Place · Level 3
Hashimoto's Thyroiditis
免疫系统认错了人, 把自家甲状腺当外敌, 一年年打成甲减。硒和碘是它的两个矿物——补对是帮手, 补过是帮凶; 麸质、十字花科的戒口大多被吓大了。药怎么吃、化验单怎么读, 这一岛讲明白。
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Chapter 1
What is Hashimoto's
What is Hashimoto's
Hashimoto's thyroiditis (HT) is one of the most common autoimmune diseases and the leading cause of hypothyroidism in developed countries:
Globally, 5–15% of women and 1–3% of men have positive anti-TPO / anti-Tg antibodiesPeak onset: women 30–60 years oldGenetic predisposition: a first-degree relative being positive raises risk roughly 5–10×
Core mechanism: the immune system mistakes thyroid peroxidase (thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake.) and thyroglobulin (Tg) for foreign threats, producing anti-TPO + anti-Tg antibodies; T cells infiltrate thyroid tissue, driving chronic inflammation; thyroid cells are slowly destroyed; T4/T3 synthesis capacity drops; eventually thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. rises and free T4 falls, producing hypothyroid symptoms.
Typical symptoms (often misattributed to 'aging' or 'depression'):
Persistent fatigue / sleepiness (even after 8–9 hours of sleep)Cold intolerance (you feel cold when others don't)Slow weight gain (diet and exercise unchanged)Dry skin / thinning hair / brittle nailsConstipationMenstrual irregularity (heavy flow / long cycles)Low mood / poor focus / brain fogSlow heart rate / low blood pressureMuscle aches / joint stiffness
Hashimoto ≠ hypothyroidism
Hashimoto is the cause (autoimmunity); hypothyroidism is the functional state (high TSH + low T4)Hashimoto can exist for years without hypothyroidism (subclinical, antibodies only), or eventually progress to lifelong hypothyroidismConversely, hypothyroidism isn't always Hashimoto — it can also be congenital, iodine deficiency, post-surgical, drug-induced, or pituitary
Why does it get its own atlas island?
This is the bridge between Atlas and the health report — the report engine's `hashimoto` rule and the 'strict gluten-free AIP for Hashimoto' debunking matrix both point here. It's also the most classic case of 'single nutrient ≠ single answer': Hashimoto simultaneously involves Se, I, D, Fe, gluten, and autoimmune modulation. 'What should I supplement for Hashimoto?' can't be answered by any single nutrient.
Globally, 5–15% of women and 1–3% of men have positive anti-TPO / anti-Tg antibodiesPeak onset: women 30–60 years oldGenetic predisposition: a first-degree relative being positive raises risk roughly 5–10×
Core mechanism: the immune system mistakes thyroid peroxidase (thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake.) and thyroglobulin (Tg) for foreign threats, producing anti-TPO + anti-Tg antibodies; T cells infiltrate thyroid tissue, driving chronic inflammation; thyroid cells are slowly destroyed; T4/T3 synthesis capacity drops; eventually thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. rises and free T4 falls, producing hypothyroid symptoms.
Typical symptoms (often misattributed to 'aging' or 'depression'):
Persistent fatigue / sleepiness (even after 8–9 hours of sleep)Cold intolerance (you feel cold when others don't)Slow weight gain (diet and exercise unchanged)Dry skin / thinning hair / brittle nailsConstipationMenstrual irregularity (heavy flow / long cycles)Low mood / poor focus / brain fogSlow heart rate / low blood pressureMuscle aches / joint stiffness
Hashimoto ≠ hypothyroidism
Hashimoto is the cause (autoimmunity); hypothyroidism is the functional state (high TSH + low T4)Hashimoto can exist for years without hypothyroidism (subclinical, antibodies only), or eventually progress to lifelong hypothyroidismConversely, hypothyroidism isn't always Hashimoto — it can also be congenital, iodine deficiency, post-surgical, drug-induced, or pituitary
Why does it get its own atlas island?
This is the bridge between Atlas and the health report — the report engine's `hashimoto` rule and the 'strict gluten-free AIP for Hashimoto' debunking matrix both point here. It's also the most classic case of 'single nutrient ≠ single answer': Hashimoto simultaneously involves Se, I, D, Fe, gluten, and autoimmune modulation. 'What should I supplement for Hashimoto?' can't be answered by any single nutrient.
人群 · 症状清单
桥本氏甲状腺炎 (Hashimoto's thyroiditis, HT) 是最常见的自体免疫疾病之一, 也是发达国家甲状腺功能减退 (甲减) 的首要原因:全球女性 5-15%、男性 1-3% 抗 thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. / 抗 Tg 抗体阳性发病高峰: 30-60 岁女性遗传倾向: 一级亲属阳性时风险约升 5-10 倍
典型症状 (常被误以为是老化或抑郁):
持续疲倦、嗜睡 (即使睡了 8-9 小时)怕冷 (别人不冷你冷)体重缓慢增加 (饮食运动没变)皮肤干燥、头发稀疏、指甲脆便秘月经异常 (经量多 / 周期长)情绪低落、注意力差、脑雾心率慢、血压低肌肉酸痛、关节僵硬
这些症状单看每一条都平平无奇, 放在一起才有意义: 它们全是甲状腺激素这个油门变小之后的下游表现——产热少了所以怕冷, 肠道蠕动慢了所以便秘, 心跳慢了所以血压偏低, 皮肤和毛囊的更新也跟着拖慢。
桥本 ≠ 甲减
桥本是病因 (自体免疫), 甲减是功能状态 (thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. 高 + T4 低)桥本可以多年没有甲减 (亚临床期, 仅抗体阳性), 也可能最终发展为终身性甲减反过来, 甲减不一定是桥本 — 也可能是先天、缺碘、手术后、药物诱导、垂体性
Diagnosis · antibodies + function + ultrasound
Confirming Hashimoto requires1. Antibodies:
Anti-thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. (TPOAb): positive in ~90% of Hashimoto patients, highly Hashimoto-specificAnti-Tg (TgAb): 60–80% positive, slightly lower specificity2. Thyroid function:
TSH (thyroid-stimulating hormone): the most sensitive screen; Hashimoto: TSH elevated (subclinical 4.5–10 mU/L, overt >10)Free T4 (FT4): in Hashimoto progression goes normal → low-normal → frankly lowFree T3 (FT3): not routinely needed, consider only if symptoms don't match TSH/FT43. Ultrasound (optional):
Diffuse hypoechogenicity + heterogeneity + pseudonodules are typical Hashimoto findingsMainly used to rule out nodular disease
Antibody positive + normal function — what to do?
