Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FASTING”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources
PubMed2006

Does Ramadan fasting affect sleep?

Experimental fasting has been shown to alter the sleep-wakefulness pattern in various species. As fasting during Ramadan is distinct from experimental fasting, the physiological and behavioural changes occurring during Ramadan fasting may differ from those occurring during experimental fasting. There has been increased interest in recent years in sleep changes and daytime sleepiness during Ramadan. Moreover, many of those who fast during Ramadan associate this fasting with increased daytime sleepiness and decreased performance. This raises the question of whether Ramadan fasting affects sleep. In this review, we discuss the findings of research conducted to assess changes in sleep pattern, chronobiology, circadian rhythms, daytime sleepiness and function and sleep architecture during the month of Ramadan. Where applicable, these findings are compared with those obtained during experimental fasting.

Activities of Daily Living↗
PubMed1997

Fast and slow skeletal muscles express a common basic profile of acetylcholinesterase molecular forms.

Recent evidence suggests that the high content of acetylcholinesterase (AChE) globular form G4, characteristic of fast muscles, is controlled by phasic high-frequency activity performed by these muscles. This indicates that inactive, though still innervated, fast muscles should be devoid of their characteristic G4 pool. Accordingly, in the absence of phasic activity, both fast and slow muscles should exhibit a common basic profile of AChE molecular forms of the slow type. We first tested this hypothesis by examining the AChE content in cultures of myotubes obtained from the fusion of satellite cells originating from fast and slow muscles. These two cell populations produced AChE molecular-form profiles of the slow type characterized by modest levels of G4 together with an increased proportion of the asymmetric forms A8 relative to A12. Second, we determined the impact of muscle paralysis on the specific content of AChE molecular forms of adult rat fast and slow muscles. Complete paralysis of hindlimb muscles was achieved by chronic superfusion of tetrodotoxin (TTX) onto the sciatic nerve. Ten days after TTX inactivation, the distributions of AChE molecular forms of both fast extensor digitorum longus (EDL) and plantaris muscles were transformed into ones resembling the slow soleus, the latter showing no significant modifications in its AChE profile. Finally, we investigated the impact of nerve-mediated phasic high-frequency stimulation of TTX-inactivated fast and slow muscles on the content of AChE molecular forms. This stimulation produced a profile of AChE molecular forms similar to that observed in control EDL muscles, indicating that phasic activation counteracted the TTX-induced transformation in the distribution of AChE molecular forms in fast EDL muscles. Together, these results are consistent with the proposal that adult fast muscles constitutively express a basic profile of AChE molecular forms of the type displayed by slow muscles, onto which varying levels of G4 are added according to the amount of phasic activity performed by the muscles.

Acetylcholinesterase↗
PubMed2001

Muscle LIM protein is upregulated in fast skeletal muscle during transition toward slower phenotypes.

Muscle LIM protein (MLP) is constitutively expressed in slow, but undetectable in fast, muscles of the rat. Here we show that MLP was upregulated at both the mRNA and protein levels under experimental conditions leading to transitions from fast to slower phenotypes. Chronic low-frequency stimulation and mechanical overloading by synergist removal both induced fast-to-slow shifts in myosin heavy chain (MHC) isoforms and expression of MLP in fast muscles. High amounts of MLP mRNA and protein were also present in fast muscles of the myotonic, hyperactive ADR mouse. Hypothyroidism evoked shifts in myosin composition toward slower isoforms and increased the MLP protein content of soleus (SOL) muscle but failed to induce MLP in fast muscles. Unweighting by hindlimb suspension elicited slow-to-fast transitions in MHC expression without altering MLP levels in SOL muscle. Hyperthyroidism shifted the MHC pattern toward faster isoforms but did not affect MLP content in SOL muscle. We conclude that alterations in MLP expression are associated with transitions from fast to slower phenotypes but not with slow-to-fast muscle fiber transitions.

Animals↗
PubMed1989

Insulin, glucagon, and catecholamines in prevention of hypoglycemia during fasting.

