In labs, Omega 5 oil has shown the potantial
of anti tumor activity against prostate cancer
So, should I drink less milk and use Omega 5 oil soft gel caps instead?
Professor James describes the benefits of the green tech
of POMEGA5
A provocative study from Harvard Medical School shows that men who eat diary products regularly have a 30 percent greater chance of suffering prostate cancer than those who eat less than half a serving per day.
How can this be?
How can this be?
Isn't milk a health food? Many of you will be shocked by these findings, but this study is the largest done yet, it is done by arguably the most respected epidemiology teams in the world and there is a physiologic explanation for the results. Milk is loaded with calcium and taking large amounts of calcium lowers blood levels of the body's form of vitamin D called 1,24 dihydroxyvitamin D that prevents cancers (2). Of course, milk is usually fortified with vitamin D, but there is so much more calcium than vitamin D in milk that the extra calcium drains vitamin D from the body.
This study shows that men who take in more than six glasses of vitamin D fortified milk per week have lower levels of vitamin D than those who take in fewer than two glasses. This tells you that you shouldn't believe everything that you hear, even if it comes from scientific studies. These studies imply that you don't need to drink milk and that taking calcium supplements may harm you. Lack of vitamin D is usually caused by lack of sunlight as very few people get the vitamin D that they need from food. Vitamin D deficiency is common in winter, particularly in people who live in the northern parts of the globe and people with dark skin.
1) Results of the Physicians Study presented at the American Association for Cancer Research in San Francisco April 4, 2000. 2) AM Barreto, GG Schwartz, R Woodruff, SC Cramer. 5-hydroxyvitamin D-3, the prohormone of 1,25-dihydroxyvitamin D-3, inhibits the proliferation of primary prostatic epithelial cells.Cancer Epidemiology Biomarkers & Prevention, 2000, Vol 9, Iss 3, pp 265-270. these findings support a potential role for vitamin D in the
Journal of Medicinal Food
Pomegranate Extracts Potently Suppress Proliferation, Xenograft Growth, and Invasion of Human Prostate Cancer Cells
To cite this paper:Martin Albrecht, Wenguo Jiang, James Kumi-Diaka, Ephraim P. Lansky, Lyndon M. Gommersall, Amit Patel, Robert E. Mansel, Ishak Neeman, Albert A. Geldof, Moray J. Campbell. Journal of Medicinal Food. September 1, 2004, 7(3): 274-283. doi:10.1089/jmf.2004.7.274.
Martin Albrecht Institute of Anatomy and Cell Biology, Philipps University, Marburg, Germany
Wenguo Jiang University Department of Surgery, University of Wales College of Medicine, Cardiff James Kumi-Diaka Division of Science, College of Liberal Arts, Florida Atlantic University, Davie, Florida, U.S.A. Ephraim P. Lansky Rimonest Ltd. Lyndon M. Gommersall Division of Medical Sciences, University of Birmingham Medical School, Birmingham, United Kingdom Amit Patel Division of Medical Sciences, University of Birmingham Medical School, Birmingham, United Kingdom Robert E. Mansel University Department of Surgery, University of Wales College of Medicine, Cardiff Ishak Neeman Rimonest Ltd. Department of Food Engineering and Biotechnology, Technion-Israel Institute of Technology, Haifa, Israel Albert A. Geldof Departments of Urology and Nuclear Medicine, VU University Medical Center, Amsterdam, The Netherlands Moray J. Campbell Division of Medical Sciences, University of Birmingham Medical School, Birmingham, United Kingdom
We completed a multicenter study of the effects of pomegranate cold-pressed (Oil) or supercritical CO2-extracted (S) seed oil, fermented juice polyphenols (W), and pericarp polyphenols (P) on human prostate cancer cell xenograft growth in vivo, and/or proliferation, cell cycle distribution, apoptosis, gene expression, and invasion across Matrigel, in vitro. Oil, W, and P each acutely inhibited in vitro proliferation of LNCaP, PC-3, and DU 145 human cancer cell lines. The dose of P required to inhibit cell proliferation of the prostate cancer cell line LNCaP by 50% (ED50) was 70 mg/mL, whereas normal prostate epithelial cells (hPrEC) were significantly less affected (ED50 5 250 mg/mL).
These effects were mediated by changes in both cell cycle distribution and induction of apoptosis. For example, the androgen-independent cell line DU 145 showed a significant increase from 11% to 22% in G2/M cells (P , .05) by treatment with Oil (35 µg/mL) with a modest induction of apoptosis. In other cell lines/treatments, the apoptotic response predominated, for example, in PC-3 cells treated with P, at least partially through a caspase 3-mediated pathway. These cellular effects coincided with rapid changes in mRNA levels of gene targets. Thus, 4-hour treatment of DU 145 cells with Oil (35 µg/mL) resulted in significant 2.3 ± 0.001-fold (mean ± SEM) up-regulation of the cyclin-dependent kinase inhibitor p21(waf1/cip1) (P < .01) and 0.6 ± 0.14-fold down-regulation of c-myc (P < .05). In parallel, all agents potently suppressed PC-3 invasion through Matrigel, and furthermore P and S demonstrated potent inhibition of PC-3 xenograft growth in athymic mice.
