Effect of Medically Supervised Prolonged Fasting Therapy on Vitamin D, B12, Body Weight, Body Mass Index, Vitality and Quality of Life: A Randomized Control Trial
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ABSTRACT: Background:
Recent research indicates prolonged fasting for more than 7 days is
SUBMITTER: Tewani G
PROVIDER: S-EPMC9619880 | biostudies-literature | 2022 Jan
REPOSITORIES: biostudies-literature
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Project description:Lower serum vitamin B12 levels have been related to adverse metabolic health profiles, including adiposity. We used a Mendelian randomization design to test whether this relation might be causal. We included two Danish population-based studies (ntotal = 9311). Linear regression was used to test for associations between (1) serum vitamin B12 levels and body mass index (BMI), (2) genetic variants and serum vitamin B12 levels, and (3) genetic variants and BMI. The effect of a genetically determined decrease in serum vitamin B12 on BMI was estimated by instrumental variable regression. Decreased serum vitamin B12 associated with increased BMI (P < 1 × 10-4). A genetic risk score based on eight vitamin B12 associated variants associated strongly with serum vitamin B12 (P < 2 × 10-43), but not with BMI (P = 0.91). Instrumental variable regression showed that a 20% decrease in serum vitamin B12 was associated with a 0.09 kg/m2 (95% CI 0.05; 0.13) increase in BMI (P = 3 × 10-5), whereas a genetically induced 20% decrease in serum vitamin B12 had no effect on BMI [-0.03 (95% CI -0.22; 0.16) kg/m2] (P = 0.74). Nevertheless, the strongest serum vitamin B12 variant, FUT2 rs602662, which was excluded from the B12 genetic risk score due to potential pleiotropic effects, showed a per allele effect of 0.15 kg/m2 (95% CI 0.01; 0.32) on BMI (P = 0.03). This association was accentuated including two German cohorts (ntotal = 5050), with a combined effect of 0.19 kg/m2 (95% CI 0.08; 0.30) (P = 4 × 10-4). We found no support for a causal role of decreased serum vitamin B12 levels in obesity. However, our study suggests that FUT2, through its regulation of the cross-talk between gut microbes and the human host, might explain a part of the observational association between serum vitamin B12 and BMI.
| S-EPMC5374184 | biostudies-literature
Project description:BackgroundEvidence suggests that fasting, during which only water is consumed, results in potentially health promoting physiological effects. However, peer-reviewed research assessing the safety of water-only fasting is lacking. To address this, we conducted a chart review to describe adverse events (AEs) that occurred during medically supervised, water-only fasting.MethodsElectronic charts from patient visits to a residential medical facility from 2006 to 2011 were reviewed. Patients who were at least 21 years of age and water-only fasted for ≥2 consecutive days with a refeeding period equal to half of the fast length were included. Out of 2539 charts, 768 visits met our inclusion and exclusion criteria. AEs were abstracted from chart notes and classified according to CTCAE (v4.03) and MedDRA (v12.1) terminology. Descriptive analysis of AEs is reported.ResultsDuring the protocol period, the highest grade AE (HGAE) in 555 visits was a grade 2 event or lower, in 212 visits it was a grade 3 event, in 1 visit it was a grade 4 event, and there were no grade 5 events. There were 2 (0.002%) visits with a serious adverse event (SAE). The majority of AEs identified were mild (n = 4490, 75%) in nature and known reactions to fasting.ConclusionsTo our knowledge, this is the most comprehensive analysis of AEs experienced during medically supervised, water-only fasting conducted to date. Overall, our data indicate that the majority of AEs experienced were mild to moderate and known reactions to fasting. This suggests that the protocol used in this study can be safely implemented in a medical setting with minimal risk of a SAE.
| S-EPMC5819235 | biostudies-literature
Project description:BackgroundBreast cancer survivors rank fatigue (e.g., decreased vitality) as their number one concern affecting quality of life. Excess adiposity is associated with decreased vitality in breast cancer survivors, yet weight loss intervention trials report inconsistent effects on this parameter.MethodsThis is a secondary analysis of the Exercise and Nutrition to Enhance Recovery and Good Health for You trial, in which 692 overweight or obese breast cancer survivors ≤5 years from diagnosis, initiated weight loss interventions, and completed assessments semi-annually for 2 years. Assessments included the Godin Leisure-Time Exercise Questionnaire and the SF-36 MOS vitality subscale as an inverse measure of fatigue. Multilevel structural equation models estimated the direct effects of physical activity on vitality and indirect effects through body mass index (BMI) changes.ResultsWithin-person findings show that at assessments with greater physical activity, BMI was significantly lower (B = -0.07, p < 0.001) and vitality was higher (B = 0.22, p < 0.001). However, there was no direct relationship between lower BMI and higher vitality (B = -0.11, p = 0.262) after controlling for the relationship of physical activity with BMI and physical activity with vitality. The between-person indirect effect of physical activity change through BMI change to vitality was significant (B = 0.03, p < 0.001). Participants whose physical activity was above the mean (B = 0.37, p < 0.001) and whose BMI was below the mean (B = -1.05, p < 0.001) were more likely to report greater vitality.ConclusionImprovements in vitality are primarily associated with increases in physical activity rather than BMI changes in this trial. Vitality was lower among survivors with higher BMI, although within-individual changes in BMI had no effect on vitality. Physical activity and weight loss share mechanistic links to vitality with physical activity potentially increasing (e.g., in an additive or synergistic manner) the effect of BMI reduction on vitality.
