Razi Journal of Medical Sciences

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Background and Aim: Iodine is essential for the production of thyroid hormones, which regulate many bodily functions, including metabolism and growth.  Thyroid hormones are closely related to the growth, development of the nervous system, and the metabolism of substances throughout the body, thus managing various aspects of the body's metabolism.
Fetal development strongly depends on thyroid and iodine metabolism, especially during critical periods of brain development (from early pregnancy to early birth), nervous system development depends on thyroid hormones and can be compromised if their function is impaired. This narrative review focuses on the role and importance of iodine during pregnancy and lactation and explains various related issues.
Materials and Methods: In this narrative review, PubMed, Web of Science, and Scopus databases, as well as SID, Irandoc, and Magiran Persian databases, were searched with appropriate keywords for related articles, and 97 articles were used for this comparative review.
Results:
Iodine during pregnancy:
Thyroid hormone production in pregnant women increases by 50% in early pregnancy. On the other hand, the increase in the mother's blood volume during pregnancy may be associated with a decrease in the concentration of nutrients and, as a result, a decrease in their concentration in the urine. During pregnancy, maternal iodine is transferred to the fetus through the placenta and is the only source of iodine for the fetus during pregnancy, so the iodine status of pregnant women directly affects the growth and development of the fetus. Insufficient iodine intake during pregnancy can lead to a range of adverse reproductive outcomes, including increased risk of perinatal and infant mortality, and intellectual impairment in children. The most severe consequence of iodine deficiency is cretinism, a condition characterized by severe physical and mental developmental delays. Iodine deficiency during pregnancy can cause serious disorders in maternal and fetal thyroid function and lead to adverse consequences in pregnancy. Studies have shown that overt hypothyroidism due to severe iodine deficiency during pregnancy is associated with adverse outcomes including spontaneous abortion, gestational hypertension, preeclampsia, and gestational diabetes. Mother's thyroid hormone plays an important role in fetal brain development. The brain is especially sensitive to iodine deficiency during its formation in the early embryonic period and after birth. During pregnancy and early lactation, the iodine needed by children is completely taken from the mother. Insufficient iodine as well as excess may cause hypothyroidism. Indeed, iodine deficiency during pregnancy is the most important preventable cause of neurodevelopmental disorders worldwide and is an important global public health issue.
Pregnant and lactating women need more iodine than other adults. In general, pregnant women need a 50% increase in iodine to produce enough thyroid hormone to meet the needs of the fetus, as well as to meet the needs of increased production and placental transfer of thyroid hormone, which is necessary for optimal fetal growth. In areas where iodine is sufficient, the mother's thyroid gland increases its iodine absorption to maintain sufficient reserves inside the thyroid. However, in moderate to severe iodine deficiency, such adaptive mechanisms may fail to maintain adequate iodine stores (4). Accordingly, the daily requirement of iodine during pregnancy increases to 250 micrograms compared to 150 micrograms for non-pregnant women.
Iodine during Lactation:
Infants are more sensitive than other age groups to abnormal changes in iodine concentration because they have the highest iodine requirement per kilogram of body weight. The development of the brain and central nervous system takes place from the second trimester of pregnancy to the age of 3 years. Breastfed infants are solely dependent on the adequate supply of iodine in breast milk for the synthesis of thyroid hormones, and the concentration of iodine in breast milk depends on the mother's dietary intake. Therefore, low maternal iodine intake inevitably predisposes lactating women and their infants to iodine deficiency. Based on this, it is clear that during this period, the mother's iodine intake should be optimal to provide enough iodine for the developing fetus.
Recommendations
Most people get relatively small amounts of iodine in their diet, so an additional source is needed to provide them with enough iodine for their daily needs and to maintain normal thyroid hormone concentrations. Salt, enriched bread and water are the main sources of iodine. WHO recommends fortification of all dietary salt with iodine as an effective and safe strategy for the control and prevention of iodine deficiency disorders (IDD) for those living in iodine-deficient and iodine-sufficient areas. Adults need 150 micrograms of iodine per day, which varies from 90 to 290 micrograms per day based on the age and physiological status of the person. Pregnant and lactating women need more iodine than other adults. 220 to 250 micrograms per day during pregnancy and 250 to 290 micrograms per day during lactation are recommended.
Accordingly, iodine supplementation during pregnancy and lactation is widely and justifiably recommended to prevent the potentially damaging and irreversible consequences of iodine deficiency on child development.
Current WHO recommendations indicate that although iodine supplementation during pregnancy is safe, it may not be justified in pregnant women with mild iodine deficiency living in iodine-sufficient countries
The timing of iodine supplementation seems to be very important in relation to pregnancy. All the evidence shows that iodine supplementation is most effective (probably the only effective agent) in preventing fetal neurologic damage if it is started before conception or in the first and early second trimester of pregnancy and continues throughout pregnancy. Given the timing of thyroid hormone action on the developing fetal brain, it is reasonable to start iodine supplementation for women prone to iodine deficiency before conception, if possible, to ensure adequate thyroid iodine stores.
WHO, UNICEF, and ICCIDD/IGN recommend a daily dose of 250 mcg potassium iodide for lactating women. Alternatively, in countries where iodine deficiency is evident, and has not been corrected by a public iodized salt program, these authorities recommend an annual depot dose of 400 mg of iodized oil orally at 6-monthly intervals for the exclusive breastfeeding mother
Conclusion: In summary, adequate iodine intake during pregnancy and lactation is vital for the health and development of the child. Considering the necessity of sufficient iodine for the development of the nervous system of the fetus and newborn and the increased need for iodine in pregnant and lactating women compared to other adults, it is recommended to take iodine supplements or iodine-rich foods during pregnancy and lactating.
 

