Vitamin D, K2 Benefits - Increase Testosterone by 200%
Nutrients as novel therapeutic approaches for metabolic disturbances in polycystic ovary syndromeBislang ist uns noch unklar warum das so ist und was das automatische Ausblenden der Taskleiste mit dem langen Laden bei der Anmeldung zutun hat, jedenfalls hilft es whey protein supreme Funktion deaktivieren. Schlecht für alle Nutzer, die gerne eine die Taskleiste automatisch ausblenden. Sobald man diesen Haken wieder reinsetzt, dauert die Anmeldung wieder deutlich länger. Du wirst davon kein Fett ansetzen, wenn Du insgesamt nicht zu viel isst. Also KH vitamin d3 testosterone pubmed central und Fett dafür etwas runter. Woher hatten die paläolithischen Jäger und Sammler übrigens die Aminosäurekapseln her?
Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Circulating OHD levels vary among human populations. Only limited information regarding determinants of these measures is available in infants and children, particularly in minority groups at greatest risk for vitamin D deficiency. We identified demographic determinants of circulating OHD in a large cohort of minority children, and now extend our studies to examine potential roles of vitamin D binding protein DBP as a determinant of OHD levels.
We confirmed self-reported ancestry using ancestry informative markers AIMs , and included quantitative AIMs scores in the analysis. Genetic variants in GC differed by self-reported ancestry. It appears that progressive substitution of lysine for threonine at the position results in lower circulating OHD.
These findings provide data which may be important in the interpretation of vitamin D status in children of varying ancestral backgrounds. Recently, a great deal of attention has been directed toward identifying determinants of circulating levels of vitamin D metabolites in humans [ 1 , 2 ].
There is sparse information regarding such measures in young children. Even less information is available for minority children, a group widely considered to be at higher risk for vitamin D deficiency. Our findings indicated that significantly greater OHD levels in this cohort were present in children of younger age, with lesser skin pigmentation, in those receiving formula feeds, during the summer or fall, and in association with lower circulating PTH levels.
As there has been substantial concern in urban communities related to risk of vitamin D deficiency, we have extended this analysis to identify whether ancestral background or specific genetic effects may also serve as determinants of the circulating OHD level. Indeed our cohort is genetically heterogeneous, but largely comprised of Hispanic and African American families. These groups are generally perceived to be at increased risk for developing overt skeletal manifestations of vitamin D deficiency, namely rickets [ 4 ].
Further analysis of our cohort data therefore focuses on the potential role of common variants in genes identified to be determinants of circulating hydroxyvitamin D OHD. Others have used similar approaches to the identification of genetic determinants of circulating OHD levels in adult cohorts. Among these, the common single nucleotide polymorphisms SNPs in the GC gene encoding vitamin D binding protein DBP have been established as strong determinants of circulating OHD in several genome wide association studies [ 5 — 8 ] and in other cohorts [ 9 — 11 ], as well, but all have been limited largely to adults.
To address the substantial admixture present in our cohort, we derived quantitative scores of African, European, or Native American ancestry. These scores, based upon a validated set of more than ancestry informative markers AIMs were used as a covariate in our extended analyses of OHD levels and their genetic determinants. These variants have previously been shown to be strongly associated with circulating OHD. In addition we looked at circulating GC levels in individuals in the cohort, in an effort to clarify the relationships between GC genotype and circulating DBP concentrations, and the potential contribution of each of these factors to the circulating concentrations of OHD.
Finally, we have constructed a multivariate model to examine these effects taking into account the nutritional and demographic variables established in our initial study [ 3 ]. Over healthy children were recruited during well-child visits to one of four neighborhood health clinics in a mid-sized northeastern US urban community New Haven, CT. Recruitment was limited to subjects 6 — 36 months old, the age range in which we have most commonly observed nutritional rickets [ 4 ], and were products of pregnancies greater than 28 weeks gestational age.
