The first stage of cardiovascular disease is damage to the endothelium. The single layer of cells lining the arteries. After this, we need to look at what then happens? Before looking at this more closely, I would like to take you back in time around one hundred and sixty years. This was when the first scientific debates about plaque development were taking place.
Rudolf Virchow and Karl von Rokitansky were the proponents of different hypotheses at this time. I am grateful to Professor Paul Rosch for providing the information on Virchow’s ideas. He provided this description in one of his newsletter.
‘Rudolph Virchow was the first to demonstrate the presence of cholesterol in atheroma in 1856. He described atherosclerosis as “endarteritis deformans” The suffix “itis” emphasized that it resulted from an inflammatory process that injured the inner lining of the arteries, and that the cholesterol deposits started to appear subsequently
Virchow was very specific about this when he wrote. ‘We cannot help regarding the process as one which has arisen out of irritation of the parts, stimulating them to new, formative actions; so far therefore it comes under our ideas of inflammation, or at least of those processes which are extremely nearly allied to inflammation.
We can distinguish a stage of irritation preceding the fatty metamorphosis, comparable to the stage of swelling, cloudiness, and enlargement which we see in other inflamed parts. I have therefore felt no hesitation in siding with the old view in this matter, and in admitting an inflammation of the inner arterial coat to be the starting point of the so-called atheromatous degeneration and the cholesterol deposits came later.’
So, even one hundred and sixty years ago, eminent professors recognised that atherosclerotic plaques started with ‘inflammation of the inner arterial coat’ a.k.a…the endothelium. The cholesterol deposits came later. Quite so. Or to put this another way, the cholesterol was not the cause of the plaque, the appearance of cholesterol in a plaque was part of the second stage of plaque development.
However, whilst agreeing on this observation, Karl Von Rokitansky had a further hypothesis.
‘Rokitansky proposed that the deposits observed in the inner layer of the arterial wall were derived primarily from fibrin and other blood elements rather than being the result of a purulent process. Subsequently, the atheroma resulted from the degeneration of the fibrin and other blood proteins and finally these deposits were modified toward a pulpy mass containing cholesterol crystals and fatty globules.’
Or, to put it another way. He believed that plaques were, in fact, blood clots, in various stages of repair. He believed this because plaques looked exactly like blood clots, and contained everything that you can see in a blood clot. Perhaps most critically, a great deal of fibrin, which is the key component of all blood clots.
However, Virchow objected to this idea on the simple basis. ‘How can a blood clot form within the arterial wall?’ Or, how can a blood clot form under the endothelium. A good point, and Rokitansky had no effective response. So he lost.
However, there is a very simple explanation as to exactly how a blood clot can be found beneath the endothelium. And this is, because the endothelium wasn’t there when the clot formed. It grew over the top of the clot afterwards. Which takes us to Endothelial Progenitor Cells (EPCs).
After my last blog, a poster made the following comment.
‘And then… the clot, now trapped under the new endothelium, becomes plaque? If true, seems a stupidly “designed” 🙂 healing process.’
Well, superficially, this is a good point. Simply incorporating clot into arterial wall, where is forms a plaque and then kills you, does not seem a great idea. However, I would ask you to consider what would happen to a blood clot, lying on an artery wall, that simply broke off and travelled down the artery. What would happen?
The answer is simple; it would jam up as the artery narrowed. This could cause a stroke, or a heart attack, or suchlike. Exactly as happens with atrial fibrillation. Where small clots that break off from the atria travel into the brain and get jammed. The body does not like blood clots floating about in the arterial system.
So this does not happen/is not allowed to happen. When the endothelium is damaged, a clot forms on top of it. It is true that a certain amount/a great deal of this clot will be shaved away into very small (not stroke creating sized) pieces, but a ‘core’ will be left. This has to be got rid of in some way.
How are you going to do this? There is only one possible way. Firstly, you cover it over with another layer of endothelium, then you attack it, break it down, and destroy it. And this is exactly and precisely what the body does.
Once a blood clot has stabilized, Endothelial Progenitor Cells (EPCs), that are manufactured in the bone marrow, and float around in the bloodstream, are attracted to the clot. They stick to it, then they grow into fully mature endothelial cells, forming a new layer of endothelium, effectively drawing the clot inside the arterial wall. Then the clot is attacked and got rid of. How?
Well, a critical fact to add in here is that. EPCs do not always become endothelial cells, they can go down another developmental pathway as well. They can become monocytes, which in turn become macrophages. Macrophages are the ‘clear up’ cells of the immune system. They attack alien material and then engulf/ingest it. After this they either exit back into the blood stream or travel directly into the lymphatic system. Whereupon they are transported to lymph glands where they are broken down and all the ‘alien material’ is disposed of.
The body is amazingly clever is it not? After endothelium is damaged, and a clot forms, EPCs not only cover over the area of damage, they can also turn into the very cells that can clear up the clot/plaque and get rid of it. So, not a stupidly designed healing process at all. One of absolute brilliance. In fact, this is probably happening inside your artery walls right now.
The problems start to occur when the process of endothelial damage is occurring too rapidly for the healing system to clear up the mess. Repeated endothelial damage and clot formation over the same spot, time and time again. At which point, instead of having clot/plaque healing we end up with clot/plaque growth and development. Or as Rokitansky put it so eloquently
‘Subsequently, the atheroma resulted from the degeneration of the fibrin and other blood proteins and finally these deposits were modified toward a pulpy mass containing cholesterol crystals and fatty globules.’
Next, clot formation and associated problems.
Dr. Malcolm Kendrick 
Thank you for a new great input on this CVD-issue – very timely for me.
I sense we are getting there. Each brilliant blog a cliffhanger…
Malcolm,
I have never really grasped why a problem that is caused by inflammation isn’t solved, but actually made worse, by taking NSAID’s – one of the items on your original list of causative agents.
Back in the 80’s, whilst being taught immunology and biochemistry, I remember the human body’s responses to infection, injury and such like being described as a “cascade”. The fold-out diagram in one of my immunology textbooks was about 3ft long and looked liked a huge, rather wonky cobweb. The number of different pathways they had discovered was astonishing – and that was 30 years ago.
The problem with many pharmaceuticals is the benefit comes from blocking a particular pathway at a particular point in the cobweb and for a period of time, this may have the desired effect.
However, one can only imagine what other spanners might be thrown in the cobweb (sorry to mix thingies) over time by altering one of these pathways. Especially if the cause of the problem remains (ie chronic inflammatory conditions). Hence long term use of NSAIDs invariably causing stomach problems (at the very least).
Obviously over simplistic but over the years I have often found this to be the best way of looking at things.
Thanks, PeggySue,
Right, but as I understand it, these drugs inhibit the COX2 receptors, but also the COX1 receptors that control the acid in the stomach. I am not sure the irritation this causes would be classed as inflammation, or be relevant to irritation of the arteries – but I am just a layman in these matters who got here because I was burned by statins!
Everything in the body is incredibly complicated, including the immune system, but unfortunately if we just explained the workings of the body by saying they were complicated, we wouldn’t get very far at all.
Since the effect isn’t huge (NSAIDs are still in use) I can’t help wondering if there is a statistical effect at work here – people who need NSAIDS aren’t as healthy as those that don’t……
Of course, maybe Dr Kendrick will fit this particular piece of the jigsaw puzzle into place in some neat way!
Danny:
Your case interests me. Similar to mine. For how long have you survived after being “fired”?
Hi David,
I’m afraid I was being a little casual in my associations (stomach problems being the first thing that came to mind when thinking of NSAID side effects). I think I was just trying to say that it is all so complex that nothing surprises me when it comes to drug effects, especially when you mess about with the immune system.
According to Dr. Wikipedia, monocytes are attracted and ‘motivated’ by inflammation signals. So, remove the signal –> no monocyte cleanup action.
Unfortunately, there are people like myself that have no inflammation markers (C-reactive, etc.), don’t smoke, not overweight, etc. (but do have very high Lp(a)) – though given my great health and no inflammation markers, I still have a very high (700+) arterial calcium score. So much so that my ex-cardiologist fired me after my refusal to take Statins. Instead, I started taking vit. K, C, and a few others.
So, in my case, at least, I am reading and watching the good doctors blog posts trying to understand what the cause of arterial atherosclerosis actually is…
Danny:
Is the vitamin K you are taking MK-7? It covers all the bases. Also, ideally, you should take vitamin A (animal form) and vitamin D. They act together to direct the calcium in your blood to your bones and teeth (where it belongs) and out of your arteries.
Joe
Joe – Yes, I’m now taking MK-7 as well as D. Also taking quite a lot of C, as well as magnesium. I have also (mostly) eliminated sugar and bread/pasta from my diet – eating a modified Paleo (with egg and dairy). Now a big believer in REAL grass-fed butter (I use Irish) in most of my cooking – NO oils like Canola, corn, etc.
Also started up an exercise program again (working on my getting my black-belt in TKD before my 60th – I’m 57 now with a Red belt.)
Am very anxious to take another calcium scoring test later this year (yes I know of the radiation risk, but I MUST know if all these changes are working!). Ironically, most (over 99%) all Cardiologist claim one CANNOT reduce or eliminate already established arterial calcium. I hope to prove them wrong – and if I am successful, I will put the test results on the Internet for all to see.
Lastly, yes JDPatten, I am still here – alive, kicking and actually quite frustrated with doctors and Cardiologists in general. After going through three of them (Cardiologists), I finally said to hell with it, I can do better on my own. All the three wanted to do was place me on a statin and a baby asprin. Nothing about diet, supplements, etc. – and certainly nothing about the WHY and HOW of arterial calcification.
I have since learned that the AMA basically dictates what doctors (in the U.S. at least) can say and do – or risk lawsuits and/or loss of their license; i.e., CVD? their answer must be a Statin and an Asprin. Our medical establishment has stopped trying to find cures and causes and turned into a wholly-owned subsidiary of the RX industry! Very sad…
Danny Evatt: Way to go taking charge of your own health! Truth be told, while there are plenty of first-rate doctors, there has never been a time when the medical establishment was looking for cures, at least not since the beginning of the 20th century, when John D. Rockefeller, sniffing around for a market for chemicals derived from the petroleum monopoly he controlled, established the Rockefeller Foundation, and, working behind the scenes gave mighty assistance to allopathic medicine wresting control of treating the ill from homeopaths and others. Our FDA was originally called the Bureau of Chemistry. This foundation was also responsible, in the 1930’s, for developing the first polio vaccine (in response to the 1916 New York City polio epidemic, which was likely caused by a virulent microbe escaping from their Manhattan lab), which were a disaster (as were the later ones). As for me, I’m ten years your senior. Twenty years a middle of the pack long-distance runner, I now do short-distance running, with once a week sprints, and body-weight exercise, to restore lost muscle mass. Eleven years of dietary tweaking, and I’ve found the sweet spot, so that I sleep like a rock, wake up feeling good every day, have no aches or pains, a better working memory, and perfectly good cognitive functioning. I also cancelled the newspaper and unplugged the phone. Last BP, in winter, was 131/78. The thing I’ve added most recently to my diet is wild greens, which appear free of charge in the garden. Here they consist of various dandelions, chickweed in the cold months, sorrel, and herbs such as rosemary, oregano, marjoram, and thyme (which have been little changed my human hands from their wild ancestors). And I think this has had an important impact on my health. I eat nothing produced in a factory, prepare all my own meals, and go shirtless for 15-30 minutes in the middle of the day during the vitamin D months, from March through September (I do this for the NO, too). Some years ago, I produced a nutrient-density database, from USDA nutrient content tables, for the major nutrients in about 200 of the commonest foods. I try to eat mainly in the top twenty or twenty-five from these lists (mostly foods mom told us to eat, but the government is telling us not to). I would be happy to email anyone a copy of this database, if anyone is interested.
