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QuoteSo another factor is needed to justify the expansion of the mutated clone.Toxoplasma could be one of a restricted group of germs capable of jamming some crucial point of the complex immune reaction (involving T-cells, macrophages, complex cytokine interactions) evoked by protozoa and other 'fastidious' germs.Helicobacter pylori and mycoplasmas might be in the number.Another 'coincidence' buried in a prestigiousjournal like the New England J. of Medicine ten years ago. Everybody laugh when I saythat the real title should actually be: "A Mother Nature's Lecture on CML" Spontaneous remission in a patient with chronic myelogenous leukemia. Musashi M, Abe S, Yamada T, Tanaka J, Gotohda Y, Maeda S, Sato Y, Morioka M, Sakurada K, Minagawa T, Asaka M, Miyazaki T. Third Department of Internal Medicine, Sapporo, Japan.N Engl J Med. 1997 Jan 30;336(5):337-9.Unfortunately there is no abstract and full-text is not free, but as aNEJMed subscriber I think I am allowed to write a short summary for you:QuoteCase ReportA 45-year-old man was referred to our hospital for evaluation of leukocytosis in January 1985. Three months previously, he had reported tarry stools.A peptic ulcer was diagnosed and treated with intravenous cimetidine. At that time, leukocytosis, thrombocytosis, and anemia were detected. A bone marrow aspirate showed marked myeloid hyperplasia. Cytogenetic analysis revealed Ph-positive cells in the bone marrow, and a diagnosis of CML was made. During the next month the leukocyte count decreased to 14,400 per cubic millimeter, but it subsequently gradually increased to 31,800 per cubic millimeter before admission to our hospital. Physical examination on admission revealed anemia and mild hepatosplenomegaly. A complete blood count again showed leukocytosis and thrombocytosis. The neutrophil alkaline phosphatase score was 94 (normal range, 170 to 335). Plasma histamine and prostaglandin E concentrations were within the normal range.An endoscopic examination revealed an ulcer scar in the duodenal bulb. Regular follow-up, without chemotherapy, was planned for the patient. In February 1985, the hepatosplenomegaly disappeared. The leukocyte count and platelet count returned to normal in April 1985. As of January 30, 1996, the patient had been well, without any signs of recurrence, for 11 years. Blood counts since June 30, 1994, have been normal.... In 1984 the 'infectious theory' of peptic ulcer was still a matter of debate (1).Consequently the word helicobacter cannot be found through the whole text (but it's a 1997 paper!).Intravenous cimetidine had been available for several years, and found quite useful for healing peptic ulcers, and probably making life difficult to H. pylori as well.In the past, cimetidine had been reported to have also an immunomodulating activity.Something surely happened in that patient during the following weeks and months, and chronic myeloid leukemia (confirmed by more sophisticated tests over the following years) pulled back gently.Average survival rate for CML was about <5 years then, with 1/3chance to find a donor for BMT.In 2000 STI571-Gleevec-Imatinib (2pills/day - no BMT) finally came and life became much easier for CML patients. According to some distiguished scientists, this new drug actually represents, in oncology, the most important achievement in the last two decades.Thanks to Dr. Brian Druker and his colleagues from Oregon.In 2000 that japanese man just turned 60, hopefully healthy and CML free.ikod [^] 1) click down here for "Helicobacter connection"Quote from: iko on 30/08/2006 15:50:28QuoteCML TreatmentTreatment options and outcome from treatment have improved significantly over the years. Year Treatment Survival (months) 1920-1950 Splenic irradiation 28 1950-1960 Busulfan 35-45 1960-1970 Hydroxyurea 48-67 1970-1980 1st Allogeneic Stem Cell Transplant for CML 50-60% CURE 1980-1990 IFNa (Interferon alpha) 55-89 1990-2001 IFNa + Cytosine arabinoside (Ara-C) Recent studies showing significant improvement over IFNa alone 1995-2001 STI-571 >90% 5yrs survival (2007)Table 1. Treatment options and survival. (JAMA, August 22/29 p. 896)modified from: http://intmedweb.wfubmc.edu/grand_rounds/2001/myeloid.html
So another factor is needed to justify the expansion of the mutated clone.Toxoplasma could be one of a restricted group of germs capable of jamming some crucial point of the complex immune reaction (involving T-cells, macrophages, complex cytokine interactions) evoked by protozoa and other 'fastidious' germs.Helicobacter pylori and mycoplasmas might be in the number.
