13th March 2018
Before putting cardiovascular disease to bed for a while and talking about other things – such as diabetes – I thought I should highlight a fact that is almost never remarked upon yet is extremely important. At least it is, if you trying to bring down the cholesterol hypothesis. The fact is this. A raised cholesterol level, or LDL level, is not a risk factor for stroke. Not even in familial hypercholesterolaemia (FH) is a raised cholesterol level a risk factor for stroke.
Here, I am quoting from a study published in the Lancet called ‘Cholesterol, diastolic blood pressure, and stroke: 13,000 strokes in 450,000 people in 45 prospective cohorts. Prospective studies collaboration.’
‘After standardization for age, there was no association between blood cholesterol and stroke except, perhaps, in those under 45 years of age when screened. This lack of association was not influenced by adjustment for sex, diastolic blood pressure, history of coronary disease, or ethnicity (Asian or non-Asian).’ 1
I think that this was a big enough study to demonstrate that, if there is any effect, it can only be tiny. Yes, the study is over twenty years old, but it was done before statins came along to distort the entire area. By which I mean after the mid-nineties, a large number of people with raised cholesterol were being put on statins, thus making any interpretation of the impact of different cholesterol levels, on stroke, almost impossible.
As for Familial Hypercholesterolaemia. The findings of the Simon Broome registry (set up in the UK to study the health impact of FH) were, as follows
‘The data also confirm our earlier findings that FH patients are not at a higher risk of fatal stroke.’ 2
Thus, a raised cholesterol level is not a risk factor for stroke, even at very high levels found in FH – even in homozygous FH (where both the subject’s genes are faulty so leading to more severe FH). Yet, and yet, statins reduce the risk of stroke. Not by much, and not to the extent that I consider the benefits to outweigh the harms, but they do. Here, plucked from a million possible articles is something from the American Heart Association
‘Millions more people worldwide may benefit from cholesterol-lowering statins after a global study showed the drugs help reduce heart attacks and strokes in people at moderate risk. The risk fell slightly further when patients also took blood pressure drugs.’ 3
The absolute figures wobble about, depending of which of the myriad studies and meta-analyses you choose to look at, but the reduction in stroke risk is about the same as the reduction in the risk of heart attacks/myocardial infarctions.
When I see facts like this, I try to use logic. The logic, in this case, goes something like this:
- Factor A (raised LDL) is not a risk factor for disease B (stroke)
- However, if you lower factor A, the risk of disease B falls
Conclusion. Something other than the lowering of Factor A is causing the reduction in the risk of disease B. If you take this thought one step further, the beneficial effect of statins on the risk of stroke, flatly contradicts the cholesterol hypothesis.
1: https://www.ncbi.nlm.nih.gov/pubmed/8551820
3: https://news.heart.org/statins-lower-heart-attack-stroke-risk-in-people-at-average-risk/
Dr. Malcolm Kendrick 
In mathematics we have “if and only if”: the missing logic in many theories of medication function it seems.
In medicine we are supposed to have. Necessary and sufficient. Necessary is a requirement for causality. Sufficient is not. in fact, few factors are necessary and sufficient as ‘host’ variation has a significant impact.
In stroke, raised LDL is neither necessary, nor sufficient. Ergo it cannot be the causal factor.
“necessary and sufficient” is the same as “if and only if”. You can write the latter as ‘iff’ which is the shortest form of all.
Dr. Kendrick, a recent Medscape article by a prominent U.S. cardiologist, Dr. John Mandrola, makes the case that there isn’t any high quality evidence which unequivocally demonstrates that statins are beneficial for reducing stroke risk. To quote:
“The statin-after-stroke quality measure mostly began after publication of the Pfizer-sponsored SPARCL trial, which also included Pfizer employees as authors. This RCT tested the hypothesis that treatment with 80 mg of atorvastatin per day would reduce the risk of fatal or nonfatal stroke in patients with a history of stroke or TIA. About 4700 patients were randomized at 205 centers.
During a median follow-up of nearly 5 years, 11.2% of patients on atorvastatin had a fatal or nonfatal stroke vs 13.1% of those on placebo. This approximate 2% absolute difference (NNT=50) barely met statistical significance (P=0.03)…. Post hoc analyses suggested a heterogeneous treatment effect based on the type of stroke: atorvastatin use reduced the risk of ischemic stroke (HR 0.78, 95% CI 0.66–0.94), however, there was an increased risk of hemorrhagic stroke (HR 1.66, 95% CI 1.08–2.55). Moreover, there was no difference in mortality between treatment groups”.
Dr. Mandrola’s incisive critique of the evidence-base is well worth reading in full: “Statins After Stroke: Don’t Take as Gospel”. https://www.medscape.com/viewarticle/884124#vp_1
@JPSand. Thank you. I thought he could have made more of:
“There was no difference in mortality between treatment groups.”
Dr K, could you please explain further your logic here :
“Something other than the lowering of Factor A is causing the reduction in the risk of disease B.
I have rewritten the 2 previous statements you made as follows to make them clearer to myself.
1 A raised LDL does not increase the stroke risk
And
2 But less LDL lowers the risk of stroke.
I don’t think your conclusion necessarily follows. It could be something else. But also it could be that there is a threshold level of LDL below which stroke risk falls…
I think you will find my conclusion does necessarily follow.
I agree!
Sorry Dr K, you miss my point.
I am not arguing for statins or for lowering LDL.
I am just suggesting that the logic you put up, does not reflect the complexity of many interacting biological processes in the body. That is why I asked you to explain further…
The problem is that there is not just A & B. There is C, D, E, F, ……..through to Z. All interacting. My suggestion of a ‘threshold level’ was an attempt to illustrate this.
Bill. I agree there are complexities in the body. However, this particular issue is not complex – it is simple. Causality can never be proven. However, it can be disproven quite easily.
If you say that x causes y. All I need to do, to disprove your hypothesis, is to find people with y who do not have x. This is concept of ‘necessary’. As in, what factor is ‘necessary’ to causes a disease. The tuberculous bacillus is necessary for TB to develop. Without it the disease cannot occur. Of course, some people can be ‘infected’ with the bacillus, yet do not get the disease – they fight it off. In which case the bacillus can be defined as necessary but not sufficient. However, if a factor is neither necessary, nor sufficient for a disease to occur, it cannot be the cause. It may accelerate the disease – which is where complexity comes in. LDL may accelerate CVD, but it cannot be the cause. It is neither necessary, nor sufficient.
I think it does, and that wider evidence from statin trials – the CHD evidence too – supports it.
I remember seeing on a Cholesterol skeptics forum years ago that cholesterol is synthesised in situ in the arteries. A drug like statin which inhibits cholesterol synthesis would reduce in situ synthesis. It would also reduce liver synthesis and lower LDL. But this would only be associated with benefit in people with excess synthesis in situ, if the excess in situ cholesterol synthesis was causal and not the LDL.
And this is exactly the pattern seen in every statin trial where there’s an attempt made by subgroup analysis to distinguish those with increased cholesterol synthesis rates.
I think Malcolm means that the statins have extra effects (like promoting NO production, if memory serves me right) that are beneficial (unless you end up crippled from muscle problems!). There were some earlier drugs that lowered cholesterol, but had no effect on cholesterol, but these got forgotten!
I have obviously been following this blog for far too long!
He said it was something else that reduces the risk. Not the LDL lowering. Maybe increased NO synthesis. Maybe slight decrease in inflammation.
No increased risk of stroke with higher cholesterol. Good.
So, stroke, in this study, I presume refers to the ischemic variety. Does ischemia above the neck necessarily mean ischemia in the chest? MI? Not?
Is there no comparable pre-statin study that relates directly to CVD?
So what is the justification for prescribing the Statin in the first place ? Especially when considering all of the negative effects they have
Justification? Money! Money, money, money, money, money! Money makes the world go ’round, the world go ’round, etc. Just check out the disclosures, voluntary and wrenched from their grubby little fists by muckraking investigators, of the so-called “experts” recommending the widespread use of statins. It’s a multi-billion dollar bonanza for the docs, the pharma bros, etc.
Have very much appreciated and followed your series of blogs on heart disease, strokes, statins et al. It is great to be more informed than my GP’s on the subject, and to take the initiative on monitoring my health rather than leaving all the responsibility to the medical profession… Well… I’ve reached 69, eating loads of fats, enjoying cakes and especially good quality icecream… I have a positive outlook, take regular exercise, don’t smoke, having a loving wifer and cat (not necessarily in that order… !!), travel regularly, play and listen to music, enjoy concerts and ballet , garden, photograph and watch wildlife , research travel , and maintain a keen interest in world events , natural history etc etc etc…. Does all this give me a positive start on increasing my potential quality and length of life.. what do you think..?? In case not, propose to vist as many countries and cultures as I can…. current total: 15-20 Greek islands, 15 Caribbean islands , all the main Spanish, French and Italian islands plus Spitzbergen and..oh yes…. 75 different countries (so far)…. How about this for a life maxim: ‘cover the earth before it covers you’, or ‘better to roll into the grave knackered shouting’what a ride’ than get to the grave in a perfectly formed body’……. It isn’t how much you have in life, it’s what you do with what you have’…….. Continued thanks for your common sense perspectives on cholesterol, heart disease and all the other NHS and BMA ‘scare-mongering’…. …
Crystal clear- let’s hope people finally understand this
Crystal clear – let’s hope people finally get this
So what causes strokes!
