High sugar consumption and poor nutrient intake among drug addicts in Oslo, Norway.

Poor dietary habits among drug addicts represent health hazards. However, very few studies have focused on dietary intake as an independent health risk factor in relation to this group. The objective of the present study was to examine the dietary habits of drug addicts living on the fringes of an affluent society. The study focused on food access, food preferences, intake of energy and nutrients, and related nutrient blood concentrations. The respondent group consisted of 123 male and seventy-two female drug addicts, who participated in a cross-sectional study that included a 24 h dietary recall, blood samples, anthropometrical measurements and a semi-structured interview concerning food access and preferences. Daily energy intake varied from 0 to 37 MJ. Food received from charitable sources and friends/family had a higher nutrient density than food bought by the respondents. Added sugar accounted for 30 % of the energy intake, which was mirrored in biomarkers. Sugar and sugar-sweetened food items were preferred by 61 % of the respondents. Of the respondents, 32 % had a TAG concentration above the reference values, while 35 % had a cholesterol concentration beneath the reference values. An elevated serum Cu concentration indicated inflammation among the respondents. Further research on problems related to the diets of drug addicts should focus on dietary habits and aim to uncover connections that may reinforce inebriation and addiction.

Quantitative studies of the metabolism of chylomicron triglycerides and cholesterol by liver and extrahepatic tissues of sheep and dogs.

Unanesthetized sheep and dogs, previously fitted with indwelling catheters in the aorta, lower vena cava, mesenteric, portal, left hepatic and jugular veins, were given constant intravenous infusions of lymph in which the chylomicron lipids were variously labeled with (3)H or (14)C. Para-aminohippuric acid was infused into the mesenteric venous catheter for measurement of portal and hepatic venous blood flow. In some animals, alternately labeled free fatty acids bound to albumin were mixed with the lymph to be infused. In both species, chylomicron triglyceride fatty acids were taken up in the region drained by the lower vena cava and portal vein and free fatty acids derived from hydrolysis of these triglycerides were extensively recycled in the blood. Direct uptake of triglyceride fatty acids also occurred in liver and accounted for about 10% of the total triglyceride fatty acids removed from the blood in sheep and 22% in dogs. In sheep, 10% and, in dogs, about 40% of these triglyceride-fatty acids were released into the blood as free fatty acids. The free fatty acids recycled from various regions accounted for a substantial fraction of the chylomicron fat eventually deposited in each tissue. Uptake of chylomicron cholesterol from the blood of sheep occurred primarily in liver and to a small extent in certain tissues drained by the portal vein. The results obtained, together with other available data, demonstrate that chylomicron triglycerides are removed primarily in extrahepatic tissues of both species, while the liver removes cholesterol contained in chylomicron "skeletons" from which most of the triglycerides have been removed. The quantitative differences between transport of chylomicron lipid in sheep and dogs may be related to known differences in the structure of their hepatic sinusoids.

Transport of L-carnitine induced by prednisolone in an established cell line (CCL 27). A possible explanation of the therapeutic effect of glucocorticoids in muscular carnitine deficiency syndrome.

Prednisolone (10(-8)--10(-5) mol/l) in the growth medium for 24 h increased the rate of uptake of L-[3H]carnitine in an established cell line (CCL 27) to 164 +/- 6% (mean +/-S.E.) of the rate observed in untreated cells. At the same time the intracellular content of free L-carnitine increased about 20%. The simultaneous addition of prednisolone (10(-6) mol/l for 24 h) and L-carnitine (10(-4) mol/l for 96 h) to the growth medium increased the rate of uptake to 225 +/- 8% (mean +/-S.E.) of that in untreated cells. The increase seemed to be mediated through an increase in number of carriers, as judged by the increase in V of the transport process with unchanged Km. Phosphodiesterase I, an enzyme mainly localized in the plasma membrane, increased its activity about 3.5 times when cells were stimulated with prednisolone. Thus, it seems that the increase in the rate of uptake of L-carnitine mediated by glucocorticoids, is part of a more general effect on the plasma membrane. The observations offer an explanation to the observed clinical improvement in patients with muscular carnitine deficiency treated with glucocorticoids and/or L-carnitine.

The effect of diphtheria toxin on the cellular uptake and efflux of L-carnitine. Evidence for a protective effect of prednisolone.

