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  知识库 -> 两性话题 -> 胸部发育什么时候才会停下来? -> 正文阅读

[两性话题]胸部发育什么时候才会停下来?

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高一生73—98,初中开始发育,不过一直不快,一年涨一个杯罩的样子,初三75d,到中考完,人瘦了,下胸围减到72,上胸围没变,高一开学后压力不是特别大…
我觉得胸部发育分为三个阶段:
第一次是10-15岁,这期间胸部会从平平无奇变成隆起,这期间由于激素发育,会导致胸部隆起但是没用什么脂肪,所以给人感觉是空空的!
第二次是15-22岁,这期间胸部是开始正式发育,最明显的是乳头开始发育,胸部会更大更成人化,到了20岁左右,胸部就已经发育的和成年女性几乎一样了!
第三次是怀孕期间,胸部会因为孕激素和雌性激素的刺激,胸部会继续增大,乳头也会继续变大,会比以前的大小大上一倍,这期间乳头发育到最大的尺寸,并且开始产生乳汁,这一次变大一定要注意,千万不要快速让胸部变大,要慢慢的来,一旦增大变快了,会导致胸部内的韧带和肌腱拉伸过长,一旦韧带和肌腱拉的过长,就会导致拉伤,拉伤之后,胸部一开始不会觉得咋样,因为胸部内充满了乳汁,可一旦哺乳了两年之后,奶水分泌过少,减少,那么胸部就会开始出现下垂,因为韧带和肌腱过度拉伸导致的无法回缩导致,这就如同弹簧被过度拉伸之后无法回缩是一个道理!
然后年轻时下垂不严重,因为体内有胶原蛋白支撑着,一旦年龄大了,胶原蛋白开始消失,慢慢的到了五十岁以后,你就会发现你的胸部下垂开始严重,到了老年了,你就是两个下垂严重的大胸了,明白了吗!
然后到了哺乳期开始后两年左右,胸部就停止发育了,不过也有个别女生还会发育,比如日本女星【冲田杏梨】,她就是一直在发育的,现在已经L罩杯了!
还有一种是疾病导致,就是俗称【巨乳症】,典型的就是日本女星【田中瞳】,她就是巨乳症导致的胸部发育,现在是L罩杯,但她这个L罩杯就是疾病导致的了,和冲田杏梨的自然发育发的好不一样了,明白了吗!
所以这就是胸部发育的三个阶段了,也是提醒大家一下,不能为了让自己奶水多就在孕期疯狂涨奶,那样对胸部是不好的,要慢慢来,一点点来,不然就会导致哺乳期之后胸部下垂难看,明白了吗!
以上内容仅代表个人意见,不喜勿喷!
我自己来说的话可能在23岁左右会停滞吧…小升初穿D,初二初三不得不买大妈款穿了 高中的体育课早操这些和家人沟通过由家人出面和学校谈尽量不参加…高中毕业80H 现在参加工作一年了内衣穿85L(外贸的那种)或者90K(欧美深杯款式)。
高中阶段是人生很重要的阶段,有这方面的疑虑要和家人做好沟通,这个阶段里不免会受到其他人的特殊眼光和风言风语。老师也不一定是一个倾诉的好选择,一定一定要和妈妈多沟通多交流,学校生活中遇到轻薄言语和行为不要隐忍!!!不要独自乱跑!!更不要觉得两三年的同学就比朝夕相处十几年的父母更了解你更爱你!!
老娘最美最性感!其他人想都做不到呢!


我大学的时候是80E现在儿子10岁了还是这样,一般大学的时候就会固定了,然后怀孕的时候还会大两到三个罩杯,生完孩子会慢慢恢复到怀孕前。
评论区蛮多人好奇80E到底是多大,发两张张图吧,用维密80E的内衣(如果有人感觉尺码不准那就是维密的问题了,与我无关)跟篮球做一个比较,就这么大。
关于下垂的问题我没有哺乳所以没有下垂,儿子一直喝奶粉喝到五岁。






