 |
|
Reply
| |
Basically, the present situation can be summed up as follows (for "aggressive, common cancers, but we will leave lung cancer aside in this post):
A diet rich in omega 6 polyunsaturated fatty acids and low in antioxidant-rich foods creates the perfect conditions for such cancers (an iron rich diet and some other co-factors also appear to play roles). If you are afflicted with such a cancer, you may be told despite some potentially horrible side effects, one should instead focus on "the positive benefit/risk ratio of Glivec for thousands of patients being treated for cancer and other life-threatening diseases," and that you should take such drugs to "fight the battle against cancer." It is not likely that you will not be told that certain dietary changes may result in complete remission.
Source for that quotation:
http://www.newsday.com/news/politics/wire/sns-ap-cancer-drug-heart-disease,0,3991287.story
Kary Mullis, inventor of PCR testing and Nobel Prize winner, has said in his autobiography that he would not take such drugs because of the toxicities involved. One point that I would make here is that the studies that are trumpeted by the mainstream media as great "successes" in the "war on cancer" are short term and are based upon entirely arbitrary criteria. For example, if a tumor shrinks, they say that it's a great success, even if the patient lives a shorter period of time and suffers terrible side effects. This is the "surrogate endpoint" - any time you are told that a surrogate endpoint is involved, I suggest you investigate the claim very carefully.
If a patient lives a month longer than those not taking the drug, but only lives a few months total (after diagnosis), ain, it's a great success, even if it causes terrible pain. And if a patient lives a certain period of time arbitrarily chosen to denote "success," that is the end of the "story" - the person could die the next day, and usually dies much sooner that people who never took such drugs, but that is not told to the public very often. This is also true for those who are give several blood transfusions in a short period of time.
|
|
|
Reply
| |
A new report sheds light on how the "war on cancer" is being lost:
QUOTE: ...Dr. Caron and colleagues conducted a study to assess the total burden of adverse health outcomes (adverse events) following childhood cancer and evaluated treatment-related risk factors. The study included 1,362 five-year survivors of childhood cancer treated in a single institution in the Netherlands between 1966 and 1996. All survivors were invited to a clinic for medical assessment of adverse events. Medical follow-up was completed for 94.3 percent of survivors (median [midpoint] follow-up, 17.0 years). At the end of follow-up the median age of the survivors was 24.4 years, with 88 percent of survivors younger than 35 years.
The researchers found that of the 1,362 survivors, 19.8 percent had no adverse events, 74.5 percent had one or more events and 24.6 percent had five or more events. Additionally, 36.8 percent of the survivors had at least one severe or life-threatening or disabling disorder, and 3.2 percent died due to an adverse event. Almost 22 percent of adverse events were severe, life-threatening or disabling, or caused death. Of those events, orthopedic disorders occurred most often, followed by second tumors, obesity, fertility disorders, psychosocial or cognitive disorders, neurologic disorders and endocrine disorders.
Of all patients treated with radiotherapy only, 55 percent had a high or severe burden of events (defined as at least two severe events or one or more life-threatening or disabling event), compared with 15 percent of patients treated with chemotherapy only and 25 percent of patients who had surgery only. Survivors of bone tumors most often had a high or severe burden of events (64 percent), while survivors of leukemia or Wilms tumor (tumor of the kidney) least often had a high or severe burden of events (12 percent each).
"In conclusion, childhood cancer survivors are at increased risk of many severe health problems, resulting in a high burden of disease during young adulthood. This will inevitably affect the survivors' quality of life and also will ultimately reduce their life expectancy... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2007/06/070626115406.htm |
|
Reply
| |
QUOTE: Submarines have periscopes. Insects have antennae. And increasingly, biologists are finding that most normal vertebrate cells have cilia, small hair-like structures that protrude like antennae into the surrounding environment to detect signals that control cell growth. In a new study published in the June 29 issue of Cell, Fox Chase Cancer Center researchers describe the strong link between ciliary signaling and cancer and identify the rogue engineers responsible for dismantling the cell's antenna... Why cilia come and go on normal cells is not entirely understood, but scientists increasingly suspect that it may play a role in timing the cell division process. Commonly, cancer cells have entirely lost their cilia, and this absence may help explain why tumors fail to respond properly to environmental cues that cause normal cells to stop growing. Hence, the discovery that too much HEF1 and Aurora A cause cilia to disassemble provides important hints into what may be happening in cancers... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2007/06/070628162636.htm |
|
Reply
| |
A new report on colorectal cancer contains the following passage:
QUOTE: For example, a cancer-causing agent or a hormone may find its way from the bloodstream to the outer membrane of a cell. After its arrival, it sets off a chain of reactions, or signals, inside the cell. Some of these signals take the form of certain enzymes activating others. Eventually, the “news�?reaches the genetic material inside the cell nucleus, where changes resulting in uncontrolled growth--cancer--or some other cell behavior are made. UNQUOTE.
