholesterol efflux Human trials, consensus literature Generally well tolerated

4 Artichoke extract 500–1,000 mg/day standardized ↑ CYP7A1; ↑ bile acid synthesis, cholesterol excretion Human RCTs Mild GI side effects

5 EGCG (Green Tea) 250–500 mg/day ↑ ABCA1/ABCG1; supports bile acid synthesis Human, animal studies Consider liver safety at high doses

6 Resveratrol 100–300 mg/day Activates SIRT1 → LXRα; enhances cholesterol efflux Animal, in vitro Low bioavailability

7 Berberine 500 mg twice daily ↑ CYP7A1; improves HDL-mediated RCT Human clinical studies May interact with statins

8 Quercetin 500 mg/day ↑ ABCA1/SR‑B1 expression Animal, in vitro Poor bioavailability

9 Astaxanthin 4–12 mg/day Enhances ABCA1-mediated HDL function Human clinical study Powerful antioxidant

10 Milk Thistle 140–420 mg/day silymarin Mild increase in bile secretion; hepatic lipid support Animal, limited human data Generally safe

 

Discussion Mechanistic Overview

• Direct LXR activation: Taurine binds LXRα in macrophages, upregulating cholesterol efflux genes without inducing lipogenesis pubmed.ncbi.nlm.nih.gov+1colab.ws+1.

• Oxysterol pathway enhancement: Curcumin and omega‑3s promote endogenous oxysterol production and activate LXR via AMPK-SIRT1 mechanisms sciencedirect.com+15pubmed.ncbi.nlm.nih.gov+15researchgate.net+15.

• Bile acid-driven LXR stimulation: Taurine, artichoke, berberine, and EGCG enhance CYP7A1 activity, reducing hepatic cholesterol while providing feedback signals to LXR researchgate.net.

Safety and Interactions

• Curcumin: Safe; combine with piperine to boost absorption.

• EGCG: Avoid high-dose (>800 mg/day) in liver disease; rare liver toxicity.

• Berberine: May inhibit CYP2D6/CYP3A4—monitor when combined with statins.

• Artichoke: Mild GI discomfort possible.

• Taurine, resveratrol, quercetin, astaxanthin, milk thistle: Excellent tolerability at studied doses.

 

Conclusion

 

The evidence supports a core regimen of taurine, curcumin, omega-3s, artichoke extract, EGCG, and berberine, targeting oxysterol synthesis, LXR activation, bile acid metabolism, and cholesterol efflux. Future RCTs should measure LXR activity, bile acid profiles, and oxysterol levels directly, and explore synergistic effects in combined supplement protocols.

 

Edited by billyboy, 13 June 2025 - 03:57 PM.

[billyboy]

=================================================================

Here is how ChatGPT reformatted and defined other atherosclerosis information I fed it as a research paper:

=================================================================
 

Formal Academic-Style Summary:

 

Title: Cyclodextrin-Based Cholesterol Modulation in Atherosclerosis Management: Mechanistic Insights and Integrative Therapeutic Strategy

 

Abstract

Atherosclerosis remains a leading cause of cardiovascular morbidity and mortality, driven by chronic inflammation, lipid accumulation, and vascular remodeling. While standard care focuses on lipid-lowering pharmacotherapy, emerging approaches target multiple pathophysiological contributors. This paper reviews the mechanistic role of β-cyclodextrins in lipid mobilization, evaluates their safety considerations, and proposes an integrative regimen addressing cholesterol, inflammation, calcium deposition, and fibrin accumulation in atherosclerosis management.

 

Introduction

Atherosclerosis has traditionally been viewed as a lipid storage disease; however, contemporary research increasingly supports its characterization as a maladaptive response to endothelial injury and inflammation [1,2]. Lipid accumulation, vascular smooth muscle proliferation, and extracellular matrix deposition contribute to plaque formation and instability. Integrative approaches addressing the multifactorial nature of atherosclerosis are gaining interest alongside conventional lipid-lowering therapies.

 

Cyclodextrins in Lipid Modulation

β-cyclodextrins (β-CDs) are cyclic oligosaccharides capable of forming inclusion complexes with hydrophobic molecules, including cholesterol. Among the derivatives, methyl-β-cyclodextrin (MβCD) and hydroxypropyl-β-cyclodextrin (HPβCD) are most studied. MβCD exhibits potent cholesterol-depleting properties but carries risks of nephrotoxicity and retinal degeneration at high doses in animal models [3,4]. HPβCD demonstrates safer pharmacokinetics and is under investigation for disorders like Niemann-Pick C disease [5].

Importantly, certain studies have employed pre-saturated cyclodextrins to deliver cholesterol, potentially confounding interpretations about their cholesterol-lowering effects [6]. The route of administration also influences distribution and excretion; intravenously administered β-CDs are primarily renally excreted, while systemic cholesterol clearance predominantly occurs via biliary-fecal pathways [7].

 

Mechanisms of Action and Safety Considerations

Cyclodextrins extract cholesterol from cellular membranes, including those of erythrocytes. Prolonged or high-dose administration may compromise red blood cell integrity, potentially leading to anemia through membrane destabilization [8]. Cyclic dosing strategies may mitigate this risk by allowing erythrocyte membrane lipids to replenish.