Overall, this study demonstrates significant antitumor activity of pomegranate-derived materials against human prostate cancer.
Journal of Medicinal Food
Chemopreventive Effects of Pomegranate Seed Oil on Skin Tumor Development in CD1 Mice
To cite this paper:Justin J. Hora, Emily R. Maydew, Ephraim P. Lansky, Chandradhar Dwivedi. Journal of Medicinal Food. October 1, 2003, 6(3): 157-161. doi:10.1089/10966200360716553.
Justin J. Hora Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD, U.S.A Emily R. Maydew Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD, U.S.A Ephraim P. Lansky
Rimonest Ltd., Horev Center, Haifa, Israel Chandradhar Dwivedi Department of Pharmaceutical Sciences, College of Pharmacy, South Dakota State University, Brookings, SD, U.S.A
Pomegranate seed oil was investigated for possible skin cancer chemopreventive efficacy in mice.
In the main experiment, two groups consisting each of 30, 4-5-week-old, female CD1 mice were used. Both groups had skin cancer initiated with an initial topical exposure of 7,12-dimethylbenzanthracene and with biweekly promotion using 12-O-tetradecanoylphorbol 13-acetate (TPA). The experimental group was pretreated with 5% pomegranate seed oil prior to each TPA application.
Tumor incidence, the number of mice containing at least one tumor, was 100% and 93%, and multiplicity, the average number of tumors per mouse, was 20.8 and 16.3 per mouse after 20 weeks of promotion in the control and pomegranate seed oil-treated groups, respectively (P < .05).
In a second experiment, two groups each consisting of three CD1 mice were used to assess the effect of pomegranate seed oil on TPA-stimulated ornithine decarboxylase (ODC) activity, an important event in skin cancer promotion. Each group received a single topical application of TPA, with the experimental group receiving a topical treatment 1 h prior with 5% pomegranate seed oil. The mice were killed 5 h later, and ODC activity was assessed by radiometric method. The experimental group showed a 17% reduction in ODC activity. Pomegrante seed oil (5%) significantly decreased (P < .05) tumor incidence, multiplicity, and TPA-induced ODC activity.
Overall, the results highlight the potential of pomegranate seed oil as a safe and effective chemopreventive agent against skin cancer.
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On January 23, 1998 researchers at the Harvard Medical School released a major study providing conclusive evidence that IGF-1 is a potent risk factor for prostate cancer. Should you be concerned? Yes, you certainly should, particularly if you drink milk produced in the United States.
IGF-1 or insulin-like growth factor 1 is an important hormone that is produced in the liver and body tissues. It is a polypeptide and consists of 70 amino acids linked together. All mammals produce IGF-1 molecules very similar in structure and human and bovine IGF-1 are completely identical. IGF-1 acquired its name because it has insulin-like activity in fat (adipose) tissue and has a structure that is very similar to that of proinsulin. The body's production of IGF-1 is regulated by the human growth hormone and peaks at puberty. IGF-1 production declines with age and is only about half the adult value at the age of 70 years. IGF-1 is a very powerful hormone that has profound effects even though its concentration in the blood serum is only about 200 ng/mL or 0.2 millionth of a gram per milliliter (1-4).
IGF-1 and cancer
IGF-1 is known to stimulate the growth of both normal and cancerous cells(2,5). In 1990 researchers at Stanford University reported that IGF-1 promotes the growth of prostate cells(2). This was followed by the discovery that IGF-1 accelerates the growth of breast cancer cells(6-8). In 1995 researchers at the National Institutes of Health reported that IGF-1 plays a central role in the progression of many childhood cancers and in the growth of tumours in breast cancer, small cell lung cancer, melanoma, and cancers of the pancreas and prostate(9). In September 1997 an international team of researchers reported the first epidemiological evidence that high IGF-1 concentrations are closely linked to an increased risk of prostate cancer(10). Other researchers provided evidence of IGF-1's link to breast and colon cancers(10,11).
The January 1998 report by the Harvard researchers confirmed the link between IGF-1 levels in the blood and the risk of prostate cancer. The effects of IGF-1 concentrations on prostate cancer risk were found to be astoundingly large - much higher than for any other known risk factor. Men having an IGF-1 level between approximately 300 and 500 ng/mL were found to have more than four times the risk of developing prostate cancer than did men with a level between 100 and 185 ng/mL. The detrimental effect of high IGF-1 levels was particularly pronounced in men over 60 years of age. In this age group men with the highest levels of IGF-1 were eight times more likely to develop prostate cancer than men with low levels. The elevated IGF-1 levels were found to be present several years before an actual diagnosis of prostate cancer was made(12).
