Costul metabolic al zahărului: fructoza și creșterea globală a riscurilor pentru sănătatea copiilor. O analiză critică

Introduction

In Europe, the consumption of sugar among children and adolescents has significantly exceeded the recommendations set by public health authorities⁽¹⁾. Recent studies show that approximately 33% of their sugar intake comes from sweetened beverages, which are a major source of added sugars in the diet⁽²⁾. While sugars naturally occur in many foods – such as fruits, vegetables, certain cereals, and dairy products –, these natural sugars are essential components of a balanced diet. In contrast, added sugars, which are used to enhance taste and sensory appeal, are not recommended in high doses for children’s diets. Although these sugars are a significant source of energy (calories), they offer little nutritional benefit and can contribute to metabolic imbalances. Moreover, added sugars can displace more nutritious foods in the diet, as children often prefer sweet flavors over foods that provide a wider range of essential nutrients.

During the process of dietary diversification, parents frequently encounter challenges when introducing new foods to their children’s diets. It typically takes an average of ten to thirteen exposures for a child to become familiar with a new food. However, with sweet foods, a single exposure is usually enough to create a strong and lasting preference⁽²⁾. Uncontrolled, this preference for sweetness may have negative health effects, as it is linked to various metabolic abnormalities and an increased risk of developing serious health issues, such as obesity, type 2 diabetes and cardiovascular diseases⁽³⁾. Excessive sugar consumption, particularly during childhood, can foster unhealthy eating behaviors that may persist into adulthood, thereby raising long-term health risks.

This article aims to critically assess the impacts of fructose consumption during childhood on metabolic health. It will integrate current perspectives on the underlying pathophysiological mechanisms and explore potential public health intervention strategies.

Sugar composition and dietary sources

Sugar is a simple carbohydrate composed of two monosaccharides: glucose and fructose. Both glucose and fructose can be found naturally as monosaccharides in fruits and honey, and they are also present in the form of sucrose, a disaccharide made up of a combination of the two sugars. Fructose has a higher sweetening power than glucose, being capable of inducing a more intense perception of sweetness at the same concentrations⁽⁴⁾. Additionally, although both monosaccharides share the same molecular chemical formula (C₆H₁₂O₆), they differ in their chemical structure: glucose is classified as an aldohexose, while fructose is a ketohexose, which gives them distinct metabolic properties.

Glucose is efficiently utilized by most cells in the body, being essential for energy production through glycolysis and stored as glycogen. In contrast, fructose is primarily metabolized in the liver, where its processing bypasses key regulatory steps of glycolysis. This can result in lipid accumulation and metabolic dysfunctions if consumed in excess⁽⁵⁾. One argument supporting the notion that fructose is more metabolically harmful than glucose is that fructose metabolism generates greater oxidative stress, a contributing factor to cardiovascular and metabolic diseases, cognitive decline and general aging⁽⁶⁾.

In nature, fructose is typically not found in its free form; it is accompanied by dietary fiber, as seen in fruits, which helps slow its digestion and absorption. This slower process limits the harmful effects of high fructose concentrations⁽⁷⁾. Thus, this mechanism helps reduce the metabolic burden on the liver, compared to concentrated and refined sources, such as high-fructose corn syrup (HFCS)⁽⁸⁾. HFCS is produced industrially from corn starch through a process that converts glucose into fructose, with concentrations ranging from 42% to 90%⁽⁹⁾. It is one of the most widely used added sugars in the food industry due to its low production cost, ease of use, and its ability to enhance the organoleptic properties (taste, texture) and shelf life of processed food products⁽¹⁰⁾.

In Europe, the use of HFCS in sweetened beverages – which is the primary source of added sugars in children’s diets – is relatively low compared to the United States. Instead, the most commonly used added sugar is sucrose, a disaccharide composed of approximately 50% fructose⁽¹¹⁾. The following studies referenced in this article will primarily refer to HFCS, as this form of fructose has been the most extensively investigated in the scientific literature. However, it is important to emphasize that the potentially harmful substance remains the same – fructose.