Things that make one say, “Hmmmm”. And would one not expect the factors that cause heart attacks to cause strokes? Aren’t both just damage caused by the blockage of blood flow to an organ, be it the heart or the brain? And isn’t the “benefit” of statins their reduction of inflammation, which can be more safely achieved by other means, like dietary regimes (which some members want to ban from discussion)?
annie. I feel that I could be accused of keeping the dietary regime discussion bobbing along on the surface of these blogs. I really do think that the food industry has a lot to answer for regarding stuff sold “as food” over the last 100 or so years, (and certainly responsible for the promotion of much ill health). However, it is in a perfect position to be redeemed by promoting good, real food, and thus keeping Big Pharma at bay. Hurrah.
So, are we talking the anti inflammatory effect of statins? My brain aches; I’m thinking too much.
JanB, another benefit of statins is that they are antimicrobial. Unfortunately statins will also poison the mitochondria and gut microbiome.
Good point, I’ve been wanting to ask that here for some time. Don’t antibiotics also damage mitochondria throughout the body and hence cause (lasting?) damage and accelerated aging? It is also well known that they decimate gut bacteria and I have always wondered why folks aren’t given new seed bacteria after a course of oral antibiotics. What about the iodine protocol, wouldn’t one expect that to also have these effects?
On the other hand, the odd course of antibotics has been known to help the CVD situation by clearing out chronic nests of infection and hence lowering overall inflammation.
There was also some hype about old broad spectrum antibiotics killing cancer cells a few years back but it seems the initial promising results did not translate into that much of a success:
https://www.ncbi.nlm.nih.gov/pubmedhealth/behindtheheadlines/news/2017-06-12-antibiotics-and-vitamin-c-could-kill-cancer-cells/
I don’t nderstand. What am I missing?
I guess the statin business is thriving on pure confusion.
The problem with you Dr. Kendrick is that you are too logical.
Dear Dr Kendrick You are truly the answer to a maiden’s prayer. I was just about to email you to ask about statins and stroke and then found the relevant information in your latest blog post. I met an Indian woman at the gym, who was working to improve mobility of her affected arm through exercises in the swimming pool and steam room. She is highly motivated and conscientious about doing what she can for her health and fitness. We talked about health and doctors. I told her about the drop in income to GP practices from the loss of ancillary services to the private sector and how doctors are paid for the drugs included in the NICE guidelines – ie statins and not antibiotics. She told me she was on statins. I talked about my understanding of the research findings and patients I had dealt with in a GP practice as a psychologist, who were clearly suffering statin side effects and were in groups that could not possibly benefit from the drugs (women, men over 65, diabetics). Next time I see her, I’ll tell her about your blog. Many thanks for all the good (life saving) work you do. Kind regards Suzanne Looms
Suzanne,
Could you explain what you mean by ancillary services and private sector? Also, are you saying doctors get kickbacks on prescribing certain drugs? Here in the US, so far as I know, doctors only make money on chemo drugs.
I would not use the word kickback. Part of the payment system for GPs in the UK is predicated on things such as, measuring cholesterol levels, then lowering them. This is the Quality Outcome Framework system (QoF). Around 40% of the total income of GPs is based on the QoF system. Clearly, prescribing statins is only a small part of this work. Others things included measuring blood pressure, and blood sugar levels and suchlike – then lowering them – if high. It is bonkers system designed to create polypharmacy with all the attendant health problems this brings.
so…a GP’s income in NHS is partly derived by measuring things they may not feel inclined to measure…the lazy so and so’s need an incentive….or, to put another way…get the Practice Nurse to do the measuring and then ultimately prescribing as to what the computer dictates. Go further down the line….get the patient to hand in regular B/P measurements done on their own machine, in their own home….and bingo!
Medicine is getting almost like putting in our own fuel for the car, submitting our gas and electric readings on line, using hand held scanners to save expensive (minimum wage) operators’ time and energy at the supermarket checkout.
Best of all…..as the placard in the car park states :-
“THIEVES OPERATE IN THIS HOSPITAL CARPARK”.
Watch out docs…..you will soon be redundant.
Jennifer: My wife and I just got a letter from our GP telling us she’s going to retire at the end of May. The response from both of us was, “Good for her.” My own feeling is that she’s already done more than her share of good in this world. As for getting a new one (she sent a long list of possibilities), I’m going to wait as long as I wish. Why would a healthy person go to the doctor? Medicine doesn’t do health. What I’ve learned here and elsewhere has made a greater improvement in my health than any medical treatment I’ve ever had (and the best medical advice I’ve ever gotten came from our retiring doctor, to get a Senior Pass-which allows free access to all national parks-and now I drink deeply of nature on a weekly basis) And how many will I have to try out to find a real doctor? Not particularly delighted at the prospect. Our retiring doctor prescribed statins to both of us at different times, but didn’t bat an eye when we declined. Same with the flu shot, and any other conventional treatment we declined. Lucky we were! For nearly thirty years!
Gary. It makes me wonder how and why we have become embroiled in this escalating need to have repeated visits to see a GP, ( or Practice Nurse), especially when we did not even feel unwell in the first place. (portal of entry = “well women/men clinics).
The time I used to spend having various tests routinely repeated would have been better spent walking in the woods. Many tests resulted in ‘doubling the dose’, or ‘let’s add this tablet’, such that more tests needed to be repeated again. And there they have us! Who dares to jump off the roundabout?
I did, but not without much consternation.
AnnaM, sorry to disillusion you, but US docs get MAJOR kickbacks from pharma companies. No, it’s not some guy with slicked-back hair and a 5-o’clock shadow passing a grubby envelope of unmarked bills under a table to a doc in a smoke-filled room. It’s far more sophisticated and elegant than that. If you read Dr. Catherine Shanahan’s book, “Deep Nutrition”, she describes how she turned down an offer to join a successful practice with a big bonus plan for the docs that prescribed the most of certain drugs — who do you think funded the “bonus program”? Funded research, a chance to publish in prestigious journals, weekend retreats to attend “seminars” sponsored by pharma companies (while your spouse and kids spend the weekend skiing free at the resort where the “seminar” is held), a little “thank you” gift at Christmas of that top-rated $175/bottle Cab Sauv you read about, etc., etc. How many published articles are there describing the “successful trials” of a drug, then the authors turn out to be docs doing some “moonlight consulting” for the drug’s manufacturer, etc.? The kickbacks are nothing new. Back in the 1990s, muckraking docs like Ben Goldacre wrote about these goings on, all to no avail. Did you know that the US pharmaceutical industry gets the largest number of, and largest value, fines of any US industry? These aren’t even a slap on the wrist – more like a tap on the wrist.
That is all very depressing. I wonder if anyone here knows what the situation is in Oz. Unfortunately I do not ‘know’ myself..
@Bill in Oz….judging by how angry my mum’s doc got when I got her off the statins I reckon there’s a fair chance that kick-backs feature prominently in Australia….especially after I wrote the doc an evidence brief about the dangers of statins and over-hyped results….that she ‘didn’t have time to look into”
And yet, statins are still somewhat revered. I am meeting my cousin for a pub lunch this week, both of us mature ladies, still care about what we look like, a few hair streakshere and there, She feels protected that her GP has now put her on statins, joining her husband. How can I prick her bubble, I won’t of course. And who will live the longest, we both are involved with animal welfare, walk our beloved dogs, so fairly active, laugh a lot, enjoy a drink with our meal, love our families to death, and our creatures. Good home cooking, buy, peel and cook proper food, advice our children have taken on board. It is all a bit confusing this medical advice lark.
Who owns our bodies I would like to know. Just to add Dr Kendrick, my son is off to the Isle of Islay for a few days, birding, distillery visiting more like. Have a wonderful London meeting.
Sylvia, I used to feel protected until the horrible side effects kicked in. I now introduce the topic and learn to exit when I’m hitting a brick wall.
At least try to warn her about the side-effects that she may or may not get, and warn her that these need not happen immediately – 3 years in my case. Also some people report that statins damage their muscles permanently. I don’t know, but I imagine these may be people who persist with their statins when they can feel the side effect.
I agree with Sylvia – some of the adverse effects may not be recognised either by the person or their GP, such as memory lapses which are put down to ‘getting old’. My mother in law ended up having her brain frazzled after several years on a high dose of statins – by the time we realised what statins can do to the brain, it was too late. Irreversible muscle damage and type 2 diabetes are also adverse effects I’m sure your cousin would like to avoid – so perhaps advise her to take note of any strange symptoms that may start even after several months on statins. In some cases it can take years for things to appear by which time it’s not linked with the statins, but actually is.
