[iko (OP)]

WOW! Ikod,

I am stunned.  I like you have a connection to leukemia and children.  Don't give up keep pushing someone will listen... I am listening.  I want to talk to you about this very fascinating area on COD Liver Oil.

I am a Pedi Oncologist in USA... we don't often talk about alternative medical practice/methods...but I agree with you.  We cannot be satisfied with the stalemate of the last several years.

Best wishes.

Hi Cod 4 ALL,

welcome to this forum.
I must thank you and congratulate you for your nickname.
(But keep in mind that AML should be more cod-responding!)
Wish you a connection to leukemia not so tight as mine.
I think this matter is not alternative at all,
but pure, crystal-clear and neglected Science!
Enjoy bits and pieces around here

ikoD  [^]

[Cod 4 ALL]

Ikod,

I am slowly working my way through this fascinating thread- a clear demonstration of your open thought and ability to define the critical question that plague families of children with cancer.

WHY MY CHILD?
I want to offer a few points to ponder, I don't know the answers myself but perhaps someone can add to the thought as we work through this monster.

1.  Genetic changes seen in patients with leukemia have been demonstrated clonal changes among WBC's in the so called "Guthrie cards" now routinely collected at birth to "screen" for treatable genetic diseases.  This work has been widely reported and thought to support the Knudson "two-hit" theory of cancer development - meaning it takes two separate but cooperating events to cause cancer.

my point and questions this... could these "clonal changes" and Vitamin D deficiency cooperate to PUSH and individual toward leukemia.  The obvious argument against this is that not all patients have demonstrated "clonal" changes.  But could this be a CLUE?

2.  If you consider the simple CBC differential as a person ages... there is a predicted "switch" that occurs in children between the ages of 2-4 where the number or relative percentage of lymphocytes goes from a dominate position of say 50-60% of the total WBC's to a much lower 30-40%.  This may not be related and I certainly don't know the answer why this happens - but it has always "bothered" me as there must be a logical if not scientific reason... the deeper question here is ...

Most children develop leukemia during this same time period...the thought I have had for years is what is the connection....if any.

3.  If we accept that Vitamin D deficiency is only the tip of the problem, I think it has been stated that overall vitamin D plays many roles but roughly divided you can say one is BONE development and two roughly lumped together "CELL SIGNALING" mechanisms.  This brings me to my question about the possible association of Vitamin D and OSTEOSARCOMA.

Is it possible that during the adolescent growth spurt the relative amount of vitamin D available for "CELL SIGNALING" events is decreased - thereby creating a "deficiency state" that promotes bone tumor formation?

I will stop here... for now.  Thanks for listening.

Best wishes

[Cod 4 ALL]

IkoD,
Thanks for the welcome.  I must say when I created my "nickname" I did not intend to put "all" in CAPS - guess it happened for a reason.  I understand why AML would be more likely to be a COD responding condition based on what is known about the VDR.

Do we know what the level of 25(OH)D is among patients newly diagnosed?  For that matter do we know how or if 25(OH)D3 influences lymphocyte populations.  The reason I ask is I have been reading quite a bit lately about using the ABSOLUTE LYMPHOCYTE COUNT during induction chemotherapy as a way to identify patients at "risk" of relapse and survival.

It would seem if we could "modify" the ALC when low using (MYSTERY AGENT) we may be able to "stimulate" ones natural anticancer defenses.  I cannot help myself to think there is some way to link this to your interest - I just don't have the knowledge.  Of course it would help if we knew what the target was?  What do you think NK cells? TH2, TH1?


Below is an excerpt from the abstract.  This should be easy to find with the info provided.

CONCLUSIONS:
"ALC is a simple, statistically powerful measurement for patients with de novo AML and ALL. The results, when combined with previous studies, demonstrate that ALC is a powerful new prognostic factor for a range of malignancies. These findings suggest a need for further exploration of postchemotherapy immune status and immune-modulating cancer therapies. Cancer 2008. © 2007 American Cancer Society."
Cancer Volume 112, Issue 2 , Pages 407 - 415

[iko (OP)]

Interesting point Cod 4 ALL,

and crossing "vitamin D deficiency" and lymphopenia on PubMed database gives just ONE citation, 18yrs old russian paper: good for a start, isn't it?

[Development of vitamin D deficiency and immunologic disorders in children with glomerulonephritis]
[Article in Russian]

Sergeev IN, Pletsityĭ KD, Rusnak FI, Spirichev VB.
Biochemical symptoms of vitamin D deficiency and a sharp reduction in the number of T-lymphocytes in the peripheral blood were recorded in children suffering from glomerulonephritis. During the combined therapy using the compound "oksidevit " (1-hydroxyvitamin D3) the parameters characterizing D-vitamin providing became normal, and the number of T-lymphocytes in the peripheral blood was recovered.

Vopr Pitan. 1990 Jul-Aug;(4):28-31.
I'm used to cosidering hypothetical COD-related effects as combined by omega-3, vitamin D3 and vitamin A plus a strong placebo effect.  Yes, a placebo for parents and patients that feel lost against the mysterious enemy but have this old remedy, a relic from the past (number one superfood?), a precious nutrient useful to recover over the months and years.
We had all the scheduled pills over the hours...but 'COD' was our particular thing, that had been so good to our family in the past.  A special care.
At the end of maintenance, when all drugs are suspended and you just follow regular check-ups, 'cod' is always there, to help and defend you...just in case.
Focusing too much on vitamin D effects might lead to the same negative results observed with vitamin A in the eighties...

Speaking of why giving stinky "cod" instead of specific synthetic substances, let's borrow this note from the anti-oxidant topic of the Forum:

quote:
A quote from the article is "Just because a food with a certain compound in it is beneficial to health, it does not mean a pill with the same compound in is"

That's exactly right. A pill sometimes works better than the original food and viceversa.

Scientists versus Mother Nature and her tricks

In the late '70s researchers opened their enormous freezers where thousands of serum samples from blood donors had been stocked since over 10yrs before. They wanted to test vitamin A concentration (knowing that it is well preserved in frozen samples) and look for a correlation with cancer incidence in those individuals. Experimental data in animals had demonstrated a positive effect of retinoic acid on precancerous lesions.
They found a strong inverse relation between vitamin A concentration and risk of tumor. All the media started recommending vitamin A to prevent or even fight cancer.
Few years later a proper RCT (randomized clinical trial) was started: a group of nurses and doctors took either a certain dose of vitamin A or a placebo every day for years. The conclusion of the study was disappointing: no difference in cancer incidence with or without vitamin A.
Some clever mind offered an explanation for this: vitamin A had been found increased in blood donors who had lower risk of cancer because it had been eaten together with some other more effective anticancer compounds.
Here we go with all the broccoli, cabbage, cauliflowers and so on...they are rich of vitamin A and probably have other mysterious anticancer factors.

iko


Addendum:
Vitamin A instead of cod liver oil would play the same trick...if you gave vit.A to patients because the ones taking 'cod' had higher levels of retinoic acid in their blood and were doing better (hypothesis!), you could get poor results because you are not giving together Vit.D and a bit of omega-3 fatty acids, the original recipe.

:mudneddA
 Vitamin D instead of cod liver oil would play the same trick...if you gave vit.D to patients because the ones taking 'cod' had higher levels of vitamin D3 in their blood and were doing better (hypothesis!), you could get poor results because you are not giving together Vit.A and a bit of omega-3 fatty acids, the original recipe.

Do we know what the level of 25(OH)D is among patients newly diagnosed?  For that matter do we know how or if 25(OH)D3 influences lymphocyte populations.  The reason I ask is I have been reading quite a bit lately about using the ABSOLUTE LYMPHOCYTE COUNT during induction chemotherapy as a way to identify patients at "risk" of relapse and survival.

Good question, unfortunately the 2005 Mansoura study from Egypt is the only one showing a profund vitamin D deficiency in every leukemic child at diagnosis, 3mts and 1 year.

Low turnover bone disease in Egyptian children with acute leukemia.

El-Ziny MA, Al-Tonbary YA, Salama OS, Bakr AA, Al-Marsafawy H, Elsharkawy AA.
Endocrinology Unit, Pediatric Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt.

The aim of this work was to study bone turnover markers, calcium homeostasis and bone mineral density (BMD) in children with acute leukemia at diagnosis, after induction chemotherapy, and during maintenance therapy to delineate abnormalities present. After evaluation of L2-L4 BMD using dual-energy X-ray absorptiometry in patients with acute myeloid and lymphoid leukemia at presentation and after treatment, the results were compared to 352 healthy age- and sex-matched Egyptian controls. Calcium homeostasis parameters and bone turnover biochemical markers (serum osteocalcin and urinary deoxypyridinoline) were also assayed and the results were compared to 12 healthy age- and sex-matched controls. Osteopenia was observed at diagnosis and during treatment in patients with acute leukemia. At diagnosis osteopenia was observed in 27 patients (62.8%): 10 (23.3%) had non severe osteopenia and 17 (39.5%) had severe osteopenia. This low BMD persisted in those who were followed up. Parathyroid hormone (PTH) (pg/ml) levels demonstrated non significant differences between children with acute leukemia at different stages of therapy and controls, while, 25 (OH) D3 (ng/ml) was significantly lower in acute leukemia patients at different stages of therapy compared to controls (p<0.001). Osteocalcin (ng/ml) is significantly lower in patients at different stages of the disease compared to controls (p<0.001) but there was no significant difference between patients at different stages of therapy. Deoxy-pyridoline cross links showed non-significant difference between the different types of acute leukemia and with controls. Osteopenia is a significant problem in children with acute leukemia at presentation and after chemotherapy. Osteopenia in acute leukemia appears to be of the low turnover type (decreased osteoblastic activity and decreased bone mineralization).

Hematology. 2005 Aug;10(4):327-33.
You should see the table with vitD serum levels!
I wrote an e-mail to this Author in 2006, citing the Shanghai report.
No reply.  Then I was lucky to find this forum.

[iko (OP)]

BTW, vitD3 is good for HIV-related lymphopenia as well!  []

A potential role for vitamin D on HIV infection?

Villamor E.
Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA. evillamo@hsph.harvard.edu

Despite advances in the knowledge of vitamin D's potent immunomodulatory activity, its role on HIV disease progression is unknown. Decreased concentrations of 1alpha,25-hydroxyvitamin D3, or 1,25(OH)2D, the active form of vitamin D, have been reported among HIV-infected people and attributed to defects in renal hydroxylation and increased utilization. A few studies also described low levels of 25-hydroxyvitamin D3, 25(OH)D, the vitamin obtained from solar synthesis and diet. An inverse association between 1,25(OH)2D concentrations and mortality has been reported from a small cohort of HIV-infected adults, and some cross-sectional studies have indicated positive correlations between 1,25(OH)2D and CD4+ cell counts. Additional observational studies are needed to confirm the associations between vitamin D status and HIV disease progression. These investigations would provide useful insights on the potential role of vitamin D supplementation to HIV-infected persons and the planning of intervention trials.

Nutr Rev. 2006 May;64(5 Pt 1):226-33.



P.S.
I'll do my best to reply point 1-3 from your previous post.
Deep questions need more thinking...

   

http://dowhatnow.typepad.com/do_what_now/images/2007/09/04/codliver_oil.jpg
http://www.nlm.nih.gov/exhibition/ephemera/images/child29.jpg

[iko (OP)]

Do we know what the level of 25(OH)D is among patients newly diagnosed?  For that matter do we know how or if 25(OH)D3 influences lymphocyte populations.  The reason I ask is I have been reading quite a bit lately about using the ABSOLUTE LYMPHOCYTE COUNT during induction chemotherapy as a way to identify patients at "risk" of relapse and survival.


CONCLUSIONS:
"ALC is a simple, statistically powerful measurement for patients with de novo AML and ALL. The results, when combined with previous studies, demonstrate that ALC is a powerful new prognostic factor for a range of malignancies. These findings suggest a need for further exploration of postchemotherapy immune status and immune-modulating cancer therapies. Cancer 2008. © 2007 American Cancer Society."
Cancer Volume 112, Issue 2 , Pages 407 - 415

It's not your fault, I know it, but this makes me feel old and useless.
Almost thirty years have past, studying kinetics and differentiation of the bad 'clones', ignoring the initial causes, testing any remedy... and here we are, counting total circulating lymphocytes to predict an early death.  Where is Science?
I apologize, tomorrow it will be much better.

[Cod 4 ALL]

IkoD,

I agree with you... but this is hard to ignore, there are other papers citing the effect among solid tumors in children.  I should add the original evidence was found in adults following stem cell transplant.

The Mansoura, Egypt data will require more analysis on my part.  It is clearly interesting that they show Vit D deficiency at diagnosis... I think they were looking at this as a clue to the BMD problems seen with ALL therapy.  But before I make wrong assumptions I will need to review the full manuscript and data tables.

This "ALC" effect is real.  But what does it mean?  Is it yet another clue?  Your reply is like others that I have discussed this with.  Everyone cannot believe how we missed this.

Kind of feels like COD and the LOST but not forgotten Shanghai report.  Thanks for the reminder to not FOCUS too much on VIT D3.  I will be in touch.

[iko (OP)]

...A massive vitamin D 'tsunami' is coming closer,
spinning out of the scientific literature circuit:
will flu vaccination campaigns be the first casualties?

Epidemic influenza and vitamin D.

Cannell JJ, Vieth R, Umhau JC, Holick MF, Grant WB, Madronich S, Garland CF, Giovannucci E.
Atascadero State Hospital, 10333 El Camino Real, Atascadero, CA 93422, USA.

In 1981, R. Edgar Hope-Simpson proposed that a 'seasonal stimulus' intimately associated with solar radiation explained the remarkable seasonality of epidemic influenza. Solar radiation triggers robust seasonal vitamin D production in the skin; vitamin D deficiency is common in the winter, and activated vitamin D, 1,25(OH)2D, a steroid hormone, has profound effects on human immunity. 1,25(OH)2D acts as an immune system modulator, preventing excessive expression of inflammatory cytokines and increasing the 'oxidative burst' potential of macrophages. Perhaps most importantly, it dramatically stimulates the expression of potent anti-microbial peptides, which exist in neutrophils, monocytes, natural killer cells, and in epithelial cells lining the respiratory tract where they play a major role in protecting the lung from infection. Volunteers inoculated with live attenuated influenza virus are more likely to develop fever and serological evidence of an immune response in the winter. Vitamin D deficiency predisposes children to respiratory infections. Ultraviolet radiation (either from artificial sources or from sunlight) reduces the incidence of viral respiratory infections, as does cod liver oil (which contains vitamin D). An interventional study showed that vitamin D reduces the incidence of respiratory infections in children. We conclude that vitamin D, or lack of it, may be Hope-Simpson's 'seasonal stimulus'.

Epidemiol Infect. 2006 Dec;134(6):1129-40. Epub 2006 Sep 7.




Note: ... Vitamin D deficiency predisposes children to respiratory infections .
from: Rickets Today - Children Still Need Milk and Sunshine

Nicholas Bishop,M.D.  University of Sheffield
...
Rickets may have severe consequences. It is strongly associated with pneumonia in young children in developing countries. In a case–control study at the Ethio-Swedish Children's Hospital in Addis Ababa,3 Muhe and colleagues demonstrated an incidence of rickets among children with pneumonia that was 13 times as high as that among control children, after adjustment for family size, birth order, crowding, and months of exclusive breast-feeding. The relative risk of death for the children with rickets as compared with the children without rickets was 1.7. Furthermore, bony deformity of the pelvis in women leads to obstructed labor and increased perinatal morbidity and mortality.
...
Children in developed countries need calcium, too. There is clear evidence from prospective studies of dietary supplementation that increased calcium intake during childhood results in increased calcium retention and increased bone mass.8 Young adults with a history of greater milk consumption have a higher total-body bone mass than those with lower intake after the influence of body size is taken into account.9 Calcium, vitamin D, and phosphate are essential nutrients for the growing skeleton. Wherever children live, they should follow Grandma's advice: "Drink up your milk, and go play outside."

N.Engl.J.Med. 1999 341(: 602-604.

http://www.goworldtravel.com/ex/aspx/articleGuid.c009fecc-3cc7-4134-b9d5-d203d0111eb3/xe/article.htm

Connection vitD&low lymphs:  Infantile rickets reduces lymphocyte survival

http://cat.inist.fr/?aModele=afficheN&cpsidt=18348812

I might spend $19 for this full-text about VitD+ASA!    http://www.ncbi.nlm.nih.gov/pubmed/18414055?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Infantile rickets reduces lymphocyte survival

EL HODHOD Moustafa A., NASSAR May Fouad, IBRAHIM Abla Y.
Department of Pediatric, Faculty of Medicine, Ain Shams University, Cairo 11566, EGYPTE
Department of Clinical Pathology, Faculty of Medicine, Ain Shams University Specialized Hospital, Cairo, EGYPTE


Increased incidence of infections had long been recognized in rachitic patients who were also described to have impaired lymphocytic functions.
 This study was designed to assess different apoptotic changes in peripheral lymphocytes in patients with infantile rickets in its various stages and to correlate these findings with the frequency of infection in this disease. The study included 24 rachitic patients with a mean age of 17.88 ± 7.65 months compared with 16 healthy matching controls. There were 7 rachitic patients who were in the active stage, 11 in the healing stage, and 6 in the healed stage. The enrolled cases were subjected to a full history and clinical examination. X-ray of extremities was performed, in addition to the laboratory tests including serum calcium, phosphorus, and alkaline phosphatase as well as direct immunofluorescence using flow cytometry with dual staining technique to check for apoptotic changes in peripheral lymphocytes. The results of the present study showed that the early apoptotic cells percent (EAC%), the late apoptotic and/or necrotic cells percent (LA and/or NC%), the NC%, and the total abnormal cells (%) of the lymphocytes were higher in the rachitic patients compared with healthy controls; although only the latter showed statistical significance. The EAC% of lymphocytes showed a trend to increase accompanied by a simultaneous decrease in the LA and/or NC% with the progression toward the healed rickets stage. The current study also showed a trend of the EAC% and LA and/or NC% of the lymphocytes to decrease with the doses of vitamin D shock therapy given to the rachitic patients. A significant positive correlation was demonstrated between the EAC% and the total abnormal cells (%) of the peripheral lymphocytes and the rate of chest infection in the rachitic cases in the 3 months previous to the study.
In conclusion, rickets does not increase the rate of infection through local causes or immune cell dysfunction only, but it entails disturbed lymphocyte survival. The increased apoptotic tendency of peripheral lymphocytes in rickets is reversed with vitamin D therapy, which further emphasizes the importance of early prevention and proper treatment of such a disease.

Nutrition research 2006, 26 (11), 561-566.

[iko (OP)]

Putting Cod 4 ALL questions in the right order...to reply properly asap.

1.  Genetic changes seen in patients with leukemia have been demonstrated clonal changes among WBC's in the so called "Guthrie cards" now routinely collected at birth to "screen" for treatable genetic diseases.  This work has been widely reported and thought to support the Knudson "two-hit" theory of cancer development - meaning it takes two separate but cooperating events to cause cancer.

my point and questions this... could these "clonal changes" and Vitamin D deficiency cooperate to PUSH and individual toward leukemia.  The obvious argument against this is that not all patients have demonstrated "clonal" changes.  But could this be a CLUE?

Not every leukemia shows clonal changes, as far as I know.
If plenty of immature white cells don't stop dividing, seem unable to differentiate and manage to reach circulating blood from the bone marrow, invading other organs...
well something must be definitely wrong, and it shouldn't matter so much whether they came from one or more 'clones' out of control.
Timo Timonen's hypothesis shows exactly this: vitamin D deficiency in some patients might contribute to let some precursor cells, damaged by a previous infection (viral flu, mycoplasma?) escape from control and start the disease.
In some patients, of course.
We know from the 'Shanghai report' that daily doses of vitamins A and D (actually cod liver oil!) -taken for at least one year- could be able to reduce leukemia incidence to half or 1/3.
It's not much, but we (parents) should give it a chance and offer this protection to our sick children, to avert relapse risk. 

2.  If you consider the simple CBC differential as a person ages... there is a predicted "switch" that occurs in children between the ages of 2-4 where the number or relative percentage of lymphocytes goes from a dominate position of say 50-60% of the total WBC's to a much lower 30-40%.  This may not be related and I certainly don't know the answer why this happens - but it has always "bothered" me as there must be a logical if not scientific reason... the deeper question here is ...

Most children develop leukemia during this same time period...the thought I have had for years is what is the connection....if any.

I'm not your expert for this.  I simply thought that lymphocyte pool is expanded during the first 3-5 years of life for physiological reasons (proper immunological setting under thymus-nodes-spleen control, Ig genes rearrangement etc.), so this state of hyperactivity may more easily get in trouble if something (a reaction to a common pathogen) goes wrong.
Vitamin D deficiency may play a role.

3.  If we accept that Vitamin D deficiency is only the tip of the problem, I think it has been stated that overall vitamin D plays many roles but roughly divided you can say one is BONE development and two roughly lumped together "CELL SIGNALING" mechanisms.  This brings me to my question about the possible association of Vitamin D and OSTEOSARCOMA.

Is it possible that during the adolescent growth spurt the relative amount of vitamin D available for "CELL SIGNALING" events is decreased - thereby creating a "deficiency state" that promotes bone tumor formation?

Why not?
Some time ago I couldn't find any study about VitD levels in patients with osteosarcoma.
At least we HAVE 2-3 papers about VitD deficiency in leukemia!

[iko (OP)]

We know from the 'Shanghai report' that daily doses of vitamins A and D (actually cod liver oil!) -taken for at least one year- could be able to reduce leukemia incidence to half or 1/3.
It's not much, but we (parents) should give it a chance and offer this protection to our sick children, to avert relapse risk. 

Yes, an autoquote.
Waiting for cod4ALL and his comments on the 'Mansoura report' and those striking data about vitamin D deficiency at 0-3-12 months after a diagnosis of childhood leukemia (47 cases: further studies are obviously needed...in the next 2-3 decades).

http://www.uvadvantage.org/portals/0/pres/video/video/slides/slide100.jpg

for at least one year

Why such a long lag-phase of cod-therapy is needed before achieving a significant anti-leukemia effect?  Could this be bound mainly to a vitamin D action?

Well, simple minds can only give simple answers:

If proper levels of vitamin D are needed to counteract leukemia onset, a deficient child (and most humans seem to be vitamin D deficient these days!) gets a relatively small amount of the sunshine vitamin from daily doses of cod liver oil.   Maybe vitamin A helps, together with omega-3 fatty acids and vitamin E, but daily vitamin D through 'cod' is about 400 I.U.
Not much to treat deficiency, so it could take longer to reach adequate concentrations and work properly.

Maybe vitamin A helps

This is a recent medical hypothesis: vitamin A could prevent toxicity of vitamin D and cooperate with vitamin K too...most of the fat-soluble vitamins together!
Isn't it wonderful?   []

Vitamin D toxicity redefined: vitamin K and the molecular mechanism.

Masterjohn C.
Weston A. Price Foundation, 4200 Wisconsin Ave., NW, Washington, DC 20016, United States. ChrisMasterjohn@gmail.com

The dose of vitamin D that some researchers recommend as optimally therapeutic exceeds that officially recognized as safe by a factor of two; it is therefore important to determine the precise mechanism by which excessive doses of vitamin D exert toxicity so that physicians and other health care practitioners may understand how to use optimally therapeutic doses of this vitamin without the risk of adverse effects. Although the toxicity of vitamin D has conventionally been attributed to its induction of hypercalcemia, animal studies show that the toxic endpoints observed in response to hypervitaminosis D such as anorexia, lethargy, growth retardation, bone resorption, soft tissue calcification, and death can be dissociated from the hypercalcemia that usually accompanies them, demanding that an alternative explanation for the mechanism of vitamin D toxicity be developed.
The hypothesis presented in this paper proposes the novel understanding that vitamin D exerts toxicity by inducing a deficiency of vitamin K. According to this model, vitamin D increases the expression of proteins whose activation depends on vitamin K-mediated carboxylation; as the demand for carboxylation increases, the pool of vitamin K is depleted. Since vitamin K is essential to the nervous system and plays important roles in protecting against bone loss and calcification of the peripheral soft tissues, its deficiency results in the symptoms associated with hypervitaminosis D. This hypothesis is circumstantially supported by the observation that animals deficient in vitamin K or vitamin K-dependent proteins exhibit remarkable similarities to animals fed toxic doses of vitamin D, and the observation that vitamin D and the vitamin K-inhibitor Warfarin have similar toxicity profiles and exert toxicity synergistically when combined.
The hypothesis further proposes that vitamin A protects against the toxicity of vitamin D by decreasing the expression of vitamin K-dependent proteins and thereby exerting a vitamin K-sparing effect. If animal experiments can confirm this hypothesis, the models by which the maximum safe dose is determined would need to be revised. Physicians and other health care practitioners would be able to treat patients with doses of vitamin D that possess greater therapeutic value than those currently being used while avoiding the risk of adverse effects by administering vitamin D together with vitamins A and K.

Med Hypotheses. 2007;68(5):1026-34.

Masterjohn's hypothesis about cooperation between these three fat-soluble vitamins is just fascinating.
If proper levels of vitamin A were required to avoid vitamin D toxicity, or to optimize its effects, giving cod liver oil containing Vitamins A and D (text-string from the Shanghai report!) would be much better and safer than recommending vitamin D supplementation alone.
Ancient studies first suggested this protective effect, and they are properly cited in the article:

11) Thoenes F.    Uber die Korrelation von vitamin A and D.
       Deutsch Med Woch 1935;61:2079.

12) Morgan AF, Kimmel l, Hawkins NC.    A comparison of the hypervitaminoses induced by irradiated ergosterol and fish liver oil concentrates.
       J Biol Chem  1937;120(1):85-102.

13) Clark I, Basset CAL.    The amelioration of hypervitaminosis D in rats with vitamin A.
       J Exp Med  1962;115:147-56.




New recipe

"Physicians and other health care practitioners would be able to treat patients with doses of vitamin D that possess greater therapeutic value than those currently being used while avoiding the risk of adverse effects by administering vitamin D together with vitamins A and K."

Med Hypotheses. 2007;68(5):1026-34.

And here we go with cod liver oil (containing vitamins A and D) plus spinaches, cabbage, cauliflower, and other green leafy vegetables (rich of vitamin K)!
We might even give rosemary (carnosic acid) and sesamolin a chance.
And never forget orange juice! (but that's another story)  []

[Cod 4 ALL]

I am a little busy right now I will properly reply as I have more time to compile my thoughts.  Sorry - not lack of interest just time.

[iko (OP)]

I am a little busy right now I will properly reply as I have more time to compile my thoughts.  Sorry - not lack of interest just time.

Take your time cod4ALL,
I'll wait.   I've been around here for almost 2 years!  []

I hope you had enough time to check this out:

Connection vitD&low lymphs:  Infantile rickets reduces lymphocyte survival
http://cat.inist.fr/?aModele=afficheN&cpsidt=18348812

[iko (OP)]

Could by any chance the old remedy, a relic from the past,
an inexpensive nutrient containing vitamins A and D,
help leukemic patients in the long run, AFTER treatment?
According to this recent study, the answer is yes.

Differentiation-inducing liposoluble vitamin deficiency may explain
frequent secondary solid tumors after hematopoietic stem cell transplantation
Minireview.

Gedikoglu G, Altinoz MA.

Secondary cancers are among the most threatening long-term health problems of hematopoetic stem cell- transplant (HSCT) patients. There are several lines of evidence indicating the possibility of a prolonged Vitamin A deficiency for solid tumor-type secondary cancers: I- Solid tumors such as oral cavity, head/neck region squamous carcinomas, skin cancers and melanomas, where lowered Vitamin A concentrations and chemo-preventing activity of its derivatives (retinoids) are most explicitly proven, arise much more frequently than others. II- Early monitorings: A significant retinol deficiency in HSCT patients is detectable along with a severity of mucositis and the vulnerability to infection. III- Monitoring of other liposoluble vitamins: Vitamin D, a differentiation-inducing vitamin like Vitamin A, showed a sustained decrease. Another similarity of these two vitamins is that they also depend on intestinal absorption and are decreased due to bowel injury by conditioning agents and chronic graft-versus-host disease. IV- Peroxidative reactions and inflammation can directly exhaust retinol levels despite sufficient intake. Considering the similar inhibitory role of Vitamin D analogs (deltanoids) on squamous carcinomas, skin tumors and melanomas, we propose that animal studies and extended vitamin surveillance studies in HSCT patients may unfold a preventive strategy against long-term complications.

Neoplasma. 2008;55(1):1-9.

[iko (OP)]

Some news come out crossing "Vitamin D" and "leukemia" on PubMed database.
A study from Valparaiso, Chile, published in January 2008:
Vitamin D administration to leukemic children for 1 year!!!

http://www.a-i-a.com/puyuhuapi/images/valparaiso.jpg

Effect of 1,25(OH)2-vitamin D on bone mass in children with acute lymphoblastic leukemia.

Díaz PR, Neira LC, Fischer SG, Teresa Torres MC, Milinarsky AT, Giadrosich VR, Arriagada MM, Arinoviche RS, Casanova DM.
Pediatric Hemato-Oncology Department, Viña del Mar School of Medicine, University of Valparaíso, Chile.

BACKGROUND: Calcitriol deficit has been described in patients with acute lymphoblast leukemia (ALL). The aim of this randomized case-control trial is to investigate the effectiveness of calcitriol administration during the first year of treatment to protect bone mass. Sixteen children recently diagnosed with ALL, aged 1.7 to 11.5 years, average 5.5, completed the study. Anthropometrical measurements, food intake record, physical activity, and bone pain were registered. Dual energy x-ray absorptiometry was performed at the completion of remission induction chemotherapy (after 1 mo) to measure bone mineral density (BMD) at hip, lumbar spine and whole body, and total bone mineral content and 1 year after. Half of them were randomly assigned to receive calcitriol during 1 year.
STATISTICAL: Kruskal-Wallis, Wilcoxon, Mann-Whitney, and Spearman.
RESULTS: Both groups had similar anthropometric measurements and bone densitometric variables increments. Spine BMD significantly increased in calcitriol supplemented children with lower baseline BMD (r=-0.78 and P<0.05).

CONCLUSIONS: One-year calcitriol administered to recently diagnosed ALL children did not show impact on bone mass. Greater increment in lumbar spine bone mass was observed in patients who received calcitriol and had lower baseline BMD.

J Pediatr Hematol Oncol. 2008 Jan;30(1):15-9.

Never mind.  A 'near-miss' for cod liver oil maniacs and vitamin D fanatics.
The 'Shanghai report' and the 'Mansoura study' are not even mentioned.
Neither this thread in the Naked Scientists Forum is cited!  []

Plasma levels of vitamin D before and after treatment were not measured and the Authors apologize for that.
Unfortunately only calcitriol, the active form of vitamin D has been given to these children, not vitamin D3 or ultraviolet exposure.

Far away from suspecting a vit D deficiency, measuring it and providing proper treatment:

...

Treatment of vitamin D deficiency with 1,25(OH2)D (calcitriol) or analogues of 1,25(OH2)D (paricalcitol, doxercalciferol)

are inappropriate, ineffective, dangerous and contraindicated.

JJ Cannell et al.  2008 excellent and concise review available full-text online!

http://www.vitamindcouncil.org/PDFs/diagnosis-vitdd.pdf

Diagnosis and treatment of vitamin D deficiency.

Cannell JJ, Hollis BW, Zasloff M, Heaney RP.
Atascadero State Hospital, 10333 El Camino Real, Atascadero, California 93422, USA. jcannell@ash.dmh.ca.gov

The recent discovery--in a randomised, controlled trial--that daily ingestion of 1100 IU of colecalciferol (vitamin D) over a 4-year period dramatically reduced the incidence of non-skin cancers makes it difficult to overstate the potential medical, social and economic implications of treating vitamin D deficiency. Not only are such deficiencies common, probably the rule, vitamin D deficiency stands implicated in a host of diseases other than cancer. The metabolic product of vitamin D is a potent, pleiotropic, repair and maintenance, secosteroid hormone that targets > 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. A common misconception is that government agencies designed present intake recommendations to prevent or treat vitamin D deficiency. They did not. Instead, they are guidelines to prevent particular metabolic bone diseases. Official recommendations were never designed and are not effective in preventing or treating vitamin D deficiency and in no way limit the freedom of the physician--or responsibility--to do so. At this time, assessing serum 25-hydroxy-vitamin D is the only way to make the diagnosis and to assure that treatment is adequate and safe. The authors believe that treatment should be sufficient to maintain levels found in humans living naturally in a sun-rich environment, that is, > 40 ng/ml, year around. Three treatment modalities exist: sunlight, artificial ultraviolet B radiation or supplementation. All treatment modalities have their potential risks and benefits. Benefits of all treatment modalities outweigh potential risks and greatly outweigh the risk of no treatment. As a prolonged 'vitamin D winter', centred on the winter solstice, occurs at many temperate latitudes, < or = 5000 IU (125 microg) of vitamin D/day may be required in obese, aged and/or dark-skinned patients to maintain adequate levels during the winter, a dose that makes many physicians uncomfortable.

Expert Opin Pharmacother. 2008 Jan;9(1):107-18.

[iko (OP)]

Diagnosis and treatment of vitamin D deficiency.

Cannell JJ, Hollis BW, Zasloff M, Heaney RP.
Atascadero State Hospital, 10333 El Camino Real, Atascadero, California 93422, USA. jcannell@ash.dmh.ca.gov

The recent discovery--in a randomised, controlled trial--that daily ingestion of 1100 IU of colecalciferol (vitamin D) over a 4-year period dramatically reduced the incidence of non-skin cancers makes it difficult to overstate the potential medical, social and economic implications of treating vitamin D deficiency. Not only are such deficiencies common, probably the rule, vitamin D deficiency stands implicated in a host of diseases other than cancer. The metabolic product of vitamin D is a potent, pleiotropic, repair and maintenance, secosteroid hormone that targets > 200 human genes in a wide variety of tissues, meaning it has as many mechanisms of action as genes it targets. A common misconception is that government agencies designed present intake recommendations to prevent or treat vitamin D deficiency. They did not. Instead, they are guidelines to prevent particular metabolic bone diseases. Official recommendations were never designed and are not effective in preventing or treating vitamin D deficiency and in no way limit the freedom of the physician--or responsibility--to do so. At this time, assessing serum 25-hydroxy-vitamin D is the only way to make the diagnosis and to assure that treatment is adequate and safe. The authors believe that treatment should be sufficient to maintain levels found in humans living naturally in a sun-rich environment, that is, > 40 ng/ml, year around. Three treatment modalities exist: sunlight, artificial ultraviolet B radiation or supplementation. All treatment modalities have their potential risks and benefits. Benefits of all treatment modalities outweigh potential risks and greatly outweigh the risk of no treatment. As a prolonged 'vitamin D winter', centred on the winter solstice, occurs at many temperate latitudes, < or = 5000 IU (125 microg) of vitamin D/day may be required in obese, aged and/or dark-skinned patients to maintain adequate levels during the winter, a dose that makes many physicians uncomfortable.

Expert Opin Pharmacother. 2008 Jan;9(1):107-18.

I know you cannot read it and I'm perfectly aware that most people aren't interested in Dr. Cannell's crusade on vitamindcouncil.com as well.
These days people read messages like these:

"Keep away from the sun to avoid cancer"

"multivitamin pills shorten your life"

Something must be wrong around here.
So, before we hear the usual folks blaming vitamin D supporters for huge profits from celebrity and vitamin pills plus UV lamps market, let me report the final words of this superb review by John Cannell and his colleagues.
Please do read the complete article: if you had enough time to read this crap page, you MUST find a few minutes for real Science!

http://www.vitamindcouncil.org/PDFs/diagnosis-vitdd.pdf

...
To the authors' knowledge, plaintiffs' attorneys are not yet involved in the vitamin D debate.   After the findings of Lappe et al. (1), it may only be a matter of time until lawsuits against physicians begin to appear, claiming that physicians dispensed sun-avoidance advice, but negligently failed to diagnose and treat the consequent vitamin D deficiency, leading to fatal cancers.   Unless the future literature fails to support the present, such medical malpractice suits may become commonplace.

Finally, physicians and policy-makers should understand that much of the future of vitamin D is out of their hands.   Inexpensive high-dose supplements are now widely available to the American public over-the-counter and to the world via the Internet.   Sunlight remains free.   A Google search for 'vitamin D' reveals several million hits.   After the Canadian Cancer Society recently recommended 1000 IU/day for all Canadian adults in the wintertime, vitamin D disappeared off the shelves, causing a shortage during the summer.

The pleiotropic actions and unique pharmacology of vitamin D mean educated patients, on their own, can entirely control their own tissue levels of this steroid, through either UVB exposure or over-the-counter supplementation.   Given the attitudes that some in mainstream medicine have about any substance with the word 'vitamin' in it (105), the public and not the medical profession may be the first to enter the vitamin D era.

reference 105:

Battling quackery: attitudes about micronutrient supplements in American academic medicine.

Goodwin JS, Tangum MR.
Center on Aging, The University of Texas Medical Branch, Galveston 77555-0460, USA.

...sorry, $15 to read even the only abstract!!!  []

Arch Intern Med. 1998 Nov 9;158(20):2187-91.

[iko (OP)]

WOW! Folks, I'm stunned too...

so much time has passed, the "resurrection of vitamin D" is going fast and many scientific reports are invading the medical literature.
Still, Googling this particular text-string: " vitamin D deficiency in leukemia "...you find absolutely no result.    It will be a long way.

ikoD


BTW, today, typing: "vitamin D deficiency in " gives you a 120,000 round figure.
                   "vitamin C deficiency in " gives you 18,100 citations.

http://www.greenhealthspot.com/images/2007/11/09/sunshine.jpg

...it's just about time to change the title of this "ancient" thread:

from "Cod Liver Oil and Childhood Leukemia" to a more intriguing "Vitamin D deficiency in Leukemia?"


From now on, this highly specific text-string "works" on Google!

[iko (OP)]

September 1999...November 2007:

 "Play it again Timo!"

Are sunlight deprivation and influenza epidemics associated with the onset of acute leukemia?

Timonen T, Näyhä S, Koskela T, Pukkala E.
Department of Internal Medicine, Oulu University Hospital, Oulu, Finland.

Month of diagnosis of 7,423 cases of acute leukemia (AL) in Finland during 1964-2003 were linked with data on influenza and solar radiation.
Acute myeloblastic leukemia (AML) showed the highest risk in the dark season. During the light season, the incidence decreased by 58% (95% confidence interval, 16-79%) per 1,000 kJ/m(2)/d increase of solar radiation. Independent of solar radiation, AML increased by 9% (95% confidence interval, 0-19%) during influenza epidemics. Reoccurring at the same time annually, darkness-related vitamin D deficiency and influenza could cause successive and co-operative mutations leading to AL with a short latency.

Haematologica. 2007 Nov;92(11):1553-6.

Free full-text available on line:
http://www.haematologica.org/cgi/reprint/92/11/1553?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&andorexacttitle=and&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&volume=92&firstpage=1553&resourcetype=HWCIT

...Surprisingly enough, the "Shanghai report" is not mentioned in the whole article.


Nobody is perfect. []

...
Getting close

…In late 1999 a team of Finnish pediatricians investigate bone turn over in children suffering from cancer (40% leukemias) at completion of therapy. They find abnormal data related to calcium and bone metabolism that explain the high incidence of osteoporosis and pathological fractures observed in these patients. Together with calcium, vitamin D is found significantly lower (P<0.0001). These alterations are referred to bone invasion by cancer initially, but most of all to chemotherapy damage later. These Authors suggest to consider a controlled clinical trial to evaluate the possibility of vitamin D and calcium supplementation.


Click down here to see the abstract:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10531569&query_hl=2&itool=pubmed_docsum

Suprisingly, in 1999, writing from the very same country (Finland) the bright hematologist T.T.Timonen gets published in Ann.Hematol. "A hypothesis concerning deficiency of sunlight, cold temperature, and influenza epidemics associated with the onset of acute lymphoblastic leukemia in northern Finland." In the end of the summary: "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."

http://www.yukonhelmut.de/Winter/Artic1.jpg

"A hypothesis concerning deficiency of sunlight, cold temperature, and influenza epidemics associated with the onset of acute lymphoblastic leukemia in northern Finland."  by T.T. Timonen, 1999.

Click down here to see the abstract:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10525828&query_hl=6&itool=pubmed_docsum

...but all this is just supporting Mel Greaves’s hypothesis: “the final hit may be infectious”.
Dr. Timo Timonen actually introduces the concept that vitamin D3 deficiency itself might cause leukemia in some patients.

http://www.corecharacter.com/uploads/einstein3-thumb.jpg

"The whole of science is nothing more than a refinement of everyday thinking."
Albert Einstein

...
The pleiotropic actions and unique pharmacology of vitamin D mean educated patients, on their own, can entirely control their own tissue levels of this steroid, through either UVB exposure or over-the-counter supplementation.   Given the attitudes that some in mainstream medicine have about any substance with the word 'vitamin' in it, the public and not the medical profession may be the first to enter the vitamin D era.

John Jacob Cannell
http://www.vitamindcouncil.org/PDFs/diagnosis-vitdd.pdf

..."educated patients" doesn't necessarily mean that they had read up on vitamin D.
In some cases personal experience helped to solve this problem from the very start.

Many years ago, at the camping ground near the seaside where I went with my family, I noticed four elderly men around a table, playing cards.
One of the group was 'reeeally' tanned, almost black, much darker than the others.  Another friend passed by and started chatting.
After having said to the overtanned fellow: "You surely took a lot of sun this summer!",
he got this quick reply, probably the same given every day to others, over and over:

"Well, when I don't do this, I get aches and pains in the winter"


That wise old man had found out something important for his health all by himself.
He actually tested it "on his own skin"... year after year, then he drew his conclusions.
No 1988 Shanghai report, no 1999 Timo Timonen's hypothesis, and much before the "resurrection of vitamin D" (2007).

 
        
http://www.equilibriarte.org/upload/forum/070805145950-238.jpg

[iko (OP)]

Cut and paste from another thread:

Neilep, our dearest moderator, asked: "Why are colds, sore throats, colds etc so much more common in winter ?"

Easy question Neilepus amicissimus,

the answer MIGHT be right here:

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=529704

Enjoy

ikod

AWESOME !!!..Vitamin D Rules !!...If only I knew a good source of Vitamin D !! [] []

Hi Neilepus rapidofastissimus thread-makerus!

Cod liver oil is no good for 'boosting' your vitamin D: plenty of vitamin A and omega-3 fatty acids plus 'some' vitamin D.
It probably works in the long run as far as vitamin D3 is concerned (approx. 400 I.U./day).
So dear old 'cod' is still used daily in northern Europe, during months with the 'R': from September to April.
Short 'flashes' (30min.) of sushine between 10a.m. to 2p.m. at a proper latitude (no clouds please) really boost your  skin production of vitamin D3 (>20,000 I.U.)

Sorry you cannot read the complete paper previously cited by ikus.
You would be impressed by a 1918 study about flu reported in the article.

