White Striping Myopathy in Broilers: A Review of Genetic Factors and Non-Genetic Modulators

Abstract

White Striping (WS) is a macroscopic defect of the pectoralis major muscle, characterized by distinct white striations that impair meat acceptability and commercial value. It is a phenotype with polygenic inheritance, controlled by several QTLs and genes associated with muscle repair and metabolism. Beyond genetic factors, phenotypic manifestation is strongly modulated by the environment. This review integrates research on genetic predispositions and modulating factors to provide a holistic overview of WS in broilers. The defect predominantly affects heavier birds with high breast yield and elevated ultimate breast pH. LRSAM1 gene, on chromosome GGA17, is identified as a putative candidate gene as its expression co-localizes with the phenotypic QTL. Chromosome GGA5 has recently been identified as the primary genomic region of interest hosting a cluster of specific markers. Research on dietary strategies has extensively explored the manipulation of feed formulations, especially of amino acids. While results for some nutrients like methionine remain conflicting, restricting lysine during the growth phase could be an effective dietary intervention for reducing WS severity. Management offers the most practical short-term solutions, whereas selective breeding enables meaningful and permanent progress across generations, given the moderate heritability of many quality-related traits. Effective mitigation requires an integrated approach combining welfare, environmental control, and precision feeding throughout the production cycle, while acknowledging trade-offs with productivity. To meet evolving consumer expectations, the industry must embrace practices that are simultaneously scientifically rigorous, ethically responsible, and environmentally sustainable.

1. Introduction

The modern broiler industry represents the result of targeted genetic selection, supported by optimized nutrition and management, contributing to meet the protein demand of an incessantly growing world population. This has been driven in part by a marked consumer shift toward chicken meat over other meats. Key factors for this preference include its relatively lower cost, culinary versatility, desirable sensory qualities, and its reputation as a healthier meat alternative. This perception is further reinforced by the classification of red meat as “probably carcinogenic to humans” by the International Agency for Research on Cancer [1]. The widespread cultural and religious acceptability of poultry meat further sustains its demand. In response, the industry has intensified breeding programs focused on achieving rapid growth and maximizing production efficiency to meet market needs and enhance profits [2,3]. Historically, in the 1940s, the “Chicken of Tomorrow” contest radically shifted breeding goals from dual-purpose production (eggs and meat) toward maximizing meat yield, with a specific focus on breast, thighs, and drumsticks [4]. Today, we have overwhelmingly surpassed these goals. The time required for commercial birds to reach market sized weight has been significantly reduced. The average body weight at 42 days of age increased from 539 g in 1957 as represented by the Athens-Canadian Randombred strain to 2672 g in 2001 as represented by the Ross308 strain and the feed conversion ratio decreased from 2.34 to 1.43 over the same period. Although some of these performance gains are due to environmental factors, 85 to 90% has been attributed to genetics [5]. Prior to World War II, birds were selected for their live traits, since they were sold alive. The post-war shift to selling prepared carcasses in urban markets and grocery stores created an economic incentive to prioritize traits that maximized carcass yield. Subsequently, as consumer demand shifted towards specific cut-up portions, breeding programs adapted further to optimize the yield of the main carcass parts [6]. A primary target of this selection has been the pectoralis major muscle, along with improvements in growth rate and feed conversion. From 1957 to 2005, pectoralis major yield increased by 79% in males and 85% in females, achieving the intended beneficial changes [7]. However, while animals became super-efficient feed converters, the intense, unilateral selection for rapid muscle growth led to unintended consequences. Among the most prevalent are muscular myopathies, which now pose a major challenge to poultry production [8,9,10]. Myopathies are diseases arising from defects in the structural composition of muscle fibers and can sometimes appear by themselves or in combination with others. The selection for hypergrowth has profoundly altered muscle architecture, increased muscle fiber diameter, length, and number, while concurrently reducing capillary density and the capillary-to-fiber ratio. This compromised vascularization leads to insufficient oxygenation, elevated oxidative stress, and ultimately, metabolic impairment and tissue degeneration, with negative consequences for meat quality [11,12,13,14]. It is hypothesized that in chickens with a reduced capillary network, perimortem lactate is removed more slowly, leading to a faster postmortem pH decline and an increased likelihood of pale color and reduced water-holding capacity. Since the broiler breast muscle consists entirely of fast-glycolytic fibers, fiber type distribution does not play a role. Growth performance can influence the rate and extent of rigor development [11]. Perhaps the most visually distinctive of these muscle abnormalities is White Striping (WS), characterized by white striations of various quantity and thickness up to a few mm, parallel to the muscle fibers direction on the surface of the broiler breast fillet. From a chronological perspective, WS was the first abnormal breast condition observed in commercial slaughterhouses worldwide [14,15]. Of note, its prevalence is also rising in the turkey industry [16]. While WS is not a food safety issue, it has significant economic and quality implications [16,17,18,19,20,21]. In the paper published by Baldi et al. [18], the main histological alterations associated with the presence of WS included nuclear internalization, loss of cross-striations, vacuolar and hyaline degeneration, necrosis and fiber lysis, infiltration of inflammatory cells, variable cross-sectional area (with signs of both degeneration and regeneration), lipidosis, and fibrosis. A distinctive feature observed in WS samples was the increased deposition of adipocytes within the connective tissue (lipidosis), along with fat infiltration reaching the fibrillar components. Regarding proximate composition, WS-affected breasts showed significantly lower protein content (−1.1% for superficial and −0.8% for deep pectoralis major) and higher lipid content (+0.94% for superficial and +0.47% for deep pectoralis major). Additionally, WS samples were heavier and exhibited significantly higher pHu compared to normal ones. According to Barbut and Leishman [22], modern consumers demand greater transparency about food origin and production methods, with growing emphasis on ethical considerations. Since emotions play a key role in consumer food choices [23], even when the information disclosed is occasionally biased or lacks full scientific legitimacy, it remains a fact that consumers from developed countries are increasingly concerned about livestock farming and meat production practices [2]. De Carvalho et al. [24] investigated whether awareness of the underlying causes of WS and recognition of the affected breast as a “sick muscle” could influence consumer emotions, attitudes, and purchasing decisions. In this study, only 16% of consumers were already aware of WS, while 84% had never heard of it. After providing information about the myopathy, 5% of consumers decided to reject WS samples, associating the condition with “health problems,” “animal stress,” and “suffering.” WS samples showed significantly lower acceptability than normal fillets, both before and after information was provided. Interestingly, providing information about WS significantly decreased acceptability compared to the non-informed evaluation. According to the authors, this behavior may have a moral basis: consumers perceived that meat from fast-growing breeds affected by WS likely came from animals that experienced “health problems,” “stress,” and “compromised welfare.” Additionally, as concluded by Kuttappan et al. [25], consumers may also associate the high fat content of WS meat with poor nutritional quality. If this trend continues, it will result in substantial economic losses for the poultry industry, as processors would be unable to sell WS fillets for fresh retail and would instead have to downgrade and further process them [26,27,28,29]. However, although meat from birds raised under slower growth rates may offer benefits for animal welfare and social acceptability, it also comes with higher production costs, which are ultimately passed on to consumers [22]. WS is commonly assessed by visually scoring pectoralis major fillets. The most widely used classification, established by Kuttappan et al. [27], defines three severity degrees: normal (absence of striations), moderate (presence of white lines < 1 mm thick, parallel to muscle fibers), and severe (presence of white lines > 1 mm thick, parallel to muscle fibers). Subsequent studies have occasionally employed modified versions of this scale, often incorporating the percentage estimates of affected muscle surface or expanding the system to a four-point scale, adding a mild category between normal and moderate [30]. A lack of understanding of how distinct macroscopic attributes of broiler breast fillets relate to myopathies is currently impeding the development of objective classification technologies needed by the industry to assess myopathy occurrence and severity [12]. Indeed, despite their distinct phenotypes and unclear etiologies, WS, Wooden Breast (WB), and Spaghetti Meat (SM) share similar histological features. WB is characterized by a hardened consistency and pale appearance of the pectoral muscles [31], while SM presents an overall impaired integrity of the pectoralis major muscle, with a tendency toward separation of the fiber bundles, giving the muscle an appearance resembling long, thin, solid, cylindrical pasta [18]. Common histological features among these myopathies include profoundly altered muscle architecture, hypercontracted fibers with rounded profiles, nuclei internalization, multifocal myofibril degeneration (up to necrosis), as well as occasional regeneration, splitting, and fragmentation of myofibers. Additionally, alterations in perimysial and endomysial connective tissue have been observed, along with infiltration of fat and inflammatory cells [14,15]. WS is not a simple genetic flaw, but a complex, multifactorial disorder and its causes are still under investigation. While a genetic predisposition for rapid growth is the foundational cause, the actual incidence and severity of WS are modulated by non-genetic factors, including nutrition and management [9,32,33,34]. Experts in the field acknowledge that a sustainable long-term improvement depends on productivity, muscle structure, biochemical composition and the overall appeal of the meat to consumers. Progress in genomics, bioinformatics, and molecular biology has equipped poultry breeders with more precise tools for identifying and enhancing desirable traits. Genetically, many quality-related attributes are moderately inheritable, allowing selective breeding to meaningful and lasting improvements across generations [34,35]. This review synthesizes the current understanding of WS myopathy by critically examining its multifactorial etiology. It will first delineate the genetic basis established by decades of selection. It will then analyze the critical modulating roles of non-genetic factors, including dietary and rearing conditions. By integrating these perspectives, this review aims to provide a holistic view, which is essential for developing effective, sustainable mitigation strategies in modern broiler production.