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  Background : Adipokines are proteins secreted from adipose tissue that are involved in metabolism control. Adipsin is one of the adipokines that has a systemic role in lipid metabolism or physiological systems relating to energy balance. Serum levels are found to be associated with BMI, and insulin resistance in several studies. The aim of this study was to assess adipsins association with Poly Cystic Ovary Syndrome (PCOS).

  Methods: This case-control study was performed on patients who referred to the clinic of the Research Institute for Endocrine Sciences of Shahid-Beheshti University in 2011. Forty five patients with PCOS and 45 normal individuals as control group were selected by easy given sampling method and studied. Fasting adipsin and insulin serum levels were measured by Elisa method and fasting glucose serum level was measured by enzyme-calorimetric method. Data were analyzed using independent t-test, Pearson correlation coefficient and one-way ANOVA by SPSS 16 software.

  Results: Adipsin serum levels did not correlate with insulin resistance in PCOS (15.93±7.24 ng/dl in PCOS patients and 14.21±7.53 ng/dl in control group). Glucose and insulin serum levels increased in PCOS (104.1±13.4 mg/dl and 10.8±5.2 mU/L respectively) in comparison with controls and these PCOS patients had insulin resistance.

  Conclusion: This study does not show the correlation between adipsin level and PCOS. It is possible to find a relationship between PCOS and adipsin through expanding the population or limiting the age levels.

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  Background : Adiponectin is one of the adipokines derived from adipose tissue. It is involved in the regulation of glucose metabolism, Insulin Resistance (IR) and obesity-related disorders. Adiponectin in patients with Poly Cystic Ovarian Syndrome (PCOS) has a different expression. This study was performed to assess the serum levels of adiponectin in PCOS patients considering the high prevalence of insulin resistance in this patients and its relation with body mass index, fasting insulin and fasting glucose to evaluate

  Methods: This case-control study was performed on 45 PCOS patients and 45 controls being matched in regards to age and BMI . Adinopectin level was measured by ELISA. FBS and insulin were measured by glucose oxidase and ELISA method, respectively. Insulin resistance was determined by HOMA-IR.

  Results : Serum adiponectin level in PCOS subjects and healthy women did not differ statistically. There was no significant difference between fasting insulin and fasting glucose levels in PCOS subjects and healthy women. However, HOMA-IR in PCOS subjects was significantly higher than healthy women. There was a significant negative correlation between adiponectin level and BMI (p=0.035) and fasting glucose (p=0.019). However, after separation of the two groups there was no correlation between adiponectin and BMI.

