Choosing to eat tomatoes not only reduces a man’s risk of developing prostate cancer, but also shrinks the existing tumors, claims a new Italian study. Researchers theorize that the secret may lie in lycopene, the powerful anti-oxidant that makes tomatoes red. Lycopene helps neutralize harmful free radicals that are implicated in various kinds of cancer, cardiovascular problems, macular degeneration and other age-related illnesses. However, the benefit was strongest for prostate cancer.
In a bid to assess the prostate cancer-fighting properties of tomatoes, the researchers at the University of Naples conducted an experiment on rodents. For the purpose of the study, the researchers fed laboratory rats implanted with prostate cancer cells, with either a normal diet or that containing 10 percent tomato powder. The tomato powders were made from whole foods so the effects of eating the entire vegetable could be assessed as a nutritional supplement. The investigators noted that the animals fed on tomato powder exhibited slow progression of the disease and also had lower rates of prostate cancer. In contrast, those fed on a normal diet displayed no such benefits.
Joanna Owens, from Cancer Research Britain disagrees stated, “This study doesn’t provide enough evidence that tomatoes can reduce the risk of prostate cancer or prevent progression of the disease in humans. “Other risks such as age, family history and ethnicity are likely to play a much greater role than diet alone.” The study has been published in the journal ‘Cancer Prevention Research.’
New findings from the Monell Center reveal that weight gain of formula-fed infants is influenced by the type of formula the infant is consuming. The findings have implications related to the infant’s risk for the development of obesity, diabetes and other diseases later in life. “Events early in life have long-term consequences on health and one of the most significant influences is early growth rate,” said study lead author Julie Mennella, Ph.D., a developmental psychobiologist at Monell. “We already know that formula-fed babies gain more weight than breast-fed babies. But we didn’t know whether this was true for all types of formula.”
While most infant formulas are cow’s milk-based, other choices include soy-based and protein hydrolysate-based formulas. Protein hydrolysate formulas contain pre-digested proteins and typically are fed to infants who cannot tolerate the intact proteins in other formulas. In adults, pre-digested proteins are believed to act in the intestine to initiate the end of a meal, thus leading to smaller meals and intake of fewer calories. Based on this, the authors hypothesized that infants who were feeding protein hydrolysate formulas would eat less and have an altered growth pattern relative to infants feeding cow’s milk-based formula.
In the study, published online in the journal Pediatrics, infants whose parents had already decided to bottle-feed were randomly assigned at two weeks of age to feed either a cow’s milk-based formula (35 infants) or a protein hydrolysate formula (24 infants) for seven months. Both formulas contained the same amount of calories, but the hydrolysate formula had more protein, including greater amounts of small peptides and free amino acids. Infants were weighed once each month in the laboratory, where they also were videotaped consuming a meal of the assigned formula. The meal continued until the infant signaled that s/he was full.
Over the seven months of the study, the protein hydrolysate infants gained weight at a slower rate than infants fed cow milk formula. Linear growth, or length, did not differ between the two groups, demonstrating that the differences in growth were specifically attributable to weight. “All formulas are not alike,” said Mennella. “These two formulas have the same amount of calories, but differ considerably in terms of how they influence infant growth.”
When the data were compared to national norms for breast-fed infants, the rate of weight gain of protein hydrolysate infants was comparable to the breast milk standards; in contrast, infants fed cow’s milk formula gained weight at a greater rate than the same breast milk standards. Analysis of the laboratory meal revealed the infants fed the protein hydrolysate formula consumed less formula during the meal. “One of the reasons the protein hydrolysate infants had similar growth patterns to breast-fed infants, who are the gold standard, is that they consumed less formula during a feed as compared to infants fed cow’s milk formula” said Mennella. “The next question to ask is: Why do infants on cow’s milk formula overfeed?”
The findings highlight the need to understand the long-term influences of infant formula composition on feeding behavior, growth, and metabolic health. Future studies will utilize measures of energy metabolism and expenditure to examine how the individual formulas influence growth, and how each differs from breastfeeding. Also contributing to the study, which was funded by the National Institute of Child Health and Human Development, were Monell scientists Gary Beauchamp and Alison Ventura.
