When you start thinking about things in a new way it is funny where it takes you. You end up seeing connections, where you may previously only have seen confusion. You see links where they could not, or should not, seemingly exist before. In this blog, I am going to take you from migraine to sickle cell disease, and explain how they both cause CVD – and how they both do it through exactly the same underlying mechanisms.
Before reading on, perhaps you might like to think about how this can possibly work … It is always much more satisfying to work things out for yourself. Or maybe that’s just me.
To begin. As you will have picked up from this blog, I believe that cardiovascular disease (CVD) is, essentially, a disease created by endothelial damage and/or dysfunctional blood clotting. With a bit of impaired clot repair thrown in. I spend too much of my life tracking down anything, and everything, that may cause CVD to see if this hypothesis fits – or does not.
Which is why I was interested to see a headline that appeared very recently on Doctors Net (A website for doctors in the UK). It was entitled ‘Migraine cardiovascular link examined’. Up to this point, I had not realised that migraine and CVD were related. So it was something new to me:
As the article, in the BMJ, went on to say:
Young women who suffer from regular migraine attacks appear to have an increased risk of cardiovascular disease, researchers warn today.
Women are three to four times more likely to experience regular migraines. The condition has previously been linked to an increased risk of stroke, but although the physiology of migraine has close links to the vascular system, the way in which migraine increases risk of stroke is unclear.
A team led by Professor Tobias Kurth of the Institute of Public Health in Berlin, Germany, looked at this association, and the link with cardiovascular disease in general.
They used details on 115,541 women aged 25 to 42 years at baseline, taking part in the US Nurses’ Health Study II, which began in 1989. Over the 20 years of follow-up, 15% of the women were diagnosed with migraine.
Cardiovascular disease was 50% more likely among the women with migraine. Heart attack was 39% more likely, stroke 62% more likely, and these women were 73% more likely to have a revascularization procedure.
In addition, women with migraine were 37% more likely to die from cardiovascular disease than women without migraine, and the risk was not significantly altered by age, smoking, high blood pressure, or use of hormone medications.1
So here is, yet another possible cause of CVD. There was no explanation put forward in this study, it was simply an observation. However, I find that unexplained observations are where the answers lie. These are the ghosts in the machine. Truths that occasionally emerge from the dark depths of the ocean, like oarfish, or giant squid, before slipping back into the abyss.
When I see a study like this, the first thing that I do is to look for an association with blood clotting, or endothelial damage, or both. If there is no association, then my hypothesis has suffered a serious blow. On the other hand…
So, taking a deep breath, I looked around the research done in this area. There has not been a great deal, but to my relief. [Yes, I know, a true scientist should never get too attached their own ideas. But, you know what, it’s hard not to….] To my relief I found that migraine is associated with, or causes, blood clotting abnormalities – and also damage to the endothelium.
Just to quote one short section from the Stroke Association:
‘Migraine-Related Stroke – There is evidence that patients with migraine, particularly migraine with aura, have an increased risk of stroke. The mechanism for this is unclear, although migraine is associated with abnormalities of platelet, coagulation and blood vessel inner lining function, and that may contribute to an increased risk of stroke.’ 2
Just to add further to the connections that potentially open up, I was interested to stumble across a case study where a patient’s migraines were ‘cured’ by using warfarin.
An unusual case report on the possible role of warfarin in migraine prophylaxis
Background: Migraine is a complex disease whose physiopathological mechanisms are still not completely revealed.
Findings: We describe an unusual case, not yet described in literature, of a patient who reported migraine remission, but still presented aura attacks, since starting a therapy with Warfarin.
Conclusions: This case report brings out new questions on the role of the coagulation, especially the blood coagulation pathway, in migraine with aura pathogenesis, and on the possibility to use vitamin K inhibitors, Warfarin or new generation drugs, as possible therapy to use in migraine prophylaxis.3
I must admit I never saw that one coming. Migraines can be treated with warfarin? Though, I suppose, had I thought things through, I might have worked it out. Or maybe not.
Anyway, pulling this information together, we now know that migraines increase the risk of CVD, – more often strokes than heart disease. When you look deeper, you find that migraines are also associated with endothelial dysfunction, and blood clotting abnormalities.
As should be pretty obvious, this all fits perfectly with the ‘CVD is all caused by blood clotting’ hypothesis. On the other hand, if you would like to try to explain how migraines cause CVD through any another process, please let me know. Of course, it could be that another deeper process causes both blood clotting abnormalities, and migraines, but that is for another day.
Of greater interest to me is that, whilst I was studying migraine and CVD, another condition kept popping up on the search criteria. Something that was, again, completely new to me. Which is that there is a very strong association between sickle cell disease (SCD), and CVD. I had never previously thought to link these conditions. However, a number of the migraine articles pointed me towards sickle cell disease (SCD).
Sickle cell disease is a genetic condition whereby red blood cells are malformed and have a sickle shape. This accounts for the name. It is a genetic mutation that, in milder forms, is thought to to protect against malaria, because mildly sickle shaped red blood cells are more difficult for the malaria parasite to enter. However, in its more severe forms, sickle cell disease is quite damaging. Sickle cells can burst, get stuck in smaller blood vessels, form clots in blood vessels in the eyes – leading to blindness, lung and kidney problems etc.
To cut a long story short, in sickle cell disease there are all sorts of ‘clotting’ problems. There is also the potential for significant endothelial damage due to the abnormal shape and function of the red blood cells. Given this, you might expect increased risk of CVD. Which there is, as covered in the paper ‘Atherosclerosis in sickle cell disease – a review:’
‘Ischemic (lack of oxygen) complications are the major causes of morbidity and mortality in patients with sickle cell disease (SCD). The pathogenesis (what causes these problems) of these complications is poorly understood. Ischemic events in these patients have been attributed to the effects of hemoglobin polymerization, resulting in rigid, dense and sickled cells trapped in the microcirculation. Therefore, vascular occlusion is often considered to be synonymous with occlusion of microvasculature by sickled red blood cells. Several observations suggest that other factors may also play a pathogenic role. Atherosclerosis is one of these factors and may affect many arteries all over the body.’
It is fascinating what you find, when you decide to look at things from a different perspective. You start looking at the connection between migraine, CVD, and blood clotting, and end up studying sickle cell disease. I must admit that I get a great sense of satisfaction when I come across facts like this. Somewhat like completing a jigsaw puzzle. ‘Yes, hoorah, it all fits. In fact, it all fits perfectly.’
Indeed, the article on Atherosclerosis in sickle cell disease goes on to bring in Nitric Oxide and L-arginine. I have covered both of these factors in some in detail earlier on in this series. [Sorry this section a bit jargon filled]:
‘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. In recent years, investigators’ attention has been attracted by the effects of chronic hemolysis on vascular bed integrity and function in patients with congenital hemolytic anemias. Hemolysis results in the release of free hemoglobin.
On one hand, it scavenges NO by oxidizing it to nitrate and releasing red blood cell arginase. On the other hand, it hydrolyzes L-arginine, the substrate of NO synthase. Because of these effects, NO bioavailability and its action is limited. All the previous mechanisms cause impairment of NO production. NO is an important vascular relaxing factor and its deficiency would lead to large artery stiffness. In addition, NO promotes general vascular homeostasis by decreasing endothelial expression of adhesion molecules, decreasing platelet activation, and inhibiting fibroblast, smooth muscle cell and endothelial cell mitogenesis and proliferation.’
In one short section on SCD we have virtually everything I have been writing about in this series so far. There is:
- Reduced NO synthesis
- Damage to the endothelium
- Increased risk of blood clotting in general
- Increased platelet activation and adhesion
- Inhibition of endothelial cell repair and proliferation
- Increased risk of CVD and accelerated atherosclerotic plaque development
Another highly important point here is, as follows. You may recall that I said atherosclerosis almost never forms in the blood vessels in the lungs (pulmonary blood vessels). The only time it does is if you have pulmonary hypertension (high blood pressure in the blood vessels in the lungs).
Well, I just found out that if you have sickle cells disease, you are at high risk of developing atherosclerosis in the lungs:
‘The pulmonary artery is one of the common sites of atherosclerosis in sickle cell disease (SCD). Autopsy of the pulmonary artery in patients with SCD showed that approximately one-third of the patients had histological evidence of medial hypertrophy, intimal proliferation, and subintimal proliferation and fibrosis.’
Now you may not think this is particularly important, but to me it is a killer fact. Atherosclerosis in the pulmonary arteries is something so unusual that when you find it, you are looking at the mother lode. If you can cause atherosclerosis here, then you are gazing at a true underlying cause, with all other risk factors stripped out.
Here is the process (or processes) revealed. Deep joy. It is not often that I come across a fact that I had no idea existed before. Certainly not one that confirms so perfectly everything that I have been saying.
I realise that I have repeatedly stated that the primary purpose of science should be to contradict hypotheses. Here, all I have ended up doing, is providing more facts that support my own hypothesis. I would ask you to believe that I started out looking for a contradiction. I ended up with greater confirmation. Confirmation from places where I had never previously even thought to look.
1: BMJ 1 June 2016; doi: 10.1136/bmj.i2610
Do sickle cells have impaired oxygen carrying capacity?
Does the zeta potential of sickle cells equate to that of healthy RBCs?
Triptans are well known to increase risk of CV events. Was this association looked at in those migraine sufferers as an independent risk factor?
“Well known” is a concept that has been coming under greater scrutiny lately.
This small study suggests that triptans might not be so evil and that a much closer look is warranted.
Migraine attacks are believed to be caused by a dilation of blood vessels which triptans counteract.
So I can see how triptans might cause MI and stroke, but dilated blood vessels should be good against stroke and MI. Where’s he catch?
Great series. But is the ‘mystery’ of CVD really the fact that it’s caused by endothelial dysfunction (and blood clotting abnormalities), or is it rather the question of why CVD has exploded since 1900 and especially since 1950? The answer to that second question can’t be SCD, or Kawasaki’s disease, or dehydration, or vitamin C deficiency, or even smoking (which peaked decades ago) or most of the other items on the list in your previous post.
In my view, the real question is why has our vascular system got so stressed during the last century? And a lot points towards metabolic stress, both directly and indirectly (diabetes etc.), induced by nutritional changes, especially a huge rise in the consumption of sugar (= isolated fructose) and omega-6 seed oils (soy, corn, sunflower etc.) destroying the crucial n6/n3 PUFA balance.
You are most likely correct. I’d add general stress to that too.
I agree with you Mathew. I believe a lot of our problems relate to nutrition. High carbohydrate and sugar consumption plus the industrial seed oils are killing us. As Gary Fettke says. Sugar makes us hungry. Carbohydrates make us fat and polyunsaturated seed oils make us inflamed and sick.
Thanks Malcolm for another informative questioning article. I don’t know whether I would want to take warfarin because of the calcification it can cause by blocking the K pathway.
“[. . . a lot points towards metabolic stress . . . ]”
Truly perceptive remarks, Matthew.
Yup, thrombogenesis [tendency for clots to form] and atherogenesis tendency for arterial ‘plaques’ to form in the endothelial cells or arteries are a part of the process that can, down the line and as the hypothesis would have it, result in an ischemic heart attack or stroke. In themselves they are not the cause.
A lot points to chronic oxidative stress. ‘Oxidative stress’ could be regarded as a bit of a misnomer because while oxidative stress may be conveyed by reactive oxygen species (ROS) [and it often is] the ‘stress’ part doesn’t have to involve oxygen itself. Oxygen’s placement in the periodic table is telling – and it explains a lot about oxygens’ biggest claim to fame.
Oxygen is a potent electrophile [it is compulsive stealer of electrons] and, really, if the mind can accept that the theft of electrons is a frequent instance arising throughout the biochemistry that keeps us alive, and that this is the ‘process’ aspect of ‘oxidative stress’ then the mind is well on the way to grasping the real nature of ‘oxidative stress’.
But there does exist a stumbling block. ‘Oxidative stress’ and metabolism each involve the movement of electrons [exchanges or theft], so they are much the same process [sometimes referred to as oxidation and reduction] and the distinction of what’s normal and healthy and what’s not is a fuzzy one. The difference of normal, healthy, and good, as compared with excessive and potentially damaging is more down to the context in which the process can be witnessed than down to the process itself.
This revised explanation of ‘oxidative stress’ is one described in the realms of the physics that applies to biochemical dealings [the trading of electrons in [bio]chemical reactions] but there exists a lot about the spark of life whose energies are traded in the quantum domain. All this means is that electrons [generally the outermost ones that shroud an atom] can rise up the ‘quantum ladder’ when, and if, stimulated by interacting with a dose of electromagnetic radiation of just the right kind [which varies from instance to instance]. And when electrons step down from an elevated rung of the quantum ladder to the lower rung that may be ‘available for occupation’ electrons lose a bit of their energy which is commuted back to electromagnetic radiation and is emitted. Frequently this kind of radiation conforms to the description of infra-red radiation [which we know better as ‘heat’].
So the learning point is that electrons can be displaced in either of two ways. There exists the good old fashioned trading between atoms and molecules [oxidation and reduction or ‘electron theft’], and there exists the movement of outer electrons from one quantised orbital to the next, say, and back down again. It could be said, as an early day hypothesis, that too much quantum horseplay is another instance of oxidative stress. Certainly, when it is going on and where it is going on you get more ‘heat’. And while the term has attracted to it connotations it may not strictly deserve, medicine has an alternative term for the presence of more heat than is usual and calls it ‘inflammation’.
Your mention of ‘metabolic stress’ and my recourse to discussion of ‘oxidative stress’ amount to much the same thing. It is [they are], in effect, ‘electron stealing’ that is arising beyond the limits of the ‘healthy’ and ‘life giving’ [how shall we say] ‘Goldilocks zone’. And there are two sides to how it can arise. There can be too much that is promotional of oxidative stress, and not enough of the factors that would normally work as a counter [the supply of antioxidants].
As you begin with the ‘process[es]’ and work back towards those factors [external to the body] that might be placed closer to the roots of the cause[s] then a lot points to endocrine disruption [environmental factors disturbing certain hormones]. Then in turn endocrine disruption may seem to be promotional both of oxidative stress and inflammation. To become sufficiently well informed as to be able to explain the link between endocrine disruption and oxidative stress fully would be a significant advance [and I’m not there], but there is a lot about homocysteine theory, and about the synthesis of epinephrine [the consumption of methyl groups] that indicates that endocrine adjustments and disruption can be a driver of oxidative stress.
“. . . the real question is why has our vascular system got so stressed during the last century?”
Matters are far from obvious until they are pointed out, but the short and long of it is that the world we live in [the one that is developed and ‘modern’] is more disruptive to the endocrine system than is the kind of world that pre-existed it.
There do still exist peoples who live in the wilds and who hunt and gather for food. These are tribes-people, as we would call them, who live beyond the reaches of the cash economy and modernity. Sadly their traditional ways are in decline and so are their numbers. But I am prepared to bet that if a person made it their business to study these ‘free-range’ examples of homo sapiens that the rates of incidence of heart disease, of stroke, of diabetes, Parkinsons, Alzheimers, sickle cell disease, multiple-sclerosis [and heck knows what else] would be far less than they are amongst us ‘westerners’.
Viewed from the dietary angle they do not eat so much (highly glycemic) carbohydrate as we do [which p[omotes chronic hyperinsulinemia], nor do they over consume troublesome omega-6 types to the extent that we do [which some direct causes membranes of cells to become dysfunctional and is the cause of insulin resistance [thus being another pro-hyperinsulinemic factor], but there are other considerations too.
We are a species like any other – a fact that sometimes gets overlooked. Many species are light-sensitive. The natural cycles of light and dark caused by the rotation of the Earth as it orbits the sun provides cues that aspects of the endocrine system can ‘read’. Crudely speaking the body knows what time of day it is. And in higher latitudes day length varies with the seasons. Because evolution has ‘engineered’ light sensitivity into aspects of the endocrine system the body knows what time of year it is. Different species may deploy this awareness differently, but in warm-blooded mammals it is usual for the hormone cortisol to have a diurnal and circadian rhythm driven by natural light. This in turn has a cascade of influence over other physiological factors.
Too few medics have contemplated the effect of the electric light bulb [invented just about the time the ‘rot’ began setting in] on public health. It has changed the way we work, the way we sleep, and the quality of our sleep. Because we spend so much time working indoors we do not spend enough time in truly bright daylight. And paradoxically we do not spend enough time in the hours of darkness in a place that is adequately dark. Accordingly it is not unusual for westerners to suffer hypercortisolemia and/or arrhythmia of cortisol. That’s endocrine disruption on a significant scale – and its all down to the ubiquity of the electric light-bulb.
I haven’t the time to trace the source but the light levels on the wards are now becoming the subject of concern and study, an email alerted me. The lights are never off, though they may be dimmed for a few hours. Hence for longer stay in-patients the light on the wards is attracting interest for being potentially disruptive to circadian aspects of physiology, and this dysfunctional side to those cycles is seen as a potential hindrance to recovery and healing. Yup, eye masks ought to be standard issue, and they should dim them there ward-lights more and for longer.
And not only did Edison invent and develop the filament bulb but some other smart-arse mastered the vulcanisation of rubber. Beginning about eighty years ago shoemakers began trending to a preference using rubber and plastics instead of leather, first for the soles and more latterly for their uppers. Even the most open-minded person would struggle to contemplate this, but rubber soled shoes deserved to be categorised as endocrine disrupters. How so? Well . .
. . Albeit with some reluctance on account of his scepticism Maurice Ghaly devised a trial designed to test the effect of ‘Earthing’ participants upon their physiology. For no other reason than cortisol can be assessed via the collection and analysis of saliva he chose cortisol as the object of his study. He expected to prove nothing. But rather oddly what he found was that the habit of earthing had a normalising effect upon cortisol. Typically participants began hypercortisolemic [as tested via saliva] and showed signs of arrhythmia too. One participant seemed hypocortisolemic as considered within the group and the effect of earthing was to restore more normal levels and diurnal rhythms. Ghaley, the sceptic, was converted. To see is to believe. 
In the natural setting cortisol plays a big part in the preparations for winter. Through being a driver for a process called gluconeogenesis [conversion of proteins to glucose] raised levels of cortisol promote both hyperinsulinemia and lipogenesis [conversion of glucose to fats] and the fats thus synthesised get transport to fat cells for storage. Those fat stores help supplement the energy budget when food is short as opposed to plentiful and a creature may last the winter. This applies to mammals, especially, and is more pronounced where the seasonal variation in the availability of food may be greatest. It commonest amongst mammals above a certain size.
