591 replies to this topic

[Snapper]

I've been reading about Conjugated Linoleic Acid (CLA).  People will have heard of this as an easily available weight-loss supplement.  Most supplements for sale do not specify what isomers of CLA their products contain, although some do.  The isomers found in products are c9, t11 (aka 9-CLA) and t10, C12 (aka 10-CLA).  Most, if not all, products are a 50:50 ratio, i.e. 50% 9-CLA and 50% 10-CLA.

 

There are many varied and contradictory studies regarding the health benefits & side effects of these isomers in different species, and in general 10-CLA would appear to be the isomer responsible for weight loss while also having some undesirable effects, such as reduced insulin sensitivity and inducement of fatty liver.  However, 9-CLA may ameliorate the undesirable effects of 10-CLA. 

 

https://nutritionand.../1743-7075-12-4

 

As for atherosclerosis, the following article reports that the 9-CLA isomer regresses plaques, via familiar mechanisms, i.e. AMPK activation, PPAR activation etc. The blend in question is 80:20.

 

https://bpspubs.onli....1111/bcp.12948

 

9-CLA is basically Rumenic acid, an Omega-7 fatty acid.  It has previously been shown that Palmitoleic acid reduces plaque, and is also an Omega-7 fatty acid.  It would seem reasonable to assume that the Omega-7 part of CLA is what may regress plaques. 

 

Using a 50:50 blend of CLA, perhaps by adding some Palmitoleic acid as well, the level of 9-CLA would be increased in order to regress plaques.  Sea Buckthorn Oil is a source of Palmitoleic acid.

 

Also, Pomegranate seeds contain punicic acid, which may be converted to Rumenic acid in mammals, and may therefore be another good way to increase 9-CLA levels.

 

https://academic.oup...784?login=false

 

 

 

Edited by Snapper, 04 November 2022 - 01:26 PM.

[ambivalent]

Impressive mouse study comparing Atorvastatin, Fisetin with high fat control model.

 

https://www.ncbi.nlm...-etm-0-0-09457/

 

Tough to see the impact on the images, but obviously the recorded percentage plaque area diffrences are impressive.

 

Full paper:

 

https://www.ncbi.nlm...les/PMC7690243/

 

 

Edited by ambivalent, 05 November 2022 - 08:58 PM.

[aza]

I was trying to come up with a kind of process of what causes heart disease as a way to better understand and prevent it.

It could be a bit off but i think it seems reasonable.

 

mitochondrial dysfunction (fasting, exercise, ergothionine) + senescent cells-> reduced nitric oxide bio-availability/cells less effective/increased inflammation

 

Low nitric oxide production (poor diet/sun avoidance/no exercise)                          

 

high blood pressure

 

high blood glucose

 

Inflammation (exercise, fasting, diet, omega index)

 

-------

These combine together to create an environment with either a poorly functioning or highly damaged glycocalx.

 

So far, i still believe fasting is still likely to be one of the best ways to slow or reverse damage but more research is needed to find how effective it is.

 

Interestingly, if i recall correctly two common causes of glycocalx damage, high blood pressure and hyperglycemia are also two of the strongest indicators of cac progression.

 

The combination of reduced glycocalx protection, reduced blood flow, age related glycocalx degradation and constant damage with little repair is not a good one

 

I'm quite interested in ergothioneine and mushrooms at the moment. It appears to be one of the few dietary mitochondrial antioxidants that i know of, and it is associated with less mortality.

"Ergothioneine was the metabolite most strongly connected to the HCFP and was associated with a lower risk of coronary disease (HR per 1 SD increment of ergothioneine, HR=0.85, p=0.01), cardiovascular mortality (HR=0.79, p=0.002) and overall mortality (HR=0.86, p=4e-5).".

https://heart.bmj.co...ntent/106/9/691

Edited by aza, 15 November 2022 - 01:21 PM.

[aza]

The effect of ergothioneine on rat endothelium when damaged by mercury chloride in rats.

 

https://www.spandido...2/etm.2018.6079

 

Endogenous antioxidant levels and lipid peroxidation lowered to almost normal levels

Reactive oxygen species levels decreased, dramatically.

