Vitamin D

[BBC3]

Prelude to my Buoooouulll SHZIT...

Vitamin D — QuickFacts

I'd like to see a study involving these factors..:

1. Time spent in the sun every day.
2. Blood plasma cholesterol reads.
3. Vit D Levels.
4. Supplemental Exogenous Vit D Co-factor
5. Broad Blood panels with measurements on vitamins and others.
6. Standard Clearance activity as well as Drug elimination counts in and out of the sun.

IT REALLY AMAZES ME THAT THERE ARE NOT A BAZILLION STUDIES QUALIFYING THE METABOLIC DIFFERENCES IN THE BODY WITH RELATION TO SUN EXPOSURE...!?!?!?!?!?!? Really? WTF?!

It would be my belief that ANYONE who is not in the sun every day is going to suffer across the board......

I am thinking of actually attempting a high Vit D supp and keep it up for one month and see what happens. I don't think it will amount to much for me, but we will see. The difference in this test and the past one I did - Is that I will be catchin some rays..

SLIGHT TANGENT HERE...:

How to solve this riddle - whether or not Vit D levels require supplementation, and if it is even possible via a gel cap alone.

** Importantly ** and I am not so much refuting that positive results are being found in Vit D supplementation studies currently ongoing in this latest "vitamin craze", but I do SUSPECT its another chicken-or-egg syndrome which would explain why some get results and some dont. (In fact, I am going to create a thread to this process). So I would be saying that the vitamin D DEFICIENCY IN MOST would be a RESULT more often, than a CAUSE. There can be no other explanation as our bodies were built on this planet and with these CONDITIONS in mind.

To further discern this difference, which basically means FInding out WHETHER OR NOT ADDING EXOGENOUS VITAMIN D WILL RESOLVE THE MATTER.

*** I'm gonna start with a basic premise for this type of analysis which I AM GOING TO COIN "The Earth/Wind/Fire" principle. Which means that I am saying that there are (3) Mandatory Factors which MUST be included in EVERY SINGLE Biological analysis to be thorough and complete.

(1) EARTH - Meaning ENVIRONMENT. We were created of this planet's make up, and all the environmental stimulus IT IS EXPOSED TO. Ranging from the elements in the soil, to the SUN from the sky, The air we breathe, and the Methods of TRAVEL (lifestyle) to which we interact.

(2) WIND - Meaning LEARNED INTERACTION. HOW do we choose to INVOLVE with all of this? Are we eating Collard greens, rubbing our skin with them, burning them for heat, Shoving them up our asses, or just wearing them as hats or shoes.

(3) FIRE - Meaning Metabolic NET Result. What is happening to us BIOLOGICALLY due to the above two FUNCTIONS. This one being the nitty gritty with the most detail and SUBSETS ranging from Complete metabolic process (absorption, action, elimination) - TO INTERACTIONS - TO Physical Effects - TO MITIGATION (damage control/medical science).

There can not be a more thorough and COMPLETE way to analyze anything. NOTE - You will not see the first (earth) included in many prescribing info's. as it does not service them(Big Pharma) as an expense to create a demand. We will all service our direct needs first and cost effectively. There is no doubt The Demand is there without consideration. While ODDLY we forget, the EARTH created this demand!!?!?!?!!!!

(A)EARTH, What are the uncontrollable and controllable CONDITIONS/STIMULUS. This would be the easiest of the three to pin down in scope, range, consistency, and redundancy in application - yet still myriad. The second of which (B)WIND, would indeed be multifaceted as you would now be including what the subject actually does with his TIME, and what they ARE NOT TELLING You. So first you would have to beat out all the lies, both intentional and habitual unrealized. Next you would have to the qualify EARTH as to WHAT is the REAL EXPOSURE on this Principle's PATH. Then you would have to look at everything under a microscope ONCE all was qualified and quantified as REAL interaction, and given we had the knowledge to actually KNOW what we were looking at. The third being FIRE, Which is the most complex of the (3) as you are now considering the first two FACETS and then looking at all the possible metabolic resulting actions in the ANIMAL which we would be studying - as they relate. The biggest problem here being GENETICS of said subject as this is POORLY UNDERSTOOD by Medical Science. This is aside from the fact that while we can draw pictures(of what we can see) - WE ARE ONLY TRACING. Thats right you heard me. LOL. What I am saying is this. From the dawn of time medical science has been trial and error, and MOST LIKELY all stimulated from POT LUCK in OBSERVATION. As the DATA gathered began to amass, we gathered the NERVE to PROPOSE to know why, NOT REALIZING that in most cases just because we observed something resulting, this does not necc tell WHY. We have PRESUMED for the most part. Granted that with enough EXPERIENCE, and laying enough TRACE PAGES on top of each other, side by side, upside down, and layered in Adobe Photoshop, we have drawn what appear to be some CERTAIN CONCLUSIONS. Keep in mind this is based on no wrong turn back at Albuquerque... As we have become "civilized", we have gone even one step further to EXPEDITE the learning process via the torment of animals(no I'm not queer harping), tolerance of variables, and application of "Benefit outweighing Risk". Again, as we all learned back in grade school, the RISK of expedition is CARELESS MISTAKES which lead to that wrong turn risking FOREVER IRREVERSIBLE TANGENT PATHS FROM TRUEST VECTOR... You really have to wonder who wins the rabbit/turtle race in the end? Did he really?! But how can you tell me the you understand human biology as a true science when you can't even tell me definitively how much testosterone a given man produces in an hour, and forget about measuring women's hormones all together!! (That should tell us something right there...!!!!!) How can you tell me medicine is SCIENCE when all we can do is wait for sickness, and not cost effectively mitigate PREVENTIVELY, in lieu of poor habits, but given healthy/normal genetics (if there is such a thing).

