De la selectivitatea alimentară la disfuncția metabolică: explorarea potențialei legături dintre comportamentele alimentare din copilărie și PMOS la adolescente

Introduction

Polycystic ovary syndrome (PCOS), recently redefined within the broader concept of polyendocrine metabolic ovary syndrome (PMOS), represents one of the most common endocrine-metabolic disorders affecting adolescent girls and women of reproductive age. The condition is characterized by a heterogeneous clinical presentation that may include menstrual irregularities, hyperandrogenism, ovulatory dysfunction, insulin resistance, dyslipidemia and chronic low-grade inflammation. Beyond its reproductive implications, PMOS is increasingly recognized as a complex metabolic disorder associated with long-term cardiometabolic risk and reduced quality of life^(1-3,20,21).

Medical nutrition therapy (MNT) constitutes a cornerstone of PMOS management across the lifespan. Current evidence supports the role of dietary interventions in improving insulin sensitivity, body composition, metabolic parameters and menstrual function. However, most nutritional approaches focus on the management of established disease, while considerably less attention has been directed toward identifying early-life dietary patterns that may contribute to the development of metabolic dysfunction before clinical manifestations become apparent^(1,26,27,30).

Food selectivity, picky eating and food neophobia are among the most common feeding difficulties observed during childhood. While many children gradually expand their dietary repertoire, a subset continues to exhibit persistent selective eating behaviors into adolescence. These behaviors are often characterized by a preference for highly palatable, energy-dense foods and limited acceptance of vegetables, fruits, legumes, fish and other nutrient-dense food groups. Consequently, persistent food selectivity may result in reduced dietary diversity, inadequate fiber intake, suboptimal micronutrient status and unfavorable dietary patterns^(4-7).

Emerging evidence suggests that reduced dietary diversity may influence metabolic health through multiple mechanisms, including alterations in gut microbiota composition, impaired metabolic flexibility, chronic low-grade inflammation and increased cardiometabolic risk. In parallel, growing attention has been directed toward the role of the gut microbiome, dietary quality and early nutritional exposures in shaping metabolic trajectories during childhood and adolescence. These factors may be particularly relevant during puberty, a period characterized by profound hormonal, metabolic and behavioral changes^(8-16).

Despite increasing interest in both childhood feeding behaviors and adolescent PMOS, the potential relationship between persistent food selectivity and the metabolic abnormalities frequently observed in PMOS remains insufficiently explored. The existing literature tends to investigate these phenomena independently, with limited attention given to the possibility that long-standing restrictive dietary patterns may contribute to the development of an unfavorable metabolic phenotype later in life^(4-10,20-23).

In clinical practice, adolescents presenting with PMOS frequently report a history of selective eating behaviors originating in childhood. These dietary patterns are often characterized by a strong preference for refined carbohydrate-rich foods, highly palatable processed products and a limited acceptance of nutrient-dense foods. Furthermore, food selectivity frequently coexists with gastrointestinal complaints, reduced dietary variety, excess adiposity, insulin resistance and psychological difficulties, including anxiety and depressive symptoms.

Although these observations do not establish a causal relationship, they raise clinically relevant questions regarding the potential long-term metabolic consequences of persistent selective eating during critical developmental periods^(20-25).

Aim of the review

The aim of this narrative review is to explore the potential relationship between childhood food selectivity, reduced dietary diversity, gut microbiota alterations and cardiometabolic risk factors relevant to PMOS in adolescents, while highlighting the potential role of early medical nutrition therapy in prevention, risk reduction and long-term reproductive health.

Materials and method

This study was designed as a narrative review with a systematic search strategy aimed at exploring the potential relationship between childhood food selectivity, reduced dietary diversity, cardiometabolic risk and factors relevant to polyendocrine metabolic ovary syndrome (PMOS) in adolescence.

A literature search was conducted using PubMed, Scopus and Google Scholar databases. Publications from January 2014 to June 2026 were considered for inclusion. Search terms included combinations of the following keywords: “food selectivity”, “picky eating”, “food neophobia”, “ARFID”, “dietary diversity”, “gut microbiota”, “childhood nutrition”, “adolescent health”, “insulin resistance”, “metabolic syndrome”, “PCOS”, “PMOS”, “hyperandrogenism”, “cardiometabolic risk” and “medical nutrition therapy”. Boolean operators (AND, OR) were used to refine the search strategy.

