Abstract
Introduction:
The status of fat-soluble vitamins (A, D, E) across the spectrum ofHashimoto’s thyroiditis (HT), particularly regarding sex-specific patterns, remainsincompletely characterized.
Methods:
This cross-sectional study aimed to evaluate the associations of these vitamins with thyroid autoimmunity and function. We analyzed 196 adults, focusing on the 136 women stratified into healthy controls (HC), euthyroid HT (E-HT), and dysfunctional HT (HT-dys).
Results:
In women, serum vitamin A levels were significantly lower in both the E-HT and HT-dys groups compared to the HC group. Lipid-normalized vitamin E (α-tocopherol/[total cholesterol+triglycerides], αT/[TCH+TG]) was significantly reduced in the HT-dys group compared to both the HC and E-HT groups. Vitamin A levels showed an inverse association with thyroglobulin antibody (TgAb), while αT/(TCH+TG) was inversely associated with both thyroid peroxidase antibody (TPOAb) and TgAb. Among women with HT, αT/(TCH+TG) was inversely correlated with thyroid-stimulating hormone (TSH) and positively correlated with free thyroxine (FT4). An exploratory analysis indicated that this association between vitamin E and thyroid function was largely independent of TPOAb levels.
Conclusion:
This exploratory study identifies distinct associations of vitamins A and E with disease activity in women with HT, highlighting the need for longitudinal and interventional studies to further explore these relationships.
1 Introduction
Hashimoto’s thyroiditis (HT), the most prevalent autoimmune thyroid disorder, is a leading cause of hypothyroidism and demonstrates a marked female predominance (1, 2). The pathogenesis of HT involves immune-mediated thyroid destruction, in which oxidative stress acts as a key amplifier of tissue damage (3–6). Given this pathophysiology, fat-soluble vitamins have garnered interest due to their immunomodulatory and antioxidant properties.
Critical evidence gaps remain, however. Vitamin A (retinol) is essential for immune regulation, primarily through retinoid receptor-mediated T-cell modulation (7–9). Deficiency in vitamin A is known to impair thyroid hormone synthesis (10–12), yet direct assessments of vitamin A status in patients with HT are limited. Vitamin D exerts potent immunomodulatory effects (13–15). Although some supplementation trials have shown promise in reducing thyroid autoantibodies (16, 17), observational studies on the association between serum vitamin D and HT have yielded inconsistent results (18–22), leaving its role unclear. Vitamin E, particularly α-tocopherol (αT), is a key lipid-soluble antioxidant that protects against peroxidation and modulates immune function (23, 24). Although epidemiological links have been reported (25), high-quality evidence quantifying vitamin E status in HT using precise methods such as liquid chromatography–tandem mass spectrometry (LC–MS/MS) remains scarce, and the important step of lipid normalization is frequently overlooked.
These gaps point to two unresolved questions. First, the sex-specific patterns of these vitamins across the spectrum of HT, from euthyroidism to overt dysfunction, remain poorly characterized, despite the strong female predominance of the disease. Second, there is a notable lack of comprehensive studies that concurrently evaluate all three vitamins with rigorous methodology, particularly with respect to LC–MS/MS and lipid normalization for vitamin E.
Therefore, we conducted a cross-sectional study to: (1) characterize the sex-specific status of vitamins A, D, and E across HT disease categories using high-precision LC–MS/MS and lipid-normalized vitamin E levels; (2) examine the associations of these vitamins with thyroid autoimmunity (thyroid peroxidase antibody [TPOAb] and thyroglobulin antibody [TgAb]) and thyroid function (thyroid-stimulating hormone [TSH] and free thyroxine [FT4]); and (3) explore the complex relationships and potential interplay among these vitamins, autoantibodies, and thyroid function. By focusing on sex-stratified analyses and methodologically robust assessments, this study aims to provide novel insights into the potential role of these nutritional factors in HT.
2 Materials and methods
2.1 Study population
The study enrolled Chinese adults aged 18–75 years who underwent health check-ups at the Health Management Center of Foshan Hospital of Traditional Chinese Medicine between January and March 2025. All participants completed a standardized assessment, which included biochemical tests, measurements of serum vitamins (A, D, and E), thyroid function tests (TSH and FT4), thyroid autoantibody assays (TPOAb and TgAb), and thyroid ultrasonography. Exclusion criteria were as follows: (a) other thyroid diseases, such as Graves’ disease or subacute thyroiditis; (b) current or previous use of thyroid medications (e.g., levothyroxine, methimazole or propylthiouracil) or a history of thyroid surgery or radioactive iodine therapy; (c) presence of other endocrine disorders or use of hormone therapy; (d) diagnosis of malignancy; and (e) pregnancy or lactation.
Data collection followed the standardized protocols of the health check-up program. Consequently, information on certain potential confounding variables, including detailed dietary intake, use of vitamin supplements, and sunlight exposure, was not routinely collected and was therefore unavailable for adjustment.