Differential metabolism of fructose
and glucose

Although glucose and fructose are both monosaccharides with similar structures, they exhibit significant differences in terms of intestinal absorption, tissue distribution and subsequent metabolization⁽¹²⁾. Glucose is actively absorbed through sodium-dependent cotransport via the SGLT1 transporter (sodium-glucose linked transporter 1), a mechanism that relies on the sodium gradient and requires energy expenditure⁽¹³⁾. In contrast, fructose is mainly absorbed via passive, energy-independent facilita­ted diffusion, mediated by the specific transporter GLUT5 (glucose transporter type 5), which is expressed on the apical membrane of enterocytes, the epithelial cells lining the small intestine⁽¹⁴⁾. A small proportion of ingested fructose can be converted into glucose within enterocytes. However, when fructose intake is high – such as with high-fructose corn syrup – the amount absorbed surpasses the enterocytes’ capacity, directing the excess to the large intestine and the liver, the primary organ involved in fructose metabolism. A small fraction is also metabolized in the kidneys, skeletal muscles, and adipose tissue⁽¹⁵⁾.

Following absorption, glucose and fructose are transported into the bloodstream through different mechanisms. Fructose is taken up via the GLUT5 transporter, whereas glucose is predominantly transported via GLUT2, particularly to the liver⁽¹⁶⁾. Glucose is mainly utilized by the liver and muscles, where it is stored as glycogen, a process that dependents on insulin action. It is also used as an energy source by the brain, kidneys and adipose tissue⁽¹⁵⁾. Once inside the cells, both glucose and fructose undergo phosphorylation mediated by specific kinases. Glucose is phosphorylated by the enzyme glucokinase (GK), primarily in hepatocytes, while fructose is the substrate of fructokinase A (KHK-A) and fructokinase C (KHK-C), two isoforms of ketohexokinase. KHK-C is the predominant form expressed in the liver, but it is also present in the kidneys and enterocytes, while KHK-A has a broader tissue distribution⁽¹⁷⁾.

A crucial feature of fructose metabolism is its accelerated phosphorylation rate. KHK-C catalyzes this reaction with an efficiency that is approximately ten times greater than that of glucokinase acting on glucose and, notably, it is not down-regulated through negative feedback. This lack of homeostatic control promotes a rapid and massive flux of fructose to the liver⁽¹⁸⁾.

Once phosphorylated, fructose is cleaved into trioses – dihydroxyacetone phosphate (DHAP) and glyceraldehyde – which enter glycolytic pathways. These intermediates are primarily converted into lactic acid and can be further transformed into glucose, hepatic glycogen or lipids, depending on the body’s metabolic needs. Increased fructose intake is associated with enhanced de novo lipogenesis, along with reduced fatty acid oxidation, conditions that facilitate lipid accumulation in the liver and the development of hepatic steatosis⁽¹⁹⁾. These metabolic characteristics of fructose are directly related to the onset and progression of metabolic syndrome, as will be explored in the following section.

Fructose and its metabolic impact: mechanisms and toxic effects

In contemporary societies, metabolic health is increasingly compromised due to the prevalent overconsumption of energy-dense foods and beverages, which are often engineered to be highly palatable. This pattern is frequently accompanied by a sedentary lifestyle, a trend observed not only among adults but also within the pediatric population⁽²⁰⁾. Diets dominated by ultra-processed foods rich in added sugars, unhealthy fats, and nutritionally poor “empty” calories have been strongly implicated in the onset and progression of various metabolic disorders. This dietary and lifestyle shift has contributed to the global rise of metabolic syndrome⁽²¹⁾, a multifactorial condition characterized by central (visceral) obesity, atherogenic dyslipidemia (including elevated levels of LDL choleste­rol, reduced HDL cholesterol, and hypertriglyceridemia), insulin resistance and hypertension. While traditionally associated with adult populations, the prevalence of metabolic syndrome is rising alarmingly among children and adolescents, particularly in low- and middle-income countries, encompassing a wide range of global risk factors for chronic noncommunicable diseases⁽²²⁾.

