*1 AMENDMENT* AMENDMENT: It’s been pointed out to me by @F0Xit (on TH-cam) that the researchers (Study 246) should have done a Bonferroni correction on the data. For those not into statistics, if researchers perform multiple comparisons (group A vs group B), it’s common practice in statistics to perform some form of correction, because the risk of detecting an effect that isn’t truly there increases with more comparisons made. A Bonferroni correction drastically cuts down on that risk, which is why many statisticians argue for its use. If a Bonferroni correction were applied to all the data (19 comparisons), the true p-value to meet would be 0.00263 (much lower than the typical 0.05 and what I reported in the study). However, I met with a statistician here at my medical school to discuss the topic, and he argued this would be the incorrect use of a correction, because some of the measures are independent of one another. Technically, he argued none of the comparisons should have a correction applied to them, but he mentioned he could see an argument for some of the measures being corrected (6-9 of them in Table 2). So, if we assume a middle ground and a correction is applied to 9 comparisons, the p-value wanted would have to be below 0.00556. If no corrections are applied, the results are as presented (based on a p-value of 0.05). In the end, even with the most strict option (option 1), some of the effects are still significant. More are significant in the middle option, and obviously all the ones I reported are significant in the uncorrected option. Thank you to “@F0Xit” - I learned something from the comment (below), and although I wasn’t a stranger to statistical corrections, I’ll be on the lookout in 2 sample tests just as I do in multi-sample tests. “None of these measures are significant. When you have so many comparisons you need to correct the p-values. This is done with Bonferroni and with so many comparisons you should divide 0.05 by the number of comparisons (you have 19 observables in the first two tables, therefore is 0.05/19= 0.002). Bonferroni is a quite strict corrector, you may want to use Holm-Bonferroni. This study is statistically quite weak. Although, it may be useful for future meta-analyses. Note: I do medical statistics for a job.”
If you have 19 comparisons and only one of them shows a positive effect, then the p-value should be 0.00263. However, if multiple comparisons show a positive effect while none show a negative effect, the the p-value can be increased again.
Anti plaque stack: Fast 1-3 days a week (free) burpees + jog/run 4 days a week (free) niacin - flushing kind daily (super cheap) vitamin k2 daily (super cheap) psyllium husk daily (cheap) Magnesium daily (cheap if oxide, moderate cost if better form) Add-ons to the stack: Weight training 2-3 days a week (moderate price) Creatine (moderate) Protein (expensive)
HIIT. Most ischaemic events (heart attacks and stokes) occur when a plaque bursts and the outpouring of goo causes a large blood clot which then affects the heart or brain. You have to be careful starting HIIT as this additional pressure can cause plaques to burst and cause an ischaemic event. This happened to a well known BBC presenter in the UK who suffered a stroke trying HIIT.
are you implying that if we've had a bypass (ie lots of plaque), then we shouldn't be doing any HIIT? HIIT is the best way to build collateral arteries
If you had bypass, then stenosis as a result, possibly tied into bad artery. What are my choices, what testing can i do. I never had a heart attack. Im completely lost.
@@bradkeenan4428 If you have narrowed arteries from atherosclerosis then you may have had angina pains or your doctors found calcification in your Coronary arteries. If narrowing is severe then your doctors may choose to operate without you having had a heart attack. Any thought of HIIT must be discussed with your doctor.
Fascinating, I lowered my LDL 50 points in six months by upping my fiber intake, taking plant sterols, cutting out cheese and butter replaced with olive oil/ cod liver oil / black seed oil/ flaxseed oil, eating 600 calories in vegetables daily, and intermittent fasting ( not eating after 2 pm) ( also I always exercise daily so that didn’t have any effect). I’m skinny so everyone said my high cholesterol was genetics, but I proved that by following a different diet than the rest of the family and taking plant sterols I could lower my cardiovascular risk. 😅Also wanted to add that when increasing fiber intake it’s really important to up water intake if you don’t want wrinkles. 😅 I would love to see analysis on any studies on plant sterols and intermittent fasting for atherosclerosis.
Nick Norwitz lower his LDL by 75% with 12 oreo cookies in 2 weeks, he went from 420 to 111 by adding carbs back to his diet. Hes on carnivore or low carb diet.
@@beautylover8138 What are your cholesterol numbers LDL HDL and triglycerides? Before and after ? Do you have family CVD history ? What was your diet before ?
@@manojlogulic4234 Unfortunately his conclusions are BS. He is a hyper responder which is a tiny fraction of people. For the vast majority of people they should NOT eat Oreos(common sense would tell us that). They should follow a Med diet, exercise and if their LDL and apoB are high take a statin. The fact he is on carnivore diet or claims that means he is to be discounted.
@@supernova1976 I improved my LDL cholesterol from 136 to 100, dropping 36 points and shifting from high to normal. Initially, I didn't fast before the test, resulting in an LDL of 125 after a diet change and starting plant sterols. Three weeks later, it was 125, and after five months, including a trip to Ireland where I indulged but balanced it with vegetables and continued plant sterols, it dropped to 100. Even after eating Popeyes the night before my last test, my levels were normal. That was three months ago, and my cholesterol might be even lower now, despite the occasional half cookie. I struggle to maintain weight with a high fiber intake (25-28g daily), requiring 14 cups of fluid to avoid wrinkles and keep up with intermittent fasting and gym routines. My HDL rose from 52 to 61, and triglycerides fell from 120 to 83. Previously, my diet was heavy on cheese, protein shakes, pizza, and buttered popcorn. Despite a family history of high cholesterol (but low blood pressure), I was unaware of the 25g daily fiber recommendation and its impact on skin health until recently. Adjusting my fluid intake restored my skin. Sharing this in case it helps anyone!
On another note: soon new CT photon counting high resolution scanner will be able to reveal intima borders of coronary vessels, information that was previously visible only via OCT wich is highly invasive. No study as of today could compare CT and OCT conclusively because of low resolution. When more data will be available we may be able to see regression in atherosclerosis and potentially retargeting cure and habits of the observed patient.
This was an excellent presentation on the topic and worth the time to view it. It's a complex topic, you covered the key aspects people need to know to get a fuller understanding of the process of CVD.
Very interesting information! I think another thing to look at would be nattokinase supplementation. There are a couple studies that show pretty dramatic plaque reduction, but the dose had to be high enough.
The vast majority of supplements to reduce LDL and apoB have been found to be pretty much useless. Plant stanols or sterols can reduce it by 5% but a simple 5mg Rosuvastatin give you 39% reduction. nattokinase supplement unless from tested scientifically verified trial should be avoided. The famous SPORTS trial showed supplements are generally useless for LDL reduction
I'm taking 12,000 Fibrinolytic Units of nattokinase every day on an empty stomach and have never had any stomach upset. Food will deactivate the Nattokinase, so it's important to take it away from food. @@thomasmuller1850
All I know is i vastly increased my overall activity and exercise while changing nothing about diet or medications (because diet and medication changes were something my doctors and I had adjusted the previous year) and in the six months of increased exercise my cholesterol numbers were all vastly improved. Our next experiment is taking me off avortastatin for 6 months to see if I can continue to get more muscle mass with less pain (muscle pain is a potential side effect from statins that I feel was interfering with exercise) We check blood every 6 months and make a decision on what to adjust or change next. Over the past 3years I've lost 160 pounds(starting from 500) while slowly being able to stop taking various medications. We started with diet and lifestyle choices and then expanded to body building for muscle gains. Hopefully I can lose another 100 pounds over the next year and then see where I am and what needs to be the next target goal.
This was excellent! If I were to request anything from your channel, it would be that you present some analysis on soluble versus non-soluble, fiber intake, especially as it impacts those with heart disease. Keep up the good work.
This was so interesting! It looks like many presenters on youTube over simplify what cardiovascular disease is & how it's caused; it's the first time I've seen something detailed enough to help me figure out why cardiovascular disease is such a common problem in my family. I've been plant-based for 6 years and am fairly fit (not overweight). I wonder if my dietary choices are going to be helpful. I'm 71.
check out nutritionfacts. He claims heart disease is reversible with a plant based diet. Its always good to have lots of sources of info since this stuff is complex. @locutia7
Plant based doesn't say that much. For example a lot of vegans eat a lot of sugar, and they can still be called "plant based". And the problem with that is that insulin resistance is involved in all of the metabolic chronic diseases.
Diet is an important part of the equation but sedentary behaviour and pollution also increase cardiovascular disease risk (so do cigarette smoking and alcohol consumption ... and marijuana use). Controlling blood pressure is also important. I understand that 'plant based' works if it contains lots of whole fresh fruits and vegetables, whole grains etc but very few processed foods (plant based or not).
Dude. This is a beautiful explanation! Watching all of the out-of-control layers and buildups is just freaking me out even more and reminding me to keep to my good habits. Seriously, thank you!
Can I suggest that you bring in the glycocalyx and also the fact that diabetes dramatically increases the risk of CVD. If it is all explained by LDL, why does hyperglycemia and diabetes have such a dramatic effect? Everyone accepts that diabetes causes major vascular problems in the periphery, so why doesn’t it also cause problems in the coronary arteries? Another important question is why does arthrosclerosis only occur in high-pressure, high turbulent areas of the coronary arteries? Why does it never occur on the venous side?
@@miltonhondrakis2431 so how is LDL and shear stress connected? Shear stress damages the glycocalyx particularly if it is thinned out by hyperglycemia.