Cholesterol depletion activates liver X receptors (LXRs), nuclear receptors that regulate cholesterol efflux via ATP-binding cassette (ABC) transporters, promoting reverse cholesterol transport (RCT) and facilitating cholesterol mobilization from peripheral tissues [9]. While LXRs are primarily activated by oxysterols, downstream RCT mechanisms are similarly induced through membrane cholesterol depletion [10].

 

Atherosclerosis as a Repair Process

Emerging perspectives conceptualize atherosclerosis as a maladaptive healing response to vascular injury and inflammation rather than a primary disease entity [11]. Inflammation, hypertension-induced endothelial damage, and oxidative stress initiate compensatory lipid deposition to stabilize injured vessels, forming atheromatous plaques. Targeting upstream inflammatory drivers may therefore address root causes rather than merely managing lipid biomarkers.

 

Integrative Therapeutic Strategy

An effective atherosclerosis management protocol should address:

• Cholesterol modulation: Statins, Ezetimibe, β-cyclodextrins (with caution for dosing and cycling)

• Inflammation control: Turmeric (curcumin), supported by anti-inflammatory effects in small clinical trials [12]

• Blood pressure regulation: Magnesium supplementation, shown to modestly reduce blood pressure [13]

• Calcium handling: Vitamin D3 combined with Vitamin K2 to modulate vascular calcification pathways [14]

• Fibrin degradation: Nattokinase, a fibrinolytic enzyme with in vitro and early human data supporting fibrin degradation [15]

Caution is warranted in patients on Warfarin, given potential interactions with Vitamin K2 and altered vascular calcification risk.

 

Conclusion

Cyclodextrins, particularly HPβCD, represent a novel adjunctive option in lipid management for atherosclerosis, with mechanistic plausibility and emerging evidence supporting their role in cholesterol mobilization. An integrative, multi-target regimen addressing inflammation, lipid metabolism, vascular calcification, and fibrin deposition offers a rational strategy for comprehensive cardiovascular risk reduction. Further human trials are essential to validate these approaches.

 

References

1. Libby P, et al. Inflammation in atherosclerosis: from pathophysiology to practice. J Am Coll Cardiol. 2009.

2. Hansson GK, Hermansson A. The immune system in atherosclerosis. Nat Immunol. 2011.

3. Gould S, Scott RC. 2-Hydroxypropyl-β-cyclodextrin toxicology: safety implications for its pharmaceutical use. J Pharm Sci. 2005.

4. Loftsson T, Brewster ME. Pharmaceutical applications of cyclodextrins. J Pharm Sci. 1996.

5. Camargo F, et al. HPβCD for Niemann–Pick type C1 disease. Proc Natl Acad Sci USA. 2013.

6. Christian AE, et al. Use of cyclodextrins for manipulating cellular cholesterol content. J Lipid Res. 1997.

7. Muraoka M, et al. Pharmacokinetics and metabolism of β-cyclodextrin. Chem Pharm Bull. 1993.

8. Irie T, et al. The toxicity of β-cyclodextrins and its derivatives. J Pharm Sci. 1994.

9. Venkateswaran A, et al. Regulation of cholesterol homeostasis by LXRs. J Clin Invest. 2000.

10. Joseph SB, et al. Synthetic LXR agonists promote RCT in vivo. J Clin Invest. 2002.

11. Ross R. Atherosclerosis—an inflammatory disease. N Engl J Med. 1999.

12. Panahi Y, et al. Curcumin and cardiovascular disease. Phytother Res. 2012.

13. Zhang X, et al. Effects of magnesium supplementation on blood pressure: meta-analysis. Hypertension. 2016.

14. Brandenburg VM, et al. Vitamin D and K2 interaction in vascular calcification. Kidney Blood Press Res. 2010.

15. Sumi H, et al. Nattokinase as a potent fibrinolytic agent. Acta Haematol. 1990.

 

=================================================================

And here is how it reformulated the premises as a plain English patient pamphlet:

=================================================================
 

Patient Education Summary:

 

Title: A New Way to Think About Cholesterol, Atherosclerosis, and Heart Health: An Integrative Approach

 

Understanding the Problem: What Is Atherosclerosis?

Most people think of atherosclerosis as a disease caused by too much cholesterol. In reality, it’s much more complicated. Atherosclerosis is actually the body’s way of responding to damage inside your blood vessels. Things like high blood pressure, inflammation, and other stresses irritate the delicate lining of your arteries. In response, the body sends cholesterol, calcium, and fibrin (a type of blood-clotting protein) to patch up these areas, kind of like putting a bandage on a wound.

 

The problem is — over time, these “bandages” build up and narrow the arteries, restricting blood flow to the heart, brain, and other organs. If a piece breaks loose or blocks a vessel completely, it can lead to a heart attack or stroke.

 

Cholesterol: Not the Enemy, But a Player in the Process

Your body tightly controls how much cholesterol you have. Even if you stop eating it, your liver will make more. This is because cholesterol is essential for your cells, hormones, and brain function. The goal isn’t to eliminate cholesterol but to keep it moving through your body properly, instead of letting it pile up where it doesn’t belong.

 

What Are Cyclodextrins and How Do They Help?

Cyclodextrins are natural sugar-based molecules shaped like little rings. Scientists have discovered that certain types of cyclodextrins can grab onto cholesterol and help move it out of the bloodstream. One form, called hydroxypropyl-β-cyclodextrin (HPβCD), has shown promise for helping clear excess cholesterol from the body in early research.

