Shifted my LDL cholesterol from borderline pattern B over solidly into the green of pattern A. Did this by donating whole blood 4 times in a six months time period. Had to rotate between Red Cross and Community Blood Center. The small dense damaged cholesterol gets removed with the whole blood and then your body makes all brand new cholesterol.
I am interested in this. Can you give a detailed understanding. So Ldl C which is usually fir people on keto like > 200 . Does it decrease by giving blood ?
Always interested in your progress, Dave, as I suspect that I am a LMHR (68y.o. fem, non-smoker, Trig 0.71mmol/L, Hdl 2.55mmol/L, Ldl 4.57mmol/L, yes I'm in Canada). Very interested in the results of the study! Of course, my doctor is advocating a statin, but as a senior female, whose mother and grandmother survived without statins to their mid-90's, not sure if it is in my best interests. Unfortunately, NMR Lipid panel and CAC are unavailable to me to confirm my health status. I've been ketovore for nearly 3 years, other numbers are great, feel the best in years! Thanks for all your efforts in this field!
Hi, Bety, In my case I eat Whole Plant Based Diet. No oils. My TC (6 months ago) 4.2mmol/L (164mg/L), HDL 2.1mmol/L, LDL 1.9mmol/L (73mg/L), Trig. 0.36 mmol/L. I track and weight everything, no mistake - everything perfect, but was surprised about my TC. I'd have expected to to had them slightly better - not only 164mg/L but 150, 145. My 2 latest tests showed me worse data: TC 4.6mmol/L (178mg/L), HDL 1.9mmol/L, LDL 2.4mmol/L (93mg/L), Trig. 0.42 mmol/L and I've started to be panicking up to now because I misunderstood something. @Dave Feldman helped me a lot with his investigations. (I also work in technical area as he - in science/physics and this is my hobby. I wanted to do exactly what he did (prior I found his videos) . I think I'll re-introduce the olive oil again that I stopped eating 18 months ago +I'll add more avocados. Jarek/Europe.
I don't understand the massive focus again on the LDL-C value. My understanding was that the LDL value on its own was pretty meaningless, and one would need to look at the LDL particle counts for bigger and smaller LDLs respectively. Also, why is there only a focus on ApoB, and not on Apo-A1, and the ApoB/Apo a-1 ratio.
Because risk follows ApoB. The ratio is meaningless and not employed in clinical practice. It is possible that small particles are more atherogenic, but it has been conclusively proven that both can cause the formation of plaque. FH patients tend to only have the large fluffy LDL and they are at the highest risk because of the sheer number of particles.
For those of us who have moved along with the times and using decimal system, and wondering what the hell a Glucose score of 90 mg/dl or less means, according to a calculator I found, it is about 5 mmol/l ot less. Divide your mg/dl by 5 to get mmol/l, or multiply your mmol/l number by 18 to get mg/dl.
What I don't understand is, why do I keep hearing that 50% of people who have a heart attack have low to normal Cholesterol? Personally, I developed some plaque with a LDL of 82. Would it have really made that much difference going from 82 to a lower number?
If ~50% of people with high LDL get a heart attack and 50% with lower LDL get a heart attack, it's just not a good marker. Just flip a coin. Also: there is risk with low LDL and very high LDL. Total mortality goes up below 130 and above 190 or so. But I guess they like to ignore those stats. Maybe the reason people with LDL of 10 don't develop a heart attack is be cause they die early. Of infections and cancer. At least that's what the stats suggest.
I am interested in the graphing done by Precision Health as it makes some of this confusion on blood reports more understandable. My doctor has never sat down with me to discuss numbers, only calls in a statin which I refuse to take as after two years on keto I am finding that the high risk factors (triglycerides, glucose, HDL, etc.) are improving over time though my LDL is rising. Is that bad, is that good, I don't really know.
Thanks, rikwen96, for your feedback! Our goal was to create a highly visual report that "makes sense" and focuses on you. As we discussed in the video, LDL risk is more a matter of "how high for how long" rather than an individual number. It's also helpful to know if there is evidence of blockage ("plaque") in your arteries. You should discuss these things with your physician to get a better perspective of your LDL values.
Does anybody know if anything like this exists in the UK, please? I desperately need a test like this, as I have FH, osteoporosis and gut issues. I'm at a point where I'm utterly lost. My cardiologist just throws Statins at me, and they are killing me, literally. Any advice would be very welcome. Thanks. Ben.
Has PCSK9 extreme cholesterol lowering been tested long enough to reveal whether people will succumb to other problems such as Alzheimer's, reduced longevity, higher incidence of infections, cancer, etc? For example, your heart might be ticking beautifully on PCSK9s but how wonderful is that if your brain is "dead?"
I would love for one or both of these guys meet with Dr Andrew Huberman and or David Sinclair. What fascinating talks they would be. I would love to see both AH and DS labs like Dave shared with us. I remember them scratching their heads over cholesterol. I wanted to scream “Dave Feldman, Dudes!!! You need to sit down with him!!!” Great labs Dave👍 I’m a 60 yr old female and mine are similar except I don’t have high cholesterol “genetically”.
