Hi! Just thought I would provide my critique on your views on LDL’s relationship to cardiovascular disease from 1:00:36 to 1:18:06. My response to your views on LDL’s relationship to cardiovascular disease is as follows: Why reference comparatively extremely low quality epidemiological studies on LDL, that are rife for confounders and so are poor at establishing causation, and not even mention the much higher quality randomised controlled trials and the Mendelian randomisation studies that we have on this topic, where the randomisation process gets rid of confounders and therefore is much better at establishing causation? Based on the scientific evidence hierarchy we should be giving more weight to evidence higher on the scientific evidence hierarchy that is superior at establishing causation, not lower. You allude to not believing LDL/apoB is causative of cardiovascular disease with the ambulance analogy at 1:10:20. That’s actually precisely the problem with focusing on epidemiological studies as, similar to the ambulance analogy, seeing a correlation in epidemiological studies does not mean there is a causation-with epidemiological studies being inferior at inferring causation compared to randomised controlled trials and Mendelian randomisation studies. You also say at 1:16:00 that we should care more about the triglyceride and HDL ratio and care more about triglycerides and HDL compared to LDL. Let’s look at the evidence for LDL: separate meta analysis of over 200 prospective cohort studies, Mendelian randomisation studies and randomised trials including more than 2 million participants with over 20 million person years of follow up and over 150,000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of the exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. What is the evidence for the triglyceride to HDL ratio, triglycerides or HDL that includes more and higher quality evidence than this evidence I provided for LDL, with higher quality evidence ceteris paribus being higher on the scientific evidence hierarchy, that shows that the triglyceride to HDL ratio, triglycerides or HDL is more relevant in terms of their causative effect on cardiovascular disease compared to LDL?
I appreciate Matt's open-mindedness. As a scientist myself, I don't know why it is such a rare trait amongst our creed these days. It was especially frustrating working amongst clinicians in Clinical Endocrinology and Metabolism that I often heard tell their patients that no lifestyle changes can reverse their metabolic ill health. They would cite epidemiological research to underscore the futility of this approach. It was really an eye opener to me how we train people to be beholden to the greater wisdom of the medical industry to both make and break our health. All personal agency is removed - which likely is why we are where we are now.
I don't think fruit juice is a good choice no matter what. It's way too much fructose with nothing to offset it (no fiber). I can't believe you guys don't recognize that. Otherwise I agree with most of the advise. I'm Whole foods almost exclusive with no meat or dairy and my labs are near perfect. I do supplement Omega 3's and all the supplements you mentioned. No covid as yet and I'm 82, exercise regularly, sleep well with a C-pap machine, So far so good. Watch a lot of health related videos. Good info out there but also some not so good. It doesn't take long to discover who is legit and who is not.
Central Florida here, and approximately 1/2 of the year, we avoid doing any significant type of outside work in the sun. These past few weeks it has been so hot and humid that working in the shade causes excessive sweating, having to make sure to add electrolytes during the day. Both my husband and myself, late 6th decade, supplement with D3/K2/K4 or K7 to keep our levels in high normal ranges. We also have a functional doctor who tests for this throughout the year.
Hi! Just thought I would provide my critique on HighIntensityHealth’s views on LDL’s relationship to cardiovascular disease from 1:00:36 to 1:18:06. My response to HighIntensityHealth’s views on LDL’s relationship to cardiovascular disease is as follows: Why reference comparatively extremely low quality epidemiological studies on LDL, that are rife for confounders and so are poor at establishing causation, and not even mention the much higher quality randomised controlled trials and the Mendelian randomisation studies that we have on this topic, where the randomisation process gets rid of confounders and therefore is much better at establishing causation? Based on the scientific evidence hierarchy we should be giving more weight to evidence higher on the scientific evidence hierarchy that is superior at establishing causation, not lower. You allude to not believing LDL is causative of cardiovascular disease with the ambulance analogy at 1:10:20. That’s actually precisely the problem with focusing on epidemiological studies as, similar to the ambulance analogy, seeing a correlation in epidemiological studies does not mean there is a causation-with epidemiological studies being inferior at inferring causation compared to randomised controlled trials and Mendelian randomisation studies. You also say at 1:16:00 that we should care more about the triglyceride and HDL ratio and care more about triglycerides and HDL compared to LDL. Let’s look at the evidence for LDL: separate meta analysis of over 200 prospective cohort studies, Mendelian randomisation studies and randomised trials including more than 2 million participants with over 20 million person years of follow up and over 150,000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of the exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C. What is the evidence for the triglyceride to HDL ratio, triglycerides or HDL that includes more and higher quality evidence than this evidence I provided for LDL, with higher quality evidence ceteris paribus being higher on the scientific evidence hierarchy, that shows that the triglyceride to HDL ratio, triglycerides or HDL is more relevant in terms of their causative effect on cardiovascular disease compared to LDL?
