24th September 2017
‘The flow of rivers and streams in their boundaries . . . the circulation of the blood in our arteries and veins . . . the flight of the insect, the bird and the airplane; the movement of a ship in the water or of a fish in the depths . . . these are all, in major degree, varied expressions of the laws of fluid mechanics … Everywhere we find fluids and solids in reactive contact, usually in relative motion; and everywhere in this domain, the laws of fluid mechanics must control.
Application of the laws of fluid mechanics to the natural conditions in the circulatory system reveals a rational and demonstrable basis for the localization, inception, and progressive development of atherosclerosis.
Atherosclerosis does not occur at random locations. It does occur uniformly at specific sites of predilection that can be precisely defined, predicted, and produced by applying the principles of fluid mechanics. The areas of predilection for atherosclerosis are consistently found to be the segmental zones of diminished lateral pressure produced by the forces generated by the flowing blood.
Such segmental zones of diminished lateral pressure are characterized by tapering, curvature, bifurcation, branching, and external attachment. Serpentine flow in a relatively straight vessel also produces segmental zones of diminished lateral pressure.
Although these anatomic configurations occur in many variations of geometry, their common feature is a pattern of blood flow conducive to the production of localized areas of diminished lateral pressure. This is the initial stimulus.
Atherosclerosis may therefore be considered to be the biologic response of blood vessels to the effect of the laws of fluid mechanics, that is, the diminished lateral pressure generated by the flowing blood at sites of predilection determined by local hydraulic specifications in the circulatory system.’1
Not my words, and quite poetic I suppose. What does it mean. It means, if you accept what is written, is that atherosclerosis forms exactly where you would expect it to form – if the initial stimulus is ‘diminished lateral pressure’.
My last blog was primarily a looking at the primary stimulus for the initial formation of atherosclerotic plaques. I like to use the term biomechanical stress. I am not entirely certain if this means anything. But the general idea is that atherosclerotic plaques start at the points in blood vessels where there is the greatest ‘biomechanical stress.’
Several people who know far more about fluid dynamics questioned this. I think that they are all probably right in what they say, and the mathematics are well beyond my understanding. However, what I do know, and what are facts, are the following:
- Atherosclerotic plaques inevitably occur where is there is tapering, curvature, bifurcation, branching and areas of external attachment.
- Plaques never develop in veins, regardless of tapering, curvature and branding and suchlike.
- Plaques never develop in the arteries and veins in your lungs – unless you develop pulmonary hypertension (raised blood pressure in the lungs) – though a caveat applies.
- Plaques often appear on one side of an artery, and not the other (i.e., they do not encircle the artery).
- If you take a vein from the leg, and use it as a coronary artery bypass graft, it will rapidly develop atherosclerotic plaques.
Therefore, whatever term you want to use, however, you wish to understand it, it is clear that in order to get a plaque to start, you need to apply some form of ‘stress’ to the blood vessel, and the blood pressure needs to be at a certain level – or else nothing will happen. This is true, no matter what the LDL level, or the blood sugar level, or whether you smoke, or [insert any one of eight thousand risk factors here].
Ergo, there must be some form of damage occurring at the point of high biomechanical stress, that triggers plaque development. Under biomechanical stress, the first part of the artery to suffer will be the endothelium – the layer of cells that lines the arteries. If endothelial cells are stressed, damaged, or dysfunctional, this is the trigger for plaques to start:
‘In view of the ever-increasing prevalence of ischaemic heart disease in the developed and developing world, it has become imperative to identify and investigate mechanisms of early, potentially reversible pre-atherosclerotic changes in the endothelium. To date, the most clearly defined and well-understood early precursor of atherosclerosis is Endothelial Dysfunction. In fact, Endothelial Dysfunction can be regarded as the primum movens of atherosclerotic disease.’2
I guess that primum movens is Latin for ‘the single most really important thing.’
In short, you damage the endothelium, and that releases the atherosclerotic dogs of war. What sort of things are known to increase endothelial stress/damage. Here is a list, off the top of my head, of a few factors that have been identified.
- Smoking
- Air pollution
- Diabetes
- Cocaine use
- Dehydration
- Infections/sepsis
- Systemic Lupus Erythematosus (SLE)
- Lead
- Stress hormones
- Avastin
- Omeprazole
- Cushing’s disease
- Kawasaki’s disease.
I could go on, and on, but I think that is enough to be going on with. All of these factors have been demonstrated to cause significant damage to the endothelium – in different ways – and there is another thing that they all do. They all increase the risk of dying of CVD. Some of them enormously increase the risk. A young woman with SLE has an increased risk of dying of CHD of 5000% (relative risk increase).
When you are looking at a 5000% increase in risk you are, without the slightest shadow of a doubt, looking at a cause.
The only other increased risk I have ever seen to match this, or in fact beat this, is in young people with sickle cell anaemia where the increased risk of stroke is 33,000% (relative increase in risk). Yes, not many young people get strokes, but an increase of 33,000% is difficult to argue with.
Why do they get so many strokes? It is, in part, because the ‘sickle’ shaped red blood cells clump together more easily than normal shaped red blood cells. Once they clump together, they form clots, and these clots block arteries. Often in the brain – but also elsewhere. It is not as simple as this, but that will do for now.
There is another thing about sickle cells anaemia that I find of great interest. It is the only condition (at least the only condition I have come across), where atherosclerotic plaques can form in the lungs – at normal blood pressure.3
Why does this happen? Well sickle cells are not round and smooth. They are crescent shaped, and spiky at the ends, and stiffer than normal red blood cells, and they are more likely to cause mechanical damage to the endothelium.
‘A further mechanism of endothelial dysfunction is attributed to the rigidity of sickled erythrocytes (red blood cells) causing mechanical injury to the endothelial cells.’3
In addition:
‘The sickling process leads to vascular occlusion, tissue hypoxia and subsequent reperfusion injury, thus inducing inflammation and endothelial injury. This causes a blunted response to nitric oxide (NO) synthase inhibition.’3
Yes, our old friend Nitric Oxide again. Put simply, sickle cells crash into, and damage endothelial cells, which then stop producing as much NO. This endothelial dysfunction then leads on to atherosclerosis. All of this happens with no other risk factors present, and in arteries where atherosclerosis is normally never seen. Which means that we are looking very directly at cause, and effect. Physical damage to endothelial cells, no other factors required.
Now, I am aware that many people wonder why my series on what causes heart disease/cardiovascular has been so long and meandering. One major reason is that there is so much to try and find out, and explain. Also, and perhaps more critically, if you are going to try and understand cardiovascular disease fully, you must attempt to fit everything together, and that does take time.
For example, you must explain how: SLE, sickle cell anaemia, Kawasaki’s disease, omeprazole, diabetes, smoking and infections (to name but seven) can all cause CVD when, superficially, there is nothing to link them. Certainly none of the established, mainstream, risk factors.
There is no point in saying that, yes, they all cause heart disease, and that’s that, just add them to the list. There is a requirement to fit them within a single process, and it must make sense. It also has to be supported by the facts – as far as that is possible.
Equally, there is no point in saying CVD is ‘multifactorial’, which is the normal defence of the mainstream when pressed on why many people, with no risk factors for CVD, still get CVD. The word “multifactorial” explains nothing, it is just an escape route for those pressed to explain the many ‘paradoxes’ or refutations that keep on appearing.
If, for example, you cannot explain how sickle cell anaemia causes atherosclerotic plaque formation, in pulmonary arteries, this means you do not understand, or do not wish to understand, the underlying process. It fits nowhere within the accepted major risk factors, yet it increases the risk of stroke by 33,000%, and causes plaques to develop in the lungs. So, you cannot just ignore it, relatively rare though it may be.
So, where have we got to? Where we have got to, I believe is to demonstrate that the trigger factor for CVD is damage to the endothelium. If you don’t damage the endothelium nothing else happens. The damage happens at well recognised places where the biomechanical stress is at its greatest. Which means that, with no biomechanical stress, there can be no atherosclerotic plaques.
However, it takes more than just biomechanical stress. You also have to have, at least one, extra factor present to trigger endothelial dysfunction. Then … next episode.
References:
1: From Chapter 8 Coronary Heart Disease: The Dietary Sense and Nonsense: George V. Mann: 9781857560725: Amazon.com: Books
Dr. Malcolm Kendrick 
Thank you Dr Kendrick. I hope you are enjoying good health.
Atherosclerosis may therefore be considered to be the biologic response of blood vessels to the effect of the laws of fluid mechanics, that is, the diminished lateral pressure generated by the flowing blood at sites of predilection determined by local hydraulic specifications in the circulatory system.?
Repair with the wrong material?? with stuff that happens to be present for other reasons?
I don’t know but it seems to me that the wrong guys are being accused.
So instead of drugs we need to be re-engineered?
Maybe we just need some more vit K2.
.
So, wouldn’t reducing blood pressure (essential hypertension) to say, <=130 / 80 via drugs be of benefit? I know you've previously said that all cause mortality isn't affected by the reduction of moderately raised blood pressure, but isn't stroke reduction a good thing? A stroke may not kill you immediately but the long term ramifications can be significant… before your eventual demise.
Mark,
Dr Kendrick has also previously said that elevated blood pressure is the result of the narrowing of vessels due to CVD, not the other way around.
Perhaps that’s out of date?
Hm. Fight-or flight response, grueling sports activity, scary movies — they all MOMENTARILY increase BP.
Enough to start the damage? Then that damage increases BP . . .
Modern chronic stress syndrome. Certainly enough.
I have CAC 70 w low blood pressure, never had high ever…. hmmm
“…and the blood pressure needs to be at a certain level – or else nothing will happen.”
I can easily imagine that the BP threshold level would be different for different people and other variables within an individual. Riskier to chop wood than to jog?
Can you cite a ballpark threshold?
Though that certain level is required for something to happen, it’s not on your list of “factors”. ??
(Will we eventually get definitive lists?)
What a cliff hanger! Wicked!
I did not know about the Mann book. I will get a copy, it looks like it will be suitable reading.
Another good one.
Another analogy perhaps – sort of reminds me of ox box lake formation: flowing, meandering water…different flow rates at bends in the terrain…erosion and deposits at the bends (always in the same place)… Silt, stones, debris carried in the flowing water (i.e. that one extra factor e.g. high amount of small LDL particles…stress hormones or whatever risk factor you favour) and so on aiding the erosion on the outside bend and being deposited elsewhere.
That extra factor…for those in the 27% (wasn’t it?) with no conventional risk factors (who have had a CVD incident) that’s the problem in identification and future prevention…but can conventional risk factors be that easily confirmed as the additional factor/culprit anyway?
,
Fluoride belongs on that list too.
http://fluoridealert.org/studytracker/?effect=cardio-2&sub=&type=&start_year=&end_year=&show=10&fulltext=&fantranslation=
This is getting more exciting than many thrillers I have read. And more worthwhile!
I’ve looked for an answer to this before but haven’t found one. If family history increases one’s risk of developing heart disease, what is it in the history that increases that risk? If it is just adherence to lifestyle choices copied from family, eg smoking, sedentary habits,diet etc. then that is within the power of the individual to change, but if it is (also) genetically caused then is there something in the genetic makeup that causes predisposition to endothelial stress/damage? This is a statement from the website of the British Heart Foundation:
Genes can pass on the risk of cardiovascular disease
If they can, what mechanism do they pass on? Please ignore this if I’ve missed some blindingly obvious explanation.
Fluid mechanics are the guys who proved that the bumble bee cannot fly. I wonder if the writer meant shear stress more than a threshold value when he was talking of diminished lateral pressure, because the lateral pressure diminishes 72 times a minute over the whole artery, but the entire arterial system doesn’t become clogged with plaque.
Incidentally, given the importance of NO, I can see where the O comes from, but where does the N come from? Is it recycled, or do we get it from our diets? And if the latter, protein is the only N-rich food I can think of, so how do vegetarians fare?
Diminished lateral pressure. How diminished?
I’m thinking that what might be meant is a diminishment to well below ambient pressure such that the endothelial cells rupture from within.
JD,
The idea of rupturing from within never occurred to me, I must admit.
Following on from your suggestion, there’s another possible mechanism for flexing the endothelium the wrong way. If a small section of arterial muscle were to go into spasm, such that it contracts while the rest of the artery is relaxing, you could get reversed localized bending stresses in the endothelium.
Martin,
It is explained here.
https://www.britannica.com/science/nitric-oxide
and there;
https://en.wikipedia.org/wiki/Nitric_oxide_synthase
and here i guess;
https://en.wikipedia.org/wiki/Biological_functions_of_nitric_oxide
Dietary nitrate is also an important source of nitric oxide in mammals. Green, leafy vegetables and some root vegetables (such as beetroot) have high concentrations of nitrate.[17] When eaten and absorbed into the bloodstream, nitrate is concentrated in saliva (about 10-fold) and is reduced to nitrite on the surface of the tongue by a biofilm of commensal facultative anaerobic bacteria.[18] This nitrite is swallowed and reacts with acid and reducing substances in the stomach (such as ascorbate) to produce high concentrations of nitric oxide. The purpose of this mechanism to create NO is thought to be both sterilization of swallowed food, to prevent food poisoning, and to maintain gastric mucosal blood flow.[19]
Thanks, Gaetan. Thinks: must eat more spinach ;o)
So what is the effect of oral antibiotics on this process ? Is it damaged and if so does it restore over time ?
I think it is a mistake to assume vegetables and fruits don’t contain any proteins.
Foods rich in l-arginine and l-citrulline play a major role in the nitric oxide pathway and NO metabolism in the endothelium. Since the endothelium is the major “organ” to produce NO, which has many biological effects, damage to or a degradation of the endothelium inhibits NO production, which then results in changes in vasoreactivity, increase in BP, etc., which all increase the risk of CVD.
Andrew,
Good points about the roles of l-arginine and l-citrulline in the NO pathway . . . but it is worth bearing in mind that the impulse for the epithelial cells to producer NO is the shear force of the blood on the proteinaceous hairs that connect to the epithelial cells’ cytoplasm and extend through the glycoprotein matrix of the glycocalyx.
It is the forces on the glycocalyx and its hairs that are transmitted to the epithelial cells that stimulate the NO production. So, compromising the glycocalyx is all that is required to prejudice the power of the epithelium to producing protective NO.
See:
“High Glucose Attenuates Shear-Induced Changes in Endothelial Hydraulic Conductivity by Degrading the Glycocalyx” 2013
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0078954
It does seem odd that something that on the face of it might seem very destructive, like high sheer forces, in fact, is just the thing that stimulates the protective NO.
Antony,
It makes sense for NO production to increase with shear force. As the heart pumps and relaxes, blood flows past an area of endothelium now fast, now slow. If the endothelium produces NO at a constant rate, the fast flow will receive less NO per cc than the slow flow, leading to differing concentrations of NO along the length of the blood vessel.
Because shear force increases with flow rate, increasing NO production with increased shear force will help to maintain a uniform concentration of NO.
Very goo
Oh, Dr Kendrick, the more answers postulated, the more questions there are!
Reading this intriguing post I wonder if it has been a “smart” move of me to avoid all NO- “supplements” for 20 years?
Well, evidently I am not dead and still kicking!
And I am at 70 years evidently an anecdotal “poster boy” for Big Pharma CVD-resistance.
It’s all very interesting. You raise good questions but give almost no answers. Do you have the answers? Especially non-standard practical advice about CVD prevention. I hope to see someday all your findings together in one good article or book.
read what causes heart disease Part I to XXXVII.
You will definitely get answers, and in his books as well.
Once you understand the process, the answers become clear, I hope.
Yes, the result of reading your books and these articles has meant that a lifetime of avoiding all medication has been vindicated. The out come has been good health for me. However my husband who has done the same has labile blood pressure which at times is very high. When are we going to get some guidance on what can we do ourselves, other than avoid the obvious risk factors that you have outlined. Where does labile blood pressure fit into the CVD picture?