2. Methodological Framework

A literature search was conducted between October 2025 and February 2026 using the following scientific databases: PubMed, Scopus, Web of Science, and Google Scholar. Peer-reviewed articles relevant to the scope of the review were included, along with additional studies cited in the primary selection. The main inclusion criterion was the relevance of the topic to the present review. No numerical threshold based on citation counts was applied as an exclusion criterion to avoid bias against recent or specialized contributions. The available literature on WS in broilers is broad and covers various aspects (e.g., meat quality, histology, genetics, nutrition). Therefore, the search strategy was specifically tailored to identify studies on the genetic and non-genetic causes of WS. Search terms included: “White Striping Myopathy”, “Broiler Myopathies”, “Broiler Breast Myopathy”, “White Striping Genes”, “White Striping Heritability”, “Genetic Correlation White Striping”, “White Striping Quantitative Trait Loci”, “Broiler Chromosome White Striping”, “Candidate Genes White Striping”, “White Striping Nutrition”, “White Striping Amino Acids”, “White Striping Feeding Strategy”, “White Striping Mitigation Strategies”. Selected papers were examined to identify recurring themes related to genetic and non-genetic factors of WS. Following a manual screening process to include, discuss, and link only meaningful studies, a total of 48 papers were deemed relevant and used for the present review.

