Blood Clots May Be the Root Cause of All Heart Disease
STORY AT-A-GLANCE In this interview, repeat guest Dr.
Malcolm Kendrick, a board-certified family physician and author of the book, “ The Clot Thickens: The Enduring Mystery of Heart Disease ,” reviews the underlying mechanisms for heart disease, which for the last century has been the leading cause of death in the U.S. Of all the books he's written, this is my favorite, as it goes into great detail, giving you the biological understanding of the process of atherosclerosis leading to heart attacks and strokes. He also has solid strategies for lowering your cardiovascular disease risk. Incidentally, once you understand the disease process, then you can also understand how both COVID-19 and the COVID jab can contribute to heart disease. When asked why he's taken such an interest in heart disease, Kendrick replies:
“When I was training as a student in medicine, Scotland had the highest rate ofheart disease in the world. Early on the answer for why was, ‘Oh, well, it'sbecause we have such terrible diet, and we eat rubbish food like deep friedMars bars.'So, you eat too much saturated fat, the saturated fat gets turned intocholesterol in your bloodstream, and then it's absorbed into arteries and formsnarrowings and thickenings, which all sounds plausible if you don't think aboutit too hard.But I also happen to go to France quite a lot, and what I noticed about Francewas, they eat a lot of saturated fat. They eat more, in fact, than anyone else inEurope, and certainly more than Scotland. So, [this saturated fat] hypothesiscertainly didn't work for the French. They have the highest saturated fat intakein Europe and lowest rate of heart disease, and this has been the case fordecades.If you took all the risk factors for France and Scotland [such as smoking, highblood pressure and diabetes], then the French had slightly [higher risk],according to conventional thinking. But, in fact, they had one-fifth [the rateamong age-matched men].So, I thought, this is interesting. It doesn't make much sense according to whatwe're told. Then while I was in medical school, a tutor in cardiology said ... LDLcannot cross the endothelium. At the time, I didn't know what LDL was, nor did Iknow what the endothelium was, but it sounded important.She had been looking at heart disease as a different process for decades ... So,I think that's really where I got started. Once you start questioning what theproblem is, you end up questioning more and more and you start thinking, gosh,this is just nonsense, isn't it? This whole hypothesis is just nonsense. So, Istarted picking it apart.”
The Thrombogenic Hypothesis
“The Clot Thickens” is Kendrick's effort to explain an alternative hypothesis for what actually causes heart disease. If it's not saturated fat and cholesterol, what is it? In 1852, a Viennese researcher, Karl von Rokitansky, developed what he called the encrustation hypothesis of heart disease. Today, this hypothesis has been renamed the thrombogenic hypothesis. ‘Thrombo' stands for thrombosis, i.e., blood clots, and ‘genesis' means the cause of, or the start of. So, the thrombogenic hypothesis is that blood clots are the basic pathology that causes all heart disease.
We know blood clots cause the final event incardiovascular disease. We know blood clots causeplaques to grow. Why won't you accept that blood clotsare the thing that starts heart disease in the firstplace? Because then we have one process all the waythrough, and it makes sense, because it fits with whatyou can see. ~ Dr. Malcolm Kendrick
In a nutshell, when a blood clot forms on your artery wall, which can happen for a number of reasons, it will typically be covered over and dissolved. A problem arises, however, if the blood clot is not fully eliminated and another blood clot forms in the same ‘vulnerable' area. This then becomes what's conventionally referred to as atherosclerotic plaque.
“The atherosclerotic plaque is basically a buildup of blood clot, repair, bloodclot, repair, blood clot, repair,”
Kendrick explains.
“If the blood clotting processis faster than the repair process, you have a plaque that gradually grows andeventually thickens the artery wall until it narrows suficiently that the finalblood clot, on top of the existing plaque, is the thing that can cause a heartattack or stroke ...If you cut through the plaque and look at it, it almost looks like tree rings. Youcan see there's been a clot, repair, clot, repair, clot, repair, clock, repair over theyears.It's widely accepted that a blood clot forming on an existing plaque will causethe plaque to grow in size. You can find 10,000 papers saying that this is thecase. What the mainstream won't accept is that a blood clot on a healthy arterywall can initiate the whole process.So, to an extent, all I'm saying to people is, well, we know blood clots cause thefinal event. We know blood clots cause plaques to grow. Why won't you acceptthat blood clots are the thing that starts it in the first place? Because then wehave one process all the way through, and it makes sense, because it fits withwhat you can see.”
