故事
头发变白 · 色素是怎么停下的
头发的颜色由毛囊里的色素细胞一根根染上,它们和背后的干细胞储备慢慢耗尽,新长的头发就白了。这里讲衰老、氧化、压力和遗传各起什么作用,以及哪些原因值得查。
最后更新:
先读这一段 头发白了,不是长好的头发褪了色,而是毛囊不再往新长出来的那段头发里放色素。
科普内容,不替代医师诊断或处方;有症状或在服药请咨询医师。
故事路径
第 1 章
头发的颜色从哪来
Where hair color comes from
头发白了,不是长好的头发褪了色,而是毛囊不再往新长出来的那段头发里放色素。
头发的颜色叫黑色素,由毛囊底部毛球里的黑素细胞(专门造色素的细胞)制造,再递给旁边正在变成发丝的细胞。黑褐色和偏红黄的两种黑色素比例不同,就有了黑发、棕发、红发。
这条色素生产线只在头发的生长期开工,退行期停工,休止期没有。每长一根新头发,毛球里都要有一批黑素细胞上岗,它们由毛囊上部的一小群黑素干细胞补充。
发丝一长出头皮,就是没有活细胞的角蛋白,颜色在毛囊里已经定好。所以白发是长出来时就白,不是黑发长在头上慢慢变白。
头发的颜色叫黑色素,由毛囊底部毛球里的黑素细胞(专门造色素的细胞)制造,再递给旁边正在变成发丝的细胞。黑褐色和偏红黄的两种黑色素比例不同,就有了黑发、棕发、红发。
这条色素生产线只在头发的生长期开工,退行期停工,休止期没有。每长一根新头发,毛球里都要有一批黑素细胞上岗,它们由毛囊上部的一小群黑素干细胞补充。
发丝一长出头皮,就是没有活细胞的角蛋白,颜色在毛囊里已经定好。所以白发是长出来时就白,不是黑发长在头上慢慢变白。
机制 · 灰发和白发差在哪
单看一根头发,白发里完全没有装着色素的小颗粒(黑素小体),灰发里还剩一些,只是稀稀落落。发丝的角蛋白本身是淡黄色的,没有色素挡着,光在发丝里反射、折射,看上去就是白的。满头花白,多数是黑发和白发混在一起:每个毛囊各走各的周期、各有各的储备,哪个先用完,哪根就先白。
毛球里的色素单位很小:一个黑素细胞大约只服务 5 个正在变成发丝的细胞,皮肤表皮里一个黑素细胞要服务约 36 个(Kumar 综述)。而且造色素本身是一条带着氧化反应的化学线,过氧化氢在毛囊里堆积一章会用到这一点。
头发本身怎么长、怎么掉,是毛囊里的另一条线,脱发 · 先分清是哪一种讲的是它。
第 2 章
色素干细胞慢慢耗尽
The pigment reserve runs out
随年龄变白,大致分两步,都发生在毛囊里。
第一步在毛球:一根接一根头发长下去,毛球里的黑素细胞造的色素越来越少。造色素的关键酶酪氨酸酶活性下降,色素递不出去,有的黑素细胞干脆凋亡。这时头发先变浅、变灰。
第二步在毛囊上部:负责补充黑素细胞的黑素干细胞储备也耗光了。在小鼠和老年人的毛囊里都看到,这些干细胞本该安静待命,却在原地提前成熟、被用掉,储备补不回来。到了这一步,变白基本不可逆(O'Sullivan 综述)。
这也是白了的头发很少再黑回来的原因:毛囊里已经没有能补位的造色素细胞了。
第一步在毛球:一根接一根头发长下去,毛球里的黑素细胞造的色素越来越少。造色素的关键酶酪氨酸酶活性下降,色素递不出去,有的黑素细胞干脆凋亡。这时头发先变浅、变灰。
