Actor James Gandolfini’s sudden and tragic passing has cruelly reminded us about the seriousness and unpredictability of cardiovascular disease.
Sudden death in middle age is most often caused by underlying coronary heart disease (CHD).
One has to wonder, in light of current knowledge and modern technology, why we can not prevent such devastating events. One explanation may be the fact that CHD often is a very unpredictable disorder. In some cases, serious disturbances in heart rhythm (ventricular fibrillation) leading to sudden death is the first symptom. This is usually caused by an abrupt blockage of one of the coronary arteries that supply blood to the muscle of the left ventricle of the heart.
Recently, on the website Lecturepad, Thomas Dayspring MD and James A Underberg MD reflected on the teachable moment G
Gandolifini’s untimely demise presents. Lecturepad is one of my favourite websites for medical information. It needs a registration, but I presume everyone can have one, and it is definitively worthwhile. Their educational material is top class and up to date.
Dayspring and Underberg suggest that “if modern diagnostic blood tests were routinely performed and any discovered abnormalities were treated with proper lifestyle and appropriate pharmacological intervention, premature death from CHD would likely disappear”.
The Dreaded Plaque Rupture
In their article, Dayspring and Underberg point out that “humans do not die from severely narrowed or blocked coronary arteries or pipes” as we have often been lead to believe. “The fact is that the real cause of heart attack is the presence of small, obstructive cholesterol laden plaques that suddenly rupture and rapidly induce blood clots that obstruct the artery, which causes blood flow to the heart to be blocked, leading to injury or death of heart muscle”.
They don’t go into details about what cause plaque formation and why plaques rupture. A plaque that is prone to rupture can not be detected by a blood sample, an electrocardiogram (ECG), an exercise test, an ultrasound of the heart or a coronary calcium scan. Even coronary angiography usually can not differ between a rupture-prone plaque and a stable plaque. One of the biggest questions in cardiology today is how we can detect plaques that are prone to rupture from those who are not. Dayspring and Underberg on the other hand point out that “the only absolute requirement for plaque development is the presence of cholesterol in the artery: although there are additional heart risk factors like smoking, hypertension, obesity, family history, diabetes, kidney disease, etc., none of those need to be present”.
Cholesterol and Risk
Measurements of blood cholesterol have traditionally been used for risk testing. In particular, blood levels of low density lipoprotein cholesterol (LDL-C) are used to assess risk and to guide therapy. Lowering LDL-C is considered an important target to reduce the risk of future CHD, and among patients with known cardiovascular disease.
However, measuring cholesterol levels in the blood may be misleading, because cholesterol circulating in our blood will not cause plaque unless it settles in the arterial wall. According to Doctors Dayspring and Underberg ” The graveyard and coronary care units are filled with individuals whose pre-death cholesterol levels were perfect. We now understand that the major way cholesterol gets into the arteries is as a passenger, in protein-enwrapped particles, called lipoproteins”. They believe that we have much better biomarkers than blood cholesterol to assess cardiovascular risk.
They write: “Particle entry into the artery wall is driven by the amount of particles (particle number) not by how much cholesterol they contain. CHD is very often found in those with normal total or LDL cholesterol levels in the presence of a high LDL particle number (LDL–P). By far, the most common underlying condition that increases LDL particle concentration is insulin resistance, or prediabetes, a state where the body actually resists the action of the sugar controlling hormone insulin. This is the most common scenario where patients have significant heart attack risk with perfectly normal cholesterol levels. The good news is that we can easily fix this, sometimes without medication.”
The Role of Sugar and Carbohydrates
In general, most methods that lower LDL-C have some ability to lower LDL-P. However, there are some differences. In order to lower LDL-C, most doctors will recommend eating less fat and cholesterol from meat and dairy products. Statin therapy significantly lowers LDL-C. Therapies may affect the LDL particle number differently. Interventions that will lower LDL-C more than LDL-P include statins, estrogen replacement therapy, some antiretrovirals, and a low-fat, high-carbohydrate diet. Interventions that lower LDL-P more than LDL-C include fibrates, niacin, pioglitazone, omega-3 fatty acids, exercise, and Mediterranean and low-carbohydrate diets.
