Lumen: The lumen of the artery is the hole in the middle that the blood flows through.
The artery wall: The artery wall is made up of three layers: Endothelium/intima, media and adventitia
The endothelium: Usually thought of as a single layer of endothelial cells than line the lumen of the artery. [The layer may be more than one cell thick]. This layer of endothelium acts as a barrier to blood, or anything in the blood, leaking from the lumen into the artery wall. There is a bit of space, sometime called the intima just under the endothelial cells.
The media: This layer is mostly made up smooth muscle cells and elastic tissue. The muscle can contract or relax, depending on circumstances
The adventitia: This outermost layer is mainly made up of collagen. It is very strong and keeps the artery in shape.
The atherosclerotic plaque: The areas of thickening and narrowing of arteries (in heart disease). These are usually found between the endothelium and the media – smooth muscle layer. They lie beneath the endothelium – within the artery wall itself. The area often referred to as the intimal layer of the artery.
The elevator pitch
Various people who work in business tell me of something called the ‘elevator sales pitch’. So-called, because of a (highly unlikely) situation whereby you find yourself in an elevator (which we in the UK call a lift) with a rich, famous, person. You have a short space of time to outline your idea to them, what it is, what it means, and why it is of value. They then hand over a hundred million dollars to invest in you, and your idea. Or something like that anyway.
Whilst the elevator pitch is clearly a mythical beast, the general point is reasonable. You should be able – or you should at least attempt – to condense your ideas into a very short space of time, before people get bored and walk away. Well, clearly I have miserably failed on this, as I am now writing part twenty-seven of my idea(s) on heart disease. In truth, I am planning on the elevator breaking down for about ten hours between floors to give me the time needed.
Recently, though, I have been speaking to a number of people who have successful careers in business, music, the arts and suchlike. I have been trying out my elevator pitch on them. Admittedly the elevator I am thinking of is in the Burj Khalifa in Dubai, but I am trying. So, here goes. Doors close on the elevator. Me and Bill Gates…
Me. ‘Forget diet, forget cholesterol, the real cause of heart disease is blood clotting.’
Bill Gates looks at his watch. ‘You have one minute.’
Me. ‘Blood clots can form and stick to the inside of artery walls. They then get absorbed into the artery wall itself where, normally, they are cleared away by specialised white blood cells. But if blood clots keep forming rapidly, at the same point, or the blood clots are bigger and more difficult to shift when they form, they cannot be cleared away quickly enough and so end up stuck inside the artery wall. This leads to a build-up of blood clot residue, and remnants, in the artery wall itself. Which means that repeated episodes of clotting, over time, build into thickenings, and narrow the larger arteries, mainly in the heart and the neck, growing somewhat like tree rings. These areas of damage are usually called atherosclerotic plaques.
In time, the process of blood clotting, over a vulnerable area, leads to heart attacks and strokes as the final, fatal blood clot forms over an area of the artery that is already thickened and narrowed. In short, atherosclerotic plaques are the remnants of blood clots. Heart attacks and strokes are the end result of the same processes that caused plaques to form in the first place. Heart disease is a disease of abnormal blood clotting. It is as simple as that. The end.’
Ping. Elevator door opens and Bill Gates walks out.
Do you think he believed me? Of course not. Heart disease is caused by cholesterol, end of.
Bill Gates: ‘Who was that complete idiot in the lift, make sure he never gets the chance to speak to me again.’
Man in black suit: ‘OK boss.’
I should point out that I have never spoken to Bill Gates, and almost certainly never will. I merely used his name as an example of someone that you might try to convince using an elevator sales pitch.
I also know that my sales pitch will just seem like the most complete nonsense to most people. How can I possibly claim that atherosclerotic plaques are blood clots, when no-one else in the entire world is saying it? Am I not simply a flat-Earther? Indeed, am I not a lonely flat-Earther baying at the moon. At least the moon currently passing overheard, to join all the other moons that clearly fall into a big basket on the other side of the Earth – to be returned from time to time by an enormous dung beetle.
I like to think not, because the ‘blood clotting’ hypothesis fits all known facts about cardiovascular disease. In fact, many people have proposed the ‘blood clotting theory’ of CVD over, what is now, hundreds of years. From Rokitansky to Duguid to Smith – and many more. Here, from a paper written in 1993 called ‘Fibrin as a factor in Atherosclerosis’, co-authored by Elspeth Smith.
[Just to first remind everyone that Fibrin is a critical element of blood clots (along with platelets). Fibrin is made up of short strings of a protein called fibrinogen. When the clotting system (clotting cascade) is activated, the end result is that fibrinogen is stuck together end to end, in order to create long sticky strands of fibrin that entangle themselves around the clot and bind it all together.]
‘After many years of neglect, the role of thrombosis in myocardial infarction is being reassessed. It is increasingly clear that all aspects of the haemostatic system are involved: not only in the acute occlusive event, but also in all stages of atherosclerotic plaque development from the initiation of atherogenesis to the expansion and growth of large plaques.
Infusion of recombinant tissue plasminogen activator (rt-PA) into healthy men with no evidence of thrombotic events or predisposing conditions elicited significant production of crosslinked fibrin fragment D-dimer. Thus, in apparently healthy human subjects there appears to be a significant amount of fibrin deposited within arteries, and this should give pause for thought about the possible relationship between clotting and atherosclerosis.
It also provides in vivo biochemical support for the numerous morphological studies in which mural fibrin and microthrombi have been observed adherent to both apparently normal intima and atherosclerotic lesions. It should be noted that these observations are based on the human and not just the animal model.
In 1852 Rokitansky discussed the “atheromatous process” (sic) and asked “In what consists the nature of the disease?” He suggests “The deposit is an endogenous product derived from the blood, and for the most part from the fibrin of the arterial blood”.
One hundred years later Duguid demonstrated fibrin within, and fibrin encrustation on fibrous plaques, and small fibrin deposits on the intima of apparently normal arteries. These observations have been amply confirmed but, regrettably, the emphasis on cholesterol and lipoproteins was so overwhelming that it was another 40 years before Duguid’s observations had a significant influence on epidemiological or intervention studies of haemostatic factors in coronary heart disease.’
Unfortunately, since that paper was written the emphasis on cholesterol and lipoproteins has become even more overwhelming, and research into blood clotting and atherosclerosis has faded to almost nothing. It appears that the vast sums of money to be made from cholesterol lowering has completely distorted research into this area. All the funding, and all the international experts, have charged into the blind-alleyway that is the cholesterol hypothesis.
In a kind of supreme irony, in 1992 Pfizer were also travelling down the blood clotting route. I have (mentioned before) possibly the only remaining copy of a small booklet entitled ‘Pathologic Triggers New Insights into cardiovascular risk.’ And I quote:
‘Several features of mature plaques, such as their multi-layered patterns, suggests that platelet aggregation and thrombus formation are key elements in the progression of atherosclerosis. Platelets are also known to provide a rich source of growth factors, which can stimulate plaque development.
Given the insidious nature of atherosclerosis, it is vital to consider the role of platelets and thrombosis in the process, and the serious events that may be triggered once plaque are already present.’
Of course, this leaflet was promotional, for their product doxazosin. Doxazosin lowers blood pressure and also has effects on urinary retention. However, in this leaflet, they were trying to promote its effects on blood clotting factors. Basically, doxazosin reduces fibrinogen levels and plasminogen activator inhibitor – 1 (PAI-1). Plasminogen is activated by tissue plasminogen activator (tPA) which then becomes plasmin, an enzyme that slices fibrin apart, and breaks down blood clots. PAI-1 stops this happening, so makes clots more difficult to break down.
To quote, again.
‘These recent studies suggest that doxazosin may have a range of significant antithrombotic effects in many patients, in addition to its proven beneficial effects on hypertension and hyperlipidaemia. Following doxazosin treatment, a reduction of platelet aggregation and a tendency towards dissociation, together with a reduction in fibrinogen levels, might prevent excessive degrees of thrombosis at the site of vascular injury. In addition, reduced levels of PAI-1, and increased tPA capacity with doxazosin might stimulate fibrinolysis and early clot dissolution at these sites, and prevent the evolution of an acute coronary event.’
So there, couldn’t have put it better myself.
Then Pfizer bought Warner-Lambert, who made atorvastatin/Lipitor. The focus became Lipitor and lipids, lipids, lipids. Lo it came to pass that Pfizer never mentioned blood clotting ever again, lest it interfere with the LDL story. Pity really, because mighty Pfizer got it right in 1992. Smith got it right in 1993, Duguid got it right in the 1940s, and Rokitansky was right in 1852. Of course, there have been many others who got it right too. Many, sadly, lost to history.
At some point this, the blood clotting hypothesis, the correct hypothesis will win. Maybe that time will be now.
I realise some people may still wonder (if they have not read what I have written before) how the blood clot ends up within the artery wall/beneath the endothelium.
The reason is as follows. If the endothelium is damaged, a clot will form, sitting on the inside of the arterial wall. Once the clot has stabilised, and been reduced in size by fibrinolysis, the remainder of the clot will be covered over by Endothelial Progenitor Cells (EPCs) that float around in the bloodstream and are attracted to areas of endothelial damage.
After a layer of EPCs has grown over the clot, and converted themselves into mature endothelial cells the blood clot will now, effectively, be sitting inside the artery wall. Underneath a new layer of endothelium. Thus, clot becomes plaque.
Just noticed that the hyper-link is imprecise on two counts. First is the nature of the link itself. Second relates to the target which is more a general page and not specific.
The link has a space where it shouldn’t have. Try http://circ.ahajournals.org/content/92/5/1355.full
A Definition of Advanced Types of Atherosclerotic Lesions and a Histological Classification of Atherosclerosis
Contains detailed diagrams and photos of plaques together with detailed descriptions.
Thanks for that. I must have copied it out wrongly. It is fascinating stuff… for those of us who are fascinated by such things.
Wow Malcolm that is an interesting theory. So would it be worth looking at fibrin levels in the blood rather than cholesterol ?
A couple of years ago I ran across a list of risk factors for heart attack. At the top of the list was fibrin (or fibrinogen) level in the blood. Diabetes was right up there also. Cholesterol and/or LDL-C were way down. I can’t seem to find it now, will keep looking.
The Scottish Heart Health study, done by Hugh Tunstall Pedoe. He then went on to set up the MONICA study for the WHO.
This is not the list I was looking for but and interesting article by Life Extension on the subject:
Thanks Eliot. Anyone have sny idea of how to reduce fibrinogen level?
There is a list on this video – c1 minute into the time. This could be the list you mean.
Well worth watching beyond the list, of course.
Not sure what happened to my attempt to link to the video.
Try search engine with “Cholesterol hypothesis is wrong” + Kendrick.
Video certainly does still exist.
Brilliant.. Finally , a theory that makes sense to me.. I have been wondering why FASTING is the most potent health intervention we have.. and generally ignored for any other theory..
It’s not about weight loss or calorie restriction.. it’s about white blood cells dying back during a fast.. Rebooting stems cells to create brand new blood cells upon refeeding.. that stops the blood clotting referred to in your blog.. Young healthy white blood cells performing as evolution intended.. that’s why humans are meant to fast then feast..,
“I have been wondering why FASTING is the most potent health intervention we have.”
Fasting is a good way to interrupt a bad run of hyperphagia and hyperinsulinemia, and done right it presents an opportunity for fat cells to release some fat stores, and for those general cells of the body to begin burning as ketone bodies. Search the web and you may find research indicating emerging evidence that this helps remap components of the epigenome, .. .but this field is a new one.
Personally I think that to maintain membrane potentials in accord with natures preferences is to remove one of the most potent impediments to good health. Again this field is a new one.
The following linked article is written with cancer in the spotlight, as if that isn’t intriguing enough, but I wonder if the basic principle may be applicable to other chronic diseases and I am in the act of trying to satisfy the suggestions by another that it is.
Oh no, did it again! For some reason, your nick does not raise alarms with me, so I started reading your post, the first paragraph of which sounded perfectly reasonable. This stopped at the mention of membrane potentials. Who posted this again?
At least I’ll promise to have a look at the link and maybe post a critique.
Don’t know about cancer but fasting has definitely been shown to work in many chronic diseases.
Dear Dr Kendrick
Your articles fascinate me. I was taught in 1968 as a very young and green student nurse about the cause of CHD being atherosclerosis. Many years later working in general practice, it all changed with the drug companies financing CHD clinics and telling us all we need Statins ( a bit like the ‘Flu jabs!!)
It seems few medics understand the need for cholesterol in our bodies – should they not ask why so many people have dementia when so many elderly patients take these dreadful statins and have low fat diets. i am now retired and tell everyone to have a full fat enjoyable diet, maybe smaller portions, and keep moving. Oh and a glass of wine also goes down well. Cheers! Thank you for your newsletters, keep up the good work.
On Mon, Mar 6, 2017 at 10:03 AM, Dr. Malcolm Kendrick wrote:
> Dr. Malcolm Kendrick posted: “Lumen: The lumen of the artery is the hole > in the middle that the blood flows through.The artery wall: The artery wall > is made up of three layers: Endothelium/intima, media and adventitia The > endothelium: Usually thought of as a single layer of endothe” >
We humans have abilities and faculties that far exceed those of plants. When you look to the cells of animals (that includes us) and to cells of plants the similarities are striking. Each conform to the type ‘eukaryotic’, each have the means to synthesise mevalonate (the acetyl and mevalonate pathway), from this each can synthesise important biochemicals called sterols, and each have need of an enzyme called HMG-CoA reductase. But there certain differences that are striking too. Animals synthesise cholesterol as their sterol of choice, and they can fashion component molecules called phsopholipds. The most evident difference appears in the cell membranes. The membranes of animals bear little resemblance to the membrane of plants. Animals rely upon a structure called a ‘lipid bilayer’ to fashion membranes. They simply could not be possible without (at some time in the past) nature acquired the capacity to synthesise cholesterol. The primary structural components of membranes are cholesterol and phospholipds. I have yet to satisfy myself of this fully, but the phsophate group of the phospholipds that are assimilated into membranes may be the biophysical explanation for how we do so much more than can plants. Without the biophysical side to biochemistry we would not sense so well, would not move so readily, nor even think so well. It can still be an effort to think clearly — especially for the statin faithful.
your elevator pitch had already convinced me.
Why do clots sometimes break off and lodge themselves, for example in the brain?
Is it to do with not being sticky enough?
Thank you for all I have learnt.
Your theory on CVD is very much in line with what I read years ago in WDDTY. It makes a lot of sense. Do you think that endothelium damage is likely if someone has plaque psoriasis?
Good question, QueenKETO. That’s something that’s had me wondering too.
I think the endothelium lining arteries is very different to the skin. A different mechanism, I think. But it is an interesting thought.
It’s my understanding that there is a connection between psoriasis and CVD. For instance:
At least that’s what we were told about my father, who suffered a double pulmonar embolism at age 31, plus several VTE episodes later on. He had psoriasis from a young age.
Interesting. However, Venous thromboembolism (VTE) is not truly CVD, at least not in my definition. The clot (in VTE) form in veins – then travels into the lungs – where it sticks. Of course, it is a blood clot, blocking an artery. But the clot is created in a completely different way, due to blood stasis in a vein – then activation of the internal clotting system. There is nothing in the arteries, no atherosclerosis or suchlike. I shall, however, read the entire article to see what they found in more detail.
I’m just wondering about dwindling collagen levels as we age. Are our blood vessels affected as much as our faces? I’m starting to look as if I’ve been knitted and that might not bode well for what’s going on inside. Just a thought.
This is the most simplest explanation I have read to date. Thank you for writing it so clearly. I keep trying to explain about cholesterol not being bad to people and they look at me like I’m a Flat Earther …
Big Pharma have no interest in curing people, they are in existence to make money.
Great new input as always 🙂
I just had my own “elevator pitch” with a young man from a company which is going to offer us a new heating system in our old house. He evaluated our present system and then presented alternatives together with different length of the guaranties involved, 6, 10 and 18 years respectively. Looking into our present “risk factors” we evaluated the alternatives and then went into the “lift”.
Contrary to Bill Gates this guy was very open to further input when we mentioned LCHF since he had already, due to some tendencies to gain weight, been fighting along that LCHF-road and was rather well informed. In my one minut (turned out to be 10 minutes) pitch I told my CVD story (and my wife’s DT2 one) and mentioned that I had not experienced any problems at all working hard with my shovel for a couple of hours in the morning to clear away the snow that had fallen during the night and blocked the access to our house. This situation is otherwise typical for new “events” for CVD sufferers – sudden high intensity physical work in icy, hard northern winds.
You tend to believe what you are advocating if your own body is supporting your views as in this morning case. When I had to cancel my lecture “LCHF for your health” scheduled for december due to my pneumonia it was quite the opposite situation.
Many thanks, Dr Kendrick, for your excellent article. I have just test driven it on my non-medically inclined husband and he was most receptive. He is a political anorac, and so enjoyed the background story of how history manages to ignore or dismiss fundamental facts, when money is involved.( pharmaceuticals, in this case). I managed to ‘keep up ‘ with the technical stuff, and I seem to think that much has not changed since my student days of the 1960s. I believe that eating unadulterated foods is the basis for the health of bodily functions; also, avoidance of as many toxic contaminants as possible, (prophylactic pharmacy reigns high), in order to reduce the inflammatory response to as low a level as possible.
That’s about as good as I can manage on an individual basis, and it’s working quite well so far.
Recently had an ultrasound on my feet to investigate arthritis. The radiologist commented that there was calcium in a blood vessel in my foot. I asked whether it was inside the blood vessel or outside the wall of it but he couldn’t say. I know I haven’t got any calcium or plaque in my coronary arteries (because I had CT angiogram prior to heart surgery to replace bicuspid aortic valve) so I’m wondering what other places plaque can be laid down other than in the coronary arteries and how much this is a risk too.
One possible “explanation”. Common in diabetics with peripheral neuropathy.
Why do blood clots break off and get stuck in the brain? Because they are travelling through ever-narrowing tubes until they get to the one that is too narrow for them to get through. Why do they break off? dunno.
thanks for that, the ever narrowing part? I had worked out, the “dunno” part as to why they break off, I am still hopeful that someone knows!
Thank you once again, Dr K. We seem to be getting there… I have a question: as the blood clot/plaque forms within the artery wall, presumably it cannot break off to travel about and cause a blockage in smaller blood vessels elsewhere? Therefore an actual “heart attack” is caused solely by atherosclerosis completely blocking the artery to the heart? And strokes are caused by blood clots elsewhere breaking off and travelling to where they can get no further? And pulmonary blockages too? If so, do we need to look at what we can do to prevent those blood clots forming, as well as the heart artery ones? Sorry, that is more than one question!
Heart attacks are caused by a blood clot forming that is big enough to complete block a coronary artery. Clots that form on main arteries in the neck (carotid arteries) can break off and travel to the brain, and get stuck, causing a stroke. Pulmonary blockages are caused by clots forming in veins in the legs (a different process of blood clotting), these then travel up to the heart, through the heart, and get stuck in the lungs – leading to a pulmonary embolism.
Thank you, Dr K for taking the time to clarify that for me. Much appreciated.
Regarding strokes, another related cause is venous blood clots passing through a PFO and thence travelling from heart to brain. Or, blood stasis at the site of a PFO or atrial septal aneurysm can also travel to the brain.
I should clarify, the blood stasis at the PFO causes it to clot, which then travels to the brain.
Very interesting Doctor.
Which begs the question, how do we prevent the formation of blood clots, or how exactly blood clots are formed inside our blood vessels ?
If you damage the endothelial cells, a clot will form at that point. How do you prevent this? Keep the endothelium healthy and reduce things in the blood that can cause endothelial damage e.g. smoking, which reduces NO synthesis, the substance which both protects the endothelium and stops blood clots forming. Raised blood sugar also causes endothelial damage, as do certain stress hormones, as does lead and cadmium and air pollutants, homocysteine, PPIs (e.g. omeprazole) and etc. etc. etc. Things that improve endothelial health are such things as exercise, vitamin D, NO itself (produced in the skin in response to sunlight), l-carnitine, l-arginine, vitamin C, vitamin(s) B, Yoga, meditation etc. etc.
Thank you for that, I have printed it out so will not lose it this time.
Got this; got that – from earlier Roman Numerals. But what are the etc. etc. etc.s? And the etc. etc.s?? You’ll eventually have a definitive list, yes?
Indeed. I shall have a longer list. Not sure if it will be absolutely definitive.
I have a number of red haired friends who avoid the sun like the plague. Is there a correlation between redheads and CVD since they may be lacking in Vit D and NO synthesis?
“Finally, I will put together, what I believe, are the ten (or so) best things you can do to protect yourself from CVD.”
It’s almost the one year anniversary of that initial promise, Dr. Kendrick. Should we assume that the list has finally arrived? In the form of:
“Raised blood sugar also causes endothelial damage, as do certain stress hormones, as does lead and cadmium and air pollutants, homocysteine, PPIs (e.g. omeprazole) and etc. etc. etc. Things that improve endothelial health are such things as exercise, vitamin D, NO itself (produced in the skin in response to sunlight), l-carnitine, l-arginine, vitamin C, vitamin(s) B, Yoga, meditation etc. etc.”
Or to put it in another form:
1. Avoid stress
2. Avoid lead, cadmium and other pollutants, PPIs.
3. Keep homosysteine levels low
5. Get a some sunlight/vitamin D
6. Take l-carnitine supplements
7. Take l-arginine supplements
8. Take vitamin C supplements
9. Take a vitamin B complex supplement
10. Practice yoga or other forms of meditation.
That’s essentially “10 or so things” people can do to protect themselves from CVD. Feel free to edit my list, or further elaborate on all the etceteras.
It took a while, but we finally got here. Or so it seems. But the final word is yours.
Thanks for the journey, Doc!
“If you damage the endothelial cells, a clot will form at that point”
If the plaque lies between the endothelium and the artery walls, when they perform an atherectomy to remove plaque, which effectively means they push a fancy apple corer up the blood vessel, they have to remove the endothelium with the plaque, exposing the blood vessel wall underneath.
How come this endothelium-free area of artery wall doesn’t immediately clot over?
Lots of anti-platelets help. Also they can completely clot over, and sometimes do.
tl;dr: scabs form in the arteries. DON’T lick your scabs! Here are things that pick the scabs. Here are things that heal them . . .
. . . I’d also add hyperinsulinemia from IR (plus high carb diets)
The vascular surgeon told me to walk through the pain and revascularise myself (Peripheral Arterial Disease) which has worked pretty well. However he also told me I must go back on a statin to “stabilise” the plaque. Hmmm, I didn’t do that, “stabilise” = calcify and I already saw what calcification did to my kitchen drain, literally – the Man From Dyno-Rod used a video camera as he chipped away at the calcified crud, which hopefully won’t recur as I fitted a water softener forty years after the house was built. I previously feared the drains would need complete renewal or relining (stents?)
Thanks to you I have continued to walk in the sun this winter, even when the Arctic blast has been so dire I was picking gravel out of my teeth, keeping the Vitamin D and NO up (hopefully). LCHF/keto with lots of nutrition undiluted by valueless carbs and Omega 6 seed oils, probably including l-carnitine from the delectable local grass-fed meats and liver. I’ve also added vitamin C and l-arginine, oh and vitamin K2 and Co-Q10 and magnesium on the basis you can never be too careful. I’ll let you know if it worked by not dying yet.
Thanks to Robb Wolf for retweeting this
which I found hugely entertaining.
Fascinating, as always. My family history of CVD is horrible. With no male making it past 49 years without MI or stroke, with some having trouble in their 30’s. I’ve researched Vit K2, mk4, Vit C and others (tried the K2 for a while) . The calcium subject seems involved somehow, and interestingly, I have hashimoto’s and related, low blood calcium. I am in my middle 50’s and have not yet had a CVD cardiac event. I did have Afib at age 33 due to thyroid failure. I was also on Crestor for a decade. Doctors quote a study that shows heavy statin (Crestor) use as a proven plaque reduction agent. Many promote a veggie diet that has been said to be proven to reduce plaque, tried this too, with intestinal distress. I’m happy I’ve gotten this far without an MI, and would be thrilled to live out a normal life with a healthy heart. To that end, Dr. K, can you provide a comprehensive list of known cardioprotective items?
@franklin, if you were taking Vit K2, you need Mk7 not Mk4, and you need to take Vit D3 with it to assist with your conversion of Free T4 to Free T3. Your family history of CVD could be down to a family history of thyroid mismanagement/undertreatment or non diagnosis, as the heart needs T3 and can be hereditary.
Not medically qualified but done a lot of research.
