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等級: 新手
文章: 5
註冊時間: 2008-11-28
最近來訪: 2008-12-01
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Protein in life Stage Nutrition
蛋白質的影響
Mythology of Protein Restriction for Dogs with Reduced Renal Function
對腎功能降低的狗限制蛋白質攝取其存在的神話
Dietary protein restriction has been widely accepted as a form of nutritional management for animals with reduced renal function for over four decades.
對腎臟功能降低的動物，限制蛋白質的飲食，以做為營養管理的形式已廣泛地被接受超過四十年了。
While scientific evidence has not been presented to justify this practice, it is particularly used in dogs.
當科學證據無法提出常規是正確的證明，特別是使用於狗
Advertising claims suggest that dogs with a list of urinary problems could benefit from protein restriction including those with renal insufficiency, progressive renal failure, acute renal failure, normal aging, polydipsia / polyuria, glomerulonephritis, urinary tract infection, urolithiasis, and prostatitis. The most widely accepted of these is the notion that dogs with reduced renal function or advanced age will benefit from reduced dietary protein intake.
廣告聲明提出對於有泌尿器官問題的狗，包含腎臟不適，進行性的腎衰竭，急性腎衰竭，正常老化現象，劇渴/多尿症，腎絲球腎炎，泌尿道感染，尿石症和攝護腺炎，限制牠們蛋白質攝取是有利的。最被廣泛被接受的想法是減少蛋白質攝取將有利於降低腎臟負擔或提前老化
In recent years, 10 experimental studies using dogs have been published that clarify the controversy of protein restriction. A multicenter study conducted in human medicine is also noteworthy to review.
近年來，10項以狗為實驗對象的研究澄清對蛋白質限制的爭議，控制人類藥物治療的一項被隨機化受控試驗性的研究，也值得再注意並重新探討。
A number of false assumptions about the need for reduced protein intake in regard to renal disease have been perpetuated in the literature for many years, including:
關於腎臟疾病對於必須減少蛋白質攝取的一些錯誤假設，在文獻上已存在多年，包括:
�Increased urea load causes increased workload for the kidneys
尿素大量上升導致腎臟過量負擔
�High dietary protein intake injures kidneys
高蛋白質攝取會造成腎臟損害
�High dietary protein intake causes hyperkalemia.
高蛋白質攝取將導致高血鉀症
�High dietary protein intake causes acidosis
高蛋白質攝取會引起酸中毒
�Protein intake results in uremic toxins
蛋白質攝取導致尿毒症
�Reduced protein intake slows the progression of renal disease
減少蛋白質攝取可減緩腎臟疾病發展
Recent evidence in dogs challenges the validity of the above assumptions and redirects the questions about factors that lead to the progression of renal failure. The beliefs about protein restriction will be discussed as a medical myth. The question of why the practice of reduced protein intake persists despite the lack of supportive scientific evidence is explored.
最近以狗做證明質疑上述假設的正當性，對於導致腎衰竭發展的因素，改變討論的方向。限制蛋白質攝取的信條將以醫療神話做詳述。儘管缺少科學支持的論證尚在探索，但問題在於為何減少蛋白質攝取的慣例仍持續實行。
History of Protein Restriction 限制蛋白質的沿革
Two general reasons are most commonly given to support the reduction of dietary protein in animals with renal disease. First, reduced protein may result in reduced azotemia, which limits the nausea of renal failure and allows animals to continue eating. While this premise is widely accepted, its clinical importance has not been quantified. Second, reduced protein intake may influence the course of renal failure. The origin of these notions provides some insight into their appeal and durability.