To dissect the mechanisms of the prevention of hypoglycemia during fasting, eight normal humans were studied after overnight and 3-day fasts. Prolonged fasting resulted in the expected decrements in base-line glucose production and plasma glucose, insulin, and C-peptide and increments in plasma glucagon, epinephrine, norepinephrine, growth hormone, and cortisol. After the overnight and 3-day fasts, insulin restoration (0.2 mU.kg-1.min-1) alone resulted in transient decrements in glucose production and only 15 and 19% decrements in plasma glucose, respectively. Selective glucagon deficiency (somatostatin infusion with insulin and growth hormone replacement) resulted in transient decrements in glucose production and additional 24 and 29% decrements in plasma glucose, respectively. Notably, plasma glucose plateaued under both fasting conditions in both instances. Combined alpha- and beta-adrenergic blockade (phentolamine and propranolol infusions) alone had no effect on glycemia under either fasting condition. However, progressive hypoglycemia developed during adrenergic blockade coupled with glucagon deficiency after the overnight fast (85 +/- 2 to 48 +/- 4 mg/dl, P less than 0.001) and after the 3-day fast (65 +/- 2 to 33 +/- 1 mg/dl, P less than 0.001). These were the result of both decrements in glucose production and increments in glucose clearance. Thus we conclude that during fasting 1) the prevention of hypoglycemia is not due solely to decreased insulin secretion. 2) Glucagon plays a primary counterregulatory role. Sympathochromaffin catecholamines are not normally critical but compensate and become critical when glucagon is deficient. Adrenomedullary epinephrine is probably the relevant catecholamine. 3) Other hormones, neurotransmitters, or substrate effects may, or may not, be involved; if they are, they appear to stand low in the hierarchy of glucoregulatory factors.

Adult↗
PubMed1991

Responses of protein synthesis in different skeletal muscles to fasting and insulin in rats.

The rate of protein synthesis (Ks) was measured in nine skeletal muscles from young rats (100 g body wt) after fasting and subsequent insulin infusion. An overnight fast (12 h) resulted in a fall in Ks in all muscles, but this ranged from a small nonsignificant decrease in soleus (Sol) to one-half of the fed rate in tensor fascia latae (TFL). After fasting for 36 h, Ks was significantly reduced in all muscles, although there was still a range apparent between different muscles. The response of the individual muscles to fasting was related to fiber type composition, and, in particular, the responses of the commonly studied Sol were characteristic of the highly oxidative fiber composition rather than being peculiar to Sol itself. The magnitude of the increase in Ks during an infusion of insulin (0.5 h) in the 12-h fasted rats was proportional to the magnitude of the initial response to fasting and these changes were largely reflected in changes in the rate of synthesis expressed per unit RNA (KRNA). After 36 h of fasting, Ks in the muscles responded little to the insulin stimulus, and a similar small effect on KRNA, compared with that in the 12-h fasted animals, suggests an apparent insensitivity to insulin after this longer fasting period.

Animals↗
PubMed1991

Fasting inhibits insulin-mediated glycolysis and anaplerosis in human skeletal muscle.

Euglycemic (approximately 5.5 mM) hyperinsulinemic (60 mU.m-2.min-1) clamps were performed for 2 h after a 10-h fast and after a prolonged (72-h) fast. Biopsies were obtained from the quadriceps femoris muscle before and after each clamp. The rate of whole body glucose disposal was approximately 50% lower during the clamp after the 72-h fast (P less than or equal to 0.001). The increase in carbohydrate (CHO) oxidation (which is proportional to glycolysis) during the clamp after the 10-h fast (to 13.8 +/- 1.5 mumol.kg fat free mass-1.min-1) was completely abolished during the clamp after the 72-h fast (1.7 +/- 0.6; P less than or equal to 0.001). During the clamp after the 10-h fast, postphosphofructokinase (PFK) intermediates and malate in muscle increased, whereas glutamate decreased (P less than or equal to 0.05-0.001 vs. basal) and citrate did not change. During the clamp after the 72-h fast, there were no significant changes in post-PFK intermediates or glutamate (P greater than 0.05 vs. basal), but there was a decrease in citrate (P less than or equal to 0.01 vs. basal). Euglycemic hyperinsulinemia increased glycogen synthase fractional activity in muscle under both conditions but to a greater extent after the 72-h fast (P less than or equal to 0.01). It is concluded that insulin (after 10-h fast) increases glycolytic flux and the content of malate in muscle, which is probably due to increased anaplerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Progressive alterations in lipid and glucose metabolism during short-term fasting in young adult men.

