[iko (OP)]

Hi Zoey,
I don't want to slow down your enthusiasm but...
did you check the recent post about vitamins
and antioxidants by George (another_someone)?
http://www.thenakedscientists.com/forum/index.php?topic=6661.0
This is a really tough and delicate issue.

ikod

[Zoey]

No, I hadn't read it, but thanks. Will do! What about your enthusiasm?
Zoey

[Zoey]

 I read the report and posted a reply. If you get a copy of the report can you post some of it here? I would like to read it also.

[Zoey]

Some conflicting reports from a search on cod liver oil and cancer.  It appears there is interest in researching this issue, but it needs to be cultivated.

  The bad news first. This one shows a potential negative link between cod liver oil use and risk of developing cutaneous malignant melanoma. Some concerns about the results are noted in the abstract.

2: Int J Cancer. 1997 May 16;71(4):600-4.

Diet and risk of cutaneous malignant melanoma: a prospective study of 50,757
Norwegian men and women.

Veierod MB, Thelle DS, Laake P.

Section of Medical Statistics, University of Oslo, Norway.
marit.veierod@basalmed.uio.no

The relationship between dietary habits and subsequent risk of cutaneous
malignant melanoma (CMM) was studied in 25,708 men and 25,049 women aged 16-56
years attending a Norwegian health screening in 1977-1983. Linkage to the Cancer
Registry of Norway and the Central Bureau of Statistics of Norway ensured a
complete follow-up until December 31, 1992. Diet was recorded through a
semi-quantitative food-frequency questionnaire at the time of screening, and 108
cases of CMM were identified during follow-up. Use of cod liver oil
supplementation and intake of polyunsaturated fat were associated with
significant increased risk and drinking coffee with significant decreased risk
of CMM in women. Adjusting for height, body mass index, body surface area,
education, smoking or occupational or recreational physical activity did not
change the results. No significant association was found between the incidence
of CMM and any of the dietary factors in men. Important aspects are residual
confounding by sun exposure and social class, as well as concern with multiple
comparisons.

Publication Types:
    Research Support, Non-U.S. Gov't

PMID: 9178814 [PubMed - indexed for MEDLINE]
-------------------------------------------------
Now, something looking a little more positive.
 This review speaks mostly of vitamin D in relation to development of prostate cancer. However, the author also notes growing interest in the potential role of vitamin D in other cancers as well.  The entire review is available at PubMed Central. The link to it follows this quote.

Clin Biochem Rev. 2005 February; 26(1): 21–32.
Copyright © 2005 The Australasian Association of Clinical Biochemists Inc.
Vitamin D: A Hormone for All Seasons - How much is enough? Understanding the New Pressures
Howard A Morris*
Hanson Institute, Box 14 Rundle Mall Post Office, Adelaide, SA 5000, Australia
Corresponding author.

For correspondence: Professor Howard Morris e-mail: howard.morris@imvs.sa.gov.a
*(Professor Morris was the AACB Roman Lecturer for 2004.)

"
An area of particular interest for novel vitamin D activities is the regulation of cell growth and differentiation.  It has been recognised for over 20 years that the addition of 1,25(OH)2D to culture media for cancer cell lines produced a strong inhibition of growth.  Initially studies included breast cancer and other solid tumour cells lines.37 Particular progress has been made with the study of human prostate cancer cell lines as well as normal prostate epithelial tissue and primary prostate cancer cell cultures.  The prostate functions as a vitamin D-target organ in that normal epithelial cells express the VDR and display regulation of numerous genes by 1,25(OH)2D.  A recent complementary DNA microarray analysis of primary human prostatic epithelial cells revealed that 1,25(OH)2D up-regulated at least 38 genes and 9 were significantly down-regulated.38 The highest induction of expression was the gene for the vitamin D catabolic enzyme CYP24.  The expression of similar but not identical genes was observed in primary prostate cancer cultures.  Some of these genes modulate the mitogen-activated kinase (MAPK) pathways associated with growth factor signally while others induce apoptosis or reduce cell cycling activity necessary for cell division and replication.

