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How do we stop heart disease (Atherosclerosis, Arteriolosclerosis, Arteriosclerosis, calcification)

pamojja

Senior Member
Messages
2,398
Location
Austria
I imagine in the case of my husband who has a fasting insulin of 24, and lower HbA1C than me (my fasting insulin is 2 - 4), it would be completely worthless to measure his glucose since his pancreas seems to be able to secrete endless amounts of insulin.

Remember, ptheut panicked with an insulin of 40! Having to produce any amount above 6 in the long term will invariably exhaust the pancreas. Your husband is even the perfect candidate to check a few days of fasting and postprandial blood-glucose (1 hr after finishing meal).
 

prioris

Senior Member
Messages
622
Increase Nitric Oxide (NO) synthesis in endothelial cells. Look for supplements that do this.

https://drmalcolmkendrick.org/2017/03/17/what-causes-heart-disease-part-xviii/
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Unsurprisingly, Viagra is used to treat people who have pulmonary hypertension (high blood pressure in the blood vessels in the lungs) at sea level. It is sold under the name Ravatio, for this indication – but we know that it is just Viagra. In addition, Viagra can be used to treat Raynaud’s disease, where the small blood vessels supplying the fingers and toes constrict, leading to painful cold fingers.

So, here we have a drug that can treat angina, pulmonary hypertension, erectile dysfunction and Raynaud’s disease at the same time. Thus, you can have great sex at twenty thousand feet above sea level, not get chest pain, or breathless, and stay warm at the same time. What more could a man ask for?

How does it do all these things? The answer is that it increases Nitric Oxide (NO) synthesis in endothelial cells. When it does this in the penis, it stimulates erections. In the heart, it opens up coronary arteries. In the lungs, it dilates the blood vessels, in fingers and toes it opens up arteries. So, all of the many different effects, are all due to exactly the same process – increased NO synthesis. Viagra also lowers blood pressure – as you would expect.

  • Over a seven year period, those men taking PDE5is (Viagra Cialis and the like) had a 4.7% reduction in overall mortality – compared to men who did not.
  • Those taking Viagra were 38% less likely to have a myocardial infarction
  • If you did have a myocardial infarction, those who were taking PDE5is had a 25.7% death rate. Those who were not taking PDE5is had a 40.1% death rate. So, if you were unfortunate to have a heart attack, you were 14.6% less likely (absolute risk reduction) to die if you were taking PDE5is.
Or, to shorten this even more

  • 4.7% reduction in overall mortality
  • 38% reduction in MI (relative risk reduction)
  • 14.6% reduction in death after an MI
Whilst the first figure of a 4.7% reduction in overall mortality may not sound terrible exciting, it knocks all antihypertensives and cholesterol lowering medication into a cocked hat. Even if you add them together and multiply by two – on their best day. Because 4.7% is an absolute risk reduction. [Absolute mortality reduction in the Heart Protection Study (HPS), the most positive statin trial, was 1.8% over five years]

Do I think everyone should take Viagra? Well, if you have heart failure, diabetes and a high risk of CVD – probably. Will you get a doctor to prescribe it for you, for CVD prevention? Absolutely no chance. Will anyone ever fund a study on this? With the drugs now off patent – no chance.

In the meantime, look to other things that can increase NO synthesis. L-arginine/L-citrulline does this. Potassium does this. Sunlight does this. Exercise does this. Meditation does this. Vitamin D does this, as does Vitamin C. What are you waiting for? Go for a walk in the sun and eat an orange – you will live forever.
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Gondwanaland

Senior Member
Messages
5,095
Remember, ptheut panicked with an insulin of 40! Having to produce any amount above 6 in the long term will invariably exhaust the pancreas. Your husband is even the perfect candidate to check a few days of fasting and postprandial blood-glucose (1 hr after finishing meal).
I know. He is addicted to sugar and doesn't care :(
BTW he's come back from hell already. Things were much worse before I found out about what really underlies going gluten free for your life.
 

pamojja

Senior Member
Messages
2,398
Location
Austria
L-arginine/L-citrulline does this. Potassium does this. Sunlight does this. Exercise does this. Meditation does this. Vitamin D does this, as does Vitamin C. What are you waiting for? Go for a walk in the sun and eat an orange – you will live forever.

