Cromwell is such a breath of fresh air as an old guard who recognizes new data as just that, new data with new implications which need to be explored. It shows a true scientist as opposed to the dogma all throughout the medical profession, the medical institutions and the diet nutrition camps. So glad that Dave Feldman and Nick Norwitz both chose such well respected but open minded principle investigators from the standard lipid backgrounds in Matthew Budoff and William Cromwell.
I’m here watching you incredible guys!! I’m watching 20 other podcasts and video providers on RUclips about keto, metabolic health, etc etc….. YET!!!!! I go to the doctor and it’s like going back to the 1950’s….. 😂😂😂 great podcasts!😂
My Doc had heard of lmhr when I told her about my lipid Triad .She is about 30 years old .Formerly another Doc advised me to tke a statin ...he is 50 years old.The younger ones are more knowledgable about diet , keto , metabolic health. 45:04
My LDL went up to over 300. I also had mild plaque in one artery. I went on a statin and off keto. Not sure whether to try it again. It takes so much self-research and advocacy to figure this out, while you are simultaneously dealing with the issue that got you interested in keto. It's exhausting.
We are sorry to hear it is so frustrating. Unfortunately we hear it far too often. You can try to find an experienced clinician to help you at one of these sites. We hope that helps. www.dietdoctor.com/low-carb/doctors thesmhp.org/directory/ www.diagnosisdiet.com/directory
THANK YOU Doctor for mentioning the correlation of hypothyroid and LDL!! It’s mind boggling that GP’s are so lacking in their knowledge of the two. Here’s my story…. My LDL is considered high, at 125. Total Cholesterol is 195 down from 201 (oh the horror). HDL 62. Triglycerides 31. VLDL 6. CRP 1. I am hypothyroid. In my early 60s. I’ve been following a LCHF diet and recently switched to Keto. I consume lean beef, fish, eggs etc. Plus non-starchy veggies. I cut out gluten. And all “added sugar.” I had 2 CCTA’s w Contrast, within 3 yrs of each other. Both tests “Zero blockages.” So I am not going on any Statins as my GP’s keep pushing. 25+ years ago my LDL/Tot Chol was within “normal” ranges, HDL in 40s & triglycerides in 60s, and my VLDL was 10. I wasn’t doing any specific diet other than the SAD (Standard American Diet). Nowadays LDL/Tot Chol higher but I feel fine. So I THINK I’m OK cardiovascular wise.
@@GB0066 I stated approximate age in my initial comment. Thanks. I have not yet had the Lp (a) test done. When I go to a functional medicine doctor I will request it.
Plaque does not grow initially into the inner lumen/tube diameter. it grows core backwards“ into the wall/muscle. So a CCTA catches lumen impinging plaque growth. But may not catch plaque growth that maintains lumen, but grows backwards “ into “ the wall of the artery, which is how most plaques initiate, not into the lumen first.
I have been asking this question for a while. Apparently there are no mechanistic studies demonstrating that LDL is atherogenic. In fact any lipoprotein.
I think the closest you will get to that is that foam cells collect up oxidised LDL particles. However, more current theories are that high LDL raises apoB and that causes 'sticky' blood. Atherosclerotic plaques actually contain very little LDL and I believe the LDL that has been observed tended to be oxidised. I am a believer that it is inflammation that causes plaque formation. If you have higher blood viscosity or higher blood pressure then that can cause inflammation in the arteries. The question is whether apoB really causes sticky blood and whether that is a problem in everyone, or if there is some other factor that affects it. I have high LDL but my blood viscosity has always been very good and I have good blood pressure.
Dr Cromwell insinuates that you have to have a “reason” to be on a Ketogenic diet. There are many doctors out there who say that the ketogenic diet is the “proper human diet”. That’s why I follow this lifestyle.
Is this not a cultish, unscientific way of looking at this? We can have all manner of epistimological pissing matches about "the proper human diet." What Bill did is acknowledge there may be a vast suite of reasons any INDIVIDUAL may choose to use a KD. I've used one for 25 years to manage gut and autoimmune issues. What he did was a hell of a lot more than insinuate something, he laid out a rubric for personalized medicine with the individual at the center of that process, not a highly debatable ideology.
I was eaiting %100 meat on a no-carb diet for almost 18 months. I was pre diabetic my A1C dropped way down...right up until my heart attack in 2006. From that time on I began eating no meat and things got better. For me, eating more like a gorilla and less like a cat or dog seems to work best. Genetics, epigenetics or chemistry..who knows...people are just different.
I don't much care about what Peter Attia says or thinks. He doesn't do science and he monochrome thinking with a significant bias. By his own admission, he is a knuckle head. Let's leave the science stuff to the scientists.
I am a reflexologist. We NEVER use our practice for diagnosis, treatment, therapy, etc. However, there is a heart reflex area on the foot that is never wrong. Every person on whom I have worked that had extreme sensitivity in that area has/had heart disease. The body does not lie, nor does it make mistakes.
I'd like to see some studies on those of us who are NOT Lean Mass, but are LDL hyper-responders with HDL>90 - Trigs between 70-90, who are Insulin Sensitive , and whose NMRs show very few Small Dense particles.
To the degree there is something here, this is why it's important to look at lipoproteins and not just cholesterol. It still does not answer all our questions (as is evidenced here) but different flavors of discordance can have folks with low cholesterol, high lipoproteins (which in theory would be more atherogenic) or the inverse (low lipoproteins, high cholesterol).
If you look back tens of thousands of years ago, the average person would have been a lean mass hyper responder on an animal based diet. If that were a problem, we wouldn’t be here today. We would have died out.
We don’t know what people ate tens of thousands of years ago, other than it must have been different across geography and season. We do know that people died young and rarely grew old. We also know that animals today are genetically radically different than tens of thousands of years ago.
