Repatha
Just before I head off on holiday for a couple of weeks, I thought I should make a quick comment on the Repatha trial (PCSK9- inhibitor). I have written much about this new class of cholesterol lowering drugs, and I have been highly skeptical that they would have any benefits on cardiovascular disease. [Mainly on the basis that I don’t believe raised LDL causes CVD, and these drugs have one action – to lower LDL].
As many of you will be aware, the data from a clinical trial on Repatha has just been released. It was reported by the BBC thus
‘Huge advance’ in fighting world’s biggest killer.’
An innovative new drug can prevent heart attacks and strokes by cutting bad cholesterol to unprecedented levels, say doctors. The results of the large international trial on 27,000 patients means the drug could soon be used by millions.
The British Heart Foundation said the findings were a significant advance in fighting the biggest killer in the world. Around 15 million people die each year from heart attacks or stroke. Bad cholesterol is the villain in the heart world – it leads to blood vessels furring up, becoming easy to block which fatally starves the heart or brain of oxygen.
It is why millions of people take drugs called statins to reduce the amount of bad cholesterol . The new drug – evolocumab – changes the way the liver works to also cut bad cholesterol. “It is much more effective than statins,” said Prof Peter Sever, from Imperial College London.
He organised the bit of the trial taking place in the UK with funding from the drug company Amgen. Prof Sever told the BBC News website: “The end result was cholesterol levels came down and down and down and we’ve seen cholesterol levels lower than we have ever seen before in the practice of medicine.”
And so on, and so forth. So, the Repatha trial was a huge success. Obviously, it certainly lowered LDL to levels never seen before. Or, maybe it was not quite such a huge success. Michel de Logeril, a professor of cardiology in France – who set up and ran the famous, and successful, Lyon Heart Study sent me this comment.
‘This is just junk science.
The calculated follow-up duration required to test the primary hypothesis was 4 years as written by the authors themselves (but only in the second last paragraph before the end of discussion…) but the actual median duration of follow-up has been 2.2 years; it is thus a biased trial (a similar bias as in JUPITER: 1.9 years instead of 4 years): early stop!
In addition, contrary to the misleading claims in the medias, there was no effect on both total [444 deaths with evolocumab vs. 426 with placebo] and cardiovascular [251 vs. 240] mortality; which is not unexpected with a so short a follow-up.
They pretend that they are differences for non-fatal AMI and stroke but there is no difference in AMI and stroke mortality… Very strange… It would be critical to get access to the raw clinical data to verify the clinical history of each case in both groups.
Well, in my opinion and given the present state of consciousness among US doctors, FOURIER is a flop!
Best
Michel’
What he is saying, is that there was a reported reduction in non-fatal heart attacks and stroke. And less need for revascularization procedures e.g. PCI/stents. As you may gather Professor de Logeril would like to see the raw data to verify this. There is very little chance that this will be made available.
Anyway, that was the upside.
The downside is when you look at cardiovascular deaths.
- The total number of deaths from cardiovascular disease in the Repatha group was 251
- The total number of deaths from cardiovascular disease in the placebo group was 240
- So, 11 more people died of cardiovascular disease in the Repatha group
The overall mortality data
- The total number of, overall, deaths in the Repatha group was 444
- The total number of, overall, deaths in the placebo group was 426
- So, there were 18 more deaths in those taking Repatha.
The differences here are not large enough to be statistically significant. However, there were more, not less, deaths in the Repatha group, and more, not less, CV deaths. This study was also terminated early, which is extremely bad news for any clinical trial, and casts enormous doubt on any findings. It was supposed to last four years, but was stopped at 2.2 years. Why? Were the mortality curves heading rapidly in the wrong direction.
Alongside this, should be set the knowledge the Pfizer also had a PCSK9-inhibitor undergoing clinical trials, and they pulled the plug, right in the middle of it all.
Pfizer Ends Development Of Its PCSK9 Inhibitor
‘November 1, 2016 by Larry Husten
Immune issues and diminishing efficacy doomed the new drug.
Pfizer announced on Tuesday that it was discontinuing development of bococizumab, its cholesterol-lowering PCSK9 inhibitor under development.
“The totality of clinical information now available for bococizumab, taken together with the evolving treatment and market landscape for lipid-lowering agents, indicates that bococizumab is not likely to provide value to patients, physicians, or shareholders,” the company explained.
Pfizer said that it would halt two very large ongoing cardiovascular outcome studies with bococizumab, the 17,000 patient SPIRE 1 trial and the 10,000 patient SPIRE 2 trial. The trials were fully enrolled.’
Pulling the plug when 27,000 patients had been fully enrolled. What on earth did they see. Something more than slightly worrying. I guess we will never really know, but that is one hell of a write off.
It is also interesting to note that Amgen – the company selling Repatha, has announced that:
‘Amgen to refund cholesterol drug if patients suffer heart attack
Pledge aims to convince insurers to pay for $14,000-a-year medicine.’ 2
As reported in the Financial Times.
This is a big vote of confidence … not! I think, perhaps, we are looking at a doomed drug. Probably a doomed class of drugs. Has the cholesterol hypothesis been verified, or contradicted? I know I am biased, but I know what I think.
1: http://cardiobrief.org/2016/11/01/pfizers-ends-development-of-its-pcsk9-inhibitor/
2: https://www.ft.com/content/34154cdc-0a86-11e7-ac5a-903b21361b43
Dr. Malcolm Kendrick 
Have a good holiday
My interpretation of this drug is that it is about “mass murder” in the long run.
There is a logic.
And we have seen it before!
Would it be cynical of me to point out the savings on pensions…?
Sharon, you are now thinking outside the box.
Pharma wants people alive and taking medicine for many years. Those are the dream drugs for them. Killing us prematurely makes no sense for them and takes suspicion of these profit driven people beyond the facts. I don’t think they mind harming us, because they’ll probably find another drug to treat us.
StephenT: this is what makes a successfull virus or parasite
What is particularly telling:
No mention of it’s effect on Lp(a) – I think I can guess why.
No mention of it’s effect on oxLDL – I think I can guess why.
If you read the paper – look at the comments – that paper should never have been published in the form it is in.
What causes heart disease part XIX: Donald Trump:
(don’t worry, I have linked the English language version of the article)
http://www.zeit.de/wissen/gesundheit/2017-03/donald-trump-usa-psychology-trauma-stress-increase-population/komplettansicht
The only people stressed out about Trump are those who want America to fail. They are the people who desire Socialism even though it is an experiment that has repeatedly failed. There is a lag time between the stress and the event so I would guess there will be an increase in CVD deaths during Trumps watch in the same way there was in the 1950’s following WWII. How ever they will be a result of the 8 years before the Trump watch. The U.S. was on the road to destruction – now most Americans have hope. Most of what you see in the media doesn’t even hint at the truth…
Socialism has been and still is an intellectual laziness predominantly found in the US to disqualify any fact or argument one does not like.
The article may not have covered all its bases, but a change from 50 to 80% from summer of 2016 to now is a significant change. Also, he who must not be named has a way of being omnipresent and of bending reality to the tune of his tweets. Never realized Joanne K. Rowling was that prescient about politics…
Hi Eric: A new disease Post Election Stress Syndrome that is covered by medical insurance
Eric,
Well this Trump issue is a little bit disputable to my opinion.
Being “left” all my life I still find this guy “interesting” from the health perspective. He has confronted Big Pharma on the vaccines and not least accused main stream media, MSM, as “liars”. I am just fed upp with all the Big Pharma lies I find in MSM so here I am fully on his side.
MSM= methyl sulphonyle methane?
He may have delivered a needle prick (by his standards) on vaccination, questionable as his position may be, but he’s letting Paul Ryan and his irk have their go on health insurance contrary to his election promises.
Eric – My take on Trump as well – if the DemoPulicans hate him, perhaps he is not all bad.
I have good, bad and ugly news to report this morning. A President Trump induced heart attack likely occurred in my parents neighborhood. The bad news is that a vocal, unafraid to voice his disparaging views on President Trump, liberal friend of my parents has suffered a heart attack. The good news is he is alive. I was told he was not eligible for a heart stent. As I type he is in surgery.
The ugly is that a nightmare of mine might come true. The heart attack friend is neighbors with a retired doctor. The retired doctor and my father have talked about and looking into buying viagra to help prevent heart attacks. I figure it is only time before I see in my parents retirement neighborhood, older men walking around without shirts on, soaking up the sun and popping Viagra.
I quickly e-mailed my father about the drug Doxazosin this morning. that might be a property value saving pharmaceutical.
It has little value in mentioning this bit of connection but it is on my mind. The retired doctor has two sons. I have not met the sons. I have been told that both sons are doctors that are known. One of the sons heads the cardiologist department at a name brand world known hospital in New York. That is what I was told but don’t know myself if true. Father and son are getting together next week I believe for a birthday celebration. I can imagine a topic of discussion will be the neighbor that suffered a heart attack. With that potentially Dr. Kendrick’s heart attack prevention ideas will be discussed. It’s a stretch to say that, and even so, little professional note done, but if the ideas do work, and they seem worth a try in a hospital setting, it would be nice to advance forward in a new heart disease prevention direction. A new branch on the heart prevention tree could be beneficial.
Thank you again, Dr K. I wonder what convinces newspapers to interpret the trials thus? Oh, silly me they need the advertising from the pharma companies! Have a good holiday and please don’t get pneumonia on your return.
Money?
EXTRA EXTRA bad cholesterol on verge of being eliminated. Next battle will be to cure heart disease.
Sounds like the Vytorin results. Much lower cholesterol, same CVD results. IMPROVE-IT trail Quote: “There was no reduction in all-cause or CV mortality with simvastatin+ezetimibe, though there was a reduction in MI and stroke”
Hi Franklin: Vytorin will give you a choice on what you want to be on your death certificate as a cause of death.
Dr.Kendrick
‘This is just junk science.
Another blistering attack on a highly biased and data manipulated study. This is what makes me wonder at the cognitive levels of so-called professors. May be the statin effect on the brain is demonstrated. Frankly, should I be hospitalized, may be it would be better to arrive DOA rather the be subject to some weird ideas called modern medicine.