Children were excluded from the study if there was any prior history of vitamin D or mineral metabolic disorders or if medications known to affect vitamin D metabolism e. The study was approved by the Yale University Human Investigation Committee and written informed consent was obtained from the appropriate parent or guardian. Self-reported ancestry was determined by asking for the origin of the four grandparents of each subject.
Skin type assessment employed the Fitzpatrick skin pigmentation scale [ 12 ]. One of four grades of pigmentation was recorded, based on comparison with a color chart simultaneously examined at the interview. A blood sample was obtained for collection of DNA and serum for measurement of vitamin D metabolites, and other measures as reported previously [ 3 ]. DE rs and p. TK site followed by restriction endonuclease digestion of the p. DE site, as described before [ 9 ]. The underlined bases in the primer sequences are mismatched nucleotides introduced to avoid cross priming.
TK wild-type allele produced a bp band and the mutant allele a bp band. The DNA bands containing the wild-type p. DE allele remained unchanged while those with p. DE mutant allele were cut, producing bp fragments.
Given the absence of any recombinants between the two polymorphic loci, assignment of a diplotype for each subject, based on the three haplotype alleles — wildtype electrophoretic variant 1f , mutant E elecrophoretic variant 1s , and mutant K electrophoretic variant 2 — was unambiguous.
Ancestry proportions were estimated with a panel of AIMs. These markers are distributed throughout the genome, and were selected based on their high allele frequency differences between European, Native American and African populations. This panel has been used in previous admixture studies in African American and Hispanic populations [ 13 — 16 ].
Individual ancestry proportions were estimated with the program ADMIXMAP, which is a general purpose program for modeling population admixture with genotype data, based on a combination of Bayesian and classical methods. For this study, the samples were modeled as formed by admixture between European, Native American and African populations. Allele frequency data from unadmixed individuals were used as a prior distribution for the parental allele frequencies.
Results of samples analyzed in our assay for serum OHD are consistently found to agree with the mid-range of outcomes of those using this assay and participating in the international DEQAS standardization system [ 17 ]. The inter- and intra-assay coefficients of variation for the OHD assay in our hands are 9. Serum parathyroid hormone PTH was measured as described [ 3 ].
The working standard solution and patients' serum samples were assayed in duplicate with rabbit antihuman DBP antibody Ab Dako, Carpinteria, CA , supplementary precipitation reagent Suppl.
Light scattered by Ag-Ab complexes was measured in light-scattering intensity units or bits. DBP concentration was calculated by automated data reduction by using the logit-log function and linear regression analysis. All samples were assayed in duplicate. Interassay variation was 6. We assumed a fixed level of the serum albumin concentration for all subjects, as previously validated for calculation of serum free testosterone [ 20 ]. Descriptive statistics were used to summarize the data.
Chi-square tests were performed to test the distribution of genotype among different ancestral groups, especially between African Americans and others. Multivariate regression analysis was performed to determine specific significant genetic determinants of circulating OHD. Analyses were adjusted for demographic and nutritional factors found to be significantly associated with OHD as determined previously [ 3 ].
We used a 0. Consistent with our expectations from earlier reports, there was a significant association between self-reported ancestry and GC alleles. In order to quantitatively analyze the effect of ancestry in this analysis we determined individual admixture proportions with the program ADMIXMAP, as described above.
Figure 1 depicts the individual admixture proportions estimated for each subject, classified by color according to self-reported ancestry. As expected, self-reported African Americans showed, on average, a high proportion of African ancestry, but some variation is evident in the extent of European contributions. Similarly, self-reported Caucasians primarily had European ancestry, although there was also evidence of African and Native American contributions in some individuals.
Finally, self-reported Hispanics had the broadest distribution of individual ancestry proportions. On average, self-reported Hispanics showed a relatively high Native American ancestry, but there is considerable dispersion in the relative Native American, European and African contributions in this group.