3. Genetic Factors

The literature on genetic factors involved in WS myopathy is relatively scarce, although there is a general consensus across studies that the defect is not determined by a single gene but follows a polygenic mode of inheritance, where multiple genes contribute to the phenotype. However, conclusions regarding causative factors are conflicting. WS has been extensively assessed on different genetic lines, and the results have led to heterogeneous conclusions regarding its heritability and key influencing factors, reflecting differences in the populations examined, assessment methodologies, and interactions with environmental factors. Pampouille et al. [36] conducted a Genome-Wide Association Study (GWAS) for WS on the whole population of divergent broiler lines selected for high (pHu+) and low (pHu−) ultimate breast muscle pH. The analysis revealed three Nucleotide Polymorphisms (SNPs) significantly associated with WS located on chromosomes GGA17, GGA18, and GGA1. This Quantitative Trait Loci (QTLs) mapping did not support the existence of a single major gene with large effect on WS. Instead, the pattern of associations strongly suggested that WS, like other meat quality traits studied, follows a mode of polygenic inheritance. Subsequently, intra-line QTL detection of WS was performed. While no significant SNPs were detected in the pHu− line, eight SNPs were significant at the chromosome threshold in the pHu+ line. The analysis of the pHu+ line confirmed the two regions on GGA1 and GGA17 previously detected in the entire population, and a novel region was identified on GGA20. The minor allele frequency of the SNP on GGA17 remained similar in both lines, but the marker’s effect size was significantly amplified in the pHu+ line. This disparity indicates that the genetic architecture of WS does not function in isolation; rather, it interacts dynamically with the muscle’s metabolic environment. Consequently, even in the absence of direct genomic co-localization between QTLs for WS and pHu, the physiological status of the tissue, specifically characterized by glycogen depletion and elevated final pH, acts as a critical moderator that can exacerbate the phenotypic expression of a bird’s genetic predisposition to the myopathy. In this investigation, potential candidate genes were selected based on their proximity to significant SNPs (positional candidates) and/or their biological role (functional candidates). The majority of these selected genes are implicated in muscle architecture and the restoration of fibers, adiposity, fibrosis, the structural integrity of the extracellular matrix and sarcolemma, muscle metabolism regulation, and have established links to human neuromuscular disorders. Following GWAS, 132 SNPs were identified as significantly associated with molecular phenotypes, 24 of which reached genome-wide significance. These SNPs were organized into 21 Expression Quantitative Trait Loci (eQTLs) regions distributed across 16 chromosomes. These eQTLs are classified as cis when the polymorphism is located near the gene itself (within 1 Mb), or trans when it is further away or on a different chromosome. In this study, of the 21 eQTLs regions identified, only three were cis eQTLs, while the vast majority (18 regions) were trans eQTLs, suggesting a complex regulatory network where many genes are controlled by distant genetic elements. The most significant SNP associated with WS condition was found within the Myosin Heavy Chain 15 (MYH15) gene on GGA1, involved in muscle contraction, development, and regeneration in avian species. Several co-localizations between QTL and eQTL regions were observed on chromosomes GGA4, GGA5, and GGA17. These overlaps may help pinpoint causal genes and gene networks influencing variability in meat quality traits or breast meat yield. One notable co-localization on GGA17 involved both the expression of the Leucine-Rich Repeat and Sterile Alpha Motif Containing 1 (LRSAM1) gene and WS defect. LRSAM1 showed significant regulation and appeared to be a putative candidate gene, although functional validation (e.g., knock-out studies) is still lacking. It is a positional and a functional candidate gene, since mutations in this gene have been linked to a hereditary neuropathy characterized by progressive distal muscle weakness and atrophy [37]. A cis eQTL for the neonatal myosin heavy chain form myosin, heavy chain 1F, skeletal muscle (MYH1F, 0.30 to 0.83 Mb) was found near the WS associated QTL on GGA18 (2.77 Mb). This isoform is typically expressed during early breast muscle development or muscle fiber regeneration, suggesting MYH1F may serve as a useful molecular indicator of WS in relation to the muscle repair process. However, in the absence of functional validation, it remains a positional candidate gene. The authors could not establish that a single mutation was responsible for both the molecular phenotype and WS, given the considerable distance between the QTL and eQTL positions. While the eQTL analysis suggested some candidate genes and molecular pathways associated with WS and meat quality traits, no co-localizations with WS or with meat quality traits were detected for MYH15, β-sarcoglycan gene (SGCB, GGA5), and dysferlin gene (DYSF, GGA2) after eQTL analysis. Moreover, the authors note that these genes remain relevant candidates whose effects might be influenced by mutations in coding regions, affecting protein stability or enzymatic function, or by post-translational modifications. Mutations in the SGCB gene are linked to human limb-girdle muscular dystrophy (LGMD1E). Notably, studies on transgenic β-sarcoglycan-deficient mice have shown that they develop progressive muscular dystrophy and exhibit “whitish stripes” within the muscles, a phenotype that closely resembles WS defect in broilers [38]. Subsequently, Lake et al. [30] have identified QTLs and candidate genes underlying myopathy development in a commercial broiler population with a GWAS analysis. The GWAS revealed a primary genomic region of interest, identifying six QTLs associated with WS. A total of 18 SNPs (10 significant, 8 suggestive) were linked to the WS score, all located on chromosome GGA5 within a narrow region (12.1 to 14.8 Mb), except for one marker on GGA11. Interestingly, this pattern overlapped substantially with findings for WB. Three significant windows for WS on chromosome 5 (14–15 Mb and 58–59 Mb) and 12 (9–10 Mb) identified with Bayesian multi-marker regression, complessively explained 9.8% of the genetic variance for the trait. The analysis pinpointed several top candidate genes, including Cathepsin D (CTSD), Lymphocyte-specific protein 1 (LSP1), fast skeletal troponin I2 (TNNI2), synap-totagmin 8 (SYT8), and MOB kinase activator 2 (MOB2). The authors note that mammalian homologs of these genes are linked to altered insulin expression or secretion in pancreatic beta cells. They also possess functions directly relevant to muscle pathology: TNNI2 is crucial for calcium-dependent regulation of striated muscle contraction, and LSP1 regulates neutrophil transendothelial migration, a key step in inflammation. These findings elucidate potential molecular mechanisms, connecting genetic variation to pathways involving metabolism, muscle function, and inflammatory response in the etiology of WS. Chromosome GGA5 also contains several genes that show evidence of strong selection sweeps in commercial purebred broiler lines selected for breast muscle growth and feed efficiency [39]. Among these, are the SRY-box transcription factor 6 (SOX6) located in a candidate region (10.65–11.09 Mb), which encodes a Sry-related transcription factor that promotes early chondroblast differentiation, playing a critical role in differentiation and proliferation of chondrocytes as well as normal fiber type differentiation of fetal skeletal muscle in mice. Also within this genomic region is Actin, alpha, cardiac muscle 1 (ACTC1) (31.06–31.82 Mb), encoding cardiac muscle alpha actin, a protein which plays an important role in fetal development as well as cell survival, differentiation and development of muscle. Furthermore, the Syntaxin binding protein 6 (STXBP6), which has a potential pleiotropic effect on bone tissue and fecundity traits, is found in the same region [39]. Earlier QTL mapping studies had identified loci for fatness traits on this chromosome. Specifically, Lagarrigue et al. [40] identified a significant QTL for fatness on the distal region of GGA5 (124–165 cM). This genomic region included several genes involved in lipid metabolism, such as those encoding lipoprotein receptors, fatty acid desaturases or transcription factors involved in regulation of fatty acid synthesis. Subsequently, Le Mignon et al. [41] refined the characterization of this locus using an integrated genomics approach. Their analysis confirmed a QTL with a substantial effect of 1.03 phenotypic standard deviation and led to a reduction of its confidence interval on GGA5 from 31 cM (156–187 cM) to 18 cM (166–184 cM). This refinement substantially decreased the number of positional candidate genes from approximately 100 to 46. Overall, these results imply that the defect is influenced by the cumulative effect of many genetic variants, each with a small individual effect, which aligns with the complex and multifactorial nature of the myopathy. Lake et al. [30] reported a high prevalence of WS at approximately 80% in Cobb500, with sexual dimorphism (73% in females vs. 87% in males; p < 0.001). The estimated heritability for WS was 0.50 ± 0.06, a value intermediate to previous reports [9,42], underscoring that heritability is specific to the population and environment studied. Notably, a very high genetic correlation (0.88 ± 0.04) was found between WS and WB myopathy, suggesting these conditions are closely related and may represent variations in the same disorder. The correlation with body weight at 13 days and body weight at 7 weeks (0.15 and 0.09, respectively) was low. Studies on lines selected for different traits report higher heritability. For instance, Alnahhas et al. [42], working with two broiler lines divergently selected for ultimate pH of the pectoralis major, estimated, in the whole population, the heritability of WS to be 0.65 and of the intramuscular fat content of the pectoralis major muscle to be 0.83, with a high genetic correlation with WS (0.64). The genetic correlations of WS with body weight (0.33), breast meat yield (0.68), and pectoralis major yield (0.73) were significant, meaning that selection for these traits is genetically linked to a higher incidence and severity regardless of the line. A total of 50.7% breasts were affected by WS, with a higher incidence of WS in pHu+ line (moderate p < 0.001 and severe p < 0.0001) regardless of the sex, indicating that genetics is a major determinant of this defect in the studied lines. The positive correlation reported between breast muscle pHu and the increased degree of WS may be due to the fact that birds with the highest degree of WS also exhibited the highest breast muscle yield and it is negatively related to muscle glycogen reserve and positively related to pHu in broilers. One hypothesis is that the depletion of glycogen reserves observed in the pHu+ line would be a predisposing metabolic environment for WS development [43]. Accordingly, Pampouille et al. [36] recorded a higher proportion of normal breast fillets in the pHu− line than in the pHu+ line (57.3 vs. 32.4%, respectively) and incidence of severe WS was higher in the pHu+ line than in the pHu− line (27.7 vs. 4.3%, respectively; p < 0.001). Regarding sex, within the pHu− line, the proportion of normal fillets was significantly higher in females than in males (17.7 vs. 14.2%, respectively; p < 0.05) [42]. Females of the pHu+ line presented higher frequency of moderately white striped breast fillets compared to females of the pHu− line (12.5 vs. 8.1%, respectively; p < 0.05), while males of the two lines showed similar incidences (8.9 vs. 7.2%, respectively). The incidence of severe WS was higher in the pHu+ than in the pHu− line for both sexes (12 vs. 2%, respectively; p < 0.05). A strong genetic correlation was also found with the intramuscular fat content of the pectoralis major muscle, but not with its lipid oxidation index. While confirming a substantial genetic role, this study also refines the understanding by linking WS more closely to the genetics of pectoralis major muscle metabolism and development than to general growth rate, in fact WS was not found to be significantly correlated with abdominal fat percentage nor with leg percentage in the whole population and within each of the two divergent lines. The authors suggest that high genetic correlation between WS and intramuscular fat content of the pectoralis major muscle also indicates that the latter measurement could be used as a valuable quantitative indirect criterion of selection against WS. However, studies conducted by Aviagen researchers [9,32], using different methodologies and lines, provided a contrasting perspective that emphasized the dominance of non-genetic factors. In particular, Bailey et al. [9] estimated the genetic basis of three breast muscle myopathies and their relationship with growth and yield. Analyzing two pure pedigree broiler lines with different selection histories, Line A, selected for high breast yield, and Line B, selected for moderate breast yield, they found a higher incidence of myopathies in Line A. The genetic parameters for these defects were similar between lines. The study reported low to moderate heritability estimates for the myopathies. Specifically, the heritability for WS was 0.338 in Line A and 0.185 in Line B, indicating that while WS has a larger genetic component than other myopathies, it is still predominantly influenced by non-genetic factors. For WS, genetic and phenotypic correlations with body weight and breast yield were low in both lines. These findings have two major implications: first, the genetic factors driving growth and yield appear independent from those predisposing to myopathies; second, birds of any size or yield can be affected. Thus, while selection history influences incidence, Bailey et al. [9] concluded that it is not the primary driver of myopathy expression. The authors emphasized that understanding and managing non-genetic factors is vital for reducing incidence, although genetic progress through direct selection against WS remains possible. In a subsequent study, Bailey et al. [32] expanded their analysis using a purebred commercial broiler line, providing updated genetic estimates, reaffirming the modest role of genetics. Specifically, the heritability for WS was estimated at 0.25, aligning with the previously reported data and confirming it as the myopathy with the strongest, yet still limited, genetic component. The dominance of non-genetic factors indicates that differences in management, nutrition, and environment are the primary drivers of the variation observed in myopathy incidence and severity, even in a genetically selected line. The genetic and phenotypic correlations between WS and body weight, WS, and breast yield were low. The consistently low correlations across both studies suggest that decades of intense selection for growth and yield have not inadvertently increased the genetic propensity for these muscle disorders. Based on this evidence, the authors conclude that a significant reduction in breast myopathies cannot be achieved through selection on production traits alone. They advocate for a holistic approach, where managing non-genetic factors is prioritized for immediate impact, complemented by direct genetic selection against the myopathies themselves for long-term improvement. Bailey et al. [9,32] heritability estimates are notably lower than those obtained from Alnahhas et al. [42]. A key methodological difference may partly explain this divergence: Bailey et al. [9,32] used a 4-point observed scale, which typically yields lower values, whereas Alnahhas et al. [42] estimated heritability on an underlying continuous scale. Livingston et al. [44] concluded that genetic background may influence the expression of WS along with egg storage period and time-limited feeding, reinforcing the multifactorial nature of this condition. Their study compared broilers from two distinct male genetic strains: a growth strain selected for rapid body weight gain and a yield strain selected for high breast meat yield. The results revealed a clear genetic influence on WS severity. Broilers from the growth strain exhibited a significantly greater WS muscle score compared to those from the yield strain (2.47 vs. 2.04, respectively; p < 0.01), with 66% of yield-strain birds showing only mild or no signs of WS. This difference was linked to growth rate, as WS scores were positively correlated with body weight across both genetic backgrounds (0.44; p < 0.01). While the yield strain produced birds with lower WS scores, it showed greater susceptibility to WB myopathy, indicating a divergent myopathy profile. These findings, however, differ from other studies, such as Trocino et al. [45], which reported no significant overall difference in WS incidence between a standard breast yield commercial strain and a high breast yield strain. In this study, although severe WS was significantly less frequent in the standard genotype (−10%), overall WS prevalence was similar between the two lines (74 vs. 75%). The authors concluded that genotype had only a moderate effect on growth and did not substantially alter myopathy occurrence. They hypothesized that the high growth rate common to both modern hybrids or the insufficient difference in final body weight (3207 vs. 3130 g; p < 0.01) might explain the comparable WS incidence. In contrast, gender and early feed restriction significantly influenced performance, meat quality, and breast abnormalities. The occurrence or the degree of WS did not differ between females and males, despite significant differences in live weight (2845 vs. 3492 g), whereas the occurrence of WB was twice as frequent in males (16.3 vs. 8.0%). While genetic line had limited impact on WS in these modern fast-growing hybrids, gender and nutritional management, particularly early feed restriction, played a more decisive role in influencing myopathy occurrence. Russo et al. [46] evaluated the prevalence of WS in medium and heavy commercial broilers reared in Italy and found no correlation between genetics or sanitary status of the flock and WS. The overall prevalence of WS in medium and heavy broilers was 70.2% and 82.51%, respectively. Mean WS score and severe WS lesions prevalence resulted highly correlated with the mean body weight and with average daily gain. The interplay between genetic strain and other production variables has been further clarified by predictive modeling and studies on different lineages. Aguirre et al. [8] proposed a predictive model to investigate the incidence and severity of WS including in the model parameters such as sex, age, strain, live weight categories, and breast weight categories. Broilers aged 6 weeks and 8 weeks were associated with a significant greater probability of higher severity of WS scores compared to 4-week-old broilers. As for strain, results showed that high breast yield strains were associated with significant higher odds of increasing WS severity scores compared to the standard strain. Heavier breast fillets, particularly >750 g, were overwhelmingly associated with higher WS severity (p < 0.0001). The study concludes that breast weight is the primary driver of WS severity, followed by genetic strain and age. The developed model provides a quantitative tool for the poultry industry to assess WS risk based on measurable growth factors. A direct comparison of conventional and slower-growing lines provided further evidence for the impact of intense genetic selection. Given that the use of slower-growing strains has been suggested as an alternative to decrease incidence and severity of WS [2], Santos et al. [47] evaluated WS in 2 conventional strains vs. 12 slower-growing strains, categorized based on growth rate (fast, moderate and slow). Broilers were processed at two target weights (for conventional and slower-growing strains: TW1 at 34 and 48 d targeting 2.1 kg; TW2 at 48 and 62 d targeting 3.2 kg, respectively). Results showed that the total incidence of WS was significantly affected by category, target weight, strain, and sex. When body weight was included as a covariate, the effect of sex disappeared. A significant target weight × category interaction was observed. As birds grew from TW1 to TW2, WS incidence increased significantly. At TW1, conventional and fast strains had similar incidences, which were higher than moderate and slow strains. At TW2, conventional strains had the highest incidence, followed by fast and moderate strains, with slow strains having the lowest. The average WS score increased from TW1 to TW2. At TW1, conventional and fast strains had similar average scores, which were higher than those of moderate and slow strains. At TW2, the average score increased with growth rate, following the hierarchy: conventional > fast > moderate > slow. Correlation analysis revealed that breast yield was positively correlated with WS incidence across all categories. Conversely, drumstick, thigh, and wing yields were negatively correlated with WS incidence in several categories. Dixon [48] also found a greater incidence of WS in fast-growing strains (Ross308, Cobb500, Hubbard Flex) compared to slower-growing birds (The Hubbard JA757). The incidence of WS for birds at 42 d (63 to 78%) was similar to those reported by Santos et al. [47] (53 to 80%). Slower-growing birds slaughtered at 60 d had significantly lower WS score and significantly more abdominal fat and heavier leg weights than the other breeds. The authors attribute this result to birds’ behavior, as they were more active. Dixon [48] concluded that slower-growing broilers may be a viable commercial option taking into account improved meat quality, higher retail price, and decreased welfare issues. Panisson et al. [49] assessed WS incidence of three different genetic lineages of broilers: Embrapa021 (moderate growth), Cobb500 and Ross308 (rapid growth), fed with three different dietary nutrient densities. The lowest incidences of WS were found for Embrapa021 lineage compared to the other lineages (p < 0.05), regardless of diet. From what they observed, the Cobb and Ross lineages, subject to a greater degree of selection, were more likely to present some degree of WS as their age increases. A concise overview of the described findings is presented in

Table 1. Summary of the studies cited related to WS and genetics.

