Black & White
Used the sample of women of child-bearing age from the Second National Health and Examination Survey to examine the relationship between hemoglobin and iron status for blacks and whites.
Black women had a significantly lower mean hemoglobin value (126 +/- 12 g/L) than white women (134 +/- 11 g/L).
Evaluation of the screening performance of hemoglobin found that race-specific anemia criteria (10 g/L difference) yielded a comparable sensitivity and specificity in detecting iron deficiency for both races. In contrast, a fixed anemia criterion did not yield comparable screening performances for the two races.
This functional evaluation supports considering race-specific anemia criteria for screening iron deficiency.
Johnson-Spear MA & Yip R: Hemoglobin difference between black and white women with comparable iron status: justification for race-specific anemia criteria [see comments].Am J Clin Nutr, 1994 Jul, 60:1, 117-21.
Anemia, Iron and Blood Doping
Athletes tend to have lower hemoglobin concentrations than their sedentary counterparts. Sports anemia is a false anemia. It is a beneficial adaptation to aerobic exercise caused by an expanded plasma volume that dilutes red blood cells. Athletes can develop a true anemia usually from iron deficiency. This can hinder athletic performance. Iron supplements may be needed in women endurance athletes. The author feels blood doping, using recombinant and human erythropoietin (REPO) is a definite health risk.
"Sports Anemia, Iron Supplements, and Blood Doping", Eichner, E. Randy, Medicine and Science in Sports and Exercise, 1992;S315-S318.
Copper Deficiency and Neutropenia
A case report of a 68-year-old female patient who was hospitalized for severe anemia and neutropenia after receiving total parenteral nutrition for over 2.5 years. She was found to have low levels of copper and ceruloplasmin, and the bone marrow showed presence of ringed sideroblasts and vacuolated immature cells.
The patient was initially given .85 mg of copper chloride (which is equivalent to .4 mg of elemental copper) daily for 12 days, followed by 2.5 mg of copper chloride or 1.2 mgs of elemental copper daily for a total of 34 days as a bolus injection. After 2 months her hemoglobin had risen from 6.3 to 10.5 g/dl, and the number of granulocytes from .14 to 4.0 x 109/l. It is noted ceruloplasmin is important for the conversion of iron from its ferris to its ferric, more absorbable, form. Also the low activity of the copper-containing enzyme superoxide dismutase may also cause anemia since copper:zinc SOD contains 60% of the copper in erythrocytes.
Low copper:zinc SOD levels may accelerate the membrane defect because of decreased capacity to prevent superoxide concentrations in the cell membrane. It is believed copper is related closely to the development of granulocytes.
As total parenteral nutrition increases, copper deficiency is reported with increasing frequency. Copper is important in maintaining normal hematopoiesis.
"Anemia and Neutropenia in A Case of Copper Deficiency: Role of Copper in Normal Hematopoiesis", Hirase, Nobuhisa, et al, ACTA Hematologica, 1992;87:195-197.
Folic acid, a water-soluble vitamin, has been used since the 1940s to treat some cases of macrocytic anemia without neurologic disease. Folate deficiency is best diagnosed with red blood cell folate levels along with macrocytosis and/or megaloblastic anemia.
In addition to reversing overt deficiency, the vitamin may reduce the incidence of neural tube defects by 45% in women who receive 400 micrograms per day. It is recommended that all women of childbearing age take 400 micrograms of folate per day.
Elevations in homocysteine levels, a metabolite intimately associated with folate, are also being found with increasing regularity in those with cardiovascular diseases. Homocysteine levels are reduced by folic acid administration. Therefore, there is some biologic plausibility, but not currently direct proof, for the assumption that folate supplements may prevent heart disease, stroke, and peripheral arterial disease.
Controlled trials should take place before widespread food supplementation with folate is carried out on a large scale because of the possibility of outbreaks of permanent B12-related neurologic damage in those with undiagnosed pernicious anemia. However, if a patient has a premature cardiovascular event and has minimal risk factors, ordering a test to determine homocysteine level may be advisable, and if elevated, treating with folic acid supplement as long as B12 deficiency does not coexist.
Swain RA & St Clair L: The role of folic acid in deficiency states and prevention of disease. J Fam Pract, 1997 Feb, 44:2, 138-44.