@@Canigobackwe do have stable nitrogen isotope testing to make reasonable inference. If people died young, it was likely related to trauma, infection, not chronic disease. What is the evidence that the human genome is radically different from tens of thousands of years ago?
Not the human genome. The nutritional and genetic content of animals today are radically different than 5000 years ago. Mankind has had a dramatic influence on the environment. The animal meat we eat today is entirely different.
I am LMHR - on ketovore with high LDL, on treatment for metastatic cancer since 2021. My GP was not interested in the interplay of my diet and LDL in view of my medical history😢 My GP is only interested in putting me on statins with the myriad of side effects- which I refused as I am doing very well.
With respect to cancer, are you intentionally using metabolic therapy as your primary cancer treatment therapy? More specifically, metabolic therapy for cancer as developed and described by Dr Thomas Seyfried, PhD of Boston College. Metabolic therapy for cancer involves a low carbohydrate diet and fasting to lower glucose and insulin levels which are the primer instigators and drivers of cancer.
I'm right there with you. July 2021 and this stupid medication causes a rise in ldl on top of the LMHR. Idk what to do. I I have minimal calcium but uts calcium. I have cvd. Hard to know.
I had moderate plaque in 1 coronary artery that changed to mild plaque as my LDL climbed from 103 to 203 and then higher over 1 year and 5 months while I changed to and continued the low carb diet. My other coronary arteries changed from mild to no significant plaque and my calcium changed from mild to non observed and in one artery predominantly calcified to some calcification and non calcified plaque. My BMI ranges from 18 to 19.
@@advait2062 I had 2 coronary CT angiograms at the same place and same machine at the Houston Medical Center. I also had multiple lipid profile tests over time including regular profiles in the usual manner. I also had 2 lipid fraction tests that showed type A least likely to have a coronary event on both tests. The first lipid fraction was not fasted. The second fasted fraction showed a dramatic increase in lipid particle numbers. My apoB was done on the first fraction test and was very high. My lp(a) was
@@advait2062 I posted a reply that did not show up. Take 2: I had 2 coronary CT angiograms at the same place and machine at the Houston Medical Center 1 year and 5 months apart. I had the usual lipid profiles over time starting in 2018 to the present. When fasted the triglycerides that have never been high decreased the HDL increased showing that my reverse cholesterol synthesis works well. I had 2 lipid fractions done 3 months apart and both were type A least likely to have a coronary event. The first fraction was not fasted, the second fraction test was fasted and showed a dramatic increase in lipid particles. ApoB was very high. I reversed my disease because I went on the low carb diet that gives significantly less sugar to stimulate glp-1. The makers of the glp-1 receptor agonist Semaglutide in their paper to clinicians states that help-1 is stimulated by sugar. Glp-1 and the glp-1 receptor work through TRPV1 on the lymphatic sensory nerves that send the signal to peripheral and central nervous systems. This stimulates insulin and can cause hyperinsulinemia and the hypothalamus where it decreases inhibition of gonadotropin releasing hormones (GnRH) that then over stimulate Luteinizing hormone (LH) and follicle stimulating hormone (FSH). FSH increases sex hormone binding globulin (SHBG) that binds testosterone and estrogen. Not a good thing in older people with little or no estrogen as estrogen deficiency leads to osteoporosis. Both glp-1 and TRPV1 cause sodium loss at the kidney known as hyponatremia and this stimulates the osmosensors TRPV4 and piezo-1. A preprint December 2023 article for The Lancet publication shows a double-blind study that glp-1 Semaglutide supplied by and funded by Novo Nordisk the makers of Semaglutide caused bone mineral density (BMD) loss in adults at risk of osteoporosis. They wonder if the bone breakdown is due to weight loss and less demand and therefore stimulation of bone formation. Obviously hyponatremia causes bone breakdown because bones are where the body stores sodium. Another very large study that references NHANES (national health and nutrition) shows that chronic mild hyponatremia causes BMD loss especially in the spine and hip. SHBG-bound estrogen unavailability and sodium loss causes BMD loss. Fracture of the spine is associated with a significantly shortened life span. Finally here’s the atherosclerosis part;) TRPV4 is found in the transcriptome of active atherosclerosis along with klf4. This inflammatory phenotype leads to a dangerously thin fibrous cap at risk of rupture and then myocardial infarction and stroke. The key: stop over stimulating the natriuretics glp-1 and TRPV1. There is a big study that addresses hyponatremia in psychotropics especially in combination with other psychotropic drugs or other diuretics and I am pointing out glp-1 RA or simply glp-1 and normal or high carbohydrate/sugar consumption. Not only did I reverse my atherosclerosis but I also reversed my severe osteoporosis acquired in only 3 years on oxcarbazepine that up-regulates TRPV1 while eating a normal carbohydrate diet.
@@advait2062 I have responded twice but neither has shown up. Maybe too lengthy of a post. In summary 2 coronary CT angiograms at the same machine at the Houston Medical Center. 2 lipid fraction tests both type A and dramatically increased numbers of particles when fasted. Regular lipid panels, never high triglycerides. Fasted decreased TG and increased HDL showing good reverse cholesterol synthesis. December 2023 preprint of The Lancet has double-blind study showing bone density loss in the spine and hip after 52 weeks of treatment with Semaglutide the glp-1 receptor agonist. Another study shows mild chronic hyponatremia causes osteoporosis. Glp-1 and TRPV1 are natriuretics that cause sodium loss that leads to chronic mild hyponatremia now shown in studies including NHANES (national health and nutrition data base) data that chronic, mild hyponatremia causes bone loss and osteoporosis of the spine and hip. Hyponatremia stimulates TRPV4 found in the transcriptome of active atherosclerosis along with klf4. This leads to a thin fibrous cap, rupture, myocardial infarction and stroke. Statins stimulate TRPV1!