Wow. That’s a cracker. Thank you x 1000
Another post from Malcolm Kendrick… love Mar
On Sun, Sep 24, 2017 at 1:55 PM, Dr. Malcolm Kendrick wrote:
> Dr. Malcolm Kendrick posted: “24th September 2017 ‘The flow of rivers and > streams in their boundaries . . . the circulation of the blood in our > arteries and veins . . . the flight of the insect, the bird and the > airplane; the movement of a ship in the water or of a fish in the dept” >
I think it would behoove us all to remember that, while likely all, or nearly all, of us will suffer some degree of endothelial damage as we go through life, there is a repair process functioning as well. So preventing or stabilization of CVD would involve both behaviors that reduce the amount of damage and encourage the repair process. I’m part way through the THINCS essays, and one thing that sticks with me is that the risk from elevated BP is not linear. My 142/84 at 68 carries no greater mortality risk than 120/80. Seems to me that the simple fact of aging is going to cause some rise in BP without there necessarily being any underlying pathology. Could be that white-coat syndrome, and it not being properly taken gives a higher reading. In any case, I don’t feel particularly diseased, just slightly decrepit.
I kind of remember reading that those who lived outside of our civilization didn’t have that rise in BP over their lifetime. But it’s also possible that a slight rise over a lifetime is insignificant.
Also my understanding is to get a real accurate reading of BP necessitates taking it at different times during the day and even in different positions, like standing and sitting. But this is never done. Also those home devices seem to give different reading than in the doctor’s office.
Unfortunately the way BP is measured with a cuff on the upper arm is a poor method for determining your true blood pressure as it just measures your BP in the upper arm at a moment in time. What is more important is your central blood pressure, i.e., that pressure which is generated in your left ventricle. This is the true BP and is the pressure exerted on the brain, kidneys and heart. Hence why people that have had heart attacks and strokes often have normal BP because the pressure in the arm was reportedly within normal limits, yet their central BP was very high. One can have a high central BP yet “normal” by conventional upper arm BP measurements and therefore its important to measure and treat if necessary central BP rather than a peripheral brachial BP in the upper arm.
You surely must use ghost writers…………
When the heart beats – the muscle contracts and crimps shut arteries causing a reverse pressure wave ( similar to water-hammer in pipes) that travels backwards – away from the heart – until it is absorbed by the flexibility of the arteries. I think this is why the arteries near the heart are more likely to get damaged. The more flexible the arteries – the better they are at absorbing this shock wave. The curves again will be hight pressure points – any irregularity would increase local pressure.
It is fluid dynamics complicated by elastic arteries.
So any cause that increases the damage – high BP, low NO can be a factor. I’ve wondered if small clots from other places might act similar to sickle cells?
Stress – adrenalin – contracts arteries – reducing the elastic nature. Also increases clotting ..
https://en.wikipedia.org/wiki/Fight-or-flight_response#Reaction
Insulin is involved in the ACTH response –
The problem is when is a correlation causative – and what is the direction of the arrow of causation?
Most of what we think we know about this comes from ungrounded – or poorly grounded narratives.
The problem is that patients want answers – and there are lots of confident MD’s willing to spread narratives – it takes longer to explain what we don’t know than to parrot a narrative. Medicine is based on billable procedures not (mis?)educating patients.
I’m really enjoying the most recent few essays youve written here. I have a sense of something very interesting and important being revealed.
I’m quite relieved that we only have to concern oursleves with the Navier-Stokes equations rather than attempting to understand the utterances of the high priests of the cholesterol religion and all of their breakaway sects.
🙂
But I am also wondering how those cases of heart failure without significant vascular disease are going to fit in?
BTW the Schrödinger wave equation of quantum fame is in some ways related to the Navier-Stokes equations. There’s plenty of complexity to contemplate there without needing to invoke cholesterol.
Really? I’m roughly familiar with both (being an EE, I’m much more solidly versed in Maxwell’s equations), but I don’t recall Navier-Stokes capturing quantum effects. Please elaborate….
This makes me curious as to the potential causes for the significant increase in rates of CVD amongst astronauts, who I’d assume would be selected on high levels of health.
“Apollo Lunar Astronauts Show Higher Cardiovascular Disease Mortality: Possible Deep Space Radiation Effects on the Vascular Endothelium” https://www.nature.com/articles/srep29901
Well, the abstract of the article you linked seems to answer that question.
Sorry, worded that very badly, not my wheel house 🙂 I was thinking that the connection between damage to the endothelium leading (directly) to CVD is supportive of Dr Kendrick’s chain of reasoning; hence, finding the “smoking gun” may be easier than many think, i.e. just hunt for other mechanisms of damage.
They conclude that deep space radiation, particularly the energetic heavy particles, damages the endothelium.
Veins lie shallower than arteries, and have thinner muscular walls, so the venous endothelium must sustain more damage than the arterial endothelium. Yet there is no mention of venous plaque. So one must conclude that it is damage to the endothelium, plus [something unique to arteries], that initiates plaque.
Perhaps CVD is two processes. One causes damage. The other repairs the damage. There could be many causes as you describe, but if the repair process is working well then the damage would not accumulate. Thus it could be that only when the ongoing repair process is damaged that CVD results.
I would agree.
So what processes damage the repair process ?
Dear Bill in Oz
That is the question that has us on the edge of our seats.
“An Integrated Approach for the Mechanism Responsible for Atherosclerotic Plaque Regression” by AA Francis, in Exp. Clin. Cardiology, 2011;16(3):77-86
Andrew Larwood
Plaque regression is possible and good to know. According to article:
“Atherosclerosis is initiated by the response of endothelial cells (ECs) to injury caused by myriad noxious stimuli including hyperglycemia, hypertension, hyperlipidemia, infectious agents, obesity, modified lipoproteins, homocysteine, nicotine, free radicals, altered changes in arterial blood flow shear stress and normal spontaneous metabolic damage”
Looks like carbohydrate restriction would slow plaque progression.
An excellent offering Andrew . . . damn, yet another must read article.
Thank you
Lateral pressure (builds and) diminishes 72 times per minute causing localised forces (stress) to come and go at the same rate. Stress causes strain, which is when the material stretches as a result of the force. If the pressure profile is fairly constant throughout the circulatory system supplied by the left ventricular the elastic response profile of the vessels will depend on local geometric features, material thicknesses and material properties. If oxidised or glycated LDL has caused inflammatory response in/on endothelial cells how would this affect the materials elastic properties? Would the ability of the vessel wall to stretch under pressure be diminished? Would a threshold be reached where elastic limits were exceeded? Would this cause tearing and the formation of lesions which are then the same as cuts on external skin – immune response, swelling, build up of protective scab (containing cholesterol).
Single simple solution? Consume less sugar and carbs in diet to reduce blood glucose to reduce occurrence of glycation of proteins (including LDL). With lower blood glucose, insulin will reduce, the kidneys will not retain salt as much so less water retention needed to maintain concentration gradients so less hydrostatic pressure arising so less blood pressure required to maintain delivery of required blood flow, so vessel wall elasticity limits not exceeded.
When is your next book devoted to heart disease coming out?
Writing deadline end of November. probably spring 2018
I m glad to read this. And will buy it when it is published.
But I am also aware that the more distractions there are, the harder this deadline will be to achieve….
I am not writing like you, but to be honest I am finding it very difficult to deal or absorb, the flood of information, links and opinions put forward here. Bewildering !
Martin, good point . . . many papers that I have come across seem to focus on reduced shear stress at the artery wall as the driving factor for atheroma development; however, these areas *also* seem to correspond with diminished lateral pressure. So, is the correspondence between reduced shear stress and atheroma location simply an association . . . or is it the diminished lateral pressure that provides the association? It may be that both these physical correspondences are simply associations and that something else is involved.
To move from association to probable cause there needs to be some physiology. There are studies presenting the notion that epithelium, via the glycocalyx, can respond to shear stress. High shear stress keeps NO at a higher level. Reduced shear stress . . . less protective NO.
On top of this there is another possible association presented in this study: “Is arterial wall-strain stiffening an additional process responsible for atherosclerosis in coronary bifurcations?”. The 2011 study presents evidence that that the beating heart produces areas of increased stiffness (the sort of stiffness in a material produced when you stretch it) . . . Why should this predispose those areas to an atheroma? They refer to evidence that shows endothelial tissue supported on a “stiffened substrate” produces less NO as a possibility. (Umm . . . ).
The paper does echo ideas from other sources talking about ” . . . vascular remodelling (an adaptive process characterised by modified blood vessel morphology and function, allowing the vessel to cope with the physiological and pathological conditions). In other words the artery will respond to cope with changes in their environment . . . which brings me to Subbotin and his expanding intimal layers.
“Excessive intimal hyperplasia in human coronary arteries before intimal lipid depositions is the initiation of coronary atherosclerosis and constitutes a therapeutic target”
I think this idea has more legs.
I thought of an immediate corollary – what cause(s) might increase the friction of the endothelium/glycocalyx against the blood? Kind of the effect of the sickle cells in reverse. This one could run and run . . .
Diminished lateral pressure? I have trouble understanding the concept. Maybe I am too moored in the physics. Does anybody understand what Mann is talking about?
Lateral pressure must be compressive force acting in a plane parallel to an object’s surface, such as the ground pressing on the side walls of a basement. In the case of an artery (or a tube), thie force could be aligned axially along the tube wall or tangentially (around the circumference).
A fluid flowing inside of a tube will generate friction and hence exert lateral, axial pressure inside the wall. But clearly, faster flow = more pressure = more potential damage, so a diminishing would be a good thing. And if he is talking about variation, e.g. because of turbulence, it’s going to be both ways from a mean. So this is clearly not what he’s talking about.
Next, any pressure (static or dynamic) inside the tube is going to exert a normal (i.e. perpendicular to the surface) onto the inside of the wall. Due to the elasticity of the tube material, this gets converted into tangential force inside the wall material. But what it does, it stretches the wall material, so it exerts tensile stress inside the wall. Strictly speaking, introduction of tangential, circumferential tension could be considered a reduction of pressure. On the other hand, an unpressurized tube has a constant diameter precisely because it is free of tangential forces.
Maybe he was talking about dynamic effects? Consider a curve in the tube. The outside wall is going to take more dynamic pressure, which is exactly why the turns of a river left to its own will meander ever more over time. On the inside wall, you would get a lowered pressure because of the Bernoulli effect, but it is hard to see how this would be harmful. On top of that, the current hogs to the outside of the bend, so there is very little flow on the inner side anyway.
Am I just to dense to understand what Mann was trying to say with that statement?
If you artificially bend an artery, such as by putting someone’s elbow in a plaster cast for some months, does it become more prone to plaques?
Did not pay much attention to the hydraulic discussion until today. There seem to be separate categories and problems to look at:
a) HYDRAULIC REMODELLING which is normal, happens in everyone, and starts in early age regardless of primitive or modern era. No endothelial damage required. Intima thickening from hydraulic effect should not be called plaque, a confusing term.
b) DIET INDUCED REMODELLING. This causes a disease state with endothelial damage, fatty streaks, necrotic cores, intraplaque hemorrhage, blood clots etc..
c) DRUG INDUCED REMODELLING. Example would be statins, Q10 reduced, K2 reduced, diabetes increased, cell signalling affected etc..
d) MODERN CHEMICAL EFFECTS. Food additives, pesticides, fungicides, herbicides etc.
e) GENETIC COMPONENTS
Here’s something else I have been pondering.
Pesticides used to be mostly organochlorines. Farmers sprayed them with gay abandon, and even my father used them in the garden – and allotment – up until he read Silent Spring, which caused him to junk them. A big problem is that they have very long environmental persistence, so like the lead tetraethyl from petrol they may well still be around. Plus just because they were banned in the West didn’t mean we stopped producing them, we continued selling them to the Third World, from where we are importing food to this day. Even if they are no longer used there (unknown).
They were replaced by organophosphates, which vary a lot in toxicity from Sarin (pretty instantly lethal) to glyphosate (allegedly very harmless but now known not to be so). These are less environmentally persistent but are still being sprayed and thus constantly replaced in the environment and our food.
I will predict there has been NO research into the effects of a combination of organochlorines and organophosphates.
Would be VERY interesting to see a timeline of these substances vs. a timeline of CVD and other “modern” diseases.
Most farmers I know now use them only when there is an ongoing or imminent infestation, not prophylactically as used to be the case. Except for glyphosate, used not only on GMO crops but for pre-harvest dessication of wheat, rape etc. This was routine in the USA, Canada, etc. from where we import a lot of our bread wheat. The adoption in the UK is much more recent, less than a decade ago farmers here were dessicating their rape by heading and windrowing it – laying it in rows on top of the stalks then combining it later. Now rape for your heart healthy margarine and UK wheat for your essential biscuits and cakes is likely to carry glyphosate residues (ties back to work by Stephanie Seneff).
Food for thought . . .
Is there any way to determine how much damage I’ve already suffered? Is there a way to repair damage with feedback to know it has been fixed?
It does seem the emphasis of the hypothesis is shifting to the health of the endothelium under the mechanical stress of blood stream turbulence at points of maximum load. After all, if the endothelium is not breached then the repair mechanism is never called into action.
How far advanced is the science of endothelium health? Has it been deeply researched?
A couple of interesting papers on the functioning of DHA and its role in endothelial health. Of particular significance is the conservation of DHA in animal biochemistry for a very long (geologically speaking) time, and the high flexibility of the molecule in the context of cell membranes. Not sure of the effects of quantum tunnelling in DHA though.
Click to access pdfft
Click to access 12944_2017_Article_514.pdf
Your comment made me think of a Facebook group that is all about vit D, which also plays an important part in endothelial function. I googled it and there were endless papers for it, but I picked this one, https://www.ncbi.nlm.nih.gov/pubmed/25488441
Add thyroid to the list of factors.
“Low normal T4? Highish TSH (thyrotropin)? Rejoice: you may live an extra three years, according to the Rotterdam Study, which measured these at the age of 50. Participants with low-normal thyroid function went on to live up to 3.5 years longer overall and up to 3.1 years longer without CVD than participants with high-normal thyroid function.” — http://blogs.bmj.com/bmj/2017/09/25/richard-lehmans-journal-review-25-september-2017/
And if you have normal-normal thyroid function?
Another opinion – It is the lactic acid that provides the final trigger that causes damage to occur in arterial linings, but not so in veins. It is the presence of accumulated lactic acid in the smooth muscles surrounding arteries that ultimately causes plaques to form. https://jonbarron.org/anti-aging/arteries-and-veins
The things you can see on a google search – Do-it-yourself cardiac bypass surgery – made me LOL
And the the nomination for the “First smile of the day” prize goes to Randall!
@Martin Black
The actual link to the study is here:
http://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2653451
A correlative study can’t show cause and effect.
There are a lot of other papers that think the opposite is true:
http://annals.org/aim/article/741243/meta-analysis-subclinical-thyroid-dysfunction-risk-coronary-heart-disease-mortality
One can “prove” anything with correlative studies.
Of course there is also the argument if living with low T4 is really the same as living longer?
Malcolm,
What proportion of the arterial system is prone to plaques? Are you describing isolated spots or broad swathes/regions?
If the former, is there a clue here? For example, if stress is a driver then why is the whole arterial system not reacting albeit at different rates? Why the precipice effect? Is the mechanical stress highly localized enough to explain isolated reactions?
We are generally looking at isolated spots/plaques, although they can merge together. It is fully possible to have one single plaque in one coronary artery and that’s it. Enough to kill you.
“Diabetic” damage seems to start in the periphery and work inwards, ie. Peripheral Arterial Disease such as I have (and which is significantly worsened by hyperthyroid and improved when it goes back to normal, or below).
The classic explanation is that hyperglycemia damages the nerves starting at the furthest point from the spine, where the axons are finest, and the nerve damage results in the arterial damage, but how? I wasn’t told that bit.
I think that fluid mechanical stress on the arteries is a red herring in the search for the cause of damage to the arteries. The stress due to blood flow is just the instrument which causes the damage to an already weakened artery. What if the arteries are weakened by some yet unknown or unidentified cause? The blood flow in the areas which sustain the greatest stress will fail first. The level of weakness or injury to the artery will affect how high the stress needs to be to cause a “lesion”, so those with high blood pressure but relatively strong arteries will not suffer any immediate damage. Yes, reducing stress is desirable, but that will not address the real cause.
Hmm.. That makes me think of Pauling’s vitamin C deficiency hypothesis.
Dr Kendrick, Coincidentally at the same time as you put up this post, ( number 38 ) on the 24th of September, I made 2 comments on post 37. They are still waiting for moderation and so have not been read or discussed here by anyone. Could you please ‘release’ them ?
Per Dr. Joseph Mercola, some ways to naturally increase your level of nitric oxide:
Sunlight – https://articles.mercola.com/sites/articles/archive/2013/07/15/sun-exposure.aspx
Arginine –
https://articles.mercola.com/sites/articles/archive/2011/07/23/this-amino-acid-help-protect-you-from-different-diseases.aspx
Correct Breathing –
https://articles.mercola.com/sites/articles/archive/2013/11/24/buteyko-breathing-method.aspx
3 Minute High Intensity Exercise –
https://articles.mercola.com/sites/articles/archive/2013/11/24/buteyko-breathing-method.aspx
I would agree with all of these things. Mercola is not everyone’s cup of tea, but I think he gets many/most things right.
Hello
I read the first of the Mercola articles that were cited, about sun-produces vitamin D and heart attacks. Does this show in the statistics, for example southend France, Italy, Greece Turkey etc?
In part. Zoe Harcombe reviewed Ancel Keys seven country study and discovered that by far the most powerful association with CHD was latitude. There are, of course, confounders, but I often think that one of the reasons for higher CVD incidence in Asian Indians moving to Europe is a lack of sunlight.
Dr K
thanks for that reply which I followed up on Zoe H’s website. I understand better now why you are keen on sun exposure!
I am keen on anything proven to improve health and well-being and increase life expectancy. Sun exposure is pretty close to the top of my list.
This is my view on Dr. Mercola as well. You mustn’t believe all that he is writing. I though read with interest his newsletter every day. Sometimes there is a “pearl”.
Malcolm,
What do you think about the principle of “caution” which is actually my own guide-line today?
I.e. stay away from whatever you THINK may harm your health (e.g. farmed fish as just one example) and add whatever you THINK may improve your health (e.g. wild caught Alaskan salmon as one opposite example).
Not sure. Because some people have strange thoughts. My own principle is relatively straightforward. How did we used to live, or how are we designed to live. Mostly outside, mostly walking about or moving about, in the sun, mostly eating whatever (natural foodstuffs) we can get hold of, mostly socialising in smaller, supportive, tribes/villages. It seems to me whenever we study groups of people who live like that, they are very healthy and live for a long time. See under the Blue Zones. Of course it helps a great deal to have access to fresh water, a good medical system, excellent sewage systems, antibiotics, medical support in childbirth, access to year round foodstuffs, certain (vaccinations), good treatment for broken bones. In short, take the good bits from modern medicine/society, and retain as many of the good bits of traditional lifestyle.
I find Mercola to be an excellent gatekeeper, I’ve been exposed to many ideas I would not have been without him. Well worth putting up with his occasional weirdness. And he has the cojones to keep plugging away at the vaccine issue.
Ummmmm, for reasons that are obscure to me, I have never wanted to visit the Mercola website..But having read your opinion Goran & Dr Kendrick’s, I went there tonight and signed up to the daily subscription.
The ebook on hypertension looks worthwhile..
There are times when Dr Mercola seems quite far fetched, but over the years I have been impressed by the number of articles and interviews that seemed unlikely at the time have subsequently been corroborated. As has been said, he is a ‘gateway’, leading one to research further.
Bill in Oz: Dr. Mercola’s website is well worth subscribing to. I don’t read everything, but there are occasional gems, especially interviews (I usually read the transcript). I’ve gained an enormous amount of knowledge about a diverse variety of topics involving health from about five years of daily reading.
On the whole Dr Mercola has made the research road a much smoother ride. . . Particularly at the start. . . . . topic number one “How have statins damaged me?”.
I am not totally on board with everything . . . eg as a chemist, the notion of structured water is interesting but . . .
Perhaps of interest: L-Citrulline might be more effective at increasing NO levels in the blood than L-Arginine.
http://jap.physiology.org/content/early/2015/05/22/japplphysiol.00192.2014
http://jn.nutrition.org/content/early/2017/02/08/jn.116.240382.abstract
We’re getting there…can’t wait for No 39
I hope Dr Kendrick has enough X’s, V’s, and I’s in his ditty bag ;o)
L, C and M will come to the rescue!
40 is XL and 90 XC 😉
Is oral supplementation with D3 the same as sun induced endogenous vitamin D production? Since vitamin D is not widely found in food and when it is, it isn’t in vast amounts, nature must have intended us to get it via sun exposure. Can we therefore, be absolutely certain that oral supplementation of vitamin D is healthy?
Is it just about the vitamin D or the co-factors (some of which I bet we haven’t even discovered) which are produced alongside the vitamin D when skin is exposed to sunlight?
sunlight stimulates NO production as well.
“sunlight stimulates NO production as well.”
It isn’t quite so simple – Mercola provides no reference for his narrative as usual ( It is very important to check his claims) – but :
https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=sunlight+Nitric+oxide
Click to access 990635.pdf
It isn’t the just the average level of NO – it is where the NO is. A lot! Nitric oxide is highly reactive (having a lifetime of a few seconds) – thus producing it in the skin is not likely going to matter much for the heart arteries.
Nitric oxide is also generated by phagocytes as part of the human immune response – “the role of ·NO in inflammation is complex with model studies involving viral infection suggesting that this gaseous mediator can also promote inflammation” . The claim that getting exposed to NO is good for the heart is just an ungrounded narrative at this point – there are rules to limit the exposure:
https://en.wikipedia.org/wiki/Nitric_oxide#Occupational_safety_and_health
I’m more interested in the other photo-chemicals produced in the skin. Is the correlation with low vit-D and health problems due to the fact that sick people are less likely to be out-doors?
Yet I think low vit-D is involved in depression which is often co-morbid with CAD – but I once read that there are several other photo-chemicals produced in the skin – thus confounding variables ( also confounding is the reduction of the feed stock). I’ve looked, but can’t find, the other photo-chemicals produced in the skin – could be I read some ungrounded narrative – but I doubt that vit-D is the only product of sun and the skin.
It appears that the NO produced in the skin lasts for a long time. I have no idea how this is achieved, as I thought NO would last about two seconds, max.
It’s also possible that sun exposure causes NO to be produced in many areas of the body, not just the skin. And possibly sun exposure has many effects on the body: vasodilation, increase connective tissue repair, etc. All of which can contribute to reduction in CVD.
sunlight stimulates NO production as well.
That’s the gist of my question: there’s an association between certain diseases and latitude which is assumed to be down to vitamin D but could it (in addition) be other factors? Could it even be that oral vitamin D on its own is harmful without the co-factors of raised NO, deep tissue IR, relaxation effects etc caused by full spectrum sunshine? Or could the latitude associations between heart attack / disease translate into altered geomagnetic differences at different latitudes?
@ Mark Johnson:
I would look at Inuit. They would not be likely to get any UV-B or much UV-A even during the artick summer. Yet, they were doing ok on a traditional diet, so one would assume that Vitamin D from seafood and marine mammals is enough.
Caveats:
1. Maybe whatever sunlight produces besides Vitamin D can be eaten also?
2. What was life expectancy in pre-modern times? Are there any data on modern Inuit that have access to medical care and decent housing but shun modern foods that are shipped / flown up?
3. What about genetic selection?
As Malcolm points out some wavelengths of sunlight do more than stimulate the production of vitamin D.
On a personal note, putting the case for winter supplementation of vit D3. . . I have a skin complaint . . . parapsoriasis (flakey areas of the skin, can become sore) . . . had since I was in early teens. On the most of the body it was hidden away, but on the top of the hand, at the base of the thumb, I would get these raw patches . . . particularly in winter. I always put it down to the cold . . . sort of like chilblains.
When It got really bad about 15 years I was given NHS UV therapy. It worked . . . ah yes, remembering an Open University program . . . UV increases ‘dermal turnover’ . . so the rate of repair was greater than the rate of skin damage.
However, I learn a few years ago that parapsoriasis is an autoimmune disease. Soon after I read a piece on the Mercola site describing on vitamin D as an important modulating element in the immune system and that it may have a role to play in autoimmune conditions . . . suddenly all fell into place. The winter increase in parapsoriasis was not caused by cold but by running low on vitamin D. Now I know why the only time the skin cleared completely was in 1976 . . . (Do you remember 1976? . . . )
So, I supplement on vit D3 during non-summer months. 10000-20000 IUs a day.
I no longer have great embarrassing red stripes of damaged skin across my stomach, and no longer have the raw patches on my hands during winter. So supplementation is worthwhile for some, (and I believe for most in the UK)
Oh I used to get that – or something highly similar – on my elbows, and one worse than the other. Like a lot of other symptoms it resolved on LCHF, and probably being outdoors a lot has helped too with the vitamin D levels, and also hopefully NO. Rebalancing fat intake away from that horrid proinflammatory Omega 6 and towards relatively chemically stable saturated and monounsaturated fats and antiinflammatory Omega 3 too.
Maybe K2 also. I forgot to mention in a recent reply another current favourite cheese I was recently introduced to – Halloumi – which can be fried in butter, or olive oil, or cut into chunks and floated in my pseudo-Bolognese sauce. Probably high nutrient food in general, I once asked a dietician which nutritious foods I should stop eating in order to cram in all my mandatory carbs but never got an answer. As you don’t.
Antony, what is the difference between pseudopsoriasis and psoriasis?
Anyway, psoriasis is treated with special 311 nm lamps by Philips. Happens to increase Vit. D production, too.
Hi Eric . . . There does seem to be a difference between psoriasis and parapsoriasis . . . psoriasis seems to be a lot more aggressive, sore red lesions. When people asked about the rough patches on my skin, they would ask if it was psoriasis. I would say that it is “sort-of psoriasis” . . . but they are not sure what it is.
About 20 years ago when I saw a skin specialist (dermatologist?) he looked at my stomach . . . his eyes lit up . . . he rushed out of the room in a state of high excitement and brought back a colleague . . . “You must see this”, barely containing himself . . . “It is an absolutely classical case of parapsoriasis . . . See, it looks like someone with red hot fingers has come up from behind and held them against the stomach”. . . . pointing out the red finger sized stripes on both sides of the stomach.
I was caught up with his enthusiasm and expectantly asked what was causing it. “We don’t know”. Somewhat stunned, I offered “Was it genetic?” He came back with an emphatic “Oh no!”.
( He should have said : “It might be but I do not think so”). Meekly, I mentioned my father came back from Korea with it, and both my sons have it. He would not be moved on the genetic front.
As I mentioned previously, the condition appears to be an autoimmune response, with belligerent, misguided T cells invading the skin making a nuisance of themselves. The chances are that the lads of the family have a genetic predisposition: perhaps we need more optimal levels of vitamin D than others? Perhaps we are less efficient in its use? Perhaps we are less adept at producing Treg cells . . . Perhaps . . .
Hello Mark.
Don’t forget that vitamin D is fat soluble and stored by the body. If we get plenty of sunshine our stored supplies should see us through until ?January. So no need for the supplement until then – and then no more once the sun rays return in early summer?
The problem is that too many people in the UK do not get enough sun during our Summer months to make enough stored vitamin D to last the Winter months.
Especially Muslim women. Many of whom are seriously vitamin D deficient.
And, I would imagine, all the people who literally will not go outside without sunscreen. It especially bothers me to see children deprived of sunlight and vitamin D.
Depending on how you choose to review the literature a good case can be made that sunlight protects against malignant melanoma. It certainly protects against many common forms of cancer. Breast, prostate, colo-rectal etc. Studies in Scandinavia demonstrate that avoiding the sun is as damaging to health as smoking. The anti-sunshine meme is more powerful and far more damaging than the anti-cholesterol meme.
Antony Sanderson
Edward Hutchinson, who posts on this blog about Vitamine D, had some evidence that it’s life in the body is not that long, and certainly not the idea of a big stock in fat on which one draws at will.
My tactic is sun in the summer and supplements in the winter
On sun bathing . . . Having gone through studies and opinions over the past 4 years I see the suntan, the production of melanin in the skin in response to UVB, as an protection against high levels of UVB and UVA radiation. The only way to get this protection is to spend time under the UVB in sunlight. At the same time you do not want to spend so much time exposed to the UVB that you end up with skin damage (sunburn). So you need to build up the tan protection. The better the tan, the longer you can stay in the Sun . . . This is not new . . 1959, Newquay England, 9 years old, we children were given a schedule for being in the Sun: 15mins first day, moving an extra 15mins the next day, then extra 30mins etc., depending on how much Sun there was.
UVA does not produce sunburn in the way that UVB does, even so, it does cause skin damage. Even though UVA has less energy than UVB it penetrates the skin to a far deeper depth, down to the dermis. At this level damaging UVA rays can give rise to melanoma.
Studies as late as 2001 began to question the assumption that UVB was the cause of melanoma and proposed UVA was the prime cause.
Ultraviolet A and melanoma: a review 2001
https://www.ncbi.nlm.nih.gov/pubmed/11312434
The sunscreens of a few years ago were designed to stop the sunburn-producing UVB (putting a crimp of your protective suntan development). But while slowing the development of a protective tan . . . they allowed melanoma-producing UVA through.
Looking at the “Analysis of Trends in US Melanoma Incidence and Mortality” 1930-2016
http://jamanetwork.com/journals/jamadermatology/article-abstract/2593033
There was a dramatic rise in melanoma from 1980 to 2016. It may be that more US citizens became more well off and spent more time, at leisure, in the sun. Perhaps they were daft enough to ignore the warnings and were not taking precautions. . . . or perhaps they had taken heed of warnings and were smothering themselves with lashings of sunscreen. And of course, during the 1980s the ‘standard’ SP factor (this might be a UK thing) rose from 8 to, these days, factor 30+. The sales of sunscreen over this time have gone up significantly. . . as well as their UVB absorption effectiveness. With the UVB out of the way . . . the UVA has a free ride to the dermis.
In recent years the true damaging nature of UVA has been realised . . . now you can buy broad spectrum sunscreen which block both UVB and UVA.
My rule now is . . . “If you cannot expose your body to the Sun without the need for a sunblock . . . you should not be leaving yourself open to the exposure” . . .
So, I build up my tan starting early in the year, staying longer and longer in the Sun. If I am beginning to overrun my safe level I put the shirt on; perhaps on the beach I get the sunshade out; perhaps sit under a parasol in a bar.
Haven’t bought any suncream for 4 years.
There is a school of thought that inappropriate diets fuel melanomas, and that certain foods and antioxidants, like tomatoes, vitamins B and D3, and astaxanthin protect the skin from sun damage. I have certainly found this to be true, having sent years dutifully slathering on the sunscreens,and suffering appalling dermatitis as a result. Nowadays I gently accustom myself to the spring sun, and haven’t burnt or touched sunscreens for years. As for the sun causing melanomas, I have long wondered why they oft occur where the sun don’t shine!
I have never used sunscreen. I try to develop a tan gradually.
Remember the ’50s and ’60s when people used to slather themselves with Brylcreem or olive oil and lie in the sun for hours, trying to get a deep, dark tan? It’s a wonder we didn’t all die of skin cancer.
Just anecdotal evidence. Here in Southern Germany, school holidays end middle of September, and many folks go to Italy, France or whereever else they can get a nice tan. Most folks with kids will actually go during the last two or three weeks of summer break, as this is when the locals in those countries are back to work, prices are lower and beaches less crowded.
