VITAMIN D & cardiac fibrosis information

[Guest guest]



this is a forward ... information I received myself today which maybe of interest to some.

Clare in Tassie

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Cardiac Disease and Adiponectin

Posted: 19 Oct 2009 03:44 AM PDT

It is known that the over activation Renin-Angiotensin- Aldosterone System(RAAS) leads to cardiac disease by fibrosis (scaring). For those who have not read my previous post on the RAAS system, please Basically, the RAAS involves the kidneys' attempts to maintain blood pressure during states of volume depletion (i.e. dehydration). Inhibition of this pathway is used to control blood pressure (i.e. ACE inhibitors). I have recently discovered an article detailing the mechanisms of how cardiac fibrosis is inhibited. And of course, it involves adiponectin and the PPAR system. But first, let me speak of the basics.Angiotensin II (the final protein of the RAAS) has several functions:

 

enhances sodium retention

causes water retention

vascular constriction (constriction of the vessel)

but also is involved with inflammation - a) cell proliferation, b) cell migration, and c) free radical production ( by a process called oxidative stress caused by NF-kB)

It is this inflammation that leads to cardiac fibrosis (scarring of the cardiac tissue). ACE inhibitors, Angiotensin II Receptor Blockers, and Aldosterone have have been used in order to protect the kidneys and heart from the inflammatory effects of Angiotensin II - as well as to control blood pressure. This is exactly what most physicians do not realize that these drug are not only important for blood pressure control but also important as anti-inflammatory drugs. However, there is another drug that I really like to use to control inflammation -- VITAMIN D. An article Fujita, 2008, showed that PPAR-alpha can inhibit Angiotensin II. How? Adiponectin stimulates its receptor on the cell wall. This later increases the activity of PPAR-alpha. PPAR-alpha then in return inhibits Angiotensin II. It is believed that a protein called AMPK is a middle element in this pathway. I have not talked about AMPK before, but its role in human metabolism is very important. This is the next blog topic. NF-kB (a protein that causes inflammation) decreases the activity of PPAR-alpha.

Recall that adiponectin is increased by Vitamin D. Therefore, this is probably the main mechanism of how Vitamin D helps to prevent cardiac fibrosis. Vitamin D also prevents coronary artery disease by inhibiting macrophages in up taking oxidized LDL. Sequestration of oxidized LDL into macrophages creates a foam cell. Click here from more information. Foam cells are the initial process in the inflammatory state causing coronary artery disease.

So this brings up the topic of the next series of my discussions - NUTRIGENOMICS. What is that? This is the science of how nutrition interacts with our genes. And it is based on nuclear receptors and calming of inflammation (i.e. NF-kB). Basically, the Western diet stimulates inflammation in our bodies causing disease. And the appropriate diet will diminish the inflammatory state. It is all about NF-kB, PPARs, adiponectin, insulin resistance, etc. If all this is too complicated, do not worry. I am going to summarize everything later this week.

I was asked what brands of Vitamin D I like. Although I do not want to favor any companies, I found two brands that are not based in pro-inflammatory vegetable oils - the NOW brand 5000 IU which is in olive oil and the Vital Choice brand 2000 IU which is in fish oil.

Fujita K, Maeda N, Sonoda M, Ohashi K, Hibuse T, Nishizawa H, Nishida M, Hiuge A, Kurata A, Kihara S, Shimomura I, Funahashi T: Adiponectin protects against angiotensin II-induced cardiac fibrosis through activation of PPAR-alpha. Arterioscler Thromb Vasc Biol. 2008 May;28(5):863-70