Plant-based Nutrition  -  Fasting  
Optimizing Healing for Degenerative Diseases  

Plant Food Matrix

   Along with the previous section on Plant-based Standards is the need for a professional worked that involves the basic food components in plant-based foods as they are related to degenerative diseases.  This is a future project that is needed and looking for support and funding. 


Plant Matrix Food Components and Degenerative Diseases

       This material is based on and taken from the book: Carcinogenic and Anticarcinogenic Food Components, [452]   published in 2006.  It is a technical work on the chemical and functional properties of food components.  The 33 contributors are all from major universities around the world.  Another technical book was used for several sections (garlic, onions, probiotics):  Phytopharmaceuticals in Cancer Chemoprevention (2005). [453]    

 Even though these Peer-review Journal studies are primarily about cancer they also relate to other degenerative diseases like Parkinson’s.  Cancer is probably the most studied degenerative disease in the world, with heart disease and diabetes coming in after it.  Brain diseases have far fewer studies but many of the finding in cancer also relate to other diseases.  The studies on food definitely can be related to other diseases. 

  1.  Plant Matrix Effects Improve Bioavailability

The research of bioactive food components have gone from discovery (In vitro Studies; Animal Studies; Epidemiology), to Clinical Studies, to Delivery (Implementation and Public Intervention).  This research led to the use of purified bioactive components or analogs as cancer preventive drugs; the use of concentrates or extracts as supplements and adjuvant therapy; the use of whole foods with these bioactive components as part of a preventative diet for cancer.  The bioactive food components modulates cancer related processes through different processes including: Apoptosis, DNA repair, Cell cycle, Carinogen metabolism, Hormonal regulation, Inflammatory response, and differentiation. 

The research started finding that the isolated bioactive component does not contain the same biological response as foods or more intact preparations.  This indicated that the food matrix has an effect in bioavailability and usage and additional components from foods may be needed (Amagase and Milner, 1993; Thiagarajan et al., 1998; Boileau et al,. 2003).  This is an important finding since it shows that the whole food matrix is needed (or a plant-based diet) and not just an individual supplement or drug.  

 Obesity is being identified as an epidemic in the U.S. and is overtaking smoking as the leading healthcare factor in the U.S. today (Stein and Colditz, 2004).  Currently in America, over 65% of all adults are considered overweight: about half of whom are considered obese.  Excess calories are associated with not only increased cancer at a number of sites (Carroll 1998; Key et al., 2003), but also with a variety of other conditions including type II diabetes, hypertension, coronary heart disease, gallbladder disease, and osteoarthritis (Hill et al., 2003). 

 Genetic makeup and environment are two more factors.  People across the globe are considered to have very similar nutrient needs for normal development and body function, allowing the calculation of RDA’s.  However, the ability of bioactive food components to delay or prevent chronic diseases such as cancer may vary considerably from person to person because the response depends on both genetic makeup and environmental exposure (Chadwick, 2004: Davis and Milner, 2004; Mathers, 2004). 

 Even where there are strong mechanistic data supporting the bioactivity of a single component from a whole food, such as lycopene from tomato or sulforaphane from broccoli, it appears that, at least in some instances, there may be health advantages obtained from the whole plant over the isolated component (Miller et al., 2002).  This may be due to the presence of vitamins or other bioactive components, to the presence of components that enhance or synergize with the key component, or to plant matrix effects that improve bioavailability of the key component (Keck it al., 2003). 

 There are differences in bioactivity between different whole foods and different extracts and products which can be related to the genetic profile and/or growing environment for the plant or animal food which may vary causing variation in the bioactive components (Brown, 2002). 

 This bioactivity variation is part of the problem in setting up a dietary strategy.  Another part of the confusion is setting dietary strategies for cancer prevention resides in the fact that not all cancers respond similarly to dietary intervention.  For example, calcium is reported to decrease risk for colon cancer, while potentially increasing prostate cancer risk (Lamprecht and Lipkin, 2003; Rodriguez et al., 2003). 

 Many bioactive components are found in whole foods, yet it is unwise to use concentration alone as the criterion for evaluating the efficacy of a food.  For example, green tea contains multiple phenolics that may act as antioxidants and appear to work most effectively when consumed together rather than separately.  However, the synergy among catechins in bringing about a physiological response is also evident (Williams et al., 2003).  For some foods, the evidence implicating a specific component over others is less compelling or lacking.  For example, processed garlic contains several bioactive compounds but it is not clear which one is the most potent, or most important, in bringing about a change in cancer incidence or tumor behavior.  Different laboratories are studying particular components (Thomason and Ali, 2003; Milner, 2004). 

 Teleologically, some foods should be more effective than others since the response depends on the consumer’s lifestyle and genetic background (Ferguson, 1999).  Defining which foods, and under what circumstances, is the major challenge that currently exists with the scientific, public health, and regulatory communities.  The literature on some foods, for example soy, garlic, green tea, broccoli, and tomatoes, is far more extensive than on others.