Hello Anglosvizzera, all who know me are aware of my views on overmedication and especially statins. Unfortunately, they smile benignly, eyes glaze over, just indulge me and say ‘ but the doctor has said’. An interest in health matters and doing their homework is not on the agenda, because the doctor knows best. Frustrating, difficult. Doctor bashing is not on my agenda, they are mostly fantastic, but, but, but.
Hi Sylvia, a cardiologist once told me “my job is to fix symptoms” and it is the “patient’s job to weigh the pros and cons” if he/she decides not to take the medicines. Unfortunately the patient has to search for the pros and cons on his own. Statins are very good at curing “high cholesterol”, effect on health is not too good. Then there will be other medical specialists and their medications to look after the adverse side effects.
Bit of a cheek his thinking he’s a cardiologist. More a snake oil peddeler.
It would appear that your friend falls into two groups particularly badly served
by statins, older people and women. It may be productive to concentrate on the evidence in these areas.
Hi David…when I’ve taken that approach with friends and family they still defer to the “experts”. I keep plugging away though
Malcolm
very interesting.
question 1: Why was the emphasis on diastolic BP, rather than systolic? I would have imagined that the pressure for forcing blood through the system was more indicative of artery health?
the figures and conclusions of the same study seem to take no account of All cause mortality. In your logic part, Factor A etc, if medicine that lowers LDL also lowers stroke risk, but that LDL is not a risk factor, then something about statins is positive, but nobody knows (or cares?) what or how it is.
I first read about the pleiotropic effects of statins here:
https://spacedoc.com/articles/benefits-of-statins-1 (part 1 of two part article)
Now if you Google pleiotropic effects of statins you get quite a few articles.
Dr. K has talked about Dr. Graveline before (Space.doc.com).
Phil
Renfrew, PA USA
I must have more vitamin C for blood vessel integrity. I would also like a lot more hours in the day just to keep up with these blogs. Has anyone got some hours they could send me?
AH – I might be able to muster one or two hours to pass on but they are not brand new – well used but in reasonable condition.
Rats, forgot to tick the boxes again
Me too !
It is 10 years since I first read ‘the Great Cholesterol Con’, and thus convinced, I wanted off the toxic statins….but my GP persuaded me to continue taking them. 5 years later, I disobeyed, and stopped them.
Today, my neighbour, in her mid 40s, newly diagnosed with type II, has been told by a Nurse Practitioner,(NOT her GP, whom she has not seen since diagnosis) that she MUST take statins, and giving her a prescription for same. So, for my own peace of mind, I am having another read of the book. My mind has not been changed in the least…..unlike the NHS practitioners, who are still dishing out scare tactics with the ‘scripts.
Where do we go from here?
“Where do we go from here?” The second edition of ‘The Great Cholesterol Con’ I imagine; out in July, Dr K said in a recent comments thread. All I can recommend is persistence. The GP who tried to put me on statins has given up – he’s not raised the matter for three or four years now.
Dearieme. I think it is good that you have managed to avoid the coercion. Having just read the insert to my neighbour’s box of statins, it has as ‘being over the age of 70 years’ , as a ‘warning’,…so that’s a quick response for me, if the subject ever raises its head.
Unfortunately, a mid-forties female who hangs on every word from NHS Choices, and feels unable to question things, is at a severe disadvantage. Any words from me will certainly fall on deaf ears, so I will not discuss the topic. I dread to think how her general health may deteriorate….lets hope she falls into a cohort which can tolerate statins. ( is there one?)
My husband has lone AF ((not cured by catheter ablation) and eventually experienced a slight stroke. The GP referred him back to his cardiologist to try and persuade him to take a statin, as he had declined the GP’s pressure to do so. I prepared a dossier of studies and citations for the Cardiologist which made the case that statins were irrelevant to stroke risk for lone AF, and that in fact, even if the slight anti inflammatory effect of statins decreased the risk of ischemic stroke, it probably increased the risk of haemorrhagic stroke. I can’t presently find the citations I had for this, just this general article about it, linked below. The cardiologist said that although this was not his area of expertise (!) he was convinced by the dossier and said he was content with H not taking statins.
GP then referred him back to neurologist at the stroke clinic for whom I prepared the same dossier. That neurologist pushed the dossier back at me, saying he declined to read it. I asked him why H should be taking statins, seeing lowering cholesterol has no effect on stroke risk in AF: was it the anti inflammatory effect? He snapped that there was no such thing as the anti inflammatory effect, and the reason for him to take statins was purely “to lower his cholesterol’ to below 4 as the goal for someone who had had a stroke. We ignored this and went away.
Eventually, H was assigned a new GP who started insisting on statins all over again. Back to another neurologist at stroke clinic.
The neurologist glared at H and asked: Why are you here? Because GP sent me in the hope you would endorse statins for me. Neurologist: There is no reason whatsoever for you to be on statins. He remains just on warfarin.
http://www.drbriffa.com/2013/10/25/higher-cholesterol-levels-associated-with-improved-outcomes-in-stroke/
Fabulous.
AnnaM might say, “Fabulous”, (and I get it, I really do), but I think this is quite a sad tale. You have two practitioners in the same specialty taking very strong yet opposite positions on commonly used medication. And unlike amie, who actually thinks, there will be some number of patients visiting either GP and / or neurologist and getting completely different advice, which the patients will most likely follow, for better or for worse. And who knows if anyone is tracking the associated outcomes.
Doctors, both GP’s and specialists are human; ie fallible. And also being human they have biases and vested interests. So don’t expect anything better from humans with some years of medicine training.
Sooooo..,Let’s count our blessings when we either meet or come to know a doctor with relatively few of them..
When I was a lowly intern as a child psychologist, I took on an adult client or two (for licensing purposes). A woman had had a car roll over her and onto her chest, pushing enough blood up into her head that her eyes bugged out and went completely bloodshot. Months later, the overt physical symptoms had disappeared but she had complained of odd psychological symptoms (such as intense discomfort in social settings, such as parties). The neurologist had performed an MRI and found nothing wrong. He had told her there was no real reason why there would be damage. So here I was, an intern with no experience interpreting imaging results, just eyeballing it and thinking that there were in fact marks that looked like lesions on her right hemisphere. When coupled with her complaints about social anxiety due to perceptual differences (which would make sense specific to right hemispheric damage), I thought there was likely damage. So I sent her to a new neurologist who confirmed the lesions and likely brain damage. Be careful whom you trust. I think specialists are most prone to it because they are not overseen and therefore critiqued.
Very good
Even if statins are beneficial, please may we be given medications that do not cause collateral damage? Also, it would beneficial if researchers could actually ascertain the actual physiological effects of these drugs.
Thanks again, Dr. Kendrick. Dead and buried it is, the cholesterol hypothesis, except to the medical industry. I’ve just finished reading the Subclinical magnesium deficiency paper for the third time, and it strikes me that this is profoundly important information. Magnesium is critical for endothelial health, among its many other roles, yet agriculture has made it difficult for anyone to get enough from even a high quality diet. What alarmist headlines do we see about mineral status, except, in the case of sodium, to reduce it? And magnesium, at least in the U.S., is not routinely assessed in the metabolic panel.
If cholesterol is not causal in ischemic stroke, how could it be causal in ischemic MI, since they have the same proximal cause?
Gary here in Oz, the need for Magnesium has been a key message within the Organic community for decades. I remember when I first heard about the importance of Magnesium in 1990 at an organics conference from an elderly organic farmer ( UK born ) named Pat Coleby. I bought 4-5 of her books & Pat became a friend and valued colleague
Many parts of older but ‘wetter’ Australia are magnesium deficient and this leads to huge range of farm animal diseases and crop deficiencies…( ‘Wetter’ because rainwater leaches Magnesium out of the top soil. In dry areas with low rainfall this does not happen; but then not much farming happens in very dry areas.
Pat’s answer was the application of dolomite to the soil which has magnesium carbonate in it.. And that has been basic to my farming and gardening ever since.
Bill in Oz: Thanks. I may pick some up as an amendment, just to be on the safe side.
Bill, with magnesium being an integral part of chlorophyl, wouldn’t one expect to get plenty of magnesium just by eating enough leafy greens (not iceberg, but e.g. rocket, lamb’s lettuce, broccoli, kale)?
Also, the wet regions of Ireland, England and northern Germany are a lush green almost year round and widely used for pastures. How could they sustain the amount of grass if they were magnesium depleted? Norther Germany is mostly sandy sediment, whereas much of England is limestone.
Eric: I think part of the explanation is in the difference between how pasture land and crop land are managed. Modern conventional agriculture is essentially a mining operation, gradually removing micro-nutrient minerals, and adding mainly NPK to achieve yields. Varieties have been selected to prosper under this regimen. Pasture land, on the other hand, properly managed, more or less mimics nature, with inputs which roughly equal outputs.
