I've been doing intermittent fasting and very low carb diet for years. My doctor was horrified at my very high LDL (and overall cholesterol) and tried very hard to get me on a statin, which I politely refused. We agreed that I would do a CAC scan instead to make sure I wasn't doing too much damage to my arteries. Fast forward a few weeks... I have a CAC score of *zero*. My arteries are perfectly clear, yet my LDL is well over 200. Something is very wrong with traditional medicine's accepted understanding of cholesterol.
Its worth noting one thing about a zero cac score on keto, (I'm a lmhr and also got zero cac score ). A Cac scan only measures calcified plaque and not soft plaque (more dangerous plaque ) .A keto diet , over time develops a healthier metabolism ,which is then better able to calcify any existing soft plaque that would not show on a cac scan . Hence , a future cac scan may then show some calcified plaque .Don't panic if that happens . As long as the cac score isn't very high , this may just be pre-existent soft plaque that eventually calcified because of the ketogenic improved metabolism. .
Same here!!! My triglycerides went down to 90 but after a two month illness in the inability to cook I had to eat what my husband gave me. When I had my blood work done for my annual check up my triglycerides had gone up over 130. He wanted to put me on a statin and I said no it’s because I have been down for two months with my back and I am unable to cook and I have to basically eat. What’s put before me. My Husband and Retired and I’m not gonna make him work all day and then figure out what the heck I can eat and not eat. When I finally get up and walk and shop and I got back into it. I’m not 100% perfect but in my home, we do not have carbohydrate foods.
I think that was Nadir Ali asking one of the questions. He’s right, we need to consider completely dismissing the Lipid/Heart hypothesis. It was wrong and doomed from the beginning.
I appreciate Dr. Budoff’s explanation for why he prescribes statins. I suspect his comment is at odds with a few watching this video, but to me it demonstrates clear, honest, and measured thinking. Thank you for posting this, Dave.
Dave. Please do a study next on newer carnivores with a CAC to see what happens. Thank you for all of your hard work. What you're doing for humanity is very important.
I have been on carnivore for 14 months. Went from insulin resistant to LMHR in 9 months. I am 54 with a CAC score of 121. Would love to be in the next study. Thanks Dave, Nick, and Dr. Budoff for everything you guys are doing. You guys are a blessing to humanity!
@@OisteinThomassenMScPharmIt was thought that plaque was irreversible until ppl doing ketogenic diet showed less plaque on scans ,cac and CT Angiogram.
NOT TRUE!. Do your research. Many cases of reduction, especially with change to a KETO or Carnivore diet and use of the supplement K2 with MK-4 & MK-7. My husband is one of those lucky people who lowered and continues to lower his CA score. He is not on a statin. @@OisteinThomassenMScPharm
I was KETO for 6 years and fell naturally into carnivore this past year due to simplicity and my new found craving for fatty beef. Best I've felt in my life! My doctor's mind is blown, but I refuse to take a statin. Never had it, never will. My LDL is routinely 250+
My respect to Dr. Budoff who - as probably every cardiologist - have had his biases but was willing to actually look at the real data. Many other scientists just stay in their own dogmas which is very sad to see them being so closed-minded...
I’ve had high cholesterol my entire life. My father was a butcher and we always had meat on the table. I used to smoke and was around second hand smoke my whole life as well. I am 56 years young and started ketovore this past December. Had my first cac scan in February and it was a score of 7. Feel amazing 🙌🏼. I can’t wait to get my blood work again and see what it’s gonna show me. My A1C said 5.8 so I’m hoping it went down.
Since going low carb over 6 years ago, HDL remained steady, Triglycerides went from 260's to 80's, Total and LDL skyrocketed (321 and 253 respectively on last labs). I also dropped my A1C from 10.1 to 5.3 (highest to lowest). Doctor has been pushing me to go on statin. I have politely declined so far.
It is encouraging to witness this new science reporting evolve. Unfortunately (my) doctors still use very old "recommendations" and feel with absolute necessity to refer to book-worn old pages, to assure themselves, in prescribing statins for high LDL rather than what is in the best interest for the individual patient. Thank you for producing a quality video of this rich caliber about an old topic that needs modern day adjustment.
@@terryolay4613 Yes, but what I was sharing is that one can get tired of looking for trouble after a while. So that’s why I’m banking the good news and over looking for trouble. Just gets old.
It's an easy conversion. Whenever they give you a cholesterol value in mg/dL, simply divide it by 38.6 to convert it to mmol/L. With triglycerides, you divide the U.S. number by 88.5. That's all there is to it.
Statins help patients become diabetic which increases heart disease risk by 10x. I applaud DF and everyone participating is reconstructing the ASCVD paradigm.
2 times. But it decreases small LDL particles, the most dangerous part of being diabetic. The risk of becoming diabetic on a statin is very low. The people that did become diabetic in the studies were already pre - diabetic.
@@danielmccarthyy If you live a WFPB Lifestyle statins are never needed and cholesterol is not an issue. High cholesterol comes from one basic dietary plan. no meat 39 years!
Thanks Dave and Nick and Dr Budoff for this incredible work, God bless you all! This is SO exciting! Dr Budoff you are a rare MD that thinks of the individual, not the rote, standard treatment path. I have high cholesterol level, like the LMHR. My cardiologist had me get a CAC and cardiac ultrasound, all normal. She stopped bugging me to take a statin, which I’ve refused from several other MD’s. My dad took one, had a cholesterol level in the 170’s got dementia, had a debilitating stroke. I don ‘t want that path for myself.
I don't know why Dr. Budoff would use statins on a person who is now low carb but has proven heart disease. He would likely agree that the heart disease is the result of years and years eating a crappy diet. If the person now eats a low carb/keto diet, and their LDL spikes upwards, the 4.7-year LMHR study shows it does not provoke plaque formation. So, I repeat. What's the statin for?
I agree, I think blood pressure is a biggger factor. I saw a study in pigs that high ldl had no effect on their coronary plaque until they raised their blood pressure
I'm reducing plaques with no statins. My inflammatory markers are quite low, lowered insulin, lowered BP, reduced resting HR from 65-70 BPM to 55-60. HDL/Trigs 78/58. Two years keto then 3 years carnivore.
@@pmccord9The only diet proven to reduce plaques was a vegetarian one. Sorry. That‘s why I can‘t stand people online selling specific diets, diet books, coachings promising a mirical healing. Because people do just think they should ignore medical advice.
@@stellasternchen when I was plant based, I was anemic, obese, B12 deficient, prediabetic, and grotesquely flatulent, with acid reflux. All that resolved with carnivore along with disappearing calcium plaques. N of one.
Let me tell you a new story. I've been low carb, more animal based, since 2018. I ate terribly all my life and in 2016 I needed a triple bypass. My goal with a low carb diet was to prevent a reoccurrence, although my cholesterol did skyrocket. I always refused a statin. In April 2024, I did experience some new, albeit fairly minor, angina. I got a new 64-slice CT angiogram. It detected the calcium and plaque in my old (i.e. native) arteries, but guess what it found in my 3 bypass grafts? Nothing. Nada. All those bypasses were "patent." Do you know what patent means? It means normal, open, clear. This aligns well with the LMHR study on people like me who go low carb. The big difference being now I'm talking about bypass grafted arteries, not original arteries.
I feel like there should be more comments here or an entire video about just this... wow. I went to your channel and watched your speech for background and context. So eating high fat low carb for the last 8 years deposited nothing, no soft plaque nor calcified plaque, in the new artery grafts that have been carrying the full load for the arteries found to be blocked in 2016?
@@ellieb2914 Yes. The bypass grafts are clear despite eating high fat low carb and seeing my LDL rise more and more the stricter I got with my diet. And thanks for checking out my speech at CoSci in Las Vegas.
@@Malcolm-Achtman That's amazing! If I may ask, are you following any supplement protocols that may prevent further plaque creation/calcification? For example K2 (MK-7).
@@ellieb2914 I've been taking K2 since 2013, after reading about it in Dr. Kate Rheaume-Bleue's book entitled "Vitamin K2 and the Calcium Paradox." I still K2 but I don't believe it's a magical solution for plaque. It can't hurt, though, so I take it. I take other heart supporting supplements, most of which are recommended by cardiologist Dr. William Davis (who I follow). He especially says to take vitamin D3 and magnesium, which I've done for years. I take a kelp supplement that provides iodine, which supports the thyroid, which is important for heart health too. I've been taking CoQ10 for about 15 years (although that one is not on Dr. Davis's list). Dr. Davis likes fish oil and I would sometimes take it, but I've moved away from that as I feel it is not necessarily helpful. I prefer getting my omega-3 from eating real fish (e.g. wild caught salmon). I take some methylated B supplements as well. And some vitamin C (whole food Camu Camu vitamin C capsules).
