In recent years, there has been a significant increase in the prevalence of autism spectrum disorder (ASD), leading to a search for answers by researchers and parents. While the exact causes of ASD remain unknown, new evidence suggests that the fats we consume in our diets may be a contributing factor.
A groundbreaking study has found a potential link between polyunsaturated fatty acids (PUFAs) in our diets and the development of autism. This discovery not only offers insight into the possible origins of ASD but also raises important questions about the long-term effects of our modern dietary habits.
The rise in autism rates has coincided with changes in our dietary patterns, particularly in the types of fats we consume. Could there be a connection between the two?
Polyunsaturated fatty acids (PUFAs) are at the center of this potential link. These fats are found in various foods, including vegetable oils, seeds, nuts, and the meat of animals fed high-PUFA diets. High-PUFA diets can negatively impact thyroid hormone utilization and gut health, leading to inflammation and metabolic issues.
A recent study uncovered a startling finding: the presence of metabolic byproducts of PUFA breakdown in umbilical cord fluid was linked to the severity of autism symptoms in children. This suggests that the waste products produced when our bodies metabolize PUFAs may have a negative impact on the neurological development of children, even before they are born.
The dietary shift towards consuming more PUFAs and fewer saturated fats over the past century may be a contributing factor to the increased prevalence of autism. This change is particularly evident in the rise in consumption of linoleic acid (LA), an omega-6 PUFA found in vegetable oils. This shift in dietary habits has not only affected humans but also the animals we consume, leading to changes in the nutritional profile of our food chain.
The science behind the link between PUFAs and autism involves the breakdown of these fats in our bodies to produce bioactive molecules called eicosanoids. Eicosanoids play important roles in inflammation and other physiological processes and are primarily derived from PUFAs. The more PUFAs we consume, the more eicosanoids our bodies produce, potentially impacting neurological development and health outcomes.
In conclusion, the types of fats we consume in our diets play a crucial role in our overall health and well-being. Understanding the potential risks associated with consuming high levels of PUFAs is essential in addressing the rise in autism rates and promoting healthier dietary habits. Por lo tanto, cuanto menos PUFA comamos, menos eicosanoides habrá alrededor del cuerpo.
La prueba definitiva: diHETrE
El estudio que descubrió la conexión entre los PUFAs y la gravedad del autismo encontró niveles elevados de un eicosanoide específico llamado diHETrE en la sangre del cordón umbilical. DiHETrE se deriva de AA y tiene propiedades inflamatorias conocidas. Su producción implica la acción de enzimas LOX, que introducen grupos hidroxilo en la cadena de ácidos grasos.
Aunque consumimos pequeñas cantidades de AA directamente en nuestra dieta, la gran mayoría proviene de la conversión de LA dietético. Esto significa que un mayor consumo de LA puede llevar a niveles más altos de AA, ya que hay más material disponible para la conversión.
Las conclusiones del estudio fueron impactantes: “Específicamente, se encontró que niveles altos de dioles derivados de AA en la sangre del cordón, incluido el diHETrE total, el 11,12-diHETrE y el 14,15-diHETrE, afectaron significativamente la gravedad de los síntomas del Trastorno del Espectro Autista (TEA). A niveles altos de 11,12-diHETrE, se asoció con discapacidad del TEA … Basado en estos hallazgos, los metabolitos derivados de AA en la sangre del cordón pueden influir en el neurodesarrollo posterior en los niños.”
Estos hallazgos sugieren que la presencia de metabolitos de PUFA (que aumentan a través de un mayor consumo de PUFAs dietéticos) durante el período fetal puede influir en el desarrollo de los síntomas del TEA a través de citoquinas inflamatorias.
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