Unfortunately for us humans the way we live, compared to how we once lived, and the trend from being ‘free-range’ to ‘civilised and ‘modern’, rather replicates the conditions of perpetual summer. The body is constantly preparing for the conditions of ‘winter’ that [in the endocronological sense] never comes. 
Harking back to those wards, every bed should have an earthing sheet fitted. And when my wife suffered an aneurysm, when those dedicated medics at Hope Hospital in Salford did so much to enhance her prognosis such that she has made a full recovery, I thought nothing of taking in an antistatic wrist-band and a bonding plug so she (her body) could tap into the reserve of electrons present in earth and thus not be short of them herself. Deficiency of electrons = impaired ability to repair, recover, or heal.
“. . . the real question is why has our vascular system got so stressed during the last century?”
Hopefully the real and inclusive answers lie embedded in the above.
I highly recommend the book, Healing is Voltage:The Handbook, Jerry L Tennant MD. Tennant has drawn heavily upon the findings of Robert O Becker whose work was written up as the book, The Body Electric: Electromagnetism and the Foundation of Life, that book is highly recommended too for its introduction to what happens to the electrical potentials of the body and tissues as a result of injury and as a co-factor to the process and progress of repair and healing.
Healing is Voltage (Tennant) is far reaching in its ramifications and many are its learning points. One of the greatest learning points is the means to perceive that pH and electricity amount to much the same thing. Alkalinity arises when a surfeit of electrons are present in a fluid and acidity arises when there is a deficit. The mind may not grasp this with ease but Tennants deft explanation does grease matters so the mind can turn them over and embrace them more readily.
The Forth Phase of Water: Beyond Solid Liquid and Water, Gerald Pollack, is radical and unconvincing idea upon first encounter that makes far more sense after giving the notion a chance and adequate contemplation. Basically within bulk liquid water can exist traces of a liquid crystal phase of water that is possible because it has been deprotonated to a particular degree – and is is incident radiation, or even ambient radiation, in the form of heat that can promote that deprotonation. Molecules thus deprotonated can take on a planar crystalline formation with layers stacking (though not rigidly) in layers. This molecules and layers have net negative charge, while isolated protons thus created rush to conjoin with unaffected water molecules to form hydronium ions within the surrounding bulk water giving rise to net positive charge there. That’s a potential difference between one region of water and another – a ‘battery’ by any other name, and the means to do work. It’s the beginnings of an energy economy that is the beginnings of the makings of the essence of life itself.
Neither Tennant, nor Becker, nor Pollack, reference Earthing theory to any extent (because the theory of earthing is new) but Tennant built upon the work of Becker to arrive at a remarkable observation and comclusion; which is this: Chronic disease and cancer associate with the prevalence of acidity about the body. And because Tennant is clear in mind that pH and potential difference (of the electrical kind) are much the same thing he posits that acidity is evidence of a deficiency of electrons! We get sick because we are deficient of electrons, and though he did not recognise the fact, we become deficient of electrons because we have ceased to have the quality and frequency of contact with ground that we used to have when we walked the earth while either barefoot, or wearing footwear fashioned from natural, as opposed to man-made, materials.
It would be remiss of me if I did not also highly recommend the book on Earthing as co-authored by Ober, Sinatra and Zucker. Now in its second edition this book includes a discussion of diabetes and makes the very same point that Matthew does; that is that rates of incidence have risen in a particular period, the period we’d call the last century, in fact with, it is reported, the trend rising even more steeply in the last half-century.
The other far reaching ramification of Earthing theory is that it invites readers of the book to think about the zeta potential of red blood cells and of the resting potential of all cells. All cells have potential. Perhaps more accurately potential differences rest upon the margin that is the membrane, hence potential difference exists between the membrane and the cells innards, and likewise between the membrane and the environment that surrounds it. The potential difference is the big driver of cell metabolism – it would appear to attract metabolites and expel wastes.
Adequate zeta potential of red blood cells (RBCs) helps keep them dispersed and in suspension in blood. It is, in fact, a relative surfeit of electrons about the membrane of the RBCs that accounts for it. When the zeta potential of RBCs falls then that presents a challenge to their suspension and even distribution and they show an observable tendency to gather in ‘social groups’. They ‘clumped’ in other words. ‘Coagulated’ might be too strong a term – though that may be the way they’re trending. Certainly the preservation (or restoration) of zeta potential is anti-coagulant by nature, and certainly it is therefore a significant obstacle along the way of the pathogenesis [process] of thromobogenesis [the formation of clots].
Ditch the Warfarin, invest in an earthing sheet and sleep on it. Because the colloidal aspects of blood have bearing upon its viscosity, and because oxidative stress and viscosity have a bearing upon hypertenstion (raised blood pressure) any indications of hypertension, be they mild or more advanced, could well be influenced for the better [3, 4].
What might the habit of earthing do fro SCD? I wished I knew of sound evidence that earthing can influence SCD for the better. I be quite surprised if, at this rather early stage in general cognitive advances, that anybody has wondered to investigate the matter.
So you prick your finger, dab the droplet of blood upon a glass slide, and take a look through a microscope. I guess you could jet off and do the same with one of the few remain ‘free-range’ homo sapiens. There are still some surviving in the Amazon rainforest. Chances are that when viewed through a slide and microscope the RBCs of our free-ranging fellow human will appear evenly dispersed about the blood on the slide while our own would appear less evenly dispersed. Now suppose you find some lush and pleasant grass, or a sandy beach to walk on, kick off your shoes, enjoy the very sensual experience of walking barefoot for an hour, then prick that finger and view the results through the microscope. If anybody is in any doubt as to what will have happened the answer, and photographic images, is to be found in the book.
The notion that light-bulbs, economic implications of agrarianism [carbs are cheap to produce, profitable to subject to process, and cheap to buy and eat], and a process called ‘vulcanisation’, could result in endocrine disruption, oxidative stress, and thence ill-health, seems way, way, left field and deserving of disbelief. But the kind of disbelief that such a proposition might incite is the kind that stems from not knowing as opposed to having done sufficient ground-work to arrive at an understanding.
There is a lot about progress that is potentially bad for an individuals health. That is precisely what Matthew indicated in his comment. It also something indicated by the breadth of evidence and reason.
Progress is seen to enhance the wealth of nations, if only with an advance in our understanding could it do the same for the health of nations.
1, http://www.earthinginstitute.net/wp-content/uploads/2013/06Dr Kendrick strikes me as practitioner who may have a microscope (or could readily access one) so perhaps he might be inspired to prick his finger before and after going to the trouble of kicking off those shoes and deliberately earthing. To see is to believe – just ask Maurice Ghaley./Ghaly__Teplitz_cortisol_study_2004.pdf
2, With modest reservations I recommend Lights Out, a book, Wiley and Formby, as an introduction to the subject matter.
4, http://www.earthinginstitute.net/?page_id=2129 [A video clip of the effect of zeta potential on RBCs]
Christopher Palmer – thank you so much for that. Highly nutritious food for thought indeed. I shall certainly try the earthing/blood examination experiment. I am full of admiration for the many who contribute so generously of their time and their knowledge on this blog site, most of all Dr. K who has brought it all about.
Thank you all.
The modern demonisation of sunshine is, i posit, an additional disruption to our health. To add insult to injury, the majority of suncreams and sunblocks on the market have some very nasty endocrine disruptors and other additives that cause further harm.
With reference to Mr Edison’s lightbulb, I read a fascinating book a few years ago that explained how the availability of artificial light altered sleeping patterns forever. Previously it was customary to go to bed at nightfall, sleep for 4-5 hours, then rise for 1-2 hours, before going back to sleep until dawn. i gather that people would often go abroad to visit their neighbours during their nocturnal waking periods!
as a PhD physicist, I feel compelled to comment.
Just let me propose a few thought experimenta: If the body needs electrons, why not isolate it on purpose and charge it negatively to supply extra electrons?
What about people who work at an ESD protected desk or workstation? Do they enjoy better health? Another observational study waiting to happen!
What about folks that get hit by lightening? Do they enjoy 10 extra years if hit by negative lighting and die within a few days if hit by a positive charge?
Frankly, I fail to follow the mechanism proposed here. An isolated, somewhat conductive body will have its charge distributed at the surface, particularly at protrusions. Further inside, the electrostatic field of these surface charges cancels so I don’t see how it could influence biochemical reactions.
As for the Ghaly paper, the link you supplied as well as the link I found via google
The study can be found here
but the full text costs the trifle of $51. I strongly suspect that the study was not double-blind, probably not even single-blind, and we are seeing the placebo effect at work.
Thank you Christopher Palmer. Earthing is something I do. We sleep on an earthing sheet and I take every opportunity to earth by walking barefoot outside everyday in the summer and when I can in winter or connect via the bands. The best is on the beach at the water line which unfortunately I don’t have ready access to. To be honest I can’t say I feel any differently but I do sleep better with it than without it. I must get a microscope and have a look at my blood as I would be interested to see what the zeta potential that Sinatra talks about is evident. From what I have read you need a darkfield microscope to see this.
Thank you for pointing out the corrupted link. This is the paper as it would be cited:
Ghaly M, Teplitz D. The biological effects of grounding the human body during sleep, as measured by cortisol levels and subjective reporting of sleep, pain and stress. J Altern Complement Med 2004 10(5):767-776.
Here’s the hyperlink:
Click to access The-effect-of-earthing-on-human-physiology-Part-1-2006.pdf
Then for good measure;
http://www.earthinginstitute.net/?page_id=131 – – a page listing links to the body of research conducted thus far.
Reference your thought experiments . .
“What about people who work at an ESD protected desk or workstation? Do they enjoy better health? Another observational study waiting to happen!”
With the aid of some electrode patches and a humble voltmeter you could devise an experiment to test human bodies for voltage. Live ones would be best and three groups would be useful.
[ESD equipment is indeed a good means to re-establish the lost former connection to ground, to redress aberrant charge that builds in the body under modern ‘western’ conditions, and to positively impact upon the bio-electric aspects to biochemistry. I initially baulked at the cost of an earthing sheet. When I fiosrt ventured to read the book I had a nasty work related and painful elbow strain whose recovery had flat-lined. With suitable care and attention I stripped some copper wire, rigged that into a helix to wear around the elbow, and linked that to the Earth pin of my domestic wiring with alligator clip and lightweight flex. I noticed nothing. But after three nights of sleeping with this arrangement I was again doeing the same physical work that would cause me to wince, the big difference was the pain had gone. Speaking subjectively the exercise seemed to have kick-started a healing process that (even prior to me thinking of this initiative) seemed to me to have stalled and was not progressing so well as it should. After that we used antistatic wristbands worn over the foot whilst sleeping. We slept better and woke feeling more refreshed.]
Voltmeter readings ought to be taken before and after, positive electrode mating to the electrode patch(es) and negative electrode linked to a grounding rod or other bonded setttng. have one group go outdoors and barefoot for an hour or so (a neat grassy lawn is ideal), have another group have contact with one form of ESD device or other (mat or wristband or footwear), and the third group continue wearing modern western style footwear made from the now commonplace non-conductive materials.
Indications are that prior to earthing those people who have been isolated when going about business as usual will register 3 volts or more on the voltmeter. (I returned 5.25 volts on myself and stared at the display in disbelief). Then have them take on the interventions advocated above and test again after a period of time. Earthing for an adequate period of time, howsoever facilitated, will reduce voltage returned to next to nothing. The success rate of any placebo max’es out at around 30%. The effect in groups one and two will be nigh on 100%. The failure rate in the third group, our control group still wearing common and familiar footwear that isolates them, will be 100%.
The positive voltage recorded on the voltmeter prior to earthing is the consequence of several species of molecules about the body’s biochemistry having been robbed of one or more electrons. Heading the list must be the hydroxide ion. That’s the ion that in numbers accounts for acidity. To produce a reading of 3.0 volts or more the numbers of individual electrons involved must be staggering. ‘Oxygen’ is the robber. It is the placement of oxygen in the periodic table and the cumber and configurations of electrons in its outer shell that make it highly electrophilic in its interactions and reactions. Oxygen is an an electron stealer. The robbing of electrons amounts to one aspect of ‘oxidative stress’.
Is being depleted of electrons bad for one’s health?
Oxidative stress (which can arise via more than one pathway and which can persist for more than one reason) has an underlying detrimental effect upon biochemistry. This underlying detrimental effect upon biochemistry could extend even to having disruptive effect upon the epigenome thence upon genetic expression. That’s the open-minded possibility I derive from having ventured to read the titles I recommended in the above comment. Under conditions of oxidative stress healthy cells struggle to replicate in precisely their own likeness (Tennant – ‘Healing is Voltage’) posits and cells trend to becoming increasing unhealthy and dysfunctional over successive generations; that being the process via which chronic disease progresses.
“Another observational study waiting to happen!”
Being inclusive, holistic, balanced, and academically mature about this then I think the study you conceive is fraught with difficulties.
Chronic diseases are typically multifactorial by nature. This presents difficulties unless the nature of multifactorialism is better appreciated and understood. That said there is much about the evidence that implicates endocrine disruption as a step in many a causal process, and then there are indications that endocrine disruption can bring about a rise in the levels of oxidative stress that prevail. But the supposed link between endocrine disruption and oxidative is stress represents a vast area to study. Expecting a definitive lesson in few words is asking too much. Having said that coming to a realisation that the materials used in modern footwear amount to endocrine disrupters through a process facilitated by chronic electrical isolation from ground is step closer to gaining improved insight into multifactorialism and its role in the etiology of chronic diseases. Likewise the ubiquity of electric light.
Anyway, the level of isolation attained in the modern world is not natural, not when you think in anthropologic and evolutionary terms. Furthermore the regions of the world where endocrine disruption and electrical isolation from ground is the greatest are the very same regions of the world where incidence of certain chronic diseases is the greatest. What is more the the rise in rates of incidence tracks the rise influence of these (and other) stated factors.
There are not many of them left but there remain some remote humans living in tribes in isolated places where the influence of the light-bulb, motor vehicles, the cash economy, shoes with rubber soles, and agrarianism has yet to impact upon their way of life. They are less sedentary than we are, spend more time outdoors than we typically do, and their whole body electrical potential will always be close to the value of ground. I hearsay that they are not troubled by diabetes, cancer, multiple sclerosis, Alzheimers, CVD, etc., (perhaps even SCD) to the extent that we ‘westerners’ are.
I cannot answer the ‘thought experiment’ precisely as you phrased it. However I gave you simple experiment you yourself could undertake and predicted the likely results based upon a more holistic understanding of the subject matter than your own. While you are about that experiment and in addition to collecting readings from the voltmeter also obtain some pin-prick blood samples to be viewed under a microscope. In accord with studies that have done this red blood cells on the slides should appear more dispersed and less coupled after earthing than before. For ‘primitive’ barefoot ‘free-ranging tribes people there would no coupling and no improvement. And if during that same experiment blood samples could be taken and pH tested. I do not no for sure but pH may trend to being less acidic after earthing.
This is beginning to get too far away from the main discussion, sorry
Christopher, sorry I missed your earlier comments. Besides Healing is Voltage, what other titles do you recommend? Thank you.
Regarding endocrine disruptors, Krimsky wrote Hormonal Chaos. It’s also due to prevalence of chemicals, at least according to the book.
in your experimentation with a voltmeter, did you ever not the sign of the voltage? Dic you ever try to measure the AC component?
I’m afraid your results may be similar to someone picking up a bilingual dictionary and happily translating away into a language he knows nothing about, all the while producing what amounts to gibberish.
Electrostatic potentials on human bodies will typically be in the range of several hundreds to several thousands of volts. In spite of the small total charges involved, this is made possible by the insulation provided by synthetic soles and flooring. If you take a garden variety digital voltmeter, it typically has an input impedance of 10 MegOhms. This is low compared to the original insulation, but not so much higher than typical resistances in the body, hence it will deplete and ground any electronstatic charge within less than a second.
Now suppose your theory that the body is like a battery (which it is not, because there is no unidirectional serial connection of elementary galvanic cells), if you were to measure the voltage
between one pole of a battery and ground, you will measure nothing once electrostatic charges have been grounded. The correct way to measure the low impedance voltage of a battery is to measure between the two poles of the battery.
It is more likely that what you measured were either AC voltages (if the voltmeter was set on AC or its autorange decided you wanted to measure AC), or you measured rectified RF. Your body will act as an antenna, and the voltmeter connected between the body and ground, due to its internal protection circuitry, will rectify some of this and display a voltage in the low volts range.
Ok, enough basic electrical engineering classes for today. I agree with Malcolm that this has taken us too far off topic!
the link you provided does not go to the Gahli paper, but rather to a paper by someone called Chevalier. That study was reasonably double blinded. I haven’t read the whole thing but I suspect the differences they see in EEG etc. are more down to antenna effects than electrostatic charges.
Their talk about the earth’s potential, but a potential must always be referenced to something. Their take on clouds and lightening is downright wrong. Thunderstorm clouds develop a charge separation within the cloud, with small ice particles transferring electrons to heavier hail. The small particles go to the top of the cloud while the hail ends up in the bottom. So a cloud is usually charged positively at its top and negatively at its bottom. This potential difference is entirely within the cloud. However, the negative charge at the cloud bottom will cause the ground beneath the cloud to be positively charged by electrostatic induction. So being grounded while under heavy cloud cover would be a bad idea according to this theory.
My take is that the body is still reasonably conductive, so it acts as a Faraday cage for the small charges that accumulate when ungrounded. These positive or negative charges will sit at the surface, effectively cancelling at the interior, so there can be no paucity or affluence of electrons within.
As Dr. Grimes points out, the explosion in CHD is over: “there has been a major decline of age-related CHD deaths internationally, by up to 80% between 1980 and 2007.”
There’s still a big increase in CHD with age, however.
My mother, born 1921, was the youngest of six children. The four youngest all died in their 40s and 50s, my mother of cancer, her sister and two brothers of heart disease. (My uncle Ken was one of Dr. Chris Barnard’s first patients. He had a plastic heart valve you could hear clicking if you put your ear to his chest.)
The two oldest lived to a decent age. Now why did the youngest all die young but the oldest not? I’m wondering if it wasn’t the Depression. Perhaps they didn’t get some vital nutrient at a crucial stage of their development. They never talked about it, but from the occasional comment and a family photo that looks like it was taken in a squatter camp, I know they had a very hard time in the 1930s.
Dr Grimes is wrong. It is certainly not over in a lot of countries round the world.
