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The objective of this study, designed as a randomized controlled prospective intervention study, was to evaluate the effect of nutritional supplementation on functional status and need of care in undernourished geriatric patients during hospitalization, and up to 6 months after discharge. Participants consisted of 46 undernourished geriatric patients from a geriatric acute care hospital aged 75 years or older without malignant disease, or need for tube feeding or parenteral nutrition. Patients in the supplement group (SG, N = 20) were offered 400 mL (2100 kJ) daily of a liquid supplement during hospital stay and 200 mL (1050 kJ) per day for the following 6 months at home. Patients in the control group (CG, N = 26) had usual care without supplements. The main outcome measure was functional status based on the Barthel Activities of Daily Living score (ADL) at hospital admission, discharge and after 6 months, with higher scores indicating greater independence and a maximum score of 100 points. In supplemented patients with good acceptance (SG+, N = 11), a median improvement of 20 points was observed between admission and discharge, and a further improvement of 5 points at home. Median changes were 0 and -10 points in supplemented patients with poor acceptance (SG-, N = 9) and 5 and 2.5 points in CG, respectively. In SG+, the proportion of independent patients (> 65 points) increased continuously from 36% at admission to 63% at discharge, to 72% after 6 months, and was significantly higher compared to CG at discharge (63% vs 19%, p < 0.05) and after 6 months (72% vs 39%, p < 0.05). 64% of the patients in SG+ improved during hospitalization, compared to 23% in CG (p < 0.05). In the six months at home, 18% of SG+ improved; none of SG+ deteriorated in hospital or at home. In contrast, deterioration of the ADL score occurred in considerable proportions of SG- (22% in hospital, 22% at home) and CG (4% at hospital, 12% at home) patients. The proportion of patients who improved was smaller in SG- (44% at hospital, 22% at home) as well as in CG (23% at hospital, 35% at home), compared to SG+. In conclusion, a positive functional course was evident in supplemented patients with good acceptance during hospitalization, and further improvement was observed during the following 6 months at home. Nutritional support may contribute to reconvalescence and recovery of undernourished geriatric patients.

To determine predictors of death, nursing home placement and hospital admission, a prospective study was carried out in a university-affiliated geriatric hospital and a general practice. One hundred and thirty-five patients consecutively admitted from home to the geriatric hospital and discharged home again (site 1), and 144 patients, aged 70 years and over, of a general practice (site 2) were recruited for a comprehensive geriatric assessment program. At baseline, none was completely dependent on others, or severely demented. At follow-up after 18 months, 46 subjects (17%) had died, 20 subjects (7%) had been institutionalized, and 79 had been admitted to hospital (28 %) in the interim. Univariate analysis demonstrated a significant association between Barthel Activities of Daily Living (ADL), Lawton-Brody Instrumental Activities of Daily Living (IADL), Mini-Mental State Examination (MMSE), Balance and Gait Evaluation, Timed “Up and Go”, Timed Test of Money Counting, Grip-Strength and Williams Board Test, and death as well as nursing home placement. Barthel-ADL were significantly correlated with hospital admission. In a logistic regression analysis, Barthel-ADL were independent predictors for death; Barthel-ADL, Timed “Up and Go”, Timed Test of Money Counting, and Williams Board Test were independent predictors for nursing home placement. No independent predictor was found for hospital admission. It is concluded that self-report and performance-based measures of functional capabilities are useful instruments to identify patients at risk for nursing home placement and death. Factors contributing to hospital admissions are other than those measured by the applied tests.