Why not Mk4? Mk7 is the plant version, Mk4 is the animal version. I don’t know of any nutrient where plant version works better in humans. Mk7 has beneficial effects, but I favour Mk4, or a mixture if you want to hedge your bets. The reason that Mk4 is criticised is because blood levels fall within hours, whereas Mk7 stays in the blood for days, but this is precisely why I think Mk4 is better. Where is it going, why does it disappear? Because as an animal version, it has a greater affinity with our cells, and is hoovered up, out of circulation and into target tissue 🙂
From my research from Chris Masterjohn’s blog I think it is good to take both Mk4 and Mk7. Currently taking Mk7 but going to throw an MK4 into the mix. Gosh I will be rattling.
I think he just did that, above your post at 12:17 pm (according to my screen, anyway). Personally, I find limiting fiber, including those in vegetables, to be helpful. I haven’t yet tried a “zero carb” diet, which is where you eat basically all meat (and maybe eggs), but I’m moving toward that.
@franklin, if you are not aware of coronary artery calcium scoring CAC, you might find it a useful test to get. It’s about $100 here in the US and it is a CT of the calcium (thickness, volume, density) in the heart arteries. The test results in an Agaston score with various ranges indicating the likely risk of a heart event. Check out “The Fat Emperor” s page (Ivor Cummins on FB or the internet for lots of the research on this test. He claims there is not a better one for revealing risk, at least risk due to a coronary blockage.
I like the elevator version. Ty. Can u give me an elevator version of how to correct this with diet? Is that possible?
Good luck with your elevator pitch. I’m certainly no fan of the media and journalists after what I’ve been through. With that hope the pitch goes well.
It reminds me of a story I was reading the other month. It was about a fellow studying light therapy and cancer. He happened to share not an elevator ride, but a short car ride with the head of cancer research at Bellevue Medical center in New York, Dr Jane Wright. This was in the late 1950s. She liked the light therapy for cancer treatment sales pitch and agreed to look into the idea further.
To start, Dr. Wright asked 15 cancer patients to spend as much time outdoors without wearing glasses or sunglasses. The result was that 14 of the 15 patients showed no more tumor development and several showed possible improvement.
Hardly definitive proof, but a nice start with hopes of further study work. Sadly it was largely the finish too. The results were ridiculed by many others. Little more work was done after that. Reputations were on the line. I can imagine there to be several potential reasons no more work was done on such a simple idea.
Do we know at what time of year this happened? If outside of Nov.-Feb., might have well been Vit D.
I have just downloaded Dr TE Levy MD JD, book, Stop America’s #1 Killer!: Proof that the origin of all coronary heart disease is a clearly reversible arterial scurvy. Levy suggest as an hypothesis that “focal scurvy – ie Vitamin c deficiency” of the cardiac arteries is the initiator of the intima inflammation which results in plaque formation which in turn leads to MI. This seems to fit Dr K’s hypothesis of intima damage and inflammation, Makes sense to me
Would this mean that I, after a heart attack in 2002 in pulmanary embolism in 2009 am being protected by the Xarelto I have been prescribed?
Elegant, rational, consistent with observed reality. What is not to like?
Your elevator pitch is missing the vital phrase mentioned later on: ‘If the endothelium is damaged, a clot will form, sitting on the inside of the arterial wall’. This provides the initial context and is your hook for the follow-up of how we can prevent the damage from occurring in the first place.
I think you might be right. My elevator pitch assumes too much prior knowledge of the subject area. But, hey, it has taken me thirty years to get to this point. I can hardly expect people to jump right on it. I need a bigger elevator.
So, I’m trying to tie this back to current health care practices. If you have high LDL-P does that imply you are at a higher clotting risk?
No. However, FH and blood clotting factor abnormalities are closely related in some families.
Well I for one hope that there never is a last part of Dr K’s explanation of heart disease, it’s too entertaining! (Unless Dr K, you turn to another of medicine’s blind alleys, and explore the somatic / genetic theory of cancer perhaps? That Rokitansky made these great insights, the significance of which was lost in the pursuit of the cholesterol red herring (or should that be golden goose?) is so reminiscent of Warburg, who declared that cancer arose from problems with the mitochondria, and stubbornly maintained to his dying day that he was right, and would be proven right, and all those who believed otherwise (i.e. everyone) were idiots! Or something like that. And as with cholesterol, the more money and effort that goes down the genetic cancer alley, the more complicated and uncooperative the whole theory becomes. Lots of your black swans among the golden geese. That would be awesome. You know you want to…)
Before going off on that tangent, I just wanted to mention statins – I know Dr K has covered them before, but a few comments mentioned them. The beneficial effect of statins, such as it is, must tie in nicely with the blood clotting explanation, as it may be due to their anti-coagulant and antioxidant effects. (And be in spite of their lowering of cholesterol – plant sterols (Benecol etc.) do lower cholesterol, but have no beneficial outcome, on the contrary, and very awkwardly for the industry, very high blood levels of plant sterols quickly cause coronary atherosclerosis.)
There is a quote that people should be like stamps. Stick to one thing until you get to your destination. Or something like that.
“Be like a postage stamp – stick to one thing until you get there” – Josh Billings
Damage to the endothelium will occur. Clots will form and be covered with new endothelial tissue.
And then be cleared.
Hey, life with all its stressors happens! Hopefully, the damage doesn’t occur so often that it accumulates. (Tree rings. Yikes!)
Perhaps this is a good place for the elevator explanation of how a normal modest clot, hidden under the endothelium, gets cleared.
By macrophages. Macrophages evolve from monoctyes which, in turn, evolve from EPCs (that do not become mature endothelial cells). As you can see the body throws the elastoplast and the clear up kit at the same time.
As you have oft stated, the body functions in a wondrous manner, and everything that occurs happens for a good reason.
So shouldn’t aspirin prevent more heart attacks than statins? As far as I know aspirin has lost its role as primary prevention in low to medium risk CVD. Of course, statins are also not so potent as primary prevention as well…
I like the theory, but I would expect preventing clotting to more greatly reduce risk
No, you wouldn’t. Because the most important factor in blood clots forming on arterial walls in exposure of the blood to tissue factor (TF), and this sets of blood clotting that virtually overwhelms most anticoagulants. However, hemophiliacs (prior to clotting factor replacement) had one fifth the risk of dying of heart disease than the surrounding population. Those with Von Willibrand disease have a fifty per cent reduction in risk.
Garlic in stead of aspirin as I do?
Nose bleeds in the Inuit.
Could you detail how nosebleed helps them a little more? I often had nosebleed and could not find any reasons for them other than, maybe to lower my blood pressure i told myself. It is purely a thought i have.
Correct me if I am wrong, but…
“in exposure of the blood” should say “is exposure of the blood.”
“and this sets of blood clotting” should say “and this sets up blood clotting.”
I think you are right.
Dr. Kendrick: Thank you very much for the interesting information about the Pfizer drug, which likely has suffered an untimely death. Also like the succinct prevention advice, to keep the endothelium healthy by NO producing behaviors. Easy to remember!
The Pfizer drug still lives. Now off patent.
But be careful. Doxazosin (Cardura) seems to cause cardiac scarring – interstitial fibrosis – that then seems to lead to heart failure.
I saw those side effects when I looked it up. So not so good to take.
How would the world look like if patents had never been invented?
It’s common name is cardura, in fact I believe my mom is taking it for blood pressure.
Gary: can you write up your list of NO producing activities? When you have time. Thank you
Sasha: I don’t know any more about what activities produce NO than what I’ve learned from Dr. Kendrick and one other site which said that raising the heart rate by 10-15 BPM, as in exercise, sets eNOS in action producing it. So, sunlight and (even moderate) exercise come to mind, and since UVA is available year-round, except in the arctic and antarctic, just going outside for a while each day seems like a good idea. Now you’ve gotten me curious. What else stimulates NO production?
Gary: I don’t know, that’s why I was gonna cheat and just ask you))) I will have to look it up and see what else supports NO production…
I think someone mentioned taking niacin?
If anyone else knows, please let us know.
Garlic, shellfish, seafood, flaxseeds, eggs, nuts, dark chocolate red wine, grape juice, blueberries pmegranate juice green tea. Exercise. All are supposed to support NO.
also found a source which gives rocket lettuce as top top source of NO, followed by rhubarb, and bottom of the top ten is beetroot.
hope we are allowed to post this, as being dietary in a way!
Frederica Huxley: Yes, beets! One of Nature’s greatest gifts to us, both root and leaves. As I understand it, it is the nitrogen compounds in them and other foods which aid NO synthesis.
Beetroot, radish and possible (eeeghh) celery?
Please give us the link to your top 10 of which beetroot is 10
Here we are:
Mr. Chris: Very interesting that the top one is arugula. I have it in my garden, and eat it 2-3 times a week. Very easy to grow, though it is a cool season plant. It has naturalized in the garden, and I don’t need to plant it any more.
This NB is not for you but aragoula is in fact rocquet lettuce. This is good news for me because I like it as well as the second highest in NO rhubarb.
BTW I don’t really like beetroot
BTW 2, I don’t know if Dr Kendricks strictures on the small connection between diet and CVD applies to NO enhancers
Thank you Mr Chris. Interestingly enough, in traditional Chinese medicine bitter flavor (in foods like arugula) are said to help the heart. How the hell did ancient Chinese know this 2000 years ago???
Hey guys, be careful not to confuse nitrate (NO3-) with nitrous oxide (NO).
Nitrates will decay into nitrites, releasing oxygen (and potentially causing oxidative stress):
2 NaNO3 –> 2 NaNO2 + 02
Nitrates may form nitrosamines which are carcinogenic, This is why nitrate in drinking water and lettuce is monitored and limited.
Nitrites can also turn into NO in the body, but I am not sure I’d want to systematically load up on nitrates.
Having a diesel engine? (joke)
Hasn’t laughing gas become popular among the young clubgoing type people? I wonder if the benefits will outweigh the disasters.
It strips you of vitamin B12, which is not a good thing.
One can imagine little robots roaming our interior highways and byways looking for clots to dissolve. Or perhaps chomp into and take elsewhere. Would that be a good idea?
They are a good idea. They are called Endothelial Progenitor Cells (EPCs) and they are little bio-bots. They spot areas of damage, cover them over, then (those EPCs that turn into macrophages) remove the detritus. Isn’t nature a fantastic thing. If I didn’t believe in evolution, I would have to believe in God… (I know, don’t tell me, you can believe in both)
Sometimes nature (or god) needs a little help 🙂
A gem, Dr Kendrick. Yes nature is indeed wonderful. Don’t know why, but it makes me think of beavers, building a dam, the river will course another way,(collaterals).
Someone in another comment mentioned fasting, from what I’ve read after approx 3-4 days of fasting autophagy occurs. Is this similar to the EPCs you are mentioning? Thank you. Here’s a link to an article on this, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3106288/
“Isn’t nature a fantastic thing.”
I marvel about this more and more the older I grow. Now and then when consulting my favorite pats of the Bible I realize that king Solomon was struck by the same sentiments when he got old but he finally turned bitter – I haven’t got so far yet.
Just think about our mitochondria – I must keep my own going as I succeeded with this very morning.
Aha, so EPCs are a differentiated cell type that retain some scope for a reversion to being pluripotent. When in receipt of a certain kind of signal from a certain region of harm they switch to a new assignment and become differentiated as macrophages.
A curious aside is that one of the 49 alternate oxides of cholesterol, 25-hydroxycholesterol, can ramp up the synthesis of cholesterol within macrophages, and equally curious is that the sulphated version of 25-hydroxycholesterol (25-HCS), sends a signal to macrophages to throttle back the synthesis of cholesterol.
Cholestane triol is another of the family of cholesterol oxides — one recognised for bringing on necrosis of smooth muscles cells.
Isn’t nature enigmatic . . .
Christopher Palmer: As I recall from a 2012 Stephanie Seneff lecture, the sulfated forms of both vitamin D and cholesterol are produced in the skin during sun exposure, thus the importance of both sun exposure and sulfur- rich foods (such as onions and garlic).
Any thoughts on Vitamin K2 (MK7)> Or is it just the “cure du jour”?
Dear Dr. Kendrick,
Thanks for yet another further insight into the real causes of heart disease.
It’s interesting that much of what we hear of in the media regarding ‘plaque’ and the need to take statins, supported as well by such ‘academic’ bodies like Public Health England, NICE and NHS England endorsing the prescription of statins, that they do not mention anything about atherosclerotic plaque regression. I attach two papers for your review, (if you have already seen them apologies), that proposes scientific evidence that atherosclerotic plaques can regress. Your thoughts on the two papers would be of interest to me specifically but probably to all your other readers.
Can your blog be sent to all members of the All Party Parliamentary Committee on Cardiovascular Disease, https://www.publications.parliament.uk/pa/cm/cmallparty/register/heart-disease.htm
I’m pretty sure they would be interested to hear your views.
Your formatting went mad. Had to edit it, may have lost your two papers. Could you try to re-send. Perhaps using a different device.
P.S. I am pretty sure they would dismiss my views within a microsecond. They would do this, without having to inconvenience themselves by even finding out what my ideas actually were.
This was so interesting and fun to read! Great approach! And very informative about heart disease!
I do elevator pitches professionally. Could not stop myself from writing one.
“Me. ‘Forget diet, forget cholesterol, the real cause of heart disease is blood clotting.’
There is one simple cause of the heart disease and strokes that plague us and the problem is solvable.
“Me. ‘Blood clots can form and stick to the inside of artery walls. They then get absorbed into the ……………………….
Heart disease is a disease of abnormal blood clotting. It is as simple as that. The end.’”
Some of us repeatedly damage our blood vessel linings by our life styles and cause internal blood clots to form in response. The pace of damage overwhelms our natural repair mechanisms causing layers of clotting to accumulate (an atherosclerotic plaque) and gradually block the vessel, ultimately triggering a heart attack. Sometimes, a clot will break away from the plaque and travel through the circulatory system to cause a stroke. The solution is to minimize blood vessel clot formation through healthy life styles that prevent blood vessel damage.
Much better than mine. Thanks.
Brian’s seems a little bit too minimal to be helpfully meaningful.
So is the theory, in part at least:
anything that increases arterial stiffness, increases clotting, due to increase chances of damage, which leads to plaques and then eventually complete occlusion?
So then is it the excessive insulin in insulin resistant diabetics that leads to greater stiffness and therefore greater likelyhood of damage and therefore clotting? Or could it be that diabetics often have fatty liver, which inhibits hepatic production of NO? this would fit with studies that have shown that agressively medicating diabetics to achieve better blood sugar control doesn’t make them live longer.
How often do diabetics have fatty liver? Especially if they aren’t insulin dependent?
Almost 100% have a degree of fatty liver.
How do you know if you have fatty liver. Do the blood tests you have at the docs test for this.
If you have low HDL and high VLDL and high fasting sugar – you will have a fatty live (almost 100% guaranteed). A scan will tell you for sure.
But if a diabetic is very slim, with a 25inch waist, trig. level of .6, HDL 3.4, fairly good control of BG what then? Does trig. level co-relate to fatty liver. …..just asking.
Yes, usually. But diabetes is not all the same thing.
Thank you for your reply. Can you or somebody out there in the ether recommend a book/study/paper which explains the differences, preferably NOT someone who recommends lots of pasta, wholemeal, natch, porridge and a good daily dose of statins. There must be someone out there. Oh yes, and it would have to be written by someone who understands that not everyone understands all the argot. That would be me, then.
My understanding of Fatty Liver Disease issue in early T2D is: High glucose levels along with high insulin levels promote the creation of the fat in the liver cells. (Fat that is not wrapped up in VLDL particles) (Insulin enables the GLUT4 transporters to pop onto the surface, allowing entry to glucose into the liver cell where it is made into fat)
For T1D there is no insulin, no functional GLUT4, but there are GLUT2 transporters that allow glucose to enter the liver cells. I have just found, but not yet read, a little study that indicates that high serum glucose up-regulates GLUT2 transporters in the liver cells. So, having high GL levels can still give you fatty liver disease.
Got it. Thank you.
Oops . . . the paper
Hepatic steatosis in type 1 diabetes – Regnell 2011
Dr Kendrick: ” the ‘blood clotting’ hypothesis fits all known facts about cardiovascular disease.”
How does it explain the fact the women mostly don’t have heart attacks until menopause?
That is not a fact, but never mind. Younger women, usually, have less CVD primarily due to the different way that they handle stressors. Less production of stress hormones, reduced sympathetic response (in the main). There is a mass of literature on this subject. Quite a lot of which I have read. However, in some countries, and populations, the differential is almost zero. Younger Brazilian women, for example, and black African american women. The menopause has no effect on CVD in women. The effect of the menopause of CVD in women is a known fact, that is not, in fact, a fact. There is not one scrap of evidence to support it, other than the fact that older women have more CVD than younger women. Same as men.
Women handle stress different from men? In what way?
I had read that higher serum ferritin levels were associated with an increased risk of heart disease and that menstruating women has lower incidence of heart disease due to lower iron levels. So all those phlebotomies were for nought
“Less production of stress hormones, reduced sympathetic response (in the main).” that’s how. Now the question is why? Because they are women and i think women are more sociable than men in general and they will turn to other women or friends to share their immediate problems. They will often find a confidant to share everything and talk. Talk and have conversations whether meaningful or meaningless. There is more but i am sure google can help you 😉
Is it a fact that women produce less stress hormones? It may be, I just never heard of it expressed that way…
They have a different reaction to many stressors.
Assessment of gender differences in stress reactivity relies primarily on measuring physiological responses to acute stressors in laboratory settings. This includes activities of the Hypothalamic-Pituitary-Adrenal (HPA) axis (eg, cortisol) and sympathetic nervous system (eg, heart rate and blood pressure). Greater acute HPA and autonomic responses have been found in adult men as compared to adult women, with the help of standard performance-related psychosocial stressors such as public speaking. Pathogenesis of cardiovascular disease, aggression, and immune suppression in men are likely to be influenced by this greater sympathoadrenal responsiveness.
HPA response patterns differ markedly between males and females. This has been demonstrated in both animal and human studies. The biochemical profile of human beings varied from that of rodents with regard to stress-related neurochemicals such as basal Adrenocorticotropic Hormone (ACTH) and corticosterone levels. While the basal level as well as variance in response to stress is uniformly higher in females of rodents, the picture is more complex in humans. A relatively higher secretion of ACTH with comparable total cortisol levels under basal conditions has been observed in men. This finding reflects an increased sensitivity of the adrenal cortex in women as compared to men. However, no gender differences are observed at the pituitary level on challenging with synthetic Human Corticotropin-Releasing Factor (h-CRF) with or without pretreatment with dexamethasone The response is different to ovine CRF or a combination of h-CRF and vasopressin with respect to ACTH secretion, with women being more responsive. etc. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3425245/
Very interesting, thank you.
I am unclear about the second paragraph. Does it mean that female rodents are more stressed out than male rodents while in humans it’s the opposite? And why do they conclude that adrenal cortex is more sensitive in women?
Dr Kendrick…..how do you propose to convince GPs regarding a better understanding of female CVD stats? Along with statinisation of post-menopausal women, we girls need someone to speak up for us.
Lies, damn lies and statistics comes to mind. We can interpret anything to suit our own ends.
Excellent paper, thank you!
In retrospect my stress response was wrecked by alternating hyperglycemia and hyperinsulinemia with corresponding hypOglycemia leading to release of cortisol, norepinephrine, epinephrine, neuropeptide Y, etc. along with glucagon. Probably the case for many/most Type 2s and insulin resistant people, “reactive hypoglycemia” which may be another cause of increased CVD risk?
Three weeks out of every month being married destressed me, but the fourth week was a killer, she suffered PMS to the extent of many symptoms of Borderline which affected me only slightly less than it affected her. I wonder how that fits in?
They don’t have time.
the link at the bottom doesn’t seem to be working?
http://circ.ahajournals.org/content  /92/5/1355.full
and yes I tried copying the whole line.
Thank you 🙂
This would sure fit hand in hand with why Vitamin E is so effective in preventing heart attacks. It also opens the door for a hard look at Rutin. Stop the clot from forming and in most cases you stop the fatal event. Harvard out of Boston has been working for several years now on stopping clots in both Veins and Arteries with Rutin. So while we focus on things that might reverse heart disease wouldn’t it be nice to avoid dying from it in the meantime?
The Harvard work will likely result in a patented drug but right now it’s using a very natural, readily available nutrient – Rutin. Xarelto (a blood thinner) took this same path. It came from a natural ingredient found in nature and now is a patented drug with a host of safety issues.
http://news.harvard.edu/gazette/story/2012/05/flavonoid-compound-can-prevent-blood-clots/ There are many papers published by this group in PubMed including several in 2015/16/17. What’s so exciting about this is Rutin appears to stop the clot from a level in the clotting cascade that catches both veins and arteries.
I never thought about how important this really is. If you can stop a clot from forming in the circulatory system (a thrombosis) you prevent almost all fatal heart attacks. Think about it.
I have dozens of links and have corresponded with several of the doctors involved in this study.
Vitamin C increases the bioavailability of Rutin.
stcrim: For once in its life Wikipedia has something useful: a list of rutin-containing foods. Number one is capers! I knew there was a reason I like them!
Whole food vitamin C not ascorbic acid.
Are saying not to take a vitamin c as supplement.
Whole food vitamin C can be a supplement. It has all the bioflavanoids in it that ascorbic acid lacks.
As far as I know, with Linus Pauling (?), ascorbic acid is vitmin C and easily dissolved in lukewarm water. I am slowly sipping about 15 grams from a large glass of water every day. Would be a ton of oranges I guess.
Gosh Dr Sjoberg 15gm per day. If I took that much I would be running all day. I do believe the ascorbic acid is a good form too. Apologies in not being able to put the dots in your name.
Anne Lucas: Here is how to do it: Write your comment as a document. If you’re using Word, go to symbols and select the one you want. If you’re using Pages, simply hold down the “o” key. The screen will display several choices; press the 2 key (or whichever in the row is correct) to select the second from the left. Then highlight, edit, copy. Then you can go back to the comment page and paste it in the box.
Thanks for that tip Gary.
But also think about the reasons we clot at all.
What happens to all the little endothelial tears without the sealing healing of clots?
Reduce heart disease by simply reducing clotting factors and risk hemorrhagic stroke? Massive gastro-intestinal hemorrhage? They can kill just as well as an MI. Ask any aware person taking warfarin what they face every day.
Life’s a balance.
Fibrinogen, fibrin, all the complex of clotting factors are necessary. Good.
Reduce the NEED for it all.
Solve that and the problem’s done.
If plaques are essentially blood clots, how do cholesterol crystals and other debris get in there?
What starts the process that ends with a blood clot? Do blood clots just form randomly and stick to artery walls for no reason other than they can?
Red blood cells are an essential part of blood clots, and the only source of cholesterol crystals is the membrane of red blood cells. Cholesterol crystals cannot come from anywhere else. Blood clots contain platelets, fibrin, Lp(a), red blood cells, plasminogen, white blood cells, VLDL, HDL, LDL. Almost everything, in fact, you can find in the blood.
Dr Louis Ignarro wrote a little book called NO More Heart Disease. A program for boosti g profuction of Nitric Oxide.All about protecting your endothelium. Based on consuming l arginine, Citrulline, vitamin C and alpha lipoic acid.etc. I used to take it but the l arginine smells and tastes like old rotten boots. I was taking it with fruit juice and a small amount of citric acid twice a day which put my trigs up to 2.5 mmol/l. As soon as I stopped the fruit juice my trigs fell and now I am low carb they are 0.07mmol/l. I have been toying with the idea to put the l arginine in capsules but for the correct dose I would have to take a lot of them. So it’s back to the drawing board. I also noticed that l arginine comes in different powders. Some have only about 1/4 teaspoon for the dose and others you have to take 2 teaspoons for the same dose. I have no idea why. Any tips on taking it would be appreciated as I really should get back into it.
Pardon my typing mistakes. 🙂
Nobel prize for medicine, fits with what Dr kendrick writes. Whats not to like?
I have ordered it. Hope it contains foods boosting NO besides beetroot and rhubarb.
It does but it also spouts the low fat and polyunsaturated seed oils crap.
Be awzre that the NO formula has been disputed in some articles. However there is no real doubt that NO supports endothelial function so what is there to lose. ☺
I have learnt that it is very rare that one book, one author, one website offers the golden key, and am just grateful to learn just something new. Of course if I feel it is crap from the beginning, I give up.
I mix some beetroot powder and add stevia drops to my arginine powder. Beets are also supposed to promote NO due to high nitrate content. (I suppose bacon might have the same effect.)
Thanks Eliot I’ll give it a try.
Eliot: Funny thing about bacon, at least here in the U.S. Some years ago there was a nitrate scare, so it is nearly impossible to find cured bacon. They now use celery powder, which also has high levels of nitrates! They call it “uncured bacon.” But Americans are still getting their nitrates, as they should.
Endothelial Cell Dysfunction > subendothelial space exposed to clotting factors
My current belief is that most diseases stem from mitochondrial dysfunction, including CVD. Eat low carb to keep blood glucose low. Reduce linoleic acid (inflammatory). Supplement micronutrients, magnesium, d3, krill oil etc,.
Hyperglycemia > ROS endothelial cell apoptosis i.e. hole in endothelium > blood clot
> scurvy due to vitamin C blocking
Linoleic acid > easily oxidized part of mitochondria + ROS > cell apoptosis
Reduced eating window > autophagy, cell repair
Perhaps this elevates the humble tomato to the top of the list of ingredients in the Med’ diet that help protect against heart disease and hence the lowering of platlet aggregation from Fruitflow the aspirin alternative
“Because tomatoes include several nutrients associated with theoretical or proven effects and are widely consumed year round, they may be considered a valuable component of a cardioprotective diet.”
So maybe the unexplained fall in CVD since the 1960s is due to the rise in pizza consumption?
Here is more fuel on the vaccine “scam” issue from Mercola.
This time pretty convincing to me at my first look.
So – this recent point on my “medical scam” list seems to stick more firmly now.
Anyone who sees serious flaws in Mercola’s arguing?
I am still open for alterations on my list.
There is a good amount of problems with vaccines, that would be nice if they were addressed.
Further reading of Levy’s book lead to the following extract:
Overall, then, a focal vitamin C deficiency in the arterial wall “degenerates” the basement membrane allowing the abnormal deposition of solutes such as calcium, cholesterol, and fats. Subsequently, there is a “proliferation” of macrophages in the basement membrane which continues as long the abnormal deposition of solutes continues. And, until vitamin C levels in the arteries normalize, abnormal deposits will continue to appear and macrophages will continue to proliferate and engulf the solutes, thereby continuing the relentless progression of atherosclerosis.
Also this ties in with the Ehkers-Danlos syndrome which is a genetic condition following defective genes affecting connective tissue including blood vessels large and small. Again Vit C seems to have benefit.
Advances in Pharmacological Sciences Volume 2011, Article ID 195271, 5 pages doi:10.1155/2011/195271
In conclusion, oral supplementation of vitamin C with metformin reverses ascorbic acid levels, reduces FBS, PMBG, and improves HbA1c. Hence, both the drugs in combination may be used in the treatment of type 2 DM to maintain good glycemic control.
Brit. Heart ., 1969, 31, 227.
Cardiac Abnormalities in the Ehlers-Danlos Syndrome
High-dose (1-4 g/d) ascorbic acid (vitamin C) therapy has been tried and, in theory, has a potential effect. Clinical studies suggest that wound healing, even in patients not deficient in vitamin C, can improve with supplementation above the recommended daily allowance. In patients with kyphoscoliosis type EDS, bleeding time, wound healing, and muscle strength seem to improve after 1 year of daily high-dose vitamin C therapy; however, high-dose vitamin C therapy is not considered the standard of care and requires medical clearance for use = another case of medical establishment attempts to denigrate the use of Vit C .
Overall Vit C seems to have a place in the avoidance and therapy of heart conditions, particularly where damage/inflammation of the cardiac arteries are concerned
I think you can increase your NO by nose breathing and not mouth breathing (as I did).
Or take Viagra (as athletes have worked out).
Have you had a chat with Uffe Ravenskov. You 2 should discuss plaque characteristics.. He came up with his own theory.. including inflammation and the role of infections and other elements in the blood in the tiny vessels feeding the arteries. Maybe inflammatory factors – high blood glucose, compromised immune system – is what causes the clotting to proliferate.
We chat often. I don’t agree with him about how plaques start – we have constructive discussions about this. I do agree that infections can, and do, cause CVD. However, this is primarily though damage to the endothelial cells and creation of plaques.
Decades ago I read an essay by E M Forster on peoples experience of coming across revelatory ideas; the sort you read about going “Yes, yes, of course – I’ll buy into that”. He was saying that when that flash of enlightenment happened the reader was already there; everything in the mind was in place, the revelation was just a piece of jigsaw that filled a ready prepared space in the mind.
So it was that when I was told that I had high cholesterol (6,5 mmol/l), and was left to believe that a heart attack was around the corner, I researched into the pathoetiology of heart disease. I found how the artery was going to become blocked, prior to the looming heart attack. I learnt that high levels of serum LDL in the arteries encouraged the infiltration of LDL particles between the endothelium cells, set up and inflammation process that led to the plaque forming. To a chemist, chemical engineer, software analyst programmer this did not sit well.
Then I developed statin induced T2D. I needed to read up on how is was going to be losing limbs. One description: high glucose (GL) levels => excessive GL in endothelial cells of the capillaries => overstressed mitochondria not equipped to deal with the high GL produce excessive reactive oxygen species which damage the cell. Inflammation process sets in to deal with the damaged cell. If epithelial damage is of sufficient size and persistence the efforts of the immune system may lead to blockage, this leads to oxygen starvation of surrounding cells => more inflammation and damage => infection => gangrene etc.
All this seemed a more reasonable explanation for what was happening in the heart than the the infiltrating LDL. Glucose was the problem. But why were coronary arteries so susceptible?
Then came the E M Forster moment: I read some work by Uffe Ravenskov. He pointed out that arteries have a capillary blood supply in their walls feeding the smooth muscle etc. ** POW** If something damages the epithelium in these narrow capillaries, be it glucose, or infection (as Uffe Ravenskov describes) we have the same ischemia (oxygen starvation) as in the peripheral capillaries => inflammation => plaque.
I have since moved on a little from this scenario . . . but for a couple of days now I have been toying with trying the elevator test.
The following may distress you, terrify you or simply confirm your suspicions:
Click to access footnotes_nov14.pdf
Thanks Eliot I’ll give it a try.
It does not distress me and is just another nail in the over medication problem that has been driven by people wanting the latest and greatest pill fix snd the pharmaceutical money tree.There are many medications that are life saving or offer a better quality of life and many reponsible doctors prescibing and this is good medicine. However I am on the dishing out end and it saddens me sometimes.
Hello Anne Lucas
Sometimes talking to people, I have the impression that they think there is pill for everything, and as for exercise, or buying real food, it is either too expensive or takes too long.
Sociology has always (?) been considered a “soft science” but to me “good” sociology based on relevant “observational” evidence is as much “hard core” science as I have found in my own discipline of metallurgy.
The article “The Epidemic of Sickness and Death from Prescription Drugs” you linked to fits so well with this view.
Could it be that the article fully confirms my present view of the total corruption in the medical field I have developed now during 17 years?
Is your mitochondria ROUNDUP ready?
What is best way to die, CVD, cancer or dementia?
Root cause of all is mitochondrial dysfunction. No ATP = no vitality = loss of function
-medications, statins, aspirin etc
-antibiotics, fungicides, herbicides, bug sprays, preservatives
-mercury, lead, aluminum, cadmium
I agree with the Roundup issue. Too much is used these days and even I have been guilty of this to get rid of weeds in my garden. We don’t use it now but unfortunately my husband sprayed round our fruit trees and it has changed the way I view my organic garden.
How are the mighty fallen! Glyphosate used to be regarded as less toxic than the detergent it was mixed with. It was even recommended as causing less damage to the soil structure and inhabitants than digging or ploughing.
I have argued on various forums against the use of glyphosate, and suggested anyone thinking it is “safe” should do some research. I was banned from a UK allotment forum for getting rather short (but certainly not abusive) with the allotmenteers who were convinced it’s use was “safe”. Since one of its effects is essentially an antibiotic they really ought to comprehend what the over use of such substances can do, and what it is possibly doing to them when they eat the crops. Never mind, it is now used in the UK for a spray on wheat shortly before harvest to desiccate the remaining green bits. So eat up your sandwiches……………………
AH Notepad: Yes, glyphosate is a very dangerous chemical which never should have been approved. Not just your sandwich, but how many items on the grocery store shelves contain wheat? The majority. And conventional meat, dairy and eggs, since soybeans are part of the feed for all of these animals. Brazil recently surpassed the U.S. in pesticide tonnage; Brazilian soybeans are grown for the European market. Nearly all of us likely have glyphosate in our systems regardless of how careful we are. Bayer/Monsanto is happily poisoning all of us.
Thank you for this information Gary. Will my current 12-15g/day of vitamin c mitigate against this?
Something I forgot to mention is that glyphosate chelates minerals in the soil, making them unavailable for plants to take up, and so they will not be available in the food you bought because you thought it would give you the minerals you need. A soil analysis might show the minerals were there, but not show they wern’t available to the plants.
I seem to recall that glyphosate was originally used to clean out pipes, chelating the minerals. It was then patented as an antibiotic before being developed as Roundup.
Yes, it was used as descaling agent to clean pipes, if I remember correctly. It binds metals. Plants use enzymes that are metalloproteins, they have a metal as part of their structure. Round Up interferes with their functioning. Apparently, gut bacteria in humans use similar enzymes.
Sasha: Yes, glyphosate functions by blocking the shikimate pathway, which our human cells don’t have, but our trillions of microbial cells do. Since it is now known that our gut microbiome is in continual communication with our brain, through the vagus nerve, and is critical to brain function, perhaps even choreographing brain function, its no wonder that it is so damaging.
Yep, brain function, immune function and who knows what other functions. Sometimes I wonder where it’s all going to get us…
Yes, via the Shikimate Pathway in the gut microbiome.
Amazing, a reference would be useful for this.
I think I saw some info on it in the book GMO Deception and then followed up on people’s names with YouTube videos. Some good scientists are saying some scary stuff… And I doubt Vit C can mitigate the damage unless it helps gut bacteria regenerate which is possible, I guess. But how do you reverse the process in which enzymes responsible for their physiological functioning are incapacitated?
AH Notepad: Yes, glyphosate specifically binds manganese. We don’t need much of it, but Mn is an absolutely critical mineral for biological function. The targeted “weeds” have adapted, and glyphosate is becoming less effective. Because of the expense of having to use more of it, or more potent combinations, some farmers have stopped using GMO seeds altogether.
Wondering now about my “Bad List” and if it is ever to be an end to it.
This very morning I received a note that a Swedish GP has been suspended after having supported Lyme disease victims in violation to the official “rules” by prescribing too long time antibiotic treatments.
It is a fact that my family is surrounded by nature with many deers entering our garden and with the associated ticks and all of us were unknowingly hit by the Lyme disease carried by these tiny creatures about ten years ago. (Today we are more on the alert!) Our cat succumbed to the disease although the veterinary categorically stated that cats do not acquire the Lyme disease. With us paying for the test she returned and confirmed the fact. (I thought previously the veterinaries were more to trust then MD’s:)
So, we all had the standard time limited antibiotic treatment and although the cat succumbed my wife fully recovered with this treatment while I myself was only partly (roughly 50 %) recovered. It was my right shoulder which had been incapacitating me for years but with the antibiotics it dramatically improved during the very first day of treatment.
Being a researcher and already sceptic to all dogmatic statements from our health care system i did my homework and realized that there was not very much science as I understand it behind the official dogmas and then I got in contact with alternative medical sources (ILADS http://www.ilads.org ) in the US and was prescribed an extended antibiotic treatment and with that treatment I haven’t had any more problems now for ten years.
It is perhaps understandable that medical practices today seem to me to be more about religion than science.
In light of yesterday Wikileaks release of CIA information, if you have not read it already you might enjoy the book Lab 257. It’s a circumstantial book on where Lymes disease came from. I’ve seen one doctor speculate, after reading the book, on why doctors loose their medical license for over prescribing antibiotics for Lymes disease. I’m not sure I entirely agree but the book make for troubling reading.
Lab 257: The Disturbing Story of the Government’s Secret Germ Laboratory Paperback
This was in now Sweden and in the US it was evidently a little more “freedom” among the GP’s who did not line up, at least ten years ago.
And, of course, I don’t doubt for a minute that there are secret “germ activities” under military umbrellas. During my mandatory service time in the military I actually was picked for special training and deep looks into all nasty innovative ways to kill people by nuclear, biological and chemical means. They evidently saw my potential 🙂
However, regarding Lyme disease they have found the bacteria involved in a guy, (Oetzi), who was buried in a glacier is Switzerland during the bronze age but showed up rather recently so here CIA must be innocent. On the other hand it wouldn’t surprise me the least if the have worked out “improvements”.
I suspect that lyme disease could be treated by vitamin C, as can many other diseases. It is possible to obtain treatment in the US because there are enough physicians who have stepped out of line. It is possible to obtain vitamin C treatment in New Zealand as they have rewritten the rules so it is now a required treatment if the patient requests it. The UK is comparatively still in the dark ages. This paper should give some hope to those seeking vitamin C treatment
which I found from a video of Suzanne Humphries at about 58 mins. The theory is that it should be enough to ease the worries of physicians who might consider such treatments.
Looking forward to the next one
Levy MD JD, Thomas E. Stop America’s #1 Killer!….
Inflammation and Vitamin C Deficiency: A Probable Mechanism for Delivering Vitamin C to Deficient Arteries
Inflammation also appears to be a major player in the development, progression, and ultimate destabilization of atherosclerotic lesions, ultimately leading to the complete obstruction of an artery (Yu and Rifai, 2000; MacCallum, 2005; Boos and Lip, 2006). Becker et al. (2001) and Corti et al. (2004) have noted that plaques prone to complications — such as sudden complete obstruction — contain large numbers of inflammatory cells, while stable plaques that have a lesser complication rate have less evidence of inflammation.
Inflammation is defined as a protective response to the injury or destruction of tissue, aiming to lessen the injuring agent and wall off (isolate) the affected area. In addition to causing other effects, inflammation also serves to attract white blood cells to the site of damage.
He also raise the interesting point on the epicardial arteries and the intramyocardial arteries; the latter rarely if ever are subject to arteriosclerosis being protected from the damaged caused by high blood pressure by the heart muscles surrounding them.
This all seems to fit in with Dr Kendrick’s hypothesis of inflammation as a cause of arteriosclerosis.
Apart from one thing. I think that inflammation is the body trying to repair itself, so it does not cause anything, but occurs ‘as a result of’ underlying damage.
Levy is saying that the underlying damaged is due to “focal scurvy” and provides evidence of Vit C deficiency in the lesions. Some of the references go back decades.
I go with atherosclerosis arising as the result of inflammation processes following some epithelial insult; however, on the damage caused by high pressure, a priori, one would expect the surface epicardial arteries (in one of which I presume my stent sits) would be under less pressure than the intracardial arteries. The embedded arteries would be under compressive forces from all sides.
I have not come across the 2 categories of arteries until your comment, and it has given a lot of food for thought, and made my ideas on the possible cause for atherosclerosis a bit wobbly. My pet scenario explaining why the heart and carotid arteries seem particularly prone to atherosclerosis centres on these vessels being under under exceptional pressure; the idea that intracardial arteries are not as prone to atherosclerosis, when one would have thought that they too should suffer the same if not greater pressures weakens that notion.
Oh dear . . . back to the drawing board.
(Do we actually know what the pressures are in these arteries? – Is there actually a correlation between the pressure in the body’s arteries and the level of atherosclerosis risk?)
(As I write, I am wondering if the difference in the situation of the 2 types of carotid arteries lies in the amount the artery is free to distend. Perhaps significant movements somehow facilitate the development of a plaque ? – Does the carotid artery also have the opportunity to distend?)
Welcome to the journey. Perhaps you can research something that I cannot find an answer to. Why does atherosclerosis not form within the heart itself- where the pressure and turbulence is at its greatest. My assumption is that there is no Tissue factor in the heart, but if anyone has researched this – I cannot find the answer. [If true, it could also be why intracardial arteries do not develop atherosclerosis].
Doc, do you mean to say that the clots that form in the left atrium, and the left atrial appendage in particular, coincident with atrial fibrillation, are not due, in part, to Tissue Factor?
Yup. These clots are created by the internal clotting factors. Which is why warfarin works so well, and why warfarin is not particularly good at stopping MIs.
Does the ineffectiveness of warfarin on MIs hold true for the NOACs as well?
“The embedded arteries would be under compressive forces from all sides.”
Damage could be due to friction from turbulent flow. That depends more on the geometry than pressure, so it should matter less whether the artery is inside the heart or external – twists turns, changes in diameter or branches will all cause turbulence.
Another and possibly more significant route to damage is strain on the vessel – i.e. pressure (stress) leads to deformation (strain) according to the elastic properties of the muscular vessel wall *and its surroundings*. In this case the support from the bulk heart muscle should help constrain the vessel.
I imagine the fatty deposits around the hearts of healthy animals (I see them before cooking them, e.g around organic grass fed lambs hearts, which I take to be healthy) are indended to both relieve the strain and to reduce shock on the external arteries particularly where they are the immediate vicinity of the myocardium If I were trying to reduce shock at the point where the arteries leave the heart I’d put a material there that would provide damping (lose energy to heat), dense saturated fat is probably well suited for that purpose – it has the right feel to it.
Ken Strain: Thank you for that explanation. I cook beef heart frequently, and it always has a thick layer of fat covering the upper part. It has different textural characteristics than fat of muscle tissue, smooth and fine-grained, with rippling on the surface like ice sometimes has. Tasty, too.
The arteries must expand slightly under pulse pressure. The ones within the heart muscle would expand less, being supported by the surrounding muscle tissue, as you say.
What interests me is, if you treat the cells of the endothelium like a mosaic lining the artery wall, do the little mosaics themselves stretch as if made of rubber or gel, or do they rigidly maintain their size and the gaps between them open up a bit? According to Dr. Levy the “grout” between the cells loses its gel-like nature and becomes watery if there is a local deficiency of vitamin C, leading to leakage and plaque formation.
Another thing: The cells of the endothelium must renew themselves like all cells. But stripping out the old cells and putting in the new ones sounds like a tricky operation, rather like replacing a fuselage panel on a jet plane while it’s flying. Presumably they all renew and replace at different times according to their own internal clocks, but statistically it must happen that occasionally all of them in an area will renew at once, leading possibly to leakage and plaque formation purely due to bad luck, not any other factor.
A third thing: How do arteries at joints like elbows and knees maintain integrity? It’s like repeatedly flexing a bit of wire — at some point it’s going to break, yet they never seem to. I wonder what the secret is?
I don’t have good answers to most of your questions (I’d be guessing). This point “But stripping out the old cells and putting in the new ones sounds like a tricky operation, rather like replacing a fuselage panel on a jet plane while it’s flying.” is a very good one. Again I certainly don’t know for sure, but I would expect the progenitor cells in the artery wall replace those in the endothelium. As you point out that’s a delicate process with blood rushing past.
Progenitor cells are produced in the bone marrow and travel about in the bloodstream. As far as I am aware, they do not exist in the artery wall.
I put a reference about stem cells in the artery wall in my response at 7:43pm on the 12th. I’ve still not read the paper properly, however, despite the intriguing abstract. (http://dx.doi.org/10.1155/2014/701571)
Accepting that the EPCs are mostly or even all transported in the blood from a distant site, that does not of itself determine whether they do their job from one side or the other of the boundary of the lumen.
Is there evidence that excludes endothelial repair from the region of the vasa vasorum, thus forcing all repair to take place from within the lumen?
More on the source of new cells. The editorial at http://atvb.ahajournals.org/content/30/10/1877 “Neointima Formation A Local Affair” by Virginia J. Hoglund, Xiu Rong Dong and Mark W. Majesky discusses exactly the “controversy” of where the progenitors come from.
I quote from the editorial ” a careful and detailed study by Daniel et al seems to leave little or no room for a role of bone marrow–derived cells as progenitors for the intimal SMCs and endothelial cells that are stable residents of a mature neointima that forms after acute vascular injury.”
I’ve not had time to read the Daniel et al. study in depth – it is substantial. I am a little concerned that the type of injury induced might be artificial and different form the usual damage that leads to atherosclerosis. It looks as though in some circumstances the cells do come from bone marrow, but not as frequently as was once “hoped” (by those interested in drug discovery, at least).
I’m not sure that the Daniel study itself says as much about endothelium as it does about smooth muscle, but reference 6 concludes : “Circulating EPCs rarely, if ever, contribute to plaque endothelium in apoE -/- mice. These findings bring into question the prevailing theory that circulating EPCs play an important role in atherogenesis”
All of these are open access.
Dual role of circulating endothelial progenitor cells in stent struts endothelialisation and neointimal regrowth: a substudy of the IN-PACT CORO trial.
De Maria GL1, Porto I2, Burzotta F1, Brancati MF1, Trani C1, Pirozzolo G1, Leone AM1, Niccoli G1, Prati F3, Crea F1.
Endothelialisation is a crucial event after percutaneous coronary intervention (PCI). Endothelial progenitor cells (EPCs) are bone marrow derived elements with reparative properties. We aimed to assess the relationship between circulating EPC levels and stent neointimal hyperplasia (NIH) using frequency domain optical coherence tomography (FD-OCT).
Patients undergoing elective PCI to native vessels and randomised to bare metal stent (BMS) alone versus BMS plus drug coated balloon (DCB) were included. At six months, angiographic follow-up and FD-OCT were performed to measure percentage neointimal hyperplasia volume obstruction (%NIHV), and percentage of uncovered stent struts (%US). Venous blood samples were obtained before the procedure and at six months to detect CD34+CD45dimKDR+ EPC levels.
Twenty patients were enrolled. A significant relationship was observed between baseline EPC levels and %NIHV (R: 0.63, p: 0.03) and %US (R: -0.56, p: 0.01) at follow-up. Both EPC levels and DCB use were independently related to %NIHV (β: 0.55; p < 0.001 and β: -0.51; p: 0.001, respectively), while only EPC levels were independently associated to %US (β: -0.52; p: 0.01). Higher %NIHV (p: 0.004) and lower %US (p: 0.005) were observed in patients with stable or increasing EPC level.
Our study shows a relationship between EPC levels and stent strut coverage, supporting a dual role for these cells in favouring stent endothelialisation but also NIH growth.
I had to wait till this morning to download that paper, which is interesting, for sure, and seems to be of very high quality.
We should never be surprised by the complexity (evolution tries every option given time). Clearly the idea remains controversial (from either side of the argument). As noted in the paper “Whether this endothelial coverage derives from the seeding of progenitor cells flowing in the blood stream and, or from mature endothelium lining the vessel wall adjacent to the stented
area, however, is controversial. Experimental models of vascular injury
have shown that bone marrow derived mononuclear cells home to
areas of endothelial denudation and accelerate endothelialisation
So there is experimental evidence from both sides, and uncertainty. The authors are modest enough to state that their paper is hypothesis raising rather than definitive.
My guess would be that both mechanisms operate under different circumstances (depending on the degree of injury, timescale, general health, inflammation, and who knows what else).
I would once again suggest, however, that the source of EPCs does not constrain how the repair process proceeds – that is a separate question.
I will disagree on this. It is, I think, a critical point. It was thought, for years, that damaged endothelium was repaired from endothelial cells adjacent to the damage. However, mature human cells cannot replicate, or split in two. Equally, if EPCs are present in the vessel wall, they can only have come from bone marrow, as they are non-differentiated cells, such that are one (can only) be produced from Stem Cells which, in turn, are primarily present in bone marrow. This is why EPCs can grow into monocytes, macrophages and/or mature endothelial cells. Which means that endothelial cells, basically, blood cells, that happen to stick to the vessel walls to line them.
Ken Strain: What I thought was odd was that they began discussing intimal smooth-muscle cells, which later became a discussion of endothelial cells, which I don’t believe are the same thing. In any case, I found this confusing.
Indeed there must be stem cells, which is why I was attracted by the first reference from a few posts above (http://dx.doi.org/10.1155/2014/701571), from which:
showed that a population of stem cell antigen 1 (Sca1)–
positive cells in the adventitia (AdvSca1) could be isolated by
immunomagnetic selection or fluorescence-activated cell
sorting for Sca1 expression and found that a significant
fraction of these progenitor cells differentiated into SMCs in
vitro. These AdvSca1 progenitor cells clustered in the border
region between the media and adventitia.”
So there appear to be hematopoitic stem cells not only in marrow, at least in mice.
That’s more than enough from me on this topic.
I look forward to seeing the evidence for the bigger point about how the EPCs and other cells get to their final location in the new tissue (wherever they start out from) That seems to be an open question, or did I miss the answer?
Thank you Dr. Kendrick for your great effort in searching for causes of CVD. A hole in the artery causing plaque is the reason that I have adopted a high fat, adequate protein, low carb diet.
My simple (under one minute) understanding of a complex problem
1. high carb intake > hyperglycaemia > limits uptake of vitamin C
2. vit C deficiency > scurvy > loss of collagen > weak artery
3. crack in artery > tissue factor in sub-endothelial cells + contact with blood plasma = coagulation cascade, thrombin formation and crack repair
Hyperglycaemia also causes mitochondrial oxidative damage leading to endothelial cell apoptosis i.e. hole in artery wall.
The hypothesis seems to be standing up well to examination by the forum participants. Any doubts on your part Dr. Kendrick? What would it take to declare victory and move on to a new topic?
I welcome all attempts to find the critical flaws in this hypothesis. However, I am somewhat preaching to the converted here. I need some more powerful attacks.
