Scientists have now proven that a lack of vitamin D1
helps damaged cholesterol (oxidized cholesterol) form plaque and that
adequate vitamin D stops damaged cholesterol from forming plaque. This
should make it painfully clear that the “public health” advice of the
American Cancer Society to use sun block and stay out of the sun has
directly contributed to heart disease in a major way in America.
The research was conducted on type II diabetics who are known to have double the risk for heart disease. It was found that they do not process cholesterol efficiently, and a lack of vitamin D was determined to be the main reason for this problem. In low vitamin D patients, their macrophages readily absorbed damaged cholesterol, turned into foam cells, and initiated the process of plaque formation.
The researchers also showed that when human macrophages are placed in a vitamin D adequate environment their uptake of cholesterol is suppressed. Of course, having adequate antioxidants on board helps prevent cholesterol from being damaged in the first place, which is why the tocotrienol form of vitamin E is so protective to your cardiovascular system.
Oh J, Weng S, Felton SK, Bhandare S, Riek A, Butler B, Proctor BM, Petty M, Chen Z, Schechtman KB, Bernal-Mizrach L, Bernal-Mizrachi C. 1,25 (OH) vitamin D inhibits foam cell formation and suppresses macrophage cholesterol uptake in patients with type 2 diabetes mellitus. Circulation 2009 August
Geriatrics and Division of Nutritional Science, Department of Medicine, and Division of Biostatistics, Washington University, St Louis, Mo.
Methods and Results— We obtained macrophages from 76 obese, diabetic, hypertensive patients with vitamin D deficiency (25-hydroxyvitamin D <80 nmol/L; group A) and 4 control groups: obese, diabetic, hypertensive patients with normal vitamin D (group B; n=15); obese, nondiabetic, hypertensive patients with vitamin D deficiency (group C; n=25); and nonobese, nondiabetic, nonhypertensive patients with vitamin D deficiency (group D; n=10) or sufficiency (group E; n=10). Macrophages from the same patients in all groups were cultured in vitamin D—deficient or 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] –supplemented media and exposed to modified low-density lipoprotein cholesterol. 1,25(OH)2D3 suppressed foam cell formation by reducing acetylated or oxidized low-density lipoprotein cholesterol uptake in diabetic subjects only. Conversely, deletion of the vitamin D receptor in macrophages from diabetic patients accelerated foam cell formation induced by modified LDL. 1,25(OH)2D3 downregulation of c-Jun N-terminal kinase activation reduced peroxisome proliferated–activated receptor- expression, suppressed CD36 expression, and prevented oxidized low-density lipoprotein–derived cholesterol uptake. In addition, 1,25(OH)2D3 suppression of macrophage endoplasmic reticulum stress improved insulin signaling, downregulated SR-A1 expression, and prevented oxidized and acetylated low-density lipoprotein–derived cholesterol uptake.
Conclusion— These results identify reduced vitamin D receptor signaling as a potential mechanism underlying increased foam cell formation and accelerated cardiovascular disease in diabetic subjects.
From press release:
Low levels of vitamin D are known to nearly double the risk of cardiovascular disease in patients with diabetes, and researchers at Washington University School of Medicine in St. Louis now think they know why.
They have found that diabetics deficient in vitamin D can’t process cholesterol normally, so it builds up in their blood vessels, increasing the risk of heart attack and stroke. The new research has identified a mechanism linking low vitamin D levels to heart disease risk and may lead to ways to fix the problem, simply by increasing levels of vitamin D.
“Vitamin D inhibits the uptake of cholesterol by cells called macrophages,” says principal investigator Carlos Bernal-Mizrachi, M.D., a Washington University endocrinologist at Barnes-Jewish Hospital. “When people are deficient in vitamin D, the macrophage cells eat more cholesterol, and they can’t get rid of it. The macrophages get clogged with cholesterol and become what scientists call foam cells, which are one of the earliest markers of atherosclerosis.”
Macrophages are dispatched by the immune system in response to inflammation and often are activated by diseases such as diabetes. Bernal-Mizrachi and his colleagues believe that in diabetic patients with inadequate vitamin D, macrophages become loaded with cholesterol and eventually stiffen blood vessels and block blood flow.
