Guest guest Posted June 20, 2008 Report Share Posted June 20, 2008 I don't know about KT, but sea salt does. I googled 'arterial plaque' + 'sea salt' and found a number of entries on the subject. Dr Brownstein researched table salt as a cause of hypertension and found nothing. So he treats such patients with sea salt and get good results. Dorothy > > Does KT have a beneficial effect on dissolving arterial plaque? > Thank You - > Lawrence > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 20, 2008 Report Share Posted June 20, 2008 I don't know about KT, but sea salt does. I googled 'arterial plaque' + 'sea salt' and found a number of entries on the subject. Dr Brownstein researched table salt as a cause of hypertension and found nothing. So he treats such patients with sea salt and get good results. Dorothy > > Does KT have a beneficial effect on dissolving arterial plaque? > Thank You - > Lawrence > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted June 20, 2008 Report Share Posted June 20, 2008 > Does KT have a beneficial effect on dissolving arterial plaque? Hello Lawrence, If you google Kombucha and arteriosclerosis (which is the plaque in the arteries) you come up with an astounding array of sites. Kombucha is definitely supposed to be very beneficial against arterial plaque. The Happy herbalist recommends a tablespoon of Kombucha vinegar daily to combat arteriosclerosis. http://www.happyherbalist.com/vinegar_recipes_for_health.htm http://www.mamaherb.com/Treatments/View.aspx?id=4002 Treatments - Treating Arteriosclerosis With Kombucha . - Mamaherb – What actually works in natural health This site claims that Kombucha contains beta carotene which is new to me. Anyway, large amounts of beta carotene increase the elasticity of the bloodvessels. SO, get stuck into your carrots ;-) ! This site makes the amazing statement that if you drink a glass of Kombucha at bedtime your symptoms of arteriosclerosis should be resolved in a month. Sounds too good to be true, but you certainly won't lose anything by following this advice. Read some of the sites under 'Kombucha and arteriosclerosis' yourself and draw your own conclusions. With very best wishes, Margret UK :-) -- +------------------ Minstrel@... --------------------+ <)))<>< http://www.therpc.f9.co.uk <)))<>< http://www.AnswersInGenesis.com - God sent His only Son into the world - - so that we might have life through Him (1 4) - Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 Thanks for the post! Christian Mathisen, DC Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 Thanks for the post! Christian Mathisen, DC Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 So what is it about a blood vessel that allows cholesterol laden LDLs in to the intima to begin with? If that could be prevented the chain of events of inflammation and scarring would be prevented. s. fuchs dc From: Christian Mathisen [mailto:cmathdc@...] Sent: Friday, October 30, 2009 7:52 AM ; Sharron Fuchs Subject: Re: Atherosclerosis Thanks for the post! Christian Mathisen, DC Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the " intima " . In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ( " fatty streak " ), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as " collagen " . The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 It is the emotional subluxation known as stress........ Danno Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. No virus found in this incoming message.Checked by AVG - www.avg.com Version: 8.5.423 / Virus Database: 270.14.39/2469 - Release Date: 10/30/09 07:52:00 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 It is the emotional subluxation known as stress........ Danno Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. No virus found in this incoming message.Checked by AVG - www.avg.com Version: 8.5.423 / Virus Database: 270.14.39/2469 - Release Date: 10/30/09 07:52:00 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 So stress hormones damage the intima and allow vessels to be ‘invaded’? s. fuchs dc From: D Beebe, D.C. [mailto:daniel.beebe@...] Sent: Friday, October 30, 2009 11:26 AM Sharron Fuchs; Subject: Re: Atherosclerosis It is the emotional subluxation known as stress........ Danno Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the " intima " . In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ( " fatty streak " ), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as " collagen " . The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. size=2 width="100%" align=center> No virus found in this incoming message. Checked by AVG - www.avg.com Version: 8.5.423 / Virus Database: 270.14.39/2469 - Release Date: 10/30/09 07:52:00 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 So stress hormones damage the intima and allow vessels to be ‘invaded’? s. fuchs dc From: D Beebe, D.C. [mailto:daniel.beebe@...] Sent: Friday, October 30, 2009 11:26 AM Sharron Fuchs; Subject: Re: Atherosclerosis It is the emotional subluxation known as stress........ Danno Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the " intima " . In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ( " fatty streak " ), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as " collagen " . The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. size=2 width="100%" align=center> No virus found in this incoming message. Checked by AVG - www.avg.com Version: 8.5.423 / Virus Database: 270.14.39/2469 - Release Date: 10/30/09 07:52:00 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 There are a whole plethora of changes that occur secondary to the release of the so called stress hormones... one of which has to do w/ membrane permeability changes....... Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures.size=2 width="100%" align=center> No virus found in this incoming message.Checked by AVG - www.avg.com Version: 8.5.423 / Virus Database: 270.14.39/2469 - Release Date: 10/30/09 07:52:00 No virus found in this incoming message.Checked by AVG - www.avg.com Version: 8.5.423 / Virus Database: 270.14.39/2469 - Release Date: 10/30/09 07:52:00 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 So, the smaller, sticker LDL will stick to the intima when the artery is unprotected by its supply of NO. If you have a lot of these smaller particles, especially the unnatural ones formed from trans and hydrogenated fats (yep there are "bad fats," Virginia) in the standard American Diet, you will get stuck. These fats are anaerobic in nature and when there is hypertriglyceridemia, there will be a shift to the smaller, denser, atherogenic form of LDL. This is my conjecture of mechanism, I have no double blind study or research university to back me up. However, A high unnatural fat diet has been known to kill people. Fix the triglycerides and we see a shift in pattern. Christian Mathisen, DC 3654 S Pacific Hwy Medford, OR 97501 cmathdc@... Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 So, the smaller, sticker LDL will stick to the intima when the artery is unprotected by its supply of NO. If you have a lot of these smaller particles, especially the unnatural ones formed from trans and hydrogenated fats (yep there are "bad fats," Virginia) in the standard American Diet, you will get stuck. These fats are anaerobic in nature and when there is hypertriglyceridemia, there will be a shift to the smaller, denser, atherogenic form of LDL. This is my conjecture of mechanism, I have no double blind study or research university to back me up. However, A high unnatural fat diet has been known to kill people. Fix the triglycerides and we see a shift in pattern. Christian Mathisen, DC 3654 S Pacific Hwy Medford, OR 97501 cmathdc@... Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 Another issue that gets overlooked is that the walls of the arteries become weak due to lack of pulsating blood flow from exercise, allowing "cracks" to occur. The body uses cholesterol to patch-up the cracks. "Move it or lose it" applies to blood vessels too - they need that great shear stress from a pounding heart to keep their elasticity and strength! Jamey Dyson, DC, CCWPAdvanced Chiropractic1295 Wallace Rd NWSalem, OR 97304503-361-3949drjdyson1@... On Oct 30, 2009, at 12:18 PM, Christian Mathisen wrote:So, the smaller, sticker LDL will stick to the intima when the artery is unprotected by its supply of NO. If you have a lot of these smaller particles, especially the unnatural ones formed from trans and hydrogenated fats (yep there are "bad fats," Virginia) in the standard American Diet, you will get stuck. These fats are anaerobic in nature and when there is hypertriglyceridemia, there will be a shift to the smaller, denser, atherogenic form of LDL. This is my conjecture of mechanism, I have no double blind study or research university to back me up. However, A high unnatural fat diet has been known to kill people. Fix the triglycerides and we see a shift in pattern. Christian Mathisen, DC3654 S Pacific HwyMedford, OR 97501cmathdcjeffnet (DOT) org Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources.s. fuchs dchttp://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdfATHEROSCLEROSISBY L. Duffy, MDAtherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System.In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops.An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong.The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel.The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima.The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material.At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary.The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 