I wonder if you, in your model, could incorporate acute MI events relating to the “out of balance” between the sympathetic and the parasympathetic nervous system as manifested by the heart rate variability noted at the actual events.
Of course it does. The actual MI is often unrelated in time to the clot. It is when the myocardial cells die, and that is not necessarily directly related to the blockage.
More powerful attacks, Dr K? God forbid! We fear for your head above the parapet as it is! I have a pet theory, which of course will be dismissed as a conspiracy theory, that every few weeks the pharma and packaged food and sugar drinks companies search out and pay trolls to shoot proponents of hypotheses like yours, (and of LCHF, research that comes down against HCLF, reversal of diabetes on LCHF, etc) down in flames. Sometimes, as recently on this blog, the target is missed, when the trolling was aimed at LCHF, which you do not espouse particularly, as your site is at the moment dealing with the causes of CVD. I notice that such attackers usually take themselves off in a huff, though I think you had to ask one nutcase to remove himself, as he was becoming a right nuisance. I think you have lots of powerful intellects posting on your hospitable site, questioning and searching, pushing for the answer. It’s a joy to watch it all unfold…
I doubt it’s a conspiracy theory, it’s called “reputation management”, I think, in the professional circles and it exists… Also, trolls are usually more convincing than John Bedson was. Either that or we are getting better…
I like to let everyone come, and put forward their arguments. It is difficult when they refuse to engage, but hey ho. You cannot say that I do not try to give everyone a chance.
Thank you for this “incorporation” though why the myocardial cells typically die in the early morning hours then begs the question.
Though in my own case that happened early in the evening.
I’ve seen on the internet some people posting this video on the cause of heart attacks. It was created by a Dr. Knut Srota. He does not seem to believe that blood clots are responsible for heart attacks. The video can be seen here:
Here on this sight I’ve some posting Dr. Thomas Cowan’s new book on heart disease. He builds upon Dr. Srota’s writings. Dr. Cowan’s has some articles on the WestonPrice sight, with one being seen here. He believes heart attacks are caused outside of the arteries.
“What Causes Heart Attacks: Part Two”
I guess, what are the argument(s) against the above posted theory?
On Göran’s question on MI: I am comfortable with Malcolm’s separation of cardiovascular disease (CVD), and the myocardial infarction (MI)
My issue is in clarifying what we call a heart attack. A few years ago I had a very bad virus (cold?) to the point that I took time off work for the first time in over 15 years. During this time my heart started missing beats. (They called them PVCs) – usually every 8 beats, but it could get up to every other beat. It seemed to wane as I recovered, but returned when I did something strenuous, or was stressed at work. Couple of months later the arrhythmia came back more persistently – Doctor: ”Your hearts all over the place”. Then months after that I went for a walk – which I ended up doing painfully slowly, I was weak and felt sick, heart rate was high, missed beats. I was sent to hospital because they thought I was having a heart attack.
Turned out I was not – no high levels of troponin. A similar episode occurred 8 months later. Virus infection followed by 2 weeks of indigestion pains in the chest which Rennies did not cure; then in the middle of the night, heart racing, thumping in the temples, missing beats all over the place; ambulance to Leeds Coronary Care unit. Verdict: no heart attack, no clots, no blockages. What they did say was that fluid in the pericardium suggested an infection.
So, I am now inclined to see the many heart attacks involve the electrical disruption of the heart causing disruption of the heart’s blood supply. This may be compounded by unstable atheromas bursting under the disruptive/disrupted beating?? and subsequent clotting would not help.
What causes the disruption . . . could be stress or excitement – high cortisol levels and issues with the sympathetic nervous system or . . . infection damaging the heart – eg the ventricular septum where some of the electrical function is centred (came across this a couple of days ago). . . . or blockage of the blood vessels causing ischemia, damaging the cells involved in regulating heart rhythm.
(I have read that something like 40% of heart attacks do not have blood clots associated with them and came across the proposal that most blood clots observed in heart attacks were produced after the MI event.)
As far as the travel insurance people go I have never had a heart attack . . . but under the above definition I have had 3 . . but got away with each of them.
Complicated, ain’t it. All myocardial infarction are ‘heart attacks’, but not all heart attacks are myocardial infarctions. Actually most myocardial infarctions do not cause heart attacks, they are silent and pass unbeknownst to the victim. Or, the heart muscle can be stunned and go into hibernation. Or you can get Takostubo…. over the past few years, physicians have come to recognize and better understand another form of heart attack. This unusual type of heart attack does not involve rupturing plaques or blocked blood vessels. It is called takotsubo cardiomyopathy, or stress cardiomyopathy. Japanese doctors, who were the first to describe this condition, named it “takotsubo” because during this disorder, the heart takes on a distinctive shape that resembles a Japanese pot used to trap an octopus. The disorder was commonly believed to be caused by sudden emotional stress, such as the death of a child, and to be far less harmful than a typical heart attack. For that reason, some had also labeled this condition “broken-heart syndrome.”
I could go on.
Your Point is well taken
NICE guidance on diabetes. Not for me. It is based on seriously flawed dietary, nutritional, biochemical and metabolic processes.
Thank you for the NICE guidelines link, Mike. Not for me either! What a load of repetitive codswallop! My A1C is below those guidelines and I keep my T2 under control with a LCHF eating pattern. The recommendations are entirely aimed at high and increasing levels of pharmaceuticals, with diet guaranteed to make the patient worse and to need more drugs to treat the deterioration. If more diabetics knew how to control their blood sugar and insulin properly a great deal of NHS money could be saved. To say nothing of misery…
“Then months after that I went for a walk – which I ended up doing painfully slowly, I was weak and felt sick, heart rate was high, missed beats.”
What you describe here is a virtual portrait of my experience of a few years ago which turned out to be paroxysmal atrial fibrillation. It came on for an hour or two at first. The episodes were always over by the time I got to an ECG. I suggest you bring your docs up to speed on this possibility. (They’re getting more aware, but it can still escape them.) Ask for a Holter monitor, which is a small 24 hour ECG devise that you wear, or an even smaller Zio Patch for 2 weeks. They record every second of your electrical activity for period you wear them. It would be good just to know for sure.
Atrial fibrillation associates with increased incidence of stroke and, unless you take up substantial life-style changes, usually gets worse over time.
(Don’t ask the cause. The only honest answer is “Dunno. Not yet, not fully.”)
This is not an attack, but I am trying to reconcile your theory with the many illustrations if you google “atherosclerosis progression” that show a slow build-up of plaque with a clot forming as the grand finale of the process when the plaque explodes like a kind of Vesuvius.
Your theory seems to account for the slow build-up phase, but not calcification or rupture.
Also an unrelated question, how does the body sense it needs to send out collateral vessels and why do they not grow fast enough to cope with arterial narrowing?
Thank you for questioning my ideas. I think the final event is often a final, fatal, blood clot. This can be due to plaque rupture – which released many pro-thromobic elements into the blood. Why does the plaque rupture? Some think due to cholesterol crystals acting to erode the ‘cap’ on the plaque. Others think otherwise. I think this event fits fairly simply into the clotting hypothesis. As to calcification. This is often what happen to areas of ‘injury’ throughout the body. Scars on the skin often calcifiy – to a lesser or greater extent. Vitamin K(s) seem to stop this happening, to an extent. Which is why warfarin appears to accelerate plaque calcification quite rapidly.
Dr. Kendrick: Also, I think his question about collateral veins was answered earlier in the series; that we are born with them, and they develop as needed, as the cardiac arteries narrow. Correct me if I’m wrong.
Antony, I take magnesium citrate powder for PVCs. Works pretty well. I take 2-3 grams twice a day. YMMV.
I was thrilled by reading K. Sroka’s 2003 paper on how the MI events were so strongly associated with the “electric circuiting”, i.e. internal special nervous system in the heart, and especially the Heart Rate Variability (HRV) issue. The almost exact moment of the MI was so strongly coupled with the lowest HRV for reason which I though couldn’t understand rather than it had to do with the sympathetic/parasympathetic balance the latter being almost non-existant at that moment.
My natural question was then how the internal nervous system of the heart was “governed” by the vagal nerv connection.
Then I by coincidence had the opportunity through an acquaintance to get connected to a heart surgeon with extended experience and who also happened to have produced a Doctoral Thesis om arterial fibrillation and rather recently. Well I had great expectations before meeting a person who must be a “great” expert on the nervous system of the heart and to discuss Sroka’s paper.
To my utter disappointment this guy didn’t have the faintest idea of what I was talking about.
My disregard for “medical experts” then hit an all time low at that very moment of meeting. My suspicion is that these “experts” are really not interested in their own profession and at least not in any “new approaches”.
In an attempt to deal with the PVCs (pre-ventricular contractions) . . . for those that have not had them, it is a bit like a car engine mistiming and reducing the pumping efficiency of the heart . . . I was given an ablation! A very competent doctor/surgeon, through a catheter, zapped the areas inside the heart that he observed were causing the PVCs. The airiness in the chest disappeared, the PVCs disappeared, and I hadn’t felt so good for 2 years. They came back 2 weeks later along with the stress airiness in the chest. I now suspect that the biggest effect of the treatment was the anaesthetic given for the actual zapping. Reduced the cortisol levels temporarily?
A couple of months later I had a ‘turn’ . . . taken to hospital with a suspected heart attack . . . but all they found was evidence of possible infection of the pericardial sack surrounding the heart. Later I did find references to pericardial infection influencing PVCs (The pericardium appears to be attached to ventricle area of the heart)
I declined an offer of a second ablation because I felt the PVCs were getting less frequent – felt I was getting ‘better’ in health generally. It took about 6 months for the PVCs to go altogether. I suspect that it took that long for the infection in the pericardium (and heart? ventricular septum?) to be dealt with.
On the other hand, I am now intrigued by your comment on how magnesium citrate helped you in your version of PVCs . . . oh no . . I cannot open another strand of research!
Antony, I’ve tried many different techniques for PVCs. Some people have results using l-arginine and taurine. I have tried those. I’ve also tried many different magnesium supplements. My favorite so far is magnesium taurate, which is magnesium + taurine. Some of them cause intense diarrhea. Try them carefully. For me, I’m not sure what helped the most. I found l-arginine (and perhaps taurine) can make my blood pressure too low, so I only take it periodically now. Magnesium also seems to cause me issues now; I feel as if I’d had enough. What I think happened is that 3+ decades of eating low fat, high carb depleted my body of vitamins and minerals. It’s taken me 3+ years to recover from that. (Went from high carb to low carb, and now low fiber and high meat.) Due to Dr. Kendrick’s discussion of Vitamin C, I started taking that, as I have a “high” Lp(a) level (also started taking l-carnitine). The problem is that a single large dose of Vitamin C makes me feel as if I’m OD-ing on vitamins. Perhaps I’ve also caught up there, and since I eat very few carbs, maybe I don’t need huge doses of Vitamin C? I’m not sure.
In the 3+ years I’ve been trying low carb, then paleo, then back to low carb, and now ketogenic diets, my PVCs went from way too many to basically zero. I should note that I have heart failure, which was diagnosed about 6 months before I sent low carb for good, so I’m also taking an ACE inhibitor and a Beta blocker. I’m sure those helped. Losing 55 pounds also helped. A ketogenic diet also helps, as supposedly the heart prefers ketones as a fuel, and heart failure is theorized to be caused by/exacerbated by insulin resistance and a failure of glucose metabolism. I’ve definitely decreased my insulin resistance.
I should also note that I decreased my exercise from 4 days/week to 3 to 2 and now to 1. Search for “Body by Science”. I go to the gym one day per week, and spend 35 minutes there (and could spend less than 20, but I do extra rotator cuff and back exercises). That’s it.
BobM: I think you’re right about exercise (meaning strenuous exercise), that 1 or 2 days a week is best, although being physically active the other days is important, too. I try to do mobility exercises (which is my warmup for the strenuous stuff) every day.
People who have had a heart transplant don’t have a nervous system connection to the brain because they can’t rejoin the vagus nerve. But the heart has its own pacemaker and starts beating by itself when they jump start it, only a bit faster than usual. It can’t react to nerve signals but can react to hormone signals in the blood e.g. adrenaline.
This makes me wonder if a test of Dr. Srota’s theory can be made by observing transplanted hearts.
In the case of spinal cord injury the sympathetic (exciting) nerves are cut but the parasympathetic (relaxing) nerves are not cut, causing low blood pressure and heart rate. If Dr. Srota is correct, this also means low risk of heart attacks for those with spinal cord injury. Don’t know if this is true.
Info from Reddit: https://www.reddit.com/r/askscience/comments/14a2m3/how_do_surgeons_connect_nerves_to_donated_organs/
It depends where the spinal cord injury/fracture occurs. Also, how much damage is done to the sympathetic and parasympathetic nerves. In general CVD rates are very high in those with spinal cord injury. I looked at this in great detail a few years ago and I was unsure how to piece it together. The problem with transplanted hearts is that you have to factor in the host immune response. The form of arterial thickening in transplanted hearts is usually very different to classical atherosclerosis – if memory serves.
“magnesium supplements… Some of them cause intense diarrhea.”
There has been so much talk of magnesium among commenters on this site that I decided I had better take some extra magnesium, despite having no symptoms of magnesium deficiency. Being on a tight budget I looked around for cheap magnesium. Magnesium sulphate fitted the bill — good old Epsom Salts.
I wasn’t sure how much to take at first, and soon learned the phrase “goes through you like a dose of salts” has a very real physical meaning. That stuff can ream your bowels out like little else.
With a holy respect for the power of salts, I now take my magnesium via a tablespoon of Epsom Salts in a hot water foot bath once a week. I have no idea if it does me any good, but it’s a very restful experience.
Incidentally, on learning that garlic is an anti-fungal, I chop a couple of cloves of garlic into the foot bath. It helps to control my athlete’s foot.
I think you could use sodium ascorbate, brine, or vitamin c for athletes foot tooo. That would not be as smelly as garlic and would not put people off talking to you to the same extent. One problem with killing things that live on your feet could raise problems if the protective organisms are killed.
May I suggest that you make magnesium oil? Take an equal amount of Epsom salts and water and heat it until the salts dissolve. Leave to cool, then pour into a spray bottle. Spray on your skin – excellent for controlling and preventing leg cramps, and for getting magnesium supplementation without causing gut havoc!
I tried the “magnesium oil”. It made the skin horribly sticky, even with light applications. I could not tell if there was any benefit, so I stopped using it.
The third commentator referenced plaque classification. The first stage is artery wall thickening and final stage many decades later is the mature plaque that fits the description of plaque formation by endothelial injury and coagulation. My belief is that the initial stages are due foam cell accumulation below the endothelium. Macrophages + oxLDL. Probably does not matter how the LDL ended up in the sub-endothelial space. Foam cell accumulation will shift some cells away from capillary blood source and induce hypoxia leading to cell apoptosis, necrosis, migration of smooth muscle cells, angiogenesis,inflammation etc.. Erosion of plaque periphery by macrophages exposes the newly formed capillaries to clotting factors. The blood clots will be small and heal over and progress similar to tree rings. Stopping the progression will stabilize the plaque. Actively growing plaques will be vulnerable to rupture resulting in a big clot.
The type of plaque you are describing can pop up anywhere in the artery unexpectedly where the endothelium damage exposes tissue to blood clotting factors. This fits with blood clotting theory. The progression from small to big plaque is missing.Deadly clots can form in areas with little plaque buildup so this is not essential. No theory can explain everything.
if only someone would listen. I am just a nobody but it seems to me when they put the stents in my family member, it wasn’t the stent that worked but the BLOOD THINNERS.
I would like some input on stent insertion especially the new drug eluded stents that carry chemotherapy to the site. It seems to me that damaging the endothelium is not such a great idea let alone the side effects systemically.
Dr Kendrick, I wonder if you could tell us a bit about where you stand on blood pressure with respect to heart disease. There is plenty of disagreement out there now. It should be below 120/80 always! No, there is a J curve! No, it’s fine for seniors if they stay under 150!
Well, that’s all while sitting in a comfy chair all relaxed, not as it varies for differing needs over the day.
Under what circumstances does BP contribute to endothelial damage and clot forming?
Here is another little book on what initiates the zinglammatory process. The Origin Of Artherosclerosis – Kenneth Kensey MD and Young I Cho. PhD. Concepts discussed are sheer stress in blood flow and whole blood viscosity worth a read.
I mean inflammatory. It has some zing but no glamour.
For what it is worth Kensey also has another book called The Blood Thinner Cure. focuses on 7 steps one of which is blood donation to reduce viscosity. Sort of explains the eskimo nose bleeds and also why menopausal women have more risk of heart attacks. It’s the bleed that is important not taking blood thinners.
“The Blood Thinner Cure condenses decades of medical research on heart diseases into an easy-to-understand explanation: injury-producing blood flow is what damages the arteries. The well-researched solution? Thin the blood so that it doesn’t injure the arteries in the first place. Based on these results, the authors have created a simple seven-step lifestyle plan that involves regular blood donation, extra fluids, and sensible lifestyle strategies.”
Thin the blood so it doesn’t injure the arteries in the first place… ho, hum. They obviously worked that one out.
So, “thinned blood” – presumably meaning under the influence of some sort of anti-coagulant?
Is that what keeps Olympic weight lifters (BP 300/265 during a lift) from MIing out on the medal stage?
I would not use the phrase ‘thinned blood’ as it has no real meaning. If someone means reduced coagulability, that is a bit better. As an aside people with haemophilia (prior to widespread use of synthetic clotting factors) had 1/5th the rate of CVD of the surrounding population. Those with antiphospholopid syndrome (Hughes syndrome) where the blood is more likely to clot are far more likely to die from CVD (strokes mainly). Olympic weight lifter are more likely to blow out an artery in their brains than have an MI. Although I cannot imagine putting that strain on the system can be highly beneficial in the long run.
Just ran across some “news” from 2012 about desmosterol’s role in clearing macrophages from the arteries. Desmosterol is the penultimate step in the creation of cholesterol. Macrophages are the garbage collectors in the arteries. They are supposed to consume other cells and junk and then dispose of it. Desmosterol helps with the disposal. Guess what – statins jams up the creation of cholesterol upstream so it also lowers desmosterol (as well as CoQ10, squalene, etc)
Here is a link:
This fits Dr K’s theory, except instead of the clots forming too rapidly maybe it’s a case of not being cleared out fast enough.
Indeed. A dynamic process. If clots form too fast, you have a problem. If clots are cleared away too slowly, you have a problem
I have never been a fan of Statins. Always suspicious of a drug that cuts off other pathways. It’s like cutting the whole tree down instead of pruning the branch. The body is an amazing machine geared to maintaining homeostasis. The pathways are there for a reason.
Anne…perfect analysis. I am always suspicious of prophylactic meds of all sorts, including some (but not all) vaccines. Statins are at the top of my list, with anti-hypertensives coming a close second. The NHS would gain by a clampdown on such prescriptions and ultimately concentrate on therapeutic prescriptions…of which there are excellent examples. Big pharma would get an awful shock, though, so it is unlikely to happen.
I am conflicted on the subject of Vit C being so effective in helping prevent or at least mitigate diseases or illnesses whether associated with CVD or other conditions. Somewhere way back in our evolution, we lost the ability to produce vit C, presumably because we were obtaining enough of it through diet. Since hunter gatherers were supposed to be big meat eaters, I would imagine that the amount of vit C obtained from the diet would be small compared with 10g daily which some profess to be protective. How is it then that human evolution lead to us not making our own Vit C if it was so important? Could it be that our recent diet has changed enough that Vit C requirements are much higher cause by something in our diets?
Have a look under the interactions of vitamin C and glucose. My own sense is that you need almost no ‘extra’ vitamin C, if you don’t eat much in the way of carbs. But if you do eat lots of carbs, the vitamin C gets burned up quickly.
Captain Cook illustrated the connection between carbs and vitamin C. Once nutritious pemmican ( fat and protein) was replaced with carbohydrate-rich ships biscuits, scurvey reared its head…..and we have been battling the need for additional vitamin C requirements ever since.
We can learn much from history, if we care to look.
I haven’t found any vitamin c interaction related problems even with large (absolutely huge in NICE terms) doses, where consideration is given to the effects so that the patient is not inconvenienced. I understand IV treatment was not permitted by NICE around 2007, but I don’t know what the current situation is.
What I did find on the NHS website was IMO laughable:
“What does the Department of Health advise?
You should be able to get all the vitamin C you need by eating a varied and balanced diet. If you take vitamin C supplements, do not take too much, because this could be harmful.
Taking less than 1,000mg of vitamin C supplements is unlikely to cause any harm.”
Better spend money on antibiotics and vaccines and procedures, it seems.
Does anyone know a reference for vitamin C practicioners?
Plus some bioflavinoids recycle what vitamin C there is. I can’t remember offhand which but I recall they can be found in multicoloured plants – the New Zealand recommendation was not just for “five a day” but “five colours a day” (salmon and prawns are honorary vegetables due to astaxanthin). Accordingly I dilute my meat, game, fish and poultry with various veggies and berries, as much for flavour as anything else and so far I’m showing no sign of the scurvy dieticians claim is inevitable from low carb diets. Obviously something else they got completely back to front.
On the 5 a day . . . On holiday I was listening to a French phone-in . . . Their topic “5 par jour’. The nutritionist said the 5 should be of different colours. One woman rang in and asked if giving her children a mixture of red peppers, green peppers, and yellow peppers, would count as three of the five. To be honest the women ringing in was clearly having a pop at the desperately sincere nutritionist fielding the questions.
While as Dr K states the glucose and Vit C molecules are very similar there is evidence of tissue Vit C deficiency in various conditions and that this situation can occur in an apparently Vit C normal. Another interesting point is that white cells can have very high concentrations of Vit C.
Another point is that Vit C is an antioxidant and DHAA (the oxidized form) is a pro-oxidant and is involved in the redox system. Glucose is not. Levy has written several books on the subject.
As to huge doses of Vit C have being effective against in fection there is a wealth of research on the sugject. A pubmed search on ascorbic lead to 50,000+ refs and many clinical papers as well. Then came the antibiotics and non-patentable molecules went out the window.
More revealing information, but for some reason I don’t automatically get notified even though when I try to “follow” the message says I’m already subscribed.
I thought the same til I realised Dr K’s notifications were turning up in my ‘junk’ mail. Hmmm, talk about conspiracies….gmail decided where to put my mail. I can tell you though that notifications regarding posts in this forum are THE most important messages I get!
Craig E: Yahoo does the same to mine. In fact, about half of the blogs I subscribe to end up in the junk box, so I just use both it and the inbox. There is dirty business going on with the censorship of information, and Google is a part of it (they handle both gmail and yahoo mail).
Any suggestions where to buy l-arginine and vitamine C powder?
I get mine on ebay. Pick a known brand and a supplier with a good feedback rating.
Christine Whitehead: how can I be sure the stuff I buy can be trusted to be safe for consumption?
I agree that artery cracks are rapidly sealed by Lp(a) and coagulation. This might not be the only way plaque forms.
Return of the lipid hypothesis.
modified small/dense LDL (glycated, oxidized) + macrophages = foam cells
If LDL enter sub-endothelial space via vasa vasorum and form foam cells then it seems plausible that plaque can be initiated.
Necrotic core and rupture of vulnerable plaque = disaster. Possibly vulnerable plaques are formed by rapid accumulation of foam cells a form of inflammation.
Small dense LDL is result of a high carb diet.
My question is can a thrombus when covered by endothelial cells develop into a vulnerable plaque? Hypoxia, angiogenesis, smooth muscle cell migration, calcification, necrosis should be involved.
Stress (cortisol) will constrict arteries and reduce blood flow to heart > M.I. Cortisol rises in morning?
Heart healthy whole grains > lectins, WGA > leaky gut > inflamed arteries
Too much polyunsaturated fats > easily oxidized LDL
Statins increase artery calcification making them stronger and less prone to fracture, hahaha.
Age is a risk factor for CVD. Less collagen, glycated collagen, less nutrient intake, stiff arteries etc.
Rambling to generate questions.
If LDL enters the artery wall via the vasa vasorum then this would happen in all artery wall, everywhere. Also vein walls.
It is hard to see why that should be so, damage to the endothelium could (at least in principle) be repaired from either side. The damage would be signalled by cytokines, attracting the right cells to fix the problem. and only where there was damage in the first place. It makes more sense to me that these cells would work in the quiet and slow moving flow within the vasa vasorum, rather than the metres/second flows in the lumen.
Of course “should be” is not a very good argument.
Following an earlier post it came to mind to ask “Where are endothelial progenitor cells found?”. The first search hit yielded this: “Recent studies report that the vascular wall contains a number of stem/progenitor cells that may contribute to vascular remodeling. Microvessels serve as the vascular niche that maintains the resident stem/progenitor cells of the tissue. Therefore, the vasa vasorum may contribute to vascular remodeling through not only its conventional function as a blood conducting tube, but also its new conceptual function as a stem cell reservoir. ”
From “Review Article Role of the Vasa Vasorum and Vascular Resident Stem Cells in Atherosclerosis” by Jun-ichi Kawabe and Naoyuki Hasebe at http://dx.doi.org/10.1155/2014/701571
I’ve not had time to read it, so if it shoots my point in the foot so be it!