This is subclinical Hashimoto — most stay stable, a fraction progress yearly to hypothyroidismCheck TSH every 6–12 months to monitor progressionNo medication or AIP diet needed; Se, I, D, Fe status worth attention
thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. 5–10 mU/L + antibody positive — what to do?
This is subclinical hypothyroidismTSH >10 or symptomatic: endocrinology will consider levothyroxineTSH 4.5–7 + asymptomatic + not preconception: usually observation + recheckPreconception / pregnancy + TSH >2.5: guidelines usually start treatment even without symptoms (ATA 2017)
Practical:
First visit: endocrinology or family doctor; self-check (symptoms + family history)First panel: TSH + FT4 + anti-TPO; optional: anti-Tg + ultrasoundIf pregnant / preconception: recheck TSH in the first 12 weeks
Chapter 2
Se + I — thyroid's two minerals
Se + I — thyroid's two minerals
The thyroid chemistry workshop depends on two minerals + a pair of opposing forces:
Iodine (I): the structural atom of T4 / T3 — no iodine = no thyroid hormone (T4 = 4 iodines, T3 = 3 iodines)
Deficiency: hypothyroidism / goiter (compensatory hypertrophy)Excess: raising population iodine intake makes more people turn antibody-positive — Denmark's two matched national surveys around a cautious iodisation programme saw thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake.-Ab positivity go from 14.3% to 23.8%, mostly in young women and at low titres (Pedersen 2011). ⚠️ That is a different claim from 'already-positive people progress faster', which this line used to attribute to the same study; that endpoint is not in itKey point: Hashimoto patients don't need iodine supplementation and shouldn't take chronic high-iodine (avoid daily large amounts of kelp / nori / spirulina; iodized salt is fine)
Selenium (Se): core cofactor of GPx (glutathione peroxidase) + deiodinases (DIO1/2/3)
Mechanisms:GPx clears H₂O₂ byproducts in thyroid cells (TPO produces H₂O₂ when synthesizing T4; high concentrations damage cells)Deiodinases convert T4 → T3 (T3 is the active hormone)Selenoprotein P provides immune modulationHashimoto RCT (Toulis 2010 meta): 200 μg/day Se × 8–12 weeks, anti-TPO antibodies drop ~40% (vs placebo ~10%)Clinical meaning: antibody drop doesn't equal disease reversal, but signals easing inflammation; long-term effect unknown⚠️ Widely mis-told: the 400 in SELECT is the vitamin E dose in IU; its selenium arm was 200 μg/day, and its diabetes signal was not significant (RR 1.07, P = .16). The significant harm signals come from other trials at that same 200 μg/day — type 2 diabetes HR 1.55 (1.03-2.33), concentrated in the highest baseline-selenium tertile (Stranges 2007), and squamous cell carcinoma HR 1.25 (1.03-1.51) (Duffield-Lillico 2003). 400 μg/day is the tolerable upper intake level, not a trial-observed harm threshold
Practical:
Se 100–200 μg/day from Brazil nuts (1–2/day) / fish / eggs / whole grains; no need for chronic supplementationI: mainly through iodized salt + occasional seaweed; no chronic kelp tabletsIf inland + no seafood: iodized salt to ensure 150 μg/day (RDA)
On 'Hashimoto must avoid all iodine': this is overstated. Ordinary daily iodine intake (iodized salt + occasional seafood) is safe; what to actually avoid is chronic high-dose iodine pills and daily large amounts of kelp / nori.
Iodine (I): the structural atom of T4 / T3 — no iodine = no thyroid hormone (T4 = 4 iodines, T3 = 3 iodines)
Deficiency: hypothyroidism / goiter (compensatory hypertrophy)Excess: raising population iodine intake makes more people turn antibody-positive — Denmark's two matched national surveys around a cautious iodisation programme saw thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake.-Ab positivity go from 14.3% to 23.8%, mostly in young women and at low titres (Pedersen 2011). ⚠️ That is a different claim from 'already-positive people progress faster', which this line used to attribute to the same study; that endpoint is not in itKey point: Hashimoto patients don't need iodine supplementation and shouldn't take chronic high-iodine (avoid daily large amounts of kelp / nori / spirulina; iodized salt is fine)
Selenium (Se): core cofactor of GPx (glutathione peroxidase) + deiodinases (DIO1/2/3)
Mechanisms:GPx clears H₂O₂ byproducts in thyroid cells (TPO produces H₂O₂ when synthesizing T4; high concentrations damage cells)Deiodinases convert T4 → T3 (T3 is the active hormone)Selenoprotein P provides immune modulationHashimoto RCT (Toulis 2010 meta): 200 μg/day Se × 8–12 weeks, anti-TPO antibodies drop ~40% (vs placebo ~10%)Clinical meaning: antibody drop doesn't equal disease reversal, but signals easing inflammation; long-term effect unknown⚠️ Widely mis-told: the 400 in SELECT is the vitamin E dose in IU; its selenium arm was 200 μg/day, and its diabetes signal was not significant (RR 1.07, P = .16). The significant harm signals come from other trials at that same 200 μg/day — type 2 diabetes HR 1.55 (1.03-2.33), concentrated in the highest baseline-selenium tertile (Stranges 2007), and squamous cell carcinoma HR 1.25 (1.03-1.51) (Duffield-Lillico 2003). 400 μg/day is the tolerable upper intake level, not a trial-observed harm threshold
Practical:
Se 100–200 μg/day from Brazil nuts (1–2/day) / fish / eggs / whole grains; no need for chronic supplementationI: mainly through iodized salt + occasional seaweed; no chronic kelp tabletsIf inland + no seafood: iodized salt to ensure 150 μg/day (RDA)
On 'Hashimoto must avoid all iodine': this is overstated. Ordinary daily iodine intake (iodized salt + occasional seafood) is safe; what to actually avoid is chronic high-dose iodine pills and daily large amounts of kelp / nori.
