The macrobiotic diet in cancer.

Macrobiotics is one of the most popular alternative or complementary comprehensive lifestyle approaches to cancer. The centerpiece of macrobiotics is a predominantly vegetarian, whole-foods diet that has gained popularity because of remarkable case reports of individuals who attributed recoveries from cancers with poor prognoses to macrobiotics and the substantial evidence that the many dietary factors recommended by macrobiotics are associated with decreased cancer risk. Women consuming macrobiotic diets have modestly lower circulating estrogen levels, suggesting a lower risk of breast cancer. This may be due in part to the high phytoestrogen content of the macrobiotic diet. As with most aspects of diet in cancer therapy, there has been limited research evaluating the effectiveness of the macrobiotic diet in alleviating suffering or prolonging survival of cancer patients. The few studies have compared the experience of cancer patients who tried macrobiotics with expected survival rates or assembled series of cases that may justify more rigorous research. On the basis of available evidence and its similarity to dietary recommendations for chronic disease prevention, the macrobiotic diet probably carries a reduced cancer risk. However, at present, the empirical scientific basis for or against recommendations for use of macrobiotics for cancer therapy is limited. Any such recommendations are likely to reflect biases of the recommender. Because of its popularity and the compelling evidence that dietary factors are important in cancer etiology and survival, further research to clarify whether the macrobiotic diet or similar dietary patterns are effective in cancer prevention and treatment is warranted.

Prediction of oxygen uptake and energy expenditure during exercise in obese women.

PURPOSE: For patients concerned with weight loss, monitoring the energy balance between daily dietary intake and exercise expenditure can be useful. Formulas commonly used to estimate the energy costs of exercise were previously derived from healthy men of normal body weight. The purpose of this study was to determine the relationship between measured and predicted exercise energy expenditure for obese women. METHODS: Oxygen uptake (VO2) was measured using respiratory gas analysis in 45 obese (92 +/- 16 kg; 40 +/- 7% fat) and 10 normal weight (control) (58 +/- 5 kg; 21 +/- 6% fat) women during progressive exercise on a motorized treadmill. VO2 was also calculated at matched workrates using a regression equation published by the American College of Sports Medicine. The relationship between predicted versus measured VO2 was determined using least squares regression analysis. RESULTS: The slope of the regression line for measured versus predicted VO2 for controls (y = 0.98x +/- 0.56; P < .001) was different than that of obese women (y = 0.75x +/- 3.06; P < .001). The slope of the regression line for controls was in close approximation to the line of identity, whereas the slope for obese was below it. Using VO2 to calculate kcal, measured energy expenditure, was significantly lower than predicted energy expenditure for obese subjects, but not for controls at several matched workrates: Stage III (213 +/- 40 versus 225 +/- 38 kcal per 30 minutes, P < .001); stage 4 (292 +/- 55 versus 340 +/- 58 kcal per 30 minutes, P < .001); and stage 5 (330 +/- 55 versus 412 +/- 70 kcal per 30 minutes, P < .001) obese measured versus obese predicted, respectively. CONCLUSIONS: The authors conclude that the standard prediction equation gives a better estimation of VO2 for women who have average body weight and body fat than for obese women. This may, in part, be due to the differences in weight and/or fat mass between these subjects and those used to derive this equation. These findings should be considered when estimates of VO2 and energy expenditure are used rather than direct measures for obese women.

Prevalence of essential fatty acid deficiency in patients with chronic gastrointestinal disorders.

Patients with chronic intestinal disorders causing malabsorption, nutritional losses through diarrhea, or catabolic illness would be expected to have essential fatty acid (EFA) deficiency (EFAD), but such deficiency has not been demonstrated in patients treated in accordance with the prevailing standard of care. We studied plasma fatty acid patterns of 56 reference or control subjects and 47 patients with chronic intestinal disorders (mostly Crohn's disease) using high-resolution capillary column gas-liquid chromatography. Patients exhibited a shift in fatty acid metabolism similar to that previously shown to be associated with EFAD. Compared with control subjects, patients had (1) decreased polyunsaturated fatty acid (PUFA) levels (43.7% v 50.4%, P < .0001), (2) increased monounsaturated fatty acid (MUFA) levels (25.8% v 22.0%, P < .0001), (3) higher ratios of mead (20:3 omega 9) to arachidonic (20:4 omega 6) acid (0.020 v 0.013, P < .04), and (4) lower concentrations of total (214 v 284 mg/dL, P < .01), saturated ([SFA] 63 v 75 mg/dL, P < .001), MUFA (56 v 63 mg/dL, P < .001), and PUFA (93 v 143 mg/dL, P < .001). Patients had metabolic shifts toward increased production of MUFA and an increased ratio of derivatives to precursors of omega 6 fatty acids, shifts that occur when cells are EFA-deficient. More than 25% of the patients had biochemical evidence of EFAD according to at least one criterion. Optimal diagnosis requires a concurrent evaluation of concentrations of fatty acids in plasma and in lipoproteins (percent fatty acids). On indices of EFA status that depend on percents, ratios, or concentrations of fatty acids or on the production of abnormal fatty acids, the patients were between patients with severe whole-body EFAD and healthy subjects, a state referred to as absolute EFA insufficiency. Patients with chronic intestinal disease should be evaluated for likely EFA deficiencies and imbalances, and treated with substantial amounts of supplements rich in EFAs, such as oral vegetable and fish oils, or intravenous lipids if necessary.

