There is a "cure" for measles. It is called Vitamin a...Cod-liver oil. As early as 1932, doctors used cod-liver oil to reduce hospital mortality by 57%, but then antibiotics became the treatment of fashion, and Vitamin A was thrown out until the mid-80's. Recent published studies have found that 72%. of hospitalized measles cases in America are Vitamin A deficient, and the worse the deficiency the worse the complications and higher the death rate. (Pediatric Nursing, Sept/Oct 1996.) Yet doctors and hospitals in New Zealand do not use Vitamin A."
J. B. Ellison M.A., M.D., D.P.H. Intensive Vitamin Therapy in Measles. The British Medical Journal Oct 15, 1932, p708-711 http://www.whale.to/a/ellison1.html
"In this country the disease afflicts most heavily the children of the poorest classes, among whom the greatest mortality is observed during the first eighteen months after weaning. Since most of them are suffering from a lack of suitable fats in the diet, it is natural to suppose that they are insufficiently furnished with vitamins A and D."---J. B. Ellison M.A., M.D., D.P.H. 1932
"Three hundred cases of measles received a concentrate of vitamins A and D during the acute stage of the disease: eleven deaths occurred in the series. In a control series of 300 cases having a similar age distribution twenty-six-deaths occurred. Evidence is brought forward in support of the view that the pulmonary complications were less severe in the treated cases than in the controls."---J. B. Ellison M.A., M.D., D.P.H. 1932
The Journal of Pediatrics November 2000 • Volume 137 • Number 5
The vitamin A paradox
Jeffrey K. Griffiths, MD, MPH & TM
Vitamin A supplementation
See related article, p 660.
Vitamin A supplementation has reduced child mortality worldwide,1 and it is one of the most important public health advances of the last century. In many countries, one half of all deaths in children under the age of 5 years can be linked to malnutrition.2 Acute respiratory tract infections (chiefly pneumonia) and diarrheal disease remain the leading causes of pediatric death worldwide, surpassing even malaria, human immunodeficiency virus, or tuberculosis. The World Health Organization has determined that pneumonia alone causes one fifth of all deaths in children under 5 years and accounts for an astounding 8.2% of all worldwide disability and premature death, when measured as disability-adjusted life years or “DALYs.”2 In a world in which food security for all is still a dream, reducing the physiologic and immunologic consequences of malnutrition is a worthy, cost-effective, and achievable goal, if not an overwhelming moral mandate.
The immunosuppression of malnutrition appears to be most related to micronutrient and vitamin deficiencies, rather than simple caloric deficiency. Restitution of the immune response by the replacement of these compounds is thus a strategy for combating childhood mortality. Supplementation effectively, and independently, complements the other 2 major strategies for improving childhood health worldwide, vaccination and improved case management.3
Vaccine development is complex, costly, and time-consuming, and the outcomes can be uncertain (eg, the rotavirus vaccine experience). It is unlikely that inexpensive, effective vaccines will be developed in the near future for all of the major respiratory and diarrheal pathogens in the developing world. Vaccine delivery will also continue to be a substantial problem. Improved case management for respiratory and diarrheal diseases can lead to dramatic decreases in mortality.4 This includes simple strategies such as administration of antibiotics for pneumonia or dysentery and oral rehydration therapy for watery diarrhea. However, antibiotic resistance has already compromised this strategy and it will continue to worsen. Thus micronutrient and vitamin supplementation can potentially lead to important public health advances, even when the other major strategies are not helpful or available. The efficacy of these substances in reducing mortality is completely independent of antibiotic resistance or vaccine availability and delivery.
VAS greatly reduces measles-specific mortality5 and has been shown to reduce overall mortality in children 6 months and older in the great majority of community studies.6 A consistent benefit against diarrheal disease has usually been noted in these trials. As a result, public health and child health authorities have recommended that all children at risk for vitamin A deficiency receive VAS, regardless of their nutritional or vitamin status. Commonly administered doses of vitamin A are 100,000 IU for infants and 200,000 IU for children 1 year of age and older, given every 4 to 6 months. VAS is often given at the same time as immunizations during mass vaccination campaigns.
