Abstract
The incidence of differentiated thyroid cancer has been increasing in the last decades all over the world. Such a steady growth cannot be entirely attributable to more intensive thyroid nodule screening and more sensitive diagnostic procedures. Several environmental factors have changed with sufficient rapidity in the same time frame and may represent credible candidates for this increase. They include modified iodine intake, lifestyle-associated risk factors, exposure to various toxic compounds, pollutants and xenobiotics, nutritional deficiencies, eating habits and comorbidities. Foremost, nutritional patterns have gained high interest as possible promoters and modifiable risk factors for thyroid cancer in recent years. The aim of this narrative review is to focus on the relationship between thyroid cancer and nutritional factors, dietary habits and obesity. Low iodine intake has been associated to increased risk of thyroid cancer, favoring the development of more aggressive histotypes. Moreover, correction of iodine deficiency can shift thyroid cancer subtypes toward less aggressive forms, without affecting the overall risk for cancer. Actually, evidence regarding the association between selenium and vitamin D deficiency and thyroid cancer is very limited, despite their well-known anti-cancer potentials, and the clinical usefulness of their supplementation is still uncertain in this setting. Albeit the relationship between single foods and thyroid cancer is difficult to examine, fish and iodine-rich foods, vegetables, and fruits might exert protective effects on thyroid cancer risk. Conversely, no clear association has been found for other foods to date. Lastly, a clear association between obesity and the risk of thyroid cancer, with more aggressive behavior, seems to emerge from most studies, likely involving variations in thyroid function and chronic inflammation mediated by cytokines, insulin, leptin and adiponectins. Although no definite association between dietary factors and thyroid cancer has been firmly established so far, some nutritional patterns, together with excessive weight, seem to play a relevant role in thyroid cancer carcinogenesis as well as in its severity and aggressiveness. These effects may play an additive role to the well-established one exerted by environmental carcinogens, such as pollutants and radiation exposure.
Acknowledgements
This review is part of the “EOLO” project (Endocrinology and Oncology Learning Objects) led by Professors Emanuela Arvat, Annamaria Colao, Andrea Isidori, Andrea Lenzi and by dr. Roberto Baldelli, which aims at increasing the knowledge on oncological endocrinology. We would like to acknowledge all the Collaborators of this project: M. Albertelli, D. Attala, A. Bianchi, A. Di Sarno, T. Feola, G. Mazziotti, A. Nervo, C. Pozza, G. Puliani, P. Razzore, S. Ramponi, S. Ricciardi, L. Rizza, F. Rota, E. Sbardella, M.C. Zatelli.
Authors’ contributions
The authors’ responsibilities were as follows: L.B., M.G., M.R.R., P.d.G., F.S. and NP were responsible for the concept of this paper and drafted the manuscript; V.A., V.B., V.R. and R.B. provided a critical review of the paper. All authors contributed to and agreed on the final version of the manuscript. All authors read and approved the final manuscript.
Competing interests
The authors declare that they have no competing interests.
Abbreviations
1,25(OH)2D3calcitriol
25OH-D325-hydroxyvitamin D
ADIPO-Radiponectin receptor 1
ATAAmerican Thyroid Association
BATbrown adipose tissue
BMIbody mass index
CHEKcheckpoint kinase
CIconfidence interval
DIOiodothyronine deiodinases
DTCdifferentiated thyroid carcinoma
EPICEuropean Prospective Investigation into Cancer and Nutrition study
FNAfine-needle aspiration
FTCfollicular thyroid cancer
GPXglutathione peroxidases
H2O2hydrogen peroxide
HAAheterocyclic aromatic amines
HRhazard ratio
IARCInternational Agency for Research on Cancer
IRinsulin resistance
MAPK signaling pathways a mitogen-activated protein kinase
NOCN-nitroso-compounds
ORodds ratio
OSAobstructive sleep apnea
PAHpolycyclic aromatic hydrocarbons
PI3Kphosphoinositide 3-kinases
PTCpapillary thyroid cancer
PUFAsn–3 polyunsaturated fatty acids
RAIradioactive iodine 131I
RETREarranged during Transfection
RRrelative risk
SEERSurveillance, Epidemiology, and End Results
SMDstandardized mean differences
TNMtumor-node-metastasis
TRKTropomyosin receptor kinase
TSHThyroid-stimulating hormone
TXNRDthioredoxin reductases
VDRvitamin D receptor
WATwhite adipose tissue
WHOWorld Health Organization