Patients with high levels of triglycerides and low high-density lipoprotein cholesterol (HDL-C) are likely to have high LDL-P despite normal or low LDL-C. Such a lipid profile is typical for individuals with overweight, obesity and the metabolic syndrome. Studies indicate that carbohydrate restriction reduces LDL particle number among these individuals.
Doctors Dayspring and Underberg believe that it is possible to reduce the risk of CHD among individuals with high LDL-P despite normal or close to normal LDL-C: “The key to understanding how comes with the knowledge that the driving forces are dietary carbohydrates, especially fructose and high-fructose corn syrup. In the past, we’ve often been told that elimination of saturated fats from the diet would help solve the problem. That was bad advice. The fact is that until those predisposed to insulin resistance drastically reduce their carbohydrate intake, sudden deaths from coronary heart disease and the exploding diabetes epidemic will continue to prematurely kill those so afflicted. While obesity and insulin resistance often co-exist, 1 out of 5, or (20%), of afflicted patients have a normal body mass index (BMI). That is why testing and correctly interpreting the right blood tests are so important. And for goodness’ sake, if you want to live longer, start reducing the amount of dietary carbohydrates, including bread, potatoes, rice, soda and sweetened beverages (including fruit juices), cereal, candy – the list is large”.
“It’s the Particles Stupid”
These are Dayspring’s and Underberg’s final remarks: “James Gandolfini’s death is a tragedy, and if history is our guide, our guess is that we will find that his passing was likely preventable. It’s important for both doctors and families to learn these lessons so that similar tragedies are prevented from occurring in our own families. Bill Clinton (also a victim of a preventable heart attack) won the 1992 election with the slogan, “It’s the economy stupid.” When it comes to heart disease, a similar quip is equally as powerful and important: “It’s the particles, stupid.””
Here is an article explaining the difference between LDL-C and LDL-P.
31 thoughts on “Heart Attack and Sudden Death. “It’s the particles stupid”.”
Fantastic article (one of your best)! As my wife and I have been living a Paleo+ lifestyle for almost a year, we have come to see very clear evidence of that which you speak. Carbs (other than plant-based, non-grain) have been rather painlessly removed from our diet, and our bloodwork shows the phenomenal benefits. Hopefully the word will spread and the AMA and AHA will finally get on board.
Thank you for your wonderful newsletter. If ever in Iceland we hope to say ‘hello.’
Thanks Ken. Appreciate your interest and hope you continue to follow my blog and share your thoughts.
Although particles are likely to have an important role, I think it’s a mistake to confer on them the ‘holy grail’ of all CHD. This same mistake was first made with TC, then LDL, and now Dayspring has become the new Ancel Keys, only now its the “particles,” stupid.
There are likely additional factors at work in CHD, which if ignored by patients the more cardio event deaths will occur. Unfortunately, the bombastic and singular-minded Dayspring is doing the public a disservice by performing just like Keys.
Before people dedicate their total focus (and unhealthy obsessions) solely on particle reduction, it might be best this time to assure quality and non-biased peer reviewed research is published and widely accepted prior to encouraging everyone to change an entire lifestyle to pursue the next blood lipid, false holy grail.
With that said, particles are another important bio-marker that individuals should be aware of and monitor, along with many others that, depending on each individual, may play a bigger role regarding prevention of cardio disease/attacks.
You’re right Art. Coronary artery disease is a multifactorial disorder. Many different mechansims contribute to atherosclerosis. However, if we’re stuck on a sideroad, it may take strong words and unilateral efforts to get us back on track.
Although I cannot totally agree with Art’s comments on the “mistakes” of LDL – since I really don’t know what he means by that – I agree with the idea the Dayspring and Underberg are oversimplifying matters.
1) “Dayspring and Underberg on the other hand point out that “the only absolute requirement for plaque development is the presence of cholesterol in the artery: although there are additional heart risk factors like smoking, hypertension, obesity, family history, diabetes, kidney disease, etc., none of those need to be present”.”