A pivotal factor in the development of metabolic dysfunction is fructose, a monosaccharide that has become increasingly prevalent in the modern diet. The marked rise in dietary fructose intake – particularly in the form of HFCS, a ubiquitous sweetener in processed foods and sugar-sweetened beverages – has been strongly linked to the pathogenesis of multiple metabolic conditions. These associations are primarily attributed to fructose’s capacity to induce oxidative stress, promote insulin resistance and activate proinflammatory signaling pathways.

In contrast to glucose, which undergoes systemic metabolism across various tissues, fructose is metabolized almost exclusively in the liver. Following absorption, it is rapidly phosphorylated to fructose-1-phosphate by the enzyme ketohexokinase (KHK). Notably, this reaction circumvents the regulatory checkpoint governed by phosphofructokinase-1 (PFK-1) – the key enzyme controlling the rate of glycolysis –, thus allowing an unregulated influx of metabolic intermediates into various biochemical pathways⁽²³⁾. The rapid hepatic metabolization of fructose results in the generation of metabolic intermediates, including dihydroxyacetone phosphate (DHAP) and glyceraldehyde, which feed into critical biochemical pathways such as de novo lipogenesis – the endogenous synthesis of fatty acids from non-lipid substrates. This pathway is a major contributor to hepatic lipid accumulation, a hallmark of non-alcoholic fatty liver disease (NAFLD)⁽²⁰⁾.

Fructose metabolism also yields substantial amounts of acetyl-CoA, a central metabolite involved in multiple anabolic and catabolic processes⁽²⁴⁾. In states of nutritional excess, the accumulation of acetyl-CoA can surpass the oxidative capacity of the tricarboxylic acid (TCA) cycle, resulting in mitochondrial saturation. Consequently, excess acetyl-CoA is rerouted toward the synthesis of long-chain fatty acids and triglycerides, thereby exacerbating hepatic steatosis, promoting atherogenic dyslipidemia and increasing the risk for atherosclerotic cardiovascular disease, a leading global cause of morbidity and mortality^(24,25).

Moreover, the high metabolic flux of fructose in he­pa­to­cytes leads to a significant consumption of adenosine triphosphate (ATP), the main intracellular energy currency. This rapid ATP depletion impairs hepatic energy homeostasis and triggers the catabolism of purine nucleotides, culminating in the overproduction of uric acid, a metabolic end-product⁽²⁶⁾. Hyperuricemia has been implicated in the pathogenesis of gout and hypertension⁽²⁷⁾. Elevated uric acid levels may also potentiate systemic inflammation and are thought to contribute to the progression of insulin resistance and low-grade chronic inflammatory states⁽²⁸⁾.

Insulin resistance and early-life fructose exposure

An increasing body of epidemiological and interventional evidence indicates a robust association between excessive dietary fructose consumption and diminished insulin sensitivity, particularly in children and adolescents. Research by Goran et al. (2012) has shown that high intake of sugar-sweetened beverages (SSBs) containing fructose is independently correlated with elevated visceral adiposity and hepatic lipid deposition, two key determinants of insulin resistance in youth⁽²⁹⁾. Complementing these findings, Schwarz et al. (2015) demonstrated that dietary fructose restriction in obese adolescents elicited significant improvements in insulin sensitivity and reductions in hepatic fat accumulation, even in the absence of appreciable weight loss, suggesting a direct metabolic effect⁽³⁰⁾.