In this study, 113 patients with modestly elevated levels of low-density lipoprotein cholesterol (210 mg/dl) and coronary artery disease were randomized to an intervention group (n=56) or a control group (n=57). The intervention program consisted of daily exercise and a low-fat diet according to the American Heart Association's recommendation phase III; patients in the control group received "usual care" rendered by their private physician. After 1 year, complete data were available for all 92 patients (intervention: n=40; control: n=52) who underwent repeat coronary angiography. During the study course, patients in the intervention group showed an increase in apolipoprotein A-I(123 +/- 18 vs 129 +/- 20 mg/dl; p0.02) and apolipoprotein A-I/B (1.3 +/- 0.4 vs 1.5 +/- 0.4; p0.01) and a decrease in apolipoprotein B (99 +/- 20 vs 89 +/- 18 mg/dl; p0.01), while apolipoprotein A-II remained unchanged (38 +/- 6 vs 38 +/- 6 mg/dl; p=NS). In the control group, there were no significant changes (apolipoprotein A-I, 124 +/- 17 vs 128 +/- 13 mg/dl; apolipoprotein A-II, 38 +/- 6 vs 39 +/- 6 mg/dl; apolipoprotein B, 100 +/- 21 vs 99 +/- 16 mg/dl; apolipoprotein A-I/B, 1.3 +/- 0.3 vs 1.4 +/- 0.5; all p=NS). As previously reported, there was a significant retardation of progression in patients in the intervention group (progression 23%, no change 45%, regression 32%) compared with the control group (progression 48%, no change 35%, regression 17%) (p0.05). Although retardation of progression was significantly associated with an increase in apolipoprotein A-I/B and a decrease in apolipoprotein B (p0.05), these gave way in multivariate analysis to changes in total cholesterol/high-density lipoprotein cholesterol, absolute levels of low-density lipoprotein cholesterol, and, in a subgroup of patients, to leisure-time physical activity (all p0.05). These data demonstrate that an intervention based on a low-fat diet and intensive physical exercise is capable of improving apolipoprotein levels, associated with retardation of progression of coronary artery disease. However, total cholesterol/high-density lipoprotein cholesterol and low-density lipoprotein cholesterol appear superior to apolipoproteins as metabolic markers for effective treatment in patients with coronary artery disease.

BACKGROUND Significant regression of coronary and femoral atherosclerotic lesions has been documented by angiographic studies using aggressive lipid-lowering treatment. This study tested the applicability and effects of intensive physical exercise and low-fat diet on coronary morphology and myocardial perfusion in nonselected patients with stable angina pectoris. METHODS AND RESULTS Patients were recruited after routine coronary angiography for stable angina pectoris; they were randomized to an intervention group (n = 56) and a control group on "usual care" (n = 57). Treatment comprised intensive physical exercise in group training sessions (minimum, 2 hr/wk), daily home exercise periods (20 min/d), and low-fat, low-cholesterol diet (American Heart Association recommendation, phase 3). No lipid-lowering agents were prescribed. After 12 months of participation, repeat coronary angiography was performed; relative and minimal diameter reductions of coronary lesions were measured by digital image processing. Change in myocardial perfusion was assessed by 201Tl scintigraphy. In patients participating in the intervention group, body weight decreased by 5% (p less than 0.001), total cholesterol by 10% (p less than 0.001), and triglycerides by 24% (p less than 0.001); high density lipoproteins increased by 3% (p = NS). Physical work capacity improved by 23% (p less than 0.0001), and myocardial oxygen consumption, as estimated from maximal rate-pressure product, by 10% (p less than 0.05). Stress-induced myocardial ischemia decreased concurrently, indicating improvement of myocardial perfusion. Based on minimal lesion diameter, progression of coronary lesions was noted in nine patients (23%), no change in 18 patients (45%), and regression in 13 patients (32%). In the control group, metabolic and hemodynamic variables remained essentially unchanged, whereas progression of coronary lesions was noted in 25 patients (48%), no change in 18 patients (35%), and regression in nine patients (17%). These changes were significantly different from the intervention group (p less than 0.05). CONCLUSIONS In patients participating in regular physical exercise and low-fat diet, coronary artery disease progresses at a slower pace compared with a control group on usual care.

To obtain reference values for comparison with malnourished geriatric patients, the nutritional status of 50 apparently healthy women aged 75 or older living independently in two old people's homes in Heidelberg was examined. All women were able to walk, and were free from overt disease and signs of mental deterioration. Anthropometric measurements (body height and weight, triceps skinfold thickness, midarm circumference) and biochemical determinations of protein and vitamin status were performed. Anthropometric parameters were similar to those obtained in "younger" samples of healthy elderly, lower than those reported in younger adults, and markedly greater than those reported in geriatric patients. The majority of biochemical findings were within normal reference ranges established for healthy young adults. Only plasma retinol concentrations were below the reference limit in 8 women (16%). These findings show clearly that even in the very old, major alterations in biochemical indicators of nutritional status are rare. Neither advanced age nor institutionalization are associated with malnutrition. This obviously suggests that malnutrition in old age is mainly related to physical and mental disabilities.