Altered fatty acid metabolism in patients with angiographically documented coronary artery disease.

Plasma lipids and fatty acids have been linked to coronary artery disease (CAD), and linoleic acid deficiency has been proposed as a risk factor for cardiovascular disease, but few studies have considered their multivariate effects or found the biochemical shifts associated with abnormal fatty acid metabolism or essential fatty acid (EFA) deficiency. We studied fatty acid patterns associated with CAD using high-resolution capillary column gas-liquid chromatography to analyze fasting plasma from 47 patients with angiographically documented CAD and 56 reference subjects. CAD patients exhibited a shift in fatty acid metabolism similar to that associated with EFA-deficient patients. Compared with reference subjects, CAD patients had (1) reduced percentages of polyunsaturated fatty acids ([PUFA] 45% v 50%, P < .001), (2) increased monounsaturated fatty acids (26% v 22%, P < .001), (3) higher ratios of Mead (20:3 omega 9) to arachidonic (20:4 omega 6) acid (0.016 v 0.013, P < .04), (4) increased levels of 16:1 omega 7 (2.10% v 1.55%, P < .001), and (5) higher concentrations of total fatty acids (356 v 284 mg/dL, P < .001), saturated fatty acids (101 v 75 mg/dL, P < .001), monounsaturated fatty acids (91 v 63 mg/dL, P < .001), PUFA (159 v 143 mg/dL, P < .01), 20:3 omega 9 (0.5 v 0.3 mg/dL, P < .01) and 16:1 omega 7 (7.7 v 4.5 mg/dL, P < .01). On indices of EFA status that depend on percentages or ratios of fatty acids or on the production of abnormal fatty acids, CAD patients were between severely EFA-deficient patients and healthy subjects, a state referred to as EFA insufficiency. Patients had metabolic shifts toward increased production of monounsaturated fatty acids and increased ratios of derivatives to precursors of omega 6 fatty acids, shifts that occur when cells are EFA-deficient. Levels of EFAs were negatively correlated with levels of saturated and monounsaturated fatty acids. The percentage of 18:2 omega 6 was positively correlated with high-density lipoprotein (HDL) cholesterol and the ratio of HDL to total cholesterol (r = .58, P < .001, and r = .61, P < .001, respectively) and negatively correlated with triglycerides and total cholesterol (r = .61, P < .001, and r = -.24, P < .01, respectively). Opposite correlations with these parameters were observed with saturated and monounsaturated fatty acids. Saturated fatty acids, total cholesterol, and indicators of EFA deficiency increased and the HDL to total cholesterol ratio and PUFA decreased the probability of CAD as measured by multivariate linear regression.(ABSTRACT TRUNCATED AT 400 WORDS)

Trans-fatty acid patterns in patients with angiographically documented coronary artery disease.

The plasma trans-fatty acids of 47 patients with angiographically documented coronary artery disease were compared with those of 56 reference subjects using high-resolution capillary column gas-liquid chromatography to test the hypothesis that trans-fatty acid intake is a risk factor for cardiovascular disease. Individual and total trans-fatty acids were higher in patients than in reference subjects (1.38 vs 1.11% for total trans-fatty acids, p < 0.003; 0.40 vs 0.31% for palmitoleic acid trans, p < 0.001; and 0.28 vs 0.22% for linoleic acid trans, p < 0.007). High-density lipoprotein (HDL) cholesterol and HDL cholesterol/total cholesterol were negatively correlated (r = -0.29, p < 0.004; and r = -0.35, p < 0.001, respectively), whereas triglycerides, total cholesterol and low-density lipoprotein cholesterol were positively correlated (r = 0.47, p < 0.001; r = 0.22, p < 0.03; r = 0.20, p < 0.05, respectively) with palmitoleic acid trans. The correlations were similar and significant for linoleic acid trans, but less strong for total trans-fatty acids (which is more difficult to measure and has greater variability). Saturated and trans-fatty acids and total cholesterol are positively associated, whereas HDL/total cholesterol and polyunsaturated fatty acids are negatively associated with coronary artery disease. These results are consistent with the hypothesis that dietary trans-fatty acids are a cardiovascular risk factor.