Puzzlingly, though acute lower respiratory tract infection (pneumonia) is the leading cause of death in children worldwide, large-scale field trials of VAS have found “no evidence for a differential impact on pneumonia by age” and that VAS “has no consistent overall protective or detrimental effect on pneumonia-specific mortality in children aged between 6 months and 5 years of age” (from the authoritative 1995 World Health Organization review of pneumonia and VAS7). How can this be possible? How can an agent that reduces overall childhood deaths by ~30% in clinical trials have no effect on the major cause of death, pneumonia?
The answer to this paradox may be an unpleasantly simple one that eliminates any simple notion that vitamin A can be given indiscriminately to all children. It appears increasingly possible that VAS is protective against pneumonia in malnourished children (who are likely to be vitamin A–deficient) and is paradoxically detrimental for adequately nourished children. Essentially, there may be a differential effect of vitamin A on the basis of the child’s vitamin A nutritional status. For example, a decreased rate of pneumonia in supplemented malnourished children might be accompanied by an increased rate in well-nourished supplemented children. Overall deaths might still fall without a decrease in the overall pneumonia rate, because deaths are concentrated in the malnourished group. In this scenario the cases of pneumonia are shifted from the group least likely to survive to the group most likely to survive.
This simple explanation fits the authoritative global meta-analysis result cited by the World Health Organization Vitamin A and Pneumonia Working Group that worldwide, deaths, but not pneumonia rates, are reduced by VAS.7 Recently, Sempertegui et al,8 my othercolleagues in Ecuador, and I found a large increase in the rate of pneumonia in well-nourished children who received low-dose (10,000 IU) weekly VAS when compared with control subjects (rate ratio = 2.21, P = .005) and a clearly protective effect of VAS for malnourished children (RR = 0.38, P = .01). We suggested that VAS may only be appropriate for targeted populations if our results are confirmed. It is squarely at the center of this evolving literature that the very important results of Fawzi et al9 in this issue
of The Journal of Pediatrics are located.
Fawzi et al9 report that VAS, given at the time of hospitalization for pneumonia and then 4 and 8 months after discharge and when compared with placebo, was associated with an apparent increased risk of respiratory tract infections (RR = 1.38, P = .005 for cough and tachypnea) and clinic visits (RR = 1.34, P = .003) over the following year in Tanzanian children aged 6 to 60 months. This effect was most prominent in children who were seronegative for HIV (RR = 1.47, P = .001 for cough and tachypnea), whereas there was an apparent reduction in the risk of cough with tachypnea in HIV-positive children (RR = 0.54, P = .13). Further extending the evidence of a differential response to vitamin A supplementation based on nutritional status, they found that this particular VAS regimen decreased the risk of acute diarrhea in children with wasting disease and increased the risk in normally nourished children and children with stunted growth during the follow-up period after their initial hospitalization (P = .01 for interaction). Overall, children who received vitamin A had a significantly lower risk of severe watery diarrhea (RR = 0.57, P = .04) but not all diarrhea when compared with placebo.
It is crucial to understand that Fawzi et al9 report important health outcome differences between subgroups that may be presumed to have varying degrees of vitamin A deficiency, based on their anthropometric nutritional states, and HIV status. These significant differences would not have been seen had they not analyzed their overall data by nutritional state or HIV status. (They have also reported that VAS decreases overall mortality in HIV-positive children10 and that VAS does not decrease but may worsen the severity of pneumonia when given during acute episodes.11) The striking results from our study in Quito, Ecuador, would have also been masked by an overall analysis that did not include nutritional status of the individual child. In the articles by Fawzi et al9 and Sempertegui et al,8 there are citations and discussions of the other meritorious studies that have suggested that VAS may be detrimental in adequately nourished children. The importance of these 2 recent studies is their attention to the issue of respiratory tract infections and the clarity and consistency of their results.
