Twelve parts and not finished yet. Oh well.
At this point I have an admission to make – having recently been thinking about things in a different way. Up to now I have been using a model which I have called the ‘four step’ process of cardiovascular disease.
- Endothelial damage
- Clot formation/dysfunctional clot formation
- Clot repair/dysfunctional clot repair
- The final, fatal, blood clot
I still think that all the parts of the model are correct. However, it is probably best to look at this more as overlapping sets, rather than steps. Whilst it is true that, until the endothelium is damaged, nothing else can happen in the process of atherosclerotic plaque development. Once endothelial damage has occurred we are not looking at step 2, step 3, step 4 – as a linear process. After the first episode of endothelial damage, all the processes can be going on, virtually simultaneously (apart from the final, fatal clot obviously).
So, the thought I wish to make at this point, is that we are looking at a dynamic process, where all processes overlap and interconnect. Endothelial damage can be going on, whilst dysfunctional clot repair is also happening, in addition to further clot formation.
I was trying to think of a good analogy. The best I could come up with was rust on paintwork on a car. Before you can get rust, you need some damage to the paintwork. After that other factors can come into play. Water, salt…. Um, water and a bit more salt…um. Well, I am sure that other things can make cars rust more quickly, but hope you get the general idea.
Thus, I have decided not to call this the four step process anymore. I shall call it the four process process. No, that is rather clumsy. I shall call it the…not sure. The quadrilateral process. The ‘four process clotting’ hypothesis of heart disease. Anyway. I hope you know what I am going on about (those that have read the previous eleven blogs may do).
The role of lipoproteins
Now I am going to take this discussion in a direction those who have followed my writing thus far, may not quite expect. I want to look at the role of lipoproteins in blood clotting. Mea Culpa. I have spent a great deal of time telling people that lipoproteins have nothing to do with CVD. This is not entirely true. They can, and do, play a role.
The reality is that virtually every substance that can be found in the blood has some influence on blood clotting – and there are an enormous number of substances in the blood. So, it should come as no real surprise to find that high density lipoprotein (HDL), low density lipoproteins (LDL) and very low density lipoproteins (VLDL) are also involved.
Just to recap on one lipoprotein, namely lipoprotein (a) (Lp(a). As I have discussed earlier Lp(a), is produced by the body to plug areas of damage to artery wall. It is found in animals that cannot synthesize vitamin C – and are therefore at high risk of scurvy. Scurvy is, primarily, a disease of connective tissue e.g. collagen (which needs vitamin C for its synthesis).
Breakdown of collagen leads to cracks in blood vessels, and Lp(a) plugs the gaps. Thus, here is one lipoprotein, the entire function of which, is to help form very strongly bound blood clots. What I wish to highlight here is that Lp(a) could also be called LDL(a). Because Lp(a) is LDL which has one different protein attached to it.
With LDL and Lp(a) being virtually identical, it should come as no surprise that LDL itself also has an impact on blood clotting, through a number of different mechanisms. Indeed, the interaction between LDL and blood clotting is mind-boggling in its complexity. I am not going into things here in too much detail, and I will just highlight one study. It has the catchy title: ‘LDL receptor cooperates with LDL receptor–related protein in regulating plasma levels of coagulation factor VIII in vivo.’ Here we go:
‘High levels of FVIII in plasma (greater than 1.5 U/mL) constitute a major risk factor for arterial and venous thrombosis in humans. Our observation that the up-regulation of hepatic LDLR protein expression in mice by gene transfer accelerated FVIII clearance from the circulation may be of therapeutic interest for patients who have elevated plasma FVIII levels. In humans, the up-regulation of LDLR protein is achieved by treatment with 3-hydroxy-3-methylglutaryl co-enzyme A (HMG-CoA) reductase inhibitors, also called statins. Statins are widely recognized in the treatment of hypercholesterolemia in humans.’ 1
What is all this about? Basically if you have fewer LDL receptors (LDLR) there will be slower clearance of factor VIII (a key blood clotting factor) and the level in the blood rises. If you increase LDL receptors, by using statins, more factor VIII will be removed, and the risk of blood clotting will fall. So, here we have statins reducing the risk of cardiovascular disease by increasing the number of LDL receptors on the liver, which causes factor VIII (a blood clotting factor) to be removed from the blood.
In addition to this LDL interacts with platelets (the key blood cells involved in blood clotting) and the more LDL you have, the greater the tendency of platelets to clump together:
‘Platelets and lipoproteins are intimately involved in the pathogenesis of a wide variety of disease including atherosclerosis, thrombosis, and coronary heart disease. Evidence accumulated over the years suggests the possibility of a direct relationship between plasma lipoproteins and the hemostatic function of platelets. A number of studies demonstrated that native LDL enhanced the platelet sensitivity to stimulation and induced platelet activation.’2
In short, LDL activates platelets, and activate platelets are the starting point for blood clot formation.
The enormous complexity of the clotting system is further revealed when we look at High Density Lipoproteins (HDL) a.k.a. ‘good’ cholesterol. It is widely accepted that HDL is protective against death from CVD. It is generally believed that this protection comes through the process of reverse cholesterol transport i.e. HDL sucks cholesterol out of plaques. [Which I do not believe]
However, this is almost certainly not how HDL works. It has other important and potent effects on blood coagulation:
‘….Furthermore, HDL stimulates the endothelial production of nitric oxide and prostacyclin, which are potent inhibitors of platelet activation. Thus, HDL’s antithrombotic actions are multiple and therefore, raising HDL may be an important therapeutic strategy to reduce the risk of arterial and venous thrombosis.’3
VLDL (triglyceride)
Finally, for now, what to triglycerides do – with regard to blood clotting? More jargon here, but a very powerful statement linking VLDL/triglyceride levels to blood clotting.
‘Activation of platelets and the coagulation cascade are intertwined. VLDL and remnant lipoprotein concentrations are often increased with the metabolic syndrome. These lipoproteins have the capacity to activate platelets and the coagulation pathway, and to support the assembly of the prothrombinase complex. VLDL also upregulates expression of the plasminogen activator inhibitor-1 gene and plasminogen activator inhibitor-1 antigen and activity, a process accompanied by platelet aggregation and clot formation. The surface membrane of activated platelets also supports the assembly and activity of the prothrombinase complex, resulting in further thrombin generation and amplification of the coagulation cascade.’4
If you don’t like the jargon, I will simplify:
- High levels of LDL increase the risk of blood clots forming
- High levels of HDL reduce the risk of blood clots forming
- VLDL/triglycerides increase the risk of blood clots forming
To this, I will just add that ‘oxidised’ LDL is particularly pro-coagulant. It reduces Nitric Oxide synthesis in the endothelium, triggers platelet activation and damages the endothelium. Thus the condition known as ‘dyslipidaemia’ is particularly dangerous. Dyslipidaemia consists of low HDL, high VLDL and more ‘oxidised’ LDL. It is usually caused by insulin resistance a.k.a. the metabolic syndrome a.k.a. pre-diabetes.
So, ahem yes, blood borne lipoproteins do have a role to play in CVD. The role is not key, but it is there. I thought I should get that off my chest.
References:
2: Yashika Gupta, V. Mallika* and D.K. Srivastava: ‘INTERACTION OF LDL AND PLATELETS IN ISCHAEMIC AND ISCHAEMIC RISK SUBJECTS’ Indian Journal of Clinical Biochemistry, 2005, 20 (1) 97 – 92
Dr. Malcolm Kendrick 
very good
Dear Malcolm
12 parts is not too long to explain such a critical illness and cause of mortality and a great series of articles.
Your four stage process is pehaps better described as a four stage or four phase equilibrium cycle – assuming, as I think you imply, that each of these are reversible processes and therefore if one encourages the reversing, positive or beneficial reaction or process, one might undo some or all of the damage and have an overall positive effect on one’s chance of suffering CVD.
Is that the ultimate outcome of your article? To suggest or show that one can not only prevent or reduce the outcome of a fatal clot and heart attack, and to actually reduce the damage already done and reduce that likelihood?
Look forward to number 13 … and the conclusion!
Lovely
Are you saying here that you have changed your mind somewhat on the role of lipoproteins? It would seem so from the use of “ahem” and “mea culpa”
I have not changed my mind. I have known for many years that LDL and HDL and VLDL have a role in clotting. So they have a (minor/secondary) role in CVD. But not through the currently accepted model. I have not really talked about this up to now as, without explaining the ‘clotting’ model, I thought it would just be too confusing. So, I have been a little economical with the facts up till now.
Brilliant, once again. Hats off to you…or “hoots mon”!
Failed CETP-inhibitor trials support that the effect of LDL and HDL on clotting is minor/secondary. All these drugs lowered LDL and raised HDL significantly, but saw absolutely no meaningful clinical improvement.
Very interesting Malcolm – does that mean that since high LDL/low HDL directly increases the risk of coagulation, and blood clots forming (i.e. there is a causation, rather than just an association) anything that reduces LDL/increases HDL is a ‘good thing’ (putting aside the side-effects for the moment)… Including statins and sterols?
And if so, why does the research on statins suggest that they have very little effect on reducing the risk of death in those who have not already suffered from heart attacks – is it because the link between high LDL/low HDL and clots forming is a weak one, or are there other factors at play??
Makes things clearer, but what are high and low levels of HDL And the others?
Thank you for all the work you put in.
Fascinated to know how you will draw all this to a conclusion.
Great input to my constantly increasing confusion about these lipids!
Reminds me of what the eminent physicist John Gofman arrived at 60 years ago when he, to the uninterested and ignorant medical establishment, sorted the blood lipoproteins of different densities with the help of the ultracentrifuge from his nuclear science activities.
Thank you Dr Kendrick for this interesting article. To Dr Sjoberg, I have a book by John Gofman about radiation. I am wondering if mammography harms the heart.
As far as I understand what I have read about Gofman I guess he wanted to compensate for his involvement in the nuclear programs during the 40-th by doing something “good” in medicine with his sophisticated equipment but when he realised that he was facing a dogmatic establishment incapable of handling his type of equipment on top of being uninterested in real science about the blood he turned his back on them and went his own way by focusing on radiation.
On top of my head I remeber he claimed that there is no ‘innocent’ low levels of X-ray exposure and tried his best to get that message across to the public. Should be in your book.
Yet more useful information. Thank you Dr K.
Thanks. I shall have to slightly amend my usual anti-statin rant.
The problem the layman has Doc, is your failure to amplify conclusions. You put forward your hypothesis and then dont explain it.
I will get there in the end.
Not too long to wait I hope?
You can’t keep us waiting another week for the next part. Such a delay cannot be accepted by the ethics committee. That would be torture. 😉
So, the good Doctor has given us something to chew on. The answer does not come immediately, we must think on this, research some more, and wait in eager anticipation for the next aspect. But based on history of this series, each new blog will carry a surprise – that I am looking forward to. Thanks for your input. The key to me that we all need to learn is that there are no easy clear cut answers. The whole CV disease process/ CV disease repair process is a complex balancing act.
I am beginning to think the good doctor is making us find our own answers. I could be wrong on that. I find myself finding more answers on my own or through each of you. He is the professor par excellence. He lays out the Course Outline and allows us to ponder. Hmmm. Super Bowl of my life.
Maryl
I believe Dr K has said two things about the end of this series:
Firstly when he reached the end there would be suggestions for how we should comport ourselves.
He also said that he suspected we would have worked out a lot of it for ouselves.
I personally havé read a lot of the books and papers that are quoted, being immobilised for the winter helped.
I think I see more clearly now. Whether that is right we will find out.
Great read, as usual.
Thank you Doc for your efforts in this very complicated subject. In the meantime I guess I still have to swallow that wee pill every day, having had a heart attack about 12 years ago. 3 stents in the right coronary artery. But still going strong so far at 69.
