23rd December 2019
Another new study
Question: If a tree falls in the forest, and there’s nobody around to hear, does it make a sound?
This is a philosophical question that has been around for some time. I shall change it slightly to the following: “If a journal publishes a study, and it doesn’t make a noise, can it make a difference?”
A couple of weeks ago the Lancet published a ridiculous study with the snappy title:
‘Application of non-HDL cholesterol for population-based cardiovascular risk stratification: results from the Multinational Cardiovascular Risk Consortium.’
Which created headlines around the world – most of which failed to understand the difference between LDL (‘bad’ cholesterol) and non-HDL cholesterol. Which may, or may not, have been deliberately done.
This study was reported as saying that twenty-five-year olds should get their cholesterol checked, because raised cholesterol is far more damaging, at a young age, than previously thought. All based on, pretty much nothing at all. I critiqued it in my last blog. It was, to use a word I rather like … bilge!
Then another study came out last week to which I was pointed by a reader of this blog… thanks. It had the even snappier title:
‘Association between hyperlipidaemia and mortality after incident acute myocardial infarction or acute decompensated heart failure: a propensity score matched cohort study and a meta-analysis.’ 1
You know that title really does not scream ‘READ ME!’ What is it about medical journals, and medical writing, which demands all enthusiasm and interest is sucked out, leaving only the driest, of dry, husks. I call it mummified prose.
What I first noticed was that it did not appear to make any headlines, anywhere, at all. Of course, making enough noise to be heard, in today’s jittery, overloaded information world, takes a lot of money and effort. Which is why the Lancet study got blanket coverage. Someone, somewhere, will have been paid a lot of money to ensure that it happened.
The money was paid because there are people who stand to make billions and billions from increased cholesterol testing, including younger people, and suggesting that “raised” cholesterol must be ‘treated’ from an ever-younger age. Perhaps you would like to guess who those people may be.
On the other hand, the study ‘Association between hyperlipidaemia and mortality after incident acute myocardial infarction or acute decompensated heart failure: a propensity score matched cohort study and a meta-analysis.’ could result in the loss of billions and billions.
Because what they found, was that, after an acute myocardial infarction (AMI), and in people with acute decompensated heart failure (ADHF) – normally caused by a previous MI – the higher the LDL level, the lower the overall mortality. They called a higher LDL level hyperlipidaemia (HLP), but it was a high LDL a.k.a. ‘bad’ cholesterol.
The ‘association’ of which they spoke, is in the exact opposite direction to that in the Lancet study. Just to repeat their main finding. Those with higher LDL levels lived the longest. Full stop, exclamation mark.
They set the study up to consider the following questions – I make no excuses for the jargon here:
‘We postulated that if a diagnosis of HLP [Hyperlipidaemia] decreases the mortality after AMI or HF [Heart Failure], then, it also lessens the magnitude of mortality risks associated with other competing comorbidities.
We tested this hypothesis, separately, in large cohorts of patients hospitalised for incident AMI and acute decompensated HF (ADHF). To compare patients with and with no HLP, we assembled 1:1 balanced groups using propensity score-matching for each study condition.
Our objectives were three-fold:
(1) to estimate the association of HLP with all-cause mortality among patients with AMI or ADHF,
(2) to determine the extent to which the association between other competing comorbidities and mortality is modified by HLP
(3) and to provide risk estimates for mortality associated with HLP after incident AMI or HF through systematic review and meta-analyses of published and current study data to place the current findings in the context of published literature.’
Here were the main results. First for those diagnosed with AMI:
- In matched patients, mortality was significantly lower among patients with Hyperlipidaemia (HLP) versus those with no Hyperlipidaemia (HLP)
- Overall mortality 2182 (50.2%) vs 2718 (62.5%)
- 5.9 vs 8.6 deaths/100 person-years of follow-up, p<0.0001.
Next for those diagnosed with acute decompensated heart failure (ADHF):
- In matched patients, mortality was significantly lower among patients with HLP versus those with no HLP
- Overall mortality 1687 (58.6%) vs 1948 (67.7%)
- 12.4 vs 16.3 deaths/100 person-years of follow-up, p<0.0001.
You may have noted that the mortality rate in these patients was very high. For those with ADHF, and lower cholesterol levels (LDL levels), the mortality rate was 16.3 deaths per 100 person years. That is a sixteen point three per-cent death rate per year. One in six.
This, therefore, is a super, exceptionally high-risk population. It is also a super exceptionally high-risk secondary CV prevention population. The exact group where statins are purported to do the most good – through the specific action of lowering LDL levels.
At this point, a short detour. I know any cardiologist reading this will be thinking – or has been taught to think: “Yes, but low cholesterol is a sign of other serious conditions, such as cancer. Ergo, it is not the low cholesterol that is damaging, it is the other underlying conditions”.
This ‘fact’ been stated for many years – without a single scrap of evidence to support it.
It was Stamler who first came up with this ‘apologia’ for much contradictory evidence about low LDL levels and increased mortality. Like many things in medicine it is universally believed, without any supportive evidence. It is true that in a very few cases, late stage terminal cancer, and late stage liver failure, the LDL levels can drop. Otherwise … nothing.
However, these researchers made sure they adjusted for this, non-existent, factor anyway.
‘Our findings were adjusted for cancer and numerous other Clinical Conditions.’
What were the conclusions of this study? Well, they were exceptionally carefully worded.
‘The findings of this study, if validated, should reinforce the importance of HLP in predicting long-term mortality after index AMI or ADHF and potentially provide guidance for subsequent management. HLP can readily be diagnosed and help recognise AMI and HF patients with lower long-term mortality.
In these patients, clinical care should not focus on certain lipid targets; rather evidence based secondary prevention strategies should be initiated.
Conversely, patients with AMI and ADHF without HLP may be considered to have increased risk for early mortality and potentially alert providers for close monitoring during hospitalisation and after discharge. Both categories of patients would profit from thoughtful tailored programme with distinctive goals of care for existing CCs.’
Let me cut to the key comment in that passage. That is, the comment regarding those patients who had HLP:
Clinical care should not focus on certain lipid targets
Clinical care should not focus on certain lipid targets
Clinical care should not focus on certain lipid targets
I thought it was so good, I should say it thrice, for that makes it true. According to Lewis Carroll anyway.
“Just the place for a Snark!” the Bellman cried,
As he landed his crew with care;
Supporting each man on the top of the tide
By a finger entwined in his hair.
“Just the place for a Snark! I have said it twice:
That alone should encourage the crew.
Just the place for a Snark! I have said it thrice:
What I tell you three times is true.”
Of course, the comment is couched in such diplomatic language that I am not absolutely sure what is meant by it, although I am pretty sure.
On that basis, I shall wind up the emotion of the language somewhat. ‘These poor people, who are dreadfully ill, who have suffered the agony of a heart attack, or severe heart failure, fare so much better when they have a high LDL level. So, for pity’s sake, I beseech thee in the name of God, do not try to lower their LDL level you mad fools. Aaaaaarrrrrrrrggggghhhhh! Gasp, bonk.’
Maybe a touch too emotive? Oh well – after reading too many clinical papers, the temptation to shout become irresistible. Creeping around in the grey and lifeless world of the passive voice is not really my style. Science should not be a place of hushed diplomacy. Science should be lively and stimulating, nay argumentative. If you’ve got something to say, shout it out. Fight for it and debate it properly.
Anyway, my original question was the following. ‘If a journal publishes a study, and it doesn’t make a noise, can it make a difference?’ The answer is, almost certainly, no. Hopefully, however, I have now made a bit of noise, and maybe this study can make a bit of difference.
1: https://bmjopen.bmj.com/content/bmjopen/9/12/e028638.full.pdf
Dr. Malcolm Kendrick 
Brilliant again Doc, I feel like I’m in the middle of a gripping novel, except this isn’t fiction, it’s real life… and real lives! You do this so well, thank you so much, for bringing clarity to a world a lot of us couldn’t hope to understand
Completely agree. I now have numerous friends in their 50s and 60s on statins. It just doesn’t make sense to me that we can only live by so many of us taking medication. Thanks to Dr M. I have absolute confidence in my decision never to have my cholesterol tested and never to take statins.I am fit and healthy, but my GP wants to keep testing my cholesterol as ‘a matter of routine’. No thanks. But thanks to Dr M.
Exactly. I stopped taking statins after developing pains and tingling in my left arm. Only then did I start looking for evidence and came across Dr Kendrick and the great cholesterol con. I still get some pains in my left arm but it has improved slightly since giving up statins. Unfortunately the nerve damage is probably irreversible. I also refuse to have my cholesterol checked.
This comment is in reply to Ian Roselman. I don’t know why there was no “Reply” option beneath his comment. Anyway, my reaction to statins (pravastatin to be exact) was in my legs, developing intermittent claudication (inability) to walk non-stop for long distances after just a few months of taking it. My max non-stop walking distance was reduced from 5+ miles to a quarter of a mile. After I wised up and took myself off the statins (and fired the cardiologist who prescribed them, saying they couldn’t possibly cause a problem) my max walking distance increased to about half a mile, then stalled there for about 8 years. I came to assume that thanks to the statins the damage was irreversible and I would be crippled for life. Then about 6 months ago I tried a new supplement, replacing pure Co-Q10 with a combination of 20mg of PQQ and 200mg of Co-Q10. I had no reason to expect that to do anything for my legs, so this could not be a placebo effect. After just 6 weeks of taking it the intermittent claudication was almost entirely gone and my max distance was back up to 5 miles, albeit quite a bit slower than it used to be (2.8 vs. 3.2 mph). After two months of taking it (it’s expensive) I reverted to Co-Q10 alone and was back down to a quarter of a mile max within 2 weeks. Going back on PQQ+Co-Q10 it took a couple of months again to get back up to 5 miles. Online research suggests it’s due to PQQ’s effect on mitochondrial function. So you might want to give it a try, Ian. If you do, it would be great to read a follow-up comment from you reporting your experience.
Greg Hill, check out the work that Bruce Ames’ did with acetyl-l-carnitine and alphalipoic acid. The ALCAR is involved in transporting fatty acids into the mitochondria and the ALA damps down the free radicals produced within the mitochondria. When he put aged rats on that combo the geriatric rats not only were as active as young rats they also had better memory than before.
This is related to another post about lipoproteins being an evolutionary advantage. Would it follow that individuals with FH who take statins should experience a higher rate of statin-related AEs than people without FH taking statins?
well done Lynda; as Dr K has pointed out many times, there is no data on statins in women: the studies were done by middle-aged men; on middle-aged men; with the conclusion … ” oh, women are just the same, it should work for them ..”
but there is much data that women (and men) do better with higher LDL levels;
Let’s see if WordPress will let me comment !
Yes brilliant again Malcolm
Cutting through all the Gordian knot which is modern day medical BS !
Great!
I couldn’t agree more as being a serious MI-victim still surviving 20 years after the one single event took place and when I decided to do the opposite of what was suggested by the establishment.
My GP is terribly insistent that I take statins again (apparently my cholesterol level came down 2 points very satisfactorily when I did) and has threatened me with dire consequences if I don’t take them, ie stroke, heart attack etc, although I am disgustingly healthy despite my age (72), lack of exercise and fondness for wine. After he had explained to me how arteries get blocked by high cholesterol, I asked him why veins aren’t affected in the same way. He, momentarily, seemed confused but said that veins are affected but less so as the blood in the arteries is travelling with much greater force and speed. I was left wondering why pipes with liquid travelling through them with greater force and speed would tend NOT to block as much as pipes with liquid dawdling along through them, but decided to leave it there as this is the only GP practice in the village! I don’t take the prescription for statins though.
sorry to hear you are harassed in this way Carole: in other circumstances, one could complain about harassment and report it.
