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Yes'm
Moving away from fruits. Targeting Monday to be completely off of fruits and starches. This will be difficult but the fall months harvest is essentially done and I don't particularly like "fresh" winter fruit.
3 Apple trees, 8 varieties
1 crab apple (edible, most flavorful, June bearing)
4 Plums, 4 varieties
3 Prunes, 2 varieties
12 Blueberries, 5 varieties
2 Persimmons
1-Comice Pear
Many Asian Pears, 5 varieties
2 Mulberry, 2 varieties
1-acia berry
1 fig, access to 2 other varieties
3 variety of strawberries
Kiwi fruit
Jujube
And the tomatoes.
Doctor says that fruit fructose is different from HFCS.
I however can feel the effects just as fast or faster.
I am going to ask for blood sugar test strips and keep a diary of food eaten.
What a wonderful garden and orchard you must have. What is jujube?
The earliest event in atherogenesis is injury to the cell layer lining the inside of the artery. Factors that do that are
"Physical injury or stress as a result of direct trauma or hypertension
Circulation of reactive oxygen species (free radicals), e.g., from smoking or air pollutants
Hyperlipidemia (high blood concentrations of LDL or VLDL)
Chronically elevated blood glucose levels
Homocysteinemia"
The injury stimulates an inflammatory response, in which certain chemicals attract specialized white blood cells to the site of injury. Loosening of the junctions between cells in the arterial lining allows fluid, lipids, and white blood cells to seep into the layer of tissue beneath the arterial lining. LDL is picked up by some of those cells, macrophages, which become what are called foam cells. These cells eventually die, leaving the lipid behind. These eventually can be seen as fatty streaks in the wall of the artery. Note that fatty streaks can be found in children, and most of us have them by age 20.
Other white cells stimulate muscle cells from within the arterial wall to grow into the fatty streaks, lifting the inner lining and forming what are called plaques. Plaques form fibrin caps. Some plaques grow slowly; others may increase in size more rapidly, with caps that are prone to rupture. Once a plaque ruptures, platelets are attracted to the area and formation of a clot begins. That causes coronary thrombosis and a heart attack.
There is a video at the link showing how this process happens. There is a lot of information in this article, some technical but much of it easy to understand.
Atherosclerotic calcification chiefly occurs in the cell layer under the arterial lining, the intima. Inflammation and lipids induce differentiation of cells which are associated with bone production and which cause the calcium to deposit in the vessel. Calcification in the layer under the intima, the media, is associated with advanced age, diabetes, and chronic kidney disease. Calcification in the media contributes to arterial stiffness, which increases risk for adverse cardiovascular events.
This article, which I posted earlier and you obviously did not read, explains that calcification associated with statins may actually be beneficial:
Calcification, which happens later in the evolution of a plaque, not the first step, may help to stabilize plaque and prevent it from increasing in size and rupturing.
Patients on statins had more calcification but the volume of plaque was smaller. Thus calcification associated with statins may reduce the amount of narrowing of the artery and reduce the risk of plaque rupture and thrombosis.
Notice that the first step in the production of atherosclerosis is damage to the vessel and inflammation. Statins also have an anti-inflammatory effect, which again tends to inhibit the formation of the fatty streak.
Cholesterol is very much involved in the production of atherosclerosis.
Quote:
Originally Posted by jaminhealth
So many doctors push high calcium intake and never mention magnesium. I take far more mag than I take calcium. A friend ended up with calcium deposits on her thyroid and had part of it removed...she listened to her doc who said Tums was a good source of calcium for her..so she sucked them for years. I've almost gotten into debates with a rheumy as she was pushing more calcium and never mentioned mag. I had a lot of research done on mag for years.
I'm been alternating with bio citrate strontium every other day and 500mg cal on the alternate day and mag every day, thru the day. I'm 73 and bone health is good.
Dr. Google knows more than any MD we can go to. We need to be our own doctors more and more.
Tums is a perfectly acceptable source of calcium. Taking Tums did not cause the calcium deposits in the thyroid. That was due to whatever disease process she had, most likely by causing inflammation in the gland.
The earliest event in atherogenesis is injury to the cell layer lining the inside of the artery. Factors that do that are
"Physical injury or stress as a result of direct trauma or hypertension
Circulation of reactive oxygen species (free radicals), e.g., from smoking or air pollutants
Hyperlipidemia (high blood concentrations of LDL or VLDL)
Chronically elevated blood glucose levels
Homocysteinemia"
The injury stimulates an inflammatory response, in which certain chemicals attract specialized white blood cells to the site of injury. Loosening of the junctions between cells in the arterial lining allows fluid, lipids, and white blood cells to seep into the layer of tissue beneath the arterial lining. LDL is picked up by some of those cells, macrophages, which become what are called foam cells. These cells eventually die, leaving the lipid behind. These eventually can be seen as fatty streaks in the wall of the artery. Note that fatty streaks can be found in children, and most of us have them by age 20.
Other white cells stimulate muscle cells from within the arterial wall to grow into the fatty streaks, lifting the inner lining and forming what are called plaques. Plaques form fibrin caps. Some plaques grow slowly; others may increase in size more rapidly, with caps that are prone to rupture. Once a plaque ruptures, platelets are attracted to the area and formation of a clot begins. That causes coronary thrombosis and a heart attack.
There is a video at the link showing how this process happens. There is a lot of information in this article, some technical but much of it easy to understand.
Atherosclerotic calcification chiefly occurs in the cell layer under the arterial lining, the intima. Inflammation and lipids induce differentiation of cells which are associated with bone production and which cause the calcium to deposit in the vessel. Calcification in the layer under the intima, the media, is associated with advanced age, diabetes, and chronic kidney disease. Calcification in the media contributes to arterial stiffness, which increases risk for adverse cardiovascular events.
This article, which I posted earlier and you obviously did not read, explains that calcification associated with statins may actually be beneficial:
Calcification, which happens later in the evolution of a plaque, not the first step, may help to stabilize plaque and prevent it from increasing in size and rupturing.
Patients on statins had more calcification but the volume of plaque was smaller. Thus calcification associated with statins may reduce the amount of narrowing of the artery and reduce the risk of plaque rupture and thrombosis.
Notice that the first step in the production of atherosclerosis is damage to the vessel and inflammation. Statins also have an anti-inflammatory effect, which again tends to inhibit the formation of the fatty streak.
Cholesterol is very much involved in the production of atherosclerosis.
Tums is a perfectly acceptable source of calcium. Taking Tums did not cause the calcium deposits in the thyroid. That was due to whatever disease process she had, most likely by causing inflammation in the gland.
No, you do not know more from Google than a single doctor does.
This is waaaayyyyy too long to read. Why should I read all that when I am in perfect health, I will not.
Did you read what I posted?
You believe what you believe, and I stick to what I believe, and have a nice day.
This is waaaayyyyy too long to read. Why should I read all that when I am in perfect health, I will not.
Did you read what I posted?
You believe what you believe, and I stick to what I believe, and have a nice day.
Doctors do not get their information from Mercola.
They also have to keep up to date to keep their licenses and board certifications.
Maybe they need to. I believe Dr. Mercola is a D.O. and I'm seeing one now for my arthritic issues and this D.O. got me off ibuprofen which was keeping blood pressure elevated. Dr. M has helped a lot of people get to the root of some of their health issues.
You do not even cite the source of your sheet long excerpt. From where and when is it?
From the last century?......:-D((
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