The diverging trends in heart disease and diabetes represent a public health paradox of immense importance.
Obesity and type 2 diabetes are well-known risk factors for coronary heart disease. However, whereas the prevalence of obesity and type 2 diabetes is increasing, the death rate from coronary heart disease is declining.
This interesting paradox was recently addressed in two separate articles written by renowned experts in The Lancet Diabetes & Endocrinology (1,2)
Although the authors share some common ground, their views differ significantly in some important areas. It is of great interest to analyze their opinion on how the current paradox should affect dietary guidelines and our interpretation of the role of calories, cholesterol, saturated fats, and carbohydrates.
The Role of LDL Cholesterol and Total Energy Consumption
The first paper entitled “Diverging global trends in heart disease and diabetes: implications for dietary guidelines” is written by Jim Mann and coworkers from New Zealand.
The paper reflects a somewhat traditional view on the subject;
The decrease in coronary heart disease can be explained by several factors, including reductions in LDL cholesterol concentrations, blood pressure, and tobacco use and more recently, improvements in medical and surgical treatment.
The authors point out that reduced consumption of saturated, and more recently trans unsaturated, fatty acids with variable increases in unsaturated fatty acids have occurred in parallel with reductions in mortality from coronary heart disease.
Although everybody knows that correlation does not prove causation, they claim this dietary change has been a major contributor to the reduction in coronary heart disease, largely because of a reduction in LDL cholesterol.
Mann and colleagues believe there is accumulating epidemiological evidence suggesting that diets high in minimally processed carbohydrate and dietary fiber are associated with reduced risk of type 2 diabetes, coronary heart disease, and some cancers.
They also claim there is data supporting the potential of such dietary advice to improve the control of diabetes and to reduce cardiometabolic risks in general.
They also point out that early recommendations about dietary carbohydrates in the 1970-80s may have been misleading because they encouraged consumption of complex rather than simple carbohydrates.
They believe such distinction is unhelpful because complex carbohydrates may be very different from those associated with reduced risk, such as minimally processed fiber-rich cereals, whole grains, legumes, pulses, vegetables, and fruits.
Nonetheless, they acknowledge that for people who are insulin resistant, intake of total carbohydrate should be at the low end of the recommended range (45-60% total energy).
Although they agree that reduced carbohydrate diets may enable more short-term weight loss than do reduced fat diets, they believe that long-term weight loss relies on compliance with a prescribed diet rather than macronutrient distribution.
They conclude that existing evidence does not support a dietary pattern that involves radical restriction of carbohydrate and unlimited fat consumption, but they don’t cite studies that have compared this approach to their preferred dietary pattern.
However, they still believe that the food industry’s replacement of fat with sugar and rapidly digested starches is likely to have contributed to the increase in energy intake that is driving the epidemic of obesity and type 2 diabetes.
Furthermore, they point out that because increased bodyweight is a much weaker risk factor for coronary heart disease than for diabetes, it is readily counterbalanced by improvements in the major coronary risk factors. This, they believe, could lead to the uncoupling of trends in type 2 diabetes and coronary heart disease.
Although I think their assumption may be correct, I believe we have still not seen the full effect of the epidemic of obesity and diabetes on the prevalence of chronic lifestyle-related disease such as cardiovascular disease, cancer and dementia.
While they suggest that changes in emphasis are needed in nutritional recommendations, they believe that reduction of saturated fats and replacement of refined grains with fiber-rich whole grains should remain central to dietary advice,
Finally, they believe that a reduction in consumption of free sugars is important to reduce total energy consumption, and they emphasize that restricting consumption of manufactured energy-dense food and reducing portion size are important.
Saturated Fatty Acid Enthusiasts and Traditionalists
The other paper, written by Dariush Mozaffarian from Boston MA, USA, is entitled “Diverging global trends in heart disease and type 2 diabetes: the role of carbohydrates and saturated fats”.
Mozaffarian addresses the subject in a different manner by taking into account recent studies on the risk associated with saturated fat intake as well as evidence suggesting that focusing entirely on the role of energy intake could be misleading.
He claims that foods rich in refined starches and sugars are the primary culprits for obesity and type 2 diabetes. He writes:
To blame dietary fat or even all calories, is incorrect. Although any calorie is energetically equivalent for short-term weight loss, a food’s long-term obesogenicity is modified by its complex effects on satiety, glucose-insulin responses, hepatic fat synthesis, adipocyte function, brain craving, the microbiome, and even metabolic expenditure.
Mozaffarian explains two opposing schools of thought when it comes to defining the role of saturated fatty acids (SFAs).
He writes: “SFA enthusiasts deem all previous nutritional evidence to be erroneous, recommending meat-and-butter rich so-called paleo diets as a route to good health.”
On the other hand, SFA traditionalists, Mozaffarian writes, “uphold the conventional paradigm that because SFAs raise LDL cholesterol, a causal risk factor for coronary heart disease, SFAs must be an important cause of coronary heart disease.”
Mozaffarian thinks both schools are wrong. He writes: “Unsurprisingly, each viewpoint is extreme, simplistic and inconsistent with the full body of contemporary evidence”.
He highlights the fact that SFAs are a heterogeneous group. Some, like palmitic acid, may have adverse metabolic effects whereas other may have metabolic benefits (3). Furthermore, SFA’s in blood and tissues are often synthesized from dietary carbohydrates.
He also points out that SFAs are obtained from foods that have ingredients that may modify its health effects. Therefore, “judging the long-term health effects of foods or diet based on macronutrient composition is unsound, often creating paradoxical food choices and product formulations.”
