But because of a personal journey, he has now gone down this whole path of cholesterol and statins and low-carb lifestyle, and really trying to say, what does the science say, what does the science support in this realm. Now, this is a polarizing topic, especially with mainstream medicine, mainstream cardiology being very much in the camp of LDL is causative of heart disease.
And Dr. Diamond is on the other side of that, saying wait a second, I don't think the evidence supports that statement. Now, I've got to be honest, this is a very important topic for me, a personal topic for me. I had a huge list of notes and I kind of went a little bit all over the place because I was just so interested in talking to him and talking about the different topics and getting his thoughts on different things. So, I apologize if this interview doesn't flow as seamlessly as I would have liked.
But I think we cover a lot of different topics. Now, quick disclaimer; if you have high cholesterol, if you are on a statin, please do not make any medical decisions or changes based on this discussion. This is merely to explore some evidence, to explore one side of this equation, hopefully in a balanced way. But if you are going to make any changes or any decisions about your medications or your health, please talk to your doctor first. Do not make any decisions based on this discussion alone.
Now, with that disclaimer, we talk a lot about the science, we talk a lot about the practicality of how this implies to individuals and a low-carb lifestyle, and we explore a number of different topics about cholesterol, LDL, statins, and their benefit. So, a couple of quick definitions, which I think we go over, but relative risk reduction versus absolute risk reduction.
So, if you have a one percent risk of something and you can reduce it down to a half of a percent, the difference, the absolute difference, is a half percent, that's the absolute risk reduction. Relative risk reduction however, I would say that's 50 percent reduction because half percent is half of one percent. So, we talk a lot about that, Dr. Diamond has been very vocal about sort of truth in advertising between those two things.
We talk about Mendelian studies and basically that's just a natural history experiment of genetic mutation and following what happens to people over time with that genetic mutation, that's called a Mendelian randomization trial, I think I use that term a little bit in here. I think hopefully that's all the definitions you need, and I hope you enjoy this discussion with professor David Diamond. You can see the full transcripts on dietdoctor.com.
Again, please realize this is not medical advice, this is just simply exploring a fascinating topic with a fascinating human being. So, enjoy this discussion with Dr. David Diamond.
Dr. David Diamond, thanks so much for joining me on the Diet Doctor Podcast.
And I just figured, well, you know, I've got a background in biology. I know a lot about the brain but not much about heart disease. Least I could do is read a few papers before I go on the medication. I read a few papers and by this time, I've now read a few thousand papers. And that has helped to guide me and my decision not to use medication. Instead, I learned about the value of low-carb diet. I was able to cut my triglycerides by 75%, raise my HDL 25%, lose a good bit of weight, feel much healthier now than I did 20 years ago.
So, I'm a strong advocate for a low-carb diet but also realizing that medication wasn't appropriate. And in the process, I've been in a sense indignant about the statin research. I actually express this when I give my talks about how I realized that the cholesterol theory, which is cholesterol causes heart disease through LDL, it's really not well-supported and frankly, what I express is the obscene profits that have been made through the food and drug industry that have maintained a hypothesis that has failed.
And I think that's so valuable because, you know, in the medical world, if you're in your own echo chamber, only hearing the same people, the same experts, the same drug companies. Although, we fall into that same risk I guess, in a low carb world, right. We can be our own echo chamber too, so we have to reach out into other areas and keep our ears open for other opinions.
Now, one of the things that you're very critical of is evidence and how we portray evidence. And we talk about evidence-based medicine all the time and we talk about what is the evidence for keto, against keto. What is your perspective as you've looked into things about the state of evidence in the medical world?
And I have to tell you that I was astounded, I was offended when I saw how the data were manipulated to greatly overstate the benefit of cholesterol lowering drugs, which actually goes back decades, originally talking about cholestyramine in a 1984 paper in which you had, starting off with about half a million men, they got that work down to about 600 people at the highest levels of cholesterol, and using an older drug cholestyramine, which lowered cholesterol.
The amazing thing was after seven and a half years, there was virtually no effect and there was no real statistically significant effect. It was a 0.4% difference between treated and untreated men. And I look at that, and what they should have said, you know something, we were wrong... lowering cholesterol didn't have any benefit whatsoever.
But they turned that 0.4% into a 24% improvement in outcome. And so, this manipulation of the data and that's using relative risk rather than the actual outcomes. So, to me, this is just not right in how you report the data to the public and to the medical field.
