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Nutrients and energy intake of black adults with sickle cell disease.

Introduction

Sickle cell disease (SCD) is a debilitating disease resulting in chronic hemolytic anemia and vaso-occlusion in almost all organs leads to significant morbidity and early death (Schnog et al., 2004). Homozygous sickle cell anemia (HbSS) is the common and incapacitating form of sickle cell disease (SCD). Fetal hemoglobin (HbF) is the dominant hemoglobin type during fetal life. In the first 12 weeks after birth, the percentage of HbF quickly declines, leaving normal hemoglobin - HbA and [HbA.sub.2]. However, in SCD the HbF may remain throughout the life cycle. Both HbSS and HbF (in adults) are abnormal hemoglobins (Schnog et al., 2004).

Healthy red blood cell (RBC) half-life is one hundred and twenty days (120), while sickled erythrocyte half-life is only seventeen (17) days. Sickled RBC causes ischemic organ damage as cells get entrapped in the microcirculation. Intravascular hemolysis in SCD results from complement recognition of sickling-induced membrane changes, cell dehydration and direct membrane damage by rigid hemoglobin polymers. Monocyte and macrophage destruction of physically entrapped cells in the microcirculation also contributes to the shortened erythrocyte lifespan (Schnog et al., 2004). Most of the complications seen in sickle cell patients can be attributed to vaso-occlusion. Vaso-occlusion is a painful crisis and accounts for the majority of SCD patients' hospitalization (Powars, Hiti, Ramicone, Johnson, & Chan, 2002). Sickle cell patients often experience excruciating pain in the lumbar spine, femur, ribs, sternum, and abdomen.

Despite the increasing awareness that nutritional factors play crucial roles in the expression of a variety of chronic diseases, their roles in sickle cell disease pathophysiology and treatment have not been fully examined. Deficiencies of both macro and micro nutrients (such as protein, vitamins A, E, B-6 and zinc) have been linked to clinical features of sickle cell disease in children. After an extensive literature search, the researcher was unable to find any study that comprehensively assessed the dietary intake of adult sickle cell patients. This researcher previously reported anthropometric and energy expenditure in an earlier publication.

In 2002, Singhal, Parker, Linsell, & Serjeant analyzed a three-day, weighed food record and found that dietary intakes of energy and protein of the SCD patients were similar to those of the controls, as were their fat and carbohydrate intakes. However, there were significant differences between the genders in each genotype. Girls with SCD had higher energy (0.39 + 0.09 MJ/kg) and carbohydrate intakes (2.32 + 0.59 g/kg) than the boys with the disease (0.37 + 0.07 MJ/kg and 2.14 g/kg), respectively. However, the boys in the control group had greater energy and carbohydrate intakes.

Another study assessed the dietary intake of individuals with SCD ages six (6) months to nineteen (19) years during acute illness and steady state. Inadequate intake was reported during illness when compared to the reference values from the 1989 Recommended Dietary Allowances (RDA) for each age group (p < 0.0002). However, three (3) weeks after hospitalization and at a steady state, their dietary intake continued to remain lower than the recommended intake, although there was a significant improvement (p< 0.01) (Fung, et al., 2001).

In an earlier study in 1992, Gray, et al. examined the dietary intake of energy, protein and other nutrients in nine (9) sickle children and nineteen healthy controls. Analyses on the following were performed to determine the children's nutritional status: a three (3) day food diary, blood, and urine specimens were all analyzed to determine the children's nutritional status. Higher dietary intakes of energy (90.6 kcal + 23.4) and protein (3.12 g/kg/day + 0.77) in sickle children were reported compared with the controls' energy (71.4 kcal + 16.8) and protein intakes (2.05g/kg/day + 0.58).

The sickle cell group however, had lower levels of urinary protein, despite higher protein intake. This could be indicative of compromised digestion and/or malabsorption as other studies have concluded (Odonkor, Addae, Yamamoto & Apatu, 1984; Finan, et al., 1988). Odonkor, et al. (1984) concluded that protein products absorption was impaired in sickle cell adolescents. The researcher found elevated urinary nitrogen excretion which was theorized to be due to increased protein catabolism as a result of inadequate intestinal supply of nitrogen and nitrogen's poor utilization. However, Heyman, et al. (1985) studied five (5) growth-retarded children with SCD and found that fat absorption and intestinal mucosal morphology were normal in all the subjects. However, the researchers found that the subjects had inadequate calorie and protein intakes.