As aforementioned, fructose metabolism markedly differs from that of glucose, notably by bypassing the regulatory checkpoint of phosphofructokinase within the glycolytic cascade. This deviation facilitates increased de novo lipogenesis, leading to excessive lipid deposition in hepatic tissues⁽¹⁹⁾. In addition to enhancing triglyceride synthesis, this alternative pathway results in elevated levels of uric acid and reactive oxygen species (ROS), both of which are recognized for their detrimental impact on insulin signaling mechanisms⁽³¹⁾. In children, these adverse effects may be further intensified due to developmental vulnerabilities and the relative immaturity of key metabolic and enzymatic regulatory systems. Jin et al. (2019) reported that elevated dietary fructose intake in adolescents is significantly associated with increased levels of systemic inflammatory markers and oxidative stress indicators – both of which are critical contributors to the development of insulin resistance⁽³²⁾. In alignment with these findings, a study demonstrated that even the intake of moderate amounts of fructose over a period of several weeks results in a measurable decline in insulin sensitivity and adverse alterations in lipid profiles among metabolically healthy adolescents⁽³³⁾.

The link between fructose intake and insulin resistance is further substantiated by research exploring its impact on hormonal regulators of appetite and glycemic control. In contrast to glucose, fructose induces a markedly attenuated secretion of key metabolic hormones such as insulin and leptin – both integral to satiety signaling and energy homeostasis – which contributes to dysregulated appetite control and increased caloric consumption⁽³⁴⁾. Supporting this, Silbernagel et al. (2011) demonstrated that fructose intake in pediatric populations was associated with inadequate suppression of circulating free fatty acids and insulin, indicative of early-stage metabolic dysfunction⁽³⁵⁾. Additionally, chronic excessive fructose consumption has been implicated in adverse alterations of gut microbiota composition and increased intestinal permeability. These gastrointestinal disturbances may potentiate insulin resistance through the promotion of low-grade systemic inflammation, as evidenced by findings from Moscovitz et al. (2021)⁽³⁶⁾.

From a public health standpoint, the accumulating evidence highlights a pressing need to curtail fructose consumption among pediatric populations, particularly in the form of sugar-sweetened beverages (SSBs). Ventura et al. (2011) reported that children with high intake of SSBs exhibit significantly elevated fasting insulin concentrations and increased HOMA-IR indices – a widely used homeostatic model for assessing insulin resistance – when compared to peers with minimal or no consumption of such beverages⁽³⁷⁾. In addition, dietary interventions aimed at replacing fructose-rich foods with complex carbohydrates or whole fruits have yielded notable improvements in metabolic parameters. For example, Lustig et al. (2016) demonstrated that substituting dietary fructose with starch in obese pediatric subjects resulted in marked enhancements in insulin sensitivity, fasting plasma glucose and hepatic function biomarkers within a span of merely nine days⁽³⁸⁾. These rapid and clinically meaningful improvements underscore the specific contributory role of fructose in the pathogenesis of insulin resistance, independent of total caloric intake or fluctuations in body weight.

The notable and swift metabolic benefits observed with fructose reduction in pediatric populations highlight a crucial window for early dietary intervention. By targeting excessive fructose intake during childhood, clinicians and public health professionals may significantly alter the progression of insulin resistance and reduce the long-term burden of cardiometabolic disease.

The role of dietary fructose
in early-onset obesity

Pediatric obesity has emerged as a critical global health issue, carrying profound long-term consequences for public health systems worldwide. Projections from the World Obesity Federation indicate a dramatic rise in obesity prevalence among children and adolescents aged 5 to 19 years old. Specifically, the number of boys affected is expected to increase from 103 million in 2020 to 208 million by 2035, while the number of girls is projected to escalate from 72 million to 175 million during the same period⁽³⁹⁾.

This alarming trend is closely associated with increased dietary intake of fructose, a monosaccharide increasingly recognized for its obesogenic properties⁽⁴⁰⁾. Fructose exerts deleterious effects on key neuroendocrine pathways responsible for appetite regulation, and has been shown to influence adipocyte differentiation and lipid storage, particularly during critical developmental windows^(10,41,42). Emerging evidence underscores the significance of early-life exposure to high levels of fructose – both in utero and during the initial postnatal period – as an independent risk factor for the onset of childhood obesity⁽⁴³⁾.