As noted by Kendrick, the conventional view is that low-density lipoprotein or LDL gets into the artery wall where it initiates plaque formation. It then, inexplicably, stops initiating plaque, and the plaque continues to grow through the addition of repeated clots. However, Kendrick says, once you start drilling down into the cholesterol, aka LDL hypothesis, the whole thing starts to fall apart. LDL simply cannot explain the disease progression. Yet despite the many holes in the theory, the idea that LDL causes heart disease is touted as an absolute, indisputable fact.
What's the Mechanism?
In order to justify a hypothesis, you need to have a mechanism of action. Once you understand the mechanism of the actual disease process, then you can put the puzzle pieces together. Kendrick begins his explanation:
“Your blood vessels are lined with endothelial cells, a bit like tiles on a wall.Endothelial cells are also covered themselves in a thing called glycocalyx. If youtry to pick up a fish, it'll slip through your fingers; it's very slippery. The reasonit's slippery is because it's covered in glycocalyx and the glycocalyx is incrediblyslippery. It's nature's Tefion.So basically, in our case, the glycocalyx [is inside] our blood vessels, to allowthe blood to travel through without it sticking, without damage occurring. So,you have this kind of damage-repellent layer on top of your endothelial cells.Now, if that layer is damaged, and then the endothelial cell itself underneath isdamaged, then the body will say, ‘Oh, we've got damage to a blood vessel, wemust have a blood clot there because we could bleed out.' So, a blood clotforms on the area of damage, and immediately stops [the bleeding].”
The blood clot doesn't just keep on growing and growing. If it did, you'd die anytime you had a blood clot. Instead, when a clot forms, other processes step in to prevent it getting too big, which is why every blood clot doesn't cause a stroke or heart attack. Once the clot has stabilized, and has been shaved down, the area is covered over by endothelial progenitor cells, made in the bone marrow, that fioat around in your blood stream. When a progenitor cell finds an area that has been damaged, it attaches itself to that area, along with others, forming a new endothelial layer. The remaining blood clot is now lying ‘within' the artery wall itself. So, basically, it's the repair process that can lead to plaque buildup within the artery wall. In time, if damage outstrips repair, this can narrow the artery and reduce blood fiow.
What Damages Endothelial Cells?
The question is, what can damage the endothelium in the first place? Here, Kendrick uses the SARS-CoV-2 mechanism as an example:
“The COVID virus enters endothelial cells through the ACE2 receptor. It prefersendothelial cells because they've got ACE2 receptors on them. It gets into theendothelial cell and starts replicating, then bursts out, damaging the cell. Bingo,you've got an area of damage.Of course, added to this, when cells have viruses within them, they send outdistress signals to the immune system saying, ‘I've been infected, come and killme,' and so the immune system starts to have a go at the endothelial cells. Thisis why you can get a problem, because the endothelial cells are being damagedand stripped off.Blood clotting occurs at the points of damage and hey, presto, you're havingclotting, you're having strokes, you're having heart attacks, which is the thingthat people at first couldn't understand [about COVID-19]. Yet it's very clear thatwhat's happening is you've got damage to the endothelial cells.Obviously, you and I both know that if you get a [COVID jab], the cells aretriggered to produce the spike protein, and these cells are sending out distressmessages saying, ‘I'm infected.' You have to be very careful if you want to sticksomething into cells that then says to the immune system, ‘Please come anddestroy me,' because that's what the immune system is going to do.But moving on from that, what other thing can cause endothelial damage? Theanswer is things like smoking. Smoke particles get out of your lungs, they gointo your blood vessels and they cause damage ... You smoke one cigarette anda whole bunch of microparticles appear in your bloodstream, which meansendothelial cells are dying.Luckily as endothelial cells die, another message is sent to the bone marrowsaying, we need more endothelial cells and it stimulates endothelial progenitorcell production. These endothelial progenitor cells rush around covering overthe areas of damage.Some smokers have enough repair going on and when you're younger, it's okay.As you get older and your repair systems begin to fail a bit, cigarette smokingbecomes more and more of a problem.”