I don’t think this is all that germaine to your main point anyway (it is the same blood).
The problem of why arteries are so prone to atherosclerosis seems to beset virtually all proposed descriptions of atherosclerosis pathogenesis. The question is why arteries and why not veins.
Ravenskov’s work around . . .
LDL, or at least the ApoB100 bit of it, is part of the innate immune system. It binds with bacteria, viruses, or other foreign matter. So you can end up with a clump of LDL particles surrounding an antigen. This is happening all over the vascular system, where ever there is infection; however, in the small capillaries in the heart’s artery wall (vasa vasorum) the external pressure on these capillaries produced by the functioning heart results in narrowing of the capillaries. This then is problematic if you have a great big LDL-antigen complex; it is not easy for it to move through the capillaries. The macrophage will phagocytose the complex and remove the problem. If the infection is too great complexes can block up the narrow capillaries and thereby starve local smooth muscle cells of oxygen => death => inflammation => plaque. In this scenario the growth of the plaque is from the inside the wall towards the lumen, rather than from the artery lumen into the wall.
(a) I have not come across evidence demonstrating that the capillaries are smaller in the heart coronary arteries than else where in the body.
(b) I do not now the relative size of capillaries and the LDL-antigen complexes to see if size is an issue.
(c) We know of other things that damage epithelial cells and promote atherosclerosis eg serum homocysteine levels. . . so there will be other mechanisms instead of/besides the above.
I may have skipped a detail, but the notion of damage to the lumen epithelium causing clotting followed by the usual process of repair should in principal work on the endothelial cells in any of the vasculature – Again why the arteries and not veins?
(PS if you are going into hospital for a stay it might be a good idea to make sure your LDL level is high enough . . . as this is protective against MRSA . . . I have a copy of a whole PhD thesis on why)
Two physics arguments might come into play:
1) Arteries have muscular walls because the pressure inside is high (especially at pulses) compared to the external pressure (and only the difference matters). Veins don’t have that function or the associated pressure difference hence little wear and tear.
2) Turbulent flow occurs where the flow is greatest, and turbulence will be worst near branches (think of an island in a river). Turbulence implies fluctuations and extremes of pressure. Blood flow in veins is gentler (we don’t feel veins for a pulse – consider how pronounced the arterial pulse is at the wrist, imagine it right at the heart).
I agree there may be something in the turbulence notion Ken . . . There is a high rate of CVD damage at the bifurcations of coronary arteries, and this hints of hydrodynamic forces damaging the epithelium leading to plaque formation.
I was sure this was the most likely cause a few years ago but I am not so sure at the moment.
The way I’d look at it is there is a battle between damage and repair. Damage could be mechanical stress e.g. turbulence or physical injury, or chemical stress – in the broadest sense. Chemical stress could include lack of NO, excess homocysteine, glucose, fructose, lead, hormones, etc,: anything that affects any of the many different cell types involved in the structure and its repair.
If the repair process is not quite adequate such that damage accrues, is it not reasonable to expect to (often) find the worst damage where the chemical and physical stresses are acting in concert?
By not quite adequate, I mean that it takes years for the damage to become significant. Perhaps 100 million heart beats. The damage is nearly repaired, but not quite.
Thank you Dr. Kendrick for pointing out the vasa vasorum LDL problem. I am following this blog with great interest.
I have been obsessed with discovering why my wife required bypass procedure 8 years ago. I think that I would have required bypass or stents if cardiologist had given me a cardiogram at that time. I am now 77 and zero medications.. Thanks to the internet there is ever increasing information on how to avoid CVD and other ailments.
To reduce stress and time spent researching I summarized the lifestyle changes required to reduce metabolic syndrome ( eat low carb, adequate protein, limit grains, etc.). Tweaking as new information surfaces. Not too stressed out about trying to understand a very complex biological system.
Looking forward to your next blog.
Andy, I echo your gratitude to Dr K. The blog is opening my eyes, giving new insights, raising new questions. I am a spritely? 66 year old . . . and follow exactly the same careful diet you describe, and thanks to this and moderate careful exercise, bit by bit, over the past couple of years I have mended from diabetes and heart arrhythmia and poor lung function. Zero medications was the goal . . . I even gave up the daily aspirin. Like you, I am utterly thankful to the Internet for the wealth of information, and although often overwhelmed by the quantity, I find it all exciting . . . (keeping the dementia at bay????)
Antony Sanderson: My sentiments exactly. The quantity is overwhelming at times (especially now with Spring calling me to the garden), but completely fascinating. Learning is great fun.
Anthony, I too had lone AF episodes, 3 times in ER last time was 7 years ago. Took no medications. Blood pressure was a bit on the high side.
Discovered mTOR and how I could modify lifestyle to improve the heart at a cellular level. Reduced glucose, protein and insulin to minimize anabolic reactions. Started intermittent fasting to down-regulate mTOR and allow cells to repair and eliminate debris. Increased micronutrients (magnesium, C, Q10, fish oil etc) and more leafy greens. High fat adequate protein and low carb meals. Not a quick fix, episodes gradually diminished in frequency and severity. This is my experience, we are all different.
Very difficult to make lifestyle changes, constant motivation helps, like this blog by Dr. Kendrick.
Andy, Thanks for that post.. I am starting out from where you were 7 years ago. Taking exactly the same path.. Fasting has made the most impact…
Some years ago, this blog gave me the courage to stick to my convictions and give up statins for good. This has made a very positive difference to my health. I would also recommend Dr Kendrick’s 2 books – particularly “Doctoring Data” – because you see how data from endless studies has been bent to fit what the specialists think they know already – it is a shocking story and in a way it simply can’t be far from the truth, because those studies were performed by the medical research establishment (if you include Big Pharma in that description) itself!
Insulin gets a big green pass on heart disease and (mostly) on cancer.
Hm. Is this not counter to the thinking here?
Please remove my address from my comment please. First time to blog.
Anne. Could you re-send. I am not able to remove your address.
I follow your blogs with great interest but never contributed until now. A year ago I got severe chest pain centered at the upper end of the sternum. After an angiogram, I was diagnosed with Takotsubo Cardiomyopathy. Coronary arteries are tortuous.I definitely suffer stress. I had to take the usual meds for MI including (80mg Atorvastatin which I declined) The Cardiologist said I must had read an article in the Star. So I told him I read all your articles and there was silence. At the moment I try to eat LCHF to prevent an MI. Also started taking Vit C & D. I will be interested when you discuss Hypothyroidism as my TSH is high and T4 low. Not on treatment yet.I wondered as the HPA axis is involved, would the low thyroid and raised adrenal hormones have contributed to the Takotsubo event. Many thanks for your time and contributions to all who suffer serious illness. Anne McB.
“In endothelial cells, glutamine is metabolized to ammonia,”
“Endothelial cells make up the inner lining of blood vessels,” said William Durante, Ph.D., professor of medical pharmacology and physiology at the MU School of Medicine and lead author of the study. “Damage or loss of these cells leads to plaque buildup within the arteries and eventually cardiovascular disease. Increased production of the protein heme oxygenase-1, or HO-1, is known to help protect against endothelial cell injury and cardiovascular disease. In our study, we wanted to understand how HO-1 protects these cells and identify a natural way to increase production of this protein.”
Ammonia, a colorless gas produced naturally in the body, has been linked to the production of HO-1. Endothelial cells can produce substantial amounts of ammonia, but the biological significance of this gas in these cells is not known. Using cultured human and mouse endothelial cells, as well as a live mouse model, the researchers studied ammonia’s effect on HO-1.
“By administering measured doses of ammonia to our models over a one-day or one-week period, we saw a 300 percent increase in the expression of HO-1,” Durante said. “We also learned that ammonia actually kick-starts a series of events that ultimately result in vascular protection.”
The researchers observed that ammonia triggers oxidative stress, which increases HO-1 production. A byproduct of HO-1 is carbon monoxide, which promotes the survival of endothelial cells.
“I think it’s very interesting that ammonia, a potentially toxic gas, offered vascular health benefits in our models,” Durante said. “Strangely enough it does this by generating carbon monoxide, another potentially toxic gas.”
Although measured amounts of ammonia delivered through drinking water proved non-toxic to mice, its direct use as a cardiovascular intervention would not always be practical.
“Ammonia is processed through the liver and ultimately excreted from the body through urine,” Durante said. “However, direct administration of ammonia could result in the accumulation of toxic amounts in the system ? especially for those with compromised liver function.”
To trigger a natural increase of ammonia, the researchers used the amino acid glutamine. Glutamine is an inexpensive and easily accessible dietary supplement.
“In endothelial cells, glutamine is metabolized to ammonia,” Durante said. “By using glutamine in our study, we were able to trigger an increase in ammonia production that also increased HO-1 without the risk of toxicity.”
Durante said the next step will be a pre-clinical trial to test glutamine’s effect on a mouse model of coronary artery disease.
“Certainly more research is needed,” Durante said. “Although our study only involved mice and in vitro cells, the results are encouraging. If further research shows that we can control the mechanism that triggers natural cardiovascular protection, it may be possible to develop new treatment protocols for coronary artery disease.”
Materials provided by University of Missouri-Columbia. Note: Content may be edited for style and length.
Xiao-Ming Liu, Kelly J. Peyton, William Durante. Ammonia promotes endothelial cell survival via the heme oxygenase-1-mediated release of carbon monoxide. Free Radical Biology and Medicine, 2017; 102: 37 DOI: 10.1016/j.freeradbiomed.2016.11.029
Dr. Kendrick: What do you think of this (in support of Dr. Ravnskov’s view perhaps)?
Association of measles and mumps with cardiovascular disease; The Japan Collaborative Cohort Study
Gary . . .
I had a quick look at the abstract of the paper. I don’t think it says too much about Dr Ravnskov’s view of the pathogenesis of atherosclerosis as such.
For the benefit of those who have not seen the abstract . . . They followed about 100,000 middle aged men and women from 1988 to 2009 . . . Asked them to fill in questionnaires at the beginning of the study asking about previous infections of mumps and measles. At the end of the study 2009 death certificates were used to find out who died of CVD. They then worked out the likelihood of dying from CVD if you had mumps, measles or both. The conclusion: “Measles and mumps, especially in case of both infections, were associated with lower risks of mortality from atherosclerotic CVD”
What I believe Dr Ravnskov’s view would be: . . . (apologies for the presumption) . . . When the mumps or measles attack occurred in youth, and if the infection was sufficiently vigorous, then fatty streaks and even plaques would form. Given time these would be dealt with by the immune system and removed. By the time of middle age it seems unlikely that damage from the earlier infection is an issue – perhaps an odd scar?
What I suspect it does show, as has been proposed by others, is that: having the actual measles and mumps infections provides the body with long term increased resistance to later general infections . . . Infections that, if not attenuated by previously gained resistance, would cause CVD in the manner Dr Ravnskov suggests.
Some might say the study simply provides evidence that CVD pathogenesis is basically an inflammatory process.
In the main paper discussion . . they speculate that the youthful infections increase the number of Treg cells in the artery wall and suppress inflammation. (They would be sitting in the artery a long time!)
Antony Sanderson: I simply meant in the sense that Dr. Ravnskov’s view, according to Dr. Kendrick, is that an infectious agent is causal in CVD. Meaning the immune system is somehow involved. There is quite a list on PubMed of diseases from which having measles in childhood offers protection.
Thanks Gary, that paper was a real find . . .
You could argue, like Ravenskov, that infection helps promote CVD. So you would predict that a severe enough infection would leave you with atherosclerotic lesions, and if anything there would be an increased mortality rate among the infected. (Opposite to what they found in the study)
But, if you survived, and years later, presumably after the damaged has been repaired or stabilised, you joined the JACC study, and you now had an improved level of general immunity; you are less likely to get an infection that would lead to further development of harmful lesions. In this case you would predict that having measles/mumps in early life would leave you less likely to suffer fatal CVD. This is what was found in the study; so looked at in this way it does support Ravenskov’s picture.
You may already have looked at some Ravenskov’s work . . . but for anyone interested it is described in . . . http://www.annclinlabsci.org/content/39/1/3.long
I should admit that I suspect that this is not the whole story. You could say that infections can damage the heart’s electrical conduction system leading to sudden cardiac arrest. This could cause death. If you have a more robust immune system (thanks to earlier infections) you would be less likely to suffer this sort of attack.
Or there could be something else . . . .
Antony Sanderson: Thanks for the link. Fascinating paper, which I’m going to have to read several times to absorb, and to see how it fits into the big picture. It appears, at first glance, to fit with Dr. Kendrick’s view of the progression of CVD, as well as giving support to an infectious element. If LDL play a non-specific role in the immune system, this would help explain why high cholesterol is protective in the elderly, which it clearly is.
Could not resist to look into ammonia and CO as being beneficial. From a quick google:
1. ammonia is byproduct of protein digestion, ensure adequate and balanced protein
2. excess ammonia increases mitochondrial oxidative stress, AMMONIA IS TOXIC
3. then BACH1 is down-regulated (represses HO-1 expression)
4. then HO-1 (increased) + free heme = CO, mitochondrial fusion proteins increased MITOFUSIN 1 & 2(good), reduced mitophagy by decreased FIS1(good)
Bottom line: looks like the mitochondria is trying to protect itself from being poisoned by ammonia. HO-1 is anti inflammatory. CO function ?
Bob M and others.
1. Love Body by Science, I have been doing it since June, once per week for 15 minutes, can’t believe the increases in strength and tone. Hadn’t done any meaningful exercise in 30 years, part of what attracted me to it was the science behind it (and the contrarian view – aerobic fitness is BS which they show with research!). Also attractive as it was developed to let “old folks” exercise with weights and avoid injury. Hate to exercise but the value to cost ratio here is just to good to ignore.
2.Here’s some good info on Vitamin C and glucose similarities and metabolic implications when low carb. This site has excellent, deep science podcasts on keto, lchf, IR, highly recommended! But Dr. K remains my goto guy for athero, thanks for all you do!
Joe: Thanks for the link. Very interesting and useful information.
I think this website has readers of a contrarian view. It took me a long time to get that way, though. For instance, for lifting weights, I used to do a ton of exercises multiple times per week. But after injuring both shoulders, I started cutting things back. I found a book called “Slow Burn”, which is similar to “Body by Science”, but doesn’t place as much emphasis on the high intensity aspect (that I remember, anyway). After shoulder surgery, I found Body by Science and started using it. I still “had” to exercise at least twice a week, though. I tried a short (only 15 minutes) of biking or other high intensity exercise, as one day per week couldn’t be enough, or so I believed. Now, I’m trying one day per week, and I think it’s great. I’ve gone from 4 to 3 to 2 and now to 1 day of exercise per week.
Also, I recommend the question-and-answer book that’s the follow-up to Body by Science. In particular, they suggest in the follow-up book some back exercises that I think are awesome. For me, those are worth the cost of the book.
Anyway, I used to be a model citizen and believed what I was told: I had to eat carbohydrates; fat and particularly saturated fat was bad; fiber was good; I had to exercise hours upon hours a week; I got fat because I ate too much or exercised too little; high cholesterol was was bad; it goes on and on. Now, I believe none of that: carbs are bad; saturated fat is not bad and is likely good; fiber is bad; exercise might have a benefit, but it’s not necessary to exercise much at all; high cholesterol is good; etc.
Yes Bob, I agree that both skepticism and a contrarian view are well represented here (and in the FB groups like Keto Saved Me that I follow). I try to follow the evidence and the science as difficult as that can sometimes be. Thanks for the tip on the follow up book, I have just been looking for back exercises, having weakness and painful spasms, perfect timing.
I think being physically active has many benefits, but exercise is unnatural. But I will do BBS for 15 min per week to be sure I keep my muscle mass if nothing else.
Joe: I highly recommend “8 Steps to a Pain-Free Back.” It’s about posture. Amazing how many benefits correct posture has! I used to periodically injure my back bending and lifting, with 2-3 days of pain. Now I can bend all day in the garden or house, and lift anything I need to with no problems.
BobM: Bingo. I was a devoted long-distance runner from mid-40’s to mid-50’s. Then I trained for and ran a marathon, which was great fun because a group of 30 of us trained, travelled, and ran together. But this was the beginning of the end of my running career. Now I run twice a week, a bit over a mile, but this is just warming up for a few intervals (only once a week for these). What was missing was strength training. I don’t like gyms (prefer to be outside), and don’t know much about weight lifting, so I do body-weight exercises (pushups, pull-ups and squats) twice a week. I’ve increased upper-body muscle mass and definition, and it feels good! When I began I couldn’t do a single pull-up; now I do four sets of seven. All the body-weight exercises I do slowly, to failure. I think strength training is the most important exercise we can do for our health.
I totally agree with you. Someone posted a link recently to an article on why one should not run, making the point that strength training is the key. Running ruins your joints and puts you off strength training which helps to keep down muscle mass loss.
Here here Gary, I too was a distance runner for some years but if we subscribe to the sheer stress theory of blood damaging the arteries, especially if your blood is too thick then constant long distance running would be detrimental. These days I run 2 or 3 times a week but only short reps up a hill for 5 to 10 mins.
Long distance running is detrimental
For the reasons I have stated or others ?
I am not sure. But the evidence on ultra runners and suchlike seems pretty clear. Increased CV damage, possibly lots of ‘silent’ infarcts and suchlike. I am a great believer in exercise, in general. But you can definitely overdo it.
smartersig: Because we are not gazelles. At no time during the evolution of the human species were we chased for hours through the savannah by predators, nor did we chase prey like hyenas (who can sustain a 45 minute chase at full tilt; they are more successful hunters than lions, who can’t do anything of the sort). Hunting required an occasional sprint, but mainly relied upon agility, strength and accuracy in hurling projectiles at prey. Occasional short bursts of running strengthen the cardiovascular system, but we need recovery; in long-distance running there is no recovery. Strength training requires recovery, too; this why I do it only twice a week, and sometimes only once. This is also why I pause a full five minutes between sets.
I agree and as an ex runner thats quite a confession. I think the main problem is the sheer stress factor of blood flow. It makes sense and no one has been able to come up with an argument to refute it. There was also some research done where 5 catagories of people were followed for a number of years. The cat’s were couch potato to serious tri athlon types. The worst longevity were the couch potatoes but the second worse were the Tri’s. The sweet spot was 2 or 3 where people did a bit but regular eg walked to work
Running is NOT bad for knees – – at least according to this:
That study does not look very scientifically designed.
“Had run at some time in their lives”??
Look at the average BMI , over 28, that is a lot of weight for pavement pounding.
Subjectively, I was told one marathon a year, perhaps OK, and it is not just the joints, its the rest of the body.
smartersig: “Because we are not gazelles . . . ” . . . No, we are not made to out-chase lions . . . nor do we sustain 45mins of running at full speed after prey; however, what we can do, and in areas of Africa are done at the present day, is track and jog after over hours antelope, keeping them moving until they collapse with exhaustion. The main reason we can do it is our cooling system – sweating. The antelope does not have this system – over heats and collapses. I have seen this in action. Heifer escaped from a farm, we chased it for over 2 hours around the village, through fields until it just sank to the group and would not/could not move. It had to be put down.
There’s a school of thought that says humans were built for endurance running. https://en.wikipedia.org/wiki/Endurance_running_hypothesis Certainly the Bushmen are noted endurance runners. They have to be because their poison arrows take an hour or two to kill an animal, so they follow their wounded prey after shooting it, otherwise it’s mongongo nuts for dinner again.
On the other hand, a marathon runner and friend of Dr. Noakes told me that the human body was built to run 10 km at the most. After that it starts getting damaged. Not that there’s any chance of me running that far. I’ve always joked that the only time you should run is when there’s a police dog chasing you ;o)
For someone with CAD (blocked arteries diagnosed by angiograms) my interest is in reversing this situation by dissolving those blood clots (plaques) between the endothelium and the media. Has there been any studies done in this area perhaps using those clot busting drugs they use after a stroke or heart attack? I was on the COMPASS drug trial taking a low doses of rivaroxaban but I had to drop out because of uncontrollable bleeding. The study has completed and I’m waiting the results although this was more of a preventative study than one to reverse blocked arteries. If one accepts Dr. Kenrick’s position that plaques are blood clots then isn’t it worthwhile studying how to shrink or dissolve these clots to prevent heart attacks in persons with blocked arteries?
There is a Dean Ornish who has published work describing reversing atherosclerosis . . . Ornish D, Brown SE, Scherwitz LW, et al. Can lifestyle changes reverse coronary heart disease? Lancet 1990;336:129-33.
The experimental work looks pretty robust. I think he describes it on YouTube.
But brace yourself . . . it is a strictly vegan diet.
There are reports that describe the generation of new blood vessels (angiogenesis) to ameliorate the effect of the blockages in the carotid arteries. There is an amazing video of an angiogram showing blood coming up to a blockage, then downstream on the other side of the blockage it starts to backfill with blood up to the other side of the blockage. So the blood has found a different route. Cannot put my hands on the URL at the moment – put will have a search around.
I have a friend who has a blockage in one of his carotid artery, but his hospital doctor assures him that compensatory blood vessels have developed . . . so they are not moved to do anything about it.
I hope this link works better than the last one I tried.
Is this the video you have in mind.
If all the participants were eating the “Standard Care Diet” before the intervention (Canada Food Guide for me) then a switch to a low fat vegan/vegetarian diet would be an improvement.
You are a star Christine . . . the video is exactly the one I had seen a couple of years ago.
(I have now saved the reference)
Anthony: Angiogenesis was evident in my wife’s heart with 90 % blockage before bypass. My understanding is that angiogenesis is the response to hypoxia. Tissue survival in action.
Antony – thanks for the Dean Ornish reference. Since my first angiogram, I have been trying to eat a more heart healthy diet (ie less meat, fats, more fruit and veg) even though I’m reading more articles that say a low carb, high fat diet is OK.
I can also report that during my second angiogram, the cardiologist said “He’s got some big, juicy collaterals” so that is helping but that’s not reversing the plaque/clots that have restricted blood flow in my arteries around the heart. The new collateral arteries where the main reason why he did not do a stent.
I should also mention that I have been on a high dose of Niacin for the many years. I beleive that has helped too.
What do you take the niacin for and how much. Has it caused you any problems
Carol, I have taken Niacin ( the flushing type) for 5 years with no real problems except the flush which for me is bearable for 15 mins. You have to start really slow 1/4 of a 100mg tablet and increasing slowly until you get the right dose A lot of the literature will say you have to take 1000 mg a day or more to get benefits and I took 1000mg ( 500mg twice a day) for 2 years but then dropped down to 250mg twice a day. I took it because I did not want statins and my cholesterol numbers are really good. Trigs 0.7 HDL 2.88 LDL 3.9 Some can be attributed to my LCHF eating too. As to this doing any good other than that, who knows as I still have rampant PAD however on angiogram of my heart I had only a very small amount of plaque in my heart.So the questions continue.
Thanks Ann, I think I will try it. Did it do anything for your blood pressure? Suppose I should stop drinking red wine as well!
I recently found some references to a study done at Baylor University in the 1960s where they showed that IV hydrogen peroxide was able to remove plaque from arteries. Has anyone (Dr K?) else heard anything about this? The only references I can find are from some dodgy websites, I can’t find the original study.
Found the following. It may be of interest as it seems that antioxidants are of value in both vascular disease and diabetes. Would P4-MAX be of value. Can’t get full text – pay barrier.
Vascul Pharmacol. 2015 Nov;74:23-37. doi: 10.1016/j.vph.2015.09.003. Epub 2015 Sep 10.
Oxidative stress in chronic vascular disease: From prediction to prevention.
Santilli F1, D’Ardes D2, Davì G2.
This review article is intended to describe the strong relationship between oxidative stress and vascular disease. Reactive oxygen species (ROS) play an important role in the pathogenesis of vascular disease: oxidative stress is intimately linked to atherosclerosis, through oxidation of LDL and endothelial dysfunction, to diabetes, mainly through advanced glycation end-products (AGEs)/receptor for AGE (RAGE) axis impairment, protein kinase C (PKC), aldose reductase (AR) and NADPH oxidase (NOX) dysfunction, and to hypertension, through renin–angiotensin system(RAS) dysfunction. Several oxidative stress biomarkers have been proposed to detect oxidative stress levels and to improve our current understanding of the mechanisms underlying vascular disease. These biomarkers include ROS-generating and quenching molecules, and ROS-modified compounds, such as F2-isoprostanes. An efficient therapeutic approach to vascular diseases cannot exclude evaluation and treatment of oxidative stress. In fact, oxidative stress represents an important target of several drugs and nutraceuticals, including antidiabetic agents, statins, renin-angiotensin system blockers, polyphenols and other antioxidants. A better understanding of the relations between atherosclerosis, diabetes, hypertension and ROS and the discovery of new oxidative stress targets will translate into consistent benefits for effective vascular disease treatment and prevention.