It gets glossed over when eminently wise doctors do it; even if they don’t understand lipids at all; and just chant the old dogma. There is no evidence statins help women; as Dr K has repeatedly pointed out.
Your GP may well get given money for prescribing statins: in many countries they are so rewarded; it is not clear if they disclose this when they attempt to foist statins on unwilling souls.
Not surprising this is not more publicised. It undermines a whole way of life
That is sooo reassuring. Another brilliant post which I treasure as a rather splendid Christmas present. Thank you, thank you thank you. And warm Christmas greetings to you and yours and to all the many followers of this blog whose comments I so much enjoy reading. All very life enriching. 🎄🌹
Hear, hear, Janet. I share your feelings – and add my good wishes to all.
Me 3!
Sacrilegiously I have no Scotch, but I will have red wine with my pheasant wrapped in bacon and eaten with mushrooms and Brussels sprouts, and I will have a small quantity of Christmas pudding covered in clotted cream, ground flaxseed and brandy.
Doing the exact opposite of what we are told seems to work. There’s now an increasing quantity of evidence to that effect, and it is always interesting to see a paper like this from researchers I have never heard of before.
Season’s Greetings to all
Chris C
Ground flaxseed for Lp(a)?
Thanks for that.
Just what I wanted for Christmas!
Thank you for such an excellent post, especially so near to Christmas!
Wishing you and yours Felicitations for the Festive Season … and in normal laguage…
Happy Christmas!!
Thank you, I will now have plenty to read over Christmas
A paradox that “bad cholesterol” is good if one has HF. Now the question is how to avoid HF in the first place. These authors have an idea:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5350035/
Mitochondrial function as a therapeutic target in heart failure
“Conclusions
The vast majority of HF trials over the past decade have been neutral, and event rates remain unacceptably high. Perhaps most alarming, no proven therapies exist for patients with worsening chronic HF or HFpEF — populations that collectively comprise the majority of the total HF population.”
While waiting for new therapies/treatments I will place my bet on a ketogenic diet.
Everyone else has said just about everything that I wanted to say, so what on earth can I find to add to all those lovely comments? Only this. Thank you so much for all your hard work and dedication Dr. Kendrick, over the past few years you have given me the confidence to make my own decisions regarding which drugs to take and which ones to avoid and I thank you for that.
My best wishes to you and yours for a very happy Christmas and a peaceful New Year.
well done Sylvia; keep off the statins; they are fungal toxins after all; fungi .. eg toadstools .. make toxins to punish animals that attempt to eat them; so was the first statin discovered in Tokyo: as a toxin from a fungus. That is how they can harm cholesterol production in the liver.
My dad was told by his doctor that his cholesterol was a bit high and that he should switch to special low cholesterol milk (more expensive). He followed those instructions religiously for many years. He was perfectly fit with no health problems, but died of a massive heart attack. I really believe the special milk did not help, if anything maybe just the opposite.
Yes, it is kind of humorous how some studies are highlighted by the press and others not. I can remember when working in the food industry we would receive calls from magazines saying, we are going to run an article on such and such…an article on a product our company sold. The magazines would ask us to buy advertising next to the article.
For awhile I worked for a very large German firm, in purchasing. One day I received a call from HQ saying to stock up on this one product. Soon sales are going to go through the roof I was told. Sure though a week or two later nearly every major TV news program and most major news papers ran pieces on this product. It was a nation wide sales blitz masquerading as news. Sales certainly went through the roof after that.
Thankyou Dr Kendrick: you are like a Guardian Angel. I wish you a wonderful Christmas and a Happy Hogmany. Irene
May I wish you, Dr Kendrick, a merry Christmas and a happy and unfrustrating New Year.
When I think of all your good work, your endless patience and lucid explanations, it seems to me that you belong to a very small group of people who are doing a huge amount of good in the world. As the toast goes,
“Here’s tae us!
Wha’s like us?
Damned few –
And they’re a’ deed”.
I shall raise a glass of single malt to you at Hogmanay. Long may you remain alive, intolerant of fools and sparkling with ideas!
An interesting article, made more interesting to me as on Election Day a good friend of ours, not yet 50, had a massive heart attack on his way to work. He doesn’t smoke, doesn’t drink, eats well (as far as I’m aware, whatever ‘well’ means) and gets plenty of exercise. He does have a stressful job though. It was completely without warning.
Luckily he works in a place where they have medics instantly available who cut off his coat, lowered his body temperature with a special blanket to chill him and got him to hospital immediately. Surgery was done straight away, stents, balloons, you name it – and now, of course, he’ll be prescribed statins and blood thinners etc. He had the further problem of falling flat on his face when it happened, fracturing several facial bones and dislodging teeth, but he was on the phone to my husband last night, sounding very positive and perky, saying he’s going to discharge himself for Christmas, having proven he can walk properly and go up and down two flights of stairs. He also told the senior surgeon how dreadful some of the food is in the hospital, and about various members of staff who need attention, having asked for a bedpan and the nurse disappeared and never came back, for example!
I am now worried about his future as he will not want to refuse statins and will probably be told to follow the standard “heart-healthy diet”. He isn’t one to go against authority (probably why his job is so stressful) but I hope he looks into de-stressing his life.
Dear Dr. Malcolm,
In the last line of the main results, it reads ‘*9* vs 8.6 deaths/100 person-years of follow-up, p<0.0001", where it should read "*5.9* vs 8.6 deaths…'
Given the context, I thought that it didn't seem right, so I checked it in the study and was about to comment in your blog when I noticed that there it is correct.
Best regards, Victor.
Dr. Malcolm Kendrick escreveu no dia segunda, 23/12/2019 à(s) 08:49:
> Dr. Malcolm Kendrick posted: “23rd December 2019 Another new study > Question: If a tree falls in the forest, and there’s nobody around to hear, > does it make a sound? This is a philosophical question that has been around > for some time. I shall change it slightly to the followin” >
The smoking gun. Statins are dead. Too bad almost nobody knows about it.
And yet, and yet, and yet, Dr Malcolm, the study you and others helped us discover has and will make a difference. It may not make news headlines this week, but it should the next.
Thank you for your efforts!
Paul Melzer
Superb.I am testimony to this.I stopped Statins in 2012 even after massive heart attcakmin2011.Now happy even after mild Stroke.Herat LVEF is 46 % and recovered almost 90 % from Stroke.NO STATINS EVEN NOW LDL is 130 This LDL is required for me to Be Happy , Healthy.
Thank you, and Merry Christmas!
Just as the statin promoters might pay to get their (rubbish) findings promoted in the lay press so they might also pay to suppress “dissident ” results. More noise thetefore needed. I will do my best to help!
Have a merry Christmas and a happy new year.
On Mon, Dec 23, 2019 at 8:50 AM Dr. Malcolm Kendrick wrote:
> Dr. Malcolm Kendrick posted: “23rd December 2019 Another new study > Question: If a tree falls in the forest, and there’s nobody around to hear, > does it make a sound? This is a philosophical question that has been around > for some time. I shall change it slightly to the followin” >
Well said, young Kendrick.
Lang may yer lum reek.
Here is another conundrum, from Zen and the art of motorcycle maintenance,
To
At the time of the dinosaurs, did two plus two make four?
Answers on a postcard please.
By the way the question is perhaps more difficult than it seems
Can you say more please? Why do you think it’s more difficult than it seems?
well, do laws of mathematics have an independent existence, from us?
I am not sure. I don’t know much about mathematics but I thought it’s often referred to as the language of science and thus should describe physical phenomena as well. And physical phenomena exists independently of us.
But, I guess, language doesn’t exist independently of us either.
Well yes, those I think are the two answers. I favour your second answer.
Merry Christmas to all here
Thank you for answering. Merry Christmas to you and all on this wonderful blog.
Good
Ah, thanks to you, the falling tree is being heard! May the sound of the crash ripple out to the wider world.
Merry Christmas and a very Happy Hogmanay.
Lipoproteins are evolutionary advantage; through being an ingenious means to transport energy they also facilitate the possibility of energy storage and of the re-release of stored energy.
Stamler is not on my Christmas card mailing list. Many of the propositions he helped propel are either wrong or too simplistic to be of value.
A question to anyone who might know: is there any data on possibility of association between FH and cancer? Is there a possibility of such association? Thank you
Sorry, to repeat: does anyone know of any data claiming possible association between familial hypercholesterolemia and cancers, specifically brain or breast cancer? Thank you
Hi Sasha, this might be what you are searching for, a study on murine women:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5690879/
Elevated tumor LDLR expression accelerates LDL cholesterol-mediated breast cancer growth in mouse models of hyperlipidemia
They blamed the cholesterol but not the mouse chow. I am not a scientist but if cancer is a metabolic disease then these researchers went down the wrong rabbit hole.
Thank you, Andy. I will read it and get back to you. I have some thoughts but don’t know if they are in the right direction…
Andy, the study you linked seems to imply that elevated numbers of LDL receptors on malignant cells’ surface promote their growth. In my opinion, it doesn’t mean that cholesterol is good and mouse chow is bad. It means that cancer cells can feed off cholesterol. Whether they feed off cholesterol better, worse or the same as off sugars, I can not say. So I don’t think this study either confirms or denies cancer as metabolic disease theory. This is my interpretation of the study you linked. If someone thinks it’s wrong, I would welcome any criticism.
As far as FH. In FH the situation is the opposite, cells are impaired in their ability to take in LDL , that’s why there’s so much of it circulating in the blood. My question is: does it make more likely, less likely or doesn’t make a difference in cells’ development of malignancies? Especially energy hungry cells like brain cells or breast tissue post-lactation cells, for example. That’s why I was asking if there’s any epidemiological data showing, for example, correlation between FH and brain cancers.
Sasha,
Uffe Ravnskkov has said many times the very high LDL as seen with FH protects against cancer and infectious diseases.
Dr John, thank you. Do you have a link to where he says that or is it in one of his books?
Also, what’s the mechanism? Is it because cells are starved for energy?
Sasha, LDL has many functions
Perhaps quality of LDL is the important factor, this is what diet regulates.
https://www.ahajournals.org/doi/10.1161/01.ATV.17.1.127
The Redox Status of Coenzyme Q10 in Total LDL as an Indicator of In Vivo Oxidative Modification
Studies on Subjects With Familial Combined Hyperlipidemia
Thank you, Andy. I will take a look.
AHNotepad, thanks for the link. I googled to see if I can find the connection, so far I have not been able to.
To my thinking, if the metabolic theory of cancer is correct, it should increase cancers, not decrease them in FH. Unless, cells somehow adapt to using other forms of fuel primarily (like sugar). I, of course, might be wrong in my thinking on this.
andy, the paper you linked contains “Familial combined hyperlipidemia (FCH), first identified by Goldstein et al,1 is a genetically and metabolically heterogeneous common lipid disorder, associated with an increased risk for cardiovascular disease.12 The trait is characterized by a multiple-type hyperlipidemia in first-degree relatives. Affected persons exhibit elevated plasma concentrations of cholesterol or triglycerides, or both………”
I question whether FCH is really a “disorder” . The “official” narrative is the cholesterol is too high in many cases, and evolution must have produced a fundamental design error. In which case, is FCH really another “error”?
Well, I think that the system of LDL transport and LDL receptors on the cells’ surface evolved for a reason. Since in FH those receptors are missing, one has to question what are the benefits and harms of such a mutation. Wikipedia talks about harms (increased atherosclerosis for some) and Ravnskov, as mentioned by Jonh H, talks about benefits: less cancers and infections. Since this is a fairly common infection, I wonder if it evolved in a response to many infections that plagued the mankind for centuries.
Sorry a correction: since this is a fairly common mutation..