I move on for now for more ponder on this and before I forget the other. But WHAT WILL BE INTERESTING ABOUT THIS ANALYSIS METHOD I am attempting, is that I am going to ATTEMPT to build it to be designed to WORK FORWARD ONLY with regard to EARTH, WIND, FIRE. Allowing ONLY a building upon the Master Sets in that order..!!! I am saying to avoid any reason for review of FEEDBACK, as the SYNTAX of the QUESTION is now found to actually BE THE ANSWER..!!!! - If syntax is CORRECT... Could this perhaps prove that a MASSIVE Failure in paradigm that medical science currently employs is the LACK OF Environmental Consideration.??!?!! Thus skipping what should logically be the FIRST STEP now blowing the whole game?? It appears to me that to properly QUALIFY the factors IN ORDER leaves none behind, THUS NO REASON to look back with doubt. You say, "yea, easy said". But really, could the failure to include EARTH in analysis in fact be the monkey wrench? So the magic test will be CAN THIS EVEN BE DONE...

There can be many real intentional and unintentional REASONS for this failure; Political, Economical, Psychological, and even Religious and Spiritual. I wont ever dare at this time.....

More CONJECTURE to COME....

And if you happened to DENOTE a SLIGHT tangent from the Vit D discussion, Thats because there was one.. LOL But I',m not known for that at all. LOL I will further tie Vit D back in to may part in this discussion. But the point with regard to Vit D for now, is that there are many variables that are UNCLEAR. I SUSPECT the SUN is a big factor here as well as diet and genetics. And that I suspect that again, scientific GROUPTHINK is tossing themselves down on a TEN INCH RAZOR BARBED THROBBER AS USUAL...

 

[Michael Scally MD]

Grossmann RE, Tangpricha V. Evaluation of vehicle substances on vitamin D bioavailability: a systematic review. Mol Nutr Food Res 2010;54(8):1055-61. Evaluation of vehicle substances on vitamin D bioavailability: A systematic review

Vitamin D insufficiency is a common medical condition. Vitamin supplements can be ingested to improve vitamin D status. It is not known if the vehicle substance that is combined with the vitamin D tablet influences the bioavailability of vitamin D. The purpose of this review is to examine the impact of different vehicles on vitamin D bioavailability. A comprehensive literature search identified studies that directly compared the absorption of vitamin D from two or more vehicles. The change in mean serum 25(OH)D per average daily dose of vitamin D supplemented was calculated and compared among the studies. We identified four clinical studies that compared two different vehicles of vitamin D. Vitamin D in an oil vehicle produced a greater 25(OH)D response than vitamin D in a powder or an ethanol vehicle in healthy subjects. There are limited studies that have compared the influence of the vehicle substance on vitamin D bioavailability. Future studies should examine bioavailability among different vehicle substances such as oil, lactose powder, and ethanol and examine if there are any differences in bioavailability among different patient populations including those with fat malabsorption.

 

[Michael Scally MD]

Wong YYE, McCaul KA, Yeap BB, Hankey GJ, Flicker L. Low vitamin D status is an independent predictor of increased frailty and all-cause mortality in older men: the Health In Men Study. Journal of Clinical Endocrinology & Metabolism. http://jcem.endojournals.org/content/early/2013/06/19/jc.2013-1702.abstract (Low vitamin D status is an independent predictor of increased frailty and all-cause mortality in older men: the Health In Men Study)

Context and objective: Hypovitaminosis D and frailty are common in the older population. We aimed to determine whether 25-hydroxyvitamin D [25(OH)D] concentrations are associated with frailty and mortality.

Design: Prospective cohort study.

Setting and participants: 4203 older men aged 70–88 years in Perth, Western Australia.

Main outcome measures: 25(OH)D was measured by immunoassay. Frailty was assessed with the 5-point FRAIL (Fatigue, Resistance, Ambulation, Illness and Loss of weight) scale. Mortality was determined from the death registry via the Western Australian Data Linkage System.

Results: At baseline, 676 (16.1%) men were frail, as defined by having ?3 deficits (FRAIL scale ? 3). In multivariate cross-sectional analysis, low vitamin D status, defined by the lowest quartile of 25(OH)D values (<52.9 nmol/l), was associated with increased prevalent frailty (odds ratio [OR] 1.96, 95% confidence interval [CI] 1.52 to 2.52) in comparison to the highest quartile of 25(OH)D values (>81.6 nmol/l). After a mean period of 5.3 years, the adjusted odds ratio of being frail at follow-up for men with low vitamin D and having zero deficit at baseline (FRAIL scale = 0) was 1.56 (95% CI 1.07 to 2.27). Low vitamin D also predicted all-cause mortality over a period of up to 9.2 years (hazards ratio 1.20, 95% CI 1.02 to 1.42), independent of baseline frailty and other covariates.

Conclusion: Hypovitaminosis D is associated with prevalent and incident frailty in older men. Hypovitaminosis D also predicts all-cause mortality, independent of frailty. The association between vitamin D and mortality is not solely dependent on the occurrence of frailty.

 

[Michael Scally MD]

Romagnoli E, Pepe J, Piemonte S, Cipriani C, Minisola S. Value and limitations of assessing vitamin D nutritional status and advised levels of vitamin D supplementations. European Journal of Endocrinology. http://www.eje-online.org/content/early/2013/07/11/EJE-13-0435.abstract (Value and limitations of assessing vitamin D nutritional status and advised levels of vitamin D supplementations)

The growing attention to the role of vitamin D in skeletal and extra-skeletal diseases over the last decade, induced an increased demand for Vitamin D determination as well as a dramatic rise of sales of vitamin D supplement.