Not really...He went from no carb to high carb diet and of course his cholesterol dropped. My GP Doc told me this would happen in 2005 if I just stopped the no carb diet I was on. My cholesterol was over 400 on no-carb. Dropped over 100 pts after quitting. Nobody got poked in the eye. Just a tiktok prank really.
Would love to hear Bret Scher's current thinking on the subject.. Is there evidence that elevated LDL that is induced by diet (keto, carnivorous, lion) pose the same risk as the FH genotype. And if there is not enough data, one way or the other to know if LMHR are at an increased risk of CVD, then is there anything else about a low-carb diet that may be concerning (ex. colon cancer, magnesium deficiency, etc).
Ketogenic therapy can be like any therapeutic intervention, having potentially beneficial or adverse effects. With ketogenic therapy, research and clinical experience indicate the vast majority of the response is beneficial, especially when initiated and maintained under clinical supervision. The increased need for hydration and electrolytes is well documented, especially in the initial transition period. Here is an article that goes into more details about potential side effects. www.dietdoctor.com/low-carb/side-effects As for LDL, that is a complicated topic in evolution. We don't have specific data on keto-induced hyperlipidemia and risk of CVD in someone with good metabolic health and no other cardiac risk factors. Dr. Matt Budoff, Dave Feldman, and others are currently investigating this question and we hope to learn more as their evidence is published. Please see the interviews we've done with Dave Feldman and Dr William Cromwell for more detailed information. Thanks for your question!
I have a TC of 398. HDL 113. Trigs 46. LDL 276. VLDL 9. Zero CAC score and BP of 90 over 60. Resting BPM of 50. Cholesterol only seems to be a issue for people with metabolic disorders or polymorphisms.
The one thing I love about this study is that Nick set out to disprove the theory. All it takes is 1 case to prove a theory wrong/ incomplete. It proved nothing but that wasn't the point of it.
So,if i want to go keto, stop statins, and my ldlc (non statin) is 210, how do I know if I will get ASCVD ? Should I go keto until I get a cac of non zero ? Until a CTA shows some amount of “vessel,disease” ? Does my lp(a) level matter ? How do I know if my HDL are super functional ? I like the idea of keto for weight loss but not enthusiastic about an accompanying stroke or MI
There was a paper on this (2012-ish?) proposing to look at mass balance rather than energy balance. Mass in minus mass out vs calories in minus calories out. Very interesting way of highlighting the inherent oversimplifications of the energy balance paradigm. Instead of "you eat too much" the paradigm would be "you store too much." Since the only way to gain mass is with insulin, an insulin sparing diet will always lead to weight loss (hence Type 1 diabetics always present with rapid weight loss in spite of gorging on food). Poke around on Google Scholar. I'm sure you can track down that paper!
He is trying to be open minded. However he hasn’t looked at the possibility that in LMHR’s or those trending that way may not have any negative effect at all from high LDLs And to reach a little further, consider the possibility that the increase in LDL’s is actually a healthy response. I think all should be looked at. I Just did a stress test with eco and everything looked exceptional including my predicted Vo2max. I am in the LMHR camp.
This research is fascinating. But a roadblock that may be impassable in benefiting from the results is access to healthcare. Right now, in the US at least, having a "healthcare team" is really only a privilege of personal wealth.
The questions that we need direct answers to are 1. Does everyone with high LDL-C have the potential to have arteriosclerosis/MI/CVD 2. Does every heart attack patient presenting in A&E have high LDL-C cholesterol? 3. What is the relationship between LDL-C and blood sugar in metabolically healthy and unhealthy individuals/patients.
All great questions. As with many things in medicine, it is rare for there to be absolutes. Instead, we talk about risk factors. High LDL can increase the risk for heart disease. But we need to ask "by how much," and "how does this differ between metabolically healthy and unhealthy individuals?" I hope the excitement surrounding LMHRs will encourage more people to seek out answers!
I would add another question. What is the correlation of lipoprotein(a), aka Lp(a) levels within the LMHR study? For those who might not be aware. Lp(a) is a type of LDL. The level of Lp(a) is known to be highly correlative with the development of plaque and CVD. People with non-detectable to low levels of Lp(a) are genetically predisposed to lower incidence of plaque and CVD. In my case, I am 60, I fit the LMHR phenotype, and I have a CAC score of zero. However, I also have a non-detectable level of Lp(a) and carry the Lp(a) null allele at marker rs41272114 on chromosome 6. People who carry who carry the Lp(a) null allele have non-detectable levels of Lp(a). Approximately 3% of the general population carries the Lp(a) null allele which genetically predisposes those people to a lower incidence of plaque and CVD. Maybe somebody can explain the reason for the strategic silence on the level of Lp(a) within the LMHR cohort study? There is a 0% chance that the sponsors, investigators, and administrators of the LMHR cohort study are unaware of the well known correlation of Lp(a) levels to the incidence of plaque and CVD. In my opinion, the level of Lp(a) should have been tested, disclosed, and correlated with the level of plaque. Persons who carry the Lp(a) null allele should have been excluded from the LMHR study or otherwise segregated into a separate statistical sub-group of the LMHR study. It is the joint burden of the sponsors, investigators, and administrators of the LMHR study to demonstrate there has been no Lp(a) related mischief with respect to the potential for undisclosed LMHR study inclusion/exclusion selection criteria on the front end of the LMHR study. The strategic silence on Lp(a) only serves to invite reasonable speculation and concern of potential mischief in pursuit of a desired LMHR study outcome.
Maybe lmhr is how evolution equips us to statin-ise ourselves by quickly lowering our ldl in the event of it being poor quality small dense ldl (with metabolic syndrome) that raises cvd risk.ie eating carbs when being lmhr has effects like a super-statin .