A study of the effect of 1,25(OH)2D on growth of a number of human prostate cancer cell lines indicated varied responses to 1,25(OH)2D with the LNCaP line being most sensitive while the DU145 cell line was unresponsive39 (Figure 5).  Further studies on the expression of the genes that determine vitamin D activity in these cell lines as well as normal prostate epithelial cells and benign prostate hyperplastic cells indicate a gradation of decreasing CYP27B1 activity as prostate epithelial cells move from normal epithelium with the highest activity through benign prostate hyperplastic epithelium with moderate activity to cancer cells with markedly repressed activity (Table 4).  Neither the expression of VDR or CYP24 demonstrates such a relationship with the development of cancer.  It is interesting that when the DU145 cancer cell, which is unresponsive to 1,25(OH)2D was treated with an inhibitor of CYP24 activity, the growth inhibition by 1,25(OH)2D was demonstrated.43 A recent immunohistochemical study of a human prostate cancer series indicated that the CYP27B1 protein was present in a significant number of these specimens.  Their data suggest that the increased expression of CYP24 or some inactivation of the CYP27B1 enzyme may be important mechanisms for reducing 1,25(OH)2D activity in many clinical prostate cancers.44

These findings all suggest that modulation of vitamin D activity through disruption of vitamin D metabolism within prostate cells may play a permissive role in the development of prostate cancer.  There is considerable epidemiological evidence that either decreased sunlight exposure or decreased vitamin D status is associated with increased risk of many cancers including prostate.  In the USA rates of cancer mortality vary inversely with exposure to sunlight (reviewed45).  A study in Finland demonstrated that men with an initial low vitamin D status were at greater risk for earlier onset prostate cancer and tumours were generally more aggressive suggesting vitamin D status may be critical during the earlier stages of prostate cancer development.  These observations have been confirmed in the United Kingdom.  Thus if a low vitamin D status is confirmed to increase the risk of prostate or any cancers, the maintenance of an adequate vitamin D status and assessment of vitamin D levels are very simple procedures that could be adopted at the population level.  Thus clinical laboratory vitamin D testing would further markedly increase.  Such a public health policy will require the identification of the level of vitamin D required to reduce the risk of cancer."
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1240026

[iko (OP)]

Some conflicting reports from a search on cod liver oil and cancer.  It appears there is interest in researching this issue, but it needs to be cultivated.

  The bad news first. This one shows a potential negative link between cod liver oil use and risk of developing cutaneous malignant melanoma. Some concerns about the results are noted in the abstract.

2: Int J Cancer. 1997 May 16;71(4):600-4.

Diet and risk of cutaneous malignant melanoma: a prospective study of 50,757
Norwegian men and women.

Veierod MB, Thelle DS, Laake P.

Hi Zoey,
I couldn't check the full-text.  Reading the abstract I could not find the sun-exposure history that now seems to be crucial in making the difference: people that experienced several 'burns'  - instead of a proper suntan achieved gradually - take a much higher risk of developing a melanoma in the following decades.
Epidemiological studies seem to have a problem when cod liver oil is concerned.
As a matter of fact, things are much more complex when you get closer...
Here there is an example.


 

Predictors for cod-liver oil supplement use--the Norwegian Women and Cancer Study.

Brustad M,Braaten T, Lund E.
Institute of Community Medicine, University of Tromso, Norway. magritt.brustad@ism.uit.no

OBJECTIVE: To assess the use of cod-liver oil supplements among Norwegian women and to examine dietary, lifestyle, demographic, and health factors associated with use of this supplement.
DESIGN: Cross-sectional study.
SETTING AND SUBJECTS: The study is based on data from a food frequency questionnaire from 1998 answered by 37,226 women aged 41-55 y, who in 1991/1992 participated in the Norwegian component of the European Prospective Investigation into Cancer and Nutrition (EPIC). The Norwegian EPIC cohort was based on a random nation-wide sample of Norwegian women.
RESULTS: Cod-liver oil supplement use was reported by 44.7% of the participating women. Subjects with higher education, high physical activity level, and body mass index (BMI) in the normal range were more likely to use cod-liver oil supplements. Consumption did also increase with increased age as well as with increased reported consumption of fruits, vegetables, fatty fish, lean fish, and vitamin D (excluding the vitamin D contribution from cod-liver oil). Energy intake was higher among cod-liver oil users than nonusers. Whole-year daily users of cod-liver oil were also more likely to take other dietary supplements (OR=2.45, 95% CI: 2.28-2.62). Never smokers were more likely to use cod-liver oil supplements than current smokers.
CONCLUSION: Use of cod-liver oil is associated with several sociodemographic factors, self-reported health issues, and intake of fish, fruit, and vegetables. When assessing the relationship between cod-liver oil use and occurrence of chronic diseases potential confounders need to be considered. Cod-liver oil use seemed not to be matched with vitamin D needs. Thus, emphasis on assessing vitamin D status by measuring levels in blood should be investigated further, in particular, among people living in northern latitudes.

Eur J Clin Nutr. 2004 Jan;58(1):128-36.

