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Exploring the potential link between vegetable oil supplementation and adverse food reactions in dogs: a preliminary study

Abstract

Background

Adverse food reactions (AFR) are a common cause of skin diseases in dogs, with a prevalence of up to 24%. Research in humans and mice has shown that a high intake of vegetable oils rich in omega-6 polyunsaturated fatty acids (n-6 PUFA) can increase the risk and severity of allergic diseases. This study aimed to investigate the association between AFR and the supplementation of vegetable oils in the canine diet.

Results

A total of 459 dogs were analyzed, with atopic dermatitis (22.66%) and adverse food reactions (AFR) (8.06%) being the most common diagnoses. Oil supplementation was recorded in 14.16% of dogs, with extra-virgin olive oil being the most common (70.77%). Dogs with AFR and concurrent AFR and CAD showed significantly higher oil supplementation rates compared to other conditions (P < 0.05; P < 0.001). No significant association was found between oil type and diagnosis (P = 0.563). After excluding EFA-supplemented dogs and those on prescription dermo diets, oil supplementation was still more prevalent in dogs with AFR compared to other conditions (29.31% vs. 10.10%, P < 0.001).

Conclusions

Vegetable oil supplementation was more frequent in dogs with AFR than in those with other dermatological conditions. This is the first study to evaluate the relationship between vegetable oil supplementation and AFR in dogs. While vegetable oil supplementation is associated with AFR, further studies are needed to establish causality and better understand the role of n-6 PUFA in the development of food allergies in dogs.

Peer Review reports

Background

Adverse food reactions (AFR) are defined as any clinically abnormal response caused by the ingestion of a food or food additive. These reactions can be categorized into immune-mediated food allergies and non-immune-based food intolerances. AFR is a common condition in dogs, with studies reporting that it is the underlying cause of skin diseases in up to 24% of affected dogs [1]. Similarly, AFRs are increasingly prevalent in humans, raising significant concerns for food safety [2]. However, measuring the true prevalence of AFR remains challenging, as many studies rely on self-reported data based on food allergy perceptions, often without the diagnostic gold standard, the oral food challenge (OFC). While food allergies are more common in children (3.9–8%) compared to adults (3.7%) [3,4,5,6,7], food intolerances and reactions to food additives affect a broader population, with prevalence estimates ranging from 5 to 20% [8,9,10].

The growing incidence of AFR in humans has prompted considerable research to understand its underlying causes [11,12,13,14]. Epidemiological studies suggest that environmental factors, such as changes in lifestyle, hygiene (hygiene hypothesis), and the timing and method of food exposure, may contribute to the increasing prevalence [15,16,17]. Other risk factors include co-existing conditions like atopic dermatitis, vitamin D insufficiency, oxidative stress, and changes in dietary fat intake, particularly the imbalance between omega-6 and omega-3 polyunsaturated fatty acids (PUFAs), which may exacerbate inflammatory responses [18,19,20,21,22,23,24,25,26]. Recent dietary shifts in Western countries, characterized by higher consumption of vegetable oils rich in omega-6 PUFAs and lower intake of omega-3-rich oily fish, may further contribute to this rise [27,28,29].

The impact of dietary n-6 and n-3 PUFAs on allergic diseases has been well studied in humans. Long-chain n-3 PUFAs, found in oily fish, have immunomodulatory effects that may reduce allergy risk, while omega-6 PUFAs, such as linoleic acid (LA) and arachidonic acid (AA), promote pro-inflammatory eicosanoids like PGE2, which increase IgE production and contribute to allergic responses [30,31,32,33,34,35,36,37,38,39,40,41,42,43,44]. A disrupted n-6/n-3 ratio is considered a critical factor in modulating immune responses, with excessive omega-6 intake linked to a higher risk of developing allergic diseases. Therefore, understanding the role of n-6 PUFA-rich oils in the diet of dogs with AFR could provide valuable insights into the potential causes and clinical implications of this condition.

While the prevalence of AFR in dogs varies widely across studies, environmental factors and differences in research methodology could contribute to these discrepancies. It remains unclear whether n-6 PUFA-rich dietary oils influence the risk of developing AFR in dogs. Notably, we observed a higher prevalence of AFR in Italy compared to other countries, possibly linked to cultural dietary practices where oil supplementation is common in dog diets [45–46]. The aim of this study was to investigate the association between oil supplementation and AFR in dogs, confirming our hypothesis that oil-enriched diets may contribute to the development of AFR in dogs.

Methods

Study population

The study included dogs presented by referral owners for dermatological examination at ten clinics in Northern Italy. Information was collected through dietary intake interviews and dermatological exams performed during initial consultations and follow-up visits. Additional details were gathered by phone when necessary. All dogs with a confirmed dermatological diagnosis were sequentially enrolled in the study. Dogs with unclear diagnoses were excluded. The diagnostic process for suspected allergic reactions involved ruling out ectoparasites (via skin scrapings, trichography, and coat brushing) and flea bite hypersensitivity (using isoxazoline treatment). Microbial infections were excluded through cytological examinations and cultures for bacterial and fungal infections, with antimicrobial treatment when required.