Yes, it takes elevated LDL levels for fatty streaks (the first step toward full-blown atherosclerotic plaques) to appear. There’s no doubt about this. However, in real life and clinical practice things are rarely either or: I suppose that you too, Axel, have seen that a multitude of risk factors need to come into picture on a population level before CVD begins to “run rampant” & thus these need to be addressed. When other risk factors enter the picture, the chances of fatty streaks developing into atherosclerotic lesions increase. And with additional risk factors, the risks of the plaque remaining vulnerable (calsified & more stable vs less stable) and then rupturing increase. Thus, the notion that we could focus on just LDL and therefore virtually eliminate CVD simply isn’t reality, at least not for now.
2) “However, measuring cholesterol levels in the blood may be misleading, because cholesterol circulating in our blood will not cause plaque unless it settles in the arterial wall. According to Doctors Dayspring and Underberg ” The graveyard and coronary care units are filled with individuals whose pre-death cholesterol levels were perfect. We now understand that the major way cholesterol gets into the arteries is as a passenger, in protein-enwrapped particles, called lipoproteins”. They believe that we have much better biomarkers than blood cholesterol to assess cardiovascular risk.”
Err… The first sentence? When there’s elevated levels of cholesterol in blood, the likelihood of plaque formation rises. What do D & U want to say here? In addition, concerning the pre-cholesterol levels: it can hardly be a surprise to these two gentlemen that sometimes these “perfect levels” simply aren’t low enough to prevent issues, due to e.g. individual variation in a multitude of issues (LDL receptor function, HDL activity, genetics etc. etc.). Nor can it be a surprise that the distinction between lipoproteins which (to simplify) act as means of transportation & cholesterol which is the stuff being transported by LDL and HDL is well-known and that their role in risk prediction is nothing new.
“3) They write: “Particle entry into the artery wall is driven by the amount of particles (particle number) not by how much cholesterol they contain. CHD is very often found in those with normal total or LDL cholesterol levels in the presence of a high LDL particle number (LDL–P)P.”
Oversimplification and/or false dilemma. Yes, a large number of particles indeed marks an increased risk. However, particle issues are often related (like they themselves state) to DM2 and not all patients or risk groups have it. In addition, the amount of cholesterol itself isn’t meaningless, either: just see figure 2 in this study
and you’ll see that patients with both high LDL-P and LDL-C aren’t that much better off than patients with low LDL-P and high LDL-C (event-free survival probabilities of roughly 0.9 vs 0.88). Clearly, this isn’t a case of either/or but BOTH/AND!
4) “Patients with high levels of triglycerides and low high density lipoprotein cholesterol (HDL-C) are likely to have high LDL-P despite normal or low LDL-C. Such a lipid profile is typical for individuals with overweight, obesity and the metabolic syndrome. Studies indicate that carbohydrate restriction reduces LDL particle number among these individuals.”
Yes, there’s some data to indicate that. However, is there data showing that carb restriction reduces CV events?
“The key to understanding how comes with the knowledge that the driving forces are dietary carbohydrates, especially fructose and high-fructose corn syrup. In the past, we’ve often been told that elimination of saturated fats from the diet would help solve the problem. That was bad advice. The fact is that until those predisposed to insulin resistance drastically reduce their carbohydrate intake, sudden deaths from coronary heart disease and the exploding diabetes epidemic will continue to prematurely kill those so afflicted”
Once again, oversimplification. It isn’t a matter of “drastically reducing” carb intake, but rather a matter of primarily a) drastically LOSING weight and secondarily b) IMPROVING the quality of the carbs (since you really can’t overeat on vegetables). And even with low carb, you need to be aware of the type of fat you eat: saturate fat isn’t exactly the ideal choice if you want to avoid insulin resistance.
So if you go low carb, go for the more vegetarian-based approach: add nuts, soy and high-quality vegetable oils, ditch butter, cream & red meat.