Effects of oral soy phosphatidylcholine on phagocytosis, arachidonate concentrations, and killing by human polymorphonuclear leukocytes.

A dietary supplement of linoleic acid (LA) as soy phosphatidylcholine (PC) or as triglyceride on polymorphonuclear leukocyte (PMNL) functions, arachidonate (AA) concentrations, AA release, and leukotriene B4 (LTB4) generation was studied in normal adults. Study 1: Eight subjects were fed PC (27 g) or placebo for 3 d in a blinded crossover experiment with PMNL assays at baseline and 4, 7, and 14 d. Study 2: Subjects were fed equal quantities of LA as PC (18 g, n = 8), safflower (SF, n = 4), or soybean oil (SY, n = 4) with PMNL assays at baseline and 48 h. Study 1: PC increased PMNL phagocytosis and killing of Candida albicans twofold (P less than 0.001) and PMNL phospholipid AA content threefold (P less than 0.001); AA release after Candida albicans stimulation increased 5.3-fold, correlating with PMNL killing (r = 0.932) and phagocytosis (r = 0.872). Study 2: PC, but not SF or SY, produced changes similar to those of study 1. With PMNL exposure to calcium ionophore A23187 or N-formyl-methionyl-leucyl-phenylalanine, PC increased LTB4 generation. Phospholipid LA, in contrast to triglyceride LA, enhanced PMNL phospholipid AA, phagocytosis, and killing.

Total parenteral nutrition-induced cyclic hypercapnia.

Excessive rates of carbohydrate infusion during total parenteral nutrition (TPN) have been reported to cause hypercapnia leading to respiratory failure or inability to wean from a ventilator. This case history illustrates the hitherto unreported syndrome of cyclic hypercapnia resulting from high rates of carbohydrate infusion during peak TPN flow rates when TPN was provided in a cyclic fashion. The patient was given TPN daily over an 18 1/2-h period followed by 5 1/2 h without nutritional support. Elevated CO2 production, increased respiratory quotient, hypercapnia, and inability to wean from a ventilator occurred during peak cycle TPN flow rates. When the same carbohydrate load was infused continuously over a 24-h period, CO2 production, respiratory quotient and PaCO2 were reduced. The patient was then able to tolerate periods of unassisted ventilation.

Behavioral effects of sucrose on preschool children.

Despite speculation that sucrose consumption affects behavior, little empirical information is available. Accordingly, this study investigated the effect of sucrose consumption on the behavior of eight preschool children. Children were tested individually using a double-blind, crossover design. On separate mornings each child received 6 ounces of juice, sweetened on one morning with sucrose and on the other with an artificial sweetener. Children were observed for 90 minutes following the drinks, alternating between 15-minute sessions of work on structured tasks and 15-minute sessions of free play. Following the sucrose drink the children showed a decrement in performance in the structured testing situation, and they demonstrated more "inappropriate" behavior during free play. These differences in behavior were most pronounced approximately 45 to 60 minutes after the drinks. Thus, the study provides objective evidence in young children of a rather subtle, yet significant, time-dependent behavior effect of sucrose ingestion.

Effects of dieting and exercise on lean body mass, oxygen uptake, and strength.

The effects of exercise on lean body mass (LBM), fat mass (FM), maximal oxygen uptake (VO2max), and quadriceps (QD) strength were studied in 72 male, mildly obese (X = 38% fat) subjects (X age, 43.5 yr) randomly assigned to one of eight treatments arranged in a 2 X 4 factorial plan with exercise (EX) and non-exercise (NE) and four diets as the two factors. Exercise consisted of a 3 d/wk, 8-wk aerobics program (70-85% maximum heart rate) accompanied by a calisthenics program. LBM was determined by whole body potassium (40K), FM by subtracting LBM from total body weight, VO2max using the Wilmore-Costill method, and QD strength with the Cybex II system. Weight loss of the combined EX (11.8 +/- 0.6 kg) (X +/- SE) and NE (9.2 +/- 0.3 kg) groups was not statistically different. LBM of the EX group was unchanged (from 63.1 +/- 1.9 to 62.5 +/- 2.1 kg), whereas in the NE group it was reduced from 62.6 +/- 1.1 to 59.3 +/- 1.2 kg (P less than 0.001) accounting for 36% of total weight loss. FM loss was greater for the EX group (11.2 +/- 1.5 kg) when compared to the NE (5.2 +/- 1.6 kg) group (P less than 0.001). The EX group exhibited an increase in VO2max from 2.9 +/- 0.3 to 3.4 +/- 0.2 1 X min-1 (P less than 0.001), whereas the NE group was unchanged (3.0 +/- 0.3 to 2.9 +/- 0.4 1 X min-1 (NS].(ABSTRACT TRUNCATED AT 250 WORDS)

Selenium deficiency with total parenteral nutrition: reversal of biochemical and functional abnormalities by selenium supplementation: a case report.

