34 replies to this topic

[Sdescon]

One of the leading causes of death is atherosclerosis induced cardiovascular disease. When we age, our arteries harden and thicken because of a build up of fatty material, plaques, and the long term inflammatory immune response which follows. When these plaques start to ulcerate and/or rupture, you have the perfect recipe for thrombus formation and the resulting stroke/heart attack/or other cardiovascular event.

The current treatments mostly try to slow down the build up of plaques, via better diet or by using statins (like zocor and crestor) and other cholesterol lowering agents.

A very promising treatment approach is trying to prevent or lessen the chronic immune inflammatory response which worsens atherosclerosis by using vaccines:

...atherosclerosis is an immune mediated chronic inflammatory disease where immune response to endogenous antigens (such as LDL related protein apoB-100, and lipid components such as oxidized phospholipids), heat shock protein 65, beta-2-glycoprotein I, or possibly exogenous antigens (possibly infectious agents) plays a role in the pathophysiology of the disease.

http://www.discovery...erosis-vaccine/

A Vaccine Against Atherosclerosis: Myth or Reality?
http://www.medscape....warticle/573048
An excellent Medscape article detailing possible targets and methods in immuno-therapy against atherosclerosis.

Is there anything else in the pipeline that acts to actually significantly reverse these plaques, rather than just slow the build up down? Something akin to a roto-rooter for the arteries maybe (preferably non-invasive and chemical rather than surgical) ?

Edited by Sdescon, 15 February 2012 - 10:34 AM.

[nowayout]

The current treatments mostly try to slow down the build up of plaques, via better diet or by using statins (like zocor and crestor) and other cholesterol lowering agents.

Funny how the pharmaceutical industry has brainwashed us with their marketing. It didn't even occur to you to mention exercise, which even in relatively small amounts has a GREATLY more beneficial effect on cardiovascular disease and mortality risk than statins, and exercise doesn't destroy muscle or increase cancer risk, unlike statins.

[Danail Bulgaria]

Sdescon, I am completely agree with You, that fighting the atheroscerosis is must for a longer life. In one previous topic, started by me (http://www.longecity...is/page__st__30) scottknl cited a research, that showed a reversal of the atherosclerotic plaques in patients with a coronary heart disease, i.e. reversal of the atherosclerosis after improving the lifestyle and the diet. The article is:
Intensive Lyfestyle Changes for Reversal of Coronary Heart Disease, Dean Ornish, MD; Larry W. Scherwitz, PhD; James H. Billings, PhD, MPH; K. Lance Gould, MD; Terri A. Merritt, MS; Stephen Sparler, MA; William T. Armstrong, MD; Thomas A. Ports, MD; Richard L. Kirkeeide, PhD; Charissa Hogeboom, PhD; Richard J. Brand, PhD. I managed to find the article in the Journal of the American Medical Association:
http://jama.ama-assn...0/23/2001.short

[Sdescon]

The current treatments mostly try to slow down the build up of plaques, via better diet or by using statins (like zocor and crestor) and other cholesterol lowering agents.

Funny how the pharmaceutical industry has brainwashed us with their marketing. It didn't even occur to you to mention exercise, which even in relatively small amounts has a GREATLY more beneficial effect on cardiovascular disease and mortality risk than statins, and exercise doesn't destroy muscle or increase cancer risk, unlike statins.

It didn't occur to me because I was posting this at 5 am without good sleep , rather than purposely omitting exercise through malice. Exercise is indeed very important, but it will only get you so far if you have poor genes and a family history of atherosclerosis. When we look at life extension however, we must maximize our ability to slow down pathological processes like atherosclerosis. This includes looking at any and all options, and not ruling out pharmaceutical management. As exercise alone optimizes your health based on genomic potential, we need that extra boost to extend life beyond our genomic limits.