Vitamin deficiencies in relation to SCD have been examined, with folic acid, vitamins B-6 and B-12 receiving noteworthy attention in recent years. In vitro studies have established that vitamin B-6 has anti-sickling properties and increases the oxygen affinity of hemoglobin S (Nelson, et al. 2002). Replicating in vitro studies to in vivo efficacy has been questioned due to the high degree of albumin-binding of B6 and because of the harm that could result from impaired oxygen ([O.sub.2]) delivery (Reed, Redding-Lallinger & Orringer 1987). Several studies conducted in children found that sickle cell patients had significantly lower vitamin B-6 levels (Nelson, et al., 2002; Segal, Miller, Brereton & Resar, 2004). Nelson, et al. (2002) calculated vitamin B-6 values by measuring serum pyridoxal 5-phosphate (PLP) concentration in subjects with SCD-SS and urinary 4-pyridoxic acid (4-PA) concentration in other subjects with SCD-SS and non sickle cell children. Seventy-seven percent (77%) had a PLP concentration below the deficiency criterion of 20 nmol/L as suggested by the 1998 Dietary Reference Intakes; while urinary 4-PA was lower in children with SCD-SS when compared with the controls (Nelson et al., 2002).

Folate, vitamins B-6 and B-12 have generated heightened interest due to the effects of their deficiencies and their relationships with homocysteine. Homocysteine is a derivative of the amino acid methionine. Homocysteine is of particular interest in SCD due to its association with vascular complications. A high level of homocysteine is associated with an increased risk of atherosclerosis, which can result in a heart attack (due to coronary artery disease) and stroke (van der Dijs et al., 2002). Deficiencies of folate, vitamin B-6 and/or vitamin B-12 may increase blood levels of homocysteine. Segal et al. (2004) studied the homocysteine, folate, vitamin B-6 and B-12 in children. The findings revealed that subjects with sickle cell anemia had concentrations of homocysteine which were only somewhat higher than those of the controls. SCD individuals had lower vitamin B-6 concentrations and comparable concentrations of folate and vitamin B-12. However, homocysteine concentration was inversely related to vitamin B-12 concentration and was not independently associated with levels of vitamin B-6 or folate (Segal et al., 2004). In studies using adults, homocysteine was significantly elevated. However, both Dhar, Bellevue, Brar, & Carmel 2004 and Lowenthal, Matthew, Cornwell & Thornley-Brown D 2000 were unable to establish a relationship between folate and homocysteine levels. Both studies revealed that folate levels were higher in sickle cell patients. It must be noted that folate supplementation is routinely prescribed to SCD patients, which raises the question of daily folic acid supplements (Reed et al., 1987). Lowenthal et al. (2000) measured plasma concentrations of homocysteine, vitamin B-12 and folate in forty-nine (49) SCD patients and sixteen (16) controls. Individuals with sickle cell disease had been prescribed folic acid (1 mg by mouth daily). The results showed that folate was 1.5 fold higher in SCD patients than in the controls. There were no significant differences in vitamin B-12 levels between both groups. The researchers hypothesized that the concentration of folate required to normalize plasma homocysteine levels in patients with sickle cell disease may be higher than that of normal controls, and that patients with sickle cell disease have a higher nutritional requirement for folic acid than the general population. Although Dhar et al. (2004) had similar findings; they concluded that hyperhomocysteinemia is independent of folate and cobalamin status. They also suggested that interventions other than folate supplementation may be required to decrease homocysteine levels.

The roles of other water soluble vitamins in the pathophysiology and treatment of SCD are not well understood due to insufficient scrutiny. Ascorbic acid (vitamin C) has been studied as a vasodilator. However, the researchers were unable to establish a relationship between vasodilation and vitamin C. (Eberhardt et al., 2003).

The fat-soluble vitamins--A, D, E, and K--have been examined for their roles in SCD. The relationships of vitamin A to growth, nutritional and hematologic status were examined in children ages 2 - 9.9 years. SCD subjects had significantly lower vitamin A levels, body mass, and higher rates of hospitalization. The results demonstrated that sickle cell children with suboptimal vitamin A levels had a 10-fold increased risk of hospitalization. The researchers theorized that a suboptimal vitamin A level was associated with increased hospitalizations and poor growth and hematologic status (Schall et al., 1996).