Diphtheria toxin added to the incubation medium reduced the rate of uptake and increased the efflux of L-[3H]carnitine in an established cell line from human heart (CCL 27, Girardi human heart cells). This resulted in a decrease in the level of intracellular carnitine to about 55% of control after exposure to 10(-8) mol/l diphtheria toxin for 24 h. As expected, a decrease in protein synthesis was found to be caused by the toxin, and this inhibition seemed to a large extent to antedate the alterations in the transport processes. Measurement of the kinetic parameters for the mechanism of uptake of L-[3H]carnitine revealed a reduction in V with unaltered Km after exposure to the toxin. We therefore suggest that diphtheria toxin imposes its effect on carnitine transport by inhibiting the synthesis of carriers. Prednisolone in the medium along with the toxin opposed its effect both on the uptake and efflux mechanism, but not on the inhibition of protein synthesis. Still, the decline in the intracellular level of carnitine was prevented by the corticoid hormone. Such a decline, accompanied by accumulation of triacyglycerols, occurs during the course of a diphtheric myocarditis. It is possible that prednisolone, by counteracting the effects of diphtheria toxin on the carnitine transport processes, could be beneficial in the treatment of this condition.

Carnitine-induced uptake of L-cartinine into cells from an established cell line from human heart (CCL 27).

L-Carnitine is actively transported into Girardi human heart cells, an established cell line from human heart. The present study was undertaken to investigate the effect of different concentrations of L-Carnitine in the growth medium on the rate of uptake of L-[3H] carnitine. Increasing the concentration of L-Carnitine from 2 to 100 mumol/l in the growth medium of cells, increased the rate of uptake of L-[3H] carnitine by about 50%. The maximal effect was reached after approx. 72 h incubation. The increase in rate seemed to be caused by synthesis of increased number of carriers, as judged by the increase of V with unchanged apparent Km for the transport process. This effect of L-carnitine could be inhibited by cycloheximide, indicating the dependence on intact protein synthesis. The morphology of the cells was studied by electron microscopy. No myofilaments were found, thus the cells are dedifferentiated and no longer typical muscular cells.

Increased pivaloylcarnitine in the liver of the sodium pivalate treated rat exposed to clofibrate.

Clofibrate, a potent peroxisomal proliferator, increased the concentration of pivaloylcarnitine (nmol/g) in rat liver (mean +/- S.D.) from 11 +/- 1 (controls) to 213 +/- 39 (clofibrate), in heart from 348 +/- 107 to 521 +/- 41 and in brown adipose tissue from 185 +/- 52 to 184 +/- 39 after administration of sodium pivalate. Clofibrate feeding increased the activity of carnitine acetyltransferase (U/mg) in liver (mean +/- S.D.) from 0.02 +/- 0.00 to 0.41 +/- 0.07 and decreased the triacylglycerol concentration (mg/g liver, mean +/- S.D.) from 33.53 +/- 4.53 to 11.03 +/- 0.71.

Carnitine uptake into human heart cells in culture.

The uptake of radiolabeled carnitine and butyrobetaine has been studied in human heart cells (CCL 27). The uptake of carinitine is 3-10-fold higher in heart cells than in fibroblasts (pmol - mug DNA-1). The uptake of carnitine increases with temperature coefficient KT of 1.6 in the interval 10-20 degrees C and with a negligible uptake at 4 and 10 degrees C. The uptake of carnitine follows Michaelis-Menten kinetics with a KM of 4.8 +/- 2.2 muM and V = 8.7 +/- 3.2 pmol - mug DNA-1 - H-1. Carnitine uptake is suppressed 90% by NaF (24MM). Butyrobetaine is taken up into heart cells to the same extent as carnitine with a KM of 5.7-17.3 muM and V = 8.7-9.3 pmol - mug DNA-1 - h-1. Butyrobetaine inhibits competitively the uptake of carnitine and carnitine inhibits the uptake of butyrobetaine to the same extent. No conversion of radiolabeled butyrobetaine to carnitine, or carnitine to methyl choline was observed intra- or extracellulary during incubation. These data are compatible with a selective transport mechanism for carnitine which is also responsible for the uptake of butyrobetaine.

Formation of pivaloylcarnitine in heart and brown adipose tissue in the rat.