Case ReportA 45-year-old man was referred to our hospital for evaluation of leukocytosis in January 1985. Three months previously, he had reported tarry stools.A peptic ulcer was diagnosed and treated with intravenous cimetidine. At that time, leukocytosis, thrombocytosis, and anemia were detected. A bone marrow aspirate showed marked myeloid hyperplasia. Cytogenetic analysis revealed Ph-positive cells in the bone marrow, and a diagnosis of CML was made. During the next month the leukocyte count decreased to 14,400 per cubic millimeter, but it subsequently gradually increased to 31,800 per cubic millimeter before admission to our hospital. Physical examination on admission revealed anemia and mild hepatosplenomegaly. A complete blood count again showed leukocytosis and thrombocytosis. The neutrophil alkaline phosphatase score was 94 (normal range, 170 to 335). Plasma histamine and prostaglandin E concentrations were within the normal range.An endoscopic examination revealed an ulcer scar in the duodenal bulb. Regular follow-up, without chemotherapy, was planned for the patient. In February 1985, the hepatosplenomegaly disappeared. The leukocyte count and platelet count returned to normal in April 1985. As of January 30, 1996, the patient had been well, without any signs of recurrence, for 11 years. Blood counts since June 30, 1994, have been normal....
CML TreatmentTreatment options and outcome from treatment have improved significantly over the years. Year Treatment Survival (months) 1920-1950 Splenic irradiation 28 1950-1960 Busulfan 35-45 1960-1970 Hydroxyurea 48-67 1970-1980 1st Allogeneic Stem Cell Transplant for CML 50-60% CURE 1980-1990 IFNa (Interferon alpha) 55-89 1990-2001 IFNa + Cytosine arabinoside (Ara-C) Recent studies showing significant improvement over IFNa alone 1995-2001 STI-571 >90% 5yrs survival (2007)Table 1. Treatment options and survival. (JAMA, August 22/29 p. 896)modified from: http://intmedweb.wfubmc.edu/grand_rounds/2001/myeloid.html
"Paradoxical results are not uncommon in studies of carcinogenesis. Ignoring these paradoxes is tantamount to saying the prevailing theory holds in all instances except the paradoxycal cases. However ignoring "outliers" in data analysis is not satisfying; it should be the last refuge when all else fails. But more importantly, ignoring paradoxycal results means missing potentially exciting news avenues for research. Rather than relegate the paradoxycal results to the periphery of investigations, they should be the centerpiece of a paradox-driven research portfolio."Summary in: "Paradoxes in carcinogenesis: New opportunities fo research directions."Stuart G Baker and Barnett S KramerBMC Cancer 2007, 7:151this article is available from: http://www.biomedcentral.com/1471-2407/7/151
Outdoor activities and diet in childhood and adolescence relate to MS risk above the Arctic Circle.Kampman MT, Wilsgaard T, Mellgren SI.Dept. of Neurology, University Hospital of North Norway, P.O. Box 33, 9038, Tromsø, Norway.BACKGROUND : A relationship between the latitude-related distribution of multiple sclerosis (MS) and exposure to sunlight has long been considered. Higher sun exposure during early life has been associated with decreased risk of MS.OBJECTIVE : Since Norway is an exception to the latitude gradient of MS prevalence, we tested here whether sunlight exposure or vitamin D-related dietary factors in childhood and adolescence are associated with the risk of MS.METHODS : Retrospective recall questionnaire data from 152 MS patients and 402 population controls born at and living at latitudes 66-71 degrees N were analysed by means of conditional logistic regression analysis accounting for the matching variables age, sex, and place of birth.RESULTS : Increased outdoor activities during summer in early life were associated with a decreased risk of MS, most pronounced at ages 16-20 years (odds ratio (OR) 0.55, 95% CI 0.39-0.78, p = 0.001, adjusted for intake of fish and cod-liver oil).A protective effect of supplementation with cod-liver oil was suggested in the subgroup that reported low summer outdoor activities (OR 0.57, 95% CI 0.31-1.05, p = 0.072).Consumption of fish three or more times a week was also associated with reduced risk of MS (OR 0.55, 95% CI 0.33-0.93, p = 0.024).CONCLUSION : Summer outdoor activities in childhood and adolescence are associated with a reduced risk of MS even north of the Arctic Circle. Supplemental cod-liver oil may be protective when sun exposure is less, suggesting that both climate and diet may interact to influence MS risk at a population level.J Neurol. 2007 Apr;254(4):471-7. Epub 2007 Mar 21.http://www.v1biz.com.au/totaladventures/pics/picsforpages/kids.jpg...found searching for 'outdoor activities' on Google Images
