Atheromata, the deposits which are partially obstructing your blood circulation right now, started forming much before you were even 10 years old .
To minimize them, you may want to decipher each of the components of your arterial plaque, as enumerated below :
- Macrophages (a type of white blood cell / WBC) : a major component
- Oxidized low-density lipoprotein (LDL) cholesterol : 2nd major component
- Aggregated platelets : smaller amount.
- Calcium : smaller amount.
- Debris : smaller amount.
- Fatty acids : smaller amount.
- T cells : sometimes present
- Connective tissues & smooth muscles : local elements.
From this list, only cholesterol & fats were singled out, on flimsy grounds, as the villains behind your lifestyle disorders .
LDLs are produced in your liver to transport cholesterol to your peripheral tissues whenever they ask for it because they need it for valid reasons. But LDLs have been found in the blood even when the peripheral cells were not signalling for it.
Those who are unaware of the microvita theory may assume that these are just mindless “deregulated” molecules – as scientists call them – which stick-up here & there haphazardly, inside your arteries.
But that leaves behind more questions unanswered. For e.g., what’s the role of macrophages in this situation – after all they are a major component of all your plaques?
Probing further will uncover more of the fine microvita intelligence which is producing & driving all these molecules inside you.
For instance, pathologists know that these macrophages have scavenger receptors on their surface which cause them to take up oxidized lipoproteins floating around & then embed themselves inside the extracellular matrix of your arterial walls as shown below .
By the time their life is over, these macrophages would have eaten several dozen LDL cholesterol molecules.
Upon death, their contents are released into their surroundings. This includes cholesterol, fatty acids & other cellular debris.
Their dispersion attracts even more macrophages towards the atherosclerotic plaque which enlarges your arterial clog. Overtime the older portions of your plaque calcify.
This is the real story behind the “saturated fat & bad cholesterol” blooper.
But why do your macrophages anchor themselves inside the connective tissues behind your blood vessel walls?
If they had shown up to perform their function as a debris remover then they should have carried the LDLs away.
Are we witnessing a new hitherto unappreciated role of your immune system’s macrophage phagocytes?
To understand what’s going on you may want to examine how the other inhabitants of your clogged arteries came about? Do these members just happen to be there?
1. The inner surface of your blood vessels is lined with a thin layer of endothelial cells which normally inhibit platelet activation.
But when this endothelial layer gets injured, your collagen, vWF (von Willebrand factors) and tissue factors from the sub-endothelium get exposed to your bloodstream.
2. Due to chemotaxis (release of cytokines…) & pathogens (if any), some of your WBCs (leukocytes) are attracted to the damaged tissues. These monocytes enter the arterial wall & become a macrophage.
3. Simultaneously platelets may be deployed to these sites of injury . Upon contact with the collagen or vWF, these platelets of yours get activated & excrete calcium ions besides other stuff.
These excretions serve to clump together the platelets & temporarily plug the broken lining.
4. Thus a blood clot may form at the site of your internal injury. Fibrinogen is converted to fibrin during their formation.
5. The aggregated platelets secrete chemicals that promote the invasion of fibroblasts from surrounding extracellular matrix into the wounded area to form more of the connective tissue (scar).
Fibroblasts are known to play a critical role in all kinds of wound healing.
6. The damaged / infected cells may also attract T lymphocytes (another type of your white blood cell).
7. Once a plaque is fully-formed, your endothelium grows over it. These protrusions come in the way of your blood flow thus inviting further lesions. Once that happens, the story repeats itself while your mound gets bigger.
8. In some regions of increased macrophage activity, macrophage-induced-enzymes erode away the fibrous membrane beneath the endothelium so that the cover separating your plaque from your blood flow in the lumen becomes thin and fragile .
9. Over time these vulnerable plaques rupture, thus triggering blood clotting which further narrows your arteries.
If these happen to be large enough, blood flow in that artery will be blocked resulting in heart attack, stroke, peripheral vascular disease symptoms and other major debilitating events .
Many a times, why do cardiovascular occlusions follow intense bouts of cardio / aerobic exercises?
Because of the higher mechanical stress they may inflict upon your old plaques, especially those which may have softened by now due to the decaying junk inside. They are easy to burst open even by the non-stop stretch & release of the blood vessels induced by your regular 72 bpm pulse-rate.
Thus your plaques are your body’s best response to the bruises sustained on the inner surfaces of your blood ‘piping’. Macrophages act as a band-aid to repair these cuts & abrasions .
As observed, this mechanism has been getting invoked a bit too frequently, right from your early childhood. Can these be avoided or atleast minimized?
Obviously it has nothing to do with your intake of cholesterol or saturated fats per se, but can that be said about… the rest of your diet? Or would you rather first marvel at the incredible group dance of cholesterol with the rest of your physical microvita?
2. Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins Basic Pathology (8th ed.). Saunders Elsevier. pp. 348-351 ISBN 978-1-4160-2973-1
Checkout what do you think this could be doing to your immune system – pushing it’s resilience to the brink…
Or go back to boost ‘your nutritional quotient‘ which is modulating your IQ & EQ today.