Until I started, you know, digging a little bit deeper and realizing it's a completely different conversation if you have the absolute risk reduction. But the fallback is there is a change, there is a difference. So, even in the statins, and I guess maybe we're jumping a little ahead here, but even in the statin trials, if there is a 1% difference, it can be a statistically significant 1% difference, which then they publicize as a 36% difference.
But it's hard to argue if there is a difference, so the question becomes when is it a big enough difference to make a clinically useful intervention, and that's a hard question to answer, isn't it?
What is actually the difference in the rate of events in people of placebo versus the treated people? You shouldn't only be told the relative risk because that's deceptive, and we know it's both in doctors and the public. When you hear about a 50% reduction in risk and that's all you hear, you think that half of all people are now not going to have a heart attack. And that's exactly what doctors interpret that.
So, again, first... I'm not against reporting a 50% risk reduced with statins, but that's got to come along with the absolute risk as well. People need to have both data forms. And the second thing is, you are right. There are numerous studies showing benefit with statins, and that benefit typically is on the order of single digits. There's never been a statin study I know of in which you actually have a double-digit improvement.
And I have to just briefly tell you, in my field of neuroscience where we actually study depression, is such a great controversy because people with mild to moderate depression, given a placebo, have actually a rather dramatic effect as a benefit. And the controversy actually is that the antidepressants only improve outcome by 10% compared to placebo.
Well, there's never been a real 10% improvement outcome of any kind with statins. So, I agree with you completely, there are studies that have shown the benefit of statins when you're looking at coronary events, as well as coronary mortality and all-cause mortality and those numbers are relatively small, but they are real.
A half of a percent difference, is that a blockbuster? But then people say, cardiovascular disease is the number one killer in the world. Millions of people are going to suffer from cardiovascular disease, so if we can make 1% difference and that's a lot of people. And in a way, that's a valid argument when you're talking about a population basis.
They've been greatly minimized by the key opinion leaders. And I've also talked about this. Now, we actually were invited to write a commentary recently by Plus One. And in that commentary, which just came out a few months ago, we reviewed the literature on adverse statin effects. And it's not small, it's extensive.
We reviewed about 60 papers published in peer-reviewed medical journals of about 20 different categories of adverse effects. The most obvious is development of type 2 diabetes. And this has really been minimized by the key opinion leaders. But when you actually look carefully, and you have an RCT and an actual trial in which you get blood samples and you look at the A1c levels and you look at fasting glucose and other insulin measures, you actually find that over the course of six years - this is in men - that there's a 5% increase in new onset type 2 diabetes.
So, this particular one was done in Finland funded by the government in which you have a spontaneous increase in type 2 diabetes with placebo as 5%. But in those that were on statins, it was actually 11%. So it's doubling in the rate of type 2 diabetes, which is a relative risk measure. But we're not talking about 1%, we're talking about a 6% increase over the course of about six years, and so, that's just one adverse effect. There are really well described cognitive effects.
We've published a paper on cognitive effects in statins, and there's actually a beautiful paper that has shown that people diagnosed with dementia, older people diagnosed with dementia, which, when they were taken off the statin, their dementia disappeared. Put them back on the statin, the dementia returned. This is not something that doctors are aware of, the extent of the adverse effects of the statins.
But even with the muscle aches, there's significant controversy. I mean, you look at the trials and they report one in 20 000, you know, risk of significant muscle aches, and of course, these are designed by the pharmaceutical companies so there's a run in period which weeds out a lot of the other people who would be intolerant, so, they're not included in the trial.
But then, my favorite is how you called out Roy Collins and, you know, how he would state there's one in 10 000 risk of statins but yet his commercially available product to test for statin myopathy risk, quotes a 29% risk. So, where do you see in trying to evaluate the evidence? Where do you see the muscle aches really lie? Where do you think that is? What is the real number?
What I am presenting today is actually Steve Nissen and Christie Ballantyne and Steve Nichols strong statin advocates, talking about muscle pain caused by statins, they're not calling it a nocebo effect. And their estimate is 40% of the people taking statins stop taking it in part because of muscle pain. So, I caught them on a video in which they're being candid about what actually happens in the clinic, why people stop taking statins.
People have less energy when they've taken statins, and we do have muscles breaking down, which contributes then to kidney disease, kidney injury. There's well-established actually public papers. So, I think we are looking at very real physiological effects that have adverse effects globally on the body.