Sasha: I have found a little bit of info concerning cholesterol and cancer from Dr. Ravnskov’s book, “Ignore the Awkward.” Some of the references are hard to run down, or are behind a paywall, but he does mention PROSPER and what I think is called the Los Angeles Veteran’s trial.
Gary, I think you are referring to the idea that people with lower cholesterol levels suffer from higher rates of cancer, right?
I am, however, looking at the FH mutation where cells lack LDL receptors. Why did this mutation develop? If, as Ravnskov says, people with FH have lower rates of infection it could have been in response to centuries of high infection rates as the result of Agricultural revolution. This is just my speculation, though.
However, every mutation, has a negative side. What’s the negative of FH mutation? The official story is that people with FH suffer from higher rates of atherosclerosis. To me that seems to go well together with Bruce Ames’ Triage Theory where he says that the body will triage to ensure short term survival. Infections kill you faster than atherosclerosis or cancer.
So, do people with FH have higher rates of atherosclerosis? And do they have higher rates of cancer?And if they do, what’s the pathomechanism for both of those processes?
Sasha: As I recall either from an earlier post or in one of Dr. Kendrick’s books, it makes a difference whether one is homozygous-these tend to die young, or heterozygous for the FH gene, who seem to live as long or longer than the rest of the population. I seem to recall those with two copies of the gene do have CVD at a higher rate and at a younger age, which would imply earlier and more rapid development of atherosclerosis, or maybe not! Bit confused on this issue, especially since a significant percentage of people suffer an MI without any blockages at all of cardiac arteries, and some die of old age with all the cardiac arteries completely blocked. As for the connection of FH and cancer, I don’t really know much, but your research will be enlightening to all of us.
Gary
You are not the only one confused. I decided that quite a lot is unknowable, and that sticking to Malcolms suggestions, plus ordinary food and exercise will probably do the trick. At least it has up to now
Gary: I googled if there’s any FH cancer connection, so far I haven’t found anything. I will look again.
Gary: I think FH isn’t the only mutation that turns deadlier once it becomes homozygous. My question also: what changes between hetero and homozygous to turn an advantageous mutation into a disadvantage?
Sasha, here is a reference about FH:
https://www.spandidos-publications.com/10.3892/mmr.2018.8904
Genetic analysis in a compound heterozygote family with familial hypercholesterolemia
Apparently homoFH has more defective genes than heteroFH , affects LDL receptors and apob100 protein on LD particles. LDL in plasma cannot be transferred to cells. For the rest of us with high or low LDL, glucose can glycate apob100 and cause mischief.
Thank you, Andy. I will read it
Sasha: I may be wrong, but it seems to me that if the result of the mutation is fewer cholesterol receptors on the cells, then two copies of the gene would further reduce the number of receptors to the point that either too many fully loaded lipoproteins continuously circulate in the blood, or insufficient cholesterol is delivered to the cells for them to function well, or both.
Mutations can be beneficial to a point and then become harmful if homozygous. I think the mutation that leads to sickle cell anemia is another such example. Double check me on this, though.
AhNotepad: on understanding genes and baking a cake
The cell nucleus contains the genetic code for producing many proteins. This is like a cookbook with many recipes. To assemble a specific protein requires input from more than one gene, this is equivalent to choosing a particular recipe from a cookbook. Gene sequence and specific molecules produce the required protein, In a recipe there are instructions and an ingredient list. What I have noticed when helping to bake a cake is that sometimes all the ingredients are not available and some substitutions are made. Sometimes the sequence of adding ingredients is mixed up, the end result can vary quite a bit but hopefully the cake is still edible.
Blaming it all on genes can be misleading. Metabolism plays a big part, even in FH or any other disease. Genetic instructions sometimes could be a bit mixed up, but that might be overcome by metabolic manipulation.
Here is one that may not be exactly what you want, http://www.ravnskov.nu/2018/11/03/cholesterol-best-friend. If you need something slightly different, using duckduckgo and searching for “ravnskov cholesterol cancer”, may reveal something better
indeed; Stamler comes from Chicago and was regarded as Keys’ hitman: ruthlessly haranguing folks into submission. A very combative character.
Of course this goes a long way to affirm the facts that Ravnskov oh so quietly pointed out ( In the woods. Still!? ) about five years ago. No one heard it then. Will anyone now?
https://bmjopen.bmj.com/content/6/6/e010401
It was through the amazing Uffe Ravnskov that I found Dr Malcom Kendrick and this wonderful blog. I wish all the readers the best of Christmases and challenging but not unbeatable New Years.
karenwatcher: Me, too! Through the THINCS website.
happy christmas
just a small glitch of the keyboard: in the HLP group the figures are: 5,9 vs.8,6 deaths 100-person-years of follow-up..which makes more sense
Dr. Kendrick, how does this article relate to the finding, which you have reported, that a large slug of statins right after an MI improves the outcome? I believe the benefit is due to the ant-inflammatory effect of the statin.
Well it can’t be due to the LDL lowering effect. However I am implacably opposed to the inflammatory explanation. It makes absolutely no sense to me. The most potent antiinflammatory agents known are steroids and they greatly increase the risk of CVD.
Dr. Kendrick, or anyone, thoughts on pro-resolving mediators for inflammation?
Hi Dr Kendrick please would you elaborate further on the ‘inflammation explanation’ – husband being pressured to take statins “to help with arterial inflammation” (CAC score of 229)
sincerest thanks for all your continued efforts – always amusing & informative
a peaceful & relaxing Christmas season to you & yours
Possibly due to one or more of the ‘beneficial side-effects’ of statins, even the volume of water to take the pills wouldn’t hurt.
If the patient is awake & aware, there is also a bit of placebo going on…. (Prove me wrong !)
Forgot to tick the boxes 😳
It’s no wonder that the study wasn’t picked up by the media given how many thousands of studies are published each year, on just about any topic. And how the average punter is supposed to make sense of any of it is anyone’s guess – especially when studies on the same topic can draw opposite conclusions.
Gullible are those who blindly follow the advice of mainstream media, that get fed headlines from study authors that are often the exact opposite of what the studes showed. Complicit are the ‘authorities’ who doggedly reinforce the crap lest their kickbacks might be withdrawn.
In a world where we are so time poor, most of us swallow it all (pill pun intended), nodding and trusting. But there are those like Dr Kendrick and the readers of, and contributors to this blog, who bother to dive deeper into the quagmire that is scientific research and seek clarity where there only seems murkyness.
This blog has kept me riveted from the moment I discovered it in 2013 and has led me to many others willing to stick their heads above the parapet to put the sword to many unproven but lucrative dogma. One of the best qualities of Dr Kendrick is that he encourages respectful debate.
Merry Christmas to all
On Mon, Dec 23, 2019, 2:50 AM Dr. Malcolm Kendrick wrote:
> Dr. Malcolm Kendrick posted: “23rd December 2019 Another new study > Question: If a tree falls in the forest, and there’s nobody around to hear, > does it make a sound? This is a philosophical question that has been around > for some time. I shall change it slightly to the followin” >
A merry Xmas and a happy new year to Dr Kendrick and all his readers.
Passionate analysis – a compelling read. Thank you Dr Kendrick
Another way of saying…. if the MI patient orders butter-fried garlic mushrooms with bacon and eggs for tomorrow’s breakfast, – he should get it . !
I see you don’t use the NHS.
Again wonderful analysis and insight you provide us. I was just sharing Dr. Kendrick’s work with a fellow I was meeting with. He is in our camp as well. As regards those who do not want their cholesterol tested, I allowed mine only because my employer is giving perks and health care spending dollars for the screening. My numbers were impressive to them. I don’t recall specifically but what I do recall clearly is that I threw out an off hand comment that these results must be due to my low carb, high good-fat diet. You can only imagine their faces…. !!! An interesting conversation ensued that only supports that people are accepting what they are being fed but are starting to be aware of the truth. I am a health care provider and struggle to do what I am told is right and what I believe is right (malpractice and risk issues abound as we know).
A blessed Christmas to all!
Thank you again, Dr. Kendrick, for a superb excision of the facts from the neurofibrillary tangles of medical fiction. Wishing you and yours Compliments of the Season, and more brilliant blogging in 2020!
How sad it is that science is manipulated by the great big ugly money making machine. Hardly credible to those of us who joined the NHS to help make a difference. Dr Kendrick, you are a bright shining light in a sea of ignorance and corruption. Thank you. Thank you. Thank you.
Seems the world is full of false news and as in the case of the Lancet report, false medical news. Unfortunately the truth doesn’t always out, ar least not to the targets of the marketing chiefs & doctors of spin.
The traditional cholesterol hypothesis denigrating all cholesterol, then just “bad” cholesterol suggests that evolution got it wrong, Darwin was wrong – we somehow evolved to naturally produce something that is bad for us and only chemicals from the big pharmaceutical manufacturers can put right the evolutionary mistakes, God’s mistakes that is!! – ( if we want to go give this a biblical slant)
Unfortunately money motivates with greater intensity than the truth & doing the right thing.
Hi Dr. Malcolm Kendrick–
I’m shooting a documentary on cholesterol, heart disease, and low carb that will take me to the UK for the last weeks of February and wanted to see if we could interview you while we’re there. I’ve reached out by email, but hadn’t heard back yet (might have gone to the spam folder…?)
See details here: https://cholesterolcode.com/documentary/
Please let us know if you’d be interested — it’s hard to imagine this documentary without your addition.
Cheers,
Dave Feldman
Sounds great to me!
Looking into your schedule I miss Sweden.
Here in Sweden we were actually among the first in the world to challenge Big Agro/Pharma with LCHF and with Dr. Annika Dahlqvist as our pioneer “hero” (an early Tim Noakes) and who finally won the victory over our medical establishment when LCHF was accepted as a ‘medical’ treatment for obesity and T2D in our health care system.
We have also our Diet Doctor, Andreas Eenfeldt who now is internationally well recognized as a proponent of LCHF.
I shall have a look in my spam, thanks. Merry Xmas
Malcolm – it makes my day ever so much better and brighter every time a new post arrives from you – thank you!
This book just came to my attention and I wondered if you have also come across this perspective: Human Heart, Cosmic Heart, by Thomas Cowan MD https://www.amazon.com/Human-Heart-Cosmic-Understand-Cardiovascular/dp/1603586199/ref=sr_1_1?keywords=human+heart%2C+cosmic+heart&qid=1566402891&s=gateway&sr=8-1 “ … In this deeply personal, rigorous, and riveting account, Dr. Cowan offers up a daring claim: Not only was Steiner correct that the heart is not a pump, but our understanding of heart disease―with its origins in the blood vessels―is completely wrong. And this gross misunderstanding, with its attendant medications and risky surgeries, is the reason heart disease remains the most common cause of death worldwide.” Haven’t read it yet, but he seems to be willing, as you are, to say that the widely accepted beliefs are completely wrong.
All best to you . . . Lianna
>
Oh no, not again! Dr. Cowan was discussed in the comment section way too many times, so let me just say that endorsing him amounts to keeping ones mind open to the point where the brains fall out.
Unfortunately (or maybe fortunately) the word “cosmic” escalates my BS antennae in to overdrive
Back to topic, some points can still be raised on the study that prompted the blog entry:
Click to access e028638.full.pdf
– They determined LDL-C through the Friedewald formula which is bound to be inaccurate at either end of the triglyceride spectrum. Not sure what that means for the results of this study.
– They “preselected” their participants in that they had to have had an AMI or ADHF. The big question is if people with high LDL-C were as likely to contract such. Framingham, if you leave out the extremely high data points, seems to say so. Newer results indicate they were less likely. If they were less likely, other factors may have been even stronger, making the results even more impressive.