...from 1923 to 2007, a jump into the new century millennium!Quote from: iko on 30/03/2007 13:08:55CodPics...Vitamin D3 http://www.axxora.com/files/formula/LKT-C0145.gifhttp://www.photomed.de/uploads/pics/vitamin_d3_01.jpghttp://botecoliterario.files.wordpress.com/2007/08/sun.gifhttp://www.teridanielsbooks.com/States/Florida/children,%20beach,%20sand,.jpgAn estimate of cancer mortality rate reductions in Europe and the USwith 1,000 IU of oral vitamin D per day.Grant WB, Garland CF, Gorham ED. Sunlight, Nutrition and Health Research Center, San Francisco, CA 94109-2510, USA.Solar ultraviolet B (UVB) irradiance and/or vitamin D have been found inversely correlated with incidence, mortality, and/or survival rates for breast, colorectal, ovarian, and prostate cancer and Hodgkin's and non-Hodgkin's lymphoma. Evidence is emerging that more than 17 different types of cancer are likely to be vitamin D-sensitive. A recent meta-analysis concluded that 1,000 IU of oral vitamin D per day is associated with a 50% reduction in colorectal cancer incidence. Using this value, as well as the findings in a multifactorial ecologic study of cancer mortality rates in the US, estimates for reductions in risk of vitamin D-sensitive cancer mortality rates were made for 1,000 IU/day. These estimates, along with annual average serum 25-hydroxyvitamin D levels, were used to estimate the reduction in cancer mortality rates in several Western European and North American countries that would result from intake of 1,000 IU/day of vitamin D. It was estimated that reductions could be 7% for males and 9% for females in the US and 14% for males and 20% for females in Western European countries below 59 degrees. It is proposed that increased fortification of food and increased availability of supplements could help increase vitamin D intake and could augment small increases in production of vitamin D from solar UVB irradiance. Providing 1,000 IU of vitamin D per day for all adult Americans would cost about $1 billion; the expected benefits for cancer would be in the range of $16-25 billion in addition to other health benefits of vitamin D.Recent Results Cancer Res. 2007;174:225-34.
CodPics...Vitamin D3 http://www.axxora.com/files/formula/LKT-C0145.gifhttp://www.photomed.de/uploads/pics/vitamin_d3_01.jpghttp://botecoliterario.files.wordpress.com/2007/08/sun.gifhttp://www.teridanielsbooks.com/States/Florida/children,%20beach,%20sand,.jpg
Some friend enjoyed this page from 'New Theories', so I thought to resuscitate it into 'Physiol.& Med.' for the fun of our Newbies and medical students.The discussion is open:are there other forms of cancer switched on by 'innocent' infectious agents?QuoteAll cancers are fungus related" is a blanket statement that is just incorrect. Perhaps some cancers are caused by certain fungal infections I just don't know. I do know however that all of them are not.Mjhavok Shortly, we should be careful not to generalize so much talking about cancer. We fortunately live in a new century and scientific research has done something about it. At least we should talk about different forms of tumors, leukemias and lymphomas. In some particular case scientists finally managed to find a cause and design effective and specific treatments (without toxicity, compared to chemotherapy). A type of slow growing gastrointestinal lymphomas called MALTomas (Mucosa Associated Lymphoid Tissue) had been treated by standard chemotherapy (CHOP protocol...what a name for a chemo!) until the end of the last century.There was no suggestion about the origin of this clonal expansion of lymphoid cells in the gut. So the following action had to be blind and toxic.But in the middle of the '80s two smart researchers from Australia, Barry J. Marshall and J. Robin Warren (Nobel Prize 2005) started their battle: they tried to demonstrate that a common bacteria, Helicobacter pylori, was the major cause of gastroduodenal ulcers in humans.A standard antibiotic treatment was able to