Statins may cause rhabdomyolysis and muscle breakdown indeed, but using them correctly at the lowest effective dose, avoiding agents which increase serum levels (ie avoiding CYP 3A4 inhibitors like grapefruit juice with zocor, lowering dose of zocor with diltiazem, etc) will reduce this risk to a minimum.

Thanks to seivtcho for the great article!

Edited by Sdescon, 15 February 2012 - 08:04 PM.

[scottknl]

If you're serious about tackling atherosclerosis in your own life, exercise is is not enough. Graveyards are full of people who tried to tackle their heart disease with exercise alone. It needs to be balanced diet and exercise both. If you really want to make sure to have longevity then CRON diet and moderate exercise is the approach to take.

[mpe]

I'm amazed people (doctors included) still cling to the flawed lipid hypothesis while completely ignoring the mechanical damage hypothesis and the proposed treatments such as Pauling and Chealation Therapy. Given that CVD only occurs in animals which do not produce their own vitamin c, you would think that reasonably intelligent, educated people (doctors etc) would make the connection en masse, but they don't or is it that they do but don't want to kill the golden goose?

Regardless if you are concerned for your own or loved ones health, you would be wise to take off the blinkers of conventional medicine and consider all options. Researching the various claims is relatively easy today, but remember to take a healthy dose of scepticism before you accept any claims as fact (follow the money).

If you have read any of my prior posts you will know I'm no fan of big Pharma . My opinions have been formed from lengthy experience both my own and that of my extended family. My father since starting on statins has had 2 strokes and heart attacks and a quad bypass, he has done everything his doctor has told him, all to no avail. My wife's parents also take statins and doctor mandated low fat diet, both suffer from hypertension, diabetes, muscle pains, cognitive decline and a complete inability to stay awake more than 30 minutes after eating. My mother wouldn't take the statins, stating she would rather take her chances on her own and is still active healthy and completely independent(just as well for my father).

Following both a Paleo style diet and Pauling therapy, I have reduced my bp from 200/120 to 128/102. I know it's not perfect but it's improving my weight has fallen from 130 to 115 kilos, my target weight is 85 kilos and my target bp is 110/70. My doctor wanted me to take statins and bp meds, but as I'm not ready to die I decided on the bp meds, vit d and k2 in addition to the Paleo and Pauling therapy but no statins. My long suffering wife is also on Paleo and Pauling therapy in support of me and her last bp check showed her at a very healthy 115/65.

I'm 55 my wife's 52, our parents are mid to late 70's, our grandparents lived into their late 80's and 90's in good health without statins and on high fat diets, but not the high fat high sugar diets of today.

[Sdescon]

As I'm relatively unaware of stuff like Paleo diet, Pauling therapy, and chelation therapy, I'd like to know whether these methods have any high quality randomized double blind studies supporting their use? The mechanical damage hypothesis, why is it superior to the lipid and inflammatory hypothesis, and are there any relatively unbiased studies supporting one over the other? I admit that I am a skeptic to these alternatives, but I am honestly curious and open to the evidence.

Remember, we're all on the same side on this forum, we want to find the best way to extend life, whether this includes pharma, non-traditional medicine, procedural/surgical interventions, or what not. It's fairly clear that exercise, diet, pharmaceuticals, and supplements alone only get us so far. A combination of methods, as long as they are managed correctly in concert may lead to the best synergistic effect.

Edited by Sdescon, 16 February 2012 - 09:45 AM.

[nowayout]

Given that CVD only occurs in animals which do not produce their own vitamin c, you would think that reasonably intelligent, educated people (doctors etc) would make the connection en masse, ...

Maybe they don't make the connection because what you claim is not true. Mice produce their own vitamin C and they can also get cardiovascular disease.

[scottknl]

As I'm relatively unaware of stuff like Paleo diet, Pauling therapy, and chelation therapy, I'd like to know whether these methods have any high quality randomized double blind studies supporting their use? The mechanical damage hypothesis, why is it superior to the lipid and inflammatory hypothesis, and are there any relatively unbiased studies supporting one over the other? I admit that I am a skeptic to these alternatives, but I am honestly curious and open to the evidence.