Authors	Year	Reference	Genetic Line	Age at Slaughter (Days)	n	Sex	WS Scale	h2 WS ± SE	Main Findings
Pampouille et al.	2018	[36]	pHu+; pHu−	42	558	m + f	0–2	-	3 significant SNPs associated with WS; major incidence in pHu+ lines
Lake et al.	2021	[30]	Cobb500	49	1193	m + f	0–3	0.50 ± 0.06	6 QTLs for WS; WS prevalence in males; genetic correlation with WB
Alnahhas et al.	2016	[42]	pHu+; pHu−	42	1349	m + f	0–2	0.65 ± 0.08	Major incidence in pHu+ lines; males more susceptible to WS than females in pHu−lines; genetic correlation with body weight, pectoralis major intramuscular fat content and yield
Bailey et al.	2015	[9]	Two purebred commercial broiler lines: for high breast yield (A) and moderate breast yield (B)	Line A: 47, Line B: 40	Line A: 42,578; Line B: 56,837	-	0–3	Line A: 0.338 ± 0.020; Line B: 0.185 ± 0.012	Higher incidence of myopathies in Line A; low genetic and phenotypic correlations with body weight and breast yield
Bailey et al.	2020	[32]	Pure bred commercial broiler line (Aviagen)	40	38,780	-	0–3	0.25 ± 0.02	Low genetic and phenotypic correlations with body weight and breast yield
Livingston et al.	2019	[44]	Growth strain selected for rapid body weight gain; yield strain selected for high breast meat yield	42	240	m	1–4	-	Greater WS score on growth strain; genetic correlation with body weight; divergent myopathy profile with WB
Trocino et al.	2015	[45]	Standard breast yield commercial strain; high breast yield strain	46	768	m + f	0–2	-	Genotype with minor effect on WS severity; WS incidence influenced by feeding regime; high overall WS incidence; WS score affected by gender
Russo et al.	2015	[46]	Medium (2.59 ± 0.13 kg); heavy (3.64 ± 0.34 kg) commercial broilers	Medium: 46; heavy: 55	22,800	m + f	0–2	-	No correlation between WS and genetics or sanitary status; mean WS score and severe WS lesions prevalence highly correlated with mean body weight and average daily gain
Aguirre et al.	2020	[8]	Standard breast yield commercial strain; high breast yield strain	28, 42 and 56	4332	m + f	0–3	-	WS score influenced by breast weight, genetic strain and age
Santos et al.	2021	[47]	2 conventional strains; 12 slower-growing strains	Conventional strains: 34, 48; slower-growing strains: 48, 62	7216	m + f	0–2	-	WS incidence affected by category, target weight, strain, and sex
Dixon	2020	[48]	Fast-growing strains (Ross308, Cobb500, Hubbard Flex); slower-growing birds (The Hubbard JA757)	Fast-growing strains: 42; slower-growing birds: 62	1600	m + f	0–2	-	Lower WS score in slower-growing birds, with more abdominal fat and heavier leg weights
Panisson et al.	2022	[49]	Moderate growth: embrapa021; rapid growth: Cobb500 and Ross308	28, 35, 42, and 49	4320	m	0–2	-	WS score influenced by breast weight, genetic strain and age, regardless of nutrient density; increasing WS severity scores in high-breast-yield strains

h² WS + SE = estimated heritability of White Striping ± standard error of the estimate.

.

