0 Members and 1 Guest are viewing this topic.
My Friend, El Gato offered to help in the search.
Revisiting Vitamin D in humans.just a few clever minds got this pointfirst, several years ago...http://www.seeli.com/Daniel/leisure/travel/Finland/landscape5.jpgA hypothesis concerning deficiency of sunlight,cold temperature, and influenza epidemics associated withthe onset of acute lymphoblastic leukemia in northern Finland. Timonen TT.University of Oulu, Department of Internal Medicine, Kajaanintie 50, FIN-90220 Oulu, Finland.Research to detect new factors contributing to the etiology of acute leukemia (AL) is urgently needed. Located between latitudes 65 degrees and 70 degrees north, the population in northern Finland is exposed to extreme seasonal alterations of ultraviolet-B light and temperature. There is also a seasonal variation of both the 25(OH)- and 1,25(OH)2-D3 vitamin serum concentrations. In the present work, the frequencies of different types and age-groups at diagnosis of AL were compared during the dark and light months of the year, to uncover seasonality. Between January 1972 and December 1986, 300 consecutive patients aged >/=16 years and diagnosed as having AL were enrolled. The observed mean monthly global solar radiation, temperature measurements, and influenza epidemics were compared with the monthly occurrence of AL. Both acute lymphoblastic leukemia (ALL) (p=0.006) and total AL (p=0.015) were diagnosed excessively in the dark and cold compared with light and warm period of the year. There was a tendency for de novo leukemia to increase also in the dark and cold, but for acute myeloid leukemia (AML) patients the excess was not significant. Age >/=65 was strongly associated with the dark and cold season (p=0.003). Significantly more ALL (p=0.005) and de novo leukemias (p=0.029) were observed during influenza epidemics than during nonepidemic periods. However, a seasonality, i. e., the fluctuation of numbers of AL cases, was not determined, either monthly or during different photo- and temperature periods or influenza epidemics; this might be due to the small numbers of patients studied. Nevertheless, it is hypothesized that sunlight deprivation in the arctic winter can lead to a deficiency of the 1, 25(OH)2D3 vitamin, which might stimulate leukemic cell proliferation and block cell differentiation through dysregulation of growth factors in the bone marrow stromal cells, causing one mutation and an overt ALL in progenitor cells damaged during the current or the previous winter by influenza virus, the other mutation.Ann Hematol. 1999 Sep;78(9):408-14.
I liked Rhode Island, wish I could afford to live there for a while and use the library. Have patterns in the development of leukemia been noted like that in Finland? In general, are more cases of leukemia diagnosed at one time of year or another? ---
You mean "understand" as finding patterns, rhyme and reason. I found reports of the "clusters" too. The problem in the reporting was the immediate assumption was that if there are a lot of cases in one area, it must be enviromental, excluding nutritional enviroments. Maybe that's why there are not more Shanghai Reports. Regards,Zoey
Quote from: Zoey on 15/04/2007 22:00:14
ConclusionVitamin D–deficiency rickets is a sunlight deficiency disease. The inability to appreciate the beneficial effect of sunlight for health had devastating consequences for both children and adults for more than 300 years. When it was finally realized that exposure to sunlight could prevent and treat rickets, this led to the recommendation that all children be exposed to sensible sunlight to maximize bone health. The fortification of milk with vitamin D eradicated rickets as a major health problem, and, therefore, it was thought to have been conquered. Rickets has, however, made an unfortunate comeback (120). The major cause of rickets in the United States is a lack of appreciation that human milk contains very little if any vitamin D to satisfy the infant’s requirement. African American women are often vitamin D deficient, and women who always wear sun protection and only take a prenatal multivitamin are also at a high risk of vitamin D insufficiency. If they provide breast milk to their infant as the sole source of nutrition, the infant will become vitamin D deficient. If the infant is not exposed to sunlight or does not receive a vitamin D supplement, the infant will inevitably develop rickets.However, the skeletal manifestations of rickets represent only the tip of the vitamin D deficiency iceberg. Vitamin D deficiency in utero and during the first year of life has devastating consequences and may imprint on the child’s life chronic diseases that will shorten