Air view of Tromso, Norway


http://www.galenfrysinger.com/Photos/norway29.jpg

     

more views from:  http://www.galenfrysinger.com/tromso,_norway.htm

[Zoey]

Considering the view, I wonder if I could find a sponsor to send me there to search for information?
  Wouldn't any study need to consider if the subjects take cod liver oil, vitamin D supplements, as well as determine any participant's vitamin D level?
  I did a quick search on vitamin D deficiency in Norway and it looks like many studies focus on deficiency in immigrant groups, so even that information is taking time to locate. How could study problems related to taking cod liver oil be overcome?

[iko (OP)]

Considering the view, I wonder if I could find a sponsor to send me there to search for information?
  Wouldn't any study need to consider if the subjects take cod liver oil, vitamin D supplements, as well as determine any participant's vitamin D level?
  I did a quick search on vitamin D deficiency in Norway and it looks like many studies focus on deficiency in immigrant groups, so even that information is taking time to locate. How could study problems related to taking cod liver oil be overcome?

It is a bit funny to focus on deficiency in immigrant groups and 'discover' vitamin D deficiency...
They are dark skinned, wear traditional clothes designed to protect you from tropical sunlight, and I am afraid they do not take cod liver oil as nutritional supplement.
We now understand why most people from northern countries are white skinned blondies!
Their skin is probably able to make vitamin D even under moonlight...

ikod



now a bit of light for this topic from "A-Z Anything in Science..."

Phototherapy

from neonatal jaundice to psoriasis,
cutaneous GVHD and vitamin D deficiency...

          
http://www-english.tamu.edu/pers/fac/myers/phototherapy.jpg
http://www.npl.co.uk/publications/news/opticalrm/issue16/new_high_dose_uva1_therapy_system..jpg
http://news.bbc.co.uk/media/images/38157000/jpg/_38157237_300beach.jpg

ikod   [^]
 

[Zoey]

I'm glad you put some light on the subject, too much yet remains in the shadows.
  I've been watching vitamin D reports for several years and am skeptical of some of what we are seeing in the media on this subject. The common theme is that migration from an area of adequate sunlight, Asia, Africa, especially, to Europe and North American Countries leads to development of D deficiency. This because dark skinned people require more time in the sunlight to produce adequate levels of D, and they are relocating to areas where they get less exposure or useful exposure than in their native countries.
  I'm wondering if there are other factors here that are not as well recognized or are not recieving as much press coverage. From the volume of headlines the last few years one would have to wonder how any population could have developed and thrived in the tropical climates. One would have to wonder too, how any population ever developed in Europe.
  If a focus of the studies is on a population likely to have high percentages of deficiency it makes good  news as a 'major public health problem."
   Because there would be more extensive news coverage, more of the reading public would become "aware" of deficiency and its symptoms. Their increased level of awareness may prompt them to go to the health food store and purchase vitamin D, whether or not they belong to the group making the news.
  Other deficiencies may also be affecting vitamin D levels, but are not being heavily 'marketed' at this time. These abstracts from PubMed, may shed another ray of light on the subject.
Zoey
1: Am J Clin Nutr. 1992 Sep;56(3):533-6.

Effect of iron on serum 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D
concentrations.

Heldenberg D, Tenenbaum G, Weisman Y.

Department of Pediatrics, Hillel-Yaffe Memorial Hospital, Hadera, Israel.

In 13 of 17 infants (aged 10.5 +/- 4.3; mean +/- SD mo) with iron-deficiency
anemia, the serum 24,25-dihydroxyvitamin D concentration was below the normal
range and in 9 of these 13 the serum 25-hydroxyvitamin D concentration was below
the normal range despite the fact that these infants received 10 micrograms
vitamin D/d from the age of 1 mo. The infants were treated with intramuscular
iron dextran (Imferon). The iron-dextran treatment increased the hemoglobin and
serum iron concentrations as well as 25-hydroxyvitamin D and
24,25-dihydroxyvitamin D concentrations. It is known that iron deficiency
impairs fat and vitamin A intestinal absorption. Therefore, it is suggested that
absorption of vitamin D may also be impaired. This may contribute to the
development of vitamin D deficiency. Iron supplementation may have improved the
absorption of vitamin D in the small intestine and hence increased the vitamin D
concentration in the plasma.