對於有腎臟疾病的動物，有兩個普遍的理由用來支持減少蛋白質飲食攝取: 第一、減少蛋白質可減少氮血症發生，可限制因腎衰竭所造成的噁心感，使動物可繼續進食。當這個假設可廣泛的被接受時，它臨床的重要性尚未被量化。第二、降低蛋白質的吸收有可能影響腎衰竭的過程。這些概念的由來，對它們的感染力和持久性，提供了一些深層領悟。
The first suggestion in the literature that ingestion of protein aggravates the clinical condition of human patients with renal insufficiency dates back to 1920. Ambard reported that uremic patients were often wasted and did poorly when they ingested meat.1 This clinical description led to efforts to alleviate the so-called “toxins of uremia” by reducing dietary protein. Newburgh and Curtis in 1928 reported the development of renal lesions in rats fed varying quantities of protein and suggested that rats fed high quantities of protein containing 75% dry liver developed renal lesions more quickly than those fed moderate protein or casein diets.2 Rodents have been widely used to study possible causative factors of progression of renal failure. Some strains of rats have a high incidence of spontaneous glomerular and tubular lesions associated with age alone.3–8
The progression and severity can be enhanced by increased dietary protein,2,9,10 sodium,4 and phosphate.11 Surgical ablation of renal mass hastens glomerular lesions as does diabetes in these rats.12–14 While these observations are limited to certain strains of rats, they have influenced many investigators by establishing the possibility of a dietary protein-induced nephropathy in other species.
在文獻中第一個建議指出，自1920年存在至今，蛋白質攝取會使臨床的腎衰竭病患症狀惡化。Ambard提出患有尿毒症之病人，當他們食用肉類時，通常是無用的或是消化不良的。1 這個臨床描述指出藉由減少蛋白質之攝取可有效減緩所謂的”尿毒症之毒素”。 在1928年Newburgh和Curtis敘述，向有腎臟機能障礙的老鼠，餵食不同含量的蛋白質，研究其腎臟發展，其中要求餵食含有百分之七十五之高含量蛋白質的乾肝臟，發現患有腎臟機能不全的速度高於餵食一般含量之高白質或是酪蛋白飲食的老鼠。2 齧齒動物過去曾被廣泛研討可能成為腎臟退化擴展的因素。有些品種的老鼠有自發性腎臟絲球體高發生率，以及單單與年齡有關聯的管性損害退化，3–8 增加蛋白質2,9,10 鈉,4和磷酸鹽11可能提高其擴展和艱苦的環境。腎功能由外科手術引起的脫落，加速腎臟絲球體的損害退化，與患有糖尿病的老鼠情況相同。12–14雖然這些言論受限於特定品種的老鼠，但證實飲食蛋白質誘導型腎病發生於其他物種的可能性之結果，已經影響了許多研究者。
The first published data in the dog linking dietary protein to renal function appeared in the 1930s. It was reported that in normal dogs glomerular filtration rate (GFR), renal blood flow (RBF), and urea clearance could be acutely increased by high protein feeding.15–17Subsequent studies by Pitts indicated that intravenous infusion of amino acids dramatically increased renal hemodynamics.