| S-EPMC7189976 | biostudies-literature
Project description: Not available
| S-EPMC10220921 | biostudies-literature
Project description:BackgroundIt is controversial whether B12 deficiency causes dementia or B12 treatment can prevent dementia.ObjectiveTo assess associations between low plasma (P-)B12 levels, B12 treatment, and risk of Alzheimer's disease (AD; primary outcome) and all-cause or vascular dementia (secondary outcomes).MethodsWe conducted a population-based cohort study using Danish registry data to assess associations between low P-B12 levels, high-dose injection or oral B12 treatment, and risk of dementia (study period 2000-2013). The primary P-B12 cohort included patients with a first-time P-B12 measurement whose subsequent B12 treatment was recorded. The secondary B12 treatment cohort included patients with a first-time B12 prescription and P-B12 measurement within one year before this prescription. For both cohorts, patients with low P-B12 levels (<200 pmol/L) were propensity score-matched 1:1 with patients with normal levels (200-600 pmol/L). We used multivariable Cox regression to compute 0-15-year hazard ratios for dementia.ResultsFor low P-B12 and normal P-B12 level groups, we included 53,089 patients in the primary P-B12 cohort and 13,656 patients in the secondary B12 treatment cohort. In the P-B12 cohort, hazard ratios for AD centered around one, regardless of follow-up period or treatment during follow-up. In the B12 treatment cohort, risk of AD was unaffected by low pre-treatment P-B12 levels, follow-up period and type of B12 treatment. Findings were similar for all-cause and vascular dementia.ConclusionWe found no associatio1n between low P-B12 levels and dementia. Associations were unaffected by B12 treatment. Results do not support routine screening for B12 deficiency in patients with suspected dementia.
| S-EPMC7990402 | biostudies-literature
Project description:PurposeThe purpose of the study was to examine the association of the gestational weight gain and prepregnancy body mass index (BMI) of low-income adolescent mothers with the risk of their children being overweight and/or obese in late adolescence.MethodsStudy subjects were low-income, primiparous adolescents (n = 360) who self-identified as black and participated in the New Mothers Study in Memphis, Tennessee, and their children. Gestational weight gain was examined as a continuous variable and also categorized into overgain, recommended gain, and undergain following the 2009 Institute of Medicine guidelines. The effects of maternal prepregnancy BMI percentiles and calculated BMI were also considered. Multivariable logistic and linear regression models were used. The main outcome measures were offspring overweight, obesity, and BMI.ResultsThirty-nine percent of offspring were overweight or obese. Higher maternal gestational weight gain increased the risk for offspring overweight and obesity. There was an interaction between gestational weight gain and prepregnancy BMI: offspring of mothers with a BMI percentile ≤76 were at greater risk of obesity with higher maternal weight gain. If mothers with a BMI percentile between the 29th and 83rd percentiles overgained, offspring were at greater risk for overweight. Using calculated BMIs, if a mother's BMI was ≤26 kg/m2, offspring risk for obesity was greater with higher gestational weight gain.ConclusionsHigh gestational weight gain had a larger effect on offspring overweight and obesity if maternal prepregnancy BMI percentile was ≤76. The gestational weight gain of primiparous adolescents who self-identified as black had an effect on offspring weight.
| S-EPMC5654683 | biostudies-literature
Project description:As not much is known about the prevalence and predictors of nutritional deficiencies among vegans in the Czech Republic, we evaluated whether supplement use and duration of adherence to the vegan diet are associated with the risk of cobalamin and iron deficiencies. Associations between self-reported supplementation and duration of vegan diet with biomarkers of cobalamin (serum cobalamin, holotranscobalamin, homocysteine, folate) and iron status (serum ferritin, iron binding capacity, transferrin and saturation of transferrin) were assessed by cross-sectional analyses of medical data from a clinical nutrition center. Data from 151 (72 females) adult vegans (age 18-67 years), who were free of major chronic diseases and 85 (40 females) healthy non-vegans (age 21-47 years) were analyzed. Overall, vegans had significantly lower cobalamin, hemoglobin and ferritin levels, but higher folate and MCV values compared to non-vegans. Vegans not using cobalamin supplements were at higher risk of low plasma cobalamin than regularly supplementing vegans (OR: 4.41, 95% CI 1.2-16.16 for cobalamin, OR: 19.18, 95% CI 1.02-359.42 for holotranscobalamin), whereas no significant differences in cobalamin status related to duration of the vegan diet were observed. Regularly supplementing vegans had similar levels of cobalamin/holotranscobalamin as non-vegans. Despite lower ferritin and hemoglobin levels, there was no indication of a higher risk of iron-deficiency among vegans. To conclude cobalamin deficiency risk depends on supplementation status and not on the duration of an exclusive vegan diet, which underlines the need to integrate cobalamin status monitoring and counselling on supplement use in routine clinical care in the Czech Republic.