#Gary. I think a lot of us would be interested to see your list of top 20 nutient-rich foods
Gill: I simply aim for both nutrients and flavor. What I eat are: Pastured meats, mainly beef, but when available, pork, lamb, and goat (my favorite of all), tongue to tail. Don’t like chicken, although I eat it in the Philippines because it tastes like food, but I eat pastured eggs every day ( I think eggs are one of the best foods). Seafood frequently, mainly wild Alaskan salmon, as well as mollusks and an occasional crustacean. Pastured raw dairy, including kefir and lots of cheese, butter, and cream. A small amount of a variety of nuts, usually including Brazil nuts, almonds, hazelnuts, pistachios, and pumpkin seeds. Well-cooked mushrooms of several varieties 2-3 times a week. Garden vegetables and fruits in season (pomegranates, figs, and berries are my favorites), but not too many of them; just enough to feed the gut microbiome. A bit of 85% or100% chocolate each day. We go out only rarely, and usually for sushi, white rice being the only grain I eat. Natto once or twice a month, but I’m particularly fond of it. I think I get sufficient K2 from dairy. Small amounts of fermented vegetables each day. Some red wine (don’t much like beer or spirits). All of these foods are easily available in California, and I know how to cook, so I eat like a king.
Danny, do you have an idea of what “high” lp(a) is? I get conflicting information about this. For instance, I got my lp(a) tested at two different facilities, and they had different definitions of “high” lp(a).
Hi
Last time my Lp(a) was tested it came out at 73, it stayed stable and then the lipidist stopped testing for it. When I asked why, he replied there is no agreement on the norms, nor on the procedure, and it is expensive so he gave up doing it
BobM: got my lp(a) tested at two different facilities, and they had different definitions of “high” lp(a).
There are three different testing techniques for Lp(a): electrophoresis, VAP and NMR, and they have different reference ranges. Effective treatments appear to be dietary.
BobM – According to my last test (before my diet and supplement changes) my Lp(a) was 106 (literally off the chart), though most of the other markers were not too terribly odd (“total” chol. under 300 at 293.) Don’t know which kind of Lp(a) test this was, i.e. electrophoresis, VAP and NMR(?) C-react, homocysteine, insulin, etc. all normal or “great”.
After studying this, there is disagreement in the medical community about Lp(a), with some stating it is THE new CVD marker, while others poo-poo it. Regardless, most agree that Statins do not lower it, though Niacin and a few other supplements do lower it somewhat (which I am now taking).
However, the NEW advertised Praluent drug at $1,000 per month should lower Lp(a) – at least that is what they advertise. Despite my third and last Cardiologist insisting I take this new concoction injection, I told him “no”, it’s new, we don’t know if Lp(a) is really the cause/result of anything and we don’t know the long-term ramifications of taking such a powerful drug – besides, I told him it may turn me into a toad! 🙂 He then fired me… and called me an “uncooperative” patient.
I am taking another blood test (on my own) soon and will report if it has lowered the Lp(a). I also hope the good doctor who runs this very informative blog, will give his opinion as to whether Lp(a) is the new holy grail or just another marker of many. 🙂
Danny Evatt: …there is disagreement in the medical community about Lp(a),…
Mostly because they have no meds to prescribe for it, although one is apparently nearing approval, and the dietary approaches are entirely contrary to consensus.
re: …Niacin and a few other supplements do lower it somewhat…
In addition to an overall dissident diet, Dr. William Davis (a cardiologist) advocates some strategies specifically for Lp(a), including high-dose DHA&EPA fish oil (higher than his basic 3 grams/day), DHEA and the niacin that you already know about.
Disclosure: I contribute on one of Dr. Davis’ blogs (where Lp(a) rarely arises as a topic).
This is brilliant, even I can understand it. Supposing statins turned out to be a healing partner, reducing inflammation?
Aren’t statins now believed to be effective because of their anti-inflammatory properties? But surely there better ways of achieving this than by a drug with so many nasty side effects? I’m putting my money on turmeric at present and it has the most amazing effect on my psoriasis. It doesn’t get rid of it but takes all the ‘fire’ out of it, so maybe it works internally as well.
How do you use the tumeric? I’m a fellow sufferer and am always looking for advice.
Hi, Old fogey – I take one capsule twice a day, a total of 800mg. If I forget or run out I see a difference after a couple of days. I buy them from H&B. I hope it works for you.
Jan
Hi JanB and Old fogey…………. I too use turmeric for my psoriasis and psoriatic arthritis. The thing to remember is that it is not particularly bioavailable; the powdered form is superior to fresh root. The best way to boost bioavailability is to use 9 parts turmeric with 1/2 part freshly ground black pepper and 1/2 part ginger powder. I mix into a paste with a little honey and take as is OR leave out the honey and add powder to soups, curries, sauces etc. Just be careful, as for some individuals turmeric can affect kidney function.
Hi Wizard, interested in what you say about how to ingest turmeric. I have a close friend who has been advised by his Consultant to take high doses of turmeric to help with my friend’s myeloma. At first, he found it hard to digest but has persevered with the dosage for the last 3 years or more. My friend has now been diagnosed with kidney damage. Could turmeric in tablet form have contributed to this situation, I wonder?
I believe the myeloma itself causes serious kidney damage, but I have heard of very encouraging news about turmeric and myeloma.
Jan (MGUS)
I cannot now remember where I read it but I think statins don’t suppress the inflammation but rather the signalling that results in the cause of the inflammation not being ‘treated’ by our natural defences.
In the same way shooting reporters reduces the incidence of mafia-like corruption in Russia.
Brilliant, as usual! I read the Great Cholesterol Con when it was first published and it pointed me on the right road to a much better understanding of how our bodies work and much better health. Look forward to all Malcolm’s information. Thankyou.
Brilliantly explained to an ordinary person. Very interested in the NSAID aspect.
Beautiful!!
Clear,concise and informative, thank you !
Pennies keep on raining down… thanks a lot !
I quit statins 3 years ago despite having had triple CABG 15 years ago. Your articles are really helping me to believe the inflammation factor. I use serrapeptase, Co Q10, and curcumin. Brilliantly concise and honest writing….glad I subscribed.
“Well, a critical fact to add in here is that. EPCs do not always become endothelial cells, they can go down another developmental pathway as well. They can become monocytes, which in turn become macrophages.”
Fascinating. So what triggers / decides which developmental path the EPCs choose?
All of this has been known for 160 years? Unconscionable that it has been ignored by allopathic medicine.
You should write a book about this. Or perhaps you already did?
Does this repeated clot formation containing cholesterol deposits still therefore confirm that cholesterol measurement is irrelevant in predicting liklihood of CVD?
But what do you think actually causes ‘The first stage of cardiovascular disease is damage to the endothelium.¹???
From: “Dr. Malcolm Kendrick” Reply-To: “Dr. Malcolm Kendrick” Date: Saturday, 13 February 2016 7:23 pm To: Linda Davies Subject: [New post] What causes heart disease part V
WordPress.com Dr. Malcolm Kendrick posted: “The first stage of cardiovascular disease is damage to the endothelium. The single layer of cells lining the arteries. After this, we need to look at what then happens? Before looking at this more closely, I would like to take you back in time around one “
Linda, is it not just wear and tear, impact of whatever is hurtling along? I think of the circulatory system in a body as being like a road network in say, a county. Cars, bicycles, lorries etc are like red blood cells, immune cells, cholesterol carriers, nutrients, glucose etc. There are quiet country roads with an occasional Sunday driver pootling along (eg lungs), and giant urban spaghetti junctions of swirling mayhem (eg heart). Roads inevitably develop pot holes, especially at fast, busy junctions. Pot holes need to be repaired – a normal ongoing process, and in come the repair teams, tarmac lorries etc (inflammation). But when there is too much heavy traffic (eg high blood glucose), too many potholes, too many temporary fixes and not enough complete surface renewal, too much rush hour, endless road works…ta dah! A pile up…
With youngsters and their perpetually grazed knees, I’ve also been thinking about how the outside of the body has the luxury of just having scar tissue drop off (or hideously peeled off), whereas inside the veins there has to be this complicated and careful system of clearing it away, albeit on a very much smaller scale.
Brilliant work as ever Dr Kendrick, thank you.
I have just watched this for the second time. Excellent. http://denversdietdoctor.com/engineer-vs-family-docs-discussing-low-carb-and-hyperinsulinemia/
Clear,concise and informative, thank you .
Always look forward to your writings. I’m wondering if cardiologists are taught this or aware of this kind of thinking, or is this as it appears to me, as detective work done by Dr. Malcolm Kendrick (not McKendrick!).
Are you going to get to coronary artery calcification? It seems like it belongs in this process.
As always, Dr. Kendrick, you are a delight to read. Amazing, the human body’s ability to, and insistence upon, healing itself, given the opportunity.
Beautiful, concise, informative.
Two points come to mind when reading the later part of the post:
“this is probably happening inside your artery walls right now” does it not usually start at birth? I recall reading a paper about formation of coronory/aortic plaques within days of birth. If so, then I’d have thought it could be expected to go on throughout life. (I’ve lost the paper, but think it was from around the 1940s or 50s, and it is probably quite famous.)
In
“The problems start to occur when the process of endothelial damage is occurring too rapidly for the healing system to clear up the mess.” The words “too rapidly” could mean either that the damage is accumulating at a rate beyond the normal healing/clearing capacity, or it could mean that the healing system becomes deranged and slows down or becomes less effective. I would guess that both routes can occur. (Perhaps this links back to the earlier question about NSAIDs, which might well slow the healing process.)
I was reminded of another paper I had glanced at “Endothelial Progenitor Cells Dysfunction and Senescence: Contribution to Oxidative Stress” by Toshio Imanishi, Hiroto Tsujioka, and Takashi Akasaka (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801859/), but now see it in a new light (the level of complexity is a bit high there, though perhaps no more than it needs to be).
Ken
Inflammation is good, it is healthy, it is healing. It drives me bonkers when people suggest that inflammation is the underlying cause of a disease. No, no, no. The most powerful anti-inflammatory agents known to man are corticosteroids a.k.a. steroids a.k.a. cortisol – in a slightly altered form. Inflammation knocked on the head by steroids, death from CVD multiplies many, many, fold. Look up Cushing’s and CVD risk. If anyone tells me CVD is an inflammatory disease once more I shall do…. what I normally do, which is to scream internally. Non-steroidal drugs also increase the risk of CVD. Get rid of inflammation and you are also (in most cases) getting rid of healing. Why would anyone wish to do this?
Macolm,
I fully agree with you that inflammation is a state which is naturally good.
Still your comment made me at first feel a little embarrassed wondering if I actually had claimed such a thing as inflammation to be a cause in my recent talk on LCHF so I had to check this up. When I summarised my talk I did that by using a ‘vicious circle’ starting with sugar and carbs and through several intermediate steps halfway the circle I arrived to highlight ‘Chronic Inflammation’ which actually triggered my present embarrassment. This step on the circle is then followed by several more steps with the typical features of the metabolic syndrome and my circle ends up with the step “Severe insulin Resistance, ‘Sugarsickness’ and CVD”
Looking now at my vicious circle I realise that I am claiming a simplified regressive chain of ’cause and effect’ if you start with the ‘endpoint’ of CVD. (It is difficult to give a talk without simplifications.)