第一份出版描述狗與蛋白質飲食對腎臟功能關聯的數據，出現在1930年代。此數據指出普通的狗，若餵食它高含量蛋白質，其腎絲球體過濾率、腎血漿流量、和尿素的廓清力將劇烈地增加。15–17 Pitts後來的調查顯示，氨基酸靜脈式灌注也會戲劇性的增加腎臟血液動力。
It should be remembered that during the 1930s and 1940s the basic parameters of kidney function were first being studied. For example, blood urea concentration as an accurate measure of kidney function and the concept of extrarenal azotemia were first reported at that time.19 It was then believed that the kidney expended considerable energy to excrete urea into the urine and that moderate restriction of protein was beneficial to human patients as contended by Addis.20 This concept fell out of favor in human medicine when it was realized that renal work is tied closely to active sodium reabsorption and that urea is passively handled. Special dietary restrictions were not thought to be needed in human patients with chronic renal failure because of the lack of evidence that a normal protein intake had a deleterious effect on the kidney. Addis reported that urea production, urea excretion, and blood urea nitrogen (BUN) increased in normal subjects when dietary protein was increased. The uselessness of urea clearance and the limitations of creatinine clearance were not appreciated at that time.21
在1930和1940年代間，腎臟功能的基本特徵才第一次被研究。舉例來說，血中尿素濃度依照腎臟功能的準確測量和腎外尿毒症的概念都是在當時第一次揭露。19而那時大家相信腎臟花費相當多能量以分泌尿素到尿液裡，然而Addis主張適當限制蛋白質的攝取，是有益於患者。20這個觀點贊同人類服用的藥物上使用，當腎功能被積極鈉緊密連接重新吸收，而尿素卻是處於被動控制。特殊飲食限制被認為不適用於慢性腎衰竭病患，因為對於正常蛋白質的攝取對腎臟有害的影響缺乏證據。Addis描述一般的實驗對象當蛋白質的攝取量上升時，其尿素的產生、尿素的分泌、和血中尿素氮將會一起增加。尿素廓清力的無效能和肌酸酐廓清率的限制因素，在當時皆無被重視。21
In 1941, Allison et al. reported on 10 dogs with kidney disease as measured by increased BUN and decreased urine specific gravity, which they felt correlated well and
were of clinical significance in determining kidney damage. They were unaware of the extrarenal and renal factors separate from GFR that might influence BUN and reported that serum creatinine concentration was not a reliable indicator of kidney damage.22 Morris subsequently developed, produced, and sold a reduced-protein diet, KD, for dogs with renal failure. He and others were influenced by the erroneous work hypertrophy concept for urea excretion advanced by Addis.20 While experimental or clinical data were never published to support the value of this or other diets, the concept was broadly accepted without challenge in the veterinary literature.23 Diets were promoted as lowering BUN and reducing urine volume.
在1941年，Allison et al.指出十隻患有腎臟疾病的狗藉由增加血中尿素氮和降低尿素的比重，這兩點可使其感受關聯性的健康，也是屬於臨床重要性之中決定腎臟損害的因素。沒有被注意到的腎外和腎臟因素被腎絲球體過濾率做分離，其有可能影響血中尿素氮，報告也指出血清肌酸酐濃度並不是一個可靠測量腎臟損害的指標。22 Morris隨後為了腎衰竭的狗開發出降低蛋白質的飲食、進而生產、分裝做銷售。事實上，他和其他人皆被Addis提出那不正確且過度澎脹的尿素分泌概念所影響。20當實驗性或臨床的資料未被出版來為此或其他飲食方式的價值性提供證據，在這觀點被概括接受的同時，卻沒有人對獸醫的學術資料提出懷疑。23促使降低血中尿素氮和減少尿素含量的飲食方式才是應該被重視的。
The notion that high protein feeding to dogs may be harmful was even adopted by the National Research Council (NRC) of the National Academy of Sciences in 1972.24 It was stated that high protein found in some commercial diets increases the workload of the liver and kidney and contributes to renal disease in dogs. There is no evidence to support this view, and the recommendation has been dropped. In contrast, there is evidence that high protein diets enhance renal function in normal dogs. This has led to confusion among veterinarians who have been told for decades that low protein diets may be beneficial for kidney function and therefore high protein diets may be deleterious to normal dogs.