 

"ACh induced concentration-dependent relaxations in PE-pre-contracted aortic rings from control and treated rats (Fig. 1A).

Treatment with HgCl2 reduced ACh-induced relaxations by up to 67.1% compared with the control group (P<0.001) and shifted the concentration-response curve to the right (Fig. 1A).

EGT inhibited the impairment of ACh-induced relaxation observed in aortic rings from HgCl2-treated rats (P<0.001"

[Snapper]

Following on from reading about the likes of CLA, Pomegranates and Palmitoleic acid, I've been looking into peroxisome proliferator-activated receptors (PPARs), which are involved with handling and metabolism of fatty acids, glucose etc.  They are also involved with promotion of reverse cholesterol transport.  Agonists of PPAR-alpha and PPAR-gamma are available on prescription as fibrates (PPAR-alpha) and thiazolidinediones (TZD, PPAR-gamma).  There are also agonists etc. found in various substances such as CLA, Pomegranates, Palmitoleic acid.

 

I think it's an area which may hold promise, and is worth investigating further. 

 

Intro

 

https://pubmed.ncbi....h.gov/12223313/

 

PPAR-alpha...

 

Metabolic function

 

https://onlinelibrar....1002/jcp.25715

 

PPAR-gamma...

 

Inhibits progression, but does not reverse atherosclerosis (?)

 

https://faseb.online...bj.20.5.A1075-b

 

Rosiglitazone (TZD) inhibits atherosclerosis in mice

 

https://pubmed.ncbi....h.gov/10953027/

 

Cholesterol efflux

 

https://www.cell.com...(01)00164-2.pdf

 

Edited by Snapper, 24 February 2023 - 01:03 PM.

[Snapper]

Lengthy atherosclerosis video (part 1) from Dr James C Roberts.  Refers to Phosphatidylcholine and reverse cholesterol transport, the Rinse formula (lecithin + safflower oil etc.) from about 43m for 5 mins, and 1hr 8m for 10 mins.  The idea seems to be that by promoting reverse cholesterol transport via PPC you can de-esterify the cholesterol esters in the arterial wall and then re-esterify them with linoleic acid, meaning they are then soluble at body temperature and can be removed from the wall.

 

Edited by Snapper, 05 April 2023 - 01:36 PM.

[Mind]

Just wanted to say thanks to all of those that have found some potential ways to reverse heart heart disease. By posting here, you are potentially saving a lot of lives.

 

Sadly, when you go to a big hospital nowadays, they do not even consider ways of reducing the damage, they just put you on meds to reduce cholesterol. That's it. Good luck.

[albedo]

Thank you all. Did someone here went through a cardiac MRI to check potential coronary disease? Had so far a couple of CT calcium scores in the US.

[Dorian Grey]

Berberine Beats Crestor?  This is BIG!  

 

https://pubmed.ncbi....h.gov/35794102/

 

Berberine treats atherosclerosis via a vitamine-like effect down-regulating Choline-TMA-TMAO production pathway in gut microbiota

 

Trimethylamine-N-oxide (TMAO) derived from the gut microbiota is an atherogenic metabolite. This study investigates whether or not berberine (BBR) could reduce TMAO production in the gut microbiota and treat atherosclerosis. Effects of BBR on TMAO production in the gut microbiota, as well as on plaque development in atherosclerosis were investigated in the culture of animal intestinal bacterial, HFD-fed animals and atherosclerotic patients, respectively.

 

We found that oral BBR in animals lowers TMAO biosynthesis in intestine through interacting with the enzyme/co-enzyme of choline-trimethylamine lyase (CutC) and flavin-containing monooxygenase (FMO) in the gut microbiota. This action was performed by BBR's metabolite dihydroberberine (a reductive BBR by nitroreductase in the gut microbiota), via a vitamine-like effect down-regulating Choline-TMA-TMAO production pathway.Oral BBR decreased TMAO production in animal intestine, lowered blood TMAO and interrupted plaque formation in blood vessels in the HFD-fed hamsters.