Remember, we're all on the same side on this forum, we want to find the best way to extend life, whether this includes pharma, non-traditional medicine, procedural/surgical interventions, or what not. It's fairly clear that exercise, diet, pharmaceuticals, and supplements alone only get us so far. A combination of methods, as long as they are managed correctly in concert may lead to the best synergistic effect.

While I agree that we're all on the same side here, I have to disagree that pharmaceuticals have any place in preventing or dealing with atherosclerosis in people without gross defects in their DNA. It is caused solely and completely by diet and behavior and can be reversed by changing diet and behavior. It is true that some people have an easier time dealing with it because of genetic advantages, but I believe people need to accept responsibility for their own lifestyles and make change where it's needed.

I'm speaking as someone who has reversed their atherosclerosis and cleaned up my lifestyle to enjoy good health.

[mpe]

Mice don't naturally suffer from CVD, the inbred genetically manipulated mice used in CVD experiments have been modified specifically to suffer from the disease.
You can make an experimental animal do just about anything if you manipulate it, feed it an unnatural diet and control it's environment; a fact which is regularly brought up in this forum when discussing any breakthrough involving experimental animals.

[Danail Bulgaria]

This is isnteresting. Has anyone been thinking about why the mice do not develope cardio - vascular diseases?

[nowayout]

Mice don't naturally suffer from CVD, the inbred genetically manipulated mice used in CVD experiments have been modified specifically to suffer from the disease.

Wild type mice certainly do suffer CVD under the right unhealthy conditions, just like humans do. In the wild they simply don't live long enough, even if they had a bad enough diet. Arguably, humans don't suffer CVD either "in the wild", if you believe what paleo people keep telling us. My money is on their not living long enough in the wild, just like the mice.

[Danail Bulgaria]

While reading all of the posts, I got the feeling, that the only one scientifically tested way to reverse the atherosclerosis is changing the diet and the lifestyle.

[mpe]

Mice don't naturally suffer from CVD, the inbred genetically manipulated mice used in CVD experiments have been modified specifically to suffer from the disease.

Wild type mice certainly do suffer CVD under the right unhealthy conditions, just like humans do. In the wild they simply don't live long enough, even if they had a bad enough diet. Arguably, humans don't suffer CVD either "in the wild", if you believe what paleo people keep telling us. My money is on their not living long enough in the wild, just like the mice.

Not naturally they dont, this article details what processes have to be followed to make lab mice get CVD and the synthetic diet they have to be fed. Not only are the mice not "wild type" but also they have to be forced to eat an unnatural diet to achieve their results.

http://jap.physiolog...650.full#ref-33

"Because mice are, in general, naturally resistant to the development of some features of CVD, especially to fatty streak progression toward atherosclerosis, we feed them a synthetic, dairy fat-derived, high-fat and high-cholesterol diet (32)."

[REBUILDER]

As I'm relatively unaware of stuff like Paleo diet, Pauling therapy, and chelation therapy, I'd like to know whether these methods have any high quality randomized double blind studies supporting their use? The mechanical damage hypothesis, why is it superior to the lipid and inflammatory hypothesis, and are there any relatively unbiased studies supporting one over the other? I admit that I am a skeptic to these alternatives, but I am honestly curious and open to the evidence.

Remember, we're all on the same side on this forum, we want to find the best way to extend life, whether this includes pharma, non-traditional medicine, procedural/surgical interventions, or what not. It's fairly clear that exercise, diet, pharmaceuticals, and supplements alone only get us so far. A combination of methods, as long as they are managed correctly in concert may lead to the best synergistic effect.

While I agree that we're all on the same side here, I have to disagree that pharmaceuticals have any place in preventing or dealing with atherosclerosis in people without gross defects in their DNA. It is caused solely and completely by diet and behavior and can be reversed by changing diet and behavior. It is true that some people have an easier time dealing with it because of genetic advantages, but I believe people need to accept responsibility for their own lifestyles and make change where it's needed.