He concludes: “To summarize, these lines of evidence – no influence on apolipoprotein b, reductions in triglyceride-rich lipoproteins and lipoprotein(a), no relation of overall intake with coronary heart disease, and no observed cardiovascular harm for most major food sources – provide powerful and consistent evidence for absence of appreciable harms of SFA’s.
Although Mozaffarian believes a reduction in consumption of starchy and sugary foods is important to reduce obesity and type 2 diabetes, he seems to write off the possibility that a radical restriction in carbohydrate consumption may be helpful.
Declining in Mortality from Coronary Heart Disease – The Role of Saturated Fats?
Although the incidence and mortality from coronary artery disease have declined, it is important to understand that the burden of the disease remains high. This is partly due to the aging of the population and the fact that people with heart disease have a better prognosis than before.
Evidence suggests that the decline in mortality from coronary heart disease seen in most western countries is due to reduction in important risk factors such as smoking, high blood pressure and blood cholesterol as well as improved medical treatments.
SFA traditionalists like Mann and colleagues usually point out that lowering of blood cholesterol has played a major role in reducing the prevalence and mortality from coronary heart disease. Furthermore, they assume that the lowering of blood cholesterol has been achieved by reducing the amount of SFA’s and trans fat in our diet.
However, Dariush Mozaffarian points out that “changes in dietary fats simply cannot explain most of the reductions in blood cholesterol in most western countries.” He cites evidence showing that “whereas blood total cholesterol fell similarly in the USA and France between 1980 and 2000, changes in dietary fats explain only about 20% of the decline in the US and virtually none of that which occurred in France (4).
Furthermore, Mozaffarian points out that ” a common mistake made by SFA traditionalists is to consider only slices of data – for example , effects of SFAs on LDL cholesterol but not their other complex effects on lipids and lipoproteins; selected ecological trend; and expedient nutrient contrasts.”
The Low Carb Denialists
The first thing that comes to mind when reading Mann’s and Mozaffarian’s viewpoints is their striking disagreement on the role of saturated fats and the importance of LDL cholesterol. Their different interpretation of the medical literature in this particular area is bewildering.
Otherwise, they seem to agree on the basic elements of a diet that is likely to positively affect both heart disease and diabetes, favoring fruits, non-starchy vegetables, nuts, yogurt, fish, vegetable oils and whole grains.
Although they believe that free sugars and processed carbohydrates should be minimized they still claim that a diet with a relatively high amount of carbohydrates is the one best suited to address the epidemic of obesity and diabetes.
Unfortunately, their approach to the possible usefulness of carbohydrate restriction is arrogant and condescending.
In a large study published last week on the trends in diabetes among US adults the prevalence of prediabetes was 37% to 38% in the overall population, and consequently 49% to 52% of the population was estimated to have either diabetes or prediabetes (5). Without intervention, prediabetes is likely to become type 2 diabetes in 10 years or less (6).
Most of the increase in diabetes is due to an increase in obesity.
The seriousness of diabetes requires that we evaluate all of the evidence that is available (7). However, both Mann and Mozaffarian completely disregard data supporting the usefulness of intensive carbohydrate restriction in people with established insulin resistance or metabolic syndrome (8, 9, 10, 11). Low-carbohydrate diets tend to lead to more weight loss, less insulin resistance, lower levels of triglyceride-rich lipoproteins, and higher levels of HDL-cholesterol.
During the last few decades, health authorities, together with the food industry have managed to create an obesogenic environment that will have disastrous consequences for public health.
Although the incidence and mortality from coronary heart disease have declined significantly, the burden of disease remains high.
But, while the experts disagree on the culprits, solutions may be hard to find.
Firstly, we must understand the complexity of the situation and abstain from extreme and simplistic viewpoints.
Although we certainly bought the cholesterol hypothesis easily from the beginning, we have to abandon the belief that it can explain everything.
We have to stop putting all the blame on dietary fats, calories and lack of exercise.
The seriousness of the diabetes epidemic does not allow us to refute contradictory evidence for the sake of preconceived notions.
70 thoughts on “Less Heart Disease Despite More Diabetes; The Role of Diet”
Good balanced piece.
I think both low/high carbers and low/high fats crowds would agree that refined carbs and excess added sugars are detrimental.
As for dietary patterns that will minimize chances of disease, I think that everyone has to experiment and see what works best for them. Weight levels are not the only indicator of health, obviously cholesterol, inflammation, and BP levels are important, as is sufficient physical movement.
As an Apoe 4 carrier, I know that SFA ramp up my LDL so I try to limit them but I certainly use flax, avocado, and walnuts sufficiently. I try to stick to good (for me, anyhow) carbs like legumes, quinoa, and sweet potato, and loads of leafy greens. I don’t eat a lot of meat but quite enjoy salmon and some other fish a few times a week.
It’s really easy to become dogmatic one way or the other and let’s face it, a lot of what we see on either side of the fence is by people trying to make it their meal ticket (small pun intended).
I’d rather advocate for people to experiment, along with input from a doctor or someone “sufficiently” informed, and then look at your numbers (BMI, waist to hip, cholesterol and ratios, BP) to see how you react. And I’d advocate doing that over time too because it’always possible that these can change over a long time.
At any rate, just wanted to say I enjoyed this read.
As usual, a great post!
