The Experiment That Shook The World Of Cardiology! | Nick Norwitz | The Proof EP
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- Опубликовано: 21 окт 2024
- Join us as Nick Norwitz discusses his intriguing self-experiment comparing the effects of Oreo cookies and statins on cholesterol levels. This thought-provoking conversation delves into:
• The unexpected lipid responses in lean individuals on low-carb diets
• Potential metabolic mechanisms behind dramatic LDL fluctuations
• Implications for personalised approaches to cholesterol management
This video offers a nuanced look at the intricate relationship between diet, metabolism, and cardiovascular biomarkers. Whether you're a health professional or simply interested in nutrition science, you'll gain valuable insights into the ongoing research in this field.
Note: This experiment is a case study and should not be interpreted as medical advice. Always consult healthcare professionals for personal health decisions.
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LMHR is just another diet related metabolic disorder. I heard one cardiologist say it was not a mystery, carbs are the bodies preferred energy source so if you are on a ketogenic diet and eat carbs, you body will start sending triglycerides instead of LDL. If you just take a statin, your body still needs energy so it must send LDL, the only fuel it has access to.
One thing I take from this is, if you are a LMHR, you should pick a diet that is compatible with your metabolism. This guy is so smart that he doesn't look smart at all. I tried to make that sound as nice as possible but an LDL of 501mg/dl is anything but smart!
Im 65 years old lost 20 lbs reducing carbs not full Keto. All my blood markers improved with the exception of LDL which went up to 150 and my doctor immediately wanted me to go on statins. Not wanting to take statins I started doing my own research. I asked for an NMR particle blood test and my doctor said that’s just for people that want to get out of taking statins. I went around the doctor and took the NMR particle test and found my small LDL-p was only 295. I sent it to my doctor with the Dave Feldman study results and she said ok just keep eating good get enough sleep and exercise. Thanks for giving lay people information to work with.
What were your typical macros? When you say reducing carbs, then what is that? Like a daily amount less than 100g, 50g, 25g, or what exactly? Net or total carbs? Trying to figure out what adjustments I can make for myself. Thanks.
This has been known for decades, at least my GP doctor knew this. I was low carb Atkins with untreated cholesterol in the range of 425 to 500. He warned me for a couple of years about following low carb...right up until my heart attacks. Switched to a vegan and mostly carb and my numbers dropped like a rock. This was almost 20 years ago. Not news for some of us that live w/high cholesterol. Does not need to be Oreos.
That's been my understanding for many years as well. Dr Greger discussed it in his egg videos, I think.
@@carinaekstrom1 yes, exactly. I think this Oreo thing was more of an experiment to measure effectiveness of outrageous internet claims and videos. Nothing to do with health or cholesterol. Greger always does a great job of summarizing peer reviewed research.
Hey I want to interview you?
@6stringcodger450 SO you were on a healthy low carb diet and then changed to vegan/carb diet and believe it to be healthier LOL
@@convid1941is the way to go. One day you will realise it.
I don't know, but I learned many years ago (probably from Dr. Greger) that lean people who eat completely plant based usually have a strong LDL rise if they start eating animal based. As well as lowering their LDL quickly if they go completely plant based again. So why is this now discussed as something so unusual? I know Norwitz didn't go plant based in the experiment, but he did make a drastic change as far as eating carbohydrates when he was completely unused to it.
But why is it just lean ppl.
I was vegetarian (not vegan... included eggs, dairy, and rarely fish) and went keto very suddenly. Dropped 50lbs easily and my cholesterol did not change.
@@jellybeanvinkler4878 I guess you were used to having cholesterol in your diet already. Generally, when people who don't eat cholesterol suddenly gets lots of it, if they are not lean they can hold some of it in their fat cells and keep it out of the blood. That's been my understanding, but I'm still learning. There are of course individual differences.
This has nothing to do with consuming animal foods.The LMHR phenomenon occurs even in vegan keto. The leaner you are and the less carbs you eat, the more your LDL goes up - independent of food source (or fat type/source, as you mentioned in your other comment regarding seed oils).
@@saintwithatie interesting, the information that vegan keto also rises ldl. I didn’t try vegan keto in the days, and always wonder about it.