An immunonephelometric procedure for determination of apolipoprotein B in human serum [Clin. Chem, 25, 221-226 (1979)] was modified by using the detergent octadecenylamine-polyoxyethylene, which may bind selectively to the phospholipid moiety of lipoproteins. Preincubation of hyperlipemic serum samples with lipases could then be omitted.

In the present investigation 238 randomly selected male individuals of the general population (age 19--41 years) and 42 age-matched male patients with recurrent renal stone formation (calcium oxalate and/or calcium phosphate) were studied under outpatient conditions without dietary restrictions. Urinary Na excretion was 207 +/- 82 mmol/24 h (range 55--570) in controls and 208 +/- 100 (range 76--575) in recurrent renal stone formers. Both in controls (r = 0.36; p less than 0.01) and in stone formers (r = 0.4; p less than 0.01) a significant correlation was observed between urinary excretion of sodium and calcium. Urinary sodium excretion was unrelated to systolic or diastolic blood pressure in normotensive or hypertensive individuals. This finding indicates that factors other than sodium are involved in the maintenance of hypertension. Urinary sodium, presumably an index of intake of nutrients, was significantly correlated to several coronary risk factors, e.g. fasting glucose, cholesterol and overweight. There existed a significant inverse relationship between fasting plasma phosphate and urinary sodium, but not between fasting plasma phosphate and serum iPTH or urinary cAMP. This finding points to some function of sodium excretion as one determinant of plasma phosphate.

The previously described procedure of direct determination of LDL-cholesterol after selective extraction of VLDL and HDL with polycations and a polycation-exchange resin has been improved by using dodecoylated poly(ethyleneimine) instead of poly(ethyleneimine). The acyl derivative has a higher affinity for lipoproteins. Disc-electrophoretic patterns of lipoproteins separated by this procedure correspond to patterns of apolipoproteins in VLDL and HDL, a finding that corroborates the conclusion that the mechanism of the selective binding of certain lipoproteins to lipophilic water-soluble polycations is based on hydrophobic interaction between the polymer and lipids located at the surface of lipoprotein particles. The procedure offers a simple possibility for direct LDL-cholesterol and LDL-triglyceride determination and for the isolation of VLDL and HDL. The mechanism of the reaction has a biochemical correlate in the action of phospholipase A2 on phospholipids.

The effects of physical exercise and normalization of serum lipoproteins on stress-induced myocardial ischemia were studied in 18 patients with coronary artery disease, stable angina pectoris, and mild hypercholesterolemia (total serum cholesterol 242 +/- 32 mg/dl). These patients underwent a combined regimen of low-fat/low-cholesterol diet and regular, supervised physical exercise at high intensity for 12 months. At 1 year serum lipoproteins has been lowered to ideal levels (serum cholesterol 202 +/- 31 mg/dl, low-density lipoproteins 130 +/- 30 mg/dl, very low-density lipoproteins 22 +/- 15 mg/dl, serum triglycerides 105 [69 to 304] mg/dl) and physical work capacity was improved by 21% (p less than .01). No significant effect was noted on high-density lipoproteins, probably as a result of the low-fat/high-carbohydrate diet. Stress-induced myocardial ischemia, as assessed by thallium-201 scintigraphy, was decreased by 54% (p less than .05) despite higher myocardial oxygen consumption. Eighteen patients matched for age and severity of coronary artery disease served as a control group and "usual medical care" was rendered by their private physicians. No significant changes with respect to serum lipoproteins, physical work capacity, maximal rate-pressure product, or stress-induced myocardial ischemia were observed in this group. These data indicate that regular physical exercise at high intensity, lowered body weight, and normalization of serum lipoproteins may alleviate compromised myocardial perfusion during stress.

Longterm treatment for 5 years of young patients with familial hypercholesterolemia was accompanied by monitoring of plasma levels of calcium, iron, sodium, parathyroid hormone and water- and fat soluble vitamins, since interference of the ion exchange resin with absorption of numerous substances as well as abnormal plasma levels of some of the above had been described in several studies. Treatment was effective in the group with good compliance (lowering of plasma cholesterol at the end of 5 years by 19% and, compared to the control group, by 23%). Adverse drug effects with respect to the above parameters were not found. Plasma levels of carotinoides and vitamin E were elevated in the patients according to elevated concentrations of lipoproteins which are carriers of these vitamins.

