January, 2012

Grape seed extract proves toxic to head and neck cancer cells

Reprinted with permission of Life Extension

January 30, 2012. Researchers at the University of Colorado report online on January 19, 2012 in the journal Carcinogenesis that grape seed extract shows an ability to reduce the growth of head and neck squamous cell carcinoma when administered to cell cultures and mice.
"It's a rather dramatic effect," commented lead researcher Rajesh Agarwal, PhD, who is a professor at the University of Colorado Skaggs School of Pharmacy and Pharmaceutical Sciences. "Cancer cells are fast-growing cells. Not only that, but they are necessarily fast growing. When conditions exist in which they can't grow, they die."

Dr Agarwal and his associates tested the effects of grape seed extract in cultures of human head and neck squamous cell carcinoma as well as normal human epidermal cells. The researchers observed a reduction in growth, along with cell cycle arrest and programmed cell death in the cancerous cells. Grape seed was found to damage the DNA of the cancer cells while inhibiting its repair. The authors attribute grape seed's growth inhibitory, DNA-damaging and apoptotic effects to the accumulation of intracellular reactive oxygen species, a phenomenon that was reversed by the administration of the antioxidant N-acetylcysteine. Similarly, in an experiment involving mice that received transplanted head and neck squamous cell carcinoma tumors, animals that received grape seed extract had a reduction in cancer cell growth compared with those who did not receive the extract. In both experiments, healthy tissue remained unharmed.

"We saw absolutely no toxicity to the mice, themselves," Dr Agarwal emphasized. "I think the whole point is that cancer cells have a lot of defective pathways and they are very vulnerable if you target those pathways. The same is not true of healthy cells."
The researchers hope to test grape seed in human patients who have failed first line therapies.

 

 

 

Higher vitamin D levels predict improved survival among colorectal cancer patients

Reprinted with permission of Life Extension

January 27, 2012. An article published online on January 25, 2012 in Cancer Epidemiology, Biomarkers and Prevention reports an association between higher prediagnostic levels of vitamin D and increased survival among patients with colorectal cancer.

The study evaluated the association between serum vitamin D levels and mortality among 1,202 men and women enrolled in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, which recruited over 520,000 participants from 1992 to 1998. Subjects in the current study were diagnosed with colorectal cancer between enrollment and June, 2003. Blood samples obtained upon recruitment were analyzed for serum 25-hydroxyvitamin D [25(OH)D]. Over a mean follow-up period of 73 months, 444 deaths due to colorectal cancer and 97 deaths from other causes occurred.

Men and women whose serum vitamin D levels were among the top 20 percent of participants had a 31 percent lower risk of dying from colorectal cancer and a 33 percent lower risk of mortality from any cause compared to those whose levels were among the lowest 20 percent. Having a high vitamin D level was protective against cancers of both the colon and the rectum. When subjects were analyzed according to calcium intake, a significant protective effect of vitamin D was observed only among those with high dietary calcium.

"If verified in other studies, calcium supplementation in combination with vitamin D may be potentially useful for improved survival in colorectal cancer patients," the authors write. "This large and comprehensive study, based on the EPIC cohort has shown that higher blood vitamin D levels before colorectal cancer diagnosis are associated with reduction in colorectal cancer-specific and overall mortality. Further prognostic studies among cancer patients are needed to determine whether 25(OH)D levels at diagnosis and post-diagnosis correlate with those measured prior to diagnosis, and influence all-cause and disease-specific survival among colorectal cancer patients."

 

 

 

Luteolin shows promise as an agent to reduce colon cancer cell growth

Reprinted with permission of Life Extension

January 23, 2012. In an article published today in the journal BMC Gastroenterology, Korean researchers report a benefit for the flavonoid luteolin, which occurs in some fruits and vegetables, in reducing the growth of cultured colon cancer cells.

In earlier research, Professor Jung Han Yoon Park of Hallym University in Chuncheon and colleagues found that luteolin decreases the growth of colon cancer cells by stimulating programmed cell death (apoptosis) and cell cycle arrest. In the current study, the team cultured the cells with luteolin and/or insulin-like growth factor-1 (IGF-1), which stimulates cancer growth.

A reduction in the secretion of insulin-like growth factor II (IGF-II) occurred in colon cancer cells treated with luteolin, and a decline in levels of IGF receptor precursor protein was observed within two hours. IGF-II occurs in higher levels in colon cancer cells compared to normal colon cells, and is believed to induce uncontrolled cell division and growth in cancer. When administered with IGF-1, luteolin also inhibited IGF-1's growth stimulatory effect, by affecting the cell signaling pathways that IGF-1 activates in cancer.

"Luteolin reduced IGF-I-dependent activation of the cell signaling pathways PI3K, Akt, and ERK1/2 and CDC25c," stated Jung Han Yoon Park, who is also affiliated with Kangwon National University. "Blocking these pathways stops cancer cells from dividing and leads to cell death. Our study, showing that luteolin interferes with cell signaling in colon cancer cells, is a step forward in understanding how this flavonoid works. A fuller understanding of the in vivo results is essential to determine how it might be developed into an effective chemopreventive agent."