PMID: 1503065 [PubMed - indexed for MEDLINE]


: Am J Clin Nutr. 2004 Dec;80(6 Suppl):1725S-9S.  Links
Nutritional rickets: deficiency of vitamin D, calcium, or both?Pettifor JM.
Medical Research Council Mineral Metabolism Research Unit, Department of Paediatrics, Chris Hani Baragwanath Hospital and the University of the Witwatersrand, Johannesburg, South Africa. pettiforjm@medicine.wits.ac.za

Nutritional rickets remains a public health problem in many countries, despite dramatic declines in the prevalence of the condition in many developed countries since the discoveries of vitamin D and the role of ultraviolet light in prevention. The disease continues to be problematic among infants in many communities, especially among infants who are exclusively breast-fed, infants and children of dark-skinned immigrants living in temperate climates, infants and their mothers in the Middle East, and infants and children in many developing countries in the tropics and subtropics, such as Nigeria, Ethiopia, Yemen, and Bangladesh. Vitamin D deficiency remains the major cause of rickets among young infants in most countries, because breast milk is low in vitamin D and its metabolites and social and religious customs and/or climatic conditions often prevent adequate ultraviolet light exposure. In sunny countries such as Nigeria, South Africa, and Bangladesh, such factors do not apply. Studies indicated that the disease occurs among older toddlers and children and probably is attributable to low dietary calcium intakes, which are characteristic of cereal-based diets with limited variety and little access to dairy products. In such situations, calcium supplements alone result in healing of the bone disease. Studies among Asian children and African American toddlers suggested that low dietary calcium intakes result in increased catabolism of vitamin D and the development of vitamin D deficiency and rickets. Dietary calcium deficiency and vitamin D deficiency represent 2 ends of the spectrum for the pathogenesis of nutritional rickets, with a combination of the 2 in the middle.

PMID: 15585795 [PubMed - indexed for MEDLINE]

[Zoey]

Iko,
  I guess the next obvious step is to look up iron and calcium deficiency among the same immigrant populations showing vitamin D deficiency.
Zoey

[iko (OP)]

 Because there would be more extensive news coverage, more of the reading public would become "aware" of deficiency and its symptoms. Their increased level of awareness may prompt them to go to the health food store and purchase vitamin D, whether or not they belong to the group making the news.

I don't think these news come out for commercial reasons.
Vitamins are cheap and immigrants are poor:
as usual these facts are ignored by the most...

Did you get this from cod liver oil topic?
A neat study from Switzerland:

Bone and muscle pain in vitamin D deficiency

http://www.amnesty.org/images/homepage/srilanka_june06.jpg

Short summary from:
G de Torrenté de la Jara, A Pécoud, and B Favrat

Female asylum seekers  with musculoskeletal pain:
 the importance of diagnosis and treatment of hypovitaminosis D.

Hypovitaminosis D is well known in different populations, but may be underdiagnosed in certain populations. We aim to determine the first diagnosis considered, the duration and resolution of symptoms, and the predictors of response to treatment in female asylum seekers suffering from hypovitaminosis D.
In a network comprising an academic primary care centre and nurse practitioners, in 33 female asylum seekers with complaints compatible with osteomalacia, hypovitaminosis D (serum 25-(OH) vitamin D <21 nmol/l) was diagnosed.
The patients received either two doses of 300,000 IU intramuscular cholecalciferol as well as 800 IU of cholecalciferol with 1000 mg of calcium orally, or the oral treatment only.
We recorded the first diagnosis made by the physicians before the correct diagnosis of hypovitaminosis D, the duration of symptoms before diagnosis, the responders and non-responders to treatment, the duration of symptoms after treatment, and the number of medical visits and analgesic drugs prescribed 6 months before and 6 months after diagnosis.
Prior to the discovery of hypovitaminosis D, diagnoses related to somatisation were evoked in 30 patients (90.9%). The mean duration of symptoms before diagnosis was 2.53 years. Twenty-two patients (66.7%) responded completely to treatment; the remaining patients were considered to be non-responders.
After treatment was initiated, the responders' symptoms disappeared completely after 2.84 months. The mean number of emergency medical visits fell from 0.88 six months before diagnosis to 0.39 after. The mean number of analgesic drugs that were prescribed also decreased from 1.67 to 0.85.
Conclusion
Hypovitaminosis D in female asylum seekers may remain undiagnosed, with a prolonged duration of chronic symptoms.
The potential pitfall is a diagnosis of somatisation.
Treatment leads to a rapid resolution of symptoms, a reduction in the use of medical services, and the prescription of analgesic drugs in this vulnerable population.

BMC Fam Pract. 2006 Jan 23;7:4.

Comment:

Cod liver oil instead of vitamin D3 would have sorted the same effect.

It is impressive how much time it takes (1.4-2.8 months) to reach complete resolution of the symptoms: not even all patient responded, but all of them where vitamin D deficient. One patient required seven months of treatment to be free from symptoms.

Intriguing questions:

- How many times is a vitamin D deficiency suspected in an adult complaining bone and muscle pain?