Very nice presentation and the trending graphs would be useful to most people. As an engineer I usually want the full detail as well. Also following the LMHR work closely, and more recent research showing a J curve for ACM vs. LDL-C makes me question the US and EU cutpoints for LDL. Beyond LP-IR, Met-Syn markers, and a standard lipid panel, do you consider Apo B a reasonable proxy for a CAC, or is a scan always useful?
Thanks, Chris D, for your comment. ApoB or LDL particle number (LDL-P) are more accurate measurements of the number of atherogenic particles in blood versus LDL-C. As such, persistently high ApoB or LDL-P has a much stronger association with the presence of plaque or cardiovascular events (heart attack, stroke) than LDL-C. The impact of high ApoB or LDL-P depends on how long that exposure lasts. The more years high ApoB or LDL-P is present, the more significant the effect on plaque formation. We don't have enough lab data to answer how long these values have been high in many cases. That's where some type of non-invasive imaging to detect plaque may be helpful. If CAC scoring shows a value above the 75th percentile for age, gender, and ethnicity, then the person has evidence of cardiovascular disease. In that case, more aggressive management is an appropriate consideration. If a person has a high ApoB or LDL-P and the duration of exposure is unknown non-invasive imaging may be helpful. When to get a CAC is artistic. CAC may not detect plaques in the coronary arteries in relatively younger individuals. A zero CAC does not rule out plaque in men under 45 and women under 55. In these age ranges, noncalcified plaques are often present but are undetectable by CAC. As age increases, a zero CAC takes on greater meaning. That's why many advise considering CAC in men 45 or older and women 55 or older.
I am glad that Dr. Cromwell is viewing and responding to these comments. Here are mine: 1. I dislike that the marker for metabolic syndrome in men is 40" and not some ratio to height. A 40" waist is far different for a man 5'8" tall vs. one 6'8" tall. 2. I dislike that the suggested benefit of low LDL-C is continued "through zero." While that may be true for cardiovascular risk, it is not so for other causes of morality. While I understand that this report does focus on cardiovascular risk, I believe that overall risk of dying from any and all causes is of paramount importance. 3. I dislike the fallback position that low LDL-C is necessarily better for CVD risk based upon "research." The point of Dave's research and hypothesis is exactly the opposite. So, yes, having high LDL-C is a "risk factor" while eating the Standard American Diet. However, there is NO research about any "risk" of having high LDL-C while eating a low carb, ketogenic diet. I believe that I have a high CAC score from eating a crummy high carb diet for 56 years, not because of my Low Carb / ketogenic diet for the next 7 years. Unfortunately, I can't prove this from only one data point, and I'll need to wait a few more years to check any actual plaque progression. So Dave's LMHR volunteers (and I) are guinea pigs trying to advance the science. 4. While I applaud Precision Health Reports for developing this software, etc, I am disappointed that such information is not already provided by my top tier U.S. hospital system during my annual physical.
Agree on your points. I believe my CAC of 77 is due to my horrid diet of 47 years. Thanks to the powers that recommended HCLF in the late 70s, precisely when I was a developing human. I only have a single data point as well, but I truly hope my ketogenic lifestyle is not creating further damage as a LMHR. Anxiously monitoring Dave’s research!
Thanks for your feedback! The gender and ethnicity-specific Metabolic Syndrome criteria we show are just a reflection of the current guidelines and in no way our interpretation of what is or isn't. We do agree that the categorical approach is a bit clunky. What is even better is the Metabolic Syndrome Severity score which is why we reflect as much, or even more, on that more granular score. We, too, are disappointed that this isn't well used by ALL physicians around the country. Ask you doctor to get in touch with us!
I generally follow a Paleo diet, limit my carbs to approximately 75 grams per day, and restrict my calorie intake to a daily 8-10 hour window (time-restricted eating).
@@williamcromwell2699in your opinion is LDL-C a more important marker than Apo-b? Also, do you take in consideration in the score result, Apo-a VS Apo-b? Thanks a lot and kudos on such a great talk, to both you and Dave.
My last visit with the cardiologist , the dr. was shocked that my LDL 166, Trig 179 and HDL 43. I've been on a low carb diet for about 2 yrs. You can say I'm a LMHR (BMI of 20.5). He asked me to get off the keto diet. No way in hell I'm giving up my keto. Why is my Trig so high?
GLUC: 95. CHOL: 386, HDL: 68, LDL: 302, TRIG: 79. I lift weights at home and calisthenics. So far no cramps. This is a good video: ua-cam.com/video/R6FGaR7vOHk/v-deo.html
Like in the other post using the proper plural of data, thank you for pronouncing LabCORP correctly, and not Lab-CORE. Man, that drives me up a wall! That, and when folks pronounce the L in salmon.
Protect you LDL from oxidation with a combination of, paradoxically, a low PUFA, high saturated fat diet, and lots of antioxidants (wild blueberries and 100% pomegranate juice).
this seems overly complex to confuse the average punter. 0 CAC score would beat nearly any other measurement by an order of magnitude. We also know that diabetes is about 8 times more correlated to heart disease than any LDL score while high blood pressure is about 5-6 times more correlated. Notice I never mentioned risk? That is due to no level of 'science' done on this topic to attribute any causation.