his/her life span (24, 57). In utero, vitamin D deficiency results in reduced intrauterine long bone growth and slightly shorter gestation (121). This has been linked to increased risk of osteoporosis and fractures later in life (24, 60, 61, 82, 122). Children born and raised at latitudes below 35° for the first 10 years have a 50% reduced risk of developing multiple sclerosis later in life (103, 104). Neonates who are vitamin D deficient during the first year of life are 2.4-fold more likely to develop type 1 diabetes compared with children who received 2,000 IU of vitamin D3/day (105). It has been suggested that the increased risk of developing schizophrenia may be initiated in utero and during childhood due to vitamin D deficiency (102). Muscle function, innate immunity, cellular growth and maturation, immunomodulation, insulin secretion, as well as regulation of calcium, phosphorus, and bone metabolism are all affected or controlled by vitamin D. Thus, ensuring that women during pregnancy are vitamin D sufficient and that newborns either be immediately evaluated for their vitamin D status by measuring 25(OH)D levels in cord blood or given vitamin D prophylactically should be a high priority. Vitamin D deficiency should be immediately treated with at least 1,000 IU of vitamin D2 or vitamin D3/day for the first week of life. Alternatively, a single dose of 200,000 IU of vitamin D should suffice for the first few months of life. There has been a great fear about causing vitamin D intoxication in neonates. This resulted from the poorly described outbreak of neonatal hypercalcemia in the 1950s in Great Britain (123), which led to the enactment of laws in Europe forbidding the fortification of dairy products as well as all other products with vitamin D. In 1997 the Institute of Medicine recommended that the AI for infants and children of all ages be 200 IU/d. The same recommendation was made for pregnant and lactating women. The safe upper limit for infants ages 0–12 months was 1,000 IU/d and for children older than 1 year of age, 2,000 IU/d. However, it is now obvious based on the historical literature (14–16) as well as the recent literature (23, 24, 30, 36, 81, 86, 87) that these recommendations are inadequate without sensible sun exposure. It is well documented that neonates and children can tolerate a single dose of 200,000 IU of vitamin D2 or vitamin D3 or doses of vitamin D up to 3,000 IU/d without any untoward side effects. Indeed 400–1,000 IU/d to maintain serum 25(OH)D levels between 30–50 ng/ml should be the goal, just as it is in adults. Infants and children have routinely received 400–2,000 IU vitamin D2 or vitamin D3/day for the first years of life without any reports of toxicity (23, 80, 105, 107). Typically, doses of more than 50,000 IU/d of vitamin D2 were found to cause toxicity (12–14). In Canada, it is recommended that all infants receive 400 IU/d from birth. This recommendation has been successfully implemented and has not resulted in any reported cases of vitamin D intoxication or hypercalcemia. I believe that the 200 IU of vitamin D that is recommended by the American Academy of Pediatrics is suboptimal (124). This dose may prevent overt rickets but will not prevent vitamin D deficiency. Hopefully, history will not repeat itself. The widespread concern about any direct sun exposure increasing the risk of the relatively benign and nonlethal squamous and basal cell cancers needs to be put into perspective. It is chronic excessive exposure to sunlight and sunburning experiences during childhood that increases risk of nonmelanoma skin cancer (125). Melanoma, one of the most feared cancers because of its ability to rapidly metastasize before it is obvious to either the patient or physician, has been branded as a sun-induced skin cancer. However, most melanomas occur on the least sun-exposed areas, and it has been reported that occupational exposure to sunlight decreases risk of melanoma (125). The 30-year campaign to recommend abstinence from sun exposure has not stemmed the increase in skin cancer incidence (125). It is curious that in the 1930s and 1940s, when children were encouraged to be exposed to sunlight and artificial UV radiation to treat rickets, the incidence of skin cancer did not increase. Thus, there needs to be a reevaluation of the beneficial effect of sensible exposure to sunlight as noted by the Australian College of Dermatologists and the Cancer Council Australia, which recommend a balance between avoiding an increase risk of skin cancer and achieving enough UV radiation to maintain adequate vitamin D levels. Holick MF.Resurrection of vitamin D deficiency and ricketsJ Clin Invest. 2006 Aug;116(:2062-72.