The following papers can be downloaded in full. Risk getting diabetes on the one hand or, as individuals, take new drugs with the near certainty that you will NOT BENEFIT.
http://www.nature.com/articles/srep39982
Association between reductions in low-density lipoprotein cholesterol with statin therapy and the risk of new-onset diabetes: a meta-analysis
http://www.nejm.org/doi/full/10.1056/NEJMoa1615664
Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease
Zoe Harcombe has reported on both.. Another damning report.
I despair
“This is what makes me wonder at the cognitive levels of so-called professors”.
I suspect you may be measuring the wrong variable. Have you looked at their bank-account levels?
Tom: Self preservation is a motivator, speak up and you are out the door.
This sentence amused me:
““The end result was cholesterol levels came down and down and down and we’ve seen cholesterol levels lower than we have ever seen before in the practice of medicine.”
Since cholesterol is required by the body, how can that result be considered a success? At some point it is surely clear that low cholesterol would starve the brain of a vital raw material.
@Malcolm Was absolutely no reason given for stopping the trial? Are they claiming that it would be unethical to withhold this wonderful treatment from the placebo group – what other reason could there be other than a serious side effect?
I guess I would be classed as ‘statin intolerant’, but I’m going nowhere near PCSK9 inhibitors!
David, the focus is on winning the war on bad cholesterol , that is why the results are astounding. The scientists have almost eliminated bad cholesterol. Good cholesterol will then replace bad cholesterol. Health issues will be addressed when this is accomplished. Don’t give up hope, the scientists are regrouping for the final assault on bad cholesterol. Stopping the trial was a strategic
diversion tactic to confuse the enemy. That is the nature of war.
Peter at hyperlipid has had an email from a PR company representing Amgen, see his blog. They say:
“FOURIER was an event-driven study and was to conclude when least 1,630 hard major adverse cardiovascular event (MACE) events were accumulated. Amgen expected the study to run for 43 months with a 2 percent annual event rate in the placebo arm. However, the annual event rate in the placebo arm exceeded 3 percent and led to a faster accumulation of hard MACE events. Since the relative risk reduction in the hard MACE composite endpoint grew from 16 percent in the first year to 25 percent beyond 12 months, Amgen anticipates that a longer duration trial would have led to further relative risk reduction.”
They don’t mention that these are the secondary end points, but Serdna gives more detail in the comments section. They only had 2907 primary end points, instead of the expected 3550 but they still stopped it early.
Peter’s original comment (that they took exception to) was: “The study was stopped early, presumably to stop the hard end points of dead patients from becoming too obvious”. (Hahahaha!)
He has now revised it to: “The study was stopped early due to an unexpected excess of combined cardiac adverse end points in the placebo arm. At this time point the 4.2% increase in relative risk of all cause mortality in the treatment arm was not statistically significant”
Berberine
Has anybody looked up the natural product (used by the Chinese for millennia) Berberine?
It apparently does the same thing in the liver as PCSK9.
Why spend $billions developing a product that probably has minimal value at best for which there is a cheap natural product?
Robert, I tried Berberine for a while, It did wonders for LDL and helped with Blood glucose. One of the botanicals that contains berberine grows in my back 40. So its perfect except that blood tests showed damage to kidneys(?) . The Doctor said that weightlifters and statin users show
elevated levels . I have forgotten the name of the “stuff”.
Did the PCSK9 inhibitor trial and developed an injection site injection urticarial as big as a dinner plate. I got talked into the trial and promised pieces of silver.
I knew better.
thanks Gary
have you recovered? (urticarial as big as a dinner plate)
Barberry is a good source of berberine, as well as vit C; should work well in vodka infusions.
Why would you want to use a substance that does the same thing as the failed pharmaceutical substance?
Why spend $billions developing a product that probably has minimal value at best for which there is a cheap natural product?
Simple – There is no perception of profit for the “cheap natural product”. Big Pharma and the medical industry are only interested in patents and the consequent huge profits and status.
Another question is why is most money spent on “curing” rather than prevention excluding vaccines. With regards to vaccines why did the US government protect Big Pharma by banning any legal action against them for injury compensation for “safe and effective vaccines. Instead the US Govt. set its own system of compensation for vaccine injuries, thus protecting Big Pharma from class actions caused by their “safe and effective vaccines”? But then many powerful politicians are directly involved in Big Pharma.
Robert, why lower LDL with anything if it doesn’t help?
Stephen: we know it doesn’t help, the sub-conscious “bad cholesterol phobia” still exists and we also have to please the doctor.
Can’t make money on plants that are in patentable!
Choking with laughter – just use the natural product – cheaper, and says it all
Why attempt to lower cholesterol at all? There’s no advantage, in fact, lowering cholesterol to unprecedented levels will created illness on an epidemic scale. The only beneficiaries of this will
be; ah yes, the Pharma industries.
Bill: What do you suggest we do with the “bad” cholesterol? A doctor will not agree with your thinking.
Why spend $billions developing a product that probably has minimal value at best for which there is a cheap natural product?
I just loved the irony – smile
Presumably the hypothesis that Cholesterol causes Heart Attacks is a now a given so all these trials have to prove is that the drug in question lowers Cholesterol more than the previous ones therefore it is more effective at reducing CVD. The fact that more peopled died using the drug can therefore be ignored. To all my many friends currently on Statins: be afraid, very afraid.
Hello Dr Kendrick, My God, what is the matter with this Prof. from Imperial College London, The British Heart Foundation, The NHS, our entire health system (bar the blessed few)? Obviously this is not a question I need any answer on because I know. It’s just the elephant in the room, and he’s taking up too much space and causing a great deal of mess!
Have a good break and I look forward to your next blog.
This is simply disgusting that anyone would claim any benefits from that study alone.
”An innovative new drug can prevent heart attacks and strokes by cutting bad cholesterol to unprecedented levels, say doctors. ”
Really? I mean who get the yellow envelops to say stuff like that?
”An innovative new drug can CAUSE heart attacks and strokes by cutting AN ESSENTIAL REPAIR MOLECULE to unprecedented levels, say doctors. ”
Andy
You are assuming that there is such a think as ‘bad’ cholesterol. Since cholesterol lowering has achieved nothing except contribute to the tidal wave of bad health we seemed to be mired in right now I fail to see the efficacy of it. I think Malcolm and his colleagues at THINCS have done a good job, over the years, in debunking the whole hypothesis (for a hypothesis it is). The current academic and medical view seems me to be based on a skewed correlation ( Keys et el) from which a giant house of cards has been erected, billions of dollars have been made and no causation has ever been properly proven, witness the subject of this article we are currently discussing. We seem to be operating in a world where correlation determines policy. Modern ‘evidence’ based medicine is a sham. The gold standard RCT method is corrupted since the outcome of the RCT seems more often than not to comply with what the sponsor wanted. Much time and effort is being put into propping up a deeply flawed system. Scientists should re- read or maybe read their Popper on the scientific method.
An acquaintance recently had a heart attack and was treated with a quadruple bypass . 58 years old. He has recovered nicely and seemed happy that his doctor told him that his cholesterol was good! As a physician how many times would you have to see the paradox to realize that the hypothesis is wrong.
Also he was an auto mechanic working in garages with less than perfect ventilation for 40 years.
CO may be the culprit.
Dr. Axel Sigurdsson MD article about Repatha (Evolocumab):
Phil
Is it coincidence that this new study had 27,000 participants, exactly like the Pfizer study that was ended prematurely last year?
https://www.theguardian.com/society/2017/mar/18/drug-which-cuts-bad-cholesterol-can-help-prevent-heart-attacks-and-strokes
Dear Dr Kendrick
So Amgen investors were right to mark the shares down after this report, but it might put a nail in cholesterol /heart disease theory, since lower LDL doesn’t do anything for your life expectancy, maybe even the opposite.
As for Pfizer, since you like scenarios, try this one:
Boss: this looks like a lousy trial
Employee: no its very good, the results show very low cholesterol.
Boss: but people don’t seem to live longer, whats the sense in having a drug that does that if the patients don’t live long enough to continue taking it?
Have a well deserved break.
Thank you
On the bococizumab:
http://www.nejm.org/doi/full/10.1056/NEJMoa1701488
“…trials of PCSK9 inhibition with bococizumab were terminated early by the sponsor owing to the development of antidrug antibodies in other studies in the program.”
Apparently some 48% of subjects had immune systems that were less than thrilled about monoclonal mouse bits floating around.
The unfortunate thing about these trials is that Repatha lowers Lp(a). For people with Lp(a), and who are doing diet/supplement/lifestyle interventions that otherwise lower CVD risk, this effect might have net benefit, but are we ever going to get clarity on that?
Reblogged this on Taking Sides.
Dr. Kendrick,
You would love to see this interview with Dr. David Diamond PhD and Andreas EinfeldtM.D. about statins etc.
https://www.dietdoctor.com/member/interviews/diamond
You can see the trailer for free but if you get a month free membership you can watch it then cancel membership before the month ends. Just put a calendar alert in your phone.
It is indisputable that statins play a much greater part in cell biochemistry than just stopping the synthesis of cholesterol in the liver cells. They can damage muscle cells leading to painful myopathy (grumble grumble), damage pancreatic cells (more grumbles) and . . . the can interfere with insulin signalling leading to insulin resistance (deafening grumbles). A common side effect of statins is short term memory problems . . . Having found a study that described how insulin was required in the brain in the processing of short term memory, it said to me that it would not be surprising if statin’s ability to promote insulin resistance was to blame. There are other possibilities; however, the point is: we should be very careful when targeting one element of our body biochemistry that it is not usefully involved elsewhere.
When I first read about PCSK9 inhibitors, like Dr K I thought “so what” . . . but then groaned when I did a little research and found that a reported side effect was short term memory loss. “Oh no not again” . . . . Further research: the brain produces PCSK9 . . . so why does it seem to be a good idea to get rid of it. Where is the risk assessment for lowering PCSK9 in the brain? Further research (today) . . . “the role of PCSK9 in the brain is controversial” . . . Well, that is a surprise.
Antony:Does not take much googling to discover problems with statins. The worst impact could be on bone derived progenitor cells used for repair of all tissue types. Result would be ageing cells without chance of replacement . Accelerated ageing.