  2.  Food Processing, Cooking and Degenerative Diseases - Journal Studies

 It is common knowledge that cooking destroys certain nutrients such as carotenoids, vitamin A, vitamin C, vitamin E, Coenzyme Q10, NADH, Alpha-Lipoic and Melatonin among other nutrients.  This would definitely not be good for cancer patients.

a. Processed Meats and Degenerative Disease
 Cancer incidence has been related to meat in numerous studies.  This is also related to the way food, especially meats are preserved, processed and cooked.  There have been several reviews including two large consensus reports from the World Cancer Reserch Fund (WCRF) (WCRF, 1997) and the Committee on Medical Aspects of Food and Nutrition Policy (Department of Health, U.K., 1998).   The WCRF concluded an association between meat and colorectal cancer and cancers of the pancreas, prostate, breast, and kidney (WCRF, 1997).   Curing meat involves adding salt, nitrate (V), or nitrate (III) to foods and the WCRF report concluded that there was possible evidence between cured meats and colorected cancer (WCRF, 1997). 

Two reviews of meat and colorectal cancer concluded a significant 49% increase risk for a daily increase of 25 grams of processed meat (Sandhu et al., 2001) and a significant 1.3-fold increased risk of processed meat and colorectal cancer (Norat et al., 2002). 

 Processed meat eating has also been associated with stomach cancer in numerous case-controlled studies.  (Correa et al., 1985; Risch et al., 1985; Buiatti et al., 1989; Ward and Lopez- Wu- Williams et al., 1990; Boeing et al., 1991; Gonzalez et al., 1991; Hishiyama and Sasaba, 1992; Ward et al., 1997; Carrillo, 1999.)

 Other cancers that have been associated with processed meat consumption include childhood leukemia, and cancers of the brain, oral cavity, pharynx, larynx, prostate, esophagus, and pancreas  (Preston-Martin et al., 1982; Norell et al., 1986; Sarasua and Savitz et al., 1994; Peters et al., 1994; Michaud et al., 2001; Ngoan et al., 2002; Rajkumar et al., 2003; Levi et al.,2004; Risch, 2003). 

 Colorectal cancer is the second leading cause of cancer death in the United States, with a reported 57,155 deaths in 1999 (Hoyert et al., 2001).  Dietary fat intake is positively correlated with colon cancer death rates (Carroll, 1991). 

 There are two major families of polyunsaturated fats in the Western diet, the n-3 nad n-6 families.  The n-6 polyunsaturated fatty acids are derived from the parent compound linoleic acid (LA, 18:2 n-6).  LA comes mainly from vegetable oils or meats.  Also part of this n-6 line are the GLA (primarily in oils) and AA (in meats, fish, eggs).  The n-3 family of PUFAs is derived from the parent compound a-linolenic acid (ALA, 18:3 n-3).  The ALA are found in vegetable oils (i.e. canola, soybean, flax) and these can be metabolized into stearidonic acid (SDA, 18:4 n-3).  SDA is found in Fish and fish oil, GM-canola oil, Echium oil and other specialty oils.  Thus humans can get their needs from vegetable sources only if desired. 

 AA can also be obtained from dietary sources, where it is only found in food products of animal origin (Taber et al., 1998).  Certain studies more clearly defined the link between dietary n-3 PUFA, with the AA cascade (including PGE2) and intestinal tumorigenesis using an in vivo model.  These studies also address a number of important issues related to diet and colorectal cancer and proposed mechanisms and fatty acids. (Petrik et al., 2002, 2000b).  Furthermore, we found that: 1. Dietary AA content is positively associated with tissue AA content.  2. Tissue AA content is positively associated with PGE2 and PGI2 levels.  3.  PGE2 and PGI2 levels are positively correlated with tumor number.  In addition adding AA to EPA more than doubled tumor number (compared to the EPA group) rather than reducing tumorigenesis as might be predicted by the peroxidation hypothesis.   

b.  Salted Foods and Degenerative Diseases
 Salt is used as a preservative and flavor enhancer.  Salt was a “convincing” risk factor for nasopharyngeal cancer and stomach cancer (WCRF, 1997).  Some case-control studies have shown a positive association between stomach cancer risk and total salt intake (La Vecchia et al., 1987; Graham et al., 1990; Nazario et al., 1993; Ramon et al., 1993) yet some other studies did not find an association.  However, foods preserved with salt have found a positive association with stomach cancer risk in case-control studies between stomach cancer risk and consumption of salted meat and fish.  (Haenszel et al., 1972; Kono et al., 1988; Buiatti et al., 1989; Demirer et al., 1990; Ward and Boeing et al., 1991; Palli et al., 1992; Ramon et al., 1993; Lee et al., 1995; Lopez-Carrillo, 1999). 

 Some other cancer sites, such as the nasopharynx, that have been associated with salted food consumption (Armstrong et al., 1983; Yu et al., 1986; Yu et al., 1989; Ning et al., 1990; Zheng et al., 1994; Srianporn et al., 1992; Yu et al., 1998),  oral cavity (Zheng et al., 1992),  esophagus (Gao et al., 1994), and colorectum (Knekt et al., 1999). 

c.  Nitrates and Degenerative Diseases 
 Nitrate (III) is added to processed meat as an antibacterial agent against Clostridium botulinum and as a cosmetic agent to react with myoglobin to produce the characteristic red-pink color of cured meats.  Nitrate (V) and nitrate (III) are known precursors for NOC (N-nitroso compounds) and thus can form NOC in meats.  NOC’s are among the most powerful chemical carinogens and have been tested in 39 different species and 6 species of primates; therefore, even small amounts in the human body could be influential in carcinogensis.