篮球是6号篮球


我小学还带的小背心,初中三年尤其初三那年长得特别快。上高一胸围破百,穿75G 现在高三75I也有点紧了 应该还会再继续长大 题主别担心 你现在穿70H试一下呢先!
乳房发育,一般可分为五期。
第一期:十岁之前,女孩乳房还没有发育,也叫发育前期。十岁之前的女孩胸部扁平,一侧或双侧的乳房能见到乳头突起。
第二期:在十岁左右,乳房发育进入第二期,此时乳头慢慢增大、隆起,出现乳晕。乳房也在逐渐隆起,软而富有弹性。乳晕明显高出乳房的皮肤表面,在皮下经常可以摸到块状物,质地稍硬,此阶段一般维持一到两年。
第三期:女孩子到了十二岁左右,乳晕色素增深,乳房乳晕都进一步增大、隆起,乳房的形状会更加的饱满。
第四期:到了十五岁左右,乳房一直在变大、变高、变得更加丰满。
第五期:在青春期行将结束之际,乳房发育也进入了其最后的发育阶段,这通常出现在十七岁左右,也叫做成熟期,这时候的乳房已经发育成型。






青春期是由激素引发的,尤其是雌激素。
10 岁左右,雌激素促使胸部脂肪堆积,导致乳房发育。
乳芽在乳头下方形成,导致乳头突出。这些圆盘状的小疙瘩可能会感到轻微疼痛、发痒或不舒服。
乳房发育一般从 8 到 12 岁开始。
乳芽形成后,乳房会继续生长并改变形状。
初次发育发生在青春期,通常在第一次月经后 1-2 年。
乳房的变化会持续一生。
女孩的乳房通常在 17-18 岁左右停止发育。
但是,由于体重的波动,到 20 多岁和 30 多岁时也会发生变化。
一侧乳房的大小和形状与另一侧略有不同是正常的。
每个人的发育时间表都是独一无二的,
乳房发育也没有 "正常值"。