Still, beginning of October usually, and this time again, marks the first mini-epedemic of colds and stomach bugs. And it hits folks who returned two or three weeks previously and should have plenty of stored Vit. D.
I have heard the theory that the immune system gets used to higher levels and is temporily weaked by dropping levels, even if the new level per se is still perfectly adequate.
For most people how much time elapses between a return from warmer climate holiday and an onset of colds, flu, etc?
Sorry , just saw the answer to my question…
What you’re describing may be due to a general weakness within the population you’re observing. One of the main markers of good health is an ability to maintain or return to homeostasis when exposed to a stressor. A young or healthy person can eat 3 pieces of cheesecake at night and wake up with normal blood sugar, for example. Not so for diabetics or those with insulin resistance.
So, what you’re seeing may be due to that. An inability to adjust to temperature/humidity/atmospheric pressure fluctuations.
Eric,
Vitamin D and flu is an important question since I have decided not to get a flu shot. Results of a quick search:
– low vitamin D level is a big risk factor, supplementation is required
– flu virus spreads faster when weather is dry and cool
– hyperglycaemia spikes negatively affect immune system (think Octoberfest)
– adequate vitamin C is beneficial
– flu virus mutates and guessing which strain to immunize against is mostly wrong
– safety of flu shots is still an issue
Strictly off topic, but I need to enthuse about another Real Scientist unafraid to reject dogma and think outside the box.
I think it was Peter at Hyperlipid who first pointed to Bill Lands 2008, but then the entire paper was unavailable. Someone else pointed to it recently, and thanks to the wonderment that is Sci-Hub
http://sci-hub.bz/10.1016/j.plipres.2007.12.001
Warning – 30 pages long but contains over 200 references so plenty of coffee and some sleepless nights required, but well worth it.
Should be read aloud to most dieticians and cardiologists who still insist in putting (LDL) cholesterol and (saturated) fat front and centre.
Should be shouted through a megaphone to the likes of The Angry Chef and Vegans.
This link does not work. And it is all in Russian… Ummmmm ?
Bill in Oz: It works here in the U.S. It takes a while for the English text to appear.
Maybe your government has blocked it? Sometimes it doesn’t work from here either, sometimes the server is just busy, it must get a serious workout. Look on Google for some other alternatives like
https://sci-hub.cc/
https://en.wikipedia.org/wiki/Sci-Hub
tells you more
if you find a mirror that works, punch in the DOI number, eg.
10.1016/j.plipres.2007.12.001
or PMID for papers from Pub-Med and usually it will pump out a PDF. Sheer unadulterated brilliance.
Bill with respect to Sci-hub. . .
First off I should say I have a MAC. I had the same situation of Russian screens when I was using Firefox. If I used Chrome – no problem . . . Then I discovered that Firefox was downloading the articles, in English, into my download folder if they were pdf files. Found buckets of them sitting there waiting to be read.
The Angry Chef may have a point of view, but he/she is wrong (and an idiot). Best ignored.
Good for a laugh though, like most dieticians spewing dogma (a small but increasing number of sensible ones though). “Know your enemy” as there’s a LOT of money behind the dogma. See also, WHO and UN who are angling to have us all on HCLF grain based vegan diets despite the health consequences.
Along the same lines of “know your enemy” Daniel Steinberg
The cholesterol controversy is over. Why did it take so long?
http://circ.ahajournals.org/content/80/4/1070
and his earlier five-paper series on the history of the Cholesterol Hypothesis
An interpretive history of the cholesterol controversy
Currently reading Malcolm’s reference
Endothelial dysfunction: the early predictor of atherosclerosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3721957/
more excellence
Re the problems which seem to be inherent in measuring blood pressure .. see article below which I came across. Personally, I have tremendous anxiety whenever my BP is measured .. when I finally relax, my systolic can decrease 20-30%, my diastolic 15-25% .. which in a way corrobates this article ..
https://spacedoc.com/articles/bp-personality-and-heart-attack
BLOOD PRESSURE, PERSONALITY, AND HEART ATTACK RISK
It was at the United States Air Force School of Aerospace Medicine in 1956 that I had my introduction to the effect of personality on blood pressure responsiveness.
We budding flight surgeons were comparing our blood pressure response during the very painful cold pressor test with our blood pressure response to the intellectual stress of subtracting the number 7 serially from 100, in our heads, as rapidly as we could ( 100-7 = 93, 93-7 = 86 etc.)
Each of us was asked to predict which stress would yield the greater blood pressure response. Naturally we all voted for the well-known cold pressor test, where you simply submerged your hand in a container of melted ice water for one minute. This is not water to which ice cubes have been added. This is water from melting ice – big difference!
Serial blood pressures were automatically recorded during the one-minute test. Our average peak blood pressure during the last ten seconds of immersion was 235/135. The extreme discomfort of this cold exposure served to make it the longest minute of your life.
Now for our surprise – our average blood pressure response during the last ten seconds of subtracting 7’s was 245/140!
We were all healthy, 25-year olds. We were told by the exercise physiologist in charge that this was a typical, normal response.
.. see article
I entered a phone-in radio quiz show with a nice cash prize. You had to answer seven questions in a row. The first few I was very relaxed, but by the time I got to six and seven my heart was pounding so hard I was afraid I’d have a seizure. I won the prize, but afterwards I reflected that I had never exercised hard enough to push my heart rate that high, because of my fear of giving myself a heart attack.
Interesting article. Just tried the serial seven test, not with a cuff but just measured pulse with a smart watch afterwards – nothing (61 bpm). But then, I have a math intensive job, and I have kids in primary and middle school, so lots of simple math practise in recent years…
I remember the feeling of wheels turning from oral exams or defending a thesis, though.
I stumbled into this article some time ago .. I have been wondering what its merit is ..
Its main claim / thesis is that “The major etiologic factor underlying myocardial infarction is a primary chemical destructive process, cause by unchecked metabolic acidosis (accumulation of acid) in the left ventricular tissue and substantially unrelated to coronary artery disease.”
here is an excerpt ..
http://www.wrf.org/alternative-therapies/g-strophantin-heart-disease.php
A NEW APPROACH FOR HEART DISEASE
Coronary artery disease is currently the leading cause of death in the United States. Despite the increasing sophistication of surgical techniques, the introduction of new techniques such as balloon angioplasty, and a number of new drugs (e.g. beta blockers, calcium antagonists), it is estimated that over 1 million heart attacks will occur this year, resulting in 500,000 deaths. In short, we do not have an adequate therapeutic solution to the problem of myocardial infarction (heart attack).
The cornerstone of therapy for treatment and prevention of myocardial infarction is to remove blockages in coronary arteries that are thought to be the cause of the infarction. This adheres to the widely accepted coronary artery thrombosis theory of infarction; that is, arteries become clogged with plaque, damaged from such things as smoking or high cholesterol. A clot forms a fissure in the plaque. The clot may shut off the blood flow of the coronary artery, causing a heart attack. It is deceptively simple: The coronary arteries are clogged. No blood can flow, so the muscles of the heart cannot be supported, and heart metabolism stops, leading to death.
In Germany, another theory of myocardial infarction has been proposed by Dr. Berthold Kern (1911-1995). Dr. Kern, while performing autopsies in Germany in the 1930s and 1940s, observed that the findings of these autopsies did not corroborate the coronary obstruction hypothesis. He began researching the literature, looking for clues as to an alternative etiology. What he found was not only a new theory that may provide the missing piece of the coronary obstruction theory, but a therapy now being used by over 5000 physicians in Germany with reportedly remarkable success.
Dr. Kern’s claims, as set forth in his 1971 informational paper, Three Ways to Cardiac Infarction, can be summarized as follows:
1. The coronary obstruction theory cannot adequately explain observed facts.
2. The major etiologic factor underlying myocardial infarction is a primary chemical destructive process, cause by unchecked metabolic acidosis (accumulation of acid) in the left ventricular tissue and substantially unrelated to coronary artery disease.
3. The regular, clinical use of oral g-strophathin (a cardiac glycoside derived from the West African plant strophanthus gratus):
* Prevents lethal myocardial tissue acidosis, and thereby
* Substantially reduces the incidence of myocardial infarction and completely prevents infarction deaths.
Dr. Kern’s observations that most myocardial infarctions occur in patients without significant obstruction of the coronary artery supplying the infracted tissue finds great support in the American peer-reviewed literature. Since 1948, over a dozen reports of post-mortem examination of infracted hearts have consistently failed to corroborate the coronary artery thrombosis theory of myocardial infarction. That is, victims of fatal heart attacks have had no evidence whatsoever of coronary occlusion.
An example of the degree of non-confirmation can be ascertained by the following quote from a 1980 article on Circulation:
“These data support the concept that an occlusive coronary thrombus has no primary role in the pathogenesis of a myocardial infarct.” The reviewer went on to note, “These reports also present clear refutation of the most common explanation used today to dismiss autopsy findings which detect no coronary thrombi, i.e. that thrombi existed at infarction but have since lysed, embolized or washed away.”
There does not appear to be any literature that effectively refutes these autopsy findings.
Another source of inconsistent data are the many reports in the literature of myocardial infarction in patients without coronary artery disease, as deduced by normal coronary angiograms. Other autopsy data has revealed widely scattered areas of necrotic tissue that produces a substantial incongruence between the area of infarction and the arterial supply.
In a 1988 editorial published in the New England Journal of Medicine titled “Twenty years of coronary bypass surgery,” Thomas Killip observed that “Neither the VA [Veterans’ Administration] nor CASS [the National Institute of Health’s Coronary Artery Surgery Study] has detected a significant difference in long-term survival between the two assigned treatment groups [surgical vs. medical] when all patients have been included…”
More recent work with coronary angioplasty and anti-thrombolytic agents has also failed to demonstrate any clear cut improvements in survival.
Dr. Kern went a step further. In his review of the literature, he came across the notion of collaterals (or anastomoses), a finely-meshed network of small blood vessels that act as natural bypass channels in the heart muscle. These collaterals have been made visible by Professor Giorgio Baroldi in studies at the Armed Forces Institute of Pathology.
Baroldi developed a technique for filling the arteries of the heart with artificial blood, a chemical substance that thickens in the blood vessels. When later the tissues were dissolved in acid, the entire structure of blood vessels in the heart was revealed. Kern hypothesized that bypass grafts were created naturally by the body via the collaterals whenever a coronary artery became blocked. Therefore, heart bypass would be redundant to a large degree.
A study by Rentrop et al in the April 1, 1988 issue of The American Journal of Cardiology has produced results completely at odds with the coronary artery blockage theory, and consistent with Kern’s hypothesis. In an accompanying editorial, Dr. Stephen Epstein of the National Heart, Lung and Blood Institute summarizes Rentrop and colleagues’ “extremely important observations.” They found that in an advanced state of the narrowing of the coronary arteries, the supply of blood to the heart muscles is fully assured via collaterals that enlarge naturally in response to the blockage. Interestingly, they observed that the more the coronaries narrow, the less danger there is of heart infarction.
Dr. Kern’s second claim, i.e. his proposed new theory of metabolic acidosis, can be summarized as follows: Metabolic conditions in the most healthy of hearts are, at best, marginal in the constantly beating left ventricle. This is the part of the heart responsible for pumping blood to most of the body, the right ventricle merely supplying the lungs. Oxygen and energy requirements are always perilously close to available supplies, and any of the several stressors may cause an oxygen/energy deficit, with deterioration in oxidative metabolism, and consequent development of acidosis. Lack of oxygen sets off the process of zymosis or fermentation metabolism, an anaerobic process, in order to produce energy in the cells. This, in turn, lowers the pH.
This lowering of the pH sets off a destructive chemical process, literally a suicide reaction of the cell. Lysozymal enzymes are released, causing cell self-digestion. This starts as a single point in the muscle, then many points, which eventually join to form a small area of necrotic tissue. Finally, a critical mass is reached, no bigger than the head of a pin, which triggers larger and larger areas of damaged tissue, resulting in infarction (heart attack).
Ideally then, the remedy to address infarction would be a restoration of pH balance to the heart muscle, thereby preventing tissue damage and fatal infarction…..
.. see article
Indeed, I communicate regularly with Carlos Monteiro – he of the myogenic theory of heart disease. There is much to commend this thinking, and there is absolutely no doubt that myocardial infarction is a complex thing, and acidosis etc. plays an important result in the end game. Tako-tsuba is a good example of purely stress induced ventricular dysfunction – sometime death – in the absence of any plaque formation. However, just because you cannot find a clot, does not mean it wasn’t there.
Ummmm this is important I think. On the 24th I made a couple of comments on this subject, as part of the previous blog by Dr Kendrick. However with the new blog being posted I suspect no one saw it.
To repeat in part : there is a website by Dr Knut Sroka in Germany : heartattacknew.com
Dr. Sroka’s remarks are interesting & I feel valuable. He also makes the comment that for 50 years in Germany, rior to Dr Kern’s research & prior to the triumph of the diet/cholesterol heart disease hypothesis, Ouabain, was the standard drug offered to relieve heart disease symptoms.
I found this section fascinating as it seems that Ouabain has been discredited and this fallen out of favour in Germany in recent years via the exact same heavy handed processes used in the English speaking world. Again for those interested here in the link.
http://heartattacknew.com/faq/what-can-be-done-to-prevent-a-heart-attack/ouabain-the-wasted-opportunity/
Dr. Sroka in turn provides a link to a 140 page pdf version of Baroldi’s 2007 book “The Etiopathologies of Coronary Heart Disease: a Heretical Theory based on morphology”
This last source I have ploughed through also. But my lack of medical knowledge makes it too hard a task. It seems that every second word is a technical medical term. ( Why could he not write in plain English ? ) But some here may be intrigued and interested.
Click to access baroldi.pdf
Reply ↓
I also thought that ouabain was available in Australia from
https://www.miherbnz.com/collections/sanum-kehlbeck/products/strophanthus-d4-80-tablets?variant=11964358913
However this site is in fact a New Zealand one. And a herbalist friend tells me that Ouabain is legally ‘banned’ in Australia due to pressure from the pharmaceutical industry here. An unpleasant surprise!
The issue of ouabain or something like it as a tonic, or an emergency restorative for the heart problems, has been on my mind for a long time, but it has been brought to the fore in the last couple of days.
I have mentioned in a previous blog that I have had 3 bad ‘turns’ in recent years. In each case there has been a coming together of an infection, significant mental stress and some sort of prior exertion. The result is persistent surging feeling in the chest (take it to be the action of cortisol`) . . . these surges often coincide with missed heart beats (to be exact PVCs); there is also a raised heart rate, and I can feel my heart beating, and in the worst ‘turns’ I can hear the pulse in my head. yet my blood pressure is low (below typically 110/68).
Each time I was taken to hospital, once by ambulance in the early hours with a suspected heart attack. Each time they came back with no MI. (Presumably they found no cardiac troponin proteins in the blood).
Before the ambulance episode (3rd turn) the pulse thumping in my head was so clear that I did not have to take my pulse to detect the PVCs . . . I could hear them!
And now to my central point ( . . . at last, you say) . . . during that 3rd turn, arriving at the local A&E, the young doctor decided there was a good chance I was having an MI. She put something under my tongue.”Let is dissolve”. The effect was steadily progressive – by the time my second abulance arrived at the Leeds Coronary Care Unit the calm was palpable . . . no head thumping, surges gone. By the time the amazingly rapid angiograph had been taken, (5:00am) I felt really ok; in fact, I felt quite the fraud. What was that magic pill?
I now suspect that the under-the-tongue pill was nitroglycerin, which I think is a vasodilator.
