Researcher András Visegrády has proposed an intriguing new idea that attempts to connect many of these observations. Rather than suggesting that autism has one simple cause, his hypothesis explores whether a particular pattern of biological change during the earliest months of life could help explain why autism develops in some children. It is an ambitious proposal that does not claim to provide definitive answers, but instead offers a fresh framework that future research can investigate.

At the heart of this idea is a naturally occurring substance called insulin-like growth factor 1, better known as IGF-1. Despite its technical name, IGF-1 performs a remarkably straightforward job. It helps regulate growth throughout the body and thus also promotes the development of the brain. During infancy, when the brain is growing at an extraordinary pace, this molecule plays an especially important role by encouraging nerve cells to mature, connect with one another, and survive.

Scientists have long suspected that IGF-1 may have some connection with autism because previous studies have found altered levels of the molecule in some children with the condition. However, these findings have never fully explained the distinctive developmental pattern often seen in autism. Many children who are later diagnosed appear to experience unusually rapid brain growth during infancy, followed by a slowing of development during early childhood. This unusual sequence has remained difficult to explain.

The hypothesis developed by András Visegrády suggests that the timing of IGF-1 activity may be just as important as its overall level. Instead of focusing on a constant shortage or excess of the growth factor, the paper proposes a two stage process. During the first year of life, IGF-1 activity may temporarily become unusually high, encouraging faster than normal growth. Later, as the body’s hormonal control systems mature, IGF-1 activity may fall too sharply, slowing developmental processes that normally continue throughout early childhood.

If this sequence occurs, it could potentially explain why researchers have observed both accelerated and slowed development at different stages in children who later receive an autism diagnosis.

The proposal reaches even further by examining events that occur before birth. Pregnancy is an extraordinarily complex biological balancing act in which both mother and baby constantly influence one another. Certain maternal conditions have repeatedly been associated with a higher likelihood of the later appearance of autism in their children, including metabolic disorders such as gestational diabetes, obesity, high blood pressure, and problems affecting fetal growth.

Rather than viewing these factors separately, the hypothesis asks whether they may sometimes interact in unexpected ways. Some pregnancy complications are linked with reduced fetal growth, while others are associated with increased insulin activity and faster growth. According to the proposed model, when these opposing influences occur together, they may create unusual changes in the newborn’s hormonal regulation after birth.

During the first months of life, babies regulate IGF-1 differently from older children or adults. Early on, insulin plays a particularly strong role in controlling this growth signal before the body’s growth hormone system gradually takes over. The review argues that this transition could represent a vulnerable developmental window. Temporary disruption during this period might first encourage excessive growth and later contribute to an abrupt slowing once hormonal control shifts.

This concept also offers possible explanations for several puzzling observations that have challenged researchers for years. It may help account for why brain imaging studies often detect early enlargement of certain brain structures before later developmental changes emerge. It could also help explain why autism presents with such remarkable diversity, since different regions of the brain may respond differently to altered growth signals. Genetic differences, environmental influences, and chance developmental variation could all shape the final outcome, even if they begin with a shared biological process.

Other findings also fit within this proposed framework. Autism is diagnosed more often in boys than girls, and the hypothesis suggests that known differences in early growth and sensitivity to growth signals might contribute to this imbalance. It also considers why autism sometimes appears repeatedly within families, while recognising that inherited genes almost certainly influence susceptibility alongside prenatal and postnatal biology. Importantly, the review does not dismiss genetics. Instead, it argues that genes, pregnancy conditions, and early hormonal regulation may all interact to shape development.

As with every scientific hypothesis, the real test comes from evidence. Visegrády outlines several ways the idea could be examined. Researchers could measure brain IGF-1 levels in infants who are at higher likelihood of developing autism, study combinations of pregnancy conditions rather than individual risk factors in isolation and investigate whether changes in early metabolism consistently predict later developmental outcomes. If future studies support these predictions, they could open new avenues for identifying children at risk earlier and perhaps even developing preventive strategies during the earliest stages of life.

Equally important is what this work does not claim. It does not suggest that IGF-1 alone causes autism, nor does it imply that all autistic people share the same biological pathway. Autism is a highly diverse condition, and the author acknowledges that many genetic and environmental influences almost certainly contribute. Instead, the review offers a unifying hypothesis that seeks to explain why so many seemingly unrelated observations point toward a common period of vulnerability during infancy.

Whether this model ultimately proves correct remains to be seen. Science advances by proposing ideas that can be tested, challenged, refined, or rejected. By bringing together evidence from brain development, pregnancy, metabolism, and endocrinology, this review encourages researchers to look beyond isolated findings and consider how the earliest months of life may shape lifelong neurodevelopment. Even if the hypothesis evolves as new evidence emerges, it provides a thought-provoking roadmap for future investigation and a reminder that understanding autism requires connecting many pieces of an exceptionally complex biological puzzle.