第二步在毛囊上部:负责补充黑素细胞的黑素干细胞储备也耗光了。在小鼠和老年人的毛囊里都看到,这些干细胞本该安静待命,却在原地提前成熟、被用掉,储备补不回来。到了这一步,变白基本不可逆(O'Sullivan 综述)。
这也是白了的头发很少再黑回来的原因:毛囊里已经没有能补位的造色素细胞了。
机制 · 干细胞为什么会被困住
黑素干细胞的储备为什么比身体里别的干细胞更早用完,还没有定论。两项研究各给了一块拼图,主要都来自小鼠:Nishimura 2005 在小鼠和老年人的毛囊里看到:衰老的黑素干细胞会在本该休眠的地方提前上色、提前成熟,等于在储备库里就被花掉了。保护这些干细胞存活的基因 Bcl2 一缺,小鼠变白就大大提前。Sun 2023 在小鼠里追踪单个干细胞,发现它们平时会在毛囊里来回移动,在待命和准备上岗两种状态之间切换;随着年龄增长,越来越多的干细胞卡在原地,不再产出黑素细胞。作者提出,让它们重新动起来也许是防白发的新思路,但这还没有在人身上试过。
要读准边界:这些是机制研究,回答的是为什么会耗尽,不是吃什么能防。O'Sullivan 综述也提醒,人的变白从毛球开始,干细胞储备耗尽是后来的事,至今没有一个公认的完整模型。
第 3 章
过氧化氢在毛囊里堆积
Hydrogen peroxide builds up
毛囊造色素,本身是一条会产生氧化副产物的化学线。其中一个副产物是过氧化氢(双氧水的主要成分),平时由过氧化氢酶拆成水和氧气。
一项用人的头发和毛囊做的研究(Wood 2009)发现:灰白头发的发干里,过氧化氢积到了毫摩尔级的浓度;灰发的毛囊里,过氧化氢酶和两种修复氧化损伤的酶几乎测不到。多出来的过氧化氢把酪氨酸酶活性中心里的一个氨基酸(甲硫氨酸)氧化了,酶越干越差,颜色就一点点变淡。
要读准它的分量:作者自己说,这是在支持一个说了很久、但证据还不够的想法。综述认为氧化损伤很可能是变白的重要推手,但人的变白至今没有公认的完整模型(O'Sullivan 综述)。
一项用人的头发和毛囊做的研究(Wood 2009)发现:灰白头发的发干里,过氧化氢积到了毫摩尔级的浓度;灰发的毛囊里,过氧化氢酶和两种修复氧化损伤的酶几乎测不到。多出来的过氧化氢把酪氨酸酶活性中心里的一个氨基酸(甲硫氨酸)氧化了,酶越干越差,颜色就一点点变淡。
要读准它的分量:作者自己说,这是在支持一个说了很久、但证据还不够的想法。综述认为氧化损伤很可能是变白的重要推手,但人的变白至今没有公认的完整模型(O'Sullivan 综述)。
误区 · 抗氧化产品能逆转白发吗
这条机制常被拿来卖东西:含过氧化氢酶的片剂、添加维生素 C 和 E 的抗白发洗发水。按机制推,它们的路很长:口服的酶是蛋白质,在消化道里会被拆开;洗发水在头皮上停留的时间很短,综述也质疑这类添加的效果(Kumar 综述)。Wood 2009 里,甲硫氨酸只是在试管里挡住了这种氧化,没有在人身上试过任何疗法。
更要紧的是色素干细胞慢慢耗尽这一步:储备一旦耗光,就算把氧化压下去,也没有细胞来造色素了。目前没有哪一种抗氧化产品被证明能让人的白发重新变黑(O'Sullivan 综述)。
第 4 章
压力会让头发变白吗
Can stress turn hair gray?