Super interesting, and demonstrates that the new diet resulted in no new calcium in (probably) in any of the arteries after. So why would Budoff prescribe statins for someone like you to lower the high LDL that is a consequence of the diet/ lifestyle that resulted in such a positive effect? Meantime those drugs will be majorly manipulating your metabolism, for the rest of your life. Wow!
Been low carb since 2018, last blood panel 2017 (I don’t think going to the doctor in the US is worth the time) until a few weeks ago. Dirty keto with lots of veggies for years, switched to ketovore since 2022. Now high fat ketovore trying to heal some inflammation issues. Now my cholesterol: LDL 505,HDL 118, Trig 62, total 635. My doctor freaked out, but I’m not overly concerned and refuse to take a statin. LMHR is real, I’ll look into getting a CAC scan if LDL is still crazy high in 6 months.
70 yo lost 70 lbs over the last year. (Keto) Cholesterol shot up to 294 LDL 221 HDL shot up to 66 TG way down from 300+ to 74. BMI from 33 to 24. Waist from 44 to 36. LDL particle size now type A (large), IR Reduced to now normal. CAC very low 30 but not zero (from 5 years ago). I work out at the gym 5 days a week followed by 20 min sauna. All markers big improvement except cholesterol. I abused my body for 69 years so I expect it will take more time to reduce the ill affects. I wonder if I have become a LMHR via my weight loss and lifestyle change. Keep up the great work.
What I recall is that, on average, statins extend your life by a day or two for every year you take them. This is for people who have not had a heart attack previously (primary prevention).
In a 2016 BMJ review performed by Ravnskov, et al, it was demonstrated that if you were over 60 years old, LDL-C was NOT associated with cardiovascular disease and was INVERSELY associated with all-cause mortality. So if a person is over 60 years old, then the level of LDL-C was absolutely worthless in predicting development/progression of arterial plaque AND the lower your LDL-C, the earlier you are going to die!!!!!!!
Im 42 year old, had a CAC done 3 years ago and i scored a 9. Ive been keto for about a year and carnivore for the last 4 months. My LDL is now 193, HDL is 70 and Triglycerides are 57. My doctor freaked out when he saw my LDL so now i am having another cac done on tuesday. So shall see how this turns out..
Dr. Budoff says he still believes that if a patient has KNOWN CAD/PLAQUE, then that individual should receive LDL-C lowering medicine(s). However, if we consider that LDL particles are "FIREFIGHTERS" that actually dampen inflammation and promote healing of the coronary endothelium, why would we want to wipe out those "FIREFIGHTERS" with statins or PCSK9 inhibitors?🧑🚒👨🚒👩🚒🧑🚒👨🚒👩🚒🧑🚒👨🚒🧑🚒
One extremely important fact that was surprisingly left out of this presentation. Anyone with existing cardiovascular disease was excluded from the study. This was defined, in part, as having a CAC score above the 75th percentile. A number of people were excluded based on this criteria alone. Had they been included there would have been a different starting result. This is beyond misleading. This study, when concluded, will prove if it is successful that if you are on a diet that elevates your lipid numbers, you are unlikely to suffer any negative affects over the next two years. That is the maximum one can learn from a study such as this one. They were told at the outset that they needed at least a five year study to have meaningful results. For a one-year study, they needed progression of plaque rather than incidence of plaque.
The study will show high LDL does not increase CVD if one fits the LMHR definition. It’s funded independently. Please donate to the next study so they can test more.
Budoff plays both sides of the argument, in a Medscape discussion recently he was extolling the ventures (lack of risk) of driving LDL down to below 50mg (
Typical nonsense expressed by the ADA. Must keep exploding the growth of the diabetic population to support the salaries and expensive lifestyles of their executives and those executives of the food industry and pharmaceutical companies who financially support the ADA.
You have to understand that diabetics have mostly small LDL particles with little cholesterol. The LDL-C value measures the cholesterol inside to estimate LDL particle quantity. This measure was developed when diabetes was a rare disease in the elderly and people had mostly larger particles, and so the normal range is adapted to those. High small particles can lead to a LDL-C in normal or even below normal range, as they carry very little cholesterol. So the LDL-C goals for diabetics need to be adapted to that.
@@stellasternchen You might want to have a look at the follow-up video on the study referenced by Budoff. It says that in Lean Mass Hyper Responders there is no relationship between small dense LDL and the coronary calcium score. The R2 and the adjusted R2 are very close to zero. So, SDLDL is not sufficient in causing calcification by itself -- it might however be in the presence of inflammation.
@@ziggywest7837 You misunderstood. I was not talking about sdLDL at all. SdLDL is not the same as small LDL. SdLDL is the smallest type of LDL that is known on the spectrum. I was referring to particles smaller then the average. And it is about the quantity of all particles that determines the risk, not the size. Note that LDL is not the same as LDL-C. Note that LDL has LDL-C inside. Note that the size of one LDL is determined by the amount of LDL-C inside. Note that the same amount of LDL-C can fit in one larger LDL or in multiple smaller ones. The same number of LDL-C can show higher risk if it fits in multiple smaller LDL then one large. I also have to explain to you that this is not about what causes the calcification but the plaque formation. The calcification is like the band-aid put on an infected wound. It shows that there is an injury, but it is not the wound itself or the inflammation inside. Quite the opposite. It prevents the puss underneath from going out sealing it off. So yea. LDL does not cause calcification, the inflammation (plaque) does. The calcification stops the plaque from rupturing, sealing it off from the blood vessel and preventing parts of it traveling to the heart or lungs when the body is no longer able to control that chronic inflammation. The inflammation that is caused by LDL injuring the vessel, causing inflammation - a vicious cycle of it as immune cells accumulating more LDL until they die which recruits more immune cells and releases toxins- is the plaque. In simple terms an open foul smelling wound with dead tissues inside. Do you think that might increase inflammation markers you can measure? Of course. But what you are trying to tell me here, is that LDL can only cause that type of wound if there is inflammation elsewhere already in the body. I don‘t get that. I‘m not immune to getting an infected wound from injuring my knee, just because I did not have a cold at the moment it happened. The fact that he did an other subgroup analysis makes me question if he just fell asleep in statistic class or if he just does not care. What he does here is called post hoc analysis. It is already a questionable method to use collected data, because you theoretically find a correlation using it that fit the conclusion that you want to draw beforehand. When doing research you normally have a question you are searching an answer for. Then you design an experiment/study around it to collect data, ensuring to select the right participants, the right number to reach statistical significance, minimizing factors that would compromise data, finding the best setting, duration etc.. This data is collected, analyzed, statistics are made. Statistical adjustments are made for any factors that might disturb findings. The findings are presented and discussed. Limitations of the studies are clearly mentioned and what kind of further research could contribute to further answer this question. Post hoc analyses are backwards. They begin with data selected for a different study question. That data is analyzed for every possible correlation there might be and from that research questions are formed from the conclusion drawn by the observed correlations. These conclusions are based on data collected not with the research question in mind, the statistics are not correctly adjusted for drawing the conclusion and the study population was not selected for it either. In other words. Proper research starts with a question and finds possible answers. Lazy research starts with some answers, draws conclusions in order to find a question fitting the answer. That is what Budoff is doing here. And then he is doing subgroup analysis. What is that? He is putting the data into several subgroups and comparing a specific variable between the subgroups. But this is very much frowned upon especially with such a small number of participants - the number of people would be far to small to be significant for anything. And now - with the sdLDL/diabetics analysis you are telling me he also did a subgroup analysis of a subgroup analysis. Jep👏 Good example of what I was taught is questionable use of statistics. If you are suspicious of big Pharma and statins and that‘s why you here - this guy is certainly working for them. He worked for a Pharma company and designed the trials for the drug vazkepa. Vazkepa is actually a very expensive version of an omega-3 supplement you can get for cheap in the supermarket/pharmacy. The trials were supposed to prove the reduction of cardiovascular events in people with coronary artery disease. Both groups (intervention, control were on other meds they needed!) My country took this drug of the market because of study manipulation. Budoff designed the trial as such, that the people in the control group were given a laxative (mineral oil) as placebo and they did not get the full dose of their meds as a result. This is how the drug vazkepa showed benefit. Those results were not reproducible in other studies without mineral oil as control. In other words. My country (Germany) is of the opinion this guy manipulated a drug trial to get a drug on the market that does not work.