Stable isotope tracers and indirect calorimetry were used to evaluate the progressive alterations in lipid and glucose metabolism after 12, 18, 24, 30, 42, 54, and 72 h of fasting in six healthy male volunteers. The rates of appearance (Ra) of glycerol and palmitic acid in plasma doubled from 2.08 +/- 0.22 and 1.63 +/- 0.20 mumol.kg-1 x min-1, respectively, after 12 h to 4.36 +/- 0.36 and 3.26 +/- 0.40 mumol.kg-1 x min-1, respectively, after 72 h of fasting (P < 0.01). Of the total increase in lipid kinetics, 60% occurred between 12 and 24 h of fasting; the greatest interval change occurred between 18 and 24 h of fasting. Glucose Ra and plasma concentration decreased by approximately 25% between 12 h (11.0 +/- 0.4 mumol.kg-1 x min-1 and 5.58 +/- 0.08 mmol/l, respectively) and 72 h (8.3 +/- 0.3 mumol.kg-1 x min-1 and 4.14 +/- 0.10 mmol/l, respectively) of fasting (P < 0.01), but no statistically significant changes occurred between 18 and 24 h of fasting. Plasma insulin decreased by approximately 50% between 12 h (64.6 +/- 12.9 pmol/l) and 72 h (30.1 +/- 7.9 pmol/l) of fasting (P < 0.001). Of the total decline in plasma insulin, 70% occurred within the first 24 h of fasting. These results demonstrate that the mobilization of adipose tissue triglycerides increases markedly between 18 and 24 h of fasting in young adult men. The early alterations in lipid metabolism are associated with a decline in circulating insulin but do not seem to be regulated by changes in glucose kinetics or plasma glucose concentrations.

Adult↗
PubMed2006

Apoptotic pathway in the rat small intestinal mucosa is different between fasting and ischemia-reperfusion.

We have previously demonstrated that fasting and ischemia-reperfusion (I/R) induced apoptosis in rat intestinal mucosa. It is widely accepted that apoptosis is induced through two main pathways. This study aimed to compare apoptotic pathways following fasting and I/R. Rats were divided into two groups: the I/R group involved occlusion of the superior mesenteric artery for 60 min, followed by 60-min reperfusion, whereas the fasting group involved fasting for 24 or 48 h. Intestinal apoptosis was assessed as percentage of fragmented DNA, by electrophoresis and by a terminal deoxynucleotidyl transferase mediated dUDP-biotin nick- end labeling (TUNEL) assay. Apoptotic proteins including death ligands/receptors and caspases were evaluated by Western blot analysis. Small intestinal mucosal height and mitochondrial dehydrogenase function were assessed. Fasting and I/R significantly induced intestinal apoptosis. Mucosal height was significantly decreased in fasting rats, and mitochondrial dysfunction was induced only by I/R. Expressions of Fas, Fas ligand, and TNF-alpha type 1 receptor were enhanced in fasting and I/R rats. After I/R, expressions of cytochrome c and cleaved caspase-9 were significantly increased. In contrast, expressions of cleaved caspase-8 and cleaved caspase-3 increased in fasting rats. Fasting promoted mucosal apoptosis via a receptor-mediated type I apoptotic pathway in the rat small intestine, and I/R induced apoptosis via a mitochondria-mediated type II pathway.

Animals↗
PubMed1994

Effect of fasting on the enterohepatic circulation of bile acids in rats.

Fasting Sprague-Dawley rats for 72 h resulted in inhibition of bile salt synthesis, reduced bile flow and bile salt secretion rate, and reduced duodenal and portal venous bile acid concentrations. The initial rate of ileal brush border membrane (BBM) taurocholate (TC) uptake was markedly reduced in the fasted group (45% of control). TC uptake by BBM was saturable, with similar maximal transport velocity for the fasted rats and controls (1.69 +/- 0.06 and 1.62 +/- 0.017 nmol.mg protein-1.min-1, respectively) but higher Michaelis-Menten constant for fasted rats than for controls (96.9 +/- 20.0 and 54.9 +/- 10.2 microM, respectively). Hepatic basolateral membrane (BLM) TC uptake was enhanced by 65% in fasted animals. Transport kinetics in BLM had a similar Michaelis-Menten constant for fasted rats and controls (31.6 +/- 8.2 and 27.3 +/- 4.7 microM, respectively), and maximal transport velocity was higher for fasted rats than for controls (1.84 +/- 0.017 and 1.11 +/- 0.014 nmol.mg protein-1.min-1). The cholesterol-to-phospholipid ratio and fluorescence anisotropy in BLM of fasted rats decreased, and the cholesterol-to-phospholipid ratio and fluorescence anisotropy increased in ileal BBM. Alterations in the enterohepatic circulation of bile acids with fasting may alter expression of transport proteins for bile salts by direct effects on synthesis or indirectly through membrane lipid compositional changes.

Animals↗
PubMed1994

Fasting enhances taurine transport by rat liver plasma membrane vesicles.

Hepatic taurine stores are maintained by biosynthesis from the sulfur-containing amino acids, methionine and cysteine, and by uptake via a Na(+)- and Cl(-)-dependent transport system, which is specific for beta-amino acids. We hypothesized that liver stores of taurine are maintained by enhanced hepatic transport during fasting when dietary sources for taurine and its precursors are diminished. Liver plasma membrane vesicles, enriched for the basolateral domain, were prepared from adult male rats fasted for 72 h and from control rats. The maximum velocity for Na(+)-dependent taurine uptake was twofold greater for the fasted group compared with the control group (0.87 +/- 0.09 vs. 0.31 +/- 0.03 nmol.mg protein-1.min-1). The apparent Michaelis constant for taurine was also greater for fasted compared with control (154.0 +/- 0.5 vs. 80.0 +/- 2.0 microM). gamma-Aminobutyric acid, but not alanine or glutamine, abolished the effect of fasting on hepatic taurine transport. To determine the effect of fasting independent of changes in the lipid microenvironment, taurine uptake was measured in proteoliposomes reconstituted by inserting detergent-solubilized membrane proteins into asolectin vesicles. Taurine uptake by proteoliposomes reconstituted from membranes prepared from the fasted group was significantly greater than from the control group. We conclude that Na(+)-dependent taurine transport is enhanced in liver plasma membranes prepared from fasted rats. Our findings imply that enhanced taurine uptake with fasting is due to either an increased number of functional carriers or activation of existing transporters.

Alanine↗
PubMed1988

Fasting in king penguin. II. Hormonal and metabolic changes during molt.

The coincidence of fast and molt in penguins is an interesting condition for investigating the factors controlling protein metabolism; avian molt involves the utilization of amino acids for synthesis of new feathers, whereas a major factor for adaptation to fasting in birds, as for mammals, is reduction in net protein breakdown. Hormonal and biochemical changes were studied in seven molting king penguins. Their initial body mass was 18 kg. It decreased by 58% over 41 days of fasting. Feather synthesis lasted for the first 3 wk of the fast. It was marked by plasma concentrations of alanine and uric acid 1.5 to 2 times those for nonmolting fast, and plasma thyroxine was increased five times. At the completion of molt all these values returned to levels comparable to those in nonmolting fast. As indicated by high plasma levels of beta-hydroxybutyrate, lipid stores were mobilized readily during molting. The fast ended by a phase of enhancement in protein utilization that was characterized by a fivefold increase in uricacidemia and coincided with an 80% drop in plasma beta-hydroxybutyrate and a fourfold increase in plasma corticosterone. These data suggest that two different hormones control the two successive periods marked by an increased protein mobilization during the molting fast, i.e., thyroxine during feather growth and corticosterone toward the end of the fast, when the molt is completed.

Aldosterone↗
PubMed1990

Relationships between plasma ketones and fasting duration in neonatal elephant seals.

Long-duration fasting in mammals can ultimately lead to stage three terminal starvation, which is characterized by depleted fat stores, a metabolic shift away from fat metabolism toward lean tissue catabolism, and a sharp decline in circulating levels of plasma fatty acids and ketone bodies. However, this biochemical shift has never been observed outside of the laboratory in a naturally fasting, nonhibernating mammal. In the current study, plasma levels of the ketone body D-beta-hydroxybutyrate (beta-HBA) were assayed in 10 Northern elephant seal pups during suckling and the postweaning fast and in 12 fasting adult seals. Plasma beta-HBA concentration in the pups was minimal during suckling (0.09 +/- 0.06 mM; n = 10) and began to increase immediately after weaning. The concentration rose until about 55 days into the fast (1.34 +/- 0.36 mM; n = 10) and then declined sharply. Within 10 days of this deflection point, the seal pups left for sea. By contrast, adult elephant seals showed consistently low levels of beta-HBA after several months of fasting (0.06 +/- 0.07 mM; n = 12). The data suggest that the duration of fasting in elephant seal pups may be determined, in part, by biochemical shifts that occur near the end of the fast and that the regulation of ketone concentration is different in fasting neonatal and adult elephant seals.

3-Hydroxybutyric Acid↗
PubMed1994

Fasting alters basal and stimulated ion transport in piglet jejunum.

Three-week-old piglets were used to study the effects of short-term fasting on jejunal ion transport. A 48-h fast significantly reduced mucosal weight, villus height, and crypt depth. Fasting increased basal short-circuit current (Isc), which reflects active ion transport, and total tissue conductance (Gt) of muscle-stripped jejunal sheets mounted in Ussing chambers. Increases in Isc evoked by carbachol, serotonin, histamine, prostaglandin E2, or Escherichia coli heat-stable enterotoxin were significantly greater in the fasted piglets. Isc responses to mucosal D-glucose were also enhanced by the fast. Under basal conditions, unidirectional and net fluxes of Na+ and Cl-, as well as serosal-to-mucosal inulin fluxes, were significantly increased in fasted piglets. In fed piglets, carbachol increased net Cl- secretion by stimulating serosal-to-mucosal Cl- flux; Gt was not affected. In fasted piglets, carbachol increased net Cl- secretion by inhibiting mucosal-to-serosal fluxes with no effect on serosal-to-mucosal fluxes. In addition, carbachol significantly inhibited mucosal-to-serosal Na+ fluxes and reduced Gt in this group. Thus a 48-h fast increased unidirectional and net ion fluxes in piglet jejunum and enhanced ion transport responses to secretory agonists. The mechanism by which carbachol stimulated net Cl- secretion was also altered by the fast. These results suggest that the absence of luminal nutrition changes the ion transport characteristics of the jejunal epithelium.

Animals↗
PubMed2004

Pyruvate dehydrogenase activation and kinase expression in human skeletal muscle during fasting.