After excluding parasitic and microbial causes, dogs with allergic symptoms underwent a homemade elimination diet consisting of a single novel protein and carbohydrate source, based on the owner’s dietary history. If a homemade diet with a novel protein and carbohydrate source was not feasible due to availability issues or owner preference, a commercial hypoallergenic diet (Anallergenic diet, Royal Canin) was used for at least eight weeks, with no additional foods or flavored supplements.

Dogs that showed improvement on the elimination diet underwent a provocation test. A relapse of clinical signs upon reintroduction of food indicated an adverse food reaction. Dogs that did not respond to the elimination diet but displayed clinical signs of atopic dermatitis were diagnosed as atopic dogs if they met the diagnostic criteria for canine atopic dermatitis (CAD).

This structured diagnostic approach ensured that only dogs with clear, definitive diagnoses were included, allowing for accurate differentiation between food-induced (AFR) and non-food-induced allergic conditions (CAD).

Survey

Dietary intake was assessed using a standardized questionnaire (Table 1), which gathered detailed information about the dog’s daily diet, including the type of diet, ingredients, oil supplementation, and the timing of dietary changes in relation to the onset of clinical signs. The questionnaire included the following questions:

  1. 1.

    Dietary type: Was the diet commercial (veterinary prescription or maintenance diet), homemade (cooked or raw), or a combination of both?

  2. 2.

    Diet composition: A detailed list of the diet’s ingredients, including the quantities and nutritional information.

  3. 3.

    Dietary changes: Was the diet modified before or after the onset of clinical signs?

  4. 4.

    Oil supplementation: What type of oil was used (e.g., extra-virgin olive, corn, sunflower)? How much was given (in teaspoons per meal)? How frequently was oil added (rated on a scale of 0–5, where 0 = never and 5 = multiple times per day)?

  5. 5.

    Dietary supplements: Were essential fatty acid (EFA) supplements included in the diet? If so, did supplementation begin before or after the onset of clinical signs?

Additional details regarding the dog’s signalment, medical history, and previous treatments were also collected. Table 1 provides the full questionnaire and response options used during the study.

Table 1 Questionnaire about dietary intake posted to owners before the referral consultation

A specific numerical score (0–5) was assigned to different frequencies for oil integration: 0 = never, 1 = a few times/year, 2 = a few times/month, 3 = a few times/week, 4 = daily, 5 = multiple times/day.

To ensure accurate temporal associations, dogs whose oil supplementation began after the onset of clinical signs, as well as those whose diets were changed before the onset of clinical signs, were excluded from the analysis.

Given the hypothesis that excessive omega-6 fatty acid (n-6) intake may contribute to the onset of food allergies, particular attention was paid to the composition of oils used in the diets. For example, extra-virgin olive oil has an n-6/n-3 ratio of approximately 13:1, while corn oil has a much higher ratio of 50:1. Other oils, such as sunflower oil (n-6/n-3 ratio around 40:1) and mixed seed oils (ranging from 20:1 to 30:1), also showed high levels of omega-6.

In a second analysis, dogs receiving EFA supplements and those fed prescription dermo diets rich in omega-3 (content > 0.6%) were excluded. The remaining dogs were then divided into two groups: those with AFR (including only AFR, AFR with CAD, and AFR with FAD (flea allergy dermatitis)) and those without AFR (all other non-allergic conditions). The prevalence of oil supplementation was then compared between these groups to assess any association with AFR.

Results

Study population

A total of 550 dogs were initially enrolled in the study, but 91 dogs were excluded due to the lack of a final diagnosis. The remaining 459 dogs, representing 69 different breeds, are summarized in Table 2. The sample included an equal number of males and females.

Table 2 Gender, age, weight, and breed of 459 dogs included in the study. Only dog breeds represented by three or more animals are listed

Diagnoses

A total of 50 different dermatological diagnoses were made across the 459 dogs. The most prevalent diagnoses were atopic dermatitis (CAD) (22.66%), adverse food reactions (AFR) (8.06%), primary superficial idiopathic pyoderma (7.84%), concurrent CAD and AFR (5.88%), demodicosis (5.88%), skin tumors (4.29%), and localized deep pyoderma (4.29%) (Table 2). The number and percentage of dogs receiving oil supplementation for each diagnosis are also shown in the table.

Table 2 Dermatological diagnoses of 459 dogs included in the study. Number and percentages of dogs supplemented with oil among animals with the same diagnosis

Survey

Dietary intake data for the dogs is detailed in Table 3. Most dogs were fed commercial pet food (59.69%), while 31.37% received a combination of commercial and homemade diets, and 8.93% were exclusively fed homemade food. Of the commercial diets, 91.24% were maintenance diets, and 8.76% were veterinary prescription diets. Among the dogs fed homemade diets, rice (62.75%) was the most common carbohydrate source, followed by potatoes (5.66%) and wheat (4.79%). The primary protein source was chicken (73.86%), followed by beef (31.59%), fish (31.37%), and lamb (5.66%).