On the one hand, people say, well, if the cardiovascular benefit is one year or five years, it's going to be 2 years or 10 years and 4% at 20 years. Okay, maybe we can make that reach, but how is the diabetes going to impact that? And we don't know the answer to that question, do we?
And what's happened with the statin advocates is they consistently take that number needed to treat- which may be small after one year- and they simply change it... one out of 100 people will actually have a benefit from statins. And then they'll say, well after 20 years, you only have to treat five or 10 people. Because that benefit will accrue over 20 years. And they refuse to say the adverse effects can also accrue.
So, if you're looking at 6% additional people who develop diabetes after about five or six years, what's going to happen after 20 years? And what's going to happen if there's actually an exponential increase in adverse effects? But once tissue starts breaking down, then you've got to be even more concerned with that happening at an even more rapid pace, especially with elderly people.
And by the way, also, the way I also present this is if the tobacco companies had the control that the drug companies have now, overlooking only with the onset of starting to take the statin after only about four years, you look at the development of cancer, it's only four years that you've started smoking, we never would have known about the link of lung cancer to smoking. So, understand, these trials were stopped really before most cancers can develop.
But when you look long-term and there's actually a nice epidemiological study looking over 10 years, you see twice the rate of breast cancer in women who are on statins chronically compared to equivalent groups of women either with high cholesterol, low cholesterol. And so, there's also evidence of cancer in men as well, but you've got to look at older population more vulnerable over a longer period of time.
Taking the evidence as a whole shows that statins reduce cardiovascular events. That's also difficult because where does the preponderates of evidence come from? It's mostly the Pharma sponsored trials. So how do we interpret Pharma sponsored trials, I mean the data is still the data, we can't- it's not like they're falsifying the data, but what is the impact the pharmaceutical companies have on the data we're seeing?
That clearly to me doesn't appear to give me any reason to accuse them of fraud because they're showing so little benefit. And again, I don't think we want to automatically demonize studies that are funded by Pharma. These are very expensive studies and it's very difficult to get government funding for long-term studies on cardiovascular disease. The other challenge is it's a very low rate at which people develop heart attacks.
About the only time you see a high rate of death is with heart failure, of which statins are actually no benefit at all, people with high cholesterol live much longer than people with low cholesterol following heart failure. But when you're looking at heart attacks, you're actually seeing in the general population such a low rate that frankly, to give the Pharma credit, it's difficult to much of a reduction in heart attacks.
You even take people with high risk of heart attacks and you'll only get about typically 3, 4, 5%. who will have heart attacks and you'll have a low rate of mortality. So, this is part of a methodological challenge for this area of research. So, now like in a cancer study you may have 50% of the people die in a short period of time. But in these heart disease studies I don't think people appreciate that there really is relatively a low rate in placebo treated people. And this is why I tell people...
I show them studies such as the Lipitor study, which was famous in the Lancet early... around 2000. Or the British Heart protection study, you're only looking at about 3% or 4% of the people who died. They're terribly uncooperative as a way to put it. And about 97% of the people don't have heart disease, and the way I also present this to people, I say, listen, you can go to your doctor and say, if I don't take the statin, if you give me a placebo... what's the likelihood in the next five years that I'll have a heart attack? And the answer is 97% likely that you will not have a heart attack. And so, to me, that's the reality of it as well.
You know, another big study, Walter Reed, that showed absolutely no statin benefit if your calcium score was zero. It showed a very small benefit if your calcium score was between one and 100. I think it was... the number needed to treat was about 100 over 10 years. But then, as that scores go over 100, all of the a sudden the number needed to treat to save one cardiovascular event- not death but cardiovascular event- goes down to 12. So, how do you think about that more laser focused approach than trying to better identify who might benefit from a statin as one part of their overall treatment program?
And I think it's actually important to go back this relates- Well, first of all, when we're talking about calcium score, I want to point out, everyone agrees high calcium score is unhealthy. I mean, it is a fact. The interesting thing is numerous studies have now come out showing that people on statins have increased their calcium score. This is also- there's no difference of opinion on this- the remarkable thing to me is now that we say, well, that must be a good thing because increasing calcium stabilizes the plaque.