@@saintwithatie Less carbs usually mean more animal products, though. And you don't have to be on a ketogenic diet for this to happen. Regarding polyunsaturated oils I'm not even convinced that they are the reason LDL goes down, it could be a replacement thing. Or maybe something else specific to such oils, they certainly aren't carbs. Maybe it's enough that they originate from plants.
Simon or Nick, have you seen this study? Association of a Low-Carbohydrate High-Fat Diet With Plasma Lipid Levels and Cardiovascular Risk | JACC: Advances Haven’t heard it addressed anywhere, but I think it’s important. It’s huge (half a million participants) and long (over 11 years), and shows a doubling of ASCVD risk in the low carb cohort. It’s observational, of course. But the magnitude of effect is impressive, especially in subgroup analysis: people on low carb whose LDL-C topped 5 mmol/L (193 mg/dL), their ASCVD hazard ratio reached 6.68.
Furthermore, even when subjects were stratified by LDL-C, ASCVD risk was significantly higher in the low carb group. For example, the low carb group with LDL-C
I saw this study recently where it was referenced as a reason to avoid low carb/ketogenic diets. It has many problems:
1. Dietary intakes were collected by a validated web-based, self-administered questionnaire
Self-administered questionnaires are known to be highly inaccurate.
2. LCHF defined as consumption of
@@DJKiwi80 I appreciate the thoughtful, researched reply. Your answers are all reasonable.
It just seems that it shouldn't be so hard to prove low carb is healthy. It's not easy to maintain the ideal you describe. Shouldn't we at least see a signal as we approach it? Not only do we see no signal in its favor, we see the opposite: low carb appears to be quite dangerous. Unless--per your suggestion--you stick to
@@mfkleven you’re welcome. I have read many studies in this space recently, since I have elevated LDL cholesterol on a ketogenic diet and want to fully understand the risks. Unfortunately, there are many studies with bold headlines, poor study design and jump to conclusions based on correlation.
Regarding your concerns, I fully understand where you are coming from. The issue with going low carb but not low enough to reach ketosis, is you will still be craving carbohydrates and end up prone to binge eating. And I doubt people in food diet questionnaires would be honest about binging and underestimate the number of calories consumed. In my experience, it's very hard to maintain a low carb diet without ketosis. Once in ketosis, its much easier to maintain since fat is very satiating and it’s difficult to overeat.
I initially went on ketogenic diet to try and resolve issues I had with joint pain and inflammation. My CRP (inflammatory maker) was up around 5 to 6 on a moderate carbohydrate diet. Ideally CRP should be under 2. Six months after starting a ketogenic diet, my CRP had dropped below 1 where it has stayed ever since. My joint pain has 100% resolved and bloodwork is perfect with the only question mark being elevated LDL cholesterol. Which is why I am interested in discussions like the one in this video!
After many hours of reading and listening to debates on this topic, I strongly suspect a long-term ketogenic diet is protective against atherosclerosis/heat disease, regardless of LDL cholesterol levels. The protective properties of the diet are probably related to its anti-inflammatory effects. Atherosclerosis is after all an inflammatory disease, and I doubt any respected cardiologist would disagree with that. I would put money on it that if we can resolve chronic inflammation in the population, without lowering LDL cholesterol, we would see a dramatic decrease in heart disease.
A good reference for anti-inflammatory effects of ketogenic diets is “The effect of a ketogenic diet on inflammation-related markers: a systematic review and meta-analysis of randomized controlled trials”. It’s a good reference since 42 studies were included in the meta-analysis.
@@mfkleven The problem is if they don't control for health BEFORE the diet, then the study does not tell you much because a lot of people go on lowcarb due to really bad issues with weight and health, diabetes, etc, they tried other things first and those didn't work, which makes them more willing to try a more restrictive diet. Anyone that can lose weight just by doing a bit more exercise and eating a few less cookies would just do that instead. Most people going on the more restrictive diets are very much forced into it by serious problems they already had and from what I've seen, their problems usually improve a lot and they usually lose a lot of weight. But on the flip side, I think it does not solve all problems of everyone and there are likely other issues we need to understand better such as degrading nutrition in all our foods, chemicals, pufa, etc. If you are comparing diets, you need to have an even comparison, not have mostly the sickest people all on just the one diet option. In fact correlational research is always not super accurate and it's even worse if there is no good attempt to control for confounders. And the reason it's 'hard' to prove one diet against another is becuase good research requires control groups, control of all known variables, etc and people are not typically willing to be randomly assigned to one specific diet and then stick wit h it long term as would be needed with gold standard scientific protocol.
