Wednesday, January 28, 2026
Impact of Fiber -Enriched Diet and Lung Cancer
5.4. Fibers-Enriched Diet
Fruit, vegetables and certain components of
plant foods, such as fiber, are associated with a reduction in systemic inflammation, obesity and metabolic syndrome, even after adjustment for important confounding variables [91].
In addition, high fiber intake has long been thought to protect against several types of cancer [92].
The mechanisms for those various health benefits seem to be linked to the modulation of the gut microbiota and metabolic pathways that fibers can induce [93].
Fiber intake is inversely associated with lung cancer risk after adjustment for status and pack-years of smoking and other lung cancer risk factors in 1,445,850 adults from studies that were conducted in the United States, Europe, and Asia [94].
Similarly, Miller et al. studied data from 478,021 individuals included in the EPIC study, and recruited from 10 European countries and who completed a dietary questionnaire [95].
After adjustment for age, smoking, height, weight and gender, there was a significant inverse association between fruit consumption and lung cancer risk in lung cancer patients. The association was strongest among current smokers at baseline [95].
Considering subtypes of lung cancer, Büchner et al., 2010 observed an inverse association between the consumption of fibers and risk of lung cancer without a clear effect on specific histological subtypes of lung cancer [96].
On the other hand, considering different sources of fibers, Bradbury et al., 2014 reported that the risk of cancer of the lung was inversely associated with fruit intake but was not associated with vegetable intake [97];
however, this association with fruit intake is restricted to smokers. In accordance with this data, Büchner et al. analyzed the effects of fruits and vegetables during a follow-up of 1830 incident cases of lung cancer; a 100 g/day increase in fruit and vegetables consumption was associated with a reduced lung cancer risk [96].
In addition, different sources of fibers do not alter positive effects, as demonstrated by Baldrick et al. that found beneficial effects in ex/smokers following a diet with high intake of fibers from legumes through anti-inflammatory mechanisms [98].
An association has been also found between total fiber intake and decreased COPD risk suggesting a beneficial impact on general lung health [99,100].
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Int J Environ Res Public Health. 2021 Mar 1;18(5):2399. doi: 10.3390/ijerph18052399
Food, Nutrition, Physical Activity and Microbiota: Which Impact on Lung Cancer?
Ersilia Nigro 1,2, Fabio Perrotta 3, Filippo Scialò 2,4, Vito D’Agnano 3, Marta Mallardo 1,2, Andrea Bianco 2,4,*, Aurora Daniele 1,2,*
Editor: Dagrun Engeset
Monday, January 26, 2026
Effect of Food and dietary Plans on Lung Cancer
5. Effects of Food and Dietary Plans on Lung Cancer
As said above, body composition and eventually the presence of sarcopenia are crucial factors determining the risk, response to therapy and therefore the prognosis of lung cancer patients.
Considering nutritional status as a determining factor of the body composition, in recent years growing attention has been paid to the choice of dietary plans as well as to performing physical activity.
Dietary schemes as well as specific foods-enriched diet influence the predisposition towards cancer disease and the response to therapies and therefore the prognosis.
The main molecular processes regulated by specific diet patterns, functional foods and physical activity in relation to cancer are the inflammation and oxidative stress.
In the next paragraphs, we report the main dietary schemes associated to body composition, response to therapy and prognosis of lung cancer patients: caloric restriction, PUFA-enriched diets, Dietary Approaches to Stop Hypertension (DASH), fibers-enriched diet and diary-enriched diet. Since a considerable variety of bioactive ingredients have been identified in foods, we will also report interesting data for single compounds.
5.1. Caloric Restriction
It is widely believed that calorie restriction can extend the lifespan of model organisms and protect against aging-related diseases, such as lung cancer.
In breast cancer, Simone et al. demonstrated that caloric restriction can augment the effects of radiation therapy as well as chemotherapy in a mouse model of breast cancer [72].
