Beauty Health for Life

In a forthcoming review article from Nutrition and Cancer: An International Journal, a publication of Routledge, researchers review available evidence that links orange juice with cancer chemoprevention. The review article, "Orange Juice and Cancer Chemoprevention" discusses the putative mechanisms involved in the process, the potential toxicity of orange juice, and the available data in terms of evidence-based medicine.

Orange juice has many potential positive effects when it comes to cancer, particularly because it is high in antioxidants from flavonoids such as hesperitin and naringinin. Evidence from previous in vitro studies has indicated that orange juice can reduce the risk of leukemia in children, as well as aid in chemoprevention against mammary, hepatic, and colon cancers. Biological effects of orange juice in vitro are largely influenced by the juices composition, which is dependent on physiological conditions of the oranges such as climate, soil, fruit maturation, and storage methods post-harvest.

The researchers acknowledge potential toxicity from orange juice if consumed in excess amounts -- especially for children, hypertensive, kidney-compromised, and diabetics. Excessive drinking of orange juice for individuals from these groups has the potential to create noxious effects, hyperkalemia, and has been associated with both food allergies and bacterial outbreaks in cases where the juice was unpasteurized. "Excessive intake of any food, even for the healthiest, can lead to oxidative status imbalance," wrote the researchers.

Further research is highly recommended to determine the biological connection between orange juice and cancer chemoprevention. Issues such as the type of cultivar and the amount consumed will also need clarification.

Overall, the review article summarizes several biological effects of orange juice that can contribute to chemoprevention, including antioxidant, antimutagenic and antigenotoxic, cytoprotective, hormonal, and cell signaling modulating effects. Orange juice has antimicrobial and antiviral action and modulates the absorption of xenobiotics. "OJ could contribute to chemoprevention at every stage of cancer initiation and progression," the researchers explained. "Among the most relevant biological effects of OJ is the juices antigenotoxic and antimutagenic potential, which was shown in cells in culture and in rodents and humans."

Also see Curry Spice Component May Help Slow Prostate Tumor Growth

Powdered turmeric has been used for centuries to treat osteoarthritis and other illnesses. Its active ingredient, curcumin, inhibits inflammatory reactions. A new study led by a research team at Ludwig-Maximilians-Universität (LMU) in Munich now shows that it can also inhibit formation of metastases.

Prostate cancer is one of the most prevalent malignancies in the Western world, and is often diagnosed only after metastatic tumors have formed in other organs. In three percent of cases, these metastases are lethal. A research team led by PD Dr. Beatrice Bachmeier at LMU Munich has been studying the mode of action of a natural product that inhibits the formation of metastases. The compound is found in turmeric, a plant that has been used for medicinal purposes for thousands of years, and is a major ingredient of curry.

Bachmeiers research centers on curcumin, the polyphenol responsible for the characteristic color of curry. Curcumin is well tolerated and is theore, in principle, suitable both for prophylactic use (primary prevention) and also for the suppression of metastases in cases where an established tumor is already present (secondary prevention). In a previous study Bachmeier and her colleagues had demonstrated that the substance reduces statistically significantly the formation of lung metastases in an animal model of advanced breast cancer.

Mitigating metastasis The new study was designed to investigate the efficacy of curcumin in the prevention of prostate cancer metastases, and to determine the agents mechanism of action. The researchers first examined the molecular processes that are abnormally regulated in prostate carcinoma cells. Breast and prostate cancers are often associated with latent or chronic inflammatory reactions, and in both cases, the tumor cells were found to produce pro-inflammatory immunomodulators including the cytokines CXCL1 und CXCL2.

The researchers went on to show that curcumin specifically decreases the expression of these two proteins, and in a mouse model, this effect correlated with a decline in the incidence of metastases. "Due to the action of curcumin, the tumor cells synthesize smaller amounts of cytokines that promote metastasis," says Bachmeier. "As a consequence, the frequency of metastasis formation in the lungs is significantly reduced, in animals with breast cancer, as we showed previously, or carcinoma of the prostate, as demonstrated in our new study."