It would be interesting to see an updated version of Grimes’ analysis using data up to 2013 or so. Also a look at how delay of death from heart attacks to later years affects the results.
I had a superficial search for such data to find clues as to what stopped the apparent decline shown by his work (if it is real, which it may not be in its entirety but it probably contains a kernel of useful information). I did not get very far for lack of the right data in a clear form.
In some locations (SW Scotland where I grew up) there have been substantial changes in the death rate especially in certain sub-groups (notably middle-aged males) which could plausibly be following the pattern Grimes saw and a large component of his finding – this is my impression, not based on looking at records.
I note the “Joseph Kraft” viewpoint which seems to have a lot of merit (CVD is roughly equal to insulin resistance or diabetes in situ or properly diagnosed diabetes – see his book for the full story), and the likely huge increase in that in the general population. That would lead one to expect a current increase in CVD, though the expected age profile is not clear. My guess would be that if we look back a few decades hence we’ll see a minumum age-corrected death rate sometime around a decade ago or even more recently.
Apart from the role of smoking (which likely played a role, but I don’t think fully explains Grimes’ results) it is not clear to me what caused the decline be observed (in his analysis, whether or not it is the whole picture). It probably involves all the causes mentioned in TGCC. I think we can expect an overall increase to be underway now, with the timing dependant on how long vascular (endothelial) damage takes to accrue and how long death can be delayed by modern medicine converting heart attacks into heart failure at a later age (among other effects).
Where I live women now smoke much more than men, and I doubt there is much difference in the rate of metabolic syndrome between women and men. It will be “interesting” to see what happens. Though perhaps the damage due to sugar/IR shows up more quickly in other ways such as in cancer or dementia.
You might find this little graph quite interesting. Whilst CHD is low in most of Western Europe, the ex-soviet counties are still way up there. CVD has not gone, it has just shifted from West to East. http://www.worldlifeexpectancy.com/cause-of-death/coronary-heart-disease/by-country/
Lots of paradoxes on those figures Doctor K, like France Belgium And Italy. Do they do less damage to their endolithium?
Do you mean lots of paradoxes for the current cholesterol hypothesis? My view is that there are no paradoxes in science. Only facts that do not fit with established dogma.
As I said when you first put this table up, it is full of paradoxes. I love these tables because they are enormous case studies country by country, which show the effects of diet, life-style, climate health care etc etc. Here are a few of the paradoxes, Italy, a carbs country if there is one, pasta at least once a day, how does that fit with LCHF? Netherlands and France, big saturated fat consumers, yet levels of CVD half those of the UK, seems to pull the rug straight out from under the feet of the saturated fat cholesterol gang? and Michel de Lorgeril’s suggestion that the French paradox is due to wine consumption, is this reinforced by the figures for Italy France and Spain.
I would be more than happy if even one of these questions were answerable.
Thank you! That link (http://www.worldlifeexpectancy.com/cause-of-death/coronary-heart-disease/by-country/) is indeed very interesting. It is remarkable to see several ex-Soviet countries with death rates 5 or 6 times higher than the figure given for the UK (which is lower than I expect, but I’m not clear on which standardisation was applied).
Curiosity led me to try several other plots from the pull-down menu – all I dare to say is that it is fascinating.
In trying to understand this a little better, I came across http://heart.bmj.com/content/early/2015/05/06/heartjnl-2015-307516.full which gives 2014 data for the UK, and some commentary, including, “Mortality from CVD varies widely throughout the UK, with the highest age-standardised CVD death rates in Scotland (347/100 000) and the North of England (320/100 000 in the North West). ”
I wonder what was the equivalent number for the WOSCOPS population? (Or some other population near the -WOS- peak of CVD mortality.)
Of course the problem is to find comparable data standardised to the same population. On the ISDScotland web site I found one table of standardised CVD death rates for males listing 408.2/100,000 in 2005, falling to 268.7/100,000 in 2014.
I too dug around a bit into the French figures, there are as you would expect wide regional variations, the northern formerly heavily industrialised zones ard above the national average, whilst around Lyon, the figures are 30% below the already low average, wine foie gras, duck etc? My bet goes on lifestyle and diet.
By the way Dr K, I should have referred to apparent paradoxes.
Dr. Grimes is not saying that CVD is no more. He is saying that it was at epidemic proportions but has now fallen to “normal” levels as might be predicted from poor diet, lack of exercise, smoking — all the usual risk factors.
IOW, in the past there was an unusual risk factor operating, but it is no longer an influence. Also, he refers specifically to the UK, and is more concerned with the policy implications of dealing with a flood of elderly people who in the past would have been expected to die of CVD but are now still alive, rather than with the clinical factors at play. But he will present some thoughts on the medical side of things.
He also presents evidence from the US, bolstering his argument that there was an epidemic. I found the autopsies of healthy young men who died in battle very telling:
“Dalen and colleagues also report autopsy findings in US soldiers killed in wars. In the young men who died in the Korean war (1951–1953), pathological evidence of CHD was found in 77%. This had fallen to 45% in those who died in the Vietnam war (1968–1978), and to 8.5% in those who died in the Iraq and Afghanistan wars (2000–2011). There is clearly a major decrease of the pathological basis of CHD, corresponding to the decrease of deaths in the general population.”
I suppose we can agree that in Western countries (including Japan), CVD pretty abruptly appeared in the 1920s, hit a peak in the 50s – 70s, and just as the misguided recommendation to cut fats, replace remaining fats with PUFA and instead eat lots of carbs was beginning to kick in, CVD rates began to go down, contrary to what we would have expected. It has continued to stay low in spite of more people working or being alert (facebook etc.) at all hours since.
We should try to understand what caused this rise and decline, and, sad as the current rise in some countries may be, it can serve to test our hypotheses.
Martin quoted from the Dalen study (autopsies of US soldiers from Korean to Afghanistan wars). This study was subject to lots of discussion at the time. Apparently, smoking has not gone down in the US military, there is round the clock ad lib. feeding with free pizza, fries and burgers from vending machines, and requirements for physical fitness and exercise had to be lowered in order to be able to fill the ranks.
So is the decline both of atherosclerosis in younger males as well as the general reduction in CVD due do better prevention (low fat, high PUFA, high carb, high veg, low sodium, blood pressure treatment, preventive statin use) and treatment (statins, stents) – I guess we are not inclined to believe so here?
Less air polution (coal and wood burning stoves, traffic, industry) – maybe! What is the situation in the former SU? Are there differences between country and city?
Less radiation? There was quite a bit of worldwide exposure into the 70s. Maybe in the former SU, folks are seeing exposure from Chernobyl and various poorly contained military sites. Why has it taken until the 90s for CVD to rise? Does it take “heart healthy” diet + radiation? what is the situation in other emerging countries that have not seen an extra radiation load after atmospheric testing was ended?
Better food safety and general hygene? One could argue that Western food safety has declined since the 70s, also Soviet food was probably not bad per se. Also, too much hygene is not necessarily a good thing.
Antibiotics? Probably not. They are helpful in getting a handle on chronic inflammation caused by bacteria, but they can also wipe out helpful gut bacteria, and I wonder what the effect on mitochondria is. We have vast differences in prescription rates in Western countries, likely with no apparent effect on CVD. Also, antibiotics were available in the East, and I doubt their use skyrocketed after the Iron Curtain fell.
Rotten teeth? Reading about Weston Price’s travels in the 30s and accounts from the 1950s and 60s, tooth decay was rampant throughout most industrialized countries. Growing up in Western Germany in the 70s, most adults from middle age had lots of repaired cavities or even dentures and where complaining about rheumatism, and I remember kids my age who had ruins for teeth before they entered school.
How was the tooth decay epedemic stopped anyway? Does it correlate to a decline in CVD some 10 – 20 years later? What about the former SU then and now?
What of suspect foods such as milk powder, partially hydrogenated vegetable oils and excessive PUFA use in the West and in the former SU?
Drug use? It probably has gone up and shifted to more harmful drugs continuously since the 60s until today in the West but its still not like a majority of the population are doing illegal drugs.
Antidepressives? They started hitting the anglophone countries in the 80s en masse but not so much or somewhat later elsewhere.
Many things to ponder and test…
You need only look about here in the U.S. and see that children are getting heavier at younger and younger ages and know that what Matthew says has merit. I also have to wonder if these terrible dietary and more sedentary lifestyles of younger people might also contribute to so many behavioral problems. You see it a lot in public schools here. The behavior problems are so out of control that many schools are actually “policed”. I don’t want to get into a social discussion here as the reasons for these things are multi factorial. However, I see younger and younger adults with terrible weight problems, depression, body image issues, and learning problems, and issues with rage. I am amazed at the numbers of mid life to slightly older people with diabetes. It seems once you have the dreaded diabetes or “pre-diabetes” states at younger ages, you are headed for trouble with virtually every other body system. They will, one by one, begin to fail. I have never seen so many people on so many medications at such young ages. I was on no less than 10 up to 15 while on statins. I was miserable. I am off these for 3 years now. I have better metabolic numbers than ever before, better lipid profile (triglycerides) and have begun to feel like my “old self” only younger. What is wrong with this picture? I do believe that I consumed way too much sugar at one time and that I was headed for disaster. I am a work in progress and hope I always will be. The latest statistics seem to agree with Matthew’s assertion. And, so do I. I hate to see our country or yours spend so much money on a condition (not a disease, Dr. Kendrick) that is so preventable. I also hate to see us go off the deep end and demonize all sugar and other carbs. I know that is not a popular opinion, but I don’t think sugar or liquor or cigarettes are going away anytime soon. We will hopefully learn to better stewards of these commodities.
I miss the days when people died of “natural causes” rather than “all cause mortality”. Feeling a little nostalgic here.
Hi, 15 meds is a lot to take. Are you off them all now. Where you on any on blood pressure. How did you manage to come off them all.
Mary, as per our previous comments I am with you all the way, also being medication-free for over 3 years now. I agree that it will take time to right the wrongs of over medicalisation of pseudo conditions, the sins of over consumption of sugar, and the heartache of tobacco use.
But we have to be upbeat, and acknowlege that advances are slowly being made on these fronts.
I want to be optimistic, but whilst watching ( on telly) all the festivities in London over the last weekend, I was astounded at the excessive number of overweight / obese individuals dancing and marching through London. It brought it home to me just how unhealthy our nation has become, and the pent-up ill health about to explode on our people. Have we become immune to obesity and the inflicted disabilities associated with it? Is it because we have been conditioned to believe that there will be a medical solution to every ill?
It is an uphill struggle, but we must not give up. The general public deserve to be better educated about the tragedy of modern diets and lifestyles, and the Internet is playing a positive role.
Hi Malcolm Kendrick
Yet some pieces that fit puzzelspillet.
I believe you are closer to the causes (Yes Causes, not the cause) to erosclerosis than anny sources I have met during my search for the causes in 10 years.
At the same time you also, consciously or unconsciously, have given some tools to curb the erosclerosis prosesses, or reverse the processes.
Identify the reasons for your erosclerosis and eliminate them.
Thank you for your work.
Reflecting on your series, I am wondering if the high prevelance of heart disease and cvd amongst former cancer patients is related to the treatment drugs (as is often suggested) or the “healthy lifestyle” i.e. nutritional adjustments after the ordeal (my assumption).
How does this situation fit into your framework?
Once more a fascinating post, and to express it in ‘modern speak’, cholesterol is SO not there! Thank you.
I get aura migraines. Now I’m terrified!
Get your iron down. I mentioned Cu and Mn before. They have an essential role in iron metabolism. Look up foods high in Cu and Mn.
Migraine is associated with an increased risk of deep white matter lesions, subclinical posterior circulation infarcts and brain iron accumulation (kruit, 2010)
Diana and Alison: Best food sources of Cu and Mn:
Cu in mg/100g Mn in mg/100g
Beef liver 14.57 Pine nut 8.8
Spiruluna 6.13 Hazelnut 6.2
Oysters, cooked 4.29 Oat bran 5.6
Chocolate 3.23 Pecan 4.5
Cashew 2.21 Pumpkin seed 4.5
Sunflower seed 1.83 Chocolate 4.2
Brazilnut 1.74 Whole wheat flour 4.1
Hazelnut 1.72 Walnut 3.4
Sesame tahini 1.61 Bulgur, dry 3.0
Walnuts 1.59 Macadamia nut 3.0
Lobster 1.55 Coconut meat 2.5
Pine nut 1.32 Almond 2.3
Pistachio 1.29 Sunflower seed 2.1
Pumpkin seed 1.27 Peanut 2.1
Pecan 1.19 Buckwheat flour 2.0
Alaskan king crab 1.18 Spirulina 1.9
Almonds 0.99 Garlic, raw 1.7
Shitake mushroom0.89 Cashew 1.7
Compiled from USDA data
Not sure that that paper would be any kind of comfort to a migraine sufferer. It has certainly scared me re my husband.
Sorry! But it was Dr. Kendrick who brought the migraine link, not me.
If it is too much iron in the brain then you have some possibilities how to try to deal with it. Phlebotomy, leeches, sauna, exercise, dietary adjustments, iron chelators… look it up.
It is interesting that aspirin brings relief. Salicylates bind iron in vitro but who knows what exactly happens in vivo?
I do not trust aspirin much, I would opt for willow bark or other natural painkillers instead.
willowbark, as you are surely aware, is pretty much the same thing as aspirin. Maybe some difference about the composition of salicates and also some other stuff thrown it. It may be nice, but is is also much less controllable what you are actually going to take.
Apparently, ibuprufen, especially when taken in low dose at the very onset, is more effective than aspirin in suppressing attacks.
“willowbark, as you are surely aware, is pretty much the same thing as aspirin.”
I am surely aware that willow bark is NOT the same thing as aspirin.
“also some other stuff thrown it” counts too, IMO.
I tend to trust herbalists more than pharmacists.
Not sure about herbalists. Have been seeing one for 6 months for my blood pressure and its not working. Probably going to stop.
I cannot comment on your herbalist but I can comment on willow bark (extract).
From UMU, just quick:
“The use of willow bark dates to the time of Hippocrates (400 BC) when people were advised to chew on the bark to reduce fever and inflammation. Willow bark has been used throughout the centuries in China and Europe, and continues to be used today for the treatment of pain (particularly low back pain and osteoarthritis), headache, and inflammatory conditions, such as bursitis and tendinitis. The bark of white willow contains salicin, which is a chemical similar to aspirin (acetylsalicylic acid). In combination with the herb’s powerful anti-inflammatory plant compounds (called flavonoids), salicin is thought to be responsible for the pain-relieving and anti-inflammatory effects of the herb. In fact, in the 1800s, salicin was used to develop aspirin. White willow appears to bring pain relief more slowly than aspirin, but its effects may last longer.
Willow bark is used to ease pain and reduce inflammation. Researchers believe that the chemical salicin, found in willow bark, is responsible for these effects. However, studies show several other components of willow bark, including plant chemicals called polyphenols and flavonoids, have antioxidant, fever-reducing, antiseptic, and immune-boosting properties. Some studies show willow is as effective as aspirin for reducing pain and inflammation (but not fever), and at a much lower dose. Scientists think that may be due to other compounds in the herb. More research is needed.”
On the second thought… chewing willow bark (and leaves) should be more potent than extract, because it is personalized. Plants are able to recognize signs of your disease and manufacture defensive compounds on demand. Widely exploited by animals, and noted by Stephen Harrod Buhner:
“The Lost Language of Plants”
“Chimpanzees are, as well, exceedingly particular about which part of the plant they choose. They only use the pith of the Vernonia; it is lowest in toxic sesquiterpene lactones and highest in the steroidal glycosides. Chimpanzees actively test Asphilia plants for activity by holding a leaf in their mouth for extended periods of time before deciding to pick it or go on to another. As they sit, allowing their vomeronasal organs (VNOs) to analyze the chemical content of their chosen plant, in return, the plant, as it does with spider mites, analyzes the saliva of the chimpanzee. In a short period of time, the plant begins altering its chemical production to enhance the necessary chemicals needed by the chimpanzee for healing.”
So which herbs would you recommend for high blood pressure.
“So which herbs would you recommend for high blood pressure.”
I’m sorry, John, I am not here to recommend anything, and besides, I know nothing about you.
Garlic, peppermint tea, chewing on milk thistle seeds… the list is long.
In response to John: in many ways herbalism is more advanced than pharmacology. The body raises BP in response to some stressors on the body. The job of an herbalist is to identify what the imbalances are and to treat the body not “BP”. Herbalism treats patterns, not diseases. Hence, one of the main principles of Chinese Medicine for example: same disease – different treatments, different diseases – same treatments.
Thanks. after 6 months do you think I should stick with it even though I haven’t seen any results or try another herbalist.
Yeah, you should have seen results by now, IMO. If you are in UK, you have a Chinese herbalist with international reputation – Mazin al Khafaji. His focus is dermatology (psoriasis, etc ) but he would probably know a good internal medicine TCM herbalist.
If you are not in UK, let me know and I’ll see what I can find out.
Also, I don’t know what your numbers are but look into “Modern Medical Myths ” to a see if your numbers are of concern…
Thanks. I contacted this guy. He gave me a name of someone in West Yorkshire. Unfortunately the cost is a little too much for me. The herbs alone work out at over £100 a month. Thanks for replying though.
Diana, sorry, the concept of the plant leaf (or, for that matter, the dead and dried bark) knowing what I need seems a little too new-agey and tree-huggy to me. Let’s assume this mechanism exists. What’s in it for the plant?
” the dead and dried bark”
Who says the bark is dead?
“What’s in it for the plant?”
I do not get your question. What do you mean?
Possibly thinking what I am thinking. Why would a plant go out of its way to help an animal that is, effectively, eating it.
Bark is not dead but inhabited by endophytic microbes (bacteria, fungi) that protect their host plant against biotic and abiotic stress. The endophytes produce tons of bioactive compounds, actually it is rather not the plant being the source of these compounds but primarily the microbes (see for instance Newman, 2015). In case of pathogenic attack, the production of the defence compounds is induced – that is produced on demand – in response to elicitors etc.
This phenomenon is exploited by pharma industry – we use plant derived compounds to heal our (animal) diseases.
“Endophytic and epiphytic microbes as “sources” of bioactive agents” (Newman, 2015)
So, possibly what happens when sick chimps is chewing on the leaves: the leaf that is far from dead recognized it is damaged, “concludes” that it is being attacked and starts to defend itself, responding to the presence of infection, stress, PAMPs (pathogen-associated molecular patterns) etc., and starts manufacturing various metabolites (with partial, or full involvement of its endophytic microbes). The chimp profits, and probably does not even pay the bill.