Unfortunately, as seems to be the rule rather than the exception, the authors of this study being reported on do not appear to realize that AA metabolites probably are the main "cancer causing agent" in most cases of colorectal cancer in the West.
Source of passage cited: http://1-news.org/world-news/Study-says-normal-but-out-of-control-enzyme
-may-be-culprit-that-signals-some-cells-to-become-cancer/ |
|
Reply
| |
From a new study:
"...The main substances that link inflammation to cancer via oxidative/nitrosative stress are prostaglandins and cytokines..."
Source: Int J Cancer. 2007 Sep 24;121(11):2381-2386.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=
ShowDetailView&TermToSearch=17893868&ordinalpos=12&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum |
|
Reply
| |
A new report sheds light on a better and simpler way to understand cancer. It's just to bad most scientists are lost in a world of things like genes, which are rarely the underlying cause of cancer (instead, what "turned on" or damaged the gene is).
QUOTE: "When cells reach the point where they divide constantly, instead of only when needed, they are cancer cells."
Instead, multicellular organisms use a seemingly inefficient process to replace lost cells, Pepper said. An organ such as the skin calls upon skin-specific stem cells to produce intermediate cells that in turn produce skin cells.
Although great at their job, the new skin cells are evolutionary dead ends. The cells cannot reproduce.
Losing the ability to reproduce was part of the evolutionary path single-celled organisms had to take to become multicellular, Pepper said.
What was in it for the single cells?
"Probably they got to be part of something more powerful," Pepper said. "Something that was hard to eat and good at eating other things..."
"Organisms are just a bunch of cells," he said.
"If you understand the conditions under which they cooperate, you can understand the conditions under which cooperation breaks down. Cancer is a breakdown of cooperation..." UNQUOTE.
Source: http://www.sciencedaily.com/releases/2007/12/071219130310.htm |
|
Reply
| |
Here are 2 original studies claiming that EFAD is a promoting condition for tumorigenesis:
Prostaglandins Leukot Essent Fatty Acids. 1997 Mar;56(3):239-44.
Dietary deficiency or enrichment of essential fatty acids modulates tumorigenesis in the whole body of cobalt-60-irradiated mice.
Eynard AR, Manzur T, Moyano A, Quiroga P, Muñoz S, Silva SM.
Instituto Biologia Celular (FCM-UNC), CONICET, Cordoba, Argentina.
The effect of dietary polyunsaturated fatty acids (PUFAs) on whole body-induced tumorigenesis was assayed in mice fed on essential fatty acid sufficient (EFAS) or essential fatty acid deficient (EFAD) diets following cobalt-60 irradiation. Four groups of mice were maintained, one on a control stock diet and three on experimental diets: a) without added fat (fat free, FF); b) containing 5% olein (O), rich in n-9; and c) containing 5% corn oil, rich in n-6 EFA (CO). Only mice fed on FF or O diets showed clinical and biochemical signs of EFAD. Total incidence of tumors showed an increase in FF (P < 0.02) and O (P < 0.03) mice. Tumors developed mostly in the liver in each of the EFAD groups (P < 0.001). Slight promoting activity on lung tumorigenesis was recorded in the CO group when this parameter was compared in EFAD and EFA sufficient mice. It may be concluded that, when a tumor initiator injures the body as a whole, EFAD, achieved either through a fat-free or an oleic-supplemented diet, behaves as a general promoting condition for tumorigenesis. The borderline tumorigenic effect of n-6 corn oil on the lungs suggests that this effect, when present, is target specific.
PMID: 9089806
Nutrition. 1999 Mar;15(3):208-12.
Differential effects of dietary Oenothera, Zizyphus mistol, and corn oils, and essential fatty acid deficiency on the progression of a murine mammary gland adenocarcinoma.
Muñoz SE, Piegari M, Guzmán CA, Eynard AR.
I Cátedra de Histología, FCM, Córdoba, Argentina.
