Colon Support
CLINICAL STUDIES ON THE FOLLOWING INGREDIENTS:
VITAMIN C
Circulating vitamin C and digestive system cancers: Mendelian randomization study *
Abstract
Background & aims: Vitamin C is an antioxidant with a potential role in the prevention of digestive system cancers, but there is yet no consensus whether vitamin C has a causal role in these cancers. The aim of this study was to utilize Mendelian randomization to decipher the potential causal associations of vitamin C with risk of digestive system cancers.
Methods: Ten genetic variants previously found to be significantly associated with circulating vitamin C were used as instrumental variables. Effect size estimates for the genetic associations of the vitamin C-associated genetic variants with six major malignancies of digestive system were obtained from the FinnGen (N = 309 154) and UK Biobank (N = 367 542) studies. Results from the two studies were combined using meta-analysis.
Results: Genetically predicted higher circulating vitamin C showed a suggestive association with lower risk of small intestine and colorectal cancer after accounting for multiple testing. The odds ratio per 1 standard deviation increment in circulating vitamin C was 0.55 (95% confidence interval 0.32-0.94; P = 0.029) for small intestine cancer and 0.84 (95% confidence interval 0.73-0.96; P = 0.013) for colorectal cancer. There was a suggestive association between genetically predicted higher circulating vitamin C with lower risk of liver cancer in FinnGen but no association in the meta-analysis (odds ratio 0.69; 95% CI 0.36-1.32; P = 0.265). Genetically predicted circulating vitamin C was not associated with cancers of the esophagus, stomach, or pancreas.
Conclusion: This Mendelian randomization study indicates that vitamin C might play a role in the prevention of small intestine and colorectal cancer.
Source: Larsson SC, Mason AM, Vithayathil M, Carter P, Kar S, Zheng JS, Burgess S. Circulating vitamin C and digestive system cancers: Mendelian randomization study. Clin Nutr. 2022 Sep;41(9):2031-2035. doi: 10.1016/j.clnu.2022.07.040. Epub 2022 Aug 7. PMID: 35986965; PMCID: PMC7613472.
FOLATE (VITAMIN B9)
Folate intake and risk of colorectal cancer: a systematic review and up-to-date meta-analysis of prospective studies *
Abstract
Purpose: Colorectal cancer is one of the most commonly diagnosed and deadly cancers worldwide. Epidemiological studies on the relationship between folate intake and the risk of colorectal cancer have reported inconsistent findings since folate fortification in the USA. For this situation, we conducted a large number of data analyses to study the relationship between folate intake and colorectal cancer risk.
Methods: PubMed and EMBASE databases were used to search the literature systematically. Eligible studies were reviewed and meta-analyzed to assess the relationship.
Results: A total of 24 cohort studies involving 37 280 patients and 6 165 894 individuals were included. The results showed that high folate intake was associated with a reduced risk of colorectal cancer. The combined relative risk (RR) for the highest intake compared with the lowest was 0.88 [95% confidence interval (CI), 0.83-0.92, P = 10 -4 ). Further studies indicated that the increase of folate intake may decrease the risk of colorectal cancer in people with medium or high alcohol consumption (RR = 0.97, 95% CI: 0.96-0.99, P = 0.008; RR = 0.95, 95% CI: 0.92-0.98, P = 0.003), but not in non-drinkers (RR = 1.00, 95% CI: 0.98-1.02, P = 0.827). Next, high folate intake may decrease the risk of colon cancer (RR = 0.86, 95% CI: 0.81-0.92, P = 10 -4 ) but not rectal cancer (RR = 0.92, 95% CI: 0.84-1.02, P = 0.112). Additionally, the result that high folate intake may decrease the risk of colorectal cancer was observed in the USA and Europe but not in other regions.
Conclusion: High folate intake may be protective against colon cancer, particularly in people with middle or high alcohol consumption, but it still needs to be further confirmed.
Source: Fu H, He J, Li C, Deng Z, Chang H. Folate intake and risk of colorectal cancer: a systematic review and up-to-date meta-analysis of prospective studies. Eur J Cancer Prev. 2023 Mar 1;32(2):103-112. doi: 10.1097/CEJ.0000000000000744. Epub 2022 May 11. PMID: 35579178.
