This condition can cause a feedback loop in which contact between bacteria and epithelial cells leads to dysregulation of mucosal immune response. This contact can lead to a bacterial biofilm, formed when bacteria attach themselves to the surfaces of the aqueous environment in the gut and begin to secrete substances that allow them to affix onto the epithelium. The interaction between bacteria and epithelial cells elevates inflammation, leading to increased thinning of the mucus and direct host-bacteria interaction. The thali approach, however, combats this cycle in two different ways: by suppressing bacterial growth with anti-microbial phytochemicals , and by reducing the opportunity for inflammation to occur. One molecular pathway involved in such a cycle involves interleukin 6 . This cytokine is normally expressed during acute inflammatory responses, and among other effects, upregulates the transcription factor STAT3. In the nucleus, STAT3 promotes cell prolifteration and differentiation as well as upregulating anti-apoptosis genes. When IL6 is chronically elevated, it can lead to an apoptosis-resistant, constantly expanding T-cell population in the intestinal mucosa. These cells can further contribute to chronic inflammation. Just as a certain diet may promote chronic inflammation, a change in diet can help to restore health. Various bio-active compounds, including anthocyanins, have demonstrated antioxidant activity, reducing local amounts of reactive oxygen species. Low levels of reactive oxygen species can lower the expression of some inflammatory genes, including IL6, bato bucket and relieve the stresses on both the intestinal microbiota and epithelial cells caused by chronic inflammation.
In a study of pigs, we found that supplementing a high-calorie diet with purple potatoes that contains anthocyanins led to a six-fold reduction in levels of interleukin-6 compared to high-fat diet control. Colorectal cancer killed nearly 774,000 people worldwide in 2015, and nearly an estimated 50,630 deaths in 2018 in America making it the third leading cause of cancer-related deaths in the United States in women and second in men. Virtually all cases of CRC are considered to result from an interplay of exogenous and endogenous factors with respect to the variable contribution from each factor . Some non-modifiable risk factors include old age and family history of CRC. Other risk factors, however, are associated with lifte style or behaviors and thus can be changed. These modifiable risk factors include smoking, obesity, low physical activity, deficiency of dietary fiber, deficiency of vitamin D, deficiency of folate, high intake of red and processed meat, and alcohol consumption. Some of these risk factors, however, are closely related. For example, inadequate fiber intake and excessive fat intake are dietary risk factors which tend to lead to a lack of exercise which ultimately may contribute to obesity, particularly in combination. In the US, 40 percent of adults are obese, and so the risk factors discussed are common mainly due to the modern Western lifte style. Therefore, it is no surprise that nearly half of the CRC cases arise in the developed nations. The Western diet in its current form contains more risk factors than the calorie and fat content. Foods that contain heterocyclic amines , polycyclic aromatic hydrocarbons , and emulsifiers can also contribute to carcinogenesis. HCA and PAH are produced in meats when they are fried or grilled over an open flame. These substances have been proved to damage the DNA of colonocytes and potentially promote risk of colon cancer. Emulsifiers are used in foods like ice cream to ensure an even distribution of fat molecules. Recent evidence suggests, however, that emulsifiers promote intestinal inflammation, creating an environment that favors colon carcinogenesis in mice. Some of these risk factors, however, are closely related. For example, inadequate fiber intake and excessive fat intake are dietary risk factors. These tend to lead to a lack of exercise, which ultimately contributes to obesity. In the US, 40 percent of adults are obese, and so the risk factors discussed are common mainly due to the modern Western life style. Therefore, it is no surprise that nearly half of CRC cases arise in developed nations. However, colon cancer has a long development period . This gives ample time for life style changes to take place, including diet-based intervention.
Chronic inflammation, a condition that is promoted by dietary risk factors also contributes to the development of cancer, even in humans. Patients with inflammatory bowel disease have a significantly increased risk of developing CRC, while long-term aspirin treatment is associated with a significantly decreased risk of CRC . The mechanisms by which chronic inflammation promotes tumor development often involve the immune system. For example, the IL6/STAT pathway discussed earlier is also implicated in cancer formation. Over expression of IL6 leads to excess STAT3 transcription, causing unwanted cell prolifteration not only in T cells but also in the intestinal epithelium. Another inflammatory cytokine of note is TNF α. While the intestinal bacteria can promote inflammation, they may also affect the likelihood of CRC more directly. Once the intestinal mucus layer is thinned, and direct bacterial-epithelial cell interactions occur, certain bacterial strains promote tumor development. E. coli strains bearing the pks island are of particular interest. This genetic locus codes for the secondary metabolite colibactin, along with the enzymes necessary for its production. Colibactin has been shown to crosslink with DNA, producing double-stranded breaks. Furthermore, pks+ E. coli strains have been shown to be prevalent in CRC patients. In one study, nearly two-thirds of CRC patients had pks+ E. coli strains in their intestinal bacteria. In the same study, pks+ E. coli also existed in about 20 percent of healthy individuals. Colibactin, however, is a reactive and short-lived protein, requiring close contact with epithelial cells to cause DNA damage. A healthy mucosal barrier keeps colibactin at a distance and reduces the chance of affecting the intestinal epithelium. Evidence for the pathogenic relationship between diets, Fusobacterium nucleatum, and CRC has been emerging. The F. nucleatum levels have been shown to be higher in CRC than in adjacent normal mucosa. Utilizing the molecular pathological epidemiology paradigm and methods, a recent study has shown the association of fiber-rich diets with decreased risk of F. nucleatum-detectable CRC, but not that of F. nucleatum-undetectable CRC .