There are studies that have found a positive association in nitrate (III) foods, such as hot dogs and bacon and esophageal cancer (Rogers et al., 1995), nasopharyngeal cancer (Ward et al., 2000), noncardia gastric cancer (Mayne et al., 2001), pancreatic cancer (Cross et al., 2004), and childhood leukemia and brain cancer (Kuijten et al., 1990; Peteres et al., 1994; Saraus and Savitz, 1994).   

d.  Cooking Methods and Degenerative Diseases 
 Cooking methods are possibly contributing to the risk of both stomach and colorectal cancers (WCRF, 1997).   Of seven case-control studies that have investigated the effect of cooking on colorectal cancer risk, three showed an increased risk for frying (Peters et al., 1989; Gerhardson de Verdier et al., 1991; Butler et al., 2003) and two found an increased risk for grilling/barbecuing (Gerhardsson de Verdier et al., 1991; Wohlleb et al., 1990).  Frying/grilling has also been associated with an increased risk of pancreatic cancer (Norell et al., 1986) and lung cancer (Sinha et al., 1998a) and in general (Lyon and Mahoney, 1988; Young and Wolf, 1988; Kampman et al., 1999.) 

 The degree that meat is cooked also has an effect on risk of some cancers.  Out of seven studies investigating the role of meat doneness on colorectal adenoma or cancer, five found a significant risk of meat that was well-done.  (Gerhardson de Verdier et al., Lang et al., 1994; Sinha et al., 1999; Nowell et al., 2002; Butler et al., 2003).  Also well-done meat has been associated with an increased risk of lung cancer (Sinha et al., 1998a) and also breast cancer (Zheng et al., 1998). 

 Mutagens are formed at high-temperature cooking methods, such as pan frying and grilling, are heterocyclic aromatic amines (HAAs).  HAAs are found in meat the highest when cooking methods are pan-frying and grilling/barbecuing.  In 1993, the International Agency for Research on Cancer found that there was sufficient evidence from experimental animal studies to conclude that the HAAs IQ, MeIQ, MeIQx, and PhIP were carcinogenic (IARC, 1993).   The most abundant HAAs in cooked meat are PhIP and MelQx.  Over twenty individual HAAs have been identified, most of which are potent bacterial mutagens and at least 10 of which have been found to induce tumors in laboratory animals. 

 Using meat doneness as a surrogate of HAA exposure, elevated risks have been shown for colorectal adenoma in case-control studies: (Probst-Hensch et al., 1997; Sinha et al., 1999), as well as cancers of the colorectum (Gerhardsson de Verdier et al., 1991; Lang et al., 1994; Kampman et al., 1999),  stomach (Ward et al., 1997), breast (Zheng et al, 1998), lung (Sinha et al, 2000), and prostate ( Norrish et al., 1999).  A few other studies found no association. 

 PAHs are mutagenic compounds formed in foods processed by smoking, such as meat, as well in meat cooked by grilling/barbecuing.  Meat cooked over a flame results in fat/meat juices dripping onto the hot fire, which yields flames containing a number of PAHs.  These PAHs adhere to the surface of the food.  Benzoapyrene (BaP) is one of the most potent PAH carcinogens in animals studies and can induce leukaemia as well as gastric, pulmonary, forestomach, esophageal, and tounge tumors in rodents (Culp et al., 1998).  Grilled and well-done steak, hamburgers, and chicken contain the highest levels of BaP.   

 Acrylamide is listed by the World Health Organization as a probable human carcinogen, and IARC concluded that it is “probably carcinogenic to humans” (IARC, 1994).  Acrylamide is formed at high temperatures from the reaction between certain amino acids, such as asparagines, and certain sugars.  Acylamide formation increases with increasing temperatures.  These substances are formed in protein-rich foods, but the highest levels are formed in carbohydrate-rich foods, such as potato chips.  Acrylamide has been shown to be mutagenic in a mouse cell line (Besaratinia and Pfeifer, 2003) and studies in rodents, acrylamide administered via different routes increased the risk of cancers of the lung, skin, reproductive tract, thyroid, mammary gland, brain, central nervous system, and oral cavity (Bull et al., 1984; Johnson et al., 1986; Dearfield et al., 1995; Friedman et al., 1995). 

A human study did not find any increased risk for cancer however this study did not consider the content of all foods therefore exposure may have been underestimated. (Mucci et al., 2003).   A second study looked at fried foods as a risk factor in a case controlled study of 527 individuals with laryngeal cancer (Bosetti et al, 2002).  This study found significant elevated risks for beef/veal (1.6-fold risk), fried fish/shellfish (3-fold risk), fried eggs (1.9-fold risk), and fried potatoes (1.9-fold risk).   Fried and baked potatoes have been shown to be among the major sources of dietary arylamide.  Yet another study showed no risk of fried and baked potatoes for certain cancers for humans (Pelucchi et al, 2003).  This area is just beginning to be explored with humans and further studies are needed.  

