Investigating the Impact of Selenium Deficiency on Thyroid Function in Iodine-Deficient New Zealand Women | Chapter 8 | Achievements and Challenges of Medicine and Medical Science Vol. 7

This narrative review aimed to present the current situation in New Zealand women who are mostly selenium and iodine deficient across their lifespans. The prevalence of thyroid disease in New Zealand women is about 5% and increased to 7%-14% in women over 50 years of age. The importance of selenium is widely recognised. Selenium plays a crucial role in metabolic, immune-endocrine, and cellular homeostasis, owing to its antioxidant and anti-inflammatory properties. Changes in selenium status may affect immune response, neurodegeneration, cardiovascular disease, and cancer. The biological actions of selenium are mostly mediated through the expression of at least 30 selenoproteins, coded by 25 genes with the 21st amino acid selenocysteine at their active centre. Selenoenzymes, selenoprotein P and glutathione peroxidase are present in human plasma and can be used as a biomarker of selenium nutritional status. The thyroid gland has a high tissue concentration of the essential micronutrient selenium (Se), more than the liver, skeletal muscles or any other organ or tissue. Thyroid dysfunction is a significant health issue in New Zealand, with women being 4.5 times more likely than men to have thyroid disorders.  For the North Island, but not for the South Island, selenium intakes have improved after increased importation of high-Se Australian and other imported wheat, because the soil in New Zealand is poor in selenium. According to the most recent 2008/09 New Zealand Nutrition Survey (NZANS), selenium intakes increased from 1997 to 2008/09. The 2023 study indicated that overall plasma selenium concentrations were higher in those living in the Nort Island (93µg/L) than in those (85.4µg/L) in the South Island.   Plasma selenium concentrations around 95 µg/L are sufficient to saturate glutathione peroxidase activity although more selenium is required to saturate selenoprotein P than to optimise GPx. In New Zealand women low plasma levels of selenium intake and low levels in the food supply have been observed in women of childbearing age and postmenopausal. Inadequate selenium status was noted in postpartum women, breastfeeding women and their infants. This situation somehow creates a vicious cycle of selenium deficiency. The finding of low plasma selenium concentrations in women who were also iodine deficient was an indicator of high thyroid dysfunction which might present itself with overt hypothyroidism, subclinical hyperthyroidism and thyroid autoimmune disorder. Current studies noted that most healthy elderly women had selenium intakes marginal to iodine intakes. Due to a lack of oestrogen, they are put at risk of compromised thyroid function. Selenium supplementation with selenomethionine (SeMet) or selenium selenite might improve selenium deficiency and slow thyroid destruction by thyroid autoantibodies. Hormone replacement therapy and antidepressant and antianxiety medication cannot decrease the symptoms of thyroid dysfunction.

 

Author (s) Details

 

Ljiljana Jowitt
Faculty of Health and Environmental Sciences, The School of Public Health and Interdisciplinary Studies, AUT University, 90 Akoranga Drive, North Shore Campus, AZ Building Level 4, P.O. Box 92006, 1142, Auckland, New Zealand.

 

 

Please see the book here:- https://doi.org/10.9734/bpi/acmms/v7/2659

A Review on Ethnicity and Type 2 Diabetes in Pacific Adults in New Zealand | Chapter 12 | Recent Updates in Disease and Health Research Vol. 8

 

This review presented ethnic characteristics of type 2 diabetes in Pacific Island adults in New Zealand. Diabetes mellitus is one out of four non-communicable diseases (NCDs), which represents a set of metabolic disorders with chronic hyperglycaemia due to defects of insulin secretion, insulin action, or both. If left untreated or undiagnosed, diabetes mellitus leads to confusion, coma, or death due to ketoacidosis. Pacific Island people in New Zealand with a specific Polynesian phenotype originate from the islands in the Pacific Ocean such as Samoa, the Cook Islands, Tonga, Niue, Tokelau, Papua New Guinea, Vanuatu, Kiribati, Fiji, Solomon Islands, Nauru, and French Polynesia. Therefore, they may have similar genetic and cultural origins. Pacific Island populations were attracted to New Zealand by the prospect of employment and were welcomed as a solution to workforce shortages in unskilled and semi-skilled occupations. About 42% of the Pacific population live in the 10% most deprived areas of the country, with poorer housing and overcrowding, which suggests that the incidence of diabetes is higher for people living in the most deprived areas, compared with people living in the least deprived areas. Socioeconomic inequalities, low education and unemployment create remarkable psychological distress. Changes in diet rich in sugars, tobacco use, and harmful use of alcohol have resulted in a profound reduction in physical activity and increased obesity rates in adults and children. The “thrifty genotype” hypothesis can explain the current increase in the prevalence of obesity in New Zealanders of Polynesian descent.

Obesity and type 2 diabetes are major challenges for Pacific Island adults, and they still have comparatively higher rates of obesity (68%) and diagnosed diabetes (13%), ten years earlier than any other ethnic group in New Zealand. Overweight and obesity have been linked to lower serum 25-OHD concentrations, impaired insulin action, glucose metabolism, and various metabolic processes in adipose and lean (muscle) tissue. Central or visceral fat is more metabolically active than subcutaneous fat, causing dysmetabolism of fatty acids and increased influx of free fatty acids into the splanchnic circulation. Besides storing fat, adipose tissue releases molecules commonly referred to as adipokines which may support β- cell failure and the development of type 2 diabetes in Pacific people. Antihypertensive and anti-lipid (statin) therapy was lowest among Pacifica people. The blood levels of triglycerides were the lowest in the Pacific population. However, HbA1C was significantly higher among Pacific people than among Māori, who had higher HbA1C than New Zealand Europeans. Interestingly, as a group, Pacific Island populations are neither hyperinsulinaemic nor insulin-resistant using HOMA-IR. This Polynesian phenotype is linked to the metabolic disorders of gout and type 2 diabetes mellitus, due to the presence of visceral obesity owing to its strong association with insulin resistance, metabolic syndrome, type 2 diabetes, and cardiovascular disease.

 

Author(s)details:-

Dr. Ljiljana M. Jowitt
Faculty of Health and Environmental Sciences, School of Public Health and Interdisciplinary Health Studies, Auckland University of Technology, New Zealand.

Please See the book here :- https://doi.org/10.9734/bpi/rudhr/v8/704