Now you're getting a bid too excited ;), we still will die. By the way, (though I would doubt Bill Sardi on many points) has anyone read this article?

http://knowledgeofhealth.com/three-arterial-cleansing-regimens/
http://knowledgeofhealth.com/three-arterial-cleansing-regimens/
Three non-prescription anti-plaque regimes have been described:
  • The vitamin C + lysine application for lipoprotein-a demonstrated by Linus Pauling and Matthis Rath
  • The chondroitin sulfate/lecithin reduction of arterial plaque as described by Lester morrison MD
  • The L-arginin/Vitamin D3 regimen described by J. Joseph Prendergast MD

Personally started with Pauling's, through TYP also Prendergast's, and finally this Sardi article made my trial Chondroitin sulfate at 5 g/d for 8 months, but never reordered due to its high price:
http://knowledgeofhealth.com/the-ma...l-molecule-20-years-before-cholesterol-drugs/
http://knowledgeofhealth.com/the-ma...l-molecule-20-years-before-cholesterol-drugs/
In retrospect exactly after that high dose trial of CS my walking-disability lifted..
 

Gondwanaland

Senior Member
Messages
5,095
Now you're getting a bid too excited ;)
I just love that ironic touch of Dr. Kendrick :woot:
Personally started with Pauling's, through TYP also Prendergast's, and finally this Sardi article made my trial Chondroitin sulfate at 5 g/d for 8 months,
How about all of them at the same time? I am scared of taking Lysine because - really, the severe vasoconstriction I get from it probably means I am very low on B2 (?) :confused: So combining it with arginine would be more feasible (and B2 of course).
 

prioris

Senior Member
Messages
622
Now you're getting a bid too excited ;), we still will die. By the way, (though I would doubt Bill Sardi on many points) has anyone read this article?



Personally started with Pauling's, through TYP also Prendergast's, and finally this Sardi article made my trial Chondroitin sulfate at 5 g/d for 8 months, but never reordered due to its high price:
http://knowledgeofhealth.com/the-ma...l-molecule-20-years-before-cholesterol-drugs/
In retrospect exactly after that high dose trial of CS my walking-disability lifted..

Excellent info pamojja.

Well he did say - i didn't excerpt it - not dying of CVD increases ones
chances of dying of cancer ... LOL

I take nattokinase/serrapeptase for plaque but increasing nitric oxide synthesis is important too
 

pamojja

Senior Member
Messages
2,398
Location
Austria
I just love that ironic touch of Dr. Kendrick :woot:

How about all of them at the same time? I am scared of taking Lysine...

A targeted and slender regimen would be really best. However, some like me have so many issues (PAD, lungs, liver, kidneys, hormones, anemia, infections and inflammation, allergies, PEM, ...) that each targeted regimen added up with all others to an all-compassing one. Which also could be considered the 'kitchen-sink' or 'shot-gun' approach. But it worked so well that I paid it's price, being broken. :(

I really envy Dr. Davis, who beside diet, get enough benefit from D3, K2, fish-oil, a bid iodine and Armour alone.

In your case would also experiment with high lysine foods:

http://nutritiondata.self.com/foods-000083000000000000000-w.html
 

prioris

Senior Member
Messages
622
High Lp(a) level, .. more difficult to break down blood clots

L-Carnitine can reduce Lp(a)

https://drmalcolmkendrick.org/2017/01/16/what-causes-heart-disease-part-xxiv/
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On the positive side, after sixty-one million years, or so, evolution came up with a partial solution to the early stages of scurvy. Namely, the synthesis of a substance to block the cracks in the blood vessel walls, and control the bleeding. This substance is, or course, lipoprotein (a).

Lipoprotein (a) (Lp(a)) is synthesized in the liver, and it travels around in the bloodstream, looking for any cracks in blood vessels walls a.k.a. damaged endothelium. When a crack is spotted Lp(a) is attracted to the area and sticks very firmly, and cannot easily be removed. Of course, the rest of the blood clotting system also moves into action, so all hell breaks loose. Therefore Lp(a) becomes mixed up with platelets, red blood cells, fibrin, and almost everything else in the blood, including all the other lipoproteins.