    C.    Flavonoids in Fruits and Vegetables - Journal Studies

 Flavonoids are present in edible plants such as fruits, vegetables, nuts, seeds, tea, olive oil, and red wine.  The beneficial effects of flavonoids have been known for a long time and used in folk medicine.  Flavonoids exert a wide range of biochemical and pharmacological effects (Middleton et al., 2000). 
 
 A form of physiological cell death is called apoptosis.  It is characterized by cell shrinkage, blebbing of the plasma membrane, and chromatin condensation associated with DNA cleavage into approximately 200-base pair fragments.  There are many compounds from natural resources, including flavonoids, that have been reported to exert anticancer effects which are mediated by apoptotic cell death.  There are numerous dietary flavonoids that have been able to induce apoptosis in different cells including human leukemia HL-60 cells (Wang et al., 1999; Lee et al., 2002; Chen et al., 2003; Shen et al., 2003), colorectal carcinoma cells (COLO2050) and hepatocellular carcinoma cells (SK-Heb) (Lee et al. 2002).  Their capacity to induce apoptosis is generally linked to the  number of hydroxyl groups.  

 Flavonoids have also proven to induce apoptosis in numerous cancer cell lines (prostate, pancreas, liver, lung, colon, bladder) by various mechanisms (Tyagi et al., 2002; Chan et al., 2002; Kumi-Diaka et al., 2000; Gupta et al., 2001; Hastak et al., 2003; Chung et al., 2001; Buchler et al., 2003; Hsu et al., 2004; Kuo and Lin, 2003; Nguyen et al., 2003b; 2003c; Tyagi et al., 2003; Iwashita et al., 2000). 

 Humans possess antioxidant systems to protect against free reactive oxygen species (ROS).  Protection against oxidative damage is one property attributed to flavonoids.  When considering flavonoids as therapeutic agents, it is important to take into account their potential toxicity.  In the case of polyhydroxylated flavonoids they have been shown to be anti or prooxidant, under certain conditions, such as pH, concentration (flavonoids at low and high doses may act as antioxidant and a prooxidant, respectively)  (Langhton et al., 1989), and thus can act as antimutagens or mutagens.  Thus caution should be taken in ingesting flavonoids at levels above that which would be obtained for typical vegetarian diet, because higher flavonoids levels obtained by supplementation may lead to the formation of ROS and ultimately DNA damage (Skibola and Smith, 2000).   

 Cell cycle arrest can involve flavonoids.   Cell cycle progression is orchestrated by cyclin-dependent kinases (CDKs) and flavonoids are able to modulate CDK activity in different mechanisms which influence cells and cancer cells.  Studies have shown that flavonoid-induced cell cycle arrest can occur in certain cancers.  The different flavonoids  that influence certain human cancer cells, and related studies as noted:  Genistein – Breast (Singletary, et. al., 2002); Genistein – Prostate (Kobayashi, et. al., 2002); Silibinin – Prostate (Tyagi, et al., 2002); Tangeretin – Colon (Pan, et al., 2002); Morin – Oral (Brown, et. al., 2003); Acacetin – Liver (Hsu, et al., 2004); Isoliquiritigenin – Lung (Ii, et el, 2004); Isoliquiritigenin – Prostate (Kanazawa, et al., 2003); Apigenin – Prostate (Kobayashi, et al., 2002; Gupta, et al., 2002); Apigenin – Diploid fibroblasts (Lepley, et al., 1997); Luteolin – Prostate (Kobayashi, et al., 2002); Quercetin – Breast (Chio et al., 2001).   

 There is a major problem in the treatment of cancer patients with chemotherapeutics is the occurrence of drug resistance.  Naturally occurring flavonoids were evaluated in vitro, in this area (Boumendjel et al., 2002), and that flavonoids can result in an increase in the intracellular accumulation of anticancer drugs (Choi et al, 2002).   Dietary flavonoids can also effect the transport of certain drugs (Nguyen et al., 2003a) and other authors have demonstrated that various flavonoids are efficient in furnishing another way, through transient, of increasing drug concentration in tumor cells (Walle and Walle, 2003; Vaidyanathan and Walle 2003). 

 The conclusion of this section is that: Flavonoids have been reported to inhibit various events related to the cancer process including cellular oxidant stress, the cell cycle, angiogenesis, reversal of multidrug resistance, and apoptoxis.  Yet most studies and articles have been realized in vitro or in vivo at pharmacological does (i.e. doses tested are significantly higher than those that would exist in human plasma after consumption of whole foods).  Moreover, little is known about flavonoid dietary intakes, absorption, metabolism, or interaction with other nutrients at the usual levels of dietary intake.  At present, it appears difficult to evaluate the benefits of flavonoid derivatives found in food and beverages in the prevention of cancer due to a lack of precise content of flavonoids in food and an insufficient number of cohort studies and in vivo studies.  

    D.   Carotenoids Potential in Plant Tissue Matrix - Journal Studies

 Carotenoids are components of edible fruits and vegetables and are thought to reduce the damage caused by free radicals to cell membranes and associated receptors, they also modulate cell immune responses, and inhibit initiated tumor cells.  Carotenoids are the most abundant class of pigments in nature.  They are yellow, orange, and red pigments present in many commonly eaten fruits and vegetables.  Approximately 600 carotenoids are found in nature. 