The study was conducted in accordance with the Declaration of Helsinki, and was approved by the Ethics Committee of Foshan Hospital of Traditional Chinese Medicine.
2.2 Data collection
2.2.1 Anthropometry
Height and weight were measured with participants wearing light clothing and without shoes. Body mass index (BMI) was calculated as weight in kilograms divided by the square of height in meters (kg/m2). After a 10-min rest, systolic and diastolic blood pressure (SBP and DBP) were measured three times on the right arm using an appropriately sized cuff; the average of the three readings was recorded.
2.2.2 Biochemical analyses
Fasting venous blood samples were collected after an 8- to 12-h overnight fast to minimize dietary influences on metabolic parameters and vitamin levels. All samples were drawn between 7:00 and 9:00 a.m. to reduce diurnal variation. Fasting plasma glucose (FPG) was measured using the hexokinase/G-6-PDH method. Enzymatic methods were used to assess triglycerides (TG) and total cholesterol (TC) with glycerol-3-phosphate kinase and cholesterol esterase-cholesterol oxidase, respectively. Low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were measured by direct methods. Uric acid (UA) was determined by uricase method. Creatinine (Cr) was measured via the sarcosine oxidase method, and urea was measured using urease rate method. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and γ-glutamyl transferase (GGT) levels were measured by kinetic assays.
2.2.3 Thyroid function and autoantibodies
Serum FT4 and TSH levels were quantified using chemiluminescence immunoassays on a Siemens ADVIA Centaur XP analyzer. Serum concentrations of TPOAb and TgAb were determined by electrochemiluminescence immunoassays on a Roche Cobas 6,000 analyzer.
2.2.4 Vitamin analysis
Serum concentrations of vitamin A (retinol), vitamin D (25-hydroxyvitamin D, 25[OH]D), and vitamin E (α-tocopherol, α-T) were quantified by LC–MS/MS. Analyses were performed using an AB SCIEX 5500+QTrap mass spectrometer coupled to a Shimadzu Nevera X2 LC system and commercially available isotope-dilution mass spectrometry (IDMS) kits (Chromsystems Instruments & Chemicals GmbH, Gräfelfing, Germany). Intra- and inter-assay coefficients of variation were both below 10%. Given the strong lipid dependence of tocopherol transport, α-T concentrations were normalized to total lipids using the ratio α-tocopherol/(total cholesterol+triglycerides) (αT/[TCH+TG]). The normalization minimizes confounding from interindividual variations in lipid metabolism and better reflects tissue-available vitamin E status (26, 27).
2.2.5 Thyroid ultrasonography
Thyroid ultrasound examinations were performed by senior sonographers, each with a minimum of 10 years of thyroid imaging experience, using a high-resolution B-mode ultrasound system (MyLab Class C, Esaote, Italy). Participants were positioned supine with the necks slightly extended.
2.3 Definition and grouping
HT was diagnosed based on the presence of thyroid autoantibody positivity (defined as TPOAb ≥ 34 IU/mL and/or TgAb ≥ 115 IU/mL) and characteristic heterogeneous echotexture with diffuse or patchy hypoechogenicity on thyroid ultrasonography (28).
Participants were stratified into three groups according to their autoantibody status and thyroid function: healthy controls (HC) (thyroid autoantibody negative [TPOAb < 34 IU/mL and TgAb < 115 IU/mL] with normal thyroid function [TSH 0.6–4.8 mIU/L, FT4 12–20.2 pmol/L]), euthyroid HT (E-HT) (positive for TPOAb and/or TgAb, with maintained euthyroidism), and dysfunctional HT (HT-dys) (positive for TPOAb and/or TgAb, with biochemically confirmed subclinical [TSH > 4.8 mIU/L and FT4 12–20.2 pmol/L] or overt hypothyroidism [TSH > 4.8 mIU/L and FT4 < 12 pmol/L]).
Serum 25(OH)D < 20 ng/mL was defined as vitamin D deficiency, in according with the Endocrine Society guidelines (29).
2.4 Statistical analysis
Statistical analyses were performed using SPSS version 27.0 (IBM Corp., Armonk, NY, USA). Continuous variables are presented as mean ± standard deviation (SD) and categorical variables as number (%). Intergroup differences were assessed using t-tests, χ2 tests, or one-way ANOVA with LSD post-hoc tests, as appropriate.
For the female cohort, multivariable linear regression (enter method) was used to identify determinants of thyroid autoimmunity and function. Covariates were selected a priori based on biological plausibility and clinical relevance, including demographic factors (age), anthropometric measures (BMI, SBP and DBP), metabolic parameters (FPG, lipid profiles, UA, liver and renal function markers), and thyroid-specific parameters (thyroid function tests and autoantibodies). Multicollinearity among candidate variables was assessed using the variance inflation factor (VIF); no variables exhibited significant collinearity (all VIFs < 5), and all were retained. The analysis was conducted as a complete-case analysis owing to the absence of missing data for key variables. To test for effect modification by sex, vitamin × sex interaction terms were included in the regression models.