However, Lp(a) has a very special trick up its sleeve. It mimics plasminogen.

After a blood clot forms, anywhere in the circulation, it has to be broken down, and removed – once the blood vessel underneath it has repaired. I liken this (not very accurately) to road works. If the road surface is damaged, the repair team comes in, sets up barriers and traffic lights and suchlike, then they repair the road. Then all the barriers, and traffic lights, and suchlike, must be removed.

....

Which means that if you have a high Lp(a) level, you will develop bigger and more difficult to break down blood clots. Exactly what evolution had in mind for creatures that cannot manufacture vitamin C, and need to plug cracks in artery walls when the vitamin C level falls. However, not so good, if you want to stop atherosclerosis from developing.

Because these Lp(a) rich blood clots have to go somewhere, and the only place that they can go is to be absorbed into the artery wall itself, and then broken down. However, these clots are more difficult to break down, so, with repeated clots over the same area of artery wall, bigger and bigger plaques will grow.

...

However, there is one way to definitely reduce Lp(a) levels, and that is to take l-carnitine. Here, from a study called ‘L-carnitine reduces plasma lipoprotein(a) levels in patients with hyper Lp(a)’

‘L-carnitine, a natural compound stimulating fatty acid oxidation at the mitochondrial level, was tested in a double blind study in 36 subjects with Lp(a) levels ranging between 40-80 mg/dL, in most with concomitant LDL cholesterol and triglyceride elevations. L-carnitine (2 g/day) significantly reduced Lp(a) levels… the reduction being more dramatic in the subjects with the more marked elevations. In particular, in the L-carnitine group, 14 out of 18 subjects (77.8%) had a significant reduction of Lp(a) vs only 7 out of 18 (38.9%) in the placebo group. In a significant number of subjects the reduction of Lp(a) resulted in a return of this major cardiovascular risk parameter to the normal range.’ 4

Does this then result in a reduction in CVD risk? The answer is that I do not know, for sure. A meta-analysis of L-carnitine supplementation has been done. This consisted of five trials on three thousand people. L-carnitine supplementation did show some benefit – which did not reach statistical significance, but came very, very close.

For those of you who like a bit of statistics, here we go

‘The interaction test yielded no significant differences between the effects of the four daily oral maintenance dosages of L-carnitine (i.e., 2 g, 3 g, 4 g, and 6 g) on all-cause mortality (risk ratio [RR] = 0.77, 95% CI [0.57-1.03], P = 0.08)’5

CI [0.57 to 1.03] – close, but no cigar.

To put this into figures anyone can understand. In the intervention groups (those taking L-carnitine) there were 83 deaths. In the control group (those not taking L-carnitine) there were 106 deaths. Total study population was 3108, split in two groups: control and intervention. This gets as close to statistical significance as you can get (virtually). In fact, if this had been a statin trial, you would never have heard the end of it. ‘Ladies and gentlemen a 22% reduction in overall mortality with L-carnitine supplementation.’ [Oh, what fun statistics are].

...

What would I now recommend? If you have a high Lp(a) level take lots of vitamin C and l-carnitine and see if your Lp(a) level falls. If it does, keep taking lots of vitamin C and l-carnitine for the rest of your life. If it does not fall? Not sure.
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Valentijn

Senior Member
Messages
15,786
I haven't read this study myself, but it's loathed by Diabetes patients about as much as PACE is loathed by ME/CFS patients. The impression I got from reading discussions about it is that patients were merely told to measure blood sugar, and given no meaningful instructions on what to do with that information.

In the real world, Type 2 diabetics can very much benefit from self-testing in altering their eating habits, catching problems early, seeing how much exercise helps, etc. I've watched numerous Type 2 diabetics on forums, newly diagnosed and instructed by their doctors not to self-test, pretty much go nuts while hyperglycemic and symptomatic. They'd be miserable and flailing about blindly to try to figure out why symptoms are happening and what to do about it.

