Health Matters

Ulcerative Colitis - could oral N-Acetyl-Cysteine supplementation help patients?

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Scientists can induce an ulcerative colitis (UC) like condition in rats and pigs by intrarectal administration of acetic acid. The acid damages the colonic epithelial (lining) cells. Damaged cells release inflammatory chemicals in order to inform/warn surrounding tissue cells and bring immune cells into the area to investigate and deal with the cause/s of cell damage. Eventually the death of epithelial cells leads to ulcer formation in the rectum and colon. How acetic acid induces colitis is still unclear, but reactive oxygen species produced by the activated immune system cells plays a significant role.

Glutathione (GSH) is a tripeptide (i.e., a tiny protein.  GSH is made in the liver, which acts as a GSH reservoir. GSH is made from the essential amin acid cysteine. Being ‘essential’ means that cysteine , unlike many other amino acids, can’t be made by our bodies but must be gotten from the diet. Once made GSH is delivered via the blood stream to all body-cells. Inside body-cells it plays a critical role in protecting them against cell-damage from:

  1. immune-system-generated (microbe killing) free radicals.
  2. free radicals generated during energy production by mitochondria.
  3. many other toxins made inside body-cells .
  4. toxic agents from external sources e.g., pollution related chemicals
    1. Nitric oxide
    2. sulphur oxide
    3. cigarette smoke compounds, etc

GSH quickly neutralises these toxic agents.

The maintenance of excellent GSH levels inside cells is key to overcoming the harmful effects of immune system generated free radicals, which can damage and kill cells such as colonic epithelial cells in UC.

So, could cysteine supplementation as N-Acetylcysteine (NAC) help treat UC?

When acetic acid is used to induce ulcerative colitis, giving animals high (500mg/kg) daily oral doses of NAC inhibits:

  1. colonic epithelial cell death
  2. breakdown of normal epithelial layer structure
  3. ulcer formation
  4. formation of:
    1. free radical producing enzymes (and by implication damaging free radicals)
    2. cell death promoting signals (Caspase 3)

and raises the local hormone EGF which promotes colonic-epithelial-cell survival, proliferation, growth and migration to speed ulcer healing (Wang et al, 2013).

A study in humans, by Guijarro et al, (2008), showed that giving UC patients NAC (800mg/day – a much lower dose than used in the animal study above), in addition to 2.4 g/day mesalazine (the standard of care for most UC patients), improved clinical response rates by 50% i.e., 44% of patients responded with clinical improvement with mesalazine-only, while 66% responded to mesalazine plus NAC.

Article Written + Submitted by:

Andreas Klein Nutritionist + Remedial Therapist from Beautiful Health + Wellness
P: 0418 166 269

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