以生活方式解决生活方式病ppt课件

健康管理管理健康人生——用生活方式解决生活方式病*生活方式病 非传染性疾病 代谢类疾病、代谢综合征 富贵病、现代文明病肥胖、三高、心脑血管疾病、恶性肿瘤等一、健康管理理论**肥胖三高形成原因 吃多了 吃错了 运动少了*原因之一：吃多了安全的血糖范围时间血糖自由基*旧的的生活方式促血管老化**食物中的脂肪小肠*内脏脂肪过多增加糖尿病和心血管代谢风险AndréTchernof,etal.PhysiolRev.2013;93:359–404.*Workingmodelbywhichexcessvisceraladiposityisassociatedwithincreasedcardiometabolicrisk.Underthismodel,excessvisceraladipositymaybeamarkerofdysfunctionalsubcutaneousadiposetissue(AT)notbeingabletoexpandwhenfacinganenergysurplus(duetoitsinabilitytoexpandthroughhyperplasiaortoitsabsencesuchasinlipodystrophicstates).Undersuchcircumstances,theinabilityofsubcutaneousadiposetissuetoactasanenergybufferwillproducealipidspilloverleadingtoaccumulationoflipidsatundesiredsites(ectopicfatdeposition)withharmfulcardiometabolicconsequences.Intraabdominaladiposityimpairspancreaticb-cellfunctionTheincreasedsecretionoffreefattyacids(FFA)fromintra-abdominaladiposityalsoimpairsb-cellfunction.Authoritativereviewsonthissubjectconcludethatashort-termstimulationifinsulinsecretionisfollowedbylong-termdamagetotheβ-cellandreductionofinsulinsecretion.ExcessFFAfromintra-abdominalobesitycanthereforeinducebothinsulinresistanceandimpairedb-cellfunction–theprimarymetabolicdefectsthatunderlietype2diabetes.Hyperlipidemiaisfrequentlyassociatedwithinsulinresistancestatesasfoundintype2diabetesandobesity.Effectsoffreefattyacids(FFA)onpancreaticb-cellshavelongbeenrecognized.Acuteexposureofthepancreaticb-celltoFFAresultsinanincreaseofinsulinrelease,whereasachronicexposureresultsindesensitizationandsuppressionofsecretion.Werecentlyshowedthatpalmitateaugmentsinsulinreleaseinthepresenceofnon-stimulatoryconcentrationsofglucose.ReductionofplasmaFFAlevelsinfastedratsorhumansseverelyimpairsglucose-inducedinsulinrelease.TheseresultsimplythatphysiologicalplasmalevelsofFFAareimportantforb-cellfunction.Although,ithasbeenacceptedthatfattyacidoxidationisnecessaryforitsstimulationofinsulinsecretion,thepossiblemechanismsbywhichfattyacids(FA)affectinsulinsecretionarediscussedinthisreview.Long-chainacyl-CoA(LC-CoA)controlsseveralaspectsoftheb-cellfunctionincludingactivationofcertaintypesofproteinkinaseC(PKC),modulationofionchannels,proteinacylation,ceramide-and/ornitricoxide(NO)-mediatedapoptosis,andbindingtonucleartranscriptionalfactors.ThepresentreviewalsodescribesthepossibleeffectsofFAoninsulinsignaling.Weshowedforthefirsttimethatacuteexposureofisletstopalmitateupregulatestheintracellularinsulin-signalingpathwayinpancreaticislets.AnotheraspectconsideredinthisreviewisthesourceofFAforpancreaticislets.Inadditiontobeexportedtothemedium,lipidscanbetransferredfromleukocytes(macrophages)topancreaticisletsinco-culture.ThisprocessconsistsanadditionalsourceofFAthatmayplaysasignificantroletoregulateinsulinsecretion.J.Cell.Physiol.194:1–12,2002.*原因之二：吃错了 克里威20年法则 一旦精制碳水化合物进入一个国家，10—20年之后，糖尿病、心脑血管疾病就会如期而至。*原因之二：吃错了 哈佛膳食金字塔（2005） 美国哈佛、耶鲁等几十所大学耗资1亿美元，历时10年，跟踪10万人群得出来的重大科研结论。**原因之二：吃错了1981年詹金斯博士提出升糖指数概念，震惊了医学界。升糖指数：升糖指数是指由人体摄入的食物转化而成的血糖升高值与等量葡萄糖转化而成的血糖升高值的比值。研究发现：大米、白面与白糖的升糖指数相当。*常见主食升糖指数面条GI=81.6白面包GI=87.9玉米GI=55白米饭GI=84-88GI=83.8顿顿吃细粮，就是顿顿吃白糖！*原因之三：运动少了 细胞膜受应点退化 细胞内线粒体面积减少**代谢轨道理论:（胰岛素抵抗）血糖脂肪细胞关键是轨道改变不良生活方式轨道改变（中部肥胖）代谢综合征体能下降少吃也胖*代谢综合征 高血糖：血糖无法顺利送给细胞 高血脂：脂肪堆积在血液 脂肪肝：脂肪堆积在肝脏 动脉硬化：脂肪沉积在动脉内壁 高血压：动脉变窄阻力增大*材料不足毒素积累AB因为得不到细胞所需要的东西它们被细胞所不需要的东西给毒害了。疾病久治不愈的两大根源*1.