摘要
动脉粥样硬化是心血管疾病的主要病理变化。尽管心血管疾病病因病理十分复杂，涉及多种相关风险因素，但现有文献中已经基本接受动脉粥样硬化是一具有特征性氧化压力升高的炎性疾病。本文回顾和分析了近几十年来文献中的研究成果，梳理了复杂的心血管疾病风险因素，提出了一个动脉粥样硬化发生发展的全新的理论。由于氧化压力升高、维生素C不足、胶原合成等因素持续存在，以及这一不正常的动脉管壁修复机制的难以控制，最终导致粥样斑块的形成、管腔的狭窄、堵塞以及心肌缺血梗死。低碳医学倡导的健康饮食，最佳及个性化营养等在冠脉粥样硬化治疗及预防中起到主导作用。氧化压力升高而导致的抗氧化剂（尤其维生素C）耗竭，造成胶原蛋白合成障碍，进而引起临床疾病的机制并不限制于冠心病。这一现象也可见于骨质疏松等。这种氧化压力、抗氧化剂（维生素C）、胶原合成之间的动态变化具有较大的区域性。
Abstract
Although the pathogenesis of CVD is very complicated and involves a variety of risk factors， it has been generally recognized and accepted in the literature that atherosclerosis is an inflammatory disease characterized by elevated oxidative stress. Sufficient basic research and preliminary clinical studies show that atherosclerosis is potentially reversible. Based on the review and analysis of decades of research， we propose a new theory of atherosclerosis development. Due to the continued and usually worsening presence of the increased oxidative stress， vitamin C deficiency， collagen synthesis deficiency and other pathogenic factors， this abnormal mechanism of arterial wall repair will not stop， which eventually leads to the formation of atherosclerosis plaque， resulting in arterial stenosis， occlusion and myocardial ischemia. Low carbohydrate diet promotes health， optimal and personalized nutrition and plays a leading role in the treatment and prevention of coronary atherosclerosis. In this paper， the mechanism of coronary heart disease is not limited to coronary heart disease due to the depletion of antioxidants (especially vitamin C) caused by the increase of oxidative pressure caused by toxin increase. This phenomenon can also be seen in osteoporosis. The dynamic changes among oxidative stress， antioxidants (vitamin C)， and collagen synthesis were regional.
关键词
心血管疾病 /
动脉粥样硬化 /
维生素C
Key words
Cardiovascular disease /
Atherosclerosis /
Vitamin C
1成长， 2Thomas Levy.
冠状动脉粥样硬化病因病理及功能医学临床干预探讨[J]. 肿瘤代谢与营养电子杂志. 2019, 6(3): 365-369 https://doi.org/10.16689/j.cnki.cn11-9349/r.2019.03.019
1CHENG， Richard Zhang， 2THOMAS Levy.
Clinical intervention of coronary atherosclerosis in etiology， pathology and functional medicine[J]. Electronic Journal of Metabolism and Nutrition of Cancer. 2019, 6(3): 365-369 https://doi.org/10.16689/j.cnki.cn11-9349/r.2019.03.019
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
参考文献
1.Boos CJ， Lip GYH. Blood clotting， inflammation， and thrombosis in cardiovascular events: perspectives. Front Biosci J Virtual Libr. 2006;11:328-336.
2.Renvert S， Ohlsson O， Pettersson T， et al. Periodontitis: a future risk of acute coronary syndrome? A follow-up study over 3 years. J Periodontol. 2010;81(7):992-1000.
3.Mahendra J， Mahendra L， Kurian VM， et al. 16S rRNA-based detection of oral pathogens in coronary atherosclerotic plaque. Indian J Dent Res Off Publ Indian Soc Dent Res. 2010;21(2):248-252.
4.Kantor ED， Rehm CD， Du M， et al. Trends in dietary supplement use among US adults from 1999-2012. JAMA. 2016;316(14):1464-1474.
5.Lean ME， Leslie WS， Barnes AC， et al. Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label， cluster-randomised trial. Lancet Lond Engl. 2018;391(10120):541-551.