- How many doctors would refer their patients' improvement to a drug injected or prescribed several months before?

- How many patients would take a drug for such a long time in spite of lack of results?

ikod

[iko (OP)]

1: Am J Clin Nutr. 1992 Sep;56(3):533-6.

Effect of iron on serum 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D
concentrations.

Heldenberg D, Tenenbaum G, Weisman Y.

Department of Pediatrics, Hillel-Yaffe Memorial Hospital, Hadera, Israel.

In 13 of 17 infants (aged 10.5 +/- 4.3; mean +/- SD mo) with iron-deficiency
anemia, the serum 24,25-dihydroxyvitamin D concentration was below the normal
range and in 9 of these 13 the serum 25-hydroxyvitamin D concentration was below
the normal range despite the fact that these infants received 10 micrograms
vitamin D/d from the age of 1 mo. The infants were treated with intramuscular
iron dextran (Imferon). The iron-dextran treatment increased the hemoglobin and
serum iron concentrations as well as 25-hydroxyvitamin D and
24,25-dihydroxyvitamin D concentrations. It is known that iron deficiency
impairs fat and vitamin A intestinal absorption. Therefore, it is suggested that
absorption of vitamin D may also be impaired. This may contribute to the
development of vitamin D deficiency. Iron supplementation may have improved the
absorption of vitamin D in the small intestine and hence increased the vitamin D
concentration in the plasma.

Thanks dear Zoey!
I think I missed this one in the pile of vitamin D papers.
Restricted to patients who are actually taking supplements
and have a profund iron deficiency at the same time.
It's not the case of leukemia, of course, but it is quite
important in many other conditions...

ikod

[iko (OP)]

http://distantpeak.com/images/zoom/WIACZN/111_1164.JPG

 
http://farm1.static.flickr.com/134/326391073_f9909d1557_m.jpg
http://farm1.static.flickr.com/144/326390395_e2d00f2105_m.jpg

from:  Climbing Gran Paradiso (4061m) in Italy
        Written by Lyngve Skrede  Friday, 23 July 2004

http://distantpeak.com/web/mountains/europe/gran_paradiso 

 

[Zoey]

Hey Iko,
 Those are awesome pictures! When you return, there is one question for this topic.
  A while back I mentioned having seen a map indicating in which areas of the planet the soil is zinc depleted. As I recall some of the areas were the same in which a high incindence of vitamin A deficiency and childhood blindness also were documented. At the time I was looking up information on a possible relationship between zinc deficiency and vitamin A deficiency. It seems to me that the map was from an international group monitoring nutrient deficiencies around the world. Do you have any ideas on how I might find this information-and map? It has been several moves and computers since I had this information and my reference is lost. If we can find it, it may add another [thin] thread to this discussion.
Zoey

[Zoey]

  If an area providing food is zinc deficient, a seemingly 'good diet' may be less than adequate. From the searching tonight, could there be a link between zinc deficiency, vitamin A, and the development of leukemia?
  At the time I had the map showing areas of soil that was zinc depleted, I was getting a lot of information on Vitamin A from the Sight and Life Organization, which was involved in WHO campaigns to eradicate childhood blindness attributed to vitamin A deficiency. I had seen maps showing areas of the planet where vitamin A deficiency and childhood blindness were common. When the map on zinc deficient soil came up it seemed there might well be a correspondence, between areas of high vitamin A and zinc deficiencies.
 If we locate the map, should we look to see if there is also a correspondence between the rates of leukemia, and the areas where the soil is zinc depleted?
Zoey
Vitamin A: Zinc deficiency is thought to interfere with vitamin A metabolism in several ways: 1) Zinc deficiency results in decreased synthesis of retinol binding ...
http://lpi.oregonstate.edu/infocenter/vitamins/vitaminA/

http://www.eurekalert.org/pub_releases/2006-01/ef-rfc010906.php

 Public release date: 9-Jan-2006
[ Print Article | E-mail Article | Close Window ]

Contact: Garazi Andonegi
garazi@elhuyar.com
34-943-363-040
Elhuyar Fundazioa

Retinol for combating leukemia cells
This press release is also available in Spanish.

 

Vitamin A, also known as retinol, is present in milk, liver, egg yolk, butter and other foodstuffs and as carotene in vegetables that have a yellow-orange colour, such as carrots and pumpkins.

This vitamin is accumulated in the liver where it is transformed into retinoid. Given that vitamin A, as such, has no effect on our organism, it is the retinoids that are responsible for the physiological activity of the vitamin.

Retinoids take part in three processes: in cell death, in cell differentiation and in cell proliferation.