Studies evaluating the role of vitamin D in SCD are limited with conflicting results. One study assessed the vitamin D-25-hydroxyvitamin D (25-OHD)-status in sixty-five (65) children (5 - 18 years) with SCD in Pennsylvania, USA. Sixty-five percent (65%) of the SCD subjects had significantly lower vitamin D levels when compared to healthy children. Also, these children were at an increased risk of low vitamin status due to inadequate dietary intake of vitamin D-rich foods. Low vitamin D prevalence was highest during Spring (Buison, et al., 2004).

Another study conducted in Curacao (a tropical island) assessed vitamin D status and calcium homeostasis in children--ages 3-19 years. Although calcium homeostasis was lower in SCD patients, none of the children had hypocalcaemia. There were no differences in serum concentrations of phosphate, total protein, albumin, intact parathyroid hormone (PTH), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D when compared with healthy children. The researchers were unable to establish a relationship between PTH and 25(OH)D. It was concluded that vitamin D status of sickle cell patients in Curacao is adequate (van der Dijs, van der Klis, Muskiet & Muskiet, 1997).

Vitamin E has generated a lot of interest. Vitamin E, superoxide dismutase, glutathione peroxidase, and catalase protect the red blood cells against oxidative stress. Erythrocytes are rich in unsaturated fatty acids that are sensitive to oxidative stress. The red blood cells of individuals with SCD have elevated density and abnormal membranes. These dense cells tend to stick to neutrophils, platelets, and vascular endothelial cells, thus causing vaso-occlusion. Using an ex vivo technique, dense cells were developed and treated with known antioxidants--garlic extract, pycnogenol, alpha-lipoic acid, vitamin E, coenzyme Q(10), beta-carotene, and black and green tea extract. The results showed that dense cells could be reduced by approximately fifty percent (50%) when a cocktail of nutritional supplements is used - 6 g of aged garlic extract, 4-6 g of vitamin C, and 800 to 1200 IU of vitamin E (Ohnishi, Ohnishi & Ogunmola, 2000).

Due to depressed plasma levels of vitamin E observed in adult human studies, the researchers concluded that vitamin E may be beneficial in the treatment and management of SCD (Gbenebitse, Jaja & Kehinde, 2005; Essien, 1995). Gbenebitse, et al. (2005) examined the effect of vitamin E supplementation (300mg/day for six (6) weeks) on blood pressure, forearm blood flow, forearm vascular resistance, plasma vitamin E level and lipid peroxidation status. Findings revealed a significant increase in plasma vitamin E and forearm blood flow; while lipid peroxidation status and forearm vascular resistance significantly decreased (p<0.001). The change in plasma vitamin E concentration correlated negatively with change in lipid peroxidation status (r=-0.8; p=0.003). However, change in plasma vitamin E concentration correlated positively with change in forearm blood flow (r=0.8; p=0.006). There was an inverse correlation between change in plasma lipid peroxidation and change in forearm blood flow (r=-0.7; p=0.03). The researchers concluded that vitamin E supplementation increases forearm blood flow and reduces forearm vascular resistance and lipid peroxidation.

Vitamin K seems to be the least nutrient examined in relation to SCD. A study reported that there was no significant difference in laboratory evidence of vitamin K deficiency in a prospective study of one hundred (100) normal children with SCD to determine the prevalence of abnormal coagulation screening tests, and to evaluate potential etiologies (Raffini, et al., 2006).

The role of zinc has been extensively examined in the pathophysiology and treatment of SCD. The findings have been conflicting. However, with more sophisticated methods of zinc analysis, the weight of evidence leans towards zinc deficiency being a common and significant nutritional problem in SCD. Consequences of zinc deficiency include defects in the immune system, impaired healing of leg ulcers, adverse hematologic effects, abnormal growth and retarded sexual development. Zinc can increase the oxygen affinity of both normal and sickled-shaped erythrocytes. Thus, zinc supplements may be beneficial in managing sickle cell disease. (Mahan & Escott-Stump, 2004).