 

 

 

Grapes may protect against macular degeneration

Reprinted with permission of Life Extension

January 13, 2012. An article published online on December 8, 2011 in the journal Free Radical Biology and Medicine shows a protective effect for grapes and lutein against the development of age-related macular degeneration (AMD) in a mouse model of the disease.
In their introduction to the article, Silvia Finnemann, PhD of Fordham University's Department of Biological Sciences and her associates explain that oxidative damage and pro-oxidant lysosomal lipofuscin accumulate in the aging human eye, which causes a decline in function of the retinal pigment epithelium: the support cells for the retina's photoreceptors. The resulting dysfunction and destruction of these cells, in turn, contributes to the development of age-related macular degeneration.

For their study, Dr Finnemann's team administered diets that provided natural antioxidants, grapes or marigold extract containing the macular pigments lutein/zeaxanthin to mice bred to have increased blood vessel formation (which occurs in macular degeneration). While lutein and zeaxanthin proved to be protective to the eye, grapes showed the greatest benefit, with both compounds resulting in reduced lipofuscin accumulation and age related rod and cone photoreceptor dysfunction, prevention of blindness as well as other positive outcomes. The antioxidant properties of compounds that occur in grapes are believed to be the protective mechanism observed in the current research.

"The protective effect of the grapes in this study was remarkable, offering a benefit for vision at old age even if grapes were consumed only at young age," Dr Finnemann stated. "A lifelong diet enriched in natural antioxidants, such as those in grapes, appears to be directly beneficial for retinal pigment epithelium, and retinal health and function."

 

 

 

Majority of postmenopausal women need more vitamin D

Reprinted with permission of Life Extension

January 11, 2012. A Position Statement prepared by the European Menopause and Andropause society (EMAS) published in the January, 2012 issue of the journal Maturitas reveals an undesirably low level of vitamin D in postmenopausal women and suggests the use of vitamin D2 or vitamin D3 supplements accompanied by monitoring when needed. The text was signed by 11 international experts and defines optimal blood levels as ranging between 30 to 90 nanograms per milliliter. "We believe that many diseases can be aggravated by a chronic deficiency of vitamin D," stated project leader Faustino R. Pérez-López of the University of Zaragoza. "We analyzed the conditions and diseases that are associated with vitamin D deficiency and we recommended the intake of supplements in postmenopausal women."

Reduced vitamin D levels are estimated to affect 50 to 70 percent of Europeans. "Healthcare professionals should be aware that this is a common problem which affects a large part of the population in Europe, even those who live in sunny places," Dr Pérez-López noted. "The World Health Organisation or other relevant bodies belonging to the European Union should establish minimum requirements or recommendations on the fortification of foods with vitamin D."

Although the medical community still has not reached a consensus concerning vitamin D supplements, Dr Pérez-López remarked that "they are effective but its efficacy has not yet been accepted." He recommended that "Patients with risk factors associated with hypovitaminosis (obesity, pigmented skin, intestinal malabsorption syndromes and living in regions close to the North and South poles) should increase their intake to up to 4,000 IU per day."

"It is unknown what will happen in the future but we make our recommendations from the EMAS," he concluded. "This is the first statement on the matter in Europe directed towards menopausal women."

 

 

 

Is manganese the missing mineral in osteoporosis?

Reprinted with permission of Life Extension

January 04, 2012. A hypothesis submitted by researchers at the University of Castilla-La Mancha in Spain, published in the January, 2012 Frontiers of Bioscience Elite Edition, suggests that a lack of manganese rather than calcium could be the cause of osteoporosis, a disease characterized by progressive thinning of the bones that is common among older individuals, particularly women.

By studying deer antlers, Tomás Landete of the University's Research Institute of Hunting Resources (IREC) and his associates discovered an association between manganese depleted diets in 2005 and increased breakage. "Previous antler studies show that manganese is necessary for calcium absorption," commented Dr Landete. "Our hypothesis is that when the human body absorbs less manganese or when it is sent from the skeleton to other organs that require it, such as the brain, the calcium that is extracted at the same time is then not properly absorbed and is excreted in the urine. It is in this way that osteoporosis can slowly strike."

"Antlers grow by transferring 20% of the skeleton's calcium towards their structure," he added. "We therefore saw that it was not calcium deficiency that caused the weakening but rather the deficiency of manganese. The lack of manganese was almost as if the 'glue' that sticks calcium to antlers bones was missing."

The researchers suggest that osteoporosis caused by a lack of manganese could precede brain disorders including Alzheimer's and Parkinson's disease. A comparison of 45 osteoporosis patients and 68 subjects with osteoarthritis who underwent surgery between 2008 and 2009 found that 40 percent of those who had osteoporosis exhibited some type of cerebral dysfunction while none of those who had osteoarthritis showed signs of the condition.

"We are collecting human bones to confirm this," Dr Landete stated. "However, studies on rats in which Alzheimer's disease has been induced by aluminum intoxication show that as the severity of this disease increases, manganese levels in the bones decrease."

 

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