To put it shortly, low carb diets are woefully inadequate in the way D & U claim unless they can modify the biggest issue: weight management. And thanks to long-term follow-ups such as Foster et al and Shai et al, we know that the differences between them & other dietary approaches aren’t that drastic. So I’d rather see D & U focusing on how to help people manage on a diet of their choice instead of trying to argue that one single alternative is superior because … err, well, it really isn’t based on solid evidence.
I see no mention that a lack of magnesium in the body can also cause this. By allowing calcium free rein in the body it will deposit in the heart and any other soft tissues. The sad diet is lacking in magnesium. Up the magnesium and ditch the grains and the bad oils.
There are multiple co-factors for calcium assimilation: magnesium, boron, silica, and vit. K2. It’s vit. K2 that catalyzes the movement of calcium into bones and prevents its buildup in vascular tissue.
Calcium requires multiple co-factors for proper assimilation: magnesium, boron, silica, and vit. K2. It’s vit. K2’s role, not magnesium’s, to activate matrix-Gla protein, which prevents calcification of blood vessels and organs. In addition, K2 activates osteocalcin to transports calcium to the bones, where K2 solidifies this calcium into the bone matrix.
Thanks Annette. The issue on magnesium is interesting. There is so much we don´t know about this mineral and so much indicating that magnesium deficiency is more common than we have been lead to believe. Do you know if there are any scientific studies relating magnesium deficiency to acute heart attack?
What about inflammation in the blood vessels, inflammation causes the cholesterol to build… From Dr. Dwight Lundell’s website “Simply stated, without inflammation being present in the body, there is no way that cholesterol would accumulate in the wall of the blood vessel and cause heart disease and strokes. Without inflammation, cholesterol would move freely throughout the body as nature intended. It is inflammation that causes cholesterol to become trapped”….
And cholesterol itself can cause inflammation. See e.g. these
if you’re interested in the mechanism.
Thanks, Mie… Appreciate the input…
You´re absolutely right Katy. Inflammation probably plays an important role in atherosclerosis and coronary heart disease. Interestingly, inflammation is associated with obesity, the metabolic syndrome and type 2 diabetes. For an obese patient, losing weight usually reduces markers of inflammation. Choosing carbohydrates with a low glycemic index (GI) is usually associated with less inflammation than those with a high GI. The Mediterranean diet is an example of a diet that has been shown to reduce inflammatory markers. There are ongoing clinical trials testing the efficacy of anti-inflammatory drugs in patients with coronary heart disease.
Thanks, appreciate the information… And also, appreciate your blog…
Dr. Sigurdsson this is a brilliantly informative article which I am now sharing with our followers. Thank you! “Cereal Killers” – our new feature length documentary focuses on my own attempt to avoid a family history of CHD and type 2 diabetes (despite being v lean + apparently healthy), under the watchful eye of Prof Tim Noakes MD in Cape Town, South Africa. Cholesterol Particles and Carbohydrate Restriction feature strongly in the implementation and analysis of my 4 week medically supervised nutritional intervention – the results will astound many but not your good self I should think. The film will release in September and I would be very glad to share a sneak peek of our existing 60 minute cut with you!
Thanks Donal. Took a sneak peak at your movie. Highly interesting. I´m certainly looking forward to see it when it´s released in september. I´m impressed by your commitment and urge to look for answers. Thanks for sharing. Good luck with it all.
People just can’t get over the failed “lipid hypothesis” and simply won’t believe that saturated fat is one of the healthiest fats you can consume. After 14 years of low-carb, I have upped fat intake to about 85%, following a ketogenic plan, and just get healthier and healthier. Insulin resistance is rampant in my family and I have no doubt that without my dietary changes, I would be like my father at my age, fat, diabetic and with heart disease.
Peggy, the so-called lipid hypothesis – which states that plasma cholesterol levels & CHD are connected – is way past the point of being a mere hypothesis. The evidence is as solid as … well, can be.
And there’s nothing healthy about saturated fat: higher intakes of it haven’t been shown to produce benefit in anything.