As early as 1975, Prasad, et al. reported that plasma zinc in the erythrocytes and hair was decreased and urinary zinc excretion was increased in sickle cell anemia patients compared with controls. It is theorized that the continued hemolysis in SCD results in the hyperzincuria frequently seen in SCD patients. A more recent study examined the relationship of zinc supplementation to growth and body composition in forty-two (42) SCD-SS children from 4 - 10 years old. The children were given either 10 mg elemental Zn/d in cherry syrup (zinc group) or cherry syrup alone (control group). Dietary intakes were evaluated and anthropometric, high precision knee-height, and plasma zinc measurements were made at baseline and at three (3), six (6), and twelve (12) months. Body composition was determined every six (6) months using dual energy X-ray absorptiometry (DEXA) as were their anthropometric measurements. No significant differences were observed at baseline. At the termination of the study, the zinc group had significantly greater increases in height, sitting height, knee height, and arm circumference. Height-for-age and weight-for-age increased significantly in the control group but did not change significantly in the zinc group (Zemel, et al., 2002).

Earlier studies found iron deficiency in individuals with SCD (Rao, et al., 1983; Serjeant, et al., 1980). Determining iron deficiency has posed some difficulty for researchers. However, some researchers consider the absence of bone marrow iron as the standard to determine iron deficiency. Low serum ferritin is highly specific for the diagnosis of iron deficiency, but its sensitivity is very low in SCD because of non-specific elevation due to increased red cell turnover (Reed, et al., 1987; Koduri, 2003).

Koduri, et al. (2003) theorized that an iron deficiency was beneficial in the management and treatment of SCD. The kinetics of sickling is strongly concentration dependent such that small decreases in the mean corpuscular deoxyhemoglobin-S concentration (MCHC-S) cause a substantial delay in sickle hemoglobin polymerization. Prolongation of the "delay time of gelation" in excess of the capillary transit time may allow the erythrocyte to traverse the capillary bed to escape to the arterial side before there is rheologic impairment of the erythrocyte from polymerization of sickle hemoglobin. Overt iron deficiency lowers the MCHC-S and thereby decreases the sickling tendency and the severity of hemolysis. The clinical improvement in SCA following the induction of iron deficient erythropoiesis by repeated phlebotomies or by erythrocytapheresis has been reported (Koduri, et al., 2003).

Although selenium (Se) is well recognized for its antioxidant properties very few studies have examined selenium's role in the management and treatment of SCD. Levels of selenium and glutathione peroxidase were determined in twenty (20) sickle cell patients and fourteen (14) healthy controls. The results showed that Se and glutathione peroxidase levels were low in both plasma and whole blood. The researchers concluded that low blood Se levels and glutathione peroxidase activity may have weakened antioxidant potential in individuals with SCD (Natta, Chen & Chow, 1990).

Fowler, et al. (2010) theorized that dietary fluid and sodium intake may influence the risk for vaso-occlusion after examining 3-day food records of 21 children with SCD. The researchers found that fluid intake was significantly lower than the recommended adequate intake and sodium was higher than the upper intake limits.

The purpose of the study was to assess the dietary intake of adults with sickle cell disease and healthy controls. It is possible that by analyzing the dietary intake new approaches and therapy for the treatment and management of SCD will emerge.

Materials and Methods

This research was conducted according to the policies and procedures of Howard University Institutional Review Board (IRB) and the General Clinical Research Center (GCRC) at Howard University Hospital. Informed consent forms were obtained from all participants.

Fourteen (14) healthy controls (10 females and 4 males) with HbAA were recruited from the Howard University community--hospital and university. Eight (8) participants included African American adult females (6) and males (2), ages 18 - 69 years diagnosed with sickle cell anemia (SCA)--homozygous HbSS disease and fetal hemoglobin (HbF). Subjects with SCD were recruited from the Howard University Sickle Cell Clinic. Participants were identified and characterized by ion-exchange high-performance liquid chromatography (HPLC) of hemoglobins (Wilson, Headlee & Huismann, 1983). Individuals who were transfused within the last 30 days, requiring oxygen supplementation, had vaso- occlusion within the last 2 weeks, diagnosed with HIV/ AIDS, diabetes, cancer, and end stage renal disease--dialysis dependent were excluded from the study.