碘 · 桥本要不要戒
但碘绝不是越多越好。把碘往上推, 人群里查出抗体的人会变多: 丹麦在谨慎加碘前后做过两次同样的全国抽样, 尿碘中位数只是从轻度缺碘升到刚够, 四五年后抗 thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. 阳性率就从 14.3% 升到 23.8%, 涨得最明显的是年轻女性和低滴度那一档 (Pedersen 2011)。⚠️ 注意它测的是更多人变成抗体阳性, 不是已经阳性的人走得更快 —— 后一句站内此前写成了同一项研究的结论, 但那项研究里没有这个终点。所以桥本患者不需要额外补碘, 也别长期高碘: 加碘盐照吃没问题, 真正要躲的是天天大把海带、紫菜、螺旋藻。为什么偏偏是抗体已经阳性的人怕碘? 碘要挂上激素, 得先在甲状腺细胞里被 TPO 氧化, 而这一步本身就在制造氧化压力和双氧水。腺体已经在慢性发炎、清洁工 (GPx) 又不够用的时候, 灌进去的碘越多, 被氧化压力伤到的甲状腺细胞就越多, 免疫系统能捡到的自家碎片也越多——攻击于是更有的放矢。
碘主要靠加碘盐, 偶尔海产点缀, 别把浓缩海带片当保健品天天吃。如果你住内陆、又基本不碰海鲜, 那就靠加碘盐把每天 150 μg (推荐量) 兜住。
最后拆一个常听到的说法: 桥本必须彻底戒碘。这话说过头了。日常那点碘 (加碘盐加偶尔海产) 是安全的, 真正该避开的只是长期大剂量碘补片、和天天成把的海带紫菜。
硒 · 证据与安全窗
硒在甲状腺里还有第三份活: 通过一种叫硒蛋白 P 的分子帮着调节免疫——这也是它和桥本这种自体免疫病扯上关系的那一环。补硒对桥本到底管不管用? 眼下最像样的证据是 Toulis 2010 的一篇汇总: 每天 200 μg 硒吃 8-12 周, 抗 thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. 抗体大约降 40% (安慰剂组只降 10% 左右)。但得泼盆冷水——抗体降了不等于病好了, 只能说炎症消停了些, 长期到底改不改命还不知道。
为什么抗体降了不等于病好了? 抗体是免疫在攻击留下的痕迹, 不是甲状腺产能的读数。真正决定你怕不怕冷、犯不犯困的是激素够不够用, 那要看 thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. 和游离 T4; 抗体掉了一截而 TSH 纹丝不动, 是完全可能的。
而且硒的安全窗特别窄。这里有一个很多科普都讲反了的地方, 值得停一下: SELECT 试验里那个 400 是维生素 E 的 IU 数, 它的硒剂量是 200 μg, 而且它测到的糖尿病风险不显著 (RR 1.07, P = .16)。真正显著的信号来自另外两项试验, 而它们用的也是 200 μg/天 —— 正好是常被称作甜点区的那个量: NPC 试验里 2 型糖尿病 HR 1.55 (1.03-2.33), 且集中在基线硒本来就够的那三分之一人群 (Stranges 2007); 同一批人里鳞状细胞癌 HR 1.25 (1.03-1.51) (Duffield-Lillico 2003)。
400 μg/天是可耐受最高摄入量 (UL), 不是某个试验测出来的危害线。 所以正确的读法不是别超过 400 就安全, 而是: 硒本来就不缺的人, 补到 200 μg 也未必是净收益。
落到日常: 硒每天 100-200 μg, 巴西果吃 1-2 颗、或者从鱼、蛋、全谷里拿就够, 不必常年吞硒片。
Other nutrients · D / Fe / Zn
Other nutrients beyond Se + I:Vitamin D:
Hashimoto patients commonly have low serum 25-hydroxyvitamin D: The storage form of vitamin D in blood — the number measured to check D status. (multiple meta-analyses)Mechanism: vitamin D receptor: The cellular 'socket' that vitamin D plugs into to carry out its instructions. regulates Treg / Th17 balance, influencing autoimmunityD RCT effects on antibodies are mixed — some show drops, some show nonePractical: test 25(OH)D once; <20 ng/mL — supplement 1000–4000 IU/day; 30–50 ng/mL maintenance
Iron (ferritin):
Hashimoto + iron deficiency is very common (especially reproductive-age women with heavy periods)Low iron impairs thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. activity (TPO is a heme enzyme); even during treatment, low iron blunts levothyroxine effectTarget: ferritin >70 ng/mL (general 30 is enough, but Hashimoto + hair loss + fatigue justify higher)
Zinc (Zn):
Zn is a cofactor of deiodinases + thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. receptorClinical impact small, normal diet is enough — no need for extra supplementation
B12 + folate:
Hashimoto co-occurs with atrophic gastritis + pernicious anemia at ~10–15% (both autoimmune)If fatigue + Hashimoto → add B12 + homocysteine check
On 'Hashimoto superfood' marketing:
There is no such thing as a Hashimoto superfoodChia seeds / blueberries / matcha / mushroom powder have no Hashimoto-specific evidenceMediterranean style + adequate protein + diverse colored fruits and vegetables is more effective for Hashimoto than any 'superfood'
Red flags about iodine supplements:
Any 'Hashimoto / thyroid support' supplement containing >150 μg iodine: check the label — many do, and may accelerate progressionConcentrated kelp tablets contain 1000–5000+ μg iodine per tablet; Hashimoto patients should not take them chronically
Chapter 3
Diet myths · gluten/AIP/cruciferous
Diet myths · gluten/AIP/cruciferous
Three big Hashimoto diet myths (debunked in order of evidence strength):
Myth 1: All Hashimoto must be strictly gluten-free
Reality: Hashimoto + celiac co-occurrence is 5–10% (slightly above the 1% population baseline) — doesn't mean every Hashimoto patient must avoid glutenIf your Hashimoto coexists with celiac: strict gluten-free is required; gluten continuously triggers immunityIf you only have non-celiac gluten sensitivity (NCGS): evidence is mixed; some report subjective improvement, but RCT design is weakShould Hashimoto patients without a celiac diagnosis avoid gluten? No strong evidence supports it; you can try a 3-month elimination, then judge subjectively
Recommendation: first test anti-tTG IgA + total IgA + small bowel biopsy if needed to confirm celiac status, then decide whether to go strict GF. Strict gluten-free has costs of its own: higher-GI processed foods / nutrient imbalance risk / social cost / financial cost — don't take it on unnecessarily.
