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Insulin is a regulatory hormone produced by pancreatic beta cells. It lowers blood glucose by promoting cellular uptake and glycogenesis. It does not cause insulin resistance; rather, resistance occurs when cells fail to respond to insulin. In gestational diabetes, insulin secretion may increase to compensate, but the hormone itself is not the cause of resistance.

Estrogen levels rise during pregnancy and support uterine growth and vascularization. While estrogen has mild antagonistic effects on insulin, it does not significantly contribute to gestational insulin resistance. Its role is more prominent in modulating lipid metabolism and increasing hepatic protein synthesis, not in impairing glucose uptake.

Thyroxine (T4) is a thyroid hormone involved in basal metabolic rate regulation. It increases glucose absorption from the gut and enhances insulin degradation but does not directly induce insulin resistance. Thyroid dysfunction may affect glucose metabolism, but thyroxine is not a major contributor to gestational diabetes pathophysiology.

Caucasian women, particularly non-Hispanic whites, have a lower incidence of GDM. Their metabolic profile shows better insulin sensitivity and beta-cell compensation. While GDM can occur in any group, Caucasians are not considered high-risk compared to Hispanic, Asian, or African American populations.

Scandinavian populations have one of the lowest GDM rates globally. Their genetic background and dietary patterns contribute to lower insulin resistance. Population-based studies from Norway and Sweden confirm reduced GDM prevalence compared to multiethnic cohorts.

Irish ethnicity does not show elevated GDM risk in epidemiological studies. Their glucose tolerance and pregnancy outcomes align more closely with other Northern European groups. No significant data supports Irish women being at higher risk than Hispanic or Asian populations.

A history of delivering a 7-pound infant does not meet the threshold for macrosomia, which is defined as birth weight >4,000 g (8.8 pounds). Macrosomia is a clinical marker of prior glucose intolerance, but 7 pounds is within normal range and does not indicate elevated GDM risk.

A pre-pregnancy BMI of 22 kg/m² is within the normal weight range (18.5–24.9 kg/m²). Obesity (BMI ≥30 kg/m²) is a significant risk factor for GDM due to increased insulin resistance. A BMI of 22 does not confer elevated risk and reflects healthy metabolic status.

Maternal age of 20 years is not considered a risk factor for GDM. Advanced maternal age (>35 years) is associated with increased insulin resistance and beta-cell decline. Younger age groups typically have lower metabolic risk and better glucose tolerance.

Fasting threshold for GDM diagnosis is ≥95 mg/dL, not 85 mg/dL. A value of 85 mg/dL is within normal fasting range and does not meet diagnostic criteria. Fasting glucose reflects basal insulin activity and hepatic glucose output, but 85 mg/dL is below the required threshold.

The 1-hour threshold is ≥180 mg/dL, not 170 mg/dL. A 1-hour value of 170 mg/dL is elevated but not diagnostic. The 1-hour reading assesses early insulin response and glucose absorption, but 170 mg/dL falls short of the diagnostic cutoff.

The 3-hour threshold is ≥140 mg/dL, not 130 mg/dL. A value of 130 mg/dL is below the diagnostic limit and reflects adequate glucose disposal. The 3-hour value helps assess sustained insulin action, but 130 mg/dL does not meet the criteria for GDM.

A fasting glucose of 80 mg/dL is within the normal range and does not meet the diagnostic threshold. It reflects adequate basal insulin function and hepatic glucose regulation. This value is not considered abnormal in the context of GDM screening.

A fasting glucose of 100 mg/dL exceeds the diagnostic threshold but is not the criterion used for GDM diagnosis. While it may indicate impaired fasting glucose in non-pregnant adults, the GDM threshold is lower due to pregnancy-induced insulin resistance. The correct cutoff is 92 mg/dL.

A fasting glucose of 126 mg/dL meets the criteria for overt diabetes, not GDM. This value suggests pre-existing diabetes mellitus and requires immediate management. GDM is diagnosed with lower thresholds specific to pregnancy physiology, and 126 mg/dL is beyond that scope.

Preterm labor is not directly caused by macrosomia. GDM is more commonly associated with post-term pregnancies due to delayed fetal lung maturity. While poorly controlled diabetes may increase risk of polyhydramnios, which can contribute to preterm labor, macrosomia itself is not a causative factor.

Low birth weight is the opposite of macrosomia. GDM leads to fetal overgrowth due to persistent maternal hyperglycemia and fetal hyperinsulinemia. Low birth weight (<2,500 g) is more typical in conditions like placental insufficiency, hypertension, or intrauterine growth restriction, not GDM.

Fetal anemia is not a complication of macrosomia. GDM does not impair fetal erythropoiesis or cause hemolysis. Anemia may result from fetomaternal hemorrhage, isoimmunization, or parvovirus B19, but not from the metabolic effects of GDM or macrosomia.

Congenital heart defects are more common in pre-gestational diabetes, especially if poorly controlled during organogenesis (weeks 3–8). GDM typically develops later in pregnancy and does not affect early fetal cardiac development. Thus, heart defects are not a direct complication of GDM-related hyperinsulinemia.

Spina bifida is a neural tube defect linked to folate deficiency and teratogenic exposures during early pregnancy. It is not caused by fetal hyperinsulinemia or GDM. GDM develops after neural tube closure (by week 4), so it does not interfere with neural tube formation.

Cleft lip and palate result from failure of facial fusion during embryogenesis, typically between weeks 4 and 7. GDM arises later and does not affect craniofacial development. These defects are associated with genetic syndromes and maternal exposures, not insulin-mediated effects.

Restricting all carbohydrate intake is not recommended. Carbohydrates are essential for fetal energy and maternal metabolism. The focus is on choosing complex carbohydrates with low glycemic index, not eliminating them. Total restriction can lead to ketosis, which is harmful to the fetus.

Rapid weight loss is contraindicated in pregnancy. Nutritional therapy aims for adequate weight gain based on pre-pregnancy BMI. Weight loss can impair fetal growth and increase risk of nutrient deficiencies. The goal is metabolic control, not weight reduction.

Increasing protein intake exclusively does not address glucose regulation. While protein supports fetal development, GDM management requires carbohydrate control and balanced macronutrients. Excess protein without carbohydrate moderation does not prevent hyperglycemia or its complications.

High-intensity interval training is contraindicated in pregnancy with GDM due to risk of maternal hypoxia and fetal acidosis. These exercises exceed 85% of maximum heart rate, increasing catecholamine release and uterine blood flow redistribution. This can impair placental perfusion and elevate risk of preterm labor or fetal distress.

Weightlifting with heavy weights is discouraged due to increased intra-abdominal pressure and risk of valsalva-induced hypotension. Heavy resistance training may compromise venous return, reduce uteroplacental perfusion, and increase risk of musculoskeletal injury. It does not significantly improve insulin sensitivity compared to aerobic activity.

Contact sports pose risk of abdominal trauma and placental abruption. Activities like soccer or basketball involve rapid direction changes, falls, and collisions, which can lead to uterine injury, premature rupture of membranes, or fetal compromise. These are contraindicated throughout pregnancy regardless of GDM status.