Prior to admission to the General Clinical Research Center (GCRC), the subjects were asked to provide a list of foods they would have typically consumed for their meals if not participating in a study. The participants were provided the foods, meals, and beverages they identified as their typical choices. There were no dietary restrictions and participants were offered foods from all the foods groups based on the food guide pyramid (United States Department of Agriculture, 2005). Three (3) free meals were served--breakfast, lunch and dinner. Snacks (twice during the admission period) were also provided for the participants. The Howard University Hospital cafeteria provided all meals and snacks, based on the participants' requests. A weighed food intake was conducted using Ohaus SP-402 electronic balance (Bradford, MA). The balance has a capacity of 400 g and readability of 0.01 g. Foods were measured before consumption. The leftovers were also weighed. Weighed food intake, caloric, and nutrient intake were calculated by the author. Nutrient intake was analyzed using Nutritionist Pro (Version 1.3, First Data Bank Division, Hearst Corp, San Bruno, CA)

Statistical Analysis

The data were analyzed using the Statistical Package for the Social Sciences (SPSS) for Windows, Version15.0 (SPSS Inc., Chicago, IL.). Descriptive and inferential statistics were used to analyze the data. Data were presented as means + standard errors of the mean (SEM). Independent sample t-test was used to assess differences between groups. Pearson's correlation coefficient and linear regression were calculated to determine relationship between energy and nutrient intake. Multiple regression analysis was undertaken to determine which macronutrient predicted weight. Statistical significance was determined at the 5% level.

Results

The subjects in the sickle cell group had a significantly higher intake of total calories (kcal) (p<0.001) (Figure 1). The daily estimated energy requirement (EER) was calculated by multiplying the resting energy expenditure (REE) value by a sedentary activity factor of 1.2 (American Dietetic Association 2000). Based on the EER values, the participants' energy intakes were exceeded by 27.64% and 64.59% by the control and the sickle cell groups respectively.

Table 1 show that the carbohydrate and fat intakes were significantly higher in the sickle cell group. Although, the protein was comparable in both groups, the control group's intake was higher. The estimated recommended macronutrients intake was determined by using the current dietary reference intake (DRI) (Institute of Medicine 2002) for macronutrients of 45 - 65% for carbohydrate, 10 - 35% protein, and 20 - 35% for fat. The control and the sickle cell group exceeded the carbohydrate intake recommended DRI (Institute of Medicine) range by 4% and 51% respectively. The fat intake recommended range was higher by 25% in the control group and 48% in the sickle cell group.

Multiple regressions were used to determine which macronutrient variable was a significant predictor(s) for weight. No statistical significance was determined.

Saturated fat, cholesterol, and trans fatty acids intakes were significantly higher in the control group (Table 2); however, in the sickle cell group polyunsaturated fat consumption was significantly higher. According to the Dietary Guidelines for Americans (Department of Health and Human Services and United States Department of Agriculture 2005) daily intakes of < 300 mg/day for cholesterol and < 10% of total calories from saturated fats are recommended. However in both groups cholesterol intake exceeded the recommended guidelines by 107% in the control group and by 50% in the sickle cell group. Actual saturated fat intake in the control group was 12%, therefore exceeding the recommended intake. The sickle cell group's intake of 10% was within the recommended guidelines. Although, neither the DRI (Institute of Medicine) or the dietary guidelines set a maximum limit on trans fatty acids, both recommend consuming as little as possible, as increased risks for coronary heart disease exists at levels above zero. The sugar intake was significantly higher (p<0.01) in the sickle cell group compared to the control (Figure 2). The control group's fat and sugar intakes comprised approximately 60% of total calories and 66% in the sickle cell group (Figures 3 and 4).

Table 3 shows a positive relationship between abnormal hemoglobins (HbSS and HbF) and sugar intake and a negative relationship between normal hemoglobin and sugar intake significant at p=0.000.

Table 4 shows selected vitamins actual intake and the RDA (Institute of Medicine 2001, 2000, 1998, and 1997) percentage of their intake. There were statistical differences between the groups for vitamins A, B-1, B-2, and E. The participants' intake of the selected vitamins in both groups was higher than the RDA recommended values, except for vitamins D and E. In the control group vitamin D intake was less than the RDA (Institute of Medicine) by approximately 40% and 29% in the sickle cell group. Vitamin E intake was below the RDA (Institute of Medicine) by 73 and 38 % in the control and sickle cell group respectively.