...From an unspecified topic in "General Science" NSforum:Sesame seedssesame buttersesaminolsesamolinhttp://www.grainfieldsaustralia.com/US/ingredients/graphics/sesame-seeds.gifSesaminol from sesame seed induces apoptosis in human lymphoid leukemia Molt 4B cells.Miyahara Y, Hibasami H, Katsuzaki H, et al.The exposure of human lymphoid leukemia Molt 4B cells to sesaminol, a component of sesame oil led to both growth inhibition and the induction of apoptosis. Morphological change showing apoptotic bodies was observed in the cells treated with sesaminol. The fragmentation of DNA by sesaminol to oligonucleosomal-sized fragments that are characteristics of apoptosis was observed to be concentration- and time-dependent. These findings suggest that growth inhibition of Molt 4B cells by sesaminol results from the induction of apoptosis in the cells.Int J Mol Med. 2001 May;7(5):485-8.Now then, if in your frantic 'surfing' on the Web you found something like this:...According to medical authorities nothing is supposed to be effective in treating leukemia -- that's cancer of the blood. We know a doctor in the Midwest who had three children who got over leukemia just by eating sesame butter. He gave them six tablespoonfuls of sesame butter a day. Brown sesame seed butter (Tahini). That's not a very glamorous treatment for a serious illness but it worked.http://22.214.171.124/search?q=cache:GztTWKxLt78J:www.usaplaza.com/scripts/wcom_producttree.asp%3FStoreID%3D1340%26ProductID%3D48398+%22sesame+butter%22+leukemia&hl=it&gl=it&ct=clnk&cd=1...given the initial statement that "nothing is supposed to be effective", as a medical doctor you would correctly think that's a scam, a totally unproven commercial crap, just quackery.Nevertheless, as a parent of a leukemia 'survivor' you would easily consider giving her/him at least some sesame-seed bread (traditional Sicilian bread) and grissini (sesame bread sticks), so tasty and good for you. They make them fresh at the bakery just across the street, so it doesn't cost much to buy some once a week. They disappear quite quickly from the kitchen counter (beside the cod caps container). ikod http://img.alibaba.com/photo/11081131/Sesame_Bread_Stick.jpghttp://www.pccnaturalmarkets.com/health/Food_Guide/Sesame_Seed_Butter.jpg
Hi Luka.thanks for appreciating my efforts and for the discussion.It helps me to explain better the point in this topic.I'll reply shortly to your post, step by step:quote I’d read every your post on this forum. I find most of your posts interesting; some of them are mind opening. But, I was disappointed that you posted this link. http://126.96.36.199/search?q=cache:GztTWKxLt78J:www.usaplaza.com/scripts/wcom_producttree.asp%3FStoreID%3D1340%26ProductID%3D48398+%22sesame+butter%22+leukemia&hl=it&gl=it&ct=clnk&cd=1Sorry if the sesame butter story comes out from a commercial link, I had to report it anyway...you cannot find it anywhere else. A scam? A real story? I leave it open.I do not even remember how, but I found it years ago. It was easy to check on PubMed and find a "scoop", one recent positive 'in vitro' result for sesaminol against a leukemic lymphoblastic cell-line.It may be a promising result, believe me.In 1980, like other groups years before, we worked on retinoic acid versus a promyelocytic cell-line (HL-60): the bad cells stopped dividing and became mature white cells within 5days. That miracle took 10-15 years to reach the 'real' patients. These days a vitamin A derivative (retinoid) is in the standard treatment for promyelocytic leukemia (AML-M3).So the story of the doctor in the Midwest may be just fantasy, but the japanese report (actually there are two papers) is real and scientifically correct.A parent usually needs more hope, and tends to take into account even those 'fantasies'... quote How significantly is it, we can’t see from this report (the “Shanghai report”).How we do know, that if children take tablespoon of honey every day, that incidence of leukemia will be lower than if they take cod liver oil.I gave instructions to check that abstract: did you reach it? We'll do it together later on.Sorry Luka, no honey, no ascorbic acid, no aloe