Some ten years ago the Department of Cell Biology and Histology at the University of the Basque Country initiated research into how cell death was boosted by means of retinoids. It was thought that this potential could be used in the fight against cancer cells.

Clean and programmed death

Two types of death occur in cells: necrosis and apoptosis. Necrosis defines a pathological death, i.e. a death caused by a lack or deficit within the cell such as lack of oxygen or food.

On the other hand, apoptosis is the pre-programmed death of a cell. A number of cells have to die in order that our organism function correctly: for example, when the feet of a foetus are developed in the womb of a mother, at first the fingers are united by a membrane. This membrane has to disappear and, so, the cells thereof have to die off so that the hands may develop correctly. This cellular death is programmed in the embryo genes and has a concrete function. This is apoptosis.

All cells, in fact, have the necessary information to be able to undergo apoptosis but, of course, not all cells have to die. Both internal and external stimuli are what initiate this mechanism in those cases where it is necessary. Various modulating substances are involved amongst which are the retinoids.

Boosting apoptosis

Amongst these retinoids, researchers from the University of the Basque Country chose retinamide for their investigations. Retinamide is a synthetic retinoid, i.e. our body does not produce this substance naturally.

Natural retinoids are used to treat various diseases (e.g. those of the skin) but they turn out to be quite poisonous in the doses required – they are not well tolerated. This is why synthetic retinoids are created.

Specifically, the University research team analysed the effect of retinamide in certain types of leukemia - lymphoblastic leukemias. Nowadays, samples from the Hospital de Cruces in Bilbao are used in order to get these types of leukemia cells.

Lymphoblastic leukemias are, as their name indicates, a type of leukemia that affects lymphoblasts. Lymphoblasts are large cells, precursors of lymphocytes. Malign lymphoblasts are constantly dividing and they accumulate in the bone marrow impeding the formation of blood cells. In the analyses undertaken in the laboratory, it was seen that 95 % of these malign lymphoblasts died after application of retinamide. But what is the mechanism that really triggers this death?

To explain the process, the researchers analysed the action mechanism of the retinamide at a molecular level. From the analyses it was observed that the retinamide accelerated the oxidative stress within the malign cells and that this stress triggered the mechanisms leading to apoptosis. This death is normally clean and programmed death, and, to this end, a group of enzymes cut the protein inside the cell at certain sites, leading to the death of the cell in question. The death has no effect on healthy adjacent cells, does not result in swelling and the side effects are minimal.

Thus, according to what has been shown, retinamide has great potential to eliminate the lymphoblastic cells without affecting healthy lymphocytes nor the rest of the normal cells.

Made-to-measure treatment

With the molecular action mechanism understood, researchers investigated why retinamide did not affect healthy cells and they discovered other factors to explain the phenomena. So, apart from molecular mechanisms, other factors that affect the efficacy of retinamide could be clearly seen. These and others should be taken into account if a pharmaceutical to combat leukemias based on retinamide is to be marketed.

Moreover, according to the researchers, future treatment will be patient-specific. As is well known, not all patients suffering from the same illness respond in the same way to the same treatment. This is why lines of medical and pharmaceutical research increasingly mention the need to know the genetic characteristics of each patient in order to specify suitable treatment. In the case of retinamide, treatment will also be similarly specific but, before this, the trigger mechanism of the retinamide in the cells has to be known and this research will provide key data to this end.


###
 

[iko (OP)]

Hi Zoey,
thanks for the vitamin A informations (I put them in my alternative-Favourites files).
Even Zinc deficiency in leukemia is interesting and I remember it has been reported long time ago: 16 citations in PubMed since the early eighties, most impressive data from Turkish docs...
I'll study a bit more this quite complicated thing. It is a REAL puzzle even for docs.
As I told you before, in the case of ALL patients eat so frantically salty foods that any zinc deficiency is probably cured in a few days!
Vitamin A and E combined had been given in the past to leukids even in my hospital (late eighties) and no positive results were reported.
Here we go again: indirect data need confirmation and long term studies if anybody in the field is vaguely interested, but the weak epidemiological evidence from the 'Shanghai report' is there, ready to be used by all of us, scared parents of a leukemia survivor.  It is ready to be applied with no risk and maybe no result, we cannot know.
Later on carnosic acid (rosemary) + vitamin D and vitamin D analogues will come, and maybe sesame seeds flavonoids (sesamin, sesamolin...did you read my posts about it?)
It is late and I have to reply to your Helicobacter connection post!
Take care

ikod

[Zoey]

I will go back to read those posts you mention, rosemary, etc. Then we need to look at writing press releases, and letters seeking research contributions for the COL and Leukemia Awareness Campaign.
Zoey

[iko (OP)]

Why do you write COL instead of CLO?
It's another mystery to me!  []
ikod

[iko (OP)]

To realize where we are and what could be done,
this cut & paste from Complementary Med. (CLO topic)
may help...vitamindcouncil should be our lighthouse!
We might arrange to join them pretty soon.