Selected major and trace minerals are shown in Table 5. Calcium was the only mineral intake that was significantly higher (p<0.01) in the sickle cell group. Although, the calcium intake in the sickle cell group was above the adequate intake recommended by the RDA (Institute of Medicine 1997), the control group's intake was less than the RDA (Institute of Medicine 1997) by 17%. The sodium intake exceeded the limits recommended by the Dietary Guidelines for Americans (Department of Health and Human Services and United States Department of Agriculture 2005) by 192% and 235% in the control and sickle cell groups respectively. The iron consumed by the control group was 45% less than the RDA (Institute of Medicine 2001) and 31% by the sickle cell group. However, the potassium intake was below the Dietary Guidelines for Americans (Department of Health and Human Services and United States Department of Agriculture 2005) by 9.07% in the control group and 9.76 % in the sickle cell group. Also the magnesium intake was less than the RDA (Institute of Medicine 1997) by 26.13% and 23.43% in the control and sickle cell groups respectively.

The study revealed that the energy and nutrient intakes (vitamins A, E, B1, and calcium) were significantly higher in the sickle group. Total calories, fat and sugar intakes were also significantly higher in the sickle cell group (p<0.01). Carbohydrate, vitamin A and vitamin B-1 intakes were significantly higher in the sickle cell group (p<0.05). The calories from sugar and fat consumption of the sickle cell group accounted for two thirds (2/3) of their total energy intake. A positive association was observed between sugar intake and HbSS and HbF (p<0.001). However, there was a negative association between sugar intake and HbAA (p<0.000). Additional studies are required to determine the relationship among diet, cardiovascular diseases, and other chronic diseases associated with SCD.

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Judith Camele Anglin, Ph.D., R.D.

Assistant Professor

College of Health and Human Services

California State University, Long Beach

James S. Adkins, Ph.D.

Professor, Director of Graduate Studies

Department of Nutritional Sciences

Howard University

Allan A. Johnson, Ph.D., L.N.

Professor and Dean

College of Allied Health Sciences

Howard University
TABLE 1
Total Carbohydrate, Protein, and Fat Intake (1,2)

                                       Control
Nutrient   Control Group               Group
           (n=12)                      DRI Range

CHO (g)    425.42 (a) [+ or -] 25.00   282-407
PRO (g)    109.50 [+ or -] 7.83        63-219
Fat (g)    122.76 (a) [+ or -] 5.07    55.69-98

                                          S.C. (3)
Nutrient   S.C. (3) Group                 Group       p Value
           (n=8)                          DRI Range

CHO (g)    551.21 (b) * [+ or -] 62.25    253-365     0.028
PRO (g)    95.08 [+ or -] 13.44           56-196      0.159
Fat (g)    128.91 (b) ** [+ or -] 16.79   50-87       0.003

(1) Values are means [+ or -] SEM

(2) Means in a row without a common superscript differ
significantly, p [less than or equal to] 0.05

(3) S.C. represents Sickle Cell Group

* p [less than or equal to] 0.05

** p [less than or equal to] 0.01

TABLE 2
Saturated, Monounsaturated, and Polyunsaturated Fats,
Cholesterol and Trans Fatty Acids Actual Intake (1,2)

                                       Control
                                       Group
Nutrient   Control Group (n=12)        DRI Range

CHO (g)    425.42 (a) [+ or -] 25.00   282-407
PRO (g)    109.50 [+ or -] 7.83        63-219
Fat (g)    122.76 (a) [+ or -] 5.07    55.69-98

                                          S.C. (3)
                                          Group
Nutrient   S.C.3 Group (n=8)              DRI Range   p Value

CHO (g)    551.21 (b) * [+ or -] 62.25    253-365     0.028
PRO (g)    95.08 [+ or -] 13.44           56-196      0.159
Fat (g)    128.91 (b) ** [+ or -] 16.79   50-87       0.003

(1) Values are means [+ or -] SEM

(2) Means in a row without a common superscript differ
significantly, p [less than or equal to] 0.05

(3) S.C. represents Sickle Cell Group

* p [less than or equal to] 0.05

** p [less than or equal to] 0.01

TABLE 3
Pearson's Correlation coefficients (r) between Sugar Intake
and HbAA, HbSS, and HbF

Hemoglobin   Sugar Intake

HbAA
r            -0.72 *
p Value      0.000

HbSS
r            0.70 *
p Value      0.000

HbF
r            0.72 *
p Value      0.000

p [less than or equal to] 0.001

TABLE 4
Selected Vitamins Actual Intake and the RDA (1,2,3)