To test their hypothesis that environmental influences experienced by the father can be passed down to the next generation in the form of changed epigenetic information, Rando and colleagues fed different diets to two groups of male mice. The first group received a standard diet, while the second received a low-protein diet. To control for maternal influences, all females were fed the same, standard diet. Rando and colleagues observed that offspring of the mice fed the low-protein diet exhibited a marked increase in the genes responsible for lipid and cholesterol synthesis in comparison to offspring of the control group fed the standard diet.
These observations are consistent with epidemiological data from two well-known human studies suggesting that parental diet has an effect on the health of offspring. One of these studies, called the Överkalix Cohort Study, conducted among residents of an isolated community in the far northeast of Sweden, found that poor diet during the paternal grandfather’s adolescence increased the risk of diabetes, obesity and cardiovascular disease in second-generation offspring. However, because these studies are retrospective and involve dynamic populations, they are unable to completely account for all social and economic variables. “Our study begins to rule out the possibility that social and economic factors, or differences in the DNA sequence, may be contributing to what we’re seeing,” said Rando. “It strongly implicates epigenetic inheritance as a contributing factor to changes in gene function.”
The results also have implications for our understanding of evolutionary processes, says Hans A. Hofmann, PhD, associate professor of integrative biology at the University of Texas at Austin and a co-author of the study. “It has increasingly become clear in recent years that mothers can endow their offspring with information about the environment, for instance via early experience and maternal factors, and thus make them possibly better adapted to environmental change. Our results show that offspring can inherit such acquired characters even from a parent they have never directly interacted with, which provides a novel mechanism through which natural selection could act in the course of evolution.” Such a process was first proposed by the early evolutionist Jean-Baptiste Lamarck, but then dismissed by 20th century biologists when genetic evidence seemed to provide a sufficient explanation.
Taken together, these studies suggest that a better understanding of the environment experienced by our parents, such as diet, may be a useful clinical tool for assessing disease risk for illnesses, such as diabetes or heart disease. “We often look at a patient’s behavior and their genes to assess risk,” said Rando. “If the patient smokes, they are going to be at an increased risk for cancer. If the family has a long history of heart disease, they might carry a gene that makes them more susceptible to heart disease. But we’re more than just our genes and our behavior. Knowing what environmental factors your parents experienced is also important.”
The next step for Rando and colleagues is to explore how and why this genetic reprogramming is being transmitted from generation to generation. “We don’t know why these genes are being reprogrammed or how, precisely, that information is being passed down to the next generation,” said Rando. “It’s consistent with the idea that when parents go hungry, it’s best for offspring to hoard calories, however, it’s not clear if these changes are advantageous in the context of a low-protein diet.”
Georgetown University researchers suggest obese women can reduce their risk of endometrial cancer by taking vitamin D supplements.Scientists from Georgetown's Lombardi Comprehensive Cancer Center recently showed that 67 percent of obese mice fed a regular diet developed this cancer, versus only 25 percent of obese mice fed a vitamin D-supplemented diet. “In the obese mice, vitamin D offered a very strong, very significant protective effect,” says the study's lead investigator, professor of oncology Leena Hilakivi-Clarke. The findings, published in Cancer Prevention Research, also reported that vitamin D offers no protective effects for mice of normal weight. About 60 percent of mice predisposed to endometrial cancer developed it no matter what diet they were fed.
All of the mice in the study were genetically predisposed to develop endometrial cancer because they lacked one of two tumor suppressor genes. People without one of these genes are strongly predisposed to the cancer, and obesity adds a strong risk factor for the disease, researchers say. “Vitamin D has been shown to be helpful in a number of cancers, but for endometrial cancer, our study suggests it protects only against cancer that develops due to obesity,” Hilakivi-Clarke says. “Still, if these results are confirmed in women, use of vitamin D may be a wonderfully simple way to reduce endometrial cancer risk.”