Priority was given to systematic reviews, meta-analyses, randomized controlled trials, prospective cohort studies and clinical practice guidelines. Additional relevant studies were identified through manual screening of reference lists from selected articles.

Studies were included if they investigated at least one of the following topics: childhood food selectivity, dietary diversity, nutrient inadequacies, gut microbiota alterations, obesity, insulin resistance, metabolic syndrome, cardiometabolic risk or nutritional aspects of adolescent PMOS/PCOS. Studies focusing exclusively on adult populations without relevance to adolescence or metabolic outcomes were excluded.

The selected literature was analyzed and synthesized narratively. Evidence was grouped into thematic categories, including food selectivity and dietary diversity, nutritional consequences of selective eating, gut microbiota and metabolic health, cardiometabolic risk factors, potential implications for PMOS development, and opportunities for early medical nutrition therapy interventions.

Food selectivity and dietary diversity in childhood

Food selectivity is a common feeding behavior during childhood, and it is generally characterized by the rejection of familiar and unfamiliar foods, a limited food repertoire and strong preferences for specific textures, colors, tastes or food presentations. Although transient selective eating is considered a normal developmental phase in many children, persistent food selectivity may extend into adolescence and adulthood, influencing dietary quality and nutritional status^(4-7).

Several studies have demonstrated that children with persistent selective eating behaviors tend to consume fewer vegetables, fruits, legumes, fish and whole grains, while relying more heavily on refined carbohydrate-rich foods and highly palatable processed products. As a consequence, dietary diversity is often substantially reduced^(6,7,10).

Dietary diversity is increasingly recognized as an important marker of diet quality and nutritional adequacy. Reduced dietary diversity has been associated with lower intake of fiber, vitamins, minerals and bioactive compounds that contribute to metabolic health. Furthermore, dietary diversity appears to play an important role in shaping gut microbiota composition and metabolic resilience throughout childhood and adolescence^(8-10).

From a clinical perspective, persistent food selectivity may represent more than a behavioral feeding challenge. It may contribute to the establishment of long-term dietary patterns capable of influencing body composition, metabolic health and future disease risk^(4,6,7,29).

Nutritional consequences of reduced dietary diversity and selective eating

Persistent food selectivity is frequently associated with reduced dietary diversity and suboptimal nutrient intake. While selective eating may initially appear to represent a behavioral feeding issue, growing evidence suggests that prolonged dietary restriction can influence multiple aspects of nutritional status and metabolic health. The impact extends beyond isolated nutrient deficiencies, and may affect gastrointestinal function, inflammatory pathways, body composition and metabolic regulation^(6-10).

Children and adolescents with highly selective eating patterns often consume significantly lower amounts of vegetables, fruits, legumes, fish and whole grains. Consequently, an inadequate intake of dietary fiber, omega-3 fatty acids, iron, zinc, magnesium, folate and vitamin D has been repeatedly reported. These nutritional inadequacies may contribute to alterations in glucose metabolism, appetite regulation, immune function and hormonal homeostasis^(6,7,10).

Reduced dietary diversity has also been associated with lower consumption of phytochemicals and bioactive compounds that play important roles in oxidative stress regulation and inflammatory control. Such dietary patterns may therefore promote a proinflammatory metabolic environment, particularly when combined with excessive consumption of refined carbohydrates and ultra-processed foods^{(9,11,12,24,25)}.

From a developmental perspective, childhood and adolescence represent critical periods during which nutritional exposures may influence long-term metabolic trajectories. Therefore, persistent selective eating behaviors should not be viewed solely as feeding difficulties, but also as potential modifiers of future metabolic health^(17-21).

Gut microbiota, inflammation and metabolic health

The gut microbiota has emerged as a central regulator of metabolic health, influencing energy homeostasis, immune function, glucose metabolism and inflammatory responses. Dietary diversity is considered one of the strongest determinants of microbial diversity, particularly during childhood and adolescence^(11-16).

Diets characterized by a wide variety of plant foods, fruits, vegetables, legumes and whole grains promote microbial richness and the production of beneficial metabolites, including short-chain fatty acids (SCFAs). In contrast, restrictive dietary patterns dominated by refined carbohydrates and ultra-processed foods have been associated with reduced microbial diversity and dysbiosis^(11-16).

Several mechanisms have been proposed through which gut microbiota alterations may contribute to metabolic dysfunction. These include increased intestinal permeability, activation of inflammatory pathways, impaired insulin signaling and altered regulation of appetite-related hormones. Collectively, these processes may facilitate the development of insulin resistance and cardiometabolic abnormalities^(11,12,16).