Dr. Kendrick,
Very interesting article. My question is in regard to LDL particle count and particle size. I firmly believe the LDL-C number the cardiologists want is not good and that the LDL does not need to be lowered. Should I be concerned about the particle count and size and seek to reduce the count and or size? My triglycerides are 45 and HDL 62 LDL 107 and I am content with that but the LDL particle is 1392 and pattern A. I don’t think I have heard you address particle counts.
David Zirkle,
Particle size?
My triglycerides are 53 and my HDL is 80 and my LDL-C is 130 but my LDL-P is 1610. My LDL-P break down is Small: 233, Medium: 291, Large: 8910. All LDL-P numbers are from Quest Diagnostics. The Small and Medium numbers are listed as “High” and the Large number as “Optimal”. Oddly my LDL Pattern is listed as Optimal Pattern A. No units are listed for any of the Quest numbers.
See my post here: https://cholesterolcode.com/blood-pool/ . Scroll down to “Leave a Reply”, click “newest” scroll down about eight posts to post #23460 “Philip Thackray”. There are some interesting links there in my post and in Huggins reply.
See also Peter Attia MD’s very recent LDL-P (and, more generally apoB) article here: https://peterattiamd.com/measuring-cardiovascular-disease-risk-and-the-importance-of-apob-part-1/
Is LDL-P (apoB) a real problem or are there confounding variables in the data presented??
This is a very timely article and I follow this blog religiously. I don’t take stains and never would and refuse to have it checked.
But my husband had a stroke 7 years ago and has been taking clopidogrel and simvastatin ever since. He reduced his statin to 10mg after a very short time as his memory was severely affected and this improved. He has tolerated crushing fatigue ever since, being told it was the after effects of the stroke. At a recent visit to the GP he mentioned the fatigue again and the GP told him to come off the statin for a month to see what happened but not for any longer as it was not ‘safe’ to do so. My H told him he was eating low carb, healthy fat, real food so his cholesterol should be fine and asked him about NNT. The GP could not answer but mumbled something about endothelial cells, inflammation and secondary prevention. He told him come back in a month and if the fatigue has gone he’ll try a different type of statin! My H has been feeling much better without it and the fatigue has disappeared but he’s now very scared of stopping statins altogether as the GP has frightened him. Although he’s a bit miffed about losing so much Tim ego fatigue caused by the drugs! Any advice would be very welcome.
Pat,
I suggest getting your husband a copy of Malcolm Kendricks book “A Statin Nation”.
Pat,
I sympathise very much with your position. I am not a doctor, but as I understand it, the various statins do vary somewhat regarding side effects, so as a last resort I suppose if your doctor switches him to a different statin that might do the trick.
However, I rather think the best approach is to change philosophy. I don’t know how old your husband is, but if he is anything like my age (70), perhaps it is best to think that life will not last for ever whatever pills we take, so it is better to enjoy life without nasty side effects, rather than make our time a misery while possibly extending it a little.
Finally, some people find that statins damage them in ways that don’t reverse easily, so I would never fool with them again.
“perhaps it is best to think that life will not last for ever whatever pills we take, so it is better to enjoy life without nasty side effects, rather than make our time a misery while possibly extending it a little.”
Quite right, David. I’ll add to that the risk of too much testing, particularly as you get to an advanced age. They’re going to find something, and want to treat it, damn the adverse effects and risks.
My mother is 86 yo, and insists on getting regular colonoscopies, because her father died from colon cancer at 92 yo. But I think the very real risks of the procedure is not worth it (I won’t even get them at 56 yo, given the risks, and my personal low risk profile, vs. the overall risk profile for the general population). And even if they find something (assuming it’s not a false positive), what will treating it gain her in longevity vs. the negative effects on her life of the treatment process (whatever that may be)?
And after all, he died at 92 year old ! At some point we can be getting greedy. You’re going to die of something, after all. And he didn’t go through a long an painful dying process either. But she can’t see past the pain she felt in losing her father, I guess.
Two of the top three in the hundred most discussed research works of 2019 would be of interest to commenters here. https://www.altmetric.com/top100/2019/
#2 of 100 — Scientists rise up against statistical significance
More than 800 scientists call for statistical significance to be retired, and thus bring an end to hyped claims, wasted resources and missed opportunities.
#3 of 100 — Measles, Mumps, Rubella Vaccination and Autism
It’s official (again): The MMR vaccine does not cause autism. Danish researchers studied the records of more than 650,000 children and showed kids who had the MMR vaccine were actually less likely to be diagnosed with autism.
…and they finally did that parachute test ;o)
#8 of 100 — Parachute use to prevent death and major trauma when jumping from aircraft: randomized controlled trial
Parachutes don’t save people jumping out of planes, but they might help stop us from jumping to conclusions. In this satirical paper, Harvard scientists show the limitations of randomized controlled trials.
Other popular interests: AI faking images, climate change, diet, and human behavior.
Six of the top ten best-selling pharmaceuticals are for treating cancer.
https://en.wikipedia.org/wiki/List_of_largest_selling_pharmaceutical_products
Cancer is detected by mammograms, x-rays, or scans. If AI can fool us by creating artificial faces, it should be able to create artificial mammograms, x-rays, or scans that show the presence of tumors.
They wouldn’t stoop so low just to make a profit, would they? Would they? Anyone…?
Fairly sure that number three has been achieved by a refusal to record a diagnosis of any side effect following the MMR and now MMRV vaccination.
If you rely on the data collected then if it hasn’t been collected you will get the negative result they want you to get.
[I may be paranoid, but the evidence is stacking up that they really are out to get me!]
Just out of interest I have recently purchased Dr Wakefield’s ‘Callous Disregard’ to see what had actually gone on, inside the front cover in large bold typeface it says that the book is not permitted to be sold in the UK. Make of that what you will.
That’s amusing, all five of the copies I bought have that in too. 🤫😂
I posted a comment last night which has disappeared from here? As I’m new to this I’m not sure why this would be, can anyone offer a suggestion please? Was it possibly an inappropriate type of comment?
I posted a comment last night which has disappeared from here? As I’m new to this I’m not sure why this would be, can anyone offer a suggestion please? Was it possibly an inappropriate type of comment?
The Wakefield paper that caused all the fuss (and implicated bowel problems, not the MMR vaccine) was published in 1998. In the 20-odd years that have passed since then one hopes that the manufacturers have made the vaccine progressively safer.
Martin Back: They most certainly haven’t. They have no incentive to improve safety because they have no liability (in the U.S.) for injury from vaccines, as they do for drugs (such as Vioxx, for example), and while reporting vaccine injury is mandatory, there is no enforcement mechanism, and doctors are taught nothing in medical school about how to spot them. The result is that less than 1% of vaccine injuries are reported to VAERS (the Vaccine Adverse Event Reporting System). They are essentially swept under the rug. Nevertheless, over the 32 years the vaccine court has been in operation about U.S. $4.5 billion has been paid as compensation for vaccine injuries. Should have been closer to $450 billion. It is not an actual court, but an administrative procedure. There are no rules of evidence, no discovery. It is a highly contentious, adversarial system in which it is very difficult for complainants to prevail. Merck’s MMR has been in use for decades. It may not be in use much longer. It is clear that the mumps portion (the Jeryl Lyn strain, which was derived from a throat swab from the throat of Maurice Hilleman’s daughter, Leryl Lyn) is no longer effective, thus outbreaks on college campuses among the fully vaccinated (Hilleman was the CEO of Merck at the time). There is an eleven year saga in federal court in Pennsylvania. The two Merck scientists tasked with verifying efficacy of the mumps portion were told to cheat and lie in their testing. That case may be coming to a conclusion, leading to the de-licensing of the Merck MMR, as the FDA is working furiously to license the GSK version of MMR. Secondary vaccine failure is the term for this. The same thing is happening with the pertussis portion of all the licensed versions of diphtheria, tetanus and pertussis vaccines. The authorities know this, and admit it in print. What are they doing about it? Nothing at all, of course.
The new kid on the block seems to be CAC.
If you have a high Agatston score, you will die . . . unless you take statins!
Well, statins will increase calcification, so . . . ?
But there are dissenters: Maybe if you’ve spent a life exercising vigorously you’ll have a high CAC, but better off for the exercise.
There are bacterial infections that cause vessel lesions that, when healed, calcify.
A score above 100 and you’re in trouble.
A score off the charts at over 400 and you’re in deep trouble.
A score over 1,500 (yes!) and . . . what kind of trouble is that??
‘Course the only way to address high scores is a complete lifestyle change including, naturally, a powerful statin. Pfff.
Dr. Malcolm, can you shed light on this?
Take a look at this latest set of harangues, including comments and links:
Yes. Just happened to come across a video of the Dr Arthur speaking to a very intently listening Ivor Cummins where yes indeed, statins are endorsed.
Thank you for this link!
Very interesting talk between two knowledgeable people!
I couldn’t resist watching since my favorite Ivan Cummins was a part of it. I learnt a lot, not least about possible benefits of statins – a new take on this. I couldn’t believe that such a thing could exist.
Calcification score seems to be a very strong indicator of CVD risk and is strongly advocated by these two gentlemen – probably also a big business.
In my case I am sure I would hit the really high marks – to tell me that I am a CVD-victim – and from that point of view it is most likely a useless test for me – just a waste of money. And the message as far as I understand it here is, if you then get the high score numbers, to do exactly what I have been doing for many years now and that is to go low carb and keto at best. They also advocate the Kraft test, measuring insulin levels as a function of time after a meal. Insulin measurements are not easily to get at through the standard health care service but much more accessible than a calcification test.
With the Kraft test you could also see if you can get out of the diabetes trap and reverse the diabetes process. Much simpler you can do it (less reliably) by several blood glucose measurements following a meal see how fast you are getting your values back to normal. If it take many hours it is an alarm. The fasting glucose levels, though, tells you nothing of value if you are not full blown diabetic.
Two things Goran that spring to mind. The endorsement for statins is a limited endorsement. Secondly we have no confirmation that Ivor agrees.
It certainly wouldn’t convince me to re- statinate.
I have to confess I found this heavy going with several lapses of concentration. It’s over an hour long and needs another viewing. Plus there’s part 2 ! Not exactly Christmas viewing
Though I had assumed the endorsement of statins was for its anti oxidative properties due to NO . Particular concern attached to lp(a)
I think it is a complex area. Calcification per se is not dangerous, or damaging. It is, what I think of as, late stage healing. I think it rather depends on why you got the damage that cause the calcification. Intense exercise, or diabetes, or smoking. The first one, and you are doing things mostly right. The second two, and your calcification is a result of ‘damaging’ factors that are still causing problems. I reserve the right to change my mind on this.
Sorry, but just trying to get this straight: If K2 redirects calcium to the bone matrix, does that mean that potentially there would be insufficient available in the arteries to heal damaged endothelium?
Hi Frederica,
That’s an extremely excellent question!
I’ve been doing K2 as menaquinone and menatetranone – sometimes double-dosing if I feel particularly paranoid – for the past four+ years.
It’s only paranoia if you’re not actually about to die, right?
My radiology report from then stated I had a CAC of 1,609! (I just looked it up again.)
Has anything happened to my calcifications in the meantime? K2 done good; harm?
Who knows. I’m refused a second scan prescription. (Only $95 here.)
Thank you, Malcolm.
This leads to my next question.
Considering that heart surgeons complain that extensive calcification makes CABG difficult and that placing a stent becomes tricky and less effective, is there a viable alternative? (Lets presume one has not been doing things mostly right.) 😦
External Enhanced Counter-pulsation is a non-invasive alternative that promotes collaterals, bridging blockages that might be present in a calcified coronary artery.
Will collaterals really form with all that “hardening” in the way??
Very interesting Malcolm!
So, if I understand correctly, if someone has a high CAC score, doctors will prescribe statins, which do not lower CAC and likely will increase it as statins cause arterial calcification, and provide no reduction from the risk of heart disease, while ruining one’s health?