Recent findings suggest that indirect early-life exposure to fructose, whether transplacentally or via breast milk, may precipitate profound metabolic disturbances with long-term consequences^(44,45). Supporting this hypothesis, a study conducted on a cohort of Hispanic infants revealed that a six-month regimen of low-lactose, HFCS-sweetened formula – compared to breast milk or traditional lactose-based formula – was associated with early alterations in the infant gut microbiome. These microbial shifts were subsequently linked to the emergence of dietary preferences for energy-dense, high-fat and high-carbohydrate foods later in childhood⁽⁴⁶⁾.

Continued high fructose consumption throughout childhood and adolescence further exacerbates the metabolic risk. For instance, one clinical study demonstrated that daily ingestion of 350 mL of HFCS-sweetened beverages by adolescents led to the development of insulin resistance and increased visceral adiposity, both of which are well-established contributors to the pathophysiology of obesity⁽⁴⁷⁾.

Conversely, isocaloric dietary interventions that restrict fructose intake in obese pediatric subjects have shown favorable effects on body fat distribution. Specifically, reductions in visceral adipose tissue accumulation were observed despite the absence of an overall caloric deficit, indicating that fructose limitation alone may confer metabolic benefits⁽⁴⁸⁾. In addition to its negative impact on Body Mass Index (BMI), excessive fructose intake has been implicated in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) – the most prevalent form of chronic liver disease in children –, formerly known as NAFLD. A 2025 pilot study involving 41 children, aged 2.5 to 16 years old, identified a significant positive correlation between high fructose intake and MASLD incidence, thereby reinforcing the pathogenic role of fructose in pediatric hepatic steatosis^(49,50).

Importantly, the study also found that a substantial portion of fructose intake was derived from natural fruit sources, supporting the premise that the body metabolizes sugars similarly, irrespective of their origin – be it natural or processed. In this context, the pediatric endocrinologist Dr. Robert Lustig posits in his publication Fat Chance that natural fruit juice may pose an even greater metabolic risk than carbonated soft drinks, given its slightly higher fructose content – approximately 1.8 grams per ounce, compared to 1.7 grams per ounce in sugar-sweetened sodas⁽²⁾.

Given the growing body of evidence implicating fructose in the disruption of metabolic homeostasis during early developmental stages, future research should prioritize elucidating the dose-response relationships, critical windows of susceptibility, and long-term health outcomes associated with early-life exposure. Concurrently, clinical practice should integrate fructose reduction as a central element of dietary counseling and early intervention strategies for pediatric obesity and related metabolic disorders.

Dietary fructose and activation
of inflammatory pathways in pediatric physiology

Excessive intake of dietary sugars – particularly fructose – has been increasingly recognized as a significant proinflammatory stimulus, initiating a cascade of immunological responses via multiple biological mechanisms⁽⁵¹⁾. Hepatic fructose metabolism leads to elevated synthesis of uric acid, a potent inflammatory mediator known to activate components of the innate immune system⁽⁵²⁾. Additionally, fructose-induced alterations in gut microbiota composition contribute to a proinflammatory intestinal milieu. These microbial shifts favor the proliferation of pathogenic bacteria and compromise epithelial barrier integrity. In a study by Mokhtari et al. (2024), which assessed the gut microbiota of 105 six-month-old Latino infants, higher total sugar intake was associated with a significant reduction in beneficial bacterial genera such as Bacteroides and Clostridium⁽⁵³⁾. This dysbiotic state facilitates the translocation of bacterial endotoxins – such as lipopolysaccharides (LPS) – into systemic circulation, thereby potentiating systemic inflammation. The resultant chronic low-grade inflammatory state, characterized by elevated circulating proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a), has been implicated in the etiopathogenesis of numerous chronic diseases^(54,55).