@@DJKiwi80 There are three problems with the study you cite:
1. Only two of several inflammatory markers improved on a KD. Notably CRP did not, and it’s the one most strongly associated with active atherogenesis.
2. Any caloric deficit reduces inflammation. To demonstrate that the KD is uniquely anti-inflammatory, only isocaloric studies should be included. Since this meta-analysis is behind a paywall, I can’t see if they did that.
3. Even if a KD is demonstrated to reduce systemic inflammation, we cannot assume it will reduce heart disease. It makes sense mechanistically, but so does reducing cholesterol and saturated fat. To have clinical relevance, the connection must be demonstrated by outcome studies, like they have with saturated fat and LDL-lowering interventions. Until then, we’re just speculating.
This is what my doctor could not explain. Before I was living irresponsibly but my LDL was low. Now that I'm living a healthy life, low carb diet and active but my LDL is currently high.
Are you also lean?
@@nico3641 Im lean now after I switched to healthy lifestyle. That's why my LDL went up, a lot higher than when I was 50 lbs over weight
If you have a healthy diet for you (not needed to be a low carb) probably you have a stable intake of nutrients and your body is producing the LDL needed for you. With an un health diet your levels of LDL and other lipids while be in a rollercoast, going up and down... in fact a diet without a regular intake of fat usually will develope problems, as the moment you take fat your body will not be able to adjust so quick and you will stress your metabolism. Our bodies are able to produce the lipids levels needed for us, whitout need to take it in the diet (but certains vitamins of course). Also the level of these biomolecular indicators are pure bullshit, probably confusing a consequence with a cause , so in fact having whats considered nowadays as "high levels" is not so bad in fact, but the opposite.
There were studies of several decades ago which indicated high levels of sugars the responsible for cardiac problems, not the fats... but you know? the big pharma wanted to sell you their new drugs, and coca-cola and other big food industries didn't want to be considered as bad for health...
@@alejandrosunshadow6041 Fat and not sugar makes our blood thick and sticks red blood cells together because it negates the zeta potential of these cells and the endothelial lining. There were no cardiac problems in any of the 20.000+ patients of Walter Kempner who were eating white rice, fruit juice and table sugar to combat their kidney diseases. Surely if sugar was as much a problem as you say this would have been shown then.
@@11235Aodh i didn't read the studies of Walter kempner but, one question about them... what uses as control group? Because if he is using any normal nowadays diet... well, that's not proof of anything to me... and I say so because i don't think is plausible to make such a studio nowadays, precisaly due to the insane difficulty of reuniting a big enough no sugar group.
Not all sugars are the same either
In my country, we say :"it's very easy to be gay with someone else's butt."
It means that everyone has an easy solution if he doesn't have skin in the game. Once the problem belongs to you, you weigh every single molecule of LDL.
High dose Niacin lowers LDL and has also shown an increase A1C (blood glycation) results , suggesting that reducing fat in the blood would also lead to an increase in sugar as the body still needs fuel.
This study may be showing that sugar as a fuel would reduce the need to have fat in that blood for a super skinny 27yo dude
the relationship between high-dose niacin, LDL cholesterol, and A1C levels is supported by scientific evidence. Research shows that high-dose niacin can lower LDL cholesterol levels, but it can also lead to increased blood glucose levels and potentially worsen glycemic control, as reflected by higher A1C values. This effect is attributed to niacin’s impact on insulin sensitivity and glucose metabolism.
However, the claim that reducing blood fat directly leads to increased blood sugar as a fuel source is not straightforward and requires more nuanced understanding. Niacin’s effects on glucose metabolism are complex and not simply a direct substitution of glucose for fat.
The idea that "sugar as a fuel would reduce the need to have fat in the blood" is not scientifically accurate. Metabolic adjustments are more nuanced. While high doses of niacin can affect glucose metabolism, it doesn’t directly mean that increased blood sugar replaces the need for fat. The body's energy regulation is more complex and involves multiple pathways.