Thanks, Scott W, for your comment. I agree that CAC score, high blood pressure, and diabetes are critical factors to consider. That's why the Cardiometabolic Risk Report includes: 1. All major risk factors (age, smoking, blood pressure, family history of early vascular disease, lipids) 2. Clinical conditions with similar heart attack and stroke risk versus those with existing cardiovascular disease (diabetes, metabolic syndrome, chronic renal failure, abdominal aortic aneurysm) 3. Clinical history of symptomatic blockage (angina, TIA, claudication, heart attack, stroke, acute coronary syndrome) or blockage requiring intervention (angioplasty, stent, by-pass, or atherectomy) 4. History of invasive (angiography) or non-invasive imaging (CAC, other modalities) 5. Risk Enhancing Factors (over 30 unique guideline identified clinical and biomarker factors that further increase cardiovascular risk) 6. Insulin resistance factors 7. Biometrics and biomarkers All of these things must be considered to provide a complete assessment of a person's risk.
@@williamcromwell2699 Again, and I know this is a few days late, but none of these marker can be given status of 'risk'. Increased 'incidence' or 'association' sure but the standards required to show risk have not really been met (the whole metabolic ward lock in study level). Most of this is at best weak epidemiology and other levels might be in vitro mechanistic studies. Thus you are dealing with a large amount of 'might' develop rather than there is physical examples of progression such as the CAC formation of the hardened plaque to protect the formed soft plaque. On a slightly different topic what are your thoughts on the Vasa Vasorum playing a larger role in the soft plaque formation than in the standard model given to the public for decades?
@@scottw2317This is sound. As far as what causes atherosclerosis, it is oxidized cholesterol, the best currently available marker of this being oxLDL which is the only cholesterol test that you in fact do want to minimize.
@@JasonActualization without glycation damage continuously taking out the glycocalyx and inflammation at these locations the oxidised LDL do not show the same issues.
@@scottw2317 Pomegranate juice in a prospective experiment has been shown to, as the only intervention, not just reduce the progression of, but reverse plaque build-up within a year. It did this since it's one of the most potent antioxidants on the planet and reduces oxLDL. In rodents they have also directly fed them oxidized cholesterol and it reliably induced atherosclerosis. Heart disease became prevalent when we began eating seed oils that greatly potentiate the oxidation of LDL. Cigarettes increase risk of heart disease because the chemicals can oxidize LDL. I'd definitely be interested to see what your oxLDL level is and what your diet consists of. I'm glad people are waking up to this!
I do not know wheather it is SAD or funny, that the modern medicine does not recognise a truly healthy ancestral phenotype in a modern surrounding as it walks in the same room. Now add some topping. Take a person who is highly motivated and has the ability to hack a condition to the max. The mentality of a professional ultra athlete of just a typical world-class athlete. Such motivation can be seen in all areas of human endevour. Any competitive sports sees this happen, an academic pursuit for a career or a succesful economic investor taking sizable risks is no different from what Dave and many more is doing. Unlike Dave we do not have to say we are cautious. Dave has to. What happens when a poor guy like myself is willing to go the extra mile, making some radical sacrifices without aiming for anything tangiable? Does this not come to the minds of orthodox academics that this must lead into improved health outcome and in real time and possibly to some longevity promoting epigenetics in the future?
It is a shame to see people putting themselves at needless cardiovascular risk because they want to believe in Dave‘s unproven hypothesis for lean mass hyper responders. Even the current study when concluded and if successful will show nothing other than if you are on an unhealthy diet your risk of forming plaque in the next one to two years is low. The study excluded most people with positive CAC scores (anyone in the 75th percentile for their age or above) so it is meaningless that the people that were enrolled did not have abnormal CAC scores. Anyone who did was excluded from the study because they fell within the definition of existing ASCVD disease.
I have been following Dave Feldman for a while but stopped at some point because (as a scientist myself) I realized that he is off target. Like Ivor Cummins, he has an idea in his head that will probably prove to be disastrous in the long-run. The metabolic part I agree with - I have no issue with that at all. However, he is ignoring the huge problem caused by saturated fats! His ApoB is 183 - *183!* - and he ignores it. There is a way to satisfy both the metabolic AND lipidemiological aspects of the problem, yet few want to implement the solution. Here it is: strip out the saturated fats.
These are great points. I think you cracked it! Not easy but for those who are serious about this there's no other way right now. I'm sure new protein-rich foods can be developed for those who are interested in preserving their health.
Rose are you off target. Looking for answers and truth bc we can not get such from the so called experts is not sticking to an idea or one hypothesis ! You obviously have not followed Dave or even watched/listened to this whole video. Seems like you are the one who is stuck on an idea. And if your idea of saturated fat is true why are most of us who listened to such and were or are in bad shape/health here looking for answers. It's been close to 80 yrs now on the saturated fat blame and how has that been working?? Start with President Eisenhower. I am old enough to remember how removing saturated fat helped him ! I caught you on another thing, why are you here if you quit following Dave ? You're a fake no doubt.