Frankly there is nothing new here. Some people that go on a lc diet get large increases in ldl cholesterol. Those very same people can also return to their original ldl level by reintroducing carbs into their diet. What would be new is if the ldl C didn’t come down in a portion of said population.
Oxidized ldl's creates plaque. Oxidized ldl's gets created by inflammation. Inflammation is mainly a component of metabolic disease + the amount of lipoprotein(a) your liver makes(which is genetic determined). So, in short, if your a metabolic healthy person and is genetically blessed with a very low level of lipoprotein(a)....the inflammation in your body will be very low and the amount of ldl's that will oxidize, will accordingly also be very low. This person could get away with elevated ldl's for a long time. Actually, latest research is showing, having very low lp(a) levels, will dramatically lower oxidation of ldl's just by itself. Your welcome! 😉
@@robb-wolf I seriously doubt he watched more than a couple minutes before parroting the anti-statin / LDL-C is a good thing wing of the low carb RUclips crowd.
I did a very experiment similar to the Oreo demonstration in 2005 and 2006 when in my 40s. I was following low carb/no carb dieting for about 18 months. My cholesterol was through the roof between 400 and 425 roughly. I sort of ignored my doctors concerns because "I read that it is ok on the Internet if you just stay in ketosis etc". I had 2 heart attacks in 2006 and 10 days in the cardiac ward. (over $100,000 back then) Just eating the normal hospital food for that time appeared to drop about 100 points off! (it continued to drop more over time). No more fad diets and Ive gone 18 years with no problems. For me this was the most dangerous and expensive experiment I ever did. Be careful.
@@wmn8344 I went from carnivore to Mediterranean in 2006…saw little improvement and still had angina. Went vegan with no added fats or oils in 2008…saw major improvement. Cholesterol dropped to around 175 and angina disappeared and bmi down to between 23 and 24. 16 years so far. Eating like my dog almost killed me…eating like a gorilla seems to be best for my health.
@@6stringcodger450thanks for sharing, if I try to get a lot of calories from whole grains like oats I start to really feel unwell that is why I tend to eat rather carnivore but wondering about cardio risk.
Do you believe that 18 months of verified keto (beta hydroxybutyrate>=1.0 mmol) caused you to suffer 2 myocardial infarctions? I carried an umbrella every day for a week. It never rained. The day I walked out without my umbrella, it rained twice and I got hit by a car. Therefore, obviously, carrying an umbrella protects against both undesired rainfall and reckless drivers. Can't argue with facts... once you line them up one after the other. It's called the "post hoc, ergo propter hoc" fallacy of argumentation. Just because event B follows after event A does not provide a demonstration that A caused B. Your heart disease developed over many years, not 18 months. A well designed, whole food ketogenic diet causes direct improvements in vascular cell function, including the crucial cell-cell adhesion that protects the lining of your blood vessels from leaking. Keto reduced insulin load which enhances cellular catabolic cleanup functions like autophagy, further improving cell health. Keto directly drives enhanced mitochondrial function, crucial in all cells and especially muscle cells and especially that muscle called your heart. In fact, heart takes up ketones and fatty acids preferentially with glucose as only a third choice. In other words, in the time since your heart attack, we have learned an incredible amount about how, at a molecular level, keto is actually atheroprotective. It gets better. After heart attack, what do you think the difference is in the ketogenic vs non ketogenic heart? The ketogenic heart systematically fares better. Eat like a gorilla if you like. You can even do vegan keto, so no problem there either. But whatever you do, you might be fascinated to read the past 22 years of research on the biochemistry of the heart and vascular system in nutritional ketosis.
This wasn't helpful. If you are not a lean-mass hyper responder and your LDL goes up because you recently started keto, his solution appears to be to add carbs back into your diet. In other words, quit keto.
The situation is what it is. There's very little studies that ensures that Keto is safe on the long term, so at this point is just about trusting these internet celebs with their cherry-picked arguments - isn't an interest on them on keeping the low-carb wheel spinning like big pharma's ? - or take an educated decision while putting your confirmation bias aside.
Cromwell is such a breath of fresh air as an old guard who recognizes new data as just that, new data with new implications which need to be explored. It shows a true scientist as opposed to the dogma all throughout the medical profession, the medical institutions and the diet nutrition camps. So glad that Dave Feldman and Nick Norwitz both chose such well respected but open minded principle investigators from the standard lipid backgrounds in Matthew Budoff and William Cromwell.
Love it when great minds come together.
I’m here watching you incredible guys!! I’m watching 20 other podcasts and video providers on RUclips about keto, metabolic health, etc etc….. YET!!!!! I go to the doctor and it’s like going back to the 1950’s….. 😂😂😂 great podcasts!😂
My Doc had heard of lmhr when I told her about my lipid Triad .She is about 30 years old .Formerly another Doc advised me to tke a statin ...he is 50 years old.The younger ones are more knowledgable about diet , keto , metabolic health. 45:04
We need many, MANY more doctors like Dr. William Cromwell!
OUTSTANDING interview, wow!
Wonderfully informative conversation. Thank you both.
My LDL went up to over 300. I also had mild plaque in one artery. I went on a statin and off keto. Not sure whether to try it again. It takes so much self-research and advocacy to figure this out, while you are simultaneously dealing with the issue that got you interested in keto. It's exhausting.
We are sorry to hear it is so frustrating. Unfortunately we hear it far too often. You can try to find an experienced clinician to help you at one of these sites. We hope that helps.
www.dietdoctor.com/low-carb/doctors
thesmhp.org/directory/
www.diagnosisdiet.com/directory
THANK YOU Doctor for mentioning the correlation of hypothyroid and LDL!! It’s mind boggling that GP’s are so lacking in their knowledge of the two. Here’s my story….
