流行病學研究指出，美國人口當中約有百分之一受乳糜瀉影響。基於此疾病的全球性影響，科學家提出了許多解決方法，其中一個便是使用可分解小麥麩質的酵素。不過，想要評論它的效用，首先需要了解此病多一點。

乳糜瀉是一種腸道疾病，特點是吃過小麥麩質後會引起腸道的免疫反應。它的病理成因是食物中未完全分解的小麥麩質會穿過小腸壁進入血管，繼而激起小腸中的免疫反應，對小腸表面上的絨毛造成破壞。這疾病是由於消化未完的小麥麩質引起免疫反應，因此任何可以分解小麥麩質的干預都可以於某程度上舒緩乳糜瀉的影響。



現今醫學知識的進展令我們知道，對乳糜瀉病人來說，最具致病性的是小麥麩質中最多脯胺酸和穀胺醯胺的部分。因此，現在最多出現在營養補充品中和科學家最多研究的都是一些可以分解小麥麩質中這些部分的酵素。

一個史丹佛大學於二零零七發表的研究指出，組合使用可分解脯胺酸和可分解穀胺醯胺的酵素加強了於胃部環境中對小麥麩質中最具致病性部分的消化作用。這可能結予乳糜瀉病人更多膳食上的彈性。

不過，這亦不代表乳糜瀉病人這樣便可以隨意食用含小麥麩質的食物。因為酵素的分解作用，永不會達到百分之百的，所以怎也會有一少部分的小麥麩質未能成功被分解而可能引起免疫反應。

總括而言，使用酵素去治療乳糜瀉仍然欠缺相關的臨床試驗支持，但是假如當病人意外吃了小麥麩質時，它可以作為一個額外的保護關卡。

Epidemolgical studies revealed that around 1% U.S. population suffers from Celiac Disease. As this problem affects man kind worldwide, many different solutions are suggested, one of which is the use of gluten-specific enzymes. To comment on its efficacy, we have to know it in more details.

Celiac Disease is an intestinal disease characterized by the inflammatory response to dietary gluten in genetically susceptible individuals. Its pathology includes the penetrations of undigested gluten into blood stream, the subsequent stimulations and responses of the immune system localized in the small intestine, leading to destructions of the villi on the small intestine surface.


Since this disease is due to the presence of incompletely-digested gluten, any intervention that can break the intact gluten into amino acids is theoretically able to relieve the problem to a certain extent.

With the advance of the science and technology, we now know that the most pathogenic part of gluten is the proline- and glutamine- (two common amino acids) rich sequences. Thus, the enzymes usually used as supplements and under researches are those extracted from plants or micro-organisms and specific to these sequences.

A study held by Stanford University published in 2007 illustrated that the combination of a proline-specific and a glutamine-specific enzyme showed an enhanced effectiveness on the digestion of the most pathogenic sequences of gluten in gastric condition. This may suggest the light to increase the safe threshold of dietary gluten in Celiac patients, which gives them more flexibility in their gluten-restricted diets.

Yet this does not necessarily mean that with this ‘therapy’ Celiac patients can eat gluten freely afterwards because all enzymatic reactions can never attain 100% yield and there are always some pathogenic peptides left which still possibly cause inflammatory responses.

To conclude, the use of enzymes to treat or cure Celiac Disease is still lack of clinical trials to support. But it is likely to be an extra barrier to accidental ingestion of gluten for gluten-sensitive patients, in addition to our natural digestive mechanisms.



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