I'm speaking as someone who has reversed their atherosclerosis and cleaned up my lifestyle to enjoy good health.

I just started Pauling Therapy and the Paleo Diet. I'd like to know how you used chelation therapy. Did you use a physician, IV, oral, and/or what chelation agents/protocol(s) did you use? How long did it take? Any advice/lesons learned?

[nowayout]

Not naturally they dont, this article details what processes have to be followed to make lab mice get CVD and the synthetic diet they have to be fed. Not only are the mice not "wild type" but also they have to be forced to eat an unnatural diet to achieve their results.

http://jap.physiolog...650.full#ref-33

"Because mice are, in general, naturally resistant to the development of some features of CVD, especially to fatty streak progression toward atherosclerosis, we feed them a synthetic, dairy fat-derived, high-fat and high-cholesterol diet (32)."

Haha, isn't it well-known that humans are also naturally resistant to CVD unless we feed them a synthetic, dairy fat-derived, high-fat and high-cholesterol diet (also known as the American diet)?

[scottknl]

As I'm relatively unaware of stuff like Paleo diet, Pauling therapy, and chelation therapy, I'd like to know whether these methods have any high quality randomized double blind studies supporting their use? The mechanical damage hypothesis, why is it superior to the lipid and inflammatory hypothesis, and are there any relatively unbiased studies supporting one over the other? I admit that I am a skeptic to these alternatives, but I am honestly curious and open to the evidence.

Remember, we're all on the same side on this forum, we want to find the best way to extend life, whether this includes pharma, non-traditional medicine, procedural/surgical interventions, or what not. It's fairly clear that exercise, diet, pharmaceuticals, and supplements alone only get us so far. A combination of methods, as long as they are managed correctly in concert may lead to the best synergistic effect.

While I agree that we're all on the same side here, I have to disagree that pharmaceuticals have any place in preventing or dealing with atherosclerosis in people without gross defects in their DNA. It is caused solely and completely by diet and behavior and can be reversed by changing diet and behavior. It is true that some people have an easier time dealing with it because of genetic advantages, but I believe people need to accept responsibility for their own lifestyles and make change where it's needed.

I'm speaking as someone who has reversed their atherosclerosis and cleaned up my lifestyle to enjoy good health.

I just started Pauling Therapy and the Paleo Diet. I'd like to know how you used chelation therapy. Did you use a physician, IV, oral, and/or what chelation agents/protocol(s) did you use? How long did it take? Any advice/lesons learned?

I seem to have given the impression that I reversed my atherosclerosis via Pauling Therapy and the Paleo Diet. This is not true. I reversed it using a near vegan calorie restricted diet with optimal nutrition and it took me about 6 months to drop my excess weight (35 lbs) and it was another 6 months before I realized that my physical performance had increased measurably. I don't think paleo diet will reverse atherosclerosis, although some versions of it may prevent it from getting worse in most people. I believe that balancing my n6:n3 ratio of dietary fats in combination with full nutrition of all vitamins and minerals made a big difference in my results.

[niner]

I'm speaking as someone who has reversed their atherosclerosis and cleaned up my lifestyle to enjoy good health.

Scott, how did you determine that you had atherosclerosis, and that you reversed it? Did you have angiograms?

[scottknl]

I'm speaking as someone who has reversed their atherosclerosis and cleaned up my lifestyle to enjoy good health.

Scott, how did you determine that you had atherosclerosis, and that you reversed it? Did you have angiograms?

No, just running the same 10Km running course regularly between 2006 up to today. Before CR, performance would drop every year a little worse than last year all the time. Even when I was training for a 1/2 marathon race, my times didn't really improve beyond a certain time for the 10 km. After CRON my performance improved drastically, especially climbing long hills. I had high cholesterol (max 300 mg/dL and min 194 mg/dL) for about 12 years prior to CR onset in 2009. 6 months after starting CR checked cholesterol was down to 156 mg/dL and running performance was about 20% faster for the same distance over the same roads etc.