It does happen on the venous side but less common. The biggest factor is high blood pressure and the location of the arteries because arteries branch and are often curved or arched. This is where it happenes
If I understand you correctly, reducing the burden of LDL particles passing through the endothelial layer is very important. And the way to do this you say is by lowering LDL-C or even better ApoB. This makes perfect sens to me. But if I understand you correctly,.. the only (significant) way to achieve this is by reducing LDL-C / ApoB. This I find confusing. Because I would think that there are more ways to achieve this, and perhaps to such an extend that the LDL-C/ApoB level becomes less important. Maintaining a health glycogalyx (lowering glucose levels, quit smoking), reducing low-level systemic inflammation, lowering blood pressure, etc. all reduce the "permeability" of the endothelial layer. Especially when all these things are achieved through non-medical interventions. (I believe that non-medical interventions have much stronger effects than what can be achieved with medications) Exercise, as you have shown, has a plaque reducing effect. Exercise is a non-medical intervention that improves all of those goals I mentioned. All of those can be achieved through dietary interventions. Is there a specific reason you didn't mention these? Or were they simply not part of the studies that you went through? Are there even studies that look at these factors in relation to dietary interventions?
I strongly suggest reading The Clot Thickens by Dr Malcolm Kendrick. A very convincing alternative hypothesis regarding the etiology of CVD backed by a mass of references.
I also strongly recommend reading or viewing content from Dr. Malcolm Kendrick. Atherosclerosis is a disease first and foremost of chronic inflammation and repeated thrombosis brought on by metabolic dysfunction.
@@patrickweisser3185 Dr Kendrick has written 4 books to date and I recommend all of them for different viewpoint of different aspects of health and health systems.
@@patrickweisser3185does he say if eating a low inflammatory diet and fasting helps reverse at all or nah ? If it's from chronic inflammation you'd think that would help
Or Dr. Ernest Curtis's (a cardiologist) "The Cholesterol Delusion" which demonstrates the low quality and outright manipulation of the original studies that led to current medical thinking. Three of the studies are included in appendices so that the reader can see for themselves what he explains in the book.
What about vitamin K2 supplementation (MK7) ? Some MD s claim that supplementing with K2 decreases calcification inside the arteries. I've been taking vitamin K2 together with vitamin D3 for years now but I'm not convinced that it has any effect on existing calcification.
Calcification has a protective funktion preventing plaques from ruptoring. I do not know if we want that. Vitamin K is also a factor in blood clotting, and if you have arteriosclerosis, you want to prevent clotting, not promote it. Vitamin K is also an antidote for heparin blood thinners. I'm sceptic
I have watched quite many of your videos, but this was clearly the best. Your explanation was comprehensive and you went to details deep enough to understand, but not too deep to make it too complex to understand. This gave me more depth understanding, yet avoiding to be sensational. Appreciate it!
HIIT group had average LDL 2.1mmol/L +/- 0.7. This places them exactly at the threshold of plaque reversal (lowered Atheroma volume) due to low enough LDL according to some other study. This means some participants were above, some were below. It means it makes it very hard to know if any changes in plaque were because of low enough LDL of some participants or was it because of HIIT.
@@adamjackson713 it's not. We can use epidemiology to establish a cause-effect relationship. Smoking, environmental carcinogens, and others. But it's not epidemiology only: - trials of LDL-lowering drugs, - Mendelian randomization trials - animal models So, you can't have a single "study" that proves everything, but rather pieces of evidence from the hundreds of studies. The same logic is used by AIDS denialists to "disprove" the HIV-AIDS link. No single study proves that casual relationships, but still the general overwhelming consensus that HIV causes AIDS.
I did it, Nattokinase and pine bark extract once a day on an empty stomach Of course your diet should be somewhat healthy Anyway this took me 18 months, had PAD
I'm so impressed, thank you! I put this video down in my notes for your detailed description of the whole course of atherosclerosis at the cellular and molecular level, then the summary of processes to regress plaque, then your great bullet points at the end on lifestyle changes. It's like a reference for January 2024 state-of-the-art in atherosclerosis and lifestyle treatment! Thanks. (I was diagnosed with CAD after CAC 586, 97th pct, Sept 2023; I'm hunting data to strongly suggest lifestyle changes so I can stop the disease, regress plaque, and avoid PCI and bypass if possible)
Cholesterol has been found in plaques, and is generally attributed to LDL but I have never seen studies showing Apo B being present. However, I have heard of studies showing that Apo A has been found in plaques, pointing to Lp(a) being the source of the cholesterol. As I mentioned below, if you consider endothelial damage and clotting, it is known that Lp(a) is involved in the arterial damage clotting process, so, this hypothesis carries much greater weight in my mind. Research in this area seems to be lax, as there is no pharmaceutical solution to Lp(a) values.
You are what you eat. Your diet impacts your health. Lower stress, reduce obesity, get enough sleep and more exercise are key to a healthy life. Obesity in children and adults is rising across the world. Fast food and sugary drinks including fruit juices are contributing to the problem of poor health and obesity. Eat a healthy plant based diet and exercise regularly. Reduce or ELIMINATE cows milk, eggs, cheese and meat. Eat more salad greens, beans, fruit and vegetables. Eliminate fast food, snacks like cookies, cakes, chips, and sugary drinks and juices. Every adult and child should own a bicycle and ride it regularly. Regular exercise will help you sleep better. Yoga is a great stress reducer. Obesity is all too common today. Get off the couch. Get off the phone, ipad or video game. A variety of stretching and other exercises help with increased mobility. Ride to work, ride to school, ride for fun. Every city should be a bicycle city. Speak up for bicycles in your community
If you are looking for new material to cover. There was a study done on the effects of nattokinase, that showed reduction in arterial placque. I would love to hear your opinion on that study as well. There may have been some bias, I really don't know, but the only bias I could imaging, is soy bean farmers, manufacturers that produce nattokinase... This was a great video, and I appreciate you pulling back, to keep the information understandable for all.
@@Physionic I'm not even sure what a DOI number is, but I will certainly see whatever information I can find on the study. I'd really be interested to see if you can make a mechanistic correlation to the supposed outcomes.
LDL of 2.1mmol/L was the threshold when there was negative % plaque volume change observed in some study, unfortunately I only took a screenshot of the graph/results so it doesn't show study link/name. Largest reduction was with 1.1mmol/L which seems to be very low, even 2.1 seems to be very low number.
In 1997 3 Doctors wrote a book The Arginine Solution Nobel Prize Beseech proving Arginine dissolved the plaque in the arteries. Helped me a lot .I have family history of Atherosclerosis. I have none.
I didn't have time for the whole video. Usually I love your deep dives. But I'm behind on my research videos so I've saved it for late and am enjoying the timestamped summary. I appreciate you take care of your followers and appreciate our home/work pressure time constraints
I'm just a normie on the Internet who got a bit more serious about health fairly recently (~6 months ago). I've learned a lot of actionable basics during this time but this is the first time I've seen an actual in-depth (from my PoV) illustration of the atherosclerotic process. Amazing stuff, thank you for this and looking forward to seeing even more content like this!
@@stevegcqI haven't watched the video but what do you think is the correct point of view? I can tell you I am reversing my CAC with the Linus Pauling Heart Protocol 200 points down from 660 in 20 months. Even with LDL at 124 and HDL at 36.
@stevegcq This guy here is about standard medicine pretty much Dr. Ken is a step well above. And what I have done is a major step above Dr. Ken. My CAC was 660 and after 20 months it was 458. Not many people achieve this. I did it following the advice of Dr. Thomas Levy, cardiologist author of "Stop America's #1 Killer" Proof that the Origin of All Coronary Heart Disease is Clearly Reversible Arterial Scurvy. I suspect at my 3 year anniversary of my 660 score that if I did another CAC it would be down by 50% to 330 or even less....imagine that....my score is reversing as fast as it progressed.....
No mention of extended fasting and autophagy? I am a sample size of one, but I have reversed my severe arteriosclerosis in 3 months. The before and after MRIs are incredible.
@@jfdomega7938 It was roughly a semi-extreme keto diet: 1. Replaced butter with olive and avocado oils, 2. Zero sugar, not even fruits, 3. Zero rice/bread/pasta - basically only vegetables. But the important part is the extended fasting: At least one 3-day or 4-day fast per week. Often 5 days of fasting per week. And 1 or 2 meals only in non-fasting days. My only indulgence (limited) Cheese!
Have you done (or will you do) any videos specifically regarding the potential benefits of garlic for cardiovascular health? I see others claiming garlic (specifically alacin) has shown some benefit in reducing plaque burden. I’m cautiously optimistic that could be true, but I’d love to see some study data to confirm or deny that claim and you seem like the kind of chap to fairly and rationally investigate such a claim.
I've heard about Apo B for a few years but never really knew what it was until recently. From what I read it seems to be a sum of all the LDL particles and is probably a better risk predictor than LDL-C because it includes VLDL. having listened to Dave explain his Lipid Energy Model and having had high TG and VLDL it's an easy to understand concept why it's a better risk predictor. But I think the reason that HIIT didn't have much effect in the data is because of diet. Exercise burns glucose and fat but if you continue to eat in a way that puts in more sugar and fat then you're not making much of a difference.
I added 60 minutes of intense cardio, at least 5 days a week and had substantial results after a 6 month period. I coupled this with a low calorie diet focused on protein, and healthy carbs.