Another issue that gets overlooked is that the walls of the arteries become weak due to lack of pulsating blood flow from exercise, allowing "cracks" to occur. The body uses cholesterol to patch-up the cracks. "Move it or lose it" applies to blood vessels too - they need that great shear stress from a pounding heart to keep their elasticity and strength! Jamey Dyson, DC, CCWPAdvanced Chiropractic1295 Wallace Rd NWSalem, OR 97304503-361-3949drjdyson1@... On Oct 30, 2009, at 12:18 PM, Christian Mathisen wrote:So, the smaller, sticker LDL will stick to the intima when the artery is unprotected by its supply of NO. If you have a lot of these smaller particles, especially the unnatural ones formed from trans and hydrogenated fats (yep there are "bad fats," Virginia) in the standard American Diet, you will get stuck. These fats are anaerobic in nature and when there is hypertriglyceridemia, there will be a shift to the smaller, denser, atherogenic form of LDL. This is my conjecture of mechanism, I have no double blind study or research university to back me up. However, A high unnatural fat diet has been known to kill people. Fix the triglycerides and we see a shift in pattern. Christian Mathisen, DC3654 S Pacific HwyMedford, OR 97501cmathdcjeffnet (DOT) org Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources.s. fuchs dchttp://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdfATHEROSCLEROSISBY L. Duffy, MDAtherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System.In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops.An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong.The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel.The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima.The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material.At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary.The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 Hey , On this issue I would add another fact.....the weakness of the arterial/venule walls has to do with inadequate minerals ,,, adequate minerals allow strengthening of the vascular walls, increasing their imperviousness to the assault....one of the major areas where adequate mineralization of the body is imperative. Sunny Sunny Kierstyn, RN DC Fibromyalgia Care Center of Oregon 2677 Willakenzie Road, 7CEugene, Oregon, 97401541- 654-0850; Fx; 541- 654-0834www.drsunnykierstyn.com From: drjdyson1@...Date: Fri, 30 Oct 2009 12:44:49 -0700Subject: Re: Atherosclerosis Another issue that gets overlooked is that the walls of the arteries become weak due to lack of pulsating blood flow from exercise, allowing "cracks" to occur. The body uses cholesterol to patch-up the cracks. "Move it or lose it" applies to blood vessels too - they need that great shear stress from a pounding heart to keep their elasticity and strength! Jamey Dyson, DC, CCWP Advanced Chiropractic 1295 Wallace Rd NW Salem, OR 97304 503-361-3949 drjdyson1comcast (DOT) net On Oct 30, 2009, at 12:18 PM, Christian Mathisen wrote: So, the smaller, sticker LDL will stick to the intima when the artery is unprotected by its supply of NO. If you have a lot of these smaller particles, especially the unnatural ones formed from trans and hydrogenated fats (yep there are "bad fats," Virginia) in the standard American Diet, you will get stuck. These fats are anaerobic in nature and when there is hypertriglyceridemia, there will be a shift to the smaller, denser, atherogenic form of LDL. This is my conjecture of mechanism, I have no double blind study or research university to back me up. However, A high unnatural fat diet has been known to kill people. Fix the triglycerides and we see a shift in pattern. Christian Mathisen, DC 3654 S Pacific Hwy Medford, OR 97501 cmathdcjeffnet (DOT) org Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. Windows 7: It works the way you want. Learn more. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 30, 2009 Report Share Posted October 30, 2009 Hey , On this issue I would add another fact.....the weakness of the arterial/venule walls has to do with inadequate minerals ,,, adequate minerals allow strengthening of the vascular walls, increasing their imperviousness to the assault....one of the major areas where adequate mineralization of the body is imperative. Sunny Sunny Kierstyn, RN DC Fibromyalgia Care Center of Oregon 2677 Willakenzie Road, 7CEugene, Oregon, 97401541- 654-0850; Fx; 541- 654-0834www.drsunnykierstyn.com From: drjdyson1@...Date: Fri, 30 Oct 2009 12:44:49 -0700Subject: Re: Atherosclerosis Another issue that gets overlooked is that the walls of the