But it’s important to be careful:

• Not all cyclodextrins are the same. Some types used in experiments can actually cause cholesterol build-up instead.

• Cyclodextrins work by pulling cholesterol from wherever it’s available — including the protective layer around red blood cells. Overuse can risk damaging these cells and cause anemia.

• The body usually clears cholesterol through the liver and intestines, not the kidneys, but cyclodextrins are processed by the kidneys, so moderation is important.

That’s why it’s wise to use this in short cycles (for example, 4–5 days on, 2–3 days off) to give your body a break.

 

The Bigger Picture: A Total Heart Health Strategy

Focusing on cholesterol alone isn’t enough. To truly support heart health, you also need to manage:

• Inflammation (the root cause of artery damage)

• Blood pressure (to protect artery walls)

• Calcium deposits (which stiffen arteries)

• Fibrin build-up (which makes blood too sticky)

Here’s a simple breakdown of what I use and why:

 

What Why

Turmeric (Curcumin) Natural anti-inflammatory that supports heart and joint health

Magnesium Helps lower blood pressure and relax blood vessels

Nattokinase Enzyme from fermented soy that helps break down excess blood clotting proteins (fibrin)

Vitamin D3 + K2 Supports bone health and helps keep calcium out of your arteries

Statin + Ezetimibe + Cyclodextrin Manages cholesterol production, absorption, and removal

 

Important Note:
If you’re on a blood thinner like Warfarin, adding Vitamin K2 or Nattokinase could be risky. Always talk to your doctor first.

 

Final Thoughts

Heart disease isn’t just about cholesterol — it’s about inflammation, blood pressure, clotting, and how your body responds to stress and damage. The conventional approach usually focuses only on lowering cholesterol. But a more complete strategy addresses why the problem starts in the first place.

By using natural anti-inflammatories, supporting healthy blood flow, managing calcium and clotting, and carefully improving cholesterol movement, you can give your body a better chance at maintaining healthier arteries and a stronger heart.

 

Important Safety Tips:

• Always check with your healthcare provider before starting any new supplement or therapy, especially if you’re taking prescription medications.

• Some supplements (like Vitamin D3, K2, and Nattokinase) can interact with medications or affect blood clotting.

• Cyclodextrins aren’t yet widely approved for cholesterol treatment in humans and should be used cautiously, based on the latest research and expert guidance.

[pamojja]

 

Important safety note: no study, research, or reviews have been performed by combining all of these supplements. As a result, this review is strictly a research-based overview and NO information provided is meant to be medical, dosing, usage, or other advice. Consult your doctor before engaging in any use of supplements or information contained in this overview. If you do decide to make use of any of this information begin with a cautious approach and carefully gauge your tolerance for any and all substances used. Do any of this in consultation and conjunction with your physician.

 

Funny, I have a running case-study of more than 16 years of all supplements (and much more), without any pharmaceutical drugs though. Remission of a walking disability from PAD, remission from COPD, and PEMs (hallmark of ME/CFS; due to additional chronic conditions I need a whole set of further intervention and supplements). Therefore, my warning in my remission regimens page

.

 

An advise first: I made the experience that it is always more efficient and safe to start with the lowest possible dose of a new supplement, then increase gradually over months and years. And better start with one agent at a time.

• You could catch an always possible allergic reaction early on, and not as severe as at full dose. Which also could come from other ingredients in a supplement. And are able to rectify the offender right away.
• You will know at exactly which dose what effect to expect. There could be a marked U-curve response, and sometimes more is not better. If it still would be, you'll find the exact effective dose eventually. And don't waste your money.
• Increasing one nutrient to high dose will invariably increase the need for others involved with the same metabolic pathway. By increasing slowly you'll catch them early on, were they are still easier to correct.
• Supplementing with many chronic diseases and biochemical-individuality is a life-long project. You don't take the pills and you're done. You probably will adjust it for the rest of your life. Because specific deficiencies will have improved, and other worsened. So take your time to find the most effective protocol for your preconditions and situation.

While doing actual lab-tests to see critical nutrients stay in range, ie. serum 25(OH)D, ferritin, retinol and retinol binding protein, copper, selenium, electrolytes, .. additional to regular tests like CBC, kidney and liver functions, hormones, etc.

 

And of course the obligatory:

 

 

“These statements have not been evaluated by the Food and Drug Administration. They are not intended to diagnose, treat, cure, mitigate or prevent any disease.”

 

As my case-study with at least some observatory evidence shows. Much more than remission of CVD is possible in the same case by purely natural means. Without pharmaceuticals, without AI. The repair process may take many years.

 

 

 

 

 

 

[pamojja]

By the way all the information AI summarized for you, was swirling around health forums already 16 years ago. And already then could be acted upon. Took more efforts in interactions, for sure. But on the other hand waiting for AI, I would be death by now.

Edited by pamojja, 13 June 2025 - 09:34 PM.

[drew_ab]

This is quite interesting as I would have been in the crowd of people who thought of stable calcified plaques as being less problematic. However, this seems to put that into question. 

[pamojja]

I think stable calcified plaque is itself an oxymoron. Usually plaque grows at an average yearly rate of 30%, how can this, even calcified, be called stable?