“The exact mechanism of action of PCSK9 is not clear, although it is known to enhance the intracellular degradation of the low density lipoprotein (LDL) receptor” All that the researchers saw was LDL.
Andy . . .I go with the accelerated ageing. My wife called the statins ‘your old man pills’. She saw the effect they had on me the longer I took statins and marvelled at the return to (relative) youth when I stopped.
Nicola Harley in the Telegraph related the usual “Scientists say …” guff, and quoted some vainglory from a Professor Sever of Imperial College. Happily she also wrote “the findings … revealed that the drug had no impact on the rate of cardiovascular mortality.”
And yet it reduced cholesterol by gazillions of percent. You might almost wonder whether the lipid hypothesis is, to some degree or another, false. As in fake. As in bollocks. Still, it’s a livin’, eh?
Happy hols, doc.
Re the Evolocumab trial
Examining the Table 2 w.r.t. actual cause of deaths (as distinct from an addition of several fatal and non-fatal categories) it is obvious that benefits are trivial and not significant. The enthusiastic claims are an example of over enthusiastic astroturfing and agnotology. Money and status win again over lives of patients.
What’s terribly sad is that most people just read the headlines and that doctors will have no problem prescribing this even with this data right in front of them!
A friend was telling me recently about NLP techniques. One of the most basic ones – you give fact, fact, fact, INFORMATION (something you’re trying to sell or convince someone of). That BBC release sounds like something out of NLP playbook…
Thank Goodness for the wonderful honest Doctors like yourself Dr. Kendrick ! My Doctor tried to convince me to go on these drugs.I simply said no thanks. It is difficult at best to make that kind of decision always wondering if you just added another nail in your own coffin. Presenting the information in easier to understand “language” allowing us to weigh the data and make an informed decision for ourselves is a gift all of the physicians like yourself give us. Your work is appreciated more than you know !!
robert lipp: Berberine was probably their starting point, what gave them the idea. Clearly a doomed drug, as was Pfizer’s. Pharma is getting desperate to keep the profit stream going to keep investors happy, while the public is becoming more aware of how worthless and dangerous many of their products are.
Having read the authors’ paper on the Repatha FOURIER trial, it appears that the randomisation between drug and placebo was performed on a regional basis. It would therefore be interesting to see the results by region, since medical standards are likely to vary from one region to another. The four regions were NA (16.6% of patients), Europe (62.9%), Latin America (6.6%) and “Asia Pacific and South Africa” (13.9%).
Reading studies produced by bigPharma could be dangerous to your health. A black box warning.
Thanks for doing this report before going on holiday Dr K. To me it looks like another failure in the lipid theory of CVD.
How many wonder drugs are publicised each week in the media? My eyes roll when I read about yet another ‘game changing’ cancer drug. Patients are cajoled by pharma in to demanding the new, expensive drug with miniscule ‘benefits’ and no talk about damaging side effects.
I doubt there is much true consent in the NHS when it comes to statins, chemotherapy or much else. We get one side of the story and it’s always the side that sells drugs.
Patients who follow doctor’s recommendation to lower badLDL PCSK9- inhibitor is probably a better choice than statins. Shotgun approach by interfering with mevalonate pathway causes too much collateral damage. Hopefully the inhibitor will only increase LDL receptors without altering some other cellular function.
Question is, what is effect on cell being stuffed full of cholesterol.
Surely the shortcomings of statins are well known, so if you swap to a PCSK9 inhibitor you are swapping a known harm for an unknown harm. If I believed in treating cholesterol levels (which I don’t any more), I would at least want to know that my cholesterol was not going to be lowered excessively – it isn’t a poison to be driven from the body!
It’s also about swapping a drug that’s off patent for a one on it.
Have a GREAT HOLIDAY Dr. K—–I appreciate your efforts—Errett
Thanks for some more solid information to add to my armoury of arguements.
Oh, and have a good rest – we shall endeavour to survive while you take a well earned break.
Jean, I am suffering withdrawal symptoms. Being in Florida for another 2 weeks gives me lots of time to read and relax. Reading Dr. K’s old blogs and letting thoughts incubate.
“.. we’ve seen cholesterol levels lower than we have ever seen before in the practice of medicine”
Just why is that a good thing? Lower than all the extremely healthy people who have lived long, happy lives? Lower than all those who have hypocholesterolaemia?
Wouldn’t we expect a good outcome for cholesterol levels to be somewhere around what generally healthy people have?
Good Lord, deliver us!
Thank you for posting this. Have a great holiday. Stay healthy and forget all about this nonsense.
And why not just let our bodies get on with what they do best. Since my cessation of statins my cholesterol levels have gone up high. – relatively – HDL 3.4, LDL 3.4 and my trigs down to .05, not that it ever that much higher. (My diabetic nurse is practically having kittens at every appointment. Ho ho. As I understand it LDL is an essential part of the immune system and needs to be fairly high. I haven’t had a cold or even a sore throats since I stopped the vile treatment AND my HbA1c plummeted. By the way, I’m old so I NEED my cholesterol, thank you very much.
Hey, Doctor K, have a great holiday. You deserve it. ☀️☀️☀️
JanB . . . I’d kill for an HDL of 3.4 . . . to me it shows the cholesterol regulation system is spot on. And the low TGs . . . wow . . . I am led to understand that low TG levels indicate low, in your case vanishingly low, numbers of small sized LDL particles, thought by many to be an issue in cardiovascular heath. Speaking as a punter in all this, you seem to be in a very good place.
Hi Anthony – I put it all down to the fact that I have a very low carb diet to keep my blood sugars in check. No bread, no rice, no roots, no pasta, no sugar, almost no fruit except berries. You know the sort of thing. But, my word, I eat good eggs, cheese and fatty meat prodigiously and like to keep a pot of clotted cream in the fridge for a spoonful every time I pass. I’m really skinny, by the way, AND I love my green vegetables.
I eat really well, but I only eat REAL FOOD.
Cheers.
Thanks Dr Kendrick…..I was waiting for your reaction to the BBC and all the other distorted accounts of this wonder drug. I am pleased you have found time to comment before scooting off on a well earned holiday.
Thanks for another well presented heads up Dr.Kendrick.I have a ( healthy ratios) high cholesterol and can now dodge attempts to entice me onto this drug.I continue to refuse the cholesterol lowering drugs as the legitimate science does not support them.I love my levels,my body would not nuture my cholesterol production and storage if I did not require it is my standpoint.I continue to marvel at the enthusiasm of the industry and its incentivised fan base to dump frankenscience on the public,nor the creativity with which editing of findings is conducted.
What are you levels. I’m up to 8.9
“LDL-lowering potency varies between agents. Cerivastatin is the most potent, (withdrawn from the market in August, 2001 due to risk of serious rhabdomyolysis)” — https://en.wikipedia.org/wiki/Statin
Rhabdomyolysis is a condition in which damaged skeletal muscle breaks down rapidly. Perhaps the ultra-low LDL levels achievable with PCSK9 inhibitors make rhabdomyolysis more likely as a side-effect?
I am waiting for them to invent a drug that lowers LDL to zero.
“Good news – no heart attacks in the treatment group.”
“Bad news – they are all dead.”
“The totality of clinical information now available for bococizumab, taken together with the evolving treatment and market landscape for lipid-lowering agents, indicates that bococizumab is not likely to provide value to patients, physicians, or shareholders,” the company explained.”
INTERPRETATION:
– “clinical information” LDL PCSK9- inhibitors kill people who use the drug
– “evolving treatment” ie LCHF diet, avoiding LDL reducing medications
– “market landscape” ie sales of statins is declining,
-provide no value to patients, physicians or shareholders. Writing on the wall: LDL hypothesis is ready to crash
What are the British Heart Foundation on? Statins? Cholesterol lowering drugs? Or huge bungs from Big Pharma? Let’s hope they wake up and smell the (bullet proof) coffee one day soon!
They take down evidence that contradicts their support for statins
Estimated lowest mortality rates for TC blood levels
All Cause mortality 222 mg/dl 5.75 mmol/L
Non-communicable disease 210 mg/dl 5.49 mmol/L
Cardiac Disease 208 mg/dl 5.44 mmol/L
http://www.heartstats.org/documents/download.asp?nodeib=6797 This URL no longer exists? WHY?
Now on https://renegadewellness.files.wordpress.com/2011/02/cholesterol-mortality-chart.pdf
http://healthcorrelator.blogspot.co.uk/2009/12/total-cholesterol-and-cardiovascular.html
I think you have answered your own question.
I thought that manipulation of trial duration, primary end points etc had been outlawed in the early 2000s?
Excellent, erudite article Dr K. Let pseudo-science be thwarted –
I’m confused about the data. Here’s what was reported in the New York Times, which I am having trouble squaring with the figures reported in Dr. K’s piece: “Participants in the study who used Amgen’s drug for 2.2 years were 20 percent less likely to die from heart disease, have a heart attack or have a stroke (816 patients taking evolocumab had one of those outcomes, compared with 1,013 taking the placebo).
There was a 15 percent reduction in the combined risk of having a heart attack or stroke or dying from cardiovascular disease, being hospitalized for worsening chest pain, or having a stent inserted to open a blocked artery (1,344 evolocumab patients versus 1,563 placebo patients).
The absolute reduction in the risk of a heart attack or stroke was 1.3 percent at two years, Amgen said, and 2 percent at three years.”
Can someone enlighten me on this?
Jmarcus
Amgen’s drug for 2.2 years were 20 percent less likely to die from heart disease,
Downlooad the paper and in Table 2 you will find:
Evolocumab Placebo Hazard Ratio
(N = 13,784) (N = 13,780) (95% CI) P Value*
Cardiovascular
death 251 (1.8) 240 (1.7) 1.05 (0.88–1.25) 0.62
Death from
any cause 444 (3.2) 426 (3.1)
If you can demonstrate a 20% less from any of those death numbers I would like to know how they did.