Curcumin and chemoprevention

Bachmeier theore believes that curcumin may be useful in the prevention of breast and prostate cancers -- which are both linked to inflammation -- and in reducing their metastatic potential. "This does not mean that the compound should be seen as a replacement for conventional therapies. However, it could play a positive role in primary prevention -- before a full-blown tumor arises -- or help to avert formation of metastases. In this context the fact that the substance is well tolerated is very important, because one can safely recommend it to individuals who have an increased tumor risk."

A daily intake of up to 8g of curcumin is regarded as safe, and its anti-inflammatory properties have long been exploited in traditional oriental medicine. Men with benign hyperplasia of the prostate (BHP) are one possible target group for prophylaxis, as are women who have a family history of breast cancer. The agent might also be valuable as a supplement to certain cancer therapies. At all events, curcumins beneficial effects must first be confirmed in controlled clinical tests. Bachmeier is now planning such a trial in patients who suffer from therapy-resistant carcinoma of the prostate.

Obese, postmenopausal women are at greater risk for developing breast cancer and their cancers tend to be more aggressive than those in lean counterparts. A University of Colorado Cancer Center study published in the December issue of the journal Cancer Research shows how this risk might be prevented.

“By using nutrient tracers for fat and sugar, we tracked where the body stored excess calories. In lean models, excess fat and glucose were taken up by the liver, mammary and skeletal tissues. In obese models, excess fat and glucose were taken up by tumors, fueling their growth,” says Erin Giles, PhD, postdoctoral researcher at the CU Cancer Center and the paper’s lead author.

In short, if you are lean, excess calories go to healthy tissue. If you are obese, excess calories feed the tumor.

“This implies that the menopausal window may be an opportunity for women to control their breast cancer risk through weight management,” Giles says.

In this study, Giles worked with a team of scientists including postdoctoral fellows Elizabeth Wellberg and Sonali Jindal, as well as faculty members Steve Anderson, Pepper Schedin, Ann Thor and Paul Maclean. Their study also showed that tumors from obese animals had increased levels of the progesterone receptor, and this receptor appears to give tumors a metabolic advantage for growth. To extend their findings to humans, they recruited gene analysis experts David Astling and Aik-Choon Tan who analyzed 585 human breast cancers and found that human tumors expressing the progesterone receptor had the same metabolic advantage.

“Basically, we saw an abnormal metabolic response to fat and sugar in the obese that, in many ways, mirrors the response to fat and sugar in Type II diabetes,” Giles says. Noticing this similarity, the group tested the use of the common Type II diabetes drug, Metformin, in their model of postmenopausal breast cancer.

“With treatment, tumor size was dramatically decreased in the obese, and tumors showed reduced expression of the progesterone receptor,” Giles says.

Using a pre-clinical model, the investigators found that weight gain during menopause is particularly bad for those who are obese when entering menopause. Together, the results of this study suggest that the combination of obesity and weight gain during menopause can impact breast cancer in two ways. First, tumors that arise in obese women appear to have a metabolic advantage, and second, the inability to store excess calories in healthy tissues may further fuel tumor growth.

“While drugs may be useful in controlling breast cancer risk in obese, postmenopausal women, our results imply that a combination of diet and exercise may be equally if not more beneficial,” Giles says.

The group’s ongoing studies are testing whether interventions such as diet and exercise, during the period of menopausal weight gain, can improve tumor outcomes.

Disease Management Care Blog readers saw it here first.

Months ago, the DMCB presciently argued that cancer patients appetite for high expense and low yield treatments was based on more than desperation.  It said it was also based on doctors and patients quite rational realization that these treatments could rarely result in meaningful life prolongation.  In other words, while an "average" life expectancy from a particular treatment might be reported to be "only" six months, knowing that some persons make it to 12 or more months while others died immediately (zero months) could prompt a reasonable cancer patient to choose a shot at getting the twelve months.