Interest in the microbiome is particularly relevant in the context of PMOS, as emerging evidence suggests that adolescents and women with PMOS frequently exhibit alterations in gut microbial composition when compared with healthy controls. Although causality remains uncertain, these findings support the hypothesis that dietary patterns influencing microbiota diversity may contribute to metabolic disturbances associated with PMOS^(22,23).

Food selectivity and cardiometabolic risk factors

An increasing body of literature suggests that persistent selective eating may influence cardiometabolic health through both direct and indirect mechanisms. Reduced dietary quality, excessive reliance on energy-dense foods, low fiber intake and altered gut microbiota composition may collectively contribute to unfavorable metabolic outcomes^(9-12,17-19).

Several observational studies have reported associations between reduced dietary diversity and increased adiposity, poorer dietary quality and metabolic abnormalities. Although findings remain heterogeneous, evidence suggests that persistent selective eating may be associated with an increased risk of overweight, obesity, insulin resistance and metabolic syndrome components in susceptible individuals^(9,17-21).

Importantly, not all selective eaters develop obesity or metabolic dysfunction. The relationship appears to be influenced by multiple factors, including dietary composition, physical activity, socioeconomic context, psychological health and genetic susceptibility. Nevertheless, selective eating may represent an early behavioral marker of vulnerability to future metabolic disturbances^(17-21,29).

Potential implications for PMOS development in adolescence

PMOS is increasingly recognized as a multifactorial disorder involving complex interactions between genetic predisposition, environmental influences, metabolic dysfunction and lifestyle-related factors. Although the etiology of PMOS remains incompletely understood, insulin resistance, chronic low-grade inflammation, adipose tissue dysfunction and altered metabolic programming are considered central contributors to disease development and progression^(1-3,20-23).

Childhood food selectivity has traditionally been viewed as a feeding behavior concern rather than a potential metabolic risk factor. However, the cumulative effects of reduced dietary diversity, inadequate nutrient intake, poor dietary quality and gut microbiota alterations may create a biological environment that favors the development of metabolic disturbances frequently observed in adolescents with PMOS^(6-16).

Persistent preference for highly palatable refined carbohydrate-rich foods may contribute to repeated glycemic excursions, increased insulin demand and progressive impairment of insulin sensitivity. Simultaneously, low intake of fiber-rich foods, legumes, vegetables and omega-3-rich sources may reduce exposure to nutrients known to support metabolic health and inflammatory regulation^(10,17-20).

During puberty, physiological insulin resistance naturally increases as part of normal developmental processes. In susceptible individuals, pre-existing metabolic vulnerabilities may be amplified during this period, potentially facilitating the emergence of hyperinsulinemia, excess adiposity, menstrual irregularities and other clinical manifestations frequently associated with PMOS^(18-21).

Although direct evidence linking childhood food selectivity to PMOS remains limited, current knowledge supports the hypothesis that persistent restrictive eating patterns may contribute indirectly to the development of a cardiometabolic phenotype that overlaps with key metabolic characteristics of PMOS^(20-23).

Figure 1 summarizes the hypothetical pathways proposed in this review.

The conceptual framework from Figure 1 illustrates the hypothetical pathways through which persistent childhood food selectivity may contribute to metabolic disturbances relevant to PMOS development during adolescence. Reduced dietary diversity and inadequate intake of nutrient-dense foods may lead to nutritional inadequacies, gut microbiota dysbiosis, chronic low-grade inflammation and metabolic dysregulation. During puberty, these factors may interact with physiological insulin resistance and individual susceptibility, potentially contributing to the emergence of PMOS-related manifestations, including menstrual irregularities, hyperandrogenism, excess adiposity and cardiometabolic abnormalities. Although a direct causal relationship has not been established, current evidence supports the biological plausibility of these interconnected mechanisms^{(1-3,8-16,17-25)}.

Clinical perspective: lessons from medical nutrition therapy

Clinical experience frequently reveals recurring patterns that are not yet fully reflected in the scientific literature. Among adolescents presenting with PMOS, a history of childhood selective eating is commonly reported during nutritional assessment. These eating patterns are often characterized by limited dietary variety, low consumption of vegetables and legumes, preference for refined carbohydrate-rich foods and strong attraction toward highly palatable processed products.