對狗餵食高蛋白食物進而有害的這個觀點，在1972年，也被美國國家科學院的國家研究委員會所採用。24其中描述一些市面上含有高蛋白的食品，增加了肝臟和腎臟的工作量也於無形之中促成狗的腎臟疾病。沒有任何證據可以證實這項觀點，而此項建議也已經被停止了。相較之下，高蛋白質的食物可增強正常狗的腎臟功能，是有證實的。這點讓數十年以來被告知低蛋白食物可能有利於腎臟功能而高蛋白可能有害於正常健康狗兒的獸醫來說，感到困惑。
While the Addis hypothesis of work hypertrophy to excrete urea is erroneous, a more modern concept associated with glomerular hyperfiltration was proposed in the 1980s by Brenner.25 This hypothesis states that after any significant loss of renal function, surviving nephrons subsequently undergo functional and structural changes including increases in single nephron GFR and glomerular capillary pressure increases. These changes are referred to as glomerular hyperfiltration and glomerular hypertension. Micropuncture studies in rats indicate that a progressive decline in renal function is observed as a consequence of these adaptations. In addition, glomerular enlargement, hypertrophy, and glomerular mesangial deposits lead to a progressive glomerulosclerosis and eventual nephron loss. Surviving nephrons undergo further increases in filtration rate, capillary pressure, and size, setting up a vicious cycle of pathogenic renal injury. A reduction in dietary protein and/or calories has been shown to limit this process in some strains of rats.26 If this mechanism were operative in the dog, there would be good rationale to limit dietary protein.
當Addis成果假設過度膨脹分泌尿素的觀點是不正確的，Brenner在1980年代提出了有關腎絲球體高濾過率的最新觀點25。這個前提陳述，在腎臟功能有任何顯著的喪失之後，倖存的腎臟小過濾器也接著經歷了機能上和構造上的改變，包含增加了一單位小過濾器的腎臟絲球體過濾率和提高腎絲球體毛細管壓。這種變化被稱為腎絲球體高濾過率和腎絲球體高血壓。微穿刺在老鼠的研究指出，適應的結果可觀察到腎臟功能逐漸下降。因此，腎絲球體的擴大，肥大，和腎絲球間質沈積，導致累進式腎絲球體硬化，以及最後一個腎臟小過濾器喪失。倖存的小過濾器經歷了逐漸增加的過濾率，毛細管的壓力，和尺寸的改變，建立了一個因腎臟損壞而引起疾病的惡性循環。對某些品種的老鼠來說，降低飲用的蛋白質和/或卡路里，顯示其限制了此過程的產生。26若這個歷程在狗身上是有效的話，在限制飲用蛋白質的議題上，這將是一個好的理論基礎。
Experimental Studies in Dogs 以狗做為實驗性研究對象
Because of the confusion in the veterinary literature and the lack of evidence to support the use of reduced protein diets, a number of experimental studies have been performed in recent years. These studies have utilized the standard experimental model of reduced renal function and have addressed many questions when dogs received varied forms and quantities of protein at different levels of renal function. These studies represent a major quantity of work that required the sacrifice of hundreds of dogs to deliver in the aggregate a clarification of the possible role of dietary protein in the initiation, maintenance, and progression of renal dysfunction.
因為與獸醫的學術研究有出入，並且缺乏證據支持減少蛋白質食用是有益的。最近已經完成一些試驗性的研究，而這些研究利用降低腎臟功能的標準實驗性模型，對於腎臟功能程度不同的狗接收不同類型和不同數量的蛋白質，提出了許多問題。這些研究陳述，若要發表一個成果，需要犧牲上百隻的狗，以實現總數的統合，來澄清在腎臟官能不良的初期、維持、和擴展，攝取蛋白質可能發生的作用。
The measurement of progression of renal failure requires specific definition. In these studies the use of clinical signs, reduced urinary concentration capacity, elevated BUN, and elevated plasma creatinine have limited ability to detect efficacy of protein restriction. Likewise, the presence of hyperphosphatemia, acidosis, and proteinuria may be misleading depending on the experimental model and diet and may not represent a precise measure of progression. The sole most reliable method is the measure of GFR using inulin or labeled iothalamate. This is considered the gold standard to indicate progression of disease, and all other measures are considered secondary.