4. Non-Genetic Factors

4.1. Diet

Several attempts have been made to prevent the appearance of WS in broiler chickens, without fully eradicating this myopathy [34,50]. Given that WS is associated with the rapid growth of breast muscle pectoralis major, manipulating the growth trajectory through dietary means is a promising strategy [3,33,51]. Reducing the nutrient density of diets can slow broiler growth [52,53]. However, nutrition is a complex system that requires careful balancing, as even single nutrients can significantly impact performance and muscle development [54,55,56]. Broiler diet formulation prioritizes highly digestible crude protein that is easily digestible into amino acids which can be reassembled and metabolized. These formulation strategies are optimized considering nutrient digestibility, cost-effectiveness, and the final meat yield and quality [51]. While supporting rapid muscle growth demands high levels of essential amino acids and metabolizable energy, strategic restriction of specific nutrients may mitigate WS [53,57,58]. According to Livingston et al. [59], the occurrence of WS may be associated with least-cost feed formulations and the inclusion of greater amounts of synthetic amino acids. To prove this affirmation, they evaluated the effects of supplemental glutamine (0 and 1%) and arginine (0 and 0.25%) on 512 male broilers, concluding that both the supplements significantly increased body weight and feed conversion rate, but only glutamine significantly increased WS severity along with breast muscle fat percentage. Also, muscle pH (24 h postmortem) significantly increased with respect to WS scores, in agreement with the results obtained by Alnahhas et al. [42] and Pampouille et al. [36]. Zampiga et al. [60] conducted a study to assess how varying the ratio of digestible arginine to lysine in broiler feed influenced the incidence and severity of WS. The birds were divided into three dietary groups: control (standard commercial diet with four feeding phases, maintaining Arg:Lys ratios of 1.05, 1.05, 1.06, and 1.07 across the phases); ARG2 and ARG3 (fed the same base diet as control but supplemented with additional crystalline L-arginine, increasing the Arg:Lys ratio by 20% for ARG2 and 30% for ARG3 above the control levels). While growth performance and general meat quality were not significantly different between the groups, the dietary treatments did affect WS. Both ARG2 and ARG3 groups had a notably higher proportion of breast fillets with no WS compared to the control group (28 and 41 vs. 17%, respectively; p < 0.001). Moreover, the ARG3 group exhibited the lowest incidence of severe WS (11%), compared to 31% in the control group and 27% in the ARG2 group (p < 0.001). Subsequent studies focused more intently on lysine as a key lever for growth control. Ahsan et al. [55] adopted a reduction in either dietary lysine or metabolizable energy along with amino acid density during different growth phases (grower and finisher) in Ross308 and evaluated WS incidence. The occurrence of WS was significantly lower in broilers fed diets containing 85% of the recommended lysine level during the grower or combined grower-finisher phases (31.67 vs. 28.33%, respectively; p < 0.001), compared to other groups. The authors attributed this effect to a slowdown in growth, reduction in breast yield, reduced lipid synthesis, and less muscle damage, as confirmed by lower extent of histopathological lesions. In fact, WS occurs due to the myofiber degeneration followed by gradual replacement with adipose and connective tissue [13]. In contrast, reducing metabolizable energy and amino acid density failed to reduce the occurrence of WS, likely due to the compensatory feed intake [55]. This finding establishes a clear distinction between the efficacy of targeted lysine restriction versus lowering the broad dietary nutrient densities. This result confirmed a pattern previously identified by Ahsan and Cengiz [53]. Reducing the dietary digestible lysine levels during grower or grower and finisher phases significantly reduced the development of WS in broiler chickens. This reduction was again associated with a slower growth rate, reflected in lower final body weight, weight gain, and breast yield. The adoption of this strategy requires a practical compromise: accepting a moderate reduction in growth and breast yield in exchange for a significantly lower WS incidence. The effect of reduced digestible lysine density on WS was further confirmed by Meloche et al. [52]. They gave 7 different dietary treatments to broilers: 100% of primary breeder recommendations for dietary lysine; 85% of lysine for the 1st grower period; 85% of lysine for the 2nd grower period; 85% of lysine for the 1st and 2nd grower periods; 75% of lysine for the 1st grower period; 75% of lysine for the 2nd grower period; 75% of lysine for the 1st and 2nd grower periods. For WS, broilers receiving diets formulated at 75% of recommended dietary lysine concentrations for the 1st and 2nd grower periods had reduced (p < 0.05) the incidence of severe scores for WS, compared to control. This result is attributed to the reduced breast weights and yields. In a second experiment, 4 dietary treatments were tested: 100% of primary breeder recommendations for dietary lysine; 85% of lysine for the grower period; 85% of lysine for the finisher period; 85% of lysine for the grower and finisher periods. The incidence of severe scores for WS was reduced (p < 0.05) in broilers receiving diets formulated at 85% of recommended dietary lysine for the grower period (22.3%) or for the grower and finisher periods (17.8%) in comparison with the control (38.3%). Collectively, these studies converge on a key conclusion: short-term reductions in dietary lysine density are effective at reducing the severity of WS. However, identifying the critical periods during which manipulation of the growth trajectory effectively reduces myopathy with the least compromise on performance is a good half-measure, as if the duration of reduced dietary lysine is too extensive, growth performance and breast meat yield will be adversely affected. In accordance, Cruz et al. [54] concluded that increasing the level of lysine improved growth performance and carcass traits, but, on the other hand, induced the occurrence and severity of WS. They conducted two experiments: increasing the level of lysine from 12 to 28 d in the first (0.08% increments from 0.77 to 1.17%) and from 28 to 42 d in the second (0.08% increments from 0.68 to 1.07%). In the first experiment, a score of 1 occurrence increased when broilers were fed diets with 1.01% lysine and then moderately decreased, whereas a score of 2 tended to linearly increase as the level of lysine increased in both experiments. In experiment 2, a score of 1 was consistent among increasing levels of lysine, except at 0.92% of lysine, where the lowest value was observed. Furthermore, a WS score of 2 increased when broilers were fed diets with 0.92% lysine and then the score tended to decrease. The severity of WS was significantly lower when broilers were fed diet without supplemental lysine compared to broilers fed diets with 1.01% of lysine in experiment 1. In experiment 2, means of WS scores were higher (p < 0.01) in all lysine levels compared to the basal diet with 0.68% of lysine. In both trials, increasing the level of lysine increased the occurrence and severity of WS lesions, possibly because the higher levels of lysine maximized the genetic potential of the broiler, but overwhelmed the support systems that allow for normal tissue turnover. Also, according to the authors, since body weight and growth rate are direct results of increasing lysine levels, myopathies do not seem to be associated with lysine itself but with gains in performance. Thus, the relationship between lysine and WS appears to be primarily mediated through its powerful effect on growth performance. However, the mechanistic evidence of these aspects deserves to be further clarified through studies focused on the specific molecular pathways by which lysine restriction reduces WS (e.g., mTOR signaling, protein synthesis rate, satellite cell activity). Beyond mere concentration, the source of lysine also emerges as a modifiable factor. A study conducted by Bertechini et al. [61] evaluated the combined effects of lysine source (Lys-HCl vs. Lys-SO₄), calcium pidolate supplementation (present/absent), and the nutritional density (high/low), for a total of eight experimental treatments, on different parameters, including WS incidence, in high-performance broilers. As a result, the use of Lys-HCl increased the rate of WS in breast fillets compared to the use of Lys-SO₄ (53.74% vs. 42.32%, respectively; p < 0.05). Lys-SO₄ also resulted in lower 24 h post-mortem breast pH than that with Lys-HCl (5.85 vs. 5.91, respectively; p < 0.05), suggesting better glycogen utilization and reduced metabolic stress linked to WS [36,42]. The addition of calcium pidolate to the diet of broilers aged ≤21 days, combined with Lys-SO₄, further reduced WS incidence (p < 0.05), likely due to its angiogenic effect and the consequent reduced hypoxia. Nutritional density did not have a direct effect on the incidence of WS. Thus, the use of high-performance diets does not increase myopathies and the early inclusion of calcium pidolate in combination with Lys-SO₄ can help mitigate WS in broilers. This introduces an important nuance: mitigation strategies can involve not just reducing levels but also selecting more favorable forms of critical nutrients. Research on other amino acids, however, presents a more complex and less consistent picture. Another amino acid that may attenuate WS is methionine, as it is a lipotropic agent and plays many roles in avian nutrition including protein synthesis, oxidative stress prevention, transmethylation, and transsulfuration pathways [56]. To test its effect on WS, Khan et al. [62] fed 144 Cornish cross chicks with a corn-soybean meal-based diet containing 0% microalgae (control), 2% microalgae (diet 1), and diet 1 + 100% more National Research Council requirement of methionine (diet 2). The incidence of visual WS was the lowest for diet 2 vs. control (p < 0.05). Moreover, histopathological changes were minimal in diet 2 when compared to control (p < 0.05). These results demonstrated a significant effect of microalgae along with methionine supplementation in reducing the incidence of WS and myopathic lesions without affecting productivity, as the experimental diet had no significant effect on overall weight gain and feed consumption in the grower or finisher phase as well as no effect of diet on breast muscle weight or yield of breast muscle when expressed as a percentage of body weight was observed (p > 0.05). Conversely, Sachs et al. [51] compared the effects of synthetic methionine vs. natural sourced methionine on WS comparing broilers fed a conventional corn/soy diet regimen with synthetic methionine to those fed roasted cowpea and sunflower seed meal (60% corn/soy, 20% sunflower seed meal, and 20% roasted cowpea) and no synthetic methionine. The alternative group had an increase in mild WS and a decrease in severe WS compared to the group fed a control diet, with mean WS scores of 2.1 and 2.6, respectively, although this difference is not significant (p = 0.068). The faster growing birds tended to have more WS and it is possible that the difference in WS seen between the diets is a result of inefficiencies in the alternative diet regimen that thus slowed broiler growth and fat deposition. In fact, the group fed an alternative diet regimen gained less weight than the control in the starter and grower phase (p < 0.01). Conflicting results were obtained by Kuter and Önol [63], who investigated the effect of dietary methionine levels (100 and 125% of requirement) and supplemental L-carnitine (0 and 100 mg/kg) on 480 male Ross380. The authors acknowledged that increased dietary methionine levels and L-carnitine supplementation failed to inhibit the development of WS on breast fillets of broiler chickens at 39 and 49 d, as total WS score was above 50% in all experimental groups. A more generalized reduction in dietary amino acid density shows efficacy. However, apart from decreasing mean WS score, it compromises the growth and meat quality. This inconsistency suggests that methionine’s role is less straightforward and potentially context-dependent compared to the more predictable effects of lysine. A broader, less targeted approach shows efficacy but at a higher cost. Pekel et al. [58] conducted a trial on 288 Ross380 fed with three dietary levels of amino acid density (normal; 10% lower than normal; 10% or 20% lower than normal). The occurrence of normal, moderate, and severe WS fillets was 45.3, 49.1, and 5.6%, respectively. As the dietary amino acid density decreased, the occurrence of no WS breast fillets increased linearly, whereas the occurrence of moderate WS fillets and mean WS score decreased linearly (p < 0.05). WS occurrence and severity increased with higher growth rate; in fact, body weight gain decreased linearly (p < 0.05) with the decreasing dietary amino acid density and as dietary amino acid density decreased, there were linear decreases (p < 0.01) in body weight at slaughter, hot carcass weight, part weights, and hot carcass yield. The same conclusions were made by Toghyani et al. [57] who found in Ross308 that increasing amino acid density resulted in higher WS mean scores (p < 0.01), as well as enhanced breast meat yield. Reducing metabolizable energy levels density led to a significant linear decrease in WS mean scores compared to standard metabolizable energy levels. At the same time, birds fed with the standard metabolizable energy levels showed the lowest percentage of score 2 fillets (p < 0.05). Finally, a range of other dietary interventions have been explored. Bodle et al. [64] observed no significant differences in WS scoring among breasts fillets of broilers fed with six different dietary strategies: commercial reference diet; increasing the level of arginine:lysine from approximately 111% to between 120 and 125%; supplementing vitamin C at 94.4 mg vitamin C/kg feed (100 ppm on a product basis); increasing the vitamin premix supplementation 2-fold; reducing the amino acid density in only the grower phase by 15%, and feeding the exact same starter, finisher, and withdraw diets that were fed in the commercial reference diet; combining all the four strategies just mentioned. Moreover, no differences were observed in average breast weight. Sirri et al. [65] investigated whether the source (organic or inorganic) and amount of trace minerals influenced the occurrence of WS in broilers, testing four dietary treatments, including for starter, grower, and finisher diets, respectively, zinc, manganese (high: 60-50-50 mg/kg feed, low: 40-32-32 mg/kg) and copper (high: 15-12.5-12.5 mg/kg, low: 10-8-8 mg/kg). The results showed that neither the source nor the dose of the trace minerals had any significant effect on WS. The combined incidence of moderate and severe WS was consistently high, ranging from 60% to 61.1% across all groups. Specifically, the rate of severe WS was nearly identical for organic (37.8%) and inorganic (39.0%) sources, and the dosage level also yielded similar outcomes. Lee et al. [66] fed broilers with corn-soy diets and 0, 0.2, and 0.4% chitosan, a polysaccharide derived from the deacetylation of chitin, in the grower and finisher phases. At market weight, they evaluated effect of dietary chitosan on WS, underlying no significant difference for WS scores between treatment groups, though there was a significant sex effect as female broilers had lower WS score overall. Moreover, multiple test comparisons demonstrated that female broilers supplemented 0.4% chitosan had significant lower WS scores than male broilers fed 0, 0.2, 0.4% chitosan, respectively. However, no significant differences in body weight were observed between treatment groups for the duration of the study. The consistency in performance indicates that the level of dietary chitosan fed did not compromise weight gain. As fast-growing birds may need greater amounts of vitamin E (DL-α-tocopherol acetate) in their muscles for normal muscle growth, Kuttappan et al. [25] included five different diet treatments with 15, 50, 100, 200, and 400 IU/kg of vitamin E levels for broilers. Results showed that the diet treatments did not have any significant effect on the occurrence of normal, moderate, and severe degrees of WS. However, higher fillet weight was the only parameter that had a significant effect on the occurrence of WS. Bošković Cabrol et al. [67] hypothesized that microalgae (Chlorella vulgaris) could mitigate the impacts of heat stress on meat quality and included WS evaluation in their analysis. Broilers submitted to a chronic heat stress were fed diets including 0, 3, and 6% of C. vulgaris meal. Although the highest inclusion level of C. vulgaris significantly decreased feed intake and body weight, without mitigating the negative effects of a chronic heat stress on growth performance, it also did not reduce the occurrence of WS. De Castilho Heiss [68] evaluated a commercial polyphenol blend for its potential to reduce WS incidence; however, no significant effect was observed. Mudalal et al. [69] tested two levels (0.2 and 0.3 mL/L) of a herbal extract supplement (containing thymol, carvacrol, antioxidants, serotonin, and essential minerals) in drinking water on WS incidence at 34, 41, and 48 days. The herbal mix significantly reduced the incidence of WS and WB only at 34 days compared to the control group.