Interestingly, Safdie et al. analyzed patients diagnosed with a variety of malignancies (one with lung cancer) that voluntarily fasted prior to (48–140 h) and/or following (5–56 h) chemotherapy reporting a reduction in fatigue, weakness and gastrointestinal side effects while fasting [73].
The molecular mechanism of caloric restriction action is mainly related to the decrease of chemotherapy-induced inflammation and induction of energy stress resulting in increased efficacy of therapy.
In lung cancer, Caiola et al. suggested, through in vitro studies, that caloric restriction regimens may sensitize NSCLC lesions carrying KRAS mutation and LKB1 loss to cytotoxic chemotherapy through induction of energy stress [74].
Resveratrol has been proposed as an active molecule mimicking the effects of caloric restriction which may have beneficial effects against numerous diseases such as type 2 diabetes, cardiovascular diseases, and cancer [75].
The positive effects in cancer are related to by the inhibition of oxidative stress, inflammation, aging, and fibrosis [76,77].
In lung cancer, and more widely, in lung diseases resveratrol represents a promising natural compound to be used in association with other drugs [78].
Although it is clear that resveratrol has shown excellent anti-cancer properties, most of the studies were performed in vitro or in pre-clinical models. Few clinical trials have been developed on the administration of resveratrol in cancer patients [79,80].
In addition, resveratrol in its current form is not ideal as therapy because, even at very high doses, it has modest efficacy and many downstream effects [81].
The identification of the cellular targets responsible for resveratrol effects would help in the development of target specific therapies based on this drug
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Int J Environ Res Public Health. 2021 Mar 1;18(5):2399. doi: 10.3390/ijerph18052399
Food, Nutrition, Physical Activity and Microbiota: Which Impact on Lung Cancer?
Ersilia Nigro 1,2, Fabio Perrotta 3, Filippo Scialò 2,4, Vito D’Agnano 3, Marta Mallardo 1,2, Andrea Bianco 2,4,*, Aurora Daniele 1,2,*
Editor: Dagrun Engeset
Lung cancer Food and Dietary Plans (4)
4. Food and Dietary Plans in the Prevention/
Control of Lung Cancer
Common phenomena in lung cancer patients are both malnutrition and cancer cachexia [52].
The prevalence of malnutrition in lung cancer patients ranges from 34.5 to 69%, with the highest incidence in more severe patients and in those undergoing chemotherapies, immunotherapy and/or radiotherapy [53].
On the other hand, inactivity represents a major risk for loss of functional pulmonary capacities in lung cancer patients [3].
Nutritional counselling, planning of meals and use of supplements are essential approaches to counteract malnutrition and sarcopenia in lung cancer. In fact, a nutritional and life-style counselling approach is recommended to control chemotherapy response,
sarcopenia, prognosis and survival of the lung cancer patients.
Tanaka et al. (2018) demonstrated that an early nutritional intervention with a dietary counselling in lung cancer patients receiving chemotherapy efficiently counteracts weight loss and sarcopenia [54].
However, many patients do not achieve recommended dietary intake even after nutritional counselling [55].
The main nutritional approaches to prevent and
treat cancer sarcopenia are: an adequate energy intake; an adequate supply of protein for maintenance or gain of muscle; use of supplements.
An adequate protein intake can reduce the incidence and severity of sarcopenia in cancer patients [56].
It has been demonstrated that a dietary program with energy and protein rich meals and snacks can improve muscle strength and performance status of lung cancer patients [57,58].
The use of supplements in the diet for cancer patients experiencing muscle loss is becoming a very popular approach.
Several products might be useful in contrasting sarcopenia during cancer (Branched-chain amino acids, carnitine, fish oil,
Eicosapentaenoic acid (EPA), vitamins and mineral, [59]. Specifically, in lung cancer
, supplementation of diet with EPA and PUFA improves the maintenance of weight and muscle mass in advanced NSCLC patients undergoing chemotherapy as well as physical and cognitive functioning [60,61,62].