Table 3 Dietary intake data of 459 dogs included in the study

Regarding oil supplementation, 14.16% of dogs received vegetable oils (which do not contain essential fatty acids, EFA) as a supplement, while only 2.40% received dedicated EFA-based supplements. Among those receiving EFA supplements, 81.82% started supplementation after the onset of clinical signs, minimizing its relevance in preclinical associations. In contrast, 90.77% of dogs that received vegetable oils began supplementation before the onset of clinical signs, suggesting a temporal association. The most commonly used oil was extra-virgin olive oil (70.77%), followed by corn oil (10.77%), mixed seed oil (10.77%), olive oil (4.62%), and sunflower oil (3.08%). Oil was supplemented at least once daily in 73.85% of cases.

Statistical analysis and grouping

After excluding dogs whose oil supplementation started after the onset of clinical signs (1.3%) and those whose diets changed before clinical signs (7.2%), the final analysis included 420 dogs. Among these, 58 dogs (13.81%) received oil supplementation: 9 of 33 (27.27%) dogs with AFR, 7 of 22 (31.81%) with concurrent AFR and CAD, 14 of 94 (14.89%) with CAD, and 45 of 385 (11.60%) with other conditions. The frequency of oil supplementation was significantly higher in dogs with AFR and concurrent AFR and CAD/FAD compared to those with other diagnoses (P < 0.05; P < 0.001, respectively) (Fig. 1). No significant association was found between oil supplementation and other dermatological conditions. Additionally, oil supplementation was not associated with a higher frequency of AFR across different dosage groups (group 1: 35%, group 2: 92%, group 3: 56%, group 4: 40%). There was no significant association between the type of oil used and the diagnoses (P = 0.563).

Fig. 1
figure 1

Percentages of dogs supplemented with vegetable oil among animals with AFR, concurrent AFR and CAD, CAD, and other skin diseases. The percentages are based on the following numbers of dogs supplemented with vegetable oil: 11 out of 37 dogs with AFR (29.7%), 9 out of 27 dogs with concurrent AFR and CAD (33.3%), 15 out of 104 dogs with CAD (14.4%), and 30 out of 291 dogs with other skin diseases (10.3%). Only dogs supplemented with vegetable oil before the onset of clinical signs are included in the graphic. The total number of dogs under each condition is reported in Table 3

After excluding dogs receiving EFA supplementation (2.1%) and those fed prescription dermo diets (1.2%), the analysis was performed on 406 dogs. Among these, 58 dogs (14.3%) had AFR (including only AFR, AFR with CAD, and AFR with FAD) and 348 dogs (85.7%) had other diseases. The proportion of dogs with AFR who received oil supplementation was higher compared to those with other diseases (29.31% vs. 10.10%). This difference was statistically significant (P < 0.001) (Fig. 2). Additionally, 70.69% of dogs receiving oil supplementation had other diseases, compared to 88.22% of dogs not receiving oil supplementation, indicating a higher prevalence of non-allergic conditions in the latter group.

Fig. 2
figure 2

Distribution of cases by oil supplementation and diagnosis (AFR (white bars) vs. other diseases (black bars). The bar chart shows the number of cases of AFR and other diseases based on oil supplementation. The asterisk (*) indicates a statistically significant difference (p = 0.0010): The comparison reveals that the prevalence of AFR is significantly higher in the group receiving oil supplementation

Discussion

The aim of this study was to explore the association between vegetable oil inclusion in the diet and the occurrence of adverse food reactions (AFR) in dogs. Our findings suggest a significant association between vegetable oil supplementation and an increased prevalence of AFR in this population. To the best of the authors’ knowledge, this is the first veterinary study specifically addressing the relationship between oil supplementation and AFR in dogs. While extensive human literature has examined the effects of vegetable oil, particularly in relation to allergic diseases, such studies in veterinary medicine remain scarce.

In humans, high dietary intake of margarine and vegetable oils rich in n-6 polyunsaturated fatty acids (PUFA) has been linked to an increased incidence of asthma, allergic rhinitis, eczema, and allergic sensitization [47,48,49,50,51,52,53]. N-6 PUFA intake is known to enhance the risk of atopic diseases in children compared to non-atopic children [54]. While the potential impact of n-6 PUFA-rich vegetable oils on the development of food allergies in humans remains unclear, recent studies have shown that increased consumption of n-6 PUFA-rich oils can suppress tolerance induction and exacerbate allergic responses in a murine model of cow’s milk allergy [55]. N-6 PUFA may influence allergic disease by promoting the formation of inflammatory mediators [56]. Specifically, linoleic acid, a precursor of arachidonic acid, leads to the production of pro-inflammatory eicosanoids, including prostaglandin E2 (PGE2) and prostaglandin D2 (PGD2). Diets high in omega-6 oils disturb the omega-6/omega-3 ratio, tipping the balance towards pro-inflammatory mediators and resulting in increased systemic inflammation. Omega-3 fatty acids, which have anti-inflammatory properties, compete with arachidonic acid for the same enzymes (cyclooxygenase and 5-lipoxygenase), thus mitigating the inflammatory response when in balance. Disruption of this balance, particularly an increase in omega-6, promotes a stronger inflammatory response, activates dendritic cells, and shifts T-helper cell responses from type 1 to type 2. This imbalance may, in turn, increase the incidence of IgE-mediated allergic diseases [27, 43, 57,58,59,60]. It has also been demonstrated that n-6 PUFA decreases the IFNg/IL4 ratio in mice and humans [61]. N-6 PUFA acts mainly by increasing the humoral response against allergens.