Myth 2: Hashimoto must do AIP (autoimmune paleo)
AIP: eliminate all grains + legumes + nightshades + eggs + dairy + nuts + sugar + caffeine + processed foods for several weeks, then reintroduce item by itemHashimoto AIP clinical evidence: one open-label single-arm study, n=17 (Abbott 2019). Self-reported symptoms and quality of life improved, while thyroid function and thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. / Tg antibodies were all retested and none changed significantly. No control arm, and the intervention was a 10-week multidisciplinary online health-coaching programme, not the diet aloneTruth: AIP works for self-reported symptoms, likely because it removes processed foods and adds produce — not an AIP-specific effectSide effects: severe restriction can cause nutrient gaps (Ca / D / fiber / iron) + tendency toward eating disorders + social isolationRecommendation: if doing AIP, limit it to 4–8 weeks, with physician / dietitian guidance, systematic reintroduction after
Myth 3: Hashimoto can't eat cruciferous vegetables (broccoli / cabbage / cauliflower)
Cruciferous contain goitrogens, which can suppress TPO iodine uptakeBut with daily cooking + sufficient iodine, this doesn't pose a clinical problem1–2 servings of steamed/cooked cruciferous per day is safeThe real problem scenario: raw + large amounts + iodine-deficient background + Hashimoto could theoretically worsen things; but cooking destroys 80–90% of goitrogensThe health benefits of cruciferous (sulforaphane / anti-inflammatory / fiber) far outweigh the theoretical thyroid risk
Actual 'Hashimoto diet' recommendations:
Mediterranean style: vegetables + fish + whole grains + olive oil + moderate red wine + adequate proteinAvoid: ultra-processed foods + heavy refined sugar + trans fatsMaintain: protein 1.0–1.2 g/kg/day + fiber 25–40 gIndividualize: if specific foods clearly make you feel worse, exclude them individually — no need to eliminate whole food groups
Myth 1: All Hashimoto must be strictly gluten-free
Reality: Hashimoto + celiac co-occurrence is 5–10% (slightly above the 1% population baseline) — doesn't mean every Hashimoto patient must avoid glutenIf your Hashimoto coexists with celiac: strict gluten-free is required; gluten continuously triggers immunityIf you only have non-celiac gluten sensitivity (NCGS): evidence is mixed; some report subjective improvement, but RCT design is weakShould Hashimoto patients without a celiac diagnosis avoid gluten? No strong evidence supports it; you can try a 3-month elimination, then judge subjectively
Recommendation: first test anti-tTG IgA + total IgA + small bowel biopsy if needed to confirm celiac status, then decide whether to go strict GF. Strict gluten-free has costs of its own: higher-GI processed foods / nutrient imbalance risk / social cost / financial cost — don't take it on unnecessarily.
Myth 2: Hashimoto must do AIP (autoimmune paleo)
AIP: eliminate all grains + legumes + nightshades + eggs + dairy + nuts + sugar + caffeine + processed foods for several weeks, then reintroduce item by itemHashimoto AIP clinical evidence: one open-label single-arm study, n=17 (Abbott 2019). Self-reported symptoms and quality of life improved, while thyroid function and thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. / Tg antibodies were all retested and none changed significantly. No control arm, and the intervention was a 10-week multidisciplinary online health-coaching programme, not the diet aloneTruth: AIP works for self-reported symptoms, likely because it removes processed foods and adds produce — not an AIP-specific effectSide effects: severe restriction can cause nutrient gaps (Ca / D / fiber / iron) + tendency toward eating disorders + social isolationRecommendation: if doing AIP, limit it to 4–8 weeks, with physician / dietitian guidance, systematic reintroduction after
Myth 3: Hashimoto can't eat cruciferous vegetables (broccoli / cabbage / cauliflower)
Cruciferous contain goitrogens, which can suppress TPO iodine uptakeBut with daily cooking + sufficient iodine, this doesn't pose a clinical problem1–2 servings of steamed/cooked cruciferous per day is safeThe real problem scenario: raw + large amounts + iodine-deficient background + Hashimoto could theoretically worsen things; but cooking destroys 80–90% of goitrogensThe health benefits of cruciferous (sulforaphane / anti-inflammatory / fiber) far outweigh the theoretical thyroid risk
Actual 'Hashimoto diet' recommendations:
Mediterranean style: vegetables + fish + whole grains + olive oil + moderate red wine + adequate proteinAvoid: ultra-processed foods + heavy refined sugar + trans fatsMaintain: protein 1.0–1.2 g/kg/day + fiber 25–40 gIndividualize: if specific foods clearly make you feel worse, exclude them individually — no need to eliminate whole food groups
三条迷思 · 逐条拆
桥本饮食营销的三大迷思 (按证据强度排序拆解):迷思 1: 所有桥本必须严格无麸质
现实: 桥本与 celiac 共发率 5-10% (略高于人群基线 1%), 不等于所有桥本都必须戒麸质如果你的桥本同时有 celiac: 应严格戒麸质, 麸质会持续触发免疫如果只是非乳糜泻麸质敏感 (NCGS): 证据混杂; 部分人主观改善, 但 RCT 设计弱桥本但没有 celiac 诊断的人是否要戒麸质? 没有强证据支持; 可以戒 3 月试验, 再判断主观感受
建议: 先查 anti-tTG IgA + 总 IgA + 必要时小肠活检, 确定有没有 celiac, 再决定是否严格无麸质。严格无麸质本身也有成本: 升 GI 食品多、营养失衡风险、社交成本、经济成本; 不必不必要地承担。
迷思 2: 桥本必须 AIP (自体免疫古老饮食)