Lots of words, lot of things, but they make no attempt to look at the overall process. This is primarily because everyone is blinded by LDL. You have to fit LDL into the centre of any model of atherosclerosis (or you will be dismissed as a crank). The only problem is that LDL does not fit in the centre. Is has a peripheral role to play. Only when Keppler recognized that the perfect shapes of the Greeks could not explain the orbits of the planets, or comets, could he progress. Only when you accept that LDL is not at the centre of the CVD Solar System can you progress. Whoever wrote this paper is stuck with the wrong model, and will never be able to get anywhere.
An excellent Kepler parallell in my eyes.
Low LDL is certainly important in respect to, for example where it leads to a poor prognosis
Arch Intern Med. 2003;163(13):1549-1554. doi:10.1001/archinte.163.13.1549
Both low LDL cholesterol and low HDL cholesterol concentrations were associated with an increased mortality risk of infection: 2.7 (95% CI, 1.2-6.2) and 2.4 (95% CI, 1.1-5.6), respectively.
Searches on Pubmed suggest that ROS and antioxidants are involved in vascular health
Life Sci. 2015 Dec 15;143:209-16. doi: 10.1016/j.lfs.2015.11.012. Epub 2015 Nov 14.
Antioxidants and vascular health.
Oxygen free radicals and other reactive oxygen species (ROS) are common products of normal aerobic cellular metabolism, but high levels of ROS lead to oxidative stress and cellular damage. Increased production of ROS favors vascular dysfunction, inducing altered vascular permeability and inflammation, accompanied by the loss of vascular modulatory function, the imbalance between vasorelaxation and vasoconstriction,
Heart Vessels. 2011 Jan;26(1):55-63. doi: 10.1007/s00380-010-0029-9. Epub 2010 Oct 27.
Oxidative stress versus antioxidant defenses in patients with acute myocardial infarction.
Acute myocardial infarction (AMI) is a highly dynamic event, which is associated with increasing production of reactive oxygen species (ROS). The imbalance between ROS production and antioxidant defenses leads to the condition known as oxidative stress,
Curr Vasc Pharmacol. 2010 Mar;8(2):259-75.
Reactive oxygen species and antioxidants in the pathophysiology of cardiovascular disease: does the actual knowledge justify a clinical approach?
There is evidence that reactive oxygen species (ROS) are related to the development of cardiovascular disease (CVD). Results from many studies support the hypothesis that ROS released from various sources or dysfunctional mitochondrial respiratory chain play a role in the development of atherosclerosis and its complications.
Proc Soc Exp Biol Med. 1999 Dec;222(3):196-204.
On the role of vitamin C and other antioxidants in atherogenesis and vascular dysfunction.
Oxidative stress has been implicated as an important etiologic factor in atherosclerosis and vascular dysfunction. Antioxidants may inhibit atherogenesis and improve vascular function by two different mechanisms
Circulation. 1995 Mar 1;91(5):1525-32.
Protection from oxidized LDL-induced leukocyte adhesion to microvascular and macrovascular endothelium in vivo by vitamin C but not by vitamin E.
The protective effects of vitamin C on oxLDL-induced leukocyte adhesion and aggregate formation were seen at vitamin C plasma levels that can easily be reached in humans by diet or supplementation, suggesting that this could be one of the mechanisms by which vitamin C contributes to the well-documented protraction of atherogenesis as observed in large epidemiological surveys.
Thanks Mike for the references.
IMO LDL is part of the repair mechanism and is there for the same reason you find firemen at fires (and ambulancemen at road accidents). Damaged LDL = the firemen are drunk and hence all bets are off.
mikecowdrey: search for new drugs is the aim of of research. Primary cause of oxidative stress is irrelevant.
Beg to differ. ROS is at the seat of many chronic conditions and its correction has many benefits. To ignore it simply results in more Big Pharma costly but largely ineffective drugs. Remember, the Big Pharma business model is based on illness.
mikecawdrey: I was a bit too brief. Oxidant stress is irrelevant to researchers when they focus on discovering the next blockbuster drug. Sorry for causing confusion.
mikecowdery; researchers are suffering from ADD-iction syndrome. Patient has oxidative stress > ADD antioxidants
No need to REMOVE something that causes the oxidative stress.
The number one cause of oxidative stress is… oxygen.
Typo in last sentence, computer problem. Should have been “REMOVE something that causes oxidative stress”
I am not suggesting that one should stop using O2 because it is involved in oxidative stress. On the other hand at bedtime to relax I exhale and hold my breath, the CO2 is apparently beneficial. Rapid breathing not so good, slow steady breathing better.
The point I was trying to get across:
High glucose+high O2 = high ROS ie high oxidative stress, is it better to ADD antioxidants or REMOVE some glucose
Same with ADDing vitamins and minerals to a bad diet. REMOVE the junk first.
I believe the oxidative problem is central to all disease. Mitochondria generates highest ROS in process of using glucose to generate ATP. No antioxidant to stop this process exists. Excess ROS is the problem. Add corn oil to mitochondrial membrane and the end result can be cell death. Reduce ROS by HFLC and less PUFA is a good solution.
Excerpt from a study copied below. Drug development is the answer to CVD.
“A better understanding of the complexity of cellular redox reactions, development of a new class of antioxidants targeted to specific subcellular locales, and the phenotype-genotype linkage analysis for oxidative stress will likely be avenues for future research in this area as we move toward the broader use of pharmacological and regenerative therapies in the treatment and prevention of CVD.”
Andy . . . on the “. No antioxidant to stop this process exists. ” Your point that mitochondria when working in a high glucose environment producing high volumes of ROS is well made. I keep reading further that dietary antioxidants are not that effective . . . by which I assume there is difficulty getting the antioxidants inside the cell??? However, as I understand it, Co-Q10 and a number of other antioxidants produced in the cell, are available in the mitochondria, and these are nature’s way of dealing with the inevitable ROS under normal conditions.
As you point out, when the mitochondria have to deal with too much glucose damaging levels of ROS can lead to cell death. But working from the other end . . . Statins are known to => damage muscles cells (amongst other types of cells). As many on this blog know statins cripple an enzyme that is involved in the production of cholesterol. (The enzyme is involved in one step in the mevalonate pathway) Unfortunately this same pathway also produces protective Co-Q10 and other antioxidants. So, while on statins, the mitochondria in the muscle cells are bereft of their antioxidants, and are more likely to be damaged because of excessive ROS => cell damage, death => a CRIPPLED SHOULDER . . . . (who says I am not bitter)
(PS I can find no study or even reference that says that confirms that liver cells (the target for statins) preferentially take up statins and that the rest of the cells in the body are ‘safe’.
PPS I have 2 Swiss studies showing that simvastatin and atorvastatin in vitro damage pancreatic beta cells)
May be I misunderstood you. “ADD antioxidants”. This is what I believe is most important and my raison d’etre for using Vit C, possibly the most researched molecule in history.
CooQ10 is a product of the mevalonate pathway and is affected by statins in the same way as cholesterol. Merck was well aware of this and has two patents combining CoQ10 witth their two statins. Unfortunately every pharma company ignored this, could not give a damn about patients, only profit. In general if there is no perception of profit, there will be no research grants
have you read Dr Lown? Here’s a very interesting essay on angina and the history of coronary artery bypass.
You might be a bit surprised.
Thank you for the link to Dr. Lown – I didn’t know about him but there is a lot which I am not familiar with in this CVD-business.
This was certainly interesting reading and confirmed almost all of my present views on CHD and especially the uselessness (or rather dangers) with CABG.
What makes me scratch my head while reading. Dr. Lown is though what he is stating about the nitroglycerine as a prophylactic treatment rather than as an acute treatment for angina pectoris (AP). I don’t see the logic.
Well, as known, I keep away from all prescribed drugs since I don’t trust that the CVD experts know what they are talking about. With my present 2.400 IU Natural vitamin E it has for some years now looked like as if I was almost completely free from AP when being able to perform hard physical labour without any discomfort (better than for many years). However, a few days ago I was hit by an AP bout and without any obvious reason that I could point at.
There is evidently here a lot that I don’t understand but taking the overwhelmingly complexity of our physiology and metabolism my limitation may be quite understandable.
My understanding from the article is that Dr. Lown is proposing that people who have regular episodes of AP learn to live with it with the help of nitro-glycerine (NG), rather than getting a stent or balloon angioplasty or bypass. Once they learn the circumstances under which they are likely to get an attack of AP, they can take NG beforehand and avoid any pain.
Someone who gets AP “out of the blue” as you did is a different case.
Incidentally, I worked with a guy who carried his tiny little NG pills everywhere and popped them frequently. Married to a much younger woman and with a baby, he was about 45 years old and had recently had a heart attack. His hair was white at the roots and brown at the ends. I commented to a lady friend the shock of the heart attack had made his hair turn white overnight. She knew better. He dyes his hair because he wants to look younger she said.
He had been told to avoid stress at all costs. So he walked around with a permanent smile plastered to his face and tried to make a joke about everything. It was fake and really creepy. He was a construction foreman which is the last job on earth you want if you need to avoid stress, but it was the only job he could get. Nice guy, actually. I hope he survived.
How little we “know”!
Reading some other essays by Dr. Lown, I actually burst out laughing when I read this:
He should have consulted Dr. Kendrick :o)
Martin, on your contribution about Dr Lown’s Liptor (Atorvastatin?) experience . . . it stoked up vivid reminders of my experience . . . 3 years, no problem then rapidly increasing muscle damage to the point I had to have help putting my jacket on; I couldn’t raise my hands in the shower to wash my hair; having to ask the doctor “at what point will I not be able to wipe my own bum”. My wife, getting a little worried at this point, not least because of the prospect of having to deal with hygiene matters, suggested that statins may be the problem (newspapers do have their uses) . . . But it was not until a little time later when I was talking to an aged acquaintance about my ills and mentioned that it may be the statins. “Oh”, she said “I gave them up ages ago when I got the same sort of pains as you”
And this brings me to my point: There is a guy who I have seen a couple of time on the TV, and in print, defending statins. To quote him “Only 1 in 10,000” suffer any sort of muscular discomfort. I think his name was Collins.
Now, in my village there are a number of people who I know have had problems with statin muscular damage; besides me and my age acquaintance there are 2 others that I know of. That means, if our village is representative, there must be another 40,000 – 4 = 39,994 people who are taking statins without suffering. BIG PROBLEM: village only has about 3500 people. This is a serious issue . . . I want to know where to other 30,000 odd people are hiding in the village . . . spooky.
Put on your “Collins blinkers” and you’ll find most side-effects magically disappear ;o)
*Now featuring KeysVision!*
Very interesting. I always wondered about the comparative safety and survival of CABG, stenting and medical therapy. Up to now all I found was that the long term survival for stenting and medical therapy were similar and the CABG had some nasty adverse reactions including Alzheimer’s
That was the main reason for me declining this “intervention” and already known so many years ago.
It is kind of “crazy” in my eyes that the they pursue this evident “stupidity”.
JD, having read Doctoring Data I wasn’t surprised, but I was impressed. It’s an excellent article. So much money wasted in this industry that we call healthcare. The surgeons’ definition of success has no meaning for patients.
Unfortunately today it is sick care not health care.
The UK is not alone in having a National Sick Service, I heard today on BBC news Malcolm Turnbull (Australian PM) Is to dictate all nursery school children must be infected and potentially damaged by vaccines before they are allowed to attend school. This is because the unvaccinated children pose a risk (no understanding of what vaccines do). If he has a flu jab, does he not twig why he should not go near other people for a few days? Still, Australian Anti-Health Service silences surgeons who advise diabetic patients on nutrition to save having to cut off so many legs. Turnbull should look at New Zealand where vitamin C is now recognised as an effective treatment for diseases.
Stephen T: the average elderly patient is taking more than five prescription medications – See more at: http://www.mdmag.com/conference-coverage/aafp_2010/how-many-pills-do-your-elderly-patients-take-each-day#sthash.TtVvo7II.dpuf. The doctor will prescribe a pill to fix some symptom according to the standard of care. The patient feels relieved and the doctor gets paid. This has very little to do with the patients “health”. A better term to describe the health care provider would be “medicine man”.
JDPatten: convinced me that clogged arteries are not a problem. Just do something to slow down progression. Keep researching.
An interesting article. If you go near a surgeon for that sort of problem, you will end up on the operating table.
I have some personal knowledge of another popular surgery area. I went to see an orthopedist for a problem of leg pain when walking. I was diagnosed as having stenosis at the base of the spine. There was talk of surgery, scraping the inside of the spine to give the nerves more room. Internet searching turned up many tales of people more disabled after surgery than before. It also turn up someone who advised a very simple set of exercises taking three to five minutes a day. They work. However when I tell other people about them, they have that “What does he know” look.
Not much changes, really.
It is 50 odd years since I enjoyed lectures by physicians and surgeons discussing the self same symptoms and situations….each advocating polar-apart strategies to manage them.
Only pharmaceuticals could possibly be appropriate for one, while the knife was always the solution to the other. So……depends on whom our GP decides to refer us to, eh?
JD Thanks a million for the Dr Lown reference. I kept flicking past it while going through the blog but ignoring it. It made my day when reading it.
Firstly because he put into very eloquent words the feelings of many . . that techno, tick-box medicine has ousted a more circumspect humanitarian approach.
Secondly his analysis of why we are so ready to jump to surgical interventions such as inserting stents and by-passes. This revolved around to ability to perform angiograms: See a blockage, no matter how limited . . . well we better fix it anyway. He describes the downsides to this approach.
(This is exactly my experience . . . On and off I was having a heart arrhythmia, tired, breathless, occasional heart racing. During one particularly bad ‘turn’, my second one, my doctor suspected a heart attack. It turned out not to be a heart attack (no serum troponin?) but they gave me an angiogram anyway. On discussing the results with the cardiologist a little later he said “There is as small to medium blockage in one of the coronary arteries, but we might as well put in a stent”. I had the stent put in; it made not a jot of difference to my arrhythmia, to my tiredness. I now feel sure it was an unnecessary operation in a cash strapped NHS.)
Thirdly, he described angina pectoris, which I knew about as a pain in the chest, but little else. He described it is as : “Temporarily reduced blood flow to heart muscle. It is not a heart attack. It does not cause heart damage”. He also described the use of nitroglycerine as a medicine to dilate the coronary arteries, decreasing the workload on the heart. He made it clear that even in difficult cases of angina invasive procedures (by-passes etc) too often resulted in complications that were worse than the original condition.
His comments on angina pectoris interest me. I now want to know the pathogenesis of an angina attack. What causes the coronary arteries and other blood vessels to constrict => an attack. I feel it such a process may be involved in other pathogenic cardiac events.
Dr Lown is an inspiration to me, and many other doctors. A great man indeed.
Antony: an important question, copied the following explanation:
Is it possible to literally be scared to death?
Absolutely, no question about it.
Really? How does that happen?
The body has a natural protective mechanism called the fight-or-flight response, which was originally described by Walter Cannon [chairman of Harvard University’s physiology department from 1906 to 1942]. If, in the wild, an animal is faced with a life-threatening situation, the autonomic (involuntary) nervous system responds by increasing heart rate, increasing blood flow to the muscles, dilating the pupils, and slowing digestion, among other things. All of this increases the chances of succeeding in a fight or running away from, say, an aggressive jaguar. This process certainly would be of help to primitive humans, but the problem, of course, is that in the modern world there is very limited advantage of the fight-or-flight response. There is a downside to revving up your nervous system like this.
How can the fight-or-flight response lead to death?
The autonomic nervous system uses the hormone adrenaline, a neurotransmitter, or chemical messenger, to send signals to various parts of the body to activate the fight-or-flight response. This chemical is toxic in large amounts; it damages the visceral (internal) organs such as the heart, lungs, liver and kidneys. It is believed that almost all sudden deaths are caused by damage to the heart. There is almost no other organ that would fail so fast as to cause sudden death. Kidney failure, liver failure, those things don’t kill you suddenly.
What exactly happens in the heart when it’s flooded with too much adrenaline?
Adrenaline from the nervous system lands on receptors of cardiac myocytes (heart-muscle cells), and this causes calcium channels in the membranes of those cells to open. Calcium ions rush into the heart cells and this causes the heart muscle to contract. If it’s a massive overwhelming storm of adrenaline, calcium keeps pouring into the cells and the muscle just can’t relax.
There is this specially adapted system of muscle and nerve tissue in the heart—the sinoatrial (SA) node, the atrioventricular node, and the Purkinje fibers—which sets the rhythm of the heart. If this system is overwhelmed with adrenaline, the heart can go into abnormal rhythms that are not compatible with life. If one of those is triggered, you will drop dead.
What is an example of one of these deadly heart rhythms?
In most cases, it’s probably ventricular fibrillation that causes these sudden deaths from fear. Ventricular fibrillation basically causes the ventricles (lower chambers of the heart) to vibrate in a way that hampers their ability to deliver blood to the body.
What other emotional states besides fear could lead to these fatal heart rhythms?
Any strong positive or negative emotions such as happiness or sadness. There are people who have died in intercourse or in religious passion. There was a case of a golfer who hit a hole in one, turned to his partner and said, “I can die now”—and then he dropped dead. A study in Germany found an increase of sudden cardiac deaths on the days that the German soccer team was playing in the World Cup. For about seven days after the 9/11 terrorists attacks on the World Trade Center and Pentagon there was an increase of sudden cardiac death among New Yorkers.
Who is most likely to suffer from sudden death?
A predisposition to heart disease would probably increase your risk of sudden death, but it happens at all ages and can happen to otherwise healthy people.
“These clots are created by the internal clotting factors. Which is why warfarin works so well, and why warfarin is not particularly good at stopping MIs.”
What about rivaroxaban, apixaban, or edoxaban? Or dabigatran?
Malcolm, I reread the blog and comments in case I missed something. Discovered (google) that Bill Gates favourite lunch is BiG Macs and diet coke. Your opening remark to him in the elevator was “Forget diet ….”. Looks like Bill already has, should we?
Direct association between diet and the stability of human atherosclerotic plaque
Isabel Gonçalves, Elisavet Andersson Georgiadou, Sören Mattsson, Göran Skog, Luís Pedro, José Fernandes e Fernandes, Nuno Dias, Gunnar Engström, Jan Nilsson & Kristina Stenström
Scientific Reports 5, Article number: 15524 (2015)
07 April 2015
23 September 2015
22 October 2015
Mediterranean diet has been suggested to explain why coronary heart disease mortality is lower in southern than northern Europe. Dietary habits can be revealed by isotope ratio mass spectrometry (IRMS) measurement of carbon (δ13C) and nitrogen (δ15N) in biological tissues. To study if diet is associated with human plaque stability, atherosclerotic plaques from carotid endarterectomy on 56 patients (21 Portuguese and 35 Swedish) were analysed by IRMS and histology. Plaque components affecting rupture risk were measured. Swedish plaques had more apoptosis, lipids and larger cores, as well as fewer proliferating cells and SMC than the Portuguese, conferring the Swedish a more rupture-prone phenotype. Portuguese plaques contained higher δ13C and δ15N than the Swedish, indicating that Portuguese plaques were more often derived from marine food. Plaque δ13C correlated with SMC and proliferating cells, and inversely with lipids, core size, apoptosis. Plaque δ15N correlated with SMC and inversely with lipids, core size and apoptosis. This is the first observational study showing that diet is reflected in plaque components associated with its vulnerability. The Portuguese plaques composition is consistent with an increased marine food intake and those plaques are more stable than those from Swedish patients. Marine-derived food is associated with plaque stability.
I spend about 5 months of the year in southern Portugal (ranked around 4th lowest for heart disease) and have long been an admirer of their diet. I recently spent my 60th birthday in Rome and the words of Dr Macdougal quickly came back to me as I wandered around the eating establishments of Rome. Macdougal is famous for stating that heart disease is a disease of Kings and Queens. In other words as society became more affluent the more they tampered and processed a basic and healthy diet. Contrasting Italy and Portugal this is very evident, and Italy is perhaps by no means the worse culprit. Portugal is the poorer cousin of Spain Italy and France and as a result their diet is by far the healthiest. They remain true to the basic fish, salad and potatoes and although this is changing in the bigger towns the trad’ diet still prevails. In Rome its pasta, pasta and more pasta and for a change Pizza. The Italians are fat whilst the Portugese are generally slim. The articles cited states that the Portugese were found to have the more stable plaque, this is no surprise to me. One other advantage which I have stated before. Blood tests here in the Algarve are a fraction of that in the UK
When I visit my son in Sweden, I have the impressionthe Swedes eat quite a lot of fish.
Well, I don’t know if we Swedes eat more fish than other people. Our speciality is though “gravlax” which we though feast on only eat at special occasions.
By the way I don’t think we are low on the CVD-list.
Re vulnerable plaque in Sweden vs Portugal
Besides fish what else affects plaque stability? Authors might have jumped to conclusions.
More sunshine, wine, less stress in warmer climate. I am now vacationing in Florida and meditate about plaque, very relaxing, swim, siesta, read….
Whilst attempting to do a little bit of ‘catch-up’ on Dr Kendrick’s latest article, I came upon J.D. Patten’s suggestion to Goran, that he might find the article on ‘Coronary Artery Entrapment’ written and published in 2012 by Bernard Lown MD, of interest, so I decided to read it for myself.
While reading Bernard Lown’s article, I came upon the following observation which can be found at the end of the third chapter under the heading ‘Essay 31’ :-
“While the cardiologists were triumphant, something vital was leached from doctoring. It meant spending less time with patients and abandoning the ancient skills of listening as well as the consummate art of the physical examination. Some doctors felt an ache like the passing of a dear friend. Most, though, never experienced a quiver of loss. These humanitarian skills, not being taught in medical schools or mentored in hospitals, were never acquired, thus never lost”.
Oh, how true are those words. The NHS decided that ten minutes was sufficient time to listen to a patient, diagnose the problem, write a prescription and send that patient on their way, always assuming that you can even get an appointment when required.
I am of an age that I well remember going to the surgery with my mother and queueing to see the doctor, (often leaving the Surgery around 10.00 p.m. depending on the queue) who then spent a little while asking about the well-being of each member of family before saying “and how can I help you today”.
I know those days can never return, but sometimes, as a patient, you very often feel that you are crying in the wilderness and nobody really sees you and, even more rarely, really listens to you, and when you actually ask a question very rarely receive a satisfactory reply.
All the above is a little off the current topic Dr. Kendrick but absolutely true, sad to say.
I too am of a vintage when doctors were allowed to have a “placebo” effect (it used to be called “bed side manner” and much admired). Now it is case of filling boxes on QoF forms and passing the problem on to a consultant (referring being the term). They have to abide by the diktat of the “Directives”. There are doctors like Dr. K who I am sure do their best to ensure their patients get their full attention. I always wonder how Dr K manages to provide these wonderful blogs and books and his daily doctoring duties. Had the NHS more of his like, the current crisis would probably not exist.
I appreciate your comments, and agree with every word you say. I also realise that doctors today have very different work-loads, and work under very different rules. No criticism whatsoever of Dr. Kendrick was intended, as I am sure he knows. I was simply stating a fact and regret that you saw it as criticism.
I, like so many, others on this blog, am astounded at that the time that Dr. Kendrick spends on research – more power to his elbow I say. I consider that his work is really making a difference to a lot of people.
Sylvia; Dr K displays intellectual honesty, curiosity, and a desire to help everyone. A heretic in the eyes of the official medical establishment.
There might come a time when the recommendation to take 2 aspirins and come back in 2 weeks would be to read “this” book and come back if you have any questions. Drawback is that fees generated from procedures and medications would be reduced.
I omitted to say that the article written by Dr Lown was excellent, if emotive – the part where he wrote about some of his own patients, and their experiences before and after heart surgery, was truly heart-rending.
A good reason to eat your fat:
“In a well-controlled feeding study. . .Plasma Lp(a) concentrations increased in stepwise fashion as SFA [saturated fat] was reduced.”
Hi Gary, I was surprised how many smart people were involved in the study. The study was done in the last century and perhaps the small dense LDL particle was not identified. Metabolic syndrome is LOW HDL and HIGH TG. Ratio TG:HDL indicates sdLDL status.Total and LDL cholesterol fell because because the sdLDL contained less cholesterol. A good study to demonstrate this.
I will file this study under”How Smart People Promote Bad Dietary Advice”.
Before the study the cholesterol levels were in a healthy range in my estimation.