Just to add a few things to the discussion:
A point from the Mann article that I find highly misleading where they decide to lump saturated fat together with trans fats to show trends in reduction of CVD mortality, stating that: “Reduced consumption of saturated, and MORE RECENTLY trans unsaturated, fatty acids compared with intakes reported in the 1970s…”
What you could read from this, is that the trend started with the reduction of saturated fats and the trans fat effect came much later on.
Data from the Minnesota Heart Survey begs to differ, showing that the consumption of trans fats steadily decreased by ” 32 percent in men and 35 percent in women” from 1980 to 2009.
In the article they also point out that: “In middle-income and low-income countries, and in some marginalised indigenous populations, coronary heart disease mortality and prevalence of type 2 diabetes continue to increase.”
However, no efforts are made to explain the discrepancies in the divergence of trends in CVD and DM between high and low income countries. Assuming the same diatery trends are happening globally, why the difference?
“However, no efforts are made to explain the discrepancies in the divergence of trends in CVD and DM between high and low income countries. Assuming the same diatery trends are happening globally, why the difference?”
Another component of the American diet that has increased substantially in the last four decades is fructose, primarily in the form of high fructose corn syrup in processed foods and sodas (2). The roles of both LA and fructose in the current obesity epidemic are under intense scrutiny but are not well understood and seldom compared side-by-side. https://press.endocrine.org/doi/abs/10.1210/endo-meetings.2013.OABA.9.SAT-708
Dietary trends can have both overlap and divergence where food quality is concerned. For example: https://articles.orlandosentinel.com/2003-09-28/news/0309270148_1_overweight-or-obese-women-were-overweight-south-africa
You probably have mice as pets, right David? Can’t think of any other reason why anyone would be so damn attracted by mice studies – which usually don’t have that much relevance in terms of human diets. Esp. as there’s no evidence of the alleged harms of LA within currently recommended intake levels, on the contrary.
The observed drop in total cholesterol may be largely attributable to the substitution of seed oils for traditional (generally animal) fats in the food supply. This is a global phenomenon. “The incidence of obesity in the U.S. has increased from 15% to 35% in the last 40 years and is expected to rise to 42% by 2030. Paralleling this increase in obesity are a number of dietary changes, most pronounced of which is a >1000 fold increase in consumption of soybean oil from 0.01 to11.6 kg/yr/capita from 1909-1999: soybean oil consists of 50-60% linoleic acid (LA), so the energy intake from LA has increased from 2% to >7%/day.” https://press.endocrine.org/doi/abs/10.1210/endo-meetings.2013.OABA.9.SAT-708
From another article: “These findings pertain directly to a massive, population-level dietary trend. Over recent decades, more and more of the oil in the typical American diet has come first from corn, and then from soybeans. In both cases, that oil is an unusually concentrated source of omega-6, linoleic acid. The direct metabolic implication of this is immediately clear: the production of DHA is being inhibited at an enormous scale. The public health ramifications are less clear, but clearly worrisome. Is widespread interference with the production, and brain uptake of DHA, a contributing factor to trends in autism, ADD, and other disorders of behavior and cognition? Proof of causality is an elusive standard, but the proposition is every bit as plausible as it is disturbing. https://www.huffingtonpost.com/david-katz-md/dietary-fat-and-the-human_b_8089586.html
So the recommendation to replace animal fats with seed oils to lower total cholesterol resulted in lowering the intelligence of several generations of children? https://davidgillespie.org/margarine-makes-kids-stupid-enough-eat-margarine/
Seed oils lower intelligence?
They also cause global warming, infertility, unemployment and spontaneous combustion. Not to mention the fall of Rome.
Seriously Dave. Don’t believe everything you read.
Seriously Mie. Attributing an extreme viewpoint to someone you disagree with (“Don’t believe everything you read.”) does not constitute a serious argument.
It seems that – just like Bob – you too have problems understanding the difference between an argument (you know, something made with serious intention) and a comment (not necessarily made with serious intention).
Now, if you’re looking for an argument, here’s one: you’re displaying naive belief in ecological fallacies. There’s nothing inherently fattening about LA – nor any other fatty acids, for that matter.
Actually, in excess, LA does appear to be inherently fattening. “Compared with control mice fed low-fat diets or high-fat coconut oil diets for 6 months, mice fed soybean oil-rich diets gained significantly more weight, had fattier livers, and had more glucose intolerance, researcher Frances M. Sladek, PhD, of the University of California, Riverside, noted in a March 6 presentation at the Endocrine Society’s 97th annual meeting (ENDO 2015) in San Diego.” https://www.medpagetoday.com/Endocrinology/GeneralEndocrinology/50472
Yes David, in EXCESS. In MICE.
I’ve often seen people write that it’s been proven that LDL-C is a cause of heart disease but I don’t recall actually seeing the evidence supporting this. Conversely, I’ve seen plenty of evidence showing that LDL-C is a poor indicator of heart health.
And as for this Mann guy, he lost me when he suggested that correlations can be used to attribute causation. This paragraph had me shaking my head:
“Although everybody knows that correlation does not prove causation, they
claim this dietary change has been a major contributor to the reduction
in coronary heart disease, largely because of a reduction in LDL
Of course, being a cholesterol denialist you choose to close your eye on any evidence. I’ll make it simple: no (excess) LDL, no atheroma. And, of course, no one’s arguing that LDL is all there is to heart disease.
This “denialist” noticed that your ad hominem attack is entirely devoid of any citations to evidence that LDL has anything to do with CAD.