He means: why would a plant accommodate a person chewing it.
Ok, Diana, now I’m with you. It may be a little stretched for my taste, but I can follow the reasoning. For a piece of dried bark that I buy in a pharmacy, not so much.
Sorry to have another go at the chimp and the leaf. I realized what bothered me in the first place only after I had posted. I can understand that the microbes in the plant will react to plant viruses but why should they even recognize let’s say flu viruses in the chimp saliva? More likely they would recognize being eaten and produce something that tastes horrible, and even that would not save them but potentially their siblings in the other leaves from the same plant.
I understand your skepticism seeing you know next to nothing about plants. I do not wish to hijack this thread talking about plant communication and endophytes, so I’m only answering this:
“but why should they even recognize let’s say flu viruses in the chimp saliva? ”
Because they do, basic immunity principles are the same in both kingdoms. If interested, start reading maybe here:
Innate immunity in plants and animals: striking similarities and obvious differences. (Nürnberger, 2004)
“Innate immunity constitutes the first line of defense against attempted microbial invasion, and it is a well-described phenomenon in vertebrates and insects. Recent pioneering work has revealed striking similarities between the molecular organization of animal and plant systems for nonself recognition and anti-microbial defense. Like animals, plants have acquired the ability to recognize invariant pathogen-associated molecular patterns (PAMPs) that are characteristic of microbial organisms but which are not found in potential host plants. Such structures, also termed general elicitors of plant defense, are often indispensable for the microbial lifestyle and, upon receptor-mediated perception, inevitably betray the invader to the plant’s surveillance system. Remarkable similarities have been uncovered in the molecular mode of PAMP perception in animals and plants, including the discovery of plant receptors resembling mammalian Toll-like receptors or cytoplasmic nucleotide-binding oligomerization domain leucine-rich repeat proteins. Moreover, molecular building blocks of PAMP-induced signaling cascades leading to the transcriptional activation of immune response genes are shared among the two kingdoms. In particular, nitric oxide as well as mitogen-activated protein kinase cascades have been implicated in triggering innate immune responses, part of which is the production of anti-microbial compounds. In addition to PAMP-mediated pathogen defense, disease resistance programs are often initiated upon plant-cultivar-specific recognition of microbial race-specific virulence factors, a recognition specificity that is not known from animals.”
I think we need another thread for this disucssion
So do I
The pine trees and oak and cherry trees that are particular targets of the Gypsy Moth caterpillar here in New England certainly react to the onslaught. And it’s effective. But it takes the better part of two years for the trees that survive to work up the toxins necessary. They work. Caterpillars die in enormous numbers. Disgustingly.
For the caterpillar, one gobbled leaf has no effect whatsoever other than general nutrition without the huge sylvan community’s lengthy build-up.
Then, it’s only the leaf eater that suffers.
Oh me too Alison! Not what I wanted to read before bedtime. Although I did know that migraine with aura is supposed to be associated with an increased risk of stroke. Dr K’s reasoning just takes understanding it a stage further.
But forewarned is forearmed as they say. Keep reading and learning. It is better to know these things because then we stand a better chance of looking after ourselves.
Invest in an earthing sheet, Alison, and sleep on it.
This may diminish the frequency or intensity of migraines, and by restoring something called zeta potential to red blood cells (RBCs) you will reduce any rise in blood viscosity, improve circulation, discourage the tendency of RBCs to clump, and place a significant obstacle between the physics of blood whose RBCs have adequate zeta potential and the risks of a clot giving rise to either a heart attack or stroke.
I guess we are now facing a typical “Popperian corroboration” of a hypothesis?
B12 deficiency causes severe headaches, increased homocysteine and therefore strokes.
I am sure that this is a factor
I am one of those lucky people who almost never get headaches. However, many years ago, I would occasionally get what I think were the auras that people report at the start of migraines – a funny flickering distortion over a portion of my field of view. They never developed into anything worse, and I could happily eat a meal while one of these happened! I haven’t had one of these ‘auras’ – if that is what they were – for many years now, but it might suggest that the auras and the migraine are distinct phenomena.
there is migraine sans migraine. Most researchers seem to believe it is the same thing.
Thanks for your reply – I imagine it was migraine sans migraine – it is fascinating what you learn on this blog!
Excitement uncontained! Quite a few years ago I heard of a Consultant who suffered terrible migraines. They disappeared after he had coronary revascularisation. Why? He assumed due to the anti-platelet effect of Clopidogrel. I tried it out with some of my patients with severe and treatment-resistant migraine and guess what? Frequency and severity of migraine episodes dropped. Don’t report me to the GMC for this off-licence use! But the patients were happy.
Incidentally, ‘Doctoring Data’ was brandished at a meeting recently. Fancy joining me in forming the British Lifestyle Medicine movement?!
Regarding SCD: why are SCD mice protected?
There is a protective enzyme heme oxygenase and it requires copper to work. SOD also needs copper. Most people are defficient in Cu, and Mn.
Paradoxical protection from atherosclerosis and thrombosis in a mouse model of sickle cell disease (Wang, 2013)
“This apparent protective effect of SCD on atherosclerosis and thrombosis was diminished by inhibition of heme oxygenase-1 (HMOX1) using zinc protoporphyrin IX.
We conclude that SCD in mice is paradoxically protective against atherosclerosis and thrombosis, highlighting the complexity of vascular events in SCD. This protective effect is at least partially mediated by induction of HMOX1.”
Dianna, are you really “Jane Karlsson” that goes from website to website pushing your Mn and Cu deficiency theory endlessly? Why the sockpuppet moniker?
I allowed this comment through, but it is moving very close to the personal insult. My general moderating rules are 1: no attempts to advertise 2: no personal attacks 3: Nothing that I rate to be incomprehensible rants (rants are fine). Thus: That is an idiotic idea – is fine. You are an idiot – is not.
??? No idea what you are talking about.
I research plants and their endophytic microbes. Some biochemistry (and other principles) apply both to plants and animals. It is my hobby to search for them.
If you look how heme is detoxified (so that it does not damage the endothelium, you arrive to these enzymes and their co-factors.
My mistake. A well-known past poster pushed a similar pet theory as you do and, well, the similarity in tone drew a suspicion. Apologies to both. It is not a useful post, so feel free to moderate if you wish.
No problem, thanks for apologising, much appreciated. You should see some of the things I write. I have learned to sit on them overnight, delete them, and try again.
What pet theory? About the importance of copper?
Here you are, fresh from Berkeley:
Copper is Key in Burning Fat
“A new study is further burnishing copper’s reputation as an essential nutrient for human physiology. A research team led by a scientist at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) and at UC Berkeley has found that copper plays a key role in metabolizing fat.”
We find that copper is essential for breaking down fat cells so that they can be used for energy,” said Chang. “It acts as a regulator. The more copper there is, the more the fat is broken down. We think it would be worthwhile to study whether a deficiency in this nutrient could be linked to obesity and obesity-related diseases.”
Chang said that copper could potentially play a role in restoring a natural way to burn fat. The nutrient is plentiful in foods such as oysters and other shellfish, leafy greens, mushrooms, seeds, nuts and beans.”
I like the “rants are fine” part. The rest, too. Good policy!
interesting publication about copper. Do we know what plumbing pipes are traditionally used in which country? In Germany, it’s copper, with PE having taken its place in the last 10 or so years. What about other countries?
Again, there is probably a sweet spot for the copper uptake. Too much is definitely not a good thing…
“interesting publication about copper. Do we know what plumbing pipes are traditionally used in which country?”
I’m sorry I know nothing about chemistry of the buildings.
re: Do we know what plumbing pipes are traditionally used in which country?
The human race has sort of figured out that lead pipes (and lead solder), and asbestos pipes aren’t a real swell idea for residential water.
Pipe material is surely a question worthy of investigation, but there are some confounders. In many places, municipal water is not potable, so an earlier question is: do people drink it or cook with it?
Even where (or perhaps especially where) the water is potable (as in most of the US), pipe composition may be overshadowed by the water itself. Municipalities face a severe challenge in delivering pathogen-free water. They presently do this via sanitizing agents, such as non-native chloride compounds, which survive into the home (and which may be quite persistent, such as chloramine). Fluorides are also often added for other reasons.
Do these non-native halogen compounds compete with already-deficient iodine at the thyroid? Are they antagonistic to microbiome? Are there implications for CVD in these scenarios? Are epidemiological studies even asking about any this on their questionnaires?
Good point, especially as it is virtually impossible to get tab water without added chlorine in the US. Does it change gut bacteria composition?
I noticed my digestion changes within one or two days in the US. I used to attribute that to either the chlorinated water or the higher portion of meat in the food. On my last two trips, I religiously avoided tab water and high protein food, it still happened. Same happens on trips to Japan, where the water is not noticably chlorinated. So maybe it’s the flight? My preferred airline serves bottled drinks only. Oh well, maybe I should skip the tea on the next flight…
Very good again
“…reported migraine remission, but still presented aura attacks…”
I don’t understand this passage. I
have read extensively on migraine
and was under the impression that
aura was the migraine. I get aura
but not a ‘headache’. Am I not having
Is there something to do to prevent
migraine with aura? I have been LCHF
for 6 years and have had no change in
my aura frequency.
Bill – my husband used to get the full Monty – headache, vomiting and bad auras. Now, at ago 80, he just gets an occasional aura but no pain and no vomiting. He used to take a daily low dose aspirin and it really worked. Now, at the first whiff of an aura he takes a 75mg aspirin and sleeps. A rapid recovery.
We also observed that he was more vulnerable to attack if he missed a meal or was late eating.
So interesting about aspirin, it is good to know. I have always taken a homoeopathic Nat Mur as soon as I see Zig Zags, works quite soon. my migraines started after menopause, thought they were neurological as well as vascular. And having transient global amnesia episode 1. Yr ago was so scary, for some it can be linked with migraine. That is when consultant prescribed statins, which I declined, my cholesterol was too high he said. Though never very overweight, 8/12 stone, 5 ft tall, had a gut. 12 months later, LCHF diet. Seem to stick at 8’2 . Had cluster of migraines after TGA, now none for 6 months, think my brain was rebooted.
Thank you Dr Kendrick, so gripping.
Stunning. A real tour de force, if I wasn’t convinced before (I was) I am now.
The link with migraine is intriguing. Migraines have always puzzled me. I never understood why so many disparate medications can be used for migraine prophylaxis from anti-depressants (amitriptiline) anti- epileptics (topiramate) to anti- hypertensives (beta blockers and calcium channel blockers) perhaps the common theme is that that have positive effects on clotting and endothelial repair!
Time for some reading.
Endothelial damage seems to be the key?
Patients with Hepatitis C Virus infection show an increased thrombotic risk. The virus seems to do it all and do it fast: damage the endothelium and activate all kinds of mechanisms and “pathways” promoting thrombin and clot formation and down regulation of anticoagulant mechanisms. I liked the description of a number of involved factors.
I think endothelium is the safety catch. If your endothelium is healthy – nothing else happens. Damage the endothelium and all the other factors/processess can become activated.
Surely oxidative stress important. Let’s hear it again for allopurinol, known to help increase available NO. Should be on your list doc. give out to all over 50 yr olds! mmm heard something similar before. Great blog.
“If your endothelium is healthy – nothing else happens”
So, excluding invasive surgery, what are the key tests that verify healthy endothelium?
Perhaps normal blood pressure, and???
The thing is, we can do what is right to fix and/or maintain our endothelium (e.g. lchf, vit C, vit e, arginine, coq10, omega 3, manage/reduce stress, etc.) hoping all is good, how do we test (be tested) to confirm all is in fact good.
“…all is in fact good.” Or not.
Yes. Peace of mind, knowing one way or the other, where our little cells stand in the scope of our lives would go a long way to ameliorate Stress!
To me, not knowing is the worst. Then, again, the doc that refuses a test-for-knowledge to avoid an incidentaloma and its complications has a point. Waddayado?
Waddayado, yes what to do. Before going lchf (Prof Noakes motivated), when my doc said jump, I jumped. Now I have been on a 2 year voyage of discovery reading as much as I can. Fascinating and exciting voyage.
Now I would really like to know if what I have done and continue to do is making a positive difference. How to test for successful repair is the question?
What I intend to do is repeat My Coronary Artery Calcium scan that I had done a couple of years ago to see what changes may have occurred. That CAC was high, which is what put me on this quest. Good would be a drastic slowing in the rate of calcification. Better would be stoppage. Best would be a regression. The Establishment says you can’t regress. I’m trying anyway. ‘Course, the only way you can tell is with that baseline score as a reference.
Anyone out there successful at reducing your CAC score?
If this is an important fact, which I think it is. How can a person figure out if his or her Endothelium is healthy. What test is available at the present time. Can you elaborate in one of your articles what important steps we should take to get our Endothelium in tip top shape. To me this would be a huge step forward in keeping a person healthy.
Thank you for any info on this.
Nothing new about migraine… The cause of attacks was ascribed to abnormal platelet aggregation way back in the 1970s. As a result I began taking low dose aspirin, which abolished my attacks, and I still do. The theory is that aggregation causes the ischaemic symptom of aura and the headache results from the subsequent reflex vasodilatation. What is also interesting is the link with IBS, making it possible that the whole complex is the result of autonomic dysfunction. Reference available on request!
Oh well, it was news to me. References would be most welcome indeed Andrew.
This is deeply, gleamingly fascinating. Like an ancient Roman haruspex NostroKendrickus continues to pull fresh nuggets of truth from the slightly smelly corpus of medical science. Not that I wish to imply that you’re ancient.
For the first 40 years of my life I lost great slabs of time to migraine. The only remedies were resting in a dark warm place with blankets plus hot water bottle even on a hot Australian summer day, and lots of aspirin.
I’m not completely sure why they stopped after that but it was probably due to dietary changes I made after my first episode of gout – I greatly cut down on sugar and flour plus industrial foodstuffs in general (msg, preservatives, etc.). Not to current low carb levels but a big reduction nonetheless.
You’ve heard of the stone age, the iron age and so on, but I grew up in the pudding age. With every evening meal had fruit in thick syrup with lashings of custard or jam roly poly, spotted dick and so forth, and the cake tin was never empty. Its not hard to do better than that.
One other interesting thing I read recently, uric acid reacts with NO in circulation converting it to peroxynitrate. Another small piece of the jigsaw perhaps?
Yes, the Stone Age, the Bronze Age, the Pudding Age……rice pudding with jam. Mmm. Sigh. Now, though, we’re in the middle of the Toxic Age and being poisoned by much in our environment.
Aspirin seems to be cropping up here as a remedy of choice for some migraine sufferers and I remember noting that it was on the list for reducing risk of CVD.
It’s suddenly occurred to me that I’ve always looked on aspirin as an old fashioned form of NSAID, probably because it became frowned on to use aspirin as a painkiller and ibuprofen seemed to be recommended instead (period pain for example).
But of course NSAIDs are on the no no list. I think I see why but I need to think about it a bit more.
I wonder how popular it is to take a daily dose of 75mg these days?
Shouldn’t be very popular if “Modern Medical Myths” is to be believed…
Ah, yes. It was my to-be wife who introduced me to the jause age.
You know: zwetschgenknödel, marillenknödel, kaffee mit schlag.
Sigh. I’m past all that. Sad, in a way. In a way, not.
Andrew, may I ask how many milligrams of aspirin you take for migraine prophylaxis?
How fascinating. Thank you.
For many years my husband took a low dose aspirin. I had read somewhere that the blood of migraine sufferers was somewhat sticky and it seemed like a good move to use aspirin. . When his migraines were bad (and relatively frequent) and he experienced horrible and frightening auras he took it on a daily basis and it really, really worked and he would go for months without an attack. Now at the age of 80 he rarely succumbs and no longer takes a daily pill, but at the first sign of aura he takes one 75mg pill, sleeps and makes a fairly fast recovery. This is all probably a propos of nothing at all, but I just thought I’d like to share.
Thank you again, Dr. K.
Another area worth investigating is how exactly people with ordinary rbc get sick from malaria since in some parts of its complex life cycle the parasite lives in rbc.
And I have wondered why, in the six years I lived in West-Africa, i never got sick with malaria while plenty of people around me did get sick, ended up in hospital on a quinine-drip. I never found out why, but one doctor said I have probably a factor in my blood that prevents the malaria parasite to complete ints cycle. So, in fact, I’m still at a loss.
hi du, reference to migraine and warfarin
Sent from my iPad
Absolutely fascinating. It all becomes clearer and clearer. I have just given both of your books to my brother who suffered a ruptured oesophagus, followed by breathing difficulties needing ventilation, and a stroke, all while on statins. He has made little progress in two years, is thin as a wraith, words elude him, still has breathing difficulties and can barely walk. Since reading the books he has decided to come off the statin. If he improves, however slowly, I will report back. If he doesn’t improve, it may be that the damage is too great, or I should have sent the information earlier. I also sent him Uffe Ravnscroft’s latest, and Duane Graveline’s Statin Damage book. Thank you to all these brave doctors for sticking your heads above the parapet to help us all. Please don’t get those heads shot off! Humanity needs you for Sanity!
When you are facing sad things like this in you closest surrounding, I have got several cases around, and realise that it is the total corruption of medicine behind all this you are inclined to throw out your hands i despair. That is probably why we admire the firm stand of people like Uffe Ravnskov (it costed him his carrier as a young researcher) and Malcolm Kendrick.
Gay: What is the name of Dr. Ravnskov’s latest book? I have only “Ignore the Awkward!” He’s always a good read.
Gary, Uffe Ravnskov’s latest book, or anyway the one I sent my brother, is The Cholesterol Myths, exposing the fallacy that saturated fat and cholesterol cause heart disease. Amazon, Kindle. As you say, he is always a good read.
Following this blog has been like watching Poirot’s ‘little grey cells’ in action! I think you may have missed your calling…..I suffered migraines (no aura) myself for a few years as a young woman, putting them down to stress at work (especially as they were the typical ‘weekend’ migraine). Having no help from doctors at the time I eventually made the link with the large amounts of table salt I was using (and no, my blood pressure was entirely normal)…reduced the salt and the migraines went. Since then I use only sea and rock salts liberally with no effects, except for the famous Fleur de Sel Guérande – this sea salt from Brittany is absolutely delicious yet gives me migraines. It broke my heart to throw away something so expensive, but having read this, very glad I did!