Alimentary lipemia was studied in 12 healthy young men with and without exercise. Three sets of experiments were performed. While continuous exercise of 90 min duration significantly reduced postprandial triglycerides by 26% (study I), this effect could not be observed when exercise was interrupted for 5 min after each 25 min (study II). Plasma free fatty acid concentrations, in the latter experiment, were significantly higher (by 311%) than during rest. When, in a third experiment continuous exercise was compared with intermittent physical activity, the latter condition significantly increased postprandial triglyceridemia, most probably due to precipitous rises of free fatty acids on each interruption of ergometry. It is concluded that in the third experiment the balance between triglyceride removal and triglyceride synthesis was shifted toward the latter. Whether exercise lowers, leaves unaltered, or raises plasma triglyceride levels may depend on subtle changes of experimental design.

In 20 children and adolescents with familial Type IIa hyperlipoproteinemia, serum lipids and lipoproteins were examined before and during treatment with polyanion exchange resins. The composition of LDL was compared to that of healthy siblings. The patients were given Colestyramine (0.6 g/kg body weight) and Colestipol (0.5 g/kg body weight) in a cross-over study for 8 weeks each, after they had been under dietary treatment for at least 12 months. In 6 children, drug treatment had to be stopped due to side-effects. The most common complaints were gastrointestinal discomfort and constipation.

Bei 6 Personen wurde die Wirkung einer intraduodenalen Instillation von 10 naval HCl/10 min und 1 E/kg Sekretin (Boots) auf die exokrine und endokrine Pankreasfunktion untersucht. Wahrend eine Stimulierung der exokrinen Pankreasfunktion sowohl wahrend der HCl-Instillation als auch unter exogener Sekretinzufuhr beobachtet werden konnte, war eine betacytotrope Wirkung, gemessen am Blutzucker und an der Plasmainsulinkonzentration im peripheren Venenblut nur nach exogener Sekretinstimulation nachweisbar. - Die intraduodenale Instillation von 2×3 mval HCl wahrend einer intraduodenalen Glucosebelastung mit 300 ml 5%iger Glucose/20 min bei 7 Personen fuhrte zudem zu keiner Steigerung der Glucoseutilisation oder des Insulinspiegels. Nach intraduodenalem Atherreiz (3 ml), welcher zur Stimulierung eines bicarbonat- und enzymreichen Pankreassaftes fuhrt, konnten keine Zeichen einer betacytotropen Wirkung beobachtet werden, so das eine endogene Sekretinfreisetzung fur die schnellere Glucoseassimilation und grosere Insulinsekretion nach oraler Glueosezufuhr im Vergleich zur intravenosen Glucosezufuhr keine grosere physiologische Bedeutung haben durfte.

Previous studies have shown that carbohydrate induction of hypertriglyceridemia in normal subjects occurs at night and appears to be related to a rise of free fatty acids after diurnal feeding of high-carbohydrate formula diet. The present investigation was undertaken to observe the effect on 24-h triglyceride, free fatty acid, blood sugar, and plasma insulin profiles of inhibition of nocturnal lipolysis by glucose or nicotinic acid in normal subjects and in patients with type IV hyperlipoproteinemia. In 10 normal subjects and 10 patients with primary type IV hyperlipoproteinemia, plasma triglyceride, free fatty acid, blood sugar, and insulin levels were followed in short intervals for 24 h while a 2,400 cal, 80% carbohydrate, fat-free formula diet was given in six equal portions during the day (control experiments). This procedure was repeated in the same subjects, 10 of whom (5 normal subjects and 5 patients) received additional feedings of glucose between 2000 and 0600 h while the other 10 persons (5 normal subjects and 5 patients) were given nicotinic acid by intravenous infusion during the same time interval. Both procedures resulted in maintained lowering of free fatty acid levels over 24 h. Mitigation of carbohydrate-induced hypertriglyceridemia appeared to result from the additional glucose in normals and in patients. Nicotinic acid abolished the nocturnal rise of plasma triglyceride levels which in the control studies of normal subjects had resulted in approximate doubling of triglyceride levels in 24 h. The effectiveness of nicotinic acid in inhibiting nocturnal lipolysis and preventing carbohydrate-induction of hypertriglyceridemia might have consequences for management of endogenous hypertriglyceridemia.