Increasing attention has been focused on the possible use of oral ghrelin receptor (G-protein coupled receptor, GHSR-1a) agonists such as anamorelin and HM01 with the aim of exploiting the ghrelin’s orexigenic capacity [63].
Anamorelin, a ghrelin receptor agonist, has been demonstrated to be able to significantly increase lean body mass [64].
Two completed clinical trials (ROMANA1 and 2, NCT01387269 and NCT01387282, respectively), performed on lung patients with inoperable stage III or IV non-small-cell lung cancer and cachexia, demonstrated that anamorelin induces an increase in lean body mass, without modification in the handgrip [65]. A third trial from the same authors, ROMANA3 (NCT01395914) has been completed confirming the improvements in body weight and anorexia-cachexia
symptoms observed in the original trials, and demonstrating a well toleration to anamorelin administration [66].
There are currently two ongoing clinical trials (NCT03743064 and 03743051) investigating the use of anamorelin to treat non-small cell lung cancer-associated weight loss
. Both trials report changes in weight although a definitive result has not been reached. On the contrary, in vitro and vivo data are available about HM01 effects on cachexia but no clinical trials are available yet [67,68].
Regarding the molecular mechanisms underlying anamorelin effects, Garcia and colleagues found the it significantly increases GH, IGF-1 and IGFBP-3 levels with consequent body weight gain [69,70].
A very recent study compared the two ghrelin receptor agonists anamorelin (non-BBB penetrant) and HM01 (BBB penetrant), demonstrating that HM01
enhances hypothalamic neuronal activation and increases cumulative food intake compared to ghrelin and anamorelin [71]. The authors also demonstrated that HM01 and anamorelin exert potent effects on calcium mobilization, however anamorelin is potentially more susceptible to treatment-induced tolerance than HM01 due to recruitment of β-arrestin and GHSR-1a internalization [71]
Ref
Int J Environ Res Public Health. 2021 Mar 1;18(5):2399. doi: 10.3390/ijerph18052399
Food, Nutrition, Physical Activity and Microbiota: Which Impact on Lung Cancer?
Ersilia Nigro 1,2, Fabio Perrotta 3, Filippo Scialò 2,4, Vito D’Agnano 3, Marta Mallardo 1,2, Andrea Bianco 2,4,*, Aurora Daniele 1,2,*
Editor: Dagrun Engeset
Lung cancer Impact of Food Nutrtion Microbiota
Abstract
Lung cancer still represents the leading cause of cancer-related death, globally. Likewise,
malnutrition and inactivity represent a major risk for loss of functional pulmonary capacities influencing overall lung cancer severity.
Therefore, the adhesion to an appropriate
health lifestyle is crucial in the management of lung cancer patients despite the subtype of cancer.
This review aims to summarize the available knowledge about dietary approaches as well as physical activity as the major factors that decrease the risk towards lung cancer,
and improve the response to therapies.
We discuss the most significant dietary schemes positively associated to body composition and prognosis of lung cancer and the main molecular processes regulated by specific diet schemes, functional foods and physical activity, i.e., inflammation and oxidative stress.
Finally, we report evidence demonstrating that dysbiosis of lung and/or gut microbiome, as well as their interconnection (the gut–lung axis), are strictly related to dietary patterns and regular physical activity playing a
key role in lung cancer formation and progression, opening to the avenue of modulating the microbiome as coadjuvant therapy. Altogether, the evidence reported in this review highlights the necessity to consider non-pharmacological interventions (nutrition and physical activity) as effective adjunctive strategies in the management of lung cancer.
Ref
Int J Environ Res Public Health. 2021 Mar 1;18(5):2399. doi: 10.3390/ijerph18052399
Food, Nutrition, Physical Activity and Microbiota: Which Impact on Lung Cancer?
