The Relationship Between Serum Level Of Manganese And Severity Of Coronary Atherosclerosis

paymanz

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http://www.zjrms.ir/article-1-2972-en.html


Background : Trace elements such as manganese have an important role in the maintenance of the normal structure and physiology of cells. Manganese is involved in many biological processes. Therefore, an evaluation of the manganese in the atherosclerotic disease is important.
Materials and Methods : In this cross sectional study, 334 subjects, without recent cardiac event and history of collagen vascular or infectious disease were investigated. All patients divided into 4 groups to evaluate severity of coronary artery disease according to Syntax scoring system. All groups were matched in cardiovascular risk factors.
Results : The serum level of manganese in normal coronary group was 1.47±0.23 µg/L and in total atherosclerotic groups was 1.06±0.37 µg/L. The serum level of manganese was significantly lower in total atherosclerotic groups than normal group (p=0.001) and significantly decreased with severity of atherosclerosis. The serum level of manganese was significantly lower in sever atherosclerosis patients than mild and moderate coronary artery disease groups (p=0.001).
Conclusion : The finding indicated that the serum level of manganese is lower in atherosclerotic patients and it decreases with severity of atherosclerosis
 

Richiebogie

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Raspberries and bananas are tasty fruits with Manganese.

Perhaps the Richie smoothie will help unclog your arteries*!

(I have 2 of these a day):
350ml OJ
500g bananas
100g raspberries
2 teaspoons gelatine

*Always seek medical advice before embarking on a Richie smoothie.
 

goodandevil

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Anyone know which enzymes require manganese? dont know where it fits in according to the ling model. It's a transition metal with a lot of oxidatiom states sounds tricky.
 
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paymanz

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Its a long list,famous ones are anti oxidant system , exteracelluar matrix synthesizing enzymes.

Glycoproteins,in early studies on vitamin k once a reasercher used a purified diet to find symptoms of vitamin k deficiency , after they shows the bleeding symptoms he added vitamin k to cure them , but it didn't work,later they found that manganese also was lacked in their feed which is needed to produce vitamin k dependant proteins.

It is a long list of enzymes.

I don't know about ling model,but yes at certain levels manganese is toxic,and cause oxidative stress.

Edit:i still cant find that long list of enzymes that depent on manganese for activation yet, that i once read somewhere that i cant remember(it was an old paper) , anyway i will add anything i find:
The estimated daily manganese intake of Korean children aged 11-12
Mn is a component of arginase, pyruvate carboxylase, Mn superoxide dismutase (MnSOD) and galactosyltransferase. There are Mn metalloenzymes that activate glutamine synthetase, phosphatase, glycosyltransferase, kinase and decarboxylase

This one also reviews possible ways that manganese may modify atherosclerosis risk
Manganese in Health and Disease
 
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Pet Peeve

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Anyone know which enzymes require manganese? dont know where it fits in according to the ling model. It's a transition metal with a lot of oxidatiom states sounds tricky.

Superoxide dismutase 2, mitochondrial (SOD2), also known as manganese-dependent superoxide dismutase
 

BibleBeliever

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Excess of manganese is much worse than a deficiency
Are you able to elaborate? I am researching this right now. I consume many herbs very high in manganese; ginger, cardamom, cinnamon, nutmeg, cloves.
I have noticed many waters I drink can cause very negative effects, a swelling in the side, blood vessel burning and even tingling.
I keep reevaluating manganese, as I wonder if it could be a culprit.
Boron appears to be the largest antagonist, as well as carbohydrates. Interesting to study.
 

Travis

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I think manganese could be a biomarker for low fruit consumption, and the real etiological cause is low vitamin C.
This is the popular one, but there are many more. George Willis made the connection even before Pauling had written about it, but Pauling supplied the molecular details and Dr. Rath supplied the human subjects.
 

RedStaR

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Milk, oats, chocolate.

Anyway the conclusion of the study is very poor. It had no controlled variables, reading the abstract.
 

lampofred

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All this study shows is that people with atherosclerosis have low levels of serum manganese. That does not imply that increasing manganese will help fight atherosclerosis. Doing that might even have the opposite reaction.
 
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paymanz

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I think manganese could be a biomarker for low fruit consumption, and the real etiological cause is low vitamin C.
This is the popular one, but there are many more. George Willis made the connection even before Pauling had written about it, but Pauling supplied the molecular details and Dr. Rath supplied the human subjects.
Everything has its own place.

Manganese is very important for oxidation stress defense, and also connective tissue repair. Just like vitamin c.

One reason high iron intake (red meat for example)increases heart disease is because its not balanced with enough manganese,in my opinion.

High rice consumption in some Asian countries might be one reason for their good health and longevity, rice is good source of manganese.
 
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tca300

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I think manganese could be a biomarker for low fruit consumption, and the real etiological cause is low vitamin C.
This is the popular one, but there are many more. George Willis made the connection even before Pauling had written about it, but Pauling supplied the molecular details and Dr. Rath supplied the human subjects.
The vitamin C infromation seems promising, but whats your take on Dr. Broda Barnes being able to drop heart disease so heavily with just a thyroid supplement? Thank you!
 