I guess even if I had done the angiograms, it would still be a one mouse experiment.

[Sdescon]

From the New England Journal of Medicine:
Study 1: Statins

Effect of Two Intensive Statin Regimens on Progression of Coronary Disease

http://www.nejm.org/...6/NEJMoa1110874

Both regimens had striking effects on coronary disease progression, resulting in significant regression of atherosclerosis. These data indicate that coronary artery disease can regress if the favorable levels of LDL and HDL cholesterol that were attained with statin therapy in this study are achieved.

Maximal doses of rosuvastatin and atorvastatin resulted in significant regression of coronary atherosclerosis. Despite the lower level of LDL cholesterol and the higher level of HDL cholesterol achieved with rosuvastatin, a similar degree of regression of PAV was observed in the two treatment groups.

From the Journal of the American Medical Association:
Study 2: intravenous ApoA-I Milano, apolipoprotein with some promise

Effect of Recombinant ApoA-I Milano on Coronary Atherosclerosis in Patients With Acute Coronary Syndromes

http://jama.ama-assn...90/17/2292.full

Design The study was a double-blind, randomized, placebo-controlled multicenter pilot trial comparing the effect of ETC-216 or placebo on coronary atheroma burden measured by intravascular ultrasound (IVUS).

Conclusions A recombinant ApoA-I Milano/phospholipid complex (ETC-216) administered intravenously for 5 doses at weekly intervals produced significant regression of coronary atherosclerosis as measured by IVUS. Although promising, these results require confirmation in larger clinical trials with morbidity and mortality end points.

Some more background on various other pharmaceutical agents used in the prevention of plaque rupture (rather than reversal):
http://www.heartandm...rg/pdf/36/3.pdf

Edited by Sdescon, 21 February 2012 - 10:36 AM.

[Sdescon]

The ASTEROID trial, from the Journal of the American Medical Association:

http://jama.ama-assn...3/1556.full.pdf

Very simple summary:

Medication used: Rosuvastatin 40mg (Crestor) given once daily, the highest approved dose of the most potent statin. No other statin or cholesterol lowering agent to be used. Any patient on other cholesterol lowering agents were washed out for 4 weeks, and no patients were on prior statins for at least 3 months.

Test used to detect regression of atherosclerosis: IVUS (intravascular ultrasound), which measures atheroma volume. Baseline was taken from 2002 and then on 2003 over the course of a year. Multiple secondary measures such as LDL, total cholesterol, and HDL were also taken on more frequent intervals of every 3 months.

Patients: Initially, 507 patients across multiple centers spread across the US, Canada, Australia, and Europe. By the end of the study, retention of 349 patients. All enrolled had to be over 18 years old, had to have at least one obstruction of 20% or greater in any coronary vessel. Patients with poorly controlled diabetes and uncontrolled triglycerides were excluded.

Side effects and adverse events: Check Table 5 (page 7). Some are drug derived, others may be disease derived

Limitations: no control group because it would be unethical to not treat very highly diseased patients and randomize with placebo. The idea that atheroma reduction will reduce mortality is speculative but highly possible.

Conclusion: from baseline, LDL decreased by an average of ~60 mg/dL, HDL increased by 14.7% (check table 2). Table 3 and 4 show statistically significant atheroma volume decreases. Figure 2 shows an example of atheroma regression, with a reduction of volume from 10.16 mm3 to 5.81 mm3.

The next step: Finding a direct link between atheroma reduction and reduction in mortality and morbidity

Edited by Sdescon, 22 February 2012 - 07:42 AM.