Humans have been eating a high saturated fat diet for eons and never worried about APOb. Why is eating saturated fat a problem now? Maybe because it's not the proximal cause of cvd.
reports like that shown @14:50, using arbitrary cut off points, and not building a profile from direct values, are old school orthodoxy, and barely worth the paper where they are printed on. brrrrr
No examination of the actual underlying science, current "guidelines" are weak not even taking into account a CAC score or even exercise when examining CV risk. Case of presentation over substance, strip out the pretty pictures and the age old traffic light approach and you are left with an expensive test that is built on at best dubious science. Tagging Dave Feldman with a CV risk of high demonstrates the inadequacies of the approach and would frighten LMHR of which I am one - TC 606 LDL-C 506 Trigs 66 HDL-C 85 with all other biomarkers excellent and none of the 5 metabolic syndrome markers anywhere near exceeded. There's a huge amount more to this discussion, which is not going to be solved by what amounts to a sales pitch; my cash will definitely stay in my bank account until Dave's next study is complete to determine if in fact a very high LDL-C in a LMHR is in fact harmful or beneficial in the context of the immune system's operation particularly in the over 65s - time will tell, but this guy seems to adopt the msm's approach to the cause of CVD I would suggest a read of The Clot Thickens by Dr Malcolm Kendrick for an examination of the thrombotic approach, these lipid guys never have an answer to why you only get CVD in arteries and not veins despite the concentration of LDL-C being consistent in both arterial systems, he doesn't even discuss Pattern A and Pattern B LDL, very disappointed that DF would engage with this guy, listen to David Diamond and Paul Mason instead.
DF is NOT a biochemist OR a physician. I think his approach is extremely irresponsible. If you are serious about your health but insist upon keto, cut out all of the saturated fats and animal products. It's not pleasant, but it's effective.
@@maarten7 Yes, of course. You propose to just go full on evolution-denial. It's interesting how the same people will bash flat eathers, climate change deniers etc., but suggest to avoid the evolutionarily-fitted diet as much as possible.
@@Peace_Guard We are omnivores (including having the dentition of omnivores) with the intestinal tract of herbivores. It's possible that high-fat diets were necessary for evolutionary brain-growth (although so was tool-making to kill those animals) but we are now striving for longevity. Eating a low sat-fat plant-based diet will most surely extend my time upon this mortal coil. I'm not worried about what's going to happen in another 20,000 years.
@@lamondaforestry Do your research before making an asinine comment - Dr Paul Mason obtained his medical degree with honours from the University of Sydney, and also holds degrees in Physiotherapy and Occupational Health. He is a Specialist Sports Medicine and Exercise Physician. Listen and learn....
I was LMHR before Dave came along and made me feel like I wasn't a freak. My DNA testing through Color Genomics came back with NO RISK of CVD genetically. Still seeking answers but MY DR REFUSES TO PRESCRIBE A GLUCOSE MONITOR UNLESS I HAVE T2 DIABETES!!!
@@JWB671 To know post prandial glucose levels and sustained blood glucose levels- and probable insulin response. Prevent pre-diabetes. They don't allow us to know our blood sugar levels until AFTER it's too lat (I'm in the US).
Start with a CAC. They're cheap. Then get a lipid panel with ApoB and Lp(a). If you have taken care of the metabolic piece (and you should change doctors if yours won't prescribe a CGM) you can make a realistic assessment. But don't be a fool and ignore the blood-lipid numbers Huge mistake.
Shifted my LDL cholesterol from borderline pattern B over solidly into the green of pattern A. Did this by donating whole blood 4 times in a six months time period. Had to rotate between Red Cross and Community Blood Center. The small dense damaged cholesterol gets removed with the whole blood and then your body makes all brand new cholesterol.
I am interested in this. Can you give a detailed understanding. So Ldl C which is usually fir people on keto like > 200 . Does it decrease by giving blood ?
Always interested in your progress, Dave, as I suspect that I am a LMHR (68y.o. fem, non-smoker, Trig 0.71mmol/L, Hdl 2.55mmol/L, Ldl 4.57mmol/L, yes I'm in Canada). Very interested in the results of the study! Of course, my doctor is advocating a statin, but as a senior female, whose mother and grandmother survived without statins to their mid-90's, not sure if it is in my best interests. Unfortunately, NMR Lipid panel and CAC are unavailable to me to confirm my health status. I've been ketovore for nearly 3 years, other numbers are great, feel the best in years! Thanks for all your efforts in this field!
Thanks, BettyP541, for your comment. Perhaps your physician has insights into medical centers that offer CAC testing in your area/province.
Hi, Bety,
In my case
I eat Whole Plant Based Diet. No oils. My TC (6 months ago) 4.2mmol/L (164mg/L), HDL 2.1mmol/L, LDL 1.9mmol/L (73mg/L), Trig. 0.36 mmol/L.
I track and weight everything, no mistake - everything perfect, but was surprised about my TC. I'd have expected to to had them slightly better - not only 164mg/L but 150, 145.
My 2 latest tests showed me worse data:
TC 4.6mmol/L (178mg/L), HDL 1.9mmol/L, LDL 2.4mmol/L (93mg/L), Trig. 0.42 mmol/L and I've started to be panicking up to now because I misunderstood something. @Dave Feldman helped me a lot with his investigations. (I also work in technical area as he - in science/physics and this is my hobby. I wanted to do exactly what he did (prior I found his videos) .