Experimental evidence supports a carcinogenic role of F. nucleatum, as well as its role in modifying therapeutic outcomes. The amount of F. nucleatum in CRC Thissue has been associated with proximal tumor location, CpG island methylator phenotype , microsatellite instability, low-level CD3+ T cell infiltrate, high-level macrophage infiltration, and unfavorable patient survival . The amount of F. nucleatum in average increased in CRC from rectum to cecum, supporting the colorectal continuum model. Future studies should examine the role of diets, microbiota, and CRC in detailed tumor locations. Dietary prevention of CRC, then, has two intertwined aims: to reduce inflammation and to promote a healthy intestinal microbiota. As already discussed, preclinical evidence implies that dietary bio-active compounds, particularly anthocyanins, can reduce symptoms of lowgrade chronic inflammation as well as oxidative stress. It can also aid in balancing the intestinal microbiota by promoting the growth of beneficial bacteria and by reducing the populations of pro-inflammatory bacteria. Clinical trials have had mixed results, but anthocyanins and some polyphenols have shown to counteract against CRC actively. More research, however, is necessary for conclusive results. How, then, are individuals to consume enough bio-active compounds to have an effect on health? Some answers may be found in the food consumption practices of cultures with historically low CRC incidence. Parts of India, for example, have had some of the lowest CRC incidence rates in the world ; however, this status has been changing. In recent decades, dutch bucket hydroponic increasing urbanization and similar factors have led to progressively Westernized diet patterns and lifestyle. CRC incidence rates are similarly rising, lending weight to the hypothesis that the traditional Indian diet may help prevent CRC. Furthermore, Indian immigrants to Western countries have a much higher incidence of CRC compared to Indians in India. Typical components of traditional Indian meals include a broad variety of flavors, as promoted in Ayurvedic medicine, and a variety of other foods. Both are facilitated by using a thali platter to serve the meal. The traditional American main meal includes an entree , one or more carbohydrates , and one or more vegetables. This basic structure can potentially be adapted with inspiration from thali meals by reducing the size of the main dish and serving more vegetables, legumes, pulses, herbs, and spices to accompany it. A unique component to thali is the combination of many tastes and colors. The inclusion of multiple colors in a meal is desirable, because certain bio-active compounds, particularly anthocyanins are also pigments. Blue, purple, and red-purple colors in plant foods indicate high anthocyanin content. Purple-pigmented potatoes can be prepared in the same way as traditional white potatoes, but the anthocyanin content is significantly higher in the pigmented varieties. Purple sweet potatoes also contain more anthocyanins than the more common orange varieties and can be easily substituted for them. Other vegetables with red or purple cultivars include carrots, cauliflower, and cabbage. Different colors can indicate the presence of other bio-active compounds, such as orange , yellow , and red/pink . Thus, healthy bio-active compound consumption may be increased by selecting colorful vegetables. Another way to increase consumption of bio-active compounds is to increase their presence in available foods. The agricultural industry could greatly impact health by adopting food plant cultivars that produce bio-active compounds in larger amounts than is currently common.
New cultivars may need to be developed that retain desirable characteristics such as large size, pest resistance, reduced spoilage, etc., but also have high bio-active content at the time of consumption. bio-active compounds, with some exceptions, tend to deteriorate during storage. Even when compounds have not deteriorated, storage may reduce the anti-inflammatory/antioxidant activity of bio-active compounds to affect health. A second systemic change that would promote increased bio-active compound consumption involves reworking how fruits and vegetables are currently stored and processed, as well as reducing the average storage time and adapting processing to optimize the amount of bio-active compounds. Presently, “nutritional adequacy” does not consider many of the bio-active compounds discussed in this paper. Further clinical studies are needed to support and elucidate the role of bio-active compounds in the prevention and treatment of disease.More than three quarters of all plant viruses are transmitted by insects , and information regarding key biological traits of vector-borne pathogens is needed to inform effective control strategies. For example, knowledge of transmission efficiency can aid in predicting rates of pathogen spread . Another key parameter in estimating the rate of appearance of newly diseased hosts is the pathogen incubation period, the time between initial infection and when symptoms become evident. Despite the importance of transmission efficiency and incubation period with respect to the development of disease management strategies, data are often not available and, when available, are usually derived from research performed under artificial conditions such as greenhouse environments. Grapevine leaf roll-associated virus 3 , in the genus Ampelovirus, family Closteroviridae, is the primary virus species associated with grapevine leaf roll disease in vineyards of wine growing regions worldwide . GLRaV-3 can cause interveinal reddening and downward rolling in red berried grape varieties , inhibits photosynthesis, decreases vine lifespan, and reduces fruit yield and quality . GLRaV-3 is one of the most common and detrimental viruses of grapevines, and has led to economic losses of 25 % or more . Spread of GLRaV-3 in vineyards and vector-borne transmission in controlled laboratory studies were first documented in South Africa , and since then GLRaV-3 spread in vineyards and transmission by several mealybug species have been documented in wine growing regions worldwide . Although multiple grape-colonizing mealybug species transmit GLRaV-3, estimates of vector transmission efficiency vary both among and within mealybug species . GLRaV-3 is transmitted in a semi-persistent manner with no latent period required between acquisition and inoculation by vectors; transmission can occur after access periods of as little as one hour, and reaches a maximum after access periods of 24 hours . First instar mealybugs are the most efficient vectors, and mealybugs lose the ability to transmit GLRaV-3 four days after being removed from an infected source .