There are a lot of recent studies, which have shown surprising and amazing results with daily Manganese intakes reversing Arteriosclerosis. Take Manganese daily up to 10 mg even better in combination with selenium preferably selenocysteine and on top Hesperidin methyl chalcone. A maximal prevention trio
@@jesincov a well balanced combination with Niacin further significantly reduces cardiovascular risks, where by ,balanced‘ it means niacin taken together with TGM (Trimethylglycine) in accordance to your individual methylisation capacity. If someone is an under-methylisator (the majority of people are!) it is mandatory to combine niacin with TMG, if you want to protect your liver of negative effects of niacin. If you are not an under-methylisator TMG still isn’t harmful at all. So it seems reasonable for everyone taking higher doses of Niacin to always add TMG. Then this combination together with Manganese, Selenium (preferably Selenocysteine) and Hesperidine Methyl Chalcone is probably the best plaque remover combination available certainly much more effective than any statins and, if you follow the advice to combine niacin with TMG, without any negative side effects
Sorry, I’m late to the video. Just finished reading the book “The Clot Thickens” by Dr Malcolm Kendrick, any comments on his theories? My motivation, I’m recovering from a heart attack a month ago…
Kendrick has long denied the role of (LDL) cholesterol in cardiovascular disease and used confounded epidemiological studies to support his arguments. He ignored clinical trials and genetic studies as well as those epidemiological studies which refuted his claims. I haven't bothered reading his latest book but I suspect it is more off the same. Try reading an alternative viewpoint before deciding which way to go. For example, Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. It's free to read.
Good conventional info but what these studies don't address is: why are we one of the few species that develop plaques?; why do the plaques only occur in arteries just outside the heart and not in veins or elsewhere in the body?
Excellent information. I want to know why my cardiologist hasn’t informed me on any of this? All I get is go on a Statin and or Repatha plus put a Stent in. No lifestyle change conversation at all. I have a high CAC score but no symptoms and can workout very hard 2 hours a day plus 30 minute sauna 6 days a week. 58 YOM 69” 155lbs
Manganese daily up to 5mg even better in combination with selenium preferably selenocysteine and on top Hesperidin methyl chalcone. A maximal prevention trio
You mentioned that you want a thick covering of fibrosis to prevent a rupture of sorts. So what about the use of proteolytic enzymes like Nattokinase? Can that potentially do more harm than good for someone with existing CVD?
They affect the clotting cascade, which plays a role, but the ECM release is mediated by the fibroblasts, not the platelets (although the platelets also play a role in atherosclerosis, just through a different mechanism).
9:52 “you can have a perfect healthy endothelium, and if you have high levels of LDL, then that LDL can cross through the cell itself (endothelial cell, endothelial cell to cell boundaries etc.)”. Please cite where you get this information from, thank you.
And why does LDL levels need to be high for that to happen? The veins see same levels of LDL, yet at those reduced pressures and more laminar flow this does not happen. Free cholesterol crystals found in plaques are not present in the bloodstream, but are contained in the structure s of damaged red blood cells. Damage to the protective glycocalyx layer readily allows damage to the endothelial cells, and hence clotting is instigated. Many things end up in the plaques and clots that were not part of the original damage. Whether arterial endothelial damage occurs by mechanical, chemical, or stress induced hormones, etc such damage is a prerequisite for plaque and clotting. Actually, lipoproteins carry much more than fats and cholesterol,.... lipoproteins are simply the vehicle of transport having coatings of different nutrients, antioxidants, and hormones that are delivered to sites of damage to remove inflammation, calcifications, and bloated foam cells that have outlived usefulness but refuse to die. Properly coated, the lipoproteins are constantly maintaining the state of repair. Lacking these coatings of CoQ10, Vit k1, k2, Vit D, Vit C, or lack of Magnesium and other minerals the repair process slowly grinds to a stop and atherosclerosis ensues vigorously as calcium solidifies to attempt walling off the damage and exposure to the bloodstream.
@@cattleprods911 From my post...."mechanical, chemical, or stress induced hormones, etc ". The mechanical damage is largely due to high pressure causing non laminar flow and the contact of blood cells and any other cells or molecules in circulation. In sickle cell anemia the blood cells are sickle shaped (pointy ended) and those afflicted die very young from massive atherosclerosis and calcification. Our veins being subjected to lower pressure and having more laminar flow almost never develop plaques like arteries do, unless surgeons use this vein in a bypass where it serves as an artery (CABG). Those grafts plug up in 6-8 years or so. Another type of damage is chemical, as when smoking cigarettes. The new under the tongue camera can detect this damage within seconds of smoking and dead endothelium cells are found in the bloodstream. Sugar also induces chemical damage because of glycation. Diabetics mostly die of heart disease. Also, an imbalance of hormones like cortisol caused by emotional stress can wreak havoc on the glycocalyx and the endothelium.
@@cattleprods911 I forgot to include bacteria as a damager of endothelium glycocalyx. Basically that is what happens in sepsis as bacteria runs rampant destroying the glycocalyx all over the body causing multiple organ failures.. The under the tongue camera is used to check the condition of sepsis patients.
My calcium score went from 283 to 153 in a year. Looking forward to my next scan in February. Hopefully it will have gone lower again. My cardiologist said he has never seen this before. Yes, you can improve your condition with diet, exercise and the right supplements.
I'm a bit torn with this, as vitamin-C prevents calcification of plaques. That is not good at all. Calcification is a secutity measure of the body to prevent plaques from rupturing. Plaques are more dangerous if soft, as they can rupture, clot and travel to heart, lungs or brain causing infarction. Statins for example increase calcification, seen in the CAC score, stabilizing plaque and decreasing risk. What interests me is the lip(a), as we do not really have a current way how to lower it - meds are still in development. If this would be an option for individuals having that elevated through genetics, maybe they could lower their risk to those without this predisposition. So much for the carnivores: I can't hear the claim anymore, that they do not need so much vitamin C, as they do not have symptoms of scurvy... They do not get that surviving does not mean no deficency or negative effects. I'll make sure to eat my fruit and veggies to get enough for prevention of several chronic diseases.
@@stellasternchen good post , people see what they want to see . Same for these "miracle' drugs to clean up cells. Yet the body knows how to do autophagy , so senescence is not to be lightly mucked around with - just do the hard work ( HIIT or intense exercise and let the body do its job) , until better understanding comes . As for the topics at hand - if there was an easy method we would know about it . Plagues of any type are hard to remove even with direct access , teeth , bathroom walls etc , when given time to embed . They are incredibly tough and can survive extremes in nature . Given that doing the things outlined here is generally enough , to continue to live healthy - ie no more growth , then if keep strength , VO2 max , chance of a problem outside an acute infection/inflammation /over exertion/dehydration /chemical or electrolyte imbalance . Drug addicts probably survive some bad scares ( eg too much meth ) solely due to young heart - not sure a 60 year old wants a heart going crazy at 200 bps
I didn't recognize the name so I had to look him up. First bit of info, he's the author of, "The Great Cholesterol Con". Sorry Johnsavage, red flags galore. @@themekfrommars
I just listened to Prekure- prevention, with doctor Paul Mason, Decoding Atherosclerosis, and I think there's some compeling finding, going back to the 60's that high LDL is not the issue. Plant steriods may be a part of the puzzel.Thanks for your analysis ,so the average person can make wise decisions.
Nic, How certain are you of the accuracy of the model of the development of arterial plaque? Specifically, if it's just a question of LDL from consumption of saturated fats, why has the incidence of arterial plaque increased so dramatically over the last 60 years?
Yes and saturated fat consumption has also come down over that 60 years but the incidence of CAD has risen. The only good news is that modern medicine can keep us alive better after an event.
@@shauna996 But what has risen over that 60 years is consumption of seed oils and processed foods, and, of course, the $billions in profit from advertised pharmaceuticals to treat the symptoms. Hmmm
Yes this exactly, plus a lot of sugar in all the fat free foods to make them not taste like cardboard. The producers of corn syrup and the pharmaceutical companies make for a very profitable team.@@neuromax3766
Awesome 👍 I live on asprins now after a stroke 2018. Recovered 90% . Using berberine and active . I avoid milk cheese dairy red meat fat etc . So far so good.
Great topic, thanks for covering the #1 cause of death in the world. Are Dr. Esselstyn and Dr. Ornish correct when they claim a Whole Food Plant Based Diet, salt oil and sugar free, can reverse arterial plaque? What about high intensity interval training? Like high water pressure flushing out the plaque through intense vigorous exercise…
Considering that statins is the all time highest selling drug and can lower ldl makes you wonder why not only CAD is still the top killer but .... also on the rise. Maybe its because loweing ldl has no effect on CAD mortality outcomes? and that there are other factors inducing atherosclerosis.
Statins weren't commercially available until the late 1980's, yet coronary heart disease (CHD) mortality rates had been dramatically declining since the late 1960's (due to public health campaigns to reduce CHD risks: reduce smoking, reduce hypertension, diet - to reduce cholesterol, hypertension etc, increase exercise, etc). CHD mortality rates continued to dramatically drop after statins were introduced, but slowing down in the 2000's, plateaued about 2007, then started a gradual increase from about 2013. Only good news - premature CHD mortality rates (younger than 65yrs) are still much lower today than in the 60's, and earlier.
It's been on my radar. Unfortunately, those lengthier videos take me about 2-3 weeks of research, a few days for notes for the video and recording, and another week of illustrations and video editing, so it's an expensive process. I may still cover it, however.
Seed oil toxicity ....Hm, those oils have shown in RCT's as LA veterans to lower cardiovascular events. A low carb doctor, right? I have nothing against low carb diets, was on one myself with a good experience and can reccomend it to reach certain goals, fight diabetes or prediabetes etc. But I do not understand this constantly need of those diet gurus to claim the opposite of what the sum of evidence shows. I do not understand this obsession with saturated fat. High fat does not mean high saturated fat. I know, because I did make sure when I was low carb dieting to eat mostly unsaturated fat. If you exclude a good source of unsaturated fat as those frying oils does make it more difficult and you end up with butter, palm oil, lard or even worse, coconut oil.
Paul's video is based on 'The Clot Thickens' by Dr. Malcolm Kendrick who has developed the Clot Theory of plaque formation. The book presents significant analysis supporting this theory. It seems to explain the creation of plaques better than the current "burrowing" theory. Since the Clot Theory deviates from current theory supporting statins, Dr. Kendrick has been blackballed by the medical community.