Your statement suggests that the study shows a specific mechanism for a "super skinny 27yo dude," which may not be universally applicable. The effects of niacin on glucose levels and lipid metabolism can vary among individuals and are not necessarily confined to a specific demographic or body type.
In essence, your statement conflates the effects of niacin on lipid and glucose metabolism with an oversimplified view of how the body compensates for changes in fat and sugar levels.
Your statement implies a direct, simple relationship where reducing blood fat due to niacin leads directly to increased blood sugar. This oversimplifies the complex metabolic interactions. Niacin's effect on glucose is more about its impact on insulin sensitivity and glucose metabolism rather than a straightforward substitution of glucose for fat.
how was his A1C affected?
His Oreo test was only 16 days long. That is not long enough to significantly impact HbA1C.
What was the TG on the Oreos? Did they go up and make the LDL-C seem falsely lower? I would want to know what the direct LDL-C was and non-HDL-C was. Also particle count
Sorry, how did this experiment shock the world? All I see is that Nick got out of ketosis due to the reintroducing of carbs, so his elevated LDL that was caused by his ketogenic diet simply reverted back to normal. I can't get my head around how this is controversial? Can someone explain how this was not expected?
It is not news. I went through the process 18 years ago after quitting Atkins ketosis diet. My GP doc at the time fully expected the change based on his years of clinical experience and seeing so many patients doing Atkins over 30 years ago. Today everything is about getting mouse clicks on their tictoc or youtube videos. Everyone loves an Oreo...Success!
@@dfoo75au for what my opinion is worth, I fully agree with you.
The issue I have with this experiment and how it's results were presented is that many will interpret it as: Oreos lowered his LDL = junk food lowers LDL. Hence, food that raises your LDL is healthy and it is totally fine to have very high LDL.
@@Sobchak2my interpretation is that if you eat a normal American or western diet with 50%+ carbs, Increase of LDL is still bad. But when you are on low carb, your body has to find alternative energy currency via transporting lipid. In this case, the extra LDL is simply used to maintain a homeostasis. This is not medically recognized because in the past people on low carb among population is just too low to gain this insight.
Curious your total test and e2 levels considering..
Wow ! 545 ( 14.12mmol) and my Doctors worried about my total cholesterol of 6.6mmol
Wants me on a statin my hdl is good 1.6 triglycerides low @ .8
LDL..4.6
Money for the Pharmos...
It’s unclear to me why this is supposed to be a shocking experimental finding. Going from a ketogenic diet-that’s expected to increase LDL because of (likely) high saturated fat consumption-to adding carbs making it closer to a normal macro-composed diet should be expected to bring LDL back down. If anything, the surprising aspect here is the existence of individuals where the LDL can fluctuate so much, but hardly the Oreo cookies part.
Why, if someone is aware or even concerned that they are a lean mass hyper responser, would they spend 4 years on a ketogenic diet, where the outcome/consequence is an LDL of 500+? I don't get it. If he had an inkling or hypothesised adding back carbs would dramatically reduce risk, why spend four years playing Russian roulette?
Because the famous keto RUclipsrs keep saying high cholesterol is safe as long as you’re not eating carbs. I’m shocked they haven’t been sued yet.
@@tarabooartarmy3654 Who is going to sue anyone for telling the truth? The people who should be sued are those 'health' organisations paid by the highly processed food industry, including nasty, oxidative and inflammatory seed oils, to encourage people to eat unhealthy sugars that raise blood glucose levels that so often leads to diabetes. And diabetes doubles the risk of atherosclerosis. People need to research the Randle cycle if they want to be taken seriously, instead of parroting ignorant nonsense.
@tarabooartarmy3654 I could be wrong, but I doubt the PhD qualified interviewee would be susceptible to what assorted low-carb RUclips influencers say.
@@jonmoore4588 it could have been confirmation bias. All humans are susceptible from time to time. Even brilliant scientists can be at times and it can taint research. It happens when they have a reason to want to believe something, so their brain looks for things that confirm that belief even if they see other evidence that doesn’t.
That may not be the case here, but it is one possible thing that could explain ignoring the evidence.
@tarabooartarmy3654 maybe. It's a fair point. Ultimately, just conjecture on our part.
I would have liked Simon to query the context of his decision to follow a keto methodology for so long whilst LDL readings skyrocketed. That would have been really useful to understand given the nature of the conversation and topic at hand (the Statin vs carb study).