Table 2. Summary of the studies cited related to WS and diet.

Authors	Year	Reference	Genetic Line	Age at Slaughter (Days)	n	Sex	WS Scale	Supplement	Experimental Groups	Main Findings
Livingston et al.	2019	[59]	-	44	512	m	1–4	Glutamine; arginine	Supplemental glutamine (1%); arginine (0.25%) at the expense of glycine at both starter 2 and grower phases	WS severity increased with glutamine supplement
Zampiga et al.	2019	[60]	Ross308	43	1755	m	0–2	Arginine:lysine	Arginine:lysine ratio increased by 20%; ratio increased by 30% across the four feeding phases	Higher proportion of no WS in experimental groups; lowest incidence of severe WS without affecting yield in 30% arginine:lysine increased ratio
Ahsan et al.	2023	[55]	Ross308	49	300	-	0–2	Lysine; metabolizable energy; amino acid density	15% low digestible lysine in grower or grower and finisher phases; 5% low metabolizable energy and amino acid density in grower or grower and finisher phases	WS occurrence lowered with 85% lysine level, without affecting overall growth performance
Ahsan and Cengiz	2020	[53]	Ross308	49	390	m	0–2	Lysine; metabolizable energy, amino acid density	15% low digestible lysine in grower or grower and finisher phases; 5% low metabolizable energy and amino acid density in grower or grower and finisher phases	WS occurrence lowered by 85% lysine level, without affecting overall growth performance
Meloche et al.	2018	[52]	Yield Plus × Ross708	48	1386	m	0–2	Lysine	85% of lysine for 1st grower period; 85% of lysine for 2nd grower period; 85% of lysine for 1st and 2nd grower period; 75% of lysine for 1st grower period; 75% of lysine for 2nd grower period; 75% of lysine for 1st and 2nd grower period	Reduced incidence of WS severe scores with 75% of recommended dietary lysine concentrations for 1st and 2nd grower periods, compared to control
Meloche et al.	2018	[52]	Yield Plus × Ross708	61	720	m	0–2	Lysine	100% of primary breeder recommendations for dietary lysine; 85% of lysine for grower period; 85% of lysine for finisher period; 85% of lysine for grower and finisher periods	Reduced incidence of severe WS with 85% of recommended dietary lysine for grower period or for grower and finisher periods, compared to control
Cruz et al.	2017	[54]	Cobb500 × Cobb broilers	35 and 42	1200	m	0–2	Lysine	Increasing the level of lysine from 12 to 28 d (0.08% increments from 0.77 to 1.17%); from 28 to 42 d (0.08% increments from 0.68 to 1.07%)	WS occurrence and severity induced by the increased level of lysine
Bertechini et al.	2024	[61]	Cobb500	42	1440	m	0–2	Lysine (Lys-HCl vs. Lys-SO4); calcium pidolate; nutritional density	99% Lys-HCl; 99% LysSO4; presence and absence of calcium pidolate; high and low nutritional density	WS rate increased with Lys-HCl compared to the use of Lys-SO4; WS incidence further reduced with calcium pidolate addition
Khan et al.	2021	[62]	Cornish cross chicks	42	144	-	1–3	Methionine; microalgae	2% microalgae; 2% microalgae and 100% more requirement of methionine	Incidence of WS reduced with microalgae and methionine supplementation, without affecting productivity
Sachs et al.	2019	[51]	Cobb500	42	120	m + f	1–3	Methionine	Conventional corn/soy diet regimen with synthetic methionine vs. roasted cowpea and sunflower seed meal and no synthetic methionine	Increased mild WS and decreased severe WS with natural methionine, compared to synthetic methionine
Kuter and Önol	2021	[63]	Ross380	39 and 49	480	m	0–2	Methionine; L-carnitine	125% methionine; 100 mg/kg L-carnitine	No inhibition of WS
Pekel et al.	2020	[58]	Ross380	49	288	m	0–2	Amino acid density	10% and 20% lower than normal	Linear increment of no WS breast fillets with dietary amino acid density decrement; occurrence of moderate WS fillets and mean WS score linear decrement; no compromission of growth and meat quality
Toghyani et al.	2025	[57]	Ross380	42	2400	m	0–3	Amino acid density; metabolizable energy levels	+3.0% and +6.0% amino acid density; −50, −100 and −150 kcal/kg metabolizable energy levels	Linear decrease in WS mean scores with reduced metabolizable energy levels density
Bodle et al.	2018	[64]	High-yielding	45	1980	m	0–2	Arginine; lysine; vitamin C; vitamin premix; amino acid density	Increasing the level of arginine:lysine from approximately 111% to between 120 and 125%; supplementing vitamin C at 94.4 mg vitamin C/kg feed (100 ppm on a product basis); increasing the vitamin premix supplementation 2-fold; reducing the amino acid density in only the grower phase by 15%, and feeding the exact same starter, finisher, and withdraw diets that were fed in the commercial reference diet; combining all the 4 strategies	No significant differences in WS scoring
Sirri et al.	2016	[65]	Ross308	31 and 51	3600	m	0–2	Organic and inorganic trace minerals (zinc, manganese and copper)	For starter, grower, and finisher diets, respectively, organic or inorganic zinc, manganese (high: 60-50-50 mg/kg feed, low: 40-32-32 mg/kg) and copper (high: 15-12.5-12.5 mg/kg, low: 10-8-8 mg/kg)	No effects of source and dose on WS
Lee et al.	2024	[66]	Cobb500	42	126	m + f	0–2	Chitosan	0.2, and 0.4% chitosan in the grower and finisher phases	No significant difference in WS scores between treatment groups; lower WS score in female broilers
Kuttapan et al.	2012	[25]	Commercial strain	49	424	m	0–2	Vitamin E (DL-α-tocopherol acetate)	15, 50, 100, 200, and 400 IU/kg of vitamin E	No effect on WS scoring; WS occurrence affected by breast weight
Bošković Cabrol et al.	2024	[67]	Ross308	42	576	m + f	0–2	Microalga Chlorella vulgaris	3 and 6% of Chlorella vulgaris meal	No effect on WS occurrence
De Castilho Heiss et al.	2025	[68]	RossAP91	21, 28,35 and 42	1280	m	0–2	Commercial polyphenol blend	250 g/ton, 500 g/ton and 1000 g/ton of commercial polyphenol blend	No significant effects on WS
Mudalal et al.	2020	[69]	Ross500	34, 41 and 48	504	-	0–1	Natural herb extract	0.2 and 0.3 mL/L of natural herb extract	WS and WB reduction at 34 days, compared to control

summarizes the information described above.