Ersilia Nigro 1,2, Fabio Perrotta 3, Filippo Scialò 2,4, Vito D’Agnano 3, Marta Mallardo 1,2, Andrea Bianco 2,4,*, Aurora Daniele 1,2,*
Editor: Dagrun Engeset
Sunday, January 25, 2026
Lung cancer Genetic and Racial Disparities
2.3. Genetic and Racial
Disparities and Lung Cancer Susceptibility
Lung cancer risk is influenced significantly by
different racial and ethnic disparities.
Individuals with African ancestry (AA) have
higher mortality rates and incidence of lung cancer development at an earlier age compared to individuals with European ancestry (EA) due to disparities in preventive screening monitoring and treatment disparities [39,40].
In addition, there is a significant disparity in the metabolic pathways and how the body processes nicotine between AA and EA groups, as AA has lower levels of cotinine glucuronidation [41].
Non-Hispanic AA males show the highest rates of mortality and lung cancer incidence compared to all race-ethnicities [42,43].
Similarly, Primm et al. showed persistent disparities in NSCLC incidence between AA and EA men [44].
Interestingly, despite disparities in diagnosis and treatment, AA and Asian NSCLC patients demonstrate better outcomes for the same-stage cancer compared to EA patients [45].
The cause for disparities is genetic ancestry, as AA populations with LUSC have more genomic instability and aggressive molecular traits, while AA patients with LUAD have a higher frequency of PTPRT and JAK2 gene mutations [46,47].
Additionally, the Asian population demonstrates a higher frequency of STK11, TP53, and EGFR gene mutation [48],
but they have longer survival rates and higher chemotherapy responses in comparison to EA patients [49].
Ok Another study linked TP53, KRAS, and KEAP1 gene mutations with worse overall survival, whereas EGFR gene mutations are associated with a higher chance of survival [50].
Recent studies found that EA patients have higher mortality rates compared to Hispanics and Asians, and they have a higher susceptibility to lung cancer due to higher frequencies in smoking-related loci [51,52].
Many studies have revealed racial disparities in the genetic mutation profile of lung cancer patients. Compared to Japanese patients, EA-LUSC patients present a higher frequency of mutations in TP53, PIK3CA, KEAP1, and NFE2L2 genes [53].
On the contrary, EA-LUAD patients exhibit a significantly lower occurrence of EGFR mutation but an increased frequency of mutation in the PIK3CA, KEAP1, KRAS, TP53, BRAF, NF1, STK11, RBM10, and MET genes.
Weiner and Winn reported a higher prevalence
of EGFR gene mutation in the East Asian population and more predominant KRAS and STK11 gene alterations in EA and AA populations [54].
Generally, the disparities in survival rates between EA and AA populations are noticeable in patients who are young and have localized tumors [55].
The disparities also exist in histological subtype, stage, and tumor grade. Asian or Pacific Islander (API) exhibit a higher frequency of adenocarcinoma (ADC) compared to AA, EA, and American Indian/Alaska Native (AIAN) patients [56].
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International Journal of Molecular Sciences logo
Int J Mol Sci. 2025 Apr 17;26(8):3818. doi: 10.3390/ijms26083818
The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity
Enas S Alsatari 1,2, Kelly R Smith 1,2, Sapthala P Loku Galappaththi 1,2, Elba A Turbat-Herrera 1,2, Santanu Dasgupta 1,2,3,*
Editor: Robert Arthur Kratzke
Lung Cancer and Risk Factors
Ref
International Journal of Molecular Sciences logo
Int J Mol Sci. 2025 Apr 17;26(8):3818. doi: 10.3390/ijms26083818
The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity
Enas S Alsatari 1,2, Kelly R Smith 1,2, Sapthala P Loku Galappaththi 1,2, Elba A Turbat-Herrera 1,2, Santanu Dasgupta 1,2,3,*
Editor: Robert Arthur Kratzke
2.2. Environmental and Lifestyle Risk Factors
Epidemiology and risk factors involve a complex interaction of environmental, genetic mutations, and lifestyle factors that contribute to susceptibility to lung cancer and its outcomes [16,17].