This, to me, came out of nowhere. It's like increased calcium score is bad unless it's induced by the statin. Then it becomes a good thing. So, that's remarkable to me. So, what I will yield here is that there is evidence of benefit of statins given to people with high risk. And the important thing actually is there's an analysis of people in the 4S study that was done 25 years ago using someone on statin and actually, that was one of the biggest effects ever in which actually had a 4% reduction in mortality. And for secondary prevention, people already had a heart attack.
Now, when you look in the 4S study, which is so important, the people that had the same high LDL but high HDL and low triglycerides, secondary prevention, no benefit whatsoever. And this is so important, getting back to low-carb, because that's exactly what happens when people go low-carb. Their HDL rises, their triglycerides drop just like it did for me. So, what this is saying is you have a choice, okay. You can take a statin and basically have a crappy metabolic syndrome, or you can go low-carb, make all those improvements and the statin won't have any benefit over that.
So, that was good. Right, now getting back to the LDL and the environment it's in, and that's something I think we really lose perspective of because even going back to the Framingham data, same thing. There was an association, all- a complete, total association between rising LDL and rising cholesterol and risk of cardiovascular disease.
But when you see the Framingham offspring data and they break it down according to HDL levels, all of a sudden, that association is lost at higher HDL. So, it shows there's something to this more than just LDL, and it probably has to do with metabolic health like you said, a revaluation of the 4S trial, says that. Now, that being said though, you know, LDL is causative of cardiovascular disease. We heard it in 1980s with Brown and Goldstein, we heard it again last year with the European society of cardiology.
The definition of cardiovascular disease as an APO-B containing lipoprotein in a macrophage in arterial wall, therefore, it is causative. Now, with so many people certain in the medical community that it is causative, what are they missing?
So, the great thing about this drug is a completely different mechanism from statins, and initially killed people, and so those trials were stopped. So, people are dying with lower LDL and higher HDL, but after that they were able to clean up the drug, so it has almost no side effects. The CETP inhibitors, drug company has invested over a billion dollars. This was to be a blockbuster, because not only did it lower LDL, it raised HDL.
This is one of the biggest failures ever in Pharma history. So, these are the people who primary, secondary treatment with the drug, dramatically lower LDL, and absolutely no difference to coronary events or mortality, so no benefit, no harm. This, to me, is sort of the death note for the LDL hypothesis.
This is saying, no, you're lowering LDL and you're making no difference in coronary events. So, that's the first thing. The second is we have to realize there's... there's a lot of money involved in blaming LDL for heart disease. What we got is a new generation of drugs. Well, let me back off, a lot of people say it doesn't matter whether statins lower LDL or not, as long as statins provide a benefit, we don't care about the mechanism.
And that's one side of the argument which actually we can talk about. If statins have a benefit and they don't have any adverse effects, fine, who cares how they work. But what has happened is we have this new generation of drugs, that's the PCSK9 inhibitors. This drug specifically targets LDL.
So, if we actually look objectively at the research and we drop LDL and we simply accept that LDL doesn't really cause heart disease and statins work and we stop right there, that would be fine. But because the drug companies have invested over a billion dollars in the PCSK9 inhibitors, we've got to continue to target LDL. Now, part of this is I just want to talk about familial hypercholesterolemia.
These are people with extremely high LDL levels, two, three times normal. And in my papers that I've written which I'm covering in my talk today, I'm covering how people with FH, people with LDL, 200 to 300 or more, live a healthy normal life... that they have a normal lifespan. These are people who live into their 70s and 80s with total cholesterol of 400 and their LDL 300. Well, that's clearly counter to the idea that LDL is killing people. It doesn't make sense.
It is remarkable; there is a greater increase, there are greater incidents of coronary events, but the actual death rate, this goes back whether you're looking at the 1960s, to Harland's work... though the decades there have been a dozen of papers published. And Mundal et al, this is beautiful work out of Norway in which you're looking at about 5000 people documented FH in which you have no increased rate of death all-cause mortality at any age.
And in fact - this is untreated, so this is not looking at statins having an effect for people 70 years of age with FH, they have a significantly lower rate of death for the next decade compared to the general population.
And their platelets are much more reactive to epinephrine. So, you put some epinephrine in a dish with platelets, platelets coagulate, okay, they aggregate. Someone with FH, put their platelets in a dish, put in some epinephrine, they're 100 times more sensitive to epinephrine than a controlled population. Now, you don't hear much about that because no one's excited about reducing platelet aggregation, I mean who wants to give aspirin to someone who's got FH, right? There's no money in platelet aggregation, far more money in targeting LDL.