Eric I will not even pretend to be an expert on the availability of Magnesium in soils of the UK or Germany for that matter..My farming experience & knowledge is of Australia. However I do know this : where Magnesium is low in the soil, many plants do not thrive and the plants which do well are ones adapted to low levels of Magnesium in the soil.
Also plants are very good at optimising how available Magnesium is used.It’s absolutely essential for photosynthesis, so that’s where it’s mostly used.
But whether these levels are sufficient for us humans is another question.
Another point to note : Pat Colby who I mentioned above was English and migrated here to Victoria in Oz in the 1940’s. She still had a ‘plummy’ voice in her 80’s when I last saw her. So probably southern England ?
But her basis of comparison for how livestock did for her in Victoria, was the farms she worked on in England. For her the question was if they did well in England why did they do poorly in Victoria for her. From memory she was running milking goats on very sandy soil at the time. She had soil samples tested and found Magnesium was very low. She started adding dolomite to the feed when they were milked. And hey presto, problems disappeared. Later it made more sense simply spread dolomite which Calcium carbonate with about 18-30% Magnesium carbonate..
I am battling to get my head around the logic, which I interpret as:
A does not cause B
C affects A and B
Therefore, A does not cause B
Therefore, A does not cause D
I think I’m missing something.
Martin I am still having trouble getting my brain around this even after Dr K’s reply above…
1 We do know from the research cited that increasing LDL-C does not lead to an increasing stroke risk.. That at least is clear…Thank goodness..
2 When LDL-C drops ( for whatever reason ) the risk of stroke also falls. But it is not at all clear why this happens…
3: The question remains whether the lower risk of stroke is a good enough reason for attempting to lower LDL-C.. I have been reading some very well argued articles just in the last week that total mortality is higher among those with low LDL-C levels.
See PD Mangan’s Rogue Health recent articles on this. They seem very persuasive to me.
Here is Mangan’s conclusion about LDL-C is an article from yesterday :
“…Given what we know about how the brain uses cholesterol, there are good reasons to think that high cholesterol is good for brain health, and that low cholesterol, whether “natural” or achieved through diet or statins may harm the brain, and increase dementia risk, as well as risk of depression, violence, and suicide.”
So,,”the widespread practice of prescribing statins to all and sundry could increase the incidence of cognitive decline and dementia.”
http://roguehealthandfitness.com/cholesterol-for-brain-health/#comment-176618
No, as the LDL level drops, the risk of stroke does not go down. It only goes down in you take statins.
Bill in Oz, maybe the missing link is assuming that there is only one kind of LDL-C. Glycated, oxidized, small dense lipoproteins might make a difference.
Thanks for that clarification Dr K….Ummmmmm. I see !
So there is a side effect of statins which lowers stroke risk….But total mortality and other deleterious side effects are mucher higher in people with a ‘lowered’ LDL-C, ( see Mangan’s recent article ) this lowered stroke risk is outweighed by other factors and so NOT a substantial reason for taking statins either…..
Oh so interesting….all of these responses are examples of wonderful research for the good of mankind, and our animal kingdom.
Pity we might be getting blown to Kingdom Come shortly!
Excuse my cynicism.
Let me quote myself from another blog.
Aha! A bloody ha! So lowering ‘LDL cholesterol’ and raising ‘HDL cholesterol’ will save us all from heart attacks and strokes, will it? Oh no it bloody won’t. Scam indeed!
http://www.nejm.org/doi/full/10.1056/NEJMoa1609581
RESULTS
At 3 months, a 31.1% decrease in the mean LDL cholesterol level was observed with evacetrapib versus a 6.0% increase with placebo, and a 133.2% increase in the mean HDL cholesterol level was seen with evacetrapib versus a 1.6% increase with placebo. … the data and safety monitoring board recommended that the trial be terminated early because of a lack of efficacy. After a median of 26 months of evacetrapib or placebo, a primary end-point event occurred in 12.9% of the patients in the evacetrapib group and in 12.8% of those in the placebo group …
CONCLUSIONS
Although … evacetrapib had favorable effects on established lipid biomarkers, treatment with evacetrapib did not result in a lower rate of cardiovascular events than placebo among patients with high-risk vascular disease.
Indeed.
Dr Kendrick, I would be really interested in your comments to my above post about the apparent contradiction regarding increased risk of haemorrhagic stroke for AF patients who are put on statins.
There is no contradiction because statins have moderate anti-coagulant actions. So, they should, and do, increase the risk of hemorrhagic stroke. As noted in the SPARCL trial.
dearieme: 0.1% worse than worthless! The smell of money is too enticing to stop these clowns from attempting to invent new magic pills.
They still died. But they died with lower cholesterol. Which Is Good.
My sister-in-law aged 50 has had a heart attack -she is not overweight(follows a low fat diet!) exercises regularly doesn’t smoke and drinks in moderation. The cardiologist says it was due to her genetic make up -has prescribed statins blood thinner and aspirin. Is there any way she can get a second opinion as this treatment is surely a one size fits all?
Did I interpret that correctly Paul? Did you mean ….blood thinner i.e….. aspirin (OK) or,….
blood thinner AND aspirin? If that is the case, then lets hope there is good access to a phlebotomist ….(what’s the bleeding time?, as they say in the East End.)
Not 100% sure but forgot to mention the beta blockers. The cardiologist called her his ‘mysterious girl’ due to lack of risk factors including cholesterol levels lower than his own -but still prescribed statins. She is now on a number of drugs for life despite them admitting they don’t have a clue why it happened.
Exactly my current situation.
Oh yes! I was discharged after my MI with a bag of meds: aspirin, Ticagrelor, Bisoprolol, Atorvastatin,Ranitidine and GTN spray. I have refused the statins and Ranitidine and am fighting a battle over side effects with the rest!
“The cardiologist called her his ‘mysterious girl’ due to lack of risk factors …”
The great thing is to remember that ‘risk factor’ does not mean cause. All it means is that there is a correlation between ‘risk factor’ x and outcome y. Since a thousand variables could confound the relationship, it is, of itself, no good reason to identify x as a cause of y.
And, as Dr K has explained many a time, the correlation between heart attacks and cholesterol breaks down when you compare different countries – hence all the lame allusions to the “French Paradox” and so on.
Opinions may legitimately differ about whether the heart attack/cholesterol theory is conscious fraud or accidental utter balls. It does seem to me, however, that it falls into at least one of those categories.
Paul: Magnesium. Have her Mg status checked. Read Dr. DiNicolantonio’s paper (Subclinical Magnesium Deficiency) to understand why this is important, and how to properly test for it:
http://openheart.bmj.com/content/5/1/e000668
All to best to you and your sister-in-law.
Appreciated Gary -the problem is it is difficult to question the ‘experts’ providing her with advice -I know if it was my wife or myself I would be searching for the cause and would not accept the standard procedure.
Cardiometabolic complications of psychotropic drugs—
Most Frequently Prescribed Psychotropic Drugs
Xanax (alprazolam), 48.5 million.
Zoloft (sertraline), 41.4 million.
Celexa (citalopram), 39.4 million.
Prozac (fluoxetine), 28.3 million.
Ativan (lorazepam), 27.9 million.
Desyrel (trazodone HCL), 26.2 million.
Lexapro (escitalopram), 24.9 million.
————————————————————————————————————————-
Horm Mol Biol Clin Investig. 2018 Jan 10. pii: /j/hmbci.ahead-of-print/hmbci-2017-0065/hmbci-2017-0065.xml. doi: 10.1515/hmbci-2017-0065. [Epub ahead of print]
Cardiometabolic effects of psychotropic medications.
Abosi O1, Lopes S1, Schmitz S1, Fiedorowicz JG2.
Author information
Abstract
Background Many psychiatric disorders including schizophrenia, bipolar disorder and major depression convey an excess burden of cardiovascular morbidity and mortality. The medications used to treat these conditions may further adversely affect cardiovascular risk and exacerbate health disparities for vulnerable populations. There is a clinical need to appreciate the cardiometabolic adverse effects of psychotropic medications. Methods This paper reviews the most relevant cardiometabolic effects of psychotropic medications, organized around the components of metabolic syndrome. When known, the molecular and physiological mechanisms underlying any adverse cardiometabolic effects are detailed.
Results:
Many commonly used psychotropic medications, particularly antipsychotics, mood stabilizers and some antidepressants, have been independently associated with cardiometabolic risk factors such as insulin resistance, obesity and dyslipidemia. Stimulants, antidepressants that inhibit reuptake of norepinephrine, some antipsychotics and valproic acid derivatives may also increase blood pressure.
Conclusion:
Understanding, assessing and subsequently managing cardiometabolic complications of psychotropic medications are important to mitigate the excess cardiovascular morbidity and mortality in the clinical populations prescribed psychotropic medications. There is considerable variability in risk between medications and individuals. Timely management of iatrogenic cardiometabolic effects is critical.