Doc Malcolm,
Another thing. Calcification density is supposed to make a difference, right? What difference?
A reductionist might put the cause of calcification on perturbed homeostasis of smooth muscle cells.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5852633/
Role of smooth muscle cells in vascular calcification: implications in atherosclerosis and arterial stiffness
Jerome Savage
Many thanks for providing the link to Ivor Cummins’ podcast with the CAC guy Arthur Agatston.
It has a running time of 1.08.47 but worth your time and with cholesterol dominating the podcast (e.g. in the case histories they discuss), very relevant to this blog by Dr Kendrick and some of the comments (e.g. on particles).
– 1st 9 minutes deals with causes/risk factors (with chronic stress appearing on the slide).
– At around 32 mins, Dr Agatston states “calcified plaques don’t regress”, which prompts a reply/discussion from Ivor Cummins. Dr Agatston does stress a few times the importance of no new plaques (soft plaques) appearing and perhaps regression/progression of calcified plaques not as worrying.
– I’ve mentioned that cholesterol dominates the podcast but I don’t think Dr Agatston is promoting the lipid hypothesis (see the 1st 9 minutes for causes/risk factors). For example, at around 49 minutes there is a case history with a CAC of 0 but high cholesterol. Ivor Cummins comments that there was no impact by cholesterol on vascular disease.
I wish we all had access to the many tests mentioned and the good doctors doing the good work.
Thanks Charles, I will revisit & find the specific time.
Reading around the subject of the value of ascorbic acid in reducing heart disease and stroke in mammals able to synthesise it compared to humans (and a few other mammals) that cannot, I came across research that discusses the ability of red blood cells to convert oxidised ascorbic acid (DHA) back to ascorbic acid using the Glut 1 receptor. This appears to be an adaptation to our loss of the ability to synthesise ascorbic acid.
Does this carrier of vitamin C in any way account for its presence in blood clots?
Further reading around reveals [ EBioMedicine. 2015 Nov; 2(11): 1735–1750.
Published online 2015 Oct 3. doi: 10.1016/j.ebiom.2015.09.049
PMCID: PMC4740302
PMID: 26870799
Low Red Blood Cell Vitamin C Concentrations Induce Red Blood Cell Fragility: A Link to Diabetes Via Glucose, Glucose Transporters, and Dehydroascorbic Acid ] that when deprived of ascorbic acid by excess glucose at the Glut1 receptor, erythrocytes become less deformable.
Presumably this is then a mechanism for increased vascular damage by more rigid erythrocytes at stress points in the vasculature.
Dear Dr Kendrick,
Thanks for all your emails, which are very informative! They add many things to what you taught us in The Great Cholesterol Con”. And whenever I read anything related to cholesterol, I immediately think about you! Here is something I read in SciAm Top Science Stories of 2019, in relation to chimps and their lack of exercise: “Despite having normally high cholesterol levels, chimp arteries do not harden and clog. As a result, chimps do not develop humanlike heart disease or have heart attacks from occluded coronary arteries” It never occurred to the author, Herman Pontzer, that this is because high cholesterol levels have nothing to do with heart disease! Happy New Year! ”
On Mon, 23 Dec 2019, 10:50 Dr. Malcolm Kendrick, wrote:
> Dr. Malcolm Kendrick posted: “23rd December 2019 Another new study > Question: If a tree falls in the forest, and there’s nobody around to hear, > does it make a sound? This is a philosophical question that has been around > for some time. I shall change it slightly to the followin” >
Frederica Huxley
“if K2 redirects calcium…insufficient available…to heal damaged endothelium”.
What an interesting thought on the vitamin K2/arterial calcium issue (it’s an issue for me)! I don’t think I’ve seen that consideration before, but I may be wrong.
The main arterial calcification arguments being:
(1) that the arterial calcium is there for a reason or
(2) it shouldn’t be there – get rid of it and then get better.
I think, for example, both Dr Barry Sears and Dr Agatston (see the Ivor Cummins podcast link provided by Jerome Savage) express more concern over new, soft, vulnerable, dangerous plaques. I recall Dr Sears referring to calcified plaques as concreted and thus less vulnerable.
All of which has modified my approach to one of caution with vitamin K2 – I supplement with vitamin K2 as opposed to shovelling it down my throat to reduce my calcium score.
And your comment is for me another reason to proceed with caution.
Irrespective of the rights or wrongs using K2 to shift the arterial calcification, how efficacious is it?
I’ve got a few visible, white scars on my skin (which I’ve learnt from Dr Kendrick on this website is calcium). They are still there…same as always. But I’m not megadosing on K2.
Any vitamin K2 megadosers help out – vitamin k2 does shift calcium to the teeth and bones, doesn’t it? Or is it just the arterial calcium it redirects? How does it know?
Or is the calcium present in skin damaged scars and arterial damage comparing apples and pears?
Charles,
Yes yes yes . . . and yes!
All of your concerns need knowledgeable answers. It’s not really possible to learn much that’s definitive from individual experience.
Those of us on K2 are going ahead relying on biased logic at best. And, we are constantly learning more about which circle of Hell that approach can lead us to!
JDP, 03 Jan.
Noooooo, don’t stir the dogmatic pot by suggesting EECP. ! – I was “vanished” from a heart support forum for doing that.
But yes, it is claimed to enhance and encourage collateral growth, as well as improve any chronic condition that benefits from increased oxygenation / circulation.
But it’s biggest problem, is it does NOT need a ‘Cardiologist’ to administer or supervise the therapy, thereby making if financially unattractive. Hence the feigned ignorance thereof.
EECP centres can be found throughout Asia, – Thailand International Hospital, and even a clinic on the holiday island of Bali (Indonesia). But none in Australia.
Yet the American FDA approves it’s use, and their Medicare supports its’ use.
And to be pedantic, there exists more studies and trials….than PCI can boast. Both being of similar vintage…
Yet another new study:
Lipoprotein (a) is reduced in subjects testing a new drug entering phase III trials.
Is this a good thing??
https://www.nejm.org/doi/full/10.1056/NEJMoa1905239
JDPatten: Note that the endpoint is a reduction in Lp(a) levels from this novel drug. Nothing about downstream effects, or change in risk for MI, the all-important question. For the moment I remain skeptical.
Article in today’s Telegraph about Tom Watson’s weight loss & Type 2 diabetes reversal, crediting Aseem Malhotra (among others) & the low carb diet.
He refers to the public health advice that was available and the marketing messages, [particularly] about low-fat products and how this was contradicted by “footnotes” in Aseem’s book. He singles out sugar as the culprit but also removed processed foods & pasta from his diet. Blood glucose normalised within 1 month.
Ringing endorsement for Dr Kendrick’s philosophy.
It strikes me that it would be best if the number of new medical studies were culled by a factor of 10 and the remaining 90% of researchers were used to do confirmatory research on the existing work. These researchers would then get brownie points if they were able to refute the study they were studying. Over time every researcher would get a shot at executing a novel study.
David – Possibly this is what this latest from the BMJ has in mind : BMJ exposes big pharma’s interference in medical decisions – goes on :-
(related story : Why Big Pharma is jeopardizing millions of lives for profit)
BMJ Calls for Accurate Research to Back Medical Practice
The BMJ launched a global initiative calling for a reduction in the commercial influence in health care moving toward transparency. In a press release published at the same time as the first article in the collection,5 BMJ’s editor-in-chief, Dr. Fiona Godlee, said:6
“Patients and the public deserve to have evidence they can trust. Commercial influence has no place in scientific research, nor in the education and guidance of clinicians, nor in decisions about diagnosis and treatment. We hope that people around the world support our call for fundamental reforms.”
The journal plans to add more content to the collection to further understanding of the conflict of interest between commercial Industries and medical decisions.7 They brought together experts from eight nations in medicine, law and philosophy to propose fundamental cultural changes with the intention of moving away from commercial influence and closer toward independence.
In trying to balance overtesting, overdiagnosis and overtreatment against necessary procedures for diagnosis, the experts want to ensure dissemination of valid evidence “conducted as independently as possible from industries profiting from their use.” They go on to say:8
“Some see transparency as the best strategy, while others regard it as necessary but insufficient. We argue that endemic financial entanglement is distorting the production and use of healthcare evidence, causing harm to individuals and waste for health systems.”
https://www.healthnutnews.com/bmj-exposes-big-pharmas-interference-in-medical-decisions/
Sasha: Yes. As I understand it, having one copy of the sickle cell gene confers protection against malaria.
JP Patten
“calcification density is supposed to make a difference…what difference?”
Your query rang a bell from my CAC scan back in 2017 – in fact, I did request my density and volume results in addition to my CAC score. I didn’t get them…maybe next time. Maybe they have but they forgot to let me know. Back to your query…
Dr Mike Eades should be able to help with your query – here’s a link to Ivor Cummins’ Fat Emperor website where the topic of volume and density is covered:
https://thefatemperor.com/2017-3-3-dr-mike-eades-important-note-on-calcification-volume-vs-density-cac/
Basically, my take is that:
volume = amount of calcium and
density = how solid the calcification is
From the text:
– if density dominates over volume your risk may be OK
– if your CAC score increases over the years and density dominates with volume falling you do not have appreciable risk
– if volume dominates over density – it’s a major flag for unstable plaque presence.
I think I’d like to know my density and volume results from 2017, especially in the context of volume dominating over density.
Hopes this helps!
Charles,
Thanks.
Try this one. Ow. It hurt my brains first read-through. It seems you might get a completely different scoring system depending on what hospital / lab you go to. Nothing like knowing where you stand!
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4091626/
Charles,
Also:
This editorial and the article referred to sheds more light on this whole calcification scene.
https://www.sciencedirect.com/science/article/pii/S1936878X17305235
Interesting article which confirms my belief that in my severe MI-case CAC is close to a useless test and as a tool to predict my future since it would at best tell me what I already know: that my plaque is of a considerable extent and that it will never disappear. I am still surviving on my collaterals developed now more than 20 years ago but they are not not to be seen on any scans. As far as I know there is no way to get a closer look into their status except through postmortem intricate examination.
My job is thus today to not relax and keep pushing exercises to my limit in order to keep my collaterals open. I guess that I should stay with my “new” high fat lifestyle with great food (e.g. today a wild boar steak with a lot of butter sauce) and a handfull of supplements each day.
It seems to work anyway.
Actually, Goran, there is a way to visualize your collaterals – if you really wanted to.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6756702/
But, as a person in your circumstances might say, “If it ain’t broke, don’t fix it.”
I found that, with my high basic CAC level on record (No measure of density!), I am, for all purposes Medical, labelled.
I might as well go to the cardiologist’s office wearing a T shirt saying, “Wait. Nevermind, I’m going to die really soon anyway.”
JD, thank you for that reference I learnt a lot about technical improvements when looking into our hearts. Very interesting reading indeed!
And as you say (good idea!) I should have bought a T-shirt with the text “Soon to die!” already 20 years ago :).
Now it is probably too late?
At least I think so. Especially yesterday when I was “fighting” with som strenuous work in the cold, rainy and very windy weather in my garden and then was hit by my ugly angina again. I shouldn’t have done that after a meal – I will probably never learn on this point. Or perhaps it was not a bad thing to do after all since it probably helped building some new collaterals and I really need them looking at what has to b done in the garden with a new greenhouse to be raised among some other things like taking care of some fallen trees with my chain saws (I have got a new nice battery driven one on a pole to reach up in the trees to cut branches – a technical improvement I as an engineer rather take to my heart.)
Well, thanks again for improving my knowledge for what it is now worth.