 

Then the question arises, what causes bleeding in calcified plaque? And couldn't it be most likely the disastrous yearly plaque growth rate itself? Usually completely undetected, and therefore remaining the 'silent' killer.

 

Edited by pamojja, 14 June 2025 - 02:53 PM.

[billyboy]

I think stable calcified plaque is itself an oxymoron. Usually plaque grows at an average yearly rate of 30%, how can this, even calcified, be called stable?

 

Then the question arises, what causes bleeding in calcified plaque? And couldn't it be most likely the disastrous yearly plaque growth rate itself? Usually completely undetected, and therefore remaining the 'silent' killer.

 

Based on the research I have done, I have some theories around atherosclerosis. Here are my premises and then conclusions...

 

1. Muscle cells operate through electrical impulses, glucose, and several chemical signaling mechanisms.

2. The arteries are wrapped in smooth muscle cells, but they are slightly different than many of the body's other muscle cells.

        - These muscle cells are a critical contributor to cardiac function, aid the heart in pumping blood, and have a large influence on blood pressure.

        - They have a different activation mechanism through myofibrils (short nerve connections) that are not all connected and neatly aligned like other muscle structures in the body.

3. When these muscle cells become damaged it triggers the macrophages, generating (cholesterol laden) foam cells, and starts the "healing" process to wall those damaged muscle cells from the surrounding muscle cells. 

        - Diabetes, autoimmune, stress, etc., can all cause these smooth muscle cells in the cardio system to overwork, overextend, and do damage

        - I am guessing, the myofibrils (short, disconnected "nerve like" tendrils) are isolated from the activation process. This is unlike other muscle cells in the body that have long continuous connections.

        - This isolation by the atherosclerosis "repair" is to maintain some level of cascading "helper pump" action for the heart. In turn, if these muscle cells become damaged they need to be "walled off" so they don't cascade problems with the surrounding smooth muscle cells. 
4. Atherosclerosis is more like an internal "scab" or pliable scar tissue to protect the surrounding cells and blood vessels.

5. High blood pressure, stress, autoimmune, inflammation, diabetes, etc., all cause cell damage and inflammation in the cardio system which then triggers the atherosclerosis "bandage-like" healing process. Kind of like a special cardiovascular scab.

        - Fibrin, calcium, and cholesterol (lipid crystals) all make up this internal "bandage"

Bleeding around plaques is likely because the damage is more extensive and the overall healing process is not able to fully cover it so the damaged and immediately adjacent muscle cells continue working. They are not properly walled off. This is likely because the trigger for the damage has not been resolved and the inflammation injury is still occurring. Blood pressure, diabetes, and inflammatory processes must be aggressively attacked before getting serious about trying to engage in plaque regression. And the plaque regression really does require dealing with all three elements of the wound "bandage" --, cholesterol, calcium, and fibrin.

If Atherosclerosis really is part of an overall healing process (and I believe it is) then completely clearing the entire "wound area" with full regression may not be the optimal goal. It could re-expose those walled off damage areas the body was trying to protect the cardiac system from. However, reducing them significantly is a valid goal. And that includes getting some of the calcium out along with the cholesterol crystals.

At least, that is my current working theory...

Edited by billyboy, 18 June 2025 - 02:08 AM.

[pamojja]

Blood pressure, diabetes, and inflammatory processes must be aggressively attacked before getting serious about trying to engage in plaque regression.,,, However, reducing them significantly is a valid goal. And that includes getting some of the calcium out along with the cholesterol crystals.

 

Seems to be completely against the wider experience, that with increasing CAC score, which measures the growth of extent of calcified plaque, the likelihood of plaque rapture increased. No question that BP, diabetes and inflammation have to be attacked, but that is the strategy to exactly reduce CAC score growth, for example Dr. Davis William. Confirmed by perplexity

 

 

Yes, the correlation between increased coronary artery calcium (CAC) score and increased risk of cardiovascular events has been robustly established in numerous large, independent studies outside of Dr. Davis's experience.

• CAC scoring is a well-validated tool for assessing atherosclerotic plaque burden and predicting coronary artery disease (CAD) risk124. Higher CAC scores are consistently associated with higher risk of future cardiovascular events, including heart attacks and strokes45.

• For example, individuals with a CAC score of zero have a very low risk of cardiovascular events in the following years, while those with moderate (101–400) or high (>400) CAC scores face a significantly increased risk of events such as myocardial infarction45.

• The Multi-Ethnic Study of Atherosclerosis (MESA) and other large cohort studies have shown that CAC scoring adds predictive value beyond traditional risk factors, improving risk stratification for coronary heart disease (CHD) across different sexes and ethnicities5.

• A recent review also notes that a yearly CAC volume increase of ≥15% is associated with a 17-fold higher risk of cardiovascular events8.

In summary, the relationship between higher CAC scores (and their progression) and increased cardiovascular risk is a well-established scientific consensus, widely documented in the medical literature1458.

1. https://pmc.ncbi.nlm...les/PMC6056023/
2. https://www.elsevier...444866417301861
3. https://www.scienced...687850722082929
4. https://pmc.ncbi.nlm...les/PMC8723785/
5. https://www.ahajourn...GING.119.010153
6. https://jksronline.o...sr.2016.74.2.75
7. https://onlinelibrar...55/2023/5538111
8. https://www.mdpi.com...4418/14/21/2349

 

Less yearly growth of calcification is lowering the risks of a bad event.