If it’s such a clear cut concept, I would think it would be a snap to point something out that’s irrefutable. Of course you can simply want to call me names to make you feel good about yourself which is entirely your preogative but your comment is a waste of everyone’s time (as usual).
Don’t use fancy words the meaning of which you don’t understand. I characterized you as a denialist, I wasn’t using it as an argument. The arguments was here:
“no (excess) LDL, no atheroma. And, of course, no one’s arguing that LDL is all there is to heart disease”
And if you resent being called a denialist, I recommend you stop being one.
So you’re trying to tell me that calling me a “denialist” means you weren’t trying to sway the opinion of other people reading this? I would say that you actually were using it as an argument. Regardless, the use of the term is ridiculous. Are you saying I’m denying that cholesterol exists? We’re you trying to asscoiate me with a Holocaust denier? Whatever it was you were attacking me personally and not my argument so just stop, okay?
“So you’re trying to tell me that calling me a “denialist” means you weren’t trying to sway the opinion of other people reading this?”
By calling you a “denialist”? Nope. Opinions ought to be based on arguments, which I always include first and foremost.
So how about focusing on them? How would you explain the fact that having excess LDL is both necessary and sufficient condition in atherosclerosis?
“Regardless, the use of the term is ridiculous.”
I use the term in its standard meaning. If you have any beef with that, be my guest. It doesn’t change the issue at hand.
Explain something to me – we have a “wonder” drug at our disposal (statins) that is very effective at lowering LDL-C levels. I will concede that if you want to lower your LDL-C you should be taking a statin because they are without a doubt the best way to accomplish that. But if statins are so terrific at lowering LDL-C (and they are), why is heart disease still a problem? Why have we not wiped out CAD? If statins are great at lowering LDL-C and LDL-C controls our heart health then why did it take more drug-company financed studies than I can count to show finally just the slightest benefit to lowering levels of CAD via statins?
We can control LDL-C levels but when that translates to incredibly small improvements in rates of CAD and no benefit whatsoever in total mortality then isn’t that an indication that focusing on LDL-C is a waste of time? Mie, can you explain this conundrum to this cholesterol denier?
“But if statins are so terrific at lowering LDL-C (and they are), why is heart disease still a problem? Why have we not wiped out CAD?”
Because, just as I pointed out, no one’s arguing that LDL is all there is to heart disease.
Now, if LDL wasn’t relevant, then statins and/or any other form of therapy that lowers LDL in clinically significant ways (without any adverse effects on other lipid values, inflammation etc.) wouldn’t work. But they do.
“We can control LDL-C levels but when that translates to incredibly small improvements in rates of CAD and no benefit whatsoever in total mortality then isn’t that an indication that focusing on LDL-C is a waste of time?”
Define “incredibly small”. Statin therapy is the most efficient treatment currently in widespread clinical practice. And no benefit in total mortality? Please.
“Across all populations, statins were significantly more effective than control in reducing all-cause mortality (OR 0.87, 95% credible interval 0.82-0.92) and major coronary events (OR 0.69, 95% CI 0.64-0.75).”
Now, in primary prevention the differences in overall mortality tend to be attenuated as the amount of fatalities in general becomes smaller in study populations, hence pure coincidence comes into picture. They still exist in CVD mortality, which is the key here as statins are used to treat it, not e.g. diabetes, cancer etc. etc. The mere prevention of major coronary events makes them cost-efficient.
Your own hand picked stats aren’t exactly blowing my socks off. I make the claim that the benefits of statin therapy are remarkably small (if there is a benefit at all) and that if lowering LDL-C was the key to stopping heart disease then statins should do the trick and then you offer stats that exactly back up what I say. WTF? Is that the best you can do?
And then you have the chutzpah to say that nobody is claiming that LDL-C is the “heart of the disease”. Bullshit! When statin therapy is essentially the only treatment, doctors are saying that LDL-C is the heart of the disease (or that they don’t have a clue how to prevent/cure it). Sure they give lip service to “lose weight” but they don’t have a clue how to get people to do that either.
Mie – I will say you are an expert in your use of the English language, you’re very good at admitting just enough to give the impression of honesty but leaving out enough to give the wrong impression. It’s really a shame you’ve decided to be on the wrong side of this. I hope you’re well paid.
” … then you offer stats that exactly back up what I say. WTF? Is that the best you can do?”
Err, I did ask you to define “incredibly small”, didn’t I? Start with that.
And in case you can’t read, the abovementioned meta-analysis indicates a benefit overall mortality, contrary to what you claimed.
“And then you have the chutzpah to …. ”
… call your BS? Yep, certainly do.
“Mie – I will say …”
… that you decided to focus on EVERYTHING else than what’s relevant?
So then. Start by defining “incredibly small”. Please.
Alright, let’s work on that.
We have a range somewhere between “Actually harmful” and 100% effective”. Now there are some drugs that are very near 100% effective to actually preventing the disease they target – I’m thinking in terms of vaccines like polio and smallpox. I’m okay with something like that. On the other hand you have something like statins which may decrease your absolute risk for CAD by less than 1% for high risk patients but also have been shown to actually increase your risk of getting other diseases like diabetes, muscle pain/weakness, rhabdomyolysis as well as a host of other crap I wouldn’t want to get.
It’s also important to note that when it’s said that statins work in terms of all-cause mortality, they are simply extending the life of the less-than-1% it works for by 3 months. Whoopie…
So I would categorize statins in the “pathetically poor” category and possibly “actually harmful” just as one might expect a substance to work that’s intended purpose is to stop your body from producing a substance that’s critical for life.