Until further studies are conducted, she says women concerned about their risk of this disease may wish to take vitamin D supplements or spend a few more minutes each week in the sun, They also should strive to lose weight if they are carrying around too many pounds. The National Cancer Institute and the Department of Defense funded the research, which also included investigators from the National Cancer Institute, Northwestern University, Wake Forest University School of Medicine and Walter Reed Hospital.
“But we really don't know why dietary vitamin D works so well in our obese mice,” Hilakivi-Clarke says. “We are currently investigating the mechanisms, and we are hopeful that we can find an answer.”
Fish oil, when combined with epigallocatechin‑3‑gallate (EGCG—a polyphenol and antioxidant found in green tea), may affect chemical processes in the brain associated with Alzheimer's disease, according to a study published in Neuroscience Letters. This study, which used an animal (mouse) model of Alzheimer's disease, builds on previous research linking the disease to peptides (amino acid chains) called beta‑amyloids and laboratory studies suggesting that EGCG decreases memory problems and beta‑amyloid deposits in mice.
Researchers from the University of South Florida divided Alzheimer's disease‑model mice into five feeding groups. During a period of 6 months, each group was fed one of five diets: fish oil only; high‑dose EGCG; low‑dose EGCG; low‑dose EGCG and fish oil; or a regular diet (control). The researchers observed that low‑dose EGCG alone did not reduce the Alzheimer's disease-related chemical processes in the brain. However, the mice fed the combination of fish oil and EGCG had a significant reduction in amyloid deposits that have been linked with Alzheimer's disease.
Upon examination of blood and brain tissues of the mice, the researchers found high levels of EGCG in the mice that were fed the combination of fish oil and low‑dose EGCG compared with those fed low‑dose EGCG alone. A possible explanation, according to the researchers, is that fish oil enhances the bioavailability of EGCG—that is, the degree to which EGCG was absorbed into the body and made available to the brain. This effect, in turn, may contribute to the increased effectiveness of this combination. Further research is necessary, however, to determine if the combination of fish oil and EGCG affects memory or cognition, and whether it might have potential as an option for people at risk of developing Alzheimer's disease.
Giunta B, Hou H, Zhu Y, et al. Fish oil enhances anti‑amyloidogenic properties of green tea EGCG in Tg2576 mice. Neuroscience Letters. 2010;471(3):134–138.
The research is being presented at the conference of the British Society for Research on Ageing (BSRA) in Newcastle. It was conducted by scientists at the BBSRC Centre for Integrated Systems Biology of Ageing and Nutrition (CISBAN) at Newcastle University.
Working with the theory that cell senescence – the point at which a cell can no longer replicate – is a major cause of ageing the researchers set out to investigate what effect a restricted diet had on this process. By looking at mice fed a restricted diet the team found that they had a reduced accumulation of senescent cells in their livers and intestines. Both organs are known to accumulate large numbers of these cells as animals age.
Alongside this the CISBAN scientists also found that the telomeres of the chromosomes of the mice on restricted diets were better maintained despite their ageing. Telomeres are the protective 'ends' of chromosomes that prevent errors, and therefore diseases, occurring as DNA replicates throughout an organisms lifetime but they are known to become 'eroded' over time.
The adult mice were fed a restricted diet for a short period of time demonstrating that it may not be necessary to follow a very low calorie diet for a lifetime to gain the benefits the scientists found.
Chunfang Wang, the lead researcher on this project at CISBAN, said: “Many people will have heard of the theory that eating a very low calorie diet can help to extend lifespan and there is a lot of evidence that this is true. However, we need a better understanding of what is actually happening in an organism on a restricted diet. Our research, which looked at parts of the body that easily show biological signs of ageing, suggests that a restricted diet can help to reduce the amount of cell senescence occurring and can reduce damage to protective telomeres. In turn this prevents the accumulation of damaging tissue oxidation which would normally lead to age-related disease.”