  Conclusion: Despite the relationship between adiponectin levels and BMI, and as no relation is observed with PCOS, the role of this adipokine in the syndrome is unlikely. Thus, apparently increase in the amount of adiponectin will not be effective in preventing the syndrome.

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Background & Aims: Weight gain during pregnancy can affect maternal mortality, pregnancy complications, and delivery, as well as healthy fetal growth and birth weight. Studies have shown that in addition to maternal obesity, which is associated with an increased risk of gestational hypertension, gestational diabetes, stillbirth, and large for gestational age, higher gestational weight gain has also adverse effects on maternal and fetal pregnancy outcomes. Besides, being overweight during pregnancy is associated with problems with breastfeeding in the postpartum period and causes postpartum weight gain, which can persist for up to three years after delivery. This, in turn, can leads to the unfavorable outcome of labor during subsequent pregnancies.
Most weight gain during pregnancy is related to the uterus and its contents, breasts, and increased blood volume and extravascular fluid. Besides, the weight gain is due to metabolic changes that lead to an increase in cellular water. Between 20 and 30 weeks of gestation, weight gain is largely due to increased maternal fat stores, and between 30 and 40 weeks of gestation, most of the weight gain is due to fetal growth and increased extravascular fluid.
Several factors such as pre-pregnancy weight, height, ethnicity, age, parity, smoking, socioeconomic status, and daily energy consumption affect the rate of weight gain during pregnancy. Also, metabolic factors such as fat biomarkers (adipocytokines) and less rest are associated with more weight gain.  Maternal thyroid function also appears to influence maternal weight gain and may have an adverse effect on maternal and neonatal outcomes. Maternal free thyroxine (FT4) has an important relationship with maternal fat stores so that in euthyroid individuals, maternal fat stores are associated with lower FT4. While this hormone is much less related to fetal growth and increased extravascular fluid, it is associated with weight gain between 30 and 40 weeks of pregnancy. Studies on the relationship between maternal thyroid function and weight gain during pregnancy are limited in this review study, we summarized the studies that assessed the effect of maternal thyroid function on maternal weight gain.
Methods: In this systematic review, the PubMed, Web of Science, and Scopus, as well as SID, Irandoc, and Magiran (Persian databases) were searched with appropriate keywords for the English and Persian related articles up to March 2020. The comprehensive electronic literature searching was conducted independently by two authors, who were familiar with search methods and information sources, without any restrictions. Furthermore, to maximize the identification of eligible studies, review articles and the reference lists of studies included were manually evaluated as well. We also excluded non-original studies including guidelines, review articles, case reports, animal studies, commentaries, editorials, letters to the editor, meeting abstracts, as well as studies that did not provide accurate and clear data. The quality of the studies was critically appraised for their methodology and results. Two authors, blinded to study author, journal name, and institution, evaluated the quality of the studies independently. The Newcastle-Ottawa scale was used to evaluate the quality of articles for cohort studies. This scale evaluates the quality of published nonrandomized studies in terms of selection, comparability, and outcomes. In the current review, out of 121 articles (115 English articles and 6 Persian articles) in the initial search, finally, 5 eligible studies were reviewed. The results of the quality assessment of the studies showed that all 5 studies had the desired (high) quality.
Results: The results of some studies showed a strong association between maternal thyroid function and weight gain during pregnancy. Higher TSH levels and lower maternal FT4 levels in early pregnancy and lower FT4 levels in mid-pregnancy have been associated with an increased risk of overweight gain during pregnancy. The basic mechanisms associated with maternal thyroid function and maternal weight gain during pregnancy are still unclear. However, there seems to be a two-pronged effect in this regard.
Maternal weight gain in early pregnancy largely reflects maternal fat deposition, and in mid-and late pregnancy reflects increased maternal fluid and amniotic fluid and fetal, placental, and uterine growth. Studies have shown that maternal thyroxin (FT4) levels have a significant relationship with maternal fat reserves. Adipocytes increase the level of the hormone leptin, which in turn affects neurons in the hypothalamus and thus the thyrotropic axis and TSH secretion. Both cross-sectional and longitudinal studies have shown that increased leptin levels lead to higher TSH levels above the upper limit of reference. Changes in leptin levels are associated with weight gain and may affect thyroid function via hypothalamic-pituitary-thyroid stimulation.
Increased hCG levels stimulate the thyroid gland through stimulation of the TSH receptor, leading to increased FT4 and decreased TSH levels during pregnancy. Because hCG levels are highest at the end of the first trimester, TSH levels are lower early in pregnancy. However, maternal hCG levels may also affect maternal weight during pregnancy, and it has been suggested that the effect of hCG may somewhat explain the weaker association between maternal TSH levels and maternal weight during pregnancy. Studies of the association of high body mass index (BMI) with maternal FT4 may also be explained by the effect of human chorionic gonadotropin (hCG).
Conclusion: Maternal weight during pregnancy should be considered as one of the important variables in studies focusing on the effect of maternal thyroid function during pregnancy on pregnancy and child outcomes. There is insufficient data on the relationship between maternal thyroid function during pregnancy and maternal weight gain, and the underlying mechanisms are unclear. The effect of thyroid hormones on maternal weight gain seems to be implemented through several biological pathways and seems to be a two-way effect. While thyroid function has a clear effect on basal metabolism and can affect fat stores, on the other hand, maternal weight gain may lead to altered thyroid function. What is certain is that more studies are needed to gain more insight into the observed relationships and their underlying complex mechanisms, especially among pregnant women. Future research is also needed to review thyroid hormone intervention strategies in women with high pre-pregnancy BMI and low FT4, as well as their impact on lower weight gain during pregnancy and better outcome outcomes.