乳房发育又称乳腺生成,是灵长类动物的一个复杂的生理过程,贯穿女性的一生。
乳腺生成跨越几个阶段,包括产前发育、青春期和妊娠期。
到了更年期,乳房发育停止,乳房萎缩。
乳房发育的结果是在胸部形成突出和发达的结构,灵长类动物称之为乳房,主要起乳腺作用。这一过程由多种激素(和生长因子)介导,其中最重要的激素包括雌激素、孕酮、催乳素和生长激素。
乳房发育的主要调节因子是类固醇激素、雌激素和孕激素、生长激素(GH)(主要通过其分泌产物胰岛素样生长因子 1 (IGF-1))和催乳素。这些调节因子可诱导生长因子的表达,如两性胰岛素、表皮生长因子 (EGF)、IGF-1 和成纤维细胞生长因子 (FGF),而这些生长因子又在乳房的生长和成熟过程中发挥特殊作用。
在青春期,下丘脑以脉冲方式分泌促性腺激素释放激素(GnRH),会诱导垂体分泌促性腺激素、卵泡刺激素(FSH)和黄体生成素(LH)。分泌的促性腺激素通过血液循环到达卵巢,在每个月经周期中触发雌激素和孕激素的波动分泌。 在产前发育、婴儿期和儿童期,GH 和 IGF-1 水平较低,但会逐渐升高,并在青春期达到峰值,此时 GH 的搏动性分泌可增加 1.5 至 3 倍,血清 IGF-1 水平可增加 3 倍或更多。研究发现,雌激素和 GH 都是青春期乳房发育的必要条件--缺少任何一种激素,乳房都不会发育。
此外研究还发现,GH 在乳房发育中的大部分作用是通过诱导 IGF-1 的产生和分泌来实现的,因为在缺乏 GH 的情况下,服用 IGF-1 可以促进乳房发育。GH诱导IGF-1的产生和分泌几乎发生在体内所有类型的组织中,尤其是肝脏,因为肝脏是循环中约80%的IGF-1的来源,乳房局部也是如此。 尽管 IGF-1 是 GH 在乳房发育过程中起主要作用的因素,但人们发现 GH 本身也起着直接的促进作用,因为它能增加乳房基质(结缔)组织中雌激素受体(ER)的表达,而 IGF-1 则没有这种作用。除了雌激素和 GH/IGF-1 都是青春期乳房发育的必要因素外,它们还能协同促进乳房发育。
尽管 GH/IGF-1 信号在青春期乳房发育中显然是必要的,但患有拉隆综合征(Laron Syndrome)的妇女,其生长激素受体(GHR)存在缺陷,对 GH 不敏感,血清 IGF-1 水平很低,因此青春期(包括乳房发育)会推迟,尽管最终总会达到完全的性成熟。研究认为,拉隆综合征妇女相对较大的乳房是由于催乳素(已知催乳素可导致乳房增大)分泌增加所致,而催乳素是由脑垂体中分泌大量 GH 的体细胞漂移现象引起的。拉隆综合征的动物模型--GHR 基因敲除小鼠在 11 周龄时,乳腺导管发育严重受损。在任何情况下,雌性 GHR 基因敲除小鼠都能正常泌乳。
因此,有人说拉隆综合征女性患者和 GHR 基因敲除小鼠的表型是相同的,体型缩小、性成熟延迟,但泌乳正常。
在胚胎发育过程中,乳芽由外胚层生成,其中形成了小管网络。这些不发育的小管最终会变成成熟的乳腺(乳汁)导管,将乳腺小叶(乳汁的 "容器")、葡萄状的腺泡群与乳头连接起来。在青春期之前,乳芽的小管网仍然不发育且处于静止状态,男性和女性的乳房没有任何差异。
在女性青春期,雌激素与 GH/IGF-1 共同作用,通过激活 ERα(而不是 ERβ 或 GPER),使乳腺小管生长并转变为成熟的乳腺导管系统。在雌激素的影响下,导管萌发并伸长,导管顶端的球状结构--终末芽(TEBs)穿透脂肪垫,并随着导管的伸长而分支。这种情况一直持续到形成一个树状的导管分支网络,嵌入并充满整个乳房脂肪垫。雌激素除了能促进导管发育外,还能导致基质组织生长和脂肪组织积聚,以及乳头乳晕复合体增大。
孕酮与 GH/IGF-1 的作用类似于雌激素,会影响青春期及其后的乳房发育。 [孕酮受体(PR)基因剔除小鼠或用孕酮受体拮抗剂米非司酮治疗的小鼠显示出延迟(尽管最终是正常的)乳腺导管发育、 此外,还发现黄体酮主要通过诱导两性胰岛素的表达来诱导小鼠乳腺导管的生长,而两性胰岛素正是雌激素主要诱导其介导导管发育的生长因子。 此外,黄体酮从青春期开始产生适度的乳腺小叶腺泡发育(腺泡芽形成或导管侧枝化),特别是通过激活 PRB(而非 PRA),每个月经周期都会在一定程度上发生腺泡的生长和退化。 然而,只有不成熟的泡会对孕前水平的孕酮和雌激素做出反应,小叶泡的发育将停留在这一阶段,直到怀孕(如果怀孕的话)。 [除了 GH/IGF-1 外,雌激素也是黄体酮影响乳房的必要条件,因为雌激素通过诱导乳腺上皮组织中黄体酮受体(PR)的表达为乳房提供能量。