My LDL is considered high, at 125. Total Cholesterol is 195 down from 201 (oh the horror). HDL 62. Triglycerides 31. VLDL 6. CRP 1. I am hypothyroid. In my early 60s. I’ve been following a LCHF diet and recently switched to Keto. I consume lean beef, fish, eggs etc. Plus non-starchy veggies. I cut out gluten. And all “added sugar.” I had 2 CCTA’s w Contrast, within 3 yrs of each other. Both tests “Zero blockages.” So I am not going on any Statins as my GP’s keep pushing. 25+ years ago my LDL/Tot Chol was within “normal” ranges, HDL in 40s & triglycerides in 60s, and my VLDL was 10. I wasn’t doing any specific diet other than the SAD (Standard American Diet).
Nowadays LDL/Tot Chol higher but I feel fine. So I THINK I’m OK cardiovascular wise.
How old are you? Great news on your CCTA’s. 😁 Have you ever had your Lp (a) tested? If so, what was it?
@@GB0066 I stated approximate age in my initial comment. Thanks. I have not yet had the Lp (a) test done. When I go to a functional medicine doctor I will request it.
Plaque does not grow initially into the inner lumen/tube diameter. it grows core backwards“ into the wall/muscle. So a CCTA catches lumen impinging plaque growth. But may not catch plaque growth that maintains lumen, but grows backwards “ into “ the wall of the artery, which is how most plaques initiate, not into the lumen first.
Can we please have a careful walk-through of the mechanism of action for the causal role of LDL in plaque formation? Mechanism of action.
There is zero evidence that LDL is causal in plaque formation. Seek up professor Bart Kay he has a playlist of videos on this.
I have been asking this question for a while. Apparently there are no mechanistic studies demonstrating that LDL is atherogenic. In fact any lipoprotein.
I think Ivor Cummins has a good podcast with a guest who has a different model for plaque development and parties involved..
@@mikewhiting5707 Dr. Malcolm Kendrick.
I think the closest you will get to that is that foam cells collect up oxidised LDL particles. However, more current theories are that high LDL raises apoB and that causes 'sticky' blood.
Atherosclerotic plaques actually contain very little LDL and I believe the LDL that has been observed tended to be oxidised.
I am a believer that it is inflammation that causes plaque formation. If you have higher blood viscosity or higher blood pressure then that can cause inflammation in the arteries. The question is whether apoB really causes sticky blood and whether that is a problem in everyone, or if there is some other factor that affects it.
I have high LDL but my blood viscosity has always been very good and I have good blood pressure.
Amazing episode. One of the best talks I ever heard on this topic so far to date!
Thank you! Let's keep doing good science!
Dr Cromwell insinuates that you have to have a “reason” to be on a Ketogenic diet. There are many doctors out there who say that the ketogenic diet is the “proper human diet”. That’s why I follow this lifestyle.
From my perspective, proper human diet is a reason 🙂
🦆🦆🦆🦆
Is this not a cultish, unscientific way of looking at this? We can have all manner of epistimological pissing matches about "the proper human diet." What Bill did is acknowledge there may be a vast suite of reasons any INDIVIDUAL may choose to use a KD. I've used one for 25 years to manage gut and autoimmune issues. What he did was a hell of a lot more than insinuate something, he laid out a rubric for personalized medicine with the individual at the center of that process, not a highly debatable ideology.
I was eaiting %100 meat on a no-carb diet for almost 18 months. I was pre diabetic my A1C dropped way down...right up until my heart attack in 2006. From that time on I began eating no meat and things got better. For me, eating more like a gorilla and less like a cat or dog seems to work best. Genetics, epigenetics or chemistry..who knows...people are just different.
PS. Your metabolism is not similar at all to that of a gorilla.
The absolute change in risk in a normal American population on a SAD diet from statins is incremental at best.
Further there are data that conclude there is no correlation between ldl level and calcium scores.
It's too bad Peter Attia doesn't see this the same way that you fellas comprehend it.
I don't much care about what Peter Attia says or thinks. He doesn't do science and he monochrome thinking with a significant bias. By his own admission, he is a knuckle head. Let's leave the science stuff to the scientists.
The most balanced perspective on LMHR and LDL risk
I am a reflexologist. We NEVER use our practice for diagnosis, treatment, therapy, etc. However, there is a heart reflex area on the foot that is never wrong. Every person on whom I have worked that had extreme sensitivity in that area has/had heart disease. The body does not lie, nor does it make mistakes.
Haha😂
I'd like to see some studies on those of us who are NOT Lean Mass, but are LDL hyper-responders with HDL>90 - Trigs between 70-90, who are Insulin Sensitive , and whose NMRs show very few Small Dense particles.
My thoughts exactly
70% of people admitted to the hospital with a heart attack have normal ldl? How do you rationalize this?
heart attacks lower ldl pubmed.ncbi.nlm.nih.gov/26233997/
Math. Time based integral.
85% of people admitted to the hospital with a heart attack are right-handed, too.
To the degree there is something here, this is why it's important to look at lipoproteins and not just cholesterol. It still does not answer all our questions (as is evidenced here) but different flavors of discordance can have folks with low cholesterol, high lipoproteins (which in theory would be more atherogenic) or the inverse (low lipoproteins, high cholesterol).
The hospital doesn't insist that all right-hand patients take medication for right-handedness!
If you look back tens of thousands of years ago, the average person would have been a lean mass hyper responder on an animal based diet. If that were a problem, we wouldn’t be here today. We would have died out.
Not necessarily. It's not because you might die from a heart attack at 40 or 60 that you were not strong, alive, and reproducing yourself until then.
We don’t know what people ate tens of thousands of years ago, other than it must have been different across geography and season. We do know that people died young and rarely grew old. We also know that animals today are genetically radically different than tens of thousands of years ago.
