I am André Krumel Portella, MD, PhD. I investigate how early-life conditions relate to the developing brain, eating behavior, and mental and metabolic health.
Why can similar experiences lead to different health trajectories? My work with colleagues examines how biology and experience shape responsiveness to the environments we encounter throughout life.
Understanding these differences can help us ask better questions about vulnerability, resilience and opportunities for prevention.
Follow the research programme →Together with Prof. Patricia P. Silveira (silveiralab.ca), we propose that insulin helps coordinate resource allocation with behavioral priorities. Bringing life-history trade-offs, allostasis and developmental programming together may explain why early nutrition and stress leave related marks on metabolism, motivation and emotional responses.
Read the postI manage Cerebra, a 16-node high-performance computing (HPC) cluster hosted at McGill University for the Meaney and Silveira laboratories. I work within a bioinformatics and biostatistics team, supporting the computing infrastructure needed for collaborative biomedical research.
Cerebra provides shared computing, data storage and scientific software for biomedical research in the Meaney and Silveira laboratories, including genomics, epigenomics and developmental neuroscience.
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Connecting scientific claims to their sources
SABICHAO is a research tool I’m developing to help researchers explore scientific papers through the claims they make and the sources they cite. It organizes PDFs into structured, searchable content while preserving sections, paragraphs, figures, tables, and source locations.
Explore SABICHAOMapping Health Science in Public Conversation
I developed Total Presence Research Engine to help researchers explore how health science is discussed outside academic research. The platform collects scientific abstracts, news articles, and YouTube transcripts, identifies relevant passages, and organizes them into interactive maps and research briefs.
Explore Total Presence Research EngineFrom the development of food preferences to dopamine and environmental responsiveness, and the shared roots of mental and metabolic illness.
47 coauthored papers, newest first. Read the plain-language explanations, original sources and key concepts.
Showing all 47 publications
Genetic variants associated with disease across a population may differ from those associated with vulnerability to childhood adversity. This study compared both questions in more than 180,000 adults.
Insulin helps regulate brain function as well as blood sugar. In rats, restricted growth before birth changed how an emotion-related brain region responded to insulin; delivering insulin directly into that region also altered adult behavior.
In UK Biobank adults, adversity before birth and during childhood was associated with having both mental health and cardiometabolic conditions, suggesting shared developmental influences.
Across adult and adolescent cohorts, the relationship between lower birth weight and combined mental and metabolic health risk varied with a genetic score related to dopamine signaling in the striatum.
Food preferences develop through prenatal conditions, early exposure to flavors and experience with textures. This review connects sensory learning with the biological systems that regulate appetite and reward.
Genetically predicted DRD4 activity was associated with different brain responses to food cues in adolescent girls and boys, linking dopamine-related variation to attention and food valuation.
In Montreal children, a dopamine-related gene variant was associated with greater dietary responsiveness to an unhealthy local food environment. The study found no corresponding association with BMI.
Insulin acts within the brain as well as the body. This review examines how altered insulin signaling could connect early adversity with later changes in cognition, behavior and metabolic health.
Among 76 adolescents, lower predicted DRD4 expression was linked to more snack intake in less advantaged circumstances and less in more advantaged circumstances, consistent with differential susceptibility.
In Quebec adults, associations of ice-cream displays and vegetable prices with diet quality differed by a dopamine-related genetic marker, suggesting variation in responsiveness to retail food cues.
Among school-aged children, birth weight had different relationships with activity, screen time and eating in boys and girls. These behaviors did not explain body weight through one common pattern.
Lower birth weight was associated with a more energy-dense, higher-fat diet in school-aged boys, without a difference in total energy intake. The adjusted pattern was not found in girls.
This letter argues that newborns’ responses to sweetness should be compared with their baseline response to water when investigating the effects of restricted fetal growth.
This review connects prenatal growth with later food preferences through appetite hormones, stress regulation and dopamine-related reward systems, extending the thrifty phenotype hypothesis into behavior.
This letter asks whether infants born small may be especially responsive to supportive feeding conditions, using differential susceptibility to frame a question for future research.
Rats overfed early in life showed altered brain insulin signaling, dopamine-related proteins and responses to sweet food, despite similar ordinary chow intake.
Both food restriction and a high-fat prenatal diet produced smaller newborn rats and altered adult activity, with less running in males and more in females.