My ldl-p was so high they didn’t even give me a number. They just said over 3500 - but I don’t fit the LMHR profile. My hdl is low and my triglycerides are high. I am still a bit overweight but have lost almost 100 pounds in the last year on keto. It could be my thyroid causing my high ldl-p, but not sure. Just got a CAC score but they are so far behind in reading it that I won’t get the results yet for over a month. But a bad CAC score won’t deter me from my carnivore diet
Shouldnt the LMHRs be compared to people with the same BMI and body composition? The BMI of 22 is in someone lean. The control group with a bmi of 25 will no doubt have more subcutaneous and visceral fat, and likely lower muscle mass
Definitely, agree. The BMI is sufficiently different between both groups to not be ruled out as an IV influencing the result. The cohort of lean mass hyper responders (low BMI, high HDL, low trigs, and high LDL) respresenting a keto diet is only a subsample of those on a ketogenic diet and not necessarily represenatative. However, imho they may be sufficient to call into question the traditional thinking on the role of LDL, apo-B and small dense LDL on heart disease risk. Like you, I would be seriously interested in seeing what would happen if a more general sample of subjects on a keto diet were analysed.
What I don’t understand is if this study challenges the conclusions and interpretations of past evidence where they felt that lowering the LDL was a positive because it would lower lower plaque is now being ignored because of “ the data” when someone already has heart disease. I understand we don’t have a study on it yet. It would indicate that this new information and insight from this study would also have us question the conclusion that LDL is a risk factor and people with heart disease already. LDL is not causing heart disease then the fact that they already have heart disease would also mean the LDL is not contributing to heart disease in this case. Not sure what I’m missing. It is a contributing factor or it isn’t.
24:00 creo en la dieta citogénica porque creo que los carbohidratos contribuyen aumentar los triglicéridos, Y los triglicéridos al almacenamiento de grasa y la inflamación
Dave, great video. Can you please provide a link to the paper in the show notes? Also, he talks a lot about "keto" diets. Most scientists only call a diet "keto" when the person is in a ketogenic state defined by producing ketones greater than or equal to .5mmol/L. In order to determine ketosis, ketones must be measured and ketosis cannot be assumed by the food that is eaten. As you know, everyone reacts differently to a particular diet. Many internet influencers including Dr. Westman incorrectly label low-carb diets as "keto". I would like to know if the diet was a real keto diet where people were verified to be in ketosis or not a keto diet where it was just a very low carb diet. There is a huge difference in metabolism between people in a ketogenic state and people who are not in ketosis and just eat a low-carb diet.
Also if I remember correctly the participants had to have regular ketone tests over the .5 threshold. They didn’t have to bat 1000 but there was criteria for it.
Dr Sean O'Mara has tested visceral fat on long distance runners, not uncommon for them to have it. Visceral fat secretes toxins which inhibit normal gene functions that prevent arteries from calcification.
@@CashMoneyMoore There are some studies that show a correlation between ongoing high cardio and atherosclerosis. Possibly increased turbulence in blood vessels over longer periods; effectively a continuous physical assault. Some high cardio people also have high carb diets and maybe that causes an additional glycation assault on blood vessels.
@@trail.blazer YES YES YES Glycation from carbs and ROS spilled out from overworked mitochondria and super oxidative stress from long distance running.
there is a strong association with diabetes and statin usage and diabetes has the strongest association to CVD of all the factors we generally understand. Statins in general interfere with clotting and inflammation it certainly doesn't seem to be the LDL aspect. Seehausen et al (2024) has an interesting graph showing high LDL with the lowest incidence of progression based of VLDL but even high levels of VLDL and high LDL matches the best results from the low LDL group. In other words this whole lowering LDL specifically looks bunk.
Lol, no. Again, a recent study sowed a strong insulin response is protective against type2 diabetes. Insulin is not the enemy. Insulin would have to be chronically too high to induce insulin resistance, not as a response to food. The people that developed diabetes in those studies where prediabetic. We know that statins can slightly rise blood sugar. Why? Because they decrease insulin secretion. But statins also get rid of those small LDL and the high triglycerides that do come with metabolic syndrom/diabetes.
@@stellasternchen lol, yes ;) Chronic stimulation of TRPV1-> chronic stimulation and the risk of hyper secretion of insulin and then insulin resistance happens. Cells already resistant become more resistant. Why? Because insulin stimulates more TRPV1 including on cell membranes that forces glucose into cells ~independent ~ of the insulin receptor. This leads to too much glucose metabolism and ultimately reactive oxygen species production in ~excess~ of the cell’s antioxidant supply and this leads to lipid oxidation, mitochondrial and cell damage. TRPV1 on mitochondria with excess activation leads to mitochondrial destruction and ultimately cellular apoptosis. Do you know how glp-1 and TRPV1 function? Check out the 2020 Berkeley study that describes the neurolymphocrine system.
This video was now really just the answer I needed. Because my LDL is so high, HDL low and Trigltcerides very low as well as very low blood pressure. I am a female, 66 yrs old and a carnivore. Two days ago my doctor says I am a nightmare happening and I must!!!!!!!! use statins.😢
Hope you have a doctor like mine. He charts “Patient refused” and shuts up. Of course I keep sharing these videos with him so he doesn’t want me to start up again…LOL
You are certainly not alone. I am in Australia, 66 female on low carb (eat meat fish veg) ,moderate fat consumption . My LDL is always very high ,HDL high, trigl very low, sugar low. My doctor is pushing statin every time i see him which I refuse. I have tried a 2 other doctors but they also sing the same song. I am not sure what to do now.
11:25 en el contexto de una buena salud metabólica el LD L alto no debe representar una preocupación especialmente cuando es inducido por una dieta cetogénica. En pacientes que tienen trastornos metabólicos, diabetes, síndromes metabólicos el LD L es un factor de riesgo modificable. En el contexto de una buena salud metabólica no vimos al menos durante 4.7 años a sufrir más ateroesclerosis que la población en general
Where can we find the document/literature that describes and summarizes the "match analysis" for "Lundquist LMHR Study" versus the "Miami Heart Study"?
A number of medications shouldn't work by their alleged mechanism, but seem to work anyway, and it's likely because of anti-inflammatory side effects. Two that spring to mind are SSRIs for depression and doxycycline for several non-bacterial illnesses. Statins are known to have an anti-inflammatory side effect, so they have all the makings of a medication that works better than it should.
Amazing stuff. My question would have been, is there or will there be a followup to look at progression in Miami Heart to see what "normal" progression looks like. And 2) why do we think there was no association between ldl and coronary plaque in Miami Heart? Is it because they were pretty darn metabolically healthy already and their ldl was just lower? IE the metabolic health is the larger factor than just ldl
Miami heart is just a dataset from a different study they picked to compare with that had people with statins, existing plaques, did not fit in BMI with LMHR participants, do not know if they are metabolically healthy or not etc… This is comparing apples to oranges. You can‘t do a follow up if you take data from somebody else instead of collecting your own. Yes metabolic health does play a part. It also has time and time again been shown that LDL-C does not depict cardiovascular risk accurately in those that are not metabolically healthy. Framingham heart study for example. And? People with poor metabolic health have 3 other risk factors on top of that, being overweight/obesity, high blood pressure, having an sedentary lifestyle. We know that tose individuals have lower LDL-C due to their predominantly small particles full of triglycerides low in cholesterol. So we look at the trigs. Other markers that better depict risk are ApoB or LDL particle measures.
Hdl will not increase in anyone unless the structure of the phospholipids in the HDL membrane can accommodate the curvature geometry required. HDL is small and dense, and the surface curvature is tight compared with larger LDL and VLDL. To accommodate this tighter curvature, a person has to either eat small chain fatty acids in their food or make them via the gut mirobiology through a higher fibre diet. Someone really should start studying interfacial colloidal science related to surfactant curvature of membranes and effects on packing at the interface.
Hi Tony I've just had my blood work back and I have very high hdl and very high ldl If I try to lower my ldl I'm worried my hdl Will be lowered as well do you think I should not Take a statin incase my hdl goes down as well I Live in the UK And when they are talking about Numbers I can't convert the US to the UK I find it so hard to understand Any help would be appreciated.