6.Zilov AV， Abdelaziz SI， AlShammary A， et al. Mechanisms of action of metformin with special reference to cardiovascular protection. Diabetes Metab Res Rev. 2019;e3173.
7.Ito F， Sono Y， Ito T. Measurement and clinical significance of lipid peroxidation as a biomarker of oxidative stress: oxidative stress in diabetes， atherosclerosis， and chronic inflammation. Antioxid Basel Switz. 2019;8(3).
8.Mathieu P， Pibarot P， Després J-P. Metabolic syndrome: the danger signal in atherosclerosis. Vasc Health Risk Manag. 2006;2(3):285-302.
9.Maritim AC， Sanders RA， Watkins JB. Diabetes， oxidative stress， and antioxidants: a review. J Biochem Mol Toxicol. 2003;17(1):24-38.
10.Ross R. The pathogenesis of atherosclerosis. In: Braunward E， editor. Heart disease: a textbook of cardiovascular medicine. Philadelphia， PA: W. B. Saunders; 1992.
11.Fisher E， McLennan SV， Tada H， et al. Interaction of ascorbic acid and glucose on production of collagen and proteoglycan by fibroblasts. Diabetes. 1991;40(3):371-376.
12.Pauling L. Vitamin C and longevity. Agressologie. 1983;24(7):317-319.
13.Rath M， Pauling L. Hypothesis: lipoprotein(a) is a surrogate for ascorbate. Proc Natl Acad Sci U S A. 1990;87(16):6204-6207.
14.Willis GC. An experimental study of intimal ground substance in atherosclerosis. Can Med Assoc J. 1953;69(1):17-22.
15.Kulacz R， Levy T. The Toxic tooth. How a root canal could be making you sick. Med Fox Publishing; 2014.
16.Sakai N， Yokoyama T， Date C， et al. An inverse relationship between serum vitamin C and blood pressure in a Japanese community. J Nutr Sci aminol (Tokyo). 1998;44(6):853-867.
17.Scher AM. Absence of atherosclerosis in human intramyocardial coronary arteries: a neglected phenomenon. Atherosclerosis. 2000;149(1):1-3.
18.Ginter E. Marginal amin C deficiency， lipid metabolism， and atherogenesis. Adv Lipid Res. 1978;16:167-220.
19.Datey KK， Dalvi CP， Mehta NJ， et al. Ascorbic acid and experimental atherosclerosis. J Assoc Physicians India. 1968;16(9):567-570.
20.Newman HA， Zilversmit DB. Quantitative aspects of cholesterol flux in rabbit atheromatous lesions. J Biol Chem. 1962;237:2078-2084.
21.Zaitsev VF， Myasnikov LA， Kasatkina LV， et al. The effect of ascorbic ACID on experimental atherosclerosis. Cor Vasa. 1964;6:19-25.
22.Chen C， Loo G. Effect of peroxyl radicals on lecithin/cholesterol acyltransferase actiy in human plasma. Lipids. 1995;30(7):627-631.
23.Rath M， Pauling L. Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig. Proc Natl Acad Sci U S A. 1990;87(23):9388-9390.
24.Scanu AM， Pfaffinger D， Lee JC， et al. A single point mutation (Trp72-->Arg) in human apo(a) kringle 4-37 associated with a lysine binding defect in Lp(a). Biochim Biophys Acta. 1994;1227(1-2):41-45.
25.Simon JA. Vitamin C and cardiovascular disease: a review. J Am Coll Nutr. 1992;11(2):107-125.
26.Chen L， Jia R， Qiu C， et al. Hyperglycemia inhibits the uptake of dehydroascorbate in tubular epithelial cell. Am J Nephrol. 2005;25(5):459-465.
27.Cunningham JJ. The glucose/insulin system and vitamin C: implications in insulin-dependent diabetes mellitus. J Am Coll Nutr. 1998;17(2):105-108.
28.Dou C， Xu DP， Wells WW. Studies on the essential role of ascorbic acid in the energy dependent release of insulin from pancreatic islets. Biochem Biophys Res Commun. 1997;231(3):820-822.