Gerry: Very interesting. Perhaps may have something to do with the specific mineral composition of it? I’ve used sea salt from Brittany for several years, with no ill effect, but I’ve never had a migraine.
The day after aortic valve replacement (due to bicuspid aortic valve) I started to get episodes of migraine auras without headache. I discovered from a forum I’m on that quite a few people who’ve had heart surgery go on to develop episodes of migraine aura, usually without headache, immediately post surgery which continue for years sometimes, though frequency gets less. I’ve been unable to find out the cause but this study suggests that visual problems can be one of the side effects of having been on the heart lung machine, though it doesn’t say why: https://www.sciencedaily.com/releases/2009/08/090813142455.htm Still getting episodes of migraines auras two and a half years post surgery.
Another piece of the puzzle
Migraines – mine were always connected with taking artificial hormones – pill, etc. GP never knew or advised. This was before the days of The Leaflet. What GP did know about was the varicose vein, and the haemorroids, although neither of those counted as the blood clots which we were all being warned about.
Of particular interest to you in view of migraine.
Sent from my iPad
Perhaps the title of this epic series of articles should be, or should become, “What Causes the Causes of Heart Disease”. There is a whole other layer still to be looked at – the so-called ‘lifestyle’ factors of diet, exercise, stressors, sleep, sunshine and community. Epigenetics, the holobiont, and of course the microbiome.
I think that functional medicine might have useful things to say about this.
“If your endothelium is healthy – nothing else happens. Damage the endothelium and all the other factors/processess can become activated.”
What if one’s endothelium has already been (heart attack) damaged?
Should one take 100 mg of l-arginine to help the blood vessel recuperate?
It’s doubtful it would hurt. L-arginine can also help with arrhythmias (such as PVCs). I would take more than 100mg, though.
However, you might want to do some research. I just did a search for “l-arginine after heart attack”. This study suggests L-arginine is bad for people who have had a heart attack:
Six people in the test group died, versus none in the placebo group. They stopped the study early because of this.
Better to reduce aginase, so keep uric acid down with alloprurinol with the added benefit of reducing oxidative stress. Some question as to arginine supplements being lost in the gut so no overall improvement, better to make use of what you have.
So is it a waste of time taking L-arginine and other supplements.
No. However, if you have sufficient intake of all essential nutrients, vitamins etc. with your normal diet, there is not need to take anything extra. However, the RDA for most vitamins, minerals etc. were established long-long ago, and it is likely that they are almost all, completely wrong. Which probably doesn’t help much.
And the additional argument is that for some of the foods the soil etc may be poor and overused.
MK: …the RDA for most vitamins, minerals etc. were established long-long ago, and it is likely that they are almost all, completely wrong.
They may also have merely established “normal”, which is not the same as “optimal” (or perhaps even “healthy”). RDA, is of course, also just a proxy. What we really need at the moment is [optimal] titer targets, because intake composition is increasingly uncertain.
RL: …the soil etc may be poor and overused.
Further, the animal foods we eat (meat, eggs) now reflect what they are being fed. All of which implies that what we think we are getting is no longer necessarily true, and common reference sources for nutritional breakdowns of basic foods may be outdated and thus unreliable.
I supplement, but it’s a short list (about a dozen), completely reconsidered every year, and adjusted based on personal results, and as credible unconfounded science emerges.
We also need to contemplate micronutrients and non-native amendments to food-like-substances that are in need of active avoidance. Many of the “seek”, as well as the “avoid”, have material implications for CVD.
But with animals if farmers won’t add additional vitamins to they diet then animals would not be able to eat only trashy fodder (beware, very long with many references):
Another intriguing and stimulating article on the causes of CVD. Over this set of articles “What causes heart disease” the range of possibilities is so wide that it is the total opposite of the usual tunnel-visioned approach of so many cardiologists. Dr Kendick, this open minded approach of yours is undoubtedly what is needed if there is ever to be a real solution to CVD.
My female relations have always had a severe migraine problem (aura, the lot for 1-3 days at a time) from teenage to late in life with difficulty in finding relief with any drug.
It is, which I seem to remember seeing in earlier articles, a multi-factorial problem with its roots in life-style, nutrition and stress and now in genetics and simply age. After all we will all die irrespective of drugs, life style etc.
I really do look forward to seeing this article summarised for a journal review paper and a fully expanded book.
I have not been able to get the BMJ paper though logged on to the BMJ but found several by Tobias Kurth on the subject. I presume one of these is the one mentioned.
Ow! Horrendous memories:
My high school migraine auras completely blinded me. The pain caused out-of-body experiences. When each was finally ending I had to be led by hand (still blind!) to the toilet to throw up green bile.
That was 1960 to 1962, more-or-less. Migraines without aura followed for decades. A symptom that hasn’t been mentioned is stupidity. My neurologist called it migraine boggy brain.
So, perhaps all this is the reason I tested over 1,600 on my CAC (calcification) score. Anything over 400 is considered very serious indeed for coronary risk.
And, so, perhaps all this also explains why I haven’t had a migraine since my ablations for atrial fibrillation (Itself part of the migraine cascade of consequences??) just a few years ago: Anticoagulation on & off with warfarin (nasty!), dabigatran (nastier!), rivaroxaban, and now a minimal dose of apixaban for occasional arrhythmia break-through.
What if I had started taking low dose aspirin fifty-six years ago?????
Nice once again
What a coincidence. Just yesterday, I received an email from a friend who mentioned that an article was published in one of our local papers (Montreal) on the subject of migraines and CVD.
Of course this article referenced the BMJ paper (http://www.bmj.com/content/353/bmj.i2610) which you referenced in your blog. Because the news article talked about associations and links and reported relative risk ratios (and not absolute risks), I decided to look up the original report.
What I found confirmed what I suspected, i.e. this was an observational, prospective study and did not provide any scientific explanation for why such links could exist. In other words, the results reported were strictly associations, without any scientific plausibility for cause. Maybe whatever caused the migraines also caused the CVD events. (Diet related perhaps, but of course such a hypothesis was not tested.)
Another problem for me was that absolute risks were not reported, only relative. In trying to guess at the absolute risks, one can estimate that in the migraine cohort, comprised of about 24K subjects out of 115K in total, there were 1329 CVD “events”, including 223 deaths. So that suggests that about 4% of the migraine sufferers experience a CVD event and somewhat fewer than 1% died of a CVD related cause. Number of deaths in the non-migraine cohort was not reported. Since the reported hazard ratio for those in the migraine cohort was 1.5, that suggests that about 2.7% in the non-migraine cohort experience CVD events, or a difference of 1.2% between the two. This is a whole lot less “significant” than 50%.
On an anecdotal level, I suffered from migraines most of my life, even as a child, right up to the age of about 50. I had a brain CT scan done to eliminate any possible evident causes such as tumors, and was given a prescription for Sumatriptan, aka Imitrex. This drug worked effectively, but I only took it once or twice and suddenly my migraines stopped. I later discovered that my mother’s migraines also stopped suddenly when she turned about 50 years old, and she suffered them also throughout her lifetime. Since that time, I almost never get a migraine, only a slight and very infrequent headache which passes quickly. I always attributed these headaches to some kind of digestion issues, allergy-like problems cause what I ate. The fact that my mother’s migraines and mine suddenly stopped at about the same age I found to be intriguing. Otherwise I have and continue to be in excellent health.
My wife of 47 years also is a migraine sufferer. Hers have not stopped and continue to this day on a more or less cyclical basis which she treats with Imitrex. We do eat the same foods (LCHF) and to this day I have been unable to find any associations with migraines and what we eat. Although I have read many anecdotal accounts in the commentary sections of blogs about people curing their migraines when they started the LCHF diet, this did not work for my wife. I am 70 years old now and we have both been on LCHF for about 4 years, and my migraine situation has not changed due to diet. Also, I have infrequently suffered the auras (associated with migraines for some people) without any head pain and still get those from time to time today. They last about 30 minutes and pass without incidence. I have been unable to associate these events with anything special in my life. They could come about while watching TV or reading a book.
So all in all, I was not impressed with this BMJ study, and I honestly wondered why the BMJ would even publish such a poor study. IMO, this was just one the many observational studies which we see regularly published which do not prove anything (or do not even lead to a hypothesis), and seem to be published to fill space and add to the list of publications by the authors.
How very interesting reading for a firm believer in the benefits of LCHF1
Just now I am reading a recent book by Dr. David Perlmutter about the connection between the gut bacterial flora and mental diseases. Sounds convincing!
Perlmutter: is the book Grain Brain? I found it fascinating! Have you completed your “Cell” study?
Fascinating is a good word. I read “Grain Brain”, the bestseller, a while ago but now I am in his followup book “Brain Maker”.
Though I must admit that I have a problem with some American authors way of writing for lay people in a ‘selling’ persuasive style as if the reader is not capable of making own judgments. I think it is a pity that a serious author like Perlmutter has adopted this style though it seems to be very common in ‘best selling’ books about health. Often I stop reading this kind of books after a few pages but the content of this one is so fascinating and so well references I will undoubtedly read it all through though admitting getting annoyed now and then.
I might be too sensitive as an old researcher.
I missed your allusion to “THE CELL”.
It is not a book (1400 pages) that anyone will be ‘done’ with and for sure not a person like me though I have been trough it a few times now and am presently slowly progressing with the reading of the one year old sixth edition. I am a little bit worried since it is a paper back and being constantly carried around it is beginning to disintegrate.
I might spend a fortune on a bound copy in the future when it completely falls apart.
It is mainly by the reading of this work I have turned completely allergic to all categorical statement from medical doctors end especially expert cardiologists 🙂
Agree, I get annoyed and somewhat frustrated with the persistent hammering of the same point like a sales convention speech. I felt that Grain Brain written more normally could have been half the size and just as comprehensive. So am forced to speed read more words for the same value. Robert
Much prefer Dr Kendrick’s style (thank you Dr K).
The following youtube presentation may interest you.
Dr.GS: I think it is a pity that a serious author like Perlmutter has adopted this style though it seems to be very common in ‘best selling’ books about health.
Well, in this case we might be tempted to blame it on the co-author, but Dr. P. signed off on it, so I take the approach as deliberate.
It’s a tough call. The key papers are out there, but the general public does not read them, even when not hidden behind pay-walls. If they did, they’d have to learn how, given that half of medical papers are “untrue” (Horton, Lancet), and a rather larger fraction of nutrition papers are intellectual junk food (my estimate).
On any given topic where a popular book has captured the public imagination on an important issue, we usually also find that the book was not the first to raise the issue and propose solutions. Dry and sober treatments preceded, and no one read them. It takes a best-seller, and there’s some formula to that.
These books probably also represent what the author-doctors are seeing in their clinical practice, indicating compelling trends, not yet reduced to peer-reviewed RCT. They are legally and professionally obliged to be a bit vague about it all.
re: It is mainly by the reading of this work I have turned completely allergic to all categorical statement from medical doctors end especially expert cardiologists
That’s the subtext of all the dissident diet and dissident doctoring books I’ve read in the last five years, and it might be their key message. People need to engage on self-directed health, and need to become aware of how much remains to be learned, because it’s considerable.
Hi John U and fellow Quebecois. I’m one of those whose migraines completely disappeared once I began LCHF. Well, not exactly true. I had one last year, but I’d abandoned the LCHF (and paleo) way of eating then. Could be co-incidence (small sample size). I’m also not very impressed with the BMJ study when taken alone, being observational in nature and all the limitation associated with this type of study, but when you combine it with the plethora of other studies presented by Dr. Kendrick throughout the series, it’s another “piece of the puzzle” supporting the theory being discussed here; it’s another study unable to disprove the theory, in other words. Good luck finding a solution for your wife.
I suffered from occasional migraine with aura up until the age of 50. In my case I could generally associate them with my monthly cycle. I was obviously more sensitive to certain triggers (strong light, dehydration etc) at certain times of the month.
Apparently migraines disappear after menopause in approximately 15% of women. Here’s hoping ….
I’ve been eating LCHF (paleo) for over nine years now. Migraine auras loads since heart surgery (to correct a birth defect) two years ago. No triggers – mine come on out of the blue, woke up this morning with one going, it was about halfway through the aura sequence when I woke up. No headaches at all, just very tired for 24 hours after.
Maybe a bit of elaboration might tilt my belief in knowing what you are saying to actually knowing. I’m talking about this passage:
Atherosclerosis in the pulmonary arteries is something so unusual that when you find it, you are looking at the mother lode. If you can cause atherosclerosis here, then you are gazing at a true underlying cause, with all other risk factors stripped out.
At first, the fact SCD causes atherosclerosis in the pulmonary branch suggests SCD does something all other triggers don’t. I see it as a unique process rather than a true underlying cause because it doesn’t address why other triggers don’t cause atherosclerosis here as well. It’s like a Sesame Street game of which of these things is not like the others. But then, when I think about it a bit more, it seems like SCD uniqueness in its ability to damage endothelium everywhere (due to the shape of the RBCs, I imagine) is not what differentiates it from the other risk factors (triggers), but what confirms that we are dealing with a two prong process. So, it strongly supports your theory of endothelial damage followed by dysfunctional blood clotting, with a weighted effect on endothelial damage in the case of SCD, whereas the effects of something like lupus would be more heavily weight on the blood clotting.
And most important of all, IMO given the current dogma, cholesterol cannot explain how SCD causes CVD. Another black swan.
Does this sound about right?
I think so. Will give it a bit more thought.
Try this, I am interested in the role of uric acid – urate, in the whole debate, an area forgotten. http://www.sciencedirect.com/science/article/pii/S1043466611006764?
And the work life balance in society now, regardless of diet, is rather toxic. I know you say stress is a factor Dr Kendrick. The harmful neoliberalism of the last decades must play a part , if not necessarily in CVD, in other illnesses leading to it. People are not valued, greed rules.
Sorry, political again, but a fair and just society must improve health.
Another correlation for my list further up: cvd in Western countries went down just as neolib was beginning to take hold in the 80s. I, like you, would prefer to believe in a reversed causality here.
Dear Malcolm – another interesting instalment in what to me, admittedlly a dangerously knowledgeable layman, seems a very convincing hypothesis – endothelial damage and dysfunctional clotting.
Some here have asked or suggested why CVD should have increased so much since the 19th century and I echo those points about excess Omega-6 (mainly from vegetable oils but even meat is now being affected as less is grass-fed and more being raised on corn, soy etc. whihc nature never intended), Vitamin D and lack of sunshine as we sit in our offices, excess carbohydrates (as we’ve been misled about the dangers of saturated fats, asked to eat whole grains and gain 30% of our calories from carbohydrates and so on).
I have one challenge for you Malcolm since you invited these :- given NSAIDs are effective dampeners of inflammation, can you say why diclofenac (aka Voltarol) has been associated wiht an INCREASE in CVD incidence? One would have thought thee opposite might apply.
It has been withdrawn from OTC sales in the UK, USA and Canada because of this risk (see https://www.gov.uk/government/news/diclofenac-tablets-now-only-available-as-a-prescription-medicine for example) and only the gel is allowed OTC.
I’d be interested in your thoughts or knowledge on why this anti-inflammatory appears to increase the risk of CVD?
Because inflammation = healing, and if you interfere with healing the disease process will accelerate. Most/all anti-inflammatory drugs increase CVD risk. Steroids are the worst.
So then your theory for low carb diets and intermittent fasting, which have been “shown”* to reduce “inflammation” via some markers of such, is that they reduce the underlying disease/condition (such as insulin resistance) and it is that reduction in the underlying disease/condition that reduces the “inflammation”? It’s a theory that makes sense to me (though I still might apply ice to an injury–old habits die hard ;-).
* Assuming these studies actually show what they purport to show; it’s difficult to find good RCTs with this info.
PS — Thank you and others like you for developing a different perspective on things. This has taught me to open my mind regarding different theories, even if I think a theory is wrong. I’m currently reading this book:
Which I’d have never considered had I not had my mind opened by you (and others, too).
Could I ask again about aspirin? Having a quick Google this is quite widely described as a NSAID yet it is on the “good” list. Does the power of the antiplatelet effect outweigh the anti inflammatory effects?
Yes, I think it must do, or it would not work.
Is this also true of topical steroids ?
Topical steroids may not exacerbate CVD, but the resultant skin atrophy from prolonged use can be a nasty side effect. Another example of the cure potentially causing more damage than the original affliction.
Dr.K: “Because inflammation = healing, and if you interfere with healing the disease process will accelerate.”
Due to it being a suspect in a case I’m following elsewhere, and because root canal hasn’t arisen as a topic on the present blog, dental issues can be a source of chronic inflammation and/or chronic infection, and advance CVD even if you’re doing everything else right. I understand that there is a strong correlation between, for example, root canals and heart attacks, likewise an association between periodontal disease and CVD.
Dental fillings are more troublesome to correlate, due to the confounding factor of potential materials toxicity. I’m not yet persuaded that mercury fillings are worth removing, but if I had any RCs, they would be removed.
Periodontal risk is dramatically reduced by deliberate diet choices. Anecdotes abound of people arresting and reversing it with various LCHF approaches.
I think there is a whole world of chronic infection/dental infection that is interesting to look at.
You can not “remove” a root canal.
Dr.K: “I think there is a whole world of chronic infection/dental infection that is interesting to look at.”
Agreed. One is Lyme Disease (implicated in yet another CVD case I’m following). It looks like Ötzi the Iceman had it as well, which means his CVD could have been due to Lyme, or the einkorn, or some combination. But it was the arrow that got him, so mind the arrows too.
Lyme is a real problem, because the Standard of Care posture, at least in the U.S., seems to be:
☤ Yes, there’s a vaccine, but no longer available to U.S. humans because reasons.
☤ Take extraordinary precautions to avoid Lyme ticks, often as good as invisible.
☤ Self-diagnose promptly, competently and seek urgent (but effective) treatment if bit.
☣ Because if you catch it late, we’ll fumble the diagnosis, have no effective treatment and health insurance may cover nothing Lyme-related going forward.
@Sasha: “You can not ‘remove’ a root canal. ”
True. You remove the dead tooth.
Anyone facing a proposed root canal needs to do some research and make up their own mind. Hmmmm. Sounds a lot like the statin situation.
Bob Niland: you got some nutty ideas… Agriculture is bad, pull a tooth rather than do a root canal.
Bob, whole can of worms. Where do you stop? Are implants good or bad? What about teeth where the nerve has receded without any cavity, as happens for natural reasons (e.g. an incisor that can get pushed around a lot as the other teeth grow)?