4.2. Management

Beyond genetics and nutrition, management and environmental factors significantly influence the development of WS often by interacting with birds’ physiology to exacerbate metabolic stress and muscle damage. A study was conducted to evaluate the effect of cyclic or chronic heat stress on the incidence and severity of WS [70]. Arbor Acres Plus broiler chickens were assigned to three experimental groups: control (22–24 °C), chronic heat stress (raised at 32 °C from day 21 onwards) or cyclic heat stress (reared at 32 °C during the daytime only, from 08.00 to 20.00 h starting at day 21 until the end of the experiment). Overall WS incidence differed among the groups, with control group having the highest incidence followed by chronic heat stress group and cyclic heat stress (83.33%, 76.67% and 66.67%, respectively). The reverse was true for score. Chronic heat stress group had lower incidence of mild (score 1) and higher incidence of severe (score 2) in comparison with control and cyclic heat stress groups (p < 0.01). In conclusion, subjecting the birds to chronic heat stress increased the severity of WS, although the incidence was numerically higher in control group than other groups despite the lower body weight gain and lighter body weight. For the chronic heat stress group, the growth performance data provided by the authors show that animals had significant lower body weight gain and lower feed intake compared to the control group for the entire duration of the trial (days 0–42). This could partially explain the counterintuitive findings of the study, as reduced feed intake under heat stress leads to lower body weight and, consequently, lower WS incidence. Nevertheless, the relatively small sample size (n = 180 across three groups) limits statistical power, and larger studies are needed to confirm these results. Tóth et al. [71] investigated the effects of incorporating yellow mealworm (Tenebrio molitor) frass at 0%, 10%, 20%, and 30% into wood shavings bedding on WS, but no statistically significant treatment effect was detected. Across multiple studies, flooring type has been consistently found to have no significant effect on WS [72,73,74]. As the toxicity of coccidiostats in skeletal muscle, visible as focal degeneration and necrosis, has already been reported in broilers, Dalle Zotte et al. [75] have hypothesized that there might be a link with WS and anticoccidials. In their study, they investigated the impact of two coccidiosis control programs (vaccine vs. anticoccidial additive) and feeding plan (standard diets for both programs and low energy diet supplemented with enzymes for vaccinated group) on WS occurrence, observing the breast of chicks at different slaughter ages (12, 25, and 51 d) to study the myopathy’s evolution. Lesions were detected at 25 d of age in all four experimental groups, but the difference was not statistically significant. At 51 d of age, the total WS prevalence was on average very high (95.1%), with no difference among treatments. WS severity was distributed according to 4% for level 0 (treatment effect: not significant), 29.4% for level 1 (treatment effect: p < 0.05), and 66.6% for level 2 (treatment effect: p < 0.01). The prevalence of moderate WS was higher in the breasts of control and vaccine than anticoccidial group birds (36.8 and 33.5% vs. 19.1%; p < 0.05). On the contrary, the prevalence of severe WS was higher in anticoccidial than control and vaccine groups (77.6 vs. 62.6 and 61.6%, respectively; p < 0.01), and higher than in vaccine + low energy diet birds (64.4%; p < 0.05). Thus, treatments influenced the prevalence of moderate and severe WS at the commercial slaughter age. In conclusion, this study suggests that vaccination against coccidiosis has no effect on WS occurrence while anticoccidial influences the severity at commercial slaughter age. Perhaps the most direct managerial lever is feed access. Ad libitum feeding has been reported to be a critical factor that exacerbates muscular defects in broiler chickens since it leads to rapid muscle hypertrophy. On the contrary, restricted and time-limited feeding regimes reduce the incidence of WS through the alleviation of stress and the welfare improvement [44,76]. However, the biggest concern of producers is the potential reduction in growth performance [45]. Ayansola et al. [76] applied intermittent fasting and fasting protocols and visually scored WS. There were four groups: ad libitum feeding, 1 h intermittent fasting, 1.5 h intermittent fasting, 1 day of fasting every 6 d of ad libitum feeding. Results showed that WS scoring was significantly lower in the last two groups and higher in the ad libitum group (p < 0.05). In conclusion, intermittent fasting or fasting prevents the development of WS without impairing the growth performance of broiler chickens. Conversely, Trocino et al. [45] confirmed that feed restriction affected performance. On a total of 768 broilers, half of the pens were fed ad libitum during the experimental trial, the remaining half were restricted in the period 13 to 21 d of age, receiving the 80% of the quantity consumed by the broilers fed ad libitum on the previous day. The feeding regime affected broilers performance: restricting broilers from 13 to 21 d of age significantly impaired live weight at 22 d of age (p < 0.001) because of the lower feed intake and daily weight gain (−15%; −16% and −15%, respectively) during the first period compared to broilers fed ad libitum. At the end of the trial, the restricted broilers still weighed significantly less despite the compensatory growth (−2% and +4%, respectively) measured during the second period. Furthermore, early-life conditions set the stage. There is evidence that modified or suboptimal incubation conditions may affect the incidence of myopathies in poultry [77]. Livingston et al. [44] concluded that WS incidence is related to egg storage period and time-limited feeding. Eggs were stored for periods of either 1 to 7 d (short) or 8 to 14 d (long). Longer egg storage generated lower body weight (3.07 vs. 3.18 kg; p < 0.01). An interaction was observed between feeding program and egg storage period on WS scores. The WS muscle scores of ad libitum fed broilers produced from long stored eggs were significantly greater compared to those from ad libitum fed broilers produced from short stored eggs (3.15 vs. 2.58; p < 0.05), which may have been related to the body weight of broilers from long stored eggs being lower by over 100 g (p < 0.05). On the other hand, WS muscle scores were similar between feeding programs when short stored eggs were utilized. Given that incubation temperature is a variable that significantly affects embryonic development, with elevated temperatures disrupting early breast muscle development, and that genetics plays a major role on the incidence of myopathies, Vafaeinia and Yalcin [78] evaluated the effects of cyclic eggshell temperature between 10 and 14 d of embryogenesis on WS incidence, comparing two genetic strains. They tested two incubation regimes: control, at constant eggshell temperature (37.8 °C) and cyclic high temperature, where the eggshell temperature was maintained at 38.8 °C for 6 h (from 10:00 to 16:00) from days 10 to 14, with the temperature maintained at 37.8 °C for the remaining time. The overall incidence of WS was significantly linked to incubation temperature. When analyzed by genotype, however, the response differed markedly. While Cobb chickens showed no significant change in WS occurrence due to the temperature cycle, Ross chickens experienced a clear increase in the incidence of mild and severe lesions under cyclic eggshell temperature (p = 0.001). Nyuiadzi et al. [79] demonstrated that chickens hatched from eggs exposed to a short, cold temperature (15 °C for 30 min) during the last stages of incubation, had significant lower incidence of WS compared to the control-incubated group when birds were reared in optimal (control) temperatures. However, when exposed to early cold rearing temperatures (29 °C at 0 to 21 °C at 21 d of age), the incidence of WS in those males from the cold-incubated group was significantly higher than males from the control-rearing group, suggesting a possible interaction between incubation and post-hatch conditions on the incidence of myopathies. In addition, all birds were fed the same 3-phase diet that may not be suitable to optimize the growth and productive performance for conventional birds but enabled the comparisons under standardized conditions. It should be noted, however, that this study used only 64 birds, which is a small sample size for detecting interaction effects between incubation and rearing conditions; therefore, the findings should be interpreted with caution. Replication in larger, more adequately powered studies is needed to confirm these results. The effect of Stocking Density (SD) on WS has been explored in several studies. Pekel et al. [58] hypothesized that increasing SD may reduce fat accumulation in breast meat, potentially helping to lower WS severity. However, their study found no effect of SD on WS occurrence. Similarly, Cônsolo et al. [80] compared two different SD levels and reported that SD did not significantly mitigate WS occurrence or severity, although it did affect breast weight. Overall, further research focusing specifically on varying SD levels is needed. Gratta et al. [81] evaluated the effect of light restriction on the occurrence and severity of WS by comparing two photoperiods: 18 h vs. 14 h of light per 24 h cycle. During the first day of the trial, all chicks were exposed to continuous light (24L:0D). From day 2 onward, light hours were gradually reduced until reaching 18L:6D at 9 days of age. From that point, one group remained on 18L:6D, while the other group was further reduced to 16 h (at 10 days) and then to 14 h (at 11 days), after which the 14L:10D photoperiod was maintained until the end of the trial. Results showed that chickens reared with 14 h of light had a significant lower occurrence of WS-affected breasts and severe WS compared to those kept under 18 h of light. The authors concluded that light restriction can be used to limit feed intake, thereby influencing growth rate, myopathy occurrence, meat quality, and broiler behavior. Yu et al. [82] examined the effects of different photoperiods on WS by testing three lighting schedules (12L:12D, 18L:6D, and 24L:0D) over a 4-week period, with a constant light intensity of 15 lux. Results showed that photoperiod did not significantly affect WS score. In contrast, the incidence of WB increased with longer photoperiods, which also enhanced breast muscle growth rate and induced glucose metabolism disorders in the breast muscle. Flees et al. [83] investigated the effect of light intensity (2 vs. 30 lux) on WS from day 0 to 35. All birds were kept under a photoperiod of 23L:1D from day 0 to 6, and 18L:6D from day 7 to 35. However, no significant differences were observed in breast weight, breast meat yield, or mean WS score between the two light intensity treatments.

Table 3. Summary of the studies cited related to WS and the influence of management factors.

Authors	Year	Reference	Genetic Line	Age at Slaughter (Days)	n	Sex	WS Scale	Management Factor	Experimental Groups	Main Findings
Aslam et al.	2021	[70]	Arbor Acres Plus	42	180	m	0–2	Heat stress	Control (22–24 °C); chronic heat stress (raised at 32 °C from day 21 onwards); cyclic heat stress (reared at 32 °C during the daytime only, from 08.00 to 20.00 h starting at day 21 until the end of the experiment)	Highest WS incidence in control group, followed by chronic heat stress group and cyclic heat stress; Higher severity in chronic heat stressed group
Tóth et al.	2026	[71]	Ross308	42	352	m	0–2	Bedding	Yellow mealworm (Tenebrio molitor) frass at 0%, 10%, 20%, and 30% into wood shavings bedding	No significant effects on WS
Przybulinski et al.	2025	[72]	Ross408	42	1500	m	0–3	Bedding	Wood shavings, plastic flooring, a 50/50 mix of plastic flooring and wood shavings, plastic flooring with antimicrobial additives, and a 50/50 mix of antimicrobial plastic flooring and wood shavings	No significant effects on WS
Aslan et al.	2024	[73]	Ross308	42	600	m + f	0–2	Bedding	Fully littered, fully slatted, 1/3 littered + 2/3 slatted, 1/2 littered + 1/2 slatted, 2/3 littered + 1/3 slatted	No significant effects on WS
Varol Avcılar et al.	2019	[74]	Ross308	42	288	m	0–3	Bedding	Wood shavings with 0%, 25% or 50% sepiolite; rice hulls with 0%, 25% or 50% sepiolite	No significant effects on WS
Dalle Zotte et al.	2015	[75]	Ross708	12, 25 and 51	720	m	0–2	Coccidiosis control programs	Control; vaccine; vaccine + low energy diet supplemented with enzymes; anticoccidial additive	WS occurrence not affected by vaccination against coccidiosis; WS severity at commercial age influenced by anticoccidial
Ayansola et al.	2023	[76]	Abor Acres	42	384	m	0–5	Feed availability	Ad libitum feeding; 1 h intermittent fasting; 1.5 h intermittent fasting; 1 day of fasting every 6 d of ad libitum feeding	WS development prevented by intermittent fasting or fasting without impairing growth performance
Trocino et al.	2015	[45]	Standard breast yield commercial strain and high breast yield strain	46	768	m + f	0–2	Feed availability	Ad libitum feeding; feed restriction from 13 to 21 d of age	Impaired weight with feed restriction at the end of the trial
Livingston et al.	2019	[44]	Growth strain selected for rapid body weight gain; yield strain selected for high breast meat yield	42	240	m	1–4	Feed availability; egg storage time	Short-time egg storage (1 to 7 d); long-time egg storage (8 to 14 d); ad libitum feeding; time-limited feeding	Interaction between feeding program and egg storage period on WS scores
Vafaeinia and Yalcin	2025	[78]	Cobb and Ross	42	480	-	0–2	Incubation temperature	Control (37.8 °C); high incubation temperature from days 10 to 14 (38.8 °C for 6 h, from 10:00 to 16:00)	Increased WS incidence in Ross under high incubation temperature
Nyuiadzi et al.	2020	[79]	Ross308	40	64	m + f	0–2	Incubation and posthatch temperature	Incubation: control (37.6 °C) or 15 °C during 30 min on day 18 and 19; posthatch: standard rearing temperature (from 32 °C at 0 d to 21 °C at 21 d of age) or colder rearing T° (from 29 °C at 0 to 21 °C at 21 d of age)	Interaction between incubation and posthatch conditions on WS incidence
Pekel et al.	2020	[58]	Ross380	49	288	m	0–2	Stocking density	9 birds/m2 vs. 12 birds/m2	No significant effects on WS
Cônsolo et al.	2022	[80]	Cobb500	49	1755	-	0–1	Stocking density	12 vs. 15 animals per pen measuring 1.0 × 1.2 m	No significant effects on WS
Gratta et al.	2023	[81]	Fast-growing commercial crossbred	45	704	m + f	0–2	Photoperiod	18 h vs. 14 h of light per 24 h cycle	Lower occurrence of WS and severe WS for 14 h than for 18 h of light
Yu et al.	2024	[82]	-	33	216	m	0–2	Photoperiod	12 h, 18 h, and 24 h of light per 24 h cycle	No significant effects on WS
Flees et al.	2024	[83]	Ross 708 × Yield Plus	36	192	m	0–3	Light intensity	2 vs. 30 lux	No significant effects on WS

