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[reason]

While an atherosclerotic plaque initially emerges because too much cholesterol finds its way into one small portion of an artery wall, after a certain point that plaque increases in size by attracting attracting immune cells, stressing them into an inflammatory state, and ultimately killing them to add their mass to the plaque. This is not just the macrophages of the innate immune system, the cell type primarily responsible for attempting to clean up excess lipids and debris, but also T cells of the adaptive immune system. Like macrophages, T cells are attracted by the signaling associated with the inflammatory, damaged plaque environment, and promptly make the problem worse. Later still, there is a cancer-like phenomenon whereby surrounding smooth muscle cells multiply and enter the plaque, accelerating growth still further. That said, and as illustrated here, researchers are interested in trying to slow the development of plaque by reducing the attraction of immune cells to the plaque environment.

Atherosclerosis is the most common cause of life-threatening cardiovascular diseases. The disease involves chronic inflammation of the inner walls of blood vessels and within atherosclerotic plaques. For a long time, macrophages and foam cells were considered the principal agents in the formation of plaques. More recent studies, however, have focused on other immune system cells, CD8+ T cells, as it transpired that these are the immune cells most commonly found in human atherosclerotic plaques.

Scientists cultivated human atherosclerotic plaques together with CD8+ T cells from the same patient in a specially developed 3D tissue culture model. They discovered that the added CD8+ T cells were located primarily in the vicinity of newly formed blood vessels within the plaques. Further analyses using single-cell RNA sequencing and 3D microscopy revealed that the endothelial cells of these vessels express large amounts of the signaling protein CXCL12.

Following up on this discovery, the researchers investigated whether CXCL12 is involved in the recruitment of CD8+ cells by blocking the corresponding receptor (CXCR4) for this signaling protein in the T cells. "This did indeed lead to a significant reduction in CD8+ T cell migration into atherosclerosis plaques. These findings furnish new lines of approach for therapeutic strategies that could influence immune cell infiltration in atherosclerotic plaques."

Link: https://www.lmu.de/e...to-plaques.html

View the full article at FightAging

[billyboy]

Is this just treating another symptom though instead of the underlying problem? In other words, have we been so conditioned that atherosclerosis is a disease that we don't look at it as part of the healing process so that we would then focus on root causes? Some excerpts from a research paper that ChatGPT helped me with :-)

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Emerging perspectives conceptualize atherosclerosis as a maladaptive healing response to vascular injury and inflammation rather than a primary disease entity. 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.
 

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.

 

The Bigger Picture: A Total Heart Health Strategy

 

The obsession with cholesterol 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 creates the sticky patch for lesions)

Here’s a simple breakdown of what I use and 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. Warfarin and some other blood thinners have been found to induce arterial calcification. Always talk to your doctor first.

 

Edited by billyboy, Yesterday, 03:58 AM.

[billyboy]

Forgot to add Fish Oil (EPA)

Fish Oil: Reduce Triglycerides and mild anti-inflammatory

[pamojja]

For some reason, one isn't allowed to post on your first threat. So I paste here to respond:

 

 

Interesting history: Rheumatoid Arthritis since 4, Sudden Cardiac Arrest at 48 (6 stents), currently over 60. Because of RA at 4 and many years of Dr visits, I started reading medical literature in my teens and never stopped. I have come up with a research-based regimen to reverse Atherosclerosis that I believe works. It is based on a multi-factor integrated approach to treating underlying triggers and reversing the damage.

 

First, sorry for so many stents, which are known from RCTs for not saving lives at all.

 

Coronary Stenting for Non-Acute Coronary Disease Compared to Medical Therapy

 

None for mortality

 

In Summary, for those who received the stenting:

 

Benefits in NNT

• None were helped (life saved, heart attack prevented, symptoms reduced)

Harms in NNH

• 1 in 50 were harmed (complications such as bleeding, stroke, kidney damage)

 

Your initial post is confusing. As how: medical literature started as teen, is related to after you came up with an assumingly research-based regimen to reverse Atherosclerosis? Obviously in-between, more than 12 years ago a cardiac arrest, and 6 unfortunate stents (presumably in more than just one year) rather point to the strong suspicion: you still don't understand the disease-process of Arteriosclerosis?

 

Of course, it's not only an inflammation driven, but a plastering healing attempt. But nevertheless, CVD is still killer no. 1.

 

The disease process proceeds silently, at an average growth rate of 30% plaque per year (even with statins taken, as in your case). If you don't test for yearly plaque growth, you're merely guessing.