The Leeds “turn” was 4 years ago. I have worked hard to improve my body’s condition – diet and exercise, sleep and breathing (slow breaths out sharp breath in). So much fitter, leaner and in control. So, I was dismayed yesterday when I had another turn. I have had an infection that sort of came to the fore, have been under mental stress, felt the cortisol surges, decided I needed a therapeutic walk to calm me down. Half a mile down the road my ‘yomp’ speed had to be cut down, going slower and slower; I had to control the breathing to keep the chest discomfort at bay. By the time I got to this hill it was mayhem, all chest surging/PVCs/HR 140+ . . . I should have gone back home. However I was determined I could control this . . . so stopping, controlling breathing, getting the pulse down, walking 20m, stopping and controlled breathing getting pulse down, bit by bit I got to the top of the hill. It was easier after that but I did need to sit down a couple of times to get things under control. A walk that normally takes 50mins (3 miles) was cut short to 2 miles and took 2h30. Before anyone else says it . . . “What an idiot !”
To my mind I needed that nitroglycerin pill. I had thought that I might still be susceptible to “turns” – a vasodilator worked once, so why not again. I did wondered about ouabain but that is not a vasodilator. In the old movies you used to see people having an angina attack having a vial of amyl nitrate broken under their noses, but that is out of the picture.
I do not know if this sort of attack (turn) has a name so it is difficult for a doctor to deal with. Or does it have a name? Over to you.
I think nitroglycerin does vasodilate, that’s how NO was discovered, if I remember correctly. Also, if you just had tachycardia without angina during that episode, taking a vasodilator could have possibly made you feel worse, not better.
Had your thyroid checked? If not, try to get an actual TSH result, not just “it’s normal” which it may well not be. Worth doing if only to eliminate a possible and treatable cause.
When mine goes high my heart rate increases and the least exertion has it thumping. When it goes too low (overtreated) the heart rate drops and I start getting PVCs, especially when falling asleep. Probably why my poor old father had “palpitations” for years, if not decades – in retrospect he had all the classic – but undiagnosed – symptoms of hypothyroid, undoubtedly the result of most of the gland being hacked out to control his hypERthyroid when he was young. His heart was actually damaged but he still lived to be 82.
Currently mine spends long periods – 6 – 12 months – relatively stable on the same carbimazole dose, then for reasons which I can’t connect to anything dietary or environmental it will suddenly either drop like a stone or shoot off into the stratosphere, which requires some major dose tinkering until it restabilises.
Another likely possibility is a hypo, or a rapid drop in blood glucose, which can set off hypo symptoms including a cortisol surge. A glucometer and test strips may be a useful purchase, and some glucose tabs strictly for emergencies. Insulin and T3 are both “master hormones” which knock on to many other systems. Mine are both out of kilter, only leptin (another master hormone) to go and I will be doomed.
Some good points Chris.
I have thought about hypothyroidism as a possibility – or at least sub-optimal thyroid levels. There was my first ‘turn’ just after having a very bad virus? infection – Had a couple of days off work for the first time in well over a decade – with the cortisol? surges in the chest and the PVC arrhythmias (one missed beat in 8, unless I did something marginally strenuous when it could go down to missing every other beat) . . . For reasons I cannot recall I thought the infection may have triggered damage to my thyroid. I put this to my GP, adding that I was feeling a catch in my throat, wanted to cough frequently to clear it, pointed out the ultra flakey skin that covered both legs, the fact that I put on weight just looking at food . . . Even mentioned the hissing in the ears (which one source gave as a sign).
He did get the tests done . . . said there were no thyroid antibodies, the thyroid hormone level or levels were in range; however, I know now that the interpretation of the figures is notoriously insecure . . . ( what the figures were I cannot say – Now I know more I think I would like the tests redone so I can see a clearer picture.)
During the 3rd turn at Leeds Coronary Care Unit, after an ultrasound test, they suggested I might have an infection of the pericardium . . . (which does figure with the PVCs – the pericardium is attached to the left ventricle so it is in a position to do mischief). So I wondered if the pericardium remains susceptible to infection, or it may sustain a low level of infection that is normally under control until stress intervenes. On the other hand it could be that the thyroid is the weak link . . . It is the one infected.
These are the sort of things I think about (not all of the time or even often) . . . But if *I* do not think about them who else will?
PS. I do have a glucometer . . . from my diabetes days . . . and a sympathetic doctor who still sports me the free test strips.
Interesting indeed! AFAICR the current belief is that thyroid is “normal” if TSH is in single figures, yet most hypothyroids I know do NOT do or feel well unless TSH is 2 or less. I suspect the recent “discovery” that hypothyroids live longer will NOT improve this situation.
Paradoxically, probably because I have come from the hypERthyroid direction, I feel better running slightly low (higher TSH), probably because this wipes out likely spikes in its activity. Why I always try to insist on getting actual numbers – though at 38 and 44 I feel virtually dead, and at 0.001something I also feel distinctly unwell.
I am just getting over the most recent bout of overtreating a serious high, and the flaky legs and relatively rapid deposition of fat was a surprise – I am currently removing the latter by reducing dietary fat and upping the protein which seems to be digesting it nicely. Also I was getting a distinct throat itching, allied to a gum infection which I haven’t had since controlling my BG, and also blepharitis probably connected to the way my eyes got bulgy and scratchy from the high thyroid.
There’s a reciprocal relationship between gum infection and CVD, now I ponder how thyroid also fits in. Some infections can affect the heart directly – remember rheumatic fever, I think caused by strep, which has become much rarer as strep has become milder, and “strep throat” which sometimes piggybacks onto a viral infection. Hmmm . . .
OTOH my tinnitus gets worse when my thyroid is high – but there are also connections between tinnitus and hyperinsulinemia, I think Amy Berger among others had some studies on this.
I used to actually or nearly faint during childhood, and later find myself unable to stay awake mainly in an “afternoon slump”, while my “depression” symptoms got markedly worse along with the physical energy drops, and also “hangry” attacks, all of which was explained when I started testing my BG and finding the postprandial highs and post-postprandial lows: that all resolved when I got my BG under control with low carb and realised how my carb tolerance/insulin resistance varied through the day. During all that my thyroid stayed resolutely around TSH=1. Even minor infections can have major effects on insulin requirements for Type 1s, a cold may need double or more the insulin dose for a while.
Lots of possibly interlinked things . . .
Bill,
Dr. Sroka’s “teaching” is also for me intriguing and especially the part relating to the heart rate variability issue.
MI evidently occurs when this variability is close to zero which to me indicates the importance of the stress factor through the vagus nerv connection to the heart.
But again, how little we know!
Heart rate variability is the single most important measure of heart health.
Dr K
By heart rate variability, do you mean going up to 150 cycling up a hill, then in the evening sitting reading a book it’s down to say 65?
No. I mean beat to beat variation. There is a lot of research on this area, it is perfectly ignored by mainstream medicine, even though the underlying science, and research, is of high quality, and mainstream. Here, from Circulation: ‘Among all analyzed variables, a steep slope of the power-law regression line of HR variability (<−1.50) was the best univariate predictor of all-cause mortality (odds ratio, 7.9; 95% confidence interval [CI], 3.7 to 17.0; P<.0001).' Or, to put this in English. Poor heart rate variability increased the risk of overall mortality by 790%. http://circ.ahajournals.org/content/97/20/2031 Compare and contrast with…. well, anything. Because you will not find any other factor that is such a powerful predictor of early death. Yet, there is not the slightest interest in this – at all. Go figure, as they say.
Dr K
that sounds interesting. I have a Polar sports watch which has a built in fitness test, where after lying down in a dark room for five minutes, it measures the heart rate and comes up with measure of fitness. A fitness coach told me that it works by measuring the micro-variations between heart beats.
Malcolm, thank you for this informative update!
Mr. Chris, I’ve got a Polar heart rate measuring device as well. I use it to monitor my maximum pulse during my garden work outs. I though doubt that it can be used to measure HR (beat to beat) variability although I wouldn’t bet on it. I don’t think the device is that sensitive. Just now mine has gone “nuts” so I think I have to buy a new one. It is not that expensive.
On top of my head I don’t remember how the variability is measured in practice – I think Dr. Sroka describes this somewhere. As far as I remember it has something to do with the balance between the sympathetic and the parasympathetic parts of the autonomous nervous system – read the vagus nerv! I think it was the parasympathetic part that was down when it goes awry which make sense.
Hello Goran,
my Polar is an M400 and here is their stuff about how its fitness measure works:
The Polar Fitness Test is an estimate of a VO2max test. The Polar Test is 86 to 93% accurate and gives us a value that we can easily track.
The Polar Fitness Test is based on your:
Resting heart rate (Heart rate watch calculates)
Heart rate variability (Heart rate watch calculates)
Gender
Age
Height
Body weight.
I did the test a couple of times and it gives consistent results, and, as you see above it claims to measure heart rate variability. Since I take all the Malcolm writes seriously, I shall try and follow this aspect of HRV measurement up.
Goran
sorry to give you information overload!
here is the reference I found to a paper on the nit website which tested the Polar monitor with an ECG.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4751190/
the finding were that the measurements are not as good as ECG but close enough.
Since my Polar gives me a good level of fitness, perhaps I am not as decrepit as I thought!
I would think you need both systems working to have variability.
1. Taking this reference from Dr Kendrick’s comment:
http://circ.ahajournals.org/content/97/20/2031
2. and taking this sentence from the above reference:
The subjects who subsequently died also had elevated baseline blood glucose and lower cholesterol concentrations relative to those who remained alive during the follow-up.
My understanding: Does this mean that those with lower cholesterol levels in their blood had a higher all cause mortality compared to those with higher levels of cholesterol?
See https://www.heartmath.com/
HeartMath — https://www.heartmath.com/ — is all about measuring heart rate variability [HRV] .. they make a gizmo you attach to your ear which measures HRV, as well as coherence between the two ‘big nerves’ [forget their names – one for flight, the other for calm and peaceful emotions] .. I have one and use it hopefully 2 times / day .. they have interesting articles posted on their site, see: HMI Research Projects today. http://www2.heartmath.org/e/17232/IHM-Research-Projects-html/c8469g/500177279
also ..
“Learn more about the “little brain” in the heart, heart-brain interactions and how coherence leads to improved personal performance, health and well-being in the Science of the Heart online e-book. .. http://www2.heartmath.org/e/17232/ownloads-science-of-the-heart-/c4gckv/497307001 “
From what you are describing, it seems to be measuring the balance between sympathetic and parasympathetic responses. Is that what HRV indirectly measures?
What it indirectly measures is heart health. It was first used, and is still used, to monitor fetal heart health during childbirth. Loss of HRV is a sign the baby is struggling. Some researchers wondered if loss of HRV could also predict health problems in adults. It does. Exactly what is being measured is not entirely clear. Probably excess sympathetic tone, indicative of overall strain in the system.
Wouldn’t good HRV indicate a better balance between both systems since heart beat responds to sympathetic/parasympathetic inputs?
Well – thanks for interesting links but still it is difficult for me to get a coherent picture of this. It is also too much of a sales pitch for me!
Though I learned that it should be possible to evaluate the HRV by a sensitive device, not necessarily a full EKG but with a clip in the ear?
I think we are on something interesting regarding CVD.
As an off topic issue I met with relatives at a funeral today and happened to face one of my cousins together with his wife at the gathering after the funeral. He was at our age very concerned about CVD-issues since he had recently had a stent put in place so I told my own “poster boy” story of refusal and there was of course a great deal interest on their part.
Of course he was on statins and I said: “Never touch them!”. My general advice was to do just the opposite to what the health care system suggested. People tend to get stunned by such advices but it may make them start “thinking” about the official guidelines even if they consider you as an “odd” figure.
The clip measures the heart rate in the earlobe and calculates the difference over time. Very simple. You can also put your thumb directly on the instrument, sparing your earlobe.
Apparently people can train a good variability using biofeedback with the measuring device.
Mathematically, what you do is measure the time of some characteristic feature of each cycle (maximum, zero crossing or whatever), do a Fourier transform and look at the frequency spectrum. Should be possible with any optical, electrical or acoustic sensor if you have some software to do the conversion.
I am guessing a control loop specialist would have a field day. Probably a sign of a control system being driven into having too little phase margin.
When chaos theory was en vogue 30 years ago, they also looked at HVR by another name. I believe attempts to model the loop by chaos theory came to a dead end, though.
Thx for the article on Ouabain. In a nut shell I understand accumulation of acid in the left ventricular tissue is the problem. It appears that the basis of infarction is too much acid in the system, or acidosis. But Stephanie Senneff from MIT and others, suggests reversing vascular disease with SULFATED-chondroitin which I believe is acidotic. I guess I need more study.
Sunlight benefits in addition to vitamin D.
Sci Rep. 2016 Oct 12;6:34320. doi: 10.1038/srep34320.
Sequestration of ubiquitous dietary derived pigments enables mitochondrial light sensing.
Zhang D1, Robinson K1, Mihai DM1, Washington I1.
Abstract
Animals alter their physiological states in response to their environment. We show that the introduction of a chlorophyll metabolite, a light-absorbing pigment widely consumed in human diets, to Caenorhabditis elegans results in animals whose fat mass can be modulated by exposure to light, despite the worm consuming the same amount of food. In the presence of the chlorophyll metabolite, exposing the worms to light increased adenosine triphosphate, reduced oxidative damage, and increased median life spans, without an effect on animal reproduction. Mice fed a dietary metabolite of chlorophyll and exposed to light, over several months, showed reductions in systemic inflammation as measured by plasma α-macroglobulin. We propose that dietary chlorophyll metabolites can enable mitochondria to use light as an environmental cue, by absorbing light and transferring the energy to mitochondrial coenzyme Q.
Fascinating! Without question sunlight does much more than produce vitamin D. We tend to concentrate on what we know, not on what is yet to be learned.
again referencing the article I posted ..
http://www.wrf.org/alternative-therapies/g-strophantin-heart-disease.php
A NEW APPROACH FOR HEART DISEASE
What stuck in my mind was the following section re the enlargement of collaterals to circumvent arterial blockage .. is this accurate or ?? feedback appreciated
from the article ..
” etc etc …
A study by Rentrop et al in the April 1, 1988 issue of The American Journal of Cardiology has produced results completely at odds with the coronary artery blockage theory, and consistent with Kern’s hypothesis. In an accompanying editorial, Dr. Stephen Epstein of the National Heart, Lung and Blood Institute summarizes Rentrop and colleagues’ “extremely important observations.” They found that in an advanced state of the narrowing of the coronary arteries, the supply of blood to the heart muscles is fully assured via collaterals that enlarge naturally in response to the blockage. Interestingly, they observed that the more the coronaries narrow, the less danger there is of heart infarction.
etc etc “
If you reject artery blockage as a cause of heart attack, how do you explain strokes? Or do you maintain that blockages affect the brain but not the heart?
Guinea pigs — which don’t manufacture vitamin C and which get plaques like humans — are also prone to heart attacks and strokes, and respond well to the same medication as humans.
Recommendations include potassium in the diet and a stress-free environment. (Where have I heard that before? ;o) )
http://oginet.com/pgurney/index.php/the-guinea-pig-health-tips-library/heart-problems-in-guinea-pigs/
Biomechanical Stress
I am a little uncertain of what we mean by biomechanical stress. Looking through the responses there seems to be a view that forces pushing on the epithelium produced by the pressure of the blood, or that friction forces (shear stress forces) produced by the flow of the blood are of sufficient strength, (over time), to damage the epithelium. Because of the hydrodynamics of the vascular system certain areas will suffer larger forces and be more prone to damage than others. These weakened/damaged areas are susceptible to further damage from a host of biochemical agents (eg glucose, homocysteine) that provide the coup de gras => endothelial dysfunction. The level of dysfunction in these ‘favoured’ places leads to an atheroma.
I may have got this all wrong, but I do have a problem with the nature of the biomechanical stress that is implied.
In the piece at the start of this blog George Mann is quoted saying “Atherosclerosis does not occur at random locations. It does occur uniformly at specific sites of predilection that can be precisely defined, predicted, and produced by applying the principles of fluid mechanics. The areas of predilection for atherosclerosis are consistently found to be the segmental zones of diminished lateral pressure produced by the forces generated by the flowing blood”
I wasn’t sure whether his lateral pressure was caused by axial forces pressing on the artery wall or, seeing how he is talking about it being “generated by the flowing blood” he must be talking of shear stress . . . either way he talks about “diminished lateral pressure.