雌激素和孕酮水平急剧上升,妊娠晚期达到比月经周期正常水平高几百倍的水平。雌激素和孕酮导致垂体前叶分泌大量催乳素,其水平比月经周期正常水平高 20 倍。 [IGF-1 和 IGF-2 水平在妊娠期间也会因胎盘生长激素(PGH)的分泌而急剧增加。此外,雌激素、孕酮(同样特别通过 PRB)、 催乳素和其他泌乳素(如人胎盘泌乳素(hPL)和 PGH)与 GH/IGF-1 以及胰岛素样生长因子 2(IGF-2)共同作用,介导妊娠期乳房小叶肺泡发育的完成。PR 和催乳素受体(PRLR)基因敲除的小鼠都无法显示乳腺小叶的发育,而孕酮和催乳素在促进腺泡生长方面具有协同作用,这表明这两种激素在乳腺发育的这一环节中起着重要作用。除了在乳腺小叶生长中的作用外,催乳素和 hPL 还能在孕期增加乳头-乳晕复合体的大小。到孕期第四个月末,乳腺小叶成熟完成,乳房已为泌乳和母乳喂养做好充分准备。
胰岛素、糖皮质激素如皮质醇(以及延伸的促肾上腺皮质激素(ACTH))和甲状腺激素如甲状腺素(以及延伸的促甲状腺激素(TSH)和促甲状腺激素释放激素(TRH))在青春期和妊娠期的乳房发育中也起着促进作用,但人们对其了解较少/特征不清,这些激素是乳房全面功能发育所必需的。
与女性相关性荷尔蒙--雌激素和孕酮--相比,男性相关性荷尔蒙--雄激素,如睾酮和双氢睾酮(DHT),可有效抑制雌激素在乳房中的作用。在没有雄激素活性的情况下,如患有完全雄激素不敏感综合症(CAIS)的妇女,适度水平的雌激素(50 pg/mL)能够促进乳房的显著发育,CAIS 妇女的乳房体积甚至高于平均水平。由于女性卵巢分泌大量雌激素而雄激素分泌较少,男性睾丸分泌大量雄激素而雌激素分泌较少,雄激素水平高得多(约高 10 倍),而雌激素水平低得多(约低 10 倍),因此男性的乳房一般不会比女性突出或发育良好。
据报道,通过维生素 D 受体(VDR)作用的具有激素活性的维生素 D--骨化三醇,与雄激素一样,是小鼠乳腺发育的负性调节剂,例如在青春期。 [VDR 基因敲除小鼠的乳腺导管发育比野生型小鼠更广泛,乳腺发育也更早。] 此外,VDR 基因敲除还导致小鼠乳腺组织对雌激素和孕激素的反应性增加,表现为细胞对这些激素的生长反应增加。相反,研究发现 VDR 基因敲除小鼠的导管分化减少,表现为未分化的 TEB 数量增加,这一发现被解释为表明维生素 D 可能是乳腺小叶发育所必需的。因此,钙三醇通过 VDR 可能是乳腺导管发育的负调节因子,但却是乳腺小叶发育的正调节因子。
一项对妇女补充维生素 D3 的研究发现,维生素 D3 可抑制乳腺中环氧化酶-2(COX-2)的表达,从而分别降低和提高前列腺素 E2(PGE2)和转化生长因子β2(TGF-β2)的水平,而前列腺素 E2 和转化生长因子β2 是已知的乳腺发育抑制因子。此外,抑制乳腺组织中的 PGE2 与此相关,因为通过激活前列腺素 EP 受体,PGE2 能有效地诱导乳腺组织中两性胰岛素的表达,而两性胰岛素对表皮生长因子受体的激活会增加乳腺组织中 COX-2 的表达,进而产生更多的 PGE2,因此,正常乳腺组织中似乎可能存在一种由于 COX-2 而导致的自我延续、协同增殖循环。因此,COX-2在乳腺组织中的过度表达会导致雌性小鼠乳腺增生和乳腺早发育,这与VDR基因敲除小鼠的表型如出一辙,并表明VDR激活后下调的COX-2对乳腺生长有强烈的刺激作用。同样,研究还发现女性乳房中 COX-2 的活性与乳房体积呈正相关。
雌激素、孕酮和催乳素以及 GH/IGF-1 通过调节乳腺组织中各种自分泌和旁分泌生长因子的局部表达对乳腺发育产生影响,这些生长因子包括 IGF-1、IGF-2、两性胰岛素、 EGF、FGF、肝细胞生长因子(HGF)、肿瘤坏死因子 α(TNF-α)、肿瘤坏死因子 β(TNF-β)、转化生长因子 α(TGF-α)、 转化生长因子 β(TGF-β)、 heregulin、Wnt、 RANKL和白血病抑制因子(LIF)。这些因子通过激活控制细胞功能的细胞内信号级联,如 Erk、Akt、JNK 和 Jak/Stat,调节细胞的生长、增殖和分化。
根据对表皮生长因子受体(EGFR)基因敲除小鼠的研究,表皮生长因子受体(EGFR)是 EGF、TGF-α、两性胰岛素(amphiregulin)和 heregulin 的分子靶标,与胰岛素样生长因子-1 受体(IGF-1R)类似,被发现对乳腺发育至关重要。 [雌激素和孕激素主要通过诱导两性胰岛素的表达,进而激活下行表皮生长因子受体,来介导乳腺导管的发育。因此,ERα、两性胰岛素和表皮生长因子受体基因敲除小鼠对乳腺导管发育的影响在表型上相互复制。同样,用两性胰岛素或其他表皮生长因子受体配体(如 TGF-α 或 heregulin)处理小鼠,可诱导小鼠乳腺导管和乳腺小叶的发育,即使在没有雌激素和孕激素的情况下也是如此。由于 IGF-1R 和表皮生长因子受体对乳腺的发育都是独立的,而且 IGF-1 和表皮生长因子受体通过各自的受体联合应用,可协同刺激人类乳腺上皮细胞的生长,因此这些生长因子系统似乎共同作用于乳腺的发育。