@lindapestridge3073 hi Linda. Sorry for the late reply. Firstly I recommend you talk to your doctor about your concerns. I have a background in science and research, but I am not medical. I take a very high dose statin, which I would like to either lower or get off. My approach has been to reduce the dose and alter my diet at the same time. I eat a lowish carb diet, i.e., no sugar, bread, pasta, rice, potatoes, cake, snacks etc. I eat meat and lots of green veg. I have stopped using dairy but still eat cheese. I also eat as healthy as I can, so there is no processed food and only eat out about once a month. My HDL is good, and my LDL is low, but I am also very happy my triglycerides are low as well. I had my bloods done last week, and they look good. I supplement with combined D3 and K2, magnesium, and I use low salt. I restrict my eating window five days a week from 12am to 7pm. I only drink a couple of beers on a Friday and have a lowish alcohol bottle of wine over the weekend. I exercise and keep active. I live in the UK also and get my blood test results directly to my NHS account. They are all displayed in an easy to read form, placing them within or outside the required bands. You should be able to do the same. Hope this helps. But if your confused your doctor will help.
Thanks Dave, Budoff and Nick 🙏 I am on keto for couple months now, dropped my a1c to 5.5 from 7.5, ldl-c 190, ldl-p 2200, hdl 60, tg 61, didnt check my cac yet, fastin insulin 3.6 with LP-IR 37, overall feel so good after switching to keto. Love LMHR. Do i need to be concered with high ldl-p?
Being in full ketosis and taking a statin or pcsk9 inhibitors should work against the lipid energy model. Destroying the fuel needed that is transported by the ldl. Is that correct an assumption?
Lipids are transported by chylomicrons to the liver from your gut. Liver cells are the only ones capable making ketones. If stored lipids are recruited for energy production, they travel as a free fatty acids bound to albumin, not in LDL particles. It does not make any sense to me, what the lipid energy is proposing.
On low carb diet, you have low insulin thus excess fat in chylomicron is taken up and repackaged by the liver as VLDL . Excess free fatty acid is also taken up by the liver as well as by the muscles. In low insulin environment there is a lot of excess fat that cannot go to storage (due to low insulin) in fat cells, and it is not possible to float around in free fatty acid form only ,so the liver makes more VLDL. After fat in VLDL is used by the body, VLDL becomes LDL. Statin does not halt the production of VLDL but increases liver uptake of LDL.
@@virojchittchang655 What you are writing here contradict itself. You are perfectly describing a state of insulin resistance. Fat droplets on muscles, on fat cells, blood stream full of free fatty acids. Those fat deposits have been demonstrated to block insulin receptors. Fat infusions cause insulin resistance in rats. Proposed mechanisms are that this protects the mitochondria from lipid overload, as lipids are high energy, take long to burn and cause lots of free radicals that need to be neutralized before causing major damage. The other proposed reason is a mechanism preserving glucose supply to vital cells that can not exist without it in the liver, blood and brain when there is not enough. I‘ve read a study of the phenomenon of insulin resistance and reduced glucose tolerance in endurance athletes, but not in other kinds of athletes. This seems to be an effect of them being in fat metabolism for a prolonged time. Hyperinsulenemia has been shown to precede insulin resistance in the obese. What does hyperinsulenemia in the insulin sensitive cause? Low blood glucose. Anyway in both the keto diet and the prolonged endurance exercise insulin is low. We know this is reversible at least in keto by eating carbs. Glucose cures insulin resistance. Funny. Illogical. But glucose seems to get rid of the fat overload. Back to keto and the lipids. Where is the high cholesterol coming from? There is everything but. Let’s look at your text. You say we have high VLDL particles, high LDL particles, high free fatty acids and high triglycerides from diet, as they fail to be stored. If there are lots of triglycerides - we also have HDL particles picking them up by exchanging their cholesterol for TG from LDL. LDL and HDL particles, that carry many TG, are small, have less cholesterol. This model describes insulin resistance perfectly, but also explains the lipid transport during it very well. But it would result in high VLDL-C, normal or low total cholesterol, normal to low LDL-C, high to very high triglycerides and low HDL-C. Remember: LDL = particles LDL-C = cholesterol inside LDL particles. This can‘t be it. The LMHR phenotype has the opposite lipid profile: LMHR have very low VLDL-C very high TC, very high LDL-C, very high HDL-C and very low TG. 1. Why would the liver send the fatty acids from diet coming from the chylomicron anywhere during ketosis? They are needed in the liver to produce ketones and even can be stored there if not needed right away. If at all I would expect lower VLDL production and low TG send to be stored somewhere. But what I would see is tons of free fatty acids. Fat from fat cell storage is needed for ketosis and so the lipid droplets with TG‘s from fat cells are dissolved. Free fatty acids travel to the liver. But there is cholesterol in those droplets now no longer needed. And I think that is the cholesterol in our particles. It is picked up by HDL, given to LDL in exchange for some TG and brought to the liver to be excreted via bile. And the rate this is happening is overwhelming the LDL receptors of the liver, no longer able to keep it up. This results in lots of LDL full of cholesterol floating around.
It can't be either LDL is 100% the problem or LDL is zero percent of the problem. I'm coming back in 2 years and hopefully AI will have figured it out.
@@ronaldlenz5745 I suggest you go and do some proper research. If you have any doubts, go and get yourself an angiogram of your heart to see all the plaque buildup you have, Afterwards, you can thank me for saving your life.
22 min: statin used to lower ldl if existing heart disease but ldl is not a cause. Surely this strategy avoids the root cause .... carbs. In other words let's treat root cause, not symptoms
I've been doing intermittent fasting and very low carb diet for years. My doctor was horrified at my very high LDL (and overall cholesterol) and tried very hard to get me on a statin, which I politely refused. We agreed that I would do a CAC scan instead to make sure I wasn't doing too much damage to my arteries. Fast forward a few weeks... I have a CAC score of *zero*. My arteries are perfectly clear, yet my LDL is well over 200. Something is very wrong with traditional medicine's accepted understanding of cholesterol.
CAC doesn't tell you if you have arteriosclerosis. It only tells you have calcium attaching to it.
Ditto story for me
@@suzannehodgkins7197 In other words, no calcification.
Its worth noting one thing about a zero cac score on keto, (I'm a lmhr and also got zero cac score ). A Cac scan only measures calcified plaque and not soft plaque (more dangerous plaque ) .A keto diet , over time develops a healthier metabolism ,which is then better able to calcify any existing soft plaque that would not show on a cac scan . Hence , a future cac scan may then show some calcified plaque .Don't panic if that happens . As long as the cac score isn't very high , this may just be pre-existent soft plaque that eventually calcified because of the ketogenic improved metabolism. .
Same here!!! My triglycerides went down to 90 but after a two month illness in the inability to cook I had to eat what my husband gave me. When I had my blood work done for my annual check up my triglycerides had gone up over 130. He wanted to put me on a statin and I said no it’s because I have been down for two months with my back and I am unable to cook and I have to basically eat. What’s put before me. My Husband and Retired and I’m not gonna make him work all day and then figure out what the heck I can eat and not eat. When I finally get up and walk and shop and I got back into it. I’m not 100% perfect but in my home, we do not have carbohydrate foods.
I think that was Nadir Ali asking one of the questions. He’s right, we need to consider completely dismissing the Lipid/Heart hypothesis. It was wrong and doomed from the beginning.
However, it is very effective at getting statins prescribed and making money for big pharma.
I appreciate Dr. Budoff’s explanation for why he prescribes statins. I suspect his comment is at odds with a few watching this video, but to me it demonstrates clear, honest, and measured thinking. Thank you for posting this, Dave.
Dave. Please do a study next on newer carnivores with a CAC to see what happens. Thank you for all of your hard work. What you're doing for humanity is very important.
Yes!
I have been on carnivore for 14 months. Went from insulin resistant to LMHR in 9 months. I am 54 with a CAC score of 121. Would love to be in the next study. Thanks Dave, Nick, and Dr. Budoff for everything you guys are doing. You guys are a blessing to humanity!
That's awesome. They need to include folks new to carnivore like yourself to see if CAC results improve or at least stay the same.
CAC scores never improve due to the irreversibility of the condition.
@@OisteinThomassenMScPharm never say never! I've seen some post that they have improved!
@@OisteinThomassenMScPharmIt was thought that plaque was irreversible until ppl doing ketogenic diet showed less plaque on scans ,cac and CT Angiogram.