Withholding testing from Type 2 diabetics is blatantly stupid and bordering on inhumane. That said, they usually don't need to test nearly as often or as regularly as Type 1. But they certainly do need to test for a while after diagnosis, and any time meds or diet are changed, or if on insulin or another drug which can cause hypoglycemia. It's also a good idea to at least test fasting values in the morning on a daily basis to catch problems early, especially since any infection can cause glucose to skyrocket and may result in ketoacidosis.
 

pamojja

Senior Member
Messages
2,398
Location
Austria
What would I now recommend? If you have a high Lp(a) level take lots of vitamin C and l-carnitine and see if your Lp(a) level falls. If it does, keep taking lots of vitamin C and l-carnitine for the rest of your life. If it does not fall? Not sure.

If you read Linus Pauling patent http://www.google.com/patents/US5278189, it's obvious Pauling patent talked also about inhibiting binding of Lp(a) and release to and from vessel walls. Which would have even to increase overall levels temporarily, before reduction could happen.
There exists therefore a need for a drug therapy for reducing the binding of Lp(a) to vessel walls, for reducing the overall level of Lp(a) in the circulatory system and for promoting the release of existing deposits of Lp(a) on vessel walls.

There are a number of additional, already old, strategies by TYP for reducing:
Lipoprotein Checklist: Lipoprotein(a)

..Small LDL particles hugely magnify risk when Lp(a) is present. We therefore aim to eliminate small LDL particles in order to effectively treat this pattern. A useful goal is to reduce small LDL to <10% of total LDL. Another interesting aspect of the small LDL question is that LDL particle size and Lp(a) particle size seem to be connected to each other. In other words, when small LDL is present, Lp(a) is also small and may pose greater risk. This may provide another reason to eliminate small LDL, since eliminating small LDL may make Lp(a) less harmful.

Treatment of Lp(a) therefore requires attention to other abnormalities, as well, particularly LDL cholesterol and small LDL.

Lipoprotein(a) is reduced by:
  • Niacin is the most effective direct treatment for Lp(a). However, higher doses may be required than for other abnormalities like low HDL or small LDL. The niacin preparations we favor are prescription Niaspan® (Kos Pharmaceuticals) or over-the-counter Slo-Niacin® (Upsher-Smith). Both are better tolerated than over-the-counter “immediate-release” niacin, which tends to cause intolerable hot flushing. However, immediate-release niacin is otherwise safe but should not be taken more frequently than twice a day. All three preparations are very safe, with little risk of liver toxicity if taken properly. Total daily niacin doses of >500 mg should be taken with the supervision of a physician.
  • Estrogen in females may lower Lp(a) around 25%, though estrogen, of course, has other considerations that need to be fully discussed with your doctor. Testosterone can be helpful for men and reduces Lp(a) by 25%. We use testosterone cream with great success. (A common dose for men >50 years old is 50 mg twice per day of a topical cream; dosing is best based on blood levels and must be prescribed). For any hormonal preparation, we advise bio-identical human preparations, i.e, preparations that are identical to the human form, not Premarin® or other non-human forms.
  • L-carnitine can be a useful nutritional supplement; 2000–4000 mg per day (e.g., 1000 mg twice a day) can reduce Lp(a) 7–8%, and occasionally will reduce it up to 20%. The only drawback is cost; it can be pretty pricey. L-carnitine is not powerful enough to be used as sole treatment, however. It’s better as an adjunct with either niacin and/or hormones.
  • Ground flaxseed (2–3 Tbsp/day) exerts a modest effect of no more than 7% Lp(a) reduction, but it’s healthy effects on reducing LDL and perhaps small LDL make it a useful adjunct. Use it as a hot cereal or added to yogurt or other foods. The seeds must be ground (e.g., purchased ground or ground in your coffee grinder).
  • Almonds—Preferably raw or dry roasted (with no added ingredients like hydrogenated oils), ¼–1/2 cup/day, are our favorite, as they not only reduce Lp(a) but also reduce LDL and partly counteract the small LDL particle abnormality.
  • Vitamin C—1000–3000 mg/day, with reported reductions of approximately 7%.
Track Your Plaque target: If measured in nmol/l, <75 nmol/l is desirable. In mg/dl, <30 mg/dl is desirable. (However, because of the lack of standardization, “normal” values in your laboratory may vary, depending on the means of measurement; discuss with your doctor.)