Bernal-Mizrachi, an assistant professor of medicine and of cell biology and physiology, studied macrophage cells taken from people with and without diabetes and with and without vitamin D deficiency. His team, led by research assistants Jisu Oh and Sherry Weng, M.D., exposed the cells to cholesterol and to high or low vitamin D levels. When vitamin D levels were low in the culture dish, macrophages from diabetic patients were much more likely to become foam cells.
In the Aug. 25 issue of the journal Circulation, which currently is available online, the team reports that vitamin D regulates signaling pathways linked both to uptake and to clearance of cholesterol in macrophages.
“Cholesterol is transported through the blood attached to lipoproteins such as LDL, the ‘bad’ cholesterol,” Bernal-Mizrachi explains. “As it is stimulated by oxygen radicals in the vessel wall, LDL becomes oxidated, and macrophages eat it uncontrollably. LDL cholesterol then clogs the macrophages, and that’s how atherosclerosis begins.”
That process becomes accelerated when a person is deficient in vitamin D. And people with type 2 diabetes are very likely to have this deficiency. Worldwide, approximately one billion people have insufficient vitamin D levels, and in women with type 2 diabetes, the likelihood of low vitamin D is about a third higher than in women of the same age who don’t have diabetes.
The skin manufactures vitamin D in response to ultraviolet light exposure. But in much of the United States, people don’t make enough vitamin D during the winter — when the sun’s rays are weaker and more time is spent indoors.
The good news is when human macrophages are placed in an environment with plenty of vitamin D, their uptake of cholesterol is suppressed, and they don’t become foam cells. Bernal-Mizrachi believes it may be possible to slow or reverse the development of atherosclerosis in patients with diabetes by helping them regain adequate vitamin D levels.
“There is debate about whether any amount of sun exposure is safe, so oral vitamin D supplements may work best,” he says, “but perhaps if people were exposed to sunlight only for a few minutes at a time, that may be an option, too.”
He has launched a new study of diabetics who are both deficient in vitamin D and have high blood pressure. He wants to learn whether replacing vitamin D will lower blood pressure and improve blood flow. For this study, Bernal-Mizrachi is recruiting patients with type 2 diabetes ages 30 to 80 who are not taking insulin to control their blood sugar. Study volunteers also must have high blood pressure.
The research was conducted on type II diabetics who are known to have double the risk for heart disease. It was found that they do not process cholesterol efficiently, and a lack of vitamin D was determined to be the main reason for this problem. In low vitamin D patients, their macrophages readily absorbed damaged cholesterol, turned into foam cells, and initiated the process of plaque formation.
The researchers also showed that when human macrophages are placed in a vitamin D adequate environment their uptake of cholesterol is suppressed. Of course, having adequate antioxidants on board helps prevent cholesterol from being damaged in the first place, which is why the tocotrienol form of vitamin E is so protective to your cardiovascular system.
Oh J, Weng S, Felton SK, Bhandare S, Riek A, Butler B, Proctor BM, Petty M, Chen Z, Schechtman KB, Bernal-Mizrach L, Bernal-Mizrachi C. 1,25 (OH) vitamin D inhibits foam cell formation and suppresses macrophage cholesterol uptake in patients with type 2 diabetes mellitus. Circulation 2009 August
Geriatrics and Division of Nutritional Science, Department of Medicine, and Division of Biostatistics, Washington University, St Louis, Mo.
Study Abstract:
Background— Cardiovascular disease is the leading cause of death among those with diabetes mellitus. Vitamin D deficiency is associated with an increased risk of cardiovascular disease in this population. To determine the mechanism by which vitamin D deficiency mediates accelerated cardiovascular disease in patients with diabetes mellitus, we investigated the effects of active vitamin D on macrophage cholesterol deposition.Methods and Results— We obtained macrophages from 76 obese, diabetic, hypertensive patients with vitamin D deficiency (25-hydroxyvitamin D <80 nmol/L; group A) and 4 control groups: obese, diabetic, hypertensive patients with normal vitamin D (group B; n=15); obese, nondiabetic, hypertensive patients with vitamin D deficiency (group C; n=25); and nonobese, nondiabetic, nonhypertensive patients with vitamin D deficiency (group D; n=10) or sufficiency (group E; n=10). Macrophages from the same patients in all groups were cultured in vitamin D—deficient or 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] –supplemented media and exposed to modified low-density lipoprotein cholesterol. 1,25(OH)2D3 suppressed foam cell formation by reducing acetylated or oxidized low-density lipoprotein cholesterol uptake in diabetic subjects only. Conversely, deletion of the vitamin D receptor in macrophages from diabetic patients accelerated foam cell formation induced by modified LDL. 1,25(OH)2D3 downregulation of c-Jun N-terminal kinase activation reduced peroxisome proliferated–activated receptor- expression, suppressed CD36 expression, and prevented oxidized low-density lipoprotein–derived cholesterol uptake. In addition, 1,25(OH)2D3 suppression of macrophage endoplasmic reticulum stress improved insulin signaling, downregulated SR-A1 expression, and prevented oxidized and acetylated low-density lipoprotein–derived cholesterol uptake.