Thanks for this series of articles. As a scientist, I like to understand the disease mechanism or processes that the drugs are trying to resolve. Surely the medical profession’s emphasis should be on avoiding damage to the arteries in the first place rather than intervening in the repair mechanism.
Also, as cholesterol is important for brain function, is there any evidence to suggest that the blanket prescription of statins to anyone over 50 is increasing the incidence of dementia?
Sue, I’m a scientist but I try to read and observe. My brother was losing his memory until he finally stopped taking statins. Dr Mark Porter reported the same effect in his Times column. If you do a simple search for the low fat diet and anxiety or mental health, you’ll find some intriguing stuff. Stephanie Seneff at MIT in America believes statins and the low fat diet are the main suspects for Alzheimer’s. She has numerous talks on YouTube and has published extensively.
I appreciate it can be dismissed as ‘anecdotal’, but when I abandoned the low-fat diet after twenty years I felt a rapid surge of energy, both physically and mentally. I now take coconut oil each day to supply extra fuel to the brain. Dr Mary Newport in the US wrote a book on coconut oil after seeing significant improvement in her husband’s Alzheimer’s after taking it. I believe denying our brains fats and sufficient cholesterol has done huge harm to mental health.
Stephen T
I agree with you whole heartedly.
And when I finally understood what PKCS9 drugs do, turning off gene receptors, I was horrified at this madness8
Coconut oil is potent antimicrobial, antifungal… that’s why it worked on Dr. Mary Newport’s husband – until it didn’t any more (microbes adapted).
Stephen T. I’m with you all the way. Thanks for summarizing so well.
Two very good questions! My simplistic view is that statins do indeed affect the lipid balance in the body, but their method of so doing is analogous to cracking the nut with a sledgehammer.
There appears to be significant evidence both through studies and patient reported outcomes, that they do, in fact, affect cognitive function. For many years, I could not think my way out of a wet Kleenex. I think it was statins. What else?
I was blinded (both eyes, SAME [lower right] quadrant; for about 45 terrifying seconds, recovering over about 10 minutes in November 2015. Guess it was TIAs. Live in USA – no insurance, no money, so no MRI. bp was about 170/110, about 7-8 AM. None since then. I’m 63, father died at 55 of heart attack.
I am very interested in your work. Want to hang around for awhile. Very high stress job – teaching science, math, technology to behavior-challenged students.
Thank you for the continuous high quality information.
Larry
Larry K:
Have you considered your experience might
have been migraine? Scintillating scotoma.
Many people I know get this type of partial
temporary blindness.
Larry K, Look up or Google, Ocular Migraine.
A temporary blind or burry area in the visual field. This can occur with or without scintilations, which are little pin point bright white points of light, usually in the shape of circles or chevrons. Don’t get confused with migraine headaches, there is no pain involved and ocular migraines are a totally different thing. I get them sometimes when I don’t feel good. For me they last 10-20 minutes and than fade away. I must admit, it is strange to be looking at something you know is there but can’t see it.
THANK-YOU! Google images even had good representations of the phenomenon. Mine were generally zig-zag bright grey delineations around the blinded area.
Mike:
Yes, that is what I meant.
Thankyou Mike!
I have been experiencing this sort of thing for the last 31years or so. I tried explaining them to my then doctor and to opticians, none of whom seemed to remotely understand what I was talking about. I gave up!!!!!!!.
Eventually, I read an account by a migraine sufferer of the associated “visual disturbances”, so I had made some sort of connection, but still couldn’t understand why I only once suffered a full on migraine headache.
Now I know what to be looking for!
Carol
Count me in too. I’ve never experienced the actual migraine headaches, but I’ve had the visual distrubances. To me, they reminded me of an aeriel view of a campfire, surrounded by logs. The campfire seemed to keep enlarging, and the logs around the fire twinkled like they were burning too. I had several episodes of this odd phenomenon about 10 years ago and then never again. Weird stuff.
Larry;
You are a Star *
Interesting, I’m wondering why HDL increases NO2 production in the endothelium?, it does suggest there is some sort of non-inflammatory reaction between the two?
Also this suggests the PCSK9 inhibitors will also work by making more LDLR available to remove the FVIII… (PS any idea why FVIII is getting caught by LDLR?)
As ever thanks for the update, keeps my brain working!
But none of us gets our LDL measured, it is always calculated (in the UK). And if you have low triglycerides (like I do 0.4) and high HDL (like I do 3.24) then the Friedewald forumla which the labs here use to calculate LDL is very, very inaccurate !
What you need to calculate LDL with low triglycerides is the Iranian formula. A calculator using it can be found here:
http://homepages.slingshot.co.nz/~geoff36/LDL_mg.htm
Yes I’ve been using the Iranian formula since it came out a few years ago. But it’s still not accurate for LDL. I have asked for direct LDL measurement but that has been refused.
So …. high LDL is definitely bad, yet I seem to remember in previous discussions the consensus is “my LDL is x but the measurement is meaningless so who cares?”.
Others say all that matters is the HDL, triglycerides and the ratio of the two.
I don’t think I’m alone in my confusion – could we possibly have a couple of explanatory sentences please?
A reiteration of a previous post (in the post discussing Calcification and Lp(a)). High levels of Lp(a) cannot be reduced by Statins. However, it can be reduced with Niacin & a few other supplements. Additionally, the lack of sufficient vitamin C causes little LDL (Lpa) to take on the role of collagen repair, adding to/creating/increasing the likelihood, of a clot.
In my opinion, people with higher than normal LDL (or anyone for that matter) should have their Lp(a) level checked as the treatment for high Lp(a) should not be Statins (as will be prescribed by most Cardiologists) but other remedies as described in the previous post/comments.
Which is vitamin C, correct?
Danny, from the Delta intervention study it looks like simply lowering carb intake would have a significant effect on Lp(a)
‘The subjects consumed an average American diet (AAD; 36% of energy from fat) and 2 additional diets in which 7% of energy from saturated fat was replaced with either carbohydrate (CHO diet) or monounsaturated fatty acids (MUFA diet).’
…
‘Lipoprotein(a) concentrations’ increased with both the CHO (20%) and MUFA (11%) diets relative to the AAD
http://www.ncbi.nlm.nih.gov/pubmed/18065577?ordinalpos=7&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
So many of the things being discussed here can be improved by simple dietary changes: Eat fewer carbs, more saturated fats, no added polyunsaturated fats and not too much fish oil, supplement in moderation. Get a few fresh vegetables.
Harking back to the sunshine post, modest meat consumption, a little sun and not too much fibre seem to be the keys to having healthy vitD levels:
‘Meat and fibre intakes showed significant negative and positive associations respectively with rachitic and osteomalacic relative risk’
…
‘The negative association of meat intakes with rachitic and osteomalacic relative risk was curvilinear; relative risk did not fall further at meat intakes above 60 g daily. Daylight outdoor exposure showed a significant negative association with combined relative risk ‘
http://www.ncbi.nlm.nih.gov/pubmed/16351777
Eating meat will also keep your levels of vitC up.
Craig – Great points! And yes, the reduction of Lp(a) – like almost anything, is a combination of several/many things. My reduction (by over 50%) was probably due to a combination of a lower carb/no sugar diet (your points), more sunshine (I moved from dark WA state back to Texas), as well as the supplements mentioned.
Another great pointer – for everyone, not just high Lp(a) persons, is to get exercise! Out of all the things we discuss here, body movement is probably the most important. Unfortunately, when one speaks of “exercise”, we often think of gyms, weights and jogging. In reality, simply walking, standing and bending a great deal throughout the day is often enough for most people…
It is interesting that blood clots serve more functions:
Interaction of Pathogenic Vibrio Bacteria With the Blood Clot of the Pacific White Shrimp, Litopenaeus vannamei (Chaikeeratisak, 2014)
“In addition to its roles in hemostasis and wound repair, the blood clot plays an underappreciated role in innate immunity, where the established clot serves as a barrier to microbial penetration into the internal milieu and where the early clot entraps and immobilizes microbes that have entered wounds to the integuments. In this report we document the behavior of the pathogenic gram-negative bacterium Vibrio harveyi that has been entrapped in the fabric of the extracellular blood clot of one of its target organisms, the Pacific white shrimp, Litopenaeus vannamei. The freshly entrapped bacteria are held tightly by the clot, losing even Brownian motility, but by 1 h post-entrapment, a fraction of the bacteria have established small domains of fibrinolysis that enlarge progressively, enabling bacteria to escape from the clot’s embrace. Escape is dependent on the actions of both serine- and metallo-proteases released from the bacterial cells. ”
Capture of Lipopolysaccharide (Endotoxin) by the Blood Clot: A Comparative Study (Armstrong, 2013)
“n vertebrates and arthropods, blood clotting involves the establishment of a plug of aggregated thrombocytes (the cellular clot) and an extracellular fibrillar clot formed by the polymerization of the structural protein of the clot, which is fibrin in mammals, plasma lipoprotein in crustaceans, and coagulin in the horseshoe crab, Limulus polyphemus. Both elements of the clot function to staunch bleeding. Additionally, the extracellular clot functions as an agent of the innate immune system by providing a passive anti-microbial barrier and microbial entrapment device, which functions directly at the site of wounds to the integument. Here we show that, in addition to these passive functions in immunity, the plasma lipoprotein clot of lobster, the coagulin clot of Limulus, and both the platelet thrombus and the fibrin clot of mammals (human, mouse) operate to capture lipopolysaccharide (LPS, endotoxin). The lipid A core of LPS is the principal agent of gram-negative septicemia, which is responsible for more than 100,000 human deaths annually in the United States and is similarly toxic to arthropods. Quantification using the Limulus Amebocyte Lysate (LAL) test shows that clots capture significant quantities of LPS and fluorescent-labeled LPS can be seen by microscopy to decorate the clot fibrils. Thrombi generated in the living mouse accumulate LPS in vivo. It is suggested that capture of LPS released from gram-negative bacteria entrapped by the blood clot operates to protect against the disease that might be caused by its systemic dispersal.”
Since Vitamin C as well as lysine is involved in maintaining and repairing the proper way, with collagen, me thinks the first step in preventing is making sure there is always an adequate supply of both. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4447075/
The trick is of course, how do we get adequate levels? Supplements? Fruits and Veggies? We know all too well that many veggies don’t have the listed amounts by the time they arrive on our plate. Dr, Ken Walker MD (Gifford-Jones) is in his 90’s still trekking through all of Canada and telling people to get Vitamin C in a form that supposedly guarantees a better end result.
Whatever shape or for, I do believe that Vitamin C appears to play a crucial role and I for one prefer prevention over repair
Hi, do you supplement with Vitamin C and if you do how much do you take.
Harriet, I supplement with a sugar-free chewable tablets. I found that a lot of products on the supermarket shelves contained Aspartame as a sweetener, so I had a look online. I believe the FDA refused a licence for Aspartame seven times before they finally gave in to lobbying. Coca Cola use it in some of their awful drinks. So, I got some vitamin c tablets made in Preston by a company called ‘Nature’s Aid’. Each tablet is 500mg, which is 625% of the RDA. I only take one a day but two would probably be better and I know that people take much higher quantities. I understand that our bodies don’t store vitamin c, so a tablet in the morning and another at night seems to make sense.
Might I suggest a “slow release” Vitamin C”. As you point out, since vitamin C is water soluble, to keep the level up all day (and night), there are slow release varieties. Here is one that I order from Amazon: http://www.amazon.com/Foods-Vitamin-Sustained-Release-Tablets/dp/B0013P1GD6?ie=UTF8&psc=1&redirect=true&ref_=oh_aui_detailpage_o04_s00
As to dosage, since my Lp(a) is very high, I try and take from 3,000-5,000 mg (3-5 grams) per day. This is way above the “normal” amount, though the “adult dosage” is much too low in my opinion.