(Perhaps we are though happier if we don’t know so much if I should trust what I now read in the “Essays of Michel de Montaigne” where he refers the Bible. (You are not allowed to eat from the fruit of knowledge! Or you get expelled from the Paradise!) BTW Montaigne thinks it nice die when one is in my age – in his time (end of the 16th century my 73 years would probably correspond to about 60 or so.)
Goran,
Youngster: “Ugh! 95? Who would ever want to live to be that old?”
Oldster But Wiser: “A 94 year-old!”
Yes, I know. Setting yourself reasonable limits is challenging. Meeting those limits… and going beyond… is who and what you are, right?
Everything about my 75 year old body is telling me to be reasonable. But that’s not how I cut and set granite curbstones by hand along my 150 foot driveway over the last couple of years.
Trouble is that, when I do such work, I then suffer the consequence of atrial tachycardia.
Sitting back to take it easy ain’t me, but sitting there with a heart rate of 230 beats per minute ain’t either!
JD Patten
there are two fantastic things about this blog:
firstly: Dr K’s leads
secondly: comments from the regulars. About atrial tachycardia, I get very occasional, once a month or less bursts of tachycardia about 160 bpm which last two minutes. What do you do about it if anything, I wait till it goes. I am trying to identify what brings it on, so far without success!
Returning to inflammation of the blood vessels, if I may:
Here is a quote from “Giant-cell Arteritis” by Paulley and Hughes, 1960
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2098374/
“A depressive state, often concealed, invariably precedes the somatic manifestations of the disease (inflammation of the arteries) by a few weeks or months and commonly arises from the death or marriage of a near or dear one. However, deaths of cats and dogs were provocative on two occasions in this series. Deprivation other than by death – as, for example, by admission of a beloved person to hospital , especially a mental hospital – occurred in a number of our cases. Marriage of sons or daughters incurring separation, especially emigration, and ungracious treatment by relations of recently bereaved old people were recurrent features. The types of stress precipitant, and the personality make-up, are not at present distinguishable from those found by one of us in most collagen diseases, particularly rheumatoid arthritis.”
My question is, since depression causes the release of excess cortisol which has an anti-inflammatory effect, might not the body try to restore equilibrium (and healing) by increasing inflammation by some means, to override the anti-healing, anti-inflammatory effect? And hence we get the vasculitis (which is treated with more anti-inflammatory!)
Or can we think of it as “stress-induced cortisol dysfunction” ?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4263906/
“Regardless of the neuroendocrine mechanism involved, the long-term effect of chronic stress remains the same: cortisol fails to function.”
I learned a new acronym today — QALY, which stands for Quality-Adjusted Life Year.
https://en.wikipedia.org/wiki/Quality-adjusted_life_year
The basic idea is one year in perfect health is 1 QALY, death is 0 QALY, and a state of partial health is in-between, so e.g. a year with a foot amputated might be 0.7 QALY. It’s rather subjective, but it has been proposed as a way to determine if a treatment is worth the cost, by determining how many QALYs it buys you.
Some authorities maintain that there are states that are are “worse than dead” and they should count as negative QALYs.
Applying the concept to statins, Dr Kendrick says that on average statins will buy you four days of extra life. That’s approximately 0.01 QALYs. But by that time you could be a shambling zombie with Alzheimer’s, diabetic complications, and severe muscle pains, which counts in my book as a “state worse than death”, let’s say -0.5 QALYs.
How much would you be willing to spend on statins to buy -0.49 QALYs? Let’s face it, it’s not worth spending money to buy a worse quality of life. In fact, assuming you’d be willing to buy an extra year of healthy life for $100,000, the statin manufacturers should pay you $49,000 to take the damned things.
Granted, I sucked these numbers out of my thumb, but the principle stands: statins are not worth it.
Very true, and as far as I know (someone will correct me if I am wrong) that figure of 4 days doesn’t take into account the loss of fitness caused by statins – those ‘muscle pains’ are actually quite debilitating – and statin side effects probably cause people to take less exercise, and possibly fall more.
Didn’t you have a President once who opined “you can fool all of the people some of the time, and some of the people all of the time, but you can’t fool all of the people all of the time”?
Sadly, not much has changed since he said it, if you consider statins, or on this side of the pond Brexit, although there are those of doubtful ethics and morality who are working hard to achieve what Lincoln thought impossible.
JD Patten – your lp(a) comment and research link
(apologies for mistyping your second initial in my CAC density/volume comment)
Like Gary Ogden I’m skeptical, and cynical too.
– It’s positive that lp(a) is being looked into, that someone has decided to spend time and money and resources looking into it but
– It’s negative that it’s Big Pharma.
As always, it’s looking at symptoms, not causes…prevention is better than cure (ideally).
But it’s got me curious: at what point does Big Pharma decide to spend their time, money and resources to develop their medicines, especially when their coffers are overflowing and will continue to overflow for some time?
By monitoring areas where others are doing their research e.g. Matthias Rath and John Cha with their lp(a) and vit C research?
Or gathering data from cardiac wards, GPs and so on?
Or vox pops such as this website (they’d be stupid not to)?
As mentioned above, I’ll take my vitamin C and treat the symptom and get all the benefits of vitamin C at the same time. That’s assuming that any lp(a) is being caused by vitamin C deficiency.
I’m not sure if vit C deficiency is the only cause of high lp(a). I don’t know enough about it. I know lp(a) is a repair molecule. I imagine there could be numerous causes for it’s presence.
Dr John E Whitcomb 25 year MD talks about K2 and all the diseases it affects and explains the French paradox and more eg removes arterial calcium https://www.youtube.com/watch?v=jPWCJxyHAg4
Randall
Thanks!
Weston Price in honor!
That was about the best lecture I ever heard about supplements. I am evidently on the right track though I should add. back the vitamin A in my big box.
Vitamin K2 with D3 seems to bring calcium out of arteries if I understand Dr. Whitcomb right.
Your welcome. Best talk on diff between MK4 and MK7
“What’s the deal with dental flossers?”
Hold on folks! Probably, you are now thinking that I’m off topic for this instalment, and also CVD in general.
But let me explain, or rather let someone called Dr Eskander explain.
I’ve just been sent an article on dental flossing extolling the virtues of an electric toothbrush/water flosser. But there’s a bit of scaremongering first to help persuade us to invest in one these devices.
To quote the article:
“Forgoing a proper dental regime including flossing can lead to gum disease, which is essentially chronic inflammation that ups your risk of heart problems. “In a process known as atherosclerosis, plaque is able to enter the bloodstream, then the heart, before attaching itself to fatty deposits in the blood vessels” says Dr Eskander.”
Over the years, Dr Kendrick has listed many of the causes of CVD. Most recently, I think, in “What causes heart disease – part 59” he itemized 35 causes and stated “that list was just off the top of my head, I could get another fifty without much effort”.
I’ve no idea if the accumulation of dental plaque on teeth, then forming tartar then gum disease then atherosclerosis has appeared on Dr Kendrick’s radar, or anybody else’s radar.
And I’ve no idea if Dr Eskander is stating that dental plaque actually enters the bloodstream but it reads ambiguously.
And I’ve no idea what sources Dr Eskander has used for his comment. For the time being, I’ll remain cynical and skeptical and feel pretty confident in stating the the cardiac wards are probably not full of patients with serious dental problems. But I try and keep an open mind and thus thought this was worth a comment from me.
But you’ve been warned! Get flossing! (It’s good advice anyway).
Charles, Tom Levy has written about the problems of infections associated with the mouth. Particularly root canal fillings. He said that heart attacks were found to have been caused by exotic bacteria that were found in the victims root canal fillings. No doubt damaging bacteria would be available in other places in the mouth, so frequent, through cleaning would probably help.
Dental plaque is a likely place for bugs to breed, so getting rid of the plaque, or at least reducing it should help. Which brings me at last to the point. I found the amount of plaque reduced dramatically when I stopped eating most carbohydrates, especially all the wheat things, which of course have glue in them. Sorry a misprint there, should have been gluten. Nope, on second thoughts, glue will do.
Get rid of the glue, and fewer things will stick to your teeth.
Anybody have any thoughts on this?
AhNotepad: We have a micro-biome in our mouth just like we do in the entire intestinal tract (asshole to appetite, so to speak) and skin. The species vary by location in the mouth. Although the people Dr. Price studied had no toothbrushes or floss, they had excellent teeth, good health, and probably low rates of CVD, including those who ate grains. They did not eat the displacing foods of modern commerce (sugar, flour, vegetable oils, and canned foods), which is likely the explanation for this. I do not eat these, either. Since I gave up grains it has been much easier to keep from getting plaque buildup. My teeth and gums sure seem to be happier. Nevertheless, I brush and floss before bed every day, and get a twice-yearly cleaning at the dentist.
Gary – what’s the problem with canned foods ?
Jerome Savage: The ingredients. Only half kidding here. Canned foods are included in Dr. Price’s list of the “displacing foods of modern commerce.”. I suspect it was because the canned foods were less nourishing than traditional foods, and, in the case of fruits, would have had a lot of added sugar. My mother canned fruits and made jams and jellies in season, but we ate lots of nourishing foods, too.
Worse than canned ingredients is the insidious habit of lining cans with BPA plasticisers, which can leach into food.
Well, surprise, surprise … NOT. Yet another nail in the coffin of the cholesterol theory of heart disease. Sadly, as the evidence against it accumulates, the researchers are still too cowed to proclaim their results more vigorously. https://www.vitalchoice.com/article/saturated-fats-seen-to-reduce-cardio-risk-factors?mcID=902:5e0fba77abd7ac3f4f6dbf70:ot:5d0aa9fc1802c8c52477ca07:1&utm_source=cordial&utm_medium=email&utm_campaign=VCNews010620
Ugh. I never know what to do when an article says something that is wrong:
“That said, when someone’s diet contains relatively high amounts of saturated fats, most — but not all — the available evidence suggests that replacing 5% of dietary saturated fat with polyunsaturated fat reduces the risk of coronary heart disease by about 10% (Wang DD et al. 2016; Praagman J et al. 2016).”
Take a look at the Wang DD reference, here:
https://www.ncbi.nlm.nih.gov/pubmed/26429077
Their conclusion: “Our findings indicate that unsaturated fats, especially PUFAs, and/or high-quality carbohydrates can be used to replace saturated fats to reduce CHD risk.”
One might think based on that conclusion was what they did was replace saturated fats with unsaturated fats, particularly PUFAs. Did they do that? Of course not. They just followed people for some years (using food frequency questionnaires (FFQs) given every 4 years) and determined that the people who indicated (lied?) on the FFQs they ate fewer saturated fats but more PUFAs had lower rates of heart disease.
So, how can they make their conclusions? They can’t, as it’s not a randomized controlled trial. That’s why the use the meaningless “Our findings indicate…”, because they never actually did this.
By the way, guess from where the study authors were? That bastion of crapidemiology, Harvard. As soon as you see an epidemiological study is from Harvard, you should stop reading. It’s garbage.
I did not look at the other study, as I’m sure it’s garbage too.
JD Patten (and anybody else interested in CAC – coronary artery calcium – scans)
Thanks for the links – my brain hurts too. My initial thought is that a large pot of tea will be needed to accompany a second read through.
The comments in the link I’m about to provide are less demanding, being my comments from 2017 on Dr Mike Eades’ website.
Back in 2017, when I was researching CAC scans and Dr Mike Eades was still blogging (he’s active on Twitter nowadays) he kindly invited people to let him know what they’d like him to blog about:
“I’ve got plenty of ideas to post about, but I am keen on learning what people who actually read these posts want to read about. If you’ve got a topic you would like to see explored, let me know in the comments.”
So I did.
My 1st entry in the comments is dated 22 Aug 2017 near the bottom – 99/137 comments – suggesting an idiot’s guide to CAC scans because it’s so complex with concerns like density and volume and a few other suggestions.