ZINC
Correlation Between Zinc Nutritional Status with Serum Zonulin and Gastrointestinal Symptoms in Diarrhea-Predominant Irritable Bowel Syndrome: A Case-Control Study *
Abstract
Background: Zinc is known to have a critical role in the maintenance of intestinal homeostasis, immune cells, and anti-diarrheal and anti-inflammatory actions.
Aims: The aim of this study was to evaluate the correlation between zinc status with serum zonulin and gastrointestinal symptoms in diarrhea-predominant patients with irritable bowel syndrome (IBS-D).
Methods: This case-control study included 61 newly diagnosed IBS-D patients and 61 healthy matched controls. Dietary zinc intake, serum zinc, and zonulin levels were measured. IBS severity was evaluated using the IBS severity score system (IBS-SSS) questionnaire.
Results: Serum zinc levels were lower in the IBS-D group compared with the controls (p = 0.001). Serum zinc was negatively correlated with serum zonulin in IBS-D patients (r = - 0.271; p = 0.035). Also, a reverse association between the serum zinc and odds of IBS-D was found [OR = 0.979; 95% CI (0.966-0.992)].
Conclusions: Our results suggest that zinc may have a role in the pathogenesis of IBS. However, clinical trial studies are warranted to evaluate this finding.
Source: Rezazadegan M, Soheilipour M, Tarrahi MJ, Amani R. Correlation Between Zinc Nutritional Status with Serum Zonulin and Gastrointestinal Symptoms in Diarrhea-Predominant Irritable Bowel Syndrome: A Case-Control Study. Dig Dis Sci. 2022 Aug;67(8):3632-3638. doi: 10.1007/s10620-021-07368-6. Epub 2022 Jan 6. PMID: 34993680.
CLINOPTILOLITE ZEOLITE
PMA - Zeolite (Clinoptilolite) in the Management of Irritable Bowel Syndrome - a Non-Interventional Study *
Abstract
In clinical practice, the treatment of patients with irritable bowel syndrome (IBS) can be very challenging. The aims of the present non-interventional study (NIS) were to investigate the tolerability and efficacy of PMA-zeolite under everyday conditions in patients with diarrheic IBS type (IBS-D) or constipated type (IBS-C) or mixed type (IBS-M).
Methods: To document prospective data on tolerability and symptom frequency in the frame of a nationwide NIS, we recruited 204 IBS patients. The study focused on the IBS-related quality of life (measured by the SF-36 questionnaire) and improvements of IBS-related symptoms according to specific ROM-III criteria and stool consistency (Bristol stool scale). The participants documented their abdominal pain, bloating, number of bowel movements, and stool consistency through a web-based internet platform (initial and exit questionnaires) and daily diary entries over the period of intake (8 weeks).
Results: A total of 82.2% of the recruited patients had filled in the questionnaires before and after the 8-week treatment with PMA-zeolite. Seven of the eight subscales of the SF-36 improved significantly (p<0,001); the reduction in abdominal pain was especially significant (p<0,001). The diary entries confirmed the reduction in abdominal pain and revealed a significant reduction in days with bloating (p<0,001). The Bristol-stool-scale analysis showed improvements; particularly, patients with IBS-D benefited from the treatment (p<0,001).
Conclusion: The treatment duration of 8 weeks was well tolerated by most patients. Under everyday life conditions, PMA-zeolite alleviated the global IBS-related symptoms and raised the quality of life (QOL). The PMA-zeolite, thus, may represent a good adjuvant therapeutic option for patients with irritable bowel syndrome.
Source: Mosgoeller W, Muss C, Eisenwagen S, Jagsch R, Vogelsang H. PMA - Zeolite (Clinoptilolite) in the Management of Irritable Bowel Syndrome - a Non-Interventional Study. Z Gastroenterol. 2024 Mar;62(3):379-387. doi: 10.1055/a-2223-3963. Epub 2024 Jan 15. PMID: 38224685; PMCID: PMC10914565.
SPIRULINA (Arthrospira plantesis)
Effects of Spirulina supplementation in patients with ulcerative colitis: a double-blind, placebo-controlled randomized trial *
Abstract
Aim: We conducted a randomized placebo-controlled trial to assess the efficacy of Spirulina (SP) supplementation on disease activity, health-related quality of life, antioxidant status, and serum pentraxin 3 (PTX-3) levels in patients with ulcerative colitis (UC).
