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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Imbalancing nutritionally adequate diets with an excessive amount of fat calories and cholesterol has obscured the fact that intimal thickening occurs spontaneously in time on low-fat cholesterol-free diets during the aging process, and that intimal thickening can be accelerated by dietary angiotoxic "risk factors." Electron microscopy of arterial tissue from animal models identified degenerated smooth muscle cells in the fetus from sows kept on low-fat cholesterol-free diets. After birth, the degenerated smooth muscle cells increased in number with age. The presence of angiotoxic "risk factors" such as oxidized cholesterol and vitamin D3 (cholecalciferol) in the diet of such animal models increased the frequency of smooth muscle cell death in their arteries. Two types of pathology could be developed in the thoracic aorta by continuous or short term feeding of 12.5 times more vitamin D than normally present in commercial rations: 1) a diffuse fibroelastic intimal thickening in the thoracic aorta (arteriosclerosis) with no evidence of lipid deposition by continuous feeding of vitamin D or 2) an initimal thickening in the thoracic aorta and intimal thickening with foam cells and extracellular lipid deposits (atherosclerosis) in the coronary arteries after a short period of supplemental vitamin D followed by 3 to 4 months of supplement-free diets. These two types of arterial damage were identical to that in the plugs of thoracic aorta obtained as a by-product of elective coronary bypass surgery. Although all of the possible sources of oxidized cholesterol in the diet have as yet not been identified, laboratory studies have identified oxidized cholesterol as an angiotoxic factor. Since population groups that consume less vitamin D-supplemented foods, less deep fat fried cholesterol-containing foods, and less hydrogenated fats have a lower incidence of coronary heart disease than Americans, it seems judicious for food processors to reduce these previously unconsidered risk factors to a minimum. This could be done by eliminating vitamin D2 and D3 from all vitamin supplements, from all food and cereal products and from the diet of livestock 1 month before they were killed so that the intake of vitamin D is no larger than the 400 IU/quart in milk which is necessary to prevent rickets in children. Deep fat fryers, which are kept at almost 200 C for 24 hr/day, could perhaps be replaced with microwave ovens in fast food chain outlets. Processors could hydrogenate vegetable oils to a minimum trans fatty acid content and rearrange this fat with polyunsaturated fats to produce high polyunsaturated fats trans-free margarines and shortenings.
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PMID:Nutrition imbalance and angiotoxins as dietary risk factors in coronary heart disease. 21 61

The early fine structural changes in the arteries of rats induced by excess vitamin D3 perorally or parenterally were essentially similar, except the latter had a more prominent toxic effect to the vascular wall. The ultrastructural features, incidental to calcification, included the appearance of increased ground substance with a separation of collagenous and elastic fibrils, and degenerative changes in smooth muscle cells. Atherosclerosis was greatly accelerated at the sites of vascular injury when cholesterol, cholic acid and thiouracil were added to the basal diet. Calcification was initially observed in relation to elastic fibrils or degenerated cells in the upper and middle layers of the arteries, although there were few such deposits in the thickened intima of the coronary arteries. Calcium deposition could not be a direct effect of hypercalcemia, but the functional activity of smooth muscle cells did seem to promote the mineralization of calcium and phosphate. Furthermore, vitamin D-induced sclerosis did not prevent intimal thickening of the arteries when vitamin D3 was withdrawn.
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PMID:Vitamin D sclerosis in rats. 22 74

Three new diphosphonic acids, i.e. compounds containing a P-C-P bond, have been investigated for their ability to inhibit the vitamin D-induced calcification of aortas and kidneys in rats. The compounds were applied orally in various doses. All of the compounds, which had previously been shown to effectively inhibit the in vitro crystallization of apatite, markedly decreased the amount of calcium deposited in aortas and kidneys. One of the new compounds was substantially more effective than ethane-1-hydroxy-1,1-diphosphonic acid (EHDP), which was used as a reference compound. Diphosphonic acids might be used therapeutically in man against soft tissue calcification.
Atherosclerosis 1978 Aug
PMID:The inhibitory effect of new diphosphonic acids on aortic and kidney calcification in vivo. 70 89

A balanced intake of alimentary lipids is necessary for calcium and phosphorus absorption, as for growth and calcification of bone. In lipid deprivation or excess, important disorders of phospho-calcic metabolism appear particularly in young growing subjects. The qualitative content of ingested fats has, too, a great influence : lipids containing short and medium-chain fatty acids, essential fatty acids and oleic acid stimulate calcium absorption. An excess of long chain and saturated lipids, or intake of erucic acid depress calcium absorption and retention. These facts are possible pathophysiological mechanisms in human disorders: The so-called humanized milks are close to human milk regarding their capacity of stimulation of phospho-calcic absorption and growth. In these milks, oleic and linoleic triglyceride level must be increased. In adult pathology, lipidic deficiency of steatorrhea is partially responsible for calcium and vitamin D malabsorption. Conversely, lipid-calcium interactions are not one-way, and an elevated dietary calcium depresses saturated lipid absorption, and has a hypolipemic action interesting in prevention of atherosclerosis of aged patients.
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PMID:[Lipid calcium interactions in experimental and human nutrition (author's transl)]. 77 52