However, several critical points in this field remain to be clarified. We lack a clear consensus about the definition of vitamin D deficiency, insufficiency and sufficiency. The identification of different thresholds defining vitamin D status have relevant implications in clinical practice. In fact, the worldwide prevalence of low vitamin D status is highly varying according to the level of 25(OH)D utilized to define sufficiency. Therefore, the assessment of 25-hydroxyvitamin D levels may have a critical role, but a number of different technical problems associated with its determination may interfere in interpreting the results.

The hydrophobic nature of the vitamin D and the tight binding to its carrier (vitamin D binding protein, DBP), the different forms circulating in blood and the issue of standardisation are among the most important factors influencing the measurement of this metabolite. Another controversial point relies on the conflicting guidance on prevention and treatment of vitamin D deficiency endorsed by different medical and scientific communities.

In particular, uncertainty exists about how to replete vitamin D stores, how to maintain normal 25(OH)D levels after repletion, which form of vitamin D is preferable for supplementation, which route of administration and dosing regimens are advisable. Finally, concerns have been raised regarding vitamin D toxicity and its adverse effects.

 

[Dalexand]

Matthew - I live very near the Equator and expose myself to sun most days due to the nature of my work. I've been Vit D diff now for almost 3 years. I stopped about 6 months ago, thinking I was feeling better - NOT - I am supplementing with 5000 IU's daily again.

So the Sunshine Vitamintheory to me is BS.

 

[Michael Scally MD]

Ameri P, Giusti A, Boschetti M, et al. Vitamin D increases circulating IGF1 in adults: potential implication for treatment of growth hormone deficiency. European Journal of Endocrinology. http://www.eje-online.org/content/early/2013/09/04/EJE-13-0510.abstract (Vitamin D increases circulating IGF1 in adults: potential implication for treatment of growth hormone deficiency.)

Objectives: Previous studies suggested that vitamin D modulates circulating IGF1. We investigated this effect in adults and its clinical relevance in the management of growth hormone deficiency (GHD).

Design and methods: IGF1 levels were prospectively measured before and after 12 weeks of treatment with oral vitamin D3 (5000 or 7000 IU/week) vs. no intervention in 39 subjects 61.9±7.9 years old. The frequency of IGF1 values ? 50th age- and sex-specific percentile in relation to vitamin D status, as determined by the concentration of 25-hydroxyvitamin D [25(OH)D], was retrospectively assessed in 69 GHD patients (57.4±16.6 yr) on stable hormone replacement and with 25(OH)D and IGF1 concurrently measured.

Results: Five-thousand and 7000 IU vitamin D3/week significantly raised 25(OH)D by 12.7±8.4 ng/ml and 13.1±6.5 ng/ml, respectively (both P < 0.001 vs. baseline). In the 7000 IU group IGF1 levels also significantly increased by 31.3±36.7 ng/ml (P = 0.01). Neither 25(OH)D nor IGF1 significantly varied in controls. IGF1 was ? 50th percentile more frequently in GHD patients with ? 15 ng/ml than < 15 ng/ml 25(OH)D (65.9% vs. 40.0%, P < 0.05). Logistic regression with adjustment for recombinant human (rh) GH dose, vitamin D supplements, gender, use of thyroid hormones, corticosteroids or estrogen/testosterone, and season revealed a significant positive association between ? 15 ng/ml 25(OH)D and IGF1 ?50th percentile (OR 4.4, 95% CI 1.0-18.8, P < 0.05). A significant negative correlation between 25(OH)D concentrations and rhGH dose was found after correcting for age and IGF1 (? - 0.042, P < 0.01), but not after further adjusting for sex, thyroid, adrenal or gonadal replacement, and season (? - 0.037, P = 0.06).

Conclusions: Vitamin D increases circulating IGF1 in adults. As a result, a better vitamin D status may ease the achievement of normal IGF1 values in GHD.

 

[Michael Scally MD]

Hilger J, Friedel A, Herr R, et al. A systematic review of vitamin D status in populations worldwide. Br J Nutr 2013:1-23. Cambridge Journals Online - British Journal of Nutrition - Abstract - A systematic review of vitamin D status in populations worldwide

Vitamin D deficiency is associated with osteoporosis and is thought to increase the risk of cancer and CVD. Despite these numerous potential health effects, data on vitamin D status at the population level and within key subgroups are limited. The aims of the present study were to examine patterns of 25-hydroxyvitamin D (25(OH)D) levels worldwide and to assess differences by age, sex and region. In a systematic literature review using the Medline and EMBASE databases, we identified 195 studies conducted in forty-four countries involving more than 168 000 participants. Mean population-level 25(OH)D values varied considerably across the studies (range 4.9-136.2 nmol/l), with 37.3 % of the studies reporting mean values below 50 nmol/l. The highest 25(OH)D values were observed in North America. Although age-related differences were observed in the Asia/Pacific and Middle East/Africa regions, they were not observed elsewhere and sex-related differences were not observed in any region. Substantial heterogeneity between the studies precluded drawing conclusions on overall vitamin D status at the population level. Exploratory analyses, however, suggested that newborns and institutionalised elderly from several regions worldwide appeared to be at a generally higher risk of exhibiting lower 25(OH)D values. Substantial details on worldwide patterns of vitamin D status at the population level and within key subgroups are needed to inform public health policy development to reduce risk for potential health consequences of an inadequate vitamin D status.