在小鼠身上会,而且走的不是常说的压力激素那条路。
Zhang 2020 让小鼠经受束缚、连续的不可预测刺激或疼痛,三种压力都让它们长出了白毛。追下去发现,起作用的是缠在黑素干细胞旁边的交感神经(管紧张反应的那套神经):压力一来,它们一下子释放大量去甲肾上腺素,本该休眠的黑素干细胞被逼着同时分裂、成熟、离开,储备一次清空,白毛就是永久的。切掉分泌压力激素的肾上腺、排除免疫攻击,都挡不住它。
放到人身上要打折扣:这是小鼠实验,人的压力和白发之间,目前只有小型研究里观察到的同步。
Zhang 2020 让小鼠经受束缚、连续的不可预测刺激或疼痛,三种压力都让它们长出了白毛。追下去发现,起作用的是缠在黑素干细胞旁边的交感神经(管紧张反应的那套神经):压力一来,它们一下子释放大量去甲肾上腺素,本该休眠的黑素干细胞被逼着同时分裂、成熟、离开,储备一次清空,白毛就是永久的。切掉分泌压力激素的肾上腺、排除免疫攻击,都挡不住它。
放到人身上要打折扣:这是小鼠实验,人的压力和白发之间,目前只有小型研究里观察到的同步。
机制 · 白毛为什么晚一轮才出现
Zhang 2020 里有个细节,正好对上头发的颜色从哪来一章:给小鼠注射引起疼痛的药之后 5 天内,很多毛囊里的黑素干细胞已经没了,可已经上岗的黑素细胞还在继续造色素,那一轮的毛仍然是黑的。白毛要等下一轮新毛长出来、没有新的黑素细胞补位时才露出来。研究者在压力刚来时短暂压住干细胞分裂,白毛就没有出现:伤害发生在干细胞被逼着同时启动的那一刻。按这个机制推,已经长在头上的头发不会因为一次惊吓当场变白。所谓一夜白头,综述把它和斑秃(头发突然成片脱落)、休止期脱发、白癜风等联系在一起(Kumar 综述),这些需要皮肤科医生分辨。
证据 · 人的白发会变回来吗
Rosenberg 2021 把 14 位健康人的 397 根头发逐段扫描颜色,像读树的年轮一样,读出每根头发长出来时的经历。他们看到,有些已经白了的头发,后来长出的那段又有了颜色;对照捐发者自己回忆的生活事件,个别头发变白和变回来的时间,正好和压力加重、减轻的时期对得上。要读准它:这是一项小型描述性研究,只能说明这种事会发生,也可以和压力同时出现,但不能说明是压力造成的,也不知道有多常见。作者用计算模型推测,只有那些本来就快到变白门槛的头发,才可能随压力减轻暂时变回来;按色素干细胞慢慢耗尽一章的机制,储备已经耗光的毛囊没有回头路。
能拿走的是:长期压力大,值得为整个身体去处理;但别指望减压能让一头白发重新变黑。
第 5 章
遗传,以及值得查的原因
Genes, and causes worth checking
什么时候开始白、白得多快,年龄是最大的因素;综述普遍认为遗传影响很大,但遗传到底占多大份量,目前还说不清(O'Sullivan 综述)。
已经找到的一个具体位点在 IRF4 基因上:一项覆盖 6000 多名拉丁美洲人的全基因组研究发现,它和白发有关,而 IRF4 正是参与开启酪氨酸酶的基因之一(Adhikari 2016)。这是一块拼图,不是一张能算出你几岁白头的表。
少数情况下,过早变白和一个查得出、治得了的问题一起出现:
维生素 B12 缺乏,尤其是恶性贫血甲状腺功能减退:甲状腺激素本身会推动毛囊造色素白癜风:可以让一小撮头发局部变白吸烟:研究看到吸烟的人更早白,这是关联
这些多来自小型研究(Kumar 综述)。
已经找到的一个具体位点在 IRF4 基因上:一项覆盖 6000 多名拉丁美洲人的全基因组研究发现,它和白发有关,而 IRF4 正是参与开启酪氨酸酶的基因之一(Adhikari 2016)。这是一块拼图,不是一张能算出你几岁白头的表。
少数情况下,过早变白和一个查得出、治得了的问题一起出现:
维生素 B12 缺乏,尤其是恶性贫血甲状腺功能减退:甲状腺激素本身会推动毛囊造色素白癜风:可以让一小撮头发局部变白吸烟:研究看到吸烟的人更早白,这是关联
这些多来自小型研究(Kumar 综述)。
数字 · 多早算过早
按 Kumar 综述引用的标准:白种人 20 岁以前、非裔 30 岁以前开始白,算过早变白;有作者建议南亚人用 25 岁,亚洲人群还没有公认的界线。开始变白的平均年龄,白种人约 34 岁,非裔约 43.9 岁。至于营养,综述里的数据都很薄:
较早的一项研究里,恶性贫血的病人约 55% 在 50 岁前开始白,对照组是 30%。铜、铁、锌、维生素 D 的研究结论不一:一项研究看到过早变白的人血铜偏低,锌和铁并不低;另一项在印度年轻人里看到、钙、维生素 D 偏低。这些都是观察到的关联,不能说明是它们造成的。
所以有作者建议:家里没有人早白、自己却很早就白的人,可以查一下 B12、叶酸和甲状腺。
第 6 章
染发和补剂,哪些靠得住
Dyes and supplements: what holds up
随年龄变白的头发,目前没有一种被证明能让它重新变黑的药或补剂(O'Sullivan 综述)。实际的选择是这几样:
染发:仍然是主要办法,只给已经长出来的发丝上色,碰不到毛囊。永久染发剂可能伤发丝;少数人会对其中常见的对苯二胺(PPD)起皮炎,也有人染发后掉发(Kumar 综述)。染后头皮发红、发痒、起疹,就停用,去看皮肤科;嘴唇、舌头或喉咙突然肿起来,或喘不上气、咽不下东西,立即打急救电话。补剂:生物素、泛酸钙、锌、铜、硒都有人用过,结果都不理想(Kumar 综述)。真缺什么,就治什么:查出 B12 缺乏或甲减,按医生的方案治,这本身就关乎健康;头发颜色能不能回来,没有保证。
染发:仍然是主要办法,只给已经长出来的发丝上色,碰不到毛囊。永久染发剂可能伤发丝;少数人会对其中常见的对苯二胺(PPD)起皮炎,也有人染发后掉发(Kumar 综述)。染后头皮发红、发痒、起疹,就停用,去看皮肤科;嘴唇、舌头或喉咙突然肿起来,或喘不上气、咽不下东西,立即打急救电话。补剂:生物素、泛酸钙、锌、铜、硒都有人用过,结果都不理想(Kumar 综述)。真缺什么,就治什么:查出 B12 缺乏或甲减,按医生的方案治,这本身就关乎健康;头发颜色能不能回来,没有保证。
误区 · 何首乌和黑芝麻能乌发吗
中文世界里最常见的两个乌发说法:何首乌:常被用来乌发、补肝肾,但美国国立卫生研究院的数据库把它列为确证会引起临床肝损伤的药;在临床上表现明显的何首乌肝损伤里,约 10% 最终死亡或需要紧急肝移植(LiverTox 2020)。为了头发颜色去冒伤肝的险,不值得。为什么有人吃了没事、有人几个月就伤肝,中药安全 · 天然不等于安全里有细讲。黑芝麻:它只是种皮里多了些深色色素,黑芝麻乌发没有可靠的人体证据。按机制推,吃进去的色素会在消化道里被分解,不会被送到毛囊去给头发上色。
回到机制:头发的颜色是毛囊里的黑素细胞当场造出来的,靠的是它们自己和背后的干细胞储备,吃进去的颜色走不到那里。
第 7 章
什么时候该看医生
When to see a doctor
多数白发是年龄和遗传的事,不需要看病。下面这些情况,值得找医生当面看:
白发的同时有手脚麻木或针刺感、走路不稳、明显乏力、舌头疼或发红:可能是维生素 B12 缺乏,尽快去看医生查血;拖得越久,神经损伤越可能变成永久的。白发的同时特别累、比平时怕冷、体重上升、便秘:医生可能会查甲状腺。白发长在一块变白的皮肤上,或皮肤上的白斑越来越多:去皮肤科,看是不是白癜风。头发突然大片变白,或同时成片脱落:去皮肤科分辨。孩子出现白发,或家里没人早白、自己很年轻就白了不少:告诉医生,可以查 B12、叶酸和甲状腺。
这一篇是科普,不替代诊断。