The modulating effect of dietary enrichment in mistol seed oil (MO) containing 25% of alpha-linolenic acid (ALA), evening primrose oil (EPO) enriched in gamma-linolenic acid (GLA) and corn oil (CO) as sources of omega-6 and omega-9 fatty acids on the growth parameters of one transplantable mammary tumor were compared. Mice fed on different lipid formulae were inoculated with a mammary gland adenocarcinoma and different growth development tumor parameters were recorded. Results showed that corn oil feeding slowed down most of the tumor growth parameters, as did the EPO diet. MO also showed antitumor activity. Olein feeding, which induces an essential fatty acid deficiency (EFAD), increased the incidence and the multiplicity of metastases when compared with the controls. It may be concluded that a diet enriched in omega-6 fatty acids did not behave as a tumor promoter in this mammary gland tumor model. The antitumor activities of EPO and MO are corroborated in present experiments, suggesting that both oils may be of value in nutritional approaches of mammary gland tumor therapies. In addition, present data add further experimental proof about the proposed protumorigenic proneness induced by the EFAD state.
PMID: 10198915
and the following study reveals that primose oil fed rats have have 21% fewer carcinomas than the corn oil fed rats despite of having significantly higher AA levels:
Lipids. 1988 Oct;23(10):948-54.
Eicosanoid synthesis in 7,12-dimethylbenz(a)anthracene-induced mammary carcinomas in Sprague-Dawley rats fed primrose oil, menhaden oil or corn oil diet.
Abou-el-Ela SH, Prasse KW, Carroll R, Wade AE, Dharwadkar S, Bunce OR.
Department of Pharmacology and Toxicology, College of Pharmacy, University of Georgia, Athens 30602.
The comparative effects of high-fat diets (20%, w/w) on eicosanoid synthesis during mammary tumor promotion in 7,12-dimethylbenz(a)anthracene (DMBA)-induced rats were studied using diets containing 20% primrose oil (PO), 20% menhaden oil (MO) or 20% corn oil (CO). Sprague-Dawley rats fed the PO or MO diet had 21% of 24% fewer adenocarcinomas, respectively, than rats fed the CO diet. Histologically (i.e., mitotic figures, inflammatory cell infiltration and necrosis), the CO-fed rats exhibited the highest frequency of changes within tumors. Plasma fatty acid composition was significantly altered by diet, reflecting the composition of the oils which were being fed. Only the plasma of PO-fed rats contained detectable levels of gamma-linolenic acid (GLA). Arachidonic acid (AA) levels were significantly higher (p less than 0.05) in PO-fed than in CO- or MO-fed rats. MO-fed rats had significantly higher levels of plasma palmitic acid, while palmitoleic, eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids were detected only in MO-fed rats. As expected, linoleic acid (LA) and AA levels were lower (p less than 0.05) in the MO-fed rats than in PO- or CO-fed groups. The plasma of the CO-fed rats contained significantly higher levels of oleic acid. Eicosanoid synthesis in mammary carcinomas of rats fed the 20%-fat diets was 2-10 times higher than in mammary fat pads of control rats.(ABSTRACT TRUNCATED AT 250 WORDS)
PMID: 3143882
does this mean that AA is protective against cancers?? |
|
Reply
| |
| Corn oil is bad news, and as for the others, once again, if you don't start with animals that have Mead acid in their cells, then AA gets released and on small animals especially can do a lot of damage even in the short term. |
|
Reply
| |
Too bad these kinds of studies get little if any coverage by the "mainstream media:"
QUOTE: Bioactive lipid mediators are increasingly being recognized as important endogenous regulators of cell activation, signaling, apoptosis and proliferation. Most of these lipid mediators are originated from cleavage of constituents of cellular membranes under the activity of phospholipases and sphingomyelinases. One of the major cascades of bioactive lipid mediator production involves the release of arachidonic acid from membrane phospholipids followed by the formation of eicosanoids (i.e. prostaglandins, leukotrienes and lipoxins). These biologically active metabolites of arachidonic acid are emerging as key regulators of cell proliferation and neo-angiogenesis and agents that specifically target these lipid mediators are being investigated as potential anticancer drugs... UNQUOTE.
Source: Recent Patents Anticancer Drug Discov. 2006 Nov;1(3):369-82. |
|
Reply
| |
It's 2005 and the experts are still not sure which dietary factors induce carcinogenesis or blaim it on the genes at best ...
Eur J Obstet Gynecol Reprod Biol. 2005 Dec 1;123(2):139-49.
Nutrition and primary prevention of breast cancer: foods, nutrients and breast cancer risk.Hanf V, Gonder U.
Department of Obstetrics and Gynecology, University of Göttingen, Robert-Koch-Street 40, 37099 Göttingen, Germany.