[brunotto]

http://www.longecity...tin-not-so-bad/

The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor pravastatin has been reported to have a beneficial effect on reducing the new onset of diabetes as well as lowering plasma lipids. Because pravastatin is a water-soluble organic anion, it cannot easily penetrate the lipid bilayer of the cell membrane. As the precise mechanisms of the effect of pravastatin on glucose metabolism and diabetes have not been clarified, we examined the roles of the organic anion transporter family on pravastatin-treated islet and adipocyte functions. Rat oatp1/slco1a1, oatp2/slco1a4 and oatp3/slco1a5 were expressed in the pancreas, and rat oatp3/slco1a5 was also detected in rat insulinoma cell line INS-1e. Pravastatin was transported not only by oatp1/slco1a1 and oatp2/slco1a4, but also by rat oatp3/slco1a5. Pravastatin uptake into INS-1e cells was detected and this transport was inhibited by sulfobromophthalein and rifampicin, both of which are known to inhibit oatp family-mediated uptake. In addition, pravastatin enhanced the glucose-stimulated insulin secretion from INS-1e cells. When fat-loaded db/db mice were treated with pravastatin, glucose intolerance and insulin resistance were prevented. In addition, insulin secretion from isolated islets was enhanced by pravastatin. These data suggest that pravastatin has pleiotropic effects on islets through membrane transport under high fat/glucose conditions.

http://www.ncbi.nlm....pubmed/20610886

Pravastatin is a water-soluble organic anion, it cannot easily penetrate the lipid bilayer of the cell membrane ... so IMHO sparing also mithocondria, cholesterol & COQ10 synthesis of the impermeable cells (al the cells without specific transport carriers)... what about lipophilic statins and tocotrienols ?!

[brunotto]

In the present study, pravastatin was the only hydrophilic
statin used, whereas several lipophilic statins were
administered: atorvastatin, fluvastatin, simvastatin and
pitavastatin. Hydrophilic statins are distributed much more
selectively in hepatocytes compared with lipophilic statins.17
Liver cellular membranes contain organic anion transporters
that mediate uptake of hydrophilic substances into
the cell. However, because extrahepatic cellular membranes
consist of lipid bilayers, hydrophilic statins cannot penetrate
these cellular membranes and thus cannot inhibit
intracellular HMG-CoA. Hence, whereas hydrophilic statins
are prevented from entering extrahepatic tissues, lipophilic
statins might inhibit not only cholesterol synthesis in the
liver but also production of essential substances by HMGCoA
reductase reaction, such as farnesylated proteins,
heme A, dolichol and ubiquinone (coenzyme Q10; CoQ10),
in peripheral compartments.17 CoQ10, an essential factor in
oxidative energy-generating systems in mitochondria, is
synthesized from mevalonic acid in many organs including
the heart.18 The mitochondrial inner membrane of heart
muscle has high activity of polyprenyltransferase, which
attaches isoprenoids to quinone bodies and is a key enzyme
in CoQ10 biosynthesis.19 It has been also reported that
upregulated CoQ10 biosynthesis in the heart is associated
with increased activity of HMG-CoA reductase.20 Lipophilic
statins that can enter easily myocardial cells inhibit isoprenoid
expression and thereby prevent CoQ10 biosynthesis in the
heart. This process could slow down mitochondrial generation
of ATP and affect myocardial contraction. Ichihara et
al reported that in a canine experimental myocardial ischemia
model, lipophilic statins worsened myocardial contractile
dysfunction during reperfusion, whereas pravastatin did
not.12,13 They also noted that worsening of myocardial
contraction was associated with reduction of myocardial
concentrations of CoQ10 and mitochondrial respiratory
function.21 Taken together, these mechanisms could explain
the superiority of hydrophilic vs lipophilic statins observed
in the present study.

http://www.ncbi.nlm....pubmed/17721009

[nowayout]

I don't know why all the brouhaha about statins. Various studies have shown NO benefit of statins in all case mortality and morbidity endpoints (they might reduce CVD a little but they increase cancer, so the mortality difference is none). . There have been studies showing that any CVD benefit of statins is hugely dwarfed by the benefit of putting patients on a mediterranean diet instead, or having them moderately exercise instead. I don't have the exact numbers with me, but you have to treat something like 100 men with statins to prevent one CVD event over a number of years (and for women statins make no difference). The other 99 patients get no benefit from them,. only side effects. So save your money.