This shows that oreos are better than what he was eating before in regard to heart health
@@Mrm1985100 - Only if a person fully and unquestioningly accepts the cholesterol causes heart disease theory.
That theory is not supported by conventional clinical medical outcomes, if studies showing that more than half the people who have heart attacks also have cholesterol levels within standard guideline levels or lower. If those studies are correct, then LDL likely has no significant effect on cardiovascular disease, other than an after the fact association that is a follow on to the actual start of CVD.
Ultimately, nobody has scientific data to show that LMHR’s are protected from CVD, heart attacks & strokes. Regardless of how LDL is in the short term, very mutable, depending on dietary lipids, the cholesterol hypothesis still stands as the gold standard.
We need cholesterol, for a great many bodily functions. It's not just the repair media for your arteries, it's a vital building block for hormones such as testosterone and estrogen, for parts of the immune system, and for the protective myelin sheaths for your nerves, your brain is 70% cholesterol. If you inhibit the body's ability to create cholesterol(which is what statins do) all these things are inhibited, the brain especially suffers, dementia follows.
@@dennisward43 that’s why we make our own colesterol and our own saturated fat. These are not supposed to come through the digestive tract into our arteries and veins. We make our own cholesterol and stay healthy when its around 100s not 400s.
@@dennisward43 I certainly don’t condone the use of Statins OR Oreos to lower LDL. Norwitz is just show-boating. What he could have done is use a carb rich WFPB approach to change his LDL instead of the Statin, but he has tunnel vision for Keto. To be fair to him, he has done a video on adding a sweet potato to his high fat diet showing the drop in LDL. It didn’t garner much attention so he went Oreo.
As for Cholesterol - it is not an essential nutrient.
@@marcelotemer Well our ancestors have been primarily eating dietary cholestrol and saturated fat for millions of years, so I guess what you suppose and what evolution has deemed necessary for the human body are two completely separate things.
You do realise that many people die from low cholesterol.
The pseudoscientific guidelines for what the optimum level of cholesterol is, is dictated by Big Pharma to 'health' organisations (who they fund with lots of money) who make a killing out of prescribing risky cholesterol lowering drugs and so set the bar very low to make more money . Far too low.
@@davedewsnap288 The whole point of the experement was to highlight to the general public that cholesterol can be reduced without dangerous statins. Had the media been unbiased it would have made a big show about it. Unfortunately most of the media (and health associations) have been bought by the big Food and Pharma companies. so there were no big headlines. Much of the media relies on adverts from these big companies so they are not going to bite the hand that feeds them.
Our ancestors have been consuming dietary cholesterol for millions of years. My opinion is that evolution is a far more reliable source of knowledge than people paid by greedy companies to promote their recommendations for financial gain.
Cholesterol is needed in every cell of the body. It is an antioxidant and is used to repair damaged cells, like those in artery walls.
"Cholesterol helps repair cells throughout the body. It's a fat-like, waxy substance that's a key component of cell membranes, hormones, and vitamin D. Cholesterol is also found in myelin sheaths, which protect nerve cells and help nerve impulses travel more efficiently. Cholesterol recycling can also support myelin repair."
Dave Feldman showed low carb high fat switching to high carb briefly lowered LDL years ago. This is not new....
Statins vs Oreos, and could we also say statins vs seed oils?
I believe I'm a lmhr that has had a heart attack. Just because a person is thin and exercises, have been my whole life, does not mean you are immune from heart disease or diabetes, hereditary.
Dobie with natural ears? Beautiful!
Good luck with health. We’ve been excellent, 10% fat vegan x 5 yrs and restored our slim, strong health at 70, but I still can’t get LDL below 220. Frustrating! Still and forever love being vegan. Soul happy in body at last! And LOVE DOBIES!!!
@@PardieDiem what was your LDL cholestrol typically and at what age did you have a heart attack? Do you by any chance know your Lp(a) level as well?
@PardieDiem please either state your lipid numbers and state that you're on low carbs or not. Thin and exercise is NOT even part of the definition of LMHR.
@@firstchoicefarm7767 What is it exactly?
@@PardieDiem According to Norwitz, lean-mass hyper-responders have LDL above 200, HDL above 80, and triglycerides under 70. It's not a large phenotype, to put it mildly...but it does suggest more work to be done in lipidology.