@@Canigobackwe do have stable nitrogen isotope testing to make reasonable inference.
If people died young, it was likely related to trauma, infection, not chronic disease.
What is the evidence that the human genome is radically different from tens of thousands of years ago?
Not the human genome. The nutritional and genetic content of animals today are radically different than 5000 years ago. Mankind has had a dramatic influence on the environment. The animal meat we eat today is entirely different.
@@Canigoback Different but not entirely different.
I am LMHR - on ketovore with high LDL, on treatment for metastatic cancer since 2021. My GP was not interested in the interplay of my diet and LDL in view of my medical history😢 My GP is only interested in putting me on statins with the myriad of side effects- which I refused as I am doing very well.
With respect to cancer, are you intentionally using metabolic therapy as your primary cancer treatment therapy? More specifically, metabolic therapy for cancer as developed and described by Dr Thomas Seyfried, PhD of Boston College. Metabolic therapy for cancer involves a low carbohydrate diet and fasting to lower glucose and insulin levels which are the primer instigators and drivers of cancer.
I'm right there with you. July 2021 and this stupid medication causes a rise in ldl on top of the LMHR. Idk what to do. I
I have minimal calcium but uts calcium. I have cvd. Hard to know.
I had moderate plaque in 1 coronary artery that changed to mild plaque as my LDL climbed from 103 to 203 and then higher over 1 year and 5 months while I changed to and continued the low carb diet. My other coronary arteries changed from mild to no significant plaque and my calcium changed from mild to non observed and in one artery predominantly calcified to some calcification and non calcified plaque. My BMI ranges from 18 to 19.
Interesting. Can you share which tests you ran?
@@advait2062 I had 2 coronary CT angiograms at the same place and same machine at the Houston Medical Center. I also had multiple lipid profile tests over time including regular profiles in the usual manner. I also had 2 lipid fraction tests that showed type A least likely to have a coronary event on both tests. The first lipid fraction was not fasted. The second fasted fraction showed a dramatic increase in lipid particle numbers. My apoB was done on the first fraction test and was very high. My lp(a) was
@@advait2062 I posted a reply that did not show up. Take 2:
I had 2 coronary CT angiograms at the same place and machine at the Houston Medical Center 1 year and 5 months apart.
I had the usual lipid profiles over time starting in 2018 to the present. When fasted the triglycerides that have never been high decreased the HDL increased showing that my reverse cholesterol synthesis works well.
I had 2 lipid fractions done 3 months apart and both were type A least likely to have a coronary event. The first fraction was not fasted, the second fraction test was fasted and showed a dramatic increase in lipid particles.
ApoB was very high.
I reversed my disease because I went on the low carb diet that gives significantly less sugar to stimulate glp-1. The makers of the glp-1 receptor agonist Semaglutide in their paper to clinicians states that help-1 is stimulated by sugar.
Glp-1 and the glp-1 receptor work through TRPV1 on the lymphatic sensory nerves that send the signal to peripheral and central nervous systems. This stimulates insulin and can cause hyperinsulinemia and the hypothalamus where it decreases inhibition of gonadotropin releasing hormones (GnRH) that then over stimulate Luteinizing hormone (LH) and follicle stimulating hormone (FSH). FSH increases sex hormone binding globulin (SHBG) that binds testosterone and estrogen. Not a good thing in older people with little or no estrogen as estrogen deficiency leads to osteoporosis.
Both glp-1 and TRPV1 cause sodium loss at the kidney known as hyponatremia and this stimulates the osmosensors TRPV4 and piezo-1.
A preprint December 2023 article for The Lancet publication shows a double-blind study that glp-1 Semaglutide supplied by and funded by Novo Nordisk the makers of Semaglutide caused bone mineral density (BMD) loss in adults at risk of osteoporosis. They wonder if the bone breakdown is due to weight loss and less demand and therefore stimulation of bone formation.
Obviously hyponatremia causes bone breakdown because bones are where the body stores sodium.
Another very large study that references NHANES (national health and nutrition) shows that chronic mild hyponatremia causes BMD loss especially in the spine and hip.
SHBG-bound estrogen unavailability and sodium loss causes BMD loss.
Fracture of the spine is associated with a significantly shortened life span.
Finally here’s the atherosclerosis part;)
TRPV4 is found in the transcriptome of active atherosclerosis along with klf4. This inflammatory phenotype leads to a dangerously thin fibrous cap at risk of rupture and then myocardial infarction and stroke.
The key: stop over stimulating the natriuretics glp-1 and TRPV1.
There is a big study that addresses hyponatremia in psychotropics especially in combination with other psychotropic drugs or other diuretics and I am pointing out glp-1 RA or simply glp-1 and normal or high carbohydrate/sugar consumption.
Not only did I reverse my atherosclerosis but I also reversed my severe osteoporosis acquired in only 3 years on oxcarbazepine that up-regulates TRPV1 while eating a normal carbohydrate diet.
@@advait2062 I have responded twice but neither has shown up. Maybe too lengthy of a post.
In summary 2 coronary CT angiograms at the same machine at the Houston Medical Center.
2 lipid fraction tests both type A and dramatically increased numbers of particles when fasted.
Regular lipid panels, never high triglycerides. Fasted decreased TG and increased HDL showing good reverse cholesterol synthesis.
December 2023 preprint of The Lancet has double-blind study showing bone density loss in the spine and hip after 52 weeks of treatment with Semaglutide the glp-1 receptor agonist.
Another study shows mild chronic hyponatremia causes osteoporosis.
Glp-1 and TRPV1 are natriuretics that cause sodium loss that leads to chronic mild hyponatremia now shown in studies including NHANES (national health and nutrition data base) data that chronic, mild hyponatremia causes bone loss and osteoporosis of the spine and hip.