Peggy don’t listen to Mie the evidence is far from solid and has many inconsistencies, the hypothesis has never been proven, associations have been shown using epidemiological studies but these have many flaws like poor dietary intake assessment, limited lifestyle assessments and miss classification of food types/ groups. So poor associations at best.
This meta-analysis of RCTs (gold standard) showed that fat modification not reduction reduced the incidence of CHD episodes. Subgroup analysis showed reducing sat fat and replacing with starch creating a low fat diet showed no risk reduction. There was no difference in CHD mortality between groups. Results sugget unsat fats were cardio protective in terms of reducing CHD incidence not mortality but low fat diets diet reduce nothing. Despite the findings the authors still recommend to continue low fat recommendations because they are bought probably. https://www.ncbi.nlm.nih.gov/pubmed/22592684
There are many RCTs that show ad libitum high fat/ low CHO diets out perform conventional low fat/ high CHO diets in terms of lipid profiles.
Here is the most recent meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease which found no association. Prospective cohorts are the gold standard of epidemiological research.
From Mie above comments she is still recommending marg over butter lol
Nick, please. Of course no one’s forcing you to be coherent here, but …You do realize that Peggy mentioned (and I answered her about) the lipid hypothesis? The so-called “diet-heart hypothesis” is a different thing.
Wanted to elaborate a little more on my earlier response.
1. Like others, I do think your article was good and informative.
2. As a blogger myself, I can understand the article’s headline and the use of James Gandolfini’s picture. But the fact remains, there is no evidence that his death was due to “particles.”
3. Based on his appearance/physique alone, and the type of food and beverage that he likely often ate (https://tinyurl.com/ktq5kwc), he was walking heart attack waiting to happen.
4. In every episode of the Sopranos, Gandolfini’s labored breathing was obvious – my impression was that he suffered from COPD.
5. And, it’s likely he was a smoker (cigars, probably), which would have contributed to his overall health issues.
6. Yet, despite the points made in #3, #4 and #5, again, there is no evidence that he had a high LDL-P count.
7. Per the known medical science, at the time of Gandolfini’s death, he could have had low total cholesterol, low LDL-C and a low LDL particle count – people die all the time by heart attack despite a variety of low readings.
8. Instead, at the time of his death, he may have been suffering from high blood pressure, COPD, high inflammatory levels (CRP, homocysteine and etc.), low HDL and high trigycirides, compounded by typical American arterial calcification.
9. Thus, it’s entirely possible a case could be made that it wasn’t the “particles,” stupid.
In general, my point is not that LDL-P is unimportant. Rather it’s that the medical science does not yet have the empirical robustness (nor does Dayspring) that merits a conclusion that a high particle count is a for-sure, absolute death sentence, let alone the killer of Gandolfini.
Instead, cardio deaths are more likely to be a unique mixture of factors for each individual, and the medical establishment needs to help patients focus on a range of cardio/health bio-markers, not just a single one. (Having the APOE 3/4 trait, I have learned to appreciate doctors who can think beyond the ‘HIGH’ designation for some of the items on my lipid panel.)
But based on your article, I would imagine there are now a lot more people overly frightened because they have a high particle count, which Gandolfini might not even have had. Or, even worse, a lot people now decide they have nothing to worry about since their particle count is low – I mean, why care about high triglycerides, arterial bursting blood pressure and obesity when one has “low” particles, eh.
In essence, that’s why I think, in a way, Dayspring is doing a dangerous disservice. Obsessing about a single measurement usually means losing sight of the proverbial health forest.
P.S. FWIW, over the last 6 months I have completely avoided all gluten, vegetable oils, fructose, and simple carbs. My daily diet goal was to achieve 60% of my calories coming from fat, primarily saturated and mono; and, my consumption of cholesterol tripled. Just had a VAP+ blood test done and my lipids have improved significantly (achieved a 60 point drop in TC, yet my consumption of cholesterol tripled; triglycerides finally below 100; and HDL finally above 50); the various blood lipid ratios have improved, moving from high to average risk; all my inflammatory/other markers (CRP, homocysteine, LpPLA2 and fibrinogen activity are rock solid low risk); and, even my LDL particle size finally made the jump up to ‘A’ size from ‘A/B’. What’s not to like?