Copyright 2006, Track Your Plaque.

Tried all, except testesterone which would need prescription. However, at one point supplementing DHEA and other botanicals did finally normalize serum DHEA and testosterone, and Lp(a) fell to my erstwhile lowest 33 mg/dl (<30), with a highest at 66.
 
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prioris

Senior Member
Messages
622
What is abnormal HDL and abnormally low LDL levels ?

So for example
Cholesterol 275 (<200)
HDL Cholesterol 44.2 (30-70)
LDL 188.8 (91-130)

So I would think a b-complex (which has niacin) and l-carnitine would suffice.

p.s. Come to realize i have had a kidney infection for some time. also bladder and uti infection. i only noticed uti more recently. My plan is to get my urine going - get the water in the pipe (bladder and urethra) flowing - which stinging nettle (1000mg 4Xday) seems to help (and hopefully keep helping) along with proteolytic enzymes (in case of biofilms), plus throw mannose and additional herb live uva ursi (900mg 2Xday) in mix. After that i will take slightly bicarbonate of soda water to keep flushing the kidney. If i drink too much water, the kidney will feel pressure - probably because bladder can't flow well. I will keeping the water flush going - whatever it can take. never dealt with something like this so have no idea how long this will take. hopefully the kidney gets better. this should fix the lymph nodes too. here's hoping. when i have never fixed something before, there's always that uncertainty until it is solved. at least i reached point where i have some idea of what i am fighting. I did get standard kidney tests 2-3 months back and everything was normal ranges. i had to address the liver inflammation before i realized that the kidneys have a problem. not sure when kidney infection came about because was focused on liver and gallbladder. since organs are adjacent to each other, i couldn't tell where all pain was coming from. eating all that spinach with huge amounts of oxalates just added to everything.
 
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pamojja

Senior Member
Messages
2,398
Location
Austria
What is abnormal HDL and abnormally low LDL levels ?
..
So I would think a b-complex (which has niacin) and l-carnitine would suffice.

Where are your triglycerides? As I wrote page 2 of this thread:

LDL isn't necessarily bad. Small dense LDL or high LDL paricle number (of which Apo B is a approximation marker) is the one highly dangerous. Large fluffy LDL much less so.
The point with diet and LDL is, that high blood glucose spikes will drive triglycerides up. With triglycerides close to 150 mg/dl almost all your LDL is of the dangerous small dense kind. Close to 50 mg/dl the harmless fluffy kind. So two patients with a high LDL could have very different risks.

Perfect trigs should be possible with perfect post-prandial blood glucose..

However, also made the observation with lipids, that in my case the lipids didn't respond as much as I wanted to diet and supplementation (though actually improving HDL and LDL by 50% and trigs by 30% in average). Therefore drew a chart in my spreadsheet with all lab markers, comparing the different bodily functions with fluctuation in lipids..

And found in my case whenever liver enzymes rise only slightly, lipids would invariably follow. See this conversation for one explanation:

https://chriskresser.com/chris-masterjohn-on-cholesterol-and-heart-disease-part-3/