I think I'll re-introduce the olive oil again that I stopped eating 18 months ago +I'll add more avocados.
Jarek/Europe.
Excellent conversation. Thank you!
Thanks, Sean.
A very nice and balanced discussion! Enjoyed getting all those new perspectives :-)
I don't understand the massive focus again on the LDL-C value. My understanding was that the LDL value on its own was pretty meaningless, and one would need to look at the LDL particle counts for bigger and smaller LDLs respectively. Also, why is there only a focus on ApoB, and not on Apo-A1, and the ApoB/Apo a-1 ratio.
Because risk follows ApoB. The ratio is meaningless and not employed in clinical practice. It is possible that small particles are more atherogenic, but it has been conclusively proven that both can cause the formation of plaque. FH patients tend to only have the large fluffy LDL and they are at the highest risk because of the sheer number of particles.
🙌 We may be a little biased, but that was FAN-TASTIC!
Except that your report is flawed..
What would be the lipid numbers of cultures that have been long-time ketogenic practitioners, ex. Masai
For those of us who have moved along with the times and using decimal system, and wondering what the hell a Glucose score of 90 mg/dl or less means, according to a calculator I found, it is about 5 mmol/l ot less. Divide your mg/dl by 5 to get mmol/l, or multiply your mmol/l number by 18 to get mg/dl.
Amen to that. I have even created a 'cheat sheet' with my own values converted to 'Murican values. I'm in a rational country 😄
What I don't understand is, why do I keep hearing that 50% of people who have a heart attack have low to normal Cholesterol? Personally, I developed some plaque with a LDL of 82. Would it have really made that much difference going from 82 to a lower number?
If ~50% of people with high LDL get a heart attack and 50% with lower LDL get a heart attack, it's just not a good marker. Just flip a coin. Also: there is risk with low LDL and very high LDL. Total mortality goes up below 130 and above 190 or so. But I guess they like to ignore those stats. Maybe the reason people with LDL of 10 don't develop a heart attack is be cause they die early. Of infections and cancer. At least that's what the stats suggest.
No, it wouldn't. You need to lower your oxidation of LDL. Start drinking a shot of 100% pomegranate juice each day.
@@JasonActualizationwhat causes oxidation of LDL?
I think I saw that you HDLc on this test, the lmhr specified a minimum of 80 .. does this mean you no longer fit your own lmhr model ?
Dave Feldman, have you ever tested what happens when you donate blood multiple times in a specific time.?
I am interested in the graphing done by Precision Health as it makes some of this confusion on blood reports more understandable. My doctor has never sat down with me to discuss numbers, only calls in a statin which I refuse to take as after two years on keto I am finding that the high risk factors (triglycerides, glucose, HDL, etc.) are improving over time though my LDL is rising. Is that bad, is that good, I don't really know.
Thanks, rikwen96, for your feedback! Our goal was to create a highly visual report that "makes sense" and focuses on you. As we discussed in the video, LDL risk is more a matter of "how high for how long" rather than an individual number. It's also helpful to know if there is evidence of blockage ("plaque") in your arteries. You should discuss these things with your physician to get a better perspective of your LDL values.
ldl rises on keto.look up cardiologist dr Ali nadir videos he explains in depth
I personally think the keto approach is a form of Russian roulette. I agree that it's "how high for how long" when it comes to LDL.
Longer detailed videos are good! Any chance of a quick, to-the-point presentation for us time starved folks?
Does anybody know if anything like this exists in the UK, please? I desperately need a test like this, as I have FH, osteoporosis and gut issues. I'm at a point where I'm utterly lost. My cardiologist just throws Statins at me, and they are killing me, literally. Any advice would be very welcome. Thanks. Ben.
Has PCSK9 extreme cholesterol lowering been tested long enough to reveal whether people will succumb to other problems such as Alzheimer's, reduced longevity, higher incidence of infections, cancer, etc? For example, your heart might be ticking beautifully on PCSK9s but how wonderful is that if your brain is "dead?"
Yes, all of that was tested in the initial study and in the follow up of these studies. There were no adverse consequences.
I will get this. Thanks.
I would love for one or both of these guys meet with Dr Andrew Huberman and or David Sinclair. What fascinating talks they would be. I would love to see both AH and DS labs like Dave shared with us. I remember them scratching their heads over cholesterol. I wanted to scream “Dave Feldman, Dudes!!! You need to sit down with him!!!”
Great labs Dave👍 I’m a 60 yr old female and mine are similar except I don’t have high cholesterol “genetically”.
I don't think Dave Feldman's work intersects with that of David Sinclair. If anything, Sinclair is moving in the direction of WFPB diet for longevity.
@@maarten7I believe that was his point, i.e., that it would be an interesting discussion.
wish results were not blurry
Blurry to say the least. Following an animal-based keto diet with those numbers is insane.
@@maarten7 I meant blurry as in literally can't see them
What do you do if you can't afford regular blood tests that insurance doesn't cover?
Go to a community clinic where they serve low-income people.