Both pivaloylesterified antibiotics and pivalic acid cause pivaloylcarnitine excretion into urine in the rat and human. In the present study, the formation of pivaloylcarnitine, expressed as short-chain acylcarnitines has been observed in rats. The carnitine pool of the rats was radiolabeled by injection of L-[3H]butyrobetaine 24 h prior to exposure to pivalic acid injected i.p. or pivampicillin administered orally. The presence of pivaloylcarnitine in liver, heart, kidney, stomach, small intestine, testis, muscle, brown fat, white fat and serum was determined at zero time, 0.5, 2, 8 and 24 h after exposure to pivalic acid. After injection of pivalic acid, pivaloylcarnitine calculated as percent of free carnitine and short-chain acylcarnitines amounted to (mean +/- SD) 1.1 +/- 0, 15.4 +/- 2.5, 33.4 +/- 0.7 and 37.5 +/- 1.5% in the heart and 1.2 +/- 0.2, 20.6 +/- 9.5, 29.8 +/- 7.6 and 22.5 +/- 1.6% in brown fat after 0, 0.5, 2 and 8 h, respectively. 2 h after administration, pivaloylcarnitine calculated as percent of free carnitine and short-chain acylcarnitines was highest in the heart (20.9 +/- 7.6%) and brown fat (19.0 +/- 8.5%) in the pivalic acid-treated rat, and highest in the kidney (12.4 +/- 3.1%) and brown fat (10.2 +/- 2.8%) in the pivampicillin-treated rat. Pivaloylcarnitine percent in the liver was 2.8 +/- 0.6 in the pivalic acid-treated rat, 3.5 +/- 1.2 in the pivampicillin-treated rat and 1.3 +/- 0.4 in the control group. Pivaloylcarnitine concentration, nmol/g and nmol/organ, was highest in the heart and brown fat in both treatment groups. The present study suggests that the heart and the brown fat, but not the liver, play important roles in pivaloylcarnitine formation in the rat.

Formation of pivaloylcarnitine in isolated rat heart cells.

Pivaloyl-containing antibiotics and pivalic acid in man or rat have been reported to cause increased urinary carnitine loss secondary to pivaloylcarnitine generation. Pivaloylcarnitine concentration was especially high in heart after administration of pivalic acid or pivampicillin in vivo. Formation of pivaloylcarnitine was therefore studied in isolated rat heart cells in the presence of sodium pivalate. Formation of pivaloylcarnitine in rat heart cells increased with incubation time, after a lag time from 0 to 2 h and linearly up to 6 h. The formation increased with increasing concentration of sodium pivalate, followed Michaelis-Menten kinetics with an apparent Km = 348 +/- 10 microM and Vmax = 116 +/- 20 pmol.mg protein-1.h-1. Bromoacetylcarnitine inhibited the pivaloylcarnitine formation to Ki = 116 +/- 43 microM and Vmax = 107 +/- 14 pmol.mg protein-1.h-1. The uptake of carnitine in heart cells was suppressed 62-74% by deoxycarnitine (40 microM) and D-carnitine (200 microM), and 95% by NaF (5 mM), NaN3 (500 microM) or at temperature 4 degrees C. Pivaloylcarnitine inhibited carnitine uptake to 33-35% of the controls, while sodium pivalate did not. More than 90% of intracellular pivaloylcarnitine was released from the heart cells after 18 h of incubation in the absence of sodium pivalate and L-carnitine. These data show that pivalate is readily converted to pivaloylcarnitine in heart cells, in contrast to the limited conversion in hepatocytes.

[Vaccine therapy of prostate cancer]. / Vakzinetherapie des Prostatakarzinoms.

Vaccine therapy of prostate cancer has been increasingly studied in trials over the past few years. The different vaccine techniques are quite variable and are predominantly used in patients with advanced hormone-refractory prostate cancer. In this review, vaccine techniques using tumor cells, dendritic cells or poxvirus are analyzed. For theses approaches phase-III trials are being planned, have been initiated or are already completed. Many trials demonstrate the efficacy with regard to endpoints such as stimulation of the immune system and/or biochemical response and/or clinical response. Recently, one vaccine approach using autologous dendritic cells demonstrated a statistically significant prolongation of overall survival compared to placebo in patients with hormone-refractory prostate cancer. Side effects of vaccination are generally mild. At present, there are trials are being planned or are already ongoing that combine vaccine with other treatment strategies or enroll patients with earlier disease stages.

Vitamin concentrations 5 years after gastric bypass.