My second entry in the comments is dated 9 Sept 2017 – 131/137 comments. I’d obviously been away having a think, doing research, seeing various doctors and so on and come back with further questions/suggestions for a possible blog.
I mentioned (1) angiogram vs CAC scan (2) frequency for CAC scans and plaque progression and (3) echocardiogram vs CAC scan.
I was thrilled to get a detailed reply from Dr Eades. Plenty of useful stuff if you are thinking about getting a scan done or getting retested (which I am).
Sadly, the post on CAC scans never happened, which makes me very grateful for Dr Eades’ great reply.
Here’s the link:
https://proteinpower.com/kevin-hall-kickstarter-and-catching-up/
Thanks Charles. All fascinating stuff. A bit alarming about the different scanners. As with anything: buyer beware.
My sense from the recent CAC research is that scanning is far from an actually standardized done deal. More is coming out about how factoring in density can change the picture. The classic Agatston is arrived at through manipulating assumed coarse density percentiles to increase the risk score, whereas various researches indicate that increasing density – viewed on a continuous scale – is inversely proportional to risk. To a degree.
Well, somebody’s gotta be more right than somebody else.
So, now there are various papers touting their own unique scoring system.
Competition is good, right? But upsetting the applecart of “simple”, “straightforward”, standardized, and incorrect Agatston will be tough going and take a
l o o o n g
time.
JD Patten and Goran
Concerning collaterals – can I conclude that unless you have this scan done, that the presence of
collaterals is just an assumption?
Or it it established that collaterals will form once a certain level of arterial blockage has been reached?
Having a calcium score of 1500, I think I’d like to have a check for collaterals but how available and affordable is this CCC (coronary collateral circulation) scan? I’ve had enough trouble here in England getting a more mainstream CAC scan done.
Speaking of which, and JD’s comments about standardisation, I thought the global (i.e. everyone uses the same measurement) Agatston score a good thing. No need to convert from a UK measurement to an American measurement.
Time and time again American measuring differs from the UK e.g. a good example is mmol/L in UK and mg/dl in America.
With reference to different scoring systems, it seems in the interest of consistency and tracking your plaque or whatever, to return to the same hospital and CT scanner
Charles,
Well, well,
Since 20 years my main coronary arteries are definitely blocked according to the angiograms that were performed at that time. And that I am now sitting here is then the ultimate proof for existing collaterals and for my survival and here I for once agree with the cardiologists. Thus I don’t need any CAC scans or any more angiograms – I already know and I refused a second round five years ago!
Today I, BTW, made some really heavy hauling and to my surprise I didn’t experience any effort angina at all – new collaterals? This is, though a fact but, of course an assumption.
Charles,
Be careful what you wish for.
My former cardiologist pushed statins on me because my cholesterol levels were higher than he
liked. Old story. To get him off my back, I confidently submitted myself to various tests. After all, no symptoms at all. A1C was fine. Blood pressure fine. Cardiac ultrasound fine. CRP, looking for inflammation, very low. Stress test fine.
Then, overconfident, I opted for the CAC. (Only $95 here.)
Well, I am now as good as labelled for life with an Agatston of 1609. That was five and a half years ago. I’m still here!
Agatston scoring is flawed. The rough approximations of density it takes into account in the algorithm that’s used increases the risk score, whereas more recent sets of research agree that there’s actually an inverse relationship between density and risk.
I’m not saying that a high Agatston is not a matter of concern.
I am saying that a simple Agatston might well be exaggerating your risk and certainly is not telling you the whole story. The trouble with it being so standardized – its problems notwithstanding – is that any newer improved scoring system will be ignored by the Establishment.
Meantime, you’re labelled.
For me, if ever I’m threatened with a stent or CABG, I’ll insist on the collateral scan first… PROVIDED my own research tells me the test is a good one and the facility does it correctly.
But not until that threat.
Meantime meantime, look up External Enhanced CounterPulsation.
Gosh, there you go again, spreading heresy ! 🙂
CAC has just recently become not only ‘known’ in Western Australia, but our largest X-ray / Scanning company is doing a lot of …. Education.
My scan + consult with a local Cardiologist in a Denpassar / Bali Hospital cost me around $AUD 200, pricey but at that time – 2017 – CAC was not popular in WA. Obviously, nor was or is, EECP.
My score was 870 Agaston, but I knew I was beyond the pale anyway, having had a CABG x5 six months earlier.
The EECP cost around $2,000 AUD, and we opted for Bali over Thailand simply because the residency costs for 3 weeks was much less.
Yes, I’m convinced it was $$$ well-spent.
James,
So you’ve had the EECP.
What I’ve read suggests that, to be effective, you must devote some time to it with repeat sessions.
How much time did you spend in the Bali device? Feel it made a difference?
You also have me wondering about your CABG specifics.
Did you have the classic with veins replacing arteries, or the newer way with mammary arteries doing the job? I’m just wondering how capable a vein is of producing collaterals.
Starting at the beginning,.
Mammary artery used. as was a Radial Artery (arm), the Great Saphenous Vein proving mostly useless…
Anyway, that was Nov. 2016, the same time, ORBITA was published.
Normal recovery, then it started to go backwards, ie. loss of stamina and breathlessness. This was early 2017, by which time I’d discovered references to EECP.
– So I ordered the book, ‘Heal your heart with EECP’ – Braverman.
The standard therapy is 35 sessions of one hour, over 35 days. This turns out to be a compromise number , and the Chinese will do more, and more rounds if required.
– So I had 18 days of two per day with 3-4 hours between.
The Clinic claims to have done a good trade with Pensioner Aussies from the Gold Coast, and their 4 machines were…. very ‘well used’.
The first one they put me on had a problem with my irregular heart-rate, and after 8 days I’d discovered via the book, that pressures being used / recorded, were ‘marginal’. Very important as the difference between ‘placebo’ and ‘Therapeautic’ in only a handful of mm Hg.
Anyway, the ‘Reserve’ machine, coped fine on both counts.
Did I notice improvements ? – I think so. Certainly could walk further & faster on our evening strolls, and the fog of depression lifted noticeably…a not un-common side-effect of EECP. Nothing to do with being on holidays… I don’t like them !
Yes, I would support it’s use, and if / when I’m rich enough, I’ll be looking at another round, though in Thailand. (Twice the $$$$, but…)
Today my gym performance markers, 20 second sprints on a rowing machine have come back to pre- pre-Head surgery figures (2015)
Any questions ? 🙂
James DownUnder
crabsnake@hotmail.com
EECP certainly does appear to help. It was available on the NHS at one time (very strict criteria). Not sure if it has died a death, or not.
James DownUnder,
My immediate concern for myself is cardiac arrhythmia. I started with atrial fibrillation (ablated), went through atrial flutter and atrial tachycardia (both ablated) and I’m left with a variety of
premature atrial and ventricular complexes.
Heart rate irregularity, as you describe.
So, it sounds like the likes of me are not good candidates for EECP!
With my 1,609 Agatston from more than five years ago, I am of course, looking over my shoulder, keeping EECP in mind as a good hedge.
Rhythm permitting.
I’m in rural Massachusetts and there’s a suburban hospital not far from Boston, or me, that does EECP – insurance paid.
How irregular was/is your heart rate?
Here’s where I go for rhythm. It’s one of three within an hour’s drive. U S is a bit different!?
https://www.lahey.org/lhmc/department/thoracic-cardiothoracic-surgery/treatments/enhanced-external-counterpulsation/
The original EECP machine had difficulty in tracking my heart signals. Reasons could range from an intermittent fault in the leads, quality/consistency of pads,,, settings of the electronics… or software parameters. So, both Operator input and maintenance are factors and highlights the possible differences between a small provider and a larger well funded hospital which shares technical staff over many departments.
Then there may have been internal feedback from pressures ‘out of range’. Again a machine issue.
Bottom line, in my experience I’d be more concerned about the provider and their performance than your rhythm, which normally includes variability.
The cure was being put onto their spare machine which is much less used and only occasional ‘misfires’ .
My original choice was a large Thai Hospital, but wife and finances ……
US is different… There are no EECP machines in Oz, and the logical explanation would be oppo$ition from Cardiologi$t$. Hospitals also make a lot of money from (elective) heart surgery- Cath lab and CABG. The “enablers” such as health insurance and governments are locked into the current paradigm, end result is patient outcomes are sacrificed for financial gain.
Malcolm,
Do you use the CAC Score in your practice? What is your opinion of it?
https://www.bbc.com/future/article/20200108-the-medications-that-change-who-we-are
“Others have not been so lucky. Over the years, Golomb has collected reports from patients across the United States – tales of broken marriages, destroyed careers, and a surprising number of men who have come unnervingly close to murdering their wives. In almost every case, the symptoms began when they started taking statins, then promptly returned to normal when they stopped; one man repeated this cycle five times before he realised what was going on.”
Here’s a recent (February 2019) open access article from Scientific Reports: “Total cholesterol and all-cause mortality by sex and age: a prospective cohort study among 12.8 million adults”:
https://www.nature.com/articles/s41598-018-38461-y
From figure 3 I learn that low total cholesterol is in general much more strongly associated with total mortality than high cholesterol, and for people aged 75 years or more, the correlation between total cholesterol and mortality is decidedly unimpressive ( aka nonexistent in practice ). Especially at the high end.
Pity they did not measure HDL, triglycerides and so forth, but with 12.8 million adults in the cohort, I guess the data comes from the very simple and cheap health check-ups often offered to the general population.
From figure 1 we also learn that women (of a certain age) on average have much higher cholesterol than men. But live longer (that last part cannot be revealed from the figure).
In case a doctor, by mistake, manages to measure my cholesterol and wants to talk to me about (possibly) high cholesterol readings, I’ll bring this article and ask the doctor to explain.
Is that final heart attack actually due to the crystals??
It seems there’s another cogent explanation every time I turn around, and I don’t know enough to be able to know if it’s bunk or not.
https://research.msu.edu/cholesterol-crystals-studied-for-role-in-heart-attack-stroke-2/
Thanks again, Dr. K.! In summary, “It’s NOT the cholesterol. It’s NOT the cholesterol! It’s NOT the cholesterol!!” Phew, I feel so much better now!
A new study study:
Elucidation of a reason there is so much disbelief, confusion and argument over medical research.
I’ve harped here more than once about how we’re all individuals and our problems and proposed solutions to them might well not match “Mr Average’s” that RCTs present to us – no matter how well done – as the model to live up to.
https://www.ncbi.nlm.nih.gov/pubmed/?term=Lack+of+group-to-individual+generalizability+is+a+threat+to+human+subjects+research
You have beat the cholesterol horse to death, seems superfluous to keep on this subject as the literature seems to agree on this point. For some small subsets heart issues are the result of disease, genetics or toxins. But for it is a part of TOR driven aging. “TOR driven aging IS these diseases. Cancer, CHF, COPD, Ml, stroke, dementia, diabetes are all the late end stage manifestations of TOR-driven aging.” All of these increase exponentially with age.
So near 60 years of age I am going on metformin and low frequency/dose rapamycin. There are now thousands of patients on this and it is miraculous at slowing TOR driven aging and associated disease. Should make it easy to reach over 100 years of age. Rapamycintherapy.com for the particulars. Dr Green seems to be the only one to step out to test the theory and now with 4 plus years of results, seems the best way forward for life extension and disease reduction. Very cost effective, has the ability to reduce many disease causes and medical requirements of old age. Could change western medicine.
Any thoughts?
My thoughts, after listening to podcasts on this subject and reading David Sinclair’s book, are that most of the anti aging therapies are unproven and they are being hyped. I do like Dr Longo’s thinking on this, though. I don’t believe you can fool mother Nature.