Methods: Eighty patients with UC were randomly assigned to consume either 1 g/day (two 500 mg capsules/day) of SP (n = 40) or control (n = 40) for 8 weeks. Dietary intakes, physical activity, disease activity, health-related quality of life, antioxidant status, erythrocyte sedimentation rate (ESR), and serum PTX-3 levels were assessed and compared between groups at baseline and post-intervention.
Results: Seventy-three patients (91.3%) completed the trial. We observed increases in serum total antioxidant capacity levels in the SP supplementation group compared to the control group after 8 weeks of intervention (p ≤ 0.001). A within-group comparison indicated a trend towards a higher health-related quality of life score after 8 weeks of taking two different supplements, SP (p < 0.001) and PL (p = 0.012), respectively. However, there were no significant changes in participant's disease activity score in response to SP administration (p > 0.05). Similarly, changes in ESR and PTX-3 levels were comparable between groups post-intervention (p > 0.05).
Conclusions: SP improved antioxidant capacity status and health-related quality of life in patients with UC. Our findings suggest that SP supplementation may be effective as an adjuvant treatment for managing patients with UC. Larger trials with longer interventions periods are required to confirm our findings.
Source: Moradi S, Bagheri R, Amirian P, Zarpoosh M, Cheraghloo N, Wong A, Zobeiri M, Entezari MH. Effects of Spirulina supplementation in patients with ulcerative colitis: a double-blind, placebo-controlled randomized trial. BMC Complement Med Ther. 2024 Feb 29;24(1):109. doi: 10.1186/s12906-024-04400-w. PMID: 38424572; PMCID:
BLACK CUMIN SEED (Nigella sativa)
Thymoquinone extracted from black seed triggers apoptotic cell death in human colorectal cancer cells via a p53-dependent mechanism *
Abstract
For centuries, the black seed (Nigella sativa) herb and oil have been used in Asia, Middle East and Africa to promote health and fight disease. Thymoquinone (TQ), the most abundant constituent present in black seed, is a promising dietary chemopreventive agent. We investigated the effects of thymoquinone (TQ) against HCT-116 human colon cancer cells and attempted to identify its potential molecular mechanisms of action. We report that TQ inhibits the growth of colon cancer cells which was correlated with G1 phase arrest of the cell cycle. Furthermore, TUNEL staining and flow cytometry analysis indicate that TQ triggers apoptosis in a dose- and time-dependent manner. Apoptosis induction by TQ was associated with a 2.5-4.5-fold increase in mRNA expression of p53 and the downstream p53 target gene, p21WAF1. Simultaneously, we found a marked increase in p53 and p21WAF1 protein levels but a significant inhibition of anti-apoptotic Bcl-2 protein. Co-incubation with pifithrin-alpha (PFT-alpha), a specific inhibitor of p53, restored Bcl-2, p53 and p21WAF1 levels to the untreated control and suppressed TQ-induced cell cycle arrest and apoptosis. p53-null HCT-116 cells were less sensitive to TQ-induced growth arrest and apoptosis. These results indicate that TQ is antineoplastic and pro-apoptotic against colon cancer cell line HCT116. The apoptotic effects of TQ are modulated by Bcl-2 protein and are linked to and dependent on p53. Our data support the potential for using the agent TQ for the treatment of colon cancer.
Source: Gali-Muhtasib H, Diab-Assaf M, Boltze C, Al-Hmaira J, Hartig R, Roessner A, Schneider-Stock R. Thymoquinone extracted from black seed triggers apoptotic cell death in human colorectal cancer cells via a p53-dependent mechanism. Int J Oncol. 2004 Oct;25(4):857-66. PMID: 15375533.