An exploratory model-based analysis was performed to examine whether the association between lipid-normalized vitamin E (αT/[TCH+TG]) and thyroid function (TSH/FT4) operated through a pathway shared with or independent of TPOAb levels. It is critical to emphasize that this cross-sectional analysis does not imply causality or temporal sequence.
Given the exploratory nature of this study and the multiple statistical tests performed, we did not adjust for multiple comparisons (e.g., Bonferroni or false discovery rate) to avoid unduly increasing the risk of Type II errors (false negatives) and to allow for hypotheses generation. Consequently, all p-values, especially those near the conventional threshold (p < 0.05), should be interpreted with caution as hypotheses-generating rather than confirming robust associations. Statistical significance was set at p < 0.05 (two-sided).
The sample size was determined by feasibility and recruitment during the study period. No formal a priori power calculation was performed. Therefore, the analyses, particularly sex-stratified and subgroup comparisons, may be underpowered to detect modest effect sizes, and the risk of Type II errors should be considered.
Owing to the very small sample size of the male HT-dys group (n = 4), which precludes valid statistical inference, data for the male cohort are presented as descriptive only. No p-values are reported for male comparisons, and these results should be interpreted as hypothesis-generating.
3 Results
The study included 196 participants (136 women, 60 men) with a mean age of 46.3 ± 10.9 years. As summarized in Table 1, men exhibited significantly higher values than women on anthropometrics measures (height, weight, BMI), blood pressure, various metabolic markers (TG, UA, Cr, Urea), liver enzymes (ALT, GGT), thyroid hormones (FT4), and vitamin A levels (625.37 ± 257.79 ng/mL vs. 431.40 ± 116.78 ng/mL, p < 0.001). Conversely, women had significantly higher HDL-C, elevated TPOAb titers, a greater prevalence of HT (60.29% vs. 41.67%, p = 0.016) and a higher prevalence of vitamin D deficiency (26.47% vs. 5.00%, p < 0.001) compared to men.
Parameter
Male (n = 60)
Women (n = 136)
p
Age (years)
48.55 ± 10.44
45.26 ± 11.03
0.052
Height (cm)
170.53 ± 5.38
158.05 ± 5.24
<0.001
Weight (kg)
73.84 ± 9.35
57.45 ± 8.01
<0.001
BMI (kg/m2)
25.37 ± 2.77
23.00 ± 2.90
<0.001
SBP (mmHg)
129.93 ± 11.54
118.96 ± 13.23
<0.001
DBP (mmHg)
82.23 ± 9.42
73.11 ± 9.08
<0.001
FPG (mmol/L)
5.32 ± 0.96
5.11 ± 1.09
0.202
TG (mmol/L)
2.36 ± 3.84
1.28 ± 0.59
0.002
TCH (mmol/L)
5.14 ± 1.25
5.43 ± 1.06
0.102
LDL-C (mmol/L)
3.35 ± 0.99
3.40 ± 0.79
0.730
HDL-C (mmol/L)
1.17 ± 0.23
1.47 ± 0.30
<0.001
UA (μmol/L)
425.96 ± 92.89
315.03 ± 66.16
<0.001
Cr (μmol/L)
77.83 ± 14.31
60.96 ± 10.47
<0.001
Urea (mmol/L)
4.86 ± 0.96
4.38 ± 1.14
0.005
ALT (U/L)
24.87 ± 9.13
18.92 ± 13.20
0.002
AST (U/L)
22.63 ± 6.30
20.61 ± 7.76
0.077
GGT (U/L)
29.16 ± 11.07
19.79 ± 11.97
<0.001
FT4 (pmol/L)
16.83 ± 2.95
15.64 ± 3.20
0.015
TSH (mIU/L)
3.47 ± 6.40
4.93 ± 12.60
0.393
HT
25 (41.67%)
82 (60.29%)
0.016
TPOAb (IU/mL)
75.88 ± 142.24
126.36 ± 169.39
0.033
TgAb (IU/mL)
226.69 ± 575.19
326.62 ± 709.15
0.338
Vitamin A (ng/mL)
625.37 ± 257.79
431.40 ± 116.78
<0.001
25(OH)D (ng/mL)
25.53 ± 7.03
25.43 ± 10.19
0.937
Vitamin D deficiency
3 (5.00%)
36 (26.47%)
<0.001
αT (ng/mL)
10137.49 ± 3882.73
10114.23 ± 3343.67
0.968
αT/(TCH+TG) (μg/mmol)
1407.62 ± 291.90
1508.22 ± 391.66
0.076
Sex-specific baseline characteristics of the study population (n = 196).