 

Moreover, 21 patients with atherosclerosis exhibited the average decrease of plaque score by 3.2% after oral BBR (0.5 g, bid) for 4 months (*P < 0.05, n = 21); whereas the plaque score in patients treated with rosuvastatin plus aspirin, or clopidogrel sulfate or ticagrelor (4 months, n = 12) increased by 1.9%. TMA and TMAO in patients decreased by 38 and 29% in faeces (*P < 0.05; *P < 0.05), and 37 and 35% in plasma (***P < 0.001; *P < 0.05), after 4 months on BBR. BBR might treat atherosclerotic plaque at least partially through decreasing TMAO in a mode of action similar to that of vitamins.

 

 

----------------------------

 

I find this study very interesting, as the danger of TMAO has been downplayed in the past.  Seafood is high in both choline and TMA (which is metabolized to TMAO) itself (the fishy odor is actual TMA).  A seafood meal has been shown to spike urinary TMAO quite high, so why don't cultures consuming substantial dietary seafood (Japan) have notoriously wicked rates of heart disease? 

 

Another fun fact; I've seen berberine poo-pooed as as an effective supplement, as it is notoriously poorly absorbed.  This study appears to indicate berberine does its best work inside the gut.  If it never made it to the colon, it would not downregulate TMAO!  

 

Dr Been goes into the nuts & bolts here: https://www.youtube....M?feature=share

 

Chris Masterjohn does a deep dive into the choline/TMAO issue here: Does Dietary Choline Contribute to Heart Disease?

https://www.westonap...ease/#gsc.tab=0

 

"Pass the liver and egg yolks please.  And maybe some folks fasting for Lent may say pass the fish, shrimp or octopus.  Consuming these choline-rich foods will produce much better mental health than worrying in the face of contrary evidence that they are clogging your arteries."

 

These guys say lecithin & dietary choline DO cause TMAO spikes, and they are in fact harmful: Intestinal Microbial Metabolism of Phosphatidylcholine and Cardiovascular Risk

 

https://pubmed.ncbi....h.gov/23614584/

 

"Increased plasma levels of TMAO were associated with an increased risk of a major adverse cardiovascular event"

 

-----------------------------

 

Perhaps we can have our cake and eat it too?  Just have a 500mg cap of berberine with every high choline meal!  

 

Stay Healthy My Friends!  

Edited by Dorian Grey, 21 April 2023 - 10:51 PM.

[Mind]

Berberine Beats Crestor?  This is BIG!  

 

https://pubmed.ncbi....h.gov/35794102/

 

Berberine treats atherosclerosis via a vitamine-like effect down-regulating Choline-TMA-TMAO production pathway in gut microbiota

 

Trimethylamine-N-oxide (TMAO) derived from the gut microbiota is an atherogenic metabolite. This study investigates whether or not berberine (BBR) could reduce TMAO production in the gut microbiota and treat atherosclerosis. Effects of BBR on TMAO production in the gut microbiota, as well as on plaque development in atherosclerosis were investigated in the culture of animal intestinal bacterial, HFD-fed animals and atherosclerotic patients, respectively.

 

We found that oral BBR in animals lowers TMAO biosynthesis in intestine through interacting with the enzyme/co-enzyme of choline-trimethylamine lyase (CutC) and flavin-containing monooxygenase (FMO) in the gut microbiota. This action was performed by BBR's metabolite dihydroberberine (a reductive BBR by nitroreductase in the gut microbiota), via a vitamine-like effect down-regulating Choline-TMA-TMAO production pathway.Oral BBR decreased TMAO production in animal intestine, lowered blood TMAO and interrupted plaque formation in blood vessels in the HFD-fed hamsters.

 

Moreover, 21 patients with atherosclerosis exhibited the average decrease of plaque score by 3.2% after oral BBR (0.5 g, bid) for 4 months (*P < 0.05, n = 21); whereas the plaque score in patients treated with rosuvastatin plus aspirin, or clopidogrel sulfate or ticagrelor (4 months, n = 12) increased by 1.9%. TMA and TMAO in patients decreased by 38 and 29% in faeces (*P < 0.05; *P < 0.05), and 37 and 35% in plasma (***P < 0.001; *P < 0.05), after 4 months on BBR. BBR might treat atherosclerotic plaque at least partially through decreasing TMAO in a mode of action similar to that of vitamins.