The evidence of a strong link between cancer risk and a high level of IGF-1 is now indisputable. The question is why do some people have high levels while others do not? Is it all genetically ordained or could it be that diet or some other outside factor influences IGF-1 levels? Dr. Samuel Epstein of the University of Illinois is one scientist who strongly believes so. His 1996 article in the International Journal of Health Sciences clearly warned of the danger of high levels of IGF-1 contained in milk from cows injected with synthetic bovine growth hormone (rBGH). He postulated that IGF-1 in rBGH-milk could be a potential risk factor for breast and gastrointestinal cancers(13).
The milk connection
Bovine growth hormone was first synthesized in the early 1980s using genetic engineering techniques (recombinant DNA biotechnology). Small-scale industry-sponsored trials showed that it was effective in increasing milk yields by an average of 14 per cent if injected into cows every two weeks. In 1985 the Food and Drug Administration (FDA) in the United States approved the sale of milk from cows treated with rBGH (also known as BST) in large-scale veterinary trials and in 1993 approved commercial sale of milk from rBGH-injected cows(13-16). At the same time the FDA prohibited the special labeling of the milk so as to make it impossible for the consumer to decide whether or not to purchase it(13).
Concerns about the safety of milk from BST-treated cows were raised as early as 1988 by scientists in both England and the United States(14,15,17-22). One of the main concerns is the high levels of IGF-1 found in milk from treated cows; estimates vary from twice as high to 10 times higher than in normal cow's milk(13,14,23). There is also concern that the IGF-1 found in treated milk is much more potent than that found in regular milk because it seems to be bound less firmly to its accompanying proteins(13). Consultants paid by Monsanto, the major manufacturer of rBGH, vigorously attacked the concerns. In an article published in the Journal of the American Medical Association in August 1990 the consultants claimed that BST-milk was entirely safe for human consumption(16,24). They pointed out that BST-milk contains no more IGF-1 than does human breast milk - a somewhat curious argument as very few grown-ups continue to drink mother's milk throughout their adult life. They also claimed that IGF-1 would be completely broken down by digestive enzymes and therefore would have no biological activity in humans(16). Other researchers disagree with this claim and have warned that IGF-1 may not be totally digested and that some of it could indeed make its way into the colon and cross the intestinal wall into the bloodstream. This is of special concern in the case of very young infants and people who lack digestive enzymes or suffer from protein-related allergies(13,14,20,22,25).
Researchers at the FDA reported in 1990 that IGF-1 is not destroyed by pasteurization and that pasteurization actually increases its concentration in BST-milk. They also confirmed that undigested protein could indeed cross the intestinal wall in humans and cited tests which showed that oral ingestion of IGF-1 produced a significant increase in the growth of a group of male rats - a finding dismissed earlier by the Monsanto scientists(25). The most important aspect of these experiments is that they show that IGF-1 can indeed enter the blood stream from the intestines - at least in rats.
Unfortunately, essentially all the scientific data used by the FDA in the approval process was provided by the manufacturers of rBGH and much of it has since been questioned by independent scientists. The effect of IGF-1 in rBGH-milk on human health has never actually been tested and in March 1991 researchers at the National Institutes of Health admitted that it was not known whether IGF-1 in milk from treated cows could have a local effect on the esophagus, stomach or intestines(26,27).
Whether IGF-1 in milk is digested and broken down into its constituent amino acids or whether it enters the intestine intact is a crucial factor. No human studies have been done on this, but recent research has shown that a very similar hormone, Epidermal Growth Factor, is protected against digestion when ingested in the presence of casein, a main component of milk(13,23,28). Thus there is a distinct possibility that IGF-1 in milk could also avoid digestion and make its way into the intestine where it could promote colon cancer(13,22). It is also conceivable that it could cross the intestinal wall in sufficient amounts to increase the blood level of IGF-1 significantly and thereby increase the risk of breast and prostate cancers(13,14).
The bottom line
Despite assurances from the FDA and industry-paid consultants there are now just too many serious questions surrounding the use of milk from cows treated with synthetic growth hormone to allow its continued sale. Bovine growth hormone is banned in Australia, New Zealand and Japan. The European Union has maintained its moratorium on the use of rBGH and milk products from BST-treated cows are not sold in countries within the Union. Canada has also so far resisted pressure from the United States and the biotechnology lobby to approve the use of rBGH commercially. In light of the serious concerns about the safety of human consumption of milk from BST-treated cows consumers must maintain their vigilance to ensure that European and Canadian governments continue to resist the pressure to approve rBGH and that the FDA in the United States moves immediately to ban rBGH-milk or at least allow its labeling so that consumers can protect themselves against the very real cancer risks posed by IGF-1.
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