AIP: 戒所有谷物 + 豆类 + 茄科 + 蛋 + 乳 + 坚果 + 糖 + 咖啡因 + 加工食品, 数周后再逐项引入桥本 AIP 临床证据: 1 个开放标签、单臂、N=17 的小研究 (Abbott 2019): 自报症状与生活质量显著改善, 而甲功与抗 thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. / 抗 Tg 抗体都复测了, 没有任何一项出现统计学显著变化。无对照组; 干预是一整套 10 周多学科线上健康指导, 不只是 AIP 饮食真相: AIP 在改善自报症状上有用, 但很可能是因为消除了加工食品 + 增加蔬果, 不是 AIP 特异性效应副作用: 严重限制饮食可致营养缺口 (Ca / D / 纤维、铁) + 进食障碍倾向 + 社交孤立建议: 如果做 AIP, 限定 4-8 周, 有医生、营养师指导, 完成后系统再引入
迷思 3: 桥本不能吃十字花科 (西兰花、卷心菜、花椰菜)
十字花科含 goitrogens (致甲状腺肿物), 会抑制 TPO 摄碘但日常烹调 + 碘足够时不构成临床问题每天吃 1-2 份蒸/煮十字花科是安全的真正的问题情境: 生吃大量 + 缺碘背景 + 桥本, 理论上会加重; 但烹调破坏 80-90% goitrogens健康十字花科的收益 (sulforaphane / 抗炎、纤维) 远大于理论上的甲状腺风险
桥本饮食的实际建议:
地中海风格: 蔬菜 + 鱼 + 全谷 + 橄榄油 + 适量红酒 + 蛋白足避免: 超加工食品 + 大量精糖 + 反式脂肪保持: 蛋白 1.0-1.2 g/kg/天 + 纤维 25-40 g个体化: 如果某些食物明显让你不舒服, 单独排除; 不必整组戒
Marketing bust · Hashimoto
'Hashimoto must eliminate everything': no evidence — instead manufactures anxiety + raises IBS / eating disorder risk'Selenium more is better': U-shaped curve, 200 μg/day is the sweet spot; chronic >400 μg leads to T2D + hair loss
'Iodine supplement is essential': Hashimoto patients should avoid chronic high-iodine supplementation; most 'thyroid support' supplements contain 100–300 μg iodine, possibly accelerating progression
'Ashwagandha treats Hashimoto': no Hashimoto-specific RCT; ashwagandha can activate the thyroid, and patients in Hashimoto progression / at hyperthyroid risk should avoid it
'Home 24-hour salivary cortisol = adrenal fatigue = Hashimoto root cause': 'adrenal fatigue' isn't a medical diagnosis (Bornstein 2016 JCEM review rejects it); salivary testing largely stays at the marketing level
'Reverse T3 is the key': rT3 doesn't need to be tested in most cases; ATA + AACE guidelines don't recommend routine testing
'Hashimoto can never get pregnant': incorrect. Controlling thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. <2.5 + continuous levothyroxine + folate supplementation + monitoring lets most women conceive and deliver normally; but Hashimoto + pregnancy monitoring is necessary (stricter TSH target during pregnancy)
Evidence-based Hashimoto management:
1. Diagnosis + monitoring: TSH every 6–12 months; more frequently in pregnancy
2. Levothyroxine for overt hypothyroidism + some subclinical cases
3. Adequate Se 100–200 μg/day from food
4. Optimize vitamin D and iron status
5. Mediterranean style + adequate protein
6. Manage stress + sleep
7. If celiac → strict gluten-free
8. Avoid chronic high-iodine supplements
Chapter 4
Labs + levothyroxine timing
Labs + levothyroxine timing
Core lab interpretation:
thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. is the gold standard:
0.4–4.0 mU/L normal (lab-dependent)0.4–2.5 mU/L stricter standard for pregnancy / preconception (ATA 2017)4.5–10: subclinical hypothyroidism>10: overt hypothyroidism, should be treated<0.4: hyperthyroid direction, not the Hashimoto main line (but can occur in early Hashitoxicosis)
Free T4: drops as TSH rises → overt hypothyroidism
Free T3: not routinely checked; rT3 mostly unnecessary
Anti-thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. + anti-Tg: once positive, annual rechecks have low yield — focus on TSH/FT4 for progression
'TSH is normal when I feel terrible — is the test wrong?'
TSH is the laboratory gold standard, not 'how you feel'But physiologically optimal TSH may be narrower for you than the population rangeIf symptoms + mid-range TSH (2.5–4), add FT4 + anti-TPO + B12 / D / iron / sleep / depression screen — other causes may be mimicking hypothyroid presentation
Levothyroxine (Levothyroxine / Synthroid / Euthyrox) administration:
Morning, empty stomach, at least 30–60 minutes before breakfastSeparate by 4 hours from: iron + calcium + milk + magnesium + high-fiber meal + coffee + soy + Mg supplementsLong-term PPI (omeprazole etc.): lower stomach acid may reduce levothyroxine absorption, possibly requiring a higher dose. To be honest about it: the studies here contradict each other, with both positive and negative results, and no reliable figure. So the move is not to self-adjust but to recheck TSH before and after the medication change and let the number decideRecheck TSH every 6–8 weeks to adjust doseDon't randomly stop or reduce — TSH rebounds and symptoms return
Levothyroxine vs T4+T3 (Armour / synthetic):
Most patients do fine on plain T4 (levothyroxine) — the body's own deiodinases convert T4 → T3Adding T3 (liothyronine or natural desiccated thyroid): only considered in some patients with persistent symptoms despite T4 alone; evidence inconsistent (ATA 2014 doesn't strongly recommend)Natural desiccated thyroid (Armour Thyroid): contains T4 + T3 + T2, but dosing instability + most studies show no clear advantage
Pregnancy + Hashimoto:
Target TSH <2.5 mU/L throughout pregnancyLevothyroxine dose typically needs to rise 25–50% in the first trimesterFirst prenatal visit: check TSH + recheck every 4 weeks in the first half, every 6–8 weeks in the second half
thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. is the gold standard:
0.4–4.0 mU/L normal (lab-dependent)0.4–2.5 mU/L stricter standard for pregnancy / preconception (ATA 2017)4.5–10: subclinical hypothyroidism>10: overt hypothyroidism, should be treated<0.4: hyperthyroid direction, not the Hashimoto main line (but can occur in early Hashitoxicosis)
Free T4: drops as TSH rises → overt hypothyroidism
Free T3: not routinely checked; rT3 mostly unnecessary
Anti-thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. + anti-Tg: once positive, annual rechecks have low yield — focus on TSH/FT4 for progression
'TSH is normal when I feel terrible — is the test wrong?'