You are right to question the report – Fake News – The NYT is great at fake news
mikecawdery: How right you are. A drug that kills folks faster than placebo is a “wonder drug” only in the Orwellian world in which we live. Only if the objective is population reduction. Thank goodness most people still have functioning brains capable of discerning BS when it is dished out by the authorities. Here in the U.S. the media has been the willing servant of the CIA since about 1947. All fake news all the time (except the comics, puzzles, obituaries, and sports scores). Carl Bernstein’s 1976 Rolling Stone article explains how they have carried it out.
A “wonder drug”? “wonder” can have several meanings The “wonder” is why do doctors prescribe these drugs.
The NYT is retailing untruths. No lives were extended in this study. The drug appeared to be slightly deadlier than the placebo, but the difference wasn’t statistically significant. See Table 2 of the link.
http://www.nejm.org/doi/pdf/10.1056/NEJMoa1615664
Yes, the “failing NYT” did its best to encourage the public to demand the newest and exceedingly expensive drug from their doctors and their insurers.
I am no longer amazed or even sickened by such reporting – it has become the new reality. By the way, American magazines geared to women are nowadays full of ads for prescription drugs.
Wait, what?
They stopped it after two years instead of four because the event rate was 50% higher than expected?
“Although the median follow-up period
in FOURIER was originally planned to be approxi-
mately 4 years, an event rate that was approxi-
mately 50% higher than had been postulated
led to a shorter required duration of follow-up to
accrue the prespecified number of events.”
When they say “reduction in the combined risk” I think they are talking about the risk factors like cholesterol levels, trig levels etc. which they use to predict disease (i.o.w. surrogate endpoints), but which are not the same as actual deaths, heart attacks etc.
So if you are treating the numbers, these drugs are fantastic. If you are treating the disease, eh, not so much.
Keep us informed
Interesting! They are trying to make drugs that kill bad cholesterol but they don’t even know what is this ‘bad cholesterol’ and why do we have it in our bodies! Paradox, huh!
HI JAIDE; The average consumer and doctor knows the meaning of “bad”. Therefore killing “bad” cholesterol is “good”. No need to look further.
I’m just a dumb musician – I can only count to 4! Even so, I saw straight through it. 444 deaths vs 426 on placebo. It’s really NOT hard at all to look at the figures critically. What on earth was the BBC correspondent doing to provide a balanced view?
And hot on the heals of the other post is this one.
On Mon, Mar 20, 2017 at 6:40 AM, Dr. Malcolm Kendrick wrote:
> Dr. Malcolm Kendrick posted: “Repatha Just before I head off on holiday > for a couple of weeks, I thought I should make a quick comment on the > Repatha trial (PCSK9- inhibitor). I have written much about this new class > of cholesterol lowering drugs, and I have been highly skeptical t” >
Today’s Times had a good column by Dr Mark Porter on statins, PCSK9 inhibitors and how poor they are in changing real outcomes in comparison to the Mediterranean diet and lifestyle changes.
Interestingly, the NNT for statins was given as 400! Yes, one in 400 patients might benefit fractionally from statins, if you don’t include the side effects. How many patients are told this? I doubt many people are giving true consent for these supposedly preventative drugs because they’re only getting the pharma half of the story.
The NNT for blood pressure medication was given as 110.
You can see the start of the article here, but most of it is behind ‘The Times’ paywall.
http://www.thetimes.co.uk/article/dr-mark-porter-the-diet-thats-almost-as-good-as-statins-and-im-proof-that-it-works-dj7gstfls29
This will give Prof. Dr. Sir Rory Collins the opportunity to claim that “ Treat 4,000,000 and save 10,000 lives a year“. I wonder if he will take this wonderful opportunity?
Re Times ‘Paywall’. No, there is no paywall, just to register with minimum detail : nameand e-mailaddie. End of. Have just read the full article – he is rather pushing the statin front, or, is gently pushing aside by upping good diet issues. He has an e-mail addie linked to The Times, so I sent him the link to Dr Kendrick’s blog… Others can do likewise…!
Thanks for the advice. I think the tone is very much “Who’d take these if they knew and here’s something better.” But I think he’s a bit cautious to avoid the pharma-funded flack.
Dr Kendrick
Have a great holiday and come back fully refreshed to continue highlighting Big Pharma/ medical industry money-making drugs.
What on earth are the statin and PCSK9-inhibitor drugs thinking. If these things cause muscle wasting or problems for muscles? THE HEART IS A MUSCLE!
I once objected to a statin-recommending GP that they were notorious for weakening muscles. He reluctantly agreed. I said “the heart is a muscle”. He said that that was quite different. Ain’t science wonderful?
I was told the same thing. I believe I said, “You must be joking!” He wasn’t…
@ dearieme
How? Did he try to explain?
Dr. K, Maybe it is time for a new book updating us on the war against cholesterol. Suggested title : THE GREAT WAR-2017
chapter 1- why cholesterol is bad (for rabbits)
chapter 2- the final battle, bad cholesterol reduced by 60%, only 40% to go, victory is near
chapter 3- life without bad cholesterol, technology can replace it with good cholesterol
chapter 4- saturated fat is bad too, increases bad cholesterol, (the eastern front)
chapter 5- who are the rebels supporting the enemy?
chapter 6- why are patients joining the rebels?
chapter 7- Big Pharma, scientists and most doctors pledge to fight to the end
chapter 8- aftermath, end of patients
Andy, I love your chapter headings, but I think your title is a bit too close to the bone!
I’d like to add a few extra chapters, to be merged in as you see fit:
Chapter ? False recovery syndrome – why some diabetes patients seem to improve with false treatments
Chapter ? False diets – why some unapproved diets can seem to make you well – how to avoid being fooled.
Chapter ? Are those who refuse modern cholesterol lowering treatment really sane – the case for forced treatment.
Chapter ? The heart warming story of a man who refused to let his cholesterol win – even though that put him in a wheel chair.
Chapter ? How YOU can help charities help Big Pharma!
Chapter ? Stamping out false medical advice on the internet – the internet petition.
David: Agree with comment re title, 100 years is not that long ago.. Another title could be THE 100 YEAR WAR ON BAD CHOLESTEROL. The fight is real and lives are at stake. Poking fun at the opposition could be effective. Your additional chapters are good. The literary critics might consider the book as fiction.
David: The patient has to be educated. The book could be the basis of a TV series if written as a thriller based on real events. The names could be changed to protect the guilty to avoid lawsuits. TV is where average people get educated. There is nothing else that is currently available to bring the cholesterol message to the masses. How many books does the average person read? A TV series with real actors could run for many years (research is evolving) and could rival the Dr. OZ show. Personally I have lost interest in OZ, he was OK in the beginning but now is geared towards a female audience. Also he believes saturated fat is bad.
Nice one. Humorous were it not so true!
Rabbits are okay with cholesterol. It was a small number of the 49 alternate cholesterol oxides that did for them. The fact would do well for being incorporated into chapter 1.
Science News
from research organizations
Researchers study a new way to lower LDL cholesterol
Date: March 6, 2017
Source: Saint Louis University Medical Center
Summary:
Drugs targeting a nuclear receptor may be able to lower LDL (bad) cholesterol in an animal model, new findings suggest.
In a paper published in Biochemical Pharmacology, Saint Louis University researchers examined the way a nuclear receptor called REV-ERB is involved in regulating cholesterol metabolism. Their findings suggest that drugs targeting this nuclear receptor may be able to lower LDL (bad) cholesterol in an animal model.
The previous post is a word for word copy of latest news about (bad) LDL.from Science News.
Note the focus on “(bad)” and “drugs”. Motivation is money, What is the point of doing research?
If the researchers had read Dr.K’s books and followed discussions on this blog they would have learned not to associate “bad” with LDL. Is any university doing studies of the benefits of cholesterol?
The war on “(bad) LDL cholesterol” continues.
This is from Chris Masterjohn episode 16 (on familial hypercholesterema):
“Polyunsaturated fatty acids also will increase the LDL receptor, because they are more effectively esterified to cholesterol in the liver than other fats, and so if the cholesterol in the liver becomes esterified, the pool of free cholesterol declines, that increases the liver’s sense that it needs more cholesterol, increases the LDL receptor, decreases blood cholesterol – everything down from esterifying the cholesterol is very similar to what statins are doing. But the overall effect is just to move cholesterol from the blood into other compartments such as the liver, and you don’t promote the utilization of that cholesterol. So it’s not like thyroid hormone, where you’re taking cholesterol in from the blood and then you’re doing something with it because you’re ramping up the metabolic rate; you’re just basically stuffing cholesterol into those tissues, and it’s not clear that that’s ideal. ”
I think he mispoke about PUFA being esterified to cholesterol, maybe he meant that they promote esterification of cholesterol? Anyway, he’s making the point that stuffing cholesterol into the cells cannot be good.
Association between reductions in low-density lipoprotein cholesterol with statin therapy and the risk of new-onset diabetes: a meta-analysis http://www.nature.com/articles/srep39982
Statins are also carcinogenic
Cancer. 1984 May 15;53(10):2034-40.
The detection of environmental mutagens and potential carcinogens.
Ames BN.
PMID: 6367933 [PubMed – indexed for MEDLINE]
Am J Clin Nutr. 2001 Dec;74(6):714-22.
gamma-tocopherol, the major form of vitamin E in the US diet, deserves more attention.
Millionaires Keep It for Themselves (MGID)
Jiang Q1, Christen S, Shigenaga MK, Ames BN.
The detection of environmental mutagens and potential carcinogens.
Ames BN.
Cancer. 1984 May 15;53(10):2034-40. Review. No abstract available.
PMID: 6367933 [PubMed – indexed for MEDLINE]
Randall: According to this meta-analysis, the higher the percent LDL is lowered the higher the risk of developing new-onset diabetes. This new wonder drug, then, should dramatically increase the risk.
“Don’t worry, we have drugs for that”
off topic but interesting:
https://www.theguardian.com/world/2017/mar/23/italys-five-star-movement-blamed-for-surge-in-measles-cases
How many times must we state that there is no “bad cholesterol”?
There is just one cholesterol chemical molecule and it is “good” for us.
“Bad cholesterol” is a typical “fake news” and well over fifty years old by now.
Göran
Each time I see the words ” bad cholesterol” I shudder.
My body has a system for regulating my cholesterol levels, if I eat foods containing it, my body produces less, so it seems to know what I need.
I let it get on with it.