CHLORELLA VULGARIS
Chlorella vulgaris Modulates Gut Microbiota and Induces Regulatory T Cells to Alleviate Colitis in Mice *
Abstract
Chlorella vulgaris (C. vulgaris) is unicellular green algae consumed worldwide as a functional food. The immune stimulatory function of C. vulgaris is known; however, no study has elucidated its immune regulatory potential and associated microbiome modulation. In the current study, we aimed to validate the immune regulatory role of C. vulgaris mediated through two mechanisms. Initially, we assessed its ability to promote the expansion of the regulatory T cell (Treg) population. Subsequently, we investigated its impact on gut microbiota composition and associated metabolites. The supplementation of C. vulgaris altered the gut microbiota composition, accompanied by increased short-chain fatty acid (SCFAs) production in mice at homeostasis. We later used C. vulgaris in the treatment of a DSS-induced colitis model. C. vulgaris intervention alleviated the pathological symptom of colitis in mice, with a corresponding increase in Treg levels. As C. vulgaris is a safe and widely used food supplement, it can be a feasible strategy to instigate cross-talk between the host immune system and the intestinal flora for the effective management of inflammatory bowel disease (IBD).
Source: Velankanni P, Go SH, Jin JB, Park JS, Park S, Lee SB, Kwon HK, Pan CH, Cha KH, Lee CG. Chlorella vulgarisModulates Gut Microbiota and Induces Regulatory T Cells to Alleviate Colitis in Mice. Nutrients. 2023 Jul 25;15(15):3293. doi: 10.3390/nu15153293. PMID: 37571230; PMCID: PMC10421373.
KELP (Laminaria japonica) (std. to 10% fucoxanthin)
Anticancer effects of fucoxanthin and fucoxanthinol on colorectal cancer cell lines and colorectal cancer tissues *
Abstract
Colorectal cancer is one of the most malignant neoplasms worldwide. Fucoxanthin is a carotenoid present in the chloroplasts of brown seaweeds. In the present study, the anticancer effects of fucoxanthin and its metabolite, fucoxanthinol, on 6 colorectal cancer cell lines and 20 tissue samples from surgically resected clinical colorectal cancer specimens were examined using a collagen-gel droplet embedded culture drug sensitivity test (CD-DST). The in vitro sensitivity to fucoxanthin, fucoxanthinol and the anticancer drugs is expressed as T/C (%), where T is the absorbance of cells which stained by neutral red treated with carotenoids and C is the absorbance of non-staining cells. Fucoxanthin and fucoxanthinol decreased the T/C (%) of Caco-2, WiDr, HCT116, and DLD-1 cell lines at doses of 20 µM. Fucoxanthinol also decreased the T/C (%) of SW620 cells, while the T/C (%) of Colo205 cells was not reduced by treatment with either carotenoid. Specifically, the T/C (%) of Caco-2 and WiDr cells, which were incubated in carotenoid-free medium for 6 days following treatment with 20 µM fucoxanthinol for 24 h, was markedly decreased to 1.4±0.2 and 12.0±0.3%, respectively. Furthermore, fucoxanthin and fucoxanthinol decreased the T/C (%) in colorectal cancer tissue samples. Notably, 20 µM fucoxanthinol treatment resulted in a higher proportion of colorectal cancer samples with a T/C (%) of <50% (13/20, 65%) compared with samples treated with 20 µM fucoxanthin (2/20, 10%). The median T/C (%) value of 35.1% for the 20 cancers specimens treated with 20 µM fucoxanthinol was lower than the median T/C (%) values of 86.3% and 75.8% for those treated with fluorouracil and paclitaxel, respectively. These results suggested that fucoxanthin and fucoxanthinol may be of use as chemotherapeutic agents in colorectal cancer.
Source: Takahashi K, Hosokawa M, Kasajima H, Hatanaka K, Kudo K, Shimoyama N, Miyashita K. Anticancer effects of fucoxanthin and fucoxanthinol on colorectal cancer cell lines and colorectal cancer tissues. Oncol Lett. 2015 Sep;10(3):1463-1467. doi: 10.3892/ol.2015.3380. Epub 2015 Jun 16. PMID: 26622691; PMCID: PMC4533304.
References:
- https://pubmed.ncbi.nlm.nih.gov/35986965/
- https://pubmed.ncbi.nlm.nih.gov/35579178/
- https://pubmed.ncbi.nlm.nih.gov/34993680/
- https://pubmed.ncbi.nlm.nih.gov/38224685/
- https://pubmed.ncbi.nlm.nih.gov/38424572/
- https://pubmed.ncbi.nlm.nih.gov/15375533/
- https://pubmed.ncbi.nlm.nih.gov/37571230/
- https://pmc.ncbi.nlm.nih.gov/articles/PMC4533304/