 Carotenoids are relatively stable within the food matrix; however, because they are highly saturated, they are susceptible to isomerization and oxidative degradation.  Carotenoid oxidation is stimulated by light, heat, some metals, enzymes, and peroxides, and is inhibited by antioxidants.  Bioavailability of carotenoids increases upon thermal or mechanical processing of food but decreases upon dehydration, freezing, and storage.  Both mechanical homogenization and heat treatment enhance the bioavailability of carotenoids form vegetables (up to a sixfold increase) (van Het Hof et al., 2000) by breaking down cell walls.  This weakens the bonding forces between carotenoids and the plant tissues matrix, making them more accessible and enhancing cis-isomerization.  For example, a-carotene and lutein appear to be more available from juice than raw or cooked vegetables (McEligot et al., 1999). 

 The bioavailability of carotenoids is the fraction of the ingested and metabolized dose that reaches the target sites.  The bioavailability of cartenoids varies since it is affected by many factors including the fat content ingested with the carotenoids, the amount and types of carotenoids present in the diet, the dietary matrix, the crystalline structure of the carotenoid, and food processing.  Host-related factors such as nutritional status, age, and disease states have also been implicated as possible factors interfering with the bioavailability of carotenoids (IARC, 1998; van Het Hof et al., 2000).  The type and amount of fat in the diet influences the bioavailability of carotenoids in the b-carotene absorption seems to be enhanced more by long-chain triacylglycerols than by medium-chain triacylglycerols (Borel et al., 1998).  For the optimal uptake of b- and a-carotene, 3 g of fat per meal is required, and for lutein as much as 36 g is needed (Roodenburg et al., 2000).   

 There have been proposed several mechanisms of action which can contribute to cancer-preventive effects of carotenoids including antioxidant properties, effects on cell-to-cell communication, modulation of immune function, cell transformation, and induction of differentiation.  Carotenoids may also increase the activity of enzymes which intercept or scavenge free radicals (Castenmiller et al., 1999).  Positive antioxidant actions of carotenoids, particularly lycopene, have also been investigated inhuman studies (Riso et al., 1999; Porrini et al., 2002).  In addition to the above antioxidant effects of carotenoids, their cancer prevention potential includes improvement of immune response and modulation of gene expression related to cell proliferation (Goodenough and Paul, 2003).   B-carotene and lycopene have been shown to induce apoptosis in human cells. (Muller et al., 2002). 

 It has been consistently shown in epidemiological studies that individuals who consume large amounts of fruits and vegetables have a reduced risk of many cancers, including those of the esophagus, lung, stomach, colorectum, bladder and breast (World Cancer Research Fund and American Institute for Cancer Research, 1997; Riboli and Norat, 2003).  Intake of tomatoes and tomato products has recently been shown to protect against prostate cancer (Giovannucci et al., 2002). 

Two meta-analyses showed that dietary B-carotene intake protects against both breast and ovarian cancer (Gandini et al., 2000; Huncharek and Kupelnich, 2001).  Case-control studies support a protective role for lycopene, b-carotene, b-cryptoxanthin against lung, pharyngeal, esophageal, and oral cancers (Chen et al., 2002; Negri et al., 2000; La Vecchia, 2002; Wright et al., 2003).   Lycopene also appears to be associated with a protective effect against gastric cancer (De Stefani et al., 2000).  Whereas lycopene showed a protective effect against both lung and prostate cancers, b-cryptoxanthin seems to be associated with a reduction in bladder cancer risk and strongly associated with a reduction in lung cancer risk (Mannisto et al., 2000).  Yet of course there are a few studies that do not confirm some of these findings.  More research is needed, before conclusions can be made but the evidence is strongly positive that carotenes do prevent cancer and then possibly can be used to treat cancer too!

   E.   Tea and Products - protective effects - Journal Studies

 A review of recent research on the cancer preventive activities of tea and their actions in metabolism, bio-availability, and potential mechanisms of action is covered in the review articles (Yang and Wang, 1993; Katiyar and Mukhtar, 1996; Yang et al., 2002) which also indicate that the organs for which tea elicited a protective effect include the lung, skin, oral cavity, esophagus, stomach, liver, pancreas, bladder, small intestine, colon, and prostate. 

 The effects of tea consumption on human cancer has been studied expensively and has been reviewed by various scholars (Yang and Wang, 1993; Blot et al., 1996; Kohlmeier et al., 1997; Buschman, 1998; Yang et al., 2002; Higdon and Frei, 2003).  Recent studies using a more quantitative assessment of tea consumption (Sun et al., 2002) and analyzing subgroups of populations (Wu et al., 2003a) have begun to demonstrate the expected protective effect. 

     1.  Selected Plant-based Products - Journal Studies

Turmeric  - active ingredient, curcumin
 Turmeric belongs to the ginger family, and has been used for centuries as a natural food colorant and preservative.  Numerous scientific investigations, as well as millennia of experience in folk medicine, reveal the breath of therapeutic potential of this spice.  Chemopreventive properties of curcumin have been extensively investigated and well defined (reviewed in Conney et al., 1997; Gescher et al., Nagabhushan and Bhide, 1992; Surh, 1999; 200a; 2003).  Curcumin acts as both blocking and suppressing agent.  Thus, curcumin inhibits the development of chemically induced tumors of oral cavity, skin, forestomach, duodenum, and colon in rodents (Conney et al., 1997). 