So, what about ‘Chronic Inflammation’? Can it be considered as an intermediate ’cause’ for the subsequent steps or rather the effect of the previous step on the vicious circle stating a severely compromised immune system.
And yet you wrote (above):
” I have therefore felt no hesitation in siding with the old view in this matter, and in admitting an inflammation of the inner arterial coat to be the starting point of the so-called atheromatous degeneration and the cholesterol deposits came later.’”
I am very confused!
Inflammation follows damage. It is a result of damage, it is not a cause of damage. It is the damaging thing that you need to find, and stop, then the inflammation will go away. Getting rid of the inflammation may make things looks better, but is extremely unlikely to prevent damage. People talk of chronic inflammation as though it some self perpetuating mechanism that is causing damage by itself without the need to invoke any other factor. To this, I say, nonsense.
What causes inflammation? Stress or an imbalance in the Sympathetic Nervous System in relationship to the Parasypathic NS. This results in too much cortisol which leads to overproduction of lactate which might lead to stuff that forms a blood clot and once too much is present there is a heart attack. The consequence is a blocked artery but that is not the cause of MI. I think this is what the German work shows and was written about by Dr. Cowan (www.fourfoldhealing.com) and one way to convert excess lactate (maybe cortisol too) is by using ouabain or g or k-strophantin which converts the lactate to pyruvate (a fuel for the heart). At least this is how I understand his theory.
I should add. I merely quoted Virchow. These were not my words
Last September (2015), I received a diagnosis of “Tempporal Arteritis,” and began a regimen of Prednisone to “get rid of the inflammation.” “You could have a stroke, you could suddenly go blind.” Yikes! Also began a regimen of low-dose aspirin. Your posting here is the first time I’ve heard the idea that all that inflammation might be a good thing, a desired thing? I can’t tolerate aspirin, so that has stopped after terrible bruising. We are tapering off the Prednisone at 2.5 grams every 3 weeks after SED rate blood tests. When SED rate goes up instead of down, we increase the Prednisone. All of this has made me very angry as I had always insisted that I would never take steroids. Oh bother!
Well – your last comment about the chronic inflammation alleviated my embarrassment.
Huummm! Let’s take lupus erythematosus, for example, which is an inflammatory disorder but also a very high risk factor for CVD ??? Is it the lupus or the steroid based treatment ?
Both, probably. But lupus is particularly harsh on the endothelial cells.
Joanne,
Try to go really low carb.
Your blood sugar will level out together with your insulin – no spikes any more.
Your inflammation may level out as well which happened to a friend of mine who had suffered for many many years from arthritis and psoriasis. Doesn’t hurt to try.
Dr. Sjoberg,
I am in my 34th month of LCHF, having lost 45 pounds, the last 20 including IF. Then, last September, in seemingly good health, I drove out to western Colorado to visit an elderly aunt. An emergency room visit for what we thought was a reaction to the alltitude turned into going “blind and having a stroke.” The ER staff insisted that I take the first dose of Prednisone before I left the ER. I’m not diabetic and my blood test results, except now for the SED rates, are really good. I had never heard of Temporal Arteritis, and I had never taken steroids other than the occasional Medrol packs over the years. But I understood that LCHF would be anti-inflammatory and I was off all meds at the time. I’ve also been diagnosed, now 6 years ago, with macroglobulinemia, received 18 Rytuximab infusions (B cell depletion), and have been non-symptomatic now since summer of 2014. So, not as simple as it might be; it never is.
Thanks for your kind reply,
“I should add. I merely quoted Virchow. These were not my word”
Right you did – I suppose I thought you were quoting him with approval! It does make sense that inflammation is part of the healing process – just as it is elsewhere in the body.
I think when this series of blogs is complete, I will stitch them all together with cut/paste and read the whole thing right through to get a better idea of the big picture – or maybe you should end with a summary!
Joanne,
Thank you for sharing your ‘story’ with us!
I take your impressive LCHF results to my heart but I fully agree with you that you can never be categoric without leaving science behind. My experience tells me that if you visit the ER or a health practitioner with some ailment and cannot refrain from telling them that you go LCHF within a minute they will tell you why you are there. I think there is an old viking saying: ” A wise man keep his mouth shut.”
Today there are so many ‘mysterious’ diseases popping up and it is no wonder why people get suspicious of why this is happening. The dramatic increase of autism is perhaps symptomatic not to mention the present diabetic epidemic.
Myself, I turned overly suspicious against all BigPharma ‘medicine’ and have during 16 years now almost categorically ( 🙂 ) kept clear from that with a recent exception of pain killers when I tried to wean myself off from the coffee (roughly 6 – 8 cups a day) but had to give up after a serious effort of one week. My ‘drug dependence’ relating to coffee could not have been manifested itself more clearly than that.
This is potentially a most interesting valuable point. My understanding is using drugs to suppress inflammation without treating its root cause is a poor strategy as the underlying cause continues to cause damage. Statins are known for suppressing inflammation. Does that make statins a poor strategy? Taking this further, arterial wall damage and statins simply delay the inflammation driven repair processes and promote the potential for more damage – no wonder statins do not extend life as per bmj article above.
Any supporting comments?
Very good
Sorry but did the miss your reasoning on what causes a tear/break in the endothelium?
Martin, perhaps it is lack of vitamin C or other nutrients. I eat a nutrient dense diet to supply all the necessary ingredients (hopefully).
I think you want to know what “kills” endothelial cells, or at least severely weakens them such that they detach (I bet they would not do that too often if healthy).
Pressure does that from birth (sorry, there is a great old paper on that showing plaques in autopsy quite shortly after birth, but I’ve misplaced it). This damage must normally be repairable, at least until reproductive age (for the usual reason). For this kind of damage, which always occurs, the question becomes one of what slows down healing to lead to the buildup Malcolm describes (and the NSAIDs example is a fine one).
Otherwise, I suspect we can look for any cause of apoptosis of endothelial cells. I think those are quite busy cells (high ATP consumption) as producing NO requires extra energy, and they live in a tough environment, so probably have to recycle quite fast. So anything that poisons the mitochondria (e.g. statins, among many many others) will put them at increased risk. That lets in a myriad of environmental and infection-related toxins as part of the story. (Is there also necrosis? I don’t know, but I’d have thought not except in critically severe circumstances, as it is just too dangerous.)
The involvement of EPCs gives many ways in which mitochondrial toxins can slow down healing too – I’d bet those are also cells that consume a lot of ATP as they are preparing to fix endothelium. Anything that slows the process is potentially deadly. Unfortunately, the same things that damage the endothelium (except pressure and friction) also hurt the EPCs, so the healing mechanism fails at the same time as the damage needs repaired. Even worse, there will be a shortage of NO at the same time, increasing clotting.
The increasing risk with age is (as usual) a direct consequence of cells running out of good mitochondria. That lowers the threshold that a “toxin” has to reach before damage occurs faster than healing. Insulin is such a toxin, and perhaps one of the most significant endogenous “toxins” (in this context – see the work of Joseph Kraft – Diabetes Epidemic and You – for observation of the link, he concludes that DM = CVD, in most cases, due to insulin). Also, high sugar levels leads to weakening of mitochondria over time (equivalent to accelerating aging). I guess sugar might also affect EPCs if they are converting to macrophages (which I think don’t like sugar much).
The paper I referenced earlier is free to access, and although it is very complicated (as I see it), even skimming it gives some ideas of where things can go wrong.
Ken
Ken, thank you so much for the detailed explanations. They are really helping me understand what is being discussed.
Thank you. Very informative but to be honest a bit over my head. I just hope you manage to get to the end of this series of blogs before I have my family heart attack!
I’ve long wondered how blood vessels get their wherewithal for living. There’s a network of vessels culminating in capillaries that bring sustenance to every living organ of our bodies. Capillaries being what they are must be capable of supplying what they need from their own cargo. But what about larger vessels with thicker muscular walls? Aorta? Mustn’t they need an external source? Arterioles and capillaries to provide their tissue that’s not actually exposed to the cargo? This external independent network would be able to scavenge as well as supply – just like anywhere else. It could scavenge the clots we’re talking about from “behind” the lumen.
A smarter healing process, no? 🙂 Just a fantasy?
Go to Google and type in vasa vasorum.
Wasn’t vasa vasorum the key element in Uffe Ravnskov’s causality theory as harbouring the vicious organelles roaming our vessels?
Oh.
Thanks.
You can tell I haven’t been to med school.
But, do the vasa vasorum reach in to the depth of the tunica intima? It seems not.
They would have nothing to do with our clot-clearing?
Have you heard of Dr.Raths theory, that the endotelial lesions, wekness is caused by relative lack of vitamin C. Animal bodies can fabricate their own vitamin C, humans cannot. Animals do not have strokes.
my best regards
“Animals do not have strokes.”
One of my dogs did – according to the vet. It bore all the hall marks of a stroke as well.
Indeed.
My sister-in-law’s poor old dog died of a massive stroke two days ago.
Jan, did the dog eat a diet similar to dogs in the wild, or left over human food?
I’m pretty sure that poor Bubbs ate dried dog food specially formulated for older dogs. Goodness knows what it’s made up of. Maybe the canine equivalent of junk food. She was an old girl, by the way. Probably 15 or 16 years old which is ANCIENT for a big dog. But vet confirmed it was stroke.
Isn’t dry animal food high carb!
I have wondered. That would account for the obesity we see in dogs these days.
Yes dried dog food is the pits. All of it. Feed human food and tinned. 1/4 meat/ protein and fat, not too much. to 3/4 carbs. Won’t go too far wrong.
No I’m pretty sure most dry animal food, kibble is usually 100% protein. It’s completely defatted.
ellifeld: On the contrary, at least in the U. S., kibble is almost entirely grains, mainly corn, which is our national religion, though the way it is grown is exceedingly destructive. I make the food for our cats, after the two previous ones didn’t live long or well on kibble. A lot of work, but worth it-they are amazingly athletic, capable of leaping from roof to roof, a distance of about twelve feet, and their fur is soft and luxuriant. Happy and healthy they are!
http://www.petmd.com/dog/nutrition/evr_dg_carbohydrates_key_to_balanced_dog_food http://www.dogfoodadvisor.com/canine-nutrition/dog-food-carbohydrates/
Here’s my 2 cents worth about dog food although it has nothing to do with the current topic. I think webMD is completely wrong. Dogs, have the same intestinal tract as wolves, it’s straight through from one end to the other, no small intestine, large, whatever, no runiments, also it is very high acid much higher than ours. They are carnivores. They do not nibble on grass let alone grains. Grains would never enter their diet. WebMD can rationalize about grains providing energy, which is the same rationalization they use for humans. So a normal dog’s diet would be mostly meat, and some fat, if they do get any carbs it would be from the intestinal tract of the animal being eaten. Grains are a cheap filler for dog food, nothing more. As far a dry food, no living animal would eat a dry food diet and then drink massive amounts of water to makeup for the missing moisture. It’s probably why kidney disease is prevelant in pets today.
ellifeld: You are absolutely right about pet food. I have much more knowledge about feeding cats than dogs, but their diets are more similar than not. Wild felids indeed relish the intestinal contents of their prey, and I suspect canids do, too. This is their source of partially-digested plant material, and is primarily carbohydrate, since plants are. But in felids it is, on average, only about 12% of their diet, and fat only about 7%. I’ve never observed a wild felid feeding, but a domestic cat, when eating a rodent, usually, unless recently fed, eats everything, and with a bird, all but the largest outer feathers. WebMD is part of the medical industry, whose role is to promote products. I don’t believe a word any of the medical industry says. Doctors, on the other hand, I mostly trust, except those who work for pharma.