TSH is the laboratory gold standard, not 'how you feel'But physiologically optimal TSH may be narrower for you than the population rangeIf symptoms + mid-range TSH (2.5–4), add FT4 + anti-TPO + B12 / D / iron / sleep / depression screen — other causes may be mimicking hypothyroid presentation
Levothyroxine (Levothyroxine / Synthroid / Euthyrox) administration:
Morning, empty stomach, at least 30–60 minutes before breakfastSeparate by 4 hours from: iron + calcium + milk + magnesium + high-fiber meal + coffee + soy + Mg supplementsLong-term PPI (omeprazole etc.): lower stomach acid may reduce levothyroxine absorption, possibly requiring a higher dose. To be honest about it: the studies here contradict each other, with both positive and negative results, and no reliable figure. So the move is not to self-adjust but to recheck TSH before and after the medication change and let the number decideRecheck TSH every 6–8 weeks to adjust doseDon't randomly stop or reduce — TSH rebounds and symptoms return
Levothyroxine vs T4+T3 (Armour / synthetic):
Most patients do fine on plain T4 (levothyroxine) — the body's own deiodinases convert T4 → T3Adding T3 (liothyronine or natural desiccated thyroid): only considered in some patients with persistent symptoms despite T4 alone; evidence inconsistent (ATA 2014 doesn't strongly recommend)Natural desiccated thyroid (Armour Thyroid): contains T4 + T3 + T2, but dosing instability + most studies show no clear advantage
Pregnancy + Hashimoto:
Target TSH <2.5 mU/L throughout pregnancyLevothyroxine dose typically needs to rise 25–50% in the first trimesterFirst prenatal visit: check TSH + recheck every 4 weeks in the first half, every 6–8 weeks in the second half
化验单 · 各段怎么读
大致的读法是这样: 多数实验室把 0.4-4.0 mU/L 算正常; 备孕、怀孕的人标准更严, 一般压到 0.4-2.5 (ATA 2017)。落在 4.5-10 之间是亚临床甲减——还没明显症状, 但甲状腺已经在吃力; 超过 10 就是明显甲减, 该治了。反过来低于 0.4 是往甲亢方向走, 不是桥本的主线, 但桥本早期偶尔会先经历一小段甲状腺被打破、激素外漏的甲亢样阶段 (叫桥本毒症 Hashitoxicosis)。thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. 之外, 游离 T4 (Free T4) 会随 TSH 升高而往下掉, 掉到明显偏低就是甲减坐实了; 游离 T3 (Free T3) 和反 T3 (rT3) 大多不用查——网上把 rT3 说得神乎其神, 指南其实并不推荐常规测。至于抗 thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake.、抗 Tg 抗体, 一旦阳性, 年年复查它意义不大: 它证明的是免疫在攻击, 但要看病情走到哪一步, 还是盯 TSH 和 T4。
很多人会问: 我明明浑身难受, TSH 却正常, 是不是化验不准? TSH 是实验室里最硬的指标, 不会因为你难受就撒谎; 但每个人生理上最舒服的那个 TSH 点, 可能比整个人群的正常区间要窄。如果症状明显、TSH 又卡在中段 (2.5-4), 值得再查一下游离 T4、抗 TPO, 顺带看看 B12、维生素 D、铁、睡眠和情绪——很可能是别的毛病在装成甲减。
服药 · 时机与怀孕
真到了要吃药, 药通常是左甲状腺素 (Levothyroxine, 商品名 Synthroid、优甲乐等)——说穿了就是把身体缺的 T4 直接补进去。吃法有几条得记牢:早上空腹吃, 离早饭至少 30-60 分钟。和好几样东西要隔开 4 小时再碰: 铁片、钙片、牛奶、镁、高纤维的一餐、咖啡、豆制品——它们会在肠道里把药拽住, 不让它好好吸收。长期吃抑酸药 (PPI, 比如奥美拉唑) 的人留个心: 胃酸变少可能让药吸收变差。老实说, 这条的研究结论互相打架, 有说影响、有说没影响, 谁也给不出准数。所以别自己加量, 换药前后各测一次 TSH, 让数字说话。调药别急: 每 6-8 周复测一次 TSH, 再决定要不要改剂量。千万别自己停药或减量——TSH 一反弹, 那些怕冷、犯困、脑雾又全回来了。
还有人纠结要不要加 T3、或者换成天然甲状腺片。多数人光靠 T4 (左甲状腺素) 就够了, 因为身体自己的脱碘酶会把 T4 转成有活性的 T3; 只有少数人单吃 T4 症状怎么都压不下去, 才会考虑加一点 T3, 而且证据并不一致 (ATA 2014 并不强推)。天然甲状腺干制剂 (Armour Thyroid) 里 T4、T3、T2 都有, 听着更天然, 但每批剂量飘、稳定性差, 多数研究也没看出它比左甲状腺素强。
怀孕要单独拎出来说。整个孕期 thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. 目标要压在 2.5 以下, 而且左甲状腺素的需求量在头三个月通常就得往上加 25-50%——因为胎儿早期完全靠妈妈供甲状腺激素。所以一确认怀孕就该查 TSH, 前半段大约每 4 周复测一次, 后半段每 6-8 周一次。
Drug interactions · PPI / iron traps
Known drug / food interactions with levothyroxine:Reduce absorption (→ thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. ↑):
Iron supplements (Fe²⁺ chelates levothyroxine)Calcium supplements + milk + high-Ca foodsMagnesium supplementsLong-term PPIs + H2 blockers (evidence inconsistent, no reliable figure; judge by rechecking TSH)Aluminum/Mg antacids (Maalox / Tums)Bile acid binders (cholestyramine)High-fiber meal + soy products (soy milk / tofu)Coffee (immediate effect within ~30 min)
Strategy: morning empty stomach + no food for at least 30–60 min + separated from the above by at least 4 hours
Raise demand (→ need higher dose):
Pregnancy (progesterone + hCG affect SHBG → levothyroxine conversion)Estrogen therapy / oral contraceptives (SHBG ↑ → levothyroxine distribution shifts)SSRI antidepressants (sometimes)Rifampin / phenobarbital / carbamazepine (CYP3A induction accelerates metabolism)
Lower demand (→ need lower dose, otherwise hyperthyroid risk):
CorticosteroidsDopamine
Clinical alerts:
New PPI + Hashimoto: recheck TSH 6–8 weeks later; may need adjustmentPositive pregnancy test: promptly raise dose 25–50% + notify endocrinologyBrand switch: bioequivalence between manufacturers can vary ±15%; recheck TSH
'I can't manage morning dosing — can I take it in the evening?'