“Now there are some drugs that are very near 100% effective to actually preventing the disease they target – I’m thinking in terms of vaccines like polio and smallpox”
The problem is that you’re comparing two very different cases: an infectious disease caused by a micro-organism and a multifactorial disease caused by lifestyle choices. Kill the micro-organism and the disease is gone, just like that – simple as that. Treat a causal risk factor and the disease isn’t gone just like that – simple as that.
Now, there are several other reasons why statins don’t give 100% protection against hear disease.
– “Intention to treat” vs “per protocol”: usually, it’s a case of the former in medical studies (meaning that people who don’t take their medication regularly – or don’t take or drop out – get included in the final analysis. This inevitably attenuates the findings.
– Atheromas take decades to build and don’t vanish overnight. Therefore, even though LDL levels can drop pretty quickly, the plaques don’t simply melt away as quickly. It’s known that baseline situation is a pretty good predictor here, see e.g.
Consequently, the benefits can be expected to be attenuated in studies of only some years in duration.
“On the other hand you have something like statins which may decrease your absolute risk for CAD by less than 1% for high risk patients but also have been shown to actually increase your risk of getting other diseases like diabetes, muscle pain/weakness, rhabdomyolysis as well as a host of other crap I wouldn’t want to get.”
Benefits vs harms: statins reduce major coronary events more than any other known treatment, and the potential harms (which, apart from muscle pain, are relatively rare – or in the case of diabetes, a case of statin treatment causing new onset DM2 some months prior to when it would emerge anyway).
“It’s also important to note that when it’s said that statins work in terms of all-cause mortality, they are simply extending the life of the less-than-1% it works for by 3 months.”
On average, yes. Once again: this stems from the fact that whereas others get substantial benefits, others get very little.
Do you have anything better to offer, then?
“So I would categorize statins in the “pathetically poor” category and possibly “actually harmful” just as one might expect a substance to work that’s intended purpose is to stop your body from producing a substance that’s critical for life.”
Now, the physiological need for LDL is but a FRACTION of what us Westeners typically have. Statin therapy doesn’t lower LDL to the point where it would actually harm us vs the benefits, there’s no evidence of that. The only significant exception is the case of new DM2 cases, and that I already covered above.
Let’s take stock of what you’ve accomplished here – you’ve called me a name, you won’t look at evidence that challenges you beliefs simply because it’s in video form rather than written, you’ve essentially agreed with everything I’ve said but in a way that makes it seem like you’re disagreeing (which is a major talent, I hope you’re well paid for that) and now you’ve reached into the bottom of your bag of tricks and are trying to dazzle with bullshit. You’re one short step from an outright lie.
Tell me this – are you directly employed by a pharmaceutical company or do you work for a company that’s revenue comes from a pharmaceutical company?
“Let’s take stock of what you’ve accomplished here”
… which is quite a lot more than you, as you didn’t address any of what I stated above.
(And BTW, if you seriously believe I’ve agreed with you as a whole, you’re not only illiterate but also delusional.
“Tell me this – are you directly employed by a pharmaceutical company or do you work for a company that’s revenue comes from a pharmaceutical company?”
Nope, don’t work in health care sector at all. Sorry Bob, it’s just a case of me being able to bother to THINK. An alien concept to you, I know. 🙂
I didn’t ask you if you worked in the health care sector – I asked you if you worked directly for a pharmaceutical company or a company that’s income depends on pharmaceutical companies. This latest comment is one more example of your brilliance when it comes to appearing to answer a question while not actually answering the question. It’s a talent. If I were a trial lawyer I’d hate to have you up on the stand.
What exactly should have I addressed from your last comment? None of it contradicted what I’d said, it was another instance of you agreeing while appearing to disagree.
Come’n – tell us all who you work for. I am dying to know. All we know right now is that you’re totally anonymous and a fierce defender of the statin industry. Wouldn’t it be more fair for us to know a little more about you?
Err, I thought that pharmaceutical industry goes under that umbrella term? At any rate, I don’t work for Big Pharma either. And that’s where this thread ends, sorry B. 🙂
“None of it contradicted what I’d said”
Yes, let’s skip e.g. your claim about statins not reducing tot. mortality due to technicality/nit-picking (not in the previous comment). But let’s not ignore the fact that I spoke about “agreeing”, not “contradicting”: you can simply make onesided claims, fail to make meaningful comparisons, ignore realistic treatment goals etc. and not “contradict”. To make it really simple: I do not agree with you, and nothing I wrote above means I did.
So Bob, if you still choose not to comment the issue at hand but try to move the discussion further into meta-discussion or chatting about my profession – simply because you know nothing of the topic at hand – you can talk to the hand.
This is almost amusing…
Once again, my question was whether you worked for a pharmaceutical company or a company that’s revenue is earned from a pharmaceutical company. I think it’s interesting that you can’t give a simple “yes” or “no” to that question. It’s not like anyone would ever know the difference since you’re completely anonymous. You could lie your ass off and nobody would know the difference. What’s the problem, is there some little bit of integrity and morality remaining that’s holding you back from saying “no”? Conscience bothering your a little bit?
Actually nevermind, nobody’s going to believe that your comments aren’t being influenced financially in some way so it’s irrelevant who pays you. I think it’s probably a good idea to get back to the original point of both the article and my comment – where is the evidence that LDL-C is the cause of heart disease?
Mie – And while you’re scurrying around trying to find some decent evidence that LDL-C is the cause of heart disease here’s something you can have on in the background – it’s a 30 minute video of Dr. Malcolm Kendrick explaining how, through the results of various studies, LDL-C is not a risk factor for heart disease.