測量腎衰竭的擴展需要特殊的定義。這些研究使用臨床特徵，降低尿濃度的容量，提高血中尿素氮，和增加血漿肌酸酐，以限制其功能來約束蛋白質攝取的功效。同樣地，高磷酸鹽血症、酸液過多症、蛋白尿的存在，依靠試驗性模型和飲食方式，可能使人誤解，並且無法對其擴展性表現出的準確測量。測量腎臟絲球體過濾率的唯一最可靠的方法就是使用菊苣纖維或是labeled iothalamate，這都是被視為測量疾病進展的優良標準，所以其他測量方式皆是被認定做次要輔助為主。
Progression to failure may also be estimated on the basis of morphologic measures. The agreement of morphologic and functional measures is extremely complex and appears to vary with the form of renal disease or experimental model. A synthesis or comparison of functional and morphologic measures may be helpful in some cases. However, results may or may not agree. Although histologic or electron microscopic alterations may indicate something about the pathophysiology, their relationship to progression of failure may be difficult to quantify. It is commonly difficult to quantify histologic lesions because they are not uniformly distributed, there may be confusion due to compensatory hypertrophy and hyperplasia, and in some forms of disease fibrosis may obscure histologic architecture.
衰退的擴展也許可以用基本形態學測量方式來做評估。形態上和功能上測量方法的一致性相當複雜，其陳現出的結果會隨著腎臟疾病之型式或者不同的實驗性模型而改變。機能上和形能上的測量方式若互相做接合或是比較，對於某些實例來說可能是有幫助的。不過，產生的結果也許會、也有可能不會相符。雖然組織學或電子學的微小變樣可能可指示出一些關於病理生理異常的現象，但它們與衰退擴展性的關聯，要使其量化是相當困難的。量化組織的損害，困難在於它們不是一致的散佈，可能造成混淆的原因是因為代償性肥大、增殖、和疾病纖維化有可能會遮掩住組織的結構。
Results of the 10 experimental studies on dogs have failed to provide evidence of the benefit of reduced dietary protein to influence the course of renal failure.27–36 The results of these studies should allow veterinarians to disabuse themselves of the six assumptions related to protein intake set forth at the beginning of this article. It is clear that the concept of increased workload, protein intake causing injury to the kidneys, and reduced protein intake slowing the progression of renal disease are incorrect. The other three assumptions dealing with hyperkalemia, acidosis, and uremic toxin require comment. Hyperkalemia was not found in the above studies related to increased dietary protein. The ability to excrete potassium and maintain a normal serum potassium concentration until the very last stages of chronic renal failure has been studied in detail in dogs.37,38 The secretory mechanism in the distal tubule represents the major site for enhanced potassium excretion during renal failure. Potassium balance is maintained in chronically uremic dogs even in the presence of changing rates of potassium intake, changing rates of excretion of sodium, phosphorus, and ammonium. Acidosis is also uncommon due to altered tubular mechanisms in dogs with reduced renal function.39–41 The dog is unique in that the fractional reabsorption of bicarbonate increases after reduced kidney function. This enhanced ability to reabsorb bicarbonate prevents acidosis and is present in spite of tubular adjustment to regulate other electrolytes such as sodium, potassium, and phosphate. Finally, the concept of dietary protein being responsible for so-called “uremic toxin” has not been proven in any species despite extensive study.42
十種以狗為實驗性對象的研究結果，並沒有足夠的證據可證明減少飲用蛋白質對於腎臟衰竭的影響是有益處。27–36這些研究結果應該可以讓獸醫糾正自己錯誤的想法，也就是本文一開始就提出的六個有關蛋白質攝取的假設，很顯然的，增加工作量、蛋白質的攝取對腎臟造成損害、和減少飲用蛋白質可遲緩腎臟疾病擴展的這些概念都是不正確的。另外三個假設關於高血鉀症、酸中毒、 尿毒需要以下註釋，高血鉀症在以上關於增加飲用蛋白質的研究裡無法找到關聯性。分泌鉀的能力和維持一個正常血鉀濃度，直到慢性腎衰竭的最後一個階段，有在實驗對象狗的身上有做到詳細的研究。37,38腎衰竭階段，在末梢細管的分泌過程是增強鉀排泄的主要部位。患有慢性尿毒症的狗，就算正在改變鉀攝取的比率，鈉、磷和氨排泄的比率時，體內的鉀含量還是維持於平衡狀態。酸中毒是由於腎功能降低進而改變狗的管狀結構是非常罕見的。39–41狗有一個獨特的現象就是在降低腎臟功能之後，部分進行重新吸收的重碳酸鹽卻增加。進行重新吸收的重碳酸鹽，其增大的能力可防止酸中毒，當時不論管狀調整是為控制其他電解質如鈉、鉀、和磷酸鹽。最後，僅管廣泛的研討，但所謂的尿毒是因蛋白質食用而產生之觀念，不論實驗對象為任何品種，都無法被證實。42