BACKGROUND/OBJECTIVES: Few studies have investigated the effects of bariatric surgery on vitamin status in the long term. We examined changes in vitamin status up to 5 years after Roux-en-Y gastric bypass surgery. SUBJECTS/METHODS: Using a retrospectively maintained database of patients undergoing weight loss surgery, we identified all patients operated with Roux-en-Y gastric bypass at our tertiary care hospital during July 2004-May 2008. Data on vitamin concentrations and patient-reported intake of dietary supplements were collected up to July 2012. Linear mixed models were used to estimate changes in vitamin concentrations during follow-up, adjusting for age and sex. All patients were recommended daily oral multivitamin, calcium/vitamin D and iron supplements and 3-monthly intramuscular B-12 after surgery. RESULTS: Out of the 443 patients operated with gastric bypass, we included 441 (99.5%) patients with one or more measurements of vitamin concentrations (75.1% women; mean age 41.5 years, mean body mass index 46.1 kg/m(2) at baseline). At 5 years after surgery, the patients' estimated mean vitamin concentrations were either significantly higher (vitamin B-6, folic acid, vitamin B-12, vitamin C and vitamin A) or not significantly different (thiamine, 25-hydroxyvitamin D and lipid-adjusted vitamin E) compared with before surgery. Use of multivitamin, calcium/vitamin D and vitamin B-12 supplements was reported by 1-9% of patients before surgery, 79-84% of patients at 1 year and 52-83% of patients 5 years after surgery. CONCLUSIONS: In patients who underwent gastric bypass surgery, estimated vitamin concentrations were either significantly increased or unchanged up to 5 years after surgery.

Effect of testosterone propionate on levels of carnitine and testicular androgen binding protein (ABP) in rat epididymis.

Twenty-one day old rats were treated for 10 days with various doses of testosterone propionate (TP) (10 micrograms to 10 mg/day) and the levels of L-carnitine and testicular androgen binding protein (ABP) were measured in the 105,000 x g supernatant fractions of epididymis. Treatment with TP in increasing doses had a biphasic effect on the level of ABP in the epididymis; thus, with doses of TP of 10-100 micrograms/day, the ABP level was reduced in a dose-dependent way, whereas with higher doses of TP (0.2 to 1 mg/day) the extent of reduction of ABP levels was less as the dose of TP increased. Treatment with high doses (5 mg or 10 mg/day) did not change the ABP level compared with non-treated control rats. The concentration of carnitine increased linearly (log dose-response) with increasing doses of TP (10-200 micrograms/day) and there was no further increase after treatment with higher doses of TP. In adult rats TP (175 micrograms and 17.5 mg/day) reduced the level of ABP but not the level of carnitine in the epididymis. These studies suggest, therefore, that ABP is of minor importance for the supply of androgens to the carnitine-concentrating cells in the corpus and cauda epididymis.

Reduced nutritional status in an elderly population (> 70 y) is probable before disease and possibly contributes to the development of disease.

In this prospective study of elderly people, nutritional status (body mass index, triceps skinfold thickness, arm-muscle circumference, and serum albumin) was assessed in a group of recently hospitalized (< 48 h) patients (n = 311), and compared with a home-living group (n = 106). Undernutrition was present in 52.9% of males and 60.6% of females by the time of admission to the hospital. Further, 65% of the males and 69% of the females had an insufficient energy intake the month before hospitalization [males < 8372 kJ (2000 kcal) and females < 7116 kJ (1700 kcal)]. Intake of vitamins and trace elements below two-thirds of the US recommended dietary allowances was more common in the hospital group. This group was more often unable to buy food and cook dinner, had more chewing problems, and had reduced appetite for food. Reduced nutrient and energy intakes may increase the occurrence of undernutrition, with increased risk for hospitalization in vulnerable groups as a consequence.

Concentrations of the water-soluble vitamins thiamin, ascorbic acid, and folic acid in serum and cerebrospinal fluid of healthy individuals.

Thiamin, thiamin monophosphate, ascorbic acid, and folic acid were determined in serum and cerebrospinal fluid (CSF) in 31 outpatients who underwent a myelography because of back-pain. All subjects were otherwise healthy. The CSF concentration (mean +/- SD) was 8.6 +/- 3.9 nmol thiamin/L, 16.9 +/- 8.3 nmol thiamin monophosphate/L, 133 +/- 58.8 mumol ascorbic acid/L, and 44.9 +/- 13.2 nmol folic acid/L. The CSF-serum ratio was 2.1 +/- 0.8 for thiamin, 8.3 +/- 4.3 for thiamin monophosphate, 3.0 +/- 1.4 for ascorbic acid, and 3.3 +/- 0.8 for folic acid; the amount in CSF was significantly higher than in serum for each compound. These results support the existence of a saturated transport mechanism of water-soluble vitamins from serum into CSF for thiamin monophosphate, ascorbic acid, and folic acid. However, low CSF concentrations are correlated with low serum concentrations for the three vitamins. High serum concentrations should therefore be advocated to ensure high CSF concentrations.