Hey Nick, do you agree with Dr. Malcolm Kendrick when he says that LDL particles, whether large and fluffy or small and dense, play absolutely NO role in triggering/CAUSING atherosclerosis? Dr. Kendrick's reasoning stems from the fact that none of the ApoB-100 particles damage or disrupt the coronary glycocalyx or endothelium.
Prove it. Other experts don’t agree.
@@mcanqb experts also said the COVID vaccine was safe, and it wasn't and that it would save lives and it didn't save any life that was lost and that lockdowns would 'flatten the curve' and reduce transmission and none of that happened.
there has to be other factors involved - that's well known. it's a risk factor but not a cause on its own. you have to have something else going on that causes injury inflammation. most studies directly between cholesterol and heart disease/death are conflicting - you could read this
Dietary Cholesterol and Cardiovascular Risk: A Science Advisory From the American Heart Association
Any fat but especially saturated fats negate the natural zeta potential of blood cells and the endothelial lining, making them stick together (called rouleax formation). This is never a good thing.
@@mcanqb Science doesn't prove things. Proof is a mathematics term.
So, what about eating about a bunch of vegetables... that would be considered low carb... so....confused.
Strange how LMHR is one in a million, and we already have several people in the comments saying they are LMHR 🤔
Where is your evidence for claiming that LMHR is one in a million?
it's not 1 in a million among lean people on a ketogenic diet
@@atomic_poppy can’t be 1 in a million unless my family accounts for a good percentage of those! My mother and 2 siblings and I are/were all in this situation. I have 2 other siblings without the issue. Definitely genetic or epigenetic.
hereditary heterozygous familial hypercholesterolemia is what was said in the video to have a 1 in 1 million chance, not the LMHR phenotype
The discussion did not claim that LMHR is one in a million. That statistic was in the comment regarding homozygous vs heterozygous familial hypercholesterolemia.
Ask the goodly gentleman to test LPS in his gut thanks
This only confirms carbohydrates lower ldl better than statins, but nothing about having high LDL on keto is good, don't see how it helps keto
No, it confirms that bad food can increase your "good cholesterol". So you have to rethink if the "good cholesterol”is really good.
It does not mean high LDL is good. But at least you should question it if you really understand what this video is discussing.
@@lumanliu8457 He isn't wrong though, a plant based carb heavy diet (a la mcDougall's starch based diet) is better at lowering ldl than statins :).
LMHR here and im certainly hoping real scientists can figure this out before big pharma gets involved.
... guys I I think Im LMRH...
@@Iam-not-VEGAN-but- why?
Yeah this didn't change anything in the cardiology world lol except prove how dangerous keto diet is.
Hey, Sound. Good to see you! I haven't forgotten about our convo in r/Cholesterol - I've just been busy and my response will take some time to type out.
Did you watch this *entire* video? Be honest.
@@saintwithatie No, i will not watch a single minute of Norwitz until he admits keto is the one of the worst diets for heart health.
@@ladagspa2008 😥I figured as much. I'll work on that response soon.
Simon, did you challenge Nick on the poor design of his experiment-namely that it used Oreos to vilify statins, and only included one class of statins?
Both of those things were discussed.
Oreos were not used to vilify statins, which was not even the goal of this experiment. This is misinformation that keeps getting spread, even in the comments on a video explaining why this is misinformation.
14:55 The goal of this experiment was to be a provocative demonstration of the LMHR phenotype and the Lipid Energy Model - which it was adequately designed to do and which it adequately demonstrated. They actually did this experiment before (sans the statins - just demonstrating the LMHR phenotype) several times before with "healthy" carbs like sweet potatoes and had similar LDL-lowering results. However, in this particular experiment Oreos were chosen because they are more provocative than sweet potatoes and also work to highlight a paradox of a "unhealthy" food resulting in a "healthy" outcome. Nick talks about why he chose the particular statin he ended up using, and says that it would be cool to do the experiment again with different classes of statin.
Have a listen to full ep. We discuss this
@@TheProofWithSimonHill I don't know if Nick is being intentionally dense. But the controversy is not that people will think Oreos are healthy, but that statins are worthless (or that statins should be replaced with junk food). Read comments on his videos. Filled with confused people using this experiment to argue with their doctors about how worthless statins are. Statin denialism is closely tied with the keto grift that people like Nick push. Disappointed you let this slip by. There was no reason to do an experiment like this.