 Curcumin is a powerful anti-inflammatory agent with many properties in common with NSAIDs such as aspirin.  Curcumin, like other inhibitors of COX and LOX, is thought to inhibit carcinogenesis by preventing the formation of arachidonic acid metabolites (Rao et al., 1995).  The literature data also indicate that curcumin is likely to elicit tumor-suppressing properties and act in the later stages of carcinogenesis, interfering with cellular processes involved in tumor promotion and progression. (Gescher et al., 2001) Curcumin is well researched with numerous studies.

Ginger - active ingredient, gingerol
 Ginger has been used for more then 2500 years.  The chemopreventive effects of ginger and its ingredients have been reviewed (Surh, 2002a; Surh et al., 1999).  Helicobacter pylori is the primary etiological agent associated with dyspepsia, peptic ulcer disease, and development of gastric cancer.  Ginger root extracts containing the gingerols inhibited the growth of some strains of H. pylori in culture, and this activity may contribute to the chemopreventive effects of ginger on gastric carcinogenesis (Mahady et al., 2003). 

Hot chili peppers  - several active ingredients
 While the nutritional values of hot red peppers have been attributable to the relatively high content of carotenoids, vitamin C, and vitamin E, which are potent antioxidants, their pungent and irritant properties come from the alkaloid capsacin.  A population-based study conducted in Italy reported that red pepper consumption was associated with a lower rate of stomach cancer (Buiatti et al., 1989).    Moreover, researchers in Singapore have reported that hot chili pepper and its pungent ingredient capsaicin have preventive effects on ulceration of the digestive tract in humans (Yeoh et al., 1995). 

 Capsaicin has been found to inhibit chemically-induced carcinogenesis and mutagenesis in various animal models and cell culture systems, possibly through the suppression of metabolic activation of mutagens and carinogens, and antioxidant and anti-inflammatory effects (Surh et al., 1998; 2001; Surh, 200b).  Capaicin inhibited TPA-promoted mouse skin carcinogenesis (Park and Surh, 1997; Park et al., 1998).  And capsaicin has been found to preferentially suppress the growth of cancerous or transformed cells by inducing apoptosis (reviewed by Surh, 2002b). 

Rosemary - active ingredient, carnosol
 Rosemary leaves have been extensively used as a spice and flavoring agent.  Extracts for rosemary have antioxidant, anti-inflammatory, and antibacterial effects (al-Sereiti et al., 1999; Aruoma, 1996; Ho et al., 1994; 2000; Leal et al., 2003 Slamenova et al, 2002).  Several phenolic diterpenoids with antioxidant properties were isolated from rosemary leaves (Ho et al., 1994; 2000).  These include carnosol and rosmarinic acid.  Carnosol and rosemary extract exhibit potent antioxidative properties, including peroxynitrite scavenging activity (Choi et al., 2002).  Rosemary extracts have been reported to inhibit experimentally induced carcinogenesis.  Dietary supplementation of rosemary extract significantly reduced the mammary epithelial cell DNA (Singletary and Nelshoppen, 1991).  And Carnosol induced apoptosis in several acute lymphoblastic leukemia cell lines (Dorrie et al., 2001). 

Clove - active ingredient, eugenol
 Clove is used in traditional oriental medicine as an antibacterial agent.  Eugenol one of the major components is well know for its antioxidant activity (Fujisawa et al., 2002).  An extract of eugenol was found to inhibit cancer activities in mice (Kim et al, 2003; Hong et al., 2002).  Eugenol was cytotoxic and inhibited DNA synthesis in both a human salivary gland tumor cell line and normal gingival fibroblasts (Atsumi et al., 2000).  Eugenol also suppressed chemically induced mutagenesis (Rompelberg et al., 1995; 1996; Sukumaran and Kuttan, 1995; Yokota et al, 1986).  And its anticarcinogenic activity was found in mice (Zheng et al., 1992). 

From Book: Phytopharmaceuticals in Cancer Chemoprevention
Chapter on: Chemopreventive Effects of Selected Spice Ingredients, for berries, garlic, onion and probiotics 

Berries - several active ingredients
 Individuals with low fruit and berry intake experienced about twice the risk of cancer compared with those with high intake.  A statistically significant protective effect of fruit and vegetable consumption has been found in 128 of 156 dietary studies in which the results were in terms of relative risk.  More recent studies continue to confirm these earlier findings, although there are some studies not supportive of this conclusion.  Roy et al., 35  tested the effects of multiple berry extracts on angiogenesis.  Six berry extracts (wild blueberry, bilberry, cranberry, elderberry, raspberry seed, and strawberry) has a positive inhibiting of the cancer.

 Antioxidant capacity of selected berries and fruits: Blueberry, wild 93; blueberry, cultivated 62; cranberries, 94; blackberries, 53; raspberries, 49; Strawberries, 36; cherries, 34; black plums, 73; plums 62.  This is just to show the differences of some of the important berries that in different studies showed some positive effects. 