 

[RosettaWood]

We should know the importance then of Vitamin D, so not to be taken for granted. Vitamin D is a steroid vitamin, a group of fat-soluble prohormones, which encourages the absorption and metabolism of calcium and phosphorous. People who are exposed to normal quantities of sunlight do not need vitamin D supplements because sunlight promotes sufficient vitamin D synthesis in the skin.
-Rosetta

 

[Michael Scally MD]

[NO] Effects Of Vitamin D Supplements On Bone Mineral Density

Reid IR, Bolland MJ, Grey A. Effects of vitamin D supplements on bone mineral density: a systematic review and meta-analysis. The Lancet. Effects of vitamin D supplements on bone mineral density: a systematic review and meta-analysis : The Lancet

Background - Findings from recent meta-analyses of vitamin D supplementation without co-administration of calcium have not shown fracture prevention, possibly because of insufficient power or inappropriate doses, or because the intervention was not targeted to deficient populations. Despite these data, almost half of older adults (older than 50 years) continue to use these supplements. Bone mineral density can be used to detect biologically significant effects in much smaller cohorts. We investigated whether vitamin D supplementation affects bone mineral density.

Methods - We searched Web of Science, Embase, and the Cochrane Database, from inception to July 8, 2012, for trials assessing the effects of vitamin D (D3 or D2, but not vitamin D metabolites) on bone mineral density. We included all randomised trials comparing interventions that differed only in vitamin D content, and which included adults (average age >20 years) without other metabolic bone diseases. We pooled data with a random effects meta-analysis with weighted mean differences and 95% CIs reported. To assess heterogeneity in results of individual studies, we used Cochran's Q statistic and the I2 statistic. The primary endpoint was the percentage change in bone mineral density from baseline.

Findings - Of 3930 citations identified by the search strategy, 23 studies (mean duration 23•5 months, comprising 4082 participants, 92% women, average age 59 years) met the inclusion criteria. 19 studies had mainly white populations. Mean baseline serum 25-hydroxyvitamin D concentration was less than 50 nmol/L in eight studies (n=1791). In ten studies (n=2294), individuals were given vitamin D doses less than 800 IU per day. Bone mineral density was measured at one to five sites (lumbar spine, femoral neck, total hip, trochanter, total body, or forearm) in each study, so 70 tests of statistical significance were done across the studies. There were six findings of significant benefit, two of significant detriment, and the rest were non-significant. Only one study showed benefit at more than one site. Results of our meta-analysis showed a small benefit at the femoral neck (weighted mean difference 0•8%, 95% CI 0•2—1•4) with heterogeneity among trials (I2=67%, p<0•00027). No effect at any other site was reported, including the total hip. We recorded a bias toward positive results at the femoral neck and total hip.

Interpretation - Continuing widespread use of vitamin D for osteoporosis prevention in community-dwelling adults without specific risk factors for vitamin D deficiency seems to be inappropriate.

 

[Michael Scally MD]

Ashraf AP, Huisingh C, Alvarez JA, Wang X, Gower BA. Insulin resistance indices are inversely associated with vitamin D binding protein concentrations. Journal of Clinical Endocrinology & Metabolism. http://jcem.endojournals.org/content/early/2013/10/28/jc.2013-2452.abstract (Insulin resistance indices are inversely associated with vitamin D binding protein concentrations)

Context: We hypothesized that similar to the coordinated homeostatic regulation of most hormones, the concentration of free and bioavailable 25-hydroxy vitamin D [25(OH)D] will be tightly controlled by total 25(OH)D and vitamin D binding protein (VDBP); and, that the VDBP concentrations will be associated with insulin resistance status.

Objective: Our primary objective was to investigate associations between total, free and bioavailable 25(OH)D and VDBP. We also evaluated the relationships of VDBP with insulin resistance indices. Study design was cross sectional in the setting of a University children’s hospital. The relative concentration of bioavailable 25(OH)D to total 25(OH)D [bioavailable 25(OH)D /total 25(OH)D was expressed as a percentage [% bioavailable 25(OH)D].

Results: Subjects were 47, post menarchal, female adolescents, mean age 15.8 ± 1.4 years, mean BMI 23.1 ± 4.0 kg/m2. Total 25(OH)D was strongly associated with VDBP (rho = 0.57, P = <0.0001). At lower total 25(OH)D concentrations, the concentration of bioavailable 25(OH)D relative to total 25(OH)D was higher (23.8% vs. 14.9%, P<0.0001), whereas the relative concentration of free 25(OH)D was similar (P=0.44). VDBP was inversely associated with fasting insulin (rho=-0.51, P=0.0003) and HOMA-IR (rho=-0.45,P=0.002), and positively with WBISI (rho=0.33, P=0.02); these relationships were persisted after adjusting for percent fat and attenuated after adjusting for race.

Conclusion: Our data suggest that, VDBP concentrations are regulated by total 25(OH)D levels to maintain adequate concentrations of bioavailable 25(OH)D. VDBP concentrations are inversely associated with hyperinsulinemia and insulin resistance.

 

[corageon]

Vitamin D is also crucial to maintaining high Free Test levels as well as promoting optimal thyroid function.