Lots of things that we don’t have solid data on, and before we do, are propabably not worth worrying about.
@eric: “…whole can of worms.”
re: “Where do you stop?”
Indeed. On the one hand, we have ominous modern disease trends, that we didn’t formerly have, resulting in healthcare expenditures rising faster than GDP. We also observe isolated cultures living ancestral lifestyles who do not exhibit these trends (as long as they stay ancestral). So we ask: what changed, and what’s different? The list of suspects is virtually endless.
We have to prioritize, and based on inadequate, spun, and sometimes withheld supporting data.
So the steps we take are going to be in some cases mere precaution. I’ve elected, for example, to use a toothpaste free of antibiotics (like triclosan), fluoride and emulsifiers.
re: “Are implants good or bad?”
Beats me. If I were facing that option, I’d research the heck out of it before deciding. Leaving a gap where a tooth used to be has hazards too (although nothing related to CVD that I’m aware of). Not having faced root canal, I haven’t looked into it deeply, but there is controversy going back many decades. Some of the RC dissidents are the usual sky-is-falling crowd, so skepticism is warranted on both sides.
A dental association here endorses RCs, claiming “A root canal is a safe and effective procedure.” They even have a page that criticizes W.A.Price, but neglects to mention the 2009 ADA paper that concluded “More accurate epidemiologic quantification of endodontic infection and inflammation is required before definitive conclusions can be made about potential relationships between endodontic disease and CHD.”
As with almost all the ailment promotion associations at present, I distrust the dental associations. They usually also endorse Hg amalgam fillings, a diet that causes tooth decay, and added fluoride in toothpaste and water. On a sane diet, the main dental problems (caries, gingivitis and periodontitis) essentially don’t arise, and the Fl is both unnecessary and in my view a potential thyroid and microbiome hazard (and by implication in both of those, a downstream CVD risk).
Bob N, so if you’ve looked into dental issues, do you share my impression that caries problems have sort of receded compared to the 1920 – 1970s? Do you have any idea why? Fluoridated toothpaste was around before that, and its not like the average diet has gone down in carbs.
Could this be one of the reasons why CVD rates have dropped in the West?
As Craig points out above, elevated Uric Acid fits into this story.. As you say, fascinating how some of these pieces start to fall into place when you begin to look at things from a different perspective…
I continue to read and learn as much on the subject of UA as I can… if I never get gout again, it’ll be too soon! Unfortunately, once they found a pharmacological way to control UA levels in gouty patients most of the research monies dried up 😦 Taubes makes the point in his “missing chapter” that never made it into his book: http://fourhourworkweek.com/2009/10/05/gout/
There’s a gentleman in my neck of the woods (Colorado USA) named Richard J. Johnson who continues to do great work on the subject. I enjoy his youtube lectures and papers, his arguments make sense to me.. Here’s one such paper that discusses the role that elevated UA plays in Hypertension and CVD.. http://hyper.ahajournals.org/content/41/6/1183.full
“We also summarize experimental studies that demonstrate that uric acid is not inert but may have both beneficial functions (acting as an antioxidant) as well as detrimental actions (to stimulate vascular smooth muscle cell proliferation and induce endothelial dysfunction).”
A case of “the dose makes the poison” I suppose.. Chronic high UA (in western societies this is usually cause by alcohol and fructose consumption) leads to endothelial damage..
A quick search reveals a possible negative effect of high UA on Coagulation and Platelet Economy.. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1922159/
“Platelet adhesiveness and plasma thromboplastic activity were correspondingly increased in the gouty subjects.”
Thanks for the wonderful series.
KellyT, thanks for those links.
One thing that sandwiches the gouty migrainous sufferer between a rock and a hard place is that aspirin exacerbates gout, can even bring it on.
A big hello from Goutboy and Uricon.
Kelly, is it UA causing CVD and fructose causing CVD or rather fructose causing UA to go up resulting in CVD?
Both, fructose sees increase in UA but also ldls, generally nasty stuff, the liver can’t cope with high levels hence NAFL. This has only been really known for circa 5-6 years. Increase in UA from whatever cause sees decrease in nitric oxide. UA both oxidant and anti-oxidant, this might be how UA works either in blood or in cells but not clear. The point is UA levels need to be looked outside of just the cause of gout.
Kelle, re: Taubes, from your link with his missing chapter:
” Even when the New England Journal published a report from Walter Willett and his Harvard colleagues in March 2004, this same kind of nutritional illiteracy manifested itself. Willett’s article had reported that men with gout seemed to eat more meat than healthy men. But Willett, who by this time was arguably the nation’s most influential nutritional epidemiologist, later explained that they had never considered sugar consumption in their analysis because neither he nor his collaborators had been aware of the hyperuricemic effect of fructose. Willett’s co-author, Gary Curhan, a nephrologist and gout specialist with a doctorate in epidemiology, said he might have once known that fructose raised uric acid levels, but it had slipped his mind. “My memory is not what it used to be,” he said. He also acknowledged, in any case, that he never knew sucrose was half fructose.”
“Unlike Willett and his colleagues, Johnson had long been aware of the ability of fructose to raise uric acid levels, and so was studying that phenomenon in his laboratory. But it was only in the summer of 2004, he explained, three months after his NEJM editorial was published, that he realized that sucrose was half fructose and that his research of the past years was even relevant to sugar.”
So we have the leading US nutriologist and two leading research nephrologists being blissfully unaware of a piece of basic science, something they should have probably learned in high school advanced placement biology or chemestry. The mind boggles. I guess I shouldn’t be surprised about the quality of other medical recommendations.
This type of thing amuses me, but also gets me rather angry. I should take you through the saga I had in trying to find out if blood sugar machines measured only glucose, or glucose and fructose. Not sure if I really know the answer to this. But I think I do.
Well, it is worrying that many physicians have a mindset to take for granted what is said on the tin. When one takes decisions that can literally kill people, one should try to have a grasp of the full picture (which is not the same as understanding every single step). Maybe it is the need for massive rote learning in med school that discorages the attempt to stay on top of the chain of reasoning.
Anyway, for glucose monitoring, there exist lots of different methods, and after a brief scan, I would assume most should not be sensitive to fructose. However, the actual method used and its cross-sensitivity may differ between devices.
There is this sweet (literally) little project for kids:
They use urine test strips and can successfully differentiate between a glucose solution and orange juice.
There are also reports of patients getting false high readings after handling sweet food and not washing their hands properly before pricking their fingers, so I suppose you could test glucose vs. fructose solution instead of blood to know what the machine in your lab or the personal monitor you recommend to your patients does.
It is also surprisingly hard to find a breakdown of sugars rather than just total sugar for a variety of fruit and foods. I am tempted to do some sciencebuddy-style testing on some fruit myself…
In addition to the experimental approach by sciencebuddies, quick search says that most commercial devices use glucose oxidase, which is just not sensitive to fructose:
The second link (with the exception of post #3 – glucose and fructose sharing the same sum formula does not mean they are easily converted into each other) contains a few quotes and comments that are relevant to the blog here in general and the role of purines in particular.
Just listened to a fantastic youtube presentation which took place at the Low Carb conference in Vail this year. It was done by Dr. Cate Shanahan, 38 minutes, and a lot of what we have been discussing here and in Dr. K’s post was mentioned in this presentation, even Iron. Well worth a watch. Here is the link – Dr. Cate Shanahan https://youtu.be/YbpX41oCi1M .
I expect I will have to watch it a few more times to digest the high level chemistry. BTW, a number of the presentation which took place at Vail are available on YouTube. I can provide links if anyone cannot find them. Drs. Eades, Gerber, Wortman, Fung, Westman, Rosedale, and others. All good.
I watched Dr. Cate’s presentation and I am little wiser. She’s not a good presenter, unfortunately. I’m not sure she has a firm grasp of the detailed plaque-forming mechanism she postulates.
But one thing she mentioned in passing was that men have heart attacks earlier than women because they have more red blood cells, hence more iron in their bloodstream.
Athletes taking EPO to boost their RBC count should have much more iron than ordinary people. Do they have an elevated risk of heart attack? (Might be difficult to separate iron count from other heart-affecting factors of their lifestyle.)
The only reason they ‘iron causes CVD’ hypothesis was created in the first place was to explain why women had less CVD than men, seemingly especially the case prior to the menopause. It was stated that women’s CVD rate accelerated after the menopause. The fact that the rate of CVD in women accelerates after the menopause has one fatal flaw. It is not true. Yes, after the menopause women have more CVD than before. Oder men have more CVD than younger men. There is no acceleration after the menopause, this effect does not exist. A further refutation of the iron hypothesis is that face that women with diabetes have the same rate of CVD as men with diabetes. Regardless of age etc. etc. One thing that does drive me nuts in the area is that someone makes a statement – CVD in women accelerates after the menopause, (may be true, may not be), someone thinks for two seconds, then comes up with a new hypothesis as the cause of CVD ‘increased iron levels cause CVD’. Because it seems reasonable (and also because it indirectly supports the cholesterol hypothesis) it is taken up worldwide, and ends up being claimed to be a proven fact. It is not. It is a guess, based on an incorrect observation.
“A further refutation of the iron hypothesis is that face that women with diabetes have the same rate of CVD as men with diabetes. Regardless of age etc. etc. ”
Iron and Diabetes Risk (Simcox, 2013)
“Iron overload is a risk factor for diabetes. The link between iron and diabetes was first recognized in pathologic conditions—hereditary hemochromatosis and thalassemia—but high levels of dietary iron also impart diabetes risk. Iron plays a direct and causal role in diabetes pathogenesis mediated both by β cell failure and insulin resistance. Iron also regulates metabolism in most tissues involved in fuel homeostasis, with the adipocyte in particular serving an iron-sensing role. The underlying molecular mechanisms mediating these effects are numerous and incompletely understood but include oxidant stress and modulation of adipokines and intracellular signal transduction pathways.”
Yes, Martin, she is not a good presenter but I just ignored this fact. In my university years I had lot’s of poor teachers and I just learned the stuff in spite of their teaching style. Dr. Shanahan presents a model for CVD which answered a lot of questions I had. We have heard time and again how PUFA’s are bad because they cause inflammation. She deals with how this happens. She shows that it is not the LDL which is the problem (nor the particle size of the lipids – HDL is the smallest yet it is good) but it is the stuff in the LDL, the cargo, oxidized PUFA’s. If the particles become oxidized they become non-recognizable by our receptors and just stay in circulation much longer until our immune system has to step in to dispose of them. Inflammation. She shows how iron is complicit in the oxidation of the PUFA’s because it acts as a kind of catalyst to increase the oxidative process. Since men have more iron, they tend to be more susceptible to oxidized PUFA’s. High glucose levels exacerbate this problem because the LDL particle stay around in the circulation for longer, so diabetics are more at risk. She deals with how these oxidized PUFA’a end up causing fatty streaks in the arteries.
There was much more, and I had never come across such a comprehensive model which included oxidized PUFA’s, CVD, Diabetes, Iron, all related. So I was impressed and I think that I am now somewhat wiser.
According to Dr. Shanahan, the oxidised LDL particles cannot be used by the body and circulate as garbage in the blood until disposed of by the immune system, causing inflammation.
I assume that oxidised LDL counts towards the total cholesterol score.
So the measured TC will be the usable cholesterol plus any junk LDL, and the more junk, the higher the TC reading. I.e. the higher the TC the more chance of CVD — the conventional “cholesterol is bad” theory. But we know elevated cholesterol is good, if you’re over 60 anyway, so I have my doubts as to whether Dr. Shanahan has got the story right.
Fascinating!! I am also very interested in the increased CVD risk (thrombosis) for those with myeloproliferative neoplasms (MPNs) such as ET, which is one of the major causes of morbidity and mortality in these patients and how best to minimize this risk, especially as this is being diagnosed in ever younger folk.
I am not sure what to do in such cases. Aspirin? The newer anticoagulation agents?
Yea !!!! Can I get off Warfarin? Would it not be GREAT !!!!
I believe Craig and Kelly T are onto something, some of the works they cite link uricemia to endothelium damge. Here’s a recent PubMed article that reaffirms much of what is found in their links:
The number of PubMed articles in the last 20 years has grown by five; we’ve got big Pharma to thank for that. Of course, they are seeking something that will lower uric acid numbers and prevent and/or mitigate attack — another number-centric chase is on.
Could well be another piece of the puzzle.
Dr Kendrick, is this perhaps another area to test against your “the cause for what causes heart disease”? The malfunctioning of the gut enteric nervous system seems to me to be a source for another stressor “cause”.
From the article below:
… If you look at the physiology in these diseases, the gut looks fine. It’s the nerves (“enteric nervous system”) that are somehow malfunctioning.
I understand that you are presently, like me, thinking in more holistic circles about “general pathology genesis” and as you mentioned earlier it is very ‘fascinating’, in this context, to read how Dr. Perlmutter elaborates on how a ruined gut flora may create neurological disorders and possibly can be restored with a healthy gut flora and with the interest from Big Pharma being virtually nil.
I find Perlmutter’s, 2013, book “Brain Maker” well worth the ‘easy reading’. Here is a lot of food for thought about food and our general health ailments of today. Well documented!
Dr. Göran: Pharma has a finely-tuned nose for the aroma for money. You can bet they are developing gut bacterial strains they can patent.
Very interesting write up by a fellow who had a bad artery. Lots of gems, self-treatments and testing over a long period of time. Quote – As stated early on with the Track Your Plaque group – We have a surface chemistry problem and a gut problem. http://www.k-vitamins.com/index.php?page=My_Story
Mention of vitamin K again lead me in a different direction wrt statins. Inhibition of the mevalonate pathway by statins has wide ranging side effects one of which is to reduce the amount of ubiquinone, CoQ10, but vit k2 a menaquinone is also affected. Possibly also another important quinone, Pqq, which has implications for Alzheimers disease. And many more…
So there’s a plausible connection between statin use and arterial calcification via vit k reduction, and of warfarin-like anti clotting effects ditto. (warfarin and vit k oppose each other) . These come at a high cost!
So There’s is a plausible connection between arterial clacification via vit k reduction and of warfarin-like anti clotting effects. (Warfarin and vit k oppose each other). To me this is a high price to pay if you are on Warfarin. Would it be safer to take the asprin therapy. It seems right to me.
So, if “inflammation is healing” and so, by dampening or stopping or slowing this healing, NSAIDs and steroids make things worse in the long run … then there is a another implied wrinkle in your hypothesis to consider which is the statins effect on CVD.
We, thanks to you and others, now know that cholesterol is not the cause of CVD and that statins are aiming at the wrong target so to speak.
BUT they ARE often credited with a minor improvement in heart attacks (and strokes? Though of course the overall mortaility is unaffected at best and probably overall increased many now believe) and the oft-quoted mechanism is that statins are mild anti-inflammatories and dampen down damaging inflammation in the arteries … or something similar many claim.
If it is bad to impede inflammation and healing, yet statins do this and show a slight improvement in CVD incidence or patient mortality, why is this?
Or isn’t it in fact and statins don’t even do this???
Facts are tricky little blighters. My view is that the beneficial effect of statins, such it is, is primarily due to NO synthesis. Statins increase it. I find myself overcome with an urge to beat my head against the wall when people start talking about inflammation in regard to CVD.
My apologies for raising it then! Was just curious about the apparent contradiction!
Surely though repairs to the endothelial wall would include an element of inflammation?
Sent from my iPad
Should we do all that we can to try to INCREASE inflammation once it shows up? Sometimes there’s too much inflammation, getting in the way of healing. Is this not so? It’s the “conventional wisdom”.
I would have appreciated having you by my side when my last (!) cardiologist prescribed his five medicines knowing that I would never touch them and especially when he stated that he was prescribing the statins not for any bad ‘cholesterols’ but to reduce the inflammation.
Reminds me of the quote from Thomas Henry Huxley, a man who did not suffer fools – ” The great tragedy of Science — the slaying of a beautiful hypothesis by an ugly fact.”
Oh, I forgot – this is now a ‘paradox’.
If “perfect vascular health” is the balance of vascular damage and vascular healing, then vascular sickness/disease is this equation of vascular damage vs vascular healing out of balance. Which is to say, too much damage going on for a certain healing capacity or not enough healing capacity going on to repair ongoing inevitable damage… Or a combination of the two.
When I think things through in these terms, it seems to me that the “damage” side of the equation – as complex as that might be – is easiest to conceptualize and define.
We can ask the question: What causes “damage” to the vascular system? Damage that triggers a “need for repair”? (questions beget questions, and now I’m pondering if there’s such a thing as damage that doesn’t trigger a “repair” response… hope not, we’d eventually have system failure with no warning signs at all! interesting…)
Anyway.. Dr. K has listed many of the “bad actors” that cause this damage and as he’s stated the list goes on and on.. If “Perfect vascular health” is what we want, we’d be smart to limit or eliminate as much of what causes this vascular damage as possible, thus bringing this damage vs repair ratio closer to balance…
The other side of the equation, the “healing” or “repair” side is obviously a bit trickier to conceptualize and define… It’s complex as hell as Dr. K has pointed out!. And as I read through this series I’m reminded of a quote by a fave ultra-runner of mine, Barry Murray, “The body is clever and running is easy..” He was talking about the mechanics of running. How most anyone can do it. But do they do it properly and most-efficiently or do they do it improperly and less-efficiently? Or somewhere in between? That’s a different question all together…
Similarly, we can say that “The body is clever and healing is easy..” It’s in our nature and Mother Nature, over millennia, has ensured that our bodies are “clever” in that most anyone can do it.. But do we heal properly, efficiently, appropriately and effectively? Or do we heal less properly, less efficiently, less appropriately or effectively? Or do we heal somewhere in between?
Our obvious question: What causes healing? What causes repair? Can cost you many years of your life researching.. Is it a law of nature that building something is always far more complex and trickier than destroying something? If not, it probably should be… Healing/Repair is a crazy complex process, as Dr. K has pointed out! It is “clever”, in that it’s got many “backup systems” built in – one way or another the damage WILL BE REPAIRED – even if it isn’t ideal. The alternative is failure of the system/death..
So understanding this, our question “What causes healing/repair?” must become “What causes ideal healing and repair?”
Ideal healing can’t be achieve without an ideal clotting process. It appears to be the cornerstone of healing.. So, what can we do to promote an ideal clotting process? This is what I’m looking forward to learning.