 Additional studies have suggested that berry fruit both retards and reverses   77, 78  both behavioral and CNS changes that occur during aging.  If this is the case, then it may be that dietary fruits and berries may also reduce cancer incidence by altering the deleterious effects of aging.  Although the data are limited, fruits and berries may be protective through antioxidant mechanisms in preventing DNA damage, but they may also affect cell division, apoptosis, and angiogenesis (Bagchi, Debasis and Preuss, Harry, 2005).  

Saffron  - active ingredient, crocetin
 Saffron is widely used as a spice and also as a perfume or a dye and also in folklore medicine.   In a study comparing the malignant and non malignant cells to saffron, they found the malignant cells were more susceptible than the normal cells to the inhibitory effects of saffron on both DNA and RNA synthesis (Addullaev, F.I. and Fenkel, G.D., 1992).  Crocetin is in saffron and significantly inhibited genotoxicity and DNA binding and also inhibited BaP-induced neoplastic transformation (Chang, W.C. et al., 1996).  Mouse studies indicated that crocetin possesses antitumor-promoting potential (Wang, C.J. et al., 1995).  Other related studies showed positive results.

Garlic - several active ingredients
Garlic has been used for both culinary and medicinal purposes.  Recent studies have revealed that garlic is effective in preventing many chronic diseases, including cardivovascular disorders, (Brace, L.D., 2002), arthritis, (Rahman, K., 2003),  arteriosclerosis, (Durak, I. et al., 2002) and cancer (Thomson, M. And Ali, M., 2003; Banerjee, S.K., Mukherjee, P.K., and Maulik, S.K., 2003).  Garlic preparations are used as over-the-counter herbal medicines in the Western countries.  The chemopreventive activity of garlic has been well documented  (Thomson, M. and Ali, M., 2003.  Banerjee, S.K., Mukherjee, P.K., and Maulik, S.K., 2003.  Borek, C., 2001. Das, S., 2002). 

Onion - several active ingredients
 Onion is used as an ingredient in may dishes.  Onion is abundant in flavonoids, the principal flavonoid is quercetin which has strong antioxidant effects.  Over the past decades, extensive studies have been conducted to evaluate the anticancer or chemopreventive properties of quercetin with success on many mechanisms of cancer.
A study in the Netherlands revealed that onion consumption is inversely related to stomach cancer (Dorant, E. et al., 1996).  And a study in China suggested onions are associated with the risk of developing stomach, esophageal, and brain cancers (Gao, C.M. et al., 1999; Hu, J. et al., 1999).  

Probiotics - several active ingredients
 Oral probiotics are living microorganisms that, upon ingestion, affect the host in a beneficial manner by modulating mucosal and systemic immunity, as well as improving nutritional and microbial balance in the intestinal tract (Fuller, 1989; Madsen, 2001). 

 The relationship between diet, colonic microflora, and the incidence of colorectal cancer is complex.  Alterations in diet affect the growth of microflora, and particular bacterial species present in the colon can have either protective or detrimental effects on the host.  Indeed, while certain luminal bacteria have been implicated in both the pathogenesis and etiology of colon cancer (Arimochi et al, 1997; Gallaher et al., 1996; Mallett and Rowland, 1990), studies performed in animal models of colon cancer have generally demonstrated a protective effect of probiotic bacteria against tumor development (Bolognani et al., 2001; Gallaher et al., 1996; Goldin et al., 1996; Hirayama and Rafter, 2000).  The exposure of tumors to certain lactic acid bacteria results in suppression of tumor growth (Naidu et al., 1999). 

   F.  Carcinogenic and Anticarcinogenic Food Components
 
 This review of example of Plant-based Anticarcinogenic foods will give some evidence for the healing effects of plant-based diets.  Following is a review from the book: Carcinogenic and Anticarcinogenic Food Components, [454]   (2006).  And remember this is a selection of some of the major studies done on vegetables, there are many vegetables that have not yet been studied, and the following does not take into account the many studies on fruits.  

   a.  Chemopreventive/Chemoprotective Effects of Respresentative Plant Foods

Broccoli –
    Human Studies:
All Cancers -  Colditgz et al., 1985;
Bladder Cancer -  Michaud et al., 1999;
 Colon – Hara et al., 2003;
 Lung – Forntham et al., 1088i;
 Stomach – Hara et al., 2003;
    Supporting Animal Studies:
All Cancers -  Finley et al., 2001; Vang et al., 1997;
Breast -  Wattenberg et al., 1989;  
 Colon –  Vang et al., 1997; Chung et al., 2000;

Cabbage
    Human Studies:
 Bladder -  Michaud et al., 1999;
 Lung  -  Kvale et al., 1983;
 Rectum –Graham et al., 1978;
    Supporting Animal Studies:
 Bladder – Munday and Munday, 2002;
 Breast – Wattenberg et al., 1989;
 Lung – Scholar et al., 1989;
 Liver – Kassie et al., 2003;
 Rectum – Chung et al., 2003;
 Skin – Isbir et al., 2000;

Carrots
    Human Studies:
 Breast – Longnecker et al., 1997;
 Lung – Lemarchand et al., 1989;
    Supporting Animal Studies:
 Liver – Rieder et al., 1983;