I took statins for over 20 years. During this time both my parents died of heart disease despite them taking statins et al. I developed unstable angina 4 years ago and have one stent. I have deliberated over whether to continue or not with them. Dr K, and others, have helped me make my mind up to discontinue them.
It is my sole responsibility. I now take Vit c, K2, magnesium and carnetine.
One factor that always troubled my was me being told by my GP I was ‘high risk’ and be I’d be a fool to discontinue statins. I was high risk because of the angina, the stent and my family history of heart disease. I agonised over this ‘high risk’ status for a long time.
When, through further agonising, even though I’ve stopped taking them, I realised I may not have a ‘family history of heart disease’ rather a ‘family history of taking statins, bp lowering drugs and antacid medication’. It is a thought that gives me comfort.
Stergio,
I keep my unstable angina at bay with 1600 IU natural vitamin E every day since three years now. Seems to work fine in my case.
Here is an “alternative” site where I learnt about the “details”.
http://www.orthomolecular.org/search2.shtml?cx=012934609838436511334%3Aplncuzvulcg&cof=FORID%3A11&ie=UTF-8&q=Angina+vitamin+E&sa=Search&siteurl=orthomolecular.org%2Fsearch2.shtml&ref=&ss=
I hope this decision works out well for you.
I know a man whose wife was very ill with cancer for a protracted period. He developed some sort of heart murmur and was on a variety of drugs. Some time after she died, he went on holiday, and discovered he had forgotten to take his tablets. He decided to cross his fingers, and by the end of the holiday he felt so much better that he has given up all his medication! His heart problem has not recurred. He came to the conclusion that the stress of his wife’s disease had caused his heart problem, and since then he had healed.
Have you managed to shed any statin side-effects?
When my father died my mother developed AFIB. Usual meds followed. Whenever I asked whether my Mum’s newly diagnosed AFIB could have anything to do with the death of my father and the accompanying stress, all the cardio docs said no. I learned many years later that such advice was complete bollocks. At the very least stress can deplete magnesium. If I knew then what I know now I’d have argued the point with the docs and given my Mum the necessary supplements. Do you reckon they cardio docs would have listened though?
Hi David. Interesting you should mention stress. I have a mental health background and was subjected to and understand its effects!
As regards statin side effects I am a club golfer and put vague pains and aches in my left shoulder down to the game and increasing age. I was convinced I was developing arthritis. I didn’t even tell my GP about it because it’d be put down to age. Since I’ve stopped statins it’s gone.
Paul,
Interesting comment. I wonder how many side effects of any medication never get reported for one reason or another?
– At my age it’s to be expected.
– It’s probably my fault. I’m always getting things wrong.
– The doctor’s a busy person and I don’t want to be a bother.
– It’s too much trouble to see the doctor again. I’ll just put up with the effects.
– The doctor’s been so nice and taken so much trouble I don’t want to disappoint him or her.
– I’m afraid the doctor will prescribe more expensive medication or a specialist I can’t afford.
– I’m afraid the alternative medication will affect me even worse. Better the devil you know.
Good to hear that he discovered he didn’t need the drugs any more. Some people think a low carb diet is often good for afib, e.g. http://high-fat-nutrition.blogspot.co.uk/search/label/Atrial%20tachycardia%20and%20fibrillation
Did aluminium feature as an ingredient in the antacids?
Hi Christopher – Yes, aluminium can be found in antacids. I have been scripted antacids that contained aluminium as an adjuvant. I did not take it. Have also had eye drops scripted that contained Mercure ! Again, I did not take. Pharma certainly needs a drubbing and an overhaul, including those that prop them up.
Here is a list Christopher of those drugs that contain aluminium :-
Generic Name Brand Name
aluminum hydroxide and magnesium carbonate Gaviscon
aluminum hydroxide and magnesium hydroxide Maalox, Mylanta
calcium carbonate Rolaids, Tums
Yes. he was on Gaviscon.
Final analysis of Repatha trial (PCSK9- inhibitor).
– Hypothesis: PCSK9 controls LDL receptor numbers by inhibiting breakdown of LDL receptors
– Results: Liver cells forced to accept more LDL, patients died
– Conclusion: LDL should stay in the bloodstream where nature intended it to be
– What went wrong? Everyone knows that LDL-C is bad. New drugs are in development.
You hit the nail on the head, Andy S. Surely those with familial hypercholesterolaemia (spelling ?) lack LDL receptors which is why it can be so harmful. Why would big medicine/pharma want to replicate this situation In otherwise healthy people? Maybe I’m missing something here.
http://bmjopen.bmj.com/content/7/3/e013650?cpetoc
Global cardiovascular risk assessment in the primary prevention of cardiovascular disease in adults: systematic review of systematic reviews
Conclusion
The quality of existing systematic reviews was generally poor and there is currently no evidence reported in these reviews that the prospective use of global cardiovascular risk assessment translates to reductions in CVD morbidity or mortality. There are reductions in SBP, cholesterol and smoking but they may not be clinically significant given their small effect size and short duration. Resources need to be directed to conduct high-quality systematic reviews focusing on hard patient outcomes, and likely further primary RCTs.
There you have it. Medical reviews are of poor quality!
mikecawdrey, the assumption is that if you are the average person (based on the number of people sampled) the risk assessment will be applicable. We are all different, am I an average person? I am starting to suspect that most people are sick (blood pressure, hyperglycemia,overweight, CVD, etc.), there are no healthy people available for a control group.
That is probably music to big pharma’s ears. 😦
Not only that but (may also apply to the statin paper above) all such people will be put on a high carb low fat diet. That’s just in case they weren’t on one already.
May be of interest to those with statistical knowledge.
The problem with p values
https://aeon.co/essays/it-s-time-for-science-to-abandon-the-term-statistically-significant?utm_source=Aeon+Newsletter&utm_campaign=a752d8f152-EMAIL_CAMPAIGN_2017_03_24&utm_medium=email&utm_term=0_411a82e59d-a752d8f152-69493625
You have to be so damn careful with statistics. Here is another example regarding false positives I read in a book called “The Drunkard’s Walk”. The writer, physicist Leonard Mlodinow, was refused life insurance on the basis of a medical exam.
He called his doctor, who told him “As a result of your blood test, the chances are 999 out of a thousand you will be dead in five years.” The test showed he had AIDS, and the false positive rate for that test was 1/1,000. This was in 1982 when AIDS was a death sentence.
Being statistically knowledgeable, the writer realised his chance of not having AIDS was much better than 1/1,000, because he belonged to a low-risk group, namely monogamous heterosexual men, where the prevalence of AIDS was about 1/10,000. If 10,000 of his group were to be tested, they would throw up ten false positives and one real positive. So his chance of having AIDS on the basis of a positive test was actually only 1/11. (It turned out he had a rare genetic mutation that triggered the test.)
However, if he had been a drug-using homosexual where the prevalence of AIDS was 1%, if 1,000 of his group were tested they would throw up ten real positives and one false positive. So his chance of having AIDS on the basis of a positive test would be almost a certainty at 10/11.
As he says, it is vitally important to know the prevalence of whatever is being tested in the sample population, as well as the accuracy of the test.
Again, off topic, but interesting:
http://science.sciencemag.org/content/355/6331/1330.full
Accorning to this, about 2/3 of cancers due to random mutations, 30% environment, 5% genetic. I have only read the abstract so far, and an article in a general magazine summarizing this paper. I think what they are missing is that in additon to carcinogens such as cigarette smoke that actively cause mutations, there are also behavorial or environmental factors that decide whether a tumor gets to grow rapidly or not. Sugar intake, lack of vitamin D and excess DHA from fish oil come to mind. DHA is particularly interesting as it promotes angiogenesis and has been shown to cause AMD (age related macula degeneration) and prostrate cancer by promoting the growth of capillary blood vessels.
Eric, this blog is about CVD, but cancer and every other disease could have common causes, you have started a list. My list includes PUFA, linoleic acid is big.
Where did AMGEN go wrong? Theory seemed simple enough, more LDL receptors = less LDL = less CVD
– First: 27,0000 people were too many to test. On the average people do not die that quickly.
– They should have studied say 100 people but measure and studied as many parameters as possible besides (bad)LDL.
– Question that should have been answered before testing on 27,000 people: What will the extra LDL particles do to liver cells and any other cell? Will the cells be stressed and cry for help, measure cell response.
– Do not try to fool Mother Nature.
Another hypothesis is needed to explain the failed AMGEN trial.
1- Cholesterol hypothesis (LDL-C as cause of CVD) is dead
2- Particle number hypothesis (LDL-P) is emerging. Too many LDL particles cause CVD. Test is not available in Canada. Seems plausible but not convinced that the LDL-P can explain anything.
3- A new LDL-PQ hypothesis ( LDL particles number and quality). This new hypothesis will not explain everything about CVD, nothing will, but it can explain a lot.. This explanation of the new hypothesis is for the benefit of the average patient. To comprehend the LDL-PQ hypothesis, one must understand the good/bad classification of LDL particles covered in a previous post.
Why trial failed: more LDL receptors removed LDL (the good cholesterol that cells need) and left only sdLDL (the bad cholesterol) that cannot be used by cells and is not readily taken up. sdLDL sits in the bloodstream and gets glycated and oxidized, and is removed by macrophages to produce foam cells (the beginning of plaque). A cell is literally starved to death. Too many dead cells > dead tissues> dead organs > dead patients.
This new hypothesis can also be used to explain why statins are harmful, increases number of (bad) sdLDL particles, decreased number of (good) LDL particles. Same concept as in failed AMGEN trial. EASY!
But statins are good because inflammation is reduced and CVD is an inflammatory disease! True but buggering up body’s defence system is not good except in some cases like heart and liver transplants required because of statin use.
LESSON: every failure can be a learning experience.
The real question anyone should ask when a new hypothesis is proposed, is why exactly we believed the previous hypothesis, or the one before that!
David Bailey
There are two answers to your question:
1 we as a species get wiser/clevejrer all the time
2 my preferencej is that these things in the absence of real understanding, are fashions, or modes of thinking, so try to reach your own conclusion
I think the statement that as a species we get wiser/cleverer, over whatever time you pick, became false when profit became the main driver. The state the world is in today with the many the ecosystems under destruction I would suggest does not indicate an overall increase in wisdom.