Study – Vitamin D (100 micrograms) ‘heals damaged hearts’ Dr Witte (consultant cardiologist) told the BBC News website: “It’s quite a big deal, that’s as big as you’d expect from other more expensive treatments that we use, it’s a stunning effect. But in those taking the vitamin pills, the ejection fraction increased from 26% to 34% Key phrase – but the skin’s ability to manufacture vitamin D also gets less effective [with age] http://www.bbc.com/news/health-35959556
Frederica Huxely, you said
“Topical steroids may not exacerbate CVD, but the resultant skin atrophy from prolonged use can be a nasty side effect. Another example of the cure potentially causing more damage than the original affliction.”
I have heard this before but never was sure that it was true. Can you elaborate on this – what is chemistry, the process, is the damage permanent, how to reverse, etc.
Alas, I have only read this – on quite a few occasions – but have never followed through to the research.
It is true. Google topical steroid damage, a few sites dedicated just to it should come up.
The answer to “What causes ideal healing and repair?” may be more obvious / known. What may be less obvious / known (in relative terms) is how to measure progress and success for “ideal healing and repair”.
It is wonderful that key doctors and scientists are challenging (thank you Dr K and Prof Noakes and many many more) and questioning medical orthodoxy. This is a fascinating story, learning of (and watching) the (excruciatingly) slowly unfolding process as mainstream medical science changes. The problem is; we the patients don’t really have time for science to catch up by conducting 10+ year RCT’s.
Philosophically, what is far far more important to finding the correct medical orthodoxy, as necessary and fascinating as that is, is how past damage (in this case endothelial damage) can be repaired – kelly your questions – and measures of successful repair – my questions.
I have previously asked a pro lchf doctor, he ducked the questions; perhaps known unknowns or even unknown unknowns. To me it seems that eventually somebody will propose some answers to these questions.
Now when somebody can give guidance on these 2 critical questions we can set about improving the health of the general population.
As I described above, get a series of CAC scans over time; look for changes.
Insurance often doesn’t cover this, but you might consider it to be worth the less than $100. That’s what it cost me in Massachusetts.
Thanks, I am in Cape Town, it costs a lot.
I find “Brain Maker” more an more interesting and almost 100 % relating to this issue of “inflammation” and the actual sequences leading from high carb diets through insulin resistance leading to “chronic inflammation”. But it seems as if Perlmutter considers that in these late stages the inflammation is in itself a culprit – there seems to be some hesitation about the subject.
The language seems to improve along the reading by the way.
Gesendet: Sonntag, 12. Juni 2016 um 23:32 Uhr Von: "Dr. Malcolm Kendrick" <email@example.com> An: firstname.lastname@example.org Betreff: [New comment] What causes heart disease part XVI
robert lipp commented: "kelly, The answer to “What causes ideal healing and repair?” may be more obvious / known. What may be less obvious / known (in relative terms) is how to measure progress and success for "ideal healing and repair". It is wonderful that key doctors "
We are still talking about inflammation which is a 1st step leading to CVD but an explanation for the source of the inflammation (or injury to the epithelium) seems to be obscure. Yet Dr. Cate Shanahan (see previous comments above) did present what I thought were persuasive arguments suggesting that oxidized lipids contained in LDL were quite likely the culprits. She presented a chain of events which went something like this:
– many of us in N.A. eat foods high in carbs and PUFA’s. Some of these pufa’s, the ones which cause the problems, are already oxidized due to processing and exposure to oxygen at elevated temperatures. Think potato fries or any processed foods that contain pufa’s and require heat for processing.
– the carbs in the diet provide significant resources to meet the basic usual energy needs while the pufa’s get packed up into lipoprotein particles suchs as chylomicrons, VLDL’s, LDL’s, etc. to circulate in the blood for future body needs when the glucose is gone. While insulin levels are still high (say one is insulin resistant to some degree) the level of glucose remains higher for longer, and pufa’s continue to circulate, and, in the presence of oxygen and iron in the circulation, continue to oxidize. The higher the degree of insulin resistance, the longer such pufa’s remain in the oxidizing environment and the more they oxidize.
– eventually this oxidized cargo in the lipoprotein particles becomes unrecognizable to the receptors which would normally transport them through the cell membrane (unrecognizable because the APO B envelope has been altered through oxidation) so they continue to circulate and oxidize until our immune system has to step up and take care of the problem. That leads to inflammation. Fatty streak are a by-product of this clean up process that tries to rid the blood vessel of these oxidized, now modified, lipoprotein particles. All of this started by eating oxidized pufa’s. (You have to watch the presentation to appreciate all the details.)
I don’t know if this model is robust or not. But it does seem to agree with so many of the observations already presented in this blog (and comments) regarding the progression of CVD. A person whose name I can’t remember, a few posts ago mentioned that he believed that Pufa’s were more detrimental than carbs to our health. Inflammation starts the process, and this model shows what starts the inflammation, an immune response to unrecognizable bodies. Damage to the endothelium follows. Isn’t this important?
Yes, there are likely other factors which may lead to plaque formation and CVD, but if this model is viable, then at least one solution to avoid CVD can be hypothesized and tested. I would be interested to know what you all think.
BTW, Dr. Shanahan did mention that the material she presented was derived from the work of a prolific researcher/organic chemist named Dr. Gerhard Spiteller. I did not come across this name before.
If that’s the case, John U, why does atherosclerosis only occur in specific sites in the arteries? Wouldn’t the risk of developing fatty plaques be the same everywhere given this theory? I think if you reverse some of the processes, if I understand Shanahan’s hypothesis correctly, then maybe it can fit into the current hypothesis. What if the oxidized PUFAs damage the endothelium prior to setting off an immune response? Or, what if the oxidized PUFAs get incorporated into the plaque and thereafter affects the clotting factors? Maybe there’s data out there supporting this chain of events. I don’t know. I suspect Dr Kendrick sees this hypothesis as yet another morphing of the original cholesterol hypothesis.
Good observations, Stipetic. Dr. Shanahan did not answer the part about fatty plaque locations, other than to note that the areas of higher stress appeared to be more often affected, which we already knew. Regarding the Oxidized pufas cause damage to the endothelium before setting off an immune response, I would ask what is the chemistry for this damage. An immune response is usually associated with inflammation, so I would think that it is the immune response first, and damage next.
Good point. Seems like the chain of events should be immune response then injury as you mention. I haven’t read the papers on oxidized cholesterol or PUFAs. May Dr Kendrick has an idea.
Congratulations on the paper in BMJOPEN . For those of your supporters who might like to read the paper it can be downloaded at
I might add that a rapid response can be to this paper at this site.
Thanks. Been doing interveiws all morning. This was really Uffe Ravnskov’s work. I just tagged along.
Excellent PR and exposure on Sky News (Aseem Malhotra came across well as always), various newspapers (see http://www.dailymail.co.uk/health/article-3638162/Statins-waste-time-60s-Row-controversial-report-says-no-link-bad-cholesterol-heart-disease.html
Aseem even managed to get into the SKy News clip that vested interests in big pharma and food cos. were responsible for the failure to get rid of the “cholesterol is bad” theory …
Well done – where were you interviewed for?
Radio 4 and 5 and Radio Scotland and Breakfast BBC.
This may interest readers:
I have sent in a rapid response to the paper as indeed anyone can do in BMJOPEN
Comments from patients and non-medics do have an impact
I heard you on the BBC World Service at around 8:15am EDT (1:15pm GMT) while driving to work.
There was just a brief quote of you saying a study of 68,000 individuals had shown that higher LDL and overall cholesterol levels were protective in those over 60. Which was followed by some harrumphing “expert” who said words to the effect that this was just one study and means nothing when there are “decades” of studies proving that lowering cholesterol prevents stroke and heart attacks.
I might have yelled “Black swan!” at the radio…
Have you ever noticed that when a paper, or a study seems to challenge established thinking, there is always a spokesman, or an expert who is wheeled out to harrumph that many studies have shown, that there are thousands of papers that show, that more research is needed…..
As they say, opinion changes funeral by funeral
The first book I read in this area was his original book (Uffe Ravnskov’s).
I think funerals will not solve the problem of established but incorrect science – because their deputies step into their shoes! One thing that would make a difference would be if the media did more investigative journalism. I mean, right now, establishment scientists are interviewed like minor gods.
For example, I’d like to see interviewers ask why people with higher cholesterol live longer – live, on air, with the references to the evidence for that made available on a corresponding website. I’d like them to ask them about the Ancel Keys evidence against SFA’s – and push until they had to justify why leaving out most of the data made for good science. I’d like to see them ask for the raw epidemiological data that SFA’s are bad for people, and maybe mix in some testimony from T2D sufferers cured or improved by LCHF diets – asking the experts to explain. If the expert refused to participate on that basis, it should be made plain to the listeners that he/she refused the interview.
Finally, I’d like the media to invite Sir Rory Collins face people who have experienced statin side effects! I’d love to meet him in person!
Science journalists should treat these people more like politicians – which is what they have, in effect become.
You are right about this. Two points,
Much journalism consists of regurgitating press releases.
I am not convinced the academics etc would go along with it, Nina Teicholz in her book, comments that eminent academics she interviewed for her book, said that any mention of Gary Taubes would cause the termination of the interview. I think they probably feel they have a lot to lose from hostile interviews.
Thanks for this alert to a truly great paper.
Reminds me of the fact that my own cholesterol was low at the time for my very serious heart attack 17 years ago. It was in fact so low that they didn’t prescribe any statins to me at that time.
Adding my congratulations – it is great to see you all working together on this. The paper has a good sharp focus too, which helps us from other areas of science to get to grips with it.
Thanks. We keep chipping away, chipping away.
Here’s the whole paper: http://bmjopen.bmj.com/content/6/6/e010401.full.pdf+html
I am a supporter of your view. Now I need to know if its OK to carry on eating OATS and Walnuts.
Am Ang Zhang: I don’t think that anyone on the wide spectrum of diet advice would consider oats and walnuts as unhealthful. By all means, carry on. Walnuts have relatively high levels of alpha-linolenic acid, the precursor to EPA and DHA, the Omega-3 fatty acids our bodies need. Not everyone converts them well, though, so I wouldn’t neglect eating fatty fish. The Gaelics of the Outer Hebrides, specifically the Isle of Lewis, whom Dr. Price studied, ate mainly oats and fish, and enjoyed robust health.
Didn’t Bob Niland say that oats had more glucose (60%) than sugar? Fishermen would no doubt use the carbs quickly.
Dr. Kendrick: Great interview. I watched thanks to Marika Sboros. Dr. Pearson didn’t seem to have any evidence except that your are part of a minority, a few hundred people with genetic defects, and a vague allusion to studies of millions which contradict your findings. Move along, nothing to see here. The foundation is crumbling.
Just finished reading the Ravnskov paper. The study was very well done and very well reported. It should be hard for anyone to contest the results, so I suspect they will just be ignored.
During the reading, 2 things stood out for me. One was with the Goldstein and Brown (ref #4). G&B receive a Nobel Prize for their work in LDL and LDL receptors. I read their “Lecture” presentation, and indeed their work did merit great admiration. However, now after much more research has been published on LDL-C, it does seem incongruent that LDL is in any way implicated in CVD. It always seemed so to me, just because LDL and Cholesterol are important and essential and natural components of the good functioning of the body. However, I could not find any science to support this position. G&B did show that animals who were genetically modified to eliminate their LDL receptors, did develop plaque and atherosclerosis. So this fact was compelling. However,after listening to Dr. Shanahan’s presentation recently, I now wonder, what if the LDL is just not recognized by the receptors and therefore not cleared out of the bloodstream as Dr. S suggested? Would this not be similar to the case of animals with “no LDL receptors”? I would think so.
The second thing that struck me was that in some of the studies which were included in the review, vegetable oil was used to replace saturated fats as an intervention. In these case studies, it was often found that LDL levels dropped, and as Ravnskov mentions, these lower LDL levels were associated with higher mortality. Interestingly, this higher mortality was probably caused by the effects of oxidized pufa’s, and as Dr. S showed in her presentation, the measured LDL-C levels did drop but only because some of the LDL-C was deposited in the arteries as fatty streaks and not included in the assay in the blood stream. How easy it is to make mistakes when your confirmation bias is intervening.
re: “…the measured LDL-C…”
For those following the CVD detective story series, it’s important to note that LDL-C is not a measurement of any kind. It’s a calculation (that’s what the “C” stands for). It’s an old approximation, from a time before we were able to routinely measure actual LDL particles. It’s based on certain assumptions about diet (which do not hold for those doing LCHF).
If Low Density Lipoproteins matter (and they do), then they need to be actually measured, via advanced lipoprotein panel, which reports various LDL-P and other numbers. This is rarely done (patients usually have to fight for it). There are reasons for this mess, but…
LDL-C, being very rough, is consequently is apt to be a poor correlate to anything, and I love the fact that this excellent new BMJ paper shows negative outcomes for reduced LDL-C. Those supporting the use of LDL-C as a basis for reckless statin prescription need to answer it.
Perhaps they can retort with “well, it’s not a terribly meaningful metric”.☺
I suspect the paper authors were fully aware of this, and deliberately chose to not open that line of argument, in the interest of getting published. Tactical. Perhaps next time.
Here’s a cardiac physician being even more blunt about LDL-C (and TC):
re: Perhaps they can retort with “well, it’s not a terribly meaningful metric”.☺
Well, that didn’t take long:
On this side of the Atlantic, Roger Blumenthal, MD, of Johns Hopkins, said that the authors “confuse LDL-cholesterol as a biologically-prime mediator of atherosclerosis (the data behind this involves genetic, epidemiological, and high-quality randomized controlled clinical trials ) with the fact that LDL cholesterol is a fairly modest biomarker of absolute cardiovascular disease risk.”
Michael Blaha, MD, MPH, also of Johns Hopkins, said that he agrees with the authors that LDL by itself is a poor marker of risk in the elderly but thinks that the conclusions the authors drew from this observation are completely unwarranted.
Bob, There were only eleven comments on that cardiobrief when I checked just now.
Surely we here can make it much more challenging than that for them. Sign up and go for it!
The quote from Dr Baha resembles corporate blabla. Anyone figure out what he was tying to convey except carry on regardless?
re: comments on that cardiobrief
I’ll consider it. I apparently have an account on MPT, but due to running NoScript in Firefox, I don’t see any comments (or ads) and it takes some work to make them, and the reply dialog visible. I follow MPT mainly to see what’s on the radar at Consensus Medicine™.
@Eric:The quote from Dr Blaha resembles corporate blabla. Anyone figure out what he was tying to convey except carry on regardless?
He turned up again today on MPT in a new article about the futility of LDL lowering:
Paper: “Our results do not provide support for a blanket principle that lower LDL cholesterol is better for all patients in secondary prevention,”
Blaha: “It is very, very hard to make conclusions from nonrandomized retrospective studies like this,”
Somewhat O.T., but not really. I believe this passage by Feynman, which I’ve seen many times, maybe even in Dr. Kendrick’s writings, is spot on:
“In general, we look for a new law by the following process. First, we guess it. Then we compute the consequences of the guess to see what would be implied if this law that we guessed is right. Then we compare the result of the computation to nature, with experiment or experience, compare it directly with observation, to see if it works. If it disagrees with experiment it is wrong. In that simple statement is the key to science. It does not make any difference how beautiful your guess is. It does not make any difference how smart you are, who made the guess, or what his name is—if it disagrees with experiment it is wrong. That is all there is to it.”
Here’s the full video clip from YouTube:
I was delighted to see in the headline that “experts” are saying that the report must be taken with a pinch of salt. How big would this pinch have to be, and by how much would it raise a person’s blood pressure? I think we ought to know.
Dr Kendrick, have you seen this video by Dr. Bereliani? If so what do you think of it?
I would love to find a way to get Sir Rory Collins and his (closed, secretive) Oxford organisation to release all their data – which they refuse to do currently citing commercial onfidentiality. If they did, I am sure Ravnskov/Kendrick et al would have a field day.
I am also deeply suspicious of the British Heart Foundation – I would like to know what funding they get directly or indirectly from pharma or food cos.
Prof Pearson is associated with this organisation which I peddles the saturated fat = cholesterol raised = CVD story unquestioningly and who refuse to countenance any alternative.
Strange, that a charitable body like BHF would not want to advance the truth …
Will have a look when I get home. NHS computers are very cencorious
I too am highly suspicious of the BHF, I sent the following graph to them asking why it had been taken down but never got an answer. Big Pharma and KOLs no doubt objected.
Estimated lowest mortality rates for TC blood levels
All Cause mortality 222 mg/dl 5.75 mmol/L
Non-communicable disease 210 mg/dl 5.49 mmol/L
Cardiac Disease 208 mg/dl 5.44 mmol/L
http://www.heartstats.org/documents/download.asp?nodeib=6797 This URL no longer exists? WHY?
Now on https://renegadewellness.files.wordpress.com/2011/02/cholesterol-mortality-chart.pdf
Study – people who cut dietary salt also saw a 2.5% increase in cholesterol levels and a 7% boost in triglycerides. Like high blood pressure, elevated levels of cholesterol and triglycerides are risk factors for heart disease. Excessive triglycerides can also contribute to diabetes. Oh oh now what do we do? http://healthland.time.com/2011/11/09/to-salt-or-not-to-salt-study-questions-the-benefits-of-reducing-dietary-sodium/
I think Gary Taubes has good answers to this question – http://www.nytimes.com/2012/06/03/opinion/sunday/we-only-think-we-know-the-truth-about-salt.html?_r=0.
Ken Strain wrote:
“Sorry for the confusion, but I’d not anticipated anyone still thinking that salt was a major cause of trouble.”
This comment made me laugh, because it just shows the vast gulf between the informed discussion here and standard NHS advice:
If only it were easier to sort out cause, effect and coincidence.
Wouldn’t we expect an association between salt and hypertension, if only due to renal artery atheroma? – after all the kidneys control salt in the blood and also blood pressure on some timescales. I think this has been discussed on this blog. I’m not convinced that tells us much that is useful. There are probably hormonal links too, but again, what is cause and what is effect.
The whole area of risk evaluation of peripheral BP at near normal levels (up to around “age plus 100” systolic) to consequential CVD is poor. I seem to recall a post here a while ago discussing central BP measurement, which may be of interest.
Is elevated TGs a cause of T2DM, a consequence of it OR simply co-observed with it due to common cause? (Or all three.)
Insulin resistance is a necessary adaptive response, but overeating CHO puts the body in a state where a series of bad things happens, leading to things getting broken. That TGs lead to IR in already broken circumstances is not to blame the TGs.