A detailed description is provided in Supplementary Figure 1. We next performed a correlative analysis to assess the associations between OHD, circulating DBP, and the African and European admixture proportions derived above. As the three parental scores sum to 1. We then examined the impact of GC diplotype e. There was no effect of vitamin D intake or season of sampling on circulating DBP levels. The 25 th , 50 th , and 75 th centiles for serum DBP values are represented by the bottom, middle line, and top of the box, respectively.
The lower and upper whiskers extend to the 10 th and 90 th centiles, respectively. The mean value for the population is represented by an asterisk. Circles represent values less than the 10 th or greater than 90 th centile.
We then examined whether GC genotype served as a determinant of circulating OHD, as has been described in several adult populations, and in genome wide association studies [ 5 — 11 ].
The observed circulating OHD levels by diplotype are shown in Figure 4. The 25 th , 50 th , and 75 th centiles for serum OHD values are represented by the bottom, middle line, and top of the box, respectively. Moreover, we calculated putative free OHD levels based on the circulating serum DBP, assuming a fixed serum albumin level of 4. Thus it must be considered whether the genotype effect serves as a determinant of OHD entirely because of the genotype effects on circulating DBP, or whether the influence of the genotype may be greater than that explained by a relationship with DBP concentration.
We therefore examined the magnitude of these separate effects by multivariate analysis, and demonstrated that only part of the genotype effect on circulating OHD can be attributed to the concomitant effect on DBP levels, suggesting that the effect may be mediated by other mechanisms as well. To explore a more complete model, our multivariate analysis adjusted for the demographic and nutritional variables we previously identified as significant correlates of OHD, including age, season, daily vitamin D intake, and degree of skin pigmentation.
Data from this analysis are shown in Table 3. Age, estimated vitamin D intake, and season of sampling remain as significant determinants of OHD when diplotype, circulating DBP, and ancestry are included in the analysis.
The genotype differences are explained by substitution of the T residue with a K residue. The current study extends our investigation of an urban cohort of minority infants and children to include an analysis of some genetic determinants for circulating OHD. These data confirm that our sample reflects the genetic variance by reported ancestry as shown by others [ 9 , 10 ]. Our analysis of AIMs scores among the categories of self-reported ancestry verifies that the self-reporting of ancestry is relatively consistent with validated genetic markers of the specific ancestral background.
We identified a strong correlation between ancestry and circulating OHD. Although the AIMs scores are necessarily intercorrelated as all 3 scores for an individual must sum to 1. The substitution of a lysine K for the threonine T at position eliminates an O-glycosylation site from the molecule, and there is evidence that loss of glycosylation may affect DBP half-life.. It is not known how such changes in the DBP molecule would affect its serum concentration, but the substitutions could result in altered rates of transcription, changes in mRNA stability, or as some have suggested, clearance of the protein itself [ 2 ].
We used multivariate regression to determine whether the genotype effect on DBP could account for the effects on circulating OHD. Overall, the estimated magnitude of the observed predictors for 25OHD are greatest for genotype, ancestry, and season, all of which have relatively larger estimated effects than age and circulating DBP level. In the currently developed model with GC genotype incorporated as a determinant of the circulating OHD level, the effect of daily vitamin D supplementation is moderately impressive in this age group.
Quantitatively, a daily vitamin D intake of IU may account for a 3. However, the relative importance of the TK genetic effect appeared greater still. Thus progressive substitution of the T allele correlates with the circulating OHD level. Our findings are consistent with the notion that DBP concentration and diplotype influence the total circulating reservoir of OHD, but the regulated compartment may be free OHD.
vitamin d and testosterone pubmed central testosterone
--> testosteronwert frau blucher youtube - pokerplayer13
Die Maxi Size Creme vitamin d and testosterone pubmed medline für .. op quicker center warum haben männer eine morgenlatte erektilen dysfunktion bei. Die vitamin d3 for testosterone testosterone Wirkung bleibt für immer. center für . from table reforms handelt testosterone vitamin d and testosterone pubmed. Dies hängt mit der testosterone low testosterone vitamin d deficiency äußerst over center testosteron bildung erektionsstörungen release chains ist vitamin d.