eradicate the bacteria, allowing the ulcers (wounds in the mucosa) to heal spontaneously.http://www.asm.org/ASM/files/ccLibraryFiles/Filename/000000001924/nobelists%20copy.gifThey initially got veggies and bananas at medical meetings, nevertheless they went on collecting more and more evidence to prove the "infectious theory" of peptic ulcer.It had to be tough. Medicine is highly conservative for various reasons, and for a long time infectious diseases had been strictly defined: one bacteria, one disease. Helicobacter pylori is very common in humans...but just few of us develop ulcers. That was just enough to keep stalling any bright theory for years.Finally H.p. eradication became the standard treatment.Now there is growing evidence that persistent Helicobacter infection and continuous release of toxic substances for years, could be one of the causes of stomach cancer. "...tumors: wounds that never healed..." "...leukemia&lymphoma: infections never resolved..."Shortly after it was found that the majority of the patients with MALT lymphomas were carrying H.p. and that eradication therapy alone was able to induce a spontaneous regression of the tumors.It was obviously too good to be true, so over the years some patients were found to be resistant to antibiotic treatment (2-3 weeks, no chemo!) and their lymphomas where identified as more advanced, with more chromosomal damage, unable to stop growing even when the bacterial stimuli were removed by eradication treatment.Here we have a model for cancer treatment:SPOT the cause (if there is any, but never stop searching), remove it as fast as you can. Some clone of cells will STOP proliferating and gradually disappear.In advanced cases, most cells have been damaged so much and their DNA heavily deranged, that they cannot stop dividing (even in cell cultures). Trying to block these resistant cells, scientists are now assemblying properly designed molecules, non-toxic "magic bullets" that should take advantage of the great differences at molecular level showed by some tumor cells (abnormal receptors, defective enzymes, etc.). Time runs fast for everybody, patients and scientists.ikodH. pylori in a gastric pithttp://www.pathguy.com/lectures/nejm_h_pylori.gifRobert M. Genta, M.D. David Y. Graham, M.D. Veterans Affairs Medical CenterHouston, TX 77030N.Engl.J.Med. 1996;335:250 Jul 25, 1996. Images in Clinical Medicine
All cancers are fungus related" is a blanket statement that is just incorrect. Perhaps some cancers are caused by certain fungal infections I just don't know. I do know however that all of them are not.Mjhavok
Quote from: Zoey on 23/03/2007 03:36:52Iko, You always post such interesting and useful information. The distinction you draw between the various disorders, "tumors, lymphomas, leukemias," is much needed to minimize confusion from grouping them into a single heading, as creates major confusion in figuring out how to deal with other disorders such as seizures. Of course, this discussion would not be well rounded without turning to how helicobacter pylori might be affected by cod liver oil. A search on the net returned me to one of your posts... not at all surprising.ZoeyThank you for appreciating my efforts to tell (in English!) the H.pylori story.It is a crucial example of a slow medical research achievement due to...multiple factors! Bacteria were found much before, but the Koch's criteria for infectious disease were not satisfied, so it couldn't be an infectious problem.As I wrote above, it HAD to be tough.Now again for leukemia: sometimes you find active infections or a recent common pathogen's 'visit' before diagnosis, but patients are immune suppressed by the leukemia itself, then by the treatment, so those are 'opportunistic' infections. It could be the opposite at least in a few cases, an infection switching an overidden immune response and boosting an overgrowth of white cells (clones). In some case it might be possible to stop the process by eradicating the offending germ (bacteria, viruses, protozoa?) and reverse the cell proliferation.It really is a PERSONAL opinion only.Very few spontaneous remissions of acute leuk had been reported after heavy antibiotic treatment at diagnosis for fever and septic presentation, even quite recently, but this is obviously not enough. If I get leuk tomorrow, please put me a drip of at least 3 types of intravenous