HubbleRules
03-11-2006, 12:53 PM
Lenin,
Haven't found a good article specifically about the anti-inflammatory qualities of statins (although I'll continue later - there's PLENTY of info out there...).
But thought you'd be interested in this.
Researchers have found that Fish Oil in combination with low-dose Asprin is related to presence of an anti-inflammatory lipid, which is derived from the essential fatty acids in fish oil.
The researchers have now identified this lipid in plasma taken from volunteers given omega-3 fatty acids and aspirin. Human resolvin E1, the authors show, inhibits both the migration of inflammatory cells to sites of inflammation and the turning on of other inflammatory cells.
You may be right about lipid profile affecting inflammation ...
HubbleRules
:cool:
Haven't found a good article specifically about the anti-inflammatory qualities of statins (although I'll continue later - there's PLENTY of info out there...).
But thought you'd be interested in this.
Researchers have found that Fish Oil in combination with low-dose Asprin is related to presence of an anti-inflammatory lipid, which is derived from the essential fatty acids in fish oil.
The researchers have now identified this lipid in plasma taken from volunteers given omega-3 fatty acids and aspirin. Human resolvin E1, the authors show, inhibits both the migration of inflammatory cells to sites of inflammation and the turning on of other inflammatory cells.
You may be right about lipid profile affecting inflammation ...
HubbleRules
:cool:
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Lenin
03-11-2006, 01:31 PM
If you want a thought to make you DIZZY.
I've always thought that a physical microscopic attack by some agent, heretofore unknown, is responsible for that first tiny lesion on a blood vessel that decades later becaome a plaque. I've let my mind run riot on the huge number of possibilities about what that agent might be. Strep, influenza, rhinitis of a particualr strain, chicken pox, DDT, fungus, a spirochete, staph, food reaction. Of course, the attack would have gone unnoticed in regards the coronary artery but the stage would be set.
Such a cause would likely NEVER be found except by serendipity.
Like aspirin causing fewer heart attacks. Nobody believed it possible but in the 30's 40's and 50's people with arthritis and taking 10-16 aspirin a day didn't get heart disease.
It was spelled out as a platelet thing...but 10 aspirin a day is MIGHTILY anti-inflammatory. But if it weren't for the serendipity of the arthritiics aspirin would still be used only for aches and pains. Will science luck out in the same way with the plaque initiator?
(Just letting my thoughts run free here...no conclusions! :D)
I've always thought that a physical microscopic attack by some agent, heretofore unknown, is responsible for that first tiny lesion on a blood vessel that decades later becaome a plaque. I've let my mind run riot on the huge number of possibilities about what that agent might be. Strep, influenza, rhinitis of a particualr strain, chicken pox, DDT, fungus, a spirochete, staph, food reaction. Of course, the attack would have gone unnoticed in regards the coronary artery but the stage would be set.
Such a cause would likely NEVER be found except by serendipity.
Like aspirin causing fewer heart attacks. Nobody believed it possible but in the 30's 40's and 50's people with arthritis and taking 10-16 aspirin a day didn't get heart disease.
It was spelled out as a platelet thing...but 10 aspirin a day is MIGHTILY anti-inflammatory. But if it weren't for the serendipity of the arthritiics aspirin would still be used only for aches and pains. Will science luck out in the same way with the plaque initiator?
(Just letting my thoughts run free here...no conclusions! :D)
HubbleRules
03-11-2006, 03:31 PM
If you want a thought to make you DIZZY.
I've always thought that a physical microscopic attack by some agent, heretofore unknown, is responsible for that first tiny lesion on a blood vessel that decades later becaome a plaque. I've let my mind run riot on the huge number of possibilities about what that agent might be. Strep, influenza, rhinitis of a particualr strain, chicken pox, DDT, fungus, a spirochete, staph, food reaction. Of course, the attack would have gone unnoticed in regards the coronary artery but the stage would be set.
Such a cause would likely NEVER be found except by serendipity.
Like aspirin causing fewer heart attacks. Nobody believed it possible but in the 30's 40's and 50's people with arthritis and taking 10-16 aspirin a day didn't get heart disease.
It was spelled out as a platelet thing...but 10 aspirin a day is MIGHTILY anti-inflammatory. But if it weren't for the serendipity of the arthritiics aspirin would still be used only for aches and pains. Will science luck out in the same way with the plaque initiator?
(Just letting my thoughts run free here...no conclusions! :D)
Lenin,
You may be right.
I posted a while ago information I found about a theory that the 1918 Spanish Flu pandemic set-up those who were infected but survived for atherosclerosis and CHD later in life. Cohort studies show that CHD peaked around 1963 and has been declining since, about the time those who were infected in 1918 started dying out...
HubbleRules
:cool:
I've always thought that a physical microscopic attack by some agent, heretofore unknown, is responsible for that first tiny lesion on a blood vessel that decades later becaome a plaque. I've let my mind run riot on the huge number of possibilities about what that agent might be. Strep, influenza, rhinitis of a particualr strain, chicken pox, DDT, fungus, a spirochete, staph, food reaction. Of course, the attack would have gone unnoticed in regards the coronary artery but the stage would be set.
Such a cause would likely NEVER be found except by serendipity.
Like aspirin causing fewer heart attacks. Nobody believed it possible but in the 30's 40's and 50's people with arthritis and taking 10-16 aspirin a day didn't get heart disease.
It was spelled out as a platelet thing...but 10 aspirin a day is MIGHTILY anti-inflammatory. But if it weren't for the serendipity of the arthritiics aspirin would still be used only for aches and pains. Will science luck out in the same way with the plaque initiator?
(Just letting my thoughts run free here...no conclusions! :D)
Lenin,
You may be right.
I posted a while ago information I found about a theory that the 1918 Spanish Flu pandemic set-up those who were infected but survived for atherosclerosis and CHD later in life. Cohort studies show that CHD peaked around 1963 and has been declining since, about the time those who were infected in 1918 started dying out...
HubbleRules
:cool: