Impact of smoking on thyroid gland: dose-related effect of urinary cotinine levels on thyroid function and thyroid autoimmunity

Kim, Su jin; Kim, Min Joo; Yoon, Sang Gab; Myong, Jun‐Pyo; Yu, Hyeong Won; Chai, Young Jun; Choi, June Young; Lee, Kyu Eun

doi:10.1038/s41598-019-40708-1

Cited by 36 publications

(35 citation statements)

References 29 publications

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“…These findings would be consistent with an effect of smoking on thyroid-directed autoimmunity as for example widely appreciated in Graves disease and thyroidassociated ophthalmopathy [9,10]. In comparison, previous cohort studies have variably reported increased [15] and decreased [30,31] anti-TPO positivity in relation to Smoking status is categorized as never (reference category); former and current, which is divided in <20 and ≥20 cigarettes per day. β: standardized regression coefficients F female, FT4 free thyroxine, FT3 free triiodothyronine, M male, TSH thyroid stimulating hormone.…”

Section: Discussionsupporting

confidence: 85%

“…Indeed, with some exceptions, evidence has accumulated since that cigarette smoking is associated lower TSH and higher FT4 levels, whereas T3 and FT3 were also found to be higher or unaltered [9,10,12,13]. In addition, using serum or urinary cotinine as a measure of nicotine exposure it was found that smoke exposure is associated with lower TSH levels [14,15].…”

Section: Introductionmentioning

confidence: 99%

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Cigarette smoking is associated with higher thyroid hormone and lower TSH levels: the PREVEND study

et al. 2019

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Purpose The extent to which smoking is associated with thyroid stimulating hormone (TSH), free thyroxine (FT4), and free triiodothyronine (FT3) when taking account of clinical variables including alcohol consumption is unclear. We aimed to determine associations of TSH, FT4, and FT3 levels with current smoking. Methods A cross-sectional study was performed in 5766 euthyroid participants (Prevention of Renal and Vascular End-Stage Disease cohort). Current smoking was determined by self-report, categorized as never, former, and current (≤20 and >20 cigarettes per day). Smoke exposure was determined by urinary cotinine. Results Current smoking of ≤20 and >20 cigarettes per day was associated with lower TSH and higher FT3 levels. FT4 levels were higher in subjects smoking <20 cigarettes per day vs. never and former smokers. Current smokers also consumed more alcohol. Multivariable linear regression analyses adjusted for age, sex, anti-TPO autoantibody positivity, alcohol consumption, and other variables demonstrated that lower TSH, higher FT4 and higher FT3 were associated with smoking ≤20 cigarettes per day vs. subjects who never smoked (P < 0.001, P = 0.018, and P < 0.001, respectively) without a further significant incremental effect of smoking >20 cigarettes per day. In agreement, TSH was inversely, whereas FT4 and FT3 levels were positively associated with urinary cotinine (P < 0.001 for each). In contrast, alcohol consumption >30 g per day conferred higher TSH and lower FT3 levels. Conclusions Cigarette smoking is associated with modestly higher FT4 and FT3, and lower TSH levels, partly opposing effects of alcohol consumption.

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Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Cigarette smoking is associated with higher thyroid hormone and lower TSH levels: the PREVEND study

et al. 2019

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“…Additionally, the three substances (cocaine, nicotine, and opioids) that showed an interactive effect with rs8052287 on SI have been investigated previously with respect to thyroid homeostasis. Cigarette smoking appears to affect thyroid function with a dose-related effect linking cotinine levels to thyroid function and thyroid autoimmunity 46 . Cocaine abuse has been linked to the disruptions in the hypothalamic-pituitary-thyroid axis 47 and cocaine use has been suggested as a possible trigger for thyroid storm 48 .…”

Section: Discussionmentioning

confidence: 99%

Multi-environment gene interactions linked to the interplay between polysubstance dependence and suicidality

et al. 2021

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Substance dependence diagnoses (SDs) are important risk factors for suicidality. We investigated the associations of multiple SDs with different suicidality outcomes, testing how genetic background moderates these associations. The Yale-Penn cohort (N = 15,557) was recruited to investigate the genetics of SDs. The Army STARRS (Study to Assess Risk and Resilience in Servicemembers) cohort (N = 11,236) was recruited to evaluate mental health risk and resilience among Army personnel. We applied multivariate logistic regression to investigate the associations of SDs with suicidality and, in the Yale-Penn cohort, we used the structured linear mixed model (StructLMM) to study multivariate gene–environment interactions. In Yale-Penn, lifetime polysubstance dependence was strongly associated with lifetime suicidality: having five SDs showed an association with suicidality, from odds ratio (OR) = 6.77 (95% confidence interval, CI = 5.74–7.99) for suicidal ideation (SI) to OR = 3.61 (95% CI = 2.7–4.86) for suicide attempt (SA). In Army STARRS, having multiple substance use disorders for alcohol and/or drugs was associated with increased suicidality ranging from OR = 2.88 (95% CI = 2.6–3.19) for SI to OR = 3.92 (95% CI = 3.19–4.81) for SA. In Yale-Penn, we identified multivariate gene–environment interactions (Bayes factors, BF > 0) of SI with respect to a gene cluster on chromosome 16 (LCAT, p = 1.82 × 10–7; TSNAXIP1, p = 2.13 × 10−7; CENPT, p = 2.32 × 10−7; PARD6A, p = 5.57 × 10−7) for opioid dependence (BF = 12.2), cocaine dependence (BF = 12.1), nicotine dependence (BF = 9.2), and polysubstance dependence (BF = 2.1). Comorbidity of multiple SDs is a significant associated with suicidality and heritability of suicidality is partially moderated by multivariate gene interactions.

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“…A recent analysis from the Korean National Health and Examination Survey evaluated associations between urinary cotinine (a metabolite of nicotine used routinely to assess exposure to tobacco) and thyroid function [60]. There was no significant association between FT4 and urinary cotinine, but TSH was correlated negatively with the cotinine levels in men and women, and levels of anti-TPO antibodies correlated positively with cotinine in men.…”

Section: Serum Tsh As the Principal Diagnostic Marker Of Systemic mentioning

confidence: 99%

Challenges in Interpreting Thyroid Stimulating Hormone Results in the Diagnosis of Thyroid Dysfunction

Razvi

Bhana

Mrabeti

2019

Journal of Thyroid Research

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The pituitary hormone, thyrotropin (TSH), is regarded as the primary biomarker for evaluating thyroid function and is useful in guiding treatment with levothyroxine for patients with hypothyroidism. The amplified response of TSH to slight changes in thyroid hormone levels provides a large and easily measured signal in the routine care setting. Laboratories provide reference ranges with upper and lower cutoffs for TSH to define normal thyroid function. The upper limit of the range, used to diagnose subclinical (mild) hypothyroidism, is itself a matter for debate, with authoritative guidelines recommending treatment to within the lower half of the range. Concomitant diseases, medications, supplements, age, gender, ethnicity, iodine status, time of day, time of year, autoantibodies, heterophilic antibodies, smoking, and other factors influence the level of TSH, or the performance of current TSH assays. The long-term prognostic implications of small deviations of TSH from the reference range are unclear. Correction of TSH to within the reference range does not always bring thyroid and other biomarkers into range and will not always resolve the patient's symptoms. Overt hypothyroidism requires intervention with levothyroxine. It remains important that physicians managing a patient with symptoms suggestive of thyroid disease consider all of the patient's relevant disease, lifestyle, and other factors before intervening on the basis of a marginally raised TSH level alone. Finally, these limitations of TSH testing mitigate against screening the population for the undoubtedly substantial prevalence of undiagnosed thyroid disease, until appropriately designed randomised trials have quantified the benefits and harms from this approach.

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Impact of smoking on thyroid gland: dose-related effect of urinary cotinine levels on thyroid function and thyroid autoimmunity

Cited by 36 publications

References 29 publications

Cigarette smoking is associated with higher thyroid hormone and lower TSH levels: the PREVEND study

Cigarette smoking is associated with higher thyroid hormone and lower TSH levels: the PREVEND study

Multi-environment gene interactions linked to the interplay between polysubstance dependence and suicidality

Challenges in Interpreting Thyroid Stimulating Hormone Results in the Diagnosis of Thyroid Dysfunction

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