The prestigious medical journal Health Affairs has finally caught up the the DMCB.  In the latest issue, Darius Lakdawalla and colleagues surveyed 150 persons with either breast cancer (N=47, 20 of whom had advanced disease), melanoma (N=20) or other types of cancer (N=83). 

There were two surveys dealing with breast cancer and melanoma that presented two nominally equal chemotherapy treatment scenarios.  One used a "hypothetical" survival outcome based on the usual kind of "average survival" statistics.  The other presented a "hopeful" survival outcome that reported a "spread" of survival statistics that included the small number of persons with shortened as well as prolonged lifespans.  The surveys were conducted face-to-face using interviews on representative patients drawn from multiple cancer treatment centers nationwide.

According to the authors, the survey was designed to test the appetite for risk among cancer patients. Behavioral economists have long known that persons generally per the "sure bets" ($100 now) over equivalently valued "hopeful gambles" (a coin flip to win $200 or lose it all).

Its also known that persons who are not well-off have a greater appetite for the hopeful gamble.  Betting a relatively small amount with a large upside explains the luster of low odds state lotteries for socioeconomically disadvantaged persons. It could also account for the willingness of very sick cancer patients - who have little to lose - to demand long shot treatments, even if theyre toxic and experimental. 

The results showed that 77% of the survey participants perred the hopeful gamble scenario. 71% of the patients with the melanoma scenario were prepared to "bet" two years of life in return for a 20% chance of living 4½ years. Among the patients with the breast cancer scenario, 83% were willing to bet 1½ years for a 10% chance of living 4 years. 

These perences were also accompanied by a willingness to spend a lot of money to access the bet. On average, the melanoma patients were willing to pay at least $45,000, while the breast cancer scenario patients were willing to pay at least $90,000.  Persons with higher income levels were willing to pay even more.

While the authors correctly note that more research is needed, the DMCB suspects this could explain the decision-making thats leading many cancer patients to demand insurance coverage of experimental, high cost and low yield treatments.  Not only does it make intuitive sense, but popular media extolls the intrepid hero who prevails and gets the girl, wins the talent show or defeats the aliens despite little chance of winning.  Were a culture inculcated with high stakes gambles,especially if there is little to lose.

The DMCB recalls one of its middle aged patients with colon cancer that had spread to his liver.  After multiple rounds of surgery (half his liver was removed), chemo and radiation, he was swollen, sickly, tired, gaunt and moribund.  He agreed the treatments were pretty bad - until he considered the alternative.

Assuming IPAB survives, do we really think their pronouncements based on the usual approaches to comparative outcomes will really convince cancer patients to not seek hope?  Will they really determine that hope is not medically necessary?

Health conscious individuals have been closely following Vitamin D research for the past decade as volumes of scientific evidence prove this prohormone has been selected through our evolution to provide critical protection against many inflammatory and immune mediated diseases.

University of Illinois scientists have evidence that lifelong exposure to genistein, a bioactive component in soy foods, protects against colon cancer by repressing a signal that leads to accelerated growth of cells, polyps, and eventually malignant tumors.

"In our study, we report a change in the expression of three genes that control an important signaling pathway," said Hong Chen, a U of I professor of food science and human nutrition.

The cells in the lining of the human gut turn over and are completely replaced weekly, she noted. "However, in 90 percent of colon cancer patients, an important growth-promoting signal is always on, leading to uncontrolled growth and malignancies. Our study suggests that the aberrant Wnt signaling during the development of colon cancer can be regulated by soy-rich diets."

"The good news is that a diet rich in soy genistein represses those signals through epigenetic modifications at the regulatory regions of those genes," said Yukun Zhang, a doctoral student in Chens laboratory.

Consuming omega-3 fish oils can help to prevent skin cancer, according to the first clinical trial exploring the influence of fish oils on the skin immunity of humans.