Interestingly, while n-6 PUFA has been implicated in the exacerbation of allergic diseases, our study did not find an association between n-6 PUFA and canine atopic dermatitis (CAD). This may be due to the lack of enzymatic activity of D6- and D5-desaturase in the epidermis of atopic dogs, making them less susceptible to the effects of n-6 PUFA supplementation [62,63,64]. Additionally, the sensitization mechanisms may differ between AFR and CAD. In CAD, epicutaneous sensitization is more critical, while food allergens primarily sensitize via the gastrointestinal tract [65–66]. Furthermore, dietary long-chain triglycerides (LCT), such as n-6 PUFA, can slow gastric emptying and prolong allergen exposure to the immune system [67]. This prolonged exposure might increase the dose of allergens presented to the immune system, promoting the development of sensitization.

Moreover, LCTs may enhance the chylomicron-dependent absorption of food proteins and bacterial lipopolysaccharides (LPS) through mesenteric lymph nodes, which play a crucial role in oral tolerance induction [68]. LPS is a potent immune activator and could contribute to T- and B-cell activation, further enhancing allergic sensitization [69]. Additionally, chylomicrons can be phagocytosed by macrophages, facilitating antigen uptake [70–71]. These mechanisms suggest that n-6 PUFA-rich oils in the diet might enhance allergic responses by increasing the sensitivity of mast cells, possibly without increasing IgE levels.

Our study also revealed that the prevalence of AFR was higher in dogs fed veterinary prescription diets compared to those on maintenance diets, and this association was noted before the onset of clinical signs. Veterinary prescription diets are often enriched with essential fatty acids (EFAs), including both n-6 and n-3 PUFAs, which are commonly used to manage inflammatory and dermatological conditions. However, since the exact EFA composition of these diets was not analyzed through advanced laboratory techniques, the precise concentrations of omega-6 and omega-3 fatty acids in the diets were not determined, making this hypothesis speculative. Commercial maintenance diets are typically formulated to meet basic nutritional needs and may contain lower levels of EFA compared to prescription diets, which are specifically designed for clinical conditions.

Homemade diets and diets supplemented with oils can vary widely in EFA content, depending on the ingredients and types of oils used. Although the decision to feed veterinary prescription diets to clinically healthy dogs could be influenced by factors such as breed predisposition to allergies, breeder recommendations, or early subtle clinical signs not yet diagnosed as AFR, this hypothesis cannot be confirmed due to the lack of detailed dietary composition and feeding behavior data.

This study’s findings emphasize the need for future research to analyze the EFA content in both prescription and maintenance diets to better understand their potential relationship with AFR. While our results suggest a significant association between prescription diets and AFR, the causal relationship has yet to be established.

Another limitation of this study is the heterogeneous distribution of oils used in the diets. Olive oil was the most commonly used oil, though not exclusively. This variability might have influenced the results, but it also offers an intriguing perspective. Despite the predominance of olive oil, which has been linked to anti-allergic effects in murine models of ovalbumin (OVA)-induced sensitization, our study did not observe a protective effect of olive oil in dogs. In the study by Yu Ma et al., olive oil supplementation alleviated allergic symptoms in sensitized mice by increasing IL-10 levels and reducing Th2 cell-associated factors [72]. However, our findings in dogs did not support these results, suggesting that the anti-allergic effects observed in mice and humans may not directly translate to dogs.

Moreover, although studies suggest that olive oil may slow gastrointestinal transit, this could potentially influence allergen exposure time in the immune system, which might increase the risk of allergic reaction [73,74,75]. A slower gastrointestinal transit could enhance allergen contact with the immune system, contributing to the development of food allergies. However, this remains speculative and warrants further investigation.

Finally, the study population consisted of dermatological referral cases, which may not represent the general canine population, limiting the generalizability of these results. Future studies should include healthy dogs and dogs with non-dermatological conditions to assess the broader impact of oil supplementation across different populations.

Despite these limitations, our study provides valuable insights into the potential association between vegetable oil supplementation and AFR in dogs, highlighting the need for further research to establish causal relationships and explore the underlying mechanisms.

Conclusion

Despite its exploratory nature, this study offers valuable insights into the potential link between vegetable oil supplementation and adverse food reactions (AFR) in dogs. It is important to note that these findings only establish an association and do not confirm a causal relationship. As such, the results should be interpreted with caution.

Nonetheless, the observed associations underscore the need for more in-depth research to clarify the role of vegetable oils and essential fatty acids in the development or exacerbation of AFR. Future studies should focus on analyzing the specific composition and dosage of oils, as well as their interactions with other dietary components. Such research will be crucial to confirm or refute these preliminary findings and will help guide dietary recommendations for dogs with dermatological conditions.

Data availability

The data that support the findings of this study are not openly available due to reasons of sensitivity and are available from the corresponding author upon reasonable request.

Abbreviations

AFR:

Adverse Food Reactions

CAD:

Canine Atopic Dermatitis

FAD:

Flea Allergic Dermatitis

CAFR:

Canine Adverse Food Reaction

EFA:

Essential Fatty Acids

PUFA:

Polyunsaturated Fatty Acids

n-6 PUFA:

Omega-6 Polyunsaturated Fatty Acids

n-3 PUFA:

Omega-3 Polyunsaturated Fatty Acids

OFC:

Oral Food Challenge

LCT:

Long Chain Triglycerides

MLN:

Mesenteric Lymph Nodes

LPS:

Lipopolysaccharides

SPSS:

Statistical Package for the Social Sciences

SD:

Standard Deviation

kg^0.75:

Metabolic Weight (used to normalize energy requirements)

PGE2:

Prostaglandin E2

PGD2:

Prostaglandin D2

IFNg:

Interferon-gamma

IL4:

Interleukin-4

References

  1. Olivry T, Mueller RS. Evidence-based veterinary dermatology: a systematic review of the treatment of canine atopic dermatitis. Vet Dermatol. 2016;27:105–14.

    Google Scholar 

  2. Nwaru BI, Hickstein L, Panesar SS, Muraro A, Werfel T, Cardona V, et al. Prevalence of common food allergies in Europe: a systematic review and meta-analysis. Allergy. 2014;69:992–1007.

    Article  CAS  PubMed  Google Scholar 

  3. Branum AM, Lukacs SL. Food allergy among children in the united States. Pediatrics. 2009;124:1549–55.

    Article  PubMed  Google Scholar 

  4. Gupta RS, Springston EE, Warrier MR, Smith B, Kumar R, Pongracic J et al. The prevalence, severity, and distribution of childhood food allergy in the united States. Pediatrics. 2011;128.

  5. McGowan EC, Keet CA. Prevalence of food allergies in children and adults in the united States. JAMA. 2013;309:2574–5.

    Google Scholar 

  6. Skypala IJ, Venter C, Meyer R, de Jong NW, Fox AT, Groetch M, et al. The prevalence of pollen food syndrome and food allergy in adults in the UK. Clin Transl Allergy. 2011;1:11.

    Google Scholar 

  7. Venter C, Laitinen K, Vlieg-Boerstra B. Nutritional aspects in diagnosis and management of food hypersensitivity—the dietitian’s role. J Allergy Clin Immunol Pract. 2016;4:33–8.

    Google Scholar 

  8. Hodge L, Salome CM, Peat JK, Haby MM, Xuan W, Woolcock AJ. Consumption of oily fish and childhood asthma risk. Am J Respir Crit Care Med. 1998;157:1018–22.

    Google Scholar 

  9. Lessof MH, Wraith DG, Merrett TG, Merrett J, Buisseret PD. Food allergy and intolerance in 100 patients—local and systemic effects. QJM. 1983;52:361–74.

    Google Scholar 

  10. Zopf Y, Baenkler HW, Silbermann A, Hahn EG, Raithel M. The differential diagnosis of food intolerance. Dtsch Arztebl Int. 2009;106:359–69.

    PubMed  PubMed Central  Google Scholar 

  11. Kool B, Ameratunga S, Walker N, Jackson R, Lee A, Robinson E. The incidence of acute food allergy reactions in new Zealand. Clin Exp Allergy. 2016;46:548–56.

    Google Scholar 

  12. Mullins RJ, Dear KBG, Tang MLK. Characteristics of childhood peanut allergy in the Australian capital territory, 1995 to 2007. J Allergy Clin Immunol. 2009;123:689–93.

    Article  PubMed  Google Scholar 

  13. Rudders SA, Banerji A, Vassallo MF, Clark S, Camargo CA Jr. Trends in pediatric emergency department visits for food-induced anaphylaxis. J Allergy Clin Immunol. 2010;126:385–8.

    Article  PubMed  Google Scholar 

  14. Turner PJ, Baumert JL, Beyer K, Boyle RJ, Chan CH, Clark AT, et al. Can we identify patients at risk of life-threatening allergic reactions to food? Allergy. 2016;71:1241–55.

    Article  CAS  PubMed  Google Scholar 

  15. Kotz D, Simpson CR, Sheikh A. Incidence, prevalence, and trends of general practitioner-recorded diagnosis of food allergy in the united Kingdom. J Allergy Clin Immunol. 2011;127:623–30.

    Article  PubMed  Google Scholar 

  16. Lack G, Penagos M. Long-term relationship between peanut allergy and sensitization to Ara h 2 and Ara h 6 in an unselected cohort. J Allergy Clin Immunol. 2013;132:1444–6.

    Google Scholar 

  17. Untersmayr E, Vestergaard H, Malling HJ, Wöhrl S, Bindslev-Jensen C, Skov PS, et al. Incomplete digestion of codfish represents a risk factor for anaphylaxis in patients with allergy. J Allergy Clin Immunol. 2008;122:295–301.

    Google Scholar 

  18. Brough HA, et al. Epicutaneous sensitization in the development of food allergy: what is the evidence and how can this be prevented? Allergy. 2020;75:2185–205.

    Article  PubMed  Google Scholar 

  19. Oyoshi MK, et al. Epicutaneous sensitization to food allergens in atopic dermatitis: pathophysiology and clinical implications. J Allergy Clin Immunol. 2017;140:1602–8.

    Google Scholar 

  20. Nakamura T, et al. Role of skin and gut microbiota in the pathogenesis of atopic dermatitis and food allergy. Clin Exp Allergy. 2021;51:4–11.

    Google Scholar 

  21. Allen KJ, et al. Vitamin D insufficiency is associated with challenge-proven food allergy in infants. J Allergy Clin Immunol. 2013;131:1109–16.

    Article  CAS  PubMed  Google Scholar 

  22. Devereux G. The increase in the prevalence of asthma and allergy: food for thought. Nat Rev Immunol. 2006;6:869–74.

    Article  CAS  PubMed  Google Scholar 

  23. Untersmayr E, Jensen-Jarolim E. The role of protein digestibility and antacids in food allergy. Curr Opin Allergy Clin Immunol. 2006;6:214–9.

    Article  PubMed  Google Scholar 

  24. Lu KD, et al. Obesity, asthma, and the microbiome: the role of systemic inflammation. Pediatr Allergy Immunol Pulmonol. 2016;29:104–11.

    Google Scholar 

  25. Calder PC, et al. Fatty acids and inflammation: the cutting edge between food and medicine. Eur J Clin Nutr. 2017;71:1–8.

    Google Scholar 

  26. Visness CM, London SJ, Daniels JL, Kaufman JS, Yeatts KB, Siega-Riz AM, et al. Association of obesity with IgE levels and allergy symptoms in children and adolescents: results from the National health and nutrition examination survey 2005–2006. J Allergy Clin Immunol. 2009;123:1163–9.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  27. Black PN, Sharpe S. Dietary fat and asthma: is there a connection? Eur Respir J. 1997;10:6–12.

    Article  CAS  PubMed  Google Scholar 

  28. Devereux G. Early life events in asthma: an update. Acta Paediatr Suppl. 2006;95:11–4.

    Google Scholar 

  29. Devereux G, Turner SW, Craig LCA, McNeill G, Martindale S, Harbour PJ, et al. Low maternal vitamin E intake during pregnancy is associated with asthma in 5-year-old children. Am J Respir Crit Care Med. 2005;171:121–8.

    PubMed  Google Scholar 

  30. Farjadian S, Moghtaderi M, Nasiri M, Shakiba AM, Kashef S. The role of omega-3 and omega-6 fatty acids in asthma and allergic diseases. Allergol Int. 2016;65:215–22.

    Google Scholar 

  31. Furuhjelm C, Warstedt K, Larsson J, Fredriksson M, Böttcher MF, Fälth-Magnusson K, et al. Fish oil supplementation in pregnancy and lactation May decrease the risk of infant allergy. Acta Paediatr. 2009;98:1461–7.

    Article  PubMed  Google Scholar 

  32. Horrobin DF. Nutritional and medical importance of gamma-linolenic acid. Prog Lipid Res. 1992;31:163–94.

    Article  CAS  PubMed  Google Scholar 

  33. Jenmalm MC, Duchen K. Timing of allergy-preventive and Immunomodulatory dietary interventions—are prenatal, perinatal or postnatal strategies optimal? Clin Exp Allergy. 2013;43:273–8.

    Article  CAS  PubMed  Google Scholar 

  34. Makino S, Kato T, Ito K, Kashiwabara Y, Shirakawa T. Enhancement of natural killer cell activity in male students with dietary supplementation of fish oil fatty acids—a randomized, double-blind, placebo-controlled trial. J Nutr Sci Vitaminol (Tokyo). 2005;51:252–6.

    Google Scholar 

  35. Miles EA, Calder PC. Modulation of immune function by dietary fatty acids. Proc Nutr Soc. 2015;54:591–602.

    Google Scholar 

  36. Muehleisen B, Gallo RL. Vitamin D in allergic disease: shedding light on a complex problem. J Allergy Clin Immunol. 2013;131:324–9.

    Article  CAS  PubMed  Google Scholar 

  37. Nagakura T, Matsuda S, Shichijyo K, Sugimoto H, Hata K. Dietary supplementation with fish oil rich in omega-3 polyunsaturated fatty acids in children with bronchial asthma. Eur Respir J. 2000;16:861–5.

    Article  CAS  PubMed  Google Scholar 

  38. Okamoto M, Mitsunobu F, Ashida K, Mifune T, Hosaki Y, Tsugeno H, et al. Effects of dietary supplementation with n-3 fatty acids compared with n-6 fatty acids on bronchial asthma. Intern Med. 2000;39:107–11.

    Article  CAS  PubMed  Google Scholar 

  39. Palmer DJ, Sullivan T, Gold MS, Prescott SL, Heddle R, Gibson RA, et al. Randomized controlled trial of fish oil supplementation in pregnant women to reduce the risk of allergic disease in their children. Pediatr Allergy Immunol. 2013;24:513–21.

    Google Scholar 

  40. Van den Elsen LWJ, van Esch BCAM, Hofman GA, Kant J, Harmsen HJM, Willemsen LEM, et al. Dietary long chain n-3 polyunsaturated fatty acids prevent allergic sensitization to cow’s milk protein in mice. Clin Exp Allergy. 2013;43:798–810.

    Article  PubMed  Google Scholar 

  41. Wendel T, Willich SN, Balzer F. Omega-3 fatty acids and cardiac arrhythmias: preventive potential and possible mechanisms. Proc Nutr Soc. 2014;70:193–201.

    Google Scholar 

  42. Calder PC, Miles EA. Fatty acids and atopic disease. Pediatr Allergy Immunol. 2000;11:29–36.

    Article  PubMed  Google Scholar 

  43. Kankaanpää PE, Seppänen-Laakso TJ, Smit J, Hammarén JP, Räsänen L, Schmidt E, et al. Increased Linoleic acid and decreased α-linolenic acid in atopic eczema patients compared with controls. Br J Dermatol. 1999;141:72–8.

    Google Scholar 

  44. Simopoulos AP. Importance of the omega-6/omega-3 balance in health and disease: evolutionary aspects of diet. World Rev Nutr Diet. 2011;102:10–21.

    Article  CAS  PubMed  Google Scholar 

  45. Maina E, Galzerano M, Noli C. Perianal pruritus in dogs with skin disease. Vet Dermatol. 2014;25:204–9.

    Article  PubMed  Google Scholar 

  46. Proverbio D, Perego R, Spada E, Ferro E. Prevalence of adverse food reactions in 130 dogs in Italy with dermatological signs: a retrospective study. J Small Anim Pract. 2010;51:370–4.

    Article  CAS  PubMed  Google Scholar 

  47. Bolte G, Frye C, Hoelscher B, Meyer I, Wjst M, Heinrich J. Margarine consumption and allergy in children. Am J Respir Crit Care Med. 2001;163:277–9.

    Article  CAS  PubMed  Google Scholar 

  48. Haby MM, Peat JK, Marks GB, Woolcock AJ, Leeder SR. Asthma in preschool children: prevalence and risk factors. Thorax. 2001;56:589–95.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  49. Nagel G, von Mutius E, Haider D, Weinmayr G, Björkstén B, Buchele G, et al. Effects of dietary intake of n-3 and n-6 fatty acids on hay fever, asthma, and allergic sensitization in children. J Allergy Clin Immunol. 2005;115:1202–8.

    Google Scholar 

  50. Sausenthaler S, Kompauer I, Borte M, Herbarth O, Schaaf B, Berg A, et al. Margarine and butter consumption, eczema and allergic sensitization in children. The LISA birth cohort study. Allergy. 2006;61:1151–7.

    Google Scholar 

  51. Trak-Fellermeier MA, Brasche S, Winkler G, Heinrich J. Food and fatty acid intake and atopic disease in adults. Eur Respir J. 2004;23:575–82.

    Article  CAS  PubMed  Google Scholar 

  52. Von Mutius E, Weiland SK, Fritzsch C, Duhme H, Keil U. Increasing prevalence of hay fever and atopy among children in Leipzig, East Germany. Lancet. 1998;351:862–6.

    Article  Google Scholar 

  53. Winkler G, Brasche S, Heinze S, Heinrich J. Dietary intake of fatty acids and selected foods in relation to hay fever, specific and total serum IgE. Allergy. 1992;47:265–9.

    Google Scholar 

  54. Dunder T, Kuikka L, Turtinen J, Räsänen L, Uhari M. Diet, serum fatty acids, and atopic diseases in childhood. Allergy. 2001;56:425–8.

    Article  CAS  PubMed  Google Scholar 

  55. Van den Elsen LWJ, Garssen J, Willemsen LEM. Long chain n-3 polyunsaturated fatty acids in the prevention of allergic and cardiovascular disease. Curr Pharm Des. 2012;18:2375–92.

    Article  PubMed  Google Scholar 

  56. Wendell S, Halling A, Nilsson TK, Olsson R, Nyberg F. Omega-3 fatty acids reduce the risk of coronary heart disease and allergic disease in adults. Eur J Clin Nutr. 2014;68:277–82.

    Google Scholar 

  57. Gosset P, Janin A, Bureau F, Ang D, Croci C, Flamand V, et al. Immune response and transcription factor activities in bronchial epithelial cells exposed to organic dust extracts from swine confinement buildings. J Immunol. 2005;175:1051–63.

    Google Scholar 

  58. Kompauer I, Demmelmair H, Koletzko B, Heinrich J. Association of fatty acids in serum phospholipids with hay fever, specific and total Immunoglobulin E. Br J Nutr. 2004;91:91–9.

    Google Scholar 

  59. Prescott SL, Jenner PJ, Dunstan JA, Simmer K, Palmer DJ, Hiller J, et al. Role of Proinflammatory fatty acids in the development of allergic disorders. Pediatr Allergy Immunol. 2004;15:90–3.