At age four, a DRD4 variant was associated with differences in snack nutrients and habitual food choices. The laboratory pattern appeared in girls, while some reported food differences crossed both sexes.
This review connects fetal growth, brain reward and stress systems with nutritional security, asking why similar access to food can lead to different dietary outcomes.
This letter argues that prenatal influences on reward and impulse control deserve attention alongside flavor learning when explaining how food preferences develop.
In a Canadian cohort, being born small and a mother’s report of low care in her own childhood jointly predicted lower attention scores in toddlers, suggesting interacting developmental influences.
Male rats raised in smaller litters became heavier and preferred sweet food when given a choice, even though separate tests of chow and sweet-food intake showed no group difference.
Brief daily separations from newborn pups altered rat mothers’ later stress-hormone and stimulant responses, showing that neonatal interventions can also have persistent maternal effects.
Female rats exposed to early stress showed stronger stress responses and a persistent preference for palatable food, despite lower body weight and less ordinary chow intake.
An omega-3-deficient diet worsened several metabolic abnormalities in rats exposed to neonatal stress, showing that later nutrition can interact with early developmental history.
This preschool study linked fetal growth, waiting for a food reward and later fat intake in a sex-specific pattern, providing preliminary evidence for a behavioral extension of the thrifty phenotype.
This review extends the thrifty phenotype hypothesis to food preference and reward, asking whether early conditions shape behaviors that secure energy and influence later metabolic risk.
A rat experiment and an adolescent study linked aspects of early care with anxiety and blood BDNF, suggesting a possible biological marker whose meaning depends on context and genetic background.
This article examines how Brazil’s demographic and disease transitions changed pediatric care, research and training, arguing for attention to chronic conditions and health across the life course.
Early adversity increased anxiety-like behavior in rats, but hippocampal nitric oxide did not differ between groups, leaving the proposed biochemical explanation unsupported by this measure.
In a small study of preterm newborns, poorer fetal growth was associated with fewer positive facial responses to sweetness on the first day of life.
Brief neonatal handling altered adult rats’ behavioral and brain-enzyme responses to chronic stress, suggesting that early experience can modify later vulnerability at a cellular level.
This 2011 review assessed the biological rationale and then-available trials of omega-3 fatty acids in bipolar disorder, with particular attention to depressive symptoms and BDNF-related mechanisms.
Adults exposed to maternal smoking before birth had a higher carbohydrate-to-protein intake ratio, even after adjustment for fetal growth and other measured factors.
Neonatally handled rats pursued sweet food more strongly while showing fewer positive taste reactions and altered dopamine metabolism, demonstrating that wanting and liking need not move together.
Neonatal handling was associated with lower serotonin metabolism in a reward-related brain region, and imipramine reversed the increased sweet-food intake, implicating modifiable monoamine signaling.
In young Brazilian adults, the association between birth weight and physical activity depended on later education, supporting a life-course view of behavioral and social influences.
Women with severe fetal growth restriction reported a higher carbohydrate-to-protein intake ratio in young adulthood, while metabolic-syndrome prevalence was similar across growth groups.
Neonatal handling, early sweet-food exposure and a toy-containing environment each affected later sweet-food intake in rats, with the timing of experience and testing shaping the result.
In a Brazilian male cohort, fetal growth restriction and overweight during school age interacted in relation to BMI at eighteen, showing why growth trajectory matters beyond birth weight alone.
This review introduces DOHaD and compares the thrifty phenotype, developmental programming and adaptive-response models, explaining how early conditions may influence health across the life course.
A rat study found that neonatal separation could aggravate later stress effects, with sex-specific behavioral and S100B patterns that differed between blood and cerebrospinal fluid.
Neonatally handled rats ate more chocolate, but their metabolic responses varied by sex and outcome, showing that food preference and metabolic vulnerability are related but distinct questions.
Neonatally handled rats ate more sweet food but still reduced intake after sucrose, suggesting that the preference could not be explained simply by a failure of satiety.
This letter introduces the idea that contrasting social and prenatal conditions can converge on similar obesity-related outcomes, motivating the “similarities in the inequalities” framework.
Multiple behavioral tests and a diazepam challenge did not support anxiety as the simple explanation for greater adult sweet-food intake after neonatal handling.
Brief handling during the first ten days of life increased adult rats’ sweet and savory snack intake, a difference still present at fifteen months without greater ordinary chow intake or body weight.
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