The study was conducted by a team of researchers from the University of Manchester and funded by the Association for International Cancer Research, and examined the effect of taking omega-3 on 79 healthy participants.

Findings of the study, published in The American Journal of Clinical Nutrition, revealed that consuming regular doses of fish oils increases immunity to sunlight.

It directly decreases sunlight-induced immunity suppression - called immunosuppression - which affects the bodys power to combat skin cancer and infection.

Professor Lesley Rhodes, Professor of Experimental Dermatology from the Photobiology Unit Dermatology Centre at the Universitys School of Medicine and Salford Royal NHS Foundation Trust, said their study was the first of its kind conducted using humans:

"There has been research in this area carried out on mice in the past but this is the first time that there has been a clinical trial directly in people. It has taken a number of years to get to this stage and the findings are very exciting. This study adds to the evidence that omega-3 is a potential nutrient to protect against skin cancer. Although the changes we found when someone took the oil were small, they suggest that a continuous low level of chemoprevention from taking omega-3 could reduce the risk of skin cancer over an individuals lifetime."

The volunteers consumed a 4g dose of omega-3 - approximately one and a half portions of oily fish each day. Then they were exposed to either 8, 15, or 30 minutes of summer midday sun in Manchester using a specific light machine.

A number of other participants took a placebo before being exposed to the sunlight machine.

Immunosuppression was shown to be 50 percent lower in the subjects that took the omega-3 and were exposed to 8 and 15 minutes of sunshine compared with the volunteers who did not take the supplement. Little to no impact on those in the 30 minute group was shown.

The conclusions from this study are significant in the battle against skin cancer, because earlier studies have always shown that sunscreens are frequently applied incorrectly and only worn on vacation.

However, Professor Rhodes points out omega-3 is not a substitute for suntan lotion or physical protection, and that it should be seen as additional protection factor to help keep the skin from burning.

Historically, fish oil has already been associated with health benefits like protecting against cardiovascular disease, helping prevent age-related vision loss, and even slowing the growth of prostate cancer cells.

New research suggests that a compound abundant in the Mediterranean diet takes away cancer cells "superpower" to escape death.

By altering a very specific step in gene regulation, this compound essentially re-educates cancer cells into normal cells that die as scheduled.

One way that cancer cells thrive is by inhibiting a process that would cause them to die on a regular cycle that is subject to strict programming. This study in cells, led by Ohio State University researchers, found that a compound in certain plant-based foods, called apigenin, could stop breast cancer cells from inhibiting their own death.

Much of what is known about the health benefits of nutrients is based on epidemiological studies that show strong positive relationships between eating specific foods and better health outcomes, especially reduced heart disease. But how the actual molecules within these healthful foods work in the body is still a mystery in many cases, and particularly with foods linked to lower risk for cancer.

Parsley, celery and chamomile tea are the most common sources of apigenin, but it is found in many fruits and vegetables.

The researchers also showed in this work that apigenin binds with an estimated 160 proteins in the human body, suggesting that other nutrients linked to health benefits – called "nutraceuticals" – might have similar far-reaching effects. In contrast, most pharmaceutical drugs target a single molecule.

"We know we need to eat healthfully, but in most cases we dont know the actual mechanistic reasons for why we need to do that," said Andrea Doseff, associate professor of internal medicine and molecular genetics at Ohio State and a co-lead author of the study. "We see here that the beneficial effect on health is attributed to this dietary nutrient affecting many proteins. In its relationship with a set of specific proteins, apigenin re-establishes the normal profile in cancer cells. We think this can have great value clinically as a potential cancer-prevention strategy."

Doseff oversaw this work with co-lead author Erich Grotewold, professor of molecular genetics and director of Ohio States Center for Applied Plant Sciences (CAPS). The two collaborate on studying the genomics of apigenin and other flavonoids, a family of plant compounds that are believed to prevent disease.