Others have talked about “atheromatous lesions are more common at sites within the arterial system which have low shear [stress] rates” These coincide with the inner curve of bent arteries and at bifurcations.
(Hypothesis: arterial glycocalyx dysfunction is the first step in the atherothrombotic process
Noble 2008 https://www.ncbi.nlm.nih.gov/pubmed/18319293
Mann, mentioned above, and other papers I have read . . . lay the “areas of predilection” for plaque formation to be in areas of diminished shear stress. Just how damaging are these diminished shear stress/lateral pressure zones?
( High shear stress stimulates the epithelium to produce protective levels of NO . . . the areas of diminished shear stress produce less protective NO)
I’ve been doing some more outside-the-box thinking. Until the sixties or so, coal fires were ubiquitous (posh people burned logs). Power stations and gasworks also burned coal. Coke and other “smokeless” fuels were produced mainly by removing the smoke – I remember the coking plant at the bottom of the Rhondda (or one of the other Welsh Valleys). Much less common today, but still in use in many other countries, where it is mainly the poor who burn wood. I wonder if coal use and the ensuing pollution has any relationship to CVD rates in different places?
Petrol engines first came in around the start of the 20th century, automotive diesels around the 1930s. Engineering improvements have decreased the pollution per individual vehicle – this sort of thing would no longer be permissible
but on the other hand the number of vehicles has increased drastically. Again would be interesting to plot this against CVD rates in different countries.
Here’s the kicker – horses used to be in use, even when my parents were young, in agriculture and even haulage, along with steam. Maybe
HORSE MANURE IS CARDIOPROTECTIVE
I’m thinking of writing to Willett and Hu and suggesting an epidemiological study. After all it makes about as much sense as some of the bull manure they come up with.
Re labile hypertension which was mentioned .. I also have that and it is extremely difficult to treat .. in my case it is caused pretty much entirely by anxiety .. when I relax my BP is OK, when not relaxed it is not OK .. the BP pills .. all of them .. and catastrophic dosage advice from the Drs .. almost killed me .. literally
There is a very very good book on hypertension .. covers everything from A to Z plus all the Rx meds, and labile hypertension is covered briefly in it:
“Hypertension and You” by Dr S Mann .. available on Amazon or perhaps in your local library
WC Mozart, was talking recently to a herbalist friend bout stress causing hypertension. I is a great believer in Withania. It’s traditional Indian herb to help manage stress.
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What I don’t understand is the apparent “contradictions” in medicine.
For example, there’s been lots of mention on this board of the value (or rather the lack of) of stenting rather than leaving the body to its own devices by producing collaterals to supply blood to the heart. The benefits seem marginal at best, yet the medical profession still does it.
I remember Dr Kendrick mentioning a study on blood pressure, where treating even relatively high blood pressure produced no benefit. Yet the medical profession still carries on treating high blood pressure.
There’s been plenty of discussion of ischaemic stroke on this board, yet a relatively recent (2012) study (IST-3) on treating acute stroke with thrombolytics (clot-busting drugs) produced no benefit. Yet the medical profession claims the opposite, despite the evidence and carries on clot busting.
I’m sure we’d all agree that it appears to make perfect logic and sense to stent blocked blood vessels because in doing so, blood supply is restored. Equally, it appears to make perfect sense to reduce hypertension because in doing so, we obviously reduce the chances of aneurysm, stroke etc. And if a (ischaemic) stroke does happen, it appears to make perfect sense to dissolve the blood clot asap. And yet, the evidence to all of the above says, no benefit.
So what’s the answer? The medical profession carries on treating with mechanical intervention and / or drugs despite studies contradicting the “logic” and the efficacy of the intervention. Is medicine in reality impotent when it comes to CHD and Voltaire, even in the 21st Century was correct when it comes to CHD when he said: The art of medicine consists in amusing the patient while nature cures the disease?
What’s the point of evidence based medicine when the evidence is ignored? And is it we, the general public, the patients who are ultimately responsible for the situation by expecting an efficacious treatment when in reality, the doctors cannot deliver?
Too often “evidence based” medicine = dogma-based medicine. Strangely the dogma always results in profit for someone even if it fails the patient.
I have also called “evidence based ,medicine” “marketing-based marketing” which I’m pretty sure is not original but I can’t remember the source.
Just been thinking some more about other interventions eg screening, appears to make perfect sense yet the evidence suggests, no benefit to the majority and possible harm. But yet, the medical profession carries on.
Cancer treatment (chemo, surgery, radio) is a horrible treatment. Does it make sense? And why do the majority of oncologists allegedly refuse treatment if they themselves should become cancer sufferers?
Vaccination – the science again appears to make sense by introducing immunity but there are lots of studies to suggest greater harm than good. But yet vaccinations are not questioned but expanded.
Mark,
I couldn’t have expressed this more succinctly myself 🙂
Dr. Göran, your reply really cheered me up because when I was writing the post and thinking of CHD interventions I was thinking of you! I often think if I were to ever suffer a “cardiac event”, would I have the courage to refuse modern treatment like you did. From what I’ve read, an MI must be a terrifying experience and in the heat of the moment would I refuse treatment or grasp out at any help offered.
Mark,
Relating to my “MI-experience” – Yes! – it was for sure an unpleasant event at the age of 52 and it was evidently one of the most severe ones they had experienced according to the “indicators” so I was happy to have survived according to the cardiologist. The good thingwith the event was that it opened up a new interesting “research” field for me.
Well – I did not refuse the comprehensive CABG suggested to start with. It was only after having done my homework properly during a couple of month or so I “dared” refuse and all the medicines after reading more on the CVD- subject. Took me half a year.
Mark,
It strikes me that most of us commenting here on this blog have some serious disease and are looking for “good medical” advice from successful equals “outside the box” due to exactly what you so clearly see as the nonsensical essence of “main stream medicine”/NHS.
Presently I am experiencing more restrictions than usual during my present garden workouts. This deterioration I attribute this time to my respiratory system. Scratching my head and thinking of my younger days when I was a heavy smoker I got aware of ‘Chronic obstructive pulmonary disease (COPD)’.
Then I made the very serious mistake of reading what is in Wiki about COPD and was completely lost in the complexity revealed.
https://en.wikipedia.org/wiki/Chronic_obstructive_pulmonary_disease
Though I didn’t let Wiki scare me to consult the NHS since I realize the criminal futility of this “service” and where they most probably would kill me within a couple of years if they got the opportunity to put their hands on me.
What I need is a new pulse meter!
Dr. GoranI am intrigued by your use of pulse meter and how it relates to heart rate variability (HRV). Got me thinking about how fasting might be beneficial in rebooting metabolism. A quick google revealed that fasting (Ramdan) can have beneficial effect on HRV. I have been experimenting with restricting eating window. A pulse meter that measures HRV would be something that I would consider purchasing.
Andy
My Polar FT2 pulsmeter is of the simplest model and I have not seen anything about HRV measurements. Though Mr Chris mentioned in a comment above that he had a Polar M400 with these advanced features as I understood it. Well worth a try.
Anyway, trying to buy a new FT2 it was evidently out of stock so I gave my old one another chance and after cleaning the strap around the chest thoroughly it now seems to work properly again. I think I now go out into the garden again and do some digging to see if my heart is beating properly again 🙂
What I now can see on the display of my Polar FT2 is that the present garden exercise was 42 minutes long, the average pulse was 102 and the maximum was 135 and as far as I have understood it is the max rate which is important to get as high as possible.
135 is not very high and I could perhaps have stressed that to 140 if I had worked harder with the hoe but I should be around 150 so when the puls meter strap is now cleaned up and the meter works properly I have to do the same with my heart I guess.
They say that alcoholics have very clean arteries and if that is really true I should perhaps buy some more Scotch whisky. As a retired I can do what I want and just now I am enjoying a glass of white wine in front of my fireplace.
I am lucky in that I have no serious disease or condition (that I’m aware of) and like to keep it that way. Both not having anything, or knowing about it. Since I cut out refined carbs, and most other carbs, except for those in dark chocolate, I feel a lot better, more alert, an d more confident. Perhaps it’s the 12 grams of vit C every day, or the large quantities of cheese and cream, you know, those unhealthy dairy products.
Andy,
I am a recent believer in the benefits of fasting.
For the second time in my life I am presently on a five days fasting – now on the third day. It is not that difficult as i may appear at first look. It is kind of a reset of the metabolic system.
Usually I am though in a lean type of fasting and only eating in a window of about six hours and thus “fasting” during the other 18 hours every day.
Dr. Jason Fung has a lot to say about this.
I think fasting is a good thing for health. It certainly does not appear to cause any harm.
Here is what Dr. Jason Fung has tos say about the benefits of intermittent fasting.
https://www.dietdoctor.com/intermittent-fasting
Jason Fung is a good man. I like his stuff.
Might want to take a look at Rapamycin? quick improvement and turn-around
http://roguehealthandfitness.com/rapamycin-anti-aging-medicine-an-interview-with-alan-s-green-m-d/
Steve,
That is a very interesting link. I just finished Mangan’s book “Dumping Iron”.
Phil
Philip Thackray
Renfrew, PA USA
Andy,
Om my 40 min garden “excursion” this morning I was happy to note an significant improvement with an average pulse of 120 and a maximum of 145 – encouraging!
Since I am now on the fourth day of fasting the improvement might be due to the strong probability that I have now entered into a state of firm ketosis and then fueled by the ketones.
Andy,
After a second workout today I must now have a “new” heart if I should trust my pulse meter.
During the one hour exercise I read an average pulse of 128 and a maximum of 174. For me this max value is almost unbelievable since I have never measured a pulse higher than 160 in previous years.
Well, just now I though feel excellent but I don’t really trust my puls meter even if it now seems to work properly. I must make a new test tomorrow. 🙂
Could it be the ketones?
Dr. Goran,
You have convinced me, ordered a pulse meter yesterday. I have many logs to split for the fireplace, the meter will be a useful tool to measure how my heart will perform. So far I have never experienced adverse effects from physical exertion.
Re Cancer Treatments .. see this very interesting article:
The Metabolic Theory of Cancer and the Key to Cancer Prevention
and Recovery
http://articles.mercola.com/sites/articles/archive/2016/02/07/metabolic-theory-cancer.aspx
and this one which is referenced in above:
A novel therapeutic strategy for the metabolic management of cancer
https://nutritionandmetabolism.biomedcentral.com/track/pdf/10.1186/s12986-017-0178-2?site=nutritionandmetabolism.biomedcentral.com
they have to justify their jobs. it’s like cops waging war on drugs, total failure, it doesn’t work. but the lawyers, judges, social workers, psychologists, doctors, all make a living out of the so call criminals using illegal drugs.
Mark,
What may be added to your list of “medical contradictions” is that medical practices which seem to work are also constantly and viciously attacked by the medical establishment.
The prime example today may be the LCHF life style (sweeping the world today?) where natural saturated fats are an essential part. (I just bought a lamb to feed us through our cold winter from a friend of mine and he assured me that it was the fattest in the flock. His openminded wife, an MD, had still problems with the cholesterol issue and the saturated fats but felt that the ground is shaking today.) Another example of the fierce attacks is the vitamins of different kinds and where my own “life line” regarding my unstable angina, consisting of high doses of natural vitamin E, is constantly warned against.
Well, as I learned doing my “home work” a few years ago before jumping on the E-vitamin “band wagon”, the “evidens based” foundation for all these warnings are tests made with the synthetic variant of vitamin E but a fact which is never mentioned in the published “evidens based” papers carrying the serious warnings.
Today, Dr. Mercola brings this topic up in his interesting newsletter – a “pearl” this time?
https://articles.mercola.com/sites/articles/archive/2017/10/02/vitamin-e-helps-decrease-cancer-risk.aspx?utm_source=dnl&utm_medium=email&utm_content=art1&utm_campaign=20171002Z2&et_cid=DM160742&et_rid=70742303
Here he though focuses on the benefits of vitamin E fighting cancer.
There seems to be a holistic medical element involved in vitamins but which is completely ignored by the “evidens based medicine”.
Hi Göran
And of course there is an argument that intensive farming, without soil rest and rejuvenation, reduces soil quality, micronutrients, minerals etc, etc that improves the nutrient quality of the food grown in/on the land. Of course, supplements cannot be patented etc. so Big Pharma is totally against supplements. Moreover, there is little return on funding costly studies.
Regards Robert
Robert,
How very true!
Funny that you mention the importance of the soil “quality” for our health. This is actually a top subject for me today since I have promised to give a talk exactly on this subject at the Swedish Nature Conservancy Agency within a month; “The Web of the Earth”
Dr. Goran, curious about “healthy soil” as source of increasing gut micro-biome diversity by minimally washing vegetables from my garden. Garden is fertilized by chicken poo from my 6 organically fed hens. Some might consider chicken poo in soil as unhealthy.
Andy S: Manure should be well-composted before it is added to the soil, in which case it will improve soil health; a little bit goes a long way. I rather doubt soil bacteria will enhance your microbiome. Eating wholesome, high-quality food, and avoiding drugs, particularly antibiotics, will.
Chicken poo in soil is ok, chicken poo on food is probably not a good idea.
AH Notepad,
The concept is to feed the soil microbes with the chicken poop plus lots of mulched twigs, wood ashes, egg shells etc.. Hopefully there will be some benefit from acquiring a few new gut buddies from the soil. Minimal washing rather than a side dish of soil might be sufficient. More investigation is needed, there might be some connection with CVD from immune boosting gut bacteria.
I don’t recall it mentioned, but I could just have forgotten, could damage to arteries in preference to veins, be caused because the arterial blood is oxygenated and hence more reactive? The may be some contribution from the mechanical stress, but what about the chemical?
Then, why no atherosclerosis in the blood vessels in the lungs?
Much lower pressure, especially in the pulmonary veins where the oxygenated content is reinstated?
Why arteries and veins are different
The human body under various influences remodels itself to reduce the effect of the influences particularly if they are prejudicial. On a trivial level . . . if you try and touch your toes with legs straight, over time the muscle/tendons develop to accommodate such odd urges. Less trivial: if an area such as the heart is suffering lack of blood, distress signals are sent and new capillaries/vessels develop to restore a level of normality. The body is geared for remodelling.
Some, myself included, feel comfortable with the evidence that the arteries intimal layer starts off with an endothelial layer in new born, but as the person ages it gains extra layers of sub-endothelial cells: 8 months 1-2 layers; 15y 10-15 layers; 25-30 years 25-30 layers.
As the person grows the demands on the vascular system as a whole and certainly the coronary arteries grows with them. If the arteries do not modify . . . the pressure required to circulate the blood will be get higher and higher. To restore ‘normal’ pressure the intimal layer cells proliferate, allowing the arteries to expand outwards, increasing the lumen cross-sectional area, reducing the pressure, restoring normality.
How is this pressure detected? Studies such as the one below . would say that the wall strain produced in the artery wall, detected by the glycocalyx/epithelial cells, causes the epithelial cells to release less NO . . . causing the intimal layer cells to proliferate. The artery expands, the pressure normalises, the strain normalises, the NO normalises. (NB the higher pressure would reduce the pulsatile effect which might also compromise NO production)
“Is arterial wall-strain stiffening an additional process responsible for atherosclerosis in coronary bifurcations?”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3191077/ 2011
The paper describes how areas of high strain in the coronary arteries, produced by the pulsing and twisting heart, are the same locations where atheroma are found. Thickening of the intimal layer would be predicted. If the intimal layer is thick enough then adventitial capillaries that feed the medial smooth muscles are stimulated by signals from oxygen deprived intimal cells to develop into the intimal layer. The new capillaries provide a route for all sorts of mischief into the coronary artery wall. (This is very much the outside => in model of plaque development).
