Miracon Science

NSAID

Specially affected active substances and pharmaceuticals

Name of active substance Trade name Affected micronutrients
Acetylsalicylic acid Aspirin®, Thrombo ASS® Vitamin C
Acetaminophen Mexalen®, ben-u-ron® Nicotinamide
N-acetylcysteine

 

Mechanism of interaction

Mechanism of interaction
Vitamin C The sodium-dependent transport of vitamin C through the intestinal wall is inhibited by salicylates. This results in an increased excretion of vitamin C in urine and feces. This results in a decrease of vitamin C levels in tissue, gastric juice and plasma. At the same time a concomitant administration of vitamin C and ASA shows a protective effect on the gastric mucosa.
Folic acid/
Vitamin B12		 Gastrointestinal damage interferes with bioavailability and absorption. Acetylsalicylic acid increases the excretion of folic acid.
Iron Impairment of iron absorption with long-term use. The reason for this is occult gastrointestinal bleeding when taken chronically.
Nicotinamide Nicotinamide is present in the body as NAD. Damage to liver cells caused by paracetamol increases NAD consumption.
N-acetylcysteine N-acetylcysteine stimulates glutathione biosynthesis. This results in hepatocellular detoxification of paracetamol.
Vitamin E Vitamin E regulates the arachidonate metabolism. Taking NSAID at the same time has an additive effect.
Potassium The impairment of renal function when taking NSAID may cause an increase in serum potassium levels. This can lead to hyperkalemia.
Chondroprotective drugs D-Glucosamine is the basic building material of cartilage. Anabolic processes in the cartilage are stimulated and catabolic processes are reduced. They have a synergistic effect with NSAID.
Glutamine L-glutamine is the main energy substrate of the cells of the gastrointestinal tract. It is used to maintain normal intestinal function. L-glutamine protects the gastrointestinal mucosa.
Omega-3 fatty acids Act synergistically. EPA inhibits the formation of proinflammatory enzymes.

 

Consequences and possible symptoms of the interaction

Negative consequences of the interaction Possible symptoms

Vitamin C

 Decrease in vitamin C levels
  • Increased risk of oxidatively induced damage to the gastric mucosa
Folic acid/
Vitamin B12
 		 Decrease in the folic acid/
Vitamin B12-levels
 
  • Increase in homocysteine level
Iron Decrease in iron level
  • Fatigue, reduced performance, increased sensitivity to cold
  • Iron deficiency anemia (hypochromic microcytic anemia), increased lactate levels
  • Pale skin, rhagades  at corner of the mouth, glossitis, dysphagia (swallowing disorders)
  • Brittle nails, diffuse hair loss
Nicotinamide Decline of NAD level
  • Energetic state decreases
  • Hepatocellular necrosis or apoptosis
Potassium Increase in potassium level
  • Increased risk of muscle weakness
  • Bradycardia or AV block
Positive consequences of the interaction Possible symptoms
N-acetylcysteine Liver cell protection
  • Improvement of liver detoxification
Vitamin E Synergistic effect with NSAIDs
  • Support the anti-inflammatory effect
  • Depression of gastrointestinal side effects
  • Reduction of NSAID dose possible
Chondroprotective drugs Synergistic effect with NSAIDs
  • Less gastrointestinal discomfort due to NSAID reduction
Glutamine Improvement of NSAID compatibility
  • Less gastrointestinal discomfort due to NSAID reduction
Vitamin C Mucosal protection
  • Less gastrointestinal side effects
Omega-3 fatty acids Synergism
  • Lowering the need for medication and the side effects

 

Recommended Supplementation

Medical substance Recommended supplementation Dosage
NSAID Vitamin C 0.5–2 g/d p.o.
Folic acid 0.6–1 mg/d p.o.
Vitamin B12 100–1000 µg/d p.o.
Iron (Vegyferrin) 50–200 mg /d p.o.
Omega-3 fatty acids 30–35 mg EPA/DHA/kg BW/d
p.o.

 

Special instructions for use

Name of active substance Instructions for use
Vitamin C Simultaneous intake of ASA and vitamin C prevents deficiency symptoms.

Folic acid

Vitamin B12

 

 Recording of the homocysteine value in via laboratory diagnostics
Iron Time interval of two to three hours between NSAID and iron intake; simultaneous vitamin C intake for improved iron absorption and tolerance.

 

References

References
1.Abate A, Yang G, Dennery PA, Oberle S, Schröder H: Synergistic inhibition of cyclooxygenase-2 expression by vitamin E and aspirin. Free Radic Biol Med. 2000 Dec; 29(11): 1135–42.
2.Ann JY, Kim SJ, Han SP, Kim JW, Kim HJ, Do JH, Kim JG, Chang SK, Jeon WK: Effect of glutamine on the non-steroidal anti-inflammatory drug-induced bacterial translocation. Korean J Gastroenterol. 2004 Nov; 44(5): 252–8.
3.Becker JC, Grosser N, Boknik P, Schröder H, Domschke W, Pohle T: Gastroprotection by Vitamin C – a heme-oxygenase-1-dependent mechanism? Biochem Biophys Res Commun. 2003 Dec 12; 312(2): 507–12.
4.Cleland LG, James MJ, Proudman SM: The role of fish oils in the treatment of rheumatoid arthritis. Drugs. 2003; 63(9): 845–53.
5.Gröber, Uwe: Mikronährstoffe: Metabolic Tuning – Prävention – Therapie. 3., völlig überarb. u. erw. Aufl. Stuttgart: WVG, 2011.
6.Gröber, Uwe: Arzneimittel und Mikronährstoffe: Medikationsorientierte Supplementierung. 3., akt. und erw. Aufl. Stuttgart: WVG, 2014.

 

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