Professor Thomas von Zglinicki, who oversaw the research, said: “It's particularly exciting that our experiments found this effect on age-related senescent cells and loss of telomeres, even when food restriction was applied to animals in later life. We don't yet know if food restriction delays ageing in humans, and maybe we wouldn't want it. But at least we now know that interventions can work if started later. This proof of principle encourages us at CISBAN in our search for interventions that might in the foreseeable future be used to combat frailty in old patients.”
CISBAN is one of the six BBSRC Centres for Integrative Systems Biology. The centres represent a more than £40M investment by the Biotechnology and Biological Sciences Research Council (BBSRC) to support the development of systems biology in the UK. The centres are also supported by the Engineering and Physical Sciences Research Council.
Systems biology uses the study of a whole, interconnected system – a cell, an organism or even an ecosystem – with computer modelling to better make the outputs of biology more useful to scientists, policymakers and industry.
Prof Douglas Kell, BBSRC Chief Executive and keynote speaker at the BSRA Conference, said: “As lifespan continues to extend in the developed world we face the challenge of increasing our 'healthspan', that is the years of our lives when we can expect to be healthy and free from serious or chronic illness. By using a systems biology approach to investigate the fundamental mechanisms that underpin the ageing process the CISBAN scientists are helping to find ways to keep more people living healthy, independent lives for longer.”
The study was conducted in mice, some of which were fed a normal diet of rodent chow and some a 16-week diet of fructose and sucrose-enriched drinking water and trans-fat solids. Their liver tissue was then analyzed for fat content, scar tissue formation (fibrosis), and the biological mechanism of damage. This was done by measuring reactive oxygen stress, inflammatory cell type and plasma levels of oxidative stress markers, which are known to play important roles in the development of obesity-related liver disease and its progression to end-stage liver disease.
The investigators found that mice fed the normal calorie chow diet remained lean and did not have fatty liver disease. Mice fed high calorie diets (trans-fat alone or a combination of trans-fat and high fructose) became obese and had fatty liver disease.
“Interestingly, it was only the group fed the combination of trans-fat and high fructose which developed the advanced fatty liver disease which had fibrosis,” says Dr. Kohli. “This same group also had increased oxidative stress in the liver, increased inflammatory cells, and increased levels of plasma oxidative stress markers.”
Dr. Kohli hopes to further investigate the mechanism of liver injury caused by high fructose and sucrose enriched drinking water and study a therapeutic intervention of antioxidant supplementation. Antioxidants are natural defenses against oxidative stress and may reverse or protect against advanced liver damage, according to Dr. Kohli.
The investigators also would like to use this model to better understand human fatty liver disease and perform clinical trials using novel therapeutic and monitoring tools.
“Our data suggest that supplementation with pharmaceuticals agents should be tested on our new model to establish whether one is able to reverse or protect against progressive liver scarring and damage,” says Dr. Kohli.
The study was supported by grants from the National Institutes of Health and the Children's Digestive Health and Nutrition Foundation.
The study will be published in the December issue of the Journal of Alzheimer's Disease and was directed by Mercedes Unzeta, professor of the UAB Department of Biochemistry and Molecular Biology. Participating in the study were researchers from this department and from the departments of Cell Biology, Physiology and Immunology, and of Psychiatry and Legal Medicine, all of which are affiliated centres of the Institute of Neuroscience of Universitat Autònoma de Barcelona. The company La Morella Nuts from Reus and the ACE Foundation of the Catalan Institute of Applied Neurosciences also collaborated in the study.
During the development of the brain, stem cells generate different neural cells (neurons, astrocytes and oligodendrocytes) which end up forming the adult brain. Until the 1960s it was thought that the amount of neurons in adult mammals decreased with age and that the body was not able to renew these cells. Now it is known that new neurons are formed in the adult brain. This generative capacity of the cells however is limited to two areas of the brain: the olfactory bulb and the hippocampus (area related to the memory and to cognitive processes). Although the rhythm of cell proliferation decreases with age and with neurodegenerative diseases, it is known that exercise and personal well being can combat this process.