Early-life consumption of high-fructose diets is increasingly recognized as a contributing factor to the development of endothelial dysfunction, a critical early marker of cardiovascular disease. Although direct evidence from pediatric human studies remains limited, data from animal models offer important mechanistic insights. Notably, a study demonstrated that rats exposed to a high-fructose diet exhibited elevated oxidative stress within the aortic and periaortic adipose tissues, alongside vascular remodeling consistent with endothelial impairment⁽⁵⁶⁾. Additionally, the study reported a diminished anti-inflammatory response from regulatory T cells, highlighting a potential immunological pathway through which fructose may disrupt vascular homeostasis. These findings suggest that excessive fructose intake during critical developmental periods could predispose individuals to long-term cardiovascular risk. Therefore, further investigation in pediatric populations is essential to confirm these associations and to guide evidence-based nutritional guidelines for early-life dietary practices.

Emerging research indicates that excessive fructose intake during early life can adversely affect brain function and behavior through neuroinflammatory mechanisms. Animal studies have demonstrated that high-fructose diets initiated during adolescence increase brain complement expression, elevate plasma tumor necrosis factor alpha (TNF-a), and promote depressive-like behaviors, suggesting a proinflammatory state in the central nervous system⁽⁵⁷⁾. Additionally, high fructose consumption has been linked to hippocampal insulin resistance, neuroinflammation and reduced neurogenesis, which may underlie cognitive deficits⁽⁵⁸⁾. These findings underscore the potential long-term neurological consequences of excessive fructose intake during critical periods of neurodevelopment.

Emerging evidence indicates that high intake of refined sugars in early life contributes to systemic inflammation, a key mechanism in the development of immune-mediated diseases, such as asthma or type 1 diabetes mellitus. A study analyzing data from the National Health and Nutrition Examination Surveys (NHANES) found that children aged 3 to 11 years old who consumed higher amounts of SSBs exhibited increased levels of C-reactive protein (CRP), a biomarker of systemic inflammation⁽⁵⁹⁾. Elevated CRP levels in children have been linked to higher energy intake and consumption of processed foods, indicating a relationship between diet and inflammation⁽⁶⁰⁾. In the context of asthma, a cross-sectional study involving 9938 children aged 2 to 17 years old demonstrated that heavy SSB consumption (≥500 kcal/day) was associated with a twofold increase in the odds of having asthma compared to non-consumers, independent of obesity status⁽⁶¹⁾. Similarly, a systematic review and meta-analysis reported a positive association between high-fructose beverage intake and asthma prevalence in children and adolescents⁽⁶²⁾. Regarding type 1 diabetes mellitus, research indicates that higher total sugar intake may increase the risk of progression from islet autoimmunity to clinical diabetes in children, suggesting that dietary sugars could influence autoimmune processes leading to pancreatic b-cell destruction⁽⁶³⁾. These findings underscore the potential long-term health implications of excessive sugar intake during critical periods of development and highlight the importance of dietary interventions aimed at reducing added sugar consumption in early life.

Given these findings, dietary interventions aimed at mitigating systemic inflammation represent a promising strategy in pediatric health promotion. The Mediterranean diet (MD), characterized by high consumption of fruits, vegetables, whole grains, legumes, nuts and healthy fats like olive oil, has been associated with reduced levels of inflammatory markers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-a) in children and adolescents⁽⁶⁴⁾. A randomized trial involving pediatric patients with active inflammatory bowel disease demonstrated that adherence to the MD led to significant improvements in clinical scores and reductions in inflammatory markers⁽⁶⁵⁾. Additionally, higher adherence to the MD has been linked to lower airway inflammation in school-aged children, suggesting benefits for respiratory health⁽⁶⁶⁾. These findings highlight the importance of promoting anti-inflammatory dietary habits from early childhood as a preventive strategy to enhance long-term health outcomes.