Association of hypogonadism with vitamin D status: the European Male Ageing Study.
Lee DM, Tajar A, Pye SR, Boonen S, Vanderschueren D, Bouillon R, O'Neill TW, Bartfai G, Casanueva FF, Finn JD, Forti G, Giwercman A, Han TS, Huhtaniemi IT, Kula K, Lean ME, Pendleton N, Punab M, Wu FC; EMAS study group.
Collaborators (29)
Source

Arthritis Research UK Epidemiology Unit, Manchester Academic Health Science Centre, The University of Manchester, Manchester M13 9PT, UK.
Abstract
OBJECTIVE:

Interrelationships between hormones of the hypothalamic-pituitary-testicular (HPT) axis, hypogonadism, vitamin D and seasonality remain poorly defined. We investigated whether HPT axis hormones and hypogonadism are associated with serum levels of 25-hydroxyvitamin D (25(OH)D) in men.
DESIGN AND METHODS:

Cross-sectional survey of 3369 community-dwelling men aged 40-79 years in eight European centres. Testosterone (T), oestradiol (E(2)) and dihydrotestosterone were measured by gas chromatography-mass spectrometry; LH, FSH, sex hormone binding globulin (SHBG), 25(OH)D and parathyroid hormone by immunoassay. Free T was calculated from total T, SHBG and albumin. Gonadal status was categorised as eugonadal (normal T/LH), secondary (low T, low/normal LH), primary (low T, elevated LH) and compensated (normal T, elevated LH) hypogonadism. Associations of HPT axis hormones with 25(OH)D were examined using linear regression and hypogonadism with vitamin D using multinomial logistic regression.
RESULTS:

In univariate analyses, free T levels were lower (P=0.02) and E(2) and LH levels were higher (P<0.05) in men with vitamin D deficiency (25(OH)D <50?nmol/l). 25(OH)D was positively associated with total and free T and negatively with E(2) and LH in age- and centre-adjusted linear regressions. After adjusting for health and lifestyle factors, no significant associations were observed between 25(OH)D and individual hormones of the HPT axis. However, vitamin D deficiency was significantly associated with compensated (relative risk ratio (RRR)=1.52, P=0.03) and secondary hypogonadism (RRR=1.16, P=0.05). Seasonal variation was only observed for 25(OH)D (P<0.001).

CONCLUSIONS:

Secondary and compensated hypogonadism were associated with vitamin D deficiency and the clinical significance of this relationship warrants further investigation.

 

[Michael Scally MD]

Larose TL, Chen Y, Camargo CA, Jr., Langhammer A, Romundstad P, Mai XM. Factors associated with vitamin D deficiency in a Norwegian population: the HUNT Study. J Epidemiol Community Health. Factors associated with vitamin D deficiency in a Norwegian population: the HUNT Study -- Larose et al. -- Journal of Epidemiology & Community Health

Vitamin D deficiency occurs worldwide. Winter season and high Body Mass Index (BMI) are associated with low levels of serum 25-hydroxyvitamin D (25(OH)D). We estimated the prevalence of vitamin D deficiency in a Norwegian adult population and examined factors associated with vitamin D deficiency.

A cohort of 25 616 adults (19-55 years) who participated in both the second and third Nord-Trondelag Health Study (HUNT 2 (1995-1997) and HUNT 3 (2006-2008)) was established in a previous study. A 10% random sample of the cohort population was recruited for serum 25(OH)D measurements (n=2584), which was used for the current cross-sectional study. Vitamin D deficiency was defined as serum 25(OH)D level <50 nmol/L.

The overall prevalence of vitamin D deficiency was 40%, but varied by season (winter: 64%; summer: 20%). Winter season (adjusted prevalence ratio (PR): 3.16, 95% CI 2.42 to 4.12) and obesity (BMI >/=30.0 kg/m2) (PR: 1.74, 95% CI 1.45 to 2.10) were strongly associated with prevalent vitamin D deficiency. Current smoking also demonstrated an increased PR (1.41, 95% CI 1.21 to 1.65). Daily intake of cod liver oil (PR: 0.60, 95% CI 0.41 to 0.77), increased physical activity (PR: 0.80, 95% CI 0.68 to 0.95) and more frequent alcohol consumption (PR: 0.76, 95% CI 0.60 to 0.95) were associated with a reduced PR.

The prevalence of vitamin D deficiency was high in Norwegian adults. Winter season, high BMI and current smoking were positively associated, and intake of cod liver oil, increased physical activity and more frequent alcohol consumption were inversely associated with vitamin D deficiency.

 

[BBC3]

I'm kinda interested in what you interpret as "the sunshine Vitamin theory"..? The way I understand it, and historically since grade school in the early 80's, was that "Vitamin D is GENERATED in the BODY due to Sunshine exposure". I also recall society (parents/teachers) advocating that this is the reason which Vit D is supplemented in Milk, but not really sure the whole idea delivered back then... So is this what you are referring too?

Thinking about it today, and with enough knowledge to make myself a COMPLETE MORON [)][)], I would speculate that BECAUSE vitamin D is a fat Soluble vitamin - Sun exposure is creating biological conditions in the body which allow more of it into plasma circulation... My Logic behind this would be that the SKIN is nourished and protected by BODY FAT, or "Body Oils". Which MAY even be classified as "Cholesterol" while in blood circulation. So then I would be saying that since the blood is in progress of DELIVERING fat and oil to the skin, that "fat and oil" is picking up/ OR enabling Vitamin D Metabolism/mobilization.

** It would be an interesting experiment to see what other fat soluble vitamins become higher in serum count during periods of excess sun exposure...?!?!??