Our golden-retriever labrador cross, when 14 yr 8 mo old, had what looked very like a stroke, but turned out in fact to be peripheral vestibular disease. She hasn’t had any dried food for the last 7 years since the whole family, including dogs and cats, went LCHF. She was given a corticosteroid to reduce inflammation, ursodeoxycholic acid to counteract the risk of gallstones from the corticosteroid, and a formulation of 3 drugs called Candilat (here in France) to help improve her balance perception. She now gets the Candilat for 10 days each month, and is very much better for it. She gets up and down the stairs several times each day, and has very few unfortunate toilet accidents.
She worked for ten and a half years as a guide dog, and as you’d expect is very intelligent—and is showing no signs of losing her marbles. She was only fed entirely on dried dog food for the first two years of her life, as we’ve always regarded that as too highly processed, even before we realised it was high in carbs.
Indeed, we’ve looked at the formulations of dozens of different brands of dried dog foods, and the one factor they all have in common is something like 60% carb by weight. This is totally unlike the natural diet of a wild dog, and very far even from the evolved diet (table scraps) of the domestic dog.
Almost all of our nine dogs, over almost 40 years, have lived to around 15 years of age—though three are still clogging on!
The only creatures on the planet who get obese are humans and the unfortunate animals we feed.
Dog food is packed with cheap carbs, even the supposedly good stuff. Cat food will be the same. I’ve advised my friend who has a spaniel to make a friend of her local butcher and to get him to keep the cheap and fatty cuts that people don’t want. Dogs are descended from wolves and I don’t think they eat too may carbs.
Hear hear. I’m in total agreement with you.
I think polar bears can get a bit on the porky side. Prior to not eating for several months.
That’s carrying intermittent fasting a tad too far.
Dr Raaste, I agree that is a possibility. I read that the requirement for vit C increases with a high carb diet. I read a book about explorers in the Antarctic. The well prepared took lots of high carb, processed food with them. They got scurvy. The less prepared ran out of food and had to kill birds and animals to survive. They didn’t get scurvy.
When I came across this idea, that unlike most animals, humans lost the ability to make vitamin C because at some distant stage our diet was fruit-based and thus we didn’t need to make it ourselves, and that this ancient defect explains CVD, I worked out how much fruit we would have to have been eating to equal the vitamin C per kg made by animals. I think it was something ludicrous like 250 mangoes a day!
The truth is that we are not flawed, we didn’t scrape through the millennia until our ingenuity enabled us to manufacture enough vitamin C again, this time as tablets. After some digging around, I came across research describing the processes whereby humans recycle vitamin C. So the truth is that we improved, recycling is evolutionary advantage, as it is far more efficient than wastefully churning out loads of vitamin C made from scratch.
That’s not to say I don’t think extra vitamin C isn’t beneficial at times, and perhaps it helps compensate for the consequences of other deficiencies (eg the antioxidant / anti-viral effects of vitamin D).
Emma,
All what you say here is exactly what I also read in Linus Pauling’s book about vitamin C from 1976.
I haven’t come across the theory that humans can recycle vitamin C. It would firmly put paid to the old cry from doctors `’vitamin C is just expensive pee”.
Good point Emma C. We lost the ability to make our own vitamin C 10 million years ago and CVD is a recent problem. If vitamin C is somehow involved (the lack thereof), it’s secondary to something else.
Emma,
One reason given for not taking large doses of Vit C is that it is excreted so rapidly that it simply wasted – I think the current RDI is around 50 mg. A Dr Klenner in the 70s did a lot of clinical work with Vitamin C
A New Zealand farmer contracted H1N1 influenza in 2009. Well-documented on New Zealand’s version of 60 Minutes, this individual had progressed to the point of being on life support, and the doctors had nothing further to offer.
https://www.youtube.com/watch?v=VrhkoFcOMII or
This is horrible. It just occurred to me that, if certain people begin to think that inflammation is a good thing, then some other people would like to ban coffee and tea and alcohol because they reduce inflammation!
Even worse, the health authorities may want to forbid veganism because plants reduce inflammation! Even worse, they may force everyone to eat only soy because it promotes inflammation!
What a nightmare! I can imagine the PETAns demanding that people stop feeding sardines to cats because that food would not give them enough inflammation to stay alive!
Even Religious fasting practices could be forbidden.
General scenario: A is good because it causes B. If B happens to be a bad thing six months later, when all the science is complete (for a while), then A becomes a crime. Government must do something, people are dying! Don’t you see?
Perhaps Global Warming is a good thing because it is a healing process. Quick, we need more global warming! Aarrrgghh, it’s too cold, we are dying! Please, burn more coal!
We need more smog to save the planet, quickly open more Universities and promote more Generals!
I could go on, but I leave it there. We need more skepticism or we will always run about like a headless hen. Also, we need more humour. Remember Pyrrho the Skeptic. Also remember to be skeptic about skepticism!
I would agree that we need more humour. The problem is, as always, when people see something associated with illness and then, without the slightest pause, believe that it must be a cause of the illness – and must therefore be lowered. Inflammation is associated with many illnesses.
After heart attacks, the area of damage (infarcted area) becomes inflamed. In the past there was an attempt to reduce the inflammation by giving high dose steroids. End result, the damaged area did not heal, turned into a massive aneurysm, and burst. Doctors do not give high dose steroids following heart attacks anymore. The inflammation was not the cause of damage, it was the result of damage, and was the body’s attempt to heal itself.
Currently, we see exactly the same scenario played out after sports injuries. Rest Ice Compression Elevation (RICE). All of these things are designed to reduce the dreaded inflammation a.k.a. healing. I am willing to bet a large sum of money that RICE, if anyone dares to study it, will hamper healing and increase the time taken to heal. In particular the ‘I’ part.
Following any muscle strain, I always following my (very strong) instinct and apply HEAT. Ice hurts, but an appropriately applied hot water bottle soothes, perhaps hastening the healing process.
Dr. Kendrick: What about heat, in treating sports injuries? Sure seems to have helped me greatly.
If I may be so bold as to ask, what was your comparison group?
Hear, hear! Skepticism is my personal religion, and humor the only saving grace in a world full of lunatics.
Blood, when it’s not in the proper place in the body, can be very irritating. Corrosive, even.
I always thought that ice, applied right away, would help stem leakage of blood into the surrounding tissues of a strain, sprain, or bad bruise. No?
Maybe you are right, but I would suspect most of the blood that leaks does it in the first minute or so. After that, you are just clearing things up.
That’s an interesting theory about RICE. It makes sense.
It’s a pity, though, that nothing I used to believe is supported by science. I used to stretch before and after working out, then they said that stretching before was bad (muscles aren’t warm). Now, I’ve read that stretching doesn’t do much other than increasing flexibility, which may be bad. So, now I don’t stretch at all.
I used to believe a low fat diet was good, I HAD to have a flu vaccine every year, additional fiber in food was good, cholesterol in food and your blood was bad, salt in your food was bad (NEVER add salt to your food!)…The list goes on and on. And, now I don’t believe any of it. I can’t think of one thing I used to believe that I now believe. It’s disconcerting.
Dr. Kendrick
After heart attacks, the area of damage (infarcted area) becomes inflamed. In the past there was an attempt to reduce the inflammation by giving high dose steroids. End result, the damaged area did not heal, turned into a massive aneurysm, and burst.
Oops. I take it that is another example of Six weeks strict bed rest, a bright idea rapidly buried without trace along with Poldeman
If that causes it – what ends it???
Thank you Dr Kendrick. So interesting!
Can iron be involved in the formation of these plaques via endothelial cell damage? I just found this from Imperial College.
http://www3.imperial.ac.uk/newsandeventspggrp/imperialcollege/newssummary/news_10-2-2016-18-44-34
Interesting. I would simply say that any agent/factor that can damage endothelial cells has the potential to increase the risk of CVD. A number of people have hypothesized that the fact that women menstruate – thus lose blood, thus iron – may the reason why they have a reduced risk of CVD. Particularly before the menopause.
I feel I’m starting to harp on about mitochondria, but they are on the usual route to cell death and must be at the heart of the matter. That’s true for both mitochondrially-triggered apoptosis and mitochondrially-mediated apoptosis. In the latter case weakened mitochondria will need less of a prompt (signal) from the cell to trigger death.
Although I’ve not studied the mechanism in detail, iron in excess is a mitochondrial toxin (when iron and reactive oxygen species -ROS- are both high, the situation is especially bad). There is extra mitochondrial ROS in inflammation (it leads to increased IL6 etc. etc.), so we have that. Then if for any reason iron is high in those cells, we have trouble.
I didn’t have a paper discussing this in endothelium or EPCs, but there is an open access review relating to neurodegenerative distorders at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3948003/ from the abstract “The co-existence of both iron and ROS in the secluded space of the mitochondrion makes this organelle particularly prone to hydroxyl radical-mediated damage.” (The same root causes of CVD are often implicated in neurodegenerative-disease.)
A search led to another open access paper http://www.ncbi.nlm.nih.gov/pubmed/22245770
I’ve not read it, but it is about how degradation products from RBCs (such as heme, an iron-containing protein) damage endothelium. From the abstract “The mechanisms of heme toxicity are not clear but may involve lipid peroxidation, which we hypothesized would result in mitochondrial damage in endothelial cells.” – they go on to collect evidence for the mechanism.
Ken
The problem, in looking at all diseases, is that you will find abnormalities wherever you look. Which are are the key ones? I believe the answer is to try to avoid getting completely dragged down one reductionist path – or another. You must keep climbing back to look around at the bigger picture and see how everything fits together. You cannot understand a painting by examining in minute detail how the yellow paint was manufactured. Sorry if that is a rubbish analogy.
Basically my view regarding ‘Statins’ has not changed for more than a decade.
(1) With ‘Primary care…they are over prescribed /indiscriminately. Which is not the fault of the prescriber, but the politics/bureaucracy/big pharma.
(2) With ‘Secondary care’, this is a ‘fish of a different colour’. There are many justified/proven reasons why statins are of benefit.
(3) There is a ridiculous amount of ‘Propaganda’ from both sides regarding statins which is unjustified nonsense.
(4) Please try to make informed decisions. It can be deleterious to your health. I know this is difficult with so many conflicting views. Perhaps a way to start is to try to listen/read people that actually know their facts. At a guess, I would estimate that less than 10% of anything regarding statins would be without prejudice and useful.
Now! On a serious note:
I actually discovered a cure, for which there is no disease, yet.
“You must keep climbing back to look around at the bigger picture and see how everything fits together.”
This is exactly my own understanding of “science”.
I’ve got a hammer, so I’m looking for nails. The nails might help hold things together, but they are not the main part of the structure, that’s true.
The point I was trying to make is not so much that mitochondria are necessarily a big part of the story, as that they sit at a junction doing what they do: collecting “signals” and producing “outputs”. Some possible outputs are ATP (when all is well), plus ROS (when there is stress, leading to the cytokines of inflammation, for example), the retrograde response when mitochondria start to get in real trouble, or eventually the chemicals of apoptosis (when the stress reaches a critical level).