@@markhapner8499 Hmm, aspirin for arteriosclerosis has been tried. This drug blocks Cox1, and thus the synthesis of clotting factors. It did more harm then benefit.
@@markhapner8499 Hmm, aspirin for arteriosclerosis has been tried. This drug blocks Cox1, and thus the synthesis of clotting factors. It did more harm then benefit.
Thanks for your work. I would greatly appreciate it if you could provide a detailed report on the effects of lithium and boron on atherosclerosis and plaque formation. I was recently intrigued to discover the breadth of literature exploring their impact, with some studies even hypothesizing that lithium deficiency could be a contributing factor to the onset of atherosclerosis. Your perspective and rigorous analysis would be of great value for those interested in the topic.
Pedantic comment 1: If the confidence interval for the difference includes 0, you cannot conclude "no effect." All it means is that the experiment lacks the power to detect the effect, if any. Also, the confidence interval bounds the likely size of the effect, if any. Since all the indicators point in the same direction, it is reasonable to hypothesize that there is an across the board effect that could be demonstrated by a larger study -- or a meta-analysis of studies including this one.
So, if I got it right, a simplified solution to some degree would be taking omega-3, K2 (to regulate blood clotting as well as distribution of calcium that gets released from plaque), exercises & possibly antioxidants after intense exercises in intervals.
So do I. Nattokinase, Serrapeptase, and Lumberkinase all work in a similar fashion and the three can work together synergistically, but most of the research to date has been done on Nattokinase.
Regarding "general solutions": Very recently we have seen that lean healthy fit people can have both high HDL (good) and high LDL (bad) with low triglycerides (good). They are called LMHR phenotypes - Lean Mass Hyper Responders. Does it mean that reducing LDL is still part of the solution above ? Is there proof of a causal link between high LDL and cardio events, or do we have only associative hypotheses. Selective data from selective studies are mostly useless.
Multiple clinical trials have shown that lowering LDL levels by diet, lifestyle changes or drugs significantly reduces the rate of major adverse cardiovascular events (fatal and nonfatal heart attacks and strokes, and the need for revscularisation surgery). They have convinced the worldwide scientific and medical professions that high LDL is a causal risk factor for CVD. It's not the only one of course but it is undoubtedly a causal risk factor.
I'm a member in your physionics group and was looking for this report in the Mighty app, but I want able to find it. Can you give me some guidance on where I might find it?
I have request for a subject I would appreciate if you could study and present? You’re doing a really great service for us seeking logical answers. Thank you.
6:57 “if the level of LDL is too high, LDL gets stuck.” You gloss over this statement without showing data that confirms controlling LDL levels prevents this mechanism from occurring. This is the key statement supporting the widespread use of Statins.
My ldl is 3.44 mmol/l = 133 mg/dl. I want to bring it down with 200 mg Nattokinase and 1200 mg red yeast rise powder after the first meal/day. Is this a good idea? I'm 70 years old male, 62 kilos.
Thanks for your analysis, Nic. Sounds like the kind of study that would never be published it a company had funded it. Un fortunately, my guess is that there are so many confounding issues there that were not controlled. Also, from a personal experience view point - if you don't change the diet, a little HIIT isn't going to cure you.
Nick I wanna give you interesting case study about myself. I started 1 mg of finasteride and I am on 120 mg testosterone a week. I have been on the testosterone for years now. And finasteride for 2 weeks. After two weeks my HDL went from 6 to 50. I am a high dht converter and I found this to be very interesting
The Dr. LINUS PAULING protocol works! I started on it way back some 15 years ago as my alternative to conventional med interventions. However, I noticed the see-saw effect of reverting increased BP by taking Vitamin D3 K2 MK7, lots of anti oxidants and anti inflammatory food. Also avoided processed and ultra processed foods, seed oils. Many of my friends who did the same thing were able to get pass cardio vascular disease. I am now 77 years old and still healthy
HIIT study. The exact size was then determined by the difference between the cross-sectional area of the atherosclerotic segment and the lumen of the artery (inner edge). That is, the difference may have been due to exercise dilating the diameter of the artery and the atheroma remaining the same. Which we know from previous research that HIIT exercise dilates blood vessels.
Thank you for your analysis of Atherosclerosis! Can you share your thoughts on the functions of stem cells, the difference between general and specialized stem cells, as well as the action of stem cells when rebuilding the body's broken down cells and tissues. A large part of the population in the Western world is attacked by osteoarthritis after they have passed the age of 60. I assume that part of the cause lies in autoimmune conditions, which develop inflammation, especially in the joints. Autoimmune inflammation is known to attack the body's own cells, and in osteoarthritis, stem cells are prevented from rebuilding the cartilage in the joints. Can you confirm this?
How about MCT's and coconut oil? As I seem to remember seeing studies that these had a positive effect?? Though both are triglycerides, is it the case that some triglycerides are more equal than others??
Aiming for June or so - depends if I get my first author paper published in time (it's a requirement for graduation). We've received comments on the paper from the reviewers and I'm running experiments to address their comments now. Fingers crossed!
Some additions: Keto diet (already kind of specified) The following supplements, but not at the same time: Mg supplement Vitamin K2 - MK7 (only 1 every 3 days) Sunshine or d3 supplement Nattokinase - breaks up fibring - caution: blood thinner warning Chanca Piedra - loosen calcium deposits - blood thinner warning Inositol and as mentioned, exercise.
Serrapeptase inhibits vascular inflammation, seems important. Mechanistic studies demonstrated that SRP significantly inhibited the LPS-induced production of proinflammatory cytokines such as IL-2, IL-1, IL-6, and TNF-α in aortic tissue. Furthermore, it also inhibited LPS-induced oxidative stress in the aortas of mice, whereas the expression and activity of monocyte chemoattractant protein-1 (MCP-1) decreased after SRP treatment. In conclusion, SRP has the ability to reduce LPS-induced vascular inflammation and damage by modulating MCP-1.
*1 AMENDMENT*
AMENDMENT: It’s been pointed out to me by @F0Xit (on TH-cam) that the researchers (Study 246) should have done a Bonferroni correction on the data. For those not into statistics, if researchers perform multiple comparisons (group A vs group B), it’s common practice in statistics to perform some form of correction, because the risk of detecting an effect that isn’t truly there increases with more comparisons made. A Bonferroni correction drastically cuts down on that risk, which is why many statisticians argue for its use. If a Bonferroni correction were applied to all the data (19 comparisons), the true p-value to meet would be 0.00263 (much lower than the typical 0.05 and what I reported in the study).
However, I met with a statistician here at my medical school to discuss the topic, and he argued this would be the incorrect use of a correction, because some of the measures are independent of one another. Technically, he argued none of the comparisons should have a correction applied to them, but he mentioned he could see an argument for some of the measures being corrected (6-9 of them in Table 2). So, if we assume a middle ground and a correction is applied to 9 comparisons, the p-value wanted would have to be below 0.00556.
If no corrections are applied, the results are as presented (based on a p-value of 0.05).
In the end, even with the most strict option (option 1), some of the effects are still significant. More are significant in the middle option, and obviously all the ones I reported are significant in the uncorrected option.
Thank you to “@F0Xit” - I learned something from the comment (below), and although I wasn’t a stranger to statistical corrections, I’ll be on the lookout in 2 sample tests just as I do in multi-sample tests.
“None of these measures are significant. When you have so many comparisons you need to correct the p-values.
This is done with Bonferroni and with so many comparisons you should divide 0.05 by the number of comparisons (you have 19 observables in the first two tables, therefore is 0.05/19= 0.002).
Bonferroni is a quite strict corrector, you may want to use Holm-Bonferroni. This study is statistically quite weak. Although, it may be useful for future meta-analyses.
Note: I do medical statistics for a job.”
I just helped someone with statistics class and this stuff is fascinating but can be mentally taxing.
If you have 19 comparisons and only one of them shows a positive effect, then the p-value should be 0.00263. However, if multiple comparisons show a positive effect while none show a negative effect, the the p-value can be increased again.
Out of the 9 measures in table 2, 5 of them have a desirable effect with p
chlorine dioxide can reverse this
Thanks for your thorough look into suggestions made by peers and/or from your audience
Anti plaque stack:
Fast 1-3 days a week (free)
burpees + jog/run 4 days a week (free)
niacin - flushing kind daily (super cheap)
vitamin k2 daily (super cheap)
psyllium husk daily (cheap)
Magnesium daily (cheap if oxide, moderate cost if better form)
Add-ons to the stack:
Weight training 2-3 days a week (moderate price)
Creatine (moderate)
Protein (expensive)
What about vitamine D and omega 3?
Developers be stackin everything 😂
Berberine?
Fasting 1-3 days a week? Hmmm...
@@NThunderMy cardiologist has me on Berberine
HIIT. Most ischaemic events (heart attacks and stokes) occur when a plaque bursts and the outpouring of goo causes a large blood clot which then affects the heart or brain. You have to be careful starting HIIT as this additional pressure can cause plaques to burst and cause an ischaemic event. This happened to a well known BBC presenter in the UK who suffered a stroke trying HIIT.
are you implying that if we've had a bypass (ie lots of plaque), then we shouldn't be doing any HIIT? HIIT is the best way to build collateral arteries
@@johnhurt888 Not saying that you shouldn't. Just be careful. Certainly discuss with your doctor.
@@peterholt4806what is hiit please
If you had bypass, then stenosis as a result, possibly tied into bad artery. What are my choices, what testing can i do. I never had a heart attack. Im completely lost.
@@bradkeenan4428 If you have narrowed arteries from atherosclerosis then you may have had angina pains or your doctors found calcification in your Coronary arteries. If narrowing is severe then your doctors may choose to operate without you having had a heart attack. Any thought of HIIT must be discussed with your doctor.