 

 

----------------------------

 

I find this study very interesting, as the danger of TMAO has been downplayed in the past.  Seafood is high in both choline and TMA (which is metabolized to TMAO) itself (the fishy odor is actual TMA).  A seafood meal has been shown to spike urinary TMAO quite high, so why don't cultures consuming substantial dietary seafood (Japan) have notoriously wicked rates of heart disease? 

 

Another fun fact; I've seen berberine poo-pooed as as an effective supplement, as it is notoriously poorly absorbed.  This study appears to indicate berberine does its best work inside the gut.  If it never made it to the colon, it would not downregulate TMAO!  

 

Dr Been goes into the nuts & bolts here: https://www.youtube....M?feature=share

 

Chris Masterjohn does a deep dive into the choline/TMAO issue here: Does Dietary Choline Contribute to Heart Disease?

https://www.westonap...ease/#gsc.tab=0

 

"Pass the liver and egg yolks please.  And maybe some folks fasting for Lent may say pass the fish, shrimp or octopus.  Consuming these choline-rich foods will produce much better mental health than worrying in the face of contrary evidence that they are clogging your arteries."

 

These guys say lecithin & dietary choline DO cause TMAO spikes, and they are in fact harmful: Intestinal Microbial Metabolism of Phosphatidylcholine and Cardiovascular Risk

 

https://pubmed.ncbi....h.gov/23614584/

 

"Increased plasma levels of TMAO were associated with an increased risk of a major adverse cardiovascular event"

 

-----------------------------

 

Perhaps we can have our cake and eat it too?  Just have a 500mg cap of berberine with every high choline meal!  

 

Stay Healthy My Friends!  

 

Nice find Dorian. After reviewing this, it just reminds me of how complicated human metabolism and aging are. One can find research that supports or refutes just about any nutritional supplement or dietary intervention.

 

For people who say eggs are bad for health, I am always reminded of Emma Morano who lived to be 116, eating 2 raw eggs and meat every day. There are always outliers, and they probably skew a lot of research, especially in small sample sizes.

 

The Berberine research above is at least in animals AND humans, and a reduction in arterial plaque, no matter how small, is a dramatic result.

[Dorian Grey]

Nice find Dorian. After reviewing this, it just reminds me of how complicated human metabolism and aging are. One can find research that supports or refutes just about any nutritional supplement or dietary intervention.

 

For people who say eggs are bad for health, I am always reminded of Emma Morano who lived to be 116, eating 2 raw eggs and meat every day. There are always outliers, and they probably skew a lot of research, especially in small sample sizes.

 

The Berberine research above is at least in animals AND humans, and a reduction in arterial plaque, no matter how small, is a dramatic result.

 

Dr Brewer has an interesting take on TMAO.  He thinks kidney function is key.  Young, healthy kidneys excrete TMAO quite efficiently, but it's when kidney function starts to decline that TMAO can persist at levels that cause problems.  

 

 

It's interesting he mentions a kidney function gfr (glomerular filtration rate) above 90 as the key.  I looked back into my labs, & saw I was always better than 90, until just last year, where my result says greater than 60.  

 

I've always been a big believer in lecithin/phosphatidylcholine, & have taken PPC (polyunsaturated PC) daily over the last decade or so.  Got my first experience with angina hiking up a hill back in January.  YIKES!  So gfr dropped from 90 to 60, & Dorian has now got angina.  

[albedo]

Berberine Beats Crestor?  This is BIG!  

 

https://pubmed.ncbi....h.gov/35794102/

 

Berberine treats atherosclerosis via a vitamine-like effect down-regulating Choline-TMA-TMAO production pathway in gut microbiota

 

Trimethylamine-N-oxide (TMAO) derived from the gut microbiota is an atherogenic metabolite. This study investigates whether or not berberine (BBR) could reduce TMAO production in the gut microbiota and treat atherosclerosis. Effects of BBR on TMAO production in the gut microbiota, as well as on plaque development in atherosclerosis were investigated in the culture of animal intestinal bacterial, HFD-fed animals and atherosclerotic patients, respectively.

