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- This Natural Source of Vitamin A, D, and Omega 3s May Help Crohns
- Medications That May Interact with Ablene
- The Role of Probiotics in a Damaged Gut
- Tips for Managing Crohns
- Fiber with Crohns: A Double-Edged Sword
- Eat These Foods To Heal Your Gut
- Inflammatory Bowel Disease & L-glutamine
- Magnesium Status in Crohns Disease
- NAG for Crohns
Does Taking Zinc Help Your Crohns? Find Out.
Zinc is a component of a number of important enzymes including antioxidant enzymes like superoxide dismutase. It is also stored in multiple locations in the body. Given the importance of this mineral, zinc deficiency can cause serious complications in Crohn’s disease. Besides correcting zinc deficiency with zinc supplements, are there other ways zinc may help Crohn’s disease? Read on to find out how zinc promotes healing in Crohn’s disease; the relationship between zinc and leaky gut; and how zinc supplementation can keep you in remission.
by Brad Chase
Although required only in trace amounts, zinc is an essential mineral for humans. It has several important roles in the body. To highlight its importance in human metabolism, zinc is a component of over 300 enzymes.
The body keeps a store of 2 – 4 g of zinc. This amount of zinc is stored in various locations including the brain, prostate gland, muscles, kidneys, liver and bones.
Zinc is also important to the production of proteins as well as the utilization of genetic materials.
This trace mineral is essential to different processes in the body including wound healing, memory formation and sensory perception.
Dietary sources of zinc include red meat, seafood, wheat, seeds, nuts, dried beans, whole grains and certain fruits.
Zinc can also be found in fortified foods and in dietary supplements.
Zinc deficiency is uncommon in the general population in developed countries but it commonly affects those with certain chronic diseases. This deficiency can be caused by low zinc intake from diet. However, it is also caused by malabsorption and disease in organs known to store the mineral.
Besides people living with chronic diseases, those at the highest risk of zinc deficiency include children and the elderly.
Mild zinc deficiency can impair the body’s immune system. Therefore, low zinc level can contribute to Crohn’s disease since this inflammatory bowel disease is caused by impaired innate immunity.
The most common cause of zinc deficiency in people suffering from Crohn’s disease is diarrhea.
The increased bowel movement caused by diarrhea empties the contents of the gastrointestinal tract before macronutrients and micronutrients can be absorbed. Therefore, dietary sources of zinc as well as oral zinc supplements may fail to raise serum zinc levels.
Strangely, diarrhea is one of the first presentations of zinc deficiency. Therefore, zinc deficiency in Crohn’s disease has a tendency to perpetuate itself in a vicious circle.
Besides diarrhea, other factors may impair the absorption of zinc in the gastrointestinal tract. For example, surgical removal of sections of the intestine and inflamed lesions in the gut can reduce the amount of zinc absorbed.
Therefore, Crohn’s disease and its treatment can cause zinc deficiency.
Zinc deficiency is especially common among children diagnosed with Crohn’s disease. Unfortunately, zinc deficiency is most dangerous in this age group as it can significantly slow down growth and sexual maturity as well as increase the risks of certain chronic diseases.
To treat zinc deficiency in Crohn’s disease, it is best to first stop diarrhea.
Once this is achieved, both dietary sources of zinc and oral zinc supplements can be used to raise the amount of zinc stored in the body.
Because the plasma level of zinc is dependent on vitamins A and D, vitamin A and D deficiencies must also be addressed if present along with zinc deficiency. Studies show that vitamin D deficiency is actually common among people living with Crohn’s disease.
Therefore, vitamins A and D supplements should be added to zinc supplements in order to prevent secondary zinc deficiency.
A 1977 study published in the journal, Digestion, investigated the nature of zinc deficiency in Crohn’s disease. The researchers used different measures of zinc levels in the body to determine zinc status in 30 patients with Crohn’s disease.
The results showed that compared to healthy controls, Crohn’s disease patients had lower plasma zinc concentrations and that their sense of taste was affected by low zinc levels.
In addition, hair zinc content (a common measure of zinc status) was lower in patients with Crohn’s disease.
Lastly, the results of the study showed that plasma albumin was also lower in Crohn’s disease patients than the controls. This finding suggests that low levels of this binding protein may contribute to low plasma zinc levels in Crohn’s disease.
A 1988 study published in the Journal of the American College of Nutrition also determined zinc status in a group of 30 patients with Crohn’s disease and 19 healthy controls.
In this study, the researchers measured the concentrations of zinc in plasma, red blood cells, muscle and urine.
The results of the study showed that Crohn’s disease patients had lower plasma and red blood cells zinc levels but the zinc concentration in their muscles and urine were comparable to healthy subjects.
This result suggests that zinc deficiency in Crohn’s disease takes the form of zinc depletion within cells.
Another study published in 1988 but in the journal, Digestive Diseases and Sciences, determined the relationship between zinc bioavailability and the severity of Crohn’s disease.
For this study, 10 patients with Crohn’s disease (5 of them had active Crohn’s disease while the other 5 were in remission) were recruited.
The researchers found that serum zinc levels were lower in the patients with active Crohn’s disease than those with the inactive form of the disease. In fact, patients in the latter group had serum zinc levels comparable to those of the health participants in the control group.
Furthermore, the excretion of zinc from the body was found to be higher in those with active disease than those in remission.
The results of this study suggests that zinc deficiency in Crohn’s disease is likely caused by the high turnover of the mineral rather than impaired absorption in gastrointestinal tract.
A previous study (1981) published in the same journal found out that the severity of Crohn’s disease was directly related to the rate of zinc clearance from the body.
A 1980 study published in the journal, Gut, closely investigated the effect of malabsorption on zinc status in Crohn’s disease.
First, the researchers established that serum zinc levels were lower in patients suffering from Crohn’s disease than in healthy subjects. Then they found that patients with low serum zinc levels also have low serum albumin levels.
However, they cautioned against using albumin levels to determine zinc deficiency in Crohn’s disease because it is very likely that the body responds to low serum zinc levels by lowering the production of albumin, its carrier protein.
After investigating the absorption of zinc in the control group and Crohn’s disease patients, the researchers found that zinc is poorly absorbed in the patients (9 – 45%) than in healthy subjects (38 – 75%).
This study shows that the malabsorption of zinc is also an important factor contributing to zinc deficiency in Crohn’s disease.
A 1987 study published in the journal, Hepatogastroenterology, examined another aspect of zinc distribution in Crohn’s disease.
In this study, the researchers investigated whether the malabsorption of zinc in the intestine is caused by a defect in the transportation of the mineral across the intestinal membrane.
By challenging the brush border membrane vesicles of 20 Crohn’s disease patients and 7 healthy subjects with zinc, sodium, D-glucose and D-mannitol, the researchers presented a clearer picture of the mechanism of zinc transport during its absorption.
The vesicles challenged are found in the jejenum. They are known vehicles of zinc absorption.
The results of the study showed that the absorption of zinc across these vesicles was impaired in 40% of the patients with Crohn’s disease even though the rates of absorption of sodium, glucose and mannitol were unaffected.
A 2004 study published in the journal, Pediatric Research, investigated the differences in zinc absorption, fecal and urinary excretion as well as plasma levels between adolescents with Crohn’s disease and healthy subjects.
The researchers recruited 15 adolescents (8 – 18 years) with stable Crohn’s disease as well as 15 matched controls.
In the course of the study, the participants were placed on zinc-rich diets and also given oral and intravenous zinc supplements.
The results of the study showed that both zinc absorption and zinc plasma levels were significantly lower in the participants with Crohn’s disease compared to the control. However, fecal and urinary excretion of zinc remained the same in both groups.
The results of this study showed that zinc was being poorly absorbed in Crohn’s disease even as the body did not lower its clearance. The result of this imbalance was lower plasma zinc levels in Crohn’s disease.
A 1998 paper published in the Journal of Gastroenterology detailed the case of a woman who suffered from zinc deficiency induced by Crohn’s disease.
The authors of the paper reported that the patient developed acrodermatitis enteropathica (a skin condition) and decreased visual acuity (poor eyesight) while she was receiving total parenteral nutrition.
These conditions were recognized as signs of zinc deficiency. Therefore, she was given intravenous zinc supplement. This corrected the zinc deficiency as well as the skin and eye conditions caused by low zinc level.
A 2003 study published in the journal, Andrologia, investigated another aspect of zinc deficiency in Crohn’s disease.
The researchers found that zinc deficiency in men with Crohn’s disease contributes to low sperm count and male infertility.
It is well known that the highest store of zinc in the body is found in the prostate organ. Furthermore, zinc is needed for the production and release of sperm. Therefore, there is a need to closely monitor zinc status in men with Crohn’s disease.
In a 1991 study published in the journal, Gut, the effect of zinc deficiency on antioxidant proteins and inflammation in Crohn’s disease was investigated.
Because zinc and copper are components of antioxidant enzymes such as superoxide dismutase and metallothionein, zinc deficiency may open the gastrointestinal tract to free radical damage.
The researchers recruited 29 patients with Crohn’s disease and 12 patients with ulcerative colitis. The control group included 18 patients with colorectal cancer.
The results of the study showed that patients with Crohn’s disease and ulcerative colitis presenting with inflamed gastrointestinal mucosa had lower levels of superoxide dismutase. Metallothionein levels were reduced in patients with inflamed and non-inflamed mucosa.
This result suggests that zinc deficiency can reduce the levels of certain antioxidant enzymes dependent on the mineral. Therefore, the deficiency reduces the antioxidant cover of the gastrointestinal tract and raises the damage done by oxygen radicals.
All of these results show that zinc deficiency can worsen the gastrointestinal inflammation associated with Crohn’s disease.
The use of copper-zinc superoxide dismutase as an anti-inflammatory agent in the treatment of Crohn’s disease was strongly considered. In fact, a phase II trial of the drug completed successfully.
While zinc is often used in the management of Crohn’s disease chiefly to treat zinc deficiency, there are indications that it could serve other purposes.
A 2001 study published in the journal, Inflammatory Bowel Diseases, investigated the possibility of using zinc supplements to tighten “leaky gut” and prevent Crohn’s disease from reactivating.
“Leaky gut” is the term used to describe increased permeability in the small intestine. It is commonly experienced by patients with Crohn’s disease who are most likely to experience relapse.
For this study, the researchers recruited 12 Crohn’s disease patients who had been in remission in the last 3 months but had experienced “leaky gut” within the last 2 months. These patients were given 110 mg of oral zinc sulfate 3 times daily for 8 weeks. They were then followed up for 12 months.
The results showed that 10 out of the 12 patients did not experience “leaky gut” and had no relapse. One patient experienced increased intestinal permeability but did not relapse while the last patient relapsed.
The researchers concluded that zinc supplementation is advised for patients with Crohn’s disease in remission in order to reduce the odds of relapse.
They also believed that zinc was effective because it improved intestinal barrier function.
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