Liver enzymes especially alt and ast can be elevated in athletes due to muscle damage from training as well… especially in muscular individuals. In this scenario it does not indicate liver stress or poor metabolic health
Hey, remember when eating lots of pasta rice and starches with lots of healthy fat like partially hydrogenated seed oils/margarine was considered healthy almost unanimously by "the experts"? Maybe people of different ideas should get together and try to hash out what is true and what isn't for the good of all, imagine that.
Okay your body makes 80% of your cholesterol... so you're saying your body is poisoning you? Ring Ring....The 1950s are calling ..... They want their Ancel Keys back😂
Yo, Matt! Long time lurker, first time commenter. Love your channel. Thanks for putting out content! Also, have you heard of Dave MacLeod? @climbermacleod You two having a chat is my dream team 🤩
Thanks for having me on, guys! This was a lot of fun especially @ 01:01:49. Thank you!
Hi! Just thought I would provide my critique on your views on LDL’s relationship to cardiovascular disease from 1:00:36 to 1:18:06. My response to your views on LDL’s relationship to cardiovascular disease is as follows:
Why reference comparatively extremely low quality epidemiological studies on LDL, that are rife for confounders and so are poor at establishing causation, and not even mention the much higher quality randomised controlled trials and the Mendelian randomisation studies that we have on this topic, where the randomisation process gets rid of confounders and therefore is much better at establishing causation? Based on the scientific evidence hierarchy we should be giving more weight to evidence higher on the scientific evidence hierarchy that is superior at establishing causation, not lower.
You allude to not believing LDL/apoB is causative of cardiovascular disease with the ambulance analogy at 1:10:20. That’s actually precisely the problem with focusing on epidemiological studies as, similar to the ambulance analogy, seeing a correlation in epidemiological studies does not mean there is a causation-with epidemiological studies being inferior at inferring causation compared to randomised controlled trials and Mendelian randomisation studies.
You also say at 1:16:00 that we should care more about the triglyceride and HDL ratio and care more about triglycerides and HDL compared to LDL. Let’s look at the evidence for LDL: separate meta analysis of over 200 prospective cohort studies, Mendelian randomisation studies and randomised trials including more than 2 million participants with over 20 million person years of follow up and over 150,000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of the exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C.
What is the evidence for the triglyceride to HDL ratio, triglycerides or HDL that includes more and higher quality evidence than this evidence I provided for LDL, with higher quality evidence ceteris paribus being higher on the scientific evidence hierarchy, that shows that the triglyceride to HDL ratio, triglycerides or HDL is more relevant in terms of their causative effect on cardiovascular disease compared to LDL?
I appreciate Matt's open-mindedness. As a scientist myself, I don't know why it is such a rare trait amongst our creed these days. It was especially frustrating working amongst clinicians in Clinical Endocrinology and Metabolism that I often heard tell their patients that no lifestyle changes can reverse their metabolic ill health. They would cite epidemiological research to underscore the futility of this approach. It was really an eye opener to me how we train people to be beholden to the greater wisdom of the medical industry to both make and break our health. All personal agency is removed - which likely is why we are where we are now.
