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Chronic Inflammation and Vitamin B-6



Two key metabolic imbalances seen in the creation of the excessive catabolic physiology response are chronic inflammation and deficiencies in B vitamins.1 Therefore, is it possible that the two can somehow be related? According to Midttun et al., in their study on low plasma vitamin B-6 status in cardiovascular patients with systemic inflammation, “Low plasma concentrations of the vitamin B-6 form pyridoxal 5’-phosphate (PLP) [the physiologically active coenzyme form of vitamin B-6] have been reported in patients with high levels of inflammatory markers and with conditions associated with inflammation, including rheumatoid arthritis, cardiovascular disease, and diabetes.”2 Therefore, in my opinion, if C-reactive protein (CRP) levels are elevated, we can most likely assume that vitamin B-6 is depleted. To validate this, Midttun et al. state the following, “94% of participants with PLP below the 5th percentile had increased concentrations of 1 or several markers of inflammation.”2 One might wonder then, what is the relationship between the two and what does this mean for the inflamed patient? According to Cheng et al., in their study on plasma PLP and CRP in coronary artery disease, “CRP, a systemic marker of inflammation, has been shown to be associated with an increased risk of CAD [and] PLP acts as a coenzyme for the production of cytokines and other polypeptide mediators during the inflammatory response.”3 Based on the results of this study by Cheng et al., inflammation expedites low levels of vitamin B-6.3 Also, individuals with low PLP (<20 nmol/L) and high CRP levels (>0.6 mg/dL) are at a further enhanced risk of CAD.3


In my opinion, deficiencies in vitamin B-6 are a derivative of chronic inflammation. Chiang EP et al. corroborate my thinking in their study on the connection between chronic inflammation and vitamin B-6, “Inflammation directly affects vitamin B-6 metabolism differently in different tissues [and] the low vitamin B-6 level is unlikely to be due to a decrease in food intake or the excessive excretion of vitamin B-6.”4 Interestingly enough, Chiang EP et al. bring up a great point that inflammation lowers B-6 status and has nothing to do with diet. In conjunction with Cheng et al., this study also emphasizes the idea that B-6 status is lowered due to chronic inflammation, “A lower pyridoxal 5’-phosphate concentration in the circulation may reflect the removal of B-6 coenzymes from the circulation to meet the higher demands of certain tissues during inflammation.”4 Fundamentally, the body is mobilizing. The body wants B-6 where it needs it to be; however, inflammation takes it away from where it should be and instead uses it in areas where it does not belong. Therefore, the question then arises, is vitamin B-6 going to where it should for one to maintain their overall health? In a different study, Chiang EP et al. focus on using 50 mg of pyridoxine for 30 days as a possible treatment for vitamin B6 deficiency in rheumatoid arthritis patients where the deficiency was potentially caused by chronic inflammation.


The following was conducted from the study, “Although pyridoxine supplementation did not suppress pro-inflammatory cytokine production in patients with rheumatoid arthritis, the suboptimal vitamin B-6 status seen in rheumatoid arthritis can be corrected by 50 mg pyridoxine supplementation for 30 days.”5 Essentially, low levels of vitamin B-6 can be replenished with supplementation, but this will not reduce inflammation or cure the initial reason for the deficiency. In my observation, supplementation of vitamin B-6 can raise serum levels; however, individual nutrients will not reduce the complex metabolic problem. While vitamin B-6 supplementation seems absolutely necessary in the case of rheumatoid arthritis, this is also evidence that our ailing population needs even more.


Assuredly, all of the studies above agree that inflammation will lower B-6 status. What seems to be unclear is whether or not low B-6 can lead to inflammation. Regardless, deficiencies in micronutrients and inflammation will lead to whole body complex interactions.1 In the world of continual stress and non-stress; all complex interactions must be addressed in order for there to be a reduction in allostatic load. It is now clear that deficiencies in B-6 can be replenished, but without addressing the inflammation, the vicious cyclic circle of catabolic physiology will remain.


References


  1. Fish JA & Friedman JM. Metabolic Stress, in Matarese LE & Gottschlich MM eds., Contemporary Nutrition Support Practice: A Clinical Guide, W.B. Saunders Co., Philadelphia, pp. 539-546, 1998.

  2. Midttun et al. Low Plasma Vitamin B-6 Status Affects Metabolism through the Kynurenine Pathway in Cardiovascular Patients with Systemic Inflammation, American Society for Nutrition, Vol. 141, pp. 611-617, 2011.

  3. Cheng et al. Plasma pyridoxal 5’-phosphate and high sensitivity C-reactive protein are independently associated with an increased risk of coronary artery disease, Elsevier, Vol. 24, pp. 239-244, 2008.

  4. Chiang EP et al. Inflammation causes tissue specific depletion of vitamin B-6, Arth Res Ther, Vol. 7, pp. R1254-R1262, 2005.

  5. Chiang EP et al. Pyridoxine supplementation corrects vitamin B-6 deficiency but does not improve inflammation in patients with rheumatoid arthritis, Arth Res Ther, Vol. 7, pp. R1404-R1411, 2005.

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