The hookworms Necator americanus and Ancylostoma duodenale infect approximately 1 billion people worldwide. The prevalence of hookworm infection increases with age in children, typically reaching a plateau in late adolescence, whereas the intensity of infection may continue to increase throughout adulthood.
Hookworms cause intestinal blood loss in amounts proportional to the number of adult worms in the gut. The relationship between hookworm infection intensity and hemoglobin concentration is evident in epidemiologic studies, but may be apparent only above a threshold worm burden that is related to the iron stores of the population.
Current hookworm control efforts are focused on reducing infection load and transmission potential through periodic anthelminthic chemotherapy. Several controlled trials have demonstrated a positive impact of anthelminthic treatment on hemoglobin levels, with best results obtained in settings where iron intakes were also increased. Evidence suggests that anthelminthic programs will have modest impacts on iron deficiency anemia in the short term, with greater impacts on more severe anemia.
Hookworms are an important cause of anemia in women, who are often overlooked by current helminth control programs. Current WHO recommendations for use of anthelminthics in schoolchildren and women are reviewed. There is a need to clarify whether hookworms are an important etiology of iron deficiency anemia in preschool children.
Stoltzfus RJ et al., Hookworm control as a strategy to prevent iron deficiency. Nutr Rev, 1997 Jun, 55:6, 223-32.
Anemia in the 1st year of life should be an important warning sign to the clinician of a potential underlying nutritional deficiency. Prompt diagnosis and treatment are warranted in many cases, not only to treat the anemia but also, more important, to prevent other long-term sequelae associated with the underlying, causative deficiency.
As more information about the impact of nutrition on various aspects of health is collected and newer therapies for the treatment of disease are developed, it will be important to understand and consider the role of vitamins and minerals in a light beyond the realm of nutritional anemia.
Gallagh G & Ehrenz RA: Nutritional anemias in infancy. Clin Perinatol, 1995 Sep, 22:3, 671-92.
Investigated the role of additional folate and vitamin B-12 supplementation of the anemia of prematurity.
All patients initially received vitamin E and iron in accordance with accepted standards. Patients were randomly assigned to four groups to receive orally 0.1 mg folate/d for 4 mo, 100 micrograms vitamin B-12 intramuscularly monthly for 4 months, both supplements, or neither.
All other activities including parenteral nutrition were carried out according to established practices, irrespective of study group. By 10-12 wk, infants treated with vitamin B-12 alone or combined with folate had higher hemoglobin values than the untreated or solely folate-treated groups. These findings held true irrespective of wide variations in treatment and feeding practices. The only uncontrolled hematologic nutritional factor, selenium, showed a similar pattern of decline for 10-12 wk in all study patients, whether or not they received additional vitamin supplements.
Worthington-White DA et al., Premature infants require additional folate and vitamin B-12 to reduce the severity of the anemia of prematurity. Am J Clin Nutr, 1994 Dec, 60:6, 930-5.
Megaloblastic Anemia and Psoriasis
A case study of a 68 year old male with a 25 year history of severe psoriasis. He had been living alone for the last 6 years and had a very unbalanced diet since his wife had died. The patient had been placed on low dose methotrexate at 7.5 mg once a week. This methotrexate treatment was discontinued.
However, his symptoms persisted even though he had stopped the methotrexate. He was eventually admitted to the hospital for severe gingival bleeding, chest tightness and dizziness. He had developed a severe pancytopenia and an elevated MCV. He had hypersegmented neutrophils present in the peripheral blood smear.
Serum vitamin B12 levels were in the normal limits, anti-intrinsic factor antibodies were negative, and a Schilling's test showed no disturbance of vitamin B12 absorption. Urinary excretion of methylmalonic acid was below 10 mg per day. Folate levels in the serum and the red blood cells were found to be decreased significantly by radioimmune assay.
He was treated with a transfusion, and also eventually received a multivitamin infusion with 400 ug of folate.
It is recommended serum folate levels be analyzed and the possibility of megaloblastic anemia be kept in mind when treating patients with psoriasis, especially those on low dose methotrexate therapy.
"Megaloblastic Anemia Associated With Psoriasis: Case Report and Review of the Literature", Iwama, Atsushi, et al, Internal Medicine, January 1992;31(1):127-130.
Adoption by women of dietary practices that are based on Dietary Guidelines for Americans can promote improved general and reproductive health and can help prevent chronic disease. Additional guidance is indicated for helping prevent neural tube defects, iron deficiency anemia, and osteoporosis.