KEYWORDS:
adverse effects; anticonvulsants; antidepressive agents; antipsychotics; diabetes mellitus; dyslipidemias; lithium; metabolic syndrome; psychotropic drugs; weight gain
PMID: 29320364 DOI: 10.1515/hmbci-2017-0065
New estimates suggest that 256,000 premature deaths from cardiovascular disease — including 185,000 deaths from ischemic heart disease — in the USA may be linked to historical lead exposure in middle-aged and older adults (people currently aged 44 years or over), according to an observational study following 14,300 people for almost 20 years, published in The Lancet Public Health journal.
Previous estimates, which assumed that low-level lead exposure did not increase the risk of premature death, produced substantially fewer deaths. However, this new study finds that low-level lead exposure (between 1-5 micrograms of lead per decilitre of blood) increases the risk of premature death, especially from cardiovascular disease. Lead exposure is linked to high blood pressure, hardening of the arteries and ischemic (coronary) heart disease.
Exposure occurs from lead that remains in the environment from historic use in fuel, paint and plumbing, as well as ongoing exposures from foods, emissions from industrial sources, and contamination from lead smelting sites and lead batteries.
This study is the first to estimate the number of deaths in the United States from low-level lead exposure using a nationally-representative sample.
“Our study estimates the impact of historical lead exposure on adults currently aged 44 years old or over in the USA, whose exposure to lead occurred in the years before the study began,” says lead author Professor Bruce Lanphear, Simon Fraser University, Canada. “Today, lead exposure is much lower because of regulations banning the use of lead in petrol, paints and other consumer products, so the number of deaths from lead exposure will be lower in younger generations. Still, lead represents a leading cause of disease and death, and it is important to continue our efforts to reduce environmental lead exposure.”
The study used data from the Third National Health and Nutrition Examination Survey (NHANES-III) for 14289 people in the USA aged 20 years or older between 1988 and 1994, and the end of 2011. All participants had a medical examination, including a blood test for lead — a measure of past and ongoing exposures to lead — and a urine test for cadmium at the start of the study.
After an average of 19.3 years, 4422 people died including 1801 from cardiovascular disease and 988 from heart disease.
At the outset, the average level of lead found in the participants’ blood was 2.7 µg/dL, but ranged from less than 1 to 56 µg/dL. One in five participants (3632 people) had levels of 5 µg/dL or more, and those with the highest levels of lead in their blood were older, less educated, more likely to be male, smoke, consume larger amounts of alcohol, have less healthy diets, have higher cholesterol, and more likely to have hypertension or diabetes.
Almost one in 10 participants had lead levels that were undetectable to the blood test, so were given a reference level of 0.7 µg/dL (8%, 1150/14289 participants).
Overall, people who had high lead levels (6.7 µg/dL) were at 37% greater risk of premature death from any cause, 70% times greater risk of cardiovascular death, and double the risk of death from ischemic heart disease, compared with people with lower levels (1 µg/dL).
Using these risk levels, the authors also estimated the current proportion of deaths in adults aged 44 years or older in the USA that could have been prevented if historical exposure to lead had not occurred.
Overall, they found that up to 18% of all deaths every year in the USA (412000/2.3 million) would be among people who had levels of lead above 1 µg/dL. They estimated that 28.7% of premature cardiovascular disease deaths (256000/ 892000) could be attributable to lead exposure, including a high proportion of ischemic heart disease deaths (lead was linked to 37.4% of all IHD deaths [185000/495000]).
These results were adjusted for age, sex, household income, ethnic origin, diabetes, BMI, smoking status, alcohol consumption, diet, physical activity, and amount of cadmium in urine.
“Our study calls into question the assumption that specific toxicants, like lead, have ‘safe levels’, and suggests that low-level environmental lead exposure is a leading risk factor for premature death in the USA, particularly from cardiovascular disease,” says Professor Lanphear. “Estimating the contribution of low-level lead exposure is essential to understanding trends in cardiovascular disease mortality and developing comprehensive strategies to prevent cardiovascular disease. Currently, low levels of lead exposure are an important, but largely ignored risk factor for deaths from cardiovascular disease. Public health measures, such as abating older housing, phasing out lead-containing jet fuels, replacing lead-plumbing lines, and reducing emissions from smelters and lead battery facilities, will be vital to prevent lead exposure.”
The authors note some limitations, including that their results rely on one blood lead test taken at the start of the study and therefore cannot determine any effect of further lead exposure after the study outset. The authors were also unable to control for all potential confounding factors, such as exposure to arsenic or air pollution, which are also risk factors for cardiovascular disease.
Writing in a linked Comment, Professor Philip Landrigan, Icahn School of Medicine at Mount Sinai, USA, says: “A recurrent theme in lead poisoning research has been the realization that lead has toxic effects on multiple organ systems at relatively low levels of exposure previously thought to be safe… A key conclusion to be drawn from this analysis is that lead has a much greater impact on cardiovascular mortality than previously recognized… [The authors] suggest that the time has come to end neglect of pollution’s contribution to non-communicable diseases’ mortality and to thoroughly re-examine lead’s role in changing global patterns of cardiovascular disease.”
Note: The authors note that these estimates are comparable to the annual number of deaths in the US in people who currently smoke (483000 deaths a year). This is because the risk of death from lead exposure is lower (HR = 1.37, 95%CI = but more prevalent across the population (in the study, 90% of participants were exposed to lead). Comparatively, 20% of the US population smoke, but the risk of premature death is higher (HR=1.75 95%CI = 1.50-2.05) than for low-level lead exposure.
Story Source:
Materials provided by The Lancet. Note: Content may be edited for style and length.
Journal Reference:
Bruce Lanphear , Stephen Rauch, Peggy Auinger, Ryan W Allen , Richard W Hornung. Low-level lead exposure and mortality in US adults: a population-based cohort study. The Lancet Public Health, 2018 DOI: 10.1016/S2468-2667(18)30025-2
Hoorah. I get to say. I told you.
Indeed, you did tell us so, in XXV. A very interesting re-read.
With regards to lead and CVD, is there a link?
A researcher called Weisskopf looked at the amount of lead in bones, and the rate of CVD. He found that those with the most lead in their bones were 837% more likely to die from CVD (relative risk) [1] than those with the least lead in their bones. Now, whilst that is a relative risk, it is of the magnitude where we can safely say we are looking straight at a direct cause of CVD.
How does lead cause CVD. Most likely through the following mechanisms
Yes, we are straight back to my old friends, endothelial dysfunction and decreased nitric oxide (NO) production. In the world of cardiovascular disease, if you know where to look, all roads lead to NO.
This research on the increased risk of even low lead levels on CVD is reported in Medscpe here
https://www.medscape.com/viewarticle/894017
Slightly easier to understand.
Interesting research paper ! In which event, what treatment is available for those of us who are in the age cohort when leaded petrol was common ? Leaded petrol was withdrawn in 1986 ( I think ) here in Oz when I was almost 40. So there was exposure to lead for all the years prior to that.
I have just been reading about lead. When used in leaded petrol it was baked into tiny bricks in the engine and thus fell out of the sir very rapidly on exiting the exhaust..Within 3 meters… So lead tened to accumulate on the road surfaces and on the ground immediately close to roads. And of course heavily trafficed roads had more lead spewed out on them. Conclusion : soils of gardens close to major roads may be heavily contaminated. ( As a big gardener I’m glad never to have lived close to a major road !!)
Lead was also used on roofs here in Australia to seal joints etc…And thus the drip line on the ground where water runs off roofs can be heavily contaminated with lead..Not clever to garden such areas without knowing if there is lead present.
“people who had high lead levels (6.7 µg/dL) were at … 70% times greater risk of cardiovascular death”: did they say whether these people were at greater risk from, say, bowel, lung, or brain cancer?
Paul – second opinions
I saw all sorts of NHS experts (I’m in England) after my incident. It was futile and rage inducing – whatever their area of speciality/expertise they all sang from the same hymn sheet…talk about hitting your head against a brick wall. It always kept coming back to medication and statins. Even the NHS endocrinologist I paid the see privately.
In the end I paid to see an independent cardiologist (i.e. I was familiar with him and knew he was one of the good guys.)
That was money well spent and a very productive consultation.
Thanks Charles -I am based in North West England -know any good guys here?
Who would want to be a doctor?
How do you give advice and sleep soundly at night?
There is so much conflicting information, I don’t think it’s just my head that is spinning.
Tell the patient the facts and let him make his own mind seems to the best way forward for both patient and doctor.
But can you disentangle the facts?
From this blog I take there is no point in taking statins as a preventative strategy, the risks of side effects seem to outweigh a marginal benefit. So that just leaves those with heart disease. Do you take statins which may keep you alive for on average an extra few days?
I think I know the way most patients would go.