 

We found that oral BBR in animals lowers TMAO biosynthesis in intestine through interacting with the enzyme/co-enzyme of choline-trimethylamine lyase (CutC) and flavin-containing monooxygenase (FMO) in the gut microbiota. This action was performed by BBR's metabolite dihydroberberine (a reductive BBR by nitroreductase in the gut microbiota), via a vitamine-like effect down-regulating Choline-TMA-TMAO production pathway.Oral BBR decreased TMAO production in animal intestine, lowered blood TMAO and interrupted plaque formation in blood vessels in the HFD-fed hamsters.

 

Moreover, 21 patients with atherosclerosis exhibited the average decrease of plaque score by 3.2% after oral BBR (0.5 g, bid) for 4 months (*P < 0.05, n = 21); whereas the plaque score in patients treated with rosuvastatin plus aspirin, or clopidogrel sulfate or ticagrelor (4 months, n = 12) increased by 1.9%. TMA and TMAO in patients decreased by 38 and 29% in faeces (*P < 0.05; *P < 0.05), and 37 and 35% in plasma (***P < 0.001; *P < 0.05), after 4 months on BBR. BBR might treat atherosclerotic plaque at least partially through decreasing TMAO in a mode of action similar to that of vitamins.

 

 

----------------------------

 

I find this study very interesting, as the danger of TMAO has been downplayed in the past.  Seafood is high in both choline and TMA (which is metabolized to TMAO) itself (the fishy odor is actual TMA).  A seafood meal has been shown to spike urinary TMAO quite high, so why don't cultures consuming substantial dietary seafood (Japan) have notoriously wicked rates of heart disease? 

 

Another fun fact; I've seen berberine poo-pooed as as an effective supplement, as it is notoriously poorly absorbed.  This study appears to indicate berberine does its best work inside the gut.  If it never made it to the colon, it would not downregulate TMAO!  

 

Dr Been goes into the nuts & bolts here: https://www.youtube....M?feature=share

 

Chris Masterjohn does a deep dive into the choline/TMAO issue here: Does Dietary Choline Contribute to Heart Disease?

https://www.westonap...ease/#gsc.tab=0

 

"Pass the liver and egg yolks please.  And maybe some folks fasting for Lent may say pass the fish, shrimp or octopus.  Consuming these choline-rich foods will produce much better mental health than worrying in the face of contrary evidence that they are clogging your arteries."

 

These guys say lecithin & dietary choline DO cause TMAO spikes, and they are in fact harmful: Intestinal Microbial Metabolism of Phosphatidylcholine and Cardiovascular Risk

 

https://pubmed.ncbi....h.gov/23614584/

 

"Increased plasma levels of TMAO were associated with an increased risk of a major adverse cardiovascular event"

 

-----------------------------

 

Perhaps we can have our cake and eat it too?  Just have a 500mg cap of berberine with every high choline meal!  

 

Stay Healthy My Friends!  

 

Great finding Dorian. Also, isn't berberine what many of us have been taking in place of metformin (longevity/health span) due to the doctor prescription requirement for the latter? Good point also from Mind! So what is is the link if any with longevity, glucose update and metabolism and TMAO? Any comment? I might convert to berberine for the possible impact on arterial plaque. All this seem to me connected in some away, we know bad glucose metabolism and diabetes are risk factors for cardiovascular disease. For the time being and after my 2x non zero (but low and constant) calcium scores in US I am due to a exercise effort test and a cardiac MRI for a check.
 

[Mind]

Great finding Dorian. Also, isn't berberine what many of us have been taking in place of metformin (longevity/health span) due to the doctor prescription requirement for the latter? Good point also from Mind! So what is is the link if any with longevity, glucose update and metabolism and TMAO? Any comment? I might convert to berberine for the possible impact on arterial plaque. All this seem to me connected in some away, we know bad glucose metabolism and diabetes are risk factors for cardiovascular disease. For the time being and after my 2x non zero (but low and constant) calcium scores in US I am due to a exercise effort test and a cardiac MRI for a check.
 

 

Based upon this result and other positive research behind Berberine (some of it showing help with blood-sugar levels), I am going to start taking it more regularly. If it can reduce arterial plaque by just a tiny percentage, then it seems worth it.

