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#51
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"Phil P." wrote in message
... "CatNipped" wrote in message ... - but the only canned food they'll eat is Fancy Feast "Tender Beef Feast" (two cans in the AM and two cans in the PM, so one can a day per cat). Tender Beef Feast contains too much phosphorus (and protein) for a renal cat. If Bandit only likes beef flavor, Try Fancy Feast Grilled Beef- its much lower in phosphorus (0.88% DMB), or better still, Fancy Feast Minced Beef (0.75% phos. DMB). OK, I'll have to try that. Have you tried Pet Guard Rabbit or Venison? Both diets are very low in phosphorus (0.21%, 0.20% DMB). Wysong Gourmet Chicken and Gourmet Liver are also low in phosphorus (0.60% DMB)- if Bandit will eat them. I can't find Pet Guard locally - I didn't want to order anything online because they are *SO* picky about what there eat so I didn't want to buy a large quantity of something that will go to waste. Do you know of any large chains (PetsMart or PetCo) that carry it? snip Bandit's labs haven't changed with the addition of the canned food - snip The BUN will be high because Fancy Feast is *very* high in protein- almost 60% on a dry matter basis. Creatinine is less affected by diet. Minced Beef is a little lower in protein (54%), but its still a little too high for a renal cat. For renal cats, I've had the best luck with Hill's Prescription x/d. Its low in phosphorus (0.53% DMB) and moderate in protein (43% DMB). But most importantly, its not an acidified diet. X/d is more palatable than k/d and g/d- which I think are a little too low in protein. I've seen dramatic turnarounds in renal cats after switching to x/d from k/d. I don't think the vet is classifying her as renal - her creatinin and BUN is actually in the "normal" range, just high normal and, considering her age, the vet wanted to keep an eye on that and switch to canned food to control any future issues. Good luck, Phil Thanks for the info Phil, I'll check out the Pet Guard (if I can get it online without spending a fortune I'll take the chance it won't be used - I can always give it to the rescue group I donate to). Hugs, CatNipped |
#52
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Phil P. wrote: Steve, I'd say its enough to make people err on the side of caution since there was a direct association between dry food and IC, and also because there are no benefits of feeding dry food- unless its a dental diet, and still, the benefits are minimal and don't offset the risks. I might agree if while we are "erring" on the side of caution we were taking a look at the incidence rate of many other diseases and using the same caution. But alas that isn't the case. The carbophobics are so intent accepting the hypothesis that canned food is the cure for every disease known to cats. Point in fact it is not - and never will be. The ONLY thing that has been proven in favor of canned foods is the issue of greater excretion of water through the urine rather than the feces. Increased dilution of the urine will reduce the chance of urolith formation. Urolith formation affects less than 2% of cats at some point in thier life. That 2% statistic comes from the Veterinary Medical Data Base at Purdue It only represents a portion of the cats seen at the 26 veterinary university hospitals in N.A. A very small % of owners bring their cats to vet school hospitals. Thus, its not representative of the owned feline population that develop FLUTD or urolithiasis. Actually the stat I was trying to quote does not come from Perdue but rather from the Elizabeth Lund study. Even so - the Perdue data is a cross section of the real world. Is it likely to reflect a higher incidence of disease - yes - but the trends remain valid. 2% still represents millions of cats! Any risk is unacceptable if its an unnecessary risk. But ONLY 2 million cats. (I know 2 million is a lot) It is annoying to find a focus on canned food as a resolution uroliths, and ignore renal disease, which according to the Perdue data has had a massive increase between 1990 and 2000. In a ten year stretch the incidence in cats over 15 went from less than 1% to 11%. While everyone is scurrying around worrying about canned foods to deal with a 2% problem, we run the great risk that they will elect to provide canned foods which contain much higher levels of phos than is typically found in dry foods. It's simply the nature of the beast. Steve, many studies were done thoughout the years that looked into the possibility of dietary iodine being a causative factor in hyperthyroidism. None were ever found. If you know of one that me and our vets missed, let me know, Our patents were published in December this past year. The data that supports the patents is very clear and of course is only a tiny fraction of the clinical data that will be published over the next couple years. An assumption that any canned food is better than any dry food is erroneous and there are risks associated with anything we do. I am not opposed to canned food - I feed my own cats a canned food for the majority of their caloric intake - but I don't think it appropriate to insinuate that all dry foods are bad and all canned foods are better. Such is simply not the case by any means. I disagree. A canned food is better for a cat than an *equal quality* dry food. The dry and canned foods in the study I cited were the same brand. Agreed, if that is what Joesephine Consumer actually bought. When buying dry foods the cost per day to feed the cats is about 25% of the cost of feeding canned foods. If Josephine Consumer elects to spend a few extra bucks buying a better quality food, the same dollars spent will buy a much better quality dry food than a canned food. Not many consumers are as interested and concerned as consumers who typically read this NG. Most are looking for convenience and to some degree price, even in the premium sector. How many posts have we read even on this NG regarding the cost of any given food? If Josephine Consumer elects to spend only X dollars per month feeding her cat - then those dollars will buy a far better quality dry food than a canned food. |
#53