Hyponatremia stimulates TRPV4 found in the transcriptome of active atherosclerosis along with klf4. This leads to a thin fibrous cap, rupture, myocardial infarction and stroke.
Statins stimulate TRPV1!
Excellent!
Nick is poking the old guard in the eye and they are super uncomfortable
Not really...He went from no carb to high carb diet and of course his cholesterol dropped. My GP Doc told me this would happen in 2005 if I just stopped the no carb diet I was on. My cholesterol was over 400 on no-carb. Dropped over 100 pts after quitting. Nobody got poked in the eye. Just a tiktok prank really.
why is Crohn's always mentioned but not ulcerative colitis? is UC just not as common? is it not impacted in the same way as crohn's?
Would love to hear Bret Scher's current thinking on the subject..
Is there evidence that elevated LDL that is induced by diet (keto, carnivorous, lion) pose the same risk as the FH genotype.
And if there is not enough data, one way or the other to know if LMHR are at an increased risk of CVD, then is there anything else about a low-carb diet that may be concerning (ex. colon cancer, magnesium deficiency, etc).
Ketogenic therapy can be like any therapeutic intervention, having potentially beneficial or adverse effects. With ketogenic therapy, research and clinical experience indicate the vast majority of the response is beneficial, especially when initiated and maintained under clinical supervision. The increased need for hydration and electrolytes is well documented, especially in the initial transition period. Here is an article that goes into more details about potential side effects. www.dietdoctor.com/low-carb/side-effects
As for LDL, that is a complicated topic in evolution. We don't have specific data on keto-induced hyperlipidemia and risk of CVD in someone with good metabolic health and no other cardiac risk factors. Dr. Matt Budoff, Dave Feldman, and others are currently investigating this question and we hope to learn more as their evidence is published. Please see the interviews we've done with Dave Feldman and Dr William Cromwell for more detailed information. Thanks for your question!
Excellent interview.
I have a TC of 398. HDL 113. Trigs 46. LDL 276. VLDL 9. Zero CAC score and BP of 90 over 60. Resting BPM of 50.
Cholesterol only seems to be a issue for people with metabolic disorders or polymorphisms.
What's your age? CAC should always be mentioned together with age.
How long has your non-HDL-C been 285[mg/dL]?
Please Compare LDL/APOB with Kraft Insulin Assay Test
The one thing I love about this study is that Nick set out to disprove the theory. All it takes is 1 case to prove a theory wrong/ incomplete. It proved nothing but that wasn't the point of it.
So,if i want to go keto, stop statins, and my ldlc (non statin) is 210, how do I know if I will get ASCVD ? Should I go keto until I get a cac of non zero ? Until a CTA shows some amount of “vessel,disease” ? Does my lp(a) level matter ? How do I know if my HDL are super functional ? I like the idea of keto for weight loss but not enthusiastic about an accompanying stroke or MI
What do you think about replacing the word “calorie “ with DMI (dietary mass intake)?
There was a paper on this (2012-ish?) proposing to look at mass balance rather than energy balance. Mass in minus mass out vs calories in minus calories out. Very interesting way of highlighting the inherent oversimplifications of the energy balance paradigm.
Instead of "you eat too much" the paradigm would be "you store too much."
Since the only way to gain mass is with insulin, an insulin sparing diet will always lead to weight loss (hence Type 1 diabetics always present with rapid weight loss in spite of gorging on food).
Poke around on Google Scholar. I'm sure you can track down that paper!
He is trying to be open minded. However he hasn’t looked at the possibility that in LMHR’s or those trending that way may not have any negative effect at all from high LDLs And to reach a little further, consider the possibility that the increase in LDL’s is actually a healthy response. I think all should be looked at. I Just did a stress test with eco and everything looked exceptional including my predicted Vo2max. I am in the LMHR camp.
This research is fascinating. But a roadblock that may be impassable in benefiting from the results is access to healthcare. Right now, in the US at least, having a "healthcare team" is really only a privilege of personal wealth.
“Let the data teach us”. Great!
Bad sound quality with echo😊
The questions that we need direct answers to are
1. Does everyone with high LDL-C have the potential to have arteriosclerosis/MI/CVD
2. Does every heart attack patient presenting in A&E have high LDL-C cholesterol?
3. What is the relationship between LDL-C and blood sugar in metabolically healthy and unhealthy individuals/patients.
All great questions. As with many things in medicine, it is rare for there to be absolutes. Instead, we talk about risk factors. High LDL can increase the risk for heart disease. But we need to ask "by how much," and "how does this differ between metabolically healthy and unhealthy individuals?" I hope the excitement surrounding LMHRs will encourage more people to seek out answers!
I would add another question. What is the correlation of lipoprotein(a), aka Lp(a) levels within the LMHR study?
For those who might not be aware. Lp(a) is a type of LDL. The level of Lp(a) is known to be highly correlative with the development of plaque and CVD. People with non-detectable to low levels of Lp(a) are genetically predisposed to lower incidence of plaque and CVD.
In my case, I am 60, I fit the LMHR phenotype, and I have a CAC score of zero. However, I also have a non-detectable level of Lp(a) and carry the Lp(a) null allele at marker rs41272114 on chromosome 6. People who carry who carry the Lp(a) null allele have non-detectable levels of Lp(a). Approximately 3% of the general population carries the Lp(a) null allele which genetically predisposes those people to a lower incidence of plaque and CVD.
Maybe somebody can explain the reason for the strategic silence on the level of Lp(a) within the LMHR cohort study? There is a 0% chance that the sponsors, investigators, and administrators of the LMHR cohort study are unaware of the well known correlation of Lp(a) levels to the incidence of plaque and CVD.