For skeptical people searching for 'gold standard' treatments
here is reported a precious annotation by Dr. Cannell from the

http://www.vitamindcouncil.com

Vitamin D Newsletter

This is a periodic newsletter from the Vitamin D Council, a non-profit trying to end the epidemic of vitamin D deficiency.  If you don't want to get the newsletter, please hit reply and let us know.  We don't copyright this newsletter.
Please reproduce it and post it on Internet sites.
Remember, we are a non-profit and rely on donations to publish our newsletter and maintain our website.  Our pathetic finances are open to public inspections.  Send your tax-deductible contributions to:
The Vitamin D Council
9100 San Gregorio Road
Atascadero, CA 93422

Supplement
 
Some of you didn't get the last newsletter.  Here's a link.

http://www.vitamindcouncil.com/newsletter/2007-mar.shtml

Why is athletic performance medically important?  If you think for a minute, you'd realize that athletic performance is the same as physical performance.  What happens when physical performance is impaired?  People fall and break their hips, resulting in death, disability, or nursing home admission.  Many people don't realize how fatal falls can be in the elderly.  In 2003, the CDC reported 13,700 persons over 65 in the USA died from their falls, and 1.8 million ended up in emergency rooms for treatment of nonfatal injuries from falls.  Falls cause the majority of hip fractures, which - if they don't result in death - often result in admission to a nursing home.  That's 13,700 deaths, hundreds of thousands of surgeries, countless nursing home admissions, and tens of billions in health care costs every year from impaired athletic performance.  That's why it matters.
 
Centers for Disease Control and Prevention (CDC). Fatalities and injuries from falls among older adults--United States, 1993-2003 and 2001-2005. MMWR Morb Mortal Wkly Rep. 2006 Nov 17;55(45):1221-4. Link:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17108890&query_hl=9&itool=pubmed_DocSum
 
The scientific evidence that vitamin D reduces falls in the elderly is quite strong.  Some physicians say they must wait for randomized, placebo controlled, interventional trials, saying they need such "gold standard" evidence before they will act to prevent falls.  Here are four such "gold standard" studies:
 
Bischoff HA, et al. Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial. J Bone Miner Res. 2003 Feb;18(2):343-51.
Dhesi JK, et al.  Vitamin D supplementation improves neuromuscular function in older people who fall. Age Ageing. 2004 Nov;33(6):589-95.
Flicker L, et al.   Should older people in residential care receive vitamin D to prevent falls? Results of a randomized trial. J Am Geriatr Soc. 2005 Nov;53(11):1881-8.
Harwood RH, et al.  A randomised, controlled comparison of different calcium and vitamin D supplementation regimens in elderly women after hip fracture: The Nottingham Neck of Femur (NONOF) Study. Age Ageing. 2004 Jan;33(1):45-51.

Some say they require a meta-analysis of such "gold standard" studies, from a top-flight university, published in a respected journal, proving vitamin D reduces falls.  Here's a meta-analysis from Harvard, published is the Journal of the American Medical Association, showing vitamin D reduces falls:

Bischoff-Ferrari HA, Dawson-Hughes B, Willett WC, Staehelin HB, Bazemore MG, Zee RY, Wong JB. Effect of Vitamin D on falls: a meta-analysis. JAMA. 2004 Apr 28;291(16):1999-2006.
 
Will these "gold standard" studies prompt physicians to act?  Will older patients finally get a vitamin D blood level and appropriate treatment of their vitamin D deficiency?  No, most will not.  I wish physicians acted on scientific studies but they do not, no matter how many people are dying.  Vitamin D scientists conducting such trials are in for a rude surprise.
No matter how good their studies, no matter how well designed or meticulously conducted, no matter how good the journal, practicing physicians will continue to ignore such studies.  Practicing physicians do what they learned in medical school, do what their colleagues do, and do what the drug company salespersons say.  Very few keep abreast of medical research, unless a drug company representative puts that research under their nose.

That's why I wrote about athletic performance.  If you think about it for a minute, you'll realize that falling is a failure of athletic performance.  Anything that improves athletic performance will reduce deaths from falls.

As far as athletic performance in younger people goes, I certainly got some interesting letters.  One guy from Tennessee agreed to list his phone number in case the press wanted to call or come by and watch him do chin-ups.

...