NOT TRUE!. Do your research. Many cases of reduction, especially with change to a KETO or Carnivore diet and use of the supplement K2 with MK-4 & MK-7. My husband is one of those lucky people who lowered and continues to lower his CA score. He is not on a statin. @@OisteinThomassenMScPharm
I was KETO for 6 years and fell naturally into carnivore this past year due to simplicity and my new found craving for fatty beef. Best I've felt in my life! My doctor's mind is blown, but I refuse to take a statin. Never had it, never will. My LDL is routinely 250+
Me too
My respect to Dr. Budoff who - as probably every cardiologist - have had his biases but was willing to actually look at the real data.
Many other scientists just stay in their own dogmas which is very sad to see them being so closed-minded...
I’ve had high cholesterol my entire life. My father was a butcher and we always had meat on the table. I used to smoke and was around second hand smoke my whole life as well. I am 56 years young and started ketovore this past December. Had my first cac scan in February and it was a score of 7. Feel amazing 🙌🏼. I can’t wait to get my blood work again and see what it’s gonna show me. My A1C said 5.8 so I’m hoping it went down.
Since going low carb over 6 years ago, HDL remained steady, Triglycerides went from 260's to 80's, Total and LDL skyrocketed (321 and 253 respectively on last labs). I also dropped my A1C from 10.1 to 5.3 (highest to lowest). Doctor has been pushing me to go on statin. I have politely declined so far.
It is encouraging to witness this new science reporting evolve. Unfortunately (my) doctors still use very old "recommendations" and feel with absolute necessity to refer to book-worn old pages, to assure themselves, in prescribing statins for high LDL rather than what is in the best interest for the individual patient. Thank you for producing a quality video of this rich caliber about an old topic that needs modern day adjustment.
Not on KETO long enough to get in the study so was not selected , all other numbers in line with LMHR. Thank you Dave and DR B, keep the info coming.
lol
Zero CAC at 58 and just now at 62 yo. I’m probably done with all the testing: keeping my Zeros on file.
On long term ketosis?
@@rahvastepaabel Nope. Actually some terrible behavior for most of my life. Father had cvd and I was a heavy smoker and drunk for 35 years.
That's excellent but zero CAC doesn't mean you have no CAD. You could still have soft plaques. A better test than CAC is CCTA.
@@terryolay4613 or an ultrasound of the carotid arteries. Less radiation with a sonogram. The less we are radiated the better.
@@terryolay4613 Yes, but what I was sharing is that one can get tired of looking for trouble after a while. So that’s why I’m banking the good news and over looking for trouble. Just gets old.
I wish these papers and presentations would also detail mmol. Not everyone is American. That said, all power to you all for your crucial work.
You should be though 😜
I've convert my numbers from mmol to dl whatever it is so that I can compare the more easily.
It's an easy conversion. Whenever they give you a cholesterol value in mg/dL, simply divide it by 38.6 to convert it to mmol/L. With triglycerides, you divide the U.S. number by 88.5. That's all there is to it.
Thank you for posting these sessions
Another great video Dave and Dr. Budoff, thanks for all the very important work you and your organization does. Cheers. :)
Fantastic! thank you for all you've done getting this out there.
Statins help patients become diabetic which increases heart disease risk by 10x. I applaud DF and everyone participating is reconstructing the ASCVD paradigm.
BS
2 times. But it decreases small LDL particles, the most dangerous part of being diabetic.
The risk of becoming diabetic on a statin is very low. The people that did become diabetic in the studies were already pre - diabetic.
@@stellasternchen meat and dairy contribute greatly to diabetes.
@@WFPBFORLIFE eat your statins and enjoy thinning of the cardiac muscle and CHF!
@@danielmccarthyy If you live a WFPB Lifestyle statins are never needed and cholesterol is not an issue. High cholesterol comes from one basic dietary plan. no meat 39 years!
Thanks Dave and Nick and Dr Budoff for this incredible work, God bless you all! This is SO exciting! Dr Budoff you are a rare MD that thinks of the individual, not the rote, standard treatment path. I have high cholesterol level, like the LMHR. My cardiologist had me get a CAC and cardiac ultrasound, all normal. She stopped bugging me to take a statin, which I’ve refused from several other MD’s. My dad took one, had a cholesterol level in the 170’s got dementia, had a debilitating stroke. I don ‘t want that path for myself.
I don't know why Dr. Budoff would use statins on a person who is now low carb but has proven heart disease. He would likely agree that the heart disease is the result of years and years eating a crappy diet. If the person now eats a low carb/keto diet, and their LDL spikes upwards, the 4.7-year LMHR study shows it does not provoke plaque formation. So, I repeat. What's the statin for?
Cholesterol does not determine plaques. Blood pressure, stress, do. See Malcom Kendrick.
My BP is always perfect 🙌🏼.
I agree, I think blood pressure is a biggger factor. I saw a study in pigs that high ldl had no effect on their coronary plaque until they raised their blood pressure
I'm reducing plaques with no statins. My inflammatory markers are quite low, lowered insulin, lowered BP, reduced resting HR from 65-70 BPM to 55-60. HDL/Trigs 78/58. Two years keto then 3 years carnivore.
@@pmccord9The only diet proven to reduce plaques was a vegetarian one. Sorry. That‘s why I can‘t stand people online selling specific diets, diet books, coachings promising a mirical healing. Because people do just think they should ignore medical advice.
@@stellasternchen when I was plant based, I was anemic, obese, B12 deficient, prediabetic, and grotesquely flatulent, with acid reflux. All that resolved with carnivore along with disappearing calcium plaques. N of one.
Let me tell you a new story. I've been low carb, more animal based, since 2018. I ate terribly all my life and in 2016 I needed a triple bypass. My goal with a low carb diet was to prevent a reoccurrence, although my cholesterol did skyrocket. I always refused a statin. In April 2024, I did experience some new, albeit fairly minor, angina. I got a new 64-slice CT angiogram. It detected the calcium and plaque in my old (i.e. native) arteries, but guess what it found in my 3 bypass grafts? Nothing. Nada. All those bypasses were "patent." Do you know what patent means? It means normal, open, clear. This aligns well with the LMHR study on people like me who go low carb. The big difference being now I'm talking about bypass grafted arteries, not original arteries.
I feel like there should be more comments here or an entire video about just this... wow. I went to your channel and watched your speech for background and context. So eating high fat low carb for the last 8 years deposited nothing, no soft plaque nor calcified plaque, in the new artery grafts that have been carrying the full load for the arteries found to be blocked in 2016?
@@ellieb2914 Yes. The bypass grafts are clear despite eating high fat low carb and seeing my LDL rise more and more the stricter I got with my diet. And thanks for checking out my speech at CoSci in Las Vegas.
@@Malcolm-Achtman That's amazing! If I may ask, are you following any supplement protocols that may prevent further plaque creation/calcification? For example K2 (MK-7).
@@ellieb2914 I've been taking K2 since 2013, after reading about it in Dr. Kate Rheaume-Bleue's book entitled "Vitamin K2 and the Calcium Paradox." I still K2 but I don't believe it's a magical solution for plaque. It can't hurt, though, so I take it. I take other heart supporting supplements, most of which are recommended by cardiologist Dr. William Davis (who I follow). He especially says to take vitamin D3 and magnesium, which I've done for years. I take a kelp supplement that provides iodine, which supports the thyroid, which is important for heart health too. I've been taking CoQ10 for about 15 years (although that one is not on Dr. Davis's list). Dr. Davis likes fish oil and I would sometimes take it, but I've moved away from that as I feel it is not necessarily helpful. I prefer getting my omega-3 from eating real fish (e.g. wild caught salmon). I take some methylated B supplements as well. And some vitamin C (whole food Camu Camu vitamin C capsules).
Super interesting, and demonstrates that the new diet resulted in no new calcium in (probably) in any of the arteries after. So why would Budoff prescribe statins for someone like you to lower the high LDL that is a consequence of the diet/ lifestyle that resulted in such a positive effect? Meantime those drugs will be majorly manipulating your metabolism, for the rest of your life. Wow!
Been low carb since 2018, last blood panel 2017 (I don’t think going to the doctor in the US is worth the time) until a few weeks ago. Dirty keto with lots of veggies for years, switched to ketovore since 2022. Now high fat ketovore trying to heal some inflammation issues. Now my cholesterol: LDL 505,HDL 118, Trig 62, total 635. My doctor freaked out, but I’m not overly concerned and refuse to take a statin. LMHR is real, I’ll look into getting a CAC scan if LDL is still crazy high in 6 months.