Dietary Protein and Progression of Renal Failure in Humans
食用蛋白質對人腎衰竭的影響
The controversy of dietary protein restriction in humans had been perpetuated by anecdotal reports and uncontrolled clinical studies since the early 1960s. In view of the Brenner hypothesis, the National Institutes of Health funded an extended multicenter study, which recruited 585 patients with chronic renal failure. Patients were fed a standard protein diet and a low-protein diet for 18 to 45 months. Measurement of GFR and standard chemistry measurements were used. The mean decline in GFR at 3 years did not significantly differ between diet groups.43 Among patients with more severe renal insufficiency, a very low protein diet compared to a low protein diet did not significantly slow the progression of renal disease.
限制人們食用蛋白質的爭議，自從1960年代初期開始，就一直存在著趣聞的報導和不受約束的臨床研究到現在。鑑於Brenner的假說，其徵募了585位慢性腎衰竭患者，而這些病人各別被餵食標準的蛋白質食物和低蛋白的飲食持續18到45個月。使用腎臟絲球體滲透率測量方法和標準的化學測量方法，三年以來腎臟絲球體滲透率微不足道的減少，在不同飲食群體中並無重大的差別。而對於那些腎臟機能嚴重不足的病患來說，相當低蛋白質的飲用與普通低蛋白質攝取在腎臟疾病的擴展上，並無可觀地減緩。
Why Is Dietary Alteration Still Used if There Is No Proven Benefit?
如果飲食改變並無被證實有任何的益處，為何還要繼續使用這個方法呢?
The continued use of protein restriction in the absence of scientific evidence deserves thoughtful consideration. I would suggest that the dogma and mythology of a possible benefit are so embedded in the thought process of veterinarians and owners that these cannot be easily dislodged despite the scientific evidence. I would refer to this as the myth of dietary protein and characterize it as a negative myth.
在缺乏科學精確證據的支持下，持續使用限制蛋白質攝取的方式，必需經謓密思考的。我認為這些信條和可能有益的神話都已經深深牢固在獸醫和寵物主人的思考模式當中，僅管有科學的證實，這些想法也很難移除。但我會把它歸屬於飲用蛋白質之神話，並當它是一個消極的神話。
What is a myth? A myth is a way of making sense of a difficult and senseless world. Myths give a society a degree of relief from neurotic guilt and excessive anxiety. Philosophers, psychiatrists, and theologians tell us that humans have always needed myths. Myths are a self-interpretation of our inner selves in relation to a larger world. All societies and individuals are built on a series of myths that are not readily apparent. If we are not given myths by society, we invent them to make sense of our personal experiences.44
什麼是神話?神話是一種對於艱難無意義世界的理解方式。神話讓社會從神經性罪過和過度焦慮，獲得程度上的調劑。哲學家、精神病學家和神學家告訴我們，人類永遠都需要神話的存在。神話是我們內心的自己對於某個廣大的世界形成的自我解釋。所有的社會和個體都被建立在一連串未必全然不真實的神話。若社會沒有給予我們神話，我們將可能自行創造神話以理解個人經驗。44
There are both positive and negative myths. Positive myths support and validate our self-worth. They provide guidance and support. These positive myths are used as important patterns in human consciousness, which allow us to cope with a difficult world, as we are reminded by the psychiatrist Rollo May,44 Carl Jung,45 and philosophers Mortimer Adler46 and Joseph Campbell.47 There are many in our contemporary popular culture, though profoundly mistaken, who consider all myths as false- hood. I would consider a truly negative myth as one that misleads or has destructive effects. These could be termed pseudo myths or exaggeration and they appear to be almost magical. These are associated with beliefs without benefit or responsibility.