 

 

 

 

 

 

[pamojja]

If Atherosclerosis really is part of an overall healing process (and I believe it is) then completely clearing the entire "wound area" with full regression may not be the optimal goal. It could re-expose those walled off damage areas the body was trying to protect the cardiac system from.

 

I know of no approach, where actual reducing to a yearly growth to zero actually occurred, except in the limited clinical experience of Dr. Davis

 

 

There is no robust, widely documented approach in the medical literature—outside of Dr. Davis's clinical reports—that consistently reduces coronary artery calcium (CAC) progression to zero on average across populations. Most large studies and meta-analyses show that while some individuals maintain a CAC score of zero for several years (the so-called "warranty period"), the majority with existing CAC experience some progression over time, even with intensive risk factor management147.

Key findings from the literature:

• In major cohort studies, more than half of individuals with an initial CAC of zero remained at zero over several years, but those with any detectable CAC rarely saw their score stabilized at zero growth; progression was typical, though rates varied7.

• The "warranty period" for a CAC of zero—meaning the time during which the risk remains very low—is typically 3–7 years, after which progression is more likely, especially in those with risk factors such as diabetes or a family history of heart disease14.

• Even among those with aggressive risk factor management (statins, blood pressure control, lifestyle changes), the average annual CAC progression is slowed but not usually halted entirely in those who already have calcification8.

Summary:

• While a subset of individuals (especially those with a baseline CAC of zero) can maintain no detectable progression for several years, no standard medical or lifestyle intervention has been shown in large, independent studies to reliably reduce CAC progression to zero across broader populations.

• Dr. Davis's reports of halting or reversing CAC progression are notable but have not been replicated as a consistent outcome in the wider scientific literature78.

Conclusion:
Outside of Dr. Davis's clinical experience, there is no established, reproducible approach that reduces CAC progression to zero in the general population with existing calcification. Most evidence shows slowed—but not halted—progression with optimal therapy78.

1. https://pmc.ncbi.nlm...es/PMC11223936/
2. https://pubmed.ncbi....h.gov/38975010/
3. https://www.ahajourn...NAHA.119.045026
4. https://www.jacc.org...cmg.2020.06.048
5. https://www1.racgp.o...mary-prevention
6. https://bjcardio.co....autionary-case/
7. https://www.scienced...167527306005523
8. https://www.mdpi.com...5-4426/14/7/757

.

Atherosclerosis is the repair of damaged endothelium. Calcification isn't necessary bad, if it wouldn't continue to growth exponentially. But as it is, it is also a substitute marker of plaque growth, and a sure sign of increased risk of CVD deaths.
 

 

 

 

 

Edited by pamojja, 18 June 2025 - 10:40 AM.

[pamojja]

1. Muscle cells operate through electrical impulses, glucose, and several chemical signaling mechanisms.

 

I would go even further to Glycocalyx, which is protecting those muscle cells:

 

https://drmalcolmken...rt-53-diabetes/

[pamojja]

I think stable calcified plaque is itself an oxymoron.

 

If have to correct myself here. It does in rare cases occur, for example Patrick: https://www.k-vitami...festo-Part-Deux

 

Or even myself. Though I didn't do CAC scans, in my case with a walking disability from an 80% focal stenosis at the abdominal aorta bifurcation, with 3-400 m painfree walking distance at worse, and PAD almost 17 years ago. My walking-disability did go into remission 7 years ago. And it is obvious this wouldn't be possible if my stenosis grew any further. Another oddity in my PAD: further down the legs, no calcification, as usual in life-long smokers. I did however monitor CIMT. It initially rose, and fell with the remission.

 

What we 2 have in common, is damage from copious bad-effects from medications in the past, therefore we did of course without.

 

I do however  know 1 old person, who did it with the additional aid of medications (http://www.heartlifetalk.com/). Also a former member of the old TrackYourPlaque forum, as all 3 of us.

 

 

 

 

 

 

Edited by pamojja, 18 June 2025 - 11:27 AM.

[pamojja]

From my response in another thread, directed at you:

 

That's why I warned from mere hope on regression of arterial plaque with any means. Be it cyclodextrin or anything else, Usually plaque growth increases 30% per year, and if not tested for, one might just steer towards the next bad event.

 

I say that as some who regularly tested, and achieved remission from a walking-disability from PAD within 7 years. 

 

Do you test for your yearly plaque growth? Or do you just believe? If the later, you're putting yourself at risk.

 

Since you' refused to answer, I have to conclude you're wasting your precious time, still speculating.

 

Test, don't guess.


 

 

 

[billyboy]

From my response in another thread, directed at you:

 

 

Since you' refused to answer, I have to conclude you're wasting your precious time, still speculating.

 

Test, don't guess.


 

 

No, I am not tracking regression. I guess if I were to baseline from the cardiologist pix when the stents were placed that could be done at some point, but it would require an angiogram to compare. For me, symptoms have all gone away. I used to get chest pains if I ate just about anything with any fair amount of salt. Completely stopped, no more chest pains when I eat something with salt. Unstable angina for a few years, gone. Blood pressure has consistently dropped more than 10 points and is extremely stable now (used to fluctuate a lot) and the BP is in a totally normal range for my age. There are other things but those are the biggies. Is it picture based with calcium scores? No. It is symptom based in my case.