Steve,
I’m sure that you have seen this post from Peter Attia MD but others may find this interesting:
https://peterattiamd.com/davidsabatini/
Philip Thackray
Hi Philip Thackray: interesting discussion about rapamycin and life extension via mTOR inhibition.
Looks like rapamycin is a plant antibiotic produced by some bacteria that can arrest cell metabolism. Understanding how plants respond might shed some light what the effect would be on humans. Producing rapamycin was beneficial to the bacterium, but not for other plant life coming in contact with it. Plants also have TOR.
https://academic.oup.com/jxb/article/70/8/2211/5460007
Target of Rapamycin kinase: central regulatory hub for plant growth and metabolism
“The discovery of TOR is a perfect example of the serendipitous nature of research. It all started with the identification of a molecule produced by Streptomyces hygroscopicus, a bacterium isolated in the 1970s in a soil sample from the remote and mysterious Easter Island, known as Rapa Nui in Polynesian. This compound was thus named rapamycin (Vezina et al., 1975). Rapamycin was found to inhibit cell proliferation but the mechanism of action was unknown. “
Good luck. Let me know when you have your hundredth birthday.
Steve, I’m quite leery of “Miracle Drugs” which over time, have all turned out to be nightmares. I took a quick peek at the website you linked to and read “Rapamycin has extended the lifespan of every living thing tested in the laboratory: yeast, worms, flies, and even middle-aged mice”. No humans it appears have been studied.
Weston Price said it takes at least 3 generations to see what effect diet and other changes have on people. So, we won’t know for 3 generations of people following that approach if it really helps, or has unseen and unintended consequences. Both of the drugs you mention are very heavy duty (ie probably not safe). Please report back your experience over time, as I’m always interested to hear first hand accounts. And, as always I will change my mind if the evidence supports doing so.
Dr.John H, my understanding from reading “Nutrition and Physical Degeneration” was facial structure could be affected almost immediately, so if a mother to be ate refined carbohydrates the face would become thinner, and the teeth would no longer have enough room. Have I misunderstood?
Dr. John H: What I got from listening to that podcast was a fascinating look at basic science. Rampamycin may not have clinical applications outside its immune-suppressing function in transplant patients, but knowing about it adds to our knowledge base in biochemistry.
Perhaps a good place to start is with a few recent papers from Mikhail Blagosklonny. Two of great personal interest to me: https://www.nature.com/articles/s41419-019-1822-8 and https://www.nature.com/articles/s41419-019-1822-8. The research and human use of rapamycin and analogs is well documented. Whether Alan Green’s approach is appropriate? I may well find out for myself (fit 79 YO with mild TD2). Thank you Steve.
AhNotepad – you are right.
Gary – Good Point!
Hi Steve: had a quick look at mTOR, rapamycin, and stem cells, not very encouraging.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550632/
Stem cell guidance through the mechanistic target of rapamycin
“Loss of mTOR, such as in the aged brain, may be a factor that results in the reduction of the proliferation of active neural stem cells.”
I find Rapamycin / metformin type anti-aging approaches interesting and will certainty look forward to any formal testing with humans that occurs. However, these drugs are both generic and therefore, there is no reason for any drug company to undertake the expense of testing these drugs for their human anti-ageing potential. Perhaps some drug company will create a patentable derivative of say Rapamycin and undertake the appropriate human testing to demonstrate the human anti-ageing effect.
Until then I would be wary of taking these drug based on the anecdotal evidence of their efficacy and lack of side effects so far presented. But I do understand how someone would want to give these drugs a try.
Philip Thackray
Hi Steve: another thought about stem cells. A fat heart may be involved in AFIB among other things.
https://www.karger.com/Article/FullText/493828
Hyperglycemia Altered the Fate of Cardiac Stem Cells to Adipogenesis through Inhibiting the β-Catenin/TCF-4 Pathway
“The adult heart has been traditionally viewed as a terminally differentiated post-mitotic organ. However, the discovery of cardiac stem cells (CSCs), which have the capacity to differentiate into the various cardiac cell lineages, has dramatically changed the understanding of myocardial biology [9, 10]. A single adult heart contains numerous CSC populations, which are divided into two types. One type of CSC population may include c-Kit+ cells, but this remains controversial; the other has been identified based on the expression of Sca-1, MDR-1, or isl-1. These CSCs can differentiate into myocardial cells, endothelial cells, and fibroblasts [11-13]. Although the resident CSC population is still unclear, with debate continuing several types of resident cardiac progenitor (or stem) cells have been reported to reside in the adult heart [14]. These CSCs play a pivotal role in the maintenance of cardiac homeostasis and regeneration [15]. After heart injury, CSCs are stimulated to propagate and differentiate, then partially replace cardiomyocytes that have been damaged by ischemia or myocardial infarction [16-18]. However, the specific signal pathways of hyperglycemia that affect CSC differentiation, reduce myocardial regeneration capability, and increase the amount of epicardial fat in diabetes remain unclear [19].
Based on the findings above, we proposed the new hypothesis that high glucose may promote CSC adipogenesis, thus contributing to the low myocardial regeneration capability and high epicardial fat content in patients with diabetes.”
Can you explain the significance of including Metformin with Rapamycin as dual therapy? I must say, I don’t fancy ingesting Rapamycin for the rest of my days, unless someone can show me it is miraculous, ( and safe), in extending life.
I can remember reading an article in the past year or so saying that this was a new and popular idea that those in Silicon Valley were doing. I have my doubts it will be helpful but more power to you if you reach 100 years of age in good shape.
I met a fellow last month who is 93 years of age. If I hadn’t been told how old he was I’d never guess. He acted and looked as if he was in his 70s. He was sharp in his conversation. Had a great sense of humor. He had all kinds of energy. I didn’t ask what he secrete to a long life was, but as I got a tour of his house he was showing off his weights, and exercise equipment. He has a pool. His wife appeared young and beautiful. He also had a large liquor bar.
See? Malcolm was right, a glass or two of wine can only be beneficial !
Yes, wine in “moderation” I do believe in!
But also in good nutrition. I remember reading about the oldest person being intervjued and asked about diet preferences and told the intervjuer that had at least one egg per day for as long as she could recall.I am a large consumer of eggs myself.
https://www.bbc.co.uk/news/health-51091083
The health service and Government must always be seen to be doing something and spinners of news bites will be required to emphasize trail blazing & cutting edge initiatives. And as we know, this is more often than not arising from corporate policy re maximising profits, market share & share price.
In any case the blurb should state that it “delays” 30,000 deaths rather than saving 30,000 lives, that is, if it stands up to any kind of scrutiny.
Bwahahahahahahah!!!!!!!
John, that’s the most hilarious report I’ve seen for a long time. I understand cyanide has a strong cholesterol busting effect too, though it busts a few other things as well.
Oh, two comments vanished. First one was about the BBC report. The most hilarious thing I have read for a long time. Cyanide has a cholesterol busting effect, and it busts other things as well, as do statins, and presumably this wonder jab will have other effects (adverse no doubt). Having Matthew Hancock (he hates being called Matthew) endorse it does nothing for confidence building, as Han….sorry, Matthew 😊, likes promoting needles for everyone. He has recieved advice from Asseem Malhotra, perhaps he could go and get some more advice.
John: Heart-warming news.
One of the worst ideas I have read about recently. Forcing the liver to absorb more cholesterol than it would naturally just seems like a bad idea.
2020…..and here we go again! Yet more rubbish in the media about cholesterol.
Luckily, there couldn’t be any drawback to halving one’s cholesterol, right?
http://high-fat-nutrition.blogspot.com/2008/01/colorectal-cancer-and-cholesterol.html
The LDL-C association did get a brief mention in the discussion:
“Surprisingly, a strong association between increased LDL levels and decreased risk of colorectal cancer was identified. The explanation for this finding is unclear.”
And of course, is there a third factor causing both, Increasing LDL levels while also decreasing risk of colorectal cancer ? But of course (of course no. 2), the body doesn’t produce LDL C for nothing ! Viva cholesterol.
I had a troubling but likely helpful health event over the New Year. Thought to mention in case it could help others.
I have a colitis condition and with that not only comes stomach issues but also muscle problems. In particular when the colitis flares up badly, the back and leg muscles can cramp up painfully. As I’ll joke it’s mother natures cruel joke, make me need to rush to the bathroom but damage my legs and hurt my back to make it difficult for me to move.
So over New Years I was in a bad way with the colitis and the back was aching terribly. I decided to try an old but new idea to see if I could find relief. I’d figured in the past that not all companies were listing broth on their lunch meat label. Broth has a bunch of spices in it, spices that I’ve wondered about as being a cause of stomach irritation. So I decided to try a plain spice free diet along with avoiding all processed lunch meat.
To my relief not only has the stomach improved on this diet, but also my back and leg muscles issues have gone away, mostly. There is still some minor leg muscle pain problems. The back though feels pain free and is strong.
This latest episode with my colitis had me thinking that I’ve known or known of many people with back issues of unknown cause. Some have even had back surgery to find relief but the operation was unsuccessful. It had me thinking that possibly there are others like me, without the colitis, that have back issues likely linked to the diet. Possibly a dietary change can bring relief for some with back issues. Just a theory that is working for me at the moment, one that I thought might be helpful for others.
Soul,
That’s great that you’ve found relief.
I’m wondering about a different approach that might possibly apply.
You describe a cycle of colitis, leg and back pain, and a processed food diet. I’m wondering if pain relievers such as ibuprofen or other NSAIDs are part of the cycle. It’s well established but not widely known that the NSAIDs can trigger lymphocytic colitis, a subcategory of Microscopic Colitis. It’s called that because a biopsy and microscope are necessary for the diagnosis.
My case of lymphocytic colitis was mistaken for Crohn’s at first. Serious stuff! I will never touch another NSAID again. Ever. I’ll do a little acetaminophen in a pain pinch.
Of course, if you’ve got any sort of colitis ongoing, it’s likely that your electrolytes are depleted and/or out of balance, causing painful muscle spasm. Picture a spasming sartorius muscle. That was me.
As for lunch meat, cut it off the freshly killed animal and make it hot as soon as possible. Freeze some for later.
Thanks JDPattern – Nah, I’ve never been one to take NSAIDs. Maybe only a handful of times in my life have I taken one. I have read that before though about how they are responsible for some people’s MC. Hopefully this latest idea with avoiding broth and spices works out for the best. For I guess nearly 10 years now I’ve come ever so frustratingly close to having an answer for my MC. Not listing a food item on the ingredients listing might be my problem. There is a lunch meat that I used to eat often. it was listed as basically plain turkey. Then the turkey lunch meat maker added some new certifications onto it’s label and next thing I saw it had broth listed in the ingredients. Doing some reading I’ve seen it mentioned that this sometimes happens with labeling.
Soul,
How can you claim the broth should be detrimental for you health?
In my world it is instead the prime source for nutritional health. My guess is that it is the collagen which is the key.
Just now have my slow cocker filled with bones from a wild boar and the broth will simmer for another day to get “ready”.
New try to post!
Soul,
How can you claim the broth should be detrimental for you health?
In my world it is instead the prime source for nutritional health. My guess is that it is the collagen which is the key.
Just now have my slow cocker filled with bones from a wild boar and the broth will simmer for another day to get “ready”.
The vegans are back on Wikipedia , this time they have targeted Shawn Baker and the carnivore diet and have deleted them. This is all over social media right now.
https://www.reddit.com/r/keto/comments/ezdrr
/carnivore_diet_deleted_by_vegans_on_wikipedia/
Now, don’t be so hard on the vegans. Their foul-tempered antics are caused by the vitamin and mineral deficiencies inherent in their unnatural diet. It’s sort of like a disability or disease with them, you know?
Brilliant and biting!
So what is a more proper path for those with secondary prevention? Those who had stroke and MI? The only care offered here in US is lowering cholesterol/LDL.