研究发现,将巨乳症乳腺基质组织暴露于非巨乳症乳腺上皮组织会导致后者的腺泡形态发生和上皮增殖增加。 一项针对 HGF(而非 IGF-1 或 EGF)的中和抗体被发现可减轻乳腺上皮组织因暴露于巨乳症乳腺基质细胞而导致的增殖,这可能直接表明 HGF 与巨乳症中出现的乳房生长和增大有关。
分娩时,雌激素和孕酮迅速降至极低水平,孕酮水平甚至检测不到。 [由于雌激素和孕酮会抑制乳腺组织中催乳素受体(PRLR)的表达,从而阻止催乳素诱导的泌乳过程,因此它们的突然消失会导致催乳素开始分泌乳汁和泌乳。 [催乳素会抑制 LH 和 FSH 的分泌,进而导致雌激素和孕激素水平持续偏低,出现暂时性闭经(无月经周期)。如果没有规律的、偶发性的哺乳,使催乳素浓度居高不下,催乳素水平就会迅速下降,月经周期就会恢复,因此雌激素和孕激素水平就会恢复正常,泌乳就会停止(即直到下一次分娩,或直到诱导泌乳(即使用半乳糖生成素、雌激素和孕激素))。
乳房形态的某些因素(包括其密度)与乳腺癌有明显的关联。虽然乳房大小具有一定的遗传性,但乳房大小与癌症之间的关系并不确定。影响乳房大小的基因变异尚未确定。
通过全基因组关联研究,多种基因多态性与乳房大小有关。
其中包括 ZNF703(锌指蛋白 703)附近的 rs7816345;INHBB(抑制素 βB)侧翼的 rs4849887 和 rs17625845;ESR1(ERα)附近的 rs12173570; ZNF365(锌指蛋白 365)中的 rs7089814;PTHLH(甲状旁腺激素样激素)附近的 rs12371778;AREG(两性胰岛素)附近的 rs62314947;以及 8p11. 23(与 rs7816345 处于完全连锁不平衡状态)和 22q13 的 rs5995871(包含 MKL1 基因,已发现该基因可调节 ERα 的转录活性)。 然而,相反,一些多态性则显示乳房大小与乳腺癌风险之间存在负相关。无论如何,一项荟萃分析得出结论,乳房大小与乳腺癌风险确实存在重要关联。
循环 IGF-1 水平与女性乳房体积呈正相关。此外,IGF1 基因中常见的 19 个重复等位基因的缺失也与女性乳房体积呈正相关,还与口服避孕药期间的高 IGF-1 水平以及女性循环 IGF-1 浓度随年龄增长而下降的正常趋势减弱呈正相关。 IGF1 19-重复等位基因的流行率在不同种族群体之间存在很大差异,据报道,非洲裔美国妇女中IGF1 19-重复等位基因的缺失率最高。
患有 CAIS 的妇女对 AR 介导的雄激素作用完全不敏感,但作为一个群体,她们的乳房大小高于平均水平。尽管她们体内的雌激素水平相对较低,但她们的乳房仍高于平均水平,这表明雄激素对雌激素介导的乳房发育具有强大的抑制作用。
芳香化酶过剩综合征是一种极为罕见的疾病,其特征是明显的雌激素过多,与女性乳房发育早熟和巨乳症有关,男性同样会出现妇科乳房发育早熟(女性乳房)在完全雄激素不敏感综合征中,AR 存在缺陷,对雄激素不敏感,尽管雌激素水平相对较低(雌二醇为 50 pg/mL),但乳房发育完全,乳房体积实际上高于平均水平。 [芳香化酶缺乏症是一种雌激素过少症,其中芳香化酶有缺陷,不能合成雌激素;完全雌激素不敏感综合征是一种ERα有缺陷且对雌激素不敏感的病症,乳房完全没有发育。
【未完待续】
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高二高三是快速发育时期,涨了2个杯,但体重也跟着长得很快。
现在大二,健身了一年多,好像能保持在E cup,有时候减猛了会小,太难了。






绝大多数女性都是在18-22岁就停止发育了 题主这种这么猛的还真是少见 先排除下巨乳症吧临床表现
1.乳房巨大,鼓胀沉重,皮肤紧张;
2.胸部压迫感;
3.常伴
慢性乳腺炎
及疼痛;4.可有乳房下皮肤糜烂。
如果实在担心的话可以去医院检查一下
.
.
.
.
.
.
好羡慕
这个说不好。比如我教的初三的女生,有的是标准的太平公主,我教的初一的女生 ,有的已经完全和成人一样大了。
可以去找医生看看,因为你长的太夸张了,如果是正常的,没必要焦虑


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