Videos? Nope. If Kendrick has anything NEW to say, rephrase it here.
Oh, you mean there’s somewhere where you’ve addressed the “old” things that Kendrick has had to say? No? Didn’t think so.
Not me, but basically everyone else.
However, you can rephrase EVERYTHING what you consider relevant in his video, if it makes you feel better. I’ll point out the flaws then.
Well that’s helpful – I’ll just go out on the internet and find everything that “everybody else” has written on the topic.
Look, if you don’t want to watch the video because you know there’s no rebuttal than why not just say so. That’s the conclusion that everyone else who’s reading this is arriving at anyhow.
I don’t watch videos, full stop. If you want to use it to argue for your point, you need to explain WHY so. Just like with e.g. research articles.
Look, I’ll make it REALLY simple: just explain the first point Kendrick makes and I’ll comment on that. Just. One. Single. Point.
I don’t blame you, why watch something that directly contradicts with references to relevant studies the nonsense you spout? You’d have to be a fool to do so and the one thing you aren’t is a fool.
Once again: pick a point. One. Single. Point.
Remember several months ago when I said you were a waste of time? It still applies today.
So you just spam videos?
Bye Bob. Wish I could say it’s been a pleasure – but unlike you, I’d rather be honest. 🙂
I’d rather you be honest too.
I think you’ll find that it is! See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/
Your own study doesn’t support what you’re saying.
“Therefore, the fact that lowering LDL levels does not prevent cardiac events in 60-70% of individuals at risk contradicts the causative role of LDL. Unfortunately, it appears that the scientific and medical communities are focusing on and emphasizing biomarkers that can predict risk, without proof that these biomarkers cause the risk.”
Do you always stop reading when you get to a bit that appears to support your opinion? Read on!
“(5) In coronary atherosclerosis, the outer layers of DIT become exclusively neovascularized, and biglycan comes into direct contact with blood lipoproteins.
If the above statements stand, a simple conclusion can be reached: in coronary atherosclerosis, biglycan of the outer DIT should extract and retain LDL-C particles from newly formed capillary beds, which are known to be very permeable [133,134]. This mechanism does not require any conditioning or complicated explanatory pathways. Furthermore, as we know from observations, lipid accumulation during early stages of coronary atherosclerosis always begins in the outer layers of the coronary DIT [61,62,64,67].
The assumption that neovascularization of the outer tunica intima
is the first step in pathogenesis results in a hypothesis that produces
the simplest explanations: (1) an initial deep localization of lipid
deposition in the tunica intima, (2) a certain probability of coronary lipid deposition and atherosclerosis development when blood LDL
levels are normal if pathological neovascularization has occurred,
owing to LDL-C accessibility for contact with previously avascular
structures (biglycan, which has affinity to LDL-C, and should extract it
regardless of LDL-C levels); (3) more probable lipid deposition and
disease contraction at high blood LDL levels; (4) probability of
coronary atherosclerosis development after high LDL levels are lowered through the use of drugs, as neovascularization has already occurred and LDL-C particles appear in direct contact with previously avascular structures (biglycan, which has affinity to LDL-C and should extract it regardless LDL-C levels). At this point in the analysis, neovascularization of the coronary tunica intima appears as a cause of coronary atherosclerosis. Therefore, it logically follows that since the presence of LDL-C in plasma is a fundamental metabolic requirement for humans , theoretically there is no “safe LDL-C level” that would be 100% certain to prevent coronary atherosclerosis if intimal neovascularization has already occurred.
Therefore, the model predicts that if the coronary intima became vascularized, lipoproteins would be extracted and retained by intimal proteoglycan biglycan even if blood LDL levels were normal. However, lipoprotein extraction and deposition will be faster if LDL levels are high. These model predictions have been confirmed by clinical observations. Therefore, contrary to the accepted model, the author’s hypothesis suggests a different cause of the disease, and the opposite route for invasion of atherogeneic lipoproteins into the coronary tunica intima.”
The bit that you quoted states that “X” contradicts the causative role of LDL. So what? The bit that I quoted shows that LDL is involved in atherosclerosis, but not in the way usually stated.
Because LDL is involved in atherosclerosis, but in a different way, reducing LDL alone doesn’t reduce the RR for CHD in a large % of individuals at risk. This means that other factors need to be addressed in addition to LDL reduction.
You’re both wrong.
First of all, Bob’s quote comes from Libby (2005) which doesn’t argue that LDL isn’t a causative agent – nor can the fact that 60-70% don’t get help from lowering LDL be used to argue this. On the contrary, Libby claims that the LDL-lowering interventions are initiated too late and/or are not aggressive enough, which is the exact OPPOSITE of what Subbotin suggests. Not to mention that residual risk in clinical studies in no way contradicts the lipid hypothesis.
Next time cite an article whose writer bothers to be honest when using sources – or can understand written language.
I interpreted “Therefore, the fact that lowering LDL levels does not prevent cardiac events in 60-70% of individuals at risk ” as:-
CHD is multi-factorial (where LDL is one of the factors) and everyone is different, therefore the predominant factor varies from person to person.
Apart from that disagreement, what do do you think of Subbotin’s neovascularisation of the DIT hypothesis (where LDL is one of the factors)?
It is multifactorial, yes, but LDL is necessary for the formation of atheroma. Of course, LDL alone is a sufficient factor too.