John Jacob Cannell MD
Executive Director 





 
now a more personal note:
...sometimes pets and captive animals get more vitamin D 'attention' than humans!

ikod

http://www.greenigsociety.org/jpg/JoseAndBaby.jpg

The Green Iguana Society

Lighting: Iguanas must have a source of UVA and UVB light! UVA stimulates natural behaviors by providing a component of natural sunlight. UVB is important to iguanas for another reason. Without it, their bodies cannot manufacture vitamin D3 or properly metabolize calcium. Iguanas that are deprived of proper UV lighting suffer from a disease called Metabolic Bone Disease (MBD) which is unfortunately very common in captive iguanas. MBD causes weak bones, jaw and bone deformities and early death.

The absolute best source of UV light is the sun. Allowing your iguana to bask in the sun on a regular basis will provide it with large amounts of natural UV light. The general rule of thumb is - the more real sun your iguana has access to, the better. One thing to be aware of is that glass and plastic filter out the UV components of sunlight. It is for this reason that you cannot just set your iguana in front of a closed window in the sun. The window glass filters out most of the UV light, so your iguana will not benefit from such sunbathing in terms of vitamin D3 production (although he might enjoy this (in)activity immensely).

An additional source of UV light is special fluorescent UV bulbs available in pet stores that sell reptile supplies. Some people feel that if daily doses of real, unfiltered sunlight can be obtained on most days, then the use of artificial UV light bulbs in the iguana's enclosure is not necessary. However, The Green Iguana Society strongly recommends the use of artificial UV in addition to as much basking time in the sun as possible, to ensure that your iguana gets adequate amounts of UV. The effectiveness of real sunlight to stimulate iguanas to produce vitamin D3 varies with the time of year and latitude of your location. Therefore, the additional use of artificial UV lights acts as a safety net - especially in cool, cloudy and/or northern climates. See the Heating, Lighting and Humidity section for specific information on the proper use of UV bulbs in your iguana's enclosure.

from:  http://www.greenigsociety.org/habitatbasics.htm     

 
...What about captive humans?



Vitamin D3

     



                 

http://www.axxora.com/files/formula/LKT-C0145.gif
http://www.photomed.de/uploads/pics/vitamin_d3_01.jpg
http://www.mmaonline.net/Publications/MNMed2005/November/Images/sun.gif
http://www.teridanielsbooks.com/States/Florida/children,%20beach,%20sand,.jpg

   
 
 
 
 
 
 
 

[Zoey]

I must have been having a dyslexic moment, typing COL
Next it is time to reread your posts on this topic and pull the most salient points into an article or proposal when contacting possible supporters for mounting a public awareness campaign and\or initiating further research.
Zoey

[Zoey]

 These are two of the companies that turned up in looking for who carries out research on COL. There is more searching to do, but do either or both of these look promising?
Zoey

Seven Seas:
Alternativeley, please email info@sseas.com or write to Seven Seas Ltd, Hedon Road, Hull, HU9 5NJ, England with any queries or feedback you may have regarding the Seven Seas Cod Liver Oil range.

Over the past seven decades Seven Seas has invested heavily in scientific research, health education and the most modern manufacturing processes. Today Seven Seas is the leading health supplement brand not only in the UK and Ireland but in the Middle East, Africa, Caribbean and the Far East.

----------

Lysi: Iceland

http://www.lysi.is/is/english/about%5Fus/

The Company

Lysi Ltd. was established in 1938 by Tryggvi Olafsson and his brother Thordur. General need for vitamins A and D triggered the founding of the company.

Following, Lysi Ltd. became the biggest producer of cod liver oil fulfilling demands from USA. In the years from 1938 - 1950 Lysi Ltd. exported large quantities of it's production to "Up-John Ltd." were vitamins
A and D where extracted from the oil.
Over the past 15 years Lysi Ltd. has held the leadership among companies in the area of research and product development in marine lipids.
The firm collaborates with the University of Iceland and the Icelandic Fisheries Laboratories on a continuous basis.

The link between leadership in research and development on one side and leadership in marketing and sales on the other is an obvious one to the management and owners of Lysi Ltd.

The R&D facilities benefit substantially from a massive reorganization dating back to 1980, when the laboratory and it's function where completely redesigned and a new emphasis was placed on research and development.

Based on this unique setup and the close cooperation with leading international pharmaceutical firms and research organizations, Lysi Ltd. is commonly regarded as one of the world leading know-how centers in the field of marine oils and their utilization.

http://www.lysi.is/is/english/about%5Fus/contacts/

Arnar Halldórsson Research and Development Manager arnar@lysi.is


--------------------