Diabetes by far is the biggest risk factors for heart disease, high blood sugar damage the arterial lining.
Yes, this!
Inflammation is also a contributor.
Read a book called "The Clot Thickens". An excellent book on the subject.
@@chrismyers9951root cause is oxidative stress
Fascinating, I lowered my LDL 50 points in six months by upping my fiber intake, taking plant sterols, cutting out cheese and butter replaced with olive oil/ cod liver oil / black seed oil/ flaxseed oil, eating 600 calories in vegetables daily, and intermittent fasting ( not eating after 2 pm) ( also I always exercise daily so that didn’t have any effect). I’m skinny so everyone said my high cholesterol was genetics, but I proved that by following a different diet than the rest of the family and taking plant sterols I could lower my cardiovascular risk. 😅Also wanted to add that when increasing fiber intake it’s really important to up water intake if you don’t want wrinkles. 😅 I would love to see analysis on any studies on plant sterols and intermittent fasting for atherosclerosis.
Nick Norwitz lower his LDL by 75% with 12 oreo cookies in 2 weeks, he went from 420 to 111 by adding carbs back to his diet. Hes on carnivore or low carb diet.
@@manojlogulic4234 well that’s the one thing I can’t give up 🙃- my cookies, but I at least wait til the end of my eating period to go for it!
@@beautylover8138 What are your cholesterol numbers LDL HDL and triglycerides? Before and after ? Do you have family CVD history ? What was your diet before ?
@@manojlogulic4234 Unfortunately his conclusions are BS. He is a hyper responder which is a tiny fraction of people. For the vast majority of people they should NOT eat Oreos(common sense would tell us that). They should follow a Med diet, exercise and if their LDL and apoB are high take a statin. The fact he is on carnivore diet or claims that means he is to be discounted.
@@supernova1976 I improved my LDL cholesterol from 136 to 100, dropping 36 points and shifting from high to normal. Initially, I didn't fast before the test, resulting in an LDL of 125 after a diet change and starting plant sterols. Three weeks later, it was 125, and after five months, including a trip to Ireland where I indulged but balanced it with vegetables and continued plant sterols, it dropped to 100. Even after eating Popeyes the night before my last test, my levels were normal. That was three months ago, and my cholesterol might be even lower now, despite the occasional half cookie. I struggle to maintain weight with a high fiber intake (25-28g daily), requiring 14 cups of fluid to avoid wrinkles and keep up with intermittent fasting and gym routines. My HDL rose from 52 to 61, and triglycerides fell from 120 to 83. Previously, my diet was heavy on cheese, protein shakes, pizza, and buttered popcorn. Despite a family history of high cholesterol (but low blood pressure), I was unaware of the 25g daily fiber recommendation and its impact on skin health until recently. Adjusting my fluid intake restored my skin. Sharing this in case it helps anyone!
On another note: soon new CT photon counting high resolution scanner will be able to reveal intima borders of coronary vessels, information that was previously visible only via OCT wich is highly invasive. No study as of today could compare CT and OCT conclusively because of low resolution. When more data will be available we may be able to see regression in atherosclerosis and potentially retargeting cure and habits of the observed patient.
That sounds amazing
This was an excellent presentation on the topic and worth the time to view it. It's a complex topic, you covered the key aspects people need to know to get a fuller understanding of the process of CVD.
Nope, but my explanation ... censored.
Remember us at a million subs brother. Always loved your channel, dating almost all the way back from it’s conception
Nothing will change. Thank you. :)
Very interesting information! I think another thing to look at would be nattokinase supplementation. There are a couple studies that show pretty dramatic plaque reduction, but the dose had to be high enough.
Is there any way to become more tolerant for higher doses? The studies mention 6.000 IU, meanwhile some people vomit with only 2.000 IU.
The vast majority of supplements to reduce LDL and apoB have been found to be pretty much useless. Plant stanols or sterols can reduce it by 5% but a simple 5mg Rosuvastatin give you 39% reduction. nattokinase supplement unless from tested scientifically verified trial should be avoided. The famous SPORTS trial showed supplements are generally useless for LDL reduction
Nattokinase is scary. If it really works it's likely that it would destabilize plaque.
I'm taking 12,000 Fibrinolytic Units of nattokinase every day on an empty stomach and have never had any stomach upset. Food will deactivate the Nattokinase, so it's important to take it away from food. @@thomasmuller1850
Oh and my dosage is based on this study: www.ncbi.nlm.nih.gov/pmc/articles/PMC9441630/@@thomasmuller1850
Im a cardiovascular tech and this has been a great listen
You are providing outstanding content. Thank you for service to the public.
All I know is i vastly increased my overall activity and exercise while changing nothing about diet or medications (because diet and medication changes were something my doctors and I had adjusted the previous year) and in the six months of increased exercise my cholesterol numbers were all vastly improved.
Our next experiment is taking me off avortastatin for 6 months to see if I can continue to get more muscle mass with less pain (muscle pain is a potential side effect from statins that I feel was interfering with exercise)
We check blood every 6 months and make a decision on what to adjust or change next.
Over the past 3years I've lost 160 pounds(starting from 500) while slowly being able to stop taking various medications. We started with diet and lifestyle choices and then expanded to body building for muscle gains.
Hopefully I can lose another 100 pounds over the next year and then see where I am and what needs to be the next target goal.
Congrats on that 160lb. Finding a way to love exercise is crucial. Good luck on that next 100lb.
This was excellent! If I were to request anything from your channel, it would be that you present some analysis on soluble versus non-soluble, fiber intake, especially as it impacts those with heart disease. Keep up the good work.
Definitely can do - thanks
This was so interesting! It looks like many presenters on youTube over simplify what cardiovascular disease is & how it's caused; it's the first time I've seen something detailed enough to help me figure out why cardiovascular disease is such a common problem in my family. I've been plant-based for 6 years and am fairly fit (not overweight). I wonder if my dietary choices are going to be helpful. I'm 71.
check out nutritionfacts. He claims heart disease is reversible with a plant based diet. Its always good to have lots of sources of info since this stuff is complex. @locutia7
Nick does a great job, doesn’t he?
Yes. Since switched to a plant based diet, then you're good
Plant based doesn't say that much. For example a lot of vegans eat a lot of sugar, and they can still be called "plant based". And the problem with that is that insulin resistance is involved in all of the metabolic chronic diseases.
Diet is an important part of the equation but sedentary behaviour and pollution also increase cardiovascular disease risk (so do cigarette smoking and alcohol consumption ... and marijuana use). Controlling blood pressure is also important. I understand that 'plant based' works if it contains lots of whole fresh fruits and vegetables, whole grains etc but very few processed foods (plant based or not).
Dude. This is a beautiful explanation! Watching all of the out-of-control layers and buildups is just freaking me out even more and reminding me to keep to my good habits. Seriously, thank you!
Glad you liked it! Thanks!
kenberryMD
This was great. Thanks
Can I suggest that you bring in the glycocalyx and also the fact that diabetes dramatically increases the risk of CVD. If it is all explained by LDL, why does hyperglycemia and diabetes have such a dramatic effect? Everyone accepts that diabetes causes major vascular problems in the periphery, so why doesn’t it also cause problems in the coronary arteries? Another important question is why does arthrosclerosis only occur in high-pressure, high turbulent areas of the coronary arteries? Why does it never occur on the venous side?
Because ldl numbers aren't the cause, they are a side effect. And there's other factors that also effect it.
@@Vincent_Beers you are talking bullshit.
Look up "shear" rate in the blood and you will get your answer about high pressure coronary arteries.
@@miltonhondrakis2431 so how is LDL and shear stress connected? Shear stress damages the glycocalyx particularly if it is thinned out by hyperglycemia.
It does happen on the venous side but less common. The biggest factor is high blood pressure and the location of the arteries because arteries branch and are often curved or arched. This is where it happenes
If I understand you correctly, reducing the burden of LDL particles passing through the endothelial layer is very important. And the way to do this you say is by lowering LDL-C or even better ApoB.
This makes perfect sens to me. But if I understand you correctly,.. the only (significant) way to achieve this is by reducing LDL-C / ApoB.
This I find confusing. Because I would think that there are more ways to achieve this, and perhaps to such an extend that the LDL-C/ApoB level becomes less important.
Maintaining a health glycogalyx (lowering glucose levels, quit smoking), reducing low-level systemic inflammation, lowering blood pressure, etc. all reduce the "permeability" of the endothelial layer.
Especially when all these things are achieved through non-medical interventions. (I believe that non-medical interventions have much stronger effects than what can be achieved with medications)
Exercise, as you have shown, has a plaque reducing effect. Exercise is a non-medical intervention that improves all of those goals I mentioned. All of those can be achieved through dietary interventions. Is there a specific reason you didn't mention these? Or were they simply not part of the studies that you went through? Are there even studies that look at these factors in relation to dietary interventions?
I strongly suggest reading The Clot Thickens by Dr Malcolm Kendrick. A very convincing alternative hypothesis regarding the etiology of CVD backed by a mass of references.
I also strongly recommend reading or viewing content from Dr. Malcolm Kendrick. Atherosclerosis is a disease first and foremost of chronic inflammation and repeated thrombosis brought on by metabolic dysfunction.
@@patrickweisser3185 Dr Kendrick has written 4 books to date and I recommend all of them for different viewpoint of different aspects of health and health systems.
Yep yep yep. Pay attention here people.
@@patrickweisser3185does he say if eating a low inflammatory diet and fasting helps reverse at all or nah ? If it's from chronic inflammation you'd think that would help
Or Dr. Ernest Curtis's (a cardiologist) "The Cholesterol Delusion" which demonstrates the low quality and outright manipulation of the original studies that led to current medical thinking. Three of the studies are included in appendices so that the reader can see for themselves what he explains in the book.