What to do – and not do – about high cholesterol
Chris Masterjohn: Absolutely. So, the first thing that we need to understand is that there are good reasons and bad reasons for increases in cholesterol in the blood. So, one of the reasons that cholesterol can increase is if we’re clearing lipids from the liver. Let’s say, for example, that a person has nonalcoholic fatty liver disease and they start resolving it. Well, one of the key problems with fatty liver disease is that the lipids get stuck in the liver and they’re not being released into the bloodstream, so once you start clearing that, part of what may happen is you may get an increase in triglycerides, and you may get an increase in cholesterol in the blood. And that is a good thing because nonalcoholic fatty liver disease is not only very dangerous for the liver, but it’s actually a much stronger predictor of cardiovascular disease risk. And this is a currently emerging field, but there is one study that was done in Japanese people, and they just looked at a number of a Japanese population that was apparently healthy, and they looked to see if they had fatty liver or not, and then they followed them over a number of years. And they found that fatty liver disease increased the risk of cardiovascular disease by over fivefold; whereas, LDL cholesterol predicted it somewhat, but the study wasn’t even statistically powerful enough to make that connection to LDL cholesterol statistically significant. And then when they incorporated LDL cholesterol and metabolic syndrome in a statistical analysis, they found that LDL cholesterol and metabolic syndrome, neither of those were even significant, and nonalcoholic fatty liver disease raised the risk of cardiovascular disease by about threefold or fourfold for men and about fourteenfold for women. So, if we’re clearing lipids from the liver, then this is a good thing.

Chris Kresser: Yeah, that’s a pretty phenomenal statistic there, especially in light of some of the estimates that I’ve seen that up to one in three Americans have nonalcoholic fatty liver disease, which would really go a ways to explaining the cardiovascular disease epidemic.

Chris Masterjohn: Absolutely.

Chris Kresser: So, you’ve written about this, Chris, what you were just talking about in terms of switching to a Primal/Paleo type of diet and the lipids going up because the fatty liver is sort of unpacking itself. And you’ve written about this extensively that choline is one of the nutrients that makes that possible, so can you say a little bit more about that?

Chris Masterjohn: Sure. So, the best sources of choline are liver and egg yolks. There are also a number of other nutrients such as folate, for example, that reduces the need for choline. So, it you’re increasing your intake of liver, egg yolks, and leafy green vegetables — you know, a general increase in nutrient density in your diet — it’s very likely that if you do have fatty liver you are going to contribute to its resolution, because choline is the key nutrient that is needed to package the fats in the liver and export them into the bloodstream so they can be metabolized by other tissues. Now, like you said, one in three Americans might have fatty liver, and the best way to diagnose fatty liver, to get certainty, the least invasive way is with an ultrasound. It can also be diagnosable with MRI or biopsy.

...
 
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prioris

Senior Member
Messages
622
Triglycerides were 210 (0-200) which are a year old and probably have come down a lot due to b12 and methyl folate consumption or at least i expect them too. These are old values. I intend to get new ones this week hopefully. Once things hopefully calm down with kidney etc, i will think about getting other things measured.
 

pamojja

Senior Member
Messages
2,398
Location
Austria
also bladder and uti infection.

Remember the main argument again high dose vitamin C - expensive urine! That expense (which vitamin C really is the least) does benefit the bladder and urinary tract with its antiviral properties greatly. Got rid of a cystitis with it too.

How much Vitamin C you're using?

Triglycerides were 210

Autsch..
 
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Gondwanaland

Senior Member
Messages
5,095
In the real world, Type 2 diabetics can very much benefit from self-testing in altering their eating habits
I totally agree with you. I think the study fits in the context of the mainstream nutritional recommendations where T2D patients always have skyrocketing BS so the testing only leads to taking more and more meds. I follow many paleo/lowcarb practiotioners on the web and their patients get really mad with the previous practiotioners who made them follow the official guidelines with no dietary changes.
 

prioris

Senior Member
Messages
622
How much Vitamin C you're using?
Autsch..

Maybe a little Vitamic C currently. I tend to react to too much vitamin C in past so won't go above 1000mg. I was using Modified Citrus Pectin twice a day when I felt more kidney pain around time I ate that spinach then got kidney stones. I've been traumatized by vitamin C ... LOL. I am using Quercetin / Bromelain at moment. I am trying to make kidney more alkaline which is what kidney likes. Vitamin C may make it opposite that.

Until I found lithium orotate, i could not address tryglycerides with any supplement due to MTHFR methylation side effects. Realized I had lithium deficiency. Hopefully next results look better. Many people are in situations that unless they solve one particular problem, they can't solve another.

P.S. too traumatized to eat any spinach too ... LOL
There is a process where Vitamin C can create oxalates in body. if kidney stones didn't enter picture, i would be more amenable too it but just erring on side of caution for now.
 
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