该进来的进来2.该出去的出去3.不该进来的别进来4.不该出去的别出去四句箴言【壹】【贰】【叁】【肆】均衡的营养PM2.5污染的水农药残留、激素恢复本能的四句箴言体内垃圾坏情绪*均衡的营养适量的运动*主流治疗方法——替代疗法重大贡献：大大延长带病生存时间固有局限：只能控制，不能治愈！药物依赖，慢性损伤！加速并发症形成：高胰岛素血症！无奈的结论：终身性疾病？！*《黄帝内经》:“病非人体素有之物，能得亦能除，言不可治者，未得其术也”一、健康管理理论*治病救人的精髓病人的本能就是病人的医生，医生只是照顾病人的本能。——希波克拉底西方医学之父*金胚力配料：大豆分离蛋白、大豆肽粉、白蛋白肽、玉米肽、小麦低聚肽、啤酒酵母、菊粉、聚葡糖糖、卵磷脂、复合维生素：（维生素A、维生素D、VE、VC、VB12、VB6、VB1、VB2、烟酸、叶酸、泛酸、胡萝卜素、牛磺酸）复合微量元素：（钙、磷、镁、锌、铁、)*调理的有关问1、调理期120天：42天强化期（包括3天启动期），7天巩固期，71天维持期。2、调理期：加强期内尽量不吃保健品，因为餐包里有足够的人体所需要各种营养素；调理是排毒修复的过程，通道里如果增加营养太多，会增加负担，影响机体反应3、各期特点：42天强化期、巩固期和维持期的每周一个蛋白日，我们执行5个餐包，巩固期常规日是三个餐包，维持期常规日一个餐包4、一个周期：减重约10-20斤，血糖高85%可完全停药，尿酸高的42天基本达到正常、血压高的65%可完全停药、高血脂可完全恢复正常！*短期计划 低糖饮食：运输车（供热能慢一点） 营养强化：鼓风机（修复快一点） 适量运动：促代谢（代谢快一点）*长期计划:三个习惯一个方法 低升糖食物：少吃细粮多吃粗粮 日常营养补充：增加新陈代谢 坚持适量运动并持之以恒 每周一个蛋白日。*Workingmodelbywhichexcessvisceraladiposityisassociatedwithincreasedcardiometabolicrisk.Underthismodel,excessvisceraladipositymaybeamarkerofdysfunctionalsubcutaneousadiposetissue(AT)notbeingabletoexpandwhenfacinganenergysurplus(duetoitsinabilitytoexpandthroughhyperplasiaortoitsabsencesuchasinlipodystrophicstates).Undersuchcircumstances,theinabilityofsubcutaneousadiposetissuetoactasanenergybufferwillproducealipidspilloverleadingtoaccumulationoflipidsatundesiredsites(ectopicfatdeposition)withharmfulcardiometabolicconsequences.Intraabdominaladiposityimpairspancreaticb-cellfunctionTheincreasedsecretionoffreefattyacids(FFA)fromintra-abdominaladiposityalsoimpairsb-cellfunction.Authoritativereviewsonthissubjectconcludethatashort-termstimulationifinsulinsecretionisfollowedbylong-termdamagetotheβ-cellandreductionofinsulinsecretion.ExcessFFAfromintra-abdominalobesitycanthereforeinducebothinsulinresistanceandimpairedb-cellfunction–theprimarymetabolicdefectsthatunderlietype2diabetes.Hyperlipidemiaisfrequentlyassociatedwithinsulinresistancestatesasfoundintype2diabetesandobesity.Effectsoffreefattyacids(FFA)onpancreaticb-cellshavelongbeenrecognized.Acuteexposureofthepancreaticb-celltoFFAresultsinanincreaseofinsulinrelease,whereasachronicexposureresultsindesensitizationandsuppressionofsecretion.Werecentlyshowedthatpalmitateaugmentsinsulinreleaseinthepresenceofnon-stimulatoryconcentrationsofglucose.ReductionofplasmaFFAlevelsinfastedratsorhumansseverelyimpairsglucose-inducedinsulinrelease.TheseresultsimplythatphysiologicalplasmalevelsofFFAareimportantforb-cellfunction.Although,ithasbeenacceptedthatfattyacidoxidationisnecessaryforitsstimulationofinsulinsecretion,thepossiblemechanismsbywhichfattyacids(FA)affectinsulinsecretionarediscussedinthisreview.Long-chainacyl-CoA(LC-CoA)controlsseveralaspectsoftheb-cellfunctionincludingactivationofcertaintypesofproteinkinaseC(PKC),modulationofionchannels,proteinacylation,ceramide-and/ornitricoxide(NO)-mediatedapoptosis,andbindingtonucleartranscriptionalfactors.ThepresentreviewalsodescribesthepossibleeffectsofFAoninsulinsignaling.Weshowedforthefirsttimethatacuteexposureofisletstopalmitateupregulatestheintracellularinsulin-signalingpathwayinpancreaticislets.AnotheraspectconsideredinthisreviewisthesourceofFAforpancreaticislets.Inadditiontobeexportedtothemedium,lipidscanbetransferredfromleukocytes(macrophages)topancreaticisletsinco-culture.ThisprocessconsistsanadditionalsourceofFAthatmayplaysasignificantroletoregulateinsulinsecretion.J.Cell.Physiol.194:1–12,2002.*