The article itself seems to be full of misunderstanding and poor reasoning and therefore difficult to take that seriously. To pick some of the more obvious flaws: Subbotin claims that the current understanding of the structure of the intima is somehow flawed – however, the links he provides to support his claim do nothing of the sort. And why wouldn’t they, as this (the layout of the intima) is by no means anything new?
“Subbotin claims that the current understanding of the structure of the intima is somehow flawed – however, the links he provides to support his claim do nothing of the sort. And why wouldn’t they, as this (the layout of the intima) is by no means anything new?”
Fair enough, but does that invalidate his hypothesis i.e. LDL invades the media via neovascularisation, rather than (or perhaps as well as) via the intima? Is there any evidence to refute his hypothesis?
As a retired Electronic Engineer, I’m interested in solving problems, which is why I have an Evidence-Based Diet, Nutrition & Fitness blog, as an awful lot of people are suffering from unresolved health problems. I’ve reversed a couple of my own without using drugs, that resulted in my Endocrinologist stating “Mr Kinbrum, that’s not possible.” (Osteoporosis -2SD in my lumbar spine → 0SD, in 3 years. Pre-T2DM OGTT 8.7mmol/L @2 hours → 3.7mmol/L @2 hours, in <5 years). Psoriasis has gone from red patches & flaky scalp & eyelashes → no visible signs.
If lowering LDL doesn't solve a problem, other factors need to be addressed. For example, what do you think of https://tinyurl.com/hk6bhjb ?
"The relative risk (RR) of CHD mortality was reduced in the upper tertile (~40.9u g/d) of dietary menaquinone (K2) compared to the lower tertile (~15.1ug/d), RR 0.43, 95% CI: 0.24, 0.77.
Phylloquinone (K1) intake was not related to any of the outcomes."
Association doesn't prove causation, but the hypothesis that Vitamin K2 drastically reduces the RR for CHD mortality (by reversing calcium shift from hard tissues to soft tissues) is worth testing. A search on PubMed for ("Vitamin K2" OR menaquinone) AND CHD shows that no RCT's have been done.
Suffice it to say, I supplement with Vitamin K2 (as it was one of the supplements that I took to reverse osteoporosis). Unlike statins, there are no adverse side-effects from taking Vitamin K2. Fujita T[Author] hypothesised about calcium shift back in 1985, yet there are no RCT's on Vitamin K2.
You need to open your eyes in order to see evidence. Here’s some for ya https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3492120/
These days, Mozaffarian’s reasoning seems to go like this:
1) “SFA is not bad because it worsens lipid values compared to unsaturated fatty acids”.
2) “Sugar is bad because it … worsens lipid values compared to unsaturated fatty acids”.
Spot any problems there? 🙂
If LDL is directly linked to CHD, how come that the average LDL level of new coronaries in the US is LESS than the mean? Neither total cholesterol nor LDL actually matter. LDL-P (particle count) seems to matter a lot. Also the ratios of the various components to one another matter. Sat fat increases LDL in some people but almost inevitably improves the ratios and lowers the particle count.
If the reduction of LDL explains the drop in CHD, how come in Framingham, it actually increased it?
The problem with many experts is that they don’t actually know the literature at all.
“If LDL is directly linked to CHD, how come that the average LDL level of new coronaries in the US is LESS than the mean?”
Err, care to rephrase that? I don’t quite understand. New “coronaries”?
“Neither total cholesterol nor LDL actually matter. LDL-P (particle count) seems to matter a lot.”
False dichotomy. All of these matter. LDL-P esp. in the case of DM2/met.syndrome.
“Sat fat increases LDL in some people but almost inevitably improves the ratios and lowers the particle count.”
First of all, SFA has no effect on apoB, a marker for LDL-P (evidence from metabolic ward studies) when the point of comparison is carbs, in the standard Western contest – in other words, crappy carbs for the most part. And there’s clinical evidence that diet rich in e.g.
beef and SFA actually raises LDL-P.
Secondly, the question about ratios fails to consider the facts that raising “mere” HDL-C doesn’t seem that important in relation to lowering LDL – HDL functionality is the key. And SFA hinders e.g. the anti-inflammatory properties of HDL. So, at best, SFA is on the same level as e.g. sugar. Hardly a recommendation, right?
“If the reduction of LDL explains the drop in CHD, how come in Framingham, it actually increased it?”
Please. Reverse causation: LDL levels decrease due to e.g. conditions and disease like cancer – in addition, higher LDL levels serve as an indicator of better nutritional status. Once this is taken into account, decreasing LDL (no matter whether via diet or medication) is
beneficial. Increasing it: no.
“The problem with many experts is that they don’t actually know the literature at all.”
After that Framingham brain fart of yours, you’re certainly in no position to talk about experts not knowing anything. Dunning-Kruger, anyone?
“However, both Mann and Mozaffarian completely disregard data supporting the usefulness of intensive carbohydrate restriction in people with established insulin resistance or metabolic syndrome (8, 9, 10, 11). ”
Or perhaps they care more about HARD end-point data than risk marker data (most of which indicated not that much in terms of clinical benefit over the alternatives)?
I assume that by HARD end-point data you mean association between variables based on observational evidence.
The main reason the traditionalists believe saturated fat is bad because it may raise LDL cholesterol (a risk marker).
Nope, clinical trials with hard end points (e.g. deaths, hospitalizations etc. prevented).