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Brad wrote: Does anyone leave any room for the possibilities that the makers of dry food have corrected problems they may have had in the past after all there is a huge market out there and I am sure they want their share of it. I just hope people like PhilP keeps an open mind in changes to the dry food industry but it doesn't seem like most of the experts will leave any possibility open. And by the way have these articles used only top notch dry food like Science Diet or Iams among others in their tests or some cheap dry food since all the experts think us dry food feeders are all lazy, penny pinching, lowlifes PhilP mentions something to that effect in nearly every single post he makes. Humor is good. To answer part of your question, most studies of this nature always choose to use a pet food which is a common food. In most cases the "regular maintenance" food being used will be Purina Cat Chow or Dog Chow. For a number of reasons - it approximates the majority of what pet owners feed, it's always easily available, and is a "typical" food. To my knowledge none of the studies/reviews comparing dry versus canned have ever been done with any premium food. By the same token the canned version of the food would not be a premium food either. One would hope that by comparing average dry to average can you could extrapolate some useful information. I'm one "expert" who does not agree canned foods are manna from heaven nor the cure-all for what ails ya. I think I can qualify as an expert - even amongst those who dislike my postings. As for Phil - he's a remarkably well educated fellow and generally knows what he's talking about. As I think about it, we only disagree on two things the mania for canned foods and the use of a renal diet in early renal failure. Shortly I will win the second debate as the peer reviewed published Grade 1 evidence based trial on feline renal failure will hit the journals. (Yes I am smirking a bit Phil - but I gotta take my shots when I can get them.) Since there are some new folks here who may not have seen the legalese before - it's probably time for that. While I have been an employee of Hill's Pet Nutrition for 23 years, any opinions expressed here are mine and mine alone should in no way be construed as originating from or pertaining to the company I work for. |
#54
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Steve Crane wrote:
Phil P. wrote: Steve, I'd say its enough to make people err on the side of caution since there was a direct association between dry food and IC, and also because there are no benefits of feeding dry food- unless its a dental diet, and still, the benefits are minimal and don't offset the risks. I might agree if while we are "erring" on the side of caution we were taking a look at the incidence rate of many other diseases and using the same caution. But alas that isn't the case. The carbophobics are so intent accepting the hypothesis that canned food is the cure for every disease known to cats. Point in fact it is not - and never will be. Steve, it's too bad you can't debate without resorting to exaggerations. Do you honestly believe that people think "canned food is the cure for every disease known to cats"? Geesh..., now that's just silly. |
#55
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On 12 Jul 2005 19:15:51 -0700, "PawsForThought"
wrote: snip Steve, it's too bad you can't debate without resorting to exaggerations. Do you honestly believe that people think "canned food is the cure for every disease known to cats"? minor snip What, it's not???? aaarrrgghh!!!??!!! |
#56
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"Steve Crane" wrote in message oups.com... Phil P. wrote: Steve, I'd say its enough to make people err on the side of caution since there was a direct association between dry food and IC, and also because there are no benefits of feeding dry food- unless its a dental diet, and still, the benefits are minimal and don't offset the risks. I might agree if while we are "erring" on the side of caution we were taking a look at the incidence rate of many other diseases and using the same caution. But alas that isn't the case. The carbophobics are so intent accepting the hypothesis that canned food is the cure for every disease known to cats. Point in fact it is not - and never will be. Steve, I didn't say canned food is a "cure for every disease known to cats". However, it may prevent a few. Canned food is the first-line treatment for interstitial cystitis, crystalluria, urolithiasis, IBD, and recently, diabetes. Now, if cats with these diseases are *switched* to canned food for management and to prevent recurrence, feeding canned food from the git-go may prevent these diseases from ever developing. The ONLY thing that has been proven in favor of canned foods is the issue of greater excretion of water through the urine rather than the feces. Increased dilution of the urine will reduce the chance of urolith formation. Urolith formation affects less than 2% of cats at some point in thier life. That 2% statistic comes from the Veterinary Medical Data Base at Purdue It only represents a portion of the cats seen at the 26 veterinary university hospitals in N.A. A very small % of owners bring their cats to vet school hospitals. Thus, its not representative of the owned feline population that develop FLUTD or urolithiasis. Actually the stat I was trying to quote does not come from Perdue but rather from the Elizabeth Lund study. Even so - the Perdue data is a cross section of the real world. Is it likely to reflect a higher incidence of disease - yes - but the trends remain valid. In my experience and our vets' general practices, I think the RL incidence of FLUTD is much higher than 2%. 2% still represents millions of cats! Any risk is unacceptable if its an unnecessary risk. But ONLY 2 million cats. (I know 2 million is a lot) It is annoying to find a focus on canned food as a resolution uroliths, and ignore renal disease, which according to the Perdue data has had a massive increase between 1990 and 2000. In a ten year stretch the incidence in cats over 15 went from less than 1% to 11%. While everyone is scurrying around worrying about canned foods to deal with a 2% problem, we run the great risk that they will elect to provide canned foods which contain much higher levels of phos than is typically found in dry foods. It's simply the nature of the beast. What are you talking about? Even most of *your* dry foods are higher in phosphorus on a caloric basis than most of *your* canned foods! In addition, when consuming dry food the total phosphorus intake is *multiplied* because dry food is less digestible and therefore, the cat must eat more food, and in doing so, ingests more phosphorus and magnesium. In fact, one of the FUS studies cited in the previous edition of SACN stated the urinary magnesium concentration was *three times higher* when cats consumed a dry food than when they ate a canned diet, even though the magnesium content in the dry matter of the diets was the *same*. Steve, many studies were done thoughout the years that looked into the possibility of dietary iodine being a causative factor in hyperthyroidism. None were ever found. If you know of one that me and our vets missed, let me know, Our patents were published in December this past year. