[dqfry]

I'm grateful for the advance cancer therapy available to us - specially being from a 3rd world country where resources are limited. I'm certain that we're not to far from target therapy and even more vaccines for certain cancers (including Leukemias)

Why did my "super baby" who was breastfed for 12-months and only receive the best and most natural nutrition available is fighting such a nasty disease? Although my initial reaction was to give up the CLO, acai (Brazilian berry loaded with antioxidants), organics, and everything else I was raised on, I couldn't!

So, today is a great day because my son is still with us and he had his spoon of CLO this morning with breakfast (sometimes is virtually impossible get that spoon of CLO go down)

Lastly, I'll take the blame for Zoey's "topic-who-nobody-caresof annihilating crisis". Maybe my initial post got her excited!!!!!

Cheers

DQfry

[Zoey]

Hi DQ,
 
There's a misunderstanding about the "no care" references; a week or so ago I started a different topic. There were some misunderstandings and bad feelings so I erased the entire discussion [Sometimes when I get upset I hold my breath until I look really awful too!]. It had nothing to do with your posts at all.

Why did my "super baby" who was breastfed for 12-months and only receive the best and most natural nutrition available is fighting such a nasty disease? Although my initial reaction was to give up the CLO, acai (Brazilian berry loaded with antioxidants), organics, and everything else I was raised on, I couldn't!
-----------------------------------
You are raising important questions. So how do we start with finding answers? One thing comes to mind. When gathering information on vitamin D deficiency and seizures in children, I read that breast milk does not contain sufficient amounts to meet the needs for infants.:

"PEDIATRICS Vol. 111 No. 4 April 2003, pp. 908-910


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

CLINICAL REPORT


Prevention of Rickets and Vitamin D Deficiency: New Guidelines for Vitamin D Intake
Lawrence M. Gartner, MD, Frank R. Greer, MD, Section on Breastfeeding and Committee on Nutrition
ABSTRACT

Rickets in infants attributable to inadequate vitamin D intake and decreased exposure to sunlight continues to be reported in the United States. It is recommended that all infants, including those who are exclusively breastfed, have a minimum intake of 200 IU of vitamin D per day beginning during the first 2 months of life. In addition, it is recommended that an intake of 200 IU of vitamin D per day be continued throughout childhood and adolescence, because adequate sunlight exposure is not easily determined for a given individual. These new vitamin D intake guidelines for healthy infants and children are based on the recommendations of the National Academy of Sciences."
http://aappolicy.aappublications.org/cgi/content/full/pediatrics;111/4/908
  The focus here is on rickets prevention and it appears there is no consideration in this and similar studies to the effects of Vitamin D deficiency on suseptibility to diseases such as cancer.
 Also, the other major vitamin in CLO, vitamin A, can also be in short supply in breast milk. Just to make this more complex, zinc deficiency via breast feeding may also pose a problem with development and resistence to disease.

"European Journal of Clinical Nutrition:December 1998, Volume 52, Number 12, Pages 884-890
Moderate zinc and vitamin A deficiency in breast milk of mothers from East-Jakarta
...Conclusions: Multi-micronutrient intervention should be considered to provide a sufficient supply of zinc and vitamin A for growth of exclusively breast-fed infants"
http://www.nature.com/ejcn/journal/v52/n12/abs/1600660a.html

Some earlier posts in this discussion have information on vitamin A and zinc deficiencies and how this may affect suseptibility to developing leukemia as well.
I'm glad you had a good day and hope you will be having many of them as you see your son recover.

[paul.fr]

Now that you put your foot in the door, Paul, you may want to do some of the research for this topic too.

i only tested the water with my toes, not yet ready to go for a swim.

[Zoey]

Iko,
 My foot is firmly in my mouth! I missed the points you made above regarding the limits of this topic. So sorry and will be extra cautious now.
Zoey

[iko (OP)]

Too many nutrients have been proposed in the last few years, but their efficacy seems still unsubstantiated in most of the cases, and practical demonstrations too vague or totally absent.
It is NOT the purpose of this topic.
We have to stick to 'cod' and a vague 1988 article, especially now that dqfry joined us.
She gave us in a few words a clear and dramatic picture of the limits of this issue.


Cod liver oil used during standard treatment of leukemia, probably could just 'help' leukemic patients, perhaps counteracting a vitamin D3 deficiency that still has to be confirmed.
This positive effect has to be demonstrated in practice, and only for lack of toxicity and costs this use could be recommended before improbable officially conducted clinical trials.
We do not have detailed data from the Shanghai report as I told you: there were 'buried' in 5" diskettes so it is impossible to find out whether the 'protective' effect had been found lower or what in toddlers compared to growning-up 8-12yrs children (this was one of my questions to Dr. Shu in 1999).

iko   09/04/2007

We're free to open various topics and keep this one ultraspecific to avoid generalizations and dispersion of the few evidences I think we have.

Dqfry surely thinks that 'cod' is not so much effective, and we'd think the same thing, being in her shoes.  So I have to remind my question about age correlations with the protective' effect.  I'll try to explain my thoughts.
The infectious hypothesis, bound to an hypothetical overridden immune reaction to a common pathogen and abnormal expansion of a specific clone of lymphocytes may concern older kids, not infants and toddlers, who show lymphocyte hyperactivity even in normal conditions.  A difference bound simply to age and immunological 'activity' may be present. Concentration of the disease within the bones, with typical bone aches and very few lymphnodes enlarged and rarely fever is more common in older children.
We'll never know whether in the 1988 Shanghai study a protective effect (actually stronger in myeloid leukemia) had been found dispersed or concentrated in a particular age group.

Nevertheless, as clearly shown in those 'ancient' tables, 8% cod in controls versus 4% cod in leukemic children is significant all right, but does not mean total immunity.
My speculation is: could most of the patients benefit of a protective effect in the long run, or only patients doing already fine with standard treatments?
In this second hypothesis no adjunctive therapeutic effect could be observed.
After all this mess.

ikod

click here for a proper view:   http://www.electric-fields.bris.ac.uk/Aetiology.jpg

[Zoey]

 I just did a search on press releases from the American Academy for the Advancement of Science-not one single research report for this year is listed.

[Zoey]

iko   09/04/2007
[/quote]
My speculation is: could most of the patients benefit of a protective effect in the long run, or only patients doing already fine with standard treatments?
In this second hypothesis no adjunctive therapeutic effect could be observed.
After all this mess.

ikod

http://www.electric-fields.bris.ac.uk/Aetiology.jpg[/center]
[/quote]
Should we be looking at population studies and comparing rates of recovery?

[iko (OP)]

Should we be looking at population studies and comparing rates of recovery?

Yap!
you mean finding out survival results related to...what, age?
It's a real jungle, even different from one study to another!

...this one is from Denmark:

http://www.danmedbul.dk/Dmb_2006/0106/0106-artikler/DMB3783-4.jpg

ikod

[iko (OP)]

Hi friendos,

Cod liver oil in childhood leukemia
...and the vitamin D3 connection.
The discussion is open, waiting for a real
scientist who explains to this bunch of loonies
the difference between a 'coincidence' and real
heavy and thick scientific evidence!   []

ikod

Season and ethnicity are determinants of serum 25-hydroxyvitamin D concentrations
in New Zealand children aged 5-14 y.

Rockell JE, Green TJ, Skeaff CM, Whiting SJ, Taylor RW, Williams SM, Parnell WR, Scragg R, Wilson N, Schaaf D, Fitzgerald ED, Wohlers MW.
Department of Human Nutrition, Preventive and Social Medicine, University of Otago, Dunedin, New Zealand.

New Zealand children, particularly those of Maori and Pacific ethnicity, may be at risk for low vitamin D status because of low vitamin D intakes, the country's latitude (35-46 degrees S), and skin color. The aim of this study was to determine 25-hydroxyvitamin D concentrations and their determinants in a national sample of New Zealand children aged 5-14 y. The 2002 National Children's Nutrition Survey was designed to survey New Zealand children, including oversampling of Maori and Pacific children to allow ethnic-specific analyses. A 2-stage recruitment process occurred using a random selection of schools, and children within each school. Serum 25-hydroxyvitamin D concentration [mean (99% CI) nmol/L] in Maori children (n = 456) was 43 (38,49), in Pacific (n = 646) 36 (31,42), and in New Zealand European and Others (NZEO) (n = 483) 53 (47,59). Among Maori, Pacific, and NZEO, the prevalence (%, 99% CI) of serum 25-hydroxyvitamin D deficiency (<17.5 nmol/L) was 5 (2,12), 8 (5,14), and 3 (1,7), respectively. The prevalence of insufficiency (<37.5 nmol/L) was 41 (29,53), 59 (42,75), and 25 (15,35), respectively. Multiple regression analysis found that 25-hydroxyvitamin D concentrations were lower in winter than summer [adjusted mean difference (99% CI) nmol/L; 15 (8,22)], lower in girls than boys [5 (1,10)], and lower in obese children than in those of "normal" weight [6 (1,11)]. Relative to NZEO, 25-hydroxyvitamin D concentrations were lower in Maori [9 (3,15)] and Pacific children [16 (10,22)]. Ethnicity and season are major determinants of serum 25-hydroxyvitamin D. There is a high prevalence of vitamin D insufficiency in New Zealand children, which may or may not contribute to increased risk of osteoporosis and other chronic disease. There is a pressing need for more convincing evidence concerning the health risks associated with the low vitamin D status in New Zealand children.

J Nutr. 2005 Nov;135(11):2602-8.

Comparison of cancer mortality and incidence in New Zealand and Australia.

Skegg DC, McCredie MR.
Department of Preventive and Social Medicine, University of Otago, Dunedin.

AIMS: To compare cancer mortality and incidence data from New Zealand and Australia, in order to gauge the potential for reducing deaths from cancer in New Zealand. METHODS: For 1996 and 1997, numbers of deaths from cancer, numbers of new cases, and population data were stratified in 5-year age-groups. Numbers observed in New Zealand were compared with numbers expected from Australian rates. Age-standardized mortality and incidence rates for each sex were analysed.
RESULTS: New Zealanders of both sexes experienced more deaths from cancer than expected in every age group. If Australian rates had applied, there would have been 215 fewer cancer deaths per year in New Zealand males, and 616 fewer in females. The largest differences related to breast cancer and lung cancer in women, and colorectal cancer in both sexes. The overall incidence of cancer was higher in New Zealand, but mortality/incidence ratios were also higher for many sites--suggesting that survival after treatment has been poorer in New Zealand than in Australia. CONCLUSIONS: Considerable scope exists for reducing cancer mortality in New Zealand. For a national cancer control strategy, it will be essential to clarify reasons for the high incidence of cancer and to study survival following treatment.

N Z Med J. 2002 May 10;115(1153):205-8.

  

http://www.emiratesteamnz.com/newzealand/images/061212_01/NewZealandFloraLR.jpg
http://www.mmaonline.net/Publications/MNMed2005/November/Images/sun.gif

[iko (OP)]

Quick search for vitamin D deficiency in New Zealand:

Vitamin D deficiency in pregnant New Zealand women.

Judkins A, Eagleton C.
Department of Endocrinology, Wellington Hospital, Private Bag 7902, Wellington. carl.eagleton@ccdhb.org.nz

AIM: This aim of this study was to identify the prevalence of vitamin D deficiency in pregnant women of a Wellington general practice where 10 cases of childhood rickets had been diagnosed over the past 3 years. METHODS: Ninety pregnant women were screened for vitamin D deficiency by measuring 25-hydroxy vitamin D by DiaSorin radioimmunoassay. Recruitment into the study was over a 12-month period. A second appointment was arranged for clinical review and drawing of blood for parathyroid hormone, adjusted calcium, and alkaline phosphatase. RESULTS: 100% of women presenting to the general practice for antenatal care consented to the study.
87% of women had 25-hydroxy vitamin D levels below 50 nmol/L.
61.2% of women had a vitamin D level below 25 nmol/L consistent with severe vitamin D deficiency. 10 women had an elevated parathyroid hormone consistent with secondary hyperparathyroidism. Only 22% of our patients were veiled, and included a diverse ethnic population, including African, Maori, European, Middle Eastern, and Polynesian women. CONCLUSIONS: Vitamin D deficiency is common in young pregnant women in this general practice, and it was not only confined to veiled women or women with dark skin. This highlights the magnitude of vitamin D deficiency in the pregnant population in a New Zealand setting; this vitamin D deficiency is responsible for the re-emergence of childhood rickets.

N Z Med J. 2006 Sep 8;119(1241):U2144.

Rickets in alpacas (Lama pacos) in New Zealand.

Hill FI, Thompson KG, Grace ND.
AgResearch, Flock House Agricultural Centre, Private Bag 1900, Bulls 5242, New Zealand.

Rickets was diagnosed in two weaner alpacas from a flock showing ill thrift and lameness during the winter of 1992. Both animals had abnormally shaped ribs with occasional healing fractures, irregular thickening of growth plates and metaphyseal haemorrhages. The mean serum phosphorus concentrations of the alpacas fell during June and July, even though lambs grazing the same pasture had normal serum phosphorus concentrations and the phosphorus concentration of the pasture was considered adequate. Vitamin D deficiency may also have contributed to the osteodystrophy. The alpacas had a thick fleece during the winter, and diurnal Vitamin D, synthesis resulting from solar irradiation is likely to have been minimal, especially considering the reduced sunshine hours recorded during the 1992 winter. Surviving alpacas recovered after treatment with monosodium phosphate and an oral Vitamin D supplement. It is possible alpacas are more susceptible to deficiencies of phosphorus and Vitamin D than other grazing animals in New Zealand.

N Z Vet J. 1994 Dec;42(6):229-32.

http://www.alpacasnz.co.nz/images/aobacoverarticles.JPG

VITAMIN D
By Nic Cooper, Southern Alpacas Stud

In the early days of alpacas in New Zealand, the industry saw  many cases of carpal valgus (bent or bowed front legs)  in alpacas.  These ranged from minor to the extreme. The higher concentration appeared to be amongst the darker coloured animals, and it appeared in youngsters, particularly when autumn born, during winter. At Southern Alpacas Stud one of your first cria born, in 1990, developed extreme rickets.

The effect was quickly traced, by researchers, to a vitamin D or phosphorous deficiency, and led to a lot of breeders sprinkling di-calcium phosphate on nuts, and adding other such supplements to nut mixes.

Research in the mid 1990's (ex USA) then indicated that treatment with vitamin D alone would alleviate the clinical signs, and (ex Australia) that di-calcium phosphate was actually bad for your alpacas. But read on for 2005 information ......

Vitamin D (particularly vitamin D3 – chalecalciferol) is necessary to the alpaca to allow it to absorb calcium and phosphorous from the intestinal tract. 

Calcium is the most abundant mineral in the body, phosphorous is the second most abundant. These minerals are required for proper bone development. Many enzymes and B vitamins are activated only in the presence of Phosphorous.

Phosphate is the naturally occurring form of the element phosphorus. Phosphate deficiency is what is measured in the bloods, and we treat with a phosphorus compound.

The natural Calcium/Phosphorous ratio in bones and teeth in 2:1, (although 1.5:1 in alpaca is closer to the ideal), and vitamin D is essential for maintaining this balance correctly.

Adequate vitamin D levels also minimise the loss of these two minerals through the kidneys (in excreta).

Vitamin D3 is produced through synthesis in the alpacas skin, from the action of ultraviolet light (sunlight) on cholesterol derivatives. In New Zealand the lower latitudes, and lower altitudes reduce this production, especially in winter, especially in darker pigmented animals, and especially in animals with denser fleeces.

Vitamin D also comes from consumption of sun cured dried foods, such as hay (which has vitamin D2).  A lush grass diet in NZ also therefore limits the production of vitamin D in the alpaca.
In addition, on lush pastures, high concentrations of carotenes can tie up vitamin D making less available to the body.
...
 
updated November 2005.


complete article:   http://www.alpacasnz.co.nz/articles-vitamind.htm

[Zoey]

 There are lots of old libraries to search, something will turn up in the archives somewhere!
Oldest Library in Mexico



Oldest Library in New York



Bodleian Library, One of the Oldest in Europe



My Friend, El Gato offered to help in the search.

[iko (OP)]

My Friend, El Gato offered to help in the search.

...our two b/white cats, Winnie and Socky
would love to join El Gato in the search!
Cheers

ikod

[iko (OP)]

After meditating on the hypothesis that the reported higher cancer incidence (childhood leukemia included, I suppose) in New Zealand might be somehow partially due to a measured vitamin D deficiency, let's go back to an historical issue like the 'unproven' efficacy of cod liver oil for TB...

This paper focussed on vitamin A and zinc: the vitamin D 'tsunami' still had to come in 2002.
Vitamin A itself increases zinc absorption from a normal diet.  So with cod liver oil we actually give vitamin A that increases zinc absorption, plus vitamin D, vitamin E, omega-3 fatty acids and who knows what other 'therapic acids'.  Just wonderful.

A double-blind, placebo-controlled study of vitamin A and zinc supplementation in persons
with tuberculosis in Indonesia: effects on clinical response and nutritional status.

Karyadi E, West CE, Schultink W, Nelwan RH, Gross R, Amin Z, Dolmans WM, Schlebusch H, van der Meer JW.
SEAMEO-TROPMED Regional Center for Community Nutrition, University of Indonesia, Jakarta, Indonesia.

BACKGROUND: The results of cross-sectional studies indicate that micronutrient deficiencies are common in patients with tuberculosis. No published data exist on the effect of vitamin A and zinc supplementation on antituberculosis treatment.
OBJECTIVE: Our goal was to investigate whether vitamin A and zinc supplementation increases the efficacy of antituberculosis treatment with respect to clinical response and nutritional status.
DESIGN: In this double-blind, placebo-controlled trial, patients with newly diagnosed tuberculosis were divided into 2 groups. One group (n = 40) received 1500 retinol equivalents (5000 IU) vitamin A (as retinyl acetate) and 15 mg Zn (as zinc sulfate) daily for 6 mo (micronutrient group). The second group (n = 40) received a placebo. Both groups received the same antituberculosis treatment recommended by the World Health Organization. Clinical examinations, assessments of micronutrient status, and anthropometric measurements were carried out before and after 2 and 6 mo of antituberculosis treatment.
RESULTS: At baseline, 64% of patients had a body mass index (in kg/m(2)) < 18.5, 32% had plasma retinol concentrations < 0.70 micromol/L, and 30% had plasma zinc concentrations < 10.7 micromol/L. After antituberculosis treatment, plasma zinc concentrations were not significantly different between groups. Plasma retinol concentrations were significantly higher in the micronutrient group than in the placebo group after 6 mo (P < 0.05). Sputum conversion (P < 0.05) and resolution of X-ray lesion area (P < 0.01) occurred earlier in the micronutrient group.
CONCLUSION: Vitamin A and zinc supplementation improves the effect of tuberculosis medication after 2 mo of antituberculosis treatment and results in earlier sputum smear conversion.

Am J Clin Nutr. 2002 Apr;75(4):720-7.


from the introduction of the article:
...
In our case-control study, the proportions of tuberculosis patients and control subjects with plasma retinol concentrations < 0.70 µmol/L were 33% and 13%, respectively (4). A study from Rwanda reported vitamin A deficiency among adults with tuberculosis (5). Vitamin A deficiency increases bacterial adherence to respiratory epithelial cells (6). It has been known since the1940s that vitamin A is excreted in the urine in patients with fever (7), and this has since been confirmed in subjects with acute infections, including pneumonia (. In addition, the requirement for vitamin A during infection is raised by its increased rate of excretion and metabolism (. Studies have shown that vitamin A has an immunoprotective role against human tuberculosis. This finding has a historical basis in that cod liver oil, which is rich in vitamins A and D, was used regularly for the treatment of tuberculosis before the introduction of modern chemotherapy (9). In addition, vitamin A supplementation results in a modulation of the immune response in patients with tuberculosis (10).

free reading of the full-text article:    http://www.ajcn.org/cgi/content/full/75/4/720

The Fisheries Museum - Aalesund, Norway

http://aalesunds.museum.no/06_fiskeri/bua_750x749.jpg

from:  http://aalesunds.museum.no/21_utland/engelsk_fisheries.htm

[Zoey]

Hi Iko,
 This is interesting. There must be more research like this buried in the stacks. My exploration tonight was not successful. There are more libraries yet to visit. Maybe I'll go to Toronto's library.


 
Yorkville Branch Library opened on June 13, 1907, in what was then the city’s north end. It was the first of four libraries constructed with a $350,000 grant made by Andrew Carnegie to the Toronto Public Library in 1903. Designed by Robert McCallum, City Architect, Yorkville’s classical, Beaux Arts style is similar to libraries in many smaller Ontario communities. It features two pairs of columns, a projected portico, Doric capitals, a bracketed cornice, and stone quoins, band courses and keystones. Yorkville is now the Toronto Public Library’s oldest library.
 

[iko (OP)]

It would be worth flying to Rhode Island and check the oldest library in America (North, South and Central?).  The answer might be right there, piled up with thousands of 'vintage' papers.

http://www.projo.com/extra/2006/slavery/day1/images/day1-redwoodlibrary.jpg

Journal photo / Frieda Squires
The oldest library in America in its original building, Newport's Redwood Library and Athenaeum on Bellevue Avenue, has been in continuous use since 1750. Quaker philanthropist and slave trader Abraham Redwood Jr. purchased more than 1,300 books to help establish the library. The statue at the front of the building is George Washington, who never stepped inside the library.

from:     http://www.projo.com/extra/2006/slavery/day1/side1.htm

[iko (OP)]

Talking of 'revisiting' and looking backwards,
allow me a cut&paste from Complementary Medicine
(Cod Liver Oil topic) and final comment from the
discussion in "Epidemic influenza and vitamin D"
J.J. Cannell et al. 2006.

Revisiting Vitamin D in humans.
just a few clever minds got this point
first, several years ago...

http://www.seeli.com/Daniel/leisure/travel/Finland/landscape5.jpg

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

Timonen TT.

University of Oulu, Department of Internal Medicine, Kajaanintie 50, FIN-90220 Oulu, Finland.

Research to detect new factors contributing to the etiology of acute leukemia (AL) is urgently needed. Located between latitudes 65 degrees and 70 degrees north, the population in northern Finland is exposed to extreme seasonal alterations of ultraviolet-B light and temperature. There is also a seasonal variation of both the 25(OH)- and 1,25(OH)2-D3 vitamin serum concentrations. In the present work, the frequencies of different types and age-groups at diagnosis of AL were compared during the dark and light months of the year, to uncover seasonality. Between January 1972 and December 1986, 300 consecutive patients aged >/=16 years and diagnosed as having AL were enrolled. The observed mean monthly global solar radiation, temperature measurements, and influenza epidemics were compared with the monthly occurrence of AL. Both acute lymphoblastic leukemia (ALL) (p=0.006) and total AL (p=0.015) were diagnosed excessively in the dark and cold compared with light and warm period of the year. There was a tendency for de novo leukemia to increase also in the dark and cold, but for acute myeloid leukemia (AML) patients the excess was not significant. Age >/=65 was strongly associated with the dark and cold season (p=0.003). Significantly more ALL (p=0.005) and de novo leukemias (p=0.029) were observed during influenza epidemics than during nonepidemic periods. However, a seasonality, i. e., the fluctuation of numbers of AL cases, was not determined, either monthly or during different photo- and temperature periods or influenza epidemics; this might be due to the small numbers of patients studied. Nevertheless, it is hypothesized that sunlight deprivation in the arctic winter can lead to a deficiency of the 1, 25(OH)2D3 vitamin, which might stimulate leukemic cell proliferation and block cell differentiation through dysregulation of growth factors in the bone marrow stromal cells, causing one mutation and an overt ALL in progenitor cells damaged during the current or the previous winter by influenza virus, the other mutation.

Ann Hematol. 1999 Sep;78(9):408-14.

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. jcannell@dmhash.state.ca.us

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.


...from the final conclusion in the full-text:

  Today, in a rush from multiplex reverse transcriptase-polymerase chain reactions that rapidly subtype influenza viruses to complex mathematical formulas that explain infectivity, many of us have forgotten Hope-Simpson's simple 'seasonal stimulus' theory for the lethal crop of influenza that sprouts around the winter solstice.   The faith and humility that characterized his life and his writings insulated him from despairing that his 'seasonal stimulus' would not be sought.  Among his last published words was the suggestion that 'it might be rewarding if persons, who are in a position to do so, will look more closely at the operative mechanisms that are causing such seasonal behaviour' [3,p.241].

Dr Edgar Hope-Simpson  (1908-2003)
        
http://www.makingthemodernworld.org.uk/learning_modules/geography/05.TU.01/?section=6
http://www.astrobiology.cf.ac.uk/image15.gif

A Gloucestershire GP carefully recorded the incidence of influenza in his practice over a period of nearly 30 years. Dr Hope-Simpson obtained a picture of the timing and intensity of these cases from 1946 to 1974.
Is it possible to compare Kilbourne’s chronological model of the spread of influenza with this data?
Such a comparison indicates that there should be evidence of the following factors influencing the final picture:
- A distinct seasonal pattern, with the highest incidence in winter.
- A series of decreases in the size of epidemic waves as the population becomes immune to one particular strain of the virus.
- The appearance of a new strain with changed antigens, meaning that the body’s defence mechanism does not recognise it. The whole process of infection should then begin again.
- The presence of more than one strain of influenza in the population at any one time.
- Newly introduced strains from other parts of the world, which can be especially virulent.

for more reading click here:  http://www.makingthemodernworld.org.uk/learning_modules/geography/05.TU.01/?section=6

[Zoey]

I liked Rhode Island, wish I could afford to live there for a while and use the library. Have patterns in the development of leukemia been noted like that in Finland? In general, are more cases of leukemia diagnosed at one time of year or another?
---

[iko (OP)]

I liked Rhode Island, wish I could afford to live there for a while and use the library. Have patterns in the development of leukemia been noted like that in Finland? In general, are more cases of leukemia diagnosed at one time of year or another?
---

Hi Zoey,

I should re-check piles of papers, but I am afraid that a proper seasonality has never been reported for leukemias.
In the past, spots of lymphoma and leukemia cases called 'clusters' had been reported now and then to propose an infectious etiology for these diseases: nothing scientifically 'heavy' I must say.
Leukemia is fortunately rare enough and progression probably variable from one patient to the other, so even if you had a common infectious switch during epidemics, symptoms would follow weeks or months later.  So much for trying to understand anything!   []
Take care

ikod

[Zoey]

You mean "understand" as finding patterns, rhyme and reason. I found reports of the "clusters" too. The problem in the reporting was the immediate assumption was that if there are a lot of cases in one area, it must be enviromental, excluding nutritional enviroments. Maybe that's why there are not more Shanghai Reports.
Regards,
Zoey

[iko (OP)]

You mean "understand" as finding patterns, rhyme and reason. I found reports of the "clusters" too. The problem in the reporting was the immediate assumption was that if there are a lot of cases in one area, it must be enviromental, excluding nutritional enviroments. Maybe that's why there are not more Shanghai Reports.
Regards,
Zoey

...wait, but the chain of events:

1) epidemic - immune response - normal response - neutralizing antibody - healing
2) epidemic - immune response - overridden reaction - CLONE expansion - organ invasion

should leave plenty of space to environmental AND nutritional factors
don't you think?