白发的同时有手脚麻木或针刺感、走路不稳、明显乏力、舌头疼或发红:可能是维生素 B12 缺乏,尽快去看医生查血;拖得越久,神经损伤越可能变成永久的。白发的同时特别累、比平时怕冷、体重上升、便秘:医生可能会查甲状腺。白发长在一块变白的皮肤上,或皮肤上的白斑越来越多:去皮肤科,看是不是白癜风。头发突然大片变白,或同时成片脱落:去皮肤科分辨。孩子出现白发,或家里没人早白、自己很年轻就白了不少:告诉医生,可以查 B12、叶酸和甲状腺。
这一篇是科普,不替代诊断。
参考文献 · 12
- Kumar, A. B., Shamim, H., & Nagaraju, U. (2018). Premature graying of hair: review with updates. International Journal of Trichology, 10(5), 198-203. Narrative review. Premature graying is defined as graying before 20 years in Caucasians and before 30 years in African Americans (average onset 34 and 43.9 years); hair is pigmented only in anagen, melanogenesis is switched off in catagen and absent in telogen; a definition for Asian populations is lacking, and some authors suggest 25 years for the Indian subcontinent; each bulb melanocyte serves about 5 keratinocytes versus 36 in the epidermis; white hair lacks melanosomes, grey hair has sparse ones. Associations reported, mostly from small case-control or older studies: vitamin B12 deficiency (about 55% of patients with pernicious anemia grayed before 50 versus 30% of controls), low thyroid hormone, vitiligo, smoking, lower copper in one study that did not find lower zinc or iron, and lower ferritin, calcium and vitamin D3 in a study of young Indians; the exact cause remains unknown. Treatment should address the cause (B12 or thyroid replacement); vitamins and minerals such as biotin, calcium pantothenate, zinc, copper and selenium have not given promising results; hair dyes remain the main option, and some people get irritant dermatitis (commonly from p-phenylenediamine) or hair loss from dyeing. Some authors suggest testing serum B12, folic acid and thyroid in people with no family history of premature graying. Sudden whitening (canities subita) has been associated with alopecia areata, telogen effluvium, vitiligo and psychogenic causes. 10.4103/ijt.ijt_47_18
- O'Sullivan, J. D. B., Nicu, C., Picard, M., Chéret, J., Bedogni, B., Tobin, D. J., & Paus, R. (2021). The biology of human hair greying. Biological Reviews, 96(1), 107-128. Narrative review. Human greying invariably begins with a gradual decline in melanogenesis in the anagen hair bulb (reduced tyrosinase activity, defective melanosome transfer, apoptosis of bulb melanocytes), so it is a primary event of the bulb, not the bulge; eventually the bulge melanocyte stem cell pool becomes depleted as well, at which stage greying becomes largely irreversible. Oxidative damage likely is a crucial driver. But there is still no universally accepted model of human hair greying, the extent of genetic contributions remains unclear, and how psychoemotional stress impacts the process, and how to retard or reverse greying, are open questions. 10.1111/brv.12648
- Nishimura, E. K., Granter, S. R., & Fisher, D. E. (2005). Mechanisms of hair graying: incomplete melanocyte stem cell maintenance in the niche. Science, 307(5710), 720-724. Using melanocyte-tagged transgenic mice and aging human hair follicles, hair graying is caused by defective self-maintenance of melanocyte stem cells in the bulge niche; physiologic aging of melanocyte stem cells was associated with ectopic pigmentation or differentiation within the niche (the reserve cells mature where they should stay dormant), accelerated by Mitf mutation, and Bcl2 deficiency causes selective apoptosis of the stem cells. Mostly mouse genetics; the human part is histology of aging follicles, not an intervention. 10.1126/science.1099593