There is little difference in the structural morphology that make up veins and arteries as far as I know . . . I even found reference recently to big veins also having adventitial capillaries.
But on vein graft disease . . . the paper below asserts:
“Vein graft disease, a common affliction of veins used as arterial bypass conduits, is characterized by excessive VSMC (venous smooth muscle cells) hyperplasia (excessive proliferation) that brings about occlusive intimal thickening. VSMCs acquire a synthetic phenotype and migrate through the vessel wall, proliferating in the sub-endothelial space. In comparison, arterial bypass grafts are much less prone to remodelling. It has long been recognized that altered mechanical factors contribute to vein graft proliferation, pulsatile stretch was found to induce VSMC hyperplasia in saphenous veins but not internal mammary arteries cultured in identical conditions [67], and even venous VSMC exposed to cyclic stretch proliferate more than arterial VSMC [68]. ”
It basically says that the remodelling response was associated with pulsatile stretch (which of course resulted in stiffening) – same as that described above in arteries.
Whereas the arteries developed slowly over the years, accommodating bit by bit the gradually increasing demands . . . the vein has to deal with the pressure and wall strain full on . . . hyperplasia results in short order . . . more chaotic? . . . adventitial capillaries come to the rescue of distressed intimal cells and open the doorway to lesion development.
(One point I would query in the above is the “VSMS acquiring a synthetic phenotype and migrating through the vessel wall”. In other words . . . they found what they knew were not SMCs, so they, like many others, assumed must be transformed SMCs, that suddenly acquired the ability to proliferate AND move into the intimal layer. To me, they were in fact sub-endothelial intimal layer cells that would proliferate at the drop of a hat anyway, and were in the intimal layer in the first place.)
“Molecular mechanisms of the vascular responses to haemodynamic forces” 2006
S. LEHOUX
On AH Notepad’s question of why arteries become sclerotic and not veins. . . on the picture above . . . arteries have to suffer much more of a demanding environment than veins and are more prone to hyperplasia . . . and the rest follows.
Antony,
Increased blood flow and pressure leads to intimal thickening (remodelling). Some believe this is the beginning of arteriosclerosis and plaque. High intensity exercise therefore appears to be counterproductive. Maybe there is good plaque and bad plaque?
Dr. GoranI am intrigued by your use of pulse meter and how it relates to heart rate variability (HRV). Got me thinking about how fasting might be beneficial in rebooting metabolism. A quick google revealed that fasting (Ramdan) can have beneficial effect on HRV. I have been experimenting with restricting eating window. A pulse meter that measures HRV would be something that I would consider purchasing.
I don’t think that Ramadan is true, healthy fasting in the medical sense that fasting gurus such as Dr Fung would recognise. Food consumption in countries such as Saudi Arabia actually increases by about 40% during Ramadan. Excessive eating during night-time and then lasting out until the following sunset can’t be healthy.
Since coming across Dr Fung’s work two or three years ago I’ve done a water only fast from Thursday evening until Saturday lunchtime / afternoon each week and a 3 – 5 day water only fast three or four times a year. My longest fast has been 7 days. I train and exercise as normal throughout the fasting period and my performance only drops marginally, if at all.
My biggest “worries” initially were related to the usual stories that “health care professionals” like to peddle. Eg, you go into starvation mode (whatever that is), your stomach will eat itself, you have to eat many (carby) meals a day to keep your blood sugar “balanced”, you’ll lose muscle mass and other such bollocks. Once you accept that fasting is normal and natural and nothing bad will happen just go for it. I think the general caveat being that you are in good health before you go for extended fasting periods. My normal diet is carb restricted so perhaps that makes things a bit easier. I’ve measured blood ketones directly in the past but the strips are expensive. Generally I enter into “proper” ketosis about day 3 – 4 and I can usually tell because of a rush of a feeling of well being, increased “get up and go” and mental clarity.
I don’t know about how fasting would affect HRV but in terms of feeling “reset”, I would say very much so.
Mark, agree that Ramadan is not a good fasting model but a study showed that HRV was improved. Increasing HRV is apparently a good thing, this is what affects it:
PARASYMPATHETIC nervous system- increases HRV (relaxation, digestion, sleep, recovery, exercise, fasting)
SYMPATHETIC nervous system – lowers HRV (stress, overtraining, inflammation)
My next investigation is to decide what type of exercise is best for my age group (77+), slow and steady or push the limit at max. heart rate. A simple pulse monitor is probably all I need to track progress.
Andy S
best exercise: both of them, since I too am 78
pulse meter: this is your future, so why skimp on it? better do your own monitoring
I like Polar, because they research and turn out decent products.
what I do:
I monitor my HRV occasionally
blood pressure regularly
eat real food
exercise
supplement, we oldsters have more difficulty absorbing stuff
keep off regular medicine
visit doctors the minimum
flu vaccination (I know this isn’t PC, but it works for me)
Read this blog and the comments, as if my life depended on it (it probably does)
Mr. Chris,
Appreciate your comments, they are in line with my protocol. Polar pulse wrist monitor will arrive next week and add another dimension to monitor vital signs.
Andy,
Here is one opinion: https://www.docsopinion.com/2017/10/02/muscular-strength-longevity-strength-training/
Phil
Philip Thackray
Renfrew, PA USA
Mr Chris
RE: “flu vaccination (I know this isn’t PC, but it works for me)”
Try Garlic (lots), vit C and exercise in that order. It works for me 🙂
Robert,
Talking vitamin C and health i am convinced that it is good for your respiratory system to ward off infections. (Pauling’s teachings!)
Yesterday, after my successful workout I though felt something was “coming on” in my lungs so I went out “hard” with vitamin C to ward this off. (Last year I had a real rough experience with pneumonia.) So I had two times fifteen grams during the evening and night and which seems to have worked pretty well but today there was no workout.
Heart rate variability is not about the highest and the lowest heart rate during exercise. It concerns a regular pattern in your resting heart rate, going up and down, up and down, following a sinus curve over time. You need one of the heart math devices to measure that.
Insulin Types probably have a huge affect on the processes. Noakes shows us that there are four types of carb sensitive individuals…hopefully I got this right. The worst pumps high Insulin all day and stores any sugar up as FAT, even leaving the victim feeling starved. With the huge affect on stroke and Heart issues due to any rise in sugar, this would have to be one of the effectors.
Most heart attack victims have high blood sugar levels. Higher levels of fribrinogen as a result?
“patients with fasting glucose levels above 88 mg/dl had greater platelet dependent thrombosis than those with levels below 88 mg/dl. The authors of this study remarked: “The relationship is evident even in the range of blood glucose levels considered normal, indicating that the risk associated with blood glucose may be continuous and graded. These findings suggest that the increased CAD risk associated with elevated blood glucose may be, in part, related to enhanced platelet-mediated thrombogenesis” (Shechter 2000).” Glucose induced platelet aggregation!
Hypertension – Sustained high blood pressure compromises the integrity of the endothelium, and can cause endothelial activation and initiation of clotting (Schmieder 2010). I know you like this one as it can be enhanced by stress.
Also, you have mentioned in the past about Vit C, many vitamins and minerals are affected somewhat by high blood sugar.
A couple of differences in veins are SUGAR and OXYGEN! I wonder if there is low sugar or O2 in the Lung arteries, or they are bathed in venous blood? Could explain the low incidence of issues there?
Oh, yes, insulin does influence clotting activity, according to many references in a google search. 50% over age 60 taking insulin had clots in legs!
There seems to be different types of insulin resistant people and the worst types have higher blood glucose and more insulin. More insulin and higher glucose levels cause cascading issues: affects the fluid viscosity which probably affects pressure, may constrict vessels or impair the function, affect numerous clotting mechanisms, reduce vitamin uptake, increase surface oxidation of epithelium. when the glucose and insulin levels increase, they finally break through and damage the epithelium, and inhibit the clotting/unclotting processes. Fat accumulation and the body fat limit may also play a part, as fat increases or clots occur, sometimes new vessels form and when clots start to form, vessels or flow can re-route. I don’t know how this comes in but I believe it does add another twist. Some people may also not be as good at forming new vessels or re-routing blood flow as others. I suspect this process is also influenced by insulin, glucose.
You were going on about the clotting process how touchy it is. Lots of things could come along to inhibit this and I believe that glucose and insulin together or individually can be a part of the problem.
If you research that you may also note that many of the things Dr. Kendrick named that supposedly cause or increase risk of CVD are not independent.
Diabetes = Hyperglycemia
Cushing = Metabolic syndrome, hyperglycemia due to stress hormones
Smoking = Short term hyperglycemia (raises BG and FFA due to sympathomimetic effects)
…
There is also a strong correlation between diabetes and CVD risk, I believe, to the extent that diabetes could be said to cause it. Of course, hyperglycemia often comes with hyperlipidaemia so there is still the question of what does you in, glycation or lipid peroxidation. Enjoy your heart healthy fats.
Steve,
Interesting comment!
I wonder if me and my wife are now really “reset” after eight years on the strikt LCHF life style. According to our blood glucose measurements we are just fine/superb, with very little variation between before and after meals, all the time except when we occasionally gravely cheat (sweet plums in the garden is a great temptation so we try to give them away to innocent people passing by) when the levels easily skyrocket.
It is a sad thing that we cannot easily measure the insulin levels at home to evaluate the more important subject of insulin resistance. Dr. Kraft has added a lot of clinical knowledge on the covariation of blood glucose and insulin in a large number of his metabolically injured patients. I am now eagerly waiting for an accessible meter for home use to emerge on the market but wonder why there isn’t any meter around already. The market potential should be enormous.
Hi Dr. Thanks for taking the time. I use myself as a guinepig as well. If I was older than 65 and in bad shape, Rapamycin would probably be tried. Before that there are other options that are probably better with less possible side effects. There are only a few sites on the cutting edge and this is certainly one of the finest.
My in laws died of their blood sugar induced strokes and Cad before 68. Since I am now past the age of initial Cad danger, with a vascular ultrasound tech wife Clear vascular scans and a zero calcium score I am eating against cancer and Diabetes. Everything I touch or eat, except special occasions, is to promote good health, minimize cancer or sugar. Practice weight training 2x per week, surf when possible and hike good mileage. Changing supplements and diet around to what works best for optimal health. We are our own best physicians, but it does require extensive study and trials.
Yes the home glucose devices are not great but they seem to work ok. This is now Something I am beginning to study and apply. Have a year or two of test kits left over might as well see what I can learn. Shame on u, I give away my Raspberry jam sweetened with stevia to friends. Still some fructose though.
Disconcerting statement from a friend’s seemingly clueful doctor
“If we actually measured insulin we would find so many diabetics the NHS would be overloaded”
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It is a sad thing that we cannot easily measure the insulin levels at home to evaluate the more important subject of insulin resistance. Dr. Kraft has added a lot of clinical knowledge on the covariation of blood glucose and insulin in a large number of his metabolically injured patients. I am now eagerly waiting for an accessible meter for home use to emerge on the market but wonder why there isn’t any meter around already. The market potential should be enormous.
Dr. Göran
I wonder if it’s because it would perhaps need a paradigm shift, similar to admitting that eating fat is healthy and basing meals on 50%+ carbs isn’t. The current paradigm says that blood glucose is the problem so measuring then lowering blood glucose is the answer, whereas in reality the best glucose testing can offer is a perhaps poor surrogate marker for the real culprit.
According to Dr Kraft just about all of us eating a typical, SAD diet are metabolically compromised which is quite worrying. He has the data to back it up as well.
Dr. Kendrick:
Here’s a video that purports to show why glucose
spikes cause heart disease:
What do you think about what they say at 14:40?
OK, Dr. K
Add blood viscosity to the list as a big hitter, as everything we are looking at changes viscosity:
Nearly 300 CAD risk factors are correlated with blood viscosity
Men tend to have older blood cells that are not as flexible
women have much higher levels of younger cells, unless they stop menstruating:
“Remember the four primary determinants of blood viscosity: hematocrit, RBC deformability, RBC aggregation, and plasma viscosity. All four are highly affected by a woman’s monthly blood loss. The effect on hematocrit is obvious. RBC deformability may be less so. RBCs have a lifespan of about 100 to 120 days. Young RBCs are more flexible and deformable than older ones. Because of monthly bleeding, a woman makes more new blood cells than a man. Her blood contains about 80% more young blood cells than a man’s and about 85% fewer old blood cells. Older RBCs are also more likely aggregate than are younger RBCs. In addition, they are more fragile than younger cells and more likely to break apart, releasing hemoglobin into the plasma. Plasma free hemoglobin binds nitric oxide, reducing the ability of NO to perform its functions as a vasodilator and an inhibitor of platelet aggregation. ”
Oh yes, NO affected as well.
Cold weather increases viscosity…more CAD in the winter? and we thought this was vitamin D?
A growing number of studies point to blood viscosity’s role in cardiovascular diseases. In the 1990s, the Edinburgh Artery Study observed 4860 men between ages 45 and 59 for five years and showed that the 20% of individuals with the highest viscosity had 55% of the major cardiovascular events. Only 4% of those with low viscosity had any significant cardiovascular event. The difference in mean whole blood viscosity between the two groups of patients was statistically very significant (p = 0.0003). The relationship of blood viscosity to the occurrence of cardiovascular events was at least as strong as for diastolic blood pressure and LDL cholesterol and stronger than that of smoking.
diabetes increases blood viscosity:
“It is has been demonstrated by many investigators that diabetics have elevated blood viscosity. It is also known that red cell deformability and the osmolarity of the blood – both affected by uncontrolled blood glucose – mediate blood viscosity changes and the onset of small vessel disease. Diabetics have a higher proportion of red cells that are relatively nondeformable and which must pass through relatively long, narrow capillaries to deliver O2 and nutrients to cells. Capillaries can be smaller than erythrocyte diameter, resulting in injuries to the capillary walls. This injury is dramatically increased as erythrocyte deformability is impaired. Blindness, kidney insufficiency, and leg ischemia are the first comorbidities to appear because the associated organs are the most dependent on microperfusion for function.”
Oh yes, capillaries are mentioned too.
Blood Viscosity (BV) is higher in diabet ic patients, and might represent a risk factor for the development of insulin resistance and type 2 diabetes. The present study shows a direct relat
ionship between BV and blood glucose in non; diabetic subjects. It also suggests that, even with
in glucose values considered completely normal, individuals with higher blood sugar levels have inc reased BV comparable to that observed in subjects with prediabetes.
Stress:
A third study followed 331 men newly diagnosed with essential hypertension for up to 12 years. Patients were grouped into three categories by their diastolic blood viscosity levels: high, medium, and low. The highest tertile for diastolic viscosity were more than three times as likely to have cardiovascular events than the lowest diastolic viscosity tertile, even though all the men were hypertensive (hazard ratio = 3.42, p = 0.006).
Hydration
Plasma viscosity refers to the viscosity of the noncellular matrix of the blood. An important determinant of plasma viscosity is hydration status, and there are many others. Research published in the journal Aviation, Space, and Environmental Medicine demonstrated that dehydration increases systolic blood viscosity by 9.3% and diastolic blood viscosity by 12.5%.
Are there any studies on this aspect from CAD Victims? How about DVT on airplanes…due to hydration and viscosity changes?
Blood viscosity thus determines not only how hard the heart has to work to circulate the blood, but also the level of physical injury that the blood can cause to the inner walls of the arteries. Viscous blood has an abrasive quality that damages the endothelium during these high-shear assaults, leading to inflammation. Plaques are formed to protect these delicate areas from the constant battering of erosive, viscous blood. Plaques also form in bifurcations of the large arteries of the legs, where the blood is subject to increased shear due to the effects of gravity.