Travis

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Maybe being euthyroid allows to to synthesize collagen faster? and repair the arterial wall?

I'm not sure, but I realize that Pauling and Rath only describe one layer of the problem. Anything that increases damage to the arterial wall would contribute, like homocysteine and high blood pressure. The mechanism that Pauling describes is basically Lp(a) gets upregulated in vitamin C deficiency and this is initially done to help 'patch' microscopic holes in the arterial wall where collagen breaks down. This 'upregulation' part is the only thing that Pauling said that I could not verify independently. I simply cannot find any information on this, at all, but I have verified all of his other claims:

  • Apo(a) is the single greatest serum risk factor for cardiovascular disease. This is often found in the LDL fraction, but also in the VLDL fraction.
  • Apoliprotein(a) has a very strong lysyl-binding domain, like plasminogen. It has such high-affinity for lysyl- groups that chromatography columns packed with lysyl-sepharose is routinely used to separate it from other blood components. You would expect Apo(a), or the entire Lp(a), to then stick to the arterial walls where damaged. There are six or so other apoproteins that, when combined, make up all serum lipoproteins. Low density lipoprotein is about 50% protein and 50% lipid, and sometimes (but not always) about half of the protein consists of the Apo(a) fragment.
  • Only some animals can even get cardiovascular disease, even if you try to force it upon them.
  • Most animals synthesize their own vitamin C.
  • Vitamin C has been shown to increase collagen synthesis 300% in vitro.
  • Scurvey is characterized by broken-down collagen. It's name actually derives from the words "broken skin" in a different language. The arterial walls have a considerable amount of collagen.
But high blood pressure will always be a factor, since you can just as easily increase the rate of damage as you can decrease collagen synthesis; the end result is nearly the same. Apo(a) appears to be upregulated in this case to prevent blood leakage as it sticks to frayed collagen. It is structurally-similar to plasminogen, which is a known blood-clotting protein. Plasminogen is involved in would healing.
 
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tca300

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Maybe being euthyroid allows to to synthesize collagen faster? and repair the arterial wall?

I'm not sure, but I realize that Pauling and Rath only describe one layer of the problem. Anything that increases damage to the arterial wall would contribute, like homocysteine and high blood pressure. The mechanism that Pauling describes is basically Lp(a) gets upregulated in vitamin C deficiency and this is initially done to help 'patch' microscopic holes in the arterial wall where collagen breaks down. This 'upregulation' part is the only thing that Pauling said that I could not verify independently. I simply cannot find any information on this, at all, but I have verified all of his other claims:

  • Apo(a) is the single greatest serum risk factor for cardiovascular disease. This is often found in the LDL fraction, but also in the VLDL fraction.
  • Apoliprotein(a) has a very strong lysyl-binding domain, like plasminogen. It has such high-affinity for lysyl- groups that chromatography columns packed with lysyl-sepharose is routinely used to separate it from other blood components. You would expect Apo(a), or the entire Lp(a), to then stick to the arterial walls where damaged. There are six or so other apoproteins that, when combined, make up all serum lipoproteins. Low density lipoprotein is about 50% protein and 50% lipid, and sometimes (but not always) about half of the protein consists of the Apo(a) fragment.
  • Only some animals can even get cardiovascular disease, even if you try to force it upon them.
  • Most animals synthesize their own vitamin C.
  • Vitamin C has been shown to increase collagen synthesis 300% in vitro.
  • Scurvey is characterized by broken-down collagen. It's name actually derives from the words "broken skin" in a different language. The arterial walls have a considerable amount of collagen.
But high blood pressure will always be a factor, since you can just as easily increase the rate of damage as you can decrease collagen synthesis; the end result is nearly the same. Apo(a) appears to be upregulated in this case to prevent blood leakage as it sticks to frayed collagen. It is structurally-similar to plasminogen, which is a known blood-clotting protein. Plasminogen is involved in would healing.
Thanks for the info!
 

Travis

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The idea is that it's a protective mechanism, because without Lp(a) you would start leaking blood as the collagen production rate decreases.

Vitamin C is also thought to play a role in crosslinking collagen even after it's laid-down, so it's intimately-involved in every step of the way.
 
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paymanz

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The idea is that it's a protective mechanism, because without Lp(a) you would start leaking blood as the collagen production rate decreases.

Vitamin C is also thought to play a role in crosslinking collagen even after it's laid-down, so it's intimately-involved in every step of the way.
MMPs are interesting too
Lipid lowering by diet reduces matrix metalloproteinase activity and increases collagen content of rabbit atheroma: a potential mechanism of lesion... - PubMed - NCBI
 

Travis

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paymanz

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I wonder if they controlled for vitamin C in their lipid lowering diet? (I suppose an easy way to find out would be for me to read the study...)
Apparently they haven't.

But anyway MMPs are known to degrade connective tissue...
 

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