And the only thing stopping them is the medical profession.
Not all of them of course.
Thanks Doc, I wished I lived in your practice area.
When you take the trouble of looking into how “modern evidens based” medicin came into “being” you are up for a scary endeavor where the PR genius Albert Lasker and his “charming” wife Mary appear on top.
Paul
Sorry – I’m in Hampshire and the cardiologist I paid to see was in London, and with a high profile so was easy for find and trust.
But it is hard to find the mavericks, the sceptics and so on.
I’ve read a few more of the comments arising from your initial comment about your sister in law. It’s a familiar story for many here.
I, too, was prescribed something to lower blood pressure, which I don’t have and it certainly wasn’t the reason for ending up in intensive care.
And, strangely, several blood thinners. Nothing wrong with my blood viscosity and it certainly wasn’t the reason for ending up in intensive care.
All prescribed for life with plenty of scare mongering of what would happen if I didn’t comply.
So, non compliance has been phased in by me over time. Rightly or wrongly. Maybe stupidly, maybe not.
And none of the 5 medications I was prescribed will have any impact on my high arterial calcium score (either stopping further development or reversal of plaque – you never know!), which is the crux of the matter.
For me, that’s enough to consider total non compliance with the meds.
Also, there are quite a few here who didn’t have the conventional risk factors for their CVD incident, me included.
I haven’t changed my view that chronic stress was my downfall. One of the reasons I follow Dr Kendrick
I guess you also follow Dr Kendrick – have you gone down that route (i.e. the mind) with your sister in law?
Charles,
Yes I follow Dr Kendrick and have read both his books-not good for my health as big pharma makes my blood boil-and I do think stress has played a part with her mother recently diagnosed with Alzheimers,
I will be keeping a close eye re side effects but I’m afraid she will be compliant as she is not sceptical of the medical profession.
Thanks for your interest.
Best wishes.
Muscle mass is responsible for the majority of total body glucose utilization—- which when impaired leads to insulin resistance.
Format: AbstractSend to
Front Physiol. 2018 Feb 23;9:112. doi: 10.3389/fphys.2018.00112. eCollection 2018.
Obesity, Metabolic Syndrome, and Musculoskeletal Disease: Common Inflammatory Pathways Suggest a Central Role for Loss of Muscle Integrity.
Collins KH1,2, Herzog W1,2, MacDonald GZ1, Reimer RA1,3, Rios JL1,2,4, Smith IC1, Zernicke RF1,5,6, Hart DA1,2,7,8.
Author information
Abstract
Inflammation can arise in response to a variety of stimuli, including infectious agents, tissue injury, autoimmune diseases, and obesity. Some of these responses are acute and resolve, while others become chronic and exert a sustained impact on the host, systemically, or locally. Obesity is now recognized as a chronic low-grade, systemic inflammatory state that predisposes to other chronic conditions including metabolic syndrome (MetS).
Although obesity has received considerable attention regarding its pathophysiological link to chronic cardiovascular conditions and type 2 diabetes, the musculoskeletal (MSK) complications (i.e., muscle, bone, tendon, and joints) that result from obesity-associated metabolic disturbances are less frequently interrogated. As musculoskeletal diseases can lead to the worsening of MetS, this underscores the imminent need to understand the cause and effect relations between the two, and the convergence between inflammatory pathways that contribute to MSK damage.
Muscle mass is a key predictor of longevity in older adults, and obesity-induced sarcopenia is a significant risk factor for adverse health outcomes. Muscle is highly plastic, undergoes regular remodeling, and is responsible for the majority of total body glucose utilization, which when impaired leads to insulin resistance. Furthermore, impaired muscle integrity, defined as persistent muscle loss, intramuscular lipid accumulation, or connective tissue deposition, is a hallmark of metabolic dysfunction. In fact, many common inflammatory pathways have been implicated in the pathogenesis of the interrelated tissues of the musculoskeletal system (e.g., tendinopathy, osteoporosis, and osteoarthritis). Despite these similarities, these diseases are rarely evaluated in a comprehensive manner.
The aim of this review is to summarize the common pathways that lead to musculoskeletal damage and disease that result from and contribute to MetS.
We propose the overarching hypothesis that there is a central role for muscle damage with chronic exposure to an obesity-inducing diet. The inflammatory consequence of diet and muscle dysregulation can result in dysregulated tissue repair and an imbalance toward negative adaptation, resulting in regulatory failure and other musculoskeletal tissue damage. The commonalities support the conclusion that musculoskeletal pathology with MetS should be evaluated in a comprehensive and integrated manner to understand risk for other MSK-related conditions. Implications for conservative management strategies to regulate MetS are discussed, as are future research opportunities.
KEYWORDS:
MAPK; NFkB; bone; joint diseases; muscle; tendon
PMID: 29527173 PMCID: PMC5829464 DOI: 10.3389/fphys.2018.00112
Free PMC Article
AnnieLaurie,
I actually do know about all those rackets you mentioned above and of course it really does come down to monetary incentives one way and another. But I was referring to direct and open payments for prescribing drugs. If a doc prescribes a blood pressure pill, an antibiotic, a sleeping pill, a statin, and so forth, he does not take a cut or do markup of the price and sell it direct to the patient. But with chemo drugs, they do.
Well, let’s not give docs a pass because some mafioso doesn’t hand them actual cash. The “payments” docs get for prescribing opioids are especially disturbing in view of the fatalities associated with our opioid crisis in the US: https://www.cnn.com/2018/03/11/health/prescription-opioid-payments-eprise/index.html
And you better believe the silly hoopla over “capital punishment for drug dealers” is pure political theater and does not apply to doctors in any way.
Some of the individual payments to docs are valued in the thousands, and some docs, as noted in the article, get the equivalent of more than $25K every year. If you are a public servant, an employee of any company that might contract for services, etc., you are generally required to report any “gift” from a potential contractor that’s valued at over $25. But, if you are a doc, you can get a “consulting fee” for putting your name on a paper someone else ghost-wrote, have all your expenses paid to an “educational conference” in St. Croix, etc. It’s payola whether a doc gets a markup on a drug, or gets $25K worth of fake fees, vacations at a resort, and other gifts. And those may amount to a greater value than a markup on some specific chemo drug, because a doc can get payments for multiple drug prescriptions from multiple companies – opioids, antidepressants, statins, etc.
Thanks.
Good news!
We live at latitude 51 degrees N
Our weather forecast is already displaying UV index today:
7-10am. Index 1
10-12 noon Index 2
Noon Index 3
1-3pm Index 2
3-6 pm Index 1
Then no “risk”!
An off topic comment : I still try to keep up with what Norman Swan is doing in his Health Report program on the ABC. I think is an arrogant bugger and frequently wrong. But he still occasionally has something interesting.
And so it was this week when he interviewed a male nurse based a small remote country town in Western Australia ( no doctor in the town ) who suffered a heart attack & had to treat himself in his own clinic…
There is a transcript here:
http://www.abc.net.au/radionational/programs/healthreport/the-remote-nurse-who-treated-his-own-heart-attack/9538610#transcript
The nurse survived ! So I think it may be of interest to folks here interested in CVD…And no I am not at all recommending that this be attempted by anyone.
Very interesting interview posted today on highintensityhealth.com. Mike Mutzel interviews Jong Rho, M.D. concerning the health-promoting effects of ketogenic diets. Well worth a watch.
I had hoped that you would find some time to talk about thyroid treatment (or lack of it) in the UK. Since you last wrote about it the situation has got a whole lot worse, with more and more people having their T3 prescriptions taken away from them, and the elderly having levothyroxine prescriptions removed or dramatically reduced because they are told they don’t need them any more now they are old or in some cases the necessary treatment is never started.
Diabetes gets lots of attention from all sorts of doctors and researchers, but the thyroid is mostly ignored. People with thyroid problems need lots of help. We would be ever so grateful!
Dr Kendrick, In reponse to your reply that there is no contradiction, as there is a slightly increased risk of haemorrhagic stroke on statins, can I qualify my query: When you write: “Yet, and yet, statins reduce the risk of stroke. and cite the AHA statement that “drugs help reduce heart attacks and strokes in people at moderate risk”: Neither of these statements make the distinction between the risks for ischemic and haemorrhagic stroke and do not assess the comparative risk for these respective types of stroke for someone on statins. To further complicate matters, as I understand it, someone with AF, albeit lone AF, would not fall into the category of people at moderate risk, but of someone at higher risk of stroke.
So my question is: What are the comparative risk factors for someone with lone AF (with a history of one mild stroke) for being on statins, given that, as I understand it, even if the risk of haemorrhagic stroke were to be less than of ischemic, it is the more catastrophic type of stroke?
