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.’
Cystatin C, a blood marker of kidney function, proved significantly more accurate than the standard blood marker, creatinine, in predicting serious complications of kidney disease, in a study by researchers at the San Francisco VA Medical Center and the University of California, San Francisco. Among adults who were identified as having chronic kidney disease by high creatinine levels, the researchers found that only patients who also had abnormally high levels of cystatin C were at high risk for death, cardiovascular disease, heart failure, or kidney failure. People with high creatinine but normal cystatin C levels had risks similar to those with normal creatinine levels.
The researchers also found that a small but important segment of the study population was missed by creatinine but identified by cystatin C as being at significant risk of serious complications, according to lead author Carmen A. Peralta, MD, MAS, an SFVAMC researcher and an assistant professor of medicine in residence in the division of nephrology at UCSF.
The study of 11,909 participants appears online on December 16, 2010, in the JASN Express section of the Journal of the American Society of Nephrology. The authors analyzed patient data from two prospective studies: the Multi-Ethnic Study of Atherosclerosis and the Cardiovascular Health Study, both sponsored by the National Heart, Lung, and Blood Institute.
Principal investigator Michael G. Shlipak, MD, MPH, chief of general internal medicine at SFVAMC, said that the current study highlights a potential clinical use for cystatin C as a method for confirming a diagnosis of chronic kidney disease. Shlipak has been a leader among physicians in identifying cystatin C as an alternative, accurate, and reliable marker of kidney function.
Both cystatin C and creatinine are substances made in the body and filtered by the kidneys. High levels of the substances in the blood indicate that the kidneys are losing the ability to filter them, and thus are losing function. However, explained Peralta, creatinine is a byproduct made in muscles, so it is affected by what you eat and especially by how much muscle you have. Thus, a bodybuilder with healthy kidneys might have an elevated creatinine level because of high muscle mass, whereas a frail elderly person might have normal or even low levels of creatinine, but in fact this persons kidneys are not working well – its just that theres not much creatinine because theres not much muscle.
In contrast, cystatin C is a protein made in cells throughout the body. In studies so far, it does not seem to be that affected by age or muscle mass or diet, said Shlipak, who is also a professor in residence of medicine and epidemiology and biostatistics at UCSF.
Shlipak proposes that cystatin C, which can cost as little as $17 per test, be added as a method for confirming or staging chronic kidney disease in guidelines that are currently being formulated by nephrologists. Its vital that we have an accurate diagnostic test, because kidney disease does not show symptoms until its too late, when your kidneys have almost failed completely, he said. Being missed by creatinine is an important limitation in our current method of diagnosing kidney disease, said Peralta. Yet, she adds, being falsely identified with kidney disease through inaccurate test results can be disastrous as well. There is fear and psychological stress, particularly in communities of color, where people have a lot of friends and family members who are on dialysis, she noted. You can also be subjected to unnecessary and expensive tests and medications.
Cystic fibrosis is a genetic disease that causes a thick, sticky mucus to build up in the lungs and digestive tract. A clinical trial of a new drug called denufosol found that those given the medication for six months prevented some of the accumulation and improved performance on lung tests.
The Cystic Fibrosis Foundation estimates that about 30,000 children and adults in the United States have the condition that clogs the lungs and leads to life-threatening lung infections. The mucus also obstructs the pancreas and stops natural enzymes from helping the body break down and absorb food.
Cystic fibrosis is caused by a genetic mutation that disrupts the cystic fibrosis transmembrane regulator (CFTR) protein, an ion channel. Denufosol tetrasodium inhalation solution works by correcting ion transport in patients to enhance airway hydration and mucus clearance by increasing chloride secretion, inhibiting sodium absorption and increasing ciliary beat frequency.
Frank J. Accurso MD of the University of Colorado and colleagues included about 350 children with cystic fibrosis aged five and older in the study called TIGER-1, The Transport of Ions to Generate Epithelial Rehydration. All had a forced expiratory volume (FEV1) at least 75% of normal, indicating normal to mildly impaired lung function characteristic of early cystic fibrosis.
The patients were randomized to receive either 60 milligrams of inhaled denufosol three times daily or a matching placebo for 24 weeks. This was followed by another 24-week open-label safety extension phase.
The patients on the new medication had increase in FEV1 of 0.048 L, approximately 2% over baseline. In addition, the researchers found further lung improvement by 0.115L by the end of the open-label phase. The placebo group, when switched over to denofusol in the open-label phase, also improved by a mean 0.078 L in FEV1.
Big improvements weren't expected, says Accurso, because the drug is primarily designed to prevent or delay loss of lung function rather than act as a rescue therapy.
Denufosol appeared to be safe without serious adverse events or impaired growth of the young patients, suggesting it could be suitable as an early intervention. Intervention for cystic fibrosis early in its course has the potential to delay or prevent progressive changes that lead to irreversible airflow obstructions, the researchers say in their study published in the American Journal of Respiratory and Critical Care Medicine.
A second phase III trial, which is called TIGER-2, is ongoing which will incorporate a longer placebo-controlled treatment phase. Inspire Pharmaceuticals is targeting a potential US commercial launch of the drug for 2012, pending FDA approval.
Accurso FJ, et al “Denufosol Tetrasodium in Patients with Cystic Fibrosis and Normal to Mildly Impaired Lung Function” Am J Respir Crit Care Med 2011.