The research appears this week in the online early edition of the journal Proceedings of the National Academy of Sciences.

Though finding that apigenin can influence cancer cell behavior was an important outcome of the work, Grotewold and Doseff point to their new biomedical research technique as a transformative contribution to nutraceutical research.

They likened the technique to "fishing" for the human proteins in cells that interact with small molecules available in the diet.

"You can imagine all the potentially affected proteins as tiny fishes in a big bowl. We introduce this molecule to the bowl and effectively lure only the truly affected proteins based on structural characteristics that form an attraction," Doseff said. "We know this is a real partnership because we can see that the proteins and apigenin bind to each other."

Through additional experimentation, the team established that apigenin had relationships with proteins that have three specific functions. Among the most important was a protein called hnRNPA2.

This protein influences the activity of messenger RNA, or mRNA, which contains the instructions needed to produce a specific protein. The production of mRNA results from the splicing, or modification, of RNA that occurs as part of gene activation. The nature of the splice ultimately influences which protein instructions the mRNA contains.

Doseff noted that abnormal splicing is the culprit in an estimated 80 percent of all cancers. In cancer cells, two types of splicing occur when only one would take place in a normal cell – a trick on the cancer cells part to keep them alive and reproducing.

In this study, the researchers observed that apigenins connection to the hnRNPA2 protein restored this single-splice characteristic to breast cancer cells, suggesting that when splicing is normal, cells die in a programmed way, or become more sensitive to chemotherapeutic drugs.

"So by applying this nutrient, we can activate that killing machinery. The nutrient eliminated the splicing form that inhibited cell death," said Doseff, also an investigator in Ohio States Davis Heart and Lung Research Institute. "Thus, this suggests that when we eat healthfully, we are actually promoting more normal splice forms inside the cells in our bodies."

The beneficial effects of nutraceuticals are not limited to cancer, as the investigators previously showed that apigenin has anti-inflammatory activities.

The scientists noted that with its multiple cellular targets, apigenin potentially offers a variety of additional benefits that may even occur over time. "The nutrient is targeting many players, and by doing that, you get an overall synergy of the effect," Grotewold explained.

Doseff is leading a study in mice, testing whether food modified to contain proper doses of this nutrient can change splicing forms in the animals cells and produce an anti-cancer effect.

Frequent, regular consumption has strongest effect and is linked to more aggressive disease

Regular consumption of deep-fried foods such as French fries, fried chicken and doughnuts is associated with an increased risk of prostate cancer, and the effect appears to be slightly stronger with regard to more aggressive forms of the disease, according to a study by investigators at Fred Hutchinson Cancer Research Center.

Corresponding author Janet L. Stanford, Ph.D., and colleagues Marni Stott-Miller, Ph.D., a postdoctoral research fellow and Marian Neuhouser, Ph.D., all of the Hutchinson Center’s Public Health Sciences Division, have published their findings online in The Prostate.

While previous studies have suggested that eating foods made with high-heat cooking methods, such as grilled meats, may increase the risk of prostate cancer, this is the first study to examine the addition of deep frying to the equation.

From French fries to doughnuts: Eating more than once a week may raise risk

Specifically, Stanford, co-director of the Hutchinson Center’s Program in Prostate Cancer Research, and colleagues found that men who reported eating French fries, fried chicken, fried fish and/or doughnuts at least once a week were at an increased risk of prostate cancer as compared to men who said they ate such foods less than once a month.

In particular, men who ate one or more of these foods at least weekly had an increased risk of prostate cancer that ranged from 30 to 37 percent. Weekly consumption of these foods was associated also with a slightly greater risk of more aggressive prostate cancer. The researchers controlled for factors such as age, race, family history of prostate cancer, body-mass index and PSA screening history when calculating the association between eating deep-fried foods and prostate cancer risk.