In addition to dietary restrictions, many adolescents presenting with PMOS also report gastrointestinal complaints, particularly constipation, alongside increased rates of anxiety, depressive symptoms and body image concerns. While these observations remain largely anecdotal and require formal investigation, they raise important questions regarding potential interactions between eating behaviors, psychological health and metabolic outcomes^(24,28,29).

Clinical observations further suggest that early nutritional intervention, particularly during late childhood or shortly after menarche, may represent a valuable opportunity to improve dietary quality, support healthy body composition and reduce metabolic risk. Medical nutrition therapy focused on dietary diversity, adequate protein intake, fiber-rich foods and sustainable eating behaviors may therefore play an important preventive role long before reproductive manifestations become clinically significant^(26,27,30).

From a practical standpoint, the identification of persistent food selectivity should prompt a broader assessment of dietary quality, gastrointestinal function, psychosocial factors and metabolic health rather than being viewed solely as a behavioral feeding challenge^(26,27).

Clinical implications for pediatricians, endocrinologists and clinical dietitians

The findings summarized in this review highlight the importance of considering childhood eating behaviors within a broader metabolic health framework. Persistent food selectivity should not be regarded exclusively as a nutritional inconvenience, but may represent an early indicator of reduced dietary quality and potential future metabolic vulnerability^(4-10,17-23).

Healthcare professionals working with children and adolescents should consider routine assessment of dietary diversity, selective eating behaviors and gastrointestinal symptoms as part of comprehensive preventive care. Early identification of restrictive eating patterns may facilitate timely nutritional intervention before significant metabolic abnormalities develop^(26,27).

Particular attention may be warranted in girls with a family history of PMOS, obesity, insulin resistance, type 2 diabetes mellitus or metabolic syndrome. In these populations, proactive medical nutrition therapy may represent an opportunity to address modifiable risk factors during critical developmental windows^(1-3,20,21).

Collaboration between pediatricians, pediatric endocrinologists, gynecologists, psychologists and clinical dietitians is essential to support both metabolic and reproductive health throughout adolescence^(1,2,26,27).

Discussion

Interpretation of current evidence

The present review explored the potential relationship between childhood food selectivity and the development of metabolic abnormalities relevant to PMOS during adolescence. While the available evidence does not support a direct causal association, several interconnected pathways suggest that persistent selective eating behaviors may contribute to an unfavorable metabolic environment during critical developmental periods^(4-10,17-23).

Current literature consistently demonstrates that persistent food selectivity is associated with reduced dietary diversity, lower intake of fiber-rich and nutrient-dense foods, and greater reliance on highly palatable processed products. These dietary patterns have been linked to alterations in gut microbiota composition, impaired metabolic flexibility and increased cardiometabolic risk, all of which are recognized components of PMOS pathophysiology^(6-23).

The findings of this review support the hypothesis that childhood eating behaviors may represent an underrecognized factor within the broader network of environmental influences contributing to metabolic vulnerability during adolescence. However, the available evidence remains insufficient to establish whether food selectivity acts as an independent risk factor or merely coexists with other determinants of metabolic dysfunction^(17-23,29).

Potential biological mechanisms

Several biological mechanisms may explain the potential association between persistent food selectivity and PMOS-related metabolic disturbances. Reduced dietary diversity is frequently accompanied by inadequate intake of dietary fiber, omega-3 fatty acids, antioxidants and other bioactive compounds involved in metabolic regulation. These nutritional inadequacies may contribute to chronic low-grade inflammation, oxidative stress and impaired insulin signaling^(8-16,24,25).

Alterations in gut microbiota composition represent another plausible pathway. Diets characterized by limited diversity and low consumption of plant-based foods have been associated with reduced microbial richness and decreased production of short-chain fatty acids, compounds known to influence intestinal barrier integrity, immune function and glucose metabolism^(11-16).

Puberty may further amplify these mechanisms. Physiological insulin resistance occurring during pubertal development could interact with preexisting metabolic vulnerabilities derived from long-standing dietary patterns, potentially increasing the likelihood of hyperinsulinemia, excess adiposity and menstrual dysfunction in genetically susceptible individuals^(18-21).

Furthermore, emerging evidence suggests the existence of bidirectional interactions between dietary quality, psychological well-being, eating behaviors and metabolic health. This may partially explain the frequent coexistence of food selectivity, anxiety symptoms, body image concerns and metabolic disturbances observed in clinical practice^(24,28,29).