SLE patients with arterial events had significantly higher blood viscosity than any of the other groups, including patients with venous thrombotic events, reported Dr. Utset, who presented the findings at the 2006 meeting of the American College of Rheumatology. The data are slated for publication in a major journal later this year. Dr. Utset is continuing her exploration of blood viscosity in other rheumatologic and autoimmune diseases, including scleroderma. even the SLE patients have higher viscosity!!!!
http://www.townsendletter.com/Jan2012/measureblood0112.html
See their blood viscosity profile.
http://www.viscopedia.com/viscosity-tables/substances/whole-blood/
Click to access dc13-1374.full.pdf
“In his report, which was titled A Unifying Theory of Atherogenesis, Dr. Sloop indicated that blood viscosity was uniquely suited to predict the entire course of cardiovascular disease because blood viscosity accomplishes the following:
Accounts for the morphological similarity of atherosclerotic lesions associated with many diverse risk factors
Explains the anatomic distribution of lesions throughout the body.
Provides a role for platelet activation by turbulent blood flow caused by hyper-viscosity.
Includes an explanation of the protective role of HDL “good” cholesterol (i.e., HDL has been shown experimentally to lower viscosity).2”
With so many risk factors, we probably only have to adversely affect a few of them to tip someone into CAD. Cold, Dehydration, Diabetes, Stress, Old Blood Cell percentage or other combinations. That’s why this is so difficult with many variables and no one is looking at this. We would have to rank these variables, if we had the blood viscosity measurements and studies we could rank the blatant actors and improve our results. Some are claiming that iron is the issue and giving blood improves this, but viscosity is also affected, maybe a larger actor? How does viscosity affect clotting? Bet there is a big affect at a certain point as fluids with fillers agglomerate, especially will affect small vessels…strokes?
This may help explain why lungs and veins don’t suffer? Lower glucose and oxygen, viscosity drop in those areas? Hydration, Nattokinase and blood donation improve blood viscosity.
As an engineer measuring polymer viscosity every once in a while, fillers or the size/shape of polymer chains present several problems, so the measurement methods are key to understanding.Blood appears to shear thin, but what about in small cappilaries, which may have quite different behavior.
Look forward to your next post.
I’m glad you mentioned blood donation as a possible factor that reduces blood viscosity. All the way though reading your comment, this was in my mind. And then you came out & said it.
I wonder if low ferocrit iron levels in the blood are also associated with lower blood viscosity ?
Steve
i have looked at the links you give re blood viscosity as a factor in CVD and hypertension etc.
However almost none of the sources are by mainstream medical researchers. Virtually all of them are from a naturopathic or other alternative medical background.I wonder if this means they are less credible or reliable than otherwise ?
Another issue that while the Townsend letter article does mention that there are ways to reduce blood viscosity, none are discussed. Though I note that blood donation rates a mention in other sources. Can you elaborate further on this ?
Finally, an off topic : I note that no comments have been published for the past few days. Maybe it means that Dr Kendrick has taken himself 7 family off for a holiday rest ! At least tht is the thought that comes to mind for me. I hope it is a good break !
I was giving a couple of talks. Lots of developing presentation time needed.
So much for the hope you were taking. well earned break !
😦
Steve
Your point; “Plaques also form in bifurcations of the large arteries of the legs, where the blood is subject to increased shear due to the effects of gravity”
My reading of the literature is that plaques form where shear stress is a minimum. The rationale for the observation is that the action of blood flow shear stress on the glycocalyx/endothelium promotes protective NO production in the endothelial cells. A priori, it would seem the bifurcations would get a hammering; however, there is more turbulent flow around the bifurcations and this corresponds with lower shear stress.
WHO site and their top 10 longest living people. Interesting the difference between the sexes.
F.A.O. Steve and blood viscosity as a “big hitter” on the list of culprits.
I noted stress appeared, which got my attention as I believe that was the reason for my event (still unproven).
Of the 331 men, how was their stress identified? And at what point was their blood viscosity (BV) established, or was BV used to identify their stress?
And I’ll ask my usual question when confronted with a new risk factor/CVD hypothesis: is this easily tested? I’d imagine so – surely a simple blood test? But for those of us on blood thinning medication is there any point? It won’t be a true reading. But then again, it would be useful to measure the efficacy of the medication (for those of us experimenting with their pill cutters and missing days here and there) against a viscosity test with no medications at all.
Interesting stuff – thanks for posting it Steve.
Do blood thinners actually thin your blood or do they interfere with the clotting mechanism?
they interfere with the clotting mechanism.
That’s what I thought… This was in reference to an earlier post questioning whether “blood thinners” will affect BV.
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This has been on my mind for some time and concerns blood clotting but not in adults.
It’s claimed that “all” babies are allegedly vitamin K deficient when born and about 5-10 / 100,000 will suffer internal bleeding as a result. Because of this, vitamin K shots are routinely administered. It strikes me that if “all” babies are vitamin K deficient, isn’t this the normal state? Would it be similar to saying that this normal vitamin K (alleged) deficiency is similar to a baby’s immune system being immature upon birth and is subsequently primed by routine infection and this is how nature intended it to be?
Instead of baby’s diet / gut bacteria gradually and naturally increasing the body’s vitamin K, is it possible that routine vitamin K shots at birth have long term consequences for the clotting cascade, blood viscosity, blood vessel health etc? Is it wise of us to interfere (eg vitamin K shots, vaccinations etc) and alter the normal state just because it appears to make sense?
Steve quoted “Capillaries can be smaller than erythrocyte diameter, resulting in injuries to the capillary walls.”
My first thought was, this is a design defect.
My second thought was, what about babies? How does blood flow in their teeny tiny blood vessels? Presumably, red blood cells cannot be smaller otherwise they won’t function.
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Or could vitamin K deficiency in the mother’s diet be responsible? Modern diets tend not to have much fermented food in them…
I know some claim that vitamin K in the mother’s diet makes little to no difference in the baby’s blood vitamin K concentration but there is research that suggests otherwise.
OK, researched the Lung issue….Lower Pressure explains no plaques ! Maybe because the flow is the reverse situation of the rest of the arterial system; from small capillaries to larger arteries. But I think this is a special case because these arteries do not have muscles and the lower pressure flow is probably more Newtonian in nature.
Pulmonary vessels
“Although the total flow of blood per minute through the lungs is the same as that through the systemic circulation, the pressures are very much lower. Pressure in the pulmonary artery is typically 25/12 mm Hg (systolic/diastolic) compared with 120/80 mm Hg in the aorta and its main branches. The pressure in the lung vessels is lower because they are shorter, wider, have less muscle in their walls, and are very numerous. In particular, there are no muscular resistance vessels like those in the systemic circulation. The pulmonary vessels form a vast low-resistance capillary network which encircles the microscopic air-sacs (alveoli). Gas exchange — of oxygen for carbon dioxide — takes place between blood in the pulmonary capillaries and air in the alveoli.”
http://www.encyclopedia.com/medicine/anatomy-and-physiology/anatomy-and-physiology/blood-vessels – plus many more sites/papers saying the same thing, with measurements via a tube inserted into the arteries.
There is also lots of interesting information on vascular differences throughout the body, the size ranges and the ability of some areas of the body to actually collapse veins. Musculature of arteries and veins. Capillaries are also an area of interest as there are a couple of ranges for their diameter out there, but they seem to be mishappen, flat and random. The ranges of red blood cell diameters seems to be more tightly controlled, but can also degrade in some circumstances. Another path with lots of variables… We have to be careful though because several arteries and veins contract and expand due to musculature, chemical signals and some signals work in some areas and do the opposite in others. How is that possible, receptor types? Maybe a muscle cramp collapses a major artery in some type of CAD?
There are also valves in the veins that can cause a lot of issues. Flow is starting and stopping, ebbing and flowing with each heart beat, Changes in flow depend on gravity, orientation, fitness level, viscosity, ….add in all the rest of the variables. there are sure to be more aggressive and less aggressive areas and they may change due to all the variables. This would also explain some of the stress issues as some of the chemicals affecting vascular flow are stress related!
How about the Newtonian vs the Non-newtonian? I mentioned I measure this and nearly every polymer exhibits non-newtonian behavior. High shear rates actually break down polymer chains and shorter polymer chains are lower viscosity, could cause proteins to also break down or unfold (I have heard of this from the lab equipment mfr that they could measure this), could something like this cause damages in the vessel walls? We could then model critical regions, compare what happens at diverse ranges of blood viscosity and maybe come up with some rudimentary understanding of how viscosity and flow can damage the endothilium. There has to be something breaking down to reduce the fluid viscosity for shear thinning to occur. Fibrin, blood cells, other proteins, etc. does this set up the cascade of events to clot with damaged blood, or is damaged blood attacking the endothelial wall? We could measure each component separately to see which has the largest breakdown at higher shear rates, but we would have to limit the shear rates to what is possible to make sure we aren’t misled. I think the shear rates they show on their graphs are too high.
I am thinking of how to come up with a blood viscosity meter similar to the blood glucose meter. May not be very difficult, but would require a lot of comparisons with other methods for validation. then a huge effort to test CAD patients and controls. If it is cheap and easy and comparable then it may be a way to change medical understanding and improve outcomes. But we need to flesh out the theory and see if it fits with viscosity being an important player.
Based on all of this study, I am beginning to think there is a fast pathway and slow pathway and combinations of both,. either will get to CAD. I think this is why there are different types of strokes, also different types of heart attacks. I think there is a lot of interrelationships with numerous variables. we need to identify the big ones.
So now that we have answered the Lung question, and we have viscosity and vascular inputs as an added feature, How about the new post?
I think the idea of “thick blood” has been around for a while in naturopathy as well as various strategies to “thin” it but I’m not sure what they are.
Sasha,
Re: blood viscosity
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576907/
“Grounding is the most desirable and suitable intervention for both reducing blood viscosity and reducing inflammation simultaneously. Medical imaging tomography has been used to document cases of rapid improvement in acute inflammation after grounding. A pilot study on delayed-onset muscle soreness demonstrated a remarkable reduction of inflammatory mediators, including a reduction in white blood cell count (lymphocytes, neutrophils, and eosinophils).”
Thank you for the link, Andy
Sasha, more on blood viscosity:
Click to access dc13-1374.full.pdf
“Conclusions: The present study shows a direct relationship between blood viscosity (BV) and blood glucose in non- diabetic subjects. It also suggests that, even within glucose values considered completely normal, individuals with higher blood sugar levels have increased BV comparable to that observed in subjects with prediabetes.”
https://www.ncbi.nlm.nih.gov/pubmed/18257336
“Abstract
Fish and fish oil are rich sources of omega-3 fatty acids–essential polyunsaturated fatty acids. These acids in doses of 1 g per day have been shown to significantly reduce the all-cause mortality in post myocardial infarction (MI) patients and the risk for sudden death caused by cardiac arrhythmias. One of the recently most studied mechanisms that may contribute to this benefits of omega-3 fatty acids is their anti-arrhythmic effect. Namely, these acids influence membrane ion channels, increase ventricular fibrillation threshold and increase heart rate variability. Although the data concerning primary prevention is less straightforward than the data relating secondary prevention, it seems that the use of omega-3 fatty acids in primary prevention might be justified as well. In higher doses (2 to 4 g per day) they are used to treat hypertriglyceridemia. Potential mechanisms by which omega-3 fatty acids may reduce risk for cardiovascular disease include also antithrombotic (they decrease platelet aggregation/reactivity, reduce plasma viscosity, enhance fibrinolysis) and anti-inflammatory effects (e.g. they decrease IL-6, MCP-1, TNF), improving vascular endothelial cell function (e.g. they increase availability of nitric oxide), reducing expression of endothelial cells adhesion molecules, inhibiting smooth muscle cells migration and proliferation, and reducing blood pressure. Based upon clinical studies the use of omega-3 fatty acids should be considered today at least as a part of comprehensive secondary prevention strategy in post-MI patients. It has been also shown that adding highly concentrated omega-3 fatty acids to standard treatment in the secondary prevention of MI is cost effective versus standard treatment alone. Particularly important is that there are no significant drug interactions with omega-3 fatty acids.”
Thank you, Andy, very interesting. I remember my mom telling me that in the 60’s children in Soviet Union were made to drink “fish fat”. It didn’t taste very well, according to her…
1940’s-50’s Welfare Food Cod Liver Oil. Most children hated it – I was wierd and liked it so much that my Mum would give me half the dose, knowing that I was going to ask for more.
Yes, sounds like a good practice ))
In America in the 50’s we had to daily take a tablespoon of cod liver oil. It was foul; I had enormous problems swallowing, whilst my younger sister asked for more!
“In America in the 50’s we had to daily take a tablespoon of cod liver oil. It was foul; I had enormous problems swallowing, whilst my younger sister asked for more!”
I didn’ realise that I was your younger sister!
Andy,
Thank you for this reference to the strong physiological effect of grounding on red blood cell clotting. Very impressive in its experimental set up!
I have earlier mostly viewed upon this grounding business with strong disbelief but now I have again turned more openminded towards this as an “alternativ treatment” for whatever. Dr. Mercola is very keen on this subject.
Before reading this paper I had though been convinced by Prof. Karl Arfors of the importance of grounding his equipment when studying the blood flow in thin capillaries.
Can I ‘throw a spanner into the works”,(so to speak) and ask for your take on how an impairment of the lymphatic system could impact on the formation of arterial plaque? I ask because I have suffered from secondary lymphoedema for 13 years, after breast cancer treatment. Almost three years ago, out of the blue, I suffered a cardiac arrest at home, and was lucky to be one of the “chosen few” to survive such an event! Following angioplasty, having a stent fitted, taking statins, followed by liver damage, followed by me deciding to NEVER touch them again, which I haven’t! I am now working on becoming a mini expert on heart disease!(joking). As lymphoedema is a chronic incurable condition, I have had to learn to live with, and manage it over the years. It’s a very complex condition, and few people know much about it, including sadly many of the medical profession. (that included me 13 years ago, now I am a bit of an expert!). During my years of “surfing the net”, I have come across the mention of an association between the lymphatic system and heart disease. I suppose it follows when the job of the lymphatic system is to “sweep up the rubbish” in our bodies(putting it basically!). My question is, considering the fact there are multi millions of people in the world, diagnosed and undiagnosed with lymphatic disorders, is it possible that the damaged lymphatic system is simply not doing it’s job as well as it should, and as a result, this wayward plaque is being deposited on the arteries of these people, whatever their lifestyle?
Steve, your posts on blood viscosity were interesting. However, they are all correlational. Other than arguing that thick blood somehow is more damaging to the arteries than thinner blood, I haven’t seen any science to support this hypothesis. Like you say, it should be relatively easy to test it, maybe using cadavers or animals, but it has not been done. Mentioning blood viscosity in the same sentence as Polymers is not helpful. We are not pumping “honey” in the blood vessels. Besides, how do we explain the fact that CVD increased dramatically in the last 50 years, even though it has diminished in frequency recently. Did our ancestors have arteries different from ours? Maybe their blood was different, but, if so, we should be looking for reasons why the blood of those who suffer CVD is viscous. I think that it is more likely that whatever causes the blood to become more viscous is the real CAUSE – damage to the arteries follows. And I have read references which suggest that higher platelet “stickiness” is linked to high carb in the diet. Unfortunately there are very few papers out there which support this position. But if high carb is leading to higher “viscosity”, then maybe it is high carb, or hyperinsulinemia, or hyperglycemia, or other which might point to the real cause.
Smoking increase and decrease explains heart issue last 50 years. There is logic and papers that indicates pressure, viscosity and many other issues are possible variables.
Comments above on pfa may align with heart issues as pfa use has probably hurt many health outcomes. Look at roguehealthandfitness.com for several pfa studies, also “know your fats.”
Viscosities of blood need lots of work. New technology may help unlock issues not seen before like protein unfolding or breakdown of blood products. Also vascular issues abound as nothing is static throughout the system. Lots to look at closer for sure.
A detailed attempt at honesty in explaining how modern clinical medicine got to where it is, with some pointed advice for today’s students. Lots of history with metaphors and frank language. Refreshing – if you have the fortitude to wade through it.
http://thehealthcareblog.com/blog/2015/03/13/academic-medicine-survival-guide/