@@TheProofWithSimonHill The controversy isn't that people will think Oreos are healthy, but that statins are worthless. Statin denialism is closely tied to the keto dieting community that Nick is associated with. He already admitted there were experiments testing this with healthier carbs. There was no reason to do this experiment other than to vilify statins. Read the comments on his videos. Loads of confused people using this experiment to argue against statin treatment.
@@hiker-uy1bi Nick has clarified his position on statins - that they do work to lower LDL and that they are useful for many individuals. He has said this many, many, many, many times in videos, blogs, social media posts, etc. So the people thinking he thinks otherwise are wrong in thinking that. Why do you blame Nick for doing this experiment, rather than blaming the individuals who did not actually listen to/understand Nick's words?
He’s a charlatan and is trying to reinvent science of ASCVD. Terrible. I question the time you invested.
Could you elaborate? I watched this entire video, as well as most of the videos Nick has put out on his channel, and couldn't find anything suggesting that he is reinventing the science of ASCVD. This particular video barely touches on ASCVD.
@@saintwithatie you spent 5 hours of your life listening to this? Son! Nick doesn’t believe that lipids matter for this made up group of LMHR people. It’s dumb and NOT backed by the body of evidence and what we know happens long term by overconsumption of SF and high apob levels
@@davidwinebrennerjr4196 Yes, and it was 5 hours well-spent!
Firstly, a lot of people think that "phenotype" means that a certain group of people are 100% unique, usually due to genetics. That's not what this means. Phenotype simply means an observed characteristic. In this case, the observed characteristics are LDL cholesterol ≥200 mg/dL, HDL cholesterol ≥80 mg/dL, and Triglycerides (TG) ≤70 mg/dL upon adopting a ketogenic diet. That's it. That's the entire criteria.
The "Lean" part comes from the fact that the majority of the people exhibiting this phenotype are lean. This phenomenon has been tested and verified as a thing that consistently occurs. The leaner someone is and the more they restrict carbohydrates, the more the phenotype expresses itself. Becoming less lean or consuming more carbohydrate consistently decreases the expression of this phenotype. This phenomenon is real, however you want to label it (if you dislike labeling it as a "phenotype"). Also, the phenomenon occurs regardless of macronutrient type (simple/refined or complex carbs, saturated or unsaturated fat) or macronutrient source (plant or animal). All that is required is increasing leanness and decreasing carb consumption.
Secondly, it is not true that Nick doesn't believe that lipids (specifically LDL) matter for individuals expressing this phenotype. He will tell you plainly that he merely has a hypothesis, not a belief, but a hypothesis that is yet to be proven, which is that ASCVD risk for LMHRs is different (lesser) than other populations with similar LDL levels. Notice the verbiage here - "is lesser" is not the same as saying "doesn't matter", i.e. 0 risk. The risk may be slightly smaller, or much smaller - he doesn't know, but he has NEVER stated that he hypothesizes the risk to be 0.
His hypothesis is based on the fact that ASCVD is a complex disease with many, many factors aside from LDL. Common (lack of) understanding of the data leads many to believe that LDL is an independent risk factor for ASCVD, but this is only half of the story. "Independent risk factor" is a statistical calculation, not a physical reality. In reality, the mere presence of LDL, even in "elevated" concentrations, does not spontaneously nor necessarily lead to any specific level of plaque formation - there's an entire cascade of events that has to occur.
There exists an insurmountable amount of data suggesting that metabolic health factors GREATLY into almost every step of plaque formation. Knowing this, the question that behooves us to ask is - "How do certain states of lipid metabolism, as well as the overall state of metabolic health, interact with LDL levels to affect ASCVD risk?" This question has not been adequately explored, despite it being common (mis)understanding that it has. Where Nick and Dave come in is having an interest in this group of individuals with this unique, little-studied lipid metabolism, and above-average metabolic health in general, and performing the up-to-now undone science to help answer that question.
STUDY OREOS IN PUBMED:
Opioid reduction and enhanced recovery in orthopaedic surgery (OREOS)
THIS VIDEO IS A WASTE OF TIME!
PURE MISINFORMATION.
You’ve totally missed the point