精神學家Rollo May，44 Carl Jung，45 和哲學家 Mortimer Adler，46 和Joseph Campbell.，47提醒我們注意神話有積極的和消極之分。積極面的神話支持和承認我們自我價值，它們給予指引和鼓舞，而這些積極面的神話是用來做為人類意識的重要典範，並可允許我們對抗這艱難的世界。許多當代大眾文化，僅管深深的被誤解，被某些人認為所有的神話都是錯誤的集體。而我認為真正消極面的神話會引人入歧途或是有毀滅性的影響。這些可稱作是假的神話或只是誇大而已，可以說它們像是使用魔術產生的。這些與無益處和無信賴性的信念有關聯。
There are many types of myths: personal, societal, and professional. We use personal myths to develop our identity, image, and moral values. We use myths to define ourselves in a community. Societal myths include the New World, the Western frontier, the lone cowboy, national heroes, and the so- called American Dream. Professional myths in veterinary medicine include the images associated with the stories of James Herriott, the gentle doctor as projected by our organized profession, and the power of healing related to modern science.
神話有非常多的類型：個人型、社會型、職業型。我們用個人神話來發展身份、形象、和道德價值。在共同社會裡，我們也用神話來給本身下定義。社會型神話包含”新世界”，西方的邊境，無伴的牧童，國民英雄，和所謂的美國夢。獸醫學的職業型神話包含James Herriott故事有關的象徵形象在內，這樣子的仁慈醫生會被我們組織性職業做投射，又治癒能力和現代科學是有聯繫的。
Are there conflicts between science and myth? As it turns out, many of our scientific theories are a kind of mythology. Many scientific discoveries begin as myths or have their original questions in myths. In many ways, science is the critique of myth (W.B. Yeats).44
介於科學和神話之間是有衝突的嗎?結果發現，我們許多的科學學說算是神話學的一種。很多科學的發現都是起源於神話或是對神話有獨特的疑問。從多方面來看，科學是神話的批評性分析所產生的。(愛爾蘭詩人、劇作家-葉慈) 44
Why Relate Protein Restriction to Myth?
I suggest that we have used the myth of dietary protein restriction because it is psychologically reassuring in the face of life-threatening illness. Chronic renal failure presents multiple difficult problems in the absence of adequate medical treatment despite all efforts to date. In the absence of dialysis, which is not practical for the vast majority of animals, and renal transplantation, which is not successful in the dog because of immunologic barriers, medical treatment has little to offer. Most cases are presented late in their natural course, are usually irreversible, and are usually attendant with a uniform pattern of failure and eventual death over months. Because of these factors, a sense of frustration, embarrassment, and even guilt arises in the veterinarian and owner. Veterinarians grasp for something to offer to maintain our professional position, status, and power in this dilemma with the owner. Dietary protein restriction is simple, relatively inexpensive, and usually not harmful and has the ring of authority. We can offer vague but firm assurance of its value since it has been on the scene for so long. Owners sense this dilemma and appreciate our efforts. This is an ideal circumstance to trap oneself and the client in a false myth.
為何限制蛋白質攝取與神話有關?
我們利用限制蛋白質食用的神話，因為它是在面對致命疾病的一種心理上的安慰。所有努力成果迄今，在缺乏醫學治療的情況下，慢性腎衰竭會引起多樣困難的問題產生。缺乏洗腎的技術，對於廣大多數的動物並無實際經驗，而腎臟移植，因為免疫障礙，以狗為實驗對象時並沒有成功，由此可知，醫學的治療並無多少貢獻。大多數的例子在不能倒置的自然過程中皆接近末期才陳現出，並且伴隨相同形式的衰退和數個月後的死亡。因為這些因素，獸醫和寵物主人易產生挫敗感，陷入焦慮，甚至引起內疚感。在這與寵物主人進退兩難的困境，獸醫急切想領會某些事物來奉獻以堅守自己的專業身份、地位和權力。限制蛋白質攝取的方法是簡單的，也相對地價格低廉，通常來說不造成傷害，並且有職權集團做支持。自它已經在這個事件存在這麼久的時間來說，我們能糢糊提出但它的重要性無法保證。寵物主人理解能這個困境並感激我們所付出的努力。這是一個理想的情況來抑制陷入謬誤神話的本身和委託人。
Why Have We Chosen to Keep the Reduced Protein Myth?
為何我們選擇相信降低蛋白質的神話呢?
The myth has been maintained even in the past decade despite negative scientific evidence because the dogma has persisted about its value for the past 40 years. If we as professionals are uncertain about the facts concerning a controversy, we are likely to put ourselves in someone else’s hands who appears to have authority. Power to command this authority is in the hands of commercial advertisements that promote these special products with misleading messages. Marketing is aggressively aimed at veterinarians and owners alike. There is a profit motive for veterinarians to sell these diets. The public has a nutritional mania and preoccupation with diet in our society. Dietary change has assumed the status of medical treatment using such terms as intervention, maintenance, and correction. The profession and the public do not appreciate that advertising claims come without proof in the case of diets. Owners can easily be enrolled to accept such diet change because they feel they are involved in doing something constructive. Professional responsibility has been lost in this case. The situation can remind us that we are part of an uncritical profession with little review or standards. When scientific proof fails to justify a practice, a false myth may likely live on.
因為從四十年前，這個信條堅持它存在的重要性，僅管負面的科學證據是存在的，但過去的數十年以來一直堅守著這個神話。如果我們同樣是專家，關於爭論，對真相不能肯定，我們有可能將自己交給擁有威信的某人手中。掌控職權的能力被做為商業廣告的可靠來源，用使人誤解的訊息來宣傳這些特殊的成果。行銷方向被侵略性瞄準於獸醫和寵物主人客層，對獸醫來說，銷售這些食品是一個利益動機。在一般社會，大眾對飲食有營養品狂熱和搶先佔有的心態。飲食改變的設想是一些被稱作調停、維持、和修正的醫學治療狀態。醫生同業和大眾沒有察知廣告所宣稱的飲食並無論證。寵物主人很可能加入並接受這樣的飲食方式，原因在於他們認為他們是在做有建設性的事。既然如此，專業性職責已無影響力可言。但這個處境提醒我們，我們微弱的評論和標準是屬於無批判力的職業。當科學證據不足以表明常規是有理的，謬誤的神話很可能繼續存在。
In conclusion, the continued existence of this false myth about dietary protein is an uncomfortable reminder of the lack of sophistication, lack of critical thought, and reliance on oversimplified and attractive dogma that persists in our profession. This is only one example of many false myths, misinformation, and partial truths that are repeated from decade to decade. Until a more critical approach with standards and oversight are brought to bear in our profession, we will likely continue to be ensnared in false myths despite the presence of sound science.
總而言之，蛋白質攝取的謬誤神話持續存在是一個缺乏教養、批判性思考、和過份簡化信賴以及執意我們職業其引人注意的教理。這麼多的謬誤神話、錯誤消息和不完全事實中，只有一個例子，數十年以來被重覆著。直到一個較關鍵性帶有標準的方法，我們的職業處於監督狀態來承擔。僅管”充分科學證據原則”是存在的，但我們將可能持續陷入謬誤神話的圈套之中。
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