- Rosenberg, A. M., Rausser, S., Ren, J., Mosharov, E. V., Sturm, G., Ogden, R. T., Patel, P., Kumar Soni, R., Lacefield, C., Tobin, D. J., Paus, R., & Picard, M. (2021). Quantitative mapping of human hair greying and reversal in relation to life stress. eLife, 10, e67437. 397 hairs from 14 healthy donors (aged 9-65) were profiled for pigment along their length. White/grey hairs that naturally regain pigmentation were found across sex, ethnicities, ages and body regions; greying and reversal can occur in parallel with self-reported psychological stressors; grey hairs upregulated proteins of energy metabolism, mitochondria and antioxidant defenses; a computational model suggests a threshold-based mechanism for temporary reversibility, most likely in hairs near their greying threshold. A small descriptive study: it shows that reversal happens and can coincide with stress, not that stress causes greying or how common reversal is. 10.7554/eLife.67437
- Sun, Q., Lee, W., Hu, H., Ogawa, T., De Leon, S., Katehis, I., Lim, C. H., Takeo, M., Cammer, M., Taketo, M. M., Gay, D. L., Millar, S. E., & Ito, M. (2023). Dedifferentiation maintains melanocyte stem cells in a dynamic niche. Nature, 616(7958), 774-782. In mice, live imaging, single-cell RNA sequencing and lineage tracing showed that most melanocyte stem cells move between the hair follicle stem cell and transit-amplifying compartments and reversibly change differentiation state under local cues such as WNT; the system is maintained by reverted cells rather than a reserve exempt from change. During ageing, stranded stem cells accumulate that no longer contribute melanocyte progeny. The authors suggest modulating stem-cell mobility as a possible approach to preventing greying; nothing was tested in people. 10.1038/s41586-023-05960-6
- Wood, J. M., Decker, H., Hartmann, H., Chavan, B., Rokos, H., Spencer, J. D., Hasse, S., Thornton, M. J., Shalbaf, M., Paus, R., & Schallreuter, K. U. (2009). Senile hair graying: H2O2-mediated oxidative stress affects human hair color by blunting methionine sulfoxide repair. FASEB Journal, 23(7), 2065-2075. Human gray/white scalp hair shafts accumulate hydrogen peroxide in millimolar concentrations (FT-Raman in vivo); catalase and methionine sulfoxide reductase A and B protein are almost absent in the gray hair follicle; oxidation of methionine residues, including Met 374 in the active site of tyrosinase, limits the enzyme and leads to gradual loss of hair color. The authors frame this as support for a long-voiced but insufficiently proven concept; L-methionine prevented the oxidation only in vitro, and no treatment was tested in people. 10.1096/fj.08-125435