[Bonee]

the only problem is to convince people to eat healthy and exercise... popping a pill is too convenient

[brunotto]

I don't know why all the brouhaha about statins. Various studies have shown NO benefit of statins in all case mortality and morbidity endpoints (they might reduce CVD a little but they increase cancer, so the mortality difference is none). . There have been studies showing that any CVD benefit of statins is hugely dwarfed by the benefit of putting patients on a mediterranean diet instead, or having them moderately exercise instead. I don't have the exact numbers with me, but you have to treat something like 100 men with statins to prevent one CVD event over a number of years (and for women statins make no difference). The other 99 patients get no benefit from them,. only side effects. So save your money.

Pravastatin (and aspirin) + fish oil is the best I discovered for my psoriasis and that works without any sides, consider please thath other possibilities I had where Ciclosporine, Methotrexathe or Humira or other strong immunosopressive stuff.

I dont have high LDL issue... but I use it.

http://www.longecity...tin-not-so-bad/

Of course I take also quite a lot of Q10... you put toghther all the statins... but -be carefull- the idrophillic pravastatin is MUCH different from other lipophillic statins becose it does not penetrate the cell bilayer or mitocondria (it needs an active transport)... so it act much much more specifically on blood vesse and blood content (T-Cell, Macrophages...) and Liver.

I agree Pravastatin it's slighltly immunosopressive so it's not good for cancer (but good for psoriasis or those with high PRC or inflammatory issue)

http://www.longecity...riasis-regimen/

having cancer specially Fluvastatin is needed... so it's not true all statins allways are bad for cancer.

http://www.ncbi.nlm....pubmed/21205474

I'm on a mediterranean diet.... I'm Italian...

Edited by brunotto, 25 February 2012 - 12:54 PM.

[HighDesertWizard]

IMHO, the leading online program in the world for Reversing Atherosclerosis is Dr. William Davis' Track Your Plaque program.

I have CVD and lots of experience with researching the disease. I'm a member of TYP. You can find me at the TYP forum.

Here's the web site...

www.TrackYourPlaque.com

[Danail Bulgaria]

wccaguy, at the long run did You all in the Track Your Plaque managed to reverse the size of the plaque of patients? If You did, please tell us how.

[Sdescon]

330,000 US Veterans over the age of 75 were part of this retrospective cohort study. These were people who were free of atherosclerotic cardiovascular disease at baseline, and were followed over a number of years. The study sought to find whether statins can reduce mortality for those over 75 who do not have baseline CV disease.

 

https://jamanetwork....bstract/2767861

 

Data still looks good for statins. Along with diet and exercise, I think certain medications can be utilized to decrease risks even further than non-pharmacological interventions alone (with proper accounting for risks of said treatment of course). The key is to use a multipronged approach that prolongs healthy life using every avenue available - not instead of diet and exercise - but in concert with these techniques. Our genes and tied epigenetic effects dictate our healthspan and lifespan in a very large part, so I believe diet and exercise can only get us so far (ie our genetic maximum). For longer term life extension, this is simply not enough.

 

PS: Just realized it's been 8 or so years since I first posted on this topic. Time flies. Has anyone changed their minds since then? What other methods are you guys utilizing?

Edited by Sdescon, 02 September 2020 - 11:16 PM.

[Gal220]

Other threads

Reversing arterial plaque

Patrick Theut "Reverse CAC score & Heart Disease

 

 

External links

Protocol for elevated CAC score(also trial results for kyolic garlic+coq10) 

Combo mix based off LP protocol

 

Vit E + Time Release vit C, 6 year trial  - would love to see this repeated with k2, collagen, and aged garlic

 

Collagen melts plaque , see also Nutritional Review

Edited by Gal220, 08 September 2020 - 06:49 PM.