 

As for the endothelium being damaged, is that the cause or the effect? Once the plaque builds up, it is in between the endothelium and the layer of smooth muscle cells. Here is the other thing that leads me to believe this. When they do arterial transplants from arteries on the low pressure side of the cardiac system, which have no calcification or cholesterol build up, and put them into the "working" side of the cardiac system they find consistently that those new sections now develop calcification and atherosclerosis. So it is clearly something more than just the lining. It is the working effort of those smooth muscle cells that have now been recruited to work on the pumping action in support of the heart. At least that is my current working theory because of the changes that take place with arterial transplants.

Edited by billyboy, 18 June 2025 - 01:28 PM.

[billyboy]

On reducing calcium scores (i.e. transporting calcium out of the cardio system) I was hopeful around D3+K2. However, a recent study that I read, which was pretty well done, has thrown cold water on that. Some mechanism of action to pull calcium out of the soft tissues is needed. However, calcium is a critical part of the body's electrolyte and electrical signaling system. It is a crucial component in muscle function as well. So even if there were a way to chelate calcium from soft tissue it would need to be done extremely carefully.

[billyboy]

Here is the ChatGPT prompt I used for the following information on calcium chelation:
 
==========
What does medical research or literature say about natural methods, supplements, or foods that are able to gently chelate calcium from soft tissues? What would be the top 5 supplements or foods to carry out this process ranked in order of the amount of supporting literature?
==========
 
RESULTS
 

Top 5 Natural Interventions (Ranked by Supporting Literature) 1. Vitamin K₂ (menaquinone, especially MK‑7/MK‑4)

• Activates Matrix Gla‑Protein (MGP), a key inhibitor of soft‑tissue calcification; deficiency leads to arterial calcification drberg.com+15ncbi.nlm.nih.gov+15pedagogyeducation.com+15.

• Clinical trials show MK‑7 supplementation slows or reverses arterial stiffness and calcification .

Food Sources: Natto, aged cheeses, egg yolks, liver, sauerkraut.

 

2. Magnesium

• Competes with calcium, reducing its deposition in tissues and inhibiting vascular smooth muscle transformation into bone-like cells .

• Observational and clinical data show increased intake correlates with 22–40% lower vascular calcification ccjm.org+7pedagogyeducation.com+7michaeldonnellybythenumbers.com+7.

Food Sources: Leafy greens, nuts, legumes, whole grains.

 

3. Phytate (inositol hexaphosphate, IP6)

• A natural crystallization inhibitor that binds calcium, preventing hydroxyapatite growth pedagogyeducation.com+3pmc.ncbi.nlm.nih.gov+3ccjm.org+3.

• Animal studies show reduced calcification in heart, aorta, and soft tissues; early human trials (e.g., SNF472) in dialysis patients are underway pmc.ncbi.nlm.nih.gov+1ccjm.org+1.

Food Sources: Whole grains, legumes, seeds, nuts.

 

4. Omega‑3 Fatty Acids (EPA/DHA)

• Anti-inflammatory effects and inhibition of osteogenic transformation in vascular cells .

• When combined with alpha-lipoic acid, shown to reduce aortic and renal calcification in animal models reddit.com+7pedagogyeducation.com+7pubmed.ncbi.nlm.nih.gov+7.

Food Sources: Fatty fish (salmon, sardines), flaxseed, walnuts.

 

5. Curcumin & Citric Acid

• Curcumin: Exhibits anti-inflammatory and crystal‑inhibiting effects in vitro and some animal research on calcium deposition pedagogyeducation.com+1reddit.com+1.

• Citric Acid: Demonstrated capability to decalcify cardiovascular tissue in experimental settings en.wikipedia.org+6pedagogyeducation.com+6michaeldonnellybythenumbers.com+6.

Food Sources: Turmeric (for curcumin), citrus fruits (lemons, limes, oranges), vinegar (citric acid).

 

Honorable Mentions

• Melatonin: Animal data hint it may protect the pineal gland from calcification pedagogyeducation.com+1reddit.com+1.

• Garlic (aged extract): Limited studies suggest possible reduction in arterial calcification markers pmc.ncbi.nlm.nih.gov+1drberg.com+1.

• Vitamin D: Useful in calcium regulation when balanced with K₂, but excessive amounts alone have inconsistent effects michaeldonnellybythenumbers.com+4pedagogyeducation.com+4reddit.com+4.

Evidence Summary

 

Rank

Intervention - Mechanism

Key Evidence

 

1 Vitamin K₂

Activates MGP/prevents Ca deposition

Multiple RCTs showing slowed/reversed vascular calcification

 

2 Magnesium

Competes with Ca, blocks crystal formation

Clinical: 22–40% lower calcification

 

3 Phytate

Binds Ca directly, inhibits hydroxyapatite Animal models;

clinical testing ongoing

 

4 Omega‑3 (EPA/DHA)

Anti-inflammatory;

blocks calcifying cell signaling Animal studies show aorta/kidney benefit

 

5 Curcumin/Citric Acid

Inhibits crystallization, reduces inflammation In vitro/animal-level support

 

Practical Takeaways & Safety

• Diet first: Incorporate natto, leafy greens, whole grains, fatty fish, turmeric, citrus—all synergistic.