All one has to watch for with high vitamin C dosages, is after daily intake of about 1-2 grams, one should slowly build up the dosage over days/weeks as it may cause bloating, gas and possible loose bowels. Once the body gets used to it, there are usually no more issues.
I am a ‘6-grammer”.
Dissolved in a glass of water I sip it now an then during the day. Having read Linus Pauling’s books I tend to believe that there is something in high dose vitamin C. I doesn’t seem to hurt.
I just finished the glass from yesterday and am now to make a new glass to put on my night table.
Dr Suzanne Humphries recommends nutribiotic sodium ascorbate, can buy on Amazon or
I Herb USA.. I think we need to take care where to buy supplements, do our homework, Have only just started to take Vit C and since watching Dr Humphries will buy that brand next.
Dr Kendrick, thank you again for a damn good read. It is so helpful that you bother to give this information in a manner that we may understand.
James
Many thanks for the link.
Lp(a) It is found in animals that cannot synthesize vitamin C (Humans) – and are therefore at high risk of scurvy In short humans!
This seems to suggest that Vitamin C is of value in heart disease.
There are studies that show that it is of value. A Dr FR Klenner has many reports on its value in infections
http://www.odt.co.nz/print/126632
while Linus Pauling demonstrated its value in heart disease. But because it is not patentable it is called quackery. Human life is irrelevant in the search for money
Just trying to help – gorge on ascorbate if that is your wish – it is degraded to oxalate. Oxalate is a nephrotic poison and may form stones. What I read is levels start rising at about 1 g/d.
Ascorbate doesn’t have any magic properties, it is just a cofactor which you need enough of. Serious infection may require a lot of it, but quantity alone probably doesn’t put your immune system into turbo mode.
There could maybe be actual pharmacological effects at extreme levels in plasma, interfering with cancer and glucose metabolism (similar ring structure as glucose, same transporter), but for these you really should know what you’re doing.
Gollum
Why then did masive IV doses resolve the condition?
http://www.3news.co.nz/Living-Proof-Vitamin-C—Miracle-Cure/tabid/371/articleID/171328/default.aspx
This is the story of a NZ farmer who was condemned to death by doctors but saved by family insisting on Vit C therapy
http://www.odt.co.nz/print/126632
headed and ignored by medics is interesting.
Doctor does not always know best
The choice between turning off life support and death versus normal life following IV 50 g Vit C
I know which one I would choose but I am not medically biased.
http://www.RiordanClinic.org . Vitamin C
http://www.HealthHunterOnline.org Vitamin C
Mike, About massive vitamin C doses, am I right in thinking that these can cause stones in one of our bladders? What a choice CV disease or being cut up to the stones out!
Sent from my diPad, excuse les tipos, fautes d’orthographe etc etc.
>
Lets give our bodies plenty of quality nourishment.
I do not know.
Anecdote, miracle, ascorbate depletion, whatever. How much ascorbate did he have before the IV? Viral infections can suck up a lot of ascorbate.
I would certainly opt for ascorbate IV if there was a possible benefit (i.e. mechanism of action) for extreme doses, or just to faciliate uptake. Kidney stones would be my last problem.
All I am saying is these plasma levels are unphysiological. You cannot reach them even if you believe the fruits, I mean, fruitarians and eat 5 a day – 5 kg that is. The GI tract just does not allow it.
Since there are (mild) drawbacks to liberal use of the ascorbate powder (BTW. bodybuilder merchants usually stock it – along with other vitamins too – if your drugstore does not have these convenient 100 g cans for 3 bucks), you should ask what benefit this will give you. If you are not currently fighting a real nasty virus, my educated is that >1g /d will probably do more harm than good. It also interferes with ROS muscle rebuild signals and iron and whatnot.
That’s all I was saying.
Chris and Gollum
Most mammals excluding humans make their own vitamin C. The dog for example can increase its production some ten times when sufferering from an infection. If this is not valuable why on earth would this system have developed over millions of years?
The MHRA DAP for ascorbic acid is interesting. Since 1965 there have been a mere 70 SARs reports involving the single active constituent; this is about 8.3% of all reports suggesting that most reports involved other constituents, the implication being that the SAR may well be due to the other constituent. Furthermore, there have been only two deaths reported for ascorbic acid alone in over 50 years. Compare this with the with the 27 year total for simvastatin of 117 and 89 (in 19 years) for atorvastin single constituent deaths. These statins are prescribed like sweeties.
Going back to the DAP for ascorbic acid it might be of interest to check this for gall bladder ARs or urolithiasis. I found zero reports.
You must take account of the fact that Vitamin C is not patentable but has saved thousands of lives from scurvy. Like the work of Ko, Pedersen and Siegfried which is deliberately ignored by Big Pharma and the medical establishment 3-BP (not patentable) can get no money for clinical testing while £billions are spent on chemicals with little or evidence to support their use. Neither molecule can provided the profits which the money makers expect
An internet search on Klenner and Vitamin C/ascorbic acid might encourage you. Pubmed search on ascorbic acid comes up with 49,602 items. http://www.ncbi.nlm.nih.gov/books/NBK121338/ Is an interesting document on this much maligned vitamin.
Dear Mike,
Incredible thanks for all of the information”
In my circle of friends ans acquaintances, I am known as a Vitamine C bore. I recently broke two metatarsals, to speed recovery I upped the vitamin C to 1 gm per day with 5000 i.u. The orthopedist claimed to have rarely seen such a callouse around the breaks.
Mr. Chris,
I must say that I would love to see a proper RCT for Vitamin C. During the winter season following the NZ farmer report, as memory serves some 600+ patients died from “flu” pneumonia. I wrote/emailed the DoH and asked whether Vit C had been tried with any of the dying patients. The response was typical – we don’t keep records on that. In short the fact that 600+ had died was of no concern.
For your information, the Klenner regimen for oral therapy was to increase dosage to the point where the dose was not tolerated – diarrohea and then back off a bit. Dosage given several times a day. The IV route as a drip in that blood concentration can be maintaine and that it is all absorbed is said to be the most effective. Liposomal Vit C is said to be the best for oral administration but Big Pharma ain’t going to fund such studies.
When I started in research Governments funded most of it but then seemed to back commercial research and now even government funded research (eg Research institutes and Universities) can sell their research to Big Pharma with government getting little in return for providing tax-payers money.
The only way out is to take drug testing completely out of the hands of drug companies and have national agencies like NIH do the testing for which Pharma would be required to pay. Unfortunately, I don’t think that will ever happen.
Does that mean that statins are good if you have FH (Familial hypercholesterolemia)?
My understanding is that if you have true FH, the answer is no. This is because in that case the receptors are not working. So inducing the cell to increase receptor activity by stopping the production of cholesterol is pointless. There is good article by Zoe Harcombe on her blog reviewing a recent book on the history of the development of statins that you might find interesting.
How does one know if yoyu really have FH? Without medication my total cholesterol level is 9.
As I remember, Dr Kendrick discusses the issue of FH in his book about cholesterol. There are two kinds, a severe form in which both genes are defective and which causes a lot of problems, and a milder, much more common version where only one gene is defective. The best thing is probably to read his book (since he can’t respond to individual cases over the internet).
If you do decide to take statins, I think it is very important to watch out for side effects. There is no point in crippling yourself or destroying your memory even if statins extend your life!
Eugene
If you are worried about your total cholesterol maybe this website on its own won’t help.I use it as a base to convinced myself that my relatively high levels are not to be worried about. Mine last count was 7, I do not take statins and now don’t get asked to take them by my GP. FH is a genetic condition and I believe its treatment is complex but can include statins. If you are worried see a doctor. Good luck.
#1, The rusting car analogy is a good one since levels of oxidative stress that are not adequately countered by antioxidant process hasten the advance of disease.
#2, Endocrine disruption brought on by fear or stress seems to add to the levels of oxidative stress that prevail, does it not?
#3, Mention of oxidised lipoproteins (as in the study cited)incites a little distrust in me since to my pedantic mind lipoproteins cannot become oxidsed. Liporptoens are entities made of components. Only one or more components within lipoproteins can become oxidised. One component with particular scope for oxidation is cholesterol. Cholesterol can form up to 49 alternate oxides of cholesterol. Each of these oxides of cholesterol will have unique biochemical properies. The effect of 25-hydroxycholesterol upon cholesterol synthesis in macrophages and hepatocytes is interesting, as is the sulphated version of that oxide.
#4, Form a systems analyst perspective thrombosis requires some changes in the forces acting. Subject to my terminology being correct [platelets become ‘sticky’ and start forming clusters. Forces of attraction are at work. It could be a case that potentials resting on the surfaces of cells and platelets alter thus opossite charges attract. Alternative since intervening mediums are involved it could be a case of likes-like-like attraction where charges induce opposite charges in the intervening medium and thus the likes can attract via induction in the medium. Do any of the papers that discuss thrombosis make any reference to the electrochemical forces at work, to protonation and to deprotonation, that alters the balance of charge separation, or do they just ignore it?
Many do concede that inflammation accompanies the process, but inflammation is no more than a fancy word for heat, or more heat than is usual. What is the source of the heat> Might it be increased electrical activity at a molecular level. Insofar as I know heat could be produced by quantum effects that are inherent to biochemistry, or to by the exchange of electrons that is a big feature of how biochemical interact. Right at the roots of this is the degree of protonation / deprotonation arising, and this has consequences for the resting potentials of cells in general, and for the zeta potentials of cells held in suspension, as in blood.
LDL whether high or low (whatever that means) only relevant if any “clotting” actually needs to “happen” … so,? 🙂
Ah Chris, you have the same question as me, what is high what is low. My lipids man is convinced my LDL is too high like 135, Barry Groves in his excellent book says 215 total is too low. So what should I think, am I OK but confused?
is there a solid recognized guideline for Lp(a)? My blood test results put it at 300 mg/L (75th percentile) may indicate an independent risk factor for CAD.” 12 years ago my level was 960 mg/L and I have brought it down to about 500 with high doses of Niacin (3,000mg/day) but it still varies between 400 and 600. I have been diagnosed (via angiograms) with CAD but blockages seem to be lessening and colaterals have developed so I’ve never had a stent. I wonder if I’m at the minimum level of Lp(a) or is there more I can do? My cholesterol is fine although I am on a low dose of Lipitor, which now seems to be a good think because of my diagnosed CAD.
I contine to enjoy these articles, written for the layman to understand, and I am thankful for Dr. Kendrick sharing his observations on this very complex subject.
Gerry, I also have high Lp(a). And since Dr. Kendrick (and others) think that Lp(a) acts as a quasi-substitute for a lack of vitamin C, I also take 5 grams of C per day. I was able to lower my Lp(a) by 1/2 (also) with Niacin, though not as much as you (only 1500mg). I also take magnesium, vitamin b, c, d and fish oil. As well as Lysine as a previous poster has mentioned. There is also a theory that vitamin K will reduce existing calcium and/or Lp(a).
My CAG score was also high but no blockages. I am due for another one in a month or two. Will be interested to see if all my work can actually lower the score – or if I am destined to be come an arterial calcium statue…
Danny, thank you for your advice on vitamin c, which I will use when I buy again. Does Lysine assist vitamin c? Do you have a source you’d recommend?
Stephen – Yes, Lysine does (somewhat) assist Vitamin C, though both lysine and vitamin C assist in collagen formation, which helps the body build connective tissues, including healthy arteries. With that said, one needs to be a bit more careful with Lysine as it is an amino acid, so humans don’t need as much as vitamin C.