Data presented as mean ± SD or n (%). p-values derived from independent t-tests or χ2 tests. BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; FPG, fasting plasma glucose; TG, triglycerides; TCH, total cholesterol; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; UA, uric acid; Cr, creatinine; ALT, alanine transaminase; AST, aspartate aminotransferase; GGT, γ-glutamyl transpeptidase; Cr, creatinine; FT4, free thyroxine; TSH, thyroid-simulating hormone; HT, Hashimoto’s thyroiditis; TPOAb, thyroid peroxidase antibody; TgAb, anti-thyroglobulin antibody; 25(OH)D, 25-hydroxyvitamin D; αT, α-tocopherol; αT/(TCH+TG), α-tocopherol/(total cholesterol+triglycerides).
Analysis of the female cohort revealed significant differences in vitamin status across the study groups (Table 2). Serum vitamin A concentrations were significantly lower in both the E-HT and HT-dys groups compared to the HC group. αT/(TCH+TG) was significantly reduced in the HT-dys group (1188.95 ± 305.70 μg/mmol) compared to both the HC group (1606.03 ± 357.18 μg/mmol; 26% decrease, p < 0.05) and the E-HT group (1496.28 ± 401.09 μg/mmol; 21% decrease, p < 0.05). In contrast, no significant intergroup differences were observed in serum vitamin D levels or in the prevalence of vitamin D deficiency.
Parameter
HC
E-HT
HT-dys
p
n
54
68
14
Age (years)
44.98 ± 12.49
44.68 ± 9.55
49.21 ± 11.79
0.366
Height (cm)
158.66 ± 4.53
158.05 ± 5.74
155.65 ± 4.88
0.159
Weight (kg)
58.05 ± 6.27
57.31 ± 9.13
55.79 ± 8.50
0.643
BMI (kg/m2)
23.10 ± 2.26
22.92 ± 3.40
22.99 ± 2.63
0.943
SBP (mmHg)
119.33 ± 14.79
117.81 ± 11.80
123.14 ± 13.49
0.379
DBP (mmHg)
73.11 ± 9.08
71.66 ± 8.44
73.86 ± 9.49
0.549
FPG (mmol/L)
5.19 ± 1.61
5.01 ± 0.46
5.26 ± 0.79
0.599
TG (mmol/L)
1.20 ± 0.49
1.29 ± 0.65
1.59 ± 0.63
0.092
TCH (mmol/L)
5.38 ± 1.09
5.51 ± 0.93
5.23 ± 1.51
0.585
LDL-C (mmol/L)
3.42 ± 0.85
3.41 ± 0.67
3.25 ± 1.10
0.777
HDL-C (mmol/L)
1.44 ± 0.27
1.50 ± 0.29
1.43 ± 0.45
0.492
UA (μmol/L)
317.10 ± 76.32
308.11 ± 56.65
340.71 ± 64.73
0.235
Cr (μmol/L)
62.71 ± 12.56
59.90 ± 7.96
60.96 ± 10.47
0.283
Urea (mmol/L)
4.49 ± 1.18
4.30 ± 1.13
4.30 ± 1.00
0.639
ALT (U/L)
18.15 ± 7.84
18.48 ± 16.76
24.00 ± 8.90
0.314
AST (U/L)
20.40 ± 7.75
20.18 ± 8.04
23.49 ± 6.01
0.339
GGT (U/L)
19.67 ± 12.82
19.72 ± 11.34
20.57 ± 12.43
0.967
FT4 (pmol/L)
16.36 ± 3.04
15.82 ± 2.21
11.98 ± 5.21bc
<0.001
TSH (mIU/L)
2.30 ± 2.20
2.22 ± 1.25
28.23 ± 31.14bc
<0.001
TPOAb (IU/mL)
12.92 ± 4.18
179.68 ± 168.29a
304.93 ± 221.98bc
<0.001
TgAb (IU/mL)
19.47 ± 12.23
383.46 ± 616.99a
1235.28 ± 1400.69bc
<0.001
Vitamin A (ng/mL)
461.72 ± 118.95
419.06 ± 113.39a
374.39 ± 97.75b
0.020
25(OH)D (ng/mL)
27.04 ± 12.56
23.81 ± 7.90
27.06 ± 9.35
0.183
Vitamin D deficiency
12 (22.22%)
22 (32.36%)
2 (14.29%)
0.249
αT (ng/mL)
10562.37 ± 3104.73
10111.62 ± 3382.02
8398.36 ± 3721.27b
0.097
αT/(TCH+TG) (μg/mmol)
1606.03 ± 357.18
1496.28 ± 401.09
1188.95 ± 305.70bc
0.001
Vitamin status and clinical characteristics of the female cohort across the spectrum of Hashimoto’s thyroiditis (n = 136).