What I really find interesting in this line of thought is I WONDER how effectively positive Vitamin D would be as a topical?? It seems to me that even before the 1990's incepted perception that Vitamin E was the holy grail (even though all megadosing it ever did for me was cause heart distress - LOL) But BEFORE Everyone started touting guzzling the shit by the shot glass, it was known to people in the "skin care" industry as good to apply to injured skin. Has anyone tried breaking open some of those vitamin D gel caps and putting on scars, open wounds, or even staph infections? I wonder is Vit D in common skin lotions? Are there any studies that ANYONE is aware of for TOPICAL Vit D application..?

A little more on target. And with consideration that perhaps other fat soluble vitamins DO NOT increase in plasma concentration during sun exposure periods. WHY THEN DOES VIT D Correlate with Sun exposure?? I also recall as a youth being told that you could die from taking too many vitamins, as some are "fat soluble" and will build up quickly due to.. Do you think perhaps FAT is simply LOADED with it? Cause it sure sounds like folks are megadosing the stuff and far beyond the amounts of Vitamin D, or Vitamin A for that matter, and getting away with it not immediately negatively affecting their health..?

So we get into the subject of Biological "synthesis" of vitamins (Whatever) - but the notion being the BODY is "MAKING FROM SCRATCH" a certain vitamin or particular molecule/s..

This leading to my technical question now generated from all this - What are the required components/precursors for the body to Synthesize Vitamin D? Clearly, FAT is somewhere in the mix.. Anyone??

** And just because something is measured at higher concentrations in BLOOD SERUM - DOES NOT MEAN that we are "making" or have MORE of it. It could very well mean that inherent stores are being mobilized for use and DEPLETED AT FASTER RATES...! Someone PLEASE SHOW ME where Vitamin D is being "MANUFACTURED" in the skin. Describe to me the technical process as to how skin cells are making this or anything else for that matter... Cause - I really suspect it is simply delivered there with the fat to keep the skin healthy, and for some SKIN SERVICING REASON...

Matthew - I live very near the Equator and expose myself to sun most days due to the nature of my work. I've been Vit D diff now for almost 3 years. I stopped about 6 months ago, thinking I was feeling better - NOT - I am supplementing with 5000 IU's daily again.

So the Sunshine Vitamintheory to me is BS.

 

[Michael Scally MD]

Autier P, Boniol M, Pizot C, Mullie P. Vitamin D status and ill health: a systematic review. The Lancet Diabetes & Endocrinology. Vitamin D status and ill health: a systematic review : The Lancet Diabetes & Endocrinology

Low serum concentrations of 25-hydroxyvitamin D (25[OH]D) have been associated with many non-skeletal disorders. However, whether low 25(OH)D is the cause or result of ill health is not known. We did a systematic search of prospective and intervention studies that assessed the effect of 25(OH)D concentrations on non-skeletal health outcomes in individuals aged 18 years or older. We identified 290 prospective cohort studies (279 on disease occurrence or mortality, and 11 on cancer characteristics or survival), and 172 randomised trials of major health outcomes and of physiological parameters related to disease risk or inflammatory status. Investigators of most prospective studies reported moderate to strong inverse associations between 25(OH)D concentrations and cardiovascular diseases, serum lipid concentrations, inflammation, glucose metabolism disorders, weight gain, infectious diseases, multiple sclerosis, mood disorders, declining cognitive function, impaired physical functioning, and all-cause mortality. High 25(OH)D concentrations were not associated with a lower risk of cancer, except colorectal cancer. Results from intervention studies did not show an effect of vitamin D supplementation on disease occurrence, including colorectal cancer. In 34 intervention studies including 2805 individuals with mean 25(OH)D concentration lower than 50 nmol/L at baseline supplementation with 50 ?g per day or more did not show better results. Supplementation in elderly people (mainly women) with 20 ?g vitamin D per day seemed to slightly reduce all-cause mortality. The discrepancy between observational and intervention studies suggests that low 25(OH)D is a marker of ill health. Inflammatory processes involved in disease occurrence and clinical course would reduce 25(OH)D, which would explain why low vitamin D status is reported in a wide range of disorders. In elderly people, restoration of vitamin D deficits due to ageing and lifestyle changes induced by ill health could explain why low-dose supplementation leads to slight gains in survival.

 

[mikes75]

Supplementation with vitamin d does not incre... [Horm Metab Res. 2013] - PubMed - NCBI

 

[Michael Scally MD]

Supplementation with vitamin d does not incre... [Horm Metab Res. 2013] - PubMed - NCBI

It should be noted for the study title, "Supplementation with vitamin d does not increase serum testosterone levels in healthy males." Also, for the conclusion, "In conclusion, in subjects without significant vitamin D deficiency, there is no increase in serum testosterone after high dose vitamin D supplementation."

I do not think anyone advises not to treat Vit. D insufficiency/deficiency.

 

[Dalexand]

BBC 3 - Yes that's what I was referring too..
Thanks
Dom

 

[BBC3]

I took the time to look at this one. I found a flaw early on that disappointed me away...

Serum vitamin D and 25(OH)D levels are dependent upon several factors: cutaneous production of vitamin D3, dietary intake and intestinal absorption of D3 and D2, and the metabolic activation and subsequent conversion of vitamin D to its metabolites for excretion. Vitamin D is a secosteroid hormone that is made in the skin from 7-dehydrocholesterol upon exposure of the skin to UV-B radiation. Vitamin D is also obtained in the diet primarily from vitamin D fortified foods or by the use of vitamin D supplements [10]. However, several studies have reported differences in the bioavailability of vitamin D supplements in some populations [11]. Decreased bioavailability may be due to altered absorption of vitamin D from the small intestine or it may be due to altered metabolism of vitamin D in the body. Intestinal malabsorption disorders may cause a decrease in vitamin D absorption due to a decreased ability to absorb lipids. Obesity has also been found to be associated with decreased 25(OH)D levels and may reflect the larger body volume of obese individuals or the sequestration of vitamin D in excess adipose tissue [9].