Nonetheless, these 2 studies have important differences. Although both had the powerful advantages of being placebo-controlled, double-blind studies, different treatment regimens were used in different populations. The Tanzanian study enrolled children aged 6 to 60 months with acute pneumonia in a sea level region with a high (9%) incidence of HIV and used episodic large doses of vitamin A. The Ecuadorian study enrolled overtly healthy children aged 6 to 36 months in an urban slum community at high altitude (~9500 feet) and gave them weekly low doses of vitamin A. This regimen approximates the recommended dietary allowance and was chosen because of the purported lack of efficacy of large-dose, episodic VAS against respiratory morbidity. The respiratory outcomes for the 2 studies followed similar symptoms and signs but are not identical. Cough, cough and fever, and cough and tachypnea were separately evaluated by Fawzi et al,9 whereas in Ecuador our primary outcome variable was the incidence of acute lower respiratory tract infection (pneumonia). This was defined as tachypnea and/or lower respiratory tract secretions detected by auscultation with one or more of the following: cough, fever, or chest retractions. Diarrhea was defined as 3 or more liquid or semi-liquid stools in 24 hours or less in the Ecuadorian study and “according to a mother’s perception” in the Tanzanian one. Vitamin A was globally protective against severe watery diarrheal disease in the Tanzanian study but only in a subgroup of children aged 18 to 23 months in Ecuador. Serum retinol levels, which are admittedly only poorly representative of overall body stores, are available only for the Ecuadorian children. HIV status was only assessed in Tanzania, because pediatric HIV infection is still rare in Quito. Despite all of this, the common finding of differential effects of VAS on subgroups of children is striking. Both studies showed VAS to be protective in children with wasting disease but not in healthy children or those with stunted growth.
The potential explanations for this differential effect of VAS must include a paradoxical (and as yet uncharacterized) adverse effect of vitamin A on the immune system of healthy, vitamin A–replete children, along with a beneficial effect in deficient children. Fortes et al12 found that VAS reduced CD3+ and CD4+ cells in elderly nursing home residents, but few if any relevant data from children exist. This explanation would be a worrisome one for many reasons, including the fact that VAS and vaccines are often co-administered. Another potential explanation is that VAS in adequately nourished children may augment the immune response to inappropriate levels. As noted by Fawzi et al,9 increased cough or diarrhea may be an indication of an improved inflammatory response secondary to the pharmacologic effects of a large dose of vitamin A.
If this differential effect of VAS on pneumonia and diarrhea is real, then the public health implications are enormous. Even in countries with substantial malnutrition, there are many children who are not vitamin A deficient and who might be harmed by VAS. Targeted but not population-wide supplementation might then prove the optimal choice, minimizing harm while maximizing benefit. Mass administration campaigns, which are easiest to conduct when everyone receives the intervention, would have to be altered to include an assessment for vitamin A deficiency. This assessment would require additional time and resources and the use of simple, sound, and proven surrogate markers for vitamin A deficiency such as a low weight for age (wasting). Of course, if this nutritional assessment led to the targeting of VAS and other interventions to the children most at need, this result would be a very positive one.
Global VAS has led to important decreases in childhood mortality. Its abandonment or alteration should not be considered lightly. Nonetheless, a number of studies now suggest that VAS is good overall and bad for some. If VAS is harmful to some, then we should not shirk our responsibility to appropriately target this necessary vitamin to those who will benefit while minimizing harm to others. The subgroups of children who benefit from VAS and the subgroups who do not must be securely identified, and the exact nature and circumstances of the benefits and risks must be delineated. As it stands, children who are HIV-infected, who have wasting disease, who are at risk for severe diarrhea or for measles, or who have overt vitamin A deficiency all appear to benefit from VAS, whereas HIV-seronegative, adequately nourished children may be harmed by it. The extent of the harm is unknown. Alternative dosing regimens may need to be studied if the currently used, large, supraphysiologic doses of vitamin A are immunomodulating. Fawzi et al9 have taken us a large step toward understanding the paradox of vitamin A supplementation and are to be commended for their work.
1. Beaton GH, Martoerll L, L’Abbé KA, Edmonston B, McCabe G, Ross AC,
et al. Effectiveness of vitamin A
supplementation in control of young child morbidity and mortality in
developing countries. Final Report to CIDA (Canadian
International Development Agency). Toronto, Ontario, Canada:
International Nutrition Program, University of Toronto; 1992.
2. Anonymous. Acute respiratory infections: the forgotten pandemic. Bull WHO 1998;76:101-3.
3. Kirkwood BR, Gove S, Rogers S, Lob-Levyt J, Arthur P, Campbell H.Potential interventions for the prevention of childhood pneumonia in developing countries: a systematic review. Bull WHO 1995;73:793-8.
4. Sazawal S, Black RE. Meta analysis of intervention trials on case-management of pneumonia in community settings. Lancet 1992;340:528-33. MEDLINE
5. Hussey GD, Klein M. A randomized, controlled trial of vitamin A in children with severe measles. N Engl J Med 1990;323:160-4. MEDLINE
6. Fawzi WW, Chalmers TC, Herrera MG, Mosteller F. Vitamin A supplementation and child mortality. JAMA 1993;269:898-903. MEDLINE
7. Vitamin A and Pneumonia Working Group. Potential interventions of the prevention of childhood pneumonia in developing countries: a meta-analysis of data from field trials to assess the impact of vitamin A supplementation on pneumonia morbidityand mortality. Bull WHO 1995;73:609-19. MEDLINE
8. Sempertegui F, Estrella B, Camaniero V, Betancourt V, Izurieta R, Ortiz W, et al. The beneficial effects of weekly low-dose vitamin A supplementation on acute lower respiratoryi infections and diarrhea in Ecuadorian children. Pediatrics 1999;104:e1. MEDLINE
9. Fawzi WW, Mbise R, Spiegelman D, Fataki M, Hertzmark E, Ndossi G.Vitamin A supplements and diarrheal and respiratory tract infections among children in Dar es Salaam, Tanzania. J Pediatr 2000;137:660-7. MEDLINE
10. Fawzi WW, Mbise RL, Hertzmark E, Fataki M, Herrera MG, Ndossi G, et al. A randomized trial of vitamin A supplements in relation to mortality among HIV-infected and uninfected children in Tanzania. Pediatr Infect Dis J 1999;18:127-33. MEDLINE
11. Fawzi WW, Mbise RL, Fataki MR, Herrer MG, Kawau F, Hertzmark E, et al. Vitamin A supplements and severity of pneumonia among children admitted to hospital in Dar es Salaam,
Tanzania. Am J Clin Nutr 1998;68: 187-92. MEDLINE
12. Fortes C, Forastiere F, Agabiti N, Fano V, Pacifici R, Virgili F,et al. The effect of zinc and vitamin A supplementation on immune response in an older population. J Am Geriatr Soc 1998;46:19-26. MEDLINE
Director, Graduate Programs in Public Health, Department of Family Medicine and Community Health, Tufts University School of Medicine, Boston, MA 02111 J Pediatr 2000;137:604-7. Copyright © 2000 by Mosby, Inc. 0022-3476/2000/$12.00 + 0 9/18/111162
Taken from TOTAL WELLNESS by Dr. Joseph Pizzorno, N.D.
Vitamin A plays several essential roles in protecting us from infections. First, it is required for maintaining the integrity of the epithelial and mucosal surfaces and their secretions. THese systems constitute our first line of defense against infection. Second, vitamin A is necessary for the production and activity of several types of white cells. Deficiency can result in atrophy of the lymph glands, a decreased number of lymphocytes,and reduced B and T cell functioning.
Vitamin A deficiency is very common in developing countries. For example, in Indonesia, 236 children who received the DPT vaccination were evaluated after they received either 60,000 mcg of vitamin A or placebo. It was foudn that both the Vitamin A deficient and the supposedly vitamin A adequate (healthy) children who received the vitamin A supplement showed significantly greater antibody response to the vaccine than the children who receive the placebo. So much evidence now supports the importance of adequate levels of Vitamin A for proper immune response that the WHO's expanded program for Immunization recommends that childrenin Vitamin A deficient communties be given Vitamin A at the time of immunization.
Unfortunately, vitamin A deficiency is not unusual in the U.S. either, especially in children with significant infections. For example, in one study, when 180 children with rubeola (hard measles) were tested for Vitamin A levels, 91% were found to have levels far below normal. Supplementation with 200,000 per day for two consecutive days resulted in and 87% decrease in death rate in the children under two years of age. In another study of 123 children, those with low serum levels of Vitamin A had significantly decreased T cell counts. Administration of vitamin A restored their T cell counts to normal. Not only does vitamin A deficiency decrease the number of T cells, it also decreases T cells' ability to respond to pathogens. Severe deficiency also leads to atrophy of the Thymus and spleen and a marked decrease in the number of all white cells in the blood.
In a recent study in New York City, vitamin A levels were evaluated in 89 children younger than two years of age with measles. In 22%, they were found to be low. Children with low levels were more likely to have fevers of 40 degrees Celcius or higher (68% versus 44%), to have fever for seven days or more (54% versus 23%), and to be hospitialized (55% versus 30%). Children with low vitamin A levels also had lower measles specific antibody levels. No child in the control group of children without measles had low Vitamin A levels.
World-wide, 1.5 million children die of measles each year. The children with the severest forms of measles have the lowest serum levels of Vitamin A. Even children from communities that are not normally deficient in vitamins are still at risk of low Vitamin A levels during infection with measles. Providing as little as a single large dose (400,000 IU) of Vitamin A has resulted in a remarkable reduction in morbidity and mortality in children hospitalized with measles in Capetown, Africa resulted in reductions in Hospital stay, intensive care admissions and death rates.
Research shows that now only are children with low Vitamin A levels more likely to get measles, they also get a worse case and suffer an increased rate of side effects and death. Supplementation with even modest amounts of this cheap nutrient results in a very significant improvement in immune function."
1: Acta Paediatr Jpn. 1998 Aug;40(4):345-9.
The effect of live measles vaccines on serum vitamin A levels in healthy children.
Yalcin SS, Yurdakok K, Ozalp I, Coskun T.
Department of Social Pediatrics, Hacettepe University Institute of Child Health, Ankara, Turkey.
OBJECTIVE: Serum retinol levels have been shown to be depressed during measles infection. This study aims to demonstrate whether there is any decrease in serum vitamin A level following immunization with live viral vaccine and its relation with vaccine seroconversion in children with measles. Since many children receive measles vaccine alone or in combination with measles-mumps-rubella vaccine, we studied serum vitamin A levels and antibody levels in healthy, well-nourished children before and after immunization with monovalent and combined live attenuated measles vaccine. METHODS: The first group included 21 healthy children between the ages of 9-11 months who received live measles (Schwarz) vaccine. There were also 21 healthy children (range 14-20 months of age) who received measles-mumps-rubella Trimovax (Pasteur Merieux) vaccine. All children were tested for serum vitamin A levels before vaccination, on days 9-14 and 30-42 following both vaccinations. Measles specific antibody levels were also measured on admission and 30-42 days following vaccinations. RESULTS:
In both vaccination groups, mean serum vitamin A levels reduced significantly on days 9-14, but increased slightly on days 30-42 in the measles-mumps-rubella vaccinated group (P < 0.05). The baseline and follow-up levels of mean serum vitamin A did not differ between seroconverted and nonseroconverted cases within the measles vaccinated group.
CONCLUSION: Serum vitamin A levels are reduced following vaccination with monovalent and combined live attenuated measles vaccines.
PMID: 9745778 [PubMed - indexed for MEDLINE]
From The Cochrane Library, Issue 1, 2004. Chichester, UK: John Wiley & Sons, Ltd. All rights reserved.
Vitamin A for treating measles in children (Cochrane Review)
D'Souza RM, D'Souza R
A substantive amendment to this systematic review was last made on 28 November 2001. Cochrane reviews are regularly checked and updated if necessary.
Background: Measles is a leading cause of childhood morbidity and mortality. Vitamin A deficiency is a recognised risk factor for severe measles. The World Health Organization (WHO) recommends administration of an oral dose of 200,000 IU (or 100,000 IU in infants) of vitamin A per day for two days to children with measles in areas where vitamin A deficiency may be present.
Objectives: The purpose of this review is to determine whether vitamin A when commenced after measles has been diagnosed, is beneficial in preventing mortality, pneumonia and other complications in children.
Search strategy: MEDLINE and the Cochrane Library, Issue 4, 1999 were searched.
Selection criteria: Only randomized controlled trials in which children with measles were given vitamin A or placebo along with standard treatment were considered.
Data collection and analysis: Studies were assessed independently by two reviewers. The analysis of dichotomous outcomes was done using the StatXact software package. Sub-group analyses were done for dose, formulation, age, hospitalisation and pneumonia specific mortality. Weighted mean difference with 95% CI were calculated for continuous outcomes.
Main results: The relative risks (RR) and 95% Confidence Intervals (CI) are based on the estimates from the StatXact software package. There was no significant reduction in mortality in the vitamin A group when all the studies were pooled together (RR 0.60; 95% CI 0.32 to 1.12)(StatXact estimate). There was a 64% reduction in the risk of mortality in children who were given two doses of 200,000 IU of vitamin A (RR=0.36; 95% CI 0.14 to 0.82) as compared to placebo. Two doses of water based vitamin A were associated with a 81% reduction in risk of mortality (RR=0.19; 95% CI 0.02 to 0.85) as compared to 48% seen in two doses of oil based preparation (RR=0.52; 95% CI 0.16 to 1.40). Two doses of oil and water based vitamin A were associated with a 82% reduction in the risk of mortality in children under the age of 2 years (RR=0.18; 95% CI 0.03 to 0.61) and a 67% reduction in the risk of pneumonia specific mortality (RR=0.33; 95% CI 0.08 to 0.92). There was no evidence that vitamin A in a single dose of 200,000 IU was associated with a reduced risk of mortality among children with measles (RR=0.77; 95% CI 0.34 to 1.78). Sub-groups like age, dose, formulation, hospitalisation and case fatality in the study area were highly correlated and there were not enough studies to separate out the individual effects of these factors. There was a 47% reduction in the incidence of croup (RR=0.53; 95% CI 0.29 to 0.89), while there was no significant reduction in the incidence of pneumonia (RR=0.92; 95% CI 0.69 to 1.22) or of diarrhoea (RR=0.80; 95% CI 0.27 to 2.34). Duration of diarrhoea was measured in days and there was a reduction in its duration of almost two days WMD -1.92, 95% CI -3.40 to -0.44. Only one study evaluated otitis media and found a 74% reduction in its incidence (RR=0.26, 95% CI, 0.05 to 0.92). We did not find evidence that a single dose of 200,000 IU of vitamin A per day, given in oil-based formulation in areas with low case fatality, was associate with
Reviewers' conclusions: Although we did not find evidence that a single dose of 200,000 IU of vitamin A per day was associated with reduced mortality among children with measles, there was evidence that the same dose given for two days was associated with a reduced risk of overall mortality and pneumonia specific mortality. The effect was greater in children under the age of two years. There were no trials that compared a single dose with two doses, although the precision of the estimates of trials that used a single dose were similar to the trials that used two doses.
Citation: D'Souza RM, D'Souza R. Vitamin A for treating measles in children (Cochrane Review). In: The Cochrane Library, Issue 1, 2004. Chichester, UK: John Wiley & Sons, Ltd.
This is an abstract of a regularly updated, systematic review prepared and maintained by the Cochrane Collaboration. The full text of the review is available in The Cochrane Library (ISSN 1464-780X).
What is already known on this topic
Trials of vitamin A supplementation have failed to show a beneficial effect on morbidity in children
Experimental studies have shown that, in the presence of zinc deficiency, vitamin A supplementation fails to reverse vitamin A deficiency Coexistence of deficiencies of zinc and vitamin A could be a reason for the failure of vitamin A supplementation, but data in humans are limited
What this paper adds
Combined zinc and vitamin A supplementation is more effective in reducing persistent diarrhoea and dysentery than either vitamin A or zinc alone Zinc alone increased respiratory illnesses, but interaction between zinc and vitamin A reduced this adverse effect
Subject: FYI - Lancet Article - Zinc appears to reduce hospital stay for pneumonia
Zinc Helpful in Children With Pneumonia
Laurie Barclay, MD
May 21, 2004 b Zinc supplements reduce the duration of illness and length of hospital stay in children with pneumonia, according to the results of a randomized trial published in the May 22 issue of The Lancet. "The effects on treatment failure are striking, have significant implications for reduction of antimicrobial resistance by decreasing multiple antibiotic exposures, and could help reduce complications and death in situations where second-line drugs are not available," lead author W. Abdullah Brooks, from the International Centre for Diarrhoeal Disease Research in Dhaka, Bangladesh, says in a news release.
The rationale for this study is that zinc is reported to prevent pneumonia, to prevent and treat diarrhea, and to enhance the immune response to infection. In addition to standard hospital antibiotics, 270 children with severe pneumonia (age range, two to 23 months) received 20 mg zinc daily or placebo. Cessation of severe pneumonia was defined as no chest indrawing, respiratory rate of 50 breaths per minute or less, and oxygen saturation at least 95% on room air. Discharge from hospital was permitted when respiratory rate was 40 breaths per minute or less for 24 consecutive hours while patients were maintained only on oral antibiotics.
The group receiving zinc had reduced duration of severe pneumonia (relative hazard [RH], .07; 95% confidence interval [CI], 0.51 - 0.98), including duration of chest indrawing (RH, .80; 95% CI, 0.61 - 1.05), respiratory rate more than 50 per minute (RH, .74; 95% CI, 0.57 - 0.98), and hypoxia (RH, .79; 95% CI, 0.61 - 1.04).
Compared with the placebo group, patients in the zinc group recovered from severe pneumonia one day earlier, and their average stay in the hospital was one day shorter (RH for overall hospital duration, 0.75; 95% CI, 0.57 - 0.99). All effects were greater when children with wheezing were omitted from analysis.
The zinc supplement was safe and well tolerated. Potential cost savings are substantial, because a course of zinc treatment costs $0.15 in U.S. dollars, and one day in the study hospital costs $25.
"This study needs to be replicated in other populations, including those with and without a high prevalence of zinc deficiency and, as with zinc studies of diarrhoeal disease, should include a follow-up period to look at effects on subsequent illness," the authors write. "Additionally, both animal and human studies should also be undertaken to describe the precise mechanism by which zinc interacts with the acute phase response, including more detail on its effects on immunity. Such studies would allow the global public-health significance of these findings to be assessed, and the results best applied to improve child health and survival."
Funding for this study came from the Johns Hopkins Family Health and Child Survival Cooperative Agreement with the U.S. Agency for International Development, the U.S. Agency for International Development, core donors to the International Centre for Diarrhoeal Disease Research, and the Bangladesh Centre for Health and Population Research. The authors report no potential financial
conflicts of interest.
LEUKEMIA: Vitamin A is better, and safer, than chemo
Oncologists have for the first time tested a therapy other than chemotherapy to treat leukemia, and it worked. But it wasn't another toxic, debilitating chemical that they turned to - it was vitamin A. This simple therapy - which involved wrapping vitamin A inside bubbles of fat - reversed a rare form of leukemia in up to a third of patients. The key to the new therapy seems to be the delivery mechanism. When it's put in a lipid carrier, it retains its potency whereas earlier trials of vitamin A as an anti-carcinogen found that little of the vitamin was being absorbed by the body when it was taken orally.
Not surprisingly, it's been patented, and is being licensed as the 'drug' Lipo-Atra, even though it is essentially a form of vitamin A known as Atra, which was originally found to help leukemia patients in studies in China. It's been tested on a group of 34 patients with acute promyelocytic leukemia (APL), 10 of whom have been in remission for an average of five years, despite never having had chemotherapy.
Lead researcher Dr Elihu Estey at Texas University's Department of Leukemia said: "This is the first time we have seen patients with an acute leukemia potentially cured without use of chemotherapy. That's an important development in the field of leukemia, because traditional treatment with chemotherapy often produces side effects, even death, in patients with different kinds of leukemia than the one studied here." He said it.
(Source: Annual proceedings of the American Society of Clinical Oncology, 2004).
CLARIFICATION ON THE VITAMIN A ISSUE
Sidney MacDonald Baker, M.D. and Jaquelyn McCandless,
Internet posting on an autism parent-support list has revealed some potentially harmful misunderstanding on some parents' part concerning the use of Vitamin A. The speculation that Vitamin A may benefit children with persistent measles vaccine virus problems as has been shown for hospitalized children with acute wild measles infections has led to some parents using the mega-dosing regime with or without medical supervision with variations of dosing and agents. A recent post from a parent who was giving mega-doses to her child for 4 days in a row wanted to know if she should increase the dose even more, even though her child was showing alternating lethargy and hyperactivity, because he hadn't yet gotten what she called the "measles" rash. She stated that she had gotten this from another parent, who believed you would not have effectiveness until you got the rash. The parent was contacted immediately and told to stop all Vitamin A, and the list was given all pertinent information about the Vitamin A issue. (Her child is fine now). We felt it was important enough to alert all of you in the DAN! community of our position on this treatment.