Of itself knowing this does not answer many questions, but remembering that these processes are going on in the cells can help to disentangle the logic of disease, I’m convinced of that.
For example, we could just state the link (positive feedback, I seem to recall), between insulin and IL6, but understanding the role of mitochondria in that loop could be helpful. Mitochondrial stress and their response to stress are almost bound to link several diseases, whether that helps understanding or not is an open question.
Reductionism is needed to some extent, as living systems are far too complex to analyse in full detail. Of course one step too far ruins the result. I think, however, that as we look for the fundamentals, energy generation, ros, etc. will always be part of the story, whether the question is CVD, neuro-degenerative disease or cancer. Once the kernel is understood, all the pathways and process can be built up around it until the answer satisfies.
Ken
Plenty of unliganded iron in blood clots. Probably a much larger contributor of unliganded iron to the endothelial cells than circulating iron via iron supplementation (unliganded, of course). It’s something the Imperial College study may not have been able to distinguish, it being in vitro/ex vivo. Still, interesting study.
Ken
Many thanks for the links. I too am interested in mitochondrial damage caused by ROS. One suspects that such damage can cause a variety of conditions as yet unconsidered.
Is haemochromatosis associated with higher rates of arterial disease?
I would be grateful if you could provide information on the benefits of statins and the associated research references. The ones that I have. like the HPS study, provide but trivial efficacy rates that most patients would probably miss out on. To know that, for example, 1 in 300 will benefit is of no use to me unless I am that one which in all probability I would not be!
Too often people hold a simplistic binary understanding of food, substance A is a nutrient therefore the more the better, while substance B is toxic so avoid it altogether. In “Evolution & Healing” Nesse & Williams describe the evolved human response to infection they call “iron withholding”. While it is true that iron is an important nutrient for long time-scale processes in the human body, bacteria have a continuous urgent need of it. So on detecting infection, our bodies release leukocyte endogenous mediator which has 2 effects: 1) to raise the body temperature (fever) 2) lower the level of iron the blood (anaemia). Both are evolved short-term mechanisms of the human body acting as defences against bacteria.
Bacteria are very temperature sensitive and the 2 or 3 degrees increase involved in fever inhibits their progress whilst anaemia (iron withholding) has a similar effect. Nesse & Williams relate the story of a group of Masai who were considered to be anaemic and with the best of intentions were give iron supplements. The incidence of amoebic liver infection leapt to 88% compared with a background rate of 10% in those not given iron suppplements!
I’m happy you have brought in discussion
of the lymphatic system. The lymphatic
system is equally as extensive as the
cardiovascular system, yet it is not as well
studied nor understood. Many don’t even
know it exists.
The lymphatic system must be kept healthy
to address CVD. LCHF helps in this regard.
If cooling inflammation is a bad thing in the big picture, why is turmeric, or vitamin C or vitamin E useful with heart disease? They all have anti-inflammatory properties.
They have properties at reducing the underlying damage that drives the healing/inflammatory process.
That must be the key!
Hi Dr Kendrick
Referring to some of the comments and responses, may I quote you:
“As you age, the production of EPCs falls. If you are stressed, the production of EPCs falls. If you take steroids the production of EPCs falls. If you have kidney disease, the production of EPCs falls. Guess what. All of these things are associated with a vastly greater risk of cardiovascular disease. Vastly greater.”
So the question must be what builds/increases EPC cells (especially as none of us can escape aging)? Or is that something that comes later?
Later. However, exercise and sunshine are good
robert lipp: According to one of the papers linked to above, or in part IV, ACE inhibitors (the only drug I take) increase the numbers of EPC’s.
Gary Ogden
ACE inhibitors = blood pressure meds?
By going LCHF I have stopped blood pressure meds and am now: 120-130 / 65-75 so that route is not open to me. A win for LCHF
robert lipp: Yes, Ace inhibitors are for BP; been taking them 21 years, but wish to wean off of them, although it’s intriguing that they appear to increase EPC’s. It is possible that weaning off of them may improve my BP. I don’t know. Last BP, in December, was 131/78, which I think pretty good for a 67-year-old. One of the papers linked to above concludes that treating mild hypertension with drugs has little value. As for food, I don’t put a label on it, but I do eat few carbohydrates (no grains or legumes, and of dairy, only the fermented kind), and all the fat (pastured animal fat, and some olive oil and coconut oil) that I can stuff in the pie hole. Gobs of garden vegetables, including the wild ones-weeds to most folks- and fruits, plenty of seafood, small portions of red meat most days, organ meats weekly, and nuts. What I aim for is to a eat a great variety of tasty, nutrient-dense foods, with sufficient protein, and no limit whatsoever on fat. And avoiding dense, acellular carbohydrates, vegetable seed oils, and anything made in a factory. I drink mineral water rather than tap, and consider red wine my main medicine. Feel good every day, and haven’t been sick since 2005, when I made fundamental dietary changes. I must add that, as revolting as it is, I force down a bit of natto once a month or so, otherwise ensuring good K2 status from gouda, other cheeses, and occasional goose liver (not easy to get here in CA). The only supplement I take is that spray-on magnesium chloride. Healing takes time.
Hi Dr Kendrick
To confirm my understanding
See quote below from the following:
https://vascularcell.biomedcentral.com/articles/10.1186/2040-2384-2-6
“Therapeutic modification of EPCs
Statins
Statin therapy is associated with an increase in the number of circulating EPCs in patients with CAD [20] (Table 3). The increase in EPCs and improvement of their migratory capacity was significant as early as at 1 week after the initiation of treatment with atorvastatin, with a 3-fold increase at 3 to 4 weeks of therapy [20]. The mobilization of circulating EPCs, along with their enhanced functional activity may contribute to the beneficial effects of statins in patients with CAD [20]. The migration and incorporation of EPCs to the sites of re-endothelialization was found significantly increased after statin administration [20, 71].”
Question: does the above statins effect (increasing circulating EPC’s) tie in with the secondary treatment benefits of statin therapy after a cardiac event but no (little) benefit in primary prevention? Therefore, you did not suggest statins as a means to raise EPC’s?
Robert lip. Did you just stop the bp meds or did you just stop. I want to stop but last time I did blood pressure went up and felt ill. Do low carb but it has reduced my bo
Gary Ogden:
Many years ago i had high blood pressure
Doc prescribed blood pressure meds
2 years ago converted to LCHF
Later doc found my blood pressure 90/60
Doc stopped blood pressure meds
Blood pressure settled as indicated previously.
Doc is happy I am happy
robert lipp: Way to go! All good. I’m impressed. I’ll get there, too. It will just take me a bit longer.
Meant to say going low carb has not reduced my blood pressure although I have lost over a stone. How do you stop taking the meds without side effects
Gordon and Robert I wish low carb would reduce my bp. Only the meds seem to do that. Tried all sorts of supplements
Maybe your blood pressure is where it needs to be. It’s only comparatively recently that we have all be encouraged to be so phobic about B.P. …..since the advent of the ‘wonderful’ drugs to reduce it maybe?
JanB: Very good point. I can’t forget reading about Duane Graveline (retired astronaut/flight surgeon whose blog spacedoc is about the dangers of statins) going with his grandma to visit the sawbones in the 1930’s, when the sphygmomanometer was a relatively new contraption. Her BP was off the chart (I believe they go up to 300), yet she lived into her 90’s, finally succumbing to cancer. So, once again, good point. I think it perfectly reasonable to assume that our blood pressure is what it needs to be, and because we’re all different, we’re not all going to have the BP the little chart says we should have. So I no longer give it a moment’s thought, nor do I bother to check it at home. Treat the underlying causes, not the symptoms.
JanB. Easy to say but when you blood pressure is 160/170 over 90 when not on the meds its a bit scary. I would like to stop them but this is what it can shoot up to.
Ben, I am the same as you. Tried loads of different supplements and low carb. without the meds cannot get my bp to budge. no idea what the meds are doing to the rest of my body.
I am not clear about the issue of inflammation and the use of anti-inflammatory drugs, be they NSAIDS or other. Dr. K, you seem to be saying that inflammation is OK because it signals the body to take action to stop the cause of the inflammation. But is inflammation not causing harm just by its own actions? When we have an allergic response to food or other chemicals, is it not wise to treat the resulting inflammation with chemicals just to reduce the inflammation? When we have a fever due to infection, is it now wise to try to reduce the fever if it is very high? I thought that inflammation can cause us harm if allowed to go to excess whatever excess means. And if anti-inflammatory drugs are taken to reduce the amount of inflammation, does that automatically mean that the body’s own mechanisms to prevent the cause or causes are proportionally reduced? Is there no situation where such drugs are indicated?
Inflammation can go on to cause worse damage than the underlying problem – that is true. As with Rheumatoid Arthritis and Crohn’s disease etc. By point, which I cannot seem to explain, is that there is always something driving the inflammation. Inflammation is not a boot-straps operation whereby inflammation starts, causes damage, then more inflammation occurs. There is always an underlying driver of inflammation. Get rid of this and the inflammation goes away. Equally, many people view inflammation as always a bad thing. Inflammation is, usually, the body trying to heal itself.
I have been ready about disseminated intrvascular coagulation which is always associated with another condition – clotting gone mad. It would be interesting to see how this fits with regular clotting models.
It seems that we have a group of people with very diverse backgrounds reading and participating in this topic. Many commentators clearly have a medical or science background and then there are the rest of us who don’t but are keen on understanding what is happening with this cardiac disease and process. The more medically inclined seem cheerful in the ongoing investigation of the CVD process while others of us remain more curious about the “how do I prevent or at least delay an MI”, or at least that’s how it appears to me based on questions posed.
I read the earlier posts in this series to reground myself and again read where Doc Kendrick wrote that you can have what is commonly called a heart attack which has nothing to do with atherosclerotic plaque, but what this series will focus on is what kills you with CVD, or atherosclerotic plaque. The question growing in my mind now is what percent of MIs come from plaque versus MIs from other causes?
Other readings have stated that heart attacks from causes other than arterial blockage in nature are not insignificant so as I think about my health and what is important to delay the inevitable how concerned should I be about plaque as opposed to SNS vs PNS imbalance, etc. or are we going to discover that these all all linked? Gigantically complex for sure.
Sorry if I’m the only one with this question but it’s been nagging me.
You are not the only one 🙂
“It seems that we have a group of people with very diverse backgrounds ”
I study plants and the associated endophytic microbes, and their role in the plant life and disease. And here I am reading the heart disease blogs, and seeing some parallels to plants. Go figure…
Perhaps this helps to explain how a globally common condition such as anaemia must protective. In addition, would the practice of blood letting and donating blood contribute to better vascular health?
some people have a condition of excessively high iron in the blood, and blood donation is recommended for them.
I am surprised that no one has asked.
“why don’t we test the ‘health/disease state of the ‘Endothelium’?
Well! There is a way, a tad extreme……’Autopsy’
You can measure arterial elasticity using pulse tonometery. This can also be done with machines that measure central arterial blood pressure.
‘au contraire! Dr Kendrick
You are generalising about diagnostics that may suggest disease/health states.
I am saying, the state of the ‘endothelium’ cannot be measured unless it is put under a microscope. Which is only possible by autopsy.
“Endothelial function has boosted clinical research in this field, its use as a clinical tool in daily practice is not established, nor has any method been recommended in clinical guidelines for planning primary or secondary prevention of vascular disease.