Yes, take it on an empty stomach 4 hours after dinner before bedSome studies show evening dosing equivalent to or even better than morning (Bolk 2010 RCT)Consistency + separation from food matters more than the time itself
How to know the dose is right?
TSH in target after 6–8 weeks (general 1–2.5 mU/L on treatment, <2.5 in pregnancy)Symptoms improve (fatigue / body temperature / weight / mood)No hyperthyroid signs (palpitations / sweating / rapid weight loss / anxiety)
singh-2001-calcium-lt4-absorptionwiesner-2021-levothyroxine-food-supplements-review
Chapter 5
Decision tree + red flags
Decision tree + red flags
'I just discovered I'm anti-thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. positive / suspected Hashimoto' — step by step:
Week 1:
See endocrinology or family doctorLabs: thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. + FT4 + anti-TPO + anti-Tg + 25-hydroxyvitamin D: The storage form of vitamin D in blood — the number measured to check D status. + ferritin + B12 + CBCOptional: anti-tTG IgA + total IgA (rule out celiac)Don't start AIP / heavy supplementation / mass elimination on your own
Weeks 2–4 (after results return):
TSH >10 + symptoms: start levothyroxine; recheck in 6 weeksTSH 4.5–10 + asymptomatic: observe 6 months then retest; if fatigue / preconception → treatTSH 4.5–10 + preconception / pregnancy: start treatment (target TSH <2.5)TSH 0.4–4.5 + antibody positive: subclinical phase; monitor + nutrition optimization, no medication needed
Concurrent supplementation:
D <30 ng/mL: 1000–4000 IU/day × 8 weeks then retestFerritin <30 ng/mL: 18–65 mg Fe (per physician, alternate-day Moretti 2015 NEJM protocol) × 8 weeks retestB12 <300 pg/mL + fatigue: 1000 μg/day oral × 4 weeksSe: Brazil nuts 1–2/day, or 100–200 μg supplement × 8–12 weeks (Toulis 2010)
Lifestyle:
Mediterranean-style dietProtein 1.0–1.2 g/kg/day25–40 g fiber dailyStrength training × 2–3/week (maintain muscle, counter metabolic slowdown)Sleep 7–9 hours + stress managementLimit alcohol
Red flags (see a doctor / ER promptly):
HR <50 + temperature <35.5°C + altered consciousness: myxedema coma, immediate ERRapidly enlarging + painful goiter: subacute thyroiditis or other cause, urgent evaluationUnexplained voice change / swallowing difficulty: rule out thyroid cancer nodulePregnancy + TSH >10: requires treatment, affects fetal neurodevelopmentExtreme anxiety / palpitations / rapid weight loss: rule out early Hashitoxicosis or concurrent Graves'
'Is Hashimoto lifelong?'
Antibodies typically persist, but disease activity can fluctuateOn hormone replacement, most people have normal function + normal lifeA few have spontaneous remission and no longer need medication (case reports)The focus isn't 'cure' but 'good control': TSH in target + symptom management + cardiovascular / bone / reproductive health monitoring
Week 1:
See endocrinology or family doctorLabs: thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. + FT4 + anti-TPO + anti-Tg + 25-hydroxyvitamin D: The storage form of vitamin D in blood — the number measured to check D status. + ferritin + B12 + CBCOptional: anti-tTG IgA + total IgA (rule out celiac)Don't start AIP / heavy supplementation / mass elimination on your own
Weeks 2–4 (after results return):
TSH >10 + symptoms: start levothyroxine; recheck in 6 weeksTSH 4.5–10 + asymptomatic: observe 6 months then retest; if fatigue / preconception → treatTSH 4.5–10 + preconception / pregnancy: start treatment (target TSH <2.5)TSH 0.4–4.5 + antibody positive: subclinical phase; monitor + nutrition optimization, no medication needed
Concurrent supplementation:
D <30 ng/mL: 1000–4000 IU/day × 8 weeks then retestFerritin <30 ng/mL: 18–65 mg Fe (per physician, alternate-day Moretti 2015 NEJM protocol) × 8 weeks retestB12 <300 pg/mL + fatigue: 1000 μg/day oral × 4 weeksSe: Brazil nuts 1–2/day, or 100–200 μg supplement × 8–12 weeks (Toulis 2010)
Lifestyle:
Mediterranean-style dietProtein 1.0–1.2 g/kg/day25–40 g fiber dailyStrength training × 2–3/week (maintain muscle, counter metabolic slowdown)Sleep 7–9 hours + stress managementLimit alcohol
Red flags (see a doctor / ER promptly):
HR <50 + temperature <35.5°C + altered consciousness: myxedema coma, immediate ERRapidly enlarging + painful goiter: subacute thyroiditis or other cause, urgent evaluationUnexplained voice change / swallowing difficulty: rule out thyroid cancer nodulePregnancy + TSH >10: requires treatment, affects fetal neurodevelopmentExtreme anxiety / palpitations / rapid weight loss: rule out early Hashitoxicosis or concurrent Graves'
'Is Hashimoto lifelong?'
Antibodies typically persist, but disease activity can fluctuateOn hormone replacement, most people have normal function + normal lifeA few have spontaneous remission and no longer need medication (case reports)The focus isn't 'cure' but 'good control': TSH in target + symptom management + cardiovascular / bone / reproductive health monitoring
两周计划 · 查什么
我刚发现抗 thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. 阳性、桥本疑似一步一步怎么做:第 1 周:
看内分泌或家庭医生化验: thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. + FT4 + 抗 TPO + 抗 Tg + 25-hydroxyvitamin D: The storage form of vitamin D in blood — the number measured to check D status. + ferritin + B12 + 全血细胞可选: anti-tTG IgA + 总 IgA (排 celiac)不要自己开始 AIP / 大量补片、戒一切
第 2-4 周 (结果回来后):
TSH > 10 + 症状: 启动左甲状腺素; 6 周后复测TSH 4.5-10 + 无症状: 观察 6 月再测; 若有疲倦、备孕 → 治疗TSH 4.5-10 + 备孕、怀孕: 应启动治疗 (目标 TSH < 2.5)TSH 0.4-4.5 + 抗体阳性: 亚临床期; 监测 + 营养优化, 不需药物
伴随补:
D < 30 ng/mL: 1000-4000 IU/天 × 8 周复测Ferritin < 30 ng/mL: 18-65 mg Fe (按医生指示, 隔天 Moretti 2015 NEJM 方案) × 8 周复测B12 < 300 pg/mL + 疲倦: 1000 μg/天 口服 4 周Se: 巴西果 1-2 颗/天 或 100-200 μg 补片 8-12 周 (Toulis 2010)
生活方式:
地中海风格饮食蛋白 1.0-1.2 g/kg/天每天 25-40 g 纤维力量训练 ×2-3/周 (维持肌肉, 抗代谢减速)睡眠 7-9 小时 + 压力管理限酒
桥本就是终身的吗?