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Background & Aims: Polycystic ovary syndrome is the most common endocrine disorder of the reproductive system in women. It is associated with some diseases such as insulin resistance, type 2 diabetes, endometrial hyperplasia, increased risk of cardiovascular disease, depression and sometimes mental disorders (2). Insulin resistance is currently a common feature of polycystic ovary syndrome, which puts women at risk for type 2 diabetes, coronary artery disease, high blood pressure and obesity. According to research, 70% of women with this complication have insulin resistance (4). Insulin resistance leads to an increase in insulin levels, which stimulates androgen production in the ovarian stroma and impairs follicular development (5). In addition, research has shown that in people with polycystic ovary syndrome, some cardiovascular risk factors such as apolipoproteins (6) are also affected, which due to the mechanisms of this disease, this change in balance is formed.
Research suggests that the most important way to prevent and treat infertility disorders in people with polycystic ovary syndrome is to control their diabetes and weight (16). Although the benefits of aerobic exercise have been proven in many studies, little research has been done on intense intermittent exercise. One type of intense intermittent exercise is the Tabata exercise (5). Numerous clinical studies have reported significant aerobic, metabolic, musculoskeletal, and psychological benefits for water sports programs and intermittent swimming exercises (22).
Considering the above and the importance of treating polycystic ovary syndrome on the one hand and the importance of angiogenesis on the other hand, the researcher intends to investigate the effect of Tabata exercise in water and metformin on endostatin and in obese women with polycystic ovary syndrome.
Methods: The present research is a quantitative and applied study that was conducted with a two-group design (experimental and control) with pre-test and post-test. The statistical population of the present study consisted of all women with a body mass index of more than 29.9 in Isfahan with polycystic ovary syndrome. 30 people were selected as a sample from the community and provided they met the inclusion criteria, which were randomly assigned to the experimental group of Tabata + metformin exercise control. Subjects then completed a personal information questionnaire and blood samples were taken after 12 hours of night fasting to determine the level of research variables. In the continuation of the experimental group, the training program consisted of 12 weeks, 3 sessions per week and each session lasted 40 minutes of Tabata training in water with a special training song for 20 minutes and 10 minutes of stretching and cooling exercises. The dose of metformin prescribed in the experimental group was 500 mgr twice a day after breakfast and dinner. 48 hours after the last training session, blood samples were taken again from all subjects. Descriptive statistics and Shapiro-Wilk tests, one-way analysis of variance and Tukey's post hoc test were used to analyze the data using SPSS / 21 software at the significance level of 0.05.
Results: The results showed that exercise (F = 27.424, P = 0.001, µ = 0.329) and the interaction of exercise and time (F = 5.865, P = 0.019, µ = 0.095) had a significant effect on adiponectin in obese women with polycystic ovary syndrome. But time had no significant effect on adiponectin in obese women with polycystic ovary syndrome (F = 0.001, P = 0.972, µ = 0.001). It was also found that insulin resistance at the end of the period was significantly lower in the exercise group than the control group (P = 0.0001). In relation to apolipoprotein A, exercise (F = 0.099, P = 0.754, µ = 0.002), time (F = 1.645, P = 0.205, µ 0.029) and exercise-time interaction (F = 1.213, P = 0.275) were determined. µ = 0.021) had no significant effect on the amount of apolipoprotein A in obese women with polycystic ovary syndrome. Other findings showed exercise (F = 1.138, P = 0.291, µ = 0.020), time (F = 0.585, P = 0.448, µ = 0.010) and exercise-time interaction (F = 0.713, P = 0.402, µ = 0.013 ) Have no significant effect on the amount of apolipoprotein B in obese women with polycystic ovary syndrome.
Conclusion: The results of the present study showed that 12 weeks of Tabata exercise program in water led to a significant reduction in insulin resistance in obese women with polycystic ovary syndrome. This finding of the present study is consistent with the results of research by Harrison et al. (2012) and Esmailzadeh Tolouei et al. (2015) (20-21). Probably the reason for the decrease in insulin resistance in the present study is a decrease in factors such as weight, body mass index and fat percentage in these people after exercise.
Regarding apolipoprotein A, it can be said that apolipoprotein A catalyzes low-density lipoprotein in the blood vessel wall of the body, especially the vascular wall of adipose tissue, by activating the enzyme lipoprotein lipase. In sports activities, low-density lipoprotein catabolism develops. Therefore, it is necessary to increase apolipoprotein A, but since the increase in low-density lipoprotein was not significant in this study, the lack of increase in lipopathological catabolism ¬ can be considered a reason for not increasing apolipo protein A.
On the other hand, it has been suggested that the increase threshold of apolipo protein A is to exercise more than one hour per session and more than twelve weeks (26). However, the training protocol was followed in the study for 12 weeks, which could be one of the reasons why apolipo protein A did not change.
Finally, the fact that apolipoprotein B levels do not decrease following Tabata exercises in the present study may be justified by the fact that LDL levels do not decrease. It seems that controlling the diet by consuming less foods with high or high glycemic index and instead consuming foods with low or medium glycemic index can have a positive effect on the amount of apolipoprotein B (29). Therefore, by controlling this nutritional factor, positive changes of apolipoprotein B can be achieved after exercise. However, in the present study, subjects did not follow a specific diet. A period of Tabata training did not cause a significant change in apolipoprotein B levels in obese women with polycystic ovary syndrome.
 