The aims of this review are to give a short overview of the most commonly used methods to measure endothelial function in humans, particularly non-invasive techniques , and to summarise the clinical implications of endothelial dysfunction in the population and in individual patients. The possible future role of endothelial function measurement for individualised medicine is also considered.”
“To estimate microvascular function have been introduced, eg, the measurement of the number of cineangiographic frames that it takes to fill a distal vessel with proximal injection of contrast. The corrected Thrombolysis in Myocardial Infarction frame count provides a semiquantitative assessment of epicardial coronary blood flow.Taking the main disadvantage—the invasive nature of the above-mentioned tests—into account, noninvasive functional tests to assess the coronary microvasculature have been developed, among them positron emission tomography, myocardial perfusion imaging, blood oxygen level–dependent magnetic resonance imaging, and echocardiography,
Assessment of endothelial function may provide important information for individual patient risk, progress, and guidance of therapy.
Respectfully yours
michael
You are generalising about diagnostics that may suggest disease/health states…. True. But that is usually all that diagnostics can ever do surely?
Question: can the artery elasticity be checked (or at least a reasonable proxy) via blood pressure?
Yes. There are BP machines that measure central arterial blood pressure and arterial elasticity. No GP has one. They cost about £2K
Malcolm
There is a large Danish study from 2013 that indicates the same process of damage to the arteries accelerates atherosclerosis process.
The study was done on workers who had heavy lifting.
The study showed that the workers who had heavy lifting, which increases blood pressure , more than two days a week had a 2.6 times increase in atherosclerosis compared with workers who had no heavy lifting or had heavy lifting two times a week or less .
The concludetion of the study was that damage to the arteries by increasing blood pressure through lifting increased Atherosclerosis via micro damage to the arteries around the heart .
The conclusiontion was further that if the damage had time to heal before the lifts were repeated there was not increased atherosclerosis.
So damage to the arteries is natural and will heal . The problem is too many injuries or too often.
This study , I think supports what you write .
So the solution is to find what it is that causes your personal micro injuries too often and eliminate this cause.
There was more in this study, example, the workers moving more leisure withstand more heavy work.
This indicates that the movement accelerated the healing process.
So walking is good for you.
I love this topic , and I think you hit the spot.
I have my reasons to dwell in the tropics every winter , I think that the sun increases the healing process and that lack of sunlight prevents the healing process.
Alcon
I’m wondering if this study is as you indicate, will those who are using weights to exercise, are they actually increasing their risks?
A very good question. And yet resistance exercise is supposed to be very good, and certainly using our bodies in general is very good. Lifting weights is not quite the same as resistance. I’m thinking yoga is more like resistance – the weight of the body in various positions is what provides the resistance. It’s a way of using muscles. Perhaps the problem with jobs that involve lifting weights is that, like most anything, done repetitively it is too much.
Well, a regular amount of cardiovascular exercise must be good for keeping the heart and lungs toned and used to a good old pumping action. If the system is suddenly challenged it is surely far more able to cope with a sudden demand than an unexercised muscle would be.
As you get older you modify the regular exercise so it doesn’t become damaging in itself. I know it sounds like noddy logic but why not?
Without looking at the paper, I would first of all wonder what these people were eating every day. I would suspect a greater correlation between CVD and high carb diet than with heavy lifting. This might be another of those papers which want to get published, so denigrating carbs would not help.
is there any good news? Sent using Hushmail On Saturday, February 13, 2016 at 8:24 PM, “Dr. Malcolm Kendrick” wrote: a:hover { color:red; } a { text-decoration:none; color:#08c; } a.primaryactionlink:link,a.primaryactionlink:visited { background-color:#2585B2; color:#fff; } a.primaryactionlink:hover,a.primaryactionlink:active { background-color:#11729E!important; color:#fff!important; } WordPress.com Dr. Malcolm Kendrick posted: “The first stage of cardiovascular disease is damage to the endothelium. The single layer of cells lining the arteries. After this, we need to look at what then happens? Before looking at this more closely, I would like to take you back in time around one “
Can you please give us your conclusions on why western men get prostate cancer ?
Sorry. I don’t have any. It is not something I have looked at in any detail
A question for the group. Do some people in their 80’s and 90’s die with no atherosclerotic plaque at all? If so, has anyone ever studied what went right in those situations?
Chan, that is a very interesting question. I saw a documentary about a group of people who were 100 years old, or nearly 100 years old. One of the things they had in common was none was a vegetarian. In another documentary, scientists were dissecting a whale that died on a beach. I think it was called Inside Nature’s Giants. One scientist commented on how clean the major blood vessels were.
Chan
There was some PM work done in the 1930s in different age groups but whether there were any in their 80s and 90s . DR Ravnskov in his book Cholesterol Myths provides a lot of refs on this subject
Thanks Mike. I will check it out.
Thank you for your work!
Talking scientific attitudes I cannot refrain from now returning to Linus Pauling since I ‘Googled’ him and arrived at Wikipedia and realised that I actually didn’t know very much about his carrier and was actually chocked by reading about his outstanding integrity as a scientist.
I understand, talking integrity, why I am hooked up here at Dr. Kendrick’s blog.
Cheers to you Malcolm when I am now sipping my glass of red wine for my heart health 🙂
Goran,
There is as you probably know a Linus Pauling Institute
http://lpi.oregonstate.edu/
While Wikipedia is a source of much useful information, some controversial information has been known to have been hacked by opponents, the so-called “quackbusters”, shills of BBig Pharma.
Incidentally, many decades ago I had the pleasure of meeting him in Uganda while he was on a US fact finding mission.
Dr Kendrick, After just reading your book, The Great Cholesterol Con, I was ready to shout from the highest hill tops AT LAST, I AM NOT ALONE!! I don’t know why it’s taken me so long to ‘find’ you and your blog and book, but here I am! I feel as though a great weight has been lifted.
My question is: if you already have CVD (which I do) and I have had 2 stents AND I have high cholesterol LDL 7.7 when unmedicated ( I know, it’s not the problem) what can I do now? I exercise 5 days a week with a powerful 6 kilometer power walk, I am slim eat lots of good food – enjoy some vino; I’m happy, I live in the sunshine. Life is good. Yet, my mother, father, both grandfathers and 6 out of 10 aunties and uncles keeled over stone dead (literally dropping like stones) all under 65 with heart attacks. My brother had a heart by pass at 60 and his cholesterol unmedicated is 14 (I don’t know the break down) . I am 61 and I’m beginning to think I can hear angels 🙂 (or the groans of the underworld). I note, that all those relatives were in the Second World War in rather horrendous circumstances. My brother and I are living away from our tribe, he in Africa and me. . . . . many countries but now Australia. Could it be that stress? How to deal with known CVD?
My cardiologist is probably going to have his own event when I tell him I’m coming off the Rosuvastatin and Ezetimibe, but I have felt for YEARS this is not the way to go. If I eat a lettuce leaf and drink water, my cholesterol stays the same (as you would expect). Yet, what does a poor old duck do, when the arteries still have narrowing?
Regards
Susan Cross
>
Kerry & Sue,
Welcome! You’ll find lots of useful and interesting information in Dr Kendrick’s blog and reading older entries may help answer some of your questions.
As you live in Australia, where dietary advice is misleading to say the least, perhaps a good starting point may be to re-evaluate what you consider to be “good food”. Please take a look at this blog and the linked Credit Suisse report https://drmalcolmkendrick.org/2015/09/21/a-swiss-investment-bank-gets-it-completely-one-hundred-per-cent-right/. Obviously I have no idea what you eat, but if you are following official advice there is a good chance that what you are eating is not helping you at all.
Kerry & Sue
You may find it useful interesting to research LCHF. My wife and I have achieved considerable health improvements through this and lost more than some weight too.
Dear Dr Kendrick,
I find this series absolutely magnificent.
As I understand the process, clots result in in damage to the endothelium, and Nature has designed a very elegant repair system that involves laying a new endothelium over the damaged area and then absorbing the clot from the outside. Am I right in thinking, that just like a bicycle inner tube is not as flexible where you have repaired a puncture, so too the artery is less flexible at this point, and that this leads to a narrowing of the artery?
Is there sometimes a breakdown in the procedure for repair, which leads to clots floating around and eventually blocking access to the brain?
Since the clots contain a mixture of cholesterol dead blood cells and other junk, cholesterol good or bad, saturated fats or other fats have no direct causal mechanism in this?
Finally, statins are said to benefit those who have had heart attacks, what is the mechanism for this?
Thanks
Chris, thanks. You are right that cholesterol and saturated fats have no part to play (other than probably beneficial). I am getting to statins at a later stage.
There is sometimes a breakdown in the repair system which does lead to clots blocking arteries in the brain.
Dr Kendrick.
Once again a superb contribution presented as a multi-staged thriller that has me (and I suspect many others) enthralled and waiting for the next installment. I cannot thank you enough.
It seems to me that if the basic, normal metabolism is disordered or disrupted by age, stress, chemicals, infection or life-style choices, this can result in inflammation which in turn results in a cascade of responses that end up with a heart attack and possibly other “chronic” diseases, mitochondrial damage etc. This could be the cause of the plethora of associated “markers” for CVD. In the studies that reveal associations, the actual correlation and covariance matrices are never or rarely published. Why?
In drug trials such as those of statins, the blood levels of CoQ10 are never published despite the fact that this vital anti-oxidant is, or should be, known to be depleted by all statins. Yet this disruption of the basic, intracellular protection of the mitochondrial DNA from ROS is totally ignored. Or may be not; in the HPS it was deliberately excluded from the anti-oxidant vitamin “cocktail” which was the second treatment of this 2×2 factorial study (simvastatin + CoQ10 is a Merck US patent – 1990). The selection of only “statin tolerant” patients also seems to have ignored this fact. Why?
Personally, I suspect that life-style choices are possibly a major cause of disrupted metabolism but these human choices may well be influenced by flawed nutritional advice. I give Ancel Keys advice on carbohydrate, saturated fat and cholesterol (I understand in his latter years he changed his views on cholesterol) in the 60s-70s which was followed by epidemics of obesity, metabolic syndrome, diabetes, and Alzheimer’s. Yet Yudkin at the same time had provided EVIDENCE of the damage caused by sucrose (a very basic carbohydrate) – something which was totally ignored but is now being taken up as, surprise, surprise as a “new” finding.
Which poses the question: How much does money and status truly influence the lives of everyone. I revert, once again to Dr. Barbara Starbridge’s (JAMA, July 26, 2000—Vol 284, No. 4) 100,000 deaths p.a. from properly prescribed and properly used prescription drugs. I personally suspect that this is probably an underestimate; how many doctors would attribute a death to a drug which is widely promoted as “life-saving” while there is a myriad of “suitable” causes to attribute death? Frankly, this is entirely understandable; doing otherwise does not benefit grieving relatives.
The same (CoQ10 levels) should surely apply to D3 levels – the reduction in cholesterol inevitably diminishing the possibilities for D3 fabrication in the skin. My own D3 level was at 9ng/ml after about 3.5 years of ‘low dose’ rosuvastatin.
Kevin
On very low dose Crestor with Ezetimbe, I was down to 18 ng on D3. Have now climbed back to 38. My GP said a lot of his patients have levels of 10, and that that 38 is probably too high.
Hmm, maybe that’s why there’s a connection between low cholesterol and cancer.
Kevin and Mr Chris,
There are reports in the literature to the effect that statins do NOT affect Vit D levels, that they are the “new”Vit D with a similar structure and do the same thing metabolically. Believe it or not as you please. I prefer your evidence!