The obstetrician-gynecologist plays an important preventive role by providing basic nutritional assessment; nutrition education; counseling concerning diet, weight, and exercise; and referral for special nutritional care as needed.
The physician needs to be especially alert for serious nutrition-related problems such as eating disorders that pose a serious health risk and to stress the importance of good nutrition particularly to adolescent and elderly patients.
Anonymous: ACOG educational bulletin. Nutrition and women. Number 229, October 1996. Committee on Educational Bulletins of the American College of Obstetricians and Gynecologists. Int J Gynaecol Obstet, 1997 Jan, 56:1, 71-81.
To estimate the levels of vitamin B12 in patients with severe sickle cell disease compared to normal controls.
(43.5%) had serum vitamin B12 levels below normal values.
Patients with low B12 achieved a significant symptomatic improvement when treated with vitamin B12, 1 mg intramuscularly weekly for 12 weeks when compared with patients with normal B12 levels.
Many patients with severe sickle cell disease may suffer from unrecognized vitamin B12 deficiency.
Diminished vitamin B12 levels in patients with severe sickle cell disease. al-Momen-AK. J-Intern-Med. 1995 Jun; 237(6): 551-5.
To determine the prevalence of iron deficiency and iron deficiency anemia in the US population. (A total of 24,894 persons aged 1 year and older examined in the third National Health and Nutrition Examination Survey (1988-1994).
Nine percent of toddlers aged 1 to 2 years and 9% to 11% of adolescent girls and women of childbearing age were iron deficient; of these, iron deficiency anemia was found in 3% and 2% to 5%, respectively.
These prevalences correspond to approximately 700,000 toddlers and 7.8 million women with iron deficiency; of these, approximately 240,000 toddlers and 3.3 million women have iron deficiency anemia.
Iron deficiency occurred in no more than 7% of older children or those older than 50 years, and in no more than 1% of teenage boys and young men. Among women of childbearing age, iron deficiency was more likely in those who are minority, low income, and multiparous.
Iron deficiency and iron deficiency anemia are still relatively common in toddlers, adolescent girls, and women of childbearing age.
Looker AC et al., Prevalence of iron deficiency in the United States. JAMA, 1997 Mar 26, 277:12, 973-6.
Microcytic Anemia, Copper Deficiency and Zinc Ingestion
This is a case report of a 57-year-old man who was consuming 1,008 mgs of a zinc-amino acid chelate, which was equivalent to 810 mgs of elemental zinc daily for over 18 months, at the advice of a "nutritionist". The patient presented with microcytic anemia, and no evidence of blood loss and gastrointestinal dysfunction. The patient discontinued the zinc supplements and within 4 weeks his hemoglobin, white blood cell count, and MCV rose significantly. Eight weeks later his blood indices were virtually normal. The authors feel this anemia was due to zinc excess, causing a copper deficiency, and recommend the evaluation of a vitamin and mineral status in patients presenting with microcytic or sideroblastic anemia.
"Copper Deficiency and Microcytic Anemia Resulting From Prolonged Ingestion of Over-The-Counter Zinc", Gyorffy, Edwin J., MD and Chan, Hung, MD, The American Journal of Gastroenterology, August 1992;87(8):1054-1055.
Megaloblastic Anemia - Thiamine Responsive (Vitamin B1)
This is a 9 year study of thiamine metabolism and cellular transport involving 2 patients with thiamine-responsive megaloblastic anemia which was associated with diabetes mellitus and sensorineural deafness in their relatives and in age-matched controls.
The ratios between the content of thiamine and its phosphoesters in erythrocytes was within the normal range.
The absolute values of thiamine and thiamine compounds were reduced by 40% as compared to controls. Thiamine pyrophosphokinase activity was about 30% lower than controls.
Thiamine treatment restored the levels of thiamine and thiamine compounds to normal values, whereas kinase was unaffected.
Cells from thiamine-responsive megaloblastic anemia patients contain low levels of thiamine compounds, probably due to their inability to take up and retain physiologic concentrations of thiamine as a result of the lack of saturable, specific components of transport and reduced thiamine pyrophosphokinase.
"Thiamine Transport by Erythrocytes and Ghosts in Thiamine-Responsive Megaloblastic Anemia", Rindi, G., et al, Journal of Inher. Metab. Dis., 1992;15:231-242.
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