Reduced carnitine and ketogenesis in the pivampicillin treated rat.

Pivampicillin (630 mg/kg body wt) given daily by stomach tube induced carnitine deficiency in the rat. The carnitine concentrations after 24 days were significantly reduced to (mean +/- SD) 34 +/- 2, 27 +/- 7, 70 +/- 18, 75 +/- 16 and 49 +/- 4% of controls in plasma, liver, muscle, heart and kidney, respectively, without any further reduction after 36 days. Pivampicillin treatment reduced the carnitine concentrations in the liver of the 48 hr fasted rat to about 1/2 of the controls after 6 days. The concentration of beta-hydroxybutyrate was significantly reduced up to 14 days of treatment, and again increased. There was no significant difference in the free fatty acid concentrations between treated and control rats. Thus, pivampicillin treatment induced carnitine deficiency in the rat, but not as pronounced as seen in humans. This is possibly caused by adjustment of bacterial flora in the gut or altered renal mechanisms. The pivampicillin-treated rat, therefore, is not a useful model for pronounced carnitine deficiency in humans.

Accumulation of carnitine in rat epididymis after injection of [3H]butyrobetaine in vivo: quantitative aspects, and the effects of androgens and antiandrogens.

After i.m. injection of [3H]butyrobetaine into intact and castrated rats, the specific activity of plasma carnitine remained nearly constant over 24--96 h and epididymal uptake of carnitine was constant per unit time up to 72 h. The uptake ratio of intact to castrated rats was high at 48, 72 and 96 h after injection. Administration of estradiol valerate over 20 days reduced carnitine uptake in epididymis. This reduction was dose-dependent when estrogen was administered i.m. at 0.33--10 microgram/day levels. A maximum reduction of 90% was obtained with the 10 microgram dose. A dose increase from 33 to 100 microgram/day caused no further reduction. Norspiroxenone (2--10 mg/day) and SK 7670 (1.5 and 7.5 mg/day) were less effective than estradiol valerate (10 microgram/day) in suppressing carnitine uptake in epididymis. Epididymal carnitine uptake in estradiol valerate treated rats (33 microgram/day for 20 days) increased in a time- and dose-dependent manner under testosterone propionate treatment (50, 250, 1250 microgram/day). Carnitine uptake increased to 80% of the nonsuppressed levels when testosterone propionate was adminsitered over a 6-day period at 1250 microgram/day. Dihydrotestosterone increased epididymal carnitine uptake to the same extent as testosterone propionate. delta4-androstene-3,17-dione and 5alpha-androstane-3alpha,17beta-diol (50 microgram/day) were less effective, stimulating uptake to only 15% and 40% respectively of the testosterone propionate (250 microgram/day) stimulated levels. Changes in epididymal carnitine uptake evoked by various experimental procedures were closely paralleled by weight changes in the ventral prostate. This response resemblance indicates a similarity between the androgen sensitivity of the prostate gland and that of the carnitine uptake system in epididymis. The dose-dependent effect of estrogen on the accumulation of epididymal carnitine, together with the marked responses induced in this system by manipulation of its androgen status, support a possible use for the system as an assay for androgen or antiandrogen potency in vivo.

Androgen-dependent accumulation of carnitine by rat epididymis after injection of [3H]butyrobetaine in vivo.