The two REDS I highlight POINT OUT the failure almost as PROOF of the Gross Negligence.

(1) Vitamin D is not "made in the skin" near as I see it, but more like FOUND-IN/Delivered TO the the skin upon UV interaction. Why can't it be that FAT is a PROTECTIVE MECHANISM of the SKIN, and that VITAMIN D is PART OF THIS PROCESS?!?!? SHOW ME THE MONEY..! They can't.!! They can NOT prove whether or not vitamin D is coming from fat delivered to the skin, or MAGICALLY MANIFESTED BY SKIN CELLS. Last time I heard, if you took some skin cells which have/or don't have Vit D present, ITS NOT POSSIBLE to PROVE how the VIT D is generated... Or should I say "SYNTHESIZED"..!

(2) Vitamin D is FAT RELATED. Folks LESS LIKELY to GIVE UP that FAT may just be inclined to be less likely to have FAT IN THE SKIN TO MAKE VIT D....! This WILL CORRELATE i GUARANTEE.....

(3) I still say let me see a correlation of guys getting sun and guys not with relation to heart clogg type disease.

(4) I further wonder why all the hubbub in the past about Vitamin E and its positive attributes to skin if applied to the skin cutaneously...! I'm reading a bottle of my wifes FAT ASS RUB right now and I see Vitamin E. But NEVER have I seen a bottle of skin lotion with Vitamin D...!

APPARENTLY THE NOTION DOES NOT EXIST....! This is real funny as I am having great success removing a chemical burn scar/darkening with D3 application, and not much of it applied to date. It happens to be an awsome lube as well. MUCH BETTER than Vit E which becomes STICKY HARD and ALL KINDS OF NASTY IN A HURRY.. Sound familiar like your heart feels after gobbling that 800iu trifecta from U-NO-WHO...! I'm Planning to lube her twat with it today. I may even jamb some down in my prostate for a while... LOL :drooling:

Heres a popular brand at CVS...
Water, Glycerin, Stearic Acid, Glycol Stearate, Isopropyl Palmitate, Petrolatum, Aloe Barbadensis (Aloe Vera) Leaf Juice, Cucumis Sativus (Cucumber) Extract, Helianthus Annuus (Sunflower) Seed Oil or Glycine Soja (Soybean) Oil, Glycine Soja (Soybean) Sterol, Sodium Stearoyl-2-Lactylate, Tocopheryl Acetate (Vitamin E Acetate), Retinyl Palmitate (Vitamin A Palmitate), Sodium Acrylate/Acryloyldimethyl Taurate Copolymer, Dimethicone, Glyceryl Stearate, Cetyl Alcohol, Lecithin, Mineral Water, Sodium PCA, Potassium Lactate, Lactic Acid, Collagen Amino Acids, Urea, Fragrance, Triethanolamine, DMDM Hydantoin, Iodopropynyl Butylcarbamate, Disodium EDTA, Titanium Dioxide (CI 77891)

Heres one sold at Walgreens...
this oil-free lotion works to provide skin with an instant natural glow. It combines 48HR moisture with Broad Spectrum UVA/ UVB SPF 25 Protection. Our skin-softening formula is infused with the antioxidant Vitamin E and a lightweight-hydrating ingredient for moisture that feels clean & barely there

Heres one from WalMart... (pricey)
Active Ingredients: Homosalate (8.0%)(sunscreen), Avobenzone (3.0%)(UVA Sunscreen - YOU are the BETA), Octocrylene(now heres an interesting one - Octocrylene is an organic compound used as an ingredient in sunscreens and cosmetics. It is an ester formed by the condensation of a diphenylcyanoacrylate with 2-ethylhexanol. It is a viscous, oily liquid that is clear and colorless.
The extended conjugation of the acrylate portion of the molecule absorbs UVB and short-wave UVA (ultraviolet) rays with wavelengths from 280 to 320 nm,[1] protecting the skin from direct DNA damage. The ethylhexanol portion is a fatty alcohol, adding emollient and oil-like (water resistant) properties.
This organic compound can penetrate into the skin where it acts as a photosensitizer. This results in an increased production of free radicals under illumination.[2] Free radicals are known to induce indirect DNA damage, and an increased concentration of free radicals might have contributed to the increased incidence of malignant melanoma in sunscreen-users compared to non-users (2.25%), Ensulizole (2%)( Best yet - Other HIGH concerns: Biochemical or cellular level changes
About ENSULIZOLE: Known to produce free radicals when exposed to sunlight, leading to damage of DNA, this UVB protector may have the potential to cause cancer. Function(s): Sunscreen Agent; Ultraviolet Light Absorber; UV ABSORBER; UV FILTER. Also Contains: Water, Glycerin, Niacinamide, Isopropyl Lauroyl Sarcosinate, Nylon-12(nylon), Dimethicone(silicone), Isopropyl Isostearate(FAT), Triethanolamine(poison somewhere between ammonia and alcohol), Palmitoyl Dipeptide-7(Vit A Derivative), Palmitoyl Pentapeptide-4(fatty Solvent/carrier), Carnosine, Panthenol, Tocopheryl Acetate(Vit E), Sodium Acrylate/Sodium Acryloyldimethyl Taurate Copolymer(hardner/stabilizer), Isohexadecane(Petroleum), Pentylene Glycol, Titanium Dioxide, Stearyl Alcohol, Cetyl Alcohol, Polysorbate 80, PEG-100 Stearate, Methylparaben, Carbomer, Ethylparaben, Propylparaben, Cetearyl Alcohol, Cetearyl Glucoside(emulsifier/"mixer), Disodium EDTA, Sodium Ascorbyl Phosphate, PEG-4 Dilaurate, PEG-4 Laurate, PEG-4, Decyl Glucoside, Lactic Acid, Ammonium Polyacrylate, Benzyl Alcohol, Iodopropynyl Butylcarbamate(Preservative, "bioicide" and on the verge of OUTLAW), Dimethiconol(silicon / Anti'foamer), Behenyl Alcohol, Stearic Acid, BHT.