Clinical relevance for early medical nutrition therapy

From a clinical perspective, the findings of this review emphasize the importance of moving beyond the traditional perception of food selectivity as solely a behavioral feeding challenge. Persistent restrictive eating patterns may also represent early indicators of reduced dietary quality and potential metabolic vulnerability^(26,27).

Clinical observations frequently reveal a history of selective eating among adolescents presenting with PMOS, particularly patterns characterized by low dietary diversity, inadequate vegetable and legume consumption, and preference for refined carbohydrate-rich foods. Although observational in nature, these recurring findings highlight the importance of comprehensive nutritional assessment during childhood and early adolescence^(20-23,29).

Early medical nutrition therapy may represent a valuable opportunity to modify dietary behaviors before the onset of significant metabolic abnormalities. Interventions focused on increasing dietary diversity, improving fiber intake, optimizing protein distribution and promoting long-term dietary flexibility may contribute to healthier metabolic trajectories and potentially reduce the severity of future endocrine-metabolic manifestations^(26,27,30).

Particular attention should be given to girls presenting with additional risk factors, including family history of PCOS/PMOS, obesity, insulin resistance or type 2 diabetes mellitus. In these populations, preventive nutritional interventions may offer benefits extending beyond immediate nutritional adequacy, supporting both metabolic and reproductive health outcomes later in life^{(1-3,20,21,26)}.

Limitations and future research directions

Several limitations should be acknowledged when interpreting the findings discussed in this review. Firstly, current evidence investigating the direct relationship between childhood food selectivity and PMOS development remains limited. Most available studies examine food selectivity, dietary diversity, obesity, insulin resistance or PMOS independently rather than exploring potential longitudinal relationships between these factors.

Secondly, the majority of studies addressing selective eating behaviors are observational in nature, limiting the ability to establish causality. The heterogeneity of definitions used for picky eating, food selectivity and food neophobia further complicates comparisons across studies and may contribute to inconsistent findings.

Thirdly, multiple factors influence the development of PMOS, including genetic susceptibility, body composition, physical activity, socioeconomic factors, psychological health and environmental exposures. Consequently, food selectivity should be considered one potential contributor within a complex multifactorial framework rather than an isolated etiological factor.

Current evidence also remains insufficient to determine whether childhood food selectivity directly increases the risk of developing PMOS or whether both conditions share common biological and behavioral determinants.

Future research should prioritize prospective longitudinal studies evaluating the relationship between early eating behaviors, dietary diversity, gut microbiota composition and metabolic outcomes throughout puberty and adolescence. In addition, studies investigating whether early medical nutrition therapy can modify cardiometabolic trajectories and reduce the severity of PMOS manifestations would provide valuable clinical insights.

The integration of nutritional assessment, microbiome analysis and metabolic profiling may further improve the understanding of the pathways linking childhood eating behaviors to adolescent metabolic health.

Conclusions

Food selectivity and reduced dietary diversity are common childhood feeding behaviors that may extend beyond nutritional adequacy alone. Emerging evidence suggests that persistent restrictive dietary patterns can influence nutrient intake, gut microbiota composition, inflammatory pathways and cardiometabolic health^(6-16).

Although current literature does not support a direct causal relationship between childhood food selectivity and PMOS, several biologically plausible mechanisms may connect long-standing restrictive eating patterns with metabolic abnormalities frequently observed in affected adolescents. Reduced dietary diversity, inadequate fiber intake, altered microbiota composition and increased reliance on highly palatable processed foods may contribute to the development of an unfavorable metabolic phenotype characterized by insulin resistance, excess adiposity and chronic low-grade inflammation^(11-23).

Clinical observations further suggest that selective eating behaviors are frequently reported among adolescents presenting with PMOS, highlighting the importance of early nutritional assessment and intervention^(20-23).

Medical nutrition therapy may therefore play a valuable role not only in the management of established PMOS, but also in the early identification and modification of nutritional risk factors during critical developmental periods^(26,27,30).

Further longitudinal and interventional studies are needed to clarify the potential relationship between childhood eating behaviors and adolescent reproductive-metabolic health. Until such evidence becomes available, promoting dietary diversity, improving diet quality and addressing persistent food selectivity remain reasonable and potentially beneficial strategies for supporting long-term metabolic and reproductive outcomes.  

Autor corespondent:  Narcisa-Anamaria Covataru E-mail: narcisacovataru@gmail.com

CONFLICT OF INTEREST: none declared.

FINANCIAL SUPPORT: none declared.

This work is permanently accessible online free of charge and published under the CC-BY.