What about vitamin K2 supplementation (MK7) ? Some MD s claim that supplementing with K2 decreases calcification inside the arteries. I've been taking vitamin K2 together with vitamin D3 for years now but I'm not convinced that it has any effect on existing calcification.
I don’t know. I would need to look into it. I can do that.
@@Physionicplease do
@@Physionic yes please.
@@Physionic EDTA
Is supposed to be even better
then k2 ( mk7 )
Calcification has a protective funktion preventing plaques from ruptoring. I do not know if we want that. Vitamin K is also a factor in blood clotting, and if you have arteriosclerosis, you want to prevent clotting, not promote it. Vitamin K is also an antidote for heparin blood thinners. I'm sceptic
Thank you for your service!
Thanks for stopping by :)
I have watched quite many of your videos, but this was clearly the best. Your explanation was comprehensive and you went to details deep enough to understand, but not too deep to make it too complex to understand. This gave me more depth understanding, yet avoiding to be sensational. Appreciate it!
HIIT group had average LDL 2.1mmol/L +/- 0.7. This places them exactly at the threshold of plaque reversal (lowered Atheroma volume) due to low enough LDL according to some other study. This means some participants were above, some were below. It means it makes it very hard to know if any changes in plaque were because of low enough LDL of some participants or was it because of HIIT.
Where is the study that shows LDL causing plaques ?
@@garyroach8624 where is the study that shows we need oxigen?
When babies are born they need to take a breath to continue living, that aside the lower the LDL the higher all cause mortality. @@YuraL88
@@YuraL88 strawman argument. Just because one correlation is actually due to causation doesn't mean that other correlations are as well.
@@adamjackson713 it's not. We can use epidemiology to establish a cause-effect relationship. Smoking, environmental carcinogens, and others.
But it's not epidemiology only:
- trials of LDL-lowering drugs,
- Mendelian randomization trials
- animal models
So, you can't have a single "study" that proves everything, but rather pieces of evidence from the hundreds of studies.
The same logic is used by AIDS denialists to "disprove" the HIV-AIDS link. No single study proves that casual relationships, but still the general overwhelming consensus that HIV causes AIDS.
I did it, Nattokinase and pine bark extract once a day on an empty stomach
Of course your diet should be somewhat healthy
Anyway this took me 18 months, had PAD
I'm so impressed, thank you! I put this video down in my notes for your detailed description of the whole course of atherosclerosis at the cellular and molecular level, then the summary of processes to regress plaque, then your great bullet points at the end on lifestyle changes. It's like a reference for January 2024 state-of-the-art in atherosclerosis and lifestyle treatment! Thanks. (I was diagnosed with CAD after CAC 586, 97th pct, Sept 2023; I'm hunting data to strongly suggest lifestyle changes so I can stop the disease, regress plaque, and avoid PCI and bypass if possible)
Cholesterol has been found in plaques, and is generally attributed to LDL but I have never seen studies showing Apo B being present. However, I have heard of studies showing that Apo A has been found in plaques, pointing to Lp(a) being the source of the cholesterol. As I mentioned below, if you consider endothelial damage and clotting, it is known that Lp(a) is involved in the arterial damage clotting process, so, this hypothesis carries much greater weight in my mind. Research in this area seems to be lax, as there is no pharmaceutical solution to Lp(a) values.
AboB-100 is found in IDL, LDL, VLDL, and Lp(a).
You are what you eat. Your diet impacts your health.
Lower stress, reduce obesity, get enough sleep and more exercise are key to a healthy life.
Obesity in children and adults is rising across the world.
Fast food and sugary drinks including fruit juices are contributing to the problem of poor health and obesity.
Eat a healthy plant based diet and exercise regularly.
Reduce or ELIMINATE cows milk, eggs, cheese and meat. Eat more salad greens, beans, fruit and vegetables. Eliminate fast food, snacks like cookies, cakes, chips, and sugary drinks and juices.
Every adult and child should own a bicycle and ride it regularly.
Regular exercise will help you sleep better. Yoga is a great stress reducer.
Obesity is all too common today. Get off the couch. Get off the phone, ipad or video game.
A variety of stretching and other exercises help with increased mobility.
Ride to work, ride to school, ride for fun.
Every city should be a bicycle city.
Speak up for bicycles in your community
If you are looking for new material to cover. There was a study done on the effects of nattokinase, that showed reduction in arterial placque. I would love to hear your opinion on that study as well. There may have been some bias, I really don't know, but the only bias I could imaging, is soy bean farmers, manufacturers that produce nattokinase... This was a great video, and I appreciate you pulling back, to keep the information understandable for all.
Could you send me the DOI number of the study? I’d be happy to cover it.
@@Physionic I'm not even sure what a DOI number is, but I will certainly see whatever information I can find on the study. I'd really be interested to see if you can make a mechanistic correlation to the supposed outcomes.
@@Physionic pubmed.ncbi.nlm.nih.gov/36072877/
Thank you
@@Physionic This is what I have found. I am not sure if that is exactly what you need to find the study
LDL of 2.1mmol/L was the threshold when there was negative % plaque volume change observed in some study, unfortunately I only took a screenshot of the graph/results so it doesn't show study link/name. Largest reduction was with 1.1mmol/L which seems to be very low, even 2.1 seems to be very low number.
Will be passing your email summary on this one on to a few since I’m in the mid 50s group. Thx Nic.
Look for it next week
In 1997 3 Doctors wrote a book
The Arginine Solution
Nobel Prize Beseech proving Arginine dissolved the plaque in the arteries. Helped me a lot .I have family history of Atherosclerosis. I have none.
Thanks for your service! 😊 Could you please do a video on NATTOKINASE, serrapeptase and lumpkinase?¿?¿?¿¿
🙏🏼❤️
I didn't have time for the whole video. Usually I love your deep dives. But I'm behind on my research videos so I've saved it for late and am enjoying the timestamped summary. I appreciate you take care of your followers and appreciate our home/work pressure time constraints
I'm just a normie on the Internet who got a bit more serious about health fairly recently (~6 months ago). I've learned a lot of actionable basics during this time but this is the first time I've seen an actual in-depth (from my PoV) illustration of the atherosclerotic process. Amazing stuff, thank you for this and looking forward to seeing even more content like this!
Except the content is wrong
How is it wrong
@@stevegcqI haven't watched the video but what do you think is the correct point of view?
I can tell you I am reversing my CAC with the Linus Pauling Heart Protocol 200 points down from 660 in 20 months. Even with LDL at 124 and HDL at 36.
@@SET12DSP10 letters, first three, 'ken', second three, 'ber', third three letters, 'rey', the last two letters are, 'MD'.
@stevegcq This guy here is about standard medicine pretty much Dr. Ken is a step well above. And what I have done is a major step above Dr. Ken. My CAC was 660 and after 20 months it was 458. Not many people achieve this. I did it following the advice of Dr. Thomas Levy, cardiologist author of "Stop America's #1 Killer" Proof that the Origin of All Coronary Heart Disease is Clearly Reversible Arterial Scurvy. I suspect at my 3 year anniversary of my 660 score that if I did another CAC it would be down by 50% to 330 or even less....imagine that....my score is reversing as fast as it progressed.....
No mention of extended fasting and autophagy? I am a sample size of one, but I have reversed my severe arteriosclerosis in 3 months. The before and after MRIs are incredible.
hi there. what are you eating if you could please tell me. thanks in advance.
@@jfdomega7938 It was roughly a semi-extreme keto diet: 1. Replaced butter with olive and avocado oils, 2. Zero sugar, not even fruits, 3. Zero rice/bread/pasta - basically only vegetables.
But the important part is the extended fasting: At least one 3-day or 4-day fast per week. Often 5 days of fasting per week. And 1 or 2 meals only in non-fasting days.
My only indulgence (limited) Cheese!
Have you done (or will you do) any videos specifically regarding the potential benefits of garlic for cardiovascular health? I see others claiming garlic (specifically alacin) has shown some benefit in reducing plaque burden. I’m cautiously optimistic that could be true, but I’d love to see some study data to confirm or deny that claim and you seem like the kind of chap to fairly and rationally investigate such a claim.
I've heard about Apo B for a few years but never really knew what it was until recently. From what I read it seems to be a sum of all the LDL particles and is probably a better risk predictor than LDL-C because it includes VLDL. having listened to Dave explain his Lipid Energy Model and having had high TG and VLDL it's an easy to understand concept why it's a better risk predictor. But I think the reason that HIIT didn't have much effect in the data is because of diet. Exercise burns glucose and fat but if you continue to eat in a way that puts in more sugar and fat then you're not making much of a difference.
I added 60 minutes of intense cardio, at least 5 days a week and had substantial results after a 6 month period. I coupled this with a low calorie diet focused on protein, and healthy carbs.
Congratulations - I’m thrilled to hear about your success. :)
There are a lot of recent studies, which have shown surprising and amazing results with daily Manganese intakes reversing Arteriosclerosis.
Take Manganese daily up to 10 mg even better in combination with selenium preferably selenocysteine and on top Hesperidin methyl chalcone. A maximal prevention trio
Easy to get in diet - 3 tbsp wheat germ and some oats and almond butter gets you 7mg/day plus beta-glucans and spermidine as a bonus!
@@jpintero6330 you won’t get 1 mg manganese by your recommended diet, which however is quite good for other reasons
I’d like this to be true as I love hibiscus tea. I’ve often worried about excessive manganese
@@jesincov a well balanced combination with Niacin further significantly reduces cardiovascular risks, where by ,balanced‘ it means niacin taken together with TGM (Trimethylglycine) in accordance to your individual methylisation capacity. If someone is an under-methylisator (the majority of people are!) it is mandatory to combine niacin with TMG, if you want to protect your liver of negative effects of niacin. If you are not an under-methylisator TMG still isn’t harmful at all. So it seems reasonable for everyone taking higher doses of Niacin to always add TMG.