- Zhang, B., Ma, S., Rachmin, I., He, M., Baral, P., Choi, S., Gonçalves, W. A., Shwartz, Y., Fast, E. M., Su, Y., Zon, L. I., Regev, A., Buenrostro, J. D., Cunha, T. M., Chiu, I. M., Fisher, D. E., & Hsu, Y.-C. (2020). Hyperactivation of sympathetic nerves drives depletion of melanocyte stem cells. Nature, 577(7792), 676-681. In mice, restraint stress, chronic unpredictable stress and pain induced by resiniferatoxin all produced white hairs. The stress-induced loss of melanocyte stem cells was independent of immune attack or adrenal stress hormones: sympathetic nerves innervating the niche release a burst of noradrenaline that drives quiescent melanocyte stem cells to proliferate rapidly, then differentiate, migrate and be permanently depleted. After resiniferatoxin many follicles lost their stem cells within 5 days while the existing coat stayed black; transient suppression of stem-cell proliferation prevented greying. Mouse study; noradrenaline also switched on proliferation and differentiation genes in cultured human melanocytes, but greying in people was not studied. 10.1038/s41586-020-1935-3
- Adhikari, K., Fontanil, T., Cal, S., Mendoza-Revilla, J., Fuentes-Guajardo, M., Chacón-Duque, J. C., et al. (2016). A genome-wide association scan in admixed Latin Americans identifies loci influencing facial and scalp hair features. Nature Communications, 7, 10815. Genome-wide association scan in over 6,000 Latin Americans; reported the first locus for hair greying, SNP rs12203592 in IRF4, a gene that works with MITF in switching on tyrosinase, the key enzyme of melanin synthesis; age was the trait most correlated with greying (r = 0.56). An association study: it finds one locus, and does not say how much of greying is genetic. 10.1038/ncomms10815
- National Institute of Diabetes and Digestive and Kidney Diseases. (2020). Polygonum multiflorum. In LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. Bethesda, MD: NIDDK. Likelihood score A; latency a few days to ~6 months; ~10% of clinically apparent cases were fatal or required urgent liver transplantation. www.ncbi.nlm.nih.gov/books/NBK548795
- NHS. (2025). Hair dye reactions. Many permanent and some semi-permanent hair dyes contain PPD (paraphenylenediamine), which can irritate the skin or cause an allergic reaction; for a mild reaction stop using the dye and wash it off, and a pharmacist or GP can help. Call 999 if your lips, mouth, throat or tongue suddenly become swollen, you are breathing very fast or struggling to breathe, your throat feels tight or you are struggling to swallow, or your skin, tongue or lips turn blue, grey or pale (page last reviewed 29 December 2025). www.nhs.uk/conditions/hair-dye-reactions
- NHS. (2023). Vitamin B12 or folate deficiency anaemia: symptoms. Symptoms usually develop gradually and include feeling weak or tired, shortness of breath, headaches, palpitations, a sore or red tongue sometimes with mouth ulcers, and problems with memory; vitamin B12 deficiency can also cause neurological symptoms including numbness, pins and needles, muscle weakness, and problems with balance and coordination. See a GP if you have these symptoms; diagnosis and treatment as soon as possible matters, because some problems can be irreversible if left untreated. www.nhs.uk/conditions/vitamin-b12-or-folate-deficiency-anaemia/symptoms
- NHS. (2025). Underactive thyroid (hypothyroidism): symptoms. Symptoms may be mild and hard to notice; common symptoms include extreme tiredness, feeling cold more than usual, weight gain, constipation, difficulty concentrating, low mood. www.nhs.uk/conditions/underactive-thyroid-hypothyroidism/symptoms