80% of strokes are ischaemic. Haemorrhagic strokes tend to be more catastrophic
The studies show that statins are beneficial, the question is why. Here are two reasons, nothing to do with cholesterol or logic:
A- statins affect immune system by reducing macrophage numbers, less inflammation response
B- statins exhibit antibiotic properties thereby reducing infections
The result is short term gain but long term pain. The adverse effects will eventually outweigh the benefits. Statins poison the mitochondria and the gut microbiome, two essential components.
The problem with theory A, is that Malcolm has repeatedly pointed out that lowering inflammation is often a bad thing as far as CVD is concerned. Drugs like NSAID’s and steroids decrease inflammation and increase the risk of CVD!
I haven’t heard of B before, but assuming it is true, I can’t help wondering if statins achieve that effect by making people on average less active, and so less likely to pick up infections!
I think a useful general principle would be to establish a minimum level of effectiveness, below which a drug would not be offered. When I was offered statins, it never occurred to me to ask about the exact size of the gain, or whether that was a relative or absolute risk!
Hi David Bailey, statins have anti-inflammatory and anti-bacterial properties, I did not make this up. This might account for the pleiotropic properties of the drug. If doctor told you that one person per 100 would benefit from treatment would this affect your decision to take the drug?
“in the JUPITER trial, for composite cardiovascular events the ARD for statins vs placebo was −0.0106 (number needed to treat [NNT], 94) in people younger than 70 years and −0.0162 (NNT, 62) in those 70 years and older,29 and in the HOPE-3 trial the ARD was −0.0088 (NNT, 114) in people 65 years and younger and −0.0183 (NNT, 55) in those older than 65 years.”
FAT–it’s all about where it’s at—-location, location, location
Horm Mol Biol Clin Investig. 2018 Mar 16. pii: /j/hmbci.ahead-of-print/hmbci-2018-0012/hmbci-2018-0012.xml. doi: 10.1515/hmbci-2018-0012. [Epub ahead of print]
Obesity associated disease risk: the role of inherent differences and location of adipose depots.
Hill JH1, Solt C1, Foster MT2.
Author information
Abstract
Obesity and associated metabolic co-morbidities are a worldwide public health problem. Negative health outcomes associated with obesity, however, do not arise from excessive adiposity alone. Rather, deleterious outcomes of adipose tissue accumulation are a result of how adipocytes are distributed to individual regions in the body. Due to our increased understanding of the dynamic relationship that exists between specific adipose depots and disease risk, an accurate characterization of total body adiposity as well as location is required to properly evaluate a population’s disease risk.
Specifically, distinctive tissue depots within the body include the lower body, upper body and abdominal (deep and superficial) subcutaneous regions, as well as visceral (mesenteric and omental) regions. Upper body and visceral adipose tissues are highly associated with metabolic dysfunction and chronic disease development, whereas lower body gluteofemoral subcutaneous adipose tissue imparts protection against diet-induced metabolic derangement.
Each adipose depot functions distinctly as an endocrine organ hence it has a different level of impact on health outcomes.
Effluent from adipose tissue can modulate the functions of other tissues, whilst receiving differential communication from the rest of the body via central nervous system innervation, metabolites and other signaling molecules. More so, adipose depots contain a diverse reservoir of tissue-resident immune cells that play an integral part in both maintaining tissue homeostasis, as well as propagating metabolically-induced inflammation.
Overall, the conceptualization of obesity and associated risks needs updating to reflect the complexities of obesity. We review adipose tissue characteristics that are linked to deleterious or beneficial adipose tissue distributions.
KEYWORDS:
adipokines; adiposity; cardiovascular disease; cytokines; diabetes; immune cells; subcutaneous; visceral
PMID: 29547393 DOI: 10.1515/hmbci-2018-0012
My seventy-year-old mother-in-law has just been put on statins by her doctor. Her cholesterol is 6.0. The madness goes on.
I’m hoping to persuade her to throw them in the bin whilst she still remembers who I am.
Apologies if in wrong place, but it also mentions arethrosclerosis in the article, but not directly in relation to methylglyoxal itself.
http://theconversation.com/have-we-got-the-causes-of-type-2-diabetes-wrong-93326
John Collis, it is a relevant article because it illustrates another type of logic.
Introduction to medical logic.
A (an extracellular stimulus) affects B (an intracellular pathway) , B increases level of C ( benign under normal levels of A), C causes symptom D, develop drug E to reduce C, problem solved since C is root cause of D.
Example for a novel cure for type 2 diabetes:
A is bood glucose
B is methylglyoxal pathway
C is methylglyoxal
D is increased glucose levels, cellular damage, insulin resistance, tissue injury
E: carnosine found in red meat is effective, but saturated fat and red meat are considered to be bad. Develop a novel drug that mimics carnosine effect. There will be side effects but other drugs will take care of that problem. Diet is not important but need a doctor to monitor methylglyoxal levels.
Please,
Let me remind you that a crucial time in the “freedom of speech” regarding medical matters is now approaching with prof. Tim Noakes at stake
http://foodmed.net/2018/03/noakes-will-academic-mobsters-silence-him/
A linked article on academic mobbing was instructive. Prof Noakes is in for a long, hard struggle.
“Harper suggested that mobbing is a primal behavior that humans engage in whenever they have been encouraged by someone in a position of influence or power to view another member of a community as a threat to that community. Once that happens, patterned and predictable stages of abuse will follow, and these will not let up until the target has been eliminated from the group or so disempowered that their continued presence in the group has no significance.” — http://quillette.com/2018/03/02/academic-mob-fatal-toll/
I was wondering why today’s dieticians are so anti-LCHF. Their patients must be asking them, “So, what’s all this low-carb stuff I keep hearing about?” They will have been trained on the ‘healthy complex carbs’ theory, and will need to go back to school or do a lot of private reading to get up to speed on LCHF theory. I think they’re just too reluctant to do it.
Maybe in years to come a new generation of dieticians will be promoting LCHF, by which time the general population will have moved on to some other dietary fad ;o)
Martin, in Tim Noakes latest book he says that dietitians aren’t allowed to recommend a low carbohydrate diet and receive no training. I find it difficult to be fair to most dietitans, but low carb must sound like heresy to them. Add in a refusal to acknowledge such a serious error and vested interests and we have the unwholly mess we have today. A situation where diabetics are told to eat at least 50% of their calories from carbohydrates (glucose). Mind bogglingly damaging. How many lives has this harmed or ruined?
I believe the ultimate problem is that if one goes to school on a certain subject, one is taught what is considered to be the most modern and agreed upon as expert view on the subject matter. One then leaves with shiny new qualification, safe in the knowledge that they are now an expert. Of course anyone who challenges this person, especially if they are just a member of the public who happened to read something off the internet is just not going to be taken seriously.
After all, who are we to question the experts view. The only time this will change is when enough of the “Experts” have changed their mind and the last few will quietly shuffle their feet into the other camp – after all they wouldn’t want to find themselves contradicting the majority expert view would they.
I was just thinking about how the experts approach to a heart attack used to be 6 weeks absolute bed rest and how eventually the experts changed their minds when eventually enough people died of blood clots and strokes.
Sheep, also behave in this manner
Besides, big Pharma has already paved the way – once the nasty statins go, the very expensive Peskie 9’s are waiting in the wings – all of the benefits and none of the established side effects.
I’m sorry — maybe I never lost my 60s rebelliousness — question authority — but why would we not question the so-called “experts”, whether in medicine, religion, art or whatever? Many of us have science backgrounds, and credentials as impressive as the “experts” (many of whose “credentials” are accolades paid for by their sponsors). In this day and age especially, when so many excellent sources of technical information are available, anyone with scientific training and a willingness to spend the time can do a fair job separating the gold from the BS in information relating to diet and lifestyle. If you take the advice of some of the former editors of JAMA and Lancet on the dross that gets published, are willing to spend the time on analysis, and look at what has worked over the eons of human evolution, it is really not such a monumental task. I learned very early in my life not to buy into the “god complex” that many docs have. I daresay many of the members on this list spend more time than the average doc in keeping abreast of the latest developments in the health field. You can find this info from the original reports through your own research, and don’t have to wait for your friendly, profit-motivated pharma rep to digest and regurgitate it to you, as my of the “pros” do.
Malcolm
How did you do it, 119 comments and nothing really about diet?
Well done!
Skill
It is possible that lowering LDL via statins in all stroke patients is not beneficial, but in many circumstances it is. For example, lowering LDL is unlikely to reduce the risk of stroke in a patient who has had an ICH or a stroke related to a non-atherosclerotic cause (i.e. AFIB, vasculitis, dissection, CVST, etc). For those patient’s who infarct as a direct result of atherosclerotic disease (extracranial or intracranial stenosis), LDL lowering via statins and non-statin medications is critical to their secondary stroke reduction medication regimen. Unfortunately studies took all-comers so the magnitude of the benefit in this subgroup of stroke patients is masked.
Would you argue that a patient with diffuse atherosclerosis (extracranial, intracranial or both) and no other identified cause of stroke (i.e. Afib, dissection, etc) should not under go intense LDL lowering therapy?