In my opinion, the level of Lp(a) should have been tested, disclosed, and correlated with the level of plaque. Persons who carry the Lp(a) null allele should have been excluded from the LMHR study or otherwise segregated into a separate statistical sub-group of the LMHR study. It is the joint burden of the sponsors, investigators, and administrators of the LMHR study to demonstrate there has been no Lp(a) related mischief with respect to the potential for undisclosed LMHR study inclusion/exclusion selection criteria on the front end of the LMHR study. The strategic silence on Lp(a) only serves to invite reasonable speculation and concern of potential mischief in pursuit of a desired LMHR study outcome.
Their 1 year LMHR study has extensive blood testing and will report Lp(a) results.
Maybe lmhr is how evolution equips us to statin-ise ourselves by quickly lowering our ldl in the event of it being poor quality small dense ldl (with metabolic syndrome) that raises cvd risk.ie eating carbs when being lmhr has effects like a super-statin .
Frankly there is nothing new here. Some people that go on a lc diet get large increases in ldl cholesterol. Those very same people can also return to their original ldl level by reintroducing carbs into their diet. What would be new is if the ldl C didn’t come down in a portion of said population.
If 0 isn't 0, where are we, really?
Oxidized ldl's creates plaque. Oxidized ldl's gets created by inflammation. Inflammation is mainly a component of metabolic disease + the amount of lipoprotein(a) your liver makes(which is genetic determined).
So, in short, if your a metabolic healthy person and is genetically blessed with a very low level of lipoprotein(a)....the inflammation in your body will be very low and the amount of ldl's that will oxidize, will accordingly also be very low.
This person could get away with elevated ldl's for a long time.
Actually, latest research is showing, having very low lp(a) levels, will dramatically lower oxidation of ldl's just by itself.
Your welcome! 😉
50 years of statins. Record heart disease.
Cromwell should be ignored as much as possible. He’s a statin pusher and has made a lot of money pushing it.
Pure bull. The reason I’m (and others) are on Keto is avoidance of insulin resistance, and that alone has done miracles.
More or less problematic is still problematic
I would also like to know how much money he has been paid by statin companies.
Likely none. No way he would an author on the Oreo study dissing statins if otherwise.
There’s no money in statins. Total red herring in the low carb community.
Seriously? You watched this whole thing and THIS is your take away?
@@robb-wolf I seriously doubt he watched more than a couple minutes before parroting the anti-statin / LDL-C is a good thing wing of the low carb RUclips crowd.
After the plandemic to think science can’t be bought by big pharma is hilarious
I did a very experiment similar to the Oreo demonstration in 2005 and 2006 when in my 40s. I was following low carb/no carb dieting for about 18 months. My cholesterol was through the roof between 400 and 425 roughly. I sort of ignored my doctors concerns because "I read that it is ok on the Internet if you just stay in ketosis etc". I had 2 heart attacks in 2006 and 10 days in the cardiac ward. (over $100,000 back then) Just eating the normal hospital food for that time appeared to drop about 100 points off! (it continued to drop more over time). No more fad diets and Ive gone 18 years with no problems. For me this was the most dangerous and expensive experiment I ever did. Be careful.
What were you eating at that time and what is your current diet ? Sorry that happened to you and hope you are doing well now.
@@wmn8344 I went from carnivore to Mediterranean in 2006…saw little improvement and still had angina. Went vegan with no added fats or oils in 2008…saw major improvement. Cholesterol dropped to around 175 and angina disappeared and bmi down to between 23 and 24. 16 years so far. Eating like my dog almost killed me…eating like a gorilla seems to be best for my health.
@@6stringcodger450thanks for sharing, if I try to get a lot of calories from whole grains like oats I start to really feel unwell that is why I tend to eat rather carnivore but wondering about cardio risk.
Do you believe that 18 months of verified keto (beta hydroxybutyrate>=1.0 mmol) caused you to suffer 2 myocardial infarctions?
I carried an umbrella every day for a week. It never rained. The day I walked out without my umbrella, it rained twice and I got hit by a car. Therefore, obviously, carrying an umbrella protects against both undesired rainfall and reckless drivers. Can't argue with facts... once you line them up one after the other.
It's called the "post hoc, ergo propter hoc" fallacy of argumentation. Just because event B follows after event A does not provide a demonstration that A caused B. Your heart disease developed over many years, not 18 months. A well designed, whole food ketogenic diet causes direct improvements in vascular cell function, including the crucial cell-cell adhesion that protects the lining of your blood vessels from leaking. Keto reduced insulin load which enhances cellular catabolic cleanup functions like autophagy, further improving cell health. Keto directly drives enhanced mitochondrial function, crucial in all cells and especially muscle cells and especially that muscle called your heart. In fact, heart takes up ketones and fatty acids preferentially with glucose as only a third choice. In other words, in the time since your heart attack, we have learned an incredible amount about how, at a molecular level, keto is actually atheroprotective. It gets better. After heart attack, what do you think the difference is in the ketogenic vs non ketogenic heart? The ketogenic heart systematically fares better.
Eat like a gorilla if you like. You can even do vegan keto, so no problem there either. But whatever you do, you might be fascinated to read the past 22 years of research on the biochemistry of the heart and vascular system in nutritional ketosis.
Tks a lot for your true life experience.. I shall cut down the scale of my keto diet
This wasn't helpful. If you are not a lean-mass hyper responder and your LDL goes up because you recently started keto, his solution appears to be to add carbs back into your diet. In other words, quit keto.
If keto can be ok only if you are the lean type, don't think it's a safe diet.
The situation is what it is. There's very little studies that ensures that Keto is safe on the long term, so at this point is just about trusting these internet celebs with their cherry-picked arguments - isn't an interest on them on keeping the low-carb wheel spinning like big pharma's ? - or take an educated decision while putting your confirmation bias aside.