“The link between prostate cancer and select deep-fried foods appeared to be limited to the highest level of consumption – defined in our study as more than once a week – which suggests that regular consumption of deep-fried foods confers particular risk for developing prostate cancer,” Stanford said.

Deep frying may trigger formation of carcinogens in food

Possible mechanisms behind the increased cancer risk, Stanford hypothesizes, include the fact that when oil is heated to temperatures suitable for deep frying, potentially carcinogenic compounds can form in the fried food. They include acrylamide (found in carbohydrate-rich foods such as French fries), heterocyclic amines and polycyclic aromatic hydrocarbons (chemicals formed when meat is cooked at high temperatures), aldehyde (an organic compound found in perfume) and acrolein (a chemical found in herbicides). These toxic compounds are increased with re-use of oil and increased length of frying time.

Foods cooked with high heat also contain high levels of advanced glycation endproducts, or AGEs, which have been associated with chronic inflammation and oxidative stress. Deep-fried foods are among the highest in AGE content. A chicken breast deep fried for 20 minutes contains more than nine times the amount of AGEs as a chicken breast boiled for an hour, for example.

For the study, Stanford and colleagues analyzed data from two prior population-based case-control studies involving a total of 1,549 men diagnosed with prostate cancer and 1,492 age-matched healthy controls. The men were Caucasian and African-American Seattle-area residents and ranged in age from 35 to 74 years. Participants were asked to fill out a dietary questionnaire about their usual food intake, including specific deep-fried foods.

“To the best of our knowledge, this is the first study to look at the association between intake of deep-fried food and risk of prostate cancer,” Stanford said. However, deep-fried foods have previously been linked to cancers of the breast, lung, pancreas, head and neck, and esophagus.

Because deep-fried foods are primarily eaten outside the home, it is possible that the link between these foods and prostate cancer risk may be a sign of high consumption of fast foods in general, the authors wrote, citing the dramatic increase in fast-food restaurants and fast-food consumption in the U.S. in the past several decades.

The British Dental Health Foundation believes new scientific research presented is a further indication of a possible link between pancreatic cancer and gum disease.

The latest research, presented in the journal Gut, found one of the bacterium key in the development of gum disease was associated with a two-fold increase in risk for pancreatic cancer. The study also discovered those with non-harmful oral bacteria had a 45 per cent lower risk of pancreatic cancer.

Although researchers cannot confirm whether gum disease contributes towards a higher risk of developing pancreatic cancer, the research is a further indication of a potential link between the two diseases.

Previous research has also drawn an association between bacteria responsible for gum disease and pancreatic cancer, although in both cases it remains unclear whether the presence of particular types of bacteria are a cause or effect of pancreatic cancer.

The papers corresponding author Dominique Michaud, epidemiologist at Brown University, commented: "This is not an established risk factor. But I feel more confident that something is going on. Its something we need to understand better."

Co-lead author Jacques Izard, of the Forsyth Institute and Harvard University concurred. He said: "We need to further investigate the importance of bacteria in pancreatic cancer beyond the associated risk."

Pancreatic cancer accounted for 7,901 deaths in 20104, while only four per cent of people in England survived the disease for more than five years. Given these statistics, Chief Executive of the British Dental Health Foundation, Dr Nigel Carter OBE, believes any link between the two diseases should provide a timely reminder about the importance of good oral health.

Dr Carter said: "This research provides further ammunition to the growing belief these two diseases could be related.

"There is no escaping the fact poor oral health has some role to play, as a number of studies are now starting to show. What we must remember is oral health is relatively simple to maintain. The Foundations three key messages - brushing your teeth for two minutes twice a day using a fluoride toothpaste, cutting down on how often you have sugary foods and drinks and visiting the dentist regularly, as often as they recommend - are a great starting point for maintaining good oral health.

"If you have swollen gums that bleed regularly when brushing, bad breath, loose teeth or regular mouth infections appear, it is likely you have gum disease. If any of these symptoms persist, your dentist may be able to help you."