And so only a subset of people with FH now have this reactive, and those are the ones. The other thing to keep in mind, people with FH are just like everybody else. They are susceptible to the same risk factors. So, people with FH that smoke have a dramatically higher rate of heart disease, much more than the general population. And if you talk about stress reducing heart disease, well, the FH person is going to be more sensitive to stress.
And diabetes, so higher blood sugar is going to trigger platelet aggregation, so that FH person will be more sensitive. But to the individuals that don't have these risk factors and yet have sky high LDL, no heart disease.
And the way to look at it is there's no evidence that statins have any benefits or any other benefit as a treatment in FH because it's never been compared to placebo.
And the statin research has shown a very low effect on overall mortality. So, there's no reason to believe that the statins have any effect on population mortality from cardiovascular disease. So, clearly, and there are papers to read in the 1970s questioning why is it so much fewer people are dying from heart disease now than they did 20 years ago. That may very well be that it is better care and it's actually post-coronary care that may be reducing- it's death from heart disease that has declined over the last 40 years or so.
But probably the incidents of heart disease may be increasing with obesity and diabetes. But actually, what it should be potentially the use of antibiotics. It's actually very important because you do see a linkage of infectious disease with heart disease.
But I think there's so much controversy about being involved and being causative and we blur the lines far too often. So, I mean, would you agree that APO-B containing lipoproteins like LDL lipoprotein are involved in the atherogenic process and involved in developing cardiovascular disease?
What you've got is a harmful metabolic environment and you've got people who have high blood sugar and high blood pressure, which is causing damage to the endothelial, it's causing damage to the vasa vasorum, and potentially one could say is then you've got infection, that the LDL is found at the scene of the crime.
And again it gets to the association versus causation. I mean, the police are always found at the scene of the crime, and so one can make an argument that police have caused the crime. It's the same kind of argument. There's good evidence that LDL works with white blood cells, with macrophages to target pathogens... to target and be able to kill bad viruses and bacteria and that is why, in fact, you find LDL in damaged artery. And you also find white blood cells. Wow, this guy is saying that these white blood cells obviously must be atherogenic.
You find calcium in your artery, well, calcium must be causing heart disease and you find lots of bacteria in these arteries, well, bacteria must be causing. LDL is found along with other things inside the arteries and essentially, there's so much work showing that LDL is a part of the immune system. And when you find actually bacterial remnants, this is very common in the plaque, you find bacterial remnants.
Infection is often associated with heart disease. And so, LDL is found where you have infection. And so that helps to understand LDL's role, which is a part of our immune system. So, I would say at this point, there is no evidence of causation. And, in fact, to take it to another level, there are different kinds of LDL. And this is so important to the low-carb community because we have to see that is so obvious is that the LDL changes depending on the environment. And so, what you find is- and there's so much work by Ron Krauss and others- is that the LDL changes under the condition of low blood sugar.
So, you don't have that abnormal LDL. I mean, natural, native LDL is large- as I say- large and fluffy. And when you surround it by sugar that is glycated and oxidized, well, you end up with what's called small, dense LDL. It has much less cholesterol in it and it's much more reactive. The way to think about this is that is not the way LDL is supposed to be.
That small, dense LDL is associated with an endothelium, with the lining of the artery wall that's damaged. And so, what you got in conjunction with too much blood sugar, too much blood pressure, and then you've got damage to the wall, the LDL itself is damaged. So, I would actually say at this point, I think small, dense LDL is potentially... think of it as atherogenic. But that's because it's contributing to the noise, it's contributing to the damage. But the native LDL in a healthy person is not contributing to the damage.
The same way with LDL, there's been sufficient work looking at LDL in people who are ketogenic. There's no work I know of looking at statin effects in people that go low-carb, and my guess is who wants to fund that study, because the low-carb will blow away statins and the benefits. So, the person who's going low-carb in a sense - and I say this - and you don't know what the outcome will be because there's never been a study on low-carb and ketogenic diet and coronary outcome.
And sometimes people... really atrocious work saying that low-carb actually increase mortality, people die from low-carb... Truly awful epidemiological work. But the answer is we don't know that ketogenic diet will reduce coronary events because no one's ever shown that. It's reasonable to assume that because the biomarkers all move in the right direction, it should all be protected from coronary events. And the LDL will turn out to be completely irrelevant.