Very nice presentation and the trending graphs would be useful to most people. As an engineer I usually want the full detail as well. Also following the LMHR work closely, and more recent research showing a J curve for ACM vs. LDL-C makes me question the US and EU cutpoints for LDL. Beyond LP-IR, Met-Syn markers, and a standard lipid panel, do you consider Apo B a reasonable proxy for a CAC, or is a scan always useful?
Thanks, Chris D, for your comment.
ApoB or LDL particle number (LDL-P) are more accurate measurements of the number of atherogenic particles in blood versus LDL-C. As such, persistently high ApoB or LDL-P has a much stronger association with the presence of plaque or cardiovascular events (heart attack, stroke) than LDL-C. The impact of high ApoB or LDL-P depends on how long that exposure lasts. The more years high ApoB or LDL-P is present, the more significant the effect on plaque formation.
We don't have enough lab data to answer how long these values have been high in many cases.
That's where some type of non-invasive imaging to detect plaque may be helpful. If CAC scoring shows a value above the 75th percentile for age, gender, and ethnicity, then the person has evidence of cardiovascular disease. In that case, more aggressive management is an appropriate consideration.
If a person has a high ApoB or LDL-P and the duration of exposure is unknown non-invasive imaging may be helpful. When to get a CAC is artistic. CAC may not detect plaques in the coronary arteries in relatively younger individuals. A zero CAC does not rule out plaque in men under 45 and women under 55. In these age ranges, noncalcified plaques are often present but are undetectable by CAC. As age increases, a zero CAC takes on greater meaning. That's why many advise considering CAC in men 45 or older and women 55 or older.
@@williamcromwell2699 thank you!
I am glad that Dr. Cromwell is viewing and responding to these comments. Here are mine:
1. I dislike that the marker for metabolic syndrome in men is 40" and not some ratio to height. A 40" waist is far different for a man 5'8" tall vs. one 6'8" tall.
2. I dislike that the suggested benefit of low LDL-C is continued "through zero." While that may be true for cardiovascular risk, it is not so for other causes of morality. While I understand that this report does focus on cardiovascular risk, I believe that overall risk of dying from any and all causes is of paramount importance.
3. I dislike the fallback position that low LDL-C is necessarily better for CVD risk based upon "research." The point of Dave's research and hypothesis is exactly the opposite. So, yes, having high LDL-C is a "risk factor" while eating the Standard American Diet. However, there is NO research about any "risk" of having high LDL-C while eating a low carb, ketogenic diet. I believe that I have a high CAC score from eating a crummy high carb diet for 56 years, not because of my Low Carb / ketogenic diet for the next 7 years. Unfortunately, I can't prove this from only one data point, and I'll need to wait a few more years to check any actual plaque progression. So Dave's LMHR volunteers (and I) are guinea pigs trying to advance the science.
4. While I applaud Precision Health Reports for developing this software, etc, I am disappointed that such information is not already provided by my top tier U.S. hospital system during my annual physical.
Agree on your points. I believe my CAC of 77 is due to my horrid diet of 47 years. Thanks to the powers that recommended HCLF in the late 70s, precisely when I was a developing human. I only have a single data point as well, but I truly hope my ketogenic lifestyle is not creating further damage as a LMHR. Anxiously monitoring Dave’s research!
Thanks for your feedback!
The gender and ethnicity-specific Metabolic Syndrome criteria we show are just a reflection of the current guidelines and in no way our interpretation of what is or isn't. We do agree that the categorical approach is a bit clunky. What is even better is the Metabolic Syndrome Severity score which is why we reflect as much, or even more, on that more granular score.
We, too, are disappointed that this isn't well used by ALL physicians around the country. Ask you doctor to get in touch with us!
Dr. Cromwell, what sort of diet to you adhere to?
I generally follow a Paleo diet, limit my carbs to approximately 75 grams per day, and restrict my calorie intake to a daily 8-10 hour window (time-restricted eating).
@@williamcromwell2699 Many thanks for your reply. 🌟
@@williamcromwell2699in your opinion is LDL-C a more important marker than Apo-b? Also, do you take in consideration in the score result, Apo-a VS Apo-b? Thanks a lot and kudos on such a great talk, to both you and Dave.
@@MarillionadooxLDL is most important, ideally you want
@@JasonActualization Thanks a lot, I'll look into which la has that specific test, as the one I use simply does not do such a thorough job.
My last visit with the cardiologist , the dr. was shocked that my LDL 166, Trig 179 and HDL 43. I've been on a low carb diet for about 2 yrs. You can say I'm a LMHR (BMI of 20.5). He asked me to get off the keto diet. No way in hell I'm giving up my keto. Why is my Trig so high?
Is it always high? Fasting period before the blood work can influence. Dave Feldman has a video on this somewhere. Roughly 12h was a good time, IIRC.
You might want to try using a continuous glucose monitor for a few weeks to see if something in your diet is sabotaging your progress.
So do you consider taking statins? I have similar values and phenotype. I started a 20mg a week ago. So far, so good.
No muscle issues? I like that they're anti-inflammatory. My claves cramped so bad I couldn't walk for days after my 1st leg day on statins.
Statins?! No!!! Why would you??