Shortly, in 1918, trying to find out how influenza viruses managed to infect people and to verify relative incubation times (2-3 days), proper experiments were set up using human volunteers.  Forget the details  [xx(]...but secretions from infected patients were carefully collected, mixed up and flushed through the nostrils of brave volunteers.   []
Surprisingly enough, nothing happened afterwards, so the experiment was considered a 'fiasco'.

Only now, 90 years later, a crystal-clear explanation is ready for this.
Anti-infective properties of vitamin D were proved only 4-5 years ago, when the cathelicidin pathway was described.
Those volunteers were healthy men from the Navy.
Probably well-tanned all year round, perfectly healthy, they had been selected for not having had a flu in the previous months, to avoid an 'immunization' bias.
Maybe a good level of vitamin D helped them to block the influenza viruses quickly.

For the same reason, somewhere in 2005, most (maybe all) vitamin D supplemented patients in Dr J.Cannell department, Atascadero CA, went through a big influenza epidemic perfectly healthy.
John Cannell was the 'prepared mind', times were changing, so the vitamindcouncil.com crusade started.

One hypothesis out of many is that flu viruses do circulate all year round in humans, but give troubles in some people only in the cold season, i.e. when vitamin D levels are low.
So much for the anti-flu vaccination campaigns.

http://www.youtube.com/watch?v=enB6BuOjXY8

P.S.
The reason why Chris is not commenting on these issues is simple: he is a virology expert and knows much better than others the other side of the coin.
Everybody is waiting for final scientific proofs about vitamin D and flu, but most of all about vitamin D benefits in other dreadful diseases.
Wonderful hypotheses need extended and accurate studies to become Science.  It takes so much time.
I'm sure Chris will never have to decide from trembling hypotheses whether to give 'cod' to one of his kids or NOT.
It happened to me, after years of serious searches and rigorous evidence-based training.
That's life.

ikod

Hypothesis--ultraviolet-B irradiance and vitamin D reduce the risk of viral infections and thus their sequelae, including autoimmune diseases and some cancers.

Grant WB.
Sunlight, Nutrition, and Health Research Center, San Francisco, CA, USA. wgrant@infionline.net

Many viral infections reach clinical significance in winter, when it is cold, relative humidity is lowest and vitamin D production from solar ultraviolet-B irradiation is at its nadir. Several autoimmune diseases, such as multiple sclerosis, type 1 diabetes mellitus and asthma, are linked to viral infections. Vitamin D, through induction of cathelicidin, which effectively combats both bacterial and viral infections, may reduce the risk of several autoimmune diseases and cancers by reducing the development of viral infections. Some types of cancer are also linked to viral infections. The cancers with seemingly important risk from viral infections important in winter, based on correlations with increasing latitude in the United States, an index of wintertime solar ultraviolet-B dose and vitamin D, are bladder, prostate, testicular and thyroid cancer, Hodgkin's and non-Hodgkin's lymphoma, and, perhaps, gastric cancer. The evidence examined includes the role of viruses in the etiology of these diseases, the geographic and seasonal variation of these diseases, and the time of life when vitamin D is effective in reducing the risk of disease. In general, the evidence supports the hypothesis. However, further work is required to evaluate this hypothesis.

Photochem Photobiol. 2008 Mar-Apr;84(2):356-65. Epub 2008 Jan 7.

   

[iko (OP)]

Fifty-five years ago...

"Look, Johnnie, over there is a little spot of sunshine,
go over and play in and get your vitamin D."



http://www.uvadvantage.org/portals/0/pres/video/video/slides/slide375.jpg

[iko (OP)]

Good NEWS on D-vitamin!!!

M. A. Helou, G. Massey, G. Francis, K. Godder, J. Laver
 
Abstract:
Background: Survivors of childhood cancer are at increased risk for osteoporosis. Contributing factors include direct effects of chemotherapy and radiation therapy on bone, secondary hormone deficiencies, and chronic illness. However, vitamin D insufficiency could be a major risk factor during and after cancer therapy. Vitamin D insufficiency is common in healthy school aged children (median 25-hydroxy vitamin D [25(OH)D] = 28 ng/mL, 55% <30 ng/mL, 5% < 10 ng/mL.) Based on this data, we hypothesize that vitamin D insufficiency would be common among children with cancer. If vitamin D insufficiency is prevalent, correction may contribute to better bone health and immune responses in children with cancer. Methods: We determined the serum levels of 25(OH)D, PTH, calcium, and phosphorus for 40 children with leukemia or lymphoma currently on therapy (group 1), 34 children with leukemia or lymphoma off therapy (group 2), 16 children with solid tumors currently on therapy (group 3), and 10 children with solid tumors off therapy (group 4.) Prevalence of 25(OH)D insufficiency ( <32 ng/mL) and severe deficiency (<10 ng/mL) was compared by Chi square test to the healthy reference population (established by Weng, et al.)
Results: For the majority of patients, calcium and phosphorus levels were within normal limits. Conclusions: Vitamin D insufficiency was very common in all groups, especially in children with solid tumors on therapy (Group 3.) 25(OH)D levels did improve off therapy, but for Group 2, still remained significantly less than normal reference population (p=0.0001.)

The data suggests that vitamin D status should be determined for all children at diagnosis of malignancy with a strong recommendation to consider vitamin D supplementation during treatment and follow up.

J Clin Oncol 26: 2008 (May 20 suppl; abstr 10023)

http://www.asco.org/ASCO/Abstracts+&+Virtual+Meeting/Abstracts?&vmview=abst_detail_view&confID=55&abstractID=35975

Something is finally "moving" on the clinical research side...
I hope(dream) that many parents -on the other side- are giving 'cod for more than one year'!

Unfortunately, if vitamin D is needed mainly, and too much vitamin A is either toxic or counteracting "D" wonderful effects (J.Cannell et al. Nov.2008), we would need a special cod liver oil formula:

a moderate amount of vitamin A, plenty of D-vitamin and lots of omega-3!

This probably WAS the original cod liver oil, before they started removing D-vitamin, erroneously thinking that it was too close to toxic amounts.
Two thousands I.U. per day of vitamin D3 was considered almost toxic for humans.
What a shame: we seem to have destroyed the original formula.

From January 2008 VitaminD Newsletter:

...
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, MD

http://content.ll-0.com/vitalchoiceseafood/Cannell.John.140.jpg

http://www.vitamindcouncil.com/

http://www.lung.ca/tb/images/full_archive/006_codLiverOil.jpg

http://karmadaze.com/sunrise.jpg