Then this combination together with Manganese, Selenium (preferably Selenocysteine) and Hesperidine Methyl Chalcone is probably the best plaque remover combination available certainly much more effective than any statins and, if you follow the advice to combine niacin with TMG, without any negative side effects
Sorry, I’m late to the video. Just finished reading the book “The Clot Thickens” by Dr Malcolm Kendrick, any comments on his theories? My motivation, I’m recovering from a heart attack a month ago…
Kendrick has long denied the role of (LDL) cholesterol in cardiovascular disease and used confounded epidemiological studies to support his arguments. He ignored clinical trials and genetic studies as well as those epidemiological studies which refuted his claims. I haven't bothered reading his latest book but I suspect it is more off the same. Try reading an alternative viewpoint before deciding which way to go. For example, Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. It's free to read.
Good conventional info but what these studies don't address is: why are we one of the few species that develop plaques?; why do the plaques only occur in arteries just outside the heart and not in veins or elsewhere in the body?
Excellent information. I want to know why my cardiologist hasn’t informed me on any of this? All I get is go on a Statin and or Repatha plus put a Stent in. No lifestyle change conversation at all. I have a high CAC score but no symptoms and can workout very hard 2 hours a day plus 30 minute sauna 6 days a week. 58 YOM 69” 155lbs
My cynical opinion of cardiologist like yours is, there’s no money to be made in stopping the progression of your disease.
Supplements, other than Omega3s, were not taken into consideration in this study. What supplements may help in reducing arterial sclerosis?
Manganese daily up to 5mg even better in combination with selenium preferably selenocysteine and on top Hesperidin methyl chalcone. A maximal prevention trio
Best video on TH-cam. Thank you.
EDTA
You mentioned that you want a thick covering of fibrosis to prevent a rupture of sorts. So what about the use of proteolytic enzymes like Nattokinase? Can that potentially do more harm than good for someone with existing CVD?
They affect the clotting cascade, which plays a role, but the ECM release is mediated by the fibroblasts, not the platelets (although the platelets also play a role in atherosclerosis, just through a different mechanism).
9:52 “you can have a perfect healthy endothelium, and if you have high levels of LDL, then that LDL can cross through the cell itself (endothelial cell, endothelial cell to cell boundaries etc.)”. Please cite where you get this information from, thank you.
exactly my question
And why does LDL levels need to be high for that to happen? The veins see same levels of LDL, yet at those reduced pressures and more laminar flow this does not happen. Free cholesterol crystals found in plaques are not present in the bloodstream, but are contained in the structure s of damaged red blood cells. Damage to the protective glycocalyx layer readily allows damage to the endothelial cells, and hence clotting is instigated. Many things end up in the plaques and clots that were not part of the original damage. Whether arterial endothelial damage occurs by mechanical, chemical, or stress induced hormones, etc such damage is a prerequisite for plaque and clotting. Actually, lipoproteins carry much more than fats and cholesterol,.... lipoproteins are simply the vehicle of transport having coatings of different nutrients, antioxidants, and hormones that are delivered to sites of damage to remove inflammation, calcifications, and bloated foam cells that have outlived usefulness but refuse to die. Properly coated, the lipoproteins are constantly maintaining the state of repair. Lacking these coatings of CoQ10, Vit k1, k2, Vit D, Vit C, or lack of Magnesium and other minerals the repair process slowly grinds to a stop and atherosclerosis ensues vigorously as calcium solidifies to attempt walling off the damage and exposure to the bloodstream.
@@mozit6 what damages the glycocalyx?
@@cattleprods911 From my post...."mechanical, chemical, or stress induced hormones, etc ". The mechanical damage is largely due to high pressure causing non laminar flow and the contact of blood cells and any other cells or molecules in circulation. In sickle cell anemia the blood cells are sickle shaped (pointy ended) and those afflicted die very young from massive atherosclerosis and calcification. Our veins being subjected to lower pressure and having more laminar flow almost never develop plaques like arteries do, unless surgeons use this vein in a bypass where it serves as an artery (CABG). Those grafts plug up in 6-8 years or so. Another type of damage is chemical, as when smoking cigarettes. The new under the tongue camera can detect this damage within seconds of smoking and dead endothelium cells are found in the bloodstream. Sugar also induces chemical damage because of glycation. Diabetics mostly die of heart disease. Also, an imbalance of hormones like cortisol caused by emotional stress can wreak havoc on the glycocalyx and the endothelium.
@@cattleprods911 I forgot to include bacteria as a damager of endothelium glycocalyx. Basically that is what happens in sepsis as bacteria runs rampant destroying the glycocalyx all over the body causing multiple organ failures.. The under the tongue camera is used to check the condition of sepsis patients.
Can fasting help?
Couldn't hurt.
Thanks. Another very helpful video was full of very important information. 👍🏽💯🔥
How would you do a double blind HIIT Trial?? Would the participants not know that they were doing high intensity interval training???
Sharp thinking, and you are always looking for the right statistic and conclusion..clever scientist !
My calcium score went from 283 to 153 in a year. Looking forward to my next scan in February. Hopefully it will have gone lower again. My cardiologist said he has never seen this before. Yes, you can improve your condition with diet, exercise and the right supplements.
So what changes in your diet and supplements you made?
Subbed, glad I found you. Love studies, thanks.
The Linus Pauling method - vitamin C + lysine could be worth covering - if you haven't done so.
So underrated. The issue is, there isn't many studies done on it because it makes no one money so there isn't much to show.
@@Always_there99 That is the Pauling Protocol. Its reported, but no studies really done on the protocol itself.
What about the study using 2400mg of aged garlic? Pretty significant improvements.
I'm a bit torn with this, as vitamin-C prevents calcification of plaques. That is not good at all. Calcification is a secutity measure of the body to prevent plaques from rupturing. Plaques are more dangerous if soft, as they can rupture, clot and travel to heart, lungs or brain causing infarction. Statins for example increase calcification, seen in the CAC score, stabilizing plaque and decreasing risk.
What interests me is the lip(a), as we do not really have a current way how to lower it - meds are still in development. If this would be an option for individuals having that elevated through genetics, maybe they could lower their risk to those without this predisposition.
So much for the carnivores: I can't hear the claim anymore, that they do not need so much vitamin C, as they do not have symptoms of scurvy... They do not get that surviving does not mean no deficency or negative effects. I'll make sure to eat my fruit and veggies to get enough for prevention of several chronic diseases.
@@stellasternchen good post , people see what they want to see . Same for these "miracle' drugs to clean up cells. Yet the body knows how to do autophagy , so senescence is not to be lightly mucked around with - just do the hard work ( HIIT or intense exercise and let the body do its job) , until better understanding comes . As for the topics at hand - if there was an easy method we would know about it . Plagues of any type are hard to remove even with direct access , teeth , bathroom walls etc , when given time to embed . They are incredibly tough and can survive extremes in nature . Given that doing the things outlined here is generally enough , to continue to live healthy - ie no more growth , then if keep strength , VO2 max , chance of a problem outside an acute infection/inflammation /over exertion/dehydration /chemical or electrolyte imbalance . Drug addicts probably survive some bad scares ( eg too much meth ) solely due to young heart - not sure a 60 year old wants a heart going crazy at 200 bps
What about the effects of vitamin K-2 (mk4/mk7) in atherosclerosis?
Dr Malcolm Kendrick is No1 on this subject
It's possible, granted, but it's probably more likely that he's an absolute fruit loop.
Very intelligent comment /s
I didn't recognize the name so I had to look him up. First bit of info, he's the author of, "The Great Cholesterol Con". Sorry Johnsavage, red flags galore. @@themekfrommars
Agreed. Dr. Malcolm Kendrick has a very interesting take on the whole lipid hypothesis.
I just listened to Prekure- prevention, with doctor Paul Mason, Decoding Atherosclerosis, and I think there's some compeling finding, going back to the 60's that high LDL is not the issue. Plant steriods may be a part of the puzzel.Thanks for your analysis ,so the average person can make wise decisions.
Nic, How certain are you of the accuracy of the model of the development of arterial plaque? Specifically, if it's just a question of LDL from consumption of saturated fats, why has the incidence of arterial plaque increased so dramatically over the last 60 years?
Yes and saturated fat consumption has also come down over that 60 years but the incidence of CAD has risen. The only good news is that modern medicine can keep us alive better after an event.
@@shauna996 But what has risen over that 60 years is consumption of seed oils and processed foods, and, of course, the $billions in profit from advertised pharmaceuticals to treat the symptoms. Hmmm
@@neuromax3766 We are in agreement.
Yes this exactly, plus a lot of sugar in all the fat free foods to make them not taste like cardboard. The producers of corn syrup and the pharmaceutical companies make for a very profitable team.@@neuromax3766
@@shauna996 They want you alive, just sick as hell. Nobody wants to lose a customer.
Awesome 👍
I live on asprins now after a stroke 2018.
Recovered 90% .
Using berberine and active .
I avoid milk cheese dairy red meat fat etc .
So far so good.
@@richardjacobs7632 verify in peer reviewed medical journal.
So many people post things not proven through evidence based medicine
Thanks 👍
Great topic, thanks for covering the #1 cause of death in the world. Are Dr. Esselstyn and Dr. Ornish correct when they claim a Whole Food Plant Based Diet, salt oil and sugar free, can reverse arterial plaque? What about high intensity interval training? Like high water pressure flushing out the plaque through intense vigorous exercise…
Considering that statins is the all time highest selling drug and can lower ldl makes you wonder why not only CAD is still the top killer but .... also on the rise. Maybe its because loweing ldl has no effect on CAD mortality outcomes? and that there are other factors inducing atherosclerosis.