The Lysine I purchase is here: http://www.amazon.com/Amazing-Nutrition-Formulas-L-Lysine-Respiratory/dp/B00V3MR88G?ie=UTF8&psc=1&redirect=true&ref_=oh_aui_detailpage_o07_s00 I only take one of these per day, though I know others may take a bit more.
Vit K2
Hello, its been 6 years since this post how are ya doing?, curious to know what the results of your CAG where?. I also have very high Lp(a). Do you continue to take the Vit C im looking for supplements suggestions.
Best, Vic.
You may like to read my book. The Clot Thickens. It covers this area in some detail.
Hello, ordered it yesterday!, thank you for sharing all of your work!.
Gerry,
Few have more severely blocked arteries than myself, since 17 years now. The angiogram didn’t lie!
Though, I would never dream of taking any statins, stents or any by-pass operation from what I have learnt during these years. Malcolm’s blog just reinforces my decision to stay away from this medical craziness.
Why not get a stent?
commenting101
That was also my idea 1999 but my case was too ‘severe’ for stents to bring any benefit as they told me.
Today, though, I don’t se any benefit in such stent procedures either. The statistics are against such interventions. My own successful experience tells me that you first of all must take responsibility for your own health by changing what you put in your mouth instead of trusting a corrupt and criminal medical system to clear up the damage already done in your system. Anyway it doesn’t hurt to give a healthy lifestyle a serious try. Out with all sugar and the PUFA’s is a good start.
Has anyone read “The Cholesterol Lies” author, Prof.Dr. Walter Hartenbach? For me as a none medical person the message seemed very clear ” lowering cholesterol is often unnecessary and harmful”. I’d be interested to hear views from others.
Cholesterol is natural and essential, so lowering it makes no sense but makes lots of money. There are numerous items on here and on Zoe Harcombe’s site that explain fully and clearly.
Ann Joyce, I can only tell you that I was put on fibrates for “suspicion” of a blockage. Within a short time, (few weeks), I began to experience unabated leg pain. Also six months from initiation of fibrates, I had a blockage. After learning fibrates might be the source of my pain, I was punished and placed on a simvastatin. Although my overall cholesterol was 121, I felt like I was dying. And, yes, I had another blockage during this time. I ditched the statins over 2.5 years ago. I also ditched b/p meds, and too many others to mention. I feel like a new person. I watch carbs, but am not overly attentive to the carbs. I did get rid of vegetable oils (nasty stuff) and now only eat butter, lard, or ghee. I eat eggs too. My memory is returned somewhat and I feel better than ever. There are other things I have done, but I won’t bore you. To me, lowering cholesterol with a pill was quite harmful unless you enjoy being in pain and feeling like you have the I.Q. of a grapefruit. Not much of a choice now is it? That is just my experience and that of many I have met along the way. Just say no.
Please bore me. I would like to know what these other things are.
Hi, how did you manage to ditch the bp meds. I am on these. Went to see a cardiologist a few years ago when my gp was worried about an ecg he gave me. The cardiologist said my heart was fine but could see some damage caused by the high blood pressure. This frightened me and a few months later when the doc suggested meds I started taking them. Wish I hadn’t and now struggling and frighten to come off them due to what the cardiologist said.
I think I did; when told about it I thought it was one of the well-known Taubes or McKendrick books, unfortunately, it was not.
He is generally right, in a practical, outcome-oriented sense but a lot of the things he claimed did not seem to check out with me, plus the novelty effect was not very there, me being well-read in lchf blogosity.
His style is also pretty repetitive and much of the pages are filled with quotes from newspapers. I’d rather read Nicolai Worm, if only he would get wise to the fattening effects of plant oils..
Like other comments, I would like to know if the adjustment of views on LDL now has implications for those who have high LDL? Should these people now be listening to medical advice about lowering it?
Red letter day – new episodes from both Game of Thrones AND Dr. Kendrick! Hard to tell which conclusion will be more exciting … great help to understanding to have the role of dislipidemia in CVD put in context.
Confused.com ! 😳
The clot thickens. Oops I mean, the plot thickens.
I can’t work out how to follow the comments without making a comment myself, but I haven’t anything inspiring to say other than ‘keep on keeping on’ Dr K. You say you’ll get there and we’re with you till the end however long it takes.
Thanks for bringing these details of cholesterol to the table, Dr. K! They fit just perfectly to the information we have about 4-HNE, the toxic oxidation product caused by seed-oils (omega-6). In this study they state that: “4-HNE content
were considerably higher in unstable than in stable plaques.”
The unstable plaque: a broken balance
http://eurheartj.oxfordjournals.org/content/30/15/1821
And this study calls this toxic byproduct as The Serial Killer: “Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance”
http://www.nature.com/cdd/journal/v20/n12/full/cdd2013138a.html
and mentions, that its formation is linked to oxidized LDL particles “LDLs can be oxidized by ROS from vascular cells. This leads to the formation of HNE and other aldehydes. HNE can form adducts with apoB.”
Omega-6 oils are also obesogenic and cause insulin resistance, thus causing doubling the damage to CV-health: “Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse”
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0132672
Ari. Thanks for this information. The sooner we can get certain polyunsaturated fats (mainly omega-6) severely restricted in the human diet, the better.
The C57Bl/6 mouse fraud!
Yes Dr. K, absolutely, but be wary of the C57Bl/6 mouse!
This mouse has been breed specifically to gain weight on a fat diet:
http://www.ncbi.nlm.nih.gov/pubmed/?term=borghjid+and+feinman
“In a paper for Nutrition Metabolism in 2012, he goes into detail about this ‘zero carbs’ mouse, known as the C57BL/6 (also as B/6 or Black six ) strain. It is used in the vast majority of mouse experiments and has been selected specifically to put on weight and raise glucose in response to a high fat diet. ”
“In sum, the response of mice to a carbohydrate-free diet was greater weight gain and metabolic disruptions in distinction to the response in humans where low carbohydrate diets cause greater weight loss than isocaloric controls.”
Review all studies with this mouse in mind. We know mouse trials don’t translate well to humans but trials with these mice are pretty well garbage.
High levels of LDL increase the risk of blood clots forming
High levels of HDL reduce the risk of blood clots forming
VLDL/triglycerides increase the risk of blood clots forming
Question. For people on Warfarin, at what point does the increased risk of blood clots warrant setting a higher target range? Instead of metallic heart valves being 2.5 to 3.5, should we now encourage 3 to 4.5 as it used to be?
Comment. I have noticed two tendencies in warfarin advice over the years. The first, ignores baseline measurement of natural difference and has tightened the range before you intervene. I once went from 2.2 to 5.5 and in both cases did NOT adjust the dosage and it stabilised naturally. It is a fact that when the range is naturally wide, intervention to restrict can create even wider swings. Second, the ranges have been shifted lower, thus 2.5 to 3.5 has become 2.0 to 3.0
Driven by the immediate surprise of the efficiency of the LCHF and the amazing recovery of the health for me and my wife (seven years ago) my scientific curiosity was ‘set on fire’ and that is also why I finally arrived here at Malcolm’s blog with all well read participants.
A real “treat”!
Here someone suggested me the reading of a “thick” book, “The Rise&Fall of Modern Medicine”, by the medical journalist James Le Fanu. I had some problems at first with the book, although it is well references, since it actually was a kind of general eulogy of the “rise” of modern medicine while I myself have profoundly revolted against it since my heart attack 17 years ago. While some fundamentals are uncontroversial (e.g. antibiotics) there is an underlying claim of successful cures, “victories”, all over the medical field which in my present world view is very far from the truth especially among the most common and most serious diseases, in our present day society; obesity, diabetes, CVD, cancer and psychiatric disorders.
Still I find strong merits in Fanu’s book and not least when it relates to my present bias towards the “really thick” and fundamental textbooks concerning how “life is possible” and can possibly work. Here I am now deep down in the standard textbook of cell biology, “Molecular Biology of THE CELL”, by Alberts et al., for the third time. When Fanu gets into the cell biology our views completely overlaps.
Medicine must by necessity be dogmatic since it is based on almost total fundamental ignorance while pretending that one knows what one is doing. This is the actual crucial ‘nimbus’ which surrounds and turn the GP into a “god” in the eyes of a common help-seeker and has so been since ‘eternal’ ‘shamanistic’ times. Along this line Fanu excels in the chapter “The Mysteries of Biology” but actually all along in his book when he points towards the fortuitousness of all medical discoveries – a strong point indeed!
To put i bluntly.
We don’t have more than very faint ideas how it “works” on the fundamental cell levels (‘secondary metabolic levels’) and much less so on ‘higher’ metabolic levels. Psychiatry is here the epitome.
And that is why the statin business is the scam it is for a scientific mind.
Gofam realised this 60 years ago.
People fear fear more than anything else. Any person, or group of people, who claim to know ‘how things work’ and thus ‘how to protect you’ will always be in a powerful position (so long as enough people believe in them). Whether or not statins work is now almost irrelevant. They are now firmly believed to be protective against death, they are the cowboy with the white hat, and this is one hell of a difficult position to shift.
A wonderful way to describe how we tend to follow as sheep. As a person who refuses to become a patient in the face of all the well meant advice I’m taking my health as an individual and am being critical of the medicine that is offered.
I often think of this quote:
“Doctors are men who prescribe medicines of which they know little, to cure diseases of which they know less, in human beings of whom they know nothing.” Voltaire
Ray
No truer words were ever spoken.
High levels of LDL increase the risk of blood clots forming
High levels of HDL reduce the risk of blood clots forming
VLDL/triglycerides increase the risk of blood clots forming
Question. For people on Warfarin, at what point does the increased risk of blood clots warrant setting a higher target range? Instead of metallic heart valves being 2.5 to 3.5, should we now encourage 3 to 4.5 as it used to be?
Comment. I have noticed two tendencies in warfarin advice over the years. The first, ignores baseline measurement of natural difference and has tightened the range before you intervene. I once went from 2.2 to 5.5 and in both cases did NOT adjust the dosage and it stabilised naturally. It is a fact that when the range is naturally wide, intervention to restrict can create even wider swings. Second, the ranges have been shifted lower, thus 2.5 to 3.5 has become 2.0 to 3.0.
Several commenters have mentioned niacin therapy. Does Dr Kendrick have any comment on that, in the light of this:
In 2011, the AIM-HIGH study proved there was no benefit to adding niacin to good statin therapy despite increasing HDL from 35 to 42 mg/dl, lowering triglycerides and lowering LDL. This and other studies showing no benefit of niacin therapy (and worrisome adverse effects) should have resulted in the total cessation of niacin prescriptions, especially in patients on statins..
Yesterday, the FDA announced it was removing from the market two drugs made by Abbvie, Advicor and Simcor, which are combinations of extended release niacin plus lovastatin or simvastatin, and removed its approved indication for niacin ER plus statin for lowering CHD risk stating:
https://theskepticalcardiologist.com/category/statin-drug-therapy/
https://theskepticalcardiologist.com/category/statin-drug-therapy/
Amie
Looking at the blog page you linked to, I wonder how sceptical a cardiologist he is?
Yes, I did find much of his blog content “problematic” as they say, but it is the findings of the FDA I am concerned about.
Thank you, Dr. K. I look forward to reading this very thoroughly on my long train journey tomorrow.
How treating 2 young twins with Niemann-Pick Type C with Cyclodextrin (sugar molecules) put the spotlight this food additive. In mice, cyclodextrin was able to reduce plaque and dissolve cholesterol crystals, which some research suggests could play a role in atherosclerosis, or narrowing of the arteries. http://addiandcassi.com/drug-rare-disorder-linked-reducing-cholesterol-plaque/#comments Melted away plaques http://arstechnica.com/science/2016/04/sweet-drug-clears-cholesterol-reverses-heart-disease-and-was-found-by-parents/ Huge battle with the FDA http://projects.wsj.com/trials/#chapter=1
Randall
very interesting.