TOWARDS A UNIFIED THEORY OF DISEASE
What an endothelial cell (or any other cell) senses and reacts to:
hypoxia: induces angiogenesis, apoptosis, necrosis
hyperglycaemia (from plant starches): high glucose is toxic, ROS increased, glycates proteins, competes with vitamin C (Scurvy), cell apoptosis
toxins from minerals, plants or industrial chemicals: increased ROS, apoptosis
energy availability: mTOR anabolic/catabolic switch
ageing: accumulation of misfolded proteins, lipofuscin etc.
Omega 6 seed oils: inflammatory response, ROS, easily oxidized, a novel food in evolutionary sense
Micronutrient deficiency: magnesium, C, d3, K2, selenium etc.
ALL OF THE ABOVE IMPACT MITOCHONDRIA/ATP. No energy = no vitality, root cause of disease. Reduce the above with diet, fasting, exercise and will stabilize plaque and prevent plaque formation..
Explanation of how PLAQUE forms or how to prevent plaque formation should be confined to this list. Focusing on associated events remote from primary cause could lead to faulty conclusions and getting sucked into an INTELLECTUAL BLACK HOLE (IBH). Researchers seem to gravitate into the IBH with rewards of developing new drugs. Once sucked into IBH it appears that majority of health experts cannot escape. IBH is similar to “rabbit hole” . IBH is very common among cardiologists, researchers and PHD’s. No known antidote to IBH exists. People who seek medical advice from doctors under influence of IBH do so at their own risk. Fourth leading cause of death is caused by IBH. I am not making this up.
Take responsibility for your own health.
Examples of what researchers come up with under influence of IBH:
a) high HDL is good > develop drug to increase HDL
b) saturated fat increases blood cholesterol + cholesterol is bad = saturated fat is bad, eat corn oil
c) hyperglycaemia is associated with diabetes > develop drug to reduce blood sugar
d) fibrinogen is associated with plaque formation > search for drug to reduce fibrinogen, statins reduce fibrinogen significantly (don’t stop your statins)
e) CRP is a sign of inflammation > statins reduce CRP up to 60%, statins good
f) plaque is cause of heart attacks > develop drugs to dissolve plaque
g) coagulation can cause blood clots > aspirin, warfarin, Xareltor
h] inflammation causes heart disease > statins reduce inflammation (affects function of immune cells)
i) abdominal fat is a risk factor > could liposuction help?
j) membrane potential > more research is needed
k) high blood pressure > many drug therapies available
l) high cholesterol > recommend low fat, low cholesterol diet + statins
m) Diabetes > eat carbs for energy and stop glucose rise with insulin
n) Increase ammonia and CO > work in progress
0) megadose with antioxidants
Could add many more but will run out of letters of the alphabet.
ps This is a first draft, comments welcome.
Andy S: Hyperlipid has an interesting recent post about a study which appears to show that omega 6 seed oils are metabolically more harmful (at least in rats) than transfat.
Gary O: I follow Hyperlipid. Fortunately I never believed the hype to avoid saturated fat and switch to heart healthy margarine (ate butter instead), also avoided eating out. Canola oil regarded as healthy is off my list as well.
Back to Mitochondria: easily oxidized polyunsaturated fats in mitochondrial membrane + ROS = dysfunctional mitochondria.
Andy S: Thanks. I wonder how mitochondrial dysfunction fits into the pathogenesis of CVD. Any ideas?
Bit of tongue in cheek.But seriously, if anyone can discover the antidote for the Intellectual Black Hole there may be a NOBEL prize. The survival of the human race is at stake. The global pollution by ROUNDUP is reminiscent but on a grander scale than DDT in SILENT SPRING. I had a hopeless feeling when discovering that all food is essentially polluted with glyphosate. The FDA has increased the “safe” level because there is so much of the stuff around.
Excellent article about good vs. bad exercise for health and longevity:
Hi Gary, very good advice on how to get exercise.
I hit the gym 2 to 3 times per week, 15 min on stationary bike at moderate speed to get blood circulating followed by 20 to 30 minuted with weights at a rapid pace, followed by a sauna to activate heat shock proteins.
Gary Ogden: Burning glucose generates ROS = inflammation. High blood glucose is toxic. Carb load and run = disaster.
Running a marathon once a week and spending the rest of the time on a couch? I believe the body needs motion to improve circulation of blood to remote tissues. Be physically active at something every day, walking, gardening etc..
Andy S: I think running a marathon any time is a terrible idea. An occasional sprint is good, and strength training has many benefits, but staying active on a daily basis is crucial. I’ve been fueling almost entirely from fat for the past several years, and it works!
By the way, did DR.Squier hva her day in court? If yes, what was the outcome?? Thanks, Nissen
Thanks Dr K. You and PT Mangan are in agreement, but he is pointeing to excessive Iron as one of the culprits, He also posts a lot of other interesting findings, especially interesting is the Iron and sugar data. Might want to read through some of his postings the last few years, pretty cool stuff that supports many of your thesis!
How to avoid the hypercoagulation of aging
Avoiding the hypercoagulation of aging would be a potent strategy for fighting aging and remaining free of the diseases of aging. There are a few ways to do this.
1. Keep iron in the low normal range, via blood donation and/or iron chelators. Both can be useful, since blood donation targets total body iron, while iron chelators mop up any excess free iron.
2. Magnesium can help dissolve fibrin-red cell aggregates. It’s therefore no surprise that magnesium reduces death rates in heart attack patients, and deficiency is associated with stroke.
3. Polyphenols like EGCG (from green tea) and curcumin protect against hypercoagulation. No accident that they also chelate iron.
4. Aspirin enhances fibrinolysis. This may be one of its modes of action that protects against both heart attacks and cancer. Long-term aspirin use also results in lower levels of iron.
Is Insulin Resistance the Main Cause of Heart Disease?
Why high blood glucose relates to heart disease
Why did statins quit working after 2004 http://roguehealthandfitness.com/do-statins-work/
Hi Steve: I was ready to rush out and get leeches to reduce my iron levels. Then I did some googling and discovered that mitochondria become dysfunctional when Fe and Cu is low = low ATP. Not concerned anymore. Iron overload symptoms include low energy, erectile dysfunction etc.. For sure there are people with abnormal levels of Fe that would benefit being treated by a doctor.
When something can be measured there is a tendency to establish norms and develop medications to treat the numbers.
After reading about how necessary magnesium is for our bodies, and after enjoying many soaks containing good old Epsom Salts, someone in an earlier blog mentioned that Magnesium Oil is available. I have tried this very recently and can honestly say that I have found it very helpful in many ways. Holland & Barrett’s stock it and their assistants are generally quite knowledgeable. Not too expensive either.
You can also make your own. Get one of those little spray bottles. Buy some magnesium flakes from Holland and Barrett.
How to Make Magnesium Oil. http://www.healthextremist.com/how-to-make-magnesium-oil/
-What You Need
-1/2 cup of Magnesium Flakes
-1/2 cup of Water
-Jar or Spray Bottle to Store the Mixture
-Magnesium Oil Directions
1.Heat up ½ cup of water (not to the point of boiling)
2.Pour the water over ½ cup of magnesium flakes
3.Stir the mixture until the magnesium flakes are dissolved.
4.Let the mixture cool and store in a spray bottle or jar
5.You can apply the mixture to your skin after it has cooled enough to a comfortable temperature. You can also store the magnesium oil for future use
Thanks a lot for that. I might give it a whirl at a later date. Still have two bottles of Magnrsium Oil in hand so will use those up first, but certainly worth considering.
Same here! bought the expensive spray, and have found it very beneficial for rubbing into my ankles, but I intend to make my own from the Epsom salts which we generally use in our bath, then put the strong solution into the empty spray bottle…..ensures contents are safely labelled, which I think is important.
Jennifer, use magnesium chloride flakes for your oil rather than epsom salts. The epsom salts does not seem to dissolve well and you get crystals forming when it settles out. You do not get this with the mgcl. Even though the mgcl flakes are more expensive it is still much cheaper to make your own. Tip, keep your old mgcl oil bottles to use again .
Speaking of magnesium I use Carolyn Dean’s Pico Magnsium Re Mag
and the minerals ReMyte. I take 600 mg of elemental mag this way. No diarrhorea. also do the foot baths with epsom salts and bicarb. Magnesium advocacy group on facebook has great info on magnesium. Blood tests for mag should be red blood cell test not serum test as it gives a better picture of the level in your cells. BTW I would not make mag oil from epsom salts as it is too sticky. I either buy Ancient minerals mag chloride spray and spray approx 1/2 hour before a shower. There is another book that talks about Transdermal mag and the doses you get. ReMag and ReMyte also has a free ebook on magnesium.
Sylvia – yes, I agree with you 100%. I supplement with mag.citrate every day, without it I think I would curl up into a painful ball, but sometimes I get nighttime breakthroughs when my big toe points to the ceiling and trying to stretch it back sets off cramp in my hamstrings and stretching that out sets off cramp in my calves. Phew. At those times, I have recourse to mag. oil which works like magic, even on the stubborn big toe. At least it only happens occasionally now – when I was taking statins it would be several times a night as a result of which I became very sleep deprived. As a matter of fact, it was the cessation of cramps after I ran out of statins that alerted me to the cause of the cramp hell I was suffering. I stopped/started the statin three times to be sure then stopped. A HUGE improvement. Nearly four years ago. Hurrah!
As regards cramps, I noticed, to my surprise, that once I got serious on L-Arginine supplementation, they almost disappeared.
Are cramps a sign of not enough NO?
Mr. Chris – I haven’t a clue. Since since I began supplementing with citrulline to improve NO I can run much more easily but maybe I should try L-Arginine as well. Another supplement – groan. I practically rattle. I’ll visit that nice Mr. Amazon……
Ouch, you certainly took me back, talking about cramp. I also was a slave to it and recognise the big toe pointing to the ceiling scenario. Epsom Salts and Magnesium Oil put paid to all that. When I first discovered Dr Kendrick’s blog the discussion was concentrating on statins and their side-effects. At the time I was of the opinion that statins were probably the cause of all my aches and pains. Following encouragement from people on this site I stopped taking them and the side-effects started to ease, (many thanks to Dr Kendrick; also to David Bailey and many others for their encouragement).
So sorry, Sylvia – I pressed the thumbs down icon in error and couldn’t correct it. It was meant to be a ‘big thumbs up.’ Like you, I am immensely grateful to Dr. K and all the contributors here. A shining light in a dark and scary medical world.
Please see my reply lower down.
“Diet and CVD: death by association
If I sometimes strike a note of weary cynicism after nearly 19 years of writing these reviews, much of the blame falls on the habit of all the leading journals of printing long articles and then rubbishing them in short editorials. Here’s a classic case. Six authors spend an immense amount of time trying to quantify the association between mortality due to heart disease, stroke, or type 2 diabetes and 10 kinds of dietary intake in the United States: fruits, vegetables, nuts/seeds, whole grains, unprocessed red meats, processed meats, sugar sweetened beverages, polyunsaturated fats, seafood omega-3 fats, and sodium.
They conclude that about 45% of such deaths can be attributed to diet. Their assumptions and methods are then demolished in an editorial, which consists entirely of “How do I hate thee? Let me count the ways.” Is this fair on the authors? Or the readers? I suppose it has some value as a teaching example of how not to do association studies, but to me it seems more like cruel and unusual punishment.”
That Dr. Lehman – he has a tongue on him!
From his weekly blog (with associated links):
JDPatten: Did not pay to get the full text. Dr. Lehman seems to be upset that there could be criticism of an expensive and lengthy study in the same journal. The journal should be commended for printing critical reviews. In my humble opinion the study has very little value for people seeking dietary advice. Salt is responsible for 9.5% of deaths. Low salt is also a risk factor.
A good video on what this thread is about. I liked the part on OxLDL. https://www.youtube.com/watch?v=8uQuF9isqFo
Randall: Thanks for the link, I trust Chris.
Perhaps early stage of atherosclerosis is not atherosclerosis. Artery wall becomes thicker as part of body maturation and compensation for increased blood pressure. Do number of smooth muscle cells increase from working harder when pressure is high? Is thickening uniform?
I think one of the hardest questions to answer about CAD, is why blockages occur usually in only a few areas. (mean stent length 20.0 +/- 7.9 mm) You can watch an Angiogram Procedure on youtube and you can see the arteries eg. https://www.youtube.com/watch?v=F2bJFDvDVxg
Randall: re why blockage only in a few areas
Angiogram shows the most severely constricted areas. When considering artery inflammation that could be everywhere. Stent opens one area but new areas develop constrictions. How long this takes depends on many factors that we in this blog are trying to understand.
Warning Label : my opinions are subject to change if better information becomes available
Mr Chris, when I began fasting for around 16 hours, I began to have ‘restless’ legs in bed. Not cramps exactly. I upped my magnesium intake and the symptom disappeared. The thinking being that LCHF and relatively short fasts is going to reduce the level of insulin used when I eat, and extend the period when it’s not needed at all. However, a lower level of insulin leads to water loss. Salt and other minerals can leave the body with the water. So, I have a salt drink twice a day too.
Hi Stephen T – how interesting. Tuesday is my fasting day (24hours) and Tuesday/Wednesday night is my regular cramp night – or rather, was. I now have a little salty bone broth to keep it at bay, plus of course the usual magnesium etc.
Thanks, Jan. I like the sound of the salty bone broth.
Stephen T: Reducing salt intake is for people who follow dietary advice (USA, Canada Food Guide) a leading cause of CVD. The WHO has recently recommended increasing salt intake.
Magnesium is a muscle relaxant, I used it to reduce AFIB.
Apparently low insulin level (fasting and post prandial) is the path to health. Fat Emperor
Andy, I agree about salt and have read what Dr Kendrick says. What a mess our dietary guidelines are in. I drink my salt with coconut oil, with a little diluted lemon, so you can see what nonsense I think the official guidelines are.
Tim Noakes, Jason Fung and The Fat Emperor have convinced me about the harm of consistently high insulin.
Andy, and all magnesium advocates,
Magnesium, not so much.
Potassium, more like.
That, according to this guy:
This is about arrhythmias.
It’s my thought that odd heart contractions are probably related to odd leg contractions (Cramps!).
Anyhow, I’m not about to stop supplementing with either.
I drink Gerolsteiner water when I fast. This is a “high” mineral, carbonated water. I will also spray magnesium oil on my legs if necessary. I take in extra salt and potassium too. I can lose 6-7 pounds in a single day when fasting.
SOLUTION TO HEART DISEASE (for the consumer/patient)
(a) Impediment to solution – getting too scientific and detailed to level of protons and electrons, thousands of new molecules (and more remaining to be discovered, interactions between all molecules
Example of how scientific method is applied:
Why is jumping out of an airplane without a parachute dangerous? Variables to consider gravitational constant, acceleration, velocity at impact, drag, wind direction speed, weight of person, dimensions of person, age of person, alcohol use, drug use, clothing worn, elevation at impact point, composition of landing spot,coriolis acceleration, IQ of person.
– Perform study using mice with and without parachutes, 10,000 mice in each group, budget $10,000,000
– compare survival using statistics and relative risk comparison
-more research needs to be done due to confounding variables, some mice did not want to participate
– no recommendation how to extrapolate to human behaviour
Applicable recommendation could have been: for health reasons wait for airplane to land. Very little scientific investigation required.
(b) A detailed scientific explanation is not required to understand CVD.
– veins do not have plaque because blood pressure is very low (primary reason)
– heart arterioles and capillaries do not have plaque (low pressure, no vasa vasorum)
– large arteries have plaque (high pressure, gummed up vasa vasorum, high glucose, PUFA in LDL
(c) next – how to reduce risk by dietary means, exercise, timing of food ingestion, +
I agree, the blood pressure explanation seems obvious. People with high BP are at higher risk, BP in arteries is higher. Sheer stress causes arterial damage. Probably explains why people with average BP but high pressure jobs run into problems. There BP may be fine on examination but on a daily basis it is constantly shooting up.
People with normal BP when relaxed can get chest pain from elevated BP during stress or extreme physical exertion. Pressure in the large artery around the left ventricle squeezes the smaller arteries shut rather like a blood pressure cuff, causing pain from lack of blood to the muscle.
Per Dr. Howard Wayne http://www.heartprotect.com/chest-pain.shtml
This explanation seems outside the general understanding that the heart perfuses itself during diastole. Any muscle in the body will stop its own blood flow during flexion. The ventricles, while contracting, shut down the smaller arteries/arterioles within the muscle. Elasticity of the system allows for flow when the muscle relaxes. Narrowed vessels or stiffness in the system would compromise flow during high demand > pain from oxygen starvation.
Is it more complex than that??
I’m no expert. I’m just quoting Dr. Wayne who claims to have a range of non-invasive procedures that tell him in detail what goes on in the heart.
But thinking about it, the left ventricle is a bit of a special case. It squeezes blood into the aorta when contracting, therefore it is always contracted and resisting arterial blood flow when blood pressure is highest. All other muscles will randomly be contacted or relaxed during pressure pulses, so they will be getting a good rush of blood at least half the time.
JDPatten: re. magnesium and arrhythmias
Do not understand why the Dr. trashed Mercola and Sinatra.
The main reason I like magnesium is that it is required by mitochondria to generate ATP. No ATP no energy. Secondly it relaxes muscles, heart muscle and all other muscles. Chlorophyll molecular structure is similar to hemoglobin, one with Fe other with Mg at core. Eat leafy greens.
The doctors (not many 4) that have had me as a patient have only prescribed pills. Diet is a lifestyle and that is patients responsibility. Doctor and dietician had no clue about vitamin K2.
The doctor has no time to educate patients.
Andy S: Also, he is a fan of aerobic exercise, which I don’t think is necessarily a good idea.
One reason to at least question Mercola and Sinatra is that the stuff they “research” and tout is the stuff they themselves sell and profit from. A good reason to examine the motives of any source of information.
And, don’t forget, Dr Kendrick suggested potassium for enhanced NO – good for the endothelium.
JDP: Mercola and Sinatra inform. If they need to fund their “research” by selling vitamin pills that is not so bad. For balanced opinion I look for information from many other sources.
So, Harvard “informed” when its research – funded by the Sugar Industry – touted the innocence of… uh… sugar??
You gotta be careful with your standards. Don’t believe it just ’cause you want to. Have verifiable reasons.
Studies sponsored by pharmaceutical and food industry are always suspect. If I find something of interest I will search for confirmation from other sources. You are absolutely right, verify then trust, and be ready to change your mind if better information is discovered
Dr. Kendrick’s Potassium article here: https://drmalcolmkendrick.org/2013/03/04/potassium-your-invisible-friend/
I take food grade potassium bicarbonate available here: https://pforlife.com/ or at “do it yourself” wine making websites. I take 1/2 teaspoon (2.5 ml) which yields about 2 grams of elemental potassium. The RDA (USA) is somewhere around 4 grams. More may be optimal.
Hi Philip: I was googling while waiting for more comments. On vacation and need something to do. I was searching for impact of silicon on health when tripped over this bit of information. Copy of interesting bit:
In clinical practice great emphasis is placed on potassium loss in the etiology and intensification of cardiac arrhythmias and cardiomyopathy. Recent evidence indicates that magnesium loss may also be an important factor in these conditions. Magnesium is necessary for the integrity of the mitochondrial system, which is responsible for the maintenance of cellular potassium as well as for the metabolic, processes . Magnesium loss from the heart, as from other tissues, interferes with the cellular machinery, without which cardiac potassium cannot be maintained . Magnesium loss thus predisposes to potassium loss.
Good point. I am increasingly concerned about magnesium depletion in my elderly patients, particularly those on PPIs (omeprazole, lanzoprazole etc.). These electrolytes are tricky things.
I take magnesium everyday, but what really sorted out the nocturnal cramps was L-Arginine. The arrythmias seem to have gone too.
Nice. I take a couple of doses of this stuff per day:
Potassium bicarbonate is 39% potassium. Potassium gluconate is 16% potassium. The density of potassium bicarbonate is 2.17 g/cm^3 and the density of potassium gluconate is 1.73 g/cm^3. So the same volume of potassium bicarbonate has about 3 times the amount of potassium as potassium gluconate. I’m not arguing in favor of potassium bicarbonate over potassium gluconate, just putting the numbers out there for interested readers.
Philip Thackray: Thank you for the link. I couldn’t remember it because I only came here a couple of years ago. My doctor once cautioned about taking potassium supplements, but I’m convinced now that it is perfectly safe, and a good idea. I eat lots of potassium-rich foods, but I think I’ll begin a 1-2g supplement.
I am a bit surprised your patients are on PPI’s, given that you wrote some time back about the problems with these drugs!
Isn’t Gaviscon a better alternative for acid reflux?
I don’t start them on PPIs. Equally, they are part of NICE guidance for elderly people taking NSAIDs. So, other doctors happily start them, and never stop them…ever.
JDPatten: That is good to know. I had forgotten (so many Roman numerals). My own physician has promoted potassium-rich foods as long as I have been going to her.
I have been using ‘reduced sodium’ salt (available in all good supermarkets), which is roughly 50/50 potassium and sodium chloride for all culinary purposes. Helps to increase my potassium intake while I hope it contributes to maintaining a 12g sodium chloride (5g sodium) per day optimum. I’m not bothered about the anti-caking additives – the alternative of fish poo in “sea salt” is not an attractive idea.
Is this a tiny crack in Establishment Cardiology’s statin stonewall??
(The first item.)
A prospective study—-statin use and diabetes—
Older Australian women taking cholesterol-lowering statins face a significantly increased risk of developing diabetes, according to a University of Queensland study.
UQ School of Public Health researcher Dr Mark Jones said women over 75 faced a 33 per cent higher chance of developing diabetes if they were taking statins.
The risk increased to over 50 per cent for women taking higher doses of statins.
“We found that almost 50 per cent of women in their late seventies and eighties in the study took statins, and five per cent were diagnosed with new-onset diabetes,” Dr Jones said.
“Statins are highly prescribed in this age group but there are very few clinical trials looking at their effects on older women.
“The vast majority of research is on 40- to 70-year-old men.”
Statins, a class of drugs that lower cholesterol in the blood, are prescribed to reduce the incidence of cardiovascular events such as heart attacks and strokes.
“What’s most concerning was that we found a ‘dose effect’ where the risk of diabetes increased as the dosage of statins increased.
“Over the 10 years of the study most of the women progressed to higher doses of statins,” Dr Jones said.
“GPs and their elderly female patients should be aware of the risks.
“Those elderly women taking statins should be carefully and regularly monitored for increased blood glucose to ensure early detection and management of diabetes.”
The research was based on prescription and survey data from 8372 women born between 1921 and 1926 who are regularly surveyed as part of the Women’s Health Australia study (also known as the Australian Longitudinal Study on Women’s Health).
The research is published in Drugs and Ageing.
Materials provided by University of Queensland. Note: Content may be edited for style and length.
Very nice spot, thanks.
Another side effect discovered, there will be many more. Apparently stains alter expression of bone derived stem cells affecting repair of every body tissue.
My wife has been on statins for 7+ years since bypass. Need to find a doctor who understands statin side effects and convince her to quit the medication.
Interested if statins can cause lower back pain by effect on muscle fibres and tendons, I have suspicions that this could happen. Spine is supported and kept in alignment by muscles and tendons. Maybe statins involved in bone degeneration as well. Symptoms would take a long time to develop and therefore would not show up on studies lasting only a few years.
The belief the doctors/shamans are close to the gods and know best has been around, I guess, from the very beginning of humankind. That healing and religion is closely connected is apparent if you e.g. look into the christian bible.
I am struggling with an old friend of mine who I convinced many years ago to quit the statins but he was dragged into this again by the doctors he tend to believe more in than in what I am telling him. He is very reluctant to relate his muscle weakness or his other ailments with the statins.
When it comes to beliefs there is som much at stake.
While I was struggling with the pain induced by Simvastatin (before I realised that it was caused by the statin) there was a time when the pain seemed to spread from my (polio) leg, into my lower back.
Since I have never had back pain before or since (touch wood!), this was obviously also caused by the statin. To be honest, it is difficult to tell what precisely hurts when statin side effects bite – muscles and joints seem to hurt – and cramp.
If you could just persuade your wife to stop her statin for a week, she would probably begin to feel the difference. Even if statins do provide benefit, you have to ask yourself if they provide more benefit than exercise – which tends to get curtailed if you have muscle pain!
BACK TO THE MAIN TOPIC: WHAT CAUSES PLAQUE?
I can’t decide if plaque initiation occurs below the intima or on the lumen side. To avoid argument we could compromise and meet halfway, or maybe there is a bit of truth in both.
The restraint of “forget diet” has to be investigated. To answer this question we have to look at other species besides bipeds without feathers. The motto from Animal Farm “two legs bad, four legs good” got me thinking. Look at animals in the wild, there are less confounding variables.
GIRAFFE: blood pressure 280/180, blood vessels thicken with age to avoid rupturing under increasing pressure.Can’t find any info about their CVD. Conclusion – exercise compensates for the high blood pressure (tongue in cheek}.