The main objective of this research was to study the effect of an LMN cream-enriched diet on the neurogenesis of the brain of an adult mouse. Scientists used two groups of mice for the study. One group was given a normal diet and the other was given the same diet enriched with LMN cream. Both groups were fed during 40 days (approximately five years in humans). The analyses carried out in different brain regions demonstrated that those fed with LMN cream had a significantly higher amount of stem cells, as well as new differentiated cells, in the olfactory bulb and hippocampus.
The second objective was to verify if the LMN cream could prevent damage caused by oxidation or neural death in cell cultures. Cultures of the hippocampal and cortical cells were pretreated with LMN cream. After causing oxidative damage with hydrogen peroxide, which killed 40% of the cells, scientists observed that a pretreatment with LMN cream was capable of diminishing, and in some cases completely preventing, oxidative damage. The hippocampal and cortical cells were also damaged using amyloid beta (anomalous deposits of this protein are related to Alzheimer's disease). The results obtained were similar to those obtained using hydrogen peroxide.
These results demonstrate that an LMN diet is capable of inducing the generation of new cells in the adult brain, and of strengthening the neural networks which become affected with age and in neurogenerative processes such as Alzheimer's disease, as well as protecting neurons from oxidative and neural damage, two phenomena which occur at the origin of many diseases affecting the central nervous system.
In this study researchers have used different biochemical and molecular analysis techniques, with the help of specific antibodies, to detect different neuronal markers implied in the process of differentiation.
The group of researchers led by Dr Unzeta has spent years studying the effects oxidases have on oxidative stress as a factor implied in neurodegenerative disorders such as Parkinson and Alzheimer's disease, and the effects of different natural products with anti-inflammatory and antioxidant properties in different experimental models of Alzheimer's disease.
The study forms part of the CENIT project, which was awarded to La Morella Nuts in 2006 under the auspices of the INGENIO 2010 programme, with the objective of establishing methodologies for the design, evaluation and verification of functional foods which may protect against cardiovascular diseases and Alzheimer's disease. With 21.15m euros in funding and a duration of four years, the project has included the participation of 50 doctors and technicians from nine different companies, four universities (7 departments) and 2 research centres.
Curcumin, one of the principal components of the Indian spice turmeric, seems to delay the liver damage that eventually causes cirrhosis, suggests preliminary experimental research in the journal Gut. Curcumin, which gives turmeric its bright yellow pigment, has long been used in Indian Ayurvedic medicine to treat a wide range of gastrointestinal disorders.
Previous research has indicated that it has anti-inflammatory and antioxidant properties which may be helpful in combating disease. The research team wanted to find out if curcumin could delay the damage caused by progressive inflammatory conditions of the liver, including primary sclerosing cholangitis and primary biliary cirrhosis.
Both of these conditions, which can be sparked by genetic faults or autoimmune disease, cause the liver's plumbing system of bile ducts to become inflamed, scarred, and blocked. This leads to extensive tissue damage and irreversible and ultimately fatal liver cirrhosis.
The research team analysed tissue and blood samples from mice with chronic liver inflammation before and after adding curcumin to their diet for a period of four and a period of eight weeks.
The results were compared with the equivalent samples from mice with the same condition, but not fed curcumin.
The findings showed that the curcumin diet significantly reduced bile duct blockage and curbed liver cell (hepatocyte) damage and scarring (fibrosis) by interfering with several chemical signalling pathways involved in the inflammatory process.
These effects were clear at both four and eight weeks. No such effects were seen in mice fed a normal diet.
The authors point out that current treatment for inflammatory liver disease involves ursodeoxycholic acid, the long term effects of which remain unclear. The other alternative is a liver transplant.
Curcumin is a natural product, they say, which seems to target several different parts of the inflammatory process, and as such, may therefore offer a very promising treatment in the future.
Source: Anna Baghdasaryan, Thierry Claudel, Astrid Kosters, Judith Gumhold, Dagmar Silbert, Andrea Thüringer, Katharina Leski, Peter Fickert, Saul J Karpen, Michael Trauner. Curcumin improves sclerosing cholangitis in Mdr2-/- mice by inhibition of cholangiocyte inflammatory response and portal myofibroblast proliferation. Gut, 2010; 59: 521-530