Cyclodextrin promotes atherosclerosis regression via macrophage reprogramming (Zimmer, 2016)
http://stm.sciencemag.org/content/8/333/333ra50
“We showed that CD treatment of murine atherosclerosis reduced atherosclerotic plaque size and CC load and promoted plaque regression even with a continued cholesterol-rich diet. Mechanistically, CD increased oxysterol production in both macrophages and human atherosclerotic plaques and promoted liver X receptor (LXR)–mediated transcriptional reprogramming to improve cholesterol efflux and exert anti-inflammatory effects. In vivo, this CD-mediated LXR agonism was required for the antiatherosclerotic and anti-inflammatory effects of CD as well as for augmented reverse cholesterol transport. Because CD treatment in humans is safe and CD beneficially affects key mechanisms of atherogenesis, it may therefore be used clinically to prevent or treat human atherosclerosis.”
Recent advances in the use of cyclodextrins in antifungal formulations. (Macaev, 2013)
http://benthamscience.com/journals/current-topics-in-medicinal-chemistry/volume/13/issue/21/page/2677/
“Continuous retention of apolipoprotein B–containing lipoproteins in the subendothelial space causes a local overabundance of free cholesterol. Because cholesterol accumulation and deposition of cholesterol crystals (CCs) trigger a complex inflammatory response, we tested the efficacy of the cyclic oligosaccharide 2-hydroxypropyl-β-cyclodextrin (CD), a compound that increases cholesterol solubility in preventing and reversing atherosclerosis. We showed that CD treatment of murine atherosclerosis reduced atherosclerotic plaque size and CC load and promoted plaque regression even with a continued cholesterol-rich diet. Mechanistically, CD increased oxysterol production in both macrophages and human atherosclerotic plaques and promoted liver X receptor (LXR)–mediated transcriptional reprogramming to improve cholesterol efflux and exert anti-inflammatory effects. In vivo, this CD-mediated LXR agonism was required for the antiatherosclerotic and anti-inflammatory effects of CD as well as for augmented reverse cholesterol transport. Because CD treatment in humans is safe and CD beneficially affects key mechanisms of atherogenesis, it may therefore be used clinically to prevent or treat human atherosclerosis.”
In your title of this article, are you being funny, or did you just misspell “skeptic”? Regards, Carol Wright
Anyone here know of Lown?
Some concerned thinking, leanings toward change going on.
http://www.medscape.com/viewarticle/862417?src=soc_tw_160426-pm_mscpedt_news_lown
Known of him for many years. Great man. I talk about him quite a lot in Doctoring Data.
JDPatten
Thank you for letting us know about Lown!
It is encouraging to read that there are organisations fighting the obvious corruption in medicine. I now got the good feeling of the 70-th when I was young and fighting together with millions of young people all over the world “for a change”. But I agree that a major change in medicine has to come from the outside but sadly nothing points in this direction.
A positive sign might be that queen Elisabeth is monitoring her excellent (?) health by going LCHF. (Changes tend to go top-down!) I though wonder what she did with the birthday cake she was given from a grass root admirer.
Interesting that the Royal Family has espoused homeopathic medicine for the past 100 years – to which one may credit their robust health and longevity?
Well worth reading this Dr Lown reference
‘To this, I will just add that ‘oxidised’ LDL is particularly pro-coagulant’
Isn’t this the very thing which is increased by statins? Eg lowering the production of cholesterol via their action opposing hmgCoA reductase leads to an increase in the number of ldl receptors because cells are desperate to receive some of the dwindling cholesterol supplies. Thus more ldl is removed from circulation. However (glycated) oxLdl is not able to be removed by these ldl receptors so the proportion of it in circulation greatly increases. This is a BAD thing!
Statins have so many seriously umdesirable effects i don’t know why you’d feel even slightly embarrased for not mentioning one or two slightly useful ones.
Thank you.
http://www.bmj.com/content/353/bmj.i1246
And what about this one?
Re: “overestimation of benefits”
A lovely paper Paola yet it’s a pity it still pussyfoots a little in not completely refuting benefits which are not at all in evidence:
“Summary and conclusion
Available evidence from randomized controlled trials shows that replacement of saturated fat with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes. MCE findings add to growing evidence that incomplete publication has contributed to overestimation of benefits, and underestimation of potential risks, of replacing saturated fat with vegetable oils rich in linoleic acid.”
Not process.. but Cascade. Hence, “the Cardiovascular Disease Cascade”.
Eugene, after cholesterol level found then possible referral to lipid specialist here in UK. Other reasons why cholesterol could be high eg hypothyroidism which is blood test confirmed. Views on FH vary. Check this out eg Uve Ravnskov.
Eugene – my total cholesterol is currently 9.7. I haven’t got FH. The total is always in the 8s or 9s. It didn’t used to be that way, the total used to be just under 5. Then nine years ago I adopted a very low carb high fat diet (good fats, e.g. the fats in organically reared meat and in coconut oil) and my cholesterol steadily rose. At the same time my HDL rose loads, it’s in the upper 3’s, once reached 3.9 ! And my triglycerides fell to 0.4. That’s why my total cholesterol is high. The cholesterol ratio, that is the total with the HDL is always in the very protective range if you believe in “good” cholesterol !
Geeks only (and perhaps Dr. Subbotin)
Atherosclerosis- and age-related multinucleated variant endothelial cells in primary culture from human aorta. (Tokunaga, 2015)
“Endothelial cells were cultured from human aortas and inferior venae cavae of autopsied subjects ranging in age from infancy to 85 years. Endothelial cells in 32 of more than 100 attempted cultures were pure enough for evaluation. Emerged endothelial cells in primary culture were classified into two types: typical endothelium and variant endothelium. Typical endothelial cells were small, round to polygonal shaped, and were arranged uniformly. Their diameter ranged from 50 to 70 microns. Variant endothelial cells were larger, ranging from 100 to 200 microns in diameter, and giant endothelial cells measuring more than 250 microns in diameter were scattered among them. Variant endothelial cells were usually multinucleated and possessed endothelium-specific markers of vWF and Weibel-Palade bodies. No incorporation of [3H]thymidine was found in the nuclei of cultured variant endothelial cells. Although most cultured endothelial cells were of the typical type, variant endothelial cells were interspersed throughout the culture. The ratio of variant endothelial cells to typical cells correlated well with the severity of atherosclerosis, but less so with aging.
Although it is not clear if the multinucleated variant cells were formed before the formation of atherosclerotic plaque or after the plaque formation, they will contribute to further development of atherosclerotic lesions, which in turn cause malfunction of the cell membrane. We suggest that there is a cyclic effect of these processes for multiplication of the variant endothelial cells and advancement of atherosclerotic lesions.”
Errata: Should be: (Tokunaga, 1989), not 2015
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1880500/
Eugene and Conner. Here goes. This is the very short version and only applicable to me. Serendipity placed a huge role in my quest to feel better and more healthy. I was in horrific pain for so long and having exhausted all the prayers to the Blessed Mother (and the Big Guy above) I could muster, I happened upon a site called spacedoc. I read a book by Dr. Graveline about the dangers of statins, then read Dr. Kendrick’s first book. I also ordered Statin Nation I. I studied each of the major contributors to that film…a lot. In short, I came to understand that many of the illnesses we face today have a lot to do with oxidative stress and inflammation. I had plenty of each. Slowly, I began to change my eating habits to more natural forms of fat and vegetables. I also began to rid my life of as much stress as I could, but learned also that I could compartmentalize stress to better my life. You can’t get away from stress, you can only change how you perceive it. So the prayers helped because that is always how I handled stress in the past. I learned that prayers as I knew them, were nothing more than intense meditation or changing one’s behavior or attitude toward stress. From the time I was a child prayer always gave me a feeling that it would all be okay. I also read about bioenergetics, which fascinates me to this day. I started with purchasing a pair of all leather moccasins. I walked 1,000 steps in my yard three times per week or whenever I began to experience pain. I weaned off b/p meds, but my blood pressure remained normal or low. I had been duped into believing I had been chronically depressed all my life and that was why I had chronic pain. I decided I was not buying that one and ditched those too. To my utter surprise, I did not commit suicide. Who knew? I actually felt alive again. I learned that I was vit d deficient and from a friend of Dr. Kendrick learned to take 5,000 units per day. I also took magnesium 500 per day and coq10 to protect my heart. The rest of it I get from my diet. My diet is not high fat low carb, but rather saturated fat friendly and low carb. During the winter when it might be cold or rainy I purchased a whole body vibration machine and began to use it regularly. I saw muscle where before there was muscle waste. I have used it for quite some time and get as much from that as a brisk walk or run in a park. I still walk bare foot in my grass several times a week as well or just lay out in the grass to soak up some sun. I tried cbd oil to wean off the rest of the pain medications which heretofore I had begun to wean off naturally. I had not the first awful detox symptoms we hear tell of. I think overpriced “rehab programs” are also overrated. I do not have any significant pain. If I feel pain coming on, I get on my hypervibe on a low setting and within 10 minutes all pain is gone. Or, I take a walk barefoot outside (in the grass) and the mild pain goes away. I have pain medications just in case, but don’t really need them as before. I take virtually nothing really other than supplements as listed here and good food. I socialize more, laugh a lot, flirt a bit, and worry less. I listen to my instincts. I still pray. And, I am not quitting that. It makes me feel good and hopeful and serene. Yoga is just not my thing, but I have no problem with those who do it. Whatever works. None of these things happened in linear steps or over a short period but rather over a period of years. I may find I have cancer tomorrow and die. At least I feel human again and for that, I am eternally grateful. By the way, all lipid and metabolic levels are “normal” along with b/p. I feel good. But, to me, “normal” is never etched in stone.
What an encouraging story Mary. Thanks for sharing.
What an encouraging story Mary. Really good to read. Just goes to show how you can be set on the wrong track by others. I’m thinking of you being told you were depressed. How dreadful. Thank goodness you looked into it yourself. Carry on with what you’re doing, it obviously works.
Thanks Sue. I have been depressed when my cat died, my mom and dad or I had tough circumstances. But, is that not a natural part of the human experience that none of us save those who have no conscience can avoid? It is not. Given enough time and help, we can overcome a lot. I don’t fight those things any longer. They just have to happen and to me, they have to get better.
I agree Mary. It’s absolutely normal to be sad about something sad happening and unhappy when things go wrong. They are a human being’s way of coping just as grief is a natural response to losing a loved one. Sadly people are now told that they are ‘ill’ and given a pill, and it just makes things worse because then they feel inadequate, I aged of understanding that they are simply responding to life, which does sometimes knock us about a bit. Glad you obviously discovered that.
Mary, thank you for sharing your story. Can you tell me which sources on bioenergetics you studied?
Dr. Paul Rosch to me “wrote the book” on Energy Medicine. Look him up. He is amazing and brilliant. You can also find his articles on spacedoc. I encourage you to think outside of traditional medicine and open your mind to the many possibilities that nature can give us. Good luck!
Thank you
I have just finished my reading of “The Rise and Fall of Modern Medicine”. I my eyes this is a “great” book with a lot of unorthodox thinking outside the ‘box’. The author, James Fanu, is using the broadest of brushes to my enjoyment.
However what amazes me considering this ‘great’ attitude is that the author completely dismiss the role of our food involved in our diseases. This may be a side effect of his dismissal of the cholesterol hypothesis of Ancel Keys which he duly consider to be nonsense. It is an extraordinary fact that he doesn’t even mention sugar or PUFA’s in his book of almost 600 pages. To me this is just weird to ignore.
But how much does it take to recognise that if you are a diabetic you should not eat sugar?
Goran S,
I am glad that you enjoyed the Le Fanu’s book. He is an MD, not just a medical journalist as you referred to him in your earlier post. I just wanted to correct this description of the author in case other’s might be misled.