As to “normal” blood levels of Vit D, these have been established on a population that, as the UK CMO has stated has a high level of insufficiency/deficiency; hardly a population on which to base optimal level guidelines. I suggest that an optimal level is more likely to be in the range of 100-120 mmol/L based on my research of published research. But to get this level naturally, use of sunscreens have to be used with care – something that horrifies the manufacturers. The conversion factor between ng/ml and mmol/L is ≈ 2.5
http://www.endmemo.com/medical/unitconvert/Vitamin__D.php
9ng/ml = 20.24 mmol/L Conversion factor ≈ 2.5
38ng/ml = 94.85 mmol/L
Mike;
thank you for that. In fact, you made me check the reading which was 36.8 ng/ML of 25-OH-Vitamin D. The hospital gives a range of 30-100 ng/ml.
I like DR Kendricks blog for two reasons:
I learn a lot from him
I learn a lot from other posters
great stuff
Mr Chris
Re your reasons for liking Dr Kendrick’s blog coincide exactly with mine. He is a mine of information, his books are superb and the comments are generally stimulating. At 82 the old mind needs the exercise and he provides it in spades.
Yes, amazing what can be replaced by statins…
For the past 4.5 years (since ditching Astra Zeneca’s universal panacea) I have aimed for a D3 level of about 60ng/ml (150mmol) and have been there or thereabouts – achieved by a combination of sun (44.5N @ 600 metres), D3 supplements (5k/10k day seasonally outside summer) and (in addition) for the past two winters 5mins/day in front of a “vitamin D lamp” (4-bar UVB of relevant wavelength – from memory ca. 290-320).
That 60/150 is arguably a bit on the high side but reading the literature convinced me that it is necessary for at least one of my health issues. Pleased to say that my current GP is generally supportive.
Dear Kevin,
The thing that worries me about massive Vitamin D3 dosing is the risk of turning arteries into cement pipes from calcification! Not easy to get consistent data on this.
After watching the new Icelandic thriller on BBC 4 was intrigued to look at the health of the Island and was entirely ignorant of the fact that they are people with a long life span. Considering the volatile weather, brief low tem summers, how do they manage it.
Fish, minerals from volcanic springs, Viking genes, very small population. What is vit D and C amount in their bloods. Just a thought.
Chris,
There’s a huge amount of material on all this, my reading of which is that 10,000 IU D3 is not really very much (depends on skin type but may be as little as 10-15 mins sun). Further, any problem of calcification (if it really exists in the normal setting – absent calcium supplementation or, horror of horrors, substantial intake of calcium enriched soya products) should be (at least) counteracted by an adequate intake of K2 (doesn’t have to be Natto – just about the only revolting thing I ever encountered in Japan – since there are excellent natural alternatives in Brie de Meaux, and many other cheeses, also choucroute is tasty and useful as a condiment. The point of which is that K2 activates MGP (Matrix GLA protein), which is what steers calcium away from soft tissue and towards bone (it is probable that it actually removes existing calcium from soft tissue).
Google Hollis & Hollick for D3 & Rheaume-Bleue for K2 (of course there are many others as well).
Dr, Kendrick,
This reminds me of a study that showed how the loss of pain receptors in diabetics leads to amputations. It basically showed that external injuries needed pain signals to trigger the healing process and that once those signals were lost, due to diabetic damage, then the injury site never heals.
Are we seeing the same process in CVD? I don’t know what signalling process the internal body would use in replacement of the pain receptors but the loss of those signaling processes might prevent the body from properly healing the internal damage you are describing that finally leads to the ultimate CV event?
Regards, thanks for all your wonderful work, you are the reason I got my mom and father in-law off statins, thank you.
The use, for blood pressure, of potassium, l-arginine, garlic… etc, is now validated by the British Journal of Clinical Pharmacology!
http://www.ncbi.nlm.nih.gov/pubmed/26852373?dopt=Abstract
Many thanks – an interesting outcome that will probably be ignored.
May I remind people of the way data can be manipulated or ignored to achieve the right “story” even by respected institutions?
Anderson KM and others. JAMA 1987;257:2176-80Cholesterol and mortality. 30 years of follow-up from the Framingham study.
Anderson KM, Castelli WP, Levy D.
AbstractFrom 1951 to 1955 serum cholesterol levels were measured in 1959 men and 2415 women aged between 31 and 65 years who were free of cardiovascular disease (CVD) and cancer. Under age 50 years, cholesterol levels are directly related with 30-year overall and CVD mortality; overall death increases 5% and CVD death 9% for each 10 mg/dL. After age 50 years there is no increased overall mortality with either high or low serum cholesterol levels. There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels). Under age 50 years these data suggest that having a very low cholesterol level improves longevity. After age 50 years the association of mortality with cholesterol values is confounded by people whose cholesterol levels are falling–perhaps due to diseases predisposing to death. ( the escape “perhaps” clause)
PMID: 3560398 [PubMed – indexed for MEDLINE] and
The American Heart Association citing from the above paper claimed that: The results of the Framingham study indicate that a 1% reduction…of cholesterol corresponds to a 2% reduction in CHD risk. J C LaRosa and others. Circulation 1990; 81:1721-33 citing Framingham Study where
The CPPT results and those from the Framingham Study indicate that a 1% reduction in an individual’s total serum cholesterol level translates into an approximate 2% reduction in CHD risks. But where There is a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1 mg/dL per year drop in cholesterol levels)!!!!!
MORAL: Do not believe medical research where money and status are paramonut and scientific integrity is ignored,
( 1 mg/dL TC = 0.0259 mmol/L thus 1 mmol/L = 38.6 mg/dL)
Question: If, over 50(age) a 1 mg/dL drop in TC results in 11% overall and 14% CVD death rate increase what does a 38 mg/dL drop result in??
Ravnskov, Uffe (2010-12-01). Ignore the awkward! How the cholesterol myths are kept alive
Diseases that take 32 years to reveal themselves. Of course I know this paper. Amazing that low cholesterol protects you when you are young, then kills you when you are older – and vice versa. It is good, bad, good, cholesterol. Or would that be bad, good, bad?
I just returned from my lecture today in which the main theme of demonising the Statins.
In my talk I actually avoided all kind of epidemiological ‘proofs’, or statistics, but instead went into the very deep chemical nature and minutes of why the one and only cholesterol molecule is among our most beneficial and important building blocks in the membranes outlining our 10 000 000 000 cells comprising our bodies.
As one of the participants in this group expressed it after my talk he was very grateful for the intellectual rigour and the depth of understanding of the role of cholesterol. Uffe Ravnskov’s logic was part of that.
Goran,
The fact is that the cholesterol molecule goes back as far as the cenancestor some 2 billion years ago. In short Mother Nature has had a long time to test it and prove its value by trial and error. then in less than 80 years ago some “bright genius” declares it to be a killer; no doubt along with saturated fat. I wonder how many people this has killed?
Goran,
The fact is that the cholesterol molecule goes back as far as the cenancestor some 2 billion years ago. In short Mother Nature has had a long time to test it and prove its value by trial and error. then in less than 80 years ago some “bright genius” declares it to be a killer; no doubt along with saturated fat. I wonder how many people this has killed?
So would statins interfere with phagocytosis and thereby stop a wonderfully designed immune system from doing its job. A continual endothelium attack from a variety of causes struggles to repair itself because immune response can’t keep up. Am a bit lost in your wonderful deep science, bit like black holes. Or do the statins work further down the line in the process. My brother has finally persuaded his consultant to agree to remove statins, he feels better in two weeks. Thank you again for such a wonderfully informative read
Sylvia,
It just goes on and on.
One of the participants on my lecture today confirmed, as your brother, how his problem, with ‘pain in the muscles’, disappeared in a couple of weeks when he stopped taking the statin prescribed. All this is just a dreadful extremely advanced ‘quackery’ shame in my eyes.
Unbelievable to say the least!
Well – 200 000 000 000swedish kronor of sale each year makes it believable.
But when is it going to end and how?
Concerning Dr Mark Porter’s health column in today’s Times.
In January Dr Mark Porter embarked on a lower carb diet and today he reported the results in his column under the slightly odd title ‘The diet that’s almost as good as statins – and I’m proof that it works’.
Dr Porter reports:
“At the start of the year I embarked on a six-week trial to see whether cutting back on carbohydrates could improve my poor cholesterol profile. The results are in and I’m bowled over: I shed half a stone in weight, my cholesterol level dropped by 20 per cent, my triglycerides level by 30 per cent and, according to the risk calculator favoured by the NHS, my odds of succumbing to an early heart attack or stroke have dropped by nearly 15 per cent.” Surprisingly, he then adds, “Not quite the benefit you might expect from taking a statin, but as near as dammit.”
Dr Porter stopped taking statins after suffering memory lapses, but somehow he still believes they have a benefit. I’m not sure how that makes sense. Dr Porter urges readers to take a close look at a lower carb diet. He still takes sugar with his coffee and describes his diet as “at the upper end of what most people would regard as a low carb diet, but it was a significant reduction for me”.
The doctor still thinks butter is bad for him, but he says he ate more meat, eggs and cheese without damaging his cholesterol profile. He concludes, “My only regret is that I wish I had tried this in my twenties. . . . My local bakery and sandwich shop may regret my decision but it is low carbs for me from now on.”
A little bit of progress?
A quick question, Dr. Kendrick. Is Rokitansky’s view of early clot formation at the site of injury and subsequent generation of new endothelium over it a well accepted view today? In other words, is there any controversy today regarding step 2?
There is not really any controversy. However, not really any discussion either. Conventional thinking says cholesterol is the cause of heart disease, therefore other mechanisms of action are just, really, ignored.
Robert Lipp (15/02),
You (and others) may find this of interest http://www.clinsci.org/content/122/9/397 and this https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282536/ . Dr Sjöberg will be pleased to see some benefits of red wine http://ajcn.nutrition.org/content/92/1/161.full – study involved young people but I don’t see any obvious reason why it would not apply to older people.
A deficiency in magnesium is a factor in many health issues, especially when there is an imbalance between it and calcium. Not helped by the misguided supplementation of calcium to treat/prevent osteoporosis. Plenty of information here http://www.mgwater.com/index.shtml
Barry,
Many thanks for the references. Most useful and an example of the benefits added by commenters
Mike,
One of the things that I like about this blog is the way we share knowledge. None of us knows everything and I find the links and comments of the people posting here of great value. Doesn’t matter whether we agree or not as long as it makes us think – hopefully with an open mind.
Barry and Mike
A parachute and the mind only work when they are open
Benefits of red wine, not anymore in the UK. Chief Medical Officers says there is no safe limit. Given the new guidance says 14 units for men and women – political move to get to zero.
Move to France or Italy. : )
Barry:
Thanks, wow fascinating. The science is at my limits of comprehension but I believe I get the picture. Appreciated.
Dr Kendrick,
The items, as far as I can tell, are supportive of your “what causes heart disease” series. Is that correct?
Thanks
My personal feeling about inflammation is that it’s a marker, like “good” “cholesterol” (HDL). I think it’s a marker that there’s damage, and that damage is likely exacerbated by what they’ve been telling us to eat (in the US anyway) — vegetable oils/PUFAs and high carbohydrates (leading to high insulin and insulin resistance in those of us susceptible to that). By using intermittent fasting and a low carb/high fat diet, my markers of inflammation are now all low.
Insulin levels go up as a result of protein as well, particularly whey. It does’nt raise sugar levels however, its all a bit of a mystery.