 

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Background & Aims: Obesity and overweight and especially visceral fat accumulation are common findings in people with polycystic ovary syndrome and it has been shown that increasing body fat has a direct role in determining insulin resistance (4) Research shows that weight loss alone in women with polycystic ovary syndrome reduces insulin and androgen levels and resumes ovulation cycles (5) Research has also shown that in people with polycystic ovary syndrome, some cardiovascular risk factors such as fat profile (CHOL, TG, HDL, LDL) (7) are also affected due to The mechanisms of this disease are formed by this change in balance.
Today, restrictions on diet and physical activity are recommended by experts as a priority for these patients (3). This has led to the use of different training methods, which have also yielded different results. Among these is a type of intense periodic Tabata exercise (13). Numerous clinical studies have reported significant aerobic, metabolic, musculoskeletal, and psychological benefits for water sports programs and intermittent swimming exercises (14).
However, in view of the above, it should be noted that due to the complications of polycystic ovary syndrome, which include infertility, cardiovascular disease and insulin resistance; Reducing the symptoms and treating this disease is very important. Therefore, according to the various results that have shown the role of exercise in controlling the symptoms and complications of this disease, and since no research has been done on the effect of Tabata exercises in water on these patients. The effect of Tabata exercises on cardiovascular risk factors in patients with polycystic ovary syndrome can be of particular importance.
Methods: The present research is a quantitative and applied study that was conducted with a two-group design (experimental and control) with pre-test and post-test. The statistical population of the present study consisted of all women with a body mass index of more than 29.9 in Isfahan with polycystic ovary syndrome. 30 people were selected as a sample from the community and provided they met the inclusion criteria, which were randomly assigned to the experimental group of Tabata + metformin exercise control. Subjects then completed a personal information questionnaire and blood samples were taken after 12 hours of night fasting to determine the level of research variables. In the continuation of the experimental group, the training program consisted of 12 weeks, 3 sessions per week and each session lasted 40 minutes of Tabata training in water with a special training song for 20 minutes and 10 minutes of stretching and cooling exercises. The dose of metformin prescribed in the experimental group was 500 mgr twice a day after breakfast and dinner. 48 hours after the last training session, blood samples were taken again from all subjects. Descriptive statistics and Shapiro-Wilk tests, one-way analysis of variance and Tukey's post hoc test were used to analyze the data using SPSS / 21 software at the significance level of 0.05.