Eine neue Methode der Lipoproteinelektrophorese in Agarose-Gel wird mit der nachLees u.Hatch (1963) modifizierten Methode der Papierelektrophorese an Hand von Seren mit typischen Lipoproteinmustern verglichen. Nach den bisherigen Erfahrungen bietet die Agarose-Gel-Elektrophorese gegenuber dem Verfahren auf Papier die Vorteile einer scharferen Trennung der einzelnen Lipoproteinbanden, einer schnelleren Durchfuhrung, reproduzierbarer Aussagen uber die relative elektrophoretische Mobilitat bestimmter Lipoproteinbanden und einer densitometrischen Auswertbarkeit.

The antilipolytic effects of N6-phenylisopropyladenosine and of prostaglandin E2 were studied with adipocytes of obese volunteers before and after 4 weeks of severe energy restriction [1250 kJ (300 cal)/day] in the presence and absence of adenosine deaminase (1.6 micrograms/ml, corresponding to 320 m-units/ml). The studies were undertaken to define more clearly the role that local modulators might play in adaptation of lipid mobilization to starvation in humans. Starvation was associated with an approx. 3-fold increase in non-stimulated lipolysis. Removal of endogenous adenosine resulted in a similar increase in basal glycerol release under both conditions, averaging 2 and 2.2 mumol/180 min per 10(6) cells respectively. The sensitivity of the cells to N6-phenylisopropyladenosine and to prostaglandin E2 was not changed by starvation in the presence of adenosine deaminase. These results are discussed in terms of the possible role that local regulators might play during dietary adaption in human fat-cells in vitro.

In addition to their effect on lipids Clofibrate and related drugs can influence platelet function and fibrinolytic activity. Interaction of these drugs with coumarin anticoagulants may induce hemorrhagic complications. Therefore the effect of a new hypolipemic agent (bezafibrate) on blood coagulation and components of the fibrinolytic encyme system was investigated.15 patients on long term treatment with phenprocoumon received bezafibrate (450 or 600 mg daily) for 4 weeks. Evaluation of platelet function demonstrated a reduced platelet aggregation induced by collagen (p < 0.05) and prolongation of bleeding time (p< 0.05), dependent on the given dose. Plasma fibrinogen was reduced moderately. Examination of the fibrinolytic activity yealded a shortened euglobulin clot lysis time (p < 0.05) but no changing of inhibitors. Serum level of phenprocoumon and bezafibrate were determined to obtain data about the mechanism of drug interaction. After reduction of the phenprocoumon dose by 20.6 or 28.7% the serum phenprocoumon levels decreased by 9-3 and 30.6%, respectively.Hypo-prothrombinemia was maintained (p< 0.05). The results support the hypothesis, that hypolipemic drugs such as bezafibrate augment the anticoagulant response to phenprocoumon by increasing the affinity of the receptor site for coumarin and not by effecting the rate of metabolism.

A potassium loss of 3–11% (6.0±2.7%) of total body potassium, was produced in 6 normal subjects during the course of a metabolic balance study of 13–16 days duration using a supplemented formula diet. This resulted in the development of a marked hypokaliaemic alkalosis. There were no significant changes of blood sugar, free fatty acid and plasma insulin concentrations during intravenous (0.5 g/kg) or oral (100 g) glucose tolerance tests for control and experimental periods.

Bei 5 Normalpersonen wurde der Einflus von 7µg/kg Glukagon (Novo) i. v. auf die exokrine und endokrine Pankreasfunktion im Vergleich zur Wirkung von 1 E/kg Korpergewicht/kg Secretin (Boots) untersucht. Blutzucker und Plasmainsulinkonzentration zeigten nach Glukagonzufuhr einen raschen Anstieg und einen tragen Abfall innerhalb 60 min. Die Bicarbonatsekretion und die Amylasesekretion wiesen wahrend dieses Zeitraumes keine Veranderungen im Vergleich zur Leerperiode auf. Die nachfolgende Secretininjektion verursachte eine signifikante Steigerung der Bicarbonatsekretion.

In tierexperimentellen Untersuchungen an adrenalektomierten Ratten wurde der Einflus von Glucagon (0,1 mg/kg) auf die Insulinsekretion und den Blutzucker nach Vorbehandlung mit 200 mg/kg Diazoxid untersucht. Bei normal gefutterten Tieren war die glucagoninduzierte Insulinsekretion nach Diazoxid stark vermindert, aber nicht vollig aufgehoben. Nach 24stundigem Fasten hatte Diazoxid keine hemmende Wirkung auf die glucagonstimulierte Insulinsekretion.