Conclusion— These results identify reduced vitamin D receptor signaling as a potential mechanism underlying increased foam cell formation and accelerated cardiovascular disease in diabetic subjects.
From press release:
Low levels of vitamin D are known to nearly double the risk of cardiovascular disease in patients with diabetes, and researchers at Washington University School of Medicine in St. Louis now think they know why.
They have found that diabetics deficient in vitamin D can’t process cholesterol normally, so it builds up in their blood vessels, increasing the risk of heart attack and stroke. The new research has identified a mechanism linking low vitamin D levels to heart disease risk and may lead to ways to fix the problem, simply by increasing levels of vitamin D.
“Vitamin D inhibits the uptake of cholesterol by cells called macrophages,” says principal investigator Carlos Bernal-Mizrachi, M.D., a Washington University endocrinologist at Barnes-Jewish Hospital. “When people are deficient in vitamin D, the macrophage cells eat more cholesterol, and they can’t get rid of it. The macrophages get clogged with cholesterol and become what scientists call foam cells, which are one of the earliest markers of atherosclerosis.”
Macrophages are dispatched by the immune system in response to inflammation and often are activated by diseases such as diabetes. Bernal-Mizrachi and his colleagues believe that in diabetic patients with inadequate vitamin D, macrophages become loaded with cholesterol and eventually stiffen blood vessels and block blood flow.
Bernal-Mizrachi, an assistant professor of medicine and of cell biology and physiology, studied macrophage cells taken from people with and without diabetes and with and without vitamin D deficiency. His team, led by research assistants Jisu Oh and Sherry Weng, M.D., exposed the cells to cholesterol and to high or low vitamin D levels. When vitamin D levels were low in the culture dish, macrophages from diabetic patients were much more likely to become foam cells.
In the Aug. 25 issue of the journal Circulation, which currently is available online, the team reports that vitamin D regulates signaling pathways linked both to uptake and to clearance of cholesterol in macrophages.
“Cholesterol is transported through the blood attached to lipoproteins such as LDL, the ‘bad’ cholesterol,” Bernal-Mizrachi explains. “As it is stimulated by oxygen radicals in the vessel wall, LDL becomes oxidated, and macrophages eat it uncontrollably. LDL cholesterol then clogs the macrophages, and that’s how atherosclerosis begins.”
That process becomes accelerated when a person is deficient in vitamin D. And people with type 2 diabetes are very likely to have this deficiency. Worldwide, approximately one billion people have insufficient vitamin D levels, and in women with type 2 diabetes, the likelihood of low vitamin D is about a third higher than in women of the same age who don’t have diabetes.
The skin manufactures vitamin D in response to ultraviolet light exposure. But in much of the United States, people don’t make enough vitamin D during the winter — when the sun’s rays are weaker and more time is spent indoors.
The good news is when human macrophages are placed in an environment with plenty of vitamin D, their uptake of cholesterol is suppressed, and they don’t become foam cells. Bernal-Mizrachi believes it may be possible to slow or reverse the development of atherosclerosis in patients with diabetes by helping them regain adequate vitamin D levels.
“There is debate about whether any amount of sun exposure is safe, so oral vitamin D supplements may work best,” he says, “but perhaps if people were exposed to sunlight only for a few minutes at a time, that may be an option, too.”
He has launched a new study of diabetics who are both deficient in vitamin D and have high blood pressure. He wants to learn whether replacing vitamin D will lower blood pressure and improve blood flow. For this study, Bernal-Mizrachi is recruiting patients with type 2 diabetes ages 30 to 80 who are not taking insulin to control their blood sugar. Study volunteers also must have high blood pressure.
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