Well…based on my apoB100 measurement, my particle count is still too high but it has declined nicely. Thank you very much, Misters Saturated Fat and Cholesterol!
(My prior diet consisted of low-fat, a modest amount of junk food (simple carbs), high amount of complex carbs and high consumption of grains and fruits.)
I do agree with you. Of course we can’t allow ourselves to only look at the LDL-particle count. There are a lot of other important risk factors, some of which you mention, like smoking and high blood pressure.
Although Gandolfini’s death sparked my article, my intention was not to analyse his personal health nor his risk factors. I don’t know anything about his LDL particle count or his medical history in general. So, my intentionm was not to discuss Mr. Gandolfini’s health or trying to figure out the cause of his tragcic and sudden death. That’s up to other people to find out.
My intention was firstly to discuss the unpredictability, and sometimes dramatic consequences of a plaque rupture in a coronary artery, which is a common cause of sudden death in middle age. Secondly I wanted to highlight that among obese individuals in general, and those with the metabolic syndrome, LDL choloesterol may underestimate risk. These individuals often have high triglycerides and low HDL cholesterol. Total cholesterol and LDL-cholesterol are often not that bad. However, LDL-P and ApoB may be elevated. As you know, this may demand a different approach than the one that is usually recommended to lower LDL cholesterol.
Finally, I agree with yout that saying it is only about the particles, is an oversimplification. Furthermore, we still have a lot to learn about the clinical usefulness of LDL-P measurements, and what methods can be used to lower our LDL particle number.
In looking at his last meal link from Art above, I can’t help but notice lots of fried food. I had my heart attack after fried falafel. I can still hear the sound of it hitting the deep fat fryer in the nearby restaurant kitchen. In her book “Deep Nutrition” by Dr. Cate Shanahan, she states that she has asked her heart attack patients if they had fried food before their heart attacks, and she says that “all” of them have said yes. I don’t have the book any more, but I believe she said something about the fried aspect made any existing plaque much more likely to soften up and flake off.
I have changed many things about my diet (now low carb, real food, no sugar, more veggies, etc), and of course, no more fried food ever!
I agree with “Mi(k)e” here!
Dr Dayspring idea’s about SFA avoidance being a failed public health measure is highly problematic based on pure mathematics. The IMPACT models by Simon Capewell show that the age-adjusted mortality in US has halved since the 1960s. The decline in mean serum cholesterol levels of Americans (from 240 to the current 200mg/dl), that occurred prior to statins, explains 25% of this reduction in CHD mortality. Much more dramatic findings have been observed in North-Europe and New Zealand. In Finland, the age-adjusted CHD mortality went down 80%. Decline in cholesterol levels explains 50% of this decline in CHD mortality. The decline in cholesterol levels in Finland is almost solely explained by reduction in saturated fats. Iceland experienced a 66% decline in coronary heart disease mortality between 1981 and 2006, for which the decline in serum cholesterol largely explained by a decreased intake of saturated animal fat intake was attributed to 32% of this decline.
All in all, the public measures against SFA has been very successful, especially in Northern Europe and New Zealand. Lives has been saved.
Why have total cholesterol levels declined in most developed countries?
Europe’s leading diet-heart scholars (Pedersen et al) recently expressed themselves on the current trend in downplaying the importance of SFA reduction as expressed by certain American epidemiologists.
The importance of reducing SFA to limit CHD
Response to Hoeselaar by Pedersen et al
Campaigns against eggs has saved tens of thousands from premature death in the US.
“It is a reasonable inference that the sizable decline in per capita egg consumption in the United States in recent decades, and hence in per capita total cholesterol intake, has been one important component of the improved dietary patterns leading to a fall in mean serum cholesterol concentration in the adult population from ~ 6.08 mmol/L (235 mg/dL) in the 1950s to ~ 5.30 mmol/L (205 mg/dL) in the 1990s, and to the concomitant sustained marked reductions in mortality rates from CHD, all cardiovascular diseases, and all causes.”
