Low Sun Exposure and Vitamin D Deficiency as Risk Factors for Inflammatory Bowel Disease, With a Focus on Childhood Onset.
Photochem Photobiol. 2018 Aug 29. doi: 10.1111/php.13007. [Epub ahead of print]
Holmes EA1, Rodney Harris RM1, Lucas RM1,2.
1 National Centre for Epidemiology and Population Health, Research School of Population Health, The Australian National University, Canberra, Australia.
2 Centre for Ophthalmology and Visual Science, University of Western Australia, Perth, Australia.
- IBD in children might be associated with low sun exposure – Aug 2018
- Inflammatory Bowel Disease in children is associated with low Vitamin D, Iron (also low Zinc for Crohn’s) – Aug 2018
- Crohn's disease in black children is worse in 6 ways – Dec 2015
- Obese children with celiac disease had lower levels of vitamin D – April 2012
Overview Gut and vitamin D has the following summary
- Gut problems result in reduced absorption of Vitamin D, Magnesium, etc.
- Celiac disease has a strong genetic component.
- Most, but not all, people with celiac disease have a gene variant.
- An adequate level vitamin D seems to decrease the probability of getting celiac disease.
- Celiac disease causes poor absorption of nutrients such as vitamin D.
- Bringing the blood level of vitamin D back to normal in patients with celiac disease decreases symptoms.
- The prevalence of celiac disease, not just its diagnosis, has increased 4X in the past 30 years, similar to the increase in Vitamin D deficiency.
- Review in Nov 2013 found that Vitamin D helped
- Many intervention clinical trials for vitamin D to prevent or treat Gut problems (93 trials listed as of Jan 2017)
- All items in category gut and vitamin D
Gut category listing contains the following
130 items in GUT category - see also Overview Gut and vitamin D,
- "Ulcerative Colitis" OR UC 689 items March 2019
- "celiac disease" OR CD 1280 items Feb 2018
- "inflammatory bowel disease" OR "inflammatory bowel symptom" 1010 items as of March 2019
- Crohn's 1230 items as of Feb 2019
- Gut-Friendly forms of vitamin D
such as: bio-emulsion, topical, spray, sublingual, inhaled, injection . .
Overview Gut and vitamin D contains gut-friendly informationGut-friendly, Sublingual, injection, topical, UV, sunshine
Getting Vitamin D into your body has the following chart
Getting Vitamin D into your body also has the following
Bio-D-Mulsion Forte – especially made for those with poorly functioning guts, or perhaps lacking gallbladder
Sublingual – goes directly into bloodstream
Oil: 1 drop typically contains 400 IU, 1,000 IU, or 4,000 IU, typically not taste good
Topical – goes directly into bloodstream. Put oil on your skin, Use Aloe vera cream with Vitamin D, or make your own
Vaginal – goes directly into bloodstream. Prescription only?
Bio-Tech might be useful – it is also water soluble
Vitamin D sprayed inside cheeks 2X more response (poor gut) – RCT Oct 2015
and, those people with malabsorption problems had a larger response to spray
Inject Vitamin D quarterly into muscle, into vein, or perhaps into body cavity if quickly needed
Nanoparticles could be used to increase vitamin D getting to the gut – Oct 2015
Liposomal form on Amazon - Dec 2015
$20 for 60 servings of 2500 IU - unsure why a very low-cost gut-friendly form should not be used instead
Poor guts need different forms of vitamin D has the following
Guesses of Vitamin D response if poor gut
Bio Form Speed Duration 10 Injection: Vitamin D,
or Calcidiol or Calcitriol
Fast Long 10 Sun/UV Slow Long 10 Topical
(skin patch/cream, vagina)
Slow Normal 9? Inhaled (future) Fast Normal 8 Bio-D-Mulsion Forte Normal Normal 6 Water soluble (Bio-Tech) Normal Normal 5 Nanoemulsion
perhaps activates VDR
Normal Normal 4 Sublingual/spray
(some goes into gut)
Fast Normal 3 Coconut oil based Slow Normal 2 Food (salmon etc.) Slow Normal 2 Olive oil based (majority) Slow Normal
10= best bioavailable, 0 = worst, guesses have a range of +-2
Speed: Fast ~2-6 hours, Slow ~10-30 hours
Duration: Long ~3-6 months, Normal = ~2 months
The incidence and prevalence of inflammatory bowel disease (IBD) are increasing worldwide. Some ecological studies show increasing incidence with increasing latitude. Ambient ultraviolet radiation varies inversely with latitude, and sun exposure of the skin is a major source of vitamin D. Vitamin D deficiency is common in patients with IBD. Sun exposure and vitamin D have immune effects that could plausibly reduce, or be protective for, IBD. One quarter of new IBD cases are diagnosed in childhood or adolescence, but most research is for adult-onset IBD.
Here we review the evidence for low sun exposure and/or vitamin D deficiency as risk factors for IBD, focusing where possible on pediatric IBD, where effects of environmental exposures may be clearer.
The literature provides some evidence of a latitude gradient of IBD incidence, and evidence for seasonal patterns of timing of birth or disease onset are inconsistent. High prevalence of vitamin D deficiency occurs in people with IBD, but cannot be interpreted as being a causal risk factor. Evidence of vitamin D supplementation affecting disease activity is limited. Further research on pre-disease sun exposure and well-designed supplementation studies are required to elucidate whether these potentially modifiable exposures are indeed risk factors for IBD.
Conclusions – from PDF
Inflammatory bowel disease is complex disorder arising from a combination of genetic susceptibility and environmental exposures, including those that change the gut microbiome, resulting in immune activation. Geographic patterns of disease onset suggest a role for environmental factors that vary according to latitude. Sun exposure - either through vitamin D production only, or through a wider range of pathways, has plausible, immune mediated, actions that may reduce the risk of developing IBD. We have shown that, despite support from ecological studies related to latitude, there is little evidence to support increased disease risk according to season of birth or of a season-of-onset effect. Individual-level observational studies show high prevalence of vitamin D deficiency in IBD, but the study designs generally are unable to distinguish between low 25OHD as a risk factor rather than a disease-induced consequence. Further, they are unable to distinguish between sun exposure and vitamin D as risk factors - vitamin D supplementation studies provide limited evidence of benefits for disease activity. Thus, the individual roles of low sun exposure or vitamin D deficiency - if any - in the aetiology of IBD (particularly PIBD) remain unclear.
The incidence and prevalence of IBD are increasing worldwide in both developed and developing countries. Much of what we know about IBD has been determined from studies of adults, yet a quarter of new IBD cases are diagnosed in children or adolescents. There are suggestions from this review that 25OHD levels may be less important in PIBD than IBD, but this will require further studies that are adequately powered. There is very little work on past sun exposure in relation to IBD risk, in pediatric or adult populations. Understanding any differences in disease risk factors between pediatric and adult onset IBD may shed light on the etiology of IBD.
PDF is available free at Sci-Hub 10.1111/php.13007