Sugar consumption – policy and public health solutions

Recent epidemiological analyses across European nations reveal that the average dietary sugar intake in most countries exceeds the thresholds recommended for maintaining optimal health⁽⁶⁷⁾. In many populations, added sugars contribute to between 7% and 25% of total daily caloric intake⁽⁶⁸⁾. In response to the growing body of evidence linking excessive sugar consumption with adverse health outcomes – particularly in children and adolescents – numerous countries have implemented or are in the process of developing regulatory policies aimed at reducing population-level sugar exposure.

To attenuate the risk of obesity and associated metabolic disorders, the World Health Organization (WHO) released guidelines in 2015, recommending that free sugars account for less than 10% of total daily energy intake in both adults and children. The WHO further suggests that reducing intake to below 5% may yield additional health benefits⁽⁶⁹⁾. Free sugars encompass monosaccharides and disaccharides that are added to foods and beverages by manufacturers, cooks or consumers, as well as sugars naturally present in honey, syrups and fruit juices^(70,71). Notably, a study presented at the 2024 European Congress on Obe­sity emphasized the importance of sugar source, in addition to quantity. The study found that children who consumed sugars from whole fruits and unsweetened dairy products demonstrated a significantly lower risk of obesity compared to those whose sugar intake came predominantly from processed foods and sweetened beverages⁽⁷²⁾.

Among policy-based interventions, sugar taxation – primarily targeting sugar-sweetened beverages (SSBs) – has emerged as a widely adopted fiscal strategy to reduce added sugar intake, particularly in pediatric populations. A modeling study published in The Lancet Public Health in 2016 projected that implementation of a sugar tax in the United Kingdom could prevent approximately 81,600 cases of obesity and 19,000 cases of type 2 diabetes annually. These benefits could be further amplified through industry-led reformulation to reduce sugar content in processed foods and beverages⁽⁷³⁾. However, the effectiveness of sugar taxes has not been uniformly demonstrated. For instance, a longitudinal study conducted in Philadelphia, USA, reported no significant change in pediatric body weight two years after the enactment of a sugary drink tax⁽⁷⁴⁾. Such findings suggest that, while sugar taxes may reduce SSBs consumption, they may not, solely, be sufficient to meaningfully impact childhood obesity rates.

Public awareness and consumer education represent additional avenues for reducing sugar intake. One promising strategy involves front-of-package (FOP) labeling that clearly communicates sugar content. This is particularly important given the wide array of nomenclature used for added sugars on food labels⁽⁷⁵⁾. In a multi-country study by Hock et al. (2021), involving a cohort over 10,000 adolescents aged 10 to 17 across Australia, Canada, Chile, Mexico, the United Kingdom and the United States, simplified FOP warning labels – particularly those incorporating “high in” statements alongside clear and easily interpreted symbols – significantly influenced the participants’ perception, leading them to regard the labeled products as unhealthy⁽⁷⁶⁾. Similarly, a study involving parents of children aged 11 to 16 years old found that visual warning labels illustrating adverse health outcomes (e.g., disease risks) were significantly more effective in deterring the purchase of sugar-sweetened beverages for their children than labels providing only caloric data⁽⁷⁷⁾.

Since a considerable portion of excess sugar intake in children occurs within the household context, effective interventions must address parental behaviors and decision-making around food purchases. Research by van Ansem et al. (2014) highlights the influence of socioeconomic status, revealing that parents with lower educational attainment are more likely to purchase sugar-sweetened products, which in turn shapes their children’s dietary habits⁽⁷⁸⁾. Consequently, parental engagement through targeted nutrition education and public awareness campaigns could serve as a critical lever for promoting healthier dietary choices⁽⁷⁹⁾. A 2022 systematic review and meta-analysis by Al-Jawaldeh et al., focused on the Eastern Mediterranean region, highlights that school-based nutrition programs are being increasingly implemented, and public awareness campaigns have played a crucial role in influencing consumer behavior⁽⁸⁰⁾.