What are your thoughts on the PCSK9 inhibitors? Your post failed to mention the FOURIER trial that showed lowering LDL directly results in decreased risk of MI, ischemic stroke, and requirement for coronoary revascularization. This study also showed that evolocumab has an excellent safety profile. These results were also seen with another PCSK9 inhibitor, alirocumab, in ODYSSEY-OUTCOMES (results released, paper publication pending).
I have written about the FOURIER trial a few times. Increased overall and CV mortality (NS). Reduction in non-fatal outcomes, primarily revascularisation (not a clinical end-point, but a clinical decision). At a meeting on this study, one of the investigators admitted that participants knew if they were on, or not on, evolucamab – due to effect on LDL. So the study was unblinded, and thus subject to observer bias.
There is no such thing as intracranial stenosis. All cerebral arteries are completely plaque free (even in homozygous FH).
By the way, the entire point of my blog was that use of statins is beneficial in stroke patients. I think you should probably read it again.
It seemed the entire point of your blog was to argue that LDL reduction has no clinical benefit in the prevention of stroke, when exactly this has been shown through PCSK9 inhibition.
Intracranial stenosis does not exist? How come intracranial stenosis can be seen on CTA/MRA/conventional angiogram? Why are there guidelines on the treatment of atherosclerotic intracranial atherosclerosis? Why are there studies testing different treatment modalities for intracranial stenosis?
As for your dismissal of FOURIER due to it being ‘unblinded, and thus subject to observer bias’ – I would argue that stroke/MI/cardiac revascularization are quite objective endpoints. Observer bias would be much more important to consider if we were asking patients to rate a response on a subjective scale (ie pain, anxiety, etc), but if a person has had an MI, the troponin/EKG/angiogram aren’t going to be biased….
You say that cardiac revascularistaion is quite an objective end-point. It is not an end point. It is a clinical decision made by a cardiologist on whether or not revascularisation would be of benefit. Based on an assessment of risk factors, or which the LDL level would be important. [The increase in revascularisations cannot have been ‘acute’ in this case, as participants were ‘censored’ after the first event].
As for stroke – you are not a clinician? I have seen many people where the diagnosis of stroke is entirely subjective. Clearly not in severe stroke, but when we are talking TIA, I spend many night on call discussing with, and seeing patients with ?weakness ?difficulty communication. A decision on whether or not this is a stroke is often a completely subjective decision. I have often written down ?stroke, without any confirmatory tests. Sometimes I have decided it is not a stroke, without any further confirmation. It depends on many different factors. Do they need investigation, have they had one before, would they benefit from anticoagulation, and suchlike? So, please do not tell me that stroke is a quite an objective endpoint. Sometimes yes, sometimes no. Medicine is not black and white, which is why double blinding is so important to remove bias.
An MI is more likely to be objective, based on troponin, but the test are far from perfect and, again, subject to bias. As all diagnoses are. Many tests are borderline. EKG misses 50% of MIs. An angiogram cannot diagnose an MI. It can just tell you there is a blockage.
Two things that are very hard end-points are death, and CV death. They went up on FOURIER – something you just choose to ignore? If so, why do you choose to ignore the fact that the two hardest end points went in the ‘wrong’ direction, whilst softer, more objective end-points went in the desired direction. Does this not give pause for thought?
By the way, there clearly is stenonsis in the brain – that is what a stroke is. However, there is no atherosclerosis in the brain. Two completely different things, two completely different discussions.
The entire point of my blog was that increased LDL is not a risk factor for stroke, yet statins reduce the risk of stroke. Ergo, they cannot have been achieving this benefit through LDL lowering, but due to other ‘pleiotropic’ effects. What is your explanation? Equally, if LDL is not a risk factor for stoke, how can PKSK9 inhibition reduce the risk of stroke?
just for a laugh about diagnostic tests.
Years ago an impatient in-patient was disgusted that he would have to have his cardiac enzymes repeated over 3 days in the NHS, causing him to be hospitalised over a few days. He wanted to go private, so that they could all be assessed in one day, and get himself home.
That happened 25 years ago…maybe the NHS has got up to speed now…..I wouldn’t know, as I swapped Nursing for politics. ouch.
Pertaining to stroke I was focusing far too much on cases where we have clear imaging in support and not on those which are much more difficult to confirm (TIA, MR negative, etc). I completely concede the point and I apologize for saying it was an objective endpoint as in many cases it is unclear.
The reason I was not bringing up death and CV death (and the reason I am wondering why you are using these to support your argument) is that the increases seen in CV death 251 evolocumab vs 240 placebo and death from any cause 442 evolocumab vs 426 were not statistically significant. I would be much more concerned (of course we all would be) if these numbers were greatly disparate and statistically significant.
Autopsies on stroke patients can demonstrate atherosclerosis of intracranial vessels. Radiologists report intracranial atherosclerosis on CTA/MRA and we treat with medical management in order to tackle the risk factors for atherosclerosis (statins, antihypertensives, antihyperglycemics, smoking cessation, antiplatelets) as per the guideline recommendations regarding intracranial atherosclerosis.
I agree that statins indeed have pleiotropic effects and maybe those are the reasons they reduce the risk of stroke. I don’t have an explanation for the exact mechanism of the pleiotropic effects of statins as they have not yet been fully elucidated.
:
“Equally, if LDL is not a risk factor for stroke, how can PKSK9 inhibition reduce the risk of stroke?”
Since PCSK9 inhibitors are monoclonal antibodies they are very specific for PCSK9 so it is unlikely they are exhibiting any pleiotropic effects seen by statins. As a result, their sole mechanism of action is to reduce LDL. Since these studies show reduced risk of stroke, they offer convincing support that reducing LDL does have benefit in stroke prevention in patients with established CAD.
Thanks for the discussion – I wish it were a neurologist speaking with you instead of me (I would much prefer to be a fly-on-the-wall)!
That’s really weird, I had written out a reply yesterday but it isn’t showing up. It was long so I will just write a short version again.
1 – I apologize for saying that stroke is clearly an objective endpoint – you are right that most of the time we have clear imaging showing a stroke but there are definitely many cases where a diagnosis could go either way (i.e. TIA vs migraine/etc) or the MR is negative but a diagnosis is made on clinical exam.
2 – I chose not to talk about total death and CV death in FOURIER (and I was surprised that you are using it as support) because the differences were very small and most importantly, not statistically significant. If there was a true difference and it was caused by the drug, you would expect it to be much more pronounced (and statistically significant) in a trial of N ~27000…
3 – Yes, intracranial vessels can have stenosis. Autopsies of deceased stroke patients can demonstrate atherosclerotic disease in these vessels. Radiologists also report, verbatim ‘intracranial atherosclerosis’ on CTA and MRA and we treat these patients according to the guidelines for treating…intracranial atherosclerosis.
4 – Aren’t FOURIER and ODYSSEY-OUTCOMES actually providing evidence against your statement that LDL has no effect on stroke risk? If that were true, then in these very large studies, we would not have seen any effect on stroke. However, since PCSK9 inhibitors are monoclonoal antibodies and therefore, are very specific for their target, they are unlikely to exhibit any pleiotropic effects such as seen with statins. As a result, their mechanism of action is solely to reduce LDL. In these studies that results in decreased stroke risk. Would we start these in every patient who has has an MI/CVA? Absolutely not – the cost and NNT are too high to make that feasible. Would we start them in select patients whose mechanism of stroke is likely artery to artery as a result of atherosclerosis? Yes, definitely.
5 – The review you are using to support your argument that LDL does not impact stroke risk (i.e. the review of 45 prospective cohorts of 450k patients) did not separate ischemic and hemorrhagic stroke, and the authors even note that if there is a relation between LDL and ischemic stroke, it is likely masked by the lack of an association between LDL and hemorrhagic stroke “However, because the types of the strokes were not centrally available, the lack of any overall relation might conceal a positive association with ischaemic stroke together with a negative association with haemorrhagic stroke.” We would not expect LDL to have any impact on hemorrhagic stroke (because they are usually a result of hypertension/AVM/aneurysm/amyloid angiopathy/etc). If you search for relation between LDL and ischemic stroke (i.e. your normal process of google –> pubmed), you will find more recent studies supporting this association. In your initial post you fail to distinguish between ischemic and hemorrhagic stroke. Do you believe that LDL flat out has no impact on either, or do you think that it has no impact on hemorrhagic stroke but it might have an impact on ischemic stroke?
6 – Thanks for the discussion. I wish it were a neurologist talking to you instead of me. I’d much rather be a fly on the wall for that conversation than to continue this one.
It is not weird. I am on holiday, without internet until now. Whilst others may have a staff of thousands, I have only me
And your efforts are appreciated. Thank you for being so dedicated.
Pharmacist, being a fly on the wall has its downside. For conversations like yours (and many others here) I am a fly on the wall, with the attendant brain power. It’s interesting, but I can’t keep up 🤔