–-Jeremiah Stamler, MD, the Chairman of the Department of Preventive Medicine of the Feinberg School of Medicine (Northwestern University), 1998
Between 1970 and 1995 annual consumption decreased from 310 to 235 eggs per person in US.
BTW, Richard: it’s “Mie”, not “Mike”. I’m not using my own name, but rather referring to a local dialect in Finland (which you, being from Finland too you recognize & possibly even appreciate).
I find the way Dr Dayspring perceives heart disease highly problematic. Cholesterol is an issue of cumulative exposure. Whether someone has “normal” cholesterol at his/her last decades of the life span is less irrelevant. Besides, cholesterol levels start to plummet after the age of 65-70 due to metabolic changes in the intestine resulting lower absorption and synthesis of cholesterol. The cumulative exposure model was highlighted by the ATP-3 panel already in 2004:
“Only in populations that maintain very low levels of serum cholesterol, e.g., total cholesterol <150 mg/dL (or LDL cholesterol <100 mg/dL) throughout life do we find a near-absence of clinical CHD.19,23-28"
I thought the nonsense arguments about people dying with “normal” cholesterol levels was a thing of the cholesterol skeptics of the 1970s. There’s not a single verifiable case of atherosclerosis among people with heterozygot PCSK9 knock-out mutation who have their life-long LDL around 50s and 60s (1.5-1.8mmol/l).
https://www.youtube.com/watch?v=DFMtoafT70c (15.20min & onwards)
Moreover, coronary heart disease was nearly non-existent in the rural China of the 1980s where people kept consistently their mean total cholesterol levels around 127mg/dl. Brown & Goldstein elucidated in 1985:
“Several lines of evidence suggest that plasma levels of LDL-cholesterol in the range of 25-60 mg/dl (total plasma cholesterol of 110 to 150 mg/dl) might indeed be physiologic for human beings. First, in other mammalian species that do not develop atherosclerosis, the plasma LDL-cholesterol level is generally less than 80 mg/dl. In these animals the affinity of the LDL receptor for their own LDL is roughly the same as the affinity of the human LDL receptor for human LDL, implying that these species are designed by evolution to have similar plasma LDL levels. Second, the LDL level in newborn humans is approximately 30 mg/dl, well within the range that seems to be appropriate for receptor binding. Third, when humans are raised on a low fat diet, the plasma LDL-cholesterol tends to stay in the range of 50 to 80 mg/dl. It only reaches levels above 100 mg/dl in individuals who consume a diet rich in saturated animal fats and cholesterol that is customarily ingested in Western societies”
I am somewhat confused.
As someone who has a LDL-C of 190 and LDL-P of 2100 with 9% of the 2100 being small dense, and a triglycerides of 28 and & HDL-C of 95…I thought I was healthy. But Dayspring & Underburg do not mention particle size as being a marker for CVD…only total particle number of LDL.
The rupturing of plaque: “The fact is that the real cause of heart attack is the presence of small, obstructive cholesterol laden plaques that suddenly rupture and rapidly induce blood clots that obstruct the artery, which causes blood flow to the heart to be blocked, leading to injury or death of heart muscle”.
This is the first I have heard of rupturing plaque. I was under the impression LDL particle number was far less important as compared to the percentage of small dense LDL….which appears to be highly atherosclerotic…based on my research. Do not the small dense irritate the vascular system, causing the body to repair the irritations over and over…thus building up plaque over the most egregious insult to the vascular wall…leading to a choked off artery? Is the rupturing of plaque by D & U the same function stated differently?
Three years ago, my numbers said I was headed for a heart attack…LDL-P was over 4000 with fully 70% was small dense. And the other numbers said heart attack just around the corner.
Should I be concerned with a LDL-P at 2100? Thanks
Dexter, your high NMR LDL-P is similar to mine, along w/ ideally low risk levels on all other lipid NMR markers and total absence of metabolic disorders. This seems to occur to some of the long-term LCHF eaters, anecdotally speaking.