Ultimately, the success of such public health interventions relies on the coordinated efforts of governmental authorities, the food and beverage industry, and consumers themselves. A multisectoral approach is essential to enhance awareness of the well-established causal relationship between excessive sugar consumption during childhood and adolescence and the subsequent emergence of metabolic diseases.

Discussion

The evolving dietary patterns of modern pediatric populations, marked by an elevated intake of hypercaloric, processed foods high in added sugars, have contributed significantly to the global rise in metabolic disorders among infants, children and adolescents. A growing body of evidence supports the role of excessive sugar consumption – particularly from sugar-sweetened beverages – as a modifiable risk factor for obesity, insulin resistance and associated noncommunicable disea­ses⁽⁸¹⁾. Accordingly, this pattern of overconsumption has emerged as a pres­sing public health challenge, with consequences that extend far beyond caloric excess alone.

Of particular concern is the pervasive intake of su­gar-sweetened beverages which are heavily marketed to children and disproportionately consumed in lower socioeconomic groups. These products provide large quantities of added sugars with minimal nutritional value and have been shown to impair energy balance, appetite regulation and metabolic homeostasis^(82,83). Given the children’s innate preference for sweetness and the emerging understanding of sugar’s addictive properties⁽⁸⁴⁾, early exposure facilitates the establishment of unhealthy dietary habits that may persist into adulthood and influence long-term metabolic programming^(46,85).

Emerging longitudinal data underscore the importance of early dietary interventions. A recent study published in Science (2024) found that reducing sugar intake during the first 1000 days of life – a critical developmental window encompassing gestation through the second year of life – was associated with a 35% lower risk of type 2 diabetes and with a 20% reduction in hypertension incidence later in adulthood⁽⁸⁶⁾. These findings reinforce the need to target sugar reduction strategies during this foundational period of development.

Another important dimension warranting critical examination is the association between socioeconomic status and dietary sugar consumption. Recent studies have shown that households with lower income and educational attainment are more likely to rely on inexpensive, processed foods rich in added sugars due to economic constraints and limited access to healthier alternatives. This structural inequality contributes to disproportionate rates of pediatric obesity and related comorbidities in socioeconomically disadvantaged populations⁽⁷⁸⁾. This contributes to the unequal burden of obesity and metabolic disease across socioeconomic strata. Public health strategies that address these structural determinants – through food pricing policies, access to healthy food environments, and culturally tailored education – are critical to achieving equitable health outcomes.

While observational and experimental studies provide strong support for the association between sugar intake and pediatric metabolic health, additional longitudinal research is needed to clarify the dose-response relationships and identify the most effective points of intervention. Furthermore, clinical guidelines and preventive programs should consider integrating sugar reduction strategies as a standard component of early-life health promotion.

In summary, mitigating the health risks associated with excessive sugar consumption requires a coordinated, multidisciplinary approach involving clinicians, public health professionals, policymakers and caregivers. Promoting nutritional awareness, reformulating high-sugar products and supporting families in adopting healthier dietary habits from early childhood may serve as effective strategies to reduce the long-term burden of metabolic disease and enhance population health.

Conclusions

Fructose has emerged not merely as an energy-dense nutrient, but as a biologically active compound capable of disrupting pediatric metabolic homeostasis. Its unique hepatic metabolism contributes to early metabolic derangement, promoting insulin resistance, hepatic steatosis and systemic inflammation, hallmarks of chronic disease development. The growing body of evidence underscores the urgent need to reorient both public health policy and clinical guidelines toward early preventive strategies. Taxation of sugar-sweetened beverages, improved front-of-package labeling and targeted parental education must be reinforced, alongside nutritional counseling within pediatric care. A proactive, prevention-centered model that prioritizes the reduction of dietary fructose may prove essential for protecting future generations from the escalating burden of noncommunicable metabolic diseases.

Autor corespondent: Bogdan-Marius Istrate E-mail: istratem.bogdan@yahoo.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.