provides a concise summary of what has been described.

5. Challenges and Future Perspectives

Driven by evolving industry and consumer demands, the modern poultry sector requires continuous adaptation. The key challenge is to find solutions that balance rapid growth with the reduction of myopathies such as WS. This disorder is most prevalent in high-efficiency markets characterized by accelerated growth rates, higher slaughter weights, and prioritizing whole-carcass and piece sales. In such contexts, increasing myopathy incidence directly threatens consumer confidence, particularly regarding animal welfare perceptions. The industry can employ mitigation strategies, adjust farming practices, or utilize meat with quality defects in processed products. Genetic strategies also offer valuable tools for enhancing meat quality and will increasingly rely on the integration of genomic, transcriptomic, epigenetic, and phenotypic data into sophisticated selection models to improve precision and outcomes. Emerging insights into muscle development and gene regulation provide a critical framework for refining breeding strategies and guiding management practices. Transcriptomic and gene expression studies can reveal the molecular pathways underlying WS and identify associated markers by assessing correlations between co-expressed gene networks and key phenotypes. The use of artificial intelligence (AI) and machine learning algorithms will also speed up data processing and the extraction of meaningful biological information. Since genetic improvement depends on the quantity and quality of phenotypic data, AI can enhance the data collection accuracy for WS-related traits without disturbing the animals or altering their behavior. Additionally, automated assessment of white stripe thickness using computer vision on breast images reduces bias in WS scoring. However, genetic improvement is particularly challenging because WS is a polygenic trait influenced by both diet and environmental conditions. As whole-genome sequencing expands, and phenotypic datasets grow richer, genomic approaches will become increasingly precise and affordable. These advancements will ensure that meat quality stays at the forefront of breeding objectives, with genetics serving as a sustainable, large-scale solution. Concurrently, advances in functional genomics and epigenetics will deepen our understanding of how genes and environment interact to shape key meat traits. A historical example of how these strategies have been applied to reduce and eliminate meat defects is the progress made in addressing the pale, soft and exudative (PSE) problem in pork meat. PSE-affected pork meat was unacceptable to consumers and could not be sold; therefore, resolving the issue was essential to prevent the industry from collapsing. In this particular case, consumers have guided the direction of the industry, shifting priorities toward a balanced approach between cost and quality. A significant reduction in both the incidence and severity of the defect was achieved by identifying a single major gene (the ryanodine receptor/halothane gene) to remove animals susceptible to PSE. For WS, current research shows that the defect is polygenic with no equivalent major-effect locus identified. Although WS abnormality has an adverse effect on meat quality traits by increasing adipocyte deposition and fat infiltration, and by reducing protein content due to more intense proteolytic degradation of muscle tissue, the market price of commercial chicken breast fillet remains unchanged. This is likely because most consumers continue to purchase the product without showing concern about this condition, and the industry has not yet experienced significant economic losses from the conventional market. While a niche segment of consumers concerned about animal welfare either avoids meat consumption or purchases certified products at a premium price, this group remains too small to drive widespread structural change. Thus, unlike the pork industry where PSE created an immediate economic crisis, WS has not yet triggered a comparable market-driven response. In fact, overall poultry consumption continues to rise, indicating that WS is not currently a decisive factor for the majority of consumers. The integration of genomics with genome editing might further accelerate poultry breeding. The advent of CRISPR/Cas9 has unlocked new possibilities for targeted genetic enhancement, allowing breeders to deactivate problematic genes or introduce favorable variations without altering the species’ fundamental genetic identity. This enables the rapid introduction of desirable traits, a significant advantage over traditional selective breeding, which takes much longer. Genome sequencing has already identified productivity-associated genetic markers, and CRISPR/Cas9 makes it possible to edit multiple markers simultaneously. However, the practical application of this approach is significantly constrained by strict regulatory frameworks and ethical concerns.

6. Conclusions

Researchers continue to seek ways to alleviate the WS problem, but as no fully effective methods have been found, reducing the high rate of muscle disorders is a key challenge for animal scientists. By selecting for markers associated with QTLs, breeders can enhance meat quality outcomes indirectly but efficiently over successive generations. Unlike other livestock systems, generation intervals are short for broilers, so time does not pose a constraint on achieving genetic improvement. Nevertheless, the majority of QTLs are characterized by small phenotypic effects, lie within relatively broad confidence intervals or regions of high linkage disequilibrium, and often reside in non-coding regions of the genome, which complicates the identification of causal genes or specific genetic variants. Gene-environment interaction is clearly reflected in the wide range of heritability estimates reported in the literature. Discrepancies in heritability estimates underscore the condition’s context-dependent nature, influenced by specific populations, measurement scales, the methodology used to estimate heritability, and rearing conditions. Generally, WS does not show any breed or strain predilection, as white stripes were found in all of them across all trials, but is associated with heavy birds, particularly with high breast yield and pHu. WS incidence and severity can be evaluated exclusively on carcasses, making its phenotypic selection more difficult. To address this limitation, a practical strategy is to employ indirect selection via genetically correlated traits. This approach can be strengthened by incorporating breeding values, isolating genetic merit from environmental effects, and using Multi-Trait Selection Indices to balance and prioritize all important traits based on their economic impact and heritability. This integrated, conventional approach remains highly effective and economical for traits with moderate to high heritability, and its potential is growing with better data collection technologies. Research on dietary strategies for WS has extensively explored the manipulation of feed formulations, primarily through the inclusion or restriction of specific amino acids such as lysine, glutamine, arginine, and methionine. While results for some nutrients like methionine remain conflicting, restricting lysine during the growth phase could be an effective dietary intervention for reducing WS severity. This efficacy underscores a fundamental physiological link: WS is not an isolated defect but a systemic manifestation of metabolic and oxidative stress, systematically correlated with altered post-mortem pH and driven by an accelerated muscle growth rate. Consequently, any successful dietary mitigation strategy inevitably highlights the central compromise in modern broiler production. Long-term genetic selection targeting correlated metabolic traits (e.g., high pHu, intramuscular fat) may reduce susceptibility, but short-term solutions must focus on management, as WS expression is primarily driven by environmental factors despite its genetic basis. Management factors significantly modulate the development of WS, often by exacerbating the underlying metabolic stress associated with rapid growth. Key findings highlight the importance of a holistic approach across the production cycle. Pre-hatch management, such as prolonged egg storage, can predispose chicks to greater WS severity under ad libitum feeding regimes. During the rearing phase, chronic heat stress acts as a critical environmental amplifier, worsening WS lesion severity through hypoxia and oxidative stress. Furthermore, health management decisions, particularly the use of certain anticoccidial drugs versus vaccination, can influence the severity distribution of WS at slaughter age, adding a layer of complexity to disease control strategies. Feeding management presents a nuanced tool: while severe feed restriction can impair growth performance without reliably reducing WS, strategic intermittent fasting may offer a pathway to mitigate the myopathy without sacrificing final body weight. Type, timing, and intensity of feed restriction are crucial; mild, time-based fasting may modulate growth pattern beneficially, while severe nutrient restriction can induce stress and impair recovery, potentially negating any benefits for muscle quality. Ultimately, WS is not merely a meat defect, but rather a symptom resulting from an intensive livestock production system pushed beyond its physiological limits. It calls for a holistic assessment of the true cost of production, taking into account animal welfare, product quality, and sustainability in future breeding and management decisions.