David Bailey: Excellent question. An (outdated)hypothesis in a group situation will persist due to peer pressure, job security, loss of confidence in the organization, or financial reasons, even when emerging new information has debunked the hypothesis. This has nothing to do with “belief”. If I believe that saturated fat causes CVD and then a new hypothesis says that sugar causes CVD, I have to make a decision. Why I believed the first hypothesis is now irrelevant. For the sake of my health I have to decide what to “believe”.
LDL-C is high, you need a statin, or take niacin or…
LDL-P hypothesis seems plausible, more particles = more chance of particles getting below endothelium. How can I make use of this idea?
LDL-PQ hypothesis: number of modified lipoprotein particles is the problem. How bad is oxLDL, what can be done to prevent LDL oxidation? Diet is the answer, no medication required.
Every person has to look after their own health and choose what to believe, and keep asking questions.
Andy,
My remark about hypotheses was supposed to be aimed at those doing research rather than the rest of us – sorry for the confusion! What I meant was that shifting hypotheses should make everyone in that area worry that their subject never was based firmly enough on evidence.
Looking at it as an outsider, I think we need more people looking at the totality of the evidence from all the studies – as Dr Kendrick does – not distorting the evidence to fit in with whatever is the current hypothesis!
Does diet cause CVD?
How much effect does diet have on CVD? Made a quick summary of what effect diet might have on CVD. Probably affects cancer and dementia as well. Other items like NO are downstream of primary activators. For the use of the average patient there is no need to go into scientific explanations, similar as per car maintenance manual. Something to discuss with doctor before getting a prescription.
Blood related risk indicators for CVD (derived from blood tests):
-high TG = from high carb intake > more sdLDL
-low HDL = from low sat/mono fat intake
-TG/HDL ratio equivalent to (carb intake)/(fat intake)
-sdLDL high TG/HDL ratio = more sdLDL= more fatty streaks > plaque, sdLDL affects NO production from endothelial cells
-high glucose = from high carb diet, > ROS, immune function, endothelial cell dysfunnction
-high insulin = from high carb diet
-hs- CRP, inflammation marker, probably effect of high carb intake
– blood clotting factors (affected by diet?)
– HbA1c glycated hemoglobin from high blood glucose
Diet related effect:
-oxidized cholesterol ( eg powdered eggs in proceeded foods) = foam cells
-oxidized fats (processed foods, food reparation), inflammatory
-high PUFA (omega-6 oil, easily oxidized, inflammatory)
-high carbohydrates (= increased sdLDL), = high insulin & glucose, lower immune function
– high fructose (a carb but deserves special attention)
-low sat./mono fat (= low HDL)
– high protein intake (excess becomes glucose)
-low micronutrients (minerals & vitamins)
-heavy metals (lead, mercury etc)
-plant defence compounds (eg WGA, lectins etc.in wheat)
-Chemical poisons, (glyphosate, msg, artificial anything)
– GMO’s
Medications to improve CVD outcome
-blood pressure, very little feet on CVD, mostly side effects
-LDL-C lowering, ie statins, NNT 150? mostly side effects
-Glucose lowering medications?
-HDL increasing, not ready for prime time, disaster
-Inflammation lowering, aspirin
-Anticoagulants, rat poison
-plaque roto-rooters
I can no longer remember who to attribute it to, but a magnificent typo which deserves to be perpetrated
“cardiovascular morality”
If people want to lower LDL, and I don’t understand why they should, niacin would do it. The disadvantage is the flush after taking it. The flush can be avoided if niacin (B3) is taken in the form of niacinamide, but then it doesn’t lower cholesterol, though it will probably stop you feeling depressed about it, if you thought you needed to. Dose would be about 3g/day according to the work of Linus Pauling and Abram Hoffer. B3 is also useful in arthritis cases. As with vitamin C, B3 doesn’t have harmful side effects, and it doesn’t earn big pharma any $.
@ AH Notepad
Re Niacin
I think Peter at Hyperlipid had an article about niacin, only he used to call it acipimox or something. (It is basically Franken-niacin).
One thing leads to another and I found out that there is a “niacine receptor”.
It inhibits lipolysis. Thus it deprives you of much needed LDL, doctor is happy.
Well, sort of happy. Niacin is too cheap.
What this does to the rest of the body, well it doesn’t take Feynman to figure this out. It eludes me at the moment whether it acts on the fat pads or already on the soontobefatty liver. In any case, this is bad I think.
Vitamin preparations usually use the amide which does not stick to the receptor but could also work indirectly due to substitition effects.
Ironically, energy drinks contain huge amounts of niacine. Probably detrimental to the energizing effect, too.
These radical ideas have also occured to others and there are papers actually discussing whether the nicacin fortification in the U.S. makes people obese. Boring statistics. But could really be that effect of giving up grains is partly due to removing niacin overload.
What I don’t understand is why humans should have a niacin receptor inhibiting lipolysis.
My pet theory is that it is a bio-signal for “food came in, storage mode”. Niacine is in high quality food and even in gruel and salads there is some.
gollum, sorry, but I don’t understand if you are making a point, and if you are, what that point is.
Well my point would be: niacin will perhaps bring down the LDL and make your GP happy, however will also prevent melting the fat pads. Filled fat pads are associated with general metabolic inflexibility, metabolic syndrome, glucose intolerance, heart problems, you name it.
So is Niacin bad for you. I have just started taking. Was recommended by my Nutritionist. Hope it might also reduce m BP. Cholesterol is 8.9 and I know I shouldn’t be but I am worried about this also.
Hi Janet, from another Janet – don’t worry. It’s the ratios that count. If you don’t already know, ask for the separate hdl, ldl and triglycerides. If your hdl is high and your trigs are low then you’re laughing. Mine are 3.4 and .05 – I’m laughing. The people at the GP’s surgery, including the GP don’t seem to grasp this important fact.
Cheers
If they grasped that important fact, pharma companies’ share prices would drop.
Niacinamide is supposed not to reduce LDL. At what dose does niacin cause the problems you describe?
That is a good question.
We have the mechanism (niacin receptor) and studies plotting correlations.
For lowering lipids (when niacin was still popular) doses like 500 mg (just a rough number) were used daily.
Doctors noted that flush problem “limiting therapy”. I do not know whether patients got fatter, if so they should have noticed but well, eat less exercise more you know the drill.
So we have mechanism but no nice plots weight under niacin vs. control group. This means I do not really know.
It is however, hard to imagine that the doses used to bring down lipids will not incur this problem, since the lowering lipids effect seems to work exactly by preventing to melt the fats.
I can tell you however that I, personally, try to limit niacin (and amide) intake (from multivitamin, energy drinks, and niacin supplement), even if at 20 or 50 mg daily (can reach that with rich food and some multivitamin) the effect may be nothing to worry about.
Cholesterol: When statins trigger diabetes
Twenty-five months after the European injunction, this new adverse reaction is not included in the patient’s record for every other case.
BY JÉRÔME VINCENT
Published on 22/03/2017 at 11:14 | Point
http://www.lepoint.fr/sante/cholesterol-quand-les-statines-declenchent-le-diabete-22-03-2017-2113798_40.php
LA LISTE NOIRE DES MÉDICAMENTS
Depuis 4 ans, nous dressons la liste des médicaments dont les inconvénients l’emportent sur les bénéfices. Coûteux, ils présentent toujours une alternative et le patient -comme le médecin prescripteur- peuvent s’en dispenser. (THE BLACK LIST OF MEDICINES
For the past four years, we have been listing medicines whose disadvantages outweigh the benefits. Costly, they always present an alternative and the patient – as the prescribing physician – can dispense with it.) http://www.lepoint.fr/dossiers/sante/liste-noire-des-medicaments/index_2.php
Twenty-five months after the European injunction, this new adverse reaction is not included in the patient’s record for every other case.
Statins, which act by decreasing the synthesis of cholesterol and are prescribed to avoid cardiovascular accidents, are the best-selling drug class in the world. More than 6 million French people consume it, and the Health Insurance estimates that they are prescribed to 1 million new patients each year. Beyond the recurring polemics about their interest or uselessness,their undesirable effects on the liver and muscles are
undeniable. Recently – in 2012 – was recognized a diabetogenic effect by
European and American drug agencies. From the … (more…paywall)
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Thought might interest –
Why veins don’t develop plaque? and how arteries do.
A very simplified explanation
Lipids Health Dis. 2013; 12: 132.
Published online 2013 Sep 8. doi: 10.1186/1476-511X-12-132
PMCID: PMC3847608
“Phenotypic alterations in human saphenous vein culture induced by tumor necrosis factor-alpha and lipoproteins: a preliminary development of an initial atherosclerotic plaque model”
“The present study was the first to apply TNF-α with LDL to enhance foam cell formation, and demonstrate SMC proliferation, SMC growth, and matrix accumulation within a short duration compared to animal models”
Plaque develops in veins if environment is changed ie higher pressure, higher glucose, pulsating pressure, more oxLDL, more endothelial dysfunction. Veins in CABG?
Conclusion; fatty streak from macrophage+oxLDL is first step in plaque formation.
Endothelial cells have oxLDL receptors (LOX-1) up-regulated by endothelial dysfunction
Endothelial cell + oxLDL = injury(NFkB activation) > cell apoptosis, Q10 and HDL3 can protect EC from apoptosis. EC’s sense oxLDL in blood and send signal to macrophages to remove threat.
I had a look at the paper “Phenotypic alterations etc . . .” because I am curious about why veins appear to be less prone to atherosclerosis than arteries. I remember reading an account describing veins used in coronary bypasses, in time, developing lesions. On the face of it, as Andy states above, the issue is one of environment. The first things that come to mind and have been mentioned by others is pressure or damage from shear stress forces, stretching . . . .
The paper describes how they created the essential atherosclerotic features in section of veins . . . such as fibrous cap formation, thickening of the intimal layer, increased proliferation of smooth muscle cells, migration of smooth muscle cells, smooth muscle cell foam cells.
What is interesting is how they managed it: Take 4 ring sections of saphenous vein – put in different culture media for 14 days . . . The 4 media used . . .