A patient with multiple intestinal fistulae maintained on total parenteral nutrition for 18 months developed low serum selenium. Erythrocyte glutathione peroxidase activity was 6% of normal. Erythrocytes were not able to metabolize H2O2 as well as those from controls, although the hexose monophosphate shunt itself was intact. Granulocytes from this patient had 15% of the erythrocyte glutathione peroxidase activity found in normals. Patient granulocytes were not able to metabolize H2O2 as well as controls, although the hexose monophosphate shunt was intact. Erythrocyte glutathione peroxidase-deficient granulocytes incubated with a respiratory burst stimulant, phorbol myristate acetate, had only 60% of the hexose monophosphate shunt activity present in control granulocytes. These abnormalities were reversed with selenium supplementation. Bacterial killing of Staphylococcus aureus 502A and cardiac function were not affected by selenium deficiency. Thus, selenium deficiency resulted in biochemical and functional abnormalities of erythrocytes and granulocytes. These abnormalities were reversed with selenium supplementation.

Myocardial healing and repair after experimental infarction in the rabbit.

Adequacy of healing after acute myocardial infarction may determine the incidence of postmyocardial infarction rupture and ventricular aneurysm. Accordingly, in 36 rabbits, from 1 to 8 days after coronary ligation, and in 18 shams, we measured collagen formation and mechanical resistance of the infarcted left ventricle to stretch and rupture. Prolyl hydroxylase, an intracellular enzyme of collagen synthesis, increased from control activity of 3970 +/- 431 to 9224 +/- 643 counts/min per mg (cpm/mg) extractable protein (P less than 0.01) at 48 hours and was nearly maximal at 3 days postmyocardial infarction (14,518 +/- 2,030 cpm/mg, P less than 0.01). Lysyl oxidase, an extracellular collagen cross-linkage enzyme, increased from control activity of 29.6 +/- 4.8 to 74.7 +/- 18.8 cpm/mg extractable protein (P less than 0.01) at 72 hours and peaked at 121.5 +/- 7.3 (P less than 0.01) 4-6 days postmyocardial infarction. Hydroxyproline, a measure of collagen content, increased from control of 2.8 +/- 0.2 to 5.3 +/- 0.6 mg/g dry weight (P less than 0.05) at 72 hours and continued to increase at 8 days postmyocardial infarction (14.5 +/- 1.7 mg/g dry weight; P less than 0.01). When enzyme activities and hydroxyproline content were expressed relative to other reference bases, including DNA, tissue protein, dry weight, and total left ventricle, similar results were obtained. The mechanical properties of the infarcted left ventricle were determined by filling a balloon in the excised left ventricle until rupture. The rupture threshold in the normal left ventricle, [664 +/- 43 mm Hg (n = 16)], was not significantly different from that of the infarcted left ventricle on days 1-8 postmyocardial infarction. However, left ventricular rupture occurred more often through the myocardial infarction on days 1-4 postmyocardial infarction (59%) than on days 6 and 8 (18%; P = 0.03) when collagen content had significantly increased. Wall stress at the point of rupture in left ventricles from shams and normals was 30 +/- 2 g/mm2; tensile strength in isolated left ventricle muscle strips was 25 +/- 4 g/mm2 and in isolated scar strips at 7 days postmyocardial infarction was 59 +/- 7 g/mm2. The passive stiffness of the infarcted left ventricle increased from control of 61 +/- 5 to 94 +/- 6 mm Hg/100 microliters (P less than 0.05) at 4 days and 100 +/- 7 mm Hg/100 microliters (P less than 0.01) at 6 days postmyocardial infarction. Stiffness correlated with hydroxyproline content over the 8 days postmyocardial infarction (r = 0.599; P less than 0.001). Thus, the acutely infarcted ventricle was highly resistant to rupture during the initial 48 hours postmyocardial infarction, before any increase in collagen occurred. This result suggests that the preinfarction collagen content has an important role in preventing rupture. After 72 hours postmyocardial infarction, collagen synthesis appeared to be a determinant of infarct stiffness and resistance of the infarcted ventricle to rupture.