Glucogenesis possibly? I know my own glucose levels go up in the morning even after fasting for 48 hours
Hello
I found this paper interesting:
https://vascularcell.biomedcentral.com/articles/10.1186/2040-2384-2-6
especially since it sheds light on why statins may be effective for those who had a cardio-vascular problem, but it seems only for four weeks?
also good effects of exercise on EPCs.
This whole series is fascinating and will probably save many lives.
Mr Chris (Feb 17),
Calcification – need to ensure that you have adequate K2, magnesium, zinc and vitamin A when taking vitamin D. There is conflicting advice regarding vitamin A see http://www.westonaprice.org/health-topics/update-on-vitamins-a-and-d/ and https://www.vitamindcouncil.org/newsletter/newsletter-vitamin-a-toxicity/. What’s not disputed is that supplementing vitamin D in isolation risks calcification and taking vitamin K2 has no known adverse effects so that’s part of the problem dealt with. Magnesium is also essential and relatively safe (you will not obtain too much from food and supplementing commercial sources such as magnesium citrate in excess will result in a serious dose of the trots – not likely to continue). Regarding vitamin A it is important that you supplement the correct type. Here’s a primer from Dr Mercola http://articles.mercola.com/sites/articles/archive/2015/11/16/vitamin-a-types.aspx and an article on balancing fat-soluble vitamins http://www.jdmoyer.com/2011/01/12/how-and-why-to-balance-fat-soluble-vitamins/. Link to WP doesn’t go directly to Chris Masterjohn article which is http://www.westonaprice.org/health-topics/the-cod-liver-oil-debate/.
When I was a kid (1950s) cod liver oil supplementation was common – my mum used to give me it every day and as I’m still here and approaching 70 with no medical issues that I am aware of so it can’t have done much harm. These days I supplement vitamin D during the winter months plus vitamin A, vitamin K2 and magnesium (magnesium citrate and magnesium chloride (as saturated mag’ oil solution and applied to skin). Works for me.
Barry:
I’d been taking vitamin K2 in it’s menaquinone form (MK-7) for several years. A while ago I came across stories (Anecdote! Very unscientific.) of folks having trouble sleeping on the stuff. So, I switched from evening to morning and started sleeping better.
Now I’m experimenting with menatetranone (MK-4) because of stories that MK-7 users experience palpitations. Don’t know if it’ll help me yet, but there are plenty of stories out there.
Hm. I wonder what preponderance of stories it might take for them to become “knowledge”.
https://www.google.com/search?q=menaquinone+palpitation&ie=utf-8&oe=utf-8
JD,
Interesting. I followed your link and found various reports of issues with K2 MK-7. Never seen any report of Japanese experiencing issues related to vitamin K2 and many Japanese consume far more K2 from natto than Westerners from supplements etc. However, a supplement is not the same as consuming a natural food containing vitamin K2 (or anything else). We’re all different and react in different ways to foods/supplements so need to find what suits us best. I haven’t experienced any obvious adverse effects to MK7 so, for the time being, will continue to use it.
Out of curiosity I had a look at Dr.Rhéaume-Bleue’s website to see if she had any comments or reports regarding sleep and found this http://doctorkatend.com/what-really-causes-waking-in-the-middle-of-the-night/ . How relevant that is to your or anyone else’s sleep issues I obviously don’t know. Probably not at all in your case as changing the time of taking the supplement helped.
I always take K2, vitamin A and vitamin D supplements together and with a meal containing fat to help absorption. Does that make a difference? We’re incredibly complex and the endless biochemical reactions can be easily upset by us chucking in a handful of supplements that are out of balance with our biochemical needs.
My input now might be considered a bit off topic since it relates to cancer but might still connect with CVD since statins might induce cancer as far as I have understood it while at the same time ‘reduce inflammation’. This was the call from the ‘arrogant’ cardiologist when he made the statin prescription against my will well aware of the fact that I would never take any. If inflammation as Malcolm points out is a beneficial defence mechanism there seems to be a logic involved since taking away a defence mechanism may actually harm our bodies.
Now, my present “off topic” input to this thread is triggered by me being overwhelmed by teh reading a book about cancer and the difficulties in overthrowing the present fruitless dogmatic ‘genetic origin’ paradigm involved in cancer research and difficulties similar to what we experience in our struggle with the CVD-dogma.
The book is one of the best I have read for long. “Tripping over the truth” by Travis Christofferson and it builds on Professor Thomas Seyfried’s resurrection of the Warburg metabolic theory of cancer. Contrary to Seyfried’s book “Cancer as a metabolic disease” it is aimed at the informed layperson but at the same time with rigour and a thrilling narrative nerve which makes me gasp. It has also a reasonable price tag.
It is just fascinating to read about the struggle to be fought in order to get science at top – great reading which gives me hope.
Goran,
I can also recommend this book. I found it after you mentioned Seyfried’s book which was beyond my pocket.
I just finished reading that book. It was really interesting and expanded the topic from that of Seyfrieds book. 3-bromopyruvate attacks the cancer metabolism. Both cancer and CVD are metabolic diseases and stem from derailing from our natural diet. Too much food and too much carbohydrates makes our cells go awry. If you can keep your blood sugar to 4.5mmol/L or below, there seems to be practically no risk of getting either disease (see the statistics in this study):
http://press.endocrine.org/doi/full/10.1210/jcem.86.8.7763
It is also worth wile to study the findings of Dr’s Kraft and Stout: http://www.thefatemperor.com/blog/2015/7/26/insulin-diabetes-rootcause-dr-kraft-excerpt-and-dr-stouts-ouevre-
Ari,
Dr. Kraft with his clinical hospital documentation during many years has really added to my understanding of what is and what is not involved in the ‘metabolic syndrome’ relating to blood sugar, insulin levels/resistance and the fundamentals of DM.
Malcolm,
Cheers to you again when I am just now sipping a ‘whisky for my heart’.
This bottle was actually my ‘reward’ for giving the lecture yesterday about the importance to avoid statins at all cost.
So – our struggle is not without any real benefits 🙂
Although this whisky is of Irish origin but may have the same ‘healing’ effect on my arteries as the excellent Scottish Ardbeg 10 years which I enjoyed during the christmas.
Whiskey = Irish
Whisky = Scottish
I prefer my whisky without e-numbers (or letters) 🙂
Slàinte mhath!
You’ve had Lagavulin sixteen year? My go-to water of life!
Mine too, Patten!
I also had a chance to drink a bit of 21 year old Lagavulin, and all I can say is: Oh…My…God.
http://www.thennt.com/home-nnt/
Statins for Acute Coronary Syndrome – Blows the Directives on this
Coronary Stenting for Non-Acute Coronary Disease Compared to Medical Therapy – Blows the Directives on this
Advanced Cardiac Life Support Medications for Cardiac Arrest – Blows the Directives on this
Beta Blockers for Acute Heart Attack (Myocardial Infarction) – Blows the Directives on this
Advanced Cardiac Life Support Medications for Cardiac Arrest – Blows the Directives on this
Heparin Given for Acute Coronary Syndromes (Unstable Angina, NSTEMI, STEMI) – Blows the Directives on this
Glycoprotein Inhibitors given for Major Heart Attack (STEMI) Patients Receiving Stents or Angioplasty – Blows the Directives on this
And shows that the “benefits” of others to be doubtful or unlikely (< 1 in 20; p < 0.05 the statistical definition)
Brilliant link.
Brilliant
Mike:
Other interesting perspectives on this. The comments and links provide more nuance. Just sayin’.
http://www.medpagetoday.com/Blogs/ThirdOpinion/50273
JDPatten
Lovely. The medical establishment does love to confuse patients. That is why, instead of relative rates and hazard ratios, I prefer the probability of NO BENEFIT based on real numbers.
I read that, and felt cross!
It seemed to neglect the fact that the NNT has been introduced to try to correct for deliberate statistical manipulation introduced by big pharma and other parts of medical science. The purpose of the NNT (as I see it) is to empower a patient when faced with a doctor who is proposing to prescribe statins, or similar such medicines that are likely to do more harm than good! In an ideal world (that I used to feel I inhabited), the doctor would suggest you took a certain medicine, and you would know it was for the best!
My irritation was increased when I returned to the article and found it obscured by a form that wanted me to sign up to something to continue reading!
http://www.ncbi.nlm.nih.gov/pubmed/?term=Digoxin+British+Journal+of+Pharmacology%2C+2016
AbstractSend to:
Br J Pharmacol. 2016 Feb 16. doi: 10.1111/bph.13453. [Epub ahead of print]
Digoxin reduces atherosclerosis in apolipoprotein E-deficient mice.
Shi H1, Mao X1, Zhong Y1, Liu Y1, Zhao X1, Yu K1, Zhu R1, Wei Y1, Zhu J1, Sun H1, Mao Y1, Zeng Q1.
Author information
Abstract
BACKGROUND AND PURPOSE:
Numerous in vitro studies have suggested that digoxin suppresses inflammation and alters lipid metabolism. However, the impact of dioxin on atherosclerosis is poorly understood. The present study was conducted to determine whether digoxin affects the development of atherosclerosis in a murine atherosclerotic disease model.
EXPERIMENTAL APPROACH:
Apolipoprotein E-deficient mice maintained on a Western-type diet were administered PBS (control), low-dose digoxin (1?mg/kg per day) or high-dose digoxin (2?mg/kg per day) via intraperitoneal injection for 12?weeks.
KEY RESULTS:
Digoxin dose-dependently reduced atherosclerotic lesion formation and plasma lipid levels (reductions of 41% in total cholesterol, 54% in triglycerides, and 20% in low-density lipoprotein cholesterol in the high-dose digoxin-treated group). Moreover, treatment with digoxin markedly attenuated interleukin (IL)-17A expression and IL-17A-related inflammatory responses and increased the abundance of Tregs. Conclusions and Implications Our data demonstrate that digoxin acts as a specific antagonist of retinoid-related orphan receptor-? to decrease atherosclerosis by suppressing lipid levels and IL-17A-related inflammatory responses.
This article is protected by copyright. All rights reserved.
PMID: 26879387 [PubMed – as supplied by publisher]
http://www.peoplespharmacy.com/2016/02/18/could-digoxin-protect-your-heart-two-ways/?utm_source=The+People%27s+Pharmacy+Newsletter&utm_campaign=ad8bded124-Health-Headlines-Email+2%2F19%2F16&utm_medium=email&utm_term=0_7300006d3c-ad8bded124-220371137&ct=t%28Health_Headlines_5_29_155_28_2015%29&mc_cid=ad8bded124&mc_eid=dd7a65b962
Don’t forget that suppressing inflammation isn’t supposed to be a good thing (see above)!
So the question is does the research show digoxin reducing inflammation directly (treating the symptoms) or treating the root cause and so allowing inflammation to reduce???
Robert Lipp,
Earlier you wrote, “Statins are known for suppressing inflammation. Does that make statins a poor strategy? Taking this further, arterial wall damage and statins simply delay the inflammation driven repair processes and promote the potential for more damage – no wonder statins do not extend life as per bmj article above.”
I don’t know the timescales for these processes, but is it possible that the tiny positive effect of statins simply stores up trouble over a time-scale that is ‘conveniently’ slightly longer than the trial duration!
I mean there is the implicit assumption in these trials that if taking statins for 3 years(say) prevents a few CVD events, then taking them for 10 years will also be useful!
David Bailey:
I don’t know, somebody with more knowledge will have to respond.