I enjoyed the book because of the way he approached the evolution of medical interventions, both from a biologic perspective and from a physical one, meaning hardware. In the early part of the 20th century, many biological processes were discovered which led to the development of chemical interventions to cure diseases. From insulin and penicillin to many more antibiotics, vaccines, and hormones which provided amazing results. Furthermore, technical advances in instruments to help diagnose problems such as the fibre optic scopes and microscopic glasses used in heart surgery led to significant advances in surgical interventions. As LeFanu stated, a lot of the chemical agents were discovered by chance (or sometimes employed in a fortuitous dose to be just right to be successful). Our understanding of biological processes was not strong, but was getting better, helped along by technological innovations in hardware.
But in the second half of the century, it was the technological innovations in hardware which continued to grow immensely, while our understanding of biological processes did not appear to keep up. LeFanu was critical of the vast sums spent on epidemiological studies and little on basic science.
I don’t think that his focus in writing this book was to provide answers or advice on how to become healthy. That is why, I think, that he did not delve into any recommendations of treatment for T2D, for example.
Now on another side topic – following below.
I have been reading a book called The Modern Nutritional Diseases, 2nd edition, by Fred Ottobani and Alice Ottobani, a husband and wife collaboration – both are PhD’s. For me this book was very heavy reading, filled with low level biochemistry, meaning complicated but not with equations of reactions, just flow diagrams. However, it was written in a very clear and attention grabbing manner, such that I found myself highlighting many sections (with a yellow pen highlighter) so that I could refer back to these parts again. The authors are clearly in favor of the LCHF way of eating but they also stress the importance of many different supplements and explain how these are involved in the metabolic processes. One of the key points they dealt with in detail was the impact of an imbalance in the n3 vs n6 essential fatty acids in the diet. They showed why and how such an imbalance causes harm.
In any case, I enjoyed the book enough to want to read it again as I did with Doctoring Data. I find that reading such books only once is not enough.
So, today I had an annual visit with my dermatologist (MD, specialist in skin disorders) so re-examine my skin which is inflamed around many parts of my body in the “bathing suit” area – waist, upper thighs, inner thighs, and recently a little area started on by chest near the armpit. Biopsies have been taken in the past and a tentative diagnosis of para-psoriasis was declared – no treatment, just watch and check annually.
This time I brought with me copies of some of the pages from the Ottobanis book which dealt with biological processes related to the skin and how these processes may be driven to cause harm instead of good. I provided copies of all the references and flow diagrams of the cascades of the biochemical stages in metabolism which appeared in the book together with the supporting text.
My doctor was not at all familiar with any of this stuff, and admitted that her knowledge of biochemistry was not strong and ended back in university before medical school. She heard of Omega 3 but was unaware of Omega 6!!! She told me that she would scan the stuff I brought her but did not believe for a second that my problem could be related to my diet. When I asked her why she believed that, her response was that I was in excellent health and physical condition, so obviously diet could not be the cause. I was very deflated by this approach to treatment to say the least, but not totally surprised.
The fact is that many, many doctors are not reading any material outside of what appears in their favorite medical journals. Similarly in their medical conferences, little if anything is discussed in the area of nutritional effects on disease. She told me that if you just avoid to much fat and salt (and something else which I didn’t catch) you would be fine. Wow!
So there you have it. She is treating me for a skin disorder which is not yet defined or diagnosed, therefore its pathogenesis is uncertain, but she is sure that diet could not cause it. Maybe she is right, but this is not good doctoring IMO. Unfortunately, it is very common I suspect.
I highly recommend the book, by the way, for anyone who is not turned away by some biochemistry.
Thanks for a new reading suggestion! The ‘heavier’ the better 🙂
Just now I am enjoying “Trick and Treat” by Barry Groves.
I am also waiting for Marcia Angell’s “The Truth About the Drug Companies: How They Deceive Us and What to Do About It. Random. 2004.” to drop down in my mailbox. And then, of course, Alberts et al. is always at my bedside.
Thanks, Goran, great reading recommendations. I will order these also.
John, sometimes we have to educate our doctors. I told mine about the low carb approach to diabetes and Dr David Unwin. I leant my practice nurse ‘The Big Fat Surprise’. At the moment, I think I’m doing more to help them than the other way around.
Yes I agree, but it is a fine line to tread sometimes. You don’t want to annoy them. Mine was obviously resistant to any information that I might be willing to share. It really was a case of “I am a doctor and you really don’t know enough to diagnose yourself”. Doctors are not much different from most ordinary folks.
John U
Great, I have just bought this on Kindle, at 7 euros 80 delivered immediately it will be great value.
A lot of people have shared their stories and knowledge here. Some have even sent an answer to me personally. My thanks to all. I have not replied to them separately, because I don’t wan’t to flood this blog. I am collecting and studying the replies and try to make a good decision for my personal situation.
I am glad this has happened. I always hoped that this blog may become both a useful discussion forum and also a place where people could, possibly, help each other.
“I am glad this has happened. I always hoped that this blog may become both a useful discussion forum and also a place where people could, possibly, help each other.” Dr K.
In that case, bit of a shot in the dark, but has anyone an opinion on current treatment for normal tension glaucoma (NTG), please?
My husband, who is very myopic, or short-sighted, has been putting eye-drops in his eyes three times daily (Ganfort once and Trusopt twice) for about 10 years for NTG. Amongst other things they darken the skin around his eyes and make him look as though he’s preparing for Halloween.) I am currently trying to investigate the subject and am confused by what I read. To quote/paraphrase a little of it:
High ocular pressures can cause glaucoma.
People with normal pressures can have glaucoma so we’ll treat it as though they have high pressure and reduce the tension like we do for people with high pressures, since we don’t have any other treatment to offer. And anyway, people with NTG may have thinner corneas which could make them seem to have lower pressures than they have.
We don’t know what causes NTG but a poor blood supply or weakness in the optic nerve could make the nerve vulnerable to normal pressure.
Meanwhile some other snippets:
The eye drops are absorbed systemically via the nasopharyngeal mucosa after passage through the nasolacrimal duct. “For this reason, local ophthalmic dosing is more akin to intravenous delivery than to oral dosing”. Hence, side effects from the carbonic anhydrase inhibitors, hypotensive lipids and beta blockers can be general and not just eye-specific.
Cystoid macular oedema is associated with ocular hypotensive lipids.
Some glaucoma experts ask, “How do you distinguish patients with myopia and glaucoma from those who have myopia-related visual field defects that may mimic glaucoma – but are not destined to show progression characteristic of glaucoma?”
“The detection and treatment of possible pathological ocular complications is essential in the management of high myopia. The ocular risks associated with myopia should not be underestimated.”
“This study has confirmed a strong relationship between myopia and glaucoma. Myopic subjects had a two to threefold increased risk of glaucoma compared with that of nonmyopic subjects. The risk was independent of other glaucoma risk factors and intraocular pressures.”
“65% of untreated NGT patients showed stable glaucoma with no deterioration”.
“The probability of blindness in eyes with NTG is much lower than reported in patients with high-tension glaucoma.” (bilateral blindness 0.3+/- 0.3% at 10 years and 1.4+/- 0.8% at 20 years).
“It is now widely estimated that a larger percentage of patients with primary open-angle glaucoma (POAG) are suffering from normal tension glaucoma: probably half of all POAG patients in Europe and the majority of POAG patients in East Asia.”
If it were down to me, my gut feeling is to stop the drugs and see…..
I’very been able to reduce IOPs with acupuncture before but if your husband’s IOP is normal I don’t know what marker you’d use to see if treatment is effective. If his IOP is elevated, have him look into acupuncture.
Dr. K, I believe it is working. Thanks for hosting such a great blog.
TS,
My ‘anecdotical’ wife with manifest glaucoma (and severe T2 diabetes) on one year with strict LCHF was no more diagnosed with this disease. Her severely impaired night vision returned within this year. Checking up by the optometrist it was just perfect today. How interesting are not those homeostatic ‘anecdotes’?
TS,
Are you aware of the website http://www.fiteyes.com. The folks there describe themselves as an “Eye Pressure Research Community & Support Group.” During the past decade, the site has evolved from a simple blog written by a fellow named “Dave” to a repository of a tremendous amount of info regarding eye pressure, in general, and glaucoma, specifically. It’s necessary to create a free user account at the site in order to access all of what it offers, but in the years I’ve been dipping in and out of the site, I’ve never been bothered by unsolicited emails or had any reason to regret joining. The stated reason for requiring the registration is so users read and agree to the medical advice disclaimer.
My sincere apologies to Dr. Kendrick if it is considered ill-mannered to direct someone to another blog. I just thought the FitEyes community is a resource worth knowing about for anyone dealing with eye pressure issues, but particularly to the people who visit this blog..
Also, Dr. Kendrick, while I have your attention, I want to say I’ve read your books and been following your blog for many years and am extremely appreciative for the time, effort and information you provide so consistently and generously. As I try to expand my thinking and continue my learning, I’ve referred to your writings time and time, again. A huge “thank you” to you and also to the many thoughtful and learned commenters who frequent this blog.
TS, I would not recommend stopping medications. Not at this point anyway. As mentioned, diet can help with systemic hypertension, so it may also help with ocular hypertension. If it does, and once the pressure is back down, reducing and stopping medication can be discussed with your doctor. Until then, this is a serious condition that can lead to blindness. The bimatoprost in Ganfort is what is discoloring the skin (and possibly growing the eyelashes and can also discolor the iris). Not much you can do to avoid this–all prostaglandin analogues do this. You may want your husband to try preservative-free version of these formulations to avoid the detrimental effect of these preservatives. And in order to reduce absorption via the nasolacrimal duct, gel formulations may be an option if the timolol in Ganfort is causing his heart rate to drop too low. I’m not a big fan of drugs, but at this point, given the ramifications related to glaucoma, I wouldn’t have him stop taking the medicine without follow up with his doc.
What can you do to control high blood pressure without the meds. Would like to come off them. Trying to wean myself off them at the moment. How long does it take for blood pressure to normalise after stopping them.
That you have done.
WHAT!!! From the American Heart Association “Atherosclerosis, formerly considered a bland lipid storage disease” http://circ.ahajournals.org/content/105/9/1135.full
Thank you for posting a link to this fantastic article… So much interesting information about the role of inflammation in atherosclerosis and MI.
(And I think your quoted sentence is simply saying that the process of atherosclerosis is much more complex than we ever thought.)
So – reading this interesting paper the obvious question would be: “What causes those inflammations?” (Inflammation could reasonably not be a ’cause’?) The same as that which causes paradontitis? Could sugar here be a culprit rather than the saturated fats and cholesterol?
The paper does cover this further on, and talks about the possible role of hypertension, diabetes, obesity, infection and high levels of sugar/fat in provoking inflammation.
There was no mention of smoking or stress, but I think these should also be added to the list…
The paper went on to mention CRP levels in response to inflammation, and how high levels of this marker can indicate a pre-disposition to MI/thromboses etc.
Dr. Goran, I do believe you are right on. Now when I eat sugar (I do you know at times), my teeth actually hurt. I rinse my mouth out. My mother died at the age of 86 with all her own teeth, a dazzling smile. She always rinsed her mouth after each meal and particularly when she ate sugar. Now, she was no scholar, but I am beginning to believe she was right. Now, I think you have something there. She never had gum disease.
Yeess. An interesting read but far from easy.
I needed Dr Google on every other line!!!!
Me too Christine… And still not sure I understood all of it!