The other is we don't know, so we really shouldn't treat this as a special circumstance until we do know, and we should lump it all together. And then when you... if you go that route and that's sort of the mainstream medical community would go that route, they really point to three versions of evidence to support that any elevated LDL is going to increase your risk.
There's the Mendelian randomization, the genetic trials which we sort of talked about with FH, but there's also the PCSK9 gain-of-function, which... so, PCSK9 basically is involved in the degradation of the LDL receptors. So, if you have a higher functioning PCSK9, you're going to actually have more LDL receptors, you're going to clear the LDL faster.
So, there's a population that had a lower risk of cardiovascular disease with that gain-of-function, and thus, the development of the PCSK9 inhibitor drugs. So, just a study like that showing benefit from lower LDL with higher receptor action, I mean is that enough to say, okay, there is more evidence there to say that a lower LDL is beneficial for some people, so therefore, we should air on that side.
The recent work has targeted the PCSK9 inhibiting drugs. The thing that's so important to realize is when someone takes this drug, what they're doing is increasing their LDL receptor density, okay, which is abnormal. There are beautiful negative feedback systems to maintain LDL receptor just to the right level. This drug blocks the neative feedback so you're increasing LDL receptors, meaning where is that LDL going to go? It's going to buy into these receptors and go into the cell.
So, the cell will become chock full of LDL that shouldn't be there. The cardiologists love this because now the LDL is taken out of the blood, so you drop LDL levels by 70%. But that LDL doesn't disappear. The LDL is being crammed into liver cells, and ultimately - my prediction, they've only looked like two years now, and there's no real difference in cardiac events when you look at the PCSK9 trials.
My prediction is you're going to see a really screwed up liver. You're going to see liver damage in these cells that have too much cholesterol inside them, and so 5, 10 years down the line, you'll be looking at people that will be harmed by this drug.
One showed a 1.5% reduction with a small mortality benefit at two years. So, the proponents say, well, if we had this effect in two years, think of the effect we're going to have at 10 years. And of course, your response is what are the side effects and the risks will be at 10 years and we don't know the answer to that question.
And this is looking at about 400,000 middle aged men and they've got their cholesterol levels and they had followed them for quite a few years, seven years. The mortality rate from the lowest to the highest man was 1%, the actual mortality rate was 1%. And they have distorted this to turn it into a 400% mortality rate. So, you mentioned Mr Fit. That was an abomination of science. Framingham, I think it's all very clear.
When you look at unhealthy people, you look at LDL in an unhealthy environment. Potentially, it's either trying to save the unhealthy environment or it's a part of it. But again, it means the patient needs to sort of take his life into his own hands or her own hands. They need to take control of their own environment, they're not going to find health in a pill has been my point.
And so, the person who has diabetes and is obese thinks they're going to be protected by taking a statin, well the answer is still they're going to be very unhealthy.
The people have the kind of biomarkers you see with someone on a low carb-diet showed no benefit whatsoever with statin treatment. That tells you a little something about what to predict when we have someone that is low-carb, and therefore, they don't need the statin because there is no benefit.
But it certainly makes empiric sense. So, if I have someone on a statin, I would actually want them on a low-carb diet. One for the metabolic benefit and to help with the LDL beyond what a statin could do but also to reduce potential side effects. Now, you've pointed out to me that there was actually a paper showing some beta cell dysfunction in the pancreas, so maybe low-carb isn't going to be enough to help reduce the risk of diabetes. What do you think?
It interferes with brain cholesterol synthesis, which is essential for making memories. And so, no, I don't think it has anything to do with the person's diet, this is now just simple physiology. You interfere with cholesterol production in the brain, you're going to interfere with brain functioning.
And age is such a fascinating topic when it comes to cholesterol and LDL in general because whether it's Framingham study or whether it's the Honolulu Heart study, there are a number of different stages. Taking it together suggests there is again maybe a bimodal response in the 50s and younger, there's a tighter association between LDL and cardiovascular risk, but in the 70s and over, that association seems to flip. And you've been very big about pointing that out. So, tell us about that difference.
And in fact, what you do find is that people with the highest LDL- and there's more than 50 years of studies- people with the highest LDL actually live longer than those with low LDL. So again, it's completely inconsistent with the idea that LDL causes harm on its own. And we published this paper in BMJ Open a few years ago.