But for those eating the Standard-American-Diet (SAD), a high LDL-P seems to flag a CVD risk, even in those w/ normal LDL-C. And upon further examination, often cited by Dayspring’s discordant case analysis, these SAD usually have high TG & low HDL and accompanied by some metabolic syndromes. LDL-P seems like a valid proxy for CVD for SAD.
Is high LDL-P equally valid for CVD in LCHF, in the absence of other risky markers and metabolic syndromes? I am unsure, as most of the clinical data, research and resulting recommendations is from SAD paradigm. Is LDL-P an equally valid diagnostic indicator for all LCHFers?
Perhaps the high LDL-P in LCHF reflects a metabolic function in some LCHF, a benign, not necessarily a malignant condition. One can do n=1 self-experiment by varying the carb intake, thyroid level, selenium and etc to shoot for a LDL-P range from SAD model.
As long as all other lipid bio-markers (especially the TG/HDL ratio) are at good level and metabolically healthy, the odds are on my side. I will wait for other LCHF chase outcomes and not fret about my high LDL-P. And if one is really worried about the aberrantly high LDL-P, then take a ultrasound CIMT for plaque buildup directly, instead of using a proxy.
DEFINITELY anecdotal only Peter! I have HeFH and went onto LCHF. Think I’m the only one in the world what dunnit! The more animal, coconut and olive fats I ate the lower my LDL got. BUT, of course, no-one cares, even though Lancet has all my astounding results. My son, who is a sportsman, refused LCHF, and over this past Christmas at 34 had quintuple bypass surger. I was floored. Now his hereditary condition has stabilised on high fat, although, he will not say a word of this to his cardiologist. He was prescribed 80 mg Crestor and almost died on that alone. RHABDOMYLOSIS. anyway nobody cares. BUT, I have the proof.
The problem with low-carbers is that they do not know the history nor the foundation of the diet-heart research. The eastern Finnish cohort in the 7CS showed highest CHD mortality in the world at the baseline and subsequent follow-ups. Abdominal obesity and metabolic syndrome was extremely infrequent in the cohort which was comprised mainly of very hard-working timbermen. The participants in the cohort had never visited MickeyDee’s nor ever had a can of coca-cola in their life. Second observation comes from the nomadic Kirghiz pastorals who ate lot of organic, grass fed beef and drank a lot of organic whole-milk. Kuczynski asserted that:
“They get arteriosclerosis in an intense degree and often at an early age as shown by cardiac symptoms, nervous disordes, typical changes of the peripheral vessels, nephrosclerosis and, finally, apoplectic attacks. Even in men thirty-two years old I frequently observed arcus senilis”
.Stamler refers to Kuczysnki:
“Kuczynski (1925) reported on an Asian population at the opposite end of the dietary spectrum – nomadic Kirghiz plainsmen who habitually consumed large amounts of meat and milk. He noted high incidence of obesity, premature extensive atherosclerosis, contracted kidney, apoplexy, and arcus senilis. Their urbanized kinsmen, subsisting on more varied fare, did not exhibit such severe vascular disease”.
If one wants to understand why the AHA is concerned about SFA and dietary cholesterol, this landmark article by Jeremiah Stamler (1978) might help. Stamler asks whether the AHA has got it all wrong. Stamler sums up experimental evidence, prospective cohorts; he notes how intraindividual ( and interindividual) variation messes the results in homogenous cohorts with individual as a unit of measure. Moreover, Stamler refers to autopsy studies from low-risk population and addresses the philosophy of science in analyzing whether the ideals of science (randomized trial on humans) can be brought unproblematically into the diet-heart framework.
New meta-analysis on low-carb diets:
Low-carbohydrate diets impair flow-mediated dilatation: evidence from a systematic review and meta-analysis
When it comes to heart disease, I get the sinking feeling that I have been sold an old nag for a premium price. Thank you so much much for debunking myths. Day by day, I realize more and more that there is no way to cheat on my diet and get away with it. I am reminded of Newton’s Law – “For every action there is an opposite and equal reaction.” In my diet, it seems poor choices accumulate despite all good signs to the contrary.