The purpose of this study was to test the effectiveness of various doses of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) in an experimental rabbit model of athero-arteriosclerosis designed by Hass et al. (Amer. J. Pathol., 49 (1966) 739). This model, which involves the feeding of a hypercholesterolemic diet in conjunction with the administration of moderately high doses of vitamin D and nicotine, results in an extensive arterial disease with complicated lesions. EHDP was administered daily by subcutaneous injection at levels of 0.25, 1.0 and 2.5 mg/kg body weight beginning with the initiation of the atherogenic regimen. Results of chemical and histopathological analyses after 8 and 12 weeks of treatment indicate the following: (1) There was a dose-related inhibition of arterial calcification at 8 weeks. At 12 weeks, only the 2.5 mg/kg dose of EHDP resulted in reduced calcification. (2) EHDP administration appeared to influence arterial lipid-containing plaque formation in medium sized arteries at 12 weeks. There was no apparent effect of EHDP administration on serum cholesterol and triglyceride levels. (3) EHDP, at a dose of 2.5 mg/kg/day, inhibited the vitamin D induced hypercalcemia. (4) EHDP administration at 2.5 mg/kg/day almost totally inhibited the thromboarteritis accompanying this disease. (5) The data thus indicate that if arterial calcification is inhibited, the other morphological effects of this treatment regime are also inhibited. This effect occurred even though serum lipid levels were unaffected. The data therefore emphasize the role of calcification in the pathogenesis of this type of experimental atherosclerosis and perhaps in human disease as well.
Atherosclerosis
PMID:The effect of disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) on a rabbit model of athero-arteriosclerosis. 81 8

Oral intake of calciferol (vitamin D) was higher in patients with myocardial infarction than in controls. Having established an assay for 25-hydroxycalciferol (25-OH-D), the principal circulating form of the vitamin, we measured this compound in control subjects and patients with myocardial infarction. In controls, 25-OH-D varied with the season: levels were high in summer and low in winter. Furthermore, levels were low in control subjects above 60 years of age. In patients with myocardial infarction, normal and low values for 25-OH-D were found. It is concluded that in this region patients with myocardial infarction do not consume greater amounts of vitamin D.
Atherosclerosis 1977 Jan
PMID:Serum 25-hydroxycalciferol in myocardial infarction. 83 48

Atherosclerosis and osteoporosis are currently considered unrelated diseases. Osteoporosis involves bone calcium (Ca) loss and predominantly affects females after menopause. Atherosclerosis is an illness predominantly affecting males, and is primarily characterized by abnormal lipid metabolism. However, pathological calcification of the arterial wall is an underlying feature of atherosclerosis. Ca homeostasis is thus important in atherosclerosis as well as in osteoporosis. Men also develop osteoporosis although at a later age than women, and, as osteoporosis progresses in women, there is an accompanying calcification of arteries leading to increased incidence of atherosclerosis in aging women. Thus, during old age, both atherosclerosis and osteoporosis are prevalent in both males and females. The dramatic increase in atherosclerosis among women as they develop osteoporosis suggests that the two illnesses may be more closely related than previously realized. The use of vitamin D as a food supplement coincides with epidemic onsets of atherosclerosis and osteoporosis, and excess vitamin D induces both conditions in humans and laboratory animals. These observations suggest a role for chronic vitamin D excess in the etiology of the two illnesses. Magnesium (Mg) deficiency, nicotine, and high dietary cholesterol are contributing factors that accentuate adverse effects of vitamin D.
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PMID:Hypothesis: etiology of atherosclerosis and osteoporosis: are imbalances in the calciferol endocrine system implicated? 145 56

The influence of chronic ethanol intoxication upon vitamin D-induced damage of cardiovascular system in rats was examined. Eighty rats, divided into 16 groups according to sex and age, were intoxicated with ethanol as the only source of liquid. Control rats drank water only. After 6 months of ethanol intoxication, part of ethanol and part of water-drinking rats received 3 x 100,000 IU vitamin D/rat, in order to induce atherosclerosis and heart muscle necrosis. The results of the described experiment revealed that the degree of circulatory system damage after chronic ethanol intoxication and vitamin D treatment was dependent on the age of the animals at the beginning of the experiment. Ethanol intoxication intensified vitamin D-dependent heart muscle necrosis in young individuals. In old rats chronic alcohol intoxication diminished atherosclerosis induced by vitamin D.
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PMID:Effects of ethanol on the development of experimental atherosclerosis and cardionecrosis in rats. 239 Feb 5

The lipid composition and structure of low- and high-density lipoproteins (LDL and HDL) have been studied in children with the vitamin D-deficient rachitis. An increase of the cholesterol content in the atherogenic LDL against a background of its decrease in the antiatherogenic HDL has been revealed, that is analogous to the observed changes under the atherosclerosis development in adults. Due to the studies in the amino acidic composition and determination of the nature and quantity of the charged groups of lipoprotein particles accessible for titration definite, certain disturbance in the structure of lipoproteins are observed as such that may cause disturbances in their functional activity.
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PMID:[Structural-functional changes in plasma lipoproteins during vitamin D-deficient rickets in children]. 239 22

A variety of age-related anatomic and functional alterations in the kidney have been described. Anatomic abnormalities in the aging kidney include a decrease in kidney size, increased glomerular sclerosis, altered tubular structure, and an altered pattern of vascular flow. These anatomic abnormalities are associated with renal functional abnormalities, including decreased renal blood flow, and glomerular filtration rate. Altered renal tubular function, including impaired handling of water, sodium, acid, and glucose, may also be present. Impaired "endocrinologic" functioning manifested by changes in the renin-angiotensin system, vitamin D metabolism, and antidiuretic hormone responsiveness have been reported. The kidney is constantly exposed to the effects of a variety of potentially toxic processes. These range from environmental toxins and drugs, to a variety of chronic medical illnesses including hypertension, diabetes, and atherosclerotic disease. In this context, differentiation of "aging" effects from nephrotoxic effects resulting from these other processes is difficult. It has been argued that hypertension is an important factor in the development and progression of renal insufficiency in the elderly. The relationship between hypertension, glomerular hyperfiltration, atherosclerosis, and progressive renal dysfunction needs further study. Further research may allow the rational recommendation of interventions designed to control age-associated changes in renal function.
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PMID:Renal function in aging. 266 87


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