arteries become weak due to lack of pulsating blood flow from exercise, allowing "cracks" to occur. The body uses cholesterol to patch-up the cracks. "Move it or lose it" applies to blood vessels too - they need that great shear stress from a pounding heart to keep their elasticity and strength! Jamey Dyson, DC, CCWP Advanced Chiropractic 1295 Wallace Rd NW Salem, OR 97304 503-361-3949 drjdyson1comcast (DOT) net On Oct 30, 2009, at 12:18 PM, Christian Mathisen wrote: So, the smaller, sticker LDL will stick to the intima when the artery is unprotected by its supply of NO. If you have a lot of these smaller particles, especially the unnatural ones formed from trans and hydrogenated fats (yep there are "bad fats," Virginia) in the standard American Diet, you will get stuck. These fats are anaerobic in nature and when there is hypertriglyceridemia, there will be a shift to the smaller, denser, atherogenic form of LDL. This is my conjecture of mechanism, I have no double blind study or research university to back me up. However, A high unnatural fat diet has been known to kill people. Fix the triglycerides and we see a shift in pattern. Christian Mathisen, DC 3654 S Pacific Hwy Medford, OR 97501 cmathdcjeffnet (DOT) org Atherosclerosis This is clearly written for the lay public but it is a great description of how atherosclerosis develops. on’s is one of my most used resources. s. fuchs dc http://www.arnoldehret.org/docs/ATHEROSCLEROSIS.pdf ATHEROSCLEROSIS BY L. Duffy, MD Atherosclerosis is commonly called hardening of the arteries. It is the underlying cause of heart attacks, strokes, and poor circulation to the legs. We are going to examine the process whereby atherosclerosis develops and place it in the context of Arnold Ehret's Mucusless Diet Healing System. In the famous medical textbook on's Principles of Internal Medicine (15th Edition) we find a detailed description of how atherosclerosis develops. An artery is a flexible elastic pipe in which blood flows to various tissues. It has an inner lining called the "intima". In its healthy state it is smooth, flexible, and strong. The earliest step in the development of atherosclerosis is the formation of the fatty streak. In the blood there are lipoproteins which carry cholesterol and fatty acids. Some will diffuse between the cells lining the inside of the artery. When these lipoprotein molecules are oxidized the structures of both cholesterol and fatty acids are modified. They have deteriorated and are not biologically useful. As they accumulate in the lining of the blood vessel you can see this under the microscope as an area of fat accumulation ("fatty streak"), In addition if the person is diabetic with elevated blood sugar, molecules of sugar can stick to other molecules in the lining of the blood vessel. The second step is the arrival of white blood cells called monocytes. It is thought that they stick to receptors in the fatty streak. They are attracted to oxidized lipoprotein. This is analogous to a patrolling cop car stopping by the road when he sees an accident. The monocytes penetrate through the lining of the artery and take up residence in the intima. The third step is foam-cell formation. The monocytes in the lining of the blood vessel transform into macrophages, which ingest the fatty material. The macrophages surround a portion of fatty debris with the outer cell membrane. The membrane then is pulled to the interior of the cell as a storage particle. In other words the macrophages act as scavengers collecting the deteriorated fat and cholesterol. Under the microscope these look like cells containing foamy material. At this stage macrophages may leave the area and remove the lipid material. Also high density lipoprotein (HDL) is a molecule which brings cholesterol back to the liver. In this way the fatty area may recede or remain stationary. The fourth step is the migration and proliferation of smooth-muscle cells. The artery has a layer of muscle cells. When activated by the inflammation caused by the fatty deposits and macrophages, smooth-muscle cells move into the inner lining of the artery and begin to reproduce. The smooth-muscle cells produce fibrous material known as "collagen". The fatty streak turns into a fibrous plaque. Small blood vessels are formed. Calcium is deposited. Macrophages and smooth-muscle cells die. A mature atherosclerotic plaque is composed of hardened, scarred material which causes the artery to be narrow and stiff. Heart attacks and strokes occur when blood clots form in the narrow arteries or the atherosclerotic plaque ruptures. Windows 7: It works the way you want. Learn more. Quote Link to comment Share on other sites More sharing options...
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