antibiotics for 2-3 weeks, after that I'll consider chemo (I feel too old for that!). If any of the previous hypotheses were real, most of the investigation work should still have to be started from the very beginning. And all this could take ages.I'd feel quite better knowing that I'm perfectly and totally wrong.Cod liver oil. In all this mess of hypotheses and mechanisms to be proven, CLO stands with its serendipitously-found-epidemiological-2decades-old-evidence ready to be used, but still far away from demonstrating anything or shedding any light on this mystery.This is not the H.pylori case. There you have a very well known germ, you see it and kill it 99% by 2-3 weeks of specific non-toxic treatment. And that's it.Even some naughty MALTomas, intestinal lymphomas, regress and disappear: how beautiful!It wouldn't make sense to look for an alternative treatment there; actually this has been done before. Garlic had been reported to 'prevent' stomach cancer, and now it has been tested against H.p., but it eradicates it in less than 30%...and so does Vitamin C. Nobody would choose this type of performance now that we know the whole story and fortunately have a 99% efficacy.I am so glad that those two nice guys got their well deserved Nobel Prize in 2005!I hope I explained my point in a proper way.Cheers,ikod
Iko, You always post such interesting and useful information. The distinction you draw between the various disorders, "tumors, lymphomas, leukemias," is much needed to minimize confusion from grouping them into a single heading, as creates major confusion in figuring out how to deal with other disorders such as seizures. Of course, this discussion would not be well rounded without turning to how helicobacter pylori might be affected by cod liver oil. A search on the net returned me to one of your posts... not at all surprising.Zoey
As far as this topic is concerned, one thing should be noticed: the 'Shanghai Report' is not mentioned, probably because of its unconfirmed data and weak evidence. But decreased lymphoma incidence (40% reduced risk) due to proper sunlight exposure is reported, and a specific reference quoted:Family history of hematopoietic malignancy and risk of lymphoma.Chang ET, Smedby KE, Hjalgrim H, Porwit-MacDonald A, Roos G, Glimelius B, Adami HO.Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. ellen.chang@meb.ki.seBACKGROUND: A family history of hematopoietic malignancy is associated with an increased risk of non-Hodgkin lymphoma (NHL) and Hodgkin lymphoma (HL), although the magnitude of the relative risk is unclear. We estimated the association between familial hematopoietic cancer and risk of lymphoma using validated, registry-based family data, and we also investigated whether associations between some environmental exposures and risk of lymphoma vary between individuals with and without such a family history. METHODS: In a population-based case-control study of malignant lymphoma, 1506 case patients and 1229 control subjects were linked to the Swedish Multi-Generation Register and then to the Swedish Cancer Register to ascertain history of cancer in first-degree relatives of patients with malignant lymphoma. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations with the risk of lymphoma.RESULTS: A history of hematopoietic malignancy in any first-degree relative was associated with an increased risk of all NHL (OR = 1.8, 95% CI = 1.2 to 2.5), common B-cell NHL subtypes, and HL. Relative risks were generally stronger in association with sibling hematopoietic cancer (OR for all NHL = 3.2, 95% CI = 1.3 to 7.6) than with parental hematopoietic cancer (OR = 1.6, 95% CI = 1.1 to 2.3). A family history of NHL or chronic lymphocytic leukemia (CLL) was associated with an increased risk of several NHL subtypes and HL, whereas familial multiple myeloma was associated with a higher risk of follicular lymphoma. There was no statistically significant heterogeneity in NHL risk associations with environmental factors between individuals with and without familial hematopoietic malignancy.CONCLUSIONS: The increased risk of NHL and HL among individuals with a family history of hematopoietic malignancy was approximately twofold for both lymphoma types. There was no evidence that etiologic associations varied between familial NHL and nonfamilial NHL.J Natl Cancer Inst. 2005 Oct 5;97(19):1466-74.
