Obesity Link to Autism PDF

Study 1: - Maternal Obesity and Diabetes Link to Autism - Study in the united states - may be issues with generalizability to UK (certain ingredients used in US fast food band in the UK) 1. Risk Associations: a. Maternal prepregnancy obesity and pregestational diabetes mellit...

Study 1: - Maternal Obesity and Diabetes Link to Autism - Study in the united states - may be issues with generalizability to UK (certain ingredients used in US fast food band in the UK) 1. Risk Associations: a. Maternal prepregnancy obesity and pregestational diabetes mellitus (PGDM) are independently associated with an increased risk of ASD in children. b. The risk is most pronounced when mothers have both obesity and either PGDM or gestational diabetes. 2. Mechanisms of Risk: a. Proinflammatory Effects of Obesity: i. Obesity increases circulating proinflammatory cytokines, proteins that mediate immune responses, in pregnant women. ii. This inflammation occurs even without infection and can affect early fetal brain development. iii. In animal models, maternal obesity and high-fat diets lead to inflammation in offspring brains, linked to ASD. b. Diabetes and Intrauterine Inflammation: i. Maternal diabetes induces inflammatory conditions in intrauterine tissues, contributing to a proinflammatory environment. ii. Elevated cytokines in amniotic fluid and placental inflammation are predictors of brain injury and have been implicated in ASD development. 3. Impact on Fetal Brain: a. Maternal immune disturbances during early development and intrauterine inflammation caused by obesity and diabetes are implicated in fetal brain inflammation, a factor in ASD etiology. Study 2 - how increased steroid hormones levels in womb increase likelihood of offspring with autism - Cambridge STUDY IS ONLY ON MEN - CAN NOT BE APPLIED TO WOMEN - previously known elevated prenatal testosterone is associated with slower social and language development, better attention to detail, and more autistic traits. 1. Hormonal Differences and Autism: a. Children who later develop autism are exposed to elevated levels of prenatal steroid hormones (testosterone, progesterone, androstenedione, cortisol). b. elevated hormone levels correlate with traits such as slower social and language development and increased autistic traits. 2. Sex Differences in Autism: a. Higher production of certain steroid hormones in males may partly explain higher prevalence of autism in males compared to females, though not all statistical analyses consistently support this hypothesis. 3. Biological Markers and Timing: a. Elevated prenatal steroid hormone levels are one of the earliest non-genetic biomarkers linked to autism. b. These hormones were measured in amniotic fluid collected during amniocentesis (around 15–16 weeks of gestation), a critical period for brain development and sexual differentiation. 4. Mechanisms of Influence: a. Steroid hormones influence how genetic instructions are translated into proteins, impacting brain development during this prenatal window.  b. Elevated hormone levels during this crucial developmental period may amplify genetic risk factors for autism, aligning with other findings that highlight 15 weeks of gestation as a key period for the expression of genetic risks in the developing brain. How can we link both of these findings to additives in our food? The study and supporting research highlight the impact of food additives—particularly emulsifiers and artificial sweeteners—on maternal and offspring health, as well as broader implications for metabolism and behavior. Key points include: 1. Food Additives and Pregnancy Outcomes: a. Emulsifiers (e.g., CRN and P80) and artificial sweeteners were linked to increased risks of gestational diabetes mellitus (GDM) and large for gestational age (LGA) offspring, particularly in overweight or obese women. 2. Artificial Sweeteners and Obesity: a. Artificial sweeteners like aspartame have coincided with rising obesity rates. They alter food reward pathways by providing sweetness without caloric content, disrupting the gustatory (sensory) and postingestive (metabolic) components of food reward. b. The mesolimbic dopamine system and hypothalamus, crucial for food satisfaction and energy balance, show impaired activation with artificial sweeteners, driving cravings and food-seeking behavior. c. Functional imaging studies reveal natural sugars (e.g., glucose) suppress hypothalamic signals post-ingestion, a response not seen with sucralose. 3. Behavioral and Neurobiological Effects: a. Artificial sweeteners activate taste receptors but fail to provide metabolic satisfaction, fostering sugar dependence and altering flavor preferences. b. This incomplete activation of reward pathways contributes to overeating and the development of obesity. 4. Public Health Implications: a. The findings suggest reducing artificial sweetener consumption and addressing the role of food additives could help mitigate obesity and its associated metabolic disorders. Study 2: The study highlights concerns about the impact of food additives and contaminants on child behavior and development. Key points include: - Food Additives and ADHD: Studies suggest that eliminating additives from diets may benefit children with attention-deficit/hyperactivity disorder (ADHD). Certain additives, such as Blue 1, may cross the blood-brain barrier, although their mechanisms and broader implications require further research. - Perchlorate and Thyroid Disruption: Perchlorate, a contaminant from water or nitrate fertilizers, disrupts thyroid hormone production by interfering with iodide uptake. Thyroid hormones are vital for early brain development. - Risks to Pregnant Women: Exposure to perchlorate is particularly concerning for iodine-deficient pregnant women, as the developing fetus relies entirely on maternal thyroid hormones in the first trimester. Maternal hypothyroidism during pregnancy has been linked to cognitive deficits in children.