We reviewed and looked at every paper that looked at mortality in relation to LDL levels. There wasn't a single paper that showed increase mortality in relation to the general population in older people, that's over 60, with the highest LDL, compared to lower LDL. So, that's completely inconsistent with the hypothesis that LDL itself is causal to heart disease. Because it's not killing older people who are at the highest risk of death from stroke and coronary heart disease.
You got a blood sample from someone in the 50s or 60s, and 20 years later you look at who's died and so, you're looking years beyond and these are people who had good health to begin with and you eliminate any people that had died in the first couple of years. You're still looking 20 years later. Those who had the high LDL in their 50s and 60s are still living in the 80s and 90s.
Well, if the people who demonize LDL and say, well it causes heart disease and people die, well, if people with high LDL would just die, in their 30s or 40s, it would be so simple. But they don't. The people with high LDL are living into their 80s and 90s and even 100; we're going to hear that today that the people who are 100 years old have the highest LDL of those measured. It just simply doesn't make sense to think of this as causing heart disease.
There is an environment, a toxic environment where you will find LDL, especially in the younger people. A toxic environment has to do with smoking and high blood pressure. And so again, if we think of high LDL coming to the rescue, now, the reason why we want to think of LDL being beneficial is that people with FH have a lower rate of death.
Again, got to emphasize, it's not statins. People in their 70s have a 40% reduced rate of death because they have a normal rate of death from coronary heart disease but a lower rate of death from non-coronary heart disease in their 70s. Less death from infectious disease, less death from cancer. This is how you look at it; if you live up to your 70s with high LDL, you've got a more protective immune system, and no difference in cardiovascular death.
My first priority was to improve my own health. I have no reason to be biased to pick the studies that would basically make a point for me. If I want to be showing that LDL is not harmful and I picked those studies, but ultimately I don't care about my own high LDL. I mean, it harms my own health. So, I have no bias. I have no interest in this other than looking at good science. I want to look at all the science and come to valid conclusions as a scientist.
Because I get no money from this, I have no pay, I have no funding for my interest in cardiovascular work. It's purely a personal venture for me. I don't want to be biased, I don't want to cherry-pick the data. I'm looking at the entirety of the literature and then coming to conclusions.
Someone say ignore the LDL completely and you don't have to worry about it and some are trying to really put it into context. But it's because of work like you, because of Zoe Harcombe and Aseem Malhotra and Malcolm Kendrick. People are willing to go against the juggernaut of the medical community and Big Pharma to say wait, we need to look at this differently, that allows clinicians the ability to say, okay this is something different, there is something to this. You've put yourself out there to really help move this forward and you've gotten a lot of attacks for it. I mean, has your skin really thickened from this?
They left me out of this because I'm not a UK person, but that article was truly awful. I mean, attacking them and saying, you know, how wrong they are. But really, I don't even think... we're not coming out against Pharma, speaking for them as well, there is no bias whatsoever. I am not looking to praise LDL and I would grant that the small dense LDL, which is an abnormal LDL, may be contributing to disease along with- it's almost like LDL, small dense LDL may very well be the gas on the fire, but it didn't make the fire.
So, I don't take it personally. And oh, I actually do recall that there was a cardiologist at Duke University, who wrote a note specifically about me saying that I was causing harm to her patients, that people would all die because I was explaining how statins have adverse effects and how overall the adverse effects are greater than the benefits, to which I wrote a rebuttal to that cardiologist to reply.
So yes, there was one example I can think of which I've personally been attacked. But then again to me, it's all just science, it's not something I take personally.
And I thought that was awful, I thought that was clearly overstepping the bounds because you are not falsifying anyt data. You are helping us see data that exists, that other people did, that's either being ignored or been promoted in a different way, you're just helping us re-see that data; there's no falsification there.
From the very beginning, I just wanted to learn how is it I can make myself healthier. And what I realize is that I did ignore the LDL and I did ignore my LDL now, which is quite high and what I really care about and what matters is blood sugar triglycerides, HDL is important but it is the canary in the coal mine. You don't want to take a drug that'll raise your HDL. HDL tells you about your lifestyle, triglycerides tell you about your lifestyle telling you you're consuming too many carbohydrates. LDL doesn't tell you much.
So, I'm really approaching this as a scientist. I don't promote myself as anything, I am not making any money from this, so I welcome the opportunity to talk about it with you, thank you so much for inviting me, but frankly, I don't have anything to share as far as promoting myself.
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