70 yo lost 70 lbs over the last year. (Keto) Cholesterol shot up to 294 LDL 221 HDL shot up to 66 TG way down from 300+ to 74. BMI from 33 to 24. Waist from 44 to 36. LDL particle size now type A (large), IR Reduced to now normal. CAC very low 30 but not zero (from 5 years ago). I work out at the gym 5 days a week followed by 20 min sauna. All markers big improvement except cholesterol. I abused my body for 69 years so I expect it will take more time to reduce the ill affects.
I wonder if I have become a LMHR via my weight loss and lifestyle change.
Keep up the great work.
I read that the drugs would only extend your life a few days. Compared to the side effects I don’t think I would go on the medication 🤷🏼♀️.
What I recall is that, on average, statins extend your life by a day or two for every year you take them. This is for people who have not had a heart attack previously (primary prevention).
@@Frostbikeryes which is why they are not recommended for primary prevention. NNT is too high
In a 2016 BMJ review performed by Ravnskov, et al, it was demonstrated that if you were over 60 years old, LDL-C was NOT associated with cardiovascular disease and was INVERSELY associated with all-cause mortality. So if a person is over 60 years old, then the level of LDL-C was absolutely worthless in predicting development/progression of arterial plaque AND the lower your LDL-C, the earlier you are going to die!!!!!!!
Dr. Sara Pugh has a presentation about LDL, and in one of her slides, the text states that statins extend life by 5 minutes. 🤣🤣
@@CashMoneyMooreThey are if there is a high or very high 10 year risk.
Dr. Budoff really shines - he has all the facts right at his fingertips, and he is willing to state clear conclusions.
Im 42 year old, had a CAC done 3 years ago and i scored a 9. Ive been keto for about a year and carnivore for the last 4 months. My LDL is now 193, HDL is 70 and Triglycerides are 57. My doctor freaked out when he saw my LDL so now i am having another cac done on tuesday. So shall see how this turns out..
Keep us informed ! Ty
How did it gooooo???
Dr. Budoff says he still believes that if a patient has KNOWN CAD/PLAQUE, then that individual should receive LDL-C lowering medicine(s). However, if we consider that LDL particles are "FIREFIGHTERS" that actually dampen inflammation and promote healing of the coronary endothelium, why would we want to wipe out those "FIREFIGHTERS" with statins or PCSK9 inhibitors?🧑🚒👨🚒👩🚒🧑🚒👨🚒👩🚒🧑🚒👨🚒🧑🚒
Thank you!
One extremely important fact that was surprisingly left out of this presentation. Anyone with existing cardiovascular disease was excluded from the study. This was defined, in part, as having a CAC score above the 75th percentile. A number of people were excluded based on this criteria alone. Had they been included there would have been a different starting result. This is beyond misleading. This study, when concluded, will prove if it is successful that if you are on a diet that elevates your lipid numbers, you are unlikely to suffer any negative affects over the next two years. That is the maximum one can learn from a study such as this one. They were told at the outset that they needed at least a five year study to have meaningful results. For a one-year study, they needed progression of plaque rather than incidence of plaque.
Completely agree. Do LMHR with a starting CAC score improve! That would be great to know.
They are also comparing metabolically healthy people with ones that are not, are on statins.
The study will show high LDL does not increase CVD if one fits the LMHR definition.
It’s funded independently. Please donate to the next study so they can test more.
@@stellasternchen if the point is to show that LDL is not THE cause, then that's still valid
Fantastic Q&A, thanks!!
Budoff plays both sides of the argument, in a Medscape discussion recently he was extolling the ventures (lack of risk) of driving LDL down to below 50mg (
Typical nonsense expressed by the ADA. Must keep exploding the growth of the diabetic population to support the salaries and expensive lifestyles of their executives and those executives of the food industry and pharmaceutical companies who financially support the ADA.
You have to understand that diabetics have mostly small LDL particles with little cholesterol.
The LDL-C value measures the cholesterol inside to estimate LDL particle quantity. This measure was developed when diabetes was a rare disease in the elderly and people had mostly larger particles, and so the normal range is adapted to those.
High small particles can lead to a LDL-C in normal or even below normal range, as they carry very little cholesterol.
So the LDL-C goals for diabetics need to be adapted to that.
@@stellasternchen You might want to have a look at the follow-up video on the study referenced by Budoff. It says that in Lean Mass Hyper Responders there is no relationship between small dense LDL and the coronary calcium score. The R2 and the adjusted R2 are very close to zero. So, SDLDL is not sufficient in causing calcification by itself -- it might however be in the presence of inflammation.
@@ziggywest7837
You misunderstood. I was not talking about sdLDL at all. SdLDL is not the same as small LDL. SdLDL is the smallest type of LDL that is known on the spectrum. I was referring to particles smaller then the average. And it is about the quantity of all particles that determines the risk, not the size.
Note that LDL is not the same as LDL-C.
Note that LDL has LDL-C inside.
Note that the size of one LDL is determined by the amount of LDL-C inside.
Note that the same amount of LDL-C can fit in one larger LDL or in multiple smaller ones.
The same number of LDL-C can show higher risk if it fits in multiple smaller LDL then one large.
I also have to explain to you that this is not about what causes the calcification but the plaque formation.
The calcification is like the band-aid put on an infected wound. It shows that there is an injury, but it is not the wound itself or the inflammation inside. Quite the opposite. It prevents the puss underneath from going out sealing it off. So yea. LDL does not cause calcification, the inflammation (plaque) does. The calcification stops the plaque from rupturing, sealing it off from the blood vessel and preventing parts of it traveling to the heart or lungs when the body is no longer able to control that chronic inflammation.
The inflammation that is caused by LDL injuring the vessel, causing inflammation - a vicious cycle of it as immune cells accumulating more LDL until they die which recruits more immune cells and releases toxins- is the plaque.
In simple terms an open foul smelling wound with dead tissues inside. Do you think that might increase inflammation markers you can measure? Of course.
But what you are trying to tell me here, is that LDL can only cause that type of wound if there is inflammation elsewhere already in the body.
I don‘t get that. I‘m not immune to getting an infected wound from injuring my knee, just because I did not have a cold at the moment it happened.
The fact that he did an other subgroup analysis makes me question if he just fell asleep in statistic class or if he just does not care.
What he does here is called post hoc analysis. It is already a questionable method to use collected data, because you theoretically find a correlation using it that fit the conclusion that you want to draw beforehand.
When doing research you normally have a question you are searching an answer for.
Then you design an experiment/study around it to collect data, ensuring to select the right participants, the right number to reach statistical significance, minimizing factors that would compromise data, finding the best setting, duration etc..
This data is collected, analyzed, statistics are made. Statistical adjustments are made for any factors that might disturb findings.
The findings are presented and discussed. Limitations of the studies are clearly mentioned and what kind of further research could contribute to further answer this question.
Post hoc analyses are backwards. They begin with data selected for a different study question.
That data is analyzed for every possible correlation there might be and from that research questions are formed from the conclusion drawn by the observed correlations.
These conclusions are based on data collected not with the research question in mind, the statistics are not correctly adjusted for drawing the conclusion and the study population was not selected for it either.
In other words. Proper research starts with a question and finds possible answers.
Lazy research starts with some answers, draws conclusions in order to find a question fitting the answer.
That is what Budoff is doing here.
And then he is doing subgroup analysis.
What is that? He is putting the data into several subgroups and comparing a specific variable between the subgroups.
But this is very much frowned upon especially with such a small number of participants - the number of people would be far to small to be significant for anything.
And now - with the sdLDL/diabetics analysis you are telling me he also did a subgroup analysis of a subgroup analysis.
Jep👏 Good example of what I was taught is questionable use of statistics.
If you are suspicious of big Pharma and statins and that‘s why you here - this guy is certainly working for them.
He worked for a Pharma company and designed the trials for the drug vazkepa.
Vazkepa is actually a very expensive version of an omega-3 supplement you can get for cheap in the supermarket/pharmacy. The trials were supposed to prove the reduction of cardiovascular events in people with coronary artery disease. Both groups (intervention, control were on other meds they needed!) My country took this drug of the market because of study manipulation.
Budoff designed the trial as such, that the people in the control group were given a laxative (mineral oil) as placebo and they did not get the full dose of their meds as a result. This is how the drug vazkepa showed benefit.
Those results were not reproducible in other studies without mineral oil as control.
In other words. My country (Germany) is of the opinion this guy manipulated a drug trial to get a drug on the market that does not work.