Vitamins            Control Group (n=12)           RDA%

Vit. A (IU)         13466.47 (a) [+ or -] 410.58   199.25
Vit. D (IU)         240.55 [+ or -] 23.65          39.86
Vit. E (mg)         4.09 (a) [+ or -] 0.59         72.73
Vit. B1 (mg)        2.09 (a) [+ or -] 0.14         81.74
Vit. B6 (mg)        2.35 [+ or -] 0.25             80.77
Vit. B12 (mg)       5.39 [+ or -] 0.30             124.58
Vit. C (mg)         240.00 [+ or -] 37.88          357.80
Niacin (mg)         34.17 [+ or -] 2.09            127.80
Folate ([micro]g)   537.33 [+ or -] 47.29          34.33

Vitamins            Sickle Cell Group (n=8)         RDA%     p Value

Vit. A (IU)         19598.41 (b) [+ or -] 7967.53   335.52   0.040
Vit. D (IU)         284.90 [+ or -] 49.00           28.78    0.285
Vit. E (mg)         9.36 (b) [+ or -] 4.23          37.60    0.033
Vit. B1 (mg)        2.38 (b) [+ or -] 0.36          1.07     0.045
Vit. B6 (mg)        2.23 [+ or -] 0.45              71.54    0.586
Vit. B12 (mg)       5.52 [+ or -] 0.85              130.00   0.056
Vit. C (mg)         335.80 [+ or -] 43.33           304.58   0.377
Niacin (mg)         30.22 [+ or -] 5.56             101.47   0.094
Folate ([micro]g)   563.44 [+ or -] 71.20           40.86    0.755

(1) Values are means [+ or -] SEM

(2) Means in a row without a common superscript differ
significantly, p [less than or equal to] 0.05

(3) Means as percent of RDA

TABLE 5
Selected Minerals Actual Intake and the RDA (1,2,3)

Minerals              Control Group (n=12)         RDA %

Sodium (mg)           4380.86 [+ or -] 388.99      192.06
Potassium (mg)        4273.71 [+ or -] 520.95      9.07
Calcium (mg)          1032.34 (a) [+ or -] 85.79   17.41
Iron (mg)             24.81 [+ or -] 2.65          44.87
Magnesium (mg)        273.33 [+ or -] 25.21        26.13
Zinc (mg)             11.82 [+ or -] 0.85          18.2
Selenium ([micro]g)   104.71 [+ or -] 8.45         90.38

Minerals              Sickle Cell Group (n=8)       RDA %    p Value

Sodium (mg)           5041.79 [+ or -] 793.96       236.12   0.114
Potassium (mg)        4241.32 [+ or -] 435.65       9.76     0.762
Calcium (mg)          1361.31 (b) [+ or -] 261.14   8.90     0.005
Iron (mg)             31.08 [+ or -] 6.89           30.93    0.068
Magnesium (mg)        283.31 [+ or -] 25.60         23.43    0.681
Zinc (mg)             11.04 [+ or -] 0.85           10.4     0.475
Selenium ([micro]g)   100.80 [+ or -] 18.07         90.38    0.135

(1) Values are means [+ or - SEM

(2) Means in a row without a common superscript
differ, p [less than or equal to] 0.01

(3) Means as percent of RDA

FIGURE 1

Comparison of Actual Energy Intake and Estimated Energy
Requirments (EER) (1,2)

                    Actual Intake   EER Intake

Control Group       a               28%
Sickle Cell Group   b               65%

(1) Values are means  [+ or -] SEM

(2) Means in a column without a common superscript differ
significantly, p [less than or equal to] 0.001

Note: Table made from bar graph.

FIGURE 2

Sugar Intake (1,2)

                    Actual Intake

Control Group           a
Sickle Cell Group       b

(1) Values are means  [+ or -] SEM

(2) Means in a column without a common superscript differ
significantly, p[less than or equal to]0.01

Note: Table made from bar graph.

FIGURE 3

Fat and Sugar Intake of the Control Group

Fat Calories%     34%
Sugar Calories%   25%
Other Calories%   41%

Note: Table made from pie chart.

FIGURE 4

Fat and Sugar Intake of the Sickle Cell Group

Fat Calories% 31%
Sugar Calories% 35%
Other Calories% 34%

Note: Table made from pie chart.
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Author:Anglin, Judith Camele; Adkins, James S.; Johnson, Allan A.
Publication:Journal of the National Society of Allied Health
Article Type:Report
Date:Mar 22, 2011
Words:6187
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