Statins weren't commercially available until the late 1980's, yet coronary heart disease (CHD) mortality rates had been dramatically declining since the late 1960's (due to public health campaigns to reduce CHD risks: reduce smoking, reduce hypertension, diet - to reduce cholesterol, hypertension etc, increase exercise, etc). CHD mortality rates continued to dramatically drop after statins were introduced, but slowing down in the 2000's, plateaued about 2007, then started a gradual increase from about 2013.
Only good news - premature CHD mortality rates (younger than 65yrs) are still much lower today than in the 60's, and earlier.
I wonder if th day is more likely linked to a reducing in smokers more than anything else. But so many variables...
Thank you for all your hard work.
Would love to hear your thoughts on a video lecture by doctor Paul Mason Decoding Atherosclerosis: The clotting theory and seed oil toxicity
It's been on my radar. Unfortunately, those lengthier videos take me about 2-3 weeks of research, a few days for notes for the video and recording, and another week of illustrations and video editing, so it's an expensive process. I may still cover it, however.
Seed oil toxicity ....Hm, those oils have shown in RCT's as LA veterans to lower cardiovascular events. A low carb doctor, right? I have nothing against low carb diets, was on one myself with a good experience and can reccomend it to reach certain goals, fight diabetes or prediabetes etc. But I do not understand this constantly need of those diet gurus to claim the opposite of what the sum of evidence shows. I do not understand this obsession with saturated fat. High fat does not mean high saturated fat. I know, because I did make sure when I was low carb dieting to eat mostly unsaturated fat. If you exclude a good source of unsaturated fat as those frying oils does make it more difficult and you end up with butter, palm oil, lard or even worse, coconut oil.
Paul's video is based on 'The Clot Thickens' by Dr. Malcolm Kendrick who has developed the Clot Theory of plaque formation. The book presents significant analysis supporting this theory. It seems to explain the creation of plaques better than the current "burrowing" theory. Since the Clot Theory deviates from current theory supporting statins, Dr. Kendrick has been blackballed by the medical community.
@@markhapner8499 Hmm, aspirin for arteriosclerosis has been tried. This drug blocks Cox1, and thus the synthesis of clotting factors.
It did more harm then benefit.
@@markhapner8499 Hmm, aspirin for arteriosclerosis has been tried. This drug blocks Cox1, and thus the synthesis of clotting factors.
It did more harm then benefit.
Thank you for this wonderful explanation and analysis.
Thanks for your work. I would greatly appreciate it if you could provide a detailed report on the effects of lithium and boron on atherosclerosis and plaque formation. I was recently intrigued to discover the breadth of literature exploring their impact, with some studies even hypothesizing that lithium deficiency could be a contributing factor to the onset of atherosclerosis.
Your perspective and rigorous analysis would be of great value for those interested in the topic.
I understand that autophagy can also reduce plaque... What say you?
thank you as a budding microbiologist this was really helpful and clear.
Thank you for helping fall asleep. You are the best natural sleeping pill! Btw, if you have 8-hour lectures in the members section, I will join!
Sounds like the study needed to be longer, the statistically insignificant values were trending in each marker consistently.
Really good information. Thanks
Pedantic comment 1: If the confidence interval for the difference includes 0, you cannot conclude "no effect." All it means is that the experiment lacks the power to detect the effect, if any. Also, the confidence interval bounds the likely size of the effect, if any. Since all the indicators point in the same direction, it is reasonable to hypothesize that there is an across the board effect that could be demonstrated by a larger study -- or a meta-analysis of studies including this one.
Awesome posting! So thoughtfully and clearly explained.🙏🏻
Thanks! Informative and straightforward 👍🏼
Best ever video about the subject, as well the comments are very interesting
This channel is a fucking goldmine
So, if I got it right, a simplified solution to some degree would be taking omega-3, K2 (to regulate blood clotting as well as distribution of calcium that gets released from plaque), exercises & possibly antioxidants after intense exercises in intervals.
I wish there was a study like this for Serrapeptase.
So do I. Nattokinase, Serrapeptase, and Lumberkinase all work in a similar fashion and the three can work together synergistically, but most of the research to date has been done on Nattokinase.
Regarding "general solutions": Very recently we have seen that lean healthy fit people can have both high HDL (good) and high LDL (bad) with low triglycerides (good). They are called LMHR phenotypes - Lean Mass Hyper Responders. Does it mean that reducing LDL is still part of the solution above ? Is there proof of a causal link between high LDL and cardio events, or do we have only associative hypotheses. Selective data from selective studies are mostly useless.
Multiple clinical trials have shown that lowering LDL levels by diet, lifestyle changes or drugs significantly reduces the rate of major adverse cardiovascular events (fatal and nonfatal heart attacks and strokes, and the need for revscularisation surgery). They have convinced the worldwide scientific and medical professions that high LDL is a causal risk factor for CVD. It's not the only one of course but it is undoubtedly a causal risk factor.
I'm a member in your physionics group and was looking for this report in the Mighty app, but I want able to find it. Can you give me some guidance on where I might find it?
I have request for a subject I would appreciate if you could study and present? You’re doing a really great service for us seeking logical answers.
Thank you.
Have you considered the studies produced by Dr. Matthias Rath regarding the impact of vitamin C on cardiovascular disease ?
6:57 “if the level of LDL is too high, LDL gets stuck.” You gloss over this statement without showing data that confirms controlling LDL levels prevents this mechanism from occurring. This is the key statement supporting the widespread use of Statins.
My ldl is 3.44 mmol/l = 133 mg/dl. I want to bring it down with 200 mg Nattokinase and 1200 mg red yeast rise powder after the first meal/day. Is this a good idea?
I'm 70 years old male, 62 kilos.
Wow! Great information! Thank you!! 👏🏼👏🏼👏🏼
Can you make a video about the proper human diet in your opinion?. Or just what you eat daily. I know that topic is controversial.
I'd also be interested.
Carnivore
Does he ever mention insulin resistance or ldl particle size?
Thanks for your analysis, Nic. Sounds like the kind of study that would never be published it a company had funded it. Un fortunately, my guess is that there are so many confounding issues there that were not controlled. Also, from a personal experience view point - if you don't change the diet, a little HIIT isn't going to cure you.
Nick I wanna give you interesting case study about myself. I started 1 mg of finasteride and I am on 120 mg testosterone a week. I have been on the testosterone for years now. And finasteride for 2 weeks. After two weeks my HDL went from 6 to 50. I am a high dht converter and I found this to be very interesting
How do we figure out which omega-3 supplement is the best one to take there’s so many and you hear bad things and good things
The Dr. LINUS PAULING protocol works! I started on it way back some 15 years ago as my alternative to conventional med interventions. However, I noticed the see-saw effect of reverting increased BP by taking Vitamin D3 K2 MK7, lots of anti oxidants and anti inflammatory food. Also avoided processed and ultra processed foods, seed oils.
Many of my friends who did the same thing were able to get pass cardio vascular disease.
I am now 77 years old and still healthy
HIIT study.
The exact size was then determined by the difference between the cross-sectional area of the atherosclerotic segment and the lumen of the artery (inner edge).
That is, the difference may have been due to exercise dilating the diameter of the artery and the atheroma remaining the same. Which we know from previous research that HIIT exercise dilates blood vessels.
I wonder how daily consumption of baked goods made with manufactured plant fats affects atherosclerosis/heart?
Thank you for your analysis of Atherosclerosis!
Can you share your thoughts on the functions of stem cells, the difference between general and specialized stem cells, as well as the action of stem cells when rebuilding the body's broken down cells and tissues. A large part of the population in the Western world is attacked by osteoarthritis after they have passed the age of 60. I assume that part of the cause lies in autoimmune conditions, which develop inflammation, especially in the joints. Autoimmune inflammation is known to attack the body's own cells, and in osteoarthritis, stem cells are prevented from rebuilding the cartilage in the joints. Can you confirm this?
Good information, so What factors to detemine the plaque will occur in heart or in brain ?
do you think that Vit K2 has a significant role in atheroma/endovascular calcium regression?
How about MCT's and coconut oil? As I seem to remember seeing studies that these had a positive effect?? Though both are triglycerides, is it the case that some triglycerides are more equal than others??
Dr Essylstyn. Takes about a year for Complete reversal, but progress is seen on angio in weeks.
How does one blind and placebo exercise study? Placebo would be doing HIIT but wrong? Blinding would be doing exercises while asleep?
I very much appreciate the General Solution and Mid Point Conclusion. Thank You ! ⬆⬆
Thanks for video. What kind of fiber soluble or insoluble?
Hey Nic when will you get your Piled Higher and Deeper (PhD)?
Aiming for June or so - depends if I get my first author paper published in time (it's a requirement for graduation). We've received comments on the paper from the reviewers and I'm running experiments to address their comments now. Fingers crossed!
Some additions:
Keto diet (already kind of specified)
The following supplements, but not at the same time:
Mg supplement
Vitamin K2 - MK7 (only 1 every 3 days)
Sunshine or d3 supplement
Nattokinase - breaks up fibring - caution: blood thinner warning
Chanca Piedra - loosen calcium deposits - blood thinner warning
Inositol
and as mentioned, exercise.
Serrapeptase inhibits vascular inflammation, seems important.
Mechanistic studies demonstrated that SRP significantly inhibited the LPS-induced production of proinflammatory cytokines such as IL-2, IL-1, IL-6, and TNF-α in aortic tissue.
Furthermore, it also inhibited LPS-induced oxidative stress in the aortas of mice, whereas the expression and activity of monocyte chemoattractant protein-1 (MCP-1) decreased after SRP treatment. In conclusion, SRP has the ability to reduce LPS-induced vascular inflammation and damage by modulating MCP-1.