Fasting forces adaptive changes in whole body and skeletal muscle metabolism that increase fat oxidation and decrease the oxidation of carbohydrate. We tested the hypothesis that 40 h of fasting would decrease pyruvate dehydrogenase (PDH) activity and increase PDH kinase (PDK) isoform mRNA expression in human skeletal muscle. The putative transcriptional activators of PDK isozymes, peroxisome proliferator-activated receptor-alpha (PPAR-alpha) protein, and forkhead homolog in rhabdomyosarcoma (FKHR) mRNA were also measured. Eleven healthy adults fasted after a standard meal (25% fat, 60% carbohydrate, 15% protein) with blood and skeletal muscle samples taken at 3, 15, and 40 h postprandial. Fasting increased plasma free fatty acid, glycerol, and beta-hydroxybutyrate concentrations and decreased glucose and insulin concentrations. PDH activity decreased from 0.88 +/- 0.11 mmol acetyl-CoA. min(-1). kg wet muscle wt(-1) at 3 h to 0.62 +/- 0.10 (P = not significant) and 0.39 +/- 0.06 (P < 0.05) mmol. min(-1). kg wet mass(-1) after 15 and 40 h of fasting. Although all four PDK isoforms were expressed in human skeletal muscle, PDK-2 and -4 mRNA were the most abundant. PDK-1 and -3 mRNA abundance was approximately 1 and 15% of the PDK-2 and -4 levels, respectively. The 40-h fast had no effect on PDK-1, -2, and -3 mRNA expression. PDK-4 mRNA was significantly increased approximately 3-fold after 15 h and approximately 14-fold after 40 h of fasting. Skeletal muscle PPAR-alpha protein and FKHR mRNA abundance were unaffected by the fast. The results suggest that decreased PDH activation after 40 h of fasting may have been a function of the large increase in PDK-4 mRNA expression and possible subsequent increase in PDK protein and activity. The changes in PDK-4 expression and PDH activity did not coincide with increases in the transcriptional activators PPAR-alpha and FKHR.

Adult↗
PubMed1998

Arcuate nucleus ablation prevents fasting-induced suppression of ProTRH mRNA in the hypothalamic paraventricular nucleus.

Fasting results in reduced thyroid hormone levels and inappropriately low or normal thyroid-stimulating hormone (TSH), partly attributed to central hypothyroidism due to suppression of pro TRH gene expression in the hypothalamic paraventricular nucleus. Recently, we demonstrated that the systemic administration of leptin to fasting animals restores plasma thyroxine (T4) and proTRH mRNA in the paraventricular nucleus to normal, suggesting that the fall in circulating leptin levels during fasting acts as a signal to hypophysiotropic neurons in the paraventricular nucleus to reset the set point for feedback regulation of pro TRH mRNA by thyroid hormone. To determine whether the effect of fasting on the hypothalamic-pituitary-thyroid axis is mediated through the hypothalamic arcuate nucleus where leptin receptors are highly concentrated, we studied the effect of fasting and exogenous leptin administration on plasma thyroid hormone levels and proTRH mRNA concentration in the paraventricular nucleus in adult animals with arcuate nucleus lesions induced pharmacologically by the neonatal administration of monosodium L-glutamate (MSG). In normal animals, fasting reduced plasma T4 and TSH levels and the concentration of proTRH mRNA in the hypothalamic paraventricular nucleus. In contrast, neither fasting nor leptin administration to fasting MSG-treated animals had any significant effects on plasma thyroid hormone and TSH levels and proTRH mRNA in the paraventricular nucleus. These studies suggest that during fasting, the arcuate nucleus is essential for the normal homeostatic response of the hypothalamic-pituitary-thyroid axis and may serve as a critical locus to mediate the central actions of leptin on proTRH gene expression in the paraventricular nucleus.

Animals↗
PubMed2002

Effect of fasting for two days on the excretion of ammonium in dogs with chronic metabolic acidosis.

BACKGROUND: The source of glutamine for renal ammonium production is ultimately dietary protein in the fed state and body proteins in fasting. OBJECTIVE: Our objective was to determine if less NH(+)(4) would be excreted by fasted dogs with chronic metabolic acidosis resulting in conservation of lean body mass. METHODS: Acid-loaded fed and fasted dogs were given 10 mmol NH(4)Cl/kg for 5 days; the fasted group had food withheld on days 4 and 5. RESULTS: The renal production of NH(+)(4) was not significantly different in both acid-loaded groups, yet the rate of NH(+)(4) excretion was significantly lower in the fasted dogs (8 vs. 21 mmol NH(+)(4)/mmol creatinine). The urine pH was significantly higher (6.0 versus 5.5) while titratable acid and the urine flow rate were significantly lower in these fasted dogs. Despite nearly equal urine flow rates and Na(+) excretion rates after an infusion of saline, the fasted dogs failed to increase the rate of excretion of NH(+)(4) to rates seen in the fed group. CONCLUSIONS: The lower rate of excretion of NH(+)(4) in fasted, acidotic dogs appeared to be due to a lower distal H(+) secretion. This may help preserve lean body mass during fasting.