Cruciferous vegetables (all)
    Human Studies:
 Bladder – Michaud et al., 1999;
 Breast – Terry et al., 2001;
Colorectal – Levi et al., 1999;
Lung – Lemarchand et al., 1989;
Prostate – Cohen et al., 2000;
Stomach – Chyou et al., 1990;
    Supporting Animal Studies:
 Bladder – Munday and Munday, 2002; 
 Breast – Bresnick et al., 1990; Stoewsand et al., 1988;
Colorectal – Smth et al., 2003;
Lung – Chung et al., 2000;

Garlic
    Human Studies:
 Breast – Levi et al., 1993;
 Colon – Iscovich et al., 1992;
 Lung – Dorant et al., 1994;
 Prostate – Hsing et al., 2002;
 Stomach – Hansson et al., 1993;
    Supporting Animal Studies:
Breast – Schaffer et al., 1996;
 Colon – Cheng et al., 1995; 
 Stomach – Sparnins et al., 1988;

Tea
    Human Studies:
 All Cancers – Imai et al., 1997;
 Breast – Wu et al., 2003;
 Colon – Su and Arab, 2002;
 Esophagus – Gao et al., 1994;
 Lung – Zhong et al., 2001;
 Stomach – Setiawan et al., 2001;
    Supporting Animal Studies:
Breast – Kavanagh et al., 2001; 
 Colon – Jia and Han, 2000;
 Esophagus – Morse et al., 1997; 
 Lung – Chung et al., 1998;
 Stomach – Yamane et al., 1995; 

Tomato
    Human Studies:
 Colon – Bidoli et al., 2000;
 GI (upper) – De Stefani et al., 2000;
 Prostate – Giovannucci et al., 2002;
 Rectum – Bidoli et al, 2002;
    Supporting Animal Studies:
 Colon – Narisawa et al., 1998;
 Prostate – Boileau et al., 2003;

Soy
    Human Studies:
 Breast – Dai et al., 2001;
 Prostate – Lee et al., 2003;
    Supporting Animal Studies:
 Breast – Gallo et al., 2002;
 Prostate – Landstrom et al., 1998;

Spinach
    Human Studies:  
Breast – Longnecker et al., 1997; 
    Supporting Animal Studies:
 Rijken et al., 1999;

  b.  Chemopreventive/Chemoprotective Effects of Respresentative Spices

Spices    Chemopreventive/Chemoprotective Effects

Turmeric    Inhibition of carcinogen activation and DNA binding
   Stimulation of carcinogen detoxification through induction of
phase II enzymes
   Induction of apoptosis or differentiation in the cancerous cells
   Induction of cell cycle arrest
   Inhibition of angiogenesis, metastasis and invasion
   Inhibition of tumor promotion
Ginger   Inhibition of tumor promotion
Inhibition of TPA-induced superoxide and hydrogen
peroxide formation
   Inhibition of TPA-induced Epstein-Barr virus activation
   Induction of apoptosis and inhibition of transformation
and metastasis
Hot red pepper  Inhibition of carcinogenactivation and DNA binding
   Stimulation of carcinogen detoxification.
   Induction of apoptosis
Saffron   Suppression of two-stage mouse skin carcinogenesis
   Inhibition of experimentally induced genotoxicity
   Inhibition of nucleic acid and protein synthesis and carcinogen
-induced neoplastic transformation
Inhibition of TPA-induced hydrogen peroxide production and
mycloperoxidase activity
Garlic    Inhibition of lipid oxidation
   Augmentation of the GST activity and biosynthesis of cellular
reduced glutathione
Onion    Potentiation of cellular antioxidant capacity through up-regulation
of y-glutamyleysteine synthase
   Inhibition of DNA damage and growth of cancer cells mediated by
perturbation of microtubule polymerization
   Inhibition of EGF-Receptor signaling
   Induction of apoptosis and cell cycle arrest in cancerous cells
Clove    Inhibition of lipid peroxidation
   Anti-inflammatory, anti-mutagenic, and anti-carcinogenic effects
Rosemary   Antioxidant effect possibly by scavenging of OH radical, singlet
oxygen, and peroxynitrite
   Stimulation of carcinogen detoxification through induction of
phase II enzyme
   Inhibition of tumor promotion
   Enhancement of intracellular accumulation of chemotherapeutic
agents through inhibition of the P-glycoprotein activity
   Induction of apoptosis and cell cycle arrest in tumor cells

 From the book:  Phytopharmaceuticals in Cancer Chemoprevention (2005). [455]  


    [452]  Carcinogenic and Anticarcinogenic Food Components, edited by Wanda Baer-Dubowska, Agnieszka Bartoszek, Danuta Malejka-Giganti, Taylor and Francis Group (CRC Press), Boca Raton, FL, 2006.
    [453]  Phytopharmaceuticals in Cancer Chemoprevention, edited by Debasis Bagchi, Harry G. Preuss, CRC Press, Boca Raton, FL, 2005. 
    [454]  Carcinogenic and Anticarcinogenic Food Components, edited by Wanda Baer-Dubowska, Agnieszka Bartoszek, Danuta Malejka-Giganti, Taylor and Francis Group (CRC Press), Boca Raton, FL, 2006.
    [455]  Phytopharmaceuticals in Cancer Chemoprevention, edited by Debasis Bagchi, Harry G. Preuss, CRC Press, Boca Raton, FL, 2005.   

 

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