Ultraviolet radiation exposure and risk of malignant lymphomas.Smedby KE, Hjalgrim H, Melbye M, Torrång A, Rostgaard K, Munksgaard L, Adami J, Hansen M, Porwit-MacDonald A, Jensen BA, Roos G, Pedersen BB, Sundström C, Glimelius B, Adami HO.Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, SE-171 77 Stockholm, Sweden. karin.ekstrom@meb.ki.seBACKGROUND: The incidence of malignant lymphomas has been increasing rapidly, but the causes of these malignancies remain poorly understood. One hypothesis holds that exposure to ultraviolet (UV) radiation increases lymphoma risk. We tested this hypothesis in a population-based case-control study in Denmark and Sweden.METHODS: A total of 3740 patients diagnosed between October 1, 1999, and August 30, 2002, with incident malignant lymphomas, including non-Hodgkin lymphoma, chronic lymphocytic leukemia, and Hodgkin lymphoma, and 3187 population controls provided detailed information on history of UV exposure and skin cancer and information on other possible risk factors for lymphomas. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated by logistic regression. Statistical tests were two-sided.RESULTS: Multivariable-adjusted analyses revealed consistent, statistically significant negative associations between various measures of UV light exposure and risk of non-Hodgkin lymphoma. A high frequency of sun bathing and sunburns at age 20 years and 5-10 years before the interview and sun vacations abroad were associated with 30%-40% reduced risks of non-Hodgkin lymphoma (e.g., for sunbathing four times a week or more at age 20 versus never sunbathing, OR = 0.7, 95% CI = 0.6 to 0.9; for two or more sunburns a year at age 20 versus no sunburns, OR = 0.6, 95% CI = 0.5 to 0.. These inverse associations increased in strength with increasing levels of exposure (all P(trend)< or =.01). Similar, albeit weaker, associations were observed for Hodgkin lymphoma. There were no clear differences among non-Hodgkin lymphoma subtypes, although associations were stronger for B-cell than for T-cell lymphomas. A history of skin cancer was associated with a doubling in risks of both non-Hodgkin and Hodgkin lymphoma.CONCLUSIONS: A history of high UV exposure was associated with reduced risk of non-Hodgkin lymphoma. The positive association between skin cancer and malignant lymphomas is, therefore, unlikely to be mediated by UV exposure.J Natl Cancer Inst. 2005 Feb 2;97(3):199-209.
Ultraviolet radiation exposure and risk of malignant lymphomas.Smedby KE, Hjalgrim H, Melbye M, Torrång A, Rostgaard K, Munksgaard L, Adami J, Hansen M, Porwit-MacDonald A, Jensen BA, Roos G, Pedersen BB, Sundström C, Glimelius B, Adami HO.Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, SE-171 77 Stockholm, Sweden. karin.ekstrom@meb.ki.seBACKGROUND: The incidence of malignant lymphomas has been increasing rapidly, but the causes of these malignancies remain poorly understood. One hypothesis holds that exposure to ultraviolet (UV) radiation increases lymphoma risk. We tested this hypothesis in a population-based case-control study in Denmark and Sweden.METHODS: A total of 3740 patients diagnosed between October 1, 1999, and August 30, 2002, with incident malignant lymphomas, including non-Hodgkin lymphoma, chronic lymphocytic leukemia, and Hodgkin lymphoma, and 3187 population controls provided detailed information on history of UV exposure and skin cancer and information on other possible risk factors for lymphomas. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated by logistic regression. Statistical tests were two-sided.RESULTS: Multivariable-adjusted analyses revealed consistent, statistically significant negative associations between various measures of UV light exposure and risk of non-Hodgkin lymphoma. A high frequency of sun bathing and sunburns at age 20 years and 5-10 years before the interview and sun vacations abroad were associated with 30%-40% reduced risks of non-Hodgkin lymphoma (e.g., for sunbathing four times a week or more at age 20 versus never sunbathing, OR = 0.7, 95% CI = 0.6 to 0.9; for two or more sunburns a year at age 20 versus no sunburns, OR = 0.6, 95% CI = 0.5 to 0.. These inverse associations increased in strength with increasing levels of exposure (all P(trend)< or =.01). Similar, albeit weaker, associations were observed for Hodgkin lymphoma. There were no clear differences among non-Hodgkin lymphoma subtypes, although associations were stronger for B-cell than for T-cell lymphomas. A history of skin cancer was associated with a doubling in risks of both non-Hodgkin and Hodgkin lymphoma.CONCLUSIONS: A history of high UV exposure was associated with reduced risk of non-Hodgkin lymphoma. The positive association between skin cancer and malignant lymphomas is, therefore, unlikely to be mediated by UV exposure.J Natl Cancer Inst. 2005 Feb 2;97(3):199-209.