@@spin564 lol ;) ikr
GLUC: 95. CHOL: 386, HDL: 68, LDL: 302, TRIG: 79. I lift weights at home and calisthenics. So far no cramps. This is a good video: ua-cam.com/video/R6FGaR7vOHk/v-deo.html
I began rosuvastatin 20mg and adjusted my diet (low-carb, not saturated fats or animal products.) The results have been amazing.
I thought you were in your late 30s, you look amazing for 48 here, holy hell
Praise the Feldman
Like in the other post using the proper plural of data, thank you for pronouncing LabCORP correctly, and not Lab-CORE.
Man, that drives me up a wall!
That, and when folks pronounce the L in salmon.
They all look competent, yet you find so many different opinions. What is a man supposed to do?
Protect you LDL from oxidation with a combination of, paradoxically, a low PUFA, high saturated fat diet, and lots of antioxidants (wild blueberries and 100% pomegranate juice).
Test, test, test.
Don't stress. The cortisol will probably kill you quicker than anything else.
Buried within Feldman's report--have to search for it "Overall cardiovascular disease risk--"high".
this seems overly complex to confuse the average punter. 0 CAC score would beat nearly any other measurement by an order of magnitude. We also know that diabetes is about 8 times more correlated to heart disease than any LDL score while high blood pressure is about 5-6 times more correlated.
Notice I never mentioned risk? That is due to no level of 'science' done on this topic to attribute any causation.
Thanks, Scott W, for your comment.
I agree that CAC score, high blood pressure, and diabetes are critical factors to consider. That's why the Cardiometabolic Risk Report includes:
1. All major risk factors (age, smoking, blood pressure, family history of early vascular disease, lipids)
2. Clinical conditions with similar heart attack and stroke risk versus those with existing cardiovascular disease (diabetes, metabolic syndrome, chronic renal failure, abdominal aortic aneurysm)
3. Clinical history of symptomatic blockage (angina, TIA, claudication, heart attack, stroke, acute coronary syndrome) or blockage requiring intervention (angioplasty, stent, by-pass, or atherectomy)
4. History of invasive (angiography) or non-invasive imaging (CAC, other modalities)
5. Risk Enhancing Factors (over 30 unique guideline identified clinical and biomarker factors that further increase cardiovascular risk)
6. Insulin resistance factors
7. Biometrics and biomarkers
All of these things must be considered to provide a complete assessment of a person's risk.
@@williamcromwell2699 Again, and I know this is a few days late, but none of these marker can be given status of 'risk'. Increased 'incidence' or 'association' sure but the standards required to show risk have not really been met (the whole metabolic ward lock in study level). Most of this is at best weak epidemiology and other levels might be in vitro mechanistic studies.
Thus you are dealing with a large amount of 'might' develop rather than there is physical examples of progression such as the CAC formation of the hardened plaque to protect the formed soft plaque.
On a slightly different topic what are your thoughts on the Vasa Vasorum playing a larger role in the soft plaque formation than in the standard model given to the public for decades?
@@scottw2317This is sound. As far as what causes atherosclerosis, it is oxidized cholesterol, the best currently available marker of this being oxLDL which is the only cholesterol test that you in fact do want to minimize.
@@JasonActualization without glycation damage continuously taking out the glycocalyx and inflammation at these locations the oxidised LDL do not show the same issues.
@@scottw2317 Pomegranate juice in a prospective experiment has been shown to, as the only intervention, not just reduce the progression of, but reverse plaque build-up within a year. It did this since it's one of the most potent antioxidants on the planet and reduces oxLDL. In rodents they have also directly fed them oxidized cholesterol and it reliably induced atherosclerosis. Heart disease became prevalent when we began eating seed oils that greatly potentiate the oxidation of LDL. Cigarettes increase risk of heart disease because the chemicals can oxidize LDL. I'd definitely be interested to see what your oxLDL level is and what your diet consists of. I'm glad people are waking up to this!
I do not know wheather it is SAD or funny, that the modern medicine does not recognise a truly healthy ancestral phenotype in a modern surrounding as it walks in the same room. Now add some topping. Take a person who is highly motivated and has the ability to hack a condition to the max. The mentality of a professional ultra athlete of just a typical world-class athlete. Such motivation can be seen in all areas of human endevour. Any competitive sports sees this happen, an academic pursuit for a career or a succesful economic investor taking sizable risks is no different from what Dave and many more is doing. Unlike Dave we do not have to say we are cautious. Dave has to.
What happens when a poor guy like myself is willing to go the extra mile, making some radical sacrifices without aiming for anything tangiable? Does this not come to the minds of orthodox academics that this must lead into improved health outcome and in real time and possibly to some longevity promoting epigenetics in the future?
It is a shame to see people putting themselves at needless cardiovascular risk because they want to believe in Dave‘s unproven hypothesis for lean mass hyper responders. Even the current study when concluded and if successful will show nothing other than if you are on an unhealthy diet your risk of forming plaque in the next one to two years is low. The study excluded most people with positive CAC scores (anyone in the 75th percentile for their age or above) so it is meaningless that the people that were enrolled did not have abnormal CAC scores. Anyone who did was excluded from the study because they fell within the definition of existing ASCVD disease.
I have been following Dave Feldman for a while but stopped at some point because (as a scientist myself) I realized that he is off target. Like Ivor Cummins, he has an idea in his head that will probably prove to be disastrous in the long-run.