My ldl-p was so high they didn’t even give me a number. They just said over 3500 - but I don’t fit the LMHR profile. My hdl is low and my triglycerides are high. I am still a bit overweight but have lost almost 100 pounds in the last year on keto. It could be my thyroid causing my high ldl-p, but not sure. Just got a CAC score but they are so far behind in reading it that I won’t get the results yet for over a month. But a bad CAC score won’t deter me from my carnivore diet
There is something about Dr. Budoff that makes you stop and listen to what he has to say. He makes a lot of sense.
He's excellent
Shouldnt the LMHRs be compared to people with the same BMI and body composition? The BMI of 22 is in someone lean. The control group with a bmi of 25 will no doubt have more subcutaneous and visceral fat, and likely lower muscle mass
Definitely, agree. The BMI is sufficiently different between both groups to not be ruled out as an IV influencing the result. The cohort of lean mass hyper responders (low BMI, high HDL, low trigs, and high LDL) respresenting a keto diet is only a subsample of those on a ketogenic diet and not necessarily represenatative. However, imho they may be sufficient to call into question the traditional thinking on the role of LDL, apo-B and small dense LDL on heart disease risk. Like you, I would be seriously interested in seeing what would happen if a more general sample of subjects on a keto diet were analysed.
Thank you for sharing this video.
What I don’t understand is if this study challenges the conclusions and interpretations of past evidence where they felt that lowering the LDL was a positive because it would lower lower plaque is now being ignored because of “ the data” when someone already has heart disease.
I understand we don’t have a study on it yet. It would indicate that this new information and insight from this study would also have us question the conclusion that LDL is a risk factor and people with heart disease already. LDL is not causing heart disease then the fact that they already have heart disease would also mean the LDL is not contributing to heart disease in this case. Not sure what I’m missing. It is a contributing factor or it isn’t.
24:00 creo en la dieta citogénica porque creo que los carbohidratos contribuyen aumentar los triglicéridos,
Y los triglicéridos al almacenamiento de grasa y la inflamación
Great video, heartwarming and ....
Dave, great video. Can you please provide a link to the paper in the show notes? Also, he talks a lot about "keto" diets. Most scientists only call a diet "keto" when the person is in a ketogenic state defined by producing ketones greater than or equal to .5mmol/L. In order to determine ketosis, ketones must be measured and ketosis cannot be assumed by the food that is eaten. As you know, everyone reacts differently to a particular diet. Many internet influencers including Dr. Westman incorrectly label low-carb diets as "keto". I would like to know if the diet was a real keto diet where people were verified to be in ketosis or not a keto diet where it was just a very low carb diet. There is a huge difference in metabolism between people in a ketogenic state and people who are not in ketosis and just eat a low-carb diet.
The study is not out yet, it has not passed peer review as well.
@@stellasternchen Thanks!
Also if I remember correctly the participants had to have regular ketone tests over the .5 threshold. They didn’t have to bat 1000 but there was criteria for it.
Jim Fixx was a runner which also may have contributed to his untimely death. There’s research linking endurance athletes and heart disease.
Probably running away from bad diet and trying to fix themselves, the running helps
@@CashMoneyMooreit has to do with the increased cardiac demand of endurance athletes for longer periods of time.
Dr Sean O'Mara has tested visceral fat on long distance runners, not uncommon for them to have it. Visceral fat secretes toxins which inhibit normal gene functions that prevent arteries from calcification.
@@CashMoneyMoore There are some studies that show a correlation between ongoing high cardio and atherosclerosis. Possibly increased turbulence in blood vessels over longer periods; effectively a continuous physical assault. Some high cardio people also have high carb diets and maybe that causes an additional glycation assault on blood vessels.
@@trail.blazer YES YES YES
Glycation from carbs and ROS spilled out from overworked mitochondria and super oxidative stress from long distance running.
Statins stimulate TRPV1 that stimulates insulin secretion and hyperinsulinemia causes insulin resistance!
there is a strong association with diabetes and statin usage and diabetes has the strongest association to CVD of all the factors we generally understand. Statins in general interfere with clotting and inflammation it certainly doesn't seem to be the LDL aspect. Seehausen et al (2024) has an interesting graph showing high LDL with the lowest incidence of progression based of VLDL but even high levels of VLDL and high LDL matches the best results from the low LDL group. In other words this whole lowering LDL specifically looks bunk.
@@scottw2317👏I bet this study is a RCT? Or a randomized Mendelian study? Because those show the opposite.
@@stellasternchen why the hell would mendelian bias bs be a strong study? only vegans push that bs.
Lol, no. Again, a recent study sowed a strong insulin response is protective against type2 diabetes.
Insulin is not the enemy.
Insulin would have to be chronically too high to induce insulin resistance, not as a response to food.
The people that developed diabetes in those studies where prediabetic.
We know that statins can slightly rise blood sugar. Why? Because they decrease insulin secretion.
But statins also get rid of those small LDL and the high triglycerides that do come with metabolic syndrom/diabetes.
@@stellasternchen lol, yes ;) Chronic stimulation of TRPV1-> chronic stimulation and the risk of hyper secretion of insulin and then insulin resistance happens. Cells already resistant become more resistant. Why? Because insulin stimulates more TRPV1 including on cell membranes that forces glucose into cells ~independent ~ of the insulin receptor. This leads to too much glucose metabolism and ultimately reactive oxygen species production in ~excess~ of the cell’s antioxidant supply and this leads to lipid oxidation, mitochondrial and cell damage. TRPV1 on mitochondria with excess activation leads to mitochondrial destruction and ultimately cellular apoptosis.
Do you know how glp-1 and TRPV1 function? Check out the 2020 Berkeley study that describes the neurolymphocrine system.
6:26 los pacientes de dieta cetogénica no tenían puntajes de placa arterial significativos comparados con los de el estudio mi corazón
This video was now really just the answer I needed. Because my LDL is so high, HDL low and Trigltcerides very low as well as very low blood pressure. I am a female, 66 yrs old and a carnivore. Two days ago my doctor says I am a nightmare happening and I must!!!!!!!! use statins.😢
Hope you have a doctor like mine. He charts “Patient refused” and shuts up.
Of course I keep sharing these videos with him so he doesn’t want me to start up again…LOL
You are certainly not alone. I am in Australia, 66 female on low carb (eat meat fish veg) ,moderate fat consumption . My LDL is always very high ,HDL high, trigl very low, sugar low. My doctor is pushing statin every time i see him which I refuse. I have tried a 2 other doctors but they also sing the same song. I am not sure what to do now.
But yes..appreciate Dr Budoff
11:25 en el contexto de una buena salud metabólica el LD L alto no debe representar una preocupación especialmente cuando es inducido por una dieta cetogénica. En pacientes que tienen trastornos metabólicos, diabetes, síndromes metabólicos el LD L es un factor de riesgo modificable. En el contexto de una buena salud metabólica no vimos al menos durante 4.7 años a sufrir más ateroesclerosis que la población en general
Se considera colesterol anormalmente bajo cuando está por debajo de 40, y este es el colesterol que elimina la placa
The answer is that the higher your triglycerides are the lower the HDL is !
Where can we find the document/literature that describes and summarizes the "match analysis" for "Lundquist LMHR Study" versus the "Miami Heart Study"?
Did you include subjects with High LPa. ???
7:55 el LD L alto no aumenta la respuesta de placa
Okay, I didn't know that LMHR is not equal to FH. That's an important distinction to know.
A number of medications shouldn't work by their alleged mechanism, but seem to work anyway, and it's likely because of anti-inflammatory side effects. Two that spring to mind are SSRIs for depression and doxycycline for several non-bacterial illnesses. Statins are known to have an anti-inflammatory side effect, so they have all the makings of a medication that works better than it should.
Amazing stuff. My question would have been, is there or will there be a followup to look at progression in Miami Heart to see what "normal" progression looks like. And 2) why do we think there was no association between ldl and coronary plaque in Miami Heart? Is it because they were pretty darn metabolically healthy already and their ldl was just lower? IE the metabolic health is the larger factor than just ldl
Miami heart is just a dataset from a different study they picked to compare with that had people with statins, existing plaques, did not fit in BMI with LMHR participants, do not know if they are metabolically healthy or not etc…
This is comparing apples to oranges.
You can‘t do a follow up if you take data from somebody else instead of collecting your own.
Yes metabolic health does play a part. It also has time and time again been shown that LDL-C does not depict cardiovascular risk accurately in those that are not metabolically healthy.
Framingham heart study for example. And?
People with poor metabolic health have 3 other risk factors on top of that, being overweight/obesity, high blood pressure, having an sedentary lifestyle.