Data presented as mean ± SD or n (%). p-values derived from independent ANOVA or χ2 tests. HT, Hashimoto’s thyroiditis; HC, healthy controls; E-HT, euthyroid HT; HT-dys, dysfunctional HT; BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; FPG, fasting plasma glucose; TG, triglycerides; TCH, total cholesterol; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; UA, uric acid; Cr, creatinine; ALT, alanine transaminase; AST, aspartate aminotransferase; GGT, γ-glutamyl transpeptidase; Cr, creatinine; FT4, free thyroxine; TSH, thyroid-simulating hormone; TPOAb, thyroid peroxidase antibody; TgAb, anti-thyroglobulin antibody; 25(OH)D, 25-hydroxyvitamin D; αT, α-tocopherol; αT/(TCH+TG), α-tocopherol/(total cholesterol+triglycerides).
aGroup E-HT vs. group HC, p < 0.05.
bGroup HT-dys vs. group HC, p < 0.05.
cGroup HT-dys vs. group E-HT, p < 0.05.
Given the very limited sample size, particularly in the male HT-dys group (n = 4), data for the male cohort are presented in Supplementary Table S1 solely for descriptive purposes. No statistical comparisons between male subgroups were performed or reported, as such comparisons would be statistically unreliable.
Multivariable linear regression analysis revealed distinct determinants of thyroid autoimmunity in women (Table 3). TPOAb levels showed positive associations with both TSH (β = 3.917, 95% CI [1.162, 6.672], p = 0.006) and TgAb (β = 0.093, 95% CI [0.055, 0.131], p < 0.001), but an inverse association with αT/(TCH+TG) (β = −0.078, 95% CI [−0.152, −0.005], p = 0.038). It should be noted that this p-value for the latter association is marginal and should be considered exploratory in the context of multiple testing. Similarly, TgAb levels were positively associated with TPOAb (β = 1.878, 95% CI [1.109, 2.647], p < 0.001) and inversely associated with both vitamin A (β = −1.531, 95% CI [−2.679, −0.383], p = 0.009) and αT/(TCH+TG) (β = −0.369, 95% CI [−0.670, −0.067], p = 0.015).
Outcome
Predictor
β (95% CI)
p
TPOAb (IU/mL)
Age (years)
−1.496 (−4.252, 1.261)
0.285
Height (cm)
−2.555 (−8.568, 3.459)
0.402
Weight (kg)
1.896 (−2.354, 6.147)
0.379
BMI (kg/m2)
−8.096 (−17.643, 1.451)
0.096
SBP (mmHg)
−0.211 (−3.435, 3.013)
0.897
DBP (mmHg)
0.907 (−3.656, 5.470)
0.694
FPG (mmol/L)
−10.740 (−34.498, 13.018)
0.372
TG (mmol/L)
36.062 (−23.415, 95.539)
0.232
TCH (mmol/L)
63.699 (−11.648, 139.046)
0.097
LDL-C (mmol/L)
−70.774 (−153.312, 11.763)
0.092
HDL-C (mmol/L)
25.432 (−92.663, 143.526)
0.670
UA (μmol/L)
−0.078 (−0.531, 0.374)
0.732
Cr (μmol/L)
0.722 (−2.008, 3.452)
0.601
Urea (mmol/L)
7.885 (−16.450, 32.221)
0.522
ALT (U/L)
−0.529 (−4.265, 3.207)
0.780
AST (U/L)
0.860 (−4.905, 6.624)
0.768
GGT (U/L)
−0.503 (−3.109, 2.104)
0.703
FT4 (pmol/L)
−20.798 (−68.162, 26.566)
0.386
TSH (mIU/L)
3.917 (1.162, 6.672)
0.006
TgAb (IU/mL)
0.093 (0.055, 0.131)
<0.001
Vitamin A (ng/mL)
0.024 (−0.239, 0.287)
0.856
25(OH)D (ng/mL)
−0.909 (−3.520, 1.702)
0.492
αT (ng/mL)
−0.071 (−0.142, −0.001)
0.054
αT/(TCH+TG) (μg/mmol)
−0.078 (−0.152, −0.005)
0.038
TgAb (IU/mL)
Age (years)
12.008 (−0.253, 24.269)
0.055
Height (cm)
−9.577 (−36.661, 17.506)
0.485
Weight (kg)
1.873 (−17.315, 21.061)
0.847
BMI (kg/m2)
−0.138 (−43.639, 43.363)
0.995
SBP (mmHg)
−3.490 (−17.985, 11.005)
0.634
DBP (mmHg)
3.849 (−16.685, 24.383)
0.711
FPG (mmol/L)
−25.212 (−132.393, 81.969)
0.642
TG (mmol/L)
22.617 (−36.735, 81.969)
0.090
TCH (mmol/L)
−220.418 (−561.192, 120.357)
0.203
LDL-C (mmol/L)
275.424 (−97.174, 648.021)
0.146
HDL-C (mmol/L)
−128.415 (−659.677, 402.847)
0.633
UA (μmol/L)
0.291 (−1.746, 2.328)
0.777
Cr (μmol/L)
−5.674 (−17.925, 6.577)
0.361
Urea (mmol/L)
−37.932 (−147.400, 71.536)
0.494
ALT (U/L)
1.549 (−15.265, 18.362)
0.855
AST (U/L)
−10.153 (−36.031, 15.725)
0.439
GGT (U/L)
−5.685 (−17.371, 6.001)
0.337
FT4 (pmol/L)
−5.533 (−48.598, 37.533)
0.800
TSH (mIU/L)
−1.157 (−13.987, 11.673)
0.858
TPOAb (IU/mL)
1.878 (1.109, 2.647)
<0.001
Vitamin A (ng/mL)
−1.531 (−2.679, −0.383)
0.009
25(OH)D (ng/mL)
7.703 (−3.982, 19.388)
0.194
αT (ng/mL)
−0.200 (−0.536, 0.136)
0.241
αT/(TCH+TG) (μg/mmol)
−0.369 (−0.670, −0.067)
0.015
Determinants of thyroid autoantibodies in women: results from multivariable linear regression analysis (n = 136).
BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; FPG, fasting plasma glucose; TG, triglycerides; TCH, total cholesterol; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; UA, uric acid; Cr, creatinine; ALT, alanine transaminase; AST, aspartate aminotransferase; GGT, γ-glutamyl transpeptidase; Cr, creatinine; FT4, free thyroxine; TSH, thyroid-simulating hormone; TPOAb, thyroid peroxidase antibody; TgAb, anti-thyroglobulin antibody; 25(OH)D, 25-hydroxyvitamin D; αT, α-tocopherol; αT/(TCH+TG), α-tocopherol/(total cholesterol+triglycerides).
Regarding thyroid function in women with HT, TSH levels demonstrated a positive association with TPOAb (β = 0.024, 95% CI [0.006, 0.042], p = 0.010) but inverse associations with both FT4 (β = −3.026, 95% CI [−3.922, −2.130], p < 0.001) and αT/(TCH+TG) (β = −0.012, 95% CI [−0.020, −0.003], p = 0.009). Conversely, FT4 levels were negatively associated with TSH (β = −0.147, 95% CI [−0.191, −0.104], p < 0.010) and TPOAb (β = −0.004, 95% CI [−0.009, −0.001], p = 0.047), but positively associated with αT/(TCH+TG) (β = 0.004, 95% CI [0.002, 0.006], p = 0.005) (Table 4).
Outcome
Predictor
β (95%CI)
p
TSH
Age (years)
0.069 (−0.252, 0.390)
0.670
Height (cm)
0.592 (−0.126, 1.311)
0.104
Weight (kg)
−0.273 (−0.719, 0.172)
0.224
BMI (kg/m2)
−0.150 (−1.117, 0.817)
0.757
SBP (mmHg)
0.193 (−0.146, 0.532)
0.259
DBP (mmHg)
−0.081 (−0.532, 0.369)
0.719
FPG (mmol/L)
1.052 (−4.821, 6.924)
0.721
TG (mmol/L)
2.238 (−7.079, 11.554)
0.632
TCH (mmol/L)
11.648 (−0.969, 24.264)
0.074
LDL-C (mmol/L)
10.750 (−0.761, 22.261)
0.066
HDL-C (mmol/L)
11.767 (−0.257, 23.791)
0.055
UA (μmol/L)
0.001 (−0.056, 0.057)
0.994
Cr (μmol/L)
0.244 (−0.144, 0.633)
0.213
Urea (mmol/L)
−0.406 (−3.428, 2.615)
0.789
ALT (U/L)
−0.210 (−0.659, 0.239)
0.354
AST (U/L)
0.615 (−0.237, 1.466)
0.154
GGT (U/L)
0.224 (−0.098, 0.546)
0.168
FT4 (pmol/L)
−3.026 (−3.922, −2.130)
<0.001
TPOAb (IU/mL)
0.024 (0.006, 0.042)
0.010
TgAb (IU/mL)
0.000 (−0.004, 0.004)
0.996
Vitamin A (ng/mL)
−0.008 (−0.037, 0.022)
0.603
25(OH)D (ng/mL)
−0.100 (−0.461, 0.261)
0.581
αT (ng/mL)
−0.003 (−0.026, 0.021)
0.805
αT/(TCH+TG) (μg/mmol)
−0.012 (−0.020, −0.003)
0.009
FT4
Age (years)
0.026 (−0.044, 0.097)
0.461
Height (cm)
0.140 (−0.018, 0.298)
0.081
Weight (kg)
−0.063 (−0.162, 0.035)
0.200
BMI (kg/m2)
−0.039 (−0.252, 0.174)
0.714
SBP (mmHg)
0.038 (−0.037, 0.113)
0.319
DBP (mmHg)
0.006 (−0.093, 0.106)
0.898
FPG (mmol/L)
0.291 (−1.003, 1.585)
0.655
TG (mmol/L)
0.055 (−2.003, 2.114)
0.957
TCH (mmol/L)
−0.788 (−3.452, 1.876)
0.556
LDL-C (mmol/L)
0.629 (−1.830, 3.087)
0.611
HDL-C (mmol/L)
−0.172 (−2.911, 2.567)
0.900
UA (μmol/L)
−0.006 (−0.019, 0.006)
0.310
Cr (μmol/L)
0.067 (−0.018, 0.152)
0.120
Urea (mmol/L)
−0.249 (−0.912, 0.415)
0.456
ALT (U/L)
−0.013 (−0.113, 0.086)
0.790
AST (U/L)
0.063 (−0.128, 0.253)
0.511
GGT (U/L)
0.051 (−0.020, 0.121)
0.158
TSH (mIU/L)
−0.147 (−0.191, −0.104)
<0.001
TPOAb (IU/mL)
−0.004 (−0.009, −0.001)
0.047
TgAb (IU/mL)
0.000 (−0.001, 0.001)
0.579
Vitamin A (ng/mL)
0.001 (−0.005, 0.008)
0.715
25(OH)D (ng/mL)
−0.037 (−0.116, 0.042)
0.356
αT (ng/mL)
0.001 (−0.004, 0.006)
0.711
αT/(TCH+TG) (μg/mmol)
0.004 (0.002, 0.006)
0.005
Associations of clinical variables with thyroid function in women with Hashimoto’s thyroiditis: results from multivariable linear regression analysis (n = 82).