The metabolic part I agree with - I have no issue with that at all. However, he is ignoring the huge problem caused by saturated fats! His ApoB is 183 - *183!* - and he ignores it. There is a way to satisfy both the metabolic AND lipidemiological aspects of the problem, yet few want to implement the solution.
Here it is: strip out the saturated fats.
These are great points. I think you cracked it! Not easy but for those who are serious about this there's no other way right now. I'm sure new protein-rich foods can be developed for those who are interested in preserving their health.
Rose are you off target. Looking for answers and truth bc we can not get such from the so called experts is not sticking to an idea or one hypothesis ! You obviously have not followed Dave or even watched/listened to this whole video. Seems like you are the one who is stuck on an idea. And if your idea of saturated fat is true why are most of us who listened to such and were or are in bad shape/health here looking for answers. It's been close to 80 yrs now on the saturated fat blame and how has that been working?? Start with President Eisenhower. I am old enough to remember how removing saturated fat helped him ! I caught you on another thing, why are you here if you quit following Dave ? You're a fake no doubt.
Humans have been eating a high saturated fat diet for eons and never worried about APOb. Why is eating saturated fat a problem now? Maybe because it's not the proximal cause of cvd.
@@jerseyjim9092Correct. The problem is actually excess PUFA. Oxidized cholesterol causes atherosclerosis.
I get half my daily calories from raw kidney fat. My LDL, triglycerides, LDL, and ApoB are all very low.
reports like that shown @14:50, using arbitrary cut off points, and not building a profile from direct values, are old school orthodoxy, and barely worth the paper where they are printed on. brrrrr
No examination of the actual underlying science, current "guidelines" are weak not even taking into account a CAC score or even exercise when examining CV risk. Case of presentation over substance, strip out the pretty pictures and the age old traffic light approach and you are left with an expensive test that is built on at best dubious science. Tagging Dave Feldman with a CV risk of high demonstrates the inadequacies of the approach and would frighten LMHR of which I am one - TC 606 LDL-C 506 Trigs 66 HDL-C 85 with all other biomarkers excellent and none of the 5 metabolic syndrome markers anywhere near exceeded. There's a huge amount more to this discussion, which is not going to be solved by what amounts to a sales pitch; my cash will definitely stay in my bank account until Dave's next study is complete to determine if in fact a very high LDL-C in a LMHR is in fact harmful or beneficial in the context of the immune system's operation particularly in the over 65s - time will tell, but this guy seems to adopt the msm's approach to the cause of CVD I would suggest a read of The Clot Thickens by Dr Malcolm Kendrick for an examination of the thrombotic approach, these lipid guys never have an answer to why you only get CVD in arteries and not veins despite the concentration of LDL-C being consistent in both arterial systems, he doesn't even discuss Pattern A and Pattern B LDL, very disappointed that DF would engage with this guy, listen to David Diamond and Paul Mason instead.
DF is NOT a biochemist OR a physician. I think his approach is extremely irresponsible. If you are serious about your health but insist upon keto, cut out all of the saturated fats and animal products. It's not pleasant, but it's effective.
@@maarten7 Yes, of course. You propose to just go full on evolution-denial. It's interesting how the same people will bash flat eathers, climate change deniers etc., but suggest to avoid the evolutionarily-fitted diet as much as possible.
@@Peace_Guard We are omnivores (including having the dentition of omnivores) with the intestinal tract of herbivores. It's possible that high-fat diets were necessary for evolutionary brain-growth (although so was tool-making to kill those animals) but we are now striving for longevity.
Eating a low sat-fat plant-based diet will most surely extend my time upon this mortal coil. I'm not worried about what's going to happen in another 20,000 years.
Paul Mason is a physiotherapist he is not remotely qualified to talk about lipid profiles and CVDs
@@lamondaforestry Do your research before making an asinine comment - Dr Paul Mason obtained his medical degree with honours from the University of Sydney, and also holds degrees in Physiotherapy and Occupational Health. He is a Specialist Sports Medicine and Exercise Physician. Listen and learn....
👍👍🙏
Thanks, Uriel Wong. I appreciate your feedback!
I was LMHR before Dave came along and made me feel like I wasn't a freak. My DNA testing through Color Genomics came back with NO RISK of CVD genetically.
Still seeking answers but MY DR REFUSES TO PRESCRIBE A GLUCOSE MONITOR UNLESS I HAVE T2 DIABETES!!!
Buy a glucose monitor online and start keeping track for yourself.
@@karenblack7117 Thanks Karen but I'm told online that I need a Dr's Rx for a CGM or even just a FreeStyle Libre... I'm in the US.
@@6789uiop why do you need a cgm?
@@JWB671 To know post prandial glucose levels and sustained blood glucose levels- and probable insulin response. Prevent pre-diabetes. They don't allow us to know our blood sugar levels until AFTER it's too lat (I'm in the US).
Start with a CAC. They're cheap. Then get a lipid panel with ApoB and Lp(a). If you have taken care of the metabolic piece (and you should change doctors if yours won't prescribe a CGM) you can make a realistic assessment. But don't be a fool and ignore the blood-lipid numbers Huge mistake.