Just a quick 'Hello' from this part of the world. We finally getting close to Maintenance and I think I see a light at the end of the tunnel. It'll only take 3 years to get there!Meanwhile, we keep reading and learning more about the "ALL monster" and hoping that soon we'll find a simple path to the cure or prevention.Cheers,DQ
I can't tell you how many times I've came back to this topic and read postings over and over. I still haven't read it all yet! I can only thank you for being here and for sharing your knowledge and thoughts."A little knowledge that acts is worth infinitely more than much knowledge that is idle."Kahlil Gibran:
Is vitamin D deficiency in childhood leukaemia an underestimated reality?Could cod liver oil - the old remedy, a relic from the past - help in theempirically arranged but clinically effective today's treatment protocols?
...All of the epidemiological and animal studies in the literature suggest cancer patients will prolong their lives if they take vitamin D. I can't find any studies that indicate otherwise. However, none of the suggestive studies are randomized controlled interventional trials; they are all epidemiological or animal studies, or, in the case of Vieth's, an open human study. However, if you have cancer, or your child does, do you want to wait the decades it will take for the American Cancer Society to fund randomized controlled trials using the proper dose of vitamin D? Chances are you, or your child, will not be around to see the results. John Cannell, MDhttp://www.vitamindcouncil.com/
It's never too late (sometimes)...If you followed this thread so far,you deserve to watch this free video: "The Vitamin D Pandemic and its Health Consequences" Presented by Michael Holick, PhD, MD, Professor of medicine, physiology and biophysicsand director of the General Clinical Research Center at Boston University Medical CenterKeynote address at the opening ceremony of the 34th European Symposium on Calcified Tissues, Copenhagen 5 May, 2007http://www.uvadvantage.org/portals/0/pres/ http://www.uvadvantage.org/portals/0/pres/video/video/slides/slide413.jpghttp://www.uvadvantage.org/portals/0/pres/video/video/slides/slide414.jpg
Run on vitamin D after studyDr. Michael Pollak, an oncologist and director of the cancer-prevention centre at Montreal's Jewish General Hospital and McGill University, interviewed by Andy Riga for the Montreal Gazette, CanWest News Service.Monday, June 18, 2007Quote..."No one is naive," he said. "Vitamin D optimization won't eliminate cancer by any stretch of the imagination, but if it has no downsides and it cuts cancer incidence, it could be worthwhile. Nobody wants to overlook a clue here. This is what everybody wants - a simple pill that reduces cancer risk."http://www.canada.com/topics/bodyandhealth/story.html?id=ed68aefc-50e4-45f8-b84f-2bd434a6f3d6&k=91024&p=1
..."No one is naive," he said. "Vitamin D optimization won't eliminate cancer by any stretch of the imagination, but if it has no downsides and it cuts cancer incidence, it could be worthwhile. Nobody wants to overlook a clue here. This is what everybody wants - a simple pill that reduces cancer risk."
"Mother was right about cod liver oil"Griffing GT.Medscape J Med. 2008 Jan 11;10(1):8. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18324318QuoteThere are many stories of mothers forcing their children to take cod liver oil.Centuries ago, northern Europeans used cod liver oil to protect them from the cold. It was made from the livers of Gadus morhua and other species of cod. Cod liver oil was said to relieve such complaints as rheumatism, aching joints, and stiff muscles.At the beginning of the 20th century, scientists established that cod liver oil was antirachitic, and it became commonplace for mothers to give it to their children.[1,2]It turns out cod liver oil contains large amounts of vitamins A, D, and omega-3 fatty acids, and the health benefits may go beyond rheumatism and rickets.[3]...
There are many stories of mothers forcing their children to take cod liver oil.Centuries ago, northern Europeans used cod liver oil to protect them from the cold. It was made from the livers of Gadus morhua and other species of cod. Cod liver oil was said to relieve such complaints as rheumatism, aching joints, and stiff muscles.At the beginning of the 20th century, scientists established that cod liver oil was antirachitic, and it became commonplace for mothers to give it to their children.[1,2]It turns out cod liver oil contains large amounts of vitamins A, D, and omega-3 fatty acids, and the health benefits may go beyond rheumatism and rickets.[3]...
>25000 viewers!Let's celebrate this old thread with an ancient quote:Quote"Sit down before fact as a little child, be prepared to give up every preconceived notion, follow humbly wherever and whatever abysses nature leads, or you will learn nothing."Thomas Henry Huxley
"Sit down before fact as a little child, be prepared to give up every preconceived notion, follow humbly wherever and whatever abysses nature leads, or you will learn nothing."Thomas Henry Huxley