 

I am unaware of any serious negative side effects from Berberine.

[Brian Valerie]

One piece of information regarding a potentially negative side effect of berberine is that discussed by Rejuvant CEO Tom Weldon in his "Modern Healthspan" YouTube video.  In a study by AKG researchers Kennedy, Lithgow, et al, mice given berberine in addition to CaAKG did not have an extended lifespan beyond that of the control group, unlike the experimental group that was given CaAKG only, which did show a slightly extended lifespan and reduced frailty.  Pending further research, I'm alternating weeks of berberine and CaAKG, as I believe in cycling off of virtually all of my supplements anyway in the hope of diminishing any homeostatic tolerance effect and also to allow my body to respond to any potential build up of possibly deleterious metabolites. 

[Gal220]

Berberine Beats Crestor?  This is BIG!  

 

https://pubmed.ncbi....h.gov/35794102/

 

Berberine treats atherosclerosis via a vitamine-like effect down-regulating Choline-TMA-TMAO production pathway in gut microbiota

 

Trimethylamine-N-oxide (TMAO) derived from the gut microbiota is an atherogenic metabolite. This study investigates whether or not berberine (BBR) could reduce TMAO production in the gut microbiota and treat atherosclerosis. Effects of BBR on TMAO production in the gut microbiota, as well as on plaque development in atherosclerosis were investigated in the culture of animal intestinal bacterial, HFD-fed animals and atherosclerotic patients, respectively.

 

 

Berberine should be taken with milk thistle

" And I recommend taking it with 175 mg of Milk Thistle extract (Amazon) each time to avoid possible DNA damage from long-term use."

 

https://nootropicsex....com/berberine/

 

 

I havent read too much negative, but this article is worth checking out

 

 

Why I Do Not Recommend Berberine extract for Diabetes

https://thebloodcode...tract-diabetes/

[Gal220]

Dr Brewer has an interesting take on TMAO.  He thinks kidney function is key.  Young, healthy kidneys excrete TMAO quite efficiently, but it's when kidney function starts to decline that TMAO can persist at levels that cause problems.  

 

 

It's interesting he mentions a kidney function gfr (glomerular filtration rate) above 90 as the key.  I looked back into my labs, & saw I was always better than 90, until just last year, where my result says greater than 60.  

 

I've always been a big believer in lecithin/phosphatidylcholine, & have taken PPC (polyunsaturated PC) daily over the last decade or so.  Got my first experience with angina hiking up a hill back in January.  YIKES!  So gfr dropped from 90 to 60, & Dorian has now got angina.  

 

Little pricey, but there are probiotics that act as a third kidney to offload some of the work

 

https://kibowbiotech.com/renadyl/

https://www.amazon.c...t/dp/B00WA1VNI0

[onemanatatime]

very happy to see this thread still alive 10 years after starting, im wondering if the thread starter has done another coronary arthery scan now 10 years later to scan the progress of interventions mentioned ?

[Dorian Grey]

What the heck?  Statins stabilize arterial plaque...  By CALCIFYING THEM?  

 

https://www.verywell...-scores-1746355

 

Statins and Your Calcium Scores

 

"Several studies have now shown that treating a patient who has atherosclerosis with statins can increase the cardiac calcium score, even though elevated scores are cause for concern and often the reason for treating with statins in the first place"

 

"Investigators reviewed eight separate studies which had used intravascular ultrasound (IVUS, a catheter technique) to assess the size and composition of atherosclerotic plaques in patients treated with statins. They found two things:

 

• High-dose statin therapy tended to shrink plaques.
• While the plaques were shrinking, their composition was changing.

 

After statin therapy, the volume of lipid deposits within plaques diminished, and the volume of fibrotic cells and calcium increased. These changes—converting an unstable “soft” plaque to a more stable “hard” plaque—may render a plaque less prone to sudden rupture."

"Evidence supports the idea that statin therapy not only reduces cholesterol levels but also changes existing plaques to make them less dangerous. As part of this process, the plaques may become more calcified—and thus, the calcium score goes up. An increasing calcium score with statin therapy, therefore, may indicate treatment success, and should not be a cause for alarm".