Acidosis↗
PubMed2002

[Short-term therapeutic fasting in the treatment of chronic pain and fatigue syndromes--well-being and side effects with and without mineral supplements].

BACKGROUND: Fasting followed by vegetarian diet has shown to be an effective treatment for rheumatoid arthritis, moreover fasting is frequently used as an adjunctive treatment in chronic pain and stress/exhaustion syndromes. Data on well-being and the frequency of side effects during fasting are mostly retrospective. Mineral supplements are frequently used in order to compensate for fasting-induced tissue acidosis and to reduce side effects. There are only limited data that support this practice. OBJECTIVE: To study the effects of oral mineral supplements on common side effects and well-being during short-term fasting. PATIENTS AND METHODS: 209 consecutive inpatients with chronic pain/exhaustion syndromes were recruited. In a controlled non-randomised study design all patients underwent fasting (250 kcal; 3 l fluid intake/day) over 7 days, in study phase 1 without (n = 103) and in study phase 2 with (n = 106) concomitant prescription of standardised oral mineral supplements (3 x 2 to 3 x 3 Bullrich's Vital). Weight, blood pressure and urinary pH were recorded daily. Well-being and mood as well as common side effects (i.e. fatigue, hunger, heart burn, headache) were assessed with standardised self-reports. RESULTS: Baseline characteristics of the 209 patients (mean age 54.7 +/- 10.5 years; 83.3% female) were balanced. Both groups showed a fasting-induced decrease of blood pressure, a slight decrease in mood and well-being on days 3 and 4 with consecutive increase and moderate hunger, i.e. in the evening. Side effects and general tolerability of fasting as well as well-being and mood were not different between the groups. There were no serious side effects in both groups. CONCLUSIONS: Short-term fasting in inpatients with pain and stress syndromes is safe and well tolerated, concomitant mineral supplements have no additive benefit.

Chronic Disease↗
PubMed2003

Effects of short-term modified fasting on sleep patterns and daytime vigilance in non-obese subjects: results of a pilot study.

BACKGROUND: Periodically repeated short-term fasting is a frequently practised tradition worldwide. Empirical reports suggest that during fasting periods the quality of sleep and daytime performance are improved. The effects of a home-based 1-week modified fasting on sleep patterns and daytime vigilance and performance were analysed in 15 healthy non-obese volunteers. METHODS: Sleep was measured by polysomnography before and after a 7-day fasting period; sleep inventories with assessment of daytime performance were collected throughout the observation period. Blood samples and urine were drawn at the beginning and at the end of fasting. RESULTS: 13 subjects (12 females, 1 male; age 41.2 +/- 13.4 years; BMI 23.9 +/- 4.2 kg/m(2)) completed the fasting period; weight decreased from 66.5 +/- 11.7 kg to 63 +/- 11.9 kg. Compared to baseline, a significant decrease in arousals, a decrease in periodic leg movements (PLM) and a non-significant increase in REM sleep were observed at the end of fasting. Subjective sleep ratings showed a fasting-induced increase in global quality of sleep, daytime concentration, vigour and emotional balance. Clinical laboratory tests showed a decrease in serum magnesium; urinary melatonin excretion decreased moderately. CONCLUSION: This open pilot study demonstrates that along with a decrease in sleep arousals a 1-week fasting period promotes the quality of sleep and daytime performance in non-obese subjects. The observed decrease in PLM might point to a nutritional modification of brain dopaminergic functions. In terms of evolutionary development, an improved daytime performance during periods of food deprivation could have been beneficial for the success in search for food.

Adult↗