After i.m. injection of [3H]butyrobetaine into rats, the accumulation of carnitine into the epididymis, prostate gland, seminal vesicles, testis and heart was studied. The concentration of radiolabeled carnitine into the cauda epididymis increased linearly with time up to 72 h after the injection of the precursor, while its level in the prostate and seminal vesicles decreased rapidly. Very low levels of carnitine were found in the testis. Castration reduced the carnitine accumulation by cauda epididymis to 6% of the control levels while treatment of castrated animals with testosterone propionate (500 mug/day) partly restored the carnitine uptake. Similar treatment with 17beta-oestradiol valerate or 17alpha-hydroxyprogesterone had no effect. Surprisingly, cyproterone acetate (5 mg/day) also significantly stimulated carnitine accumulation by the epididymis to a level above that of the castrated controls. Simultaneous injection of both cyproterone acetate and testosterone propionate to castrated animals caused an additive effect of these steroids. This indicated that cyproterone acetate in this system is working as a weak androgen. Treatment of rats with 17beta-oestradiol valerate also reduced carnitine accumulation by the cauda epididymis. This is due to suppression of pituiatry gonadotrophin secretion, since concommitant treatment with testosterone propionate (500 mug/day) caused a normalization of the carnitine uptake. Treatment of intact rats with cyproterone acetate significantly reduced the epididymal weight, but not the carnitine accumulation. 17alpha-Hydroxyprogesterone treatment had no effect either on the epididymal weight or the accumulation of the carnitine. Unilateral orchiectomy reduced the carnitine accumulation by the cauda epididymis to about 40% of that occurring in the non-operated control side. This indicates that the luminal contact between the testis and epididymis or the luminal content of the epididymis itself is of importance for the androgen-dependent metabolic process occurring in the cauda epididymis. Castration or hormone treatment did not change the conversion of butyrobetaine to carnitine, or the carnitine uptake by heart. Carnitine uptake by the testis after [3H]butyrobetaine injection was rather low and this would exclude the possibility of synthesis of carnitine in the testis as a source of epididymal carnitine. Carnitine only accumulated in the cauda epididymis in vivo 4 to 96 h after injection of [3H]butyrobetaine. The presence of radioactively labeled butyrobetaine or methylcholine was not detected.

The prevalence of undiagnosed protein-calorie undernutrition in a population of hospitalized elderly patients.

OBJECTIVE: To determine the extent to which patients with objective signs of malnutrition had been diagnosed as such by physicians and the diagnosis documented in the medical record. DESIGN: Cross-sectional. SUBJECTS: All non-critically ill patients (n = 121) aged 70 years or older admitted to an Oslo hospital during a 3-week period. METHODS: Compared problem list and other elements of the medical record with observations of height, weight, triceps skinfold, midarm circumference, and arm-muscle circumference made on first weekday in hospital. Serum albumin available on 66 subjects. MAIN RESULTS: Nine patients had weight/height ratios below 60% of normal, 16 patients between 60% and 75%, and 41 patients between 74% and 90% of normal. Of these 66 patients, only 24 were recognized as malnourished on admission, only five received nutritional support, and none was diagnosed as having malnutrition at the time of discharge. CONCLUSIONS: Malnutrition is underdiagnosed and undertreated. The consequences of this are likely to be deleterious to health.

Low serum calcidiol concentration in older adults with reduced muscular function.

OBJECTIVE: To examine the association between muscular function and the serum concentrations of 25-hydroxyvitamin D (calcidiol) and 1,25-dihydroxyvitamin D (calcitriol). DESIGN: A randomized population survey. Baseline measurements of serum calcidiol and calcitriol concentrations and assessment of muscular function (hand grip strength, ability to climb stairs, outdoor activity, and fall occurrence). SETTING: The Medical department, Aker University Hospital, Oslo, and subjects' homes. PARTICIPANTS: Two hundred forty-six recently hospitalized older patients and 103 randomly selected older people living at home. MEASUREMENTS: Serum concentration of calcidiol and calcitriol in relation to muscle function. MAIN RESULTS: Reduced muscle function was associated with low calcidiol levels. In both the hospital group and the home group, calcidiol concentrations correlated positively to arm muscle strength (r = .22, P < .001; r = .37, P < .001), ability to climb stairs (r = -.16, P < .05; r = -.42, P = < .001), physical activity (r = -.27, P < .001; r = -.31, P < .001), and the absence of fall occurrences (r = -.27, P < .001; r = -.31, P = .004). Calcitriol showed an association with physical activity in the hospital group (r = -.19, P < .05), and with fall last month in the home group (r = -.22, P < .05). CONCLUSIONS: Older people with reduced muscle function often had reduced levels of calcidiol serum concentration. Low levels of calcidiol were not associated with signs of general undernutrition, such as low body mass, or with reduced arm-muscle circumference or triceps skinfold thickness. This finding may suggest a physiological role for calcidiol in muscle function. Reduced muscle strength increased disability in our older subjects, which may be improved by vitamin D supplementation in vitamin D-deficient subjects.

Nutrition problems among home-living elderly people may lead to disease and hospitalization.

Undernutrition is a major problem among hospitalized elderly patients, increasing their morbidity and mortality. Various factors can contribute to the development of reduced nutrition status. In this study, reduced appetite and taste, dental problems, and difficulties in shopping and cooking were common in an elderly population during their last month before hospital admission compared to a reference group of home-living elderly. It is likely that these nutrition habits and disabilities may contribute to reduced nutrition status and increase the need for hospitalization in old people.