----------------------

OK, I can see how if you're in deep doo-doo with heart disease, have had an attack, stents or CABG, stabilizing plaques by calcifying them might be an effective Hail Mary therapy.  What scares the heck out of me would be statins as a prophylaxis, particularly in younger patients, as calcified arteries become very difficult to work with regarding stents and or CABG.  

 

Inflate a stent in a calcified artery, & CRUNCH, the calcium fractures, which can increase stent failure and complications.  Also, try stitching a vein or artery graft into a calcified "egg-shell" coronary artery.  Snap, crackle, pop...  "Oh well, we tried".  

 

I worked as a Surgical Technologist for 35 years, and have actually witnessed surgeons attempting to do aortic aneurysm grafts with calcified tissue.  It's no fun, and the surgeons actually express doubts about success of these during the case.   "Oh crap, this guy's badly calcified.  Let's do what we can, & get out of here as fast as possible".  

Edited by Dorian Grey, 21 May 2023 - 08:16 PM.

[Mind]

Maybe this is why large meta-analyses find almost no impact on overall mortality with statin usage. The statins are lowering cholesterol, but not really getting to the root of the problem. You still have stiff calcified arteries. Statins are one of the worst "band-aid" approaches to heart disease - expensive too.

[CarlSagan]

Maybe this is why large meta-analyses find almost no impact on overall mortality with statin usage. The statins are lowering cholesterol, but not really getting to the root of the problem. You still have stiff calcified arteries. Statins are one of the worst "band-aid" approaches to heart disease - expensive too.

 

yeah , the cholesterol is a secondary effect , not the cause. (cholesterol is a protective molecule going to sites of inflammation).  macrophages / immune cells are also in plaque. furthering inflammation & tissue damage.

 

and for the low effect size u get a bunch of problems because cholesterol is needed for hormones, needed for myelin (myelin is 1 main reason why humans have such great brain function), needed for immunity , etc.

any plaque reduction seen is really unimpressive if at all. or as mentioned maybe calcifies it (would that actually be indicating more cell death? from dead cells leaving calcium behind? https://pubmed.ncbi....ih.gov/8819895/).

main effect is likely on inflammation / blood clotting which can be gained from stuff that doesnt destroy needed cholesterol

 

Bromelain might have some effect here 

Edited by CarlSagan, 30 May 2023 - 12:16 PM.

[CarlSagan]

yeah , the cholesterol is a secondary effect , not the cause. (cholesterol is a protective molecule going to sites of inflammation).  macrophages / immune cells are also in plaque. furthering inflammation & tissue damage.

 

and for the low effect size u get a bunch of problems because cholesterol is needed for hormones, needed for myelin (myelin is 1 main reason why humans have such great brain function), needed for immunity , etc.

any plaque reduction seen is really unimpressive if at all. or as mentioned maybe calcifies it (would that actually be indicating more cell death? from dead cells leaving calcium behind? https://pubmed.ncbi....ih.gov/8819895/).

main effect is likely on inflammation / blood clotting which can be gained from stuff that doesnt destroy needed cholesterol

 

Bromelain might have some effect here 

Further insight:

https://www.ncbi.nlm...les/PMC3750440/

A population-based register study in the period 1999–2007 including 118,160 subjects aged 50 + without statin use at baseline.
All-cause mortality was lower in the groups with TC or LDL-C above the recommended levels.

"In conclusion, our population-based study shows that high TC, HDL-C, or LDL-C levels in the elderly are associated with a lower all-cause mortality compared with the group with the recommended low lipoprotein level. These findings are in opposition to the recommendation that in older adults without diabetes or CVD, lipoprotein values should be below specific values. In the current study higher lipoprotein levels do not seem to influence total mortality negatively. The opposite is the case for triglycerides, where the recommended low level is associated with lower all-cause mortality, especially in women.
However, cholesterol-lowering treatment in the form of statins provides a survival benefit without correlation to cholesterol level. 

Edited by CarlSagan, 30 May 2023 - 01:17 PM.

[CarlSagan]

nattokinase shows plaque size reversal , ~ -30% , when used at 6000 units or above

https://raypeatforum...489/post-928668

Edited by CarlSagan, 31 May 2023 - 10:27 AM.