whatsoever. They may work, I don't know.I certainly know that the only scientific report on a positive effect of a nutrient, or nutritional supplement if you like, capable of reducing incidence of childhood leukemia to half or 1/3 is the 1988 paper from Shanghai published in Cancer. I've searched around, believe me...and I am not a scientist, but I've been in this field for a long time.Distinguished journal, well-done study, statistically sound.We really have to 'codcentrate' on one thing.quote I think that diet approach in understanding cause of illnesses has reached own limit long time ago.It is necessary to find “missing link” between nutrition and physical activity on one side and health and illnesses on the other side.To speculate about the possible causes of leukemia is not the aim of this topic: I suggested to read Mel Greaves's hypothesis (there are several papers about it). Vitamin D deficiency may represent one of the many "missing links" (personal opinion), but still we are not in a position to do much about it.This is no chat or fantasy.I am concerned as a parent.I am serious and I feel I carry a sort of responsability about it.A bit of help (cod liver oil) together with standard treatments could improve,starting tomorrow, the quality of life and may be (fingers crossed) even survival......one percent? 5 percent? I do not care much:just one kid who feels a bit stronger andgrows up properly in spite of chemo would do.I do not want to be alone in reminding one of the kids to take his 'cod'. The discussion here should be on how to let those parents know what nobody told them before.asap.ikodPost Scriptum: Actually I don't exactly think I am the only parent reminding 'cod': the Shanghai report has been cited around, even in the "Cod liver oil - number one superfood" commercial website.Knowing the amount of adrenaline you get in the endless months following a diagnosis of childhood leukemia,I'm pretty sure that some other parent has snagged this information and is probably doing the same thing. Let's be a bit more positive about medical progress:maybe a few open-minded consultant hematologists around the world are recommending every day 'cod' to parents of leukemic children. Following the 'Shanghai report' indications or who knows what other mysterious path or fascinating suggestion. Adopting the old fashioned "ex-adjuvantibus" criteria.Maybe. http://www.flyanglersonline.com/lighterside/dennisdickson.jpghttp://www.immunizenc.com/images/ped_andchild.jpghttp://allconsortium.dfci.harvard.edu/public/images/lewis.jpg
12. Tahini and sesame butter (just like peanut butter but from sesame) and sesame seeds. Sesame products are eaten in some cultures in place of dairy products because of their high calcium content (calcium from sesame seeds is more easily used by our bodies than calcium from milk and a higher percentage of the calcium contained actually works for us). Eaten for thousands of years, sesame seeds were believed to possess magical properties, and they contain sesamol, which fights rancidity. Another quick easy breakfast is apple slices dipped into tahini or tahini with banana or tahini on toast. Use tahini to replace peanut butter in cookies.DEBRA STARKConcordhttp://debrastark.com/portfolio_twelve.html
As the magic words, “Open, sesame!” indicate, many excellentproperties are hidden in the tiny sesame seed and these havebecome clear by the studies described above. Sesame seed willcontribute much to the health and prosperity of people throughoutthe entire world.from: Nutraceutical Functions of Sesame: A ReviewMITSUO NAMIKI Nagoya University, Nagoya, JapanCritical Reviews in Food Science and Nutrition, 47:651–673 (2007)http://www.informaworld.com/smpp/content~db=all?content=10.1080/10408390600919114
One of the CLL groups did post a long newsletter, much like you, Iko, suggesting the use of CLO in leukemia. They asked it not be reproduced so am trying to contact them about it. As per your recent posts, the focus will shift back to how to alert parents of ALL children.Zoey
It's definitely fascinating how many people (parents) and doctors disregard any kind of supportive or alternative treatment to ALL.