BMI, body mass index; SBP, systolic blood pressure; DBP, diastolic blood pressure; FPG, fasting plasma glucose; TG, triglycerides; TCH, total cholesterol; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-density lipoprotein cholesterol; UA, uric acid; Cr, creatinine; ALT, alanine transaminase; AST, aspartate aminotransferase; GGT, γ-glutamyl transpeptidase; Cr, creatinine; TSH, thyroid-simulating hormone; FT4, free thyroxine; TPOAb, thyroid peroxidase antibody; TgAb, anti-thyroglobulin antibody; 25(OH)D, 25-hydroxyvitamin D; αT, α-tocopherol; αT/(TCH+TG), α-tocopherol/(total cholesterol+triglycerides).
Interaction analysis indicated a nominally significant interaction between αT/(TCH+TG) and sex in relation to TgAb levels (p = 0.049). However, this marginal interaction effect should be interpreted with extreme caution given the number of tests performed and the lack of adjustment for multiple comparisons. No other significant interactions with sex were observed for the relationships between vitamin A and TgAb, or between αT/(TCH+TG) and TPOAb, TSH, or FT4, either in the overall population or the HT-subgroup (all p > 0.05).
Finally, an exploratory model-based analysis demonstrated that the association between αT/(TCH+TG) and thyroid function in women with HT was largely independent of TPOAb levels, with the majority of the statistical association not explained by TPOAb (Supplementary Table S2).
4 Discussion
4.1 Vitamin A
Our study demonstrates significantly lower serum vitamin A levels in women with HT compared to healthy controls (30, 31), extending earlier observations in Caucasian populations (32) to our Chinese cohort. The key novel finding is the significant inverse association between vitamin A and TgAb, in the absence of a direct association with thyroid function parameters. This specific pattern generates the hypothesis that vitamin A’s role in HT may be primarily immunological. The inverse correlation with TgAb is consistent with its established role in immune regulation, particularly in T-cell function and B-cell activity (12, 33, 34). Conversely, the lack of association with thyroid function aligns with some prior studies (32, 35), suggesting that the vitamin’s effects are likely mediated through immunoregulation rather than a direct impact on thyroid hormone synthesis. These findings positions vitamin A status as a potential modulator of the specific autoimmune response against thyroglobulin in HT.
4.2 Vitamin E
A key finding of our study is the inverse association of lipid-normalized vitamin E (αT/(TCH+TG)) with both thyroid autoantibodies (TPOAb, TgAb) and thyroid function (TSH, FT4) in women with HT. The association with autoantibodies aligns with the established immunomodulatory role of vitamin E, which includes regulating dendritic cell maturation, macrophage polarization, and T/B-cell function (23, 36, 37). More importantly, our exploratory analysis further revealed that the association between αT/(TCH+TG) and thyroid function was largely independent of TPOAb levels. This hypothesis-generating finding suggests that, beyond immunomodulation, vitamin E may influence thyroid status through more direct pathways. As a potent lipid-soluble antioxidant, vitamin E protects cellular integrity against peroxidation (38, 39). Given that thyroid hormone biosynthesis is an oxidative process dependent on peroxide generation (40), it is plausible that a lower vitamin E status could exacerbate oxidative stress within the thyroid gland, directly impairing thyrocyte function. This hypothesis is supported by experimental evidence indicating that oxidative stress modulates redox-sensitive signaling pathways critical for thyrocyte activity (41). Thus, vitamin E deficiency may contribute to pathophysiology of HT not only by promoting immune dysregulation but also by increasing the gland’s susceptibility to reactive oxygen species (ROS)-mediated damage.