Results: The results of two-way analysis of variance test showed exercise (F = 47.708, P = 0.001, µ = 0.536), time (F = 26.049, P = 0.001, µ = 0.317) and exercise-time interaction (F = 69.105, P = 0.001 (5 = 0.552) had a significant effect on adiponectin in obese women with polycystic ovary syndrome. .
Regarding leptin, it was found that exercise, time and interaction of exercise and time had a significant effect on leptin and cholesterol in obese women with polycystic ovary syndrome. Also, the results of Ben Foroni test showed that leptin and cholesterol at the end of the period were significantly lower in the exercise group than the control group.
The results also showed that exercise had a significant effect on triglyceride and LDL levels in obese women with polycystic ovary syndrome, but exercise time and interaction and time had no significant effect.
Based on the results of two-way analysis of variance, it was found that exercise and interaction between exercise and time have a significant effect on HDL in obese women with polycystic ovary syndrome, but time has a significant effect on HDL in obese women with ovarian syndrome. It did not have polycystic.
Conclusion: It seems that the increasing nature of exercise in water, which with a gradual increase in the intensity of exercise and the use of intense exercise movements that were followed in the present study, has led to an increase in energy consumption and a significant increase in adiponectin concentrations. In addition, the involvement of larger muscle masses in this method of exercise has helped to intensify this process in obese women with polycystic ovary syndrome. Findings have shown that when working in water, more muscle groups are used to overcome water resistance, and this can be useful in increasing the dynamic pressure on bones and muscles and increase energy consumption(23). It seems that this mechanism is the main cause of changes in serum adiponectin in the present study.
Intensity and duration of activity, nutritional status of individuals, blood sampling hours, calorie imbalance, rhythm of leptin wheels, etc. are affected by exercise (30). People who are more obese are more resistant to leptin, so they need more exercise to affect leptin levels (30). Modifying the leptin response to exercise can lead to insulin sensitivity and improve energy expenditure. In general, physical activity lowers leptin levels not only by reducing fat mass but also by increasing leptin sensitivity.
The results of the present study showed that eight weeks of Tabata training in water had no significant effect on cholesterol levels in obese women with polycystic ovary syndrome. Cholesterol levels are affected by the balance between endogenous cholesterol and cholesterol from food. In the present study, nutrition and stress could not be controlled. Perhaps due to the pressure and duration of the protocol, cholesterol levels in obese women with polycystic ovary syndrome did not change significantly. Because the mechanism of action of exercise in improving lipid profile is related to the enzymatic processes involved in lipid metabolism, so if exercise was done with proper nutrition, it would allow for greater enzymatic and hormonal adaptation and changes in cholesterol.
Regarding the possible mechanism of the effect of physical activity on blood lipoproteins, the findings of previous research have shown that physical activity reduces triglycerides by increasing the activity of two enzymes, lipoprotein lipase and lecithin cholesterol acyl transferase (32). It seems that longer training can be more effective on the lipid profile, while exercise affects most of the lipid profile of women with higher basal triglyceride levels (33). Also, one of the mechanisms of effect of regular physical activity is that it increases the transport and use of triglycerides by muscle (34).