Hi Everybody. The conclusion copied here:
Conclusion
Our understanding of atherosclerosis has evolved beyond the view that these lesions consist of a lifeless collection of lipid debris. Current evidence supports a central role for inflammation in all phases of the atherosclerotic process. Substantial biological data implicate inflammatory pathways in early atherogenesis, in the progression of lesions, and finally in the thrombotic complications of this disease. Clinical studies affirm correlation of circulating markers of inflammation with propensity to develop ischemic events and with prognosis after ACS. Intralesional or extralesional inflammation may hasten atheroma evolution and precipitate acute events. Circulating acute-phase reactants elicited by inflammation may not only mark increased risk for vascular events, but in some cases may contribute to their pathogenesis. This new insight into the role of inflammation in the pathobiology of atherosclerosis has initiated important new areas of direct clinical relevance. We can use inflammatory markers today for risk stratification. Future studies will gauge their utility as guides to monitor therapy. Finally, the quest to identify proximal stimuli for inflammation, as one pathogenic process in atherogenesis or trigger to lesion complication, may yield novel therapeutic targets in years to come.
The blog is undated (can’t obviously find it) though the copyright indicates 2016
Seems to me that these guys are struggling to catch up with Dr K. 😁
As Dr Sjoberg indicated lots re inflammation (hs CRP) with links to causes thereof. So it appears that Statins major benefit is reducing inflammation – but via a poor means.
Questions are:
What level of CRP is acceptable? CRP=2.06 (UKscale) : (done everything: LCHF (Prof Noakes), lower blood press (105/70), never smoked, minimal alcohol, lost weight (-22kg, BMI=23), almost daily exercise brisk walking 40 mins+ (could not do 5 mins when prescribed Statins))
And, how to lower usCRP? Curcumin?
Any suggestions will be appreciated ???
Regards Robert
The emoticon above was meant to be a broad smile somehow that did not happen, sorry
Robert Lipp
Isn’t CRP a marker, so reducing inflammation will reduce it, but no point in trying to act on it directly?
I just learnt something amazingly new to me in “Trick and Treat” by Barry Groves.
I have for many years as a “Low Carber” been aware of my improved immune system but what I now read in that book about the compromising power of ONE milk shake on the ability of the leucocytes to capture bacteria is astonishing. Evidently it was shown already 40 years ago that one leucocyte is capable of eliminating 14 bacteria per day but after the milk shake or a beer that capacity is reduced more than 90 % from 14 to 1 bacteria.
Mr Chris
Agreed: Isn’t CRP a marker, so reducing inflammation will reduce it, but no point in trying to act on it directly?
The problem is, as far as I am aware, I have done all the right things as per my post above
Copied here: (done everything: LCHF (Prof Noakes), lower blood press (105/70), never smoked, minimal alcohol, lost weight (-22kg, BMI=23), almost daily exercise brisk walking 40 mins+ (could not do 5 mins when prescribed Statins))
Yet CRP is still (I understand) too high. So if this is to be corrected at the root by diet/ natural means what more can be done (consume or do or supplement) to reduce CRP.
Suggestions will be really appreciated.
Thanks Robert
robert lipp
“Suggestions will be really appreciated.”
I will get many minuses for this opinion – but what about reconsidering LCHF diet? Not everybody responds in the same way to such a dietary intervention (and not everybody means the same when saying LCHF). You may miss fiber, micronutrients etc., too much fat may be considered as inflammatory by your body… Just an idea.
Diana and Robert Lipp,
My CRP reacts to infections like flu and nasty bout of diarrhoea contracted in Egypt, anything like that.
here is a Wikipedia link:
https://en.wikipedia.org/wiki/C-reactive_protein
which explains, I think very well, its function etc.
When you say that your levels are too high, how high are they? They normally come and go quite quickly, if they stay up you have an underlying source of inflammations, which a conscientious GP or hospital should be able to find
Diana
“Suggestions will be really appreciated.”
Thanks for your response, have been considering variations, but as you can see the “numbers” achieved are good except for CRP (2.06). Have considered less carbs (we have lots of green leafy veggies) and resistant starch. All with little logic/info. Was hoping for specific ideas – seems it will be hit and miss with expensive lipid tests.
There was an interesting letter in ‘The Times’ this week written by a doctor. He quoted research on doctors strikes showing that mortality fell during and after the strikes. When fewer people see their doctor, there are fewer questionable procedures, fewer mistakes and fewer side effects. Less medicine has its benefits.
Smile
When I was a young nurse, especially on night duty, when a patient was distressed, I always preferred to make a cup of tea and chat rather than give analgesics prescribed PRN. Not because I was so caring, all my set did this first before sometimes giving medication, use our judgement. So much medication now, side effects treated with further medication. The medical profession and our dying health service with those still caring deeply have my unstinting admiration. Dr Kendrick you are a maverick and the comments on here are fantastic.
Stephen T,
That may very well be the understatement of the century. I have to wonder too.
Saw a report today in the USA. There is no way to note on a death certificate a category that includes incidents of “physician error”. So, are we exposing our doctors to more litigation for being human or not making them accountable enough for interventions that they are not handling properly. It is a very valid question. I am not sure what the answer to that is.
Thank you for your comments. The main reason I posted the link is because I believe they are starting to move away from saturated fat as the big cause of plugging up of the arteries. To me this is a flip flop. Yes, I believe sugar damages the endothelial cells first. Then all the other stuff happens next. Why – no GLUT4 transporters in the endothelium. Cardiac Muscle has GLUT4 transporters – is that why I never read about plaque plugging up the heart?
Some things I don’t understand:
The body raises its temperature when it is suffering an infection, etc. – but we treat it as a wrong thing and think it necessary to try to lower the temperature.
The body uses inflammation to help assist in healing processes – yet inflammation is generally considered a foe rather than a friend.
The body raises blood pressure to help ageing blood vessels (among other reasons)? – yet older people want their blood pressure to be that of younger people.
The body perhaps increases eye pressure to help deal with a problem it has (sometimes caused by myopia)? – while we assume the pressure is the cause of something rather than a possible reaction.
Please correct me if this seems wrong.
Diarrhea is our friend, as is fever, perhaps inflammation and blood pressure. Why do we mess with the natural? To make a whole lot of money, that’s why and it makes some people feel smarter than others and superior.
Hi Dr Kendrick
I looked up glut4 but did not understand everything (what’s new), confused as it seems this is applicable to heart muscle (?) while we are interested in arteries and artery muscle – yes?
Regards Robert
Many thanks to all who have offered advice and information on eye pressure lowering/glaucoma. We shall certainly visit the fiteyes website Jacquie.
Any thought on baby aspirine? One of the things I would like to know is wether the benefit outweighs the possible harm. Further if taken for a while, will the damage to the body be reversed when this medication is stopped?
I still take a daily 75 mg aspirin, but I don’t take statins! The medical-industrial complex has no reason to push aspirin, and every reason to push statins! Thus my bet is that the value of aspirin is probably under-rated.
Also, aspirin also gets favourable mention as giving some protection against cancer.
Willow bark extract is more gentle to the body (stomach included), and quite potent…
http://umm.edu/health/medical/altmed/herb/willow-bark
“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.”
Inhibition of proinflammatory biomarkers in THP1 macrophages by polyphenols derived from chamomile, meadowsweet and willow bark. (Drummond, 2012)
http://onlinelibrary.wiley.com/doi/10.1002/ptr.4753/abstract
Antiinflammatory compounds in the diet can alleviate excessive inflammation, a factor in the pathogenesis of common diseases such as rheumatoid arthritis, atherosclerosis and diabetes. This study examined three European herbs, chamomile (Matricaria chamomilla), meadowsweet (Filipendula ulmaria L.) and willow bark (Salix alba L.), which have been traditionally used to treat inflammation and their potential for use as antiinflammatory agents. Aqueous herbal extracts and isolated polyphenolic compounds (apigenin, quercetin and salicylic acid, 0–100 μM) were incubated with THP1 macrophages, and interleukin (IL)-1β, IL-6 and tumour necrosis factor-alpha (TNF-α) were measured. At concentrations of 10 μM, both apigenin and quercetin reduced IL-6 significantly ( p < 0.05). Apigenin at 10 μM and quercetin at 25 μM reduced TNF-α significantly ( p < 0.05). Amongst the herbal extracts, willow bark had the greatest antiinflammatory activity at reducing IL-6 and TNF-α production. This was followed by meadowsweet and then chamomile.
According to the nnt website one person in 1667 might benefit from aspirin in terms of a first heart attack or stroke. No deaths were prevented and the site judges it ‘Red’, ‘No Benefit’.
http://www.thennt.com/nnt/aspirin-to-prevent-a-first-heart-attack-or-stroke/
I tend to believe in my “body” as being a marvellous “instrument” of telling me if I am “OK” – in the short as well as in the long run.
We have got an incredibly large number of sensors incorporated to monitor our physiology. Basically I am, for the same reason, sceptic to all those standard lab measurements done on a blood test sample to tell me to take all the medications although it is a challenge to start a discussion about the merits with your GP who is pointing to those measurements and the “guidelines” and at the same time is reaching for the prescription pad. I have been trough this a number of times and resisted on most occasions.
So in the long run my body has told me that I have turned into a pretty good shape and against all odds survived by avoiding the sugars and the PUFA’s, for 17 years now and during the last 7 by going strict on LCHF.
Still, in the short run I learnt the day before yesterday, when I had made a large pot of a classic meat stew for our guests (100 % LCHF) arriving late, that you shouldn’t overeat in the evening. Since the stew was a success among all I couldn’t resist in helping myself to several servings. And – going to bed I was again struck by my unpleasant angina of the unstable type which has been absent since I started my E-vitamine regime a couple of years ago. Evidently I am vulnerable.
So – I believe that you should “listen to your body” and incorporate whatever knowledge (could well be that you are not faring well on LCHF) to your set of concepts guiding you through the hazards of life.
At the end of the winter I always feel weary and down. This year after a miserable wet winter in the UK I have more fatigue. ? Lack of vit D. At the start of next winter will have a go with D .
Sensible enough to go to my GP for bloods if it persists. But the age thing happens does it not.
Could cut the grass, feed the baby, walk the dog, make a meal, clean the house, read a novel, with one hand tied behind my back it seemed. Have to pace myself now.
Dr Sjoberg, not just you, everyone is vulnerable. Our stomach produces most of its HCl in the first half of the day, hence a saying “Eat breakfast like a king, lunch like a prince, and dinner like pauper”. Since HCl is necessary to break down proteins, eating them late at night will create symptoms in almost everyone past certain age.
Hot of the press
N Engl J Med 2016; 374:1744-1753May 5, 2016DOI: 10.1056/NEJMoa1507750
Conclusions
In this trial, perioperative statin therapy did not prevent postoperative atrial fibrillation or perioperative myocardial damage in patients undergoing elective cardiac surgery. Acute kidney injury was more common with rosuvastatin. (Funded by the British Heart Foundation and others; STICS ClinicalTrials.gov number, NCT01573143.)
Collins is an author
Mike, is that the same Collins who said statins had few and only trivial side effects? Now that PCSK inhibitors are available and cost 12 times as much, suddenly statin advocates have discovered side effects. It’s a good job I trust these people so completely or I might think they were cynical opportunists.
120 times as much
I’m rather simplifying here, but in general, drugs work via gut flora (so do statins), which is often ignored. So what is the official “fairy tale” for PCSK inhibitors?
A-ha. Haha. Makes me want to look at their antimicrobial effects….
“When PCSK9 binds to the LDL receptor, the receptor is broken down and can no longer remove LDL cholesterol from the blood. If PCSK9 is blocked, more LDL receptors will be present on the surface of the liver and will remove more LDL cholesterol from the blood.”
(Yes, monoclonal antibodies are exepensive. For instance, Yervoy is more expensive than gold. But Yervoy only works when certain “good” commensal flora is present, otherwise not.)