However, these interactions become more significant when considering ethnic and ancestor differences.
Although smoking is the predominant cause of lung cancer, another study revealed that 10–25% of all lung cancer patients have never smoked [18].
This disparity underscores the need to investigate additional risk factors other than smoking, especially in populations where lung cancer is not related to smoking [19].
Cigarette smoking remains a major risk factor for lung cancer development. The initiation of smoking habits is mediated by peer pressure, family habits, and psychological distress [20,21].
Interestingly, Harrell et al. reported that demographic factors such as race, socioeconomic status, and pubertal development were significant predictors of early smoking initiation among schoolchildren [22].
Additionally, preventative measures for air pollution include techniques like urea-selective catalytic reduction (SCR), diesel particulate filters, and NOx storage-reduction catalysts approved to enhance air quality to avoid additional health effects from gaseous as well as particulate air pollution pollutants [23].
As a reason, there were substantial declines in lung cancer incidence in the USA from 2007 to 2018. On the other hand, there has been little change in rates among never-smokers, though rates increased significantly in Asian and Pacific Islander populations [24].
In Denmark, lung cancer trends are influenced by historical smoking patterns, where a decline in male smoking rates led to reduced incidence. In contrast, the prevalence of smoking in women remained stable for longer, contributing to a later increase in lung cancer incidence [25].
Existing evidence suggests that passive smoke is the cause of a significant proportion of lung cancer in women.
For instance, Du et al. reported that passive smoking accounts for about 17.9% of lung cancer cases among never-smoking women, most of them exposed to household smoking [26]
. Moreover, a study of Moroccan women showed that 75% of lung cancer cases were recorded in never-smokers, and LUAD was the most common subtype among passive smokers [27].
Zhu et al. reported that non-smoking people who drink tea ≥ 2 cups/day have a greater risk of lung cancer [28].
At the population level, cigarette smoking is the primary determinant of the occurrence of lung cancer [29].
Environmental factors increase the risk of developing lung cancer, such as air pollution, occupational exposure, secondhand smoke, and radiation exposure [30,31].
In China, a study by Liu et al. observed that occupational environment and meteorological conditions synergistically affect lung cancer development [32].
Furthermore, Chinese-style cooking increases lung cancer risk [33].
Moreover, long-term exposure to air pollutants such as PM2.5, NO2, and NOx significantly increases the risk of developing lung cancer [34]. The World Cancer Research Fund (WCRF) reported that drinking water with high concentrations of arsenic increases lung cancer risk, and the evidence was reported as “convincing” [35]. Additional interaction of these air pollutants with poor lifestyle and high genetic risk dramatically raises the likelihood of lung cancer occurrence [35]. Similarly, Huang et al. showed the same results [36]. However, predicting cancer associated with environmental factors like alcohol consumption and smoking can alter based on the variation in polymorphism of xenobiotic metabolizing enzymes (XME) genes [37]. Pettit et al. studied the genetic correlation between various traits and lung cancer risk, indicating a negative genetic correlation between lung cancer risk and some traits, including dietary behaviors, fitness metrics, educational attainment, and other psychosocial characteristics. On the contrary, the body mass index (BMI) showed a positive genetic correlation with the likelihood of lung cancer [38].
The relationship between lung cancer risk and dietary items like fruits, vegetables, micronutrients, phytochemicals, fat, and beverages has been studied. An increased intake of fruits, vegetables, and carotenoid-rich foods is associated with a reduced risk of developing lung cancer [35].
On the contrary, higher intake of retinol, red meat intake, processed meat intake, alcohol drinking, and dietary fat have been associated with an increased risk of lung cancer.
However, no link has been reported between the phytochemical “bioflavonoid” and lung cancer risk
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