We know that tose individuals have lower LDL-C due to their predominantly small particles full of triglycerides low in cholesterol.
So we look at the trigs.
Other markers that better depict risk are ApoB or LDL particle measures.
Metabolic health does indeed seem to be at least 10 to 20 times stronger factor/signal
I hope they measure Lp(a)
Hdl will not increase in anyone unless the structure of the phospholipids in the HDL membrane can accommodate the curvature geometry required. HDL is small and dense, and the surface curvature is tight compared with larger LDL and VLDL. To accommodate this tighter curvature, a person has to either eat small chain fatty acids in their food or make them via the gut mirobiology through a higher fibre diet. Someone really should start studying interfacial colloidal science related to surfactant curvature of membranes and effects on packing at the interface.
Hi Tony
I've just had my blood work back
and I have very high hdl
and very high ldl
If I try to lower my ldl
I'm worried my hdl
Will be lowered as well
do you think I should not
Take a statin incase my
hdl goes down as well
I Live in the UK
And when they are talking about
Numbers I can't convert the
US to the UK
I find it so hard to understand
Any help would be appreciated.
@lindapestridge3073 hi Linda. Sorry for the late reply. Firstly I recommend you talk to your doctor about your concerns. I have a background in science and research, but I am not medical. I take a very high dose statin, which I would like to either lower or get off. My approach has been to reduce the dose and alter my diet at the same time. I eat a lowish carb diet, i.e., no sugar, bread, pasta, rice, potatoes, cake, snacks etc. I eat meat and lots of green veg. I have stopped using dairy but still eat cheese. I also eat as healthy as I can, so there is no processed food and only eat out about once a month. My HDL is good, and my LDL is low, but I am also very happy my triglycerides are low as well. I had my bloods done last week, and they look good. I supplement with combined D3 and K2, magnesium, and I use low salt. I restrict my eating window five days a week from 12am to 7pm. I only drink a couple of beers on a Friday and have a lowish alcohol bottle of wine over the weekend. I exercise and keep active. I live in the UK also and get my blood test results directly to my NHS account. They are all displayed in an easy to read form, placing them within or outside the required bands. You should be able to do the same. Hope this helps. But if your confused your doctor will help.
If statins increase risk of diabetes why? Does he prescribe them?
Is ldl the best target or is it the only target
Estudio nick norwitz y Dave Feldman
Thanks Dave, Budoff and Nick 🙏 I am on keto for couple months now, dropped my a1c to 5.5 from 7.5, ldl-c 190, ldl-p 2200, hdl 60, tg 61, didnt check my cac yet, fastin insulin 3.6 with LP-IR 37, overall feel so good after switching to keto. Love LMHR. Do i need to be concered with high ldl-p?
El colesterol alto no representa una preocupación en el Marco de una dieta cetogénica y con los demás parámetros metabólicas saludables
I'm lmhr ❤ 🎉 trig to hdl is 0.6 with high ldl
Does anyone know the rationale to report the median rather than the mean? If there are outliers on the data at either extreme its good to know
When will this be published?
Would taking niacin help? 250 mg x 4 to 6 times a day
Hi Dave, you asked about getting my brownie recipe at the Keto Chow meetup in Feb. How can I get that to you?
Cuándo el colesterol HDL está alto los triglicéridos bajan
I hear a lot of negativity about statins here, however, I heard they make your CAC bigger
Being in full ketosis and taking a statin or pcsk9 inhibitors should work against the lipid energy model. Destroying the fuel needed that is transported by the ldl. Is that correct an assumption?
Lipids are transported by chylomicrons to the liver from your gut. Liver cells are the only ones capable making ketones. If stored lipids are recruited for energy production, they travel as a free fatty acids bound to albumin, not in LDL particles. It does not make any sense to me, what the lipid energy is proposing.
On low carb diet, you have low insulin thus excess fat in chylomicron is taken up and repackaged by the liver as VLDL . Excess free fatty acid is also taken up by the liver as well as by the muscles. In low insulin environment there is a lot of excess fat that cannot go to storage (due to low insulin) in fat cells, and it is not possible to float around in free fatty acid form only ,so the liver makes more VLDL. After fat in VLDL is used by the body, VLDL becomes LDL.
Statin does not halt the production of VLDL but increases liver uptake of LDL.
@@virojchittchang655
What you are writing here contradict itself. You are perfectly describing a state of insulin resistance. Fat droplets on muscles, on fat cells, blood stream full of free fatty acids. Those fat deposits have been demonstrated to block insulin receptors.
Fat infusions cause insulin resistance in rats. Proposed mechanisms are that this protects the mitochondria from lipid overload, as lipids are high energy, take long to burn and cause lots of free radicals that need to be neutralized before causing major damage.
The other proposed reason is a mechanism preserving glucose supply to vital cells that can not exist without it in the liver, blood and brain when there is not enough.
I‘ve read a study of the phenomenon of insulin resistance and reduced glucose tolerance in endurance athletes, but not in other kinds of athletes. This seems to be an effect of them being in fat metabolism for a prolonged time.
Hyperinsulenemia has been shown to precede insulin resistance in the obese.
What does hyperinsulenemia in the insulin sensitive cause? Low blood glucose.
Anyway in both the keto diet and the prolonged endurance exercise insulin is low. We know this is reversible at least in keto by eating carbs. Glucose cures insulin resistance. Funny. Illogical. But glucose seems to get rid of the fat overload.
Back to keto and the lipids. Where is the high cholesterol coming from? There is everything but. Let’s look at your text. You say we have high VLDL particles, high LDL particles, high free fatty acids and high triglycerides from diet, as they fail to be stored. If there are lots of triglycerides - we also have HDL particles picking them up by exchanging their cholesterol for TG from LDL.
LDL and HDL particles, that carry many TG, are small, have less cholesterol.
This model describes insulin resistance perfectly, but also explains the lipid transport during it very well.
But it would result in high VLDL-C, normal or low total cholesterol, normal to low LDL-C, high to very high triglycerides and low HDL-C.
Remember: LDL = particles LDL-C = cholesterol inside LDL particles.
This can‘t be it. The LMHR phenotype has the opposite lipid profile:
LMHR have very low VLDL-C very high TC, very high LDL-C, very high HDL-C and very low TG.
1. Why would the liver send the fatty acids from diet coming from the chylomicron anywhere during ketosis? They are needed in the liver to produce ketones and even can be stored there if not needed right away. If at all I would expect lower VLDL production and low TG send to be stored somewhere.
But what I would see is tons of free fatty acids. Fat from fat cell storage is needed for ketosis and so the lipid droplets with TG‘s from fat cells are dissolved. Free fatty acids travel to the liver. But there is cholesterol in those droplets now no longer needed.
And I think that is the cholesterol in our particles. It is picked up by HDL, given to LDL in exchange for some TG and brought to the liver to be excreted via bile. And the rate this is happening is overwhelming the LDL receptors of the liver, no longer able to keep it up. This results in lots of LDL full of cholesterol floating around.
It can't be either LDL is 100% the problem or LDL is zero percent of the problem. I'm coming back in 2 years and hopefully AI will have figured it out.
20:...Dr Nadir Ali ❤
plaque build up happens over time. High00 Choesterol issues are caused by one particular food group.
That's great news. Pity about all the other problems associated with a diet based on predominately red meat like colon cancer.
Pity there is no evidence to support that hypothesis.
@@ronaldlenz5745 I suggest you go and do some proper research. If you have any doubts, go and get yourself an angiogram of your heart to see all the plaque buildup you have, Afterwards, you can thank me for saving your life.
@@ronaldlenz5745Exactly
@@tomedwards1879🤣🤣🤣
So why statins?? To me it’s pretty obvious
Dr Budoff has been a waste of my time. He's not a keto guy. He'd treat high LDL with a statin. He is confusing himself & the keto science.
His approach to use of statins is disappointing
💚🏜️💚
22 min: statin used to lower ldl if existing heart disease but ldl is not a cause. Surely this strategy avoids the root cause .... carbs. In other words let's treat root cause, not symptoms
More clown show. Apob should be lower not higher and the data is clear. Eventually higher apob will result in higher plaque.
El colesterol no es el único factor de riesgo cardiovascular, también está fumar, tensión alta y diabetes o genética familiar
My LDL was 245.1
Perfect. Keep up the good work!
LDL 750 here.
Wow nice! Lean?
Wtf
Darn you got my 550 LDL beat!
@@chadfitch3293Are you on keto diet ?
@@saintjulien9707 yes
Don’t statins increase CAC?
Indeed they do…