4.3 Vitamin D
In contrast to vitamins A and E, our study found no significant association between vitamin D status and HT in the female cohort. This null finding serves as an important methodological comparator, underscoring the specificity of the associations identified for vitamins A and E, and indicating that they are not a generic feature of all fat-soluble vitamins. While some studies have reported an association between vitamin D and HT (42–44), others have not (20, 21), highlighting the persistent inconsistency in this area. Our results, obtained with a robust methodological framework, suggest that in this specific population, vitamin D status may not be a primary cross-sectional correlate of HT.
4.4 Considerations on the observed associations in women
The associations of vitamins A and E with autoimmunity and thyroid function were observed specifically in our female cohort, which aligns with the marked female predominance of HT. The potential role of sex hormones, particularly estrogens, offers a plausible biological framework for these findings. Estrogens are known to promot humoral immunity and B-cell activation, which could lower the threshold for autoimmune reactivity (45, 46). Furthermore, sex hormones may influence the metabolism and distribution of fat-soluble vitamins. For instance, estrogen can modulate genes involved in vitamin A metabolism (47), and higher fat mass in women may alter the storage of lipophilic vitamins like E (48). Thus, an estrogen-enriched microenvironment could synergize with vitamin A and E deficiencies to exacerbate the autoimmune response in HT, leading to the more robust associations observed in women. This hypothesis merits investigation in future studies measuring sex hormone levels alongside vitamin status.
4.5 Reverse causality and oxidative stress
Reverse causality must be considered as an alternative explanation for our findings. HT is characterized by chronic inflammation and elevated oxidative stress, which may increase the consumption of antioxidant vitamins A and E. Therefore, the lower vitamin levels observed across disease categories may be a consequence rather than a cause of the autoimmune process. In this scenario, low vitamin levels would serve as a biomarker of disease activity rather than a modifiable risk factor. This possibility tempers the interpretation of our findings and impacts their clinical implications: if reverse causality is the primary driver, replenishing these vitamins may not alter the underlying autoimmune pathology, though it could still improve overall antioxidant status.
4.6 Limitations
Several limitations should be acknowledged. First, the cross-sectional design precludes causal inference. Second, the small male cohort limits the generalizability of findings in men. Third, we did not adjust for key confounders, such as iodine status, menopausal status, dietary intake, supplement use, or ultraviolet exposure. Fourth, blood sampling was conducted only in winter. While this controlled for seasonal variation, it may disproportionately affect vitamin levels, particularly vitamin D (due to reduced sunlight) and vitamin E (due to potential seasonal changes in lipid metabolism). Although vitamin A levels is less subject to seasonal variation, dietary influences across seasons cannot be ruled out. Fifth, no formal a priori sample size calculation was performed, increasing the risk of Type II errors. Finally, the lack of adjustment for multiple comparisons necessitates cautious interpretation of nominal p-values.
5 Conclusion
This exploratory study identifies distinct associations of vitamins A and E with disease activity in women with HT. These findings, specifically the inverse association of vitamin A with TgAb and of vitamin E with thyroid autoimmunity and dysfunction, highlight the need for longitudinal and interventional studies to further explore the relationship between these vitamins and HT.
StatementsData availability statement
The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.
Ethics statement
The studies involving humans were approved by the Ethics Committee of Foshan Hospital of Traditional Chinese Medicine. The studies were conducted in accordance with the local legislation and institutional requirements. The participants provided their written informed consent to participate in this study.
Author contributions
QL: Conceptualization, Data curation, Formal analysis, Funding acquisition, Investigation, Visualization, Writing – original draft. DL: Data curation, Resources, Writing – review & editing. JL: Data curation, Formal analysis, Writing – review & editing. ZQ: Methodology, Project administration, Resources, Supervision, Validation, Writing – review & editing.
Funding
The author(s) declared that financial support was received for this work and/or its publication. This research was supported by the medical research subject of Foshan Health Bureau 2022, grant number 20220296. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Conflict of interest
The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Generative AI statement
The author(s) declared that Generative AI was not used in the creation of this manuscript.
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Summary
Keywords
Hashimoto’s thyroiditis, autoimmunity, thyroid function, women, vitamin A, vitamin E
Citation
Liang Q, Li D, Lin J and Qi Z (2026) Vitamin A and E status across the spectrum of Hashimoto’s thyroiditis in women: associations with autoimmunity and thyroid function. Front. Nutr. 13:1701808. doi: 10.3389/fnut.2026.1701808
Received
09 September 2025
Revised
23 January 2026
Accepted
02 February 2026
Published
19 February 2026
Volume
13 – 2026
Edited by
Patxi León-Guereño, University of Deusto, Spain
Reviewed by
Małgorzata Natalia Słoma-Krześlak, Śląskiego Uniwersytetu Medycznego, Poland
Jonas Wolf, Moinhos de Vento Hospital, Brazil
Ankur Saharan, McGill University, Canada
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Copyright
© 2026 Liang, Li, Lin and Qi.
This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Zhenhong Qi, qizhenhong82@163.com
Disclaimer
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