Topics Alert ArchiveAlert Number 47 Those Pesky Aches and PainsDate: October 5, 2004One of the common mistakes we (and our doctors!) make is attributing everything that goes wrong to CLL. If you are tired, you hurt all over, your muscles ache, heck you can feel the pain in your very bones, and nothing works, not even fistfulls of NSAIDs, why, it must be the dreaded CLL acting up, right?Not so fast, you could be dead wrong laying this at the door of the 'dragon'. You could be suffering from something that can be very easily corrected, a real cheap fix. Not only does it not cost a lot, it is not even toxic (isn't that a welcome change from the usual caveats with chemo drugs?), and it might even help you fight the CLL. What is this drug? It is called vitamin D3. I have discussed this topic before on Topics (Vitamin D3 Essential for Health) but I think it bears repeating. Below are direct quotes from a very recent paper in the prestigious Mayo Proceedings, December of 2003. You can read the whole article for free, as well as the editorial that accompanied it. I have provided the links below....In the meantime, please do discuss your vitamin D3 status with your doctor. You may want to revisit our review article "Vitamin D3: Essential for your health" on our website, to get your arms around the arguments you may need to make, to bring your doctor on board. In my opinion, it surely pays to be pro-active on this front. Do remember, unlike the general Joe Shmoe basking on the beach, as CLL patients you have significantly higher (ten times higher!) risk of skin cancer, so getting all the vitamin D3 you need from sun-bathing is not a really good option for you (Do read the article Dying to Get a Tan?. Stay in the shade, pop your doctor's recommended dose of vitamin D3 supplement with a nice cup of freshly brewed green tea (or a good glass of pinot noir!) - that should do it right by you. And get yourself some over-the-counter calcium tablets. Stop wasting good money and destroying coral reefs, while you poison yourself with mercury and other heavy metals.Be well,Chayahttp://www.clltopics.org/Alert/direct_display_alert.php?reqnum=47
Recurrence of acute leukemia in donor cells after bone marrow transplantation:documentation by in situ DNA hybridization. Mouratidou M, Sotiropoulos D, Deremitzaki K, Spathas DH, Hoffbrand AV, Prentice HG, Papanastasiou K, Tsakanikas S, Tsaftaridis P, Stamatelou M, et al. Hematology Division, Greek Anticancer Institute Athens.Donor cell leukemia after BMT has been documented in a small number of cases mainly by cytogenetic studies. We describe a case of leukemia relapse in a 16-year-old girl 1 year after BMT from her histocompatible brother. Relapse in donor cells was initially suspected on the basis of cytogenetic analysis and confirmed by DNA in situ hybridization in blast cells using a Y chromosome-specific probe.Bone Marrow Transplant. 1993 Jul;12(1):77-80.
- Parents of leukemic children will consider to give their kid some cod liver oil, instead of getting confused between hundreds of alternative and unproven nutritional supplements....and they (the parents) will immediately start feeling better...and less terrified.Why are these parents so scared?Just because they are told that their child's disease will be effectively cured in a certain percentage of cases after a series of cycles of highly toxic drugs. But in a consistent number of cases (25-30%) the disease will come back, resistent to further treatment.When this happens, more toxic cycles of chemo will be required, and may be RADIATION TREATMENT and a bone marrow transplantation. In some patients the disease comes back even after a graft, in one case out of two...After chemo and during maintenance therapy there is no official recommendation for parents:going down to the seaside or up to the mountains, to the pool or living sealed at home, staying in the shade or in the sunshine, eating this food and avoiding that...nothing.There is no confirmed evidence about these factors (are we sure?).So do what you want, but please follow your regular checkups every two weeks and then every month.In the meantime...we all wait and see if and when IT strikes again.
IT strikes back? What's IT?As I try to understand the "leukemia monster", from cytogenitics to possible causes, I always come to the same conclusion. Chemotherapy treatment is only treating the disease. It doesn't fix a possible gene lesion or DNA. So, if a certain gene translocation is present within the Leukemia cells and it's known as a pre-leukemic event (predisposition) and a second or even third event starts the Leukemia, It's possible that even after treatment the same sequence of "hits" could start the Leukemia again since the cytogenetic event/predisposition is still present.Does a BMTransplant change the individual's DNA? There was a recent discussion on this site about that. Unfortunately,I did not pay much attention to it. I still believe that viruses (like Epstein Barr and common Flu) play a major role in the Leukemia process (specially ALL) and vaccines will be the way to prevent the disease. Meanwhile, we keep hoping for a cure or prevention. Cheers,
I still believe that viruses (like Epstein Barr and common Flu) play a major role in the Leukemia process (specially ALL) and vaccines will be the way to prevent the disease. Meanwhile, we keep hoping for a cure or prevention. Cheers,
Quote from: iko on 14/04/2007 12:34:04Quote from: neilep on 13/04/2007 23:28:51Iko...would you like me to move the original garlic thread here ?Thanks me friendos,I just moved reports and abstracts here,leaving the entertaining "bagna cauda"sort of thing down there in Guest Book.I meant to keep it more scientific here.ikodAjoene (natural garlic compound): a new anti-leukaemia agent for AML therapy.Hassan HT.The reputation of garlic (Allium sativum) as an effective remedy for tumours extends back to the Egyptian Codex Ebers of 1550 b.c. Several garlic compounds including allicin and its corresponding sulfide inhibit the proliferation and induce apoptosis of several human non-leukaemia malignant cells including breast, bladder, colorectal, hepatic, prostate cancer, lymphoma and skin tumour cell lines. Ajoene (4,5,9-trithiadodeca-1,6,11-triene-9-oxide) is a garlic-derived compound produced most efficiently from pure allicin and has the advantage of a greater chemical stability than allicin. Several clinical trials and in vitro studies of ajoene have demonstrated its best-known anti-thrombosis, anti-microbial and cholesterol lowering activities. Recently, topic application of ajoene has produced significant clinical response in patients with skin basal cell carcinoma. Ajoene was shown to inhibit proliferation and induce apoptosis of several human leukaemia CD34-negative cells including HL-60, U937, HEL and OCIM-1. Also, ajoene induces 30% apoptosis in myeloblasts from chronic myeloid leukaemia patient in blast crisis. More significantly, ajoene profoundly enhanced the apoptotic effect of the two chemotherapeutic drugs: cytarabine and fludarabine in human CD34-positive resistant myeloid leukaemia cells through enhancing their bcl-2 inhibitory and caspase-3 activation activities. The two key anti-leukaemia biological actions of ajoene were the inhibition of proliferation and the induction of apoptosis. Studies have shown the anti-proliferation activity of ajoene to be associated with a block in the G2/M phase of cell cycle in human myeloid leukaemia cells. The apoptosis inducing activity of ajoene is via the mitochondria-dependent caspase cascade through a significant reduction of the anti-apoptotic bcl-2 that results in release of cytochrome c and the activation of caspase-3. Since acute myeloid leukaemia (AML) is a heterogeneous malignant disease in which disease progression at the level of CD34-positive cells has a major impact on resistance to chemotherapy and relapse and the inability to undergo apoptosis is a crucial mechanism of multi-drug resistance in AML patients. The recent findings of the potent enhancing activity of ajoene on chemotherapy-induced apoptosis in CD34-positive resistant human myeloid leukaemia cells suggest a novel promising role for the treatment of refractory and/or relapsed AML patients as well as elderly AML patients. Further studies are warranted to evaluate similar enhancing effect for ajoene in blast cells from AML patients in primary cultures before its introduction in pilot clinical study.Leuk Res. 2004 Jul;28(7):667-71.
Quote from: neilep on 13/04/2007 23:28:51Iko...would you like me to move the original garlic thread here ?Thanks me friendos,I just moved reports and abstracts here,leaving the entertaining "bagna cauda"sort of thing down there in Guest Book.I meant to keep it more scientific here.ikod
Iko...would you like me to move the original garlic thread here ?
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. email@example.comBACKGROUND: 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. firstname.lastname@example.orgBACKGROUND: 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....
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....
>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