BTW Axel, us “traditionalists” also believe that SFA is a worse option than unsaturated fatty acids, esp. PUFA – based on hard end-point clinical evidence. Silly us. 🙂
This is probably the biggest meta-analysis of both observational studies and RCT’s
“Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats”
A citation would be welcome. What studies are you referring to?
Other meta-analyses, e.g. Skeaff and Miller, have done what Chowdbury et al didn’t: examined what happens to CVD risk from 5% of tot. E from SFA gets exchanged for 5% of PUFA. It goes down.
And as for Chowdbury et al, you do realize that the inability of study participants to e.g. reach the required dietary changes, lack of statistical power in individual studies, substitution of dietary fat for carbs etc. etc. other issues in individual account for why these meta-analyses don’t show any effect without the abovementioned examination?
Are you seriously suggesting that quality of fat is irrelevant when it comes to CVD?
I do think the quality of fat matters.
Although I generally try to avoid oversimplifying, when it comes to CVD I might suggest the following order, from bad to good:
trans fat – linoleic acid – saturated fat – MUFA – omega 3
So, with regards to CVD, MUFA and omega 3 is what I would go for.
When it comes to the metabolic syndrome, I don’t recommend anyone to avoid saturated fat. More importantly, they often help people restricting their carbs which, as you know, I believe can be extremely helpful.
Ah, LA phobia has gotten to you too. Care to show any evidence pointing out that LA (which, BTW, is an essential fatty acids) is bad, within the current recommendations for consumption?
Never said LA was bad and I do realize it’s an essential fatty acid.
Care to show me your ranking order for dietary fats? Curious to know what it looks like.
“Never said LA was bad and I do realize it’s an essential fatty acid. ”
You listed LA before saturated fat which hints it is a worse option. Now, to my knowledge, there are NO trial nor observational evidence showing that SFA is less of a problem than LA – NOR e.g. evidence that shows the having a certain amount (% of tot. E) of SFA is beneficial over the same amount of Western carbs whereas there is evidence of the benefits of LA when consumed within recommended guidelines. Ths, consequently, shows in all kinds of guidelines.
If you disagree, then show me the money. I mean, evidence. 🙂
“Care to show me your ranking order for dietary fats?
There you go:
Trans fat – saturated fat – MUFA – PUFA. Based on their effects on lipid values and inflammation, though the order doesn’t really change if you think about e.g. cognition etc.
Interesting, thanks 🙂
BTW, you do realize that just because PUFA has the most beneficial effect in the recommended range of intake, there’s no reason to go overboard with it? In other words, if your intake of e.g. TFA and SFA is high & you need to lower your LDL, then it’s not reasonable to e.g. replace all SFA with only PUFA but also with MUFA. Or go for veggies and fruits.
“When it comes to the metabolic syndrome, I don’t recommend anyone to avoid saturated fat.”
Given the fact that these people are especially prone to CVD, due to lipid levels and functionality being properly messed up, I fail to see why. Care to explain why you’d deviate from clinical practice guidelines?
Currently, most practice guideline accept carbohydrate restriction for metabolic syndrome and/or type 2 diabetes.
Just look at your your neighbours on the other side of the Baltic Sea and Gulf of Bothnia.
Swedish health authorities accept carbohydrate restriction for type 2 diabetes suggesting a diet consisting of meat, fish, eggs, seafood, vegetables, legumes and vegetable proteins and fat from olive oil and butter while the content of sugar, bread, cereals, potatoes, root vegetables and rice are less than the traditional diabetes diet.
Axel, it shouldn’t be that hard to realize that SFA and low card diets aren’t synonyms.
To briefly recap why diabetics shouldn’t increase SFA consumption (compared to unsaturated fat consumption):
1) LDL levels increase.
2) LDL-P doesn’t change.
3) Endothelial function doesn’t improve.
4) Inflammation doesn’t decrease.
5) HDL functionality (which is already impaired in people with diabetes) suffers.
Any comments, Axel? I thought the point of these discussions was to learn and challenge one’s views.
Doc Axel: thanks for sharing about heart disease and what we can do to get ahead of it. Please also check out my sister’s blog that has heart, science, and a bit of fun at ALL THINGS HEART at https://allthingsheart.com/category/introduction/
From the JAHA in April
“This study of subclinical heart disease and associated risk
factors among nonelderly adult decedents found that a
decline in CAD grade over the full time period 1981–2009
was accompanied by significant reductions in elevated blood
pressure and current smoking. Importantly, the temporal
decline in CAD grade was limited to the first half of the period.
After 1994, the trend in CAD was flat (P=0.79).
significant increases in the prevalence of obesity and diabetes
in this population, and these increases likely contributed to an
end in any continued decline in CAD grade from the mid-
These findings reinforce concerns that the obesity and
diabetes epidemics may adversely affect cardiovascular
morbidity and mortality and total mortality in coming years.
Secondary prevention (eg, pharmacologic treatment) of
obesity and associated CAD risk factors (ie, hypertension,
dyslipidemia, and diabetes) can assist only so far in controlling
morbidity and mortality. Any beneficial effects of treatment
programs may be offset by failure to address the
growing numbers of persons who are obese and diabetic. The
findings presented in this study caution against complacency
about the future impact of obesity and diabetes (both
preventable conditions) based on current trends in CAD
I wasn’t aware of this paper.
It would support the hypothesis that it’s only a question of time before the epidemic of obesity and type 2 diabetes reverses the trend in mortality from coronary heart disease.
Here is another revealing epidemiological study: “Contributions of Increasing Obesity and Diabetes to Slowing Decline in Subclinical Coronary Artery Disease”