Now I really need input from my kindred spirits. I have had an angio. On this angio they seen 2 blockages in my LAD (proximal and mid) and one one the right side (distal). The LAD are severe because the stenosis are 65-70%. They want to perform a bypass operation in the near future. I have searched the internet and seen that there are several options available as there is on pump/off pump. Minimal invasion (MIDCAB) and using endoscopes (TECAB). Any input would be greatly appreciated.
“Any input would be greatly appreciated.”
Oh my God!
Well, 1999 all my arteries were blocked and still are (there are collaterals). The LAD was completely (?) blocked as I remember it on top of my head. Reading the statistics I then realised that little was to be gained by the comprehensive by-pass offered in the long run and I kindly refrained two weeks before the scheduled operation.
So I had to “change my life” instead to treat the “cause” which was obvious for me as a researcher in the natural sciences.
Most importantly. No more PUFA’s and no more sugar, a new job to reduce the stress and regular exercise – took the bike to my work everyday.
There is a lot you can do by an alternative approach (Do your home work!) and you have to use the broad brush but it does seem to work for me when I am still working with my chain saw on my last trunk delivery and then chop my fire wood. The sad thing is that Big Pharma will not make any money out of you. i am a big loss myself 🙂
The thing is I already changed my life 11 years ago. I quit smoking and started to exercise. I never was overweight. At present I have never been fitter in my entire live (I’m 50 years old now). In the last 8 years they made 4 Ct scans. Each time the calcium score got worse. The one made 6 years ago revealed moderate plaque. Guess the vitamine K I have been taken for years now, didn’t do the trick. I don’t think I am brave enough to wait and see if my heart has formed collaterals. Cut back on sugar intake in the last 2 years. Recently started cutting back on all carbohydrates and increased my vitamine C (4 grams a day).
Eugene, I wish you well in your search, for the best route for you. We are individual and not a statistic. Dr Sjoberg is very brave to take charge and follow his route. All I can say on a simple level is do some safe sunbathing to boost your D levels, which will boost your immune system.
I wish you all the best. Sylvia.
Eugene, I’d read Dr Kendrick’s view about coronary bypass operations (CABG) in ‘Doctoring Data’. Also look at the options you mention on thennt website. I’ve attached a link with the CABG statistics on benefits and a fairly long list of harms. I’m with Goran. It’s not a road I’d go down, but perhaps we all see these things different. My attitude is that the benefit would have to be clear before I’d agree to an operation. Don’t be pushed into anything.
Best wishes.
http://www.thennt.com/nnt/coronary-heart-bypass-surgery-for-prevention-of-death/
Stephen,
Thank you for this link ! It updated my old view on this. There was some scary references embedded about RCT with laser intervention.
Stephen,
Here is the scary abstract I read through your link
I didn’t even know about this laser revasculating method.
Big Pharma doesn’t surprise me any more.
———–
A blinded, randomized, placebo-controlled trial of percutaneous laser myocardial revascularization to improve angina symptoms in patients with severe coronary disease.
Leon MB1, Kornowski R, Downey WE, Weisz G, Baim DS, Bonow RO, Hendel RC, Cohen DJ, Gervino E, Laham R, Lembo NJ, Moses JW, Kuntz RE.
Abstract
OBJECTIVES:
This study was a randomized, patient- and evaluator-blinded, placebo-controlled trial in patients treated using percutaneous myocardial laser revascularization.
BACKGROUND:
Previous studies using similar therapies have been confounded by placebo bias.
METHODS:
A total of 298 patients with severe angina were randomly assigned to receive low-dose or high-dose myocardial laser channels or no laser channels, blinded as a sham procedure. The primary end point was the change in exercise duration from baseline examination to six months.
RESULTS:
The incidence of 30-day death, stroke, myocardial infarction, coronary revascularization, or left ventricular perforation occurred in two patients in the placebo, eight patients in the low-dose, and four patients in the high-dose groups (p = 0.12); 30-day myocardial infarction incidence was higher in patients receiving either low-dose or high-dose laser (nine patients) compared with placebo (no patients, p = 0.03). At six months, there were no differences in the change in exercise duration between those receiving a sham (28.0 s, n = 100), low-dose laser (33.2 s, n = 98), or high-dose laser (28.0 s, n = 98, p = 0.94) procedure. There were also no differences in the proportion of patients improving to better than Canadian Cardiovascular Society class III angina symptoms at six months. The follow-up visual summed stress single-photon-emission computed tomography scores were not significantly different from baseline in any group and were no different between groups. The modest improvement in angina symptoms assessed by the Seattle Angina Questionnaire also was not statistically different among the arms.
CONCLUSIONS:
Treatment with percutaneous myocardial laser revascularization provides no benefit beyond that of a similar sham procedure in patients blinded to their treatment status.
According to today’s Times the NHS carries out 17,000 heart bypass operations a year. In ‘Doctoring Data’ Dr Kendrick stated that there’s little or no supporting evidence to support this operation and some evidence of harm. I get the feeling that this operation is the professional pinnacle for those involved and questioning its use is close to heresy. It feels more like religion than science. Does the system care at all about informed consent?
I got the results from my bloodtest. This is the first time they measured lp(a), apo-lipoproteine A1 and apo-lipoproteine B. Values Lp(a) 1.1 g/L (should be 1.2). The doctor told me the value of lp(a) is an indication I have a genetic problem and want’s me to see an specialist in the hospital. I’m not very keen on going to a “specialist” because I will end up with a prescription for a statin which I have refused for almost a decade now. Regarding my 3 blockages in my heart my own brother asked me if I didn’t regret that decision.
Eugene,
Dr Goran referred to “collaterals” as having been his particular saving grace.
I’m wondering if collaterals might have shown up on your angiogram. Were they recognized by the radiologist if they were there? People tend to see only what they’re looking for.
I’d like to know more about collaterals myself. Do they form gradually as the arterial constriction forms, or only when that constriction starts to become critical? What lifestyle and diet changes can we make to specifically encourage collaterals? What are we doing inadvertantly that discourages them?
Anyone?
As far as I understand the collaterals don’t show up on angiograms in detail but by diffuse contrast around the blocking and not least by the back filling. I saw a video on that a while ago; it is very instructive.
http://heartattacknew.com/heart-catheter-film/
Five minutes that forever will change your view on your own disease and make you a “stranger” in the eyes of your cardiologist.
It is a, so called, Popperian refutation of the whole by-pass business and the video clearly illustrates the futility of a by-pass grafting as a “remedy” of a blockage. By accepting the grafting operation you will forever be trapped by Big Pharma with very little prospect of ever escaping.
I don’t know if I was brave but for sure I am today very happy that I refused 17 years ago and now being able to enjoy the fire wood chopping and just now relaxing in front of my fireplace with a glass of wine.
Hi! Goran, Your reference is an excellent website by Dr Knut Sroka.
He also posts the Myogenic theory of heart disease based an acidosis of the heart muscle( this has a huge number of references-always a good sign). It is important that people in general understand that heart disease and heart attack are not related in all cases. That there is also Heart failure. It is such a complex subject. Dr Sroka also references a major study by Italian pathologist -Baroldi. Baroldi showed that, in the heart, clots form AFTER a heart attack and NOT before. Baroldi also shows the extensive network of collaterals. However, I was recently diagnosed with triple vessel disease after 2 heart attacks and had a bypass surgery. Now, I have since read that what is seen an angiogram can be artifacts. But in my case so far-I had the surgery in early March 2020, I can now walk briskly for up to 1 hour with no pain in my chest. I am on an array of drugs, I am studying how to adjust my diet and I am extremely hungry in the last 4-6 weeks. I have learnt that carbohydrates, incl. sugar do not agree with me so I keep them to a minimum. I am slowly experimenting with more saturated fats. I found online-the Skeptical cardiologist and he suggested more fats, but still adheres to the statin drugs. I asked him some questions-no reply. I must say that I had very good care in the hospital in New Zealand, and in a state of the art operating theatre. At present my life has changed, but I know that I have to continue to explore how I can help myself-Dr Sroka was very clear to me on this. I have also devised a meditation process based on TM and the fact that I am an Osteopath and I am very aware of vitality or lack of vitality in the tissues. It is unfortunate that Vitalism was written out of science…few hundred years ago-this was a mistake on an enormous scale. Why? Because myself and many others in my profession see the results of engaging the vitality in patients on a daily basis and it can happen within secs to minutes in a patient one is treating. Apparently, one cannot learn TM meditation without doing a course. I have also just purchased a book on TM and the heart written by an American Doctor some years ago. I also found a paper from a University in Helsinki on the role of the lymphatics in CVD.
Hi! JD,
Collaterals. There is a time frame, so the earlier a problem starts the more collaterals form as a compensation process. Heart disease can often start in the teens years. It is also my understanding, not conveying fact here, that stress and the affects of the sympathetic nervous system overload may affect the development of collaterals.
Our bodies are truly wonderous in how it tries to respond to a process by another process.
But as you might read on my reply to Goran, the lymphatic system also plays a major role- the heart has lymphatics and dysfunction here my lead to heart failure through CONGESTION of the heart muscle-acidosis and thus weakening of heart muscle. I believe my heart attack was triggered by an intense period of exercise including weights ( I am 64 ys). The walls of heart muscle can weaken and bulge- see the website by Dr Srka…Heartattackanew.
Robin
My cycling coach is a big believer in heart zone training, he says staying in the green zone thins the wall of the heart chamber, leading to more capacity for extra volume pumping when needed, I am eighty, since I get puffed on hills, I am following his advice, grinding up hills in the lowest gear to stay in the green zone, irrespective of jeering from my family, and watching my heart rate rather than speed as I do it.
Hi! Mr Chris,
Your comments are very helpful. I will look into understanding what this means in terms of my situation. At present I would not be doing this as my grafts need to heal -how long this is I do not know. I guess it will vary according to the individual. But many thanks for this very useful information. I have noticed that I cannot lift much with my arms- a valsavra type manoeuvre is engaged here and this loads my diaphragm and impacts on the venous return-vein blood entering the heart. This function has an impact on output by the heart, although the heart ( I am really going to challenge you all here) is NOT a pump. It has a pump-like function but not like one might imagine it works as a mechanical pump. I can explain this if anyone wants a brief ( its extremely complex and lengthy to explain) explanation. I can give figures as a starting point- everyone likes numbers. The latest comprehensive scientific book on this extremely controversial topic, is by Professor Brank Furst-he is a Cardiac Anaesthesiologist. The book was written this year-2020. This ”theory” is not new. But it would challenge the original idea from the 13th Century=the beginning of the modern scientific era according to philosopher Henri Bortoft. The idea of a pump was kind of consolidated under William Harvey and the dogma on this subject would be enormous and likely be like moving all the mountains in this world.
Eugène,
Dr Kendrick often reminds us that we don’t live for ever, whatever we do. Having just come back from visiting a 95-year old guy who was ice skating a few weeks ago, and has now had a stroke, that advice seems very relevant. I think that when you reach 65+ (like me), it is better to enjoy life, not to franticly try to maximise its duration!
At one time, I thought statins were a great idea to extend my life, but once I encountered the real side effects of statins (and had unambiguously identified that statins were causing my problems), I would rather accept a slightly shorter life-span than mess about with statins.
(BTW, that does not mean that I now believe statins are useful in any way!)
Statins don’t cause you ‘muscle pains’ – they threaten to consign you in a wheel chair with a lot of pain!
we owe it or ourselves to question and know there is more than the so called orthodox route. That Dr Kendrick does this, and others of the same Ilk is remarkable, they stick their neck out and challenge. When shareholders are in the picture it gets murky. To try to live as healthy a life as possible without suffering is all we can ask, it does start with lovingly nurturing your young and making the effort to cook real food. This may help to stand us in good stead. Sorry this sounds like a patronising lecture.