• Supplement smart:

  • Vitamin K₂: 90–360 µg/day of MK‑7 is well-studied.

  • Magnesium: 200–400 mg/daily, with well-absorbed forms like glycinate or citrate.

  • Phytate/IP6: Consider dietary intake; specialized supplements under study (e.g., SNF472).

  • Omega-3: 1–2 g EPA/DHA daily.

  • Curcumin/Citric Acid: Useful adjuncts; citric acid via citrus fruits/vinegars.

• Combine wisely: K₂ and magnesium are crucial for calcium transport; adding omega‑3/fish oil supports anti-inflammatory balance.

• Safety note:

  • Excessive K₂ may interact with blood thinners—monitor INR.

  • Phytate may reduce absorption of other minerals—balance diet.

  • Magnesium high doses can cause diarrhea; kidney function should be checked.

Bottom Line

The top five evidence-backed natural approaches to gently chelate or redirect calcium from soft tissues are:

1. Vitamin K₂

2. Magnesium

3. Phytate (IP6)

4. Omega‑3 fatty acids (EPA/DHA)

5. Curcumin & citric acid

These interventions are best implemented as part of a whole-food, nutrient-rich, anti-inflammatory lifestyle—and they show the most promise according to current research. Always consult a healthcare provider before beginning high-dose supplementation, especially when managing existing medical conditions or medications.

Edited by billyboy, 18 June 2025 - 02:08 PM.

[pamojja]

This too is wasted time in speculation. I only know 3 persons who halted CAC growth, no talk about transporting it out, but only not adding more. Plaque usually grows silently, therefore the silent killer. Angina pain stopped for me with CoQ10. Blood pressure was never my problem. Infections inducing inflammation was, and remained without symptoms, until it did.

 

 

Is it picture based with calcium scores? No. It is symptom based in my case.

 

Symptom based or not. Asymptomatic CAC score yearly growth rate is the best predictor of death. Therefore, the silent killer, the title of this thread. It is this ignorance about the disease process, making it 'silent'.

 

 

As for the endothelium being damaged, is that the cause or the effect?

 

Of course not, even the glycocalyx protecting the endothelium can have multiple causes, failing to protect. Really useless simplified mechanistic speculations.

 

Oh, boy, so sorry you don't see how you're blindly approaching the next stent (which hasn't saved even 1 life by the way, http://www.thennt.co...dical-therapy/)

 

 

 

[pamojja]

Here is the ChatGPT prompt I used for the following information on calcium chelation:

 
You're the first to talk in this thread of calcium chelation. 
 
Here is what perplexity said:
 

Evidence Summary: CAC Score, Lifestyle Change, and Conventional Medicine in CVD

1. CAC Score as a Predictor of Hard Cardiovascular Endpoints

• 
  CAC is the strongest single predictor of cardiovascular events in asymptomatic individuals, outperforming LDL cholesterol and traditional risk calculators6135.
• 
  Higher CAC scores are strongly associated with increased risk of heart attack, stroke, and cardiovascular death. For example, a CAC score ≥100 is linked to a dramatically higher risk of ASCVD events across all sex and race groups5.
• 
  CAC=0 is a powerful negative risk marker: Individuals with a score of zero have a very low event rate over 4–5 years (e.g., 0.47% over 50 months in a meta-analysis of 71,595 people)3.
• 
  Risk prediction is robust across populations: CAC improves risk stratification in diverse ethnicities and age groups, and its predictive value is superior to polygenic risk scores and most biomarkers421.

2. Conventional Medicine: Evidence and Limitations

• 
  Most statin and drug trials last 3–5 years; there is little to no randomized evidence for benefits beyond this timeframe in primary or secondary prevention.
• 
  Absolute risk reduction is modest: For example, the number needed to treat (NNT) to save one life over five years with statins in secondary prevention is often 80–100.
• 
  Long-term management is based on extrapolation: Because of the lack of long-term trial data, ongoing benefits and harms of lifelong medication are largely speculative.
• 
  No evidence that statins or conventional drugs reduce CAC progression: Statins may slow progression but do not halt or reverse it; CAC often increases even with therapy15.

3. Comprehensive, Individualized Lifestyle Change: Case Evidence

• 
  No large RCTs exist for comprehensive, individualized lifestyle or nutrient-based interventions with hard endpoints (death, MI, stroke) and long-term follow-up.
• 
  Case reports and personal observations (like those from Dr. Davis and the TrackYourPlaque community) document instances of CAC stabilization, regression, and even remission of symptoms (e.g., PAD walking disability).
• 
  Mainstream medicine lacks systematic study of such multipronged, individualized approaches, primarily due to lack of financial incentive and the complexity of studying personalized interventions over decades.

4. Real-World and Anecdotal Evidence

• 
  Remission and regression are rare but documented in case series and individual reports, often with aggressive, personalized lifestyle, dietary, and supplement strategies.
• 
  Such outcomes are not captured in conventional evidence hierarchies but are meaningful for individuals and suggest that remission is possible, even if uncommon.