ELEPHANTS: blood pressure 180/120. Could only find data on elephants in zoo. Copied from research: “The two top causes of elephants dying at zoos are heart disease and arthritis. Both of these are lifestyle diseases, caused largely by two factors:
One, the elephants spend most of every day, and most of their lives, just standing around – often on concrete. Elephants in the wild, by comparison, are constantly on the move as they travel through the plains and forests to new feeding grounds and watering holes.
Two, a zoo diet is all wrong for elephants. Morfeld explains that in the wild, they eat a wide range of foods from grass to tree leaves to bamboo to bark. In captivity they eat fruits and grains and high-quality hay full of calories. And they don’t have to walk anywhere to find them.”
PRIMATES: Only zoo data available, excerpt:
“The Ape Heart Project is a European-wide research programme led by leading primate specialists at Twycross Zoo, in collaboration with The University of Nottingham, to investigate why great apes such as chimpanzees and gorillas are prone to heart disease.
Twycross Zoo CEO Dr Sharon Redrobe was responsible for initiating this long term research study over the next 10 years, which will contribute to our growing understanding of the management and welfare of primates in human care.”
WHALES: does obesith contribute to heart disease?
“A large whale heart weighing 256 pounds (116 Kg.) was dissected. The coronary arteries had extremely large right and left marginal branches, which supplied the major lateral mass of the right and left ventricles. The venous system was similar to other mammals. Crude ventricular volume and cardiac output was calculated to be 453 L. per minute based on a rate of 10 per minute. The size of the cardiac muscle fiber was similar to the human myocardium except in a fetal whale heart (wt. 1,600 Gm.) in which very small fibers were found. The aorta was found to be 20 cm. in diameter and the wall to consist of very large interwoven bundles of elastie tissue and fibrous tissue apparently devoid of muscle. There was no evidence of arteriosclerosis.”
DOMESTIC PETS- cats and dogs: Diet is everything.
Looks like a dead end. Not sure if this contributes anything worthwhile. Paradigm shifted in wrong direction?
At the risk of sounding impolite. It doesn’t really matter where you, or I, decide where plaque initiation occurs. All that matters is where does it occur. Equally, science is not a case of two people having different ideas, then compromising somewhere in the middle.
My own view on this is straightforward. Once you have damaged the endothelium (by whatever means) a clot will form at that point. This initiates the process.
If you are going to propose that the plaque starts within the artery wall, beneath the endothelium you must explain what initiates this. You must also try to explain why this does not happen in pulmonary blood vessels, or veins, and only happens in dicrete areas in arteries, almost universally those areas subjected to the greatest biomechanical stress.
Hi Dr. Kendrich; Intention was to add a bit of humour even in a serious discussion. Compromise can be absurd in some cases hence source of humour. I believe taking life too seriously is stressful and can cause demise in the long run.
Now on a serious note: we can agree that consensus does not mean mean truth. Current consensus is that plaque starts below intima with various interpretations what the process might be. Theory seems plausible.
I am in total agreement with you that a highly stressed section of artery could develop fissures and progress to plaque as you describe.
I will ponder this conundrum for a while longer.
I always thought that the capillaries supplying the walls of the arteries were lined with epithelial cells. If I am not mistaken in this, then it is conceivable that the sort of epithelial damage that might occur in the lumen of the coronary arteries, (or any arteries) could equally occur in the epithelial cells of the artery wall capillaries (vasa vasorum).
Looking at the stimulus material given at the start of this blog . . . “A definition of advanced types of atherosclerosis . . .” it clearly talks about some type VI lesions, with a unstable surface, might be prone to bleeding and thrombus formation, and so developing a new layer to the lesion. This is described as occurring on the luminal aspect of the artery – Much as Dr K describes.
The earlier 2 papers review the formation of type I, II, III lesions. I have not read these papers properly (I was rather stunned by the unrelenting detail of the third paper which I did read) . . . but at first glance, they seem to talk about an initial stage in which an area of an artery thickens – adaptive intimal thickening, often asymmetrically. It is at this place that future lesions are proposed to develop. The next stage describes the presence of macrophage foam cells in the intima.
For me the waters became just a little muddier . . .
Endothelial cells in capillaries are fenestrated – they have holes in them. They are completely different.
How very complex our physiology turns out to be when you earnestly try to understand “how it works”. (I guess that the most “scientific” explanation is the one that makes most sense in a reasonably understood context.)
Trying to understand diabetes mellitus (DM) I acquired a copy of the Joslin’s DM “bibel” in an 1970 edition some years ago and there I read that the first sign (studied by electron microscopy) of the disease was that the basal lamina in the capillaries were affected. As far as I remember this lamina was thickened which also makes sense to me thinking about the problem with the peripheral blood supply.
Well, CHD is closely connected with DM so you may wonder how this observation associates with what we discuss now.
Tissue factor (TF) is the key player here. In larger arteries TF sits under the endothelium and does not contact the bloodstream. Were it to do so, a clot would instantly form. As arteries get smaller and smaller, the endothelium becomes fenestrated (has holes in it) and TF is not present. It could not be, or the blood would instantly clot in all the smaller arteries, and we would die. Larger arteries cannot allow contact between blood and artery wall, so the endothelium is continuous, and the cells are bound tightly together – with bridges between then. In smaller vessels the contents have to be able to move in and out freely, or else there would be no point in the blood circulating. The exception to this is in the brain whereby the blood brain barrier (tightly bound endothelial cells are present in all blood vessels) there are no fenestrations. Anything moving into the brain has to be deliberately transported. Which is why the brain has to synthesize its own cholesterol, because LDL molecules cannot get past/through the endothelial (blood brain) barrier. [Which is, by the way, proof that intact endothelial cells are a perfect barrier to LDL]
Dr. Kendrick: Very interesting. Anywhere else in the body where non-fenestrated vessels exist (besides the brain and large arteries)?
Dr. Kendrick: Do we then have abundant tissue factor beneath the skin and lining of the gastrointestinal tract? Or since these tissues are full of capillaries, which must be non-fenestrated to keep us from bleeding to death, is this the source of TF in the event of injury? The interface with the outside world? Then the organs have mainly fenestrated vessels except the larger arteries?
Dr. Göran Sjoberg: Along this same line. Dr. K sent me to the dictionary yesterday to better understand the role of fenestrated capillaries; they have pores so larger ions can pass through. Is it possible then, in DM, for their thickened walls to prevent this?
I’ve always laughed at the word defenestrate which means to throw someone (or something) out a window.
How do the macrophages do their work of clearing-up if the endothelial cells they are under are so continuous? If it’s not so continuous where they need to do their work so they can get through, how is it that TF doesn’t mess things up? Is TF not present in a clot/plaque?
By exiting through the vasa vasorum. However, white blood cells can also move through endothelium when they want.
Dr K: Been away for a few days – returned to see the comment on the difference between endothelium lining arteries and arterioles and the fenestrated epithelium of the capillaries. The response did not really speak against the idea that epithelial damage (leading to clot formation and/or inflammatory reaction leading to a plaque) could equally occur on the vasa vasorum epithelial cells – even with its fenestrae – as it could on the coronary artery epithelial cells. For instance, both types of cells can be damaged by serum homocysteine. So I am now on the lookout for evidence as to whether the damage to an artery wall is initiated from the inside (lumen aspect) or from the middle of the artery wall vasa vasorum progressing towards the artery lumen. As I said before, the paper you referenced at the start of the blog clearly points to blood clotting of type VI plaques in the lumen of the artery, once the plaque has reached that stage.
I fell upon the point made above about LDL not being able to get through standard epithelial layers – and the excellent point about the effectiveness of the epithelial BBB keeping out LDL from the brain. When I first came across the idea that LDL, making its way across the epithelium, led to plaque formation, it seemed unlikely, and this idea way weakened further when researching diabetes saying that persistently high glucose levels damaged blood vessels leading sepsis and limb loss. I thought at the time that damage from high glucose levels better explained CVD, especially in view of the correlation between the increased risk of heart disease and diabetes.
I have not come across a good explanation of the mechanism by which LDL could traverse the coronary epithelium, and a mechanism that would allow for the rate of passage across the coronary epithelium to depend of the concentration of LDL (since it has been proposed that the level of atherosclerosis depends on LDL levels)
I can add a data point for elephants. For some years I kept a dried-out lump of elephant poop as an ornament. It was picked up in Etosha Pan game reserve i.e. from a wild elephant. It looked rather like a large pot scourer made of woody fibres instead of steel wool. I imagine it was composed mostly of semi-digested bark.
Moral of the story: get your roughage. After eating your rice, gnaw your chopsticks.
Made a list of parameters associated with plaque that I will have a quick look into. If anyone has ideas or volunteer to participate, please do. Purpose is to confirm a hypothesis without getting bogged down by excess scientific detail.
Consider only plaque formation on lumen side
Location: heart main branches, kidneys, neck, legs, arms, eyes
Endothelial injury as initiator of thrombus, cell apoptosis, fissure
Effect of blood composition
Presence of vasa vasorum
original lumen diameter
Fibrous cap, how formed, how long to form
Fibrous cap, does it need an endothelium
Fibrous cap stability
Structure by microscopic examination
Smooth muscle cell migration
new endothelial cell formation over thrombus
Life cycle from thrombus to mature plaque to rupture
Clearance, HDL, macrophages
Started looking into the first item on “THE LIST”, location in artery where plaques exist. To my surprise there can be plaque in legs and they can rupture and behave like plaque in coronary arteries. Focused too much on the heart, it it a very important organ. The revelation is that whatever is causing heart problems is also causing problems in every cell, tissue and organ. It is a systemic problem. What is the root cause?
Having too many specialists gives the impression that every part of the body is independent and there is a medication for it. Can anyone count the number of diseases and medications?
A question on the theory – I can remember reading years ago about the protein L-arginine. Some were writing about it as being the cure for heart disease. The theory was that L-arginine increased NO production, helped improve endothelium function and with that would help prevent a cardiac event.
I recall later reading studies that looked into L-arginine and heart disease. The studies found supplementing with the protein did not prevent heart attacks. Doing an internet search I found this article mentioning this.
“Arginine Intake and Risk of Coronary Heart Disease Mortality in Elderly Men”
“Abstract—From experimental studies, the hypothesis is derived that the amino acid arginine, the precursor of NO, could restore the impaired endothelial function and increased platelet activation observed in atherosclerosis. We investigated whether dietary intake of arginine is associated with reduced coronary heart disease risk in elderly persons. The study population consisted of 806 men aged 64 to 84 years at baseline who participated in the Zutphen Elderly Study, a population-based cohort followed up for 10 years. Information about habitual food consumption was collected by use of the cross-check dietary history method. Ninety (11.2%) of the 806 men died from coronary heart disease. Mean±SD baseline arginine intake was 4.35±1.07 g/d. Meat was the main source of arginine intake (37.1%), followed by bread (13.1%) and milk and milk products (12.1%). Arginine intake was not associated with coronary heart disease mortality. After adjustment for age, the relative risk (RR) for the medium tertile of arginine intake was 0.72 (95% CI 0.44 to 1.18), and the RR for the highest tertile was 0.71 (95% CI 0.43 to 1.19, P for trend=0.19) compared with the lowest tertile of arginine intake. After additional adjustment for history of coronary heart disease and diabetes mellitus, energy intake, body mass index, smoking habit, physical activity, and other relevant dietary and biological risk factors, the RR was 1.86 (95% CI 1.06 to 3.27) for the medium intake and 1.56 (95% CI 0.83 to 2.93) for the highest intake (P for trend=0.17). These results do not support the hypothesis that dietary arginine intake lowers the risk of coronary heart disease mortality.”
L-arginine may be harmful for heart attack patients
By Stephen Daniells, 04-Jan-2006
L-arginine amino acid supplements for heart attack patients may do more harm than good, according to a new study.
What went wrong with L-arginine? If it increases NO production and helps improve the endothelium, why wasn’t there a reduction in cardiac events observed?
HI SOUL and L-arginine studies. My background is mechanical engineering, solving problems, make sure things work. Researching medical literature is for self preservation.
Mice benefitted with L-arginine + C + E. Food composition was same for all mice.
Elderly people did not benefit, each person ate different foods.
I keep a food diary to keep my weight stable, and to monitor AFIB when I had the problem years ago.A food questionnaire is totally unreliable in predicting outcomes in a population study.
My approach is to read the studies, fix the diet, keep records, and monitor effect of adding supplements. Your health is your responsibility, takes a bit of work.
Well they didn’t test the protocol for a start and then as L-Arginine can increase friskiness maybe their hearts couldn’t stand the strain. 😀
Dr Ignarro, he of the Nobel prize for medicine, says one should supplement 4gms of L-Arginine with 200mg of LCitrulline daily. So presumably this is on top of what is naturally acquired. His book “NO more heart disease, is slightly rah rah, that is long on exhortation and short on studies. On the other hand who would fund them?
Another question, is supplemented L-Arginine bio-availble?
I find beetroot, for example, has a more dramatic effect on my BP than say roquet lettuce, even though the lettuce is top of the NO foods and beetroot is only number 10
Go figure as they say
I went back and read the entire paper. In fact the abstract is slightly misleading, in that the paper deals with dietary L-Arginine based on food questionaires, and the supplementation was from a cross-referenced paper, in which the study size was small, and the duration short.
As someone else has said, access to the stuff is very much through body-building sites. So let us turn the question on its head, the body-builders buy the stuff for improved blood flow in muscular tissue, which would seem to be from tha NO effect of arterial relaxation. Is it a placebo effect, and are they wasting their money?
Dr. Kendrick, have you seen this: “‘Huge advance’ in fighting world’s biggest killer” from the BBC? I hope you have enough data to dissect it for mere mortals like me.
I wonder what terrible malady James Gallager is suffering from, which causes his brain to write such establishment generated rubbish. I’m just making another batch of dark chocolate truffles with plenty of cream. Cholesterol? Yum yum.
Hi Solomon: Hypercholesterolaemia is the disease that needs curing and generate profit. The new drug is a huge improvement, 1 in 74 patients benefited compared to 1 in 150. The limit to how low cholesterol should be reduced is zero, nobody then would die from heart disease. Take this recommendation with a grain of salt.
It is my opinion, based on attending the HeartUK conference 18 months ago that the next step driven by Pharma is to get Hypercholestemenia (spelling?) definition levels lowered. They would like to increase membership of this group for obvious reasons
Prof Sir Nilesh Samani, the medical director at the British Heart Foundation, said: “This trial is a significant advance.
“However, the trial was stopped early after only 2.2 years of average follow-up and therefore it is difficult to be certain about the actual extent of the longer term benefit, including the impact on dying from heart disease, as well as longer term safety.”
I wonder why it (and such other trials) are always stopped “early”.
To the last sentence add: ” and don’t forget to drink your beetroot juice”.
Another good NO synthesizer.
Buy a nutri bullet, stick in a beetroot, handful of spinach leaves, half an apple or some berries, add some liquid (almond milk or even water) and blend
Smartersig, I would like to mention something that goes back 50 years, and, to my mind, illustrates early infiltration of the glorious concept of the NHS by big business.
I had my pre-natal classes in a snazzy new maternity department, and was herded round the new milk kitchen with the other expectant mothers. Oh, it was magnificent, ultra clean and full of tins of commercial baby formula….none of that NHS National Dried rubbish, and oh so much better than breast milk…..clean, convenient, full of all the stuff babies needed. Of course it was sponsored by Big Commerce, and once my baby was born, I was given the ultimatum of establishing breast feeding within 3 days(!) or, the baby would be introduced to the bottle of formula. Even for the baby, that was so much easier……and that was the job complete……off home with a couple of free tins, and hooked onto the stuff….. in fact, my second child never even got the chance to try the breast …….the preferred method was to immediately suppress my milk with a couple of tablets, and hey ho! another child hooked onto the same formula.
Kerrrrrr- ching-ing-ing..big time!
Could all that unnatural feeding contribute to the ill health we see today?
It could do, but we are also subjected to a generally poor diet, even when we think it is good. The problem there is, most of the “fresh” food is grown in an adulterated way, with plenty of glyphosate thrown around on the basis “it is so safe you could drink a tumbler full”. The way to compensate is masses of vitamin C, and plenty of other vitamins.
In my opinion it must contribute along with all the other processed foods we have all consummed over the years. We can’t beat ourselves up about it as it was the way back then. We can only march into the future with inquiring and questioning minds and be thankful for the Dr Kendrick’s of this world for giving us the opportunities to do so.
Interesting article on this no plaque tribe of people. Their infection rates are high though, could this be because of their low Cholesterol levels ?
Click to access PIIS0140-6736(17)30752-3.pdf
“few coronary artery disease risk factors, have the lowest reported levels of coronary artery disease”
According to the study summary they measured conventional risk factors. The assumption they make is LOW CAC = LOW CORONARY ARTERY DISEASE. Pay per view.
“These findings suggest that coronary atherosclerosis can be avoided in most people by achieving a lifetime with very low LDL, low blood pressure, low glucose, normal body-mass index, no smoking, and plenty of physical activity. The relative contributions of each are still to be determined.”
Very low LDL can only be achieved by drugs. Investigators were all PhD and MD, what would they think about eating more saturated fat, cholesterol, and less carbs?
“high infectious inflammatory burden”
Cause could be anything. What did they die from? Decreasing LDL does not increase hsCRP
The thinkers on this site should consult this link
Although their average life expectancy is much lower than ours we can still say that their heart disease is much lower than our sub population that marries with their age range. If we looked at westernized populations of an average age of 40 t0 50 we would find plenty of heart disease and lots of heart disease related incidents. Their diet has a lot in common with the preaching of Dr John Macdougal and his work. As for Carb’s I also associate low Carb with reducing or eliminating simple carb’s. Complex Carb’s that do not cause rapid blood sugar rises are still part of my diet.
smartersig: The average life expectancy doesn’t tell us much. If the average woman has nine children, the infant and child mortality rate must be very high, or they would quickly outstrip their resources. They do mention the above-70 population. It would be interesting to know the life expectancy of those who survived to adulthood.
Unless I suspect their diet causes a reduction in life expectancy then quite frankly I am not interested in how long they live. There are a whole multitude of reasons why they do not live as long as us but I do not want to lose sight of the wood for the trees if as the evidence suggests, they have little or no CHD. I think Zoe Harcombe has hit the nail on the head with the line ‘its not what we put in our diet but what we take out that gives us most bang for our buck’. So it is kind of sad when we get embroiled in meat V Veggie’ arguments when both can be healthy if done correctly. If what they eat plus 17000 steps per day staves off heart disease then thats all I need to know as I doubt very much that either of those two are contributing to their shorter life span.
Their average life expectancy is probably skewed by high infant and child mortality. It would be interesting to compare CVD health of their 60 and 70 year olds with that of ours. As well as other metrics: dental health, etc. My guess, it would confirm the findings of Dr. Price…
And when we have consulted, one of the things to think about is: we have to eat food contaminated by glyphosate. Next?
The Maasai have an opposite diet, high in fat and low in carbohydrate. Yet they also have a low rate of heart disease. The common factor appears to be a lot of walking.
Maasai are estimated to walk 20 km a day. The Tsimane 17,000 steps which equates to 13 km.
The other common factors may also be no sugar, no processed foods, no oil
I am inclined to agree…..unrefined diet is the key here…..I look at the shape of some very active Nurses these days, and they must walk miles in the course of a shift, ( as I did), yet due to having precious little time to take proper meals, they survive on expensive junk extracted from the hideous vending machines proliferating in our hospitals.
Oh dear….I’m off on one today.
In the Sheffield Hallam Hospital virtually every ward has a Coca Cola etc vending machine at its entrance. The most active doctor in the hospital is Dr Pepper. You will find a similar situation in most other NHS hospitals. The NHS is in the business of promoting illness and disease, it is what drives the profits of their sponsors and main controlling body.
smartersig and Jennifer.
Shocking, isn’t it. Have you been on a train lately? There is nothing, NOTHING on the trolley that I can eat. I make my journeys in to fasting days.
Same in Australia. The vending machines in hospitals are full of Coca Cola and some water. At my hospital they have signs to make healthy choices depicted by a red or green dot. Water is green coke is red however the coke is dispensed far more than the water. Even our childrens hospital has a MacDonald”s shop in the foyer. It was argued against but the “how can you deny sick kids the pleasure” argument won.
David Gillespie (davidgillespie.org) has a recent article titled, “Why Vegetable Oils Are Much More Deadly Than Cigarettes.” Aldehydes, and specifically in fast-food restaurants, because they are reheated so many times.
Thank you for this link Gary. My thoughts are the oxidation damage could be mitigated by sufficient extra vitamin C. What are your thoughts?
AH Notepad: I hadn’t thought about it, but it is probably so. It was a powerful vegetarian lobby group in Washington, D.C., called the Center For Science in the Public Interest, which pressured the fast-food industry to switch from beef fat for frying first to trans-fat, then to vegetable oil. Both Death by Food Pyramid and The Big Fat Surprise discuss this.
Sucessful angioplasty 23rd Dec 2016.
Back with vengance Feb 2017.
Faced now with choice of drug eluting stent. Surgeon wants it. I’m opposed never wanted a stent.
I feel bad because I questioned his judgement.
Compromise, drug eluting balloon angioplasty.
Stent only if dissection present or recoil is not controlled.
Follow up treatment asprin for life plus clopidigrel for 8 weeks. I am terrified about this as I see admissions for bleeding secondary to clopidegrel frequently.
I eat LCHF. Nil sugar. Healthy weight, no diabetes Cholesterol numbers better than perfect so go figure.
Only thing is I have been under severe stress.since Dec 29th. I have put on tummy fat as a result of all my natural cortisol floating around. I am convinced the stress is a contributary factor in the failure. The original stressors are still there. I have no control over them. I am trying to be calm but it is not working. I go in tomorrow but I think this new angio is heading for failure before it has begun.
Anne . . I guess you will have had the angioplasty procedure by now.
What is the moral that I learnt from my angioplasty . . .
After a very bad virus, while I was under stress at work I developed Premature Ventricular Contractions – causing missed beats – which got worse as I came under physical and mental stress. Had ‘turns’ on 3 occasions – the heart started racing, head thumping and PVC rate shot up. During the second turn my GP thought I was having a heart attack. Hospital tests were done – a small to medium blockage in one of the coronary arteries was discovered. It was decided to put a stent in, which did happen. Before the procedure everyone said you would feel much better afterwards. I did not thinks so because, even with my limited knowledge of how the heart works, such a small blockage could not be the cause of my problems.
Anyway, it didn’t do any good – PVCs still there – tiredness, weakness (of course this could have been the statins). There is ultrasound scan evidence that I had an infection of the pericardium surrounding the heart and that was causing the electrical disruption. It took a year and a half for the body to repair . . slowly beating back the infection/ repairing damage.
The moral: Stents are often put in place because ‘we can’ – even when no benefit is likely.
You were describing your situation in a previous comment: You said that you had very little stenosis in the coronary arteries . . . so I was surprised when you said the medics were offering an angioplasty.. I know little of PAD (I knew nothing 15mins ago), but what I read increased my puzzlement over the angioplasty. (I also came to understand your focus on vascular health and the importance of NO)
Anne, you have left me with a swirling mass of questions, not least because you seem to be doing all the right things and have such good blood metrics.
. . . I do wish you well and good progress in the future.
Thanks for your well wishes Anthony. It’s all over now. Sucessfull angioplasty with just the drug eluting balloon NO STENT. He has been very emphatic that if it fails within 18 months it will be the stent. He is giving himself a good margin and I made a promise i would take the clopidegrel and asprin. So I have my fingers crossed. Like you i have a swerling mass of questions. Why has my left leg been affected so badly when my right leg which had my first ordinary plasty done in 2013 is still going strong. My left leg in 2013 was totally clear. In early 2016 it only had a very small amount of plaque but none in the area I had done. By late Nov 2016 I had this blockage greater than 75% which was successfull opened in Dec 2016 but by Feb 2017 it was back. So now I am trying very hard not to react to the stressors which have been eased somewhat as I am on leave for 8 weeks practising mindfulness, meditation and hopefully after a few days will be back to having my daily walk. I am on the dreaded clopidegrel for 8 to 10 weeks. I am crossing off the days. Only 53 or 67 to go. Cardiac wise I have no idea as to whether it has progressed. Most would say highly likely but given the good condition of my right leg maybe not. However I am not about to have a coronary angiogram to find out.
So are there food to eat that would naturally help unclot. Please tell, I like to use food, instead of medicine.
David Chow: One that certainly plays a role in endothelial health is vitamin E, particularly d-tocotreinol, found most abundantly in red palm oil and annatto seeds. Easy enough to switch from whatever oil you use in cooking to red palm oil. May be better to get it from Ecuador than Indonesia, because of the orangutans. Annatto seeds can be crushed and used to flavor stews. One of the main reasons we eat healthy fats, such as those from ruminants, fish, and tropical palm and coconut, is for the fat-soluble vitamins, especially E, which acts as a preservative, but also D.