Worldwide, each year approximately one million women are newly diagnosed with breast cancer (BC), in Germany 65 new cases per 100,000 inhabitants are registered, yearly. The fact that incidence has been rising in parallel with economic development indicates that environmental factors might play a role in the causation of BC. Migrational data have pointed to nutrition as one of the more relevant external factors involved. Preventive dietary advice often includes a reduction of alcohol, red meat and animal fat and increasing the intake of vegetables, fruit and fibre and lately, phyto-estrogens from various sources. Clearly, the scientific basis for these recommendations appears sparse. The available prospective data from epidemiological studies and interventional trials do not support the overall hypothesis that higher fat-intakes are a relevant risk factor for BC development, more important seems the relative distribution of various fatty acids. A non-vegetarian eating habit (consumption of animal products) per se does not elevate BC risk, while consumption of broiled or deep fried meats cannot be ruled out as a risk factor in genetically susceptible individuals. It appears prudent to abstain from regular and increased alcohol consumption. This should be particularly true for pubescent girls, in whom glandular breast tissue is particularly vulnerable. In general, if alcohol is consumed on a regular basis, a sufficient supply of fresh vegetables and fruit is essential. While there is no overall protective effect of a high fruit and vegetable consumption speculation remains over possible beneficial effects of certain subcategories, especially brassica vegetables like broccoli, cauliflower and cabbage. In essence, regional differences in BC incidence are probably partially attributable to life long dietary habits. There is no need to adopt a foreign dietary plan in order to protect oneself against BC. Traditional western diets also have their beneficial ingredients that should be regular constituents in our meals. Lignans from traditionally made sourdough rye bread, linseed/flaxseed and berries are local sources of potentially canceroprotective phyto-estrogens. Furthermore, indole-3-carbinol rich cabbage species might contribute to BC protection by diet. Nevertheless, clear cut recommendations for or against single nutrients or secondary plant metabolites are not yet possible, lacking sufficient data on individual bioavailability, safety and long term outcome. BC prevention by dietary means therefore relies on an individually tailored mixed diet, rich in basic foods and traditional manufacturing and cooking methods.
PMID: 16316809
|
|
Reply
| |
I found an interesting book review on amazon.com (by Joel M. Kauffman) about a book entitled, "The Secret History of the War on Cancer" (by Devra Davis):
If a non-fiction book could be judged by good intentions, the perfect resume of its author, and passion for subject, this book would be rated 5-star. Its main thesis is that environmental exposures, especially workplace exposures, are the primary causes of cancer, and that exposures other than smoking are at least as important as smoking. To make a long story short, this, in my opinion, was not accomplished. What is needed in a book of this sort, besides the anguished tales of slow death from cancer or oncologists, is a clear estimate of what fraction of cancer deaths are caused by smoking, what fraction by chemical exposure, and what fraction by neither. Nothing of the sort was done. There were too few numbers and too much innuendo.
The form is good in that there is a good index and many citations with numbers in the text (the best way). Unfortunately, so many claims or suppositions are made that ten times the number of citations would not have supported them all. Writing is easy to read, with some occasional grammatical slips and misspellings.
Example after example of hazardous exposures were given, some dating back and well-known from the 18th century (scrotal cancer in chimney sweeps), workers in chemical plants using the dye intermediates (precursors) 2-aminonaphthalene and benzidine, radium-dial watch painters, blacksmiths, miners of all kinds, and many others. In no case were the cancers observed quantified so we can see how serious the numbers were by the usual method of toxicologists: deaths per 100,000 of population exposed per year. Many examples of concealing these cancers are given; this is very well done.
One of the ploys of Big Pharma in overpromoting its drugs was used throughout -- relative risk (RR) with no absolute risk (usually). And for the same reason: RR always gives bigger numbers. If you do something beneficial and the absolute risk (AR) drops from 2 in a 1,000,000 to 1 in a 1,000,000, that would be presented as a RR=0.5 or 50%, or a drop in risk of 50%, which sounds bigger. Every chart (seemingly) or table has some error in it, such as the Y-axes had no units, just numbers, but numbers of what? Or a study of electromagnetic effects that fails to include the numbers of those most exposed, even while presenting the numbers of those not exposed, and thus only RR is seen, and AR cannot be calculated.