Other things that can cause endothelial damage include: • High blood sugar levels and diabetes. The protective glycocalyx layer is made of proteins and sugars — High blood sugar damages the glycoprotein layer, thinning it down in a measurable way. High blood sugar can reduce the glycocalyx layer by as much as two-thirds. This, in turn, exposes the endothelial cells to the bloods and anything else damaging that might be there. The damage to the glycocalyx is why diabetics are prone to both arterial and capillary (small vessel) disease. You can't get atherosclerosis in the capillaries, as there's no room. Instead, the capillaries become broken down and destroyed. This in turn can cause ulcers, due to poor circulation in the skin of your legs and feet. Peripheral neuropathy as the ends of nerve cells are deprived of oxygen. Also visual problems (diabetic retinal damage) and kidney damage. Blood pressure may also become elevated as your heart has to work harder to push blood through a network of damaged/missing small blood vessels. • Heavy metals such as aluminum and lead. • High blood pressure, as it puts stress on the endothelium — Atherosclerotic plaques (atherosclerosis) doesn't occur unless the pressure is raised, adding biomechanical stress.
Repairing the Glycocalyx
As explained by Kendrick, the glycocalyx layer resembles a lawn, with slippery filaments that stick up. Within this glycocalyx layer you have nitric oxide synthase (NOS), which produces nitric oxide (NO), and you have NO itself, as well as a number of other anticoagulant proteins. The glycocalyx is actually a potent anticoagulant layer, so it stops blood clots forming. If glycocalyx is damaged, your risk of blood clotting increases. “It's a very complicated layer,” Kendrick says. “It's like a jungle full of things that say, ‘Don't stick to this, stay away from this.'” Within it, you also have albumin, protein complex produced by the liver. Albumin contains the proteins that help maintain and repair the glycocalyx. A fact that most doctors are unaware of is that, if you have a low albumin level, you're significantly more likely to die of heart disease. The good news is that while the glycocalyx layer can be rapidly destroyed, it can also be rapidly repaired. (Experiments have shown that in an area where the glycocalyx has been completely stripped off, it can be completely repaired in a single second.) Supplements like chondroitin sulfate and methylsulfonylmethane (MSM) can be helpful in this regard.
“If you try and explain that through the LDL mechanism, it just doesn't work,”
Kendrick says.
“They have discovered that if you give chondroitin sulfate as asupplement — which normally is for arthritis and stuff like that — it reduces therisk of heart disease quite considerably. How do you explain that? Well, you canexplain that because you're protecting your glycocalyx.These are the sort of things that make no sense if you like looking at theconventional ideas of heart disease, but are immediately and easily explained ifyou say, ‘We have to keep our glycocalyx healthy and we have to keep ourendothelial cells underneath them healthy.Otherwise they will be damaged and stripped off, and then we will get a bloodclot, and if we keep getting blood clots at that point, we will end up with aplaque and eventually one of the blood clots on that plaque will kill you from aheart attack or a stroke.”
Blood Flow Restriction Training
A lifestyle strategy that can help repair endothelial damage is blood fiow restriction (BFR) training. In response to BFR, your body produces vascular endothelial growth factor (VEGF), which acts as “fertilizer” for the endothelium. You can learn the ins and outs of BFR in my free BFR report . VEGF also induces the synthesis of nitric oxide (NO), a potent vasodilator, and it stimulates endothelial progenitor cells.
“NO protects the endothelium. It is anticoagulant — the most potentanticoagulant we have in the body. It's really the magic molecule forcardiovascular health,”
Kendrick says.
“At one time NO was known as Endothelial Derived Relaxation Factor (EDRF) NOwas something no one believed could possibly exist in the human body. NO isactually a free radical. Everyone says free radicals are terribly damaging andunhealthy.To that I reply, ‘Well, you may wish to know that the chemical that is the singlemost important protective chemical in the body for the cardiovascular system isan incredibly free radical called nitric oxide.”
Some anticancer drugs are designed to block VEGF, as the tumor needs angiogenesis — which is the creation of new blood vessels that are required to provide suficient ‘nutrients' Without these new blood vessels, the tumor dies off. Unfortunately, if you block VEGF, you also block NO, which then raises your risk for heart disease.
“These drugs were almost removed from the market,”
Kendrick says
, “becausedespite their anticancer activity, they were procardiovascular disease to quite ascary degree.[That's why], if you are given bevacizumab or Avastin as an anticancer drug,they now give you angiotensin converting enzyme inhibitors (ACE inhibitors),which are blood pressure lowering tablets, and ACE inhibitors have a specificimpact on bradykinin, which increases NO synthesis.”
Strategies to Lower Your Thrombotic Risk
Read the full article at the original website
References:
