Exploring the association between the consumption of beverages, fast foods, sweets, fats, and oils and the risk of gastric and pancreatic cancers: Findings from case–control study

1 Introduction

Pancreatic cancer (PC) is a highly lethal malignancy originating in the pancreas, a gland situated behind the stomach that plays a crucial role in digestive enzyme and hormone production, including insulin. With a dismal 5-year survival rate of only 10%, PC stands as one of the deadliest forms of cancer, ranking as the fifth leading cause of cancer-related deaths in developed nations and the eighth globally [1,2]. Similarly, gastric cancer (GC) is a prevalent and life-threatening cancer, ranking as the fourth most common cause of cancer mortality worldwide [3].

The intricate interplay among genetic factors, obesity, and smoking, coupled with diverse dietary patterns, contributes to the complex development of PC [4] and GC [5]. Individual risk is often influenced by a combination of these elements. Thus, regular screenings, adopting healthy lifestyle choices, and promoting early detection are paramount in effectively managing risk and enhancing outcomes for both pancreatic and GCs [6].

Emerging evidence suggests that diets rich in fast food, sugary beverages, fats, oils, and sweets may heighten the risk of both PC and GC [3]. These dietary choices are often characterized by high caloric content, saturated fats, trans fats, and added sugars, can contribute to obesity, insulin resistance, and inflammation, all recognized as risk factors for PC [7]. Salt intake has been identified as a significant risk factor for stomach cancer, as excessive salt consumption may stimulate gastric mucosa, leading to atrophic gastritis, increased DNA synthesis, cell proliferation, and the onset of GC [3]. Numerous studies have emphasized the link between various diets and the development of PC and GC, including the Western diet, the “prudent” diet, and the Mediterranean diet [7,8]. These studies have also highlighted the role of specific food groups like meat, dairy products, dietary fiber, specific fats, and nuts in this association [7,8].

Diets high in red meat and starchy foods/sweets are linked to an increased risk of both PC and GC [3,9,10,11], while insufficient consumption of fresh fruits and vegetables can elevate the risk of GC [3]. Obesity, defined by a body mass index (BMI) of 30 kg/m² or higher, is another risk factor for GC, with higher BMIs associated with increased susceptibility to the malignancy [7]. Consumption of artificially sweetened drinks and sugar-sweetened beverages (SSB) containing sweeteners like aspartame is associated with elevated PC risk [12]. A recent study found that sugar consumption and specific candy types were linked to a higher PC risk in men, with less pronounced or absent correlation in women [12].

Hyperinsulinemia and hyperglycemia have been implicated in PC formation, primarily due to insulin’s stimulating effect on cell growth [7,8]. Carcinogens in food may interact with gastrointestinal cells, altering gene expression and potentially contributing to malignancy [13]. Excessive sodium chloride consumption can damage gastrointestinal mucosa, while N-nitroso compounds dramatically increase GC risk [3]. Additionally, fried foods may also be carcinogenic, as they can lead to increased insulin resistance, contain saturated fats, and produce carcinogenic by-products during cooking [14,15].

The Gram-negative bacterium Helicobacter pylori has been classified as a class I carcinogen for GC by the World Health Organization [3]. H. pylori can influence gastric epithelial cells directly through epigenetic mechanisms or indirectly by triggering inflammation in the gastric mucosa, increasing the risk of GC development [3].

Despite extensive research, limited studies have investigated the association between fast food, sweets, fats, oils, sugary beverages, and the risk of PC and GC in Arab nations. Therefore, this study aims to fill this knowledge gap by conducting a case–control study to explore potential links between dietary habits and the development of PC and GC in the adult Jordanians.

2 Methods

3 Results

Socio-demographic and health characteristics of the study population are shown in Table 1 and were described by Al-Awwad [20]. The ages and heights of participants with PC and GC were found to be similar to those of the control group. However, there was a significant difference among PC and GC patients compared to controls in previous weight (P-value = 0.009), current weight (P-value < 0.001), previous BMI (P-value = 0.008), current BMI (P-value = 0.001), total calorie intake (P-value = 0.002), and physical activity (P-value < 0.001). Additionally, a significant difference between the three groups in a family history of cancer was detected (P-value = 0.001). The family history of cancer in controls was 31.8%, while in PC and GC cases it was 48.8 and 48.6%, respectively.

Table 2 shows the median intake of beverages, fast foods, sweets, fats, and oils of the study participants. There was a significant difference among controls and both GC and PC cases who consume sugar-sweetened fruit drinks and coffee (P-value = 0.03 and <0.001, respectively). PC cases showed the highest median intake of sugar-sweetened fruit drinks with 270 mL/day and coffee with 187.5 mL/day. Regarding fast food consumption, the GC cases had the highest intake of French fries ([145.0 (38.6–388.5 g/week)]; P-value <0.001), while controls had the highest intake of burger ([4.4 (0.0–66.2 g/week)]; P-value = 0.013). The consumption of chicken (fried or grilled) sandwiches was lower in control group ([41.6 (0.0–104.6 g/week)]; P-value <0.001). There were significant differences in consumption of added sugar, candies, biscuits, and Ma’amoul (date-stuffed cookies and nuts-stuffed cookies). The controls reported lower intake of both added sugar (25 [5.0–45.0 g/day]; P-value = 0.008) and Ma’amoul (10.5 [4.1–14.0 g/week]; P-value = 0.002). On the other hand, the consumption of candies (33.5 [12.8–115.5 g/week]; P-value = 0.003) was higher in PC cases, while biscuit consumption (33.5 [12.8–115.5 g/week]; P-value = 0.004) was higher among GC patients. The consumption of margarine, processed nuts (salted or smoked), pickled olives, olive oil, corn oil, and mayonnaise was significantly higher in the GC and PC groups compared to the control group (P < 0.05).

Regarding coffee consumption, although none of the consumption frequencies showed any association, a significant (P-value of trend = 0.004) increase in the trend of developing PC was detected, as shown in Table 3.

The findings of Table 4 reveal that the consumption of chicken sandwiches on a weekly (OR = 4.21, 95% CI = 2.19–8.09, P-value of trend < 0.001) basis was significantly associated with PC, while the risk of developing GC is associated with the consumption of chicken sandwiches on a monthly (OR = 1.78, 95% CI = 1.07–2.96, P-value of trend < 0.001) and weekly basis only (OR = 3.98, 95% CI = 2.20–7.19, P-value of trend < 0.001).

In Table 5, the findings showed that biscuit consumption was significantly associated with the risk of GC (ORs: 2.73; monthly, 2.95; weekly, and 8.52; daily, P-value of trend < 0.001). Additionally, candies’ consumption on a monthly and weekly basis was positively associated with an increased risk of PC (ORs: 2.51; monthly, and 2.0; weekly, P-value of trend = 0.019), while monthly consumption of chocolate had an inverse relationship (ORs: 0.43, P-value of trend = 0.929). Arabic sweets were significantly associated with the likelihood of a higher risk of PC (ORs: 2.11; monthly, 3.68; weekly, and 1.75, P-value of trend = 0.002).

Table 6 shows that among the GC group, margarine consumption showed a significant risk increase, with ORs of 2.80, 3.86, and 5.12 for monthly, weekly, and daily consumption, respectively (P-value of trend = 0.001). Weekly consumption of processed nuts (OR = 2.58, 95% CI = 1.29–5.17, P-value of trend = 0.011) and butter (OR = 2.07, 95% CI = 1.12–3.84, P-value of trend = 0.021) was also significantly associated with higher risk of GC. Additionally, corn oil displayed a significant trend in risk (P-value of trend < 0.001). Regarding PC, this study also revealed that margarine consumption had a significant risk increase, with ORs of 8.15 for daily consumption (P-value of trend = 0.002). Processed nuts consumption was linked to higher risk for weekly consumption (OR = 2.75, 95% CI = 1.20–6.28, P-value of trend = 0.044). Corn oil showed a significant protective effect when consumed on weekly basis (OR = 0.13, 95% CI = 0.03–0.60, P-value of trend < 0.001), and mayonnaise potentially had a protective effect for monthly consumption (P-value of trend = 0.299).

4 Discussion

This study aimed to investigate the potential association between the consumption of fast food, sweets, fats, oils, and SSB, and the likelihood of development of PC and GC among Jordanian adults. The study considered several factors, including socio-demographic characteristics, physical activity, and dietary habits, to facilitate a better understanding of these potential associations. A prospective data from a study involving up to 98,265 American adults revealed a positive association between the consumption of ultra-processed foods such as fast food, sweets, and SSB and the risk of PC [21]. This finding expands upon the existing knowledge linking ultra-processed foods with PC highlighting their potential role as carcinogens [21]. Similarly, a study investigating the association between ultra-processed foods and GC showed that there is strong evidence linking the consumption of processed meat to an increased risk of colorectal cancer [22]. Additionally, a study conducted by Kliemann et al. showed a strong evidence that consuming more salt-preserved foods and Cantonese-style salted fish raises the risk of GC [22].

The finding of a positive association between the consumption of sweets, such as candies and Arabic sweets, and an increased risk of PC aligns with existing literature [23,24]. Similarly, this association is particularly notable for those who consume candies and biscuits on a monthly or weekly basis. It is important to highlight that these findings emphasize the potential role of high sugar intake in promoting PC development. High sugar consumption can lead to elevated blood sugar levels and insulin response, which are known to be associated with PC risk. The potential mechanisms linking sugar consumption to an increased risk of PC and GC are multifaceted and complex. High sugar intake may lead to chronic hyperglycemia, insulin resistance, and elevated insulin and insulin-like growth factor levels, all of which can promote cell growth and inflammation, contributing to carcinogenesis [23]. This association was also demonstrated in few studies that have examined the relationship between added sugar consumption and the risk of PC. Lyon et al. [24] found that women who consume high amount of added sugar had a 3.7-fold higher risk of developing PC compared to women with low added sugar intakes. However, the risk was only 1.3 times in men with low added sugar intakes [24]. Nevertheless, it is crucial to note that a case–control study reported 50% increase in the risk of developing PC, although this increase did not reach statistical significance [25].

Similarly, this study reported an association between sweets consumption (candies and biscuits) and an increased risk of GC, particularly for those who showed frequent consumption. These findings suggest that the consumption of sugary sweets may have adverse impact on gastric health. It is important to note that this association could be influenced by factors such as obesity and insulin resistance, which are common risk factors for both PC and GC. As the consumption of sweeteners continues to increase globally, there have been multiple reports suggesting a potential link between sweeteners and the promotion of GC [26]. This study reported that the excessive consumption of sweets is associated with increased likelihood of developing GC. A study conducted by Castelló in 2019 found that frequent consumption of sweets was linked to a 75% higher risk of developing GC. Additionally, the study observed a slight increase in the risk of GC in individuals who consume large amounts of sweets, particularly cakes and candy [27].

The findings of this study revealed no significant difference in the risk of GC and PC associated with the intake of sugar-sweetened fruit drinks. When considering the impact of dietary choices on the risk of PC and GC, the associations with the consumption of sweetened beverages exhibited varying associations. Chan et al. [12] reported that higher consumption of sweet beverages was linked to an elevated risk of PC among men. However, these associations were inconsistent or non-existent among women. In a separate prospective study, involving US nurses and other health workers, women who consumed more than three sugar-sweetened soft drinks per week had a significantly higher risk (57% increase) of developing PC compared to women who consumed less than one sugar-sweetened soft drink per month [28]. It is worth noting that caloric sweetener content in soft drinks may differ between countries [28]. Another cohort study indicated that the consumption of SSB was found to be significantly associated with an increased risk of PC [29]. The highest risks were observed among individuals under the age of 40 [29]. Furthermore, the study revealed a clear dose–response relationship, indicating that the risk of PC increased with the quantity of SSB consumed, even as low as one drink per day [29]. The results of this study highlighted the potential link between sugar and soft drink consumption and the risk of PC, especially in the context of factors such as hyperglycemia, insulin resistance, and a high BMI. Nevertheless, based on this study, daily consumption of sugar-sweetened drinks was linked to an increased likelihood of developing both PC and GC. Additionally, type 2 diabetes and obesity, both characterized by abnormal glucose tolerance and insulin resistance, are well-established risk factors for PC [9,10,11]. High sugar consumption raises blood sugar and insulin levels, creating a favorable environment for PC cell growth [10].

In this study, the frequency of coffee consumption, specifically daily intake, was found to be significantly different between control group and GC and PC cases with OR of 1.78 (0.75–4.23) and P-value of trend = 0.004. Contrary to our findings, two cohort studies conducted as part of the International Stop Project consortium, reported no significant associations between the consumption of caffeinated and decaffeinated drinks. While considering the OR for coffee drinkers was 1.03 (95% CI: 0.94–1.13), indicating a slight increase in the risk of developing GC [30]. These studies did not provide evidence of a protective effect even for individuals with low to moderate coffee consumption. However, a non-significant 20% increased risk was reported among those with the highest coffee consumption levels [30].

Regarding fast food and its potential association with PC and GC, this study revealed that the consumption of French fries was particularly higher among individual in the GC group, with a median weekly intake of 145.0 g/week. This suggests that individuals in GC group may be more likely to consume French fries frequently. In contrast, the control group participants reported lower consumption of chicken sandwiches and burgers with a median weekly intake of 41.6 g/week for chicken sandwich and 4.4 g/week for burgers. In this study, we found an association between the consumption of chicken sandwiches and the risk of developing GC and PC. Data from a case–control study in residents of the Huaihe River Basin in China also found that the fast food pattern could increase the risk of GC, potentially due to a higher consumption of barbecue food, fried food, red meat, and seafood [31].

In this study, a positive association was observed between margarine consumption and GC with OR of 2.80 (95% CI: 1.68–4.67) for monthly consumption, 3.86 (95% CI: 2.07–7.208) for weekly consumption, and 5.12 (95% CI: 1.18–22.26) for daily consumption, with a significant P-value of trend < 0.001. Similarly, the intake of processed nuts, olive oil, and corn oil showed increasing risks with higher consumption frequencies (P-value of trend = 0.011, 0.01, and <0.001, respectively). In PC, both margarine and corn oil showed significant associations, with margarine having a significant P-value of trend of 0.002. Corn oil, when consumed daily, showed an OR of 2.55 (95% CI: 0.77–8.47) with a highly significant P-value of trend < 0.001. These findings indicate that the frequent consumption of margarine, processed nuts, and corn oil may be risk factors for both GC and PC.

There are statistically significant associations between total, saturated, and monounsaturated fat consumption, and PC, according to large prospective research [32]. The exocrine function of the pancreas, which secretes lipase, an enzyme that breaks down fat, may be a general mechanism for the association between fat consumption and PC. When fats and fatty acids from chyme enter the duodenum, they cause the release of cholecystokinin, which increases the production of pancreatic enzymes and causes pancreatic hypertrophy and hyperplasia. This might make the pancreas susceptible to other carcinogens [32,33].

In a population-based case–control research, higher intakes of both dietary saturated fatty acids and monounsaturated fatty acids were shown to be significantly associated with the development of GC [34]. Additionally, in agreement with our findings, a case–control study revealed an association between fat intake and PC, this aligning with other studies that found a link between total fat intake and PC death rates among various countries [35]. An association was identified with the consumption of margarine, while no such association was found with butter intake [35]. A study conducted in North America showed that consuming a significant amount of total fat was associated with an increased risk of developing GC [36].

High-fat diet combined with high sugar intake has been shown to significantly contribute to the development of cancer through mechanisms such as insulin resistance, inflammation, and oxidative stress [37]. These elements are typical of the Western diet, which is characterized by high consumption of red and processed meats, refined sugars, and unhealthy fats. Such dietary patterns are linked to numerous adverse health effects, including obesity, type 2 diabetes, and increased risk of certain cancers [38,39]. In contrast, the Mediterranean diet, which emphasizes the intake of fruits, vegetables, whole grains, legumes, nuts, and healthy fats like olive oil, offers protective benefits. This diet is associated with lower risk of chronic diseases [39], including PC [40] and GC [41]. Therefore, shifting from a Western diet to a Mediterranean diet can significantly improve overall health and reduce the risk of developing these serious conditions.

In GC cases, we found a positive association between processed nuts consumption on weekly or daily basis, showing higher ORs of 2.58 (95% CI: 1.29–5.17) and 2.49 (95% CI: 0.98–6.28), respectively, compared to those who rarely consume processed nuts. Similarly, for PC cases, weekly processed nuts consumption is associated with elevated ORs of 2.75 (95% CI: 1.20–6.28) compared to the control group. The prevalent variety of processed nuts typically eaten in Jordan comprises those that are salted or smoked. A recent meta-analysis of case–control and cohort studies has indicated that a high intake of salt dramatically increases the risk of GC dramatically (OR = 2.05, 95% CI, 1.60–2.62) [42]. A thorough meta-analysis of longitudinal research revealed a significant adverse impact of both total salt intake and the consumption of salt-rich foods on the occurrence of GC in the general population [43]. Numerous epidemiological studies have highlighted a connection between salt consumption and the risk of stomach cancer [44,45]. Sodium chloride, a component of salt, has been demonstrated to enhance the development of stomach cancer both in rat experiments using N-methyl-N-nitro-N-nitrosoguanidine and in human studies [46]. This detrimental effect is attributed to the damaging impact of high salt doses on the protective mucin layer that covers the stomach epithelium. Additionally, excessive salt consumption results in elevated osmotic pressure, further harming the epithelial cells. Prolonged damage to the mucous membrane eventually leads to conditions such as chronic atrophic gastritis and intestinal metaplasia, which are precursors to the development of stomach cancer [47]. A study of Eom et al. [48] indicates that the possible mechanism of AFB1 carcinogenicity may be associated to an imbalance between the capacity for bioactivation and detoxification in gastric tissue. Considering that aflatoxin B1 (AFB1) is frequently exposed to the human stomach through diets, including the consumption of nuts, and knowing that AFB1 metabolic enzymes, including CYP1A2, EPHX1, and GSTs, are expressed in human stomach tissue [48]. It was reported that 9-exo-epoxide, a reac-tive metabolite of AFB1, accumulated in the glandular sto-mach in a state of glutathione depletion [48,49]. Long-term consumption of high nitrate concentrations has been asso-ciated to an increased risk of GC. These nitrates are transformed into carcinogenic nitrites by the H. pylori bacteria found in salted, dried, and smoked foods [50].

5 Study limitations and strengths

The present study comes with certain limitations. First, recall bias is a common concern in case–control studies, particularly when gathering dietary information. Additionally, the research assistants were not blinded to the participants’ diagnoses, meaning they were aware of who had the condition and who did not. However, research assistants were extensively trained and interacted with participants in a professional and uniform manner, irrespective of their case or control status. Another limitation is the lack of biochemical levels of these micronutrients. On the other hand, this case–control study presents several strengths. These strengths encompass adjusting statistical analyses for a variety of important confounding factors, especially smoking, which is strongly associated with GC and PC, enhancing the robustness of our findings by mitigating the impact of these variables on GC risk. Other important strengths include using an ethnically validated FFQ, enrolling newly diagnosed GC cases and cancer-free controls from major hospitals to represent diverse Jordanian dietary patterns, and achieving a high compliance rate with the questionnaire, resulting in an impressive response rate exceeding 95%. In addition, the used FFQ includes cultural foods, commonly used portion sizes for each food item, and accounted for seasonal variations for a more precise estimation of participants’ dietary history.

6 Conclusion

In conclusion, this study showed a significant association between dietary choices and the risk of PC and GC in Jordanian adults. High sugar consumption and certain dietary fats increase the risk of both PC and GC. High sugar consumption, particularly from sweets like candies, was significantly associated with an increased risk of both PC and GC. Daily consumption of Arabic desserts was also linked to higher risk of PC, and consumption of biscuits was associated with risk of GC. Additionally, weekly consumption of chicken sandwiches showed associations with elevated GC and PC risks. Moreover, the study revealed that the consumption of specific fats and oils, including margarine, nuts, pickled olives, corn oil, and mayonnaise, was notably higher among PC and GC cases, highlighting the potential influence of dietary fats on cancer development. It is recommended to address the dietary factors contributing to PC and GC by highlighting the impact of diet on their development. Shifting from a Western diet to a Mediterranean diet is advised to improve overall health and lower the risk of these cancers. Promoting healthier eating habits can play a crucial role in decreasing the prevalence of PC and GC not only in Jordan but also worldwide.