If the body as a whole (muscles, adipose tissue, etc.) won’t absorb blood glucose the liver has to turn it to fat. The liver has to turn fructose to fat too (if glycogen storage is saturated).
It is no surprise that there is an association between TGs and T2DM – elevated TGs is a sign of eating too much CHO (when over fed, not in starvation when short term excess will go to glycogen instead of mostly palmitate saturated TG).
The appropriate action is to cut the sugar (and overeating). If pancreatic beta cells are still present and active in reasonable numbers, much of tne damage can be reversed.
Why do you think that salt causes renal artery atheromas? Also, if sugar isn’ getting into cells (in the absence of insulin), body won’t store it as fat, it will excrete it and patient won’t gain weight. In the old days in China diabetes was caused waisting and thirsting disease.
May be of some Use to you
Michael H. Alderman
Salt, Blood Pressure, and Human Health
Copyright © 2000 American Heart Association. All rights reserved. Print ISSN: 0194-911X. Online
Hypertension is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX
Hypertension 2000, 36:890-893
Elliott, P. Et al (1988) BMJ, 297:319-328
Folkow B (2003) Lakartidningen, 100:3142-3147
The Cochrane review of sodium and health.
Intensive support and encouragement to reduce salt intake did lead to reduction in salt eaten. It also lowered blood pressure but only by a small amount (about 1 mmHg for systolic blood pressure, less for diastolic) after more than a year. This reduction was not enough to expect an important health benefit. It was also very hard to keep to a low salt diet. However, the reduction in blood pressure appeared larger for people with higher blood pressure.
J Gen Intern Med. 2008 September; 23(9): 1297–1302
Observed associations of lower sodium with higher mortality were modest and mostly not statistically significant. However, these findings also suggest that for the general US adult population, higher sodium is unlikely to be independently associated with higher CVD or all-cause mortality.
Am J Clin Nutr. 1988 Jan;47(1):113-9.
Blood pressure response to dietary sodium restriction in healthy normotensive children.
Miller JZ, Weinberger MH, Daugherty SA, Fineberg NS, Christian JC, Grim CE.
These results suggest that compliance with modest Na restriction does not consistently lower blood pressure in normotensive children
J Am Coll Nutr. 1989 Dec;8(6):495-503.
The effect of dietary interventions to reduce blood pressure in normal humans.
Luft FC, Miller JZ, Lyle RM, Melby CL, Fineberg NS, McCarron DA, Weinberger MH, Morris CD.
Although all three interventions may benefit some hypertensive and some normal individuals, the data from these relatively short-term cross-sectional studies are insufficient to warrant generalized dietary recommendations for the normal population
I did not mean to imply that salt causes atheroma. I was iinstead suggesting that one should question the effect of reduced arterial supply to the kidneys, leading to poorer control of BP on the medium term, In that case it is plausible that the kidneys don’t do quite so well in controlling BP (on timescales of minutes or more). Of course the poor BP control could arise from microvascular damage to the kidneys, or perhaps it is both together. It would not surprise me to learn that there was often some microvascular damage seen together with atheroma (as the kidneys are sensitive in this respect).
The main point is that just because salt, BP and CVD come together, one should be reluctant to adopt a simple cause and effect model without very careful consideration. That applies to almost every observation in the area of CVD.
I doubt that it would be possible to separate these out (further than the minor residual effects seen in the Cochrane review) without a post mortem study.
In any case it appears that salt is not the risk it has been claimed to be, except in a sub-population with damaged or disfunctional kidneys.
Sorry for the confusion, but I’d not anticipated anyone still thinking that salt was a major cause of trouble.
If you reduce salt intake the body will keep blood pressure up by activating the renin angiotensin system, ending up with increaed angiotensinogen II levels. Antiotensinogen II and Nitric Oxide are mutually antagnoistic. So if you fire up the RAAS you will end up with less NO which is a bad thing – with regard to CVD. Which is why we see increased CVD mortality with low sodium intake. [And the ‘experts’ know all of this]. It is also why ACE-inhibitors reduce CVD risk, because they increase NO synthesis in the endothelium. Yes, life is simple. and everything makes sense, if you stick to basic human physiology.
So are ACE-inhibitors a good think to take for high blood pressure
Does l-arginine do this as well.
Thanks for the link – I have posted some references below. The actual numerical benefits in healthy people are trivial and also a study shows (haven’t checked if included) that those on high salt (<15g NaCl) live longer. Another case of treating the whole herd rather than a proper diagnosis for those who would benefit. Makes more money that way like the statin "7-10% risk in 10 years" 90-93% wrong diagnosis
Thought this might be interesting.
I think the real recommendation to processed food industry should be not to lower salt content in their foods but rather to cease existing and to become organic farmers (or something of that sort)… But I do that recommendation will be coming any time soon…
What is this?
“A Mobile Threadlike Structure in the Left Atrium: Cor Triatriatum, Artifact, or Thrombus?” (Markan, 2009)
A very good article on the same subject By Dr Aseem Mathotate Can be seen on www,mercole.com
What an insane medical world we are living in!
To me it seems that what you should do is almost always the opposite to what is recommended, especially when it comes to nutrition but also when i comes to medication and medical advise. The problem is to get to know, through elaborate homework, when there is a true benefit of a medicine before accepting any treatment. The best thing in my eyes is to adopt a principle of ultimate caution and keep away from the health care system until it is impossible to stay away from it for whatever reason, e.g. a broken leg.
By now I “know my heart” and realise that when being in a stressed state, as recently before a long journey, my angina showed up and really made me worry. But still I have been through this a number of times and would never dream of getting in touch with any health service since I know that they would then grab me, stent, by-pass and drug me beyond recognition.
In the unstressed condition having arrived, but still ‘worried’, at our log cabin by the mountain side in northern Sweden I had to test my “heart condition” and decided to climb the mountain side. Surprise, surprise! I behaved like a mountain goat and had almost no effort angina. Having now performed this test three days in a row with the same result convinces me that I am in little danger. On top, I am now devouring the most “forbidden” food like the fattest pork and reindeer meat available and feel great.
So, my advise is to avoid the health care system and especially screenings of all sorts as a healthy fish would avoid fishing nets at all cost.
Dr Goran, you are an inspiration. Your optimism is quite something. Goats are wonderful creatures, hardy, intelligent and amusing. You have something in common!
And I didn’t think there were any Vikings left!
I “travel” a lot using Google earth and maps, and wiki each location for things interesting. If I may ask, which area is your log cabin? That I may “travel” there. My father was, in 1918 and 1919, in the area to the East of you (WW1).
Here is the area.
For sure there are more spectacular mountains in the ridge between Sweden and Norway 100 km to the west but this most eastern mountain is presently enough for a “mountain goat” in my condition. 20 years ago I frequented those western mountains a lot, backpacking. A three week tour in the “wilderness” was an ultimate spectacular event.
Perhaps it is time to revisit and challenge the odds more severely since I at age 70 now own my own time; and health.
Found. Interesting place in June, 24 hour sun, 16.3 C daily high, 2 inches rain. Lakeside cottage (boat?) and mountain behind. What more do you want? Gallivare a small mining town. My father said the winters were terribly harsh and summers not much better but warmer with clouds of mosquitos. It was a bad time for him being ww1. He was based at Murmansk and moved between Arkangel and M.
I hope you really enjoy your time there. Me, I have realised that at 72, i don’t need to over challenge myself, so please be sensible.
I wonder if I was so very sensible today when I decided to go to the top of the mountain despite, heavy rain, 10 C and a hard wind. Well I didn’t back off and arrived at the rescue cottage at the top rather soaked and cold. I knew there was a heater inside and I had brought dry firewood in my backpack and I built a nice fire. I put my wet clothes on an number of pegs put there for this purpose.
Well I spent a few hours in the cosy cabin resting, grilling my meat on the fire and to have my clothes dry up and wait for the blizzard to pass. When I descended I had to fight some mosquitos when arriving among the trees where there is no wind. The mosquito peak will though be in about two weeks and being outdoor at lower altitudes is then really a challenge.
Anyway I am back in our own cottage now and I feel just great with a glass of wine in my hand in front of our fireplace. Evidently I don’t suffer from the physical strain – in my case it seems that it is the stress that takes it’s toll.
Quite a challenge. Blizzards are not in my league. Congratulations on your return home. Well done to those “extra arteries”grown to compensate for the original blocked ones. Amazing what our bodies can do for us.
My mother in law who will be celebrating her 98th birthday at the end of this year used to say to her daughter (my wife) that you should stay away from doctors because they will make you sick and you should stay away from hospitals because they will kill you. That is what was going through my mind when I read your post. How cynical we have become. Is it justified? Sometimes. We really have to educate ourselves.
AMEN !!! You have to be your own Health Care Advocate. No one else cares.
Hi John, not sure if I agree with your mother in law. Rather choose your doctor carefully – those that fully understand the science you follow. Like Dr K – thanks again.
I agree, stay away as long as you can from testing and routine Doctor visits.
Most ofices and labs do not do the testing right, they are too lazy.
Dr. Sjoberg—–Du ar en juvel.
An attack on Dr Ravnskov’s recent paper citing serious flaws. Are there flaws?
I thought the comments section could a very interesting battleground.
I would call them weaknesses, there is an important difference.
I just checked the comments on the cardiobrief . There were fourteen.
The people who comment here are safe.
It seems to me that progress might be made if more of the enthusiasm I see here were taken directly to the Establishment being questioned.
Why not tell these guys what the weaknesses are and what the strengths are.
Not so safe. But what’s it worth to you?
Good Point … Which would you rather be on WARFRIN or the correct Vit K. I am struggling with this decision. I would rather be on Vit K.
Warfarin, as you know is a vitamin K antagonist. If you’re wanting to supplement with say vitamin K2, you could ask your GP to prescribe one of the newer anticoagulants such as Apixaban or Rivaroxaban which act on a different pathway. Another plus is that you won’t need regular INR monitoring.
@ Dr Goran
I really do enjoy reading your posts about how you are constantly “beating the odds” with regards to your heart attack all those years ago and your colourful description of your life in Sweden.
Each time Dr Kendrick puts up a new post I always say to myself: I do hope Dr Goran has an anecdote on this!
And I’m definitely with you when you say that it’s (sadly) an almost universal truth that one has to do just about the exact opposite to what the government “health” agencies tell us to do regarding nutrition and / or medication for good health or treating chronic conditions.
I wish you many, many more years of behaving like a mountain goat! 😉
Steve (and all),
Thank you for all friendly encouragements and especially to Malcolm for an open attitude in medicine and allowing “ultimate (?) sceptics” as me to “occupy space”.
Goran. I am enjoying Dr K’s series very much, but feel unable to contribute much to the highly technical views expressed by such intelligent contributors.
I would just say, I keep coming back to the conclusion I arrived at over 3 years ago, when I seemed to just ‘see the light’. In a quiet day or two of navel-gazing I worked out that all medical interventions I had received in the previous 10 or so years had brought me to a very poor state of health. There seemed to be nothing to lose by turning my back on the GP/Nursing services, and it was the best decision I ever made. ( Dr Kendrick, I don’t mean to be rude, and I hope you won’t be offended)
If only I had the confidence to encourage others whom I see suffering like I did, to take the plunge, but I don’t. All I can do is show them how well I have become, and hope that they too may see the light before it is too late.
I constantly read round the topics of statins, anti-hypertensives and hypoglycaemics, ( all of which I was taking in high dosages for many years), and I cannot see any justification for ever re-introducing them. Quite honestly, I fail to see why I was ever prescribed any of them in the first place! I hate to say it, but I can only blame it on poorly educated medics, who have failed to keep up to date with their professional development. If they had updated their knowledge appropriately, then surely they could not fail to question their out-dated prescribing regimes…..no excuses.
As I pointed out.
“But still I have been through this a number of times and would never dream of getting in touch with any health service since I know that they would then grab me, stent, by-pass and drug me beyond recognition.”
This actually happened recently to a relative of ours who didn’t have any problem with his heart and was feeling just fine but he had a “routine” scan of some sort. When he was out shopping, being swell, he had a phone call from his sister who had been called from the hospital and she told him that he must immediately go to the hospital where he was promptly taken “care of” and he left the hospital with three stents – and to what purpose you may ask since he didn’t have any problem by the time of the scanning.
Goran, can you explain why stents don’t work? I remember reading that there’s no evidence to support their use but not why they don’t work.
As far as I understand this is that when your arteries have reached this narrowed state your homeostasis has already been at work for a long time to build collateral capillaries bypassing the closure. Otherwise I would not sit here myself or climb any mountain sides with all my main coronary arteries clogged since 17 years. And our relative didn’t experience any problem which indicates that the same homeostatic process had been at work for him as well. A stent may be helpful to some extent I guess.
Before refusing the comprehensive bypass offered I asked if there was any guaranties of a better physical performance, but no, there were no such guaranties. The only thing they firmly claimed was that the risk for a new deadly heart attack within a year would be reduced from 12 to 8 %. I still wonder how they were able to arrive at those numbers. My arteries were by the way to severely clogged to even consider any stents.
And the statistics is against the procedure since there is no difference in survival rates. Someone gave a very convincing reference a while ago at this blog. If you don’t do anything about the cause this procedure will last about 8 years and has to be ‘redone’ if possible. Since stents are foreign objects our immune system makes its best to get rid of the objects if you don’t suppress this system.
The only thing I can say is that a LCHF way of life seems to work fine in my case and especially for my severely diabetic wife. For healthy people on the other hand there is still a margin for sweets and beers but in my case I have to stick to the wine and the whisky 🙂
As far as emergency procedures go, it’s hard to argue that “stents don’t work”..
If there are Dr.s out there popping stents in for the fun of it, for the “billing pleasure”, that’s a different problem altogether…
Post-intervention intimal hyperplasia always follows, it seems…
Sheer stress causing the injury, I assume.. Then comes the clotting and remodeling, etc.
“Nevertheless, intimal hyperplasia appears to be the sole or major devastating pathological remodeling in post-interventional complications after angioplasty, bypass operations or stenting [21-23], and once begun, it is untreatable. We introduced bypass surgery, but intimal hyperplasia keeps growing in the grafted veins and arteries. We introduced angioplasty with balloon dilatation, but intimal hyperplasia grows after vessel stretching. We introduced angioplasty with stenting, but intimal hyperplasia keeps growing through the stents. We introduced stents with the best rational design – radioactive emission – but intimal hyperplasia, together with late thrombosis [24-26], again significantly hampered this innovation . We introduced drug-eluting stents, which retard growth, but intimal hyperplasia continues [28-31]. Intimal hyperplasia threatens literally every known vascular reconstructive procedure and no prophylaxis is available [32,33]. Reports evolved from very optimistic  and cautiously optimistic  to questioning the long-term effectiveness of coronary intervention [2,36-38].”
I’ve read all of Vladimir M Subbotin and William E. Stehbens papers. Very clear thinkers who ask necessary questions, like Dr. K..
Indeed. Dr. Subbotin asks the necessary questions and remarks: “the real and very sad irony stems not from biology but from our inability to notice and understand all these messages that biology sends to us.”
Hmm. Mightn’t forcing open a burdened artery squeeze shut any adjacent collaterals that are forming or trying to expand?
Same with bypass. They’d be cut away?
Collaterals are too small to show on standard scans, so no one would know they were there.
Once the collaterals are eliminated, you’d be totally dependent on the Intervention Technology.
There’s a good documentary “The Widowmaker” available on Netflix. It goes into some details of long term harms of CABG and stenting.
But I don’t know – I haven’t heard about it before. Basically there should be some kind of relief when you open up an artery with a stent. About the bypassing this is a more dubious procedure in my mind. But who knows anything but that the interventions are futile in the long run.
The only thing I have heard about the surgical procedures in the heart is that they are not without cost, not least when it comes to disturbing the “normal” working of the intricate autonomous nerve system governing the the heart muscle activity.
It is scary!
And I am happy to have been able to keep away from the knives although the fishing nets are all around.
I have cooked two deer hearts to bring along on todays mounting climb.
” A weird sceptic this Dr. Goran.”
Göran, I am curious about your reasoning: why are wine and whiskey more ok than beer? Beer has a bit of non-alcohol and non-fructose carbs, whereas wine and whiskey have no carbs beside alcohol, but quite a bid of that.
Thank you for the Subbotin paper!
As far as I understand he takes the stand of science; placing the cause-effect scenario of the unappreciated cell growth around stents and grafts into a general evolutionary context; an approach shunned by conventional medicine.
There are “Bierbauchs” but certainly no “Winebauchs” 🙂
Dr. Göran Sjöberg said, “Thank you for the Subbotin paper!”
You’re very welcome. Yes, he takes the stand of science. That’s a good way to put it. It’s what draws me to the writing of men such as Dr. Kendrick.. I can sense when men share a love of and desire to find the truth.. Subbotin is one of those, I believe.
I immediately recognized that when I read through two of my fave papers of his:
They put forward an alternate hypothesis regarding the “cause” of coronary atherosclerosis.. I’ve been pondering whether or not there’s room for this “neovascularization” process in Dr. K’s hypothesis…
I need to print out Dr. K’s series and see where these ideas might dovetail.. root out contradictions and post/email them regarding my thoughts. They are both quite accessible to curious schmucks like me – for that I thank them.
Enjoy the reading.
What role the thyroid?
According to Min-fu Bai et al (2014) hypothyroidism has an impact on the development of CHD, particularly as it affects platelet abnormalities, endothelial dysfunction, fibronolysis problems, hypercoagulability, systemic inflammation and hyperlipidaemia.
It is known that subclinical hypothyroidism (T3 normal, raised TSH usually asymptomatic) affects blood pressure, could it not also have a similar affect on the same systems as clinical hypothyroidism?
Min-fu Bai, Chuan-yuGao, Chao-kuanYang, Xian-pei Wang, Jun Liu , Da-tun Qi, You Zhang,
Pei-yuan Hao, Mu-wei Li (2014), ‘Effects of thyroid dysfunction on the severity of coronary artery lesions and its prognosis’, Journal of Cardiology, 64, pp496–500
It is not proven certain food and or drinks causes migraines. Migraine is a brain disease, coming out of the brain stem. I’m sorry, I’m Dutch so I can not explain myself well in medical English.
I suffer from chronic migraines and daily headaches. Only thing that really works for me is botox.
Still searching for another solution.
Look into acupuncture or TCM herbs. Often does wonders for migraines. Just make sure you find a good practitioner. Those disciplines can be tricky.