抗体阳性常持续, 但疾病活跃度可以波动在激素治疗下, 大多数人功能正常 + 正常生活少数人自然缓解到不需要药物 (个例)重点不在彻底根除, 而在好控制: TSH 在目标 + 症状管理 + 心血管、骨骼、生殖健康监测
Atlas links — related nutrients/systems
Hashimoto touches multiple atlas stories:`selenium` — Se U-shaped curve + selenoproteins L4`iodine` — TPO / NIS + iodized salt / excess risk + L4 thyroid animation`vitamin-d` — vitamin D receptor: The cellular 'socket' that vitamin D plugs into to carry out its instructions. + autoimmune modulation`iron` — menstruating women + TPO is a heme enzyme + alternate-day iron protocol`vitamin-b12` — co-occurs with Hashimoto, atrophic gastritis + intrinsic factor mechanism`endocrine` (system) — HPT axis + Hashimoto scenario already covered`ashwagandha` — contraindicated in Hashimoto progression / hyperthyroid risk (atlas-flagged)`spirulina` — high iodine, Hashimoto patients avoid`spirulina` + systemic immunity — Hashimoto-related warning
Atlas + Report engine: the `hashimoto` rule triggers on 'thyroid-stimulating hormone: A pituitary hormone that prods the thyroid to work — it rises when the thyroid is underactive. >4.5 + anti-thyroid peroxidase: A key enzyme that makes thyroid hormone — in Hashimoto's the immune system often attacks it by mistake. positive / diagnosed Hashimoto', recommending selenium foods + 100–200 μg/day Se (Toulis 2010 citation) + monitoring + avoidance of chronic high-iodine supplements.
Hashimoto is the most classic 'single nutrient ≠ single answer' case in the atlas: asking 'what should I supplement for Hashimoto?' has no answer in a single mineral or vitamin; the answer is adequate Se + not too much I + sufficient D + sufficient Fe + sufficient B12 + adequate protein + no strict AIP + no chronic high-iodine pills + controlled TSH + monitoring. Marketing wants to give a simple answer; reality requires this whole coordinated package.
References · 8
- Jonklaas, J., Bianco, A. C., Bauer, A. J., et al. (2014). Guidelines for the treatment of hypothyroidism: prepared by the American Thyroid Association task force on thyroid hormone replacement. Thyroid, 24(12), 1670-1751. 10.1089/thy.2014.0028
- Toulis, K. A., Anastasilakis, A. D., Tzellos, T. G., Goulis, D. G., & Kouvelas, D. (2010). Selenium supplementation in the treatment of Hashimoto's thyroiditis: a systematic review and a meta-analysis. Thyroid, 20(10), 1163-1173. 10.1089/thy.2009.0351
- Rayman, M. P. (2012). Selenium and human health. The Lancet, 379(9822), 1256–1268. 10.1016/S0140-6736(11)61452-9
- Lippman, S. M., et al. (2009). Effect of selenium and vitamin E on risk of prostate cancer (SELECT): a randomized controlled trial. JAMA, 301(1), 39–51. 10.1001/jama.2008.864
- Stranges, S., Marshall, J. R., Natarajan, R., Donahue, R. P., Trevisan, M., Combs, G. F., et al. (2007). Effects of Long-Term Selenium Supplementation on the Incidence of Type 2 Diabetes. Annals of Internal Medicine, 147(4), 217-223. THIS is where the selenium-diabetes signal comes from, and it is at 200 microg/day, not above 400: type 2 diabetes HR 1.55 (1.03-2.33), concentrated in the highest baseline-selenium tertile (HR 2.70). SELECT reported only a nonsignificant 1.07. 10.7326/0003-4819-147-4-200708210-00175
- Duffield-Lillico, A. J. (2003). Selenium Supplementation and Secondary Prevention of Nonmelanoma Skin Cancer in a Randomized Trial. Journal of the National Cancer Institute, 95(19), 1477-1481. The skin-cancer signal, also at 200 microg/day: squamous cell carcinoma HR 1.25 (1.03-1.51), total non-melanoma skin cancer HR 1.17 (1.02-1.34). SELECT never reported a skin-cancer endpoint. 10.1093/jnci/djg061
- Pedersen, I. B., Knudsen, N., Carlé, A., Vejbjerg, P., Jørgensen, T., Perrild, H., et al. (2011). A cautious iodization programme bringing iodine intake to a low recommended level is associated with an increase in the prevalence of thyroid autoantibodies in the population. Clinical Endocrinology, 75(1), 120-126. Two identical cross-sectional surveys of the general Danish population before and after cautious iodisation — NOT a follow-up of antibody-positive people. Population TPO-Ab positivity rose 14.3% to 23.8%, concentrated in young women and at low titres. It shows more people turning antibody-positive; it does not show that already-positive people progress faster. 10.1111/j.1365-2265.2011.04008.x
- Abbott, R. D., Sadowski, A., Alt, A. G. (2019). Efficacy of the Autoimmune Protocol Diet as Part of a Multi-disciplinary, Supported Lifestyle Intervention for Hashimoto’s Thyroiditis. Cureus. Open-label single-arm, n=17, a 10-week multidisciplinary online health-coaching programme (not the diet alone). Symptom and quality-of-life scores improved; thyroid function AND TPO / Tg antibodies were retested and NONE changed significantly. The story used to say antibodies were not retested. 10.7759/cureus.4556