I don't think fruit juice is a good choice no matter what. It's way too much fructose with nothing to offset it (no fiber). I can't believe you guys don't recognize that. Otherwise I agree with most of the advise. I'm Whole foods almost exclusive with no meat or dairy and my labs are near perfect. I do supplement Omega 3's and all the supplements you mentioned. No covid as yet and I'm 82, exercise regularly, sleep well with a C-pap machine, So far so good. Watch a lot of health related videos. Good info out there but also some not so good. It doesn't take long to discover who is legit and who is not.
Central Florida here, and approximately 1/2 of the year, we avoid doing any significant type of outside work in the sun. These past few weeks it has been so hot and humid that working in the shade causes excessive sweating, having to make sure to add electrolytes during the day. Both my husband and myself, late 6th decade, supplement with D3/K2/K4 or K7 to keep our levels in high normal ranges. We also have a functional doctor who tests for this throughout the year.
Hi! Just thought I would provide my critique on HighIntensityHealth’s views on LDL’s relationship to cardiovascular disease from 1:00:36 to 1:18:06. My response to HighIntensityHealth’s views on LDL’s relationship to cardiovascular disease is as follows:
Why reference comparatively extremely low quality epidemiological studies on LDL, that are rife for confounders and so are poor at establishing causation, and not even mention the much higher quality randomised controlled trials and the Mendelian randomisation studies that we have on this topic, where the randomisation process gets rid of confounders and therefore is much better at establishing causation? Based on the scientific evidence hierarchy we should be giving more weight to evidence higher on the scientific evidence hierarchy that is superior at establishing causation, not lower.
You allude to not believing LDL is causative of cardiovascular disease with the ambulance analogy at 1:10:20. That’s actually precisely the problem with focusing on epidemiological studies as, similar to the ambulance analogy, seeing a correlation in epidemiological studies does not mean there is a causation-with epidemiological studies being inferior at inferring causation compared to randomised controlled trials and Mendelian randomisation studies.
You also say at 1:16:00 that we should care more about the triglyceride and HDL ratio and care more about triglycerides and HDL compared to LDL. Let’s look at the evidence for LDL: separate meta analysis of over 200 prospective cohort studies, Mendelian randomisation studies and randomised trials including more than 2 million participants with over 20 million person years of follow up and over 150,000 cardiovascular events demonstrate a remarkably consistent dose-dependent log-linear association between the absolute magnitude of the exposure of the vasculature to LDL-C and the risk of ASCVD; and this effect appears to increase with increasing duration of exposure to LDL-C.
What is the evidence for the triglyceride to HDL ratio, triglycerides or HDL that includes more and higher quality evidence than this evidence I provided for LDL, with higher quality evidence ceteris paribus being higher on the scientific evidence hierarchy, that shows that the triglyceride to HDL ratio, triglycerides or HDL is more relevant in terms of their causative effect on cardiovascular disease compared to LDL?
Excellent conversation! Thank you very much! 🙏
Thanks 👍
Liver enzymes especially alt and ast can be elevated in athletes due to muscle damage from training as well… especially in muscular individuals. In this scenario it does not indicate liver stress or poor metabolic health
Could Vit D supplementation cause calcification say in the veins? In the heart?
Cholesterol denier. If you enjoy listening to flat earthers, you'll love Mike Mutzel.
@dr.Alo explains well about LDL
Damn! I randomly thought about this dude today after having unsubscribed from him months ago, check my feed and here he is. 😅
For me ,NAC= Bad Breath
The misinformation this guy spews is next level. It’s dangerous to platform someone who vehemently denies cholesterol. I expect better from Matt
thought exactly the same
Hey, remember when eating lots of pasta rice and starches with lots of healthy fat like partially hydrogenated seed oils/margarine was considered healthy almost unanimously by "the experts"?
Maybe people of different ideas should get together and try to hash out what is true and what isn't for the good of all, imagine that.
He’s also one of the seed oil conspiracy theorists and mis represents the studies
In which way is hé denying it?
Okay your body makes 80% of your cholesterol... so you're saying your body is poisoning you? Ring Ring....The 1950s are calling ..... They want their Ancel Keys back😂
Yo, Matt! Long time lurker, first time commenter. Love your channel. Thanks for putting out content!
Also, have you heard of Dave MacLeod? @climbermacleod You two having a chat is my dream team 🤩