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home:pathogenesis:vitamind:correlation [01.03.2012] – external edit 127.0.0.1home:pathogenesis:vitamind:correlation [10.13.2018] – [Researchers should also measure 1,25-D] sallieq
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-Many vitamin D studies suffer from methodological errors including [[home:pathogenesis:vitamind:observational_bias|bias inherent to using self-selected subjects]] and [[home:pathogenesis:vitamind:longterm|insufficient followup]], but perhaps their most egregious liability comes in mistaking correlation for causation. +Many vitamin D studies suffer from methodological errors including [[home:pathogenesis:vitamind:observational_bias|bias inherent to using self-selected subjects]] and [[home:pathogenesis:vitamind:longterm|insufficient followup]], but perhaps their most egregious liability comes in mistaking correlation for causation. (({{pubmed>long:27610068}}))
  
 It's undisputed that a wide array of studies point to the fact that 25-hydroxyvitamin D (25-D) – typically referred to in the media as vitamin D – is low in people with numerous chronic inflammatory diseases. However, these studies fail to prove that low 25-D //causes// disease. Even so, some studies assume that doubling serum levels of 25-D would drastically reduce mortality.(({{pubmed>long:21731036}})) It's undisputed that a wide array of studies point to the fact that 25-hydroxyvitamin D (25-D) – typically referred to in the media as vitamin D – is low in people with numerous chronic inflammatory diseases. However, these studies fail to prove that low 25-D //causes// disease. Even so, some studies assume that doubling serum levels of 25-D would drastically reduce mortality.(({{pubmed>long:21731036}}))
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 One of the reasons that 1,25-D isn't measured may be that it is harder to test. But another reason may be that a high 1,25-D is inconsistent with reports of vitamin D "deficiency." How can patients be said to be "deficient" in vitamin D when one of its metabolites, 1,25-D, is often several standard deviations greater than normal? One of the reasons that 1,25-D isn't measured may be that it is harder to test. But another reason may be that a high 1,25-D is inconsistent with reports of vitamin D "deficiency." How can patients be said to be "deficient" in vitamin D when one of its metabolites, 1,25-D, is often several standard deviations greater than normal?
  
-{{tag>Study_Design}}+ 
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 +{{tag> Science_behind_vitamin_D Study_Design}}
  
  
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 ===== Notes and comments ===== ===== Notes and comments =====
  
-  * Legacy content +  * Jigsaw suggests: 
-    *+    * "There are hundreds of reports of groups of sick people who have low vitaminD status, that is low levels of serum 25D as compared with healthy controls. Very few of these studies have also measured 1,25D. Some of those that have found an even better correlation between sickness and high 1,25D than between sickness and low 25D. 
 + 
 +The best illustration of the chain of causation in relation to D levels and sickness is the study below where the sick group was otherwise healthy young adults who had knee reconstructions. 
  
 +Circulating interferon-γ correlates with 1,25(OH)D ... [Cytokine. 2012] - PubMed - NCBI 
 +Circulating interferon-γ correlates with 1,25(OH)D and the 1,25(OH)D-to-25(OH)D ratio.
 +Barker T, Martins TB, Kjeldsberg CR, Trawick RH, Hill HR.
 +Source The Orthopedic Specialty Hospital, Murray, UT 84107, USA. tyler.barker@imail.org
 +Abstract The mechanism responsible for the decrease in vitamin D status (i.e., plasma or serum 25-hydroxyvitamin D (25(OH)D) concentration) during inflammatory stress is unknown in humans. Interferon (IFN)-γ is an inflammatory cytokine that regulates vitamin D metabolism in isolated immune cells, but data suggesting this regulation exists in vivo is lacking. The purpose of this study, therefore, was to associate circulating IFN-γ perturbations with 25(OH)D and 1,25-dihydroxyvitamin D (1,25(OH)D) alterations during inflammatory stress in young adults recovering from anterior cruciate ligament (ACL) reconstruction. Plasma 25(OH)D, 1,25(OH)D and IFN-γ concentrations were measured in fasting blood draw samples obtained from twelve-male patients pre-surgery and 90-m, 3-d and 7-d post-surgery. 25(OH)D decreased significantly (p<0.05) after surgery, and strikingly, tended to inversely correlate (r=-0.32, p=0.058) with IFN-γ changes from pre- to post- (i.e., 90-m, 3-d, and 7-d) surgery. Additionally, 1,25(OH)D (r=0.37, p<0.05) and the 1,25(OH)D-to-25(OH)D ratio (r=0.52, p<0.05) changes from pre- to post- (i.e., 90-m, 3-d, and 7-d) surgery correlated with those of IFN-γ. These are the first reported in vivo findings suggesting that the 25(OH)D decrease and conversion to 1,25(OH)D increase with increasing IFN-γ in the circulation. We conclude that IFN-γ contributes to the decrease in vitamin D and the conversion of vitamin D to its active hormonal form in the circulation during inflammatory insult in humans.
 +Last edited on 18 Jul 2013 04:46 pm by Jigsaw
  
 ===== References ===== ===== References =====
home/pathogenesis/vitamind/correlation.txt · Last modified: 09.14.2022 by 127.0.0.1
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