Background: (Dr. Baker) In the spring of 2002, measles virus was reliably reported to be present in the spinal fluid of some autistic children who had previously demonstrated measles vaccine virus in the lymphoid tissue of their digestive tracts. The alarm of this finding increased our incentive to come up with ideas upon which well-informed parents might base safe private decisions for their children pending a shift in public policy to address the measles virus issue. The gap between the urgency of private decisions in regard to this issue and the resistance to the very idea on the part of those responsible for public policy suggested that it might be many years before speculations about treatment of individual children with atypical presence of MV might be resolved by research in groups of children.
Very high doses of vitamin A palmitate (400,000iu per day for two consecutive days) is the only measles specific treatment for children with active acute measles. This common childhood infection may involve a sometimes fatal inflammation of the lungs (pneumonia), inflammation of the brain (encephalitis) as well as other complications that befall very sick children. Other anti-viral treatments have not been shown to work in measles. A discussion at the DAN! Think Tank in May of 2002 in Boston led to a consensus that some form of Vitamin A treatment would be worthy of consideration. Guidelines for such treatment were published in Biomedical Assessment Options For Children with Autism and Related Problems, by Pangborn, J and Baker, SM, published by the Autism Research Institute, 4182 Adams Avenue, San Diego, DA 92116 October 2002 Edition, pages 216-220.
The chronic nature of the possible measles problem in a subgroup of children in the autism spectrum led me (SMB) to consider that a lengthy treatment that pushed Vitamin A levels toward the high end of the safe range would make sense in that it answered the need of parents to observe their children over a period of a few weeks or longer to judge progress if
any should occur and it gave time for monitoring a slow increase intake to avoid surprises of toxicity. My own experience with this approach in my patients did not yield positive results. Meanwhile Dr. McCandless, inspired by Teresa Binstock's and my literature search showing this to be effective in children with wild measles and also as reported from English parents with 2-day high dosing, began suggesting that parents who fit certain criteria might try the two-day protocol, followed by maintenance doses only for at least 6 months before doing any more mega-doses. Her preliminary clinical study of salivary secretory IgA rubeola antibodies done with Dr. Ari Vojdani at Immunosciences has revealed an elevated level in 14 of 32 children tested. Those with very high levels were some of the best responders to this protocol, and other positive feedback started coming in from parents doing the protocol. Another study is almost completed checking both the serum IgG rubeola antibody level as well as the secretory IgA salivary antibody level to see how these two correlate along with clinical assessment and reports.
Seizing upon the positive implications of those reports and guided by the simplicity and safety of that approach (for which safety has been documented in studies of both well-nourished and undernourished children) I took the position that this approach might form the basis for clinical observations that could benefit children. Unfortunately, there are no generally available tests to reliably measure Vitamin A levels in the body; the assessment is primarily clinical observation. Signs of toxicity are a "scruffy" rash around the neck, headache, nausea, vomiting, lethargy, and excessive unusual hyperactivity. The few parents reporting whose children have shown any of these responses have stopped with no sequelae. Most reports have been very positive with some showing remarkable benefit. It is important to emphasize that this is not a treatment for autism generally (though the RDI is
probably very low for Vitamin A) but only for those suspected of having measles in their systems. The risks at this time do not seem to be from the protocol itself, but from misunderstandings such as related above. High doses should not be given until a skin rash is produced, for that is one sign of Vitamin A poisoning!
Based upon existing medical literature, two (2) days
of high dose vitamin A in the range of 200,000-
400,000iu of Vitamin A Palmitate is the only way of
proceeding that appears to be safe. Any further
exploration of high-dose Vitamin A therapy must be
carried out with close medical supervision. Based on
the belief that children with active measles in their
gut or brain are probably low or depleted in Vitamin
A, the criteria as outlined by Dr. McCandless for her
patients for launching into this pilot study is threeor more of the following:
-History of regression after MMR (particularly in those children who had an immediate and strong negative reaction to the vaccine or booster).
-Persistent gut problems in spite of all recommended treatments.
-More than slightly elevated IgG serum rubeola levels. -Elevated anti-myelin basic protein (MBP) and anti- neurofilament antibodies (indication of autoimmune reaction).
-Elevated secretory salivary rubeola IgA antibodies.
-Needless to say, endoscopy showing ileal lymphoid hyperplasia with vaccine strain measles by PCR, or measles in CSF studies.
Sidney M. Baker, M.D. Jaquelyn McCandless, M.D.
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