1= simple culture media;
2= media+TNFα;
3= media+TNFα+LDL;
4= media+TNFα+oxLDL
They found that TNFα by itself was sufficient to present atherosclerotic features, but LDL, and better still oxLDL, produced more developed atherosclerosis.
And . . . . . the vein managed to do this without pressure, stretching or pulsing!
Their model falls a little short in that they did not have macrophages doing their stuff. In the real situation I guess it would be the macrophages that would be producing the inflammatory TNFα.
They did not mention much on how the atherogenesis got underway other than to say that TNFα induces the endothelial dysfunction and increases the expression of Scavenger Receptors on the endothelial cells and smooth muscle cells.
Scavenger receptor? What on earth is a scavenger receptor?
Looking at “CD36, a scavenger receptor implicated in atherosclerosis” Young 2014 . . . the ScR or CD36 appears to be involved in binding loads of stuff: oxLDL and lots of other different rubbish. In principle you could get oxLDL under the epithelial layer with the help of the endothelial cells’ CD36s. The macrophage’s CD36s help swallow up oxLDL and eventually lead to foam cells – when stuff is bound to the macrophage CD36s, they set off cascades that release inflammatory cytokines.
Oh and shock . . .. platelets have CD36s which can bind oxLDL and become super activated! (COAGULATION ALERT)
They can also internalise oxLDL and these can interfere with endothelial regeneration.
Phew!
A general observation about life from start to finish.
Phase 1: slow process of foam cell/fatty streak accumulation in arteries (sub-endothelial)
Phase 2: at age 50 + or – 10 years vulnerable plaques with necrotic cores appear. Time for first and maybe last MI. Fibrous cap develops over plaque. Erosion of cap and new capillaries precipitate thrombi formation and growth of plaque. If plaque growth is slow a stable cap is formed but plaque keeps expanding unless lifestyle intervention initiated.
Phase 3A: 60+ age and CVD. If plaque growth not slowed down demise by MI is inevitable.
Phase 3B: 60+ age and slower plaque growth.. Demise by cancer or dementia.
Possible reason for my survival so far: didn’t follow guidelines, ate bacon, eggs, butter, meat, no margarine, no PUFA, read many books about diet and health (including Dr,K’s cholesterol book)
From people that I have known personally: cause of demise
– one from MI at 45
– 5 from cancer from age 62+
– 3 from ALS from age 65+
– 2 from Alhzeimers’ age 80+
The still living: toe and leg amputations , diabetes2, fatty liver, arthritis, dementia, obesity
Lesson to be learned: Theory has to be right in order to take appropriate evasive action.
I made a comment on a Facebook page, docsopinion, regarding these meds. It turned out this doctor was an investigator in this drug trial. I questioned the results of the trial. The response I received was that the trial was a success because “a well performed trial is a scientific achievement”. To me this sounds like nonsense if the drug doesn’t perform well, which it didn’t. I questioned this response and eventually led me to a deadend (no response) when I wondered why Amgen didn’t continue the trial if the results seemed so poor and it was originally scheduled to be 4 yrs not 2. Just thought this was interesting. Here’s the link to that conversation, https://www.facebook.com/DocsOpinion/posts/1390666234318623?comment_id=1391888484196398&reply_comment_id=1392366557481924&ref=notif¬if_t=share_reply¬if_id=1490037342340188
ScienceDaily reports (March 8, 2017) that researchers from the University of Salford “measured the impact on cancer stem cell metabolism of three natural substances, three experimental pharmaceuticals, and one clinical drug.” They found that “Vitamin C is up to ten times more effective at stopping cancer cell growth than pharmaceuticals. . . .”
Powerful finding, yes?
Nah!, We need to do more research, until we get the result big pharma wants, OR, vitamin C is made a controlled, prescription only drug.
Lesson learned: futile to complain about cholesterol lowering drugs and doctors that prescribe them. That is not where the solution to CVD lies. You are on your own. What destroys a healthy endothelial layer?
Back to finding the real cause. What is function of endothelial cells (EC)? What do ECs look like? What causes EC dysfunction? What is result of EC dysfunction?
A brief outline
Function: regulate NO, coagulation, vasodilation, communicate with immune system
Structure: Glycocalyx layer protects EC from erosion due to blood flow
Cause of EC dysfunction: hyperglycemia, oxLDL
Result of EC dysfunction: loss of glycoclyx, increased permeability, apoptosis, decreased NO, increased coagulation, increased inflammation, vasoconstriction, foam cell formation
J Intern Med. 2006 Apr;259(4):393-400.
Vasculoprotective properties of the endothelial glycocalyx: effects of fluid shear stress.
Gouverneur M1, Berg B, Nieuwdorp M, Stroes E, Vink H.
“Abstract
The endothelial glycocalyx exerts a wide array of vasculoprotective effects via inhibition of coagulation and leucocyte adhesion, by contributing to the vascular permeability barrier and by mediating shear stress-induced NO release. In this review, we will focus on the relationship between fluid shear stress and the endothelial glycocalyx. We will address the hypothesis that modulation of glycocalyx synthesis by fluid shear stress may contribute to thinner glycocalyces, and therefore more vulnerable endothelium, at lesion-prone sites of arterial bifurcations. Finally, we will discuss the effects of known atherogenic stimuli such as hyperglycaemia on whole body glycocalyx volume in humans and its effect on endothelial function.”
PUT DOWN THAT DONUT!
This was known 11 years ago.
Diabetes. 2006 Feb;55(2):480-6.
Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo.
Nieuwdorp M1, van Haeften TW, Gouverneur MC, Mooij HL, van Lieshout MH, Levi M, Meijers JC, Holleman F, Hoekstra JB, Vink H, Kastelein JJ, Stroes ES.
Author information
Abstract
“Hyperglycemia is associated with increased susceptibility to atherothrombotic stimuli. The glycocalyx, a layer of proteoglycans covering the endothelium, is involved in the protective capacity of the vessel wall. We therefore evaluated whether hyperglycemia affects the glycocalyx, thereby increasing vascular vulnerability. The systemic glycocalyx volume was estimated by comparing the distribution volume of a glycocalyx permeable tracer (dextran 40) with that of a glycocalyx impermeable tracer (labeled erythrocytes) in 10 healthy male subjects. Measurements were performed in random order on five occasions: two control measurements, two measurements during normoinsulinemic hyperglycemia with or without N-acetylcysteine (NAC) infusion, and one during mannitol infusion. Glycocalyx measurements were reproducible (1.7 +/- 0.2 vs. 1.7 +/- 0.3 l). Hyperglycemia reduced glycocalyx volume (to 0.8 +/- 0.2 l; P < 0.05), and NAC was able to prevent the reduction (1.4 +/- 0.2 l). Mannitol infusion had no effect on glycocalyx volume (1.6 +/- 0.1 l). Hyperglycemia resulted in endothelial dysfunction, increased plasma hyaluronan levels (from 70 +/- 6 to 112 +/- 16 ng/ml; P < 0.05) and coagulation activation (prothrombin activation fragment 1 + 2: from 0.4 +/- 0.1 to 1.1 +/- 0.2 nmol/l; d-dimer: from 0.27 +/- 0.1 to 0.55 +/- 0.2 g/l; P < 0.05). Taken together, these data indicate a potential role for glycocalyx perturbation in mediating vascular dysfunction during hyperglycemia."
Andy
You are evidently “swinging around” to find and put all pieces together to create a world view of health and nutrition that you can live with 🙂
And you have evidently arrived att the same spot I arrived at some years ago about food and health which basically spells LCHF?
Dr. Goran S.
The GLYCOCALYX (GC) was the missing link for me to understand just how bad raised blood glucose levels can be. Always believed that LCHF was healthy. Today I discovered that every endothelial cell in every blood vessel and micro-vessel has a GC barrier, heart, eyes, brain etc.. My gut feeling is that a compromised GC could also be involved in cancer and neuro-degeneration.
Researchers are busy developing medications to protect and rebuild the GC.
“Damage of the endothelial glycocalyx, which ranges from 200 to 2000 nm in thickness, decreases vascular barrier function and leads to protein extravasation and tissue oedema, loss of nutritional blood flow, and an increase in platelet and leucocyte adhesion. Thus, its protection or the restoration of an already damaged glycocalyx seems to be a promising therapeutic target both in an acute critical care setting and in the treatment of chronic vascular disease. Drugs that can specifically increase the synthesis of glycocalyx components, refurbish it, or selectively prevent its enzymatic degradation do not seem to be available.”
Until the drugs become available LCHF will have to do. Pass the bacon.
Since a was born shortly after the war, I would never advise someone to “Put down that donut!” (i.e. waste it), but to finish it but not buy another one! My theory is that it is the people who leave food on their plates that are usually the fat ones, because they order or cook food that they don’t really want, and eat their fill, content in the knowledge that they will waste the rest.
Being fat and leaving food are not necessarily associated. Many fat people eat surprisingly little, yet they are still fat. I think the theory fails, unless you have data to support it.
It appears to me that diabetics are more likely to suffer early heart disease than non-diabetics, and that diet is significant in type 2 diabetes. Therefore diet is significant. Sugar is not the only intake that will cause diabetes. For most people who post here, any excessive amount of carbohydrate will do. For people who post elsewhere they consider it is fats that cause the diabetes (don’t ask me why, that is their belief).
From the Wiki glycocalyx page:
“The enzymes and proteins listed above serve to reinforce the glycocalyx barrier against vascular and other diseases. Another main function of the glycocalyx within the vascular endothelium is that it shields the vascular walls from direct exposure to blood flow, while serving as a vascular permeability barrier.”
So degraded glycocalyx = exposure to blood = clots?
Dr K right again?
Dear Dr. Kendrick,
What are your thoughts on High LDL-P in people on a low carb diet?
Someone here said it is just an excuse to continue the diet heart dogma with a little bit different spin. But I would be interested in your opinion.
I would agree with that someone.
Right – so to be clear, would you say that diet has little/nothing to do with heart disease, unless perhaps it is so full of sugar that it gives you diabetes, which then may give you heart disease?
Slowly, slowly the tide turns.