29.Taylor AJ， Bindeman J， Feuerstein I， et al. Coronary calcium independently predicts incident premature coronary heart disease over measured cardiovascular risk factors: mean three-year outcomes in the Prospective Army Coronary Calcium (PACC) project. J Am Coll Cardiol. 2005;46(5):807-814.
30.Sharma RK， Sharma RK， Voelker DJ， et al. Cardiac risk stratification: role of the coronary calcium score. Vasc Health Risk Manag. 2010;6:603-611.
31.Simon JA， Murtaugh MA， Gross MD， et al. Relation of ascorbic acid to coronary artery calcium: the Coronary Artery Risk Development in Young Adults Study. Am J Epidemiol. 2004;159(6):581-588.
32.Ruskin S. Studies of the parallel action of vitamin C and calcium. Am J Dig Dis. 1938;5:408-411.
33.Bourne G. Vitamin C and repair of injured tissues. Lancet. 1942;2:661-664.
34.Shah SV， Alam MG. Role of iron in atherosclerosis. Am J Kidney Dis Off J Natl Kidney Found. 2003;41(3 Suppl 1):S80-S83.
35.You SA， Wang Q. Ferritin in atherosclerosis. Clin Chim Acta Int J Clin Chem. 2005;357(1):1-16.
36.Muoz M， Villar I， García-Erce JA. An update on iron physiology. World J Gastroenterol. 2009;15(37):4617-4626.
37.Fishbaine B， Butterfield G. Ascorbic acid status of running and sedentary men. Int J am Nutr Res. 1984;54(2-3):273.
38.Magazanik A， Weinstein Y， Dlin RA， et al. Iron deficiency caused by 7 weeks of intensive physical exercise. Eur J Appl Physiol. 1988;57(2):198-202.
39.a JA， Keaney JF， Raby KE， et al. Low plasma ascorbic acid independently predicts the presence of an unstable coronary syndrome. J Am Coll Cardiol. 1998;31(5):980-986.
40.Singh RB， Niaz MA， Rastogi SS， et al. Usefulness of antioxidant amins in suspected acute myocardial infarction (the Indian experiment of infarct survival-3). Am J Cardiol. 1996;77(4):232-236.
41.Dingchao H， Zhiduan Q， Liye H， Xiaodong F. The protective effects of high-dose ascorbic acid on myocardium against reperfusion injury during and after cardiopulmonary bypass. Thorac Cardiovasc Surg. 1994;42(5):276-278.
42.Tomoda H， Yoshitake M， Morimoto K， et al. Possible prevention of postangioplasty restenosis by ascorbic acid. Am J Cardiol. 1996;78(11):1284-1286.
43.Willis GC， Light AW， Gow WS. Serial arteriography in atherosclerosis. Can Med Assoc J. 1954;71(6):562-568.
44.Pauling L. Third case report on lysine-ascorbate amelioration of angina pectoris. Orthomol Med. 1993;8(3):137-138.
45.Pauling L. Case report: lysine/ascorbate-related amelioration of angina pectoris. J Orthomol Med. 1991;6(3& 4):144-146.
46.Rath M， Niedzwiecki A. Nutritional supplement program halts progression of early coronary atherosclerosis documented by ultrafast computed tomography. J Appl Nutr. 1996;48:68-78.
47.Pinto A， Bonucci A， Maggi E， et al. Anti-oxidant and anti-inflammatory actiy of ketogenic diet: new Perspectives for Neuroprotection in Alzheimer’s Disease. Antioxid Basel Switz. 2018;7(5).
48.Gershuni VM， Yan SL， Medici V. Nutritional ketosis for weight management and reversal of metabolic syndrome. Curr Nutr Rep. 2018;7(3):97-106.
49.Hanjani NA， Vafa M. Protein restriction， epigenetic diet， intermittent fasting as new approaches for preventing age-associated diseases. Int J Prev Med. 2018;9:58.
50.Vona R， Giovannetti A， Gambardella L， et al. Oxidative stress in the pathogenesis of systemic scleroderma: an overview. J Cell Mol Med. 2018;22(7):3308-3314.
PDF(966 KB)