Grossmann RE, Tangpricha V. Evaluation of vehicle substances on vitamin D bioavailability: a systematic review. Mol Nutr Food Res 2010;54(8):1055-61. Evaluation of vehicle substances on vitamin D bioavailability: A systematic review

Vitamin D insufficiency is a common medical condition. Vitamin supplements can be ingested to improve vitamin D status. It is not known if the vehicle substance that is combined with the vitamin D tablet influences the bioavailability of vitamin D. The purpose of this review is to examine the impact of different vehicles on vitamin D bioavailability. A comprehensive literature search identified studies that directly compared the absorption of vitamin D from two or more vehicles. The change in mean serum 25(OH)D per average daily dose of vitamin D supplemented was calculated and compared among the studies. We identified four clinical studies that compared two different vehicles of vitamin D. Vitamin D in an oil vehicle produced a greater 25(OH)D response than vitamin D in a powder or an ethanol vehicle in healthy subjects. There are limited studies that have compared the influence of the vehicle substance on vitamin D bioavailability. Future studies should examine bioavailability among different vehicle substances such as oil, lactose powder, and ethanol and examine if there are any differences in bioavailability among different patient populations including those with fat malabsorption.

 

[Michael Scally MD]

Perna L, Schöttker B, Holleczek B, Brenner H. Serum 25-hydroxyvitamin D and incidence of fatal and nonfatal cardiovascular events: a prospective study with repeated measurements. J Clin Endocrinol Metab 2013;98:4908-15. http://press.endocrine.org/doi/full/10.1210/jc.2013-2424

Context: Several studies suggested that low serum concentrations of 25-hydroxyvitamin D (25(OH)D) are associated with an increased risk of cardiovascular disease (CVD). However, the evidence is still inconclusive, mostly based on CVD mortality and studies with single 25(OH)D measurements.

Objective: We aimed to assess the association of 25(OH)D with fatal and nonfatal CVD in the same study population, using repeated 25(OH)D measurements and competing risks analysis.

Design: This was a population-based cohort study (ESTHER study, baseline 2000–2002). Follow-up data, including survival status, were collected after 2, 5, and 8 years. The response rate for survival was 99.9%.

Setting: Participants were recruited during a health screening examination by their general practitioners. 25(OH)D was measured in blood samples collected at baseline and the 5-year follow-up visit.

Patients or Other Participants: A total of 9949 men and women, aged 50 to 74 years at baseline, with sufficient knowledge of the German language and resident in the German state of Saarland were included in the study.

Main Outcome Measures: Outcomes included CVD, coronary heart disease (CHD), and stroke, in total and differentiated into fatal and nonfatal events.

Results: Overall, 854 study participants had a nonfatal and 176 a fatal CVD event during 8 years of follow-up. Comparing subjects with 25(OH)D levels below 30 nmol/L and above 50 nmol/L resulted in a hazard ratio of 1.27 (95% confidence interval = 1.05–1.54) for total CVD and 1.62 (95% confidence interval = 1.07–2.48) for fatal CVD in a model adjusted for important potential confounders. No significant association for nonfatal CVD was observed. In dose-response analysis, we observed an increased cardiovascular risk at 25(OH)D levels below 75 nmol/L. Results for CHD and stroke were comparable to the results obtained for the composite outcome CVD.

Conclusions: Our results support evidence that low 25(OH)D levels are associated with moderately increased risk of CVD and indicate that the observed association is much stronger for fatal than for nonfatal events.

 

[BBC3]

I thought this was a good site...

http://smartypantsvitamins.com/vitamin-d-supplements-does-the-source-matter/

I had recently posed the issue "why is vitamin D3 not included in most skin lotions"... Apparently Vitamin D3 is derived technically from either Sheeps Skin fat (Lanolin), or fish oil - As manufactured via whatever industrial processing is involved. So Lanolin in lotion is the fat source, and I guess they are making some speculation as to whether the lanolin will make a conversion to D3 once applied and exposed to sun.?/ Thats a good question..

But one point would be that it appears valuable to determine the source of the FAT for D3 manufacture in YOUR D3 supplement, as you obviously become potentially liable to any contaminants in the particular animal (Mercury from Fish oil, etc...) I HAVE noted a difference in color and viscosity in the two oils I have uncapped to apply to skin. And WHO KNOWS where they are farming the sheep to get the lanolin for processing, and WHAT the sheep are fed or exposed to. I somehow get this vision of a bunch of animals herded up in a trough eating their own shit, as opposed to Swedish sheep shaggers with loving mates cared for in the Alps.... LOL

So the answer to the question - WHY is Vitamin D3 not found in lotions WOULD APPEAR to be simply that due to being a fat soluble oil/VITAMIN, the industry is not going to take any potential risk of Overdosing you on Vitamin D3 thru skin absorption (and you know some chicks can lay on some Lotion..!)