Interesting article:
Cholesterol Paradox: A Correlate Does Not a Surrogate Make
http://www.medscape.com/viewarticle/875261
Example of medical study that is one sided – “Most cancer types just bad luck.” https://www.theatlantic.com/science/archive/2017/03/no-cancer-isnt-mostly-bad-luck/521049/
David Bailey, I was born in 1940. People were not concerned as much with heart disease as with starvation, a crust of bread was a sacred thing. I understand your point about wasting food.
But today the focus is on excess of food and choosing what to eat.
The official recommendation still is to eat low fat/high carb, but now high fat/low carb is preferred by those willing to learn the truth.
My understanding now is that CVD starts with excess blood glucose. Some say that cause of CVD is inflammation. But glucose and destruction of glycocalyx that protects endothelial cells causes inflammation.The glycocalyx also has many other functions. The donut is guilty.
Andy,
OK, but it is my contention that people eat too much partly *because* they now feel comfortable about wasting substantial amounts of food. It isn’t a coincidence that Americans, who are famous for wasting food, also have (on average of course) the largest waistlines, nor is it a coincidence, I think, that as this habit has spread to other countries, so have the problems.
Whether a person is concerned about eating less sugar, or about calories in general, if he or she feels comfortable to obtain a food item and only eat part of it, he will consume more of what he shouldn’t than he would if he followed the rule of eating all of what he buys/prepares – and therefore not buying the item next time. Next time you are in a cafe, look at which people discard the most food (disregarding those with small children).
For the last few years I have tried hard to avoid eating much sugar. There are lots of tempting things I could eat, but suppose I was in the habit of buying a piece of cake, while promising myself I’d only have a bite….
My wife wants to get a cardiologist’s blessing before stopping statin therapy. Notwithstanding the extensive statin side effects (have separate list) what are the benefits/risks of low cholesterol? My list so far is:
Benefits: NIL (cholesterol does not cause CVD)
Risks:
irritability and/or aggression
insomnia from low serotonin
A low serum cholesterol (less than 200 mg/dL [5.2 mmol/L) in patients with heart failure (HF) is associated with higher mortality
increased risk of Hemorrhagic Stroke
cholesterol Needed To Fight Cancer
increased mortality, all cause
less resistance to infection
Cholesterol Is Needed for Memory
Parkinson’s disease
lower immune system
Alzheimer’s disease
What is chance of getting cardiologist’s approval to stop statins? Any suggestions?
Chance is minimal.
The only progress i made with my mothers doctor was when i asked her to ask them why the paperwork in the statins packet says she should not take it because she is over 65… To be honest I have no idea whether it stated that… they just stopped giving her grief over them..
lol 🙂
Yes, NOT for over 65s and NOT for women…..come to think of it, NOT for anyone, though it doesn’t say that, of course.
Doesn’t it? I’m sure that was just an omission by the manufacturers. Perhaps they could send out an update.
Best hope for stopping statins might be to say “This is what we want to do” and ask for his opinion. No need to debate details at this stage, have backup data handy. Get another opinion if not co-operative.
Give cardiologist the following info:
Followed low fat /low cholesterol /low sodium diet recommendation, required CABG 8 years ago
1, LDL-C does not cause CVD, why use statins to lower cholesterol?
2. Statin therapy for women 65-74, one death prevented after treating 676 patients for 5 years, 675 patients will have possible side effects
3. CABG restenosis likely (5 to 10 years) if cause of CVD not addressed
4. CVD is mainly caused by hyperglycemia/hyperinsulinemia (diet)
5. Request agreement to discontinue statin use (muscle pain, back problems)
6. adopt high fat/low carb/moderate protein diet
7. eat saturated fat and monounsaturated fat, eliminate PUFA, restrict wheat consumption, supplement with vitamins/minerals
8. Get CAC score to monitor plaque status. (test not done in Canada, can go to USA)
9. Do complete blood tests for reference.
Why do you need to “request agreement to discontinue statins”? You can choose to do whatever you like…
Absolutely
Andy,
The trouble with your information, is that while it is probably right, it is certainly contentious.
I think the only non-contentious data is the various studies into actual health outcomes that have been done. This list of studies that show that those with higher blood cholesterol (or LDL) live, on average, slightly longer seems the most vivid illustration that something is wrong:
http://vernerwheelock.com/179-cholesterol-and-all-cause-mortality/
Andy,
My last (?) and really arrogant cardiologist had taken the standard tests before our only and one meeting but he didn’t comment any of the test results except that when he prescribed statins to me he mentioned that it was not because my cholesterol values were bad in any way but in order to treat inflammation. On the other hand my CRP values, which is the standard measure for the inflammation status as far as I have understood, he didn’t even mention. He though, all the time, knew that I would never touch any of the five drugs he prescribed so to me this was therefor an act of disrespect and on top of this insult he called me later to check if I had visited the pharmacy. What a corrupt guy in my eyes!
Anyway, at the outset of our meeting he proudly did declare that he was not the least interested in what I had been doing for 14 years and absolutely not interested in any discussion about this since it was complete nonsense to his opinion. As he stated “You can talk anyone over but not ME!” On my question if he was not the least impressed by seeing me alive and in pretty good shape since I had refused everything they had suggested he blurted: “You have just been LUCKY!”
Well I then solved my angina problem by own research, as I had done 14 years earlier, which this time led me to 1600 IU natural E-vitamin and now at 2400 IU which seems to work fairly well as I now don’t even suffer from the heavy work in my garden. With my pulse meter attached I am at every “work out” session trying to reach my maximum pulse of 160 bpm for may age
These guys do really not impress on me and my opinion is that they do more harm than good in the long run.
Dr. Goran S.: Your comments are appreciated and I will use your experience as a guide. My wife is terrified now of CVD and needs assurance, therefore need to involve cardiologist.
The “inflammation” excuse for using statins forever is not valid. Inflammation cause is hyperglycemia injury to endothelial cells and can be corrected by diet. CRP is produced by liver in response to IL-6 released by monocytes due to injury. Statins disrupt cell function (probably in most types of cells) and alter immune response. Reducing inflammation is OK for organ transplants to prevent rejection, but why for log term use.
According to today’s Times the target for doctors to prescribe statins is to be dropped to free up doctors appointments. Financial pressure is leading to some sense. Maybe they’ll ask where they’re prescribing all those drugs for diabetes when a low-carb diet can work wonders and get people drug free.
Stephen T….I did not see the article, but what do you make of this little story?
77 year old female on statins since the beginning of time……suddenly called into surgery for fasting blood tests; no explanation given as to why.
Phoned up by receptionist to say GP is satisfied with all results, and for her to continue everything as before.
Then she gets a letter to enroll on DESMOND, as she is classed as in ‘high risk’ category. (blood results do not indicate a high risk, so what is it that has triggered her referral?)
Now…..GP is obviously satisfied that the long term use of statins has not induced diabetes in this case…..but…..oh, dear it just may have an adverse effect in the future, so better get the patient educated in preventing diabetes. The inference being that it will come about by patient neglect in self-care, and not due to toxic statins.
Now if there is not a conundrum in this unfortunate tale, I will eat my nurse’s frilly cap…..better still, pour me a little tipple. ( see Dr K’s new article 1 April)
Those Indecipherable Medical Bills? They’re One Reason Health Care Costs So Much.
OT: Interesting article on the New York Times on one reason why American health care is so expensive: every procedure has to be coded, and by tweaking the code a bit you can make more money for doing much the same thing. So hospitals and doctors employ professional coders.
The medical insurers are wise to this practice so they employ their own coders to check on the service provider coders to make sure they are not being screwed. Of course, this army of clerical workers pushes up medical costs.
And if you are unfortunate enough to be uninsured, as the person in the article was, you are in for a very nasty shock when the bills hit you.
There is now a new PCSK9 trial that was published: http://www.acc.org/latest-in-cardiology/articles/2018/03/05/15/53/sat-9am-odyssey-outcomes-cv-outcomes-with-alirocumab-after-acs-acc-2018. It sounds like a great success, because “We were really pleased to see the treatment was effective and associated with a reduction in mortality.”
I meant to ask Malcolm if this study is really going to stand out for its success of cholesterol lowering, but then realized that he’d point out that it’s not clear through what mechanism the mortality was improved: ‘While the rate of all-cause death was significantly lower by 15 percent with alirocumab versus placebo (3.5 vs. 4.1 percent), there was no significant difference between the groups for CHD death (2.2 vs. 2.3 percent) and cardiovascular death (2.5 vs. 2.9 percent). ‘
Still, would be very curious to hear your opinion of it.
I will have a look at the full paper when it comes out. These studies can be very difficult to interpret. At present, however we now have two PSCK9 trials, and they appear to be showing very different outcomes. This, despite the fact that (as far as anyone knows at present) the only function of a PCSK9 is to lower LDL levels. So, we would expect them to show exactly the same outcomes, and they don’t.
The main issue with the latest trial is that alirocumab did not lower CHD or CV mortality (significantly), yet it lowered overall mortality (significantly). As the only way the PCSK9-inhibitors work is to lower LDL, and thus (according to the LDL hypothesis) CHD/CV mortality, what else could be they doing to lower overall mortality. So far, we have not been told.
The JUPITER study (on statins) was another one where CV mortality was unchanged, yet overall mortality was reduced? This was never fully explained, it just was. In fact the reduction in overall mortality was driven entirely by a reduction in cancer deaths – a result seen in no other statin trial before or since. And like both PCSK9-inhibitor studies the JUPITER study was stopped early.
Anyway, we are left with two explanations for the reduction in overall mortality with alirocumab
1: PSCK9-inhibitors have added, unexpected, beneficial effects on other diseases that are ‘pleiotropic’
2: This was a statistical artefact
It seems likely it was a statistical artefact because evolucamab showed no benefit on overall mortality (in fact morality was slightly increased vs. placebo in the FOURIER trial).
However, my main take is that neither evolucamab nor alirocumab (the two PCSK9-inhibitors) have demonstrated a reduction in CV mortality. Which should give some pause for thought, as that is exactly what they were both supposed to do.
At the same time they both managed to reduce the risk of stroke, despite the fact that a raised LDL level is not a risk factor for stroke. Which is a very clever trick.