The utter nonsense that all ionizing radiation is dangerous is in full bloom here. Never mind the facts -- that we are hit with about 1,600,000 cosmic rays per minute as determined using plastic scintillator detectors the size and shape of the human body. Study after study has shown that exposures to Xrays at 5-15 rads per year lowers cancer rates. See: Joel M. Kauffman, "Radiation Hormesis: Demonstrated, Deconstructed, Denied, Dismissed, and Some Implications for Public Policy", J. Scientific Exploration , 17(3), 389-407 (2003). To top it off, Davis worries about Xray exposure in medical imaging of .017 cGy/yr (rad/yr) for a dental set, 0.4 for a mammogram, and 6 for a body CT scan, yet hardly blinks at the typical 6000 cGy given to a cancer victim. Note that ID, CO and NM, with a background radiation level of 0.72 cG/yr have 20% lower cancer rates than AL, LA, MS with 0.22 cG/yr. Many such examples exist.
Contrarily, the Donora, PA, deadly smog of 1948 was cited repeatedly, as it was the parental home of Davis; but never with a hint that the deadly agent was some form of fluoride. See: Bryson C (2004). The Fluoride Deception, New York, NY: Seven Stories Press. Fluoride ion causes a 10% increase in over all cancer rates, including bone, breast and lung. To me it is inconceivable that a big treatise on enviromental carcinogens could leave out fluoride ion. The RR of bone cancer in boys who drink fluoridated town water is 4-7 fold (RR=4-7). See: Bassin EB et al., Age-specific fluoride exposure in drinking water and osteosarcoma (United States), Cancer Causes Control 2006;17:421-428.
And the very title of this book is misleading. The "War on Cancer" has always meant research on treatment, not the causes. The mostly useless standard treatments are not criticised for the painful waste that they are, and no promising alternative was ever even hinted at. See: Fisher B, Jeong J-H, Anderson S, Bryant J, Fisher ER, Wolmark N ( 2002). Twenty-Five-Year Follow-Up of a Randomized Trial Comparing Radical Mastectomy, Total Mastectomy, and Total Mastectomy Followed by Irradiation. New England Journal of Medicine 347(8):567-575; Moss RW (2000). Questioning Chemotherapy, Brooklyn, NY: Equinox Press.
When you have looked over the 127 questionable statements that are vetted below (or e-mail [email protected]), and you remember that only 2 or 3 serious errors will make a reader suspicious of everything in such a book, you will probably agree that Davis is less credible than she might have been, even in areas where she may be correct.
Source: http://tinyurl.com/34dvg8 |
|
Reply
| |
| This message has been deleted by the manager or assistant manager. |
|
Reply
| |
Here's a passage from a new report about "ground-breaking research:"
QUOTE: Researchers at the OU Cancer Institute have identified a new gene that causes cancer. The ground-breaking research appears April 28 in Nature’s cancer journal Oncogene.
The gene and its protein, both called RBM3, are vital for cell division in normal cells. In cancers, low oxygen levels in the tumors cause the amount of this protein to go up dramatically. This causes cancer cells to divide uncontrollably, leading to increased tumor formation... UNQUOTE.
Notice that they essentially discovered something technical (the exact gene and protein), because these "cancer causing" molecules are vital for life. The low oxygen connection to cancer is "old news." If the gene can be "turned off" in the tumor without doing any harm to other cells, it could be a "cure," but it's not clear how easy this will be. Moreover, if there is a lot of stress that led to this problem to begin with, it's likely that some other medical issue will arise, such as organ failure. It seems like many research scientists never even consider that the best they can achieve is delaying a "disease" or swapping one "disease" for another, because they never focus on the underlying stressors that lead to "disease" in the first place.
Source: http://www.sciencedaily.com/releases/2008/05/080508115829.htm |
|
Reply
| |
If cancer were cured, how would that cure be defined? What would the requirements of a cure be? Give some examples of what a cure really is? (use other deseases as an example) |
|
Reply
| |
| These are the questions you need to ask the "experts" who are "fighting the war on cancer." But don't answers that make sense, if you get any response at all. Cancer is usually the result of long-term stressors, which break down cell colony cohesion/coordination. "Inflammation" seems to be crucial, but this can easily be controlled by diet (if "essential fatty acids" are avoided, except in tiny or trace amounts). Once there is cancer present, and especially if it has spread, there may be little one can do, but experiments would need to be done to find out for sure (I'd suggest a diet that includes a lot of fresh coconut oil and a variety of antioxidant-rich food). |
|
Reply
| |
Here's a report that is relevant, though it's not stated how many different antioxidant-rich foods were studied:
http://www.sciencedaily.com/releases/2008/05/080529091128.htm |
|
|
Free Forum Hosting
Important Announcement
First
0 recommendations 
Return to All Message Boards