| S-EPMC6950550 | biostudies-literature
Project description:The aim of this study was to assess the association of vitamin B12 level and single nucleotide polymorphisms (SNPs) in vitamin B12 metabolic genes with pulmonary tuberculosis (PTB) in Chinese Han population. The plasma vitamin B12 expression level was detected using ELISA. Ten SNPs in six key genes (TCN1, TCN2, CUBN, MMACHC, FUT6, and MUT) of vitamin B12 metabolic pathway were included for genotyping by the SNPscan technique among 454 PTB patients and 467 controls. Our results found that vitamin B12 level was significantly reduced in PTB patients when compared with controls. There was no significant association between TCN1 rs526934, TCN2 rs1801198, CUBN rs7906242, rs10904861, rs1801222, MMACHC rs10789465, FUT6 rs3760776, rs3760775, MUT rs9473555, rs9381784 variants, and PTB susceptibility. TCN2 rs1801198 CC genotype, C allele was significantly associated with hypoproteinemia in PTB patients. In CUBN, rs7906242 GG genotype, G allele, rs10904861 TT genotype, and T allele were significantly related to the decreased frequency of sputum smear-positive, and rs10904861 variant affected the occurrence of drug resistance in PTB patients. In addition, the increased frequency of CUBN rs1801222 AA genotype was significantly associated with leukopenia. The decreased frequency of MUT rs9473555 CC genotype was found in the PTB patients with hypoproteinemia. However, vitamin B12 expression was not associated with the genotype distribution of above SNPs. In conclusion, vitamin B12 level was significantly decreased in PTB patients and genetic variants in vitamin B12 metabolic genes were not contributed to PTB susceptibility. Several SNPs in TCN2, CUBN, and MUT gene might associate with multiple clinical manifestations in PTB.
| S-EPMC9583150 | biostudies-literature
Project description:Transcobalamin (TC) deficiency is a rare autosomal recessive inborn error of cobalamin transport which clinically manifests in early infancy. We describe a child with TC deficiency who presented with classical clinical and lab stigmata of inborn error of vitamin B12 metabolism except normal serum B12 levels. He was started on empirical parenteral cobalamin supplements at 2 months of age; however, the definitive diagnosis could only be established at 6 years of age when a genetic evaluation revealed homozygous nonsense variation in exon 8 of the TCN2 gene (chr22:g.31019043C>T).
| S-EPMC6827761 | biostudies-literature
Project description:Coβ-4-ethylphenyl-cob(III) alamin (EtPhCbl) is an organometallic analogue of vitamin B12 (CNCbl) which binds to transcobalamin (TC), a plasma protein that facilitates the cellular uptake of cobalamin (Cbl). In vitro assays with key enzymes do not convert EtPhCbl to the active coenzyme forms of Cbl suggesting that administration of EtPhCbl may cause cellular Cbl deficiency. Here, we investigate the in vivo effect of EtPhCbl in mice and its ability, if any, to induce Cbl deficiency. We show that EtPhCbl binds to mouse TC and we examined mice that received 3.5 nmol/24h EtPhCbl (n=6), 3.5 nmol/24h CNCbl (n=7) or NaCl (control group) (n=5) through osmotic mini-pumps for four weeks. We analyzed plasma, urine, liver, spleen, submaxillary glands and spinal cord for Cbl and markers of Cbl deficiency including methylmalonic acid (MMA) and homocysteine (tHcy). Plasma MMA (mean±SEM) was elevated in animals treated with EtPhCbl (1.01±0.12 µmol/L) compared to controls (0.30±0.02 µmol/L) and CNCbl (0.29±0.01 µmol/L) treated animals. The same pattern was observed for tHcy. Plasma total Cbl concentration was higher in animals treated with EtPhCbl (128.82±1.87 nmol/L) than in CNCbl treated animals (87.64±0.93 nmol/L). However, the organ levels of total Cbl were significantly lower in animals treated with EtPhCbl compared to CNCbl treated animals or controls, notably in the liver (157.07±8.56 pmol/g vs. 603.85±20.02 pmol/g, and 443.09±12.32 pmol/g, respectively). Differences between the three groups was analysed using one-way ANOVA and, Bonferroni post-hoc test. EtPhCbl was present in all tissues, except the spinal cord, accounting for 35-90% of total Cbl. In conclusion, treatment with EtPhCbl induces biochemical evidence of Cbl deficiency. This may in part be caused by a compromised tissue accumulation of Cbl.
| S-EPMC3779197 | biostudies-literature