    Google Scholar 

  60. Theiner S, Siegl U, Heinzl G, Wilders-Truschnig M, Truschnig-Wilders M, Körmöczi G, et al. Immunophenotyping of lymphocytes in blood of patients with food intolerance: evaluation of a whole blood method. Clin Exp Allergy. 2006;36:1482–9.

    Google Scholar 

  61. Mizota T, Takahashi K, Tokuyama K, Noma H, Kaneda M, Shibata H, et al. Dietary intake of n-6 polyunsaturated fatty acids reduces interferon-γ production by T cells in asthmatic patients. Eur Respir J. 2009;34:983–90.

    Google Scholar 

  62. Schlotter YM, Vroom MW, van Schaik S, Rutten VP, Bruijnzeel-Koomen CA, Willemse T. A prospective study of the effect of a standard oligoantigenic diet on the frequency and nature of food intolerance in dogs. J Small Anim Pract. 2008;49:75–8.

    Google Scholar 

  63. Campbell WC, Faure M, Germain P, Novak N, Roth MP, Torres-Almanas A. A prospective study of fish oil and asthma in 18,533 male participants. Allergy. 1993;48:292–8.

    Google Scholar 

  64. Fuhrmann H, Heine S, Hupe A, Eule C. The effects of n-3 fatty acids on cutaneous inflammatory reactions in dogs. J Vet Med Physiol Pathol Clin Med. 2006;53:206–11.

    Google Scholar 

  65. Marsella R, Olivry T, Carlotti DN. Current evidence of skin barrier dysfunction in canine atopic dermatitis. Vet Dermatol. 2006;17:223–31.

    Google Scholar 

  66. Weala OI, Choudhary SK, Commins SP. Food allergy. Curr Gastroenterol Rep. 2018;20:17–25.

    Article  Google Scholar 

  67. Mackie A, Moutsatsou P, McDougall J, McKinley M, Simpson J, Melton L. Omega-3 and omega-6 polyunsaturated fatty acids modulate gastric emptying and satiety in obese women. Obesity. 2012;20:1034–8.

    Google Scholar 

  68. Worbs T, Bode U, Yan S, Hoffmann MW, Hintzen G, Bernhardt G, et al. Oral tolerance originates in the intestinal immune system and relies on antigen carriage by dendritic cells. J Exp Med. 2006;203:519–27.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  69. Ghoshal S, Witta J, Zhong J, de Villiers W, Eckhardt E. Chylomicrons promote intestinal absorption of lipopolysaccharides. J Lipid Res. 2009;50:90–7.

    Article  CAS  PubMed  Google Scholar 

  70. Mamo JCL, Elsegood CL, Gennat HC, Yu K. Degradation of chylomicron remnants by macrophages occurs via phagocytosis. Biochemistry. 1996;35:10210–4.

    Article  CAS  PubMed  Google Scholar 

  71. Elsegood CL, Mamo JCL. An investigation by electron microscopy of chylomicron remnant uptake by human monocyte-derived macrophages. Atherosclerosis. 2006;188:251–9.

    Article  CAS  PubMed  Google Scholar 

  72. Ma Y, Li J, Guo Y, et al. Dietary Olive oil enhances the oral tolerance of the food allergen ovalbumin in mice by regulating intestinal microecological homeostasis. J Food Biochem. 2022;46:e14297.

    Article  CAS  PubMed  Google Scholar 

  73. Thomas JE. Mechanics and regulation of gastric emptying. Physiol Rev. 1957;37:453–74.

    Article  CAS  PubMed  Google Scholar 

  74. Hunt JN, Knox JT. Regulation of gastric emptying. In: Code CF, editor. Handbook of physiology. Volume IV. Baltimore: Waverly; 1968. pp. 1917–35.

    Google Scholar 

  75. Cooke AR. Control of gastric emptying and motility. Gastroenterology. 1975;68:804–16.

    Article  CAS  PubMed  Google Scholar 

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Acknowledgements

We would like to thank Chiara Noli for her assistance in revising the manuscript and for providing critical feedback.

Funding

This study was self-funded and conducted as part of the research supported by the Belgian BOF funding. No external funding was specifically allocated for this project.

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Authors and Affiliations

Authors

Contributions

E.M. conceptualized the study, collected the cases, performed the evaluations, and wrote the manuscript. E.C. provided guidance, contributed suggestions, and critically revised the manuscript. Both authors reviewed and approved the final version of the manuscript.

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Correspondence to Elisa Maina.

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Ethics approval and consent to participate

The owners of dogs interviewed in this study were part of the study approved by the Ethical Committee of Ghent University, Belgium (EC 2013/189 for healthy dogs and EC 2013/198 for allergic dogs) and by the Deontological Committee of the Belgian government (232663/13_11_2/14). This study involved gathering information from clients regarding their dogs’ health and perspectives and is not considered experimental. Therefore, no additional ethical approval was required. The animals were treated in accordance with high ethical standards and national legislation. Informed consent to participate in the study was obtained from all clients, who were fully informed about the nature and purpose of the study.

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Not applicable.

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The authors declare no competing interests.

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Maina, E., Cox, E. Exploring the potential link between vegetable oil supplementation and adverse food reactions in dogs: a preliminary study. BMC Vet Res 21, 269 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12917-025-04720-0

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