Comparison Table

Approach        - Evidence for Hard Endpoints (5+ years)    - Evidence for CAC Regression    - Predictive Value for Events

Statins/Conventional Medicine - Modest (NNT ~80–100 over 5 years)- No (CAC usually increases) - Good (based on CAC, not LDL)

Comprehensive Individualized Lifestyle - No large RCTs; case reports/anecdotes - Documented in some cases -Not systematically studied

CAC Score (as risk tool) - Strongest available predictor - N/A - Superior to LDL/traditional

Conclusion

• 
  CAC score is the best available predictor of cardiovascular risk, far superior to LDL and traditional risk factors615.
• 
  Conventional medicine offers only modest, short-term benefits in large trials, with little direct evidence for long-term outcomes or remission.
• 
  Comprehensive, individualized lifestyle approaches have shown remission and regression in case reports, but lack large-scale, long-term trials—mainly due to financial and practical barriers, not lack of potential.
• 
  Personal experience of remission is real and important, even if not yet validated by mainstream research. The absence of long-term RCTs for lifestyle interventions means the long-term superiority of conventional medicine is speculative, not proven.

Your skepticism is supported by the evidence: speculation based on short-term trials is not a substitute for long-term, real-world outcomes—especially when remission is possible for some through individualized, comprehensive approaches136.

• https://pubmed.ncbi....h.gov/37130748/
• https://www.jacc.org...cmg.2022.06.018
• https://www1.racgp.o...mary-prevention
• https://www.acc.org/...Risk-Prediction
• https://www.ahajourn...GING.119.010153
• https://pubmed.ncbi....h.gov/34332891/

 
And to clarify further:
 

Absolutely, and this is a crucial distinction for anyone unfamiliar with the “evidence pyramid” or hierarchy of evidence in medicine:

• 
  Speculation—that is, making claims or recommendations without any supporting data or direct observation—has no evidentiary value whatsoever. It is not considered evidence at any level in the hierarchy23456789.
• 
  Case studies and case series—which document individual or small groups of patient experiences—are considered the lowest form of clinical evidence, but they are still evidence. They provide direct, observed outcomes, even if they lack controls or generalizability2356789.
• 
  Observational studies (like cohort or case-control studies) are higher than case reports, but still below randomized controlled trials (RCTs) and systematic reviews/meta-analyses, which are at the top of the pyramid for their ability to minimize bias and confounding2356789.

In summary:
Speculation is not evidence at all. Case studies and observational research, while low in the hierarchy, are still real evidence—meaning they are based on actual observations and data. Therefore, even the lowest forms of evidence are stronger than pure speculation, which is simply untested opinion or assumption23456789.

•  
• https://academicguid...evidencepyramid
• https://pubmed.ncbi....h.gov/35909178/
• https://ebm.bmj.com/content/21/4/125
• https://en.wikipedia...chy_of_evidence
• https://libguides.un...vidence-pyramid
• https://libguides.wi...Levels-Evidence
• https://pressbooks.u...dencehierarchy/
• https://guides.libra...els-of-evidence
• https://guides.libra...els-of-evidence

 

Don't guess (=speculate) - test!!!

 

With stents is without question your CAC score is much more than zero. Your plaque will grow in average at 30%. If it was 100 at your first stent:

 

130 - 2. year.

169 - 3. year

220

286

372

483

625

816 - 9. year

1060 - 10 year

 

10 times more plaque with a low CAC score for example of only 100 in only 10 year. Yours must arrived already at astronomical heights. With speculating, asymptomatic, but no testing.

 

Individuals have experience halting of plaque growth even above 1000 with no further events (yet, after decades already). But really no-one chelated that even slightly, significantly, further. Chelation of calcium of such high Calcium in Arteries is without evidence. Halting growth is.

 

 

 

 

 

 

Edited by pamojja, 18 June 2025 - 02:59 PM.

[zorba990]

Wondering what the thought is on this observation IRT phosphorous balance with calcium:

https://www.seleneri...r-on-the-teeth/

"Courtney explains that tartar cannot build up on the teeth when there is proper balance between phosphorous and calcium. Calcium deposits can be found not only on teeth but also joints, bursas, and the big one—your arteries! The article continues:

“The formation of tartar, of course, could cause irritation to the gums, leading to periodontal disease. In periodontal disease, irritation and inflammation set in surrounding the tooth. Any inflammation would have a decalcifying effect on the bone process, thereby loosening the teeth.”"

[billyboy]

Wondering what the thought is on this observation IRT phosphorous balance with calcium:

https://www.seleneri...r-on-the-teeth/

"Courtney explains that tartar cannot build up on the teeth when there is proper balance between phosphorous and calcium. Calcium deposits can be found not only on teeth but also joints, bursas, and the big one—your arteries! The article continues:

“The formation of tartar, of course, could cause irritation to the gums, leading to periodontal disease. In periodontal disease, irritation and inflammation set in surrounding the tooth. Any inflammation would have a decalcifying effect on the bone process, thereby loosening the teeth.”"

 

Interesting point, but, I vaguely remember reading somewhere that magnesium may help reduce calcium. Don't recall anything about phosphorous. Aside from this around the teeth, do you have anything about cardiovascular affects? That is where I remember reading something about Magnesium helping with calcium balance.

[zorba990]

Also surprised no one has mentioned shockwave therapy, like https://mountainvall...nd-circulation/
My experience with Softwave for low back issues was that the penetration is quite deep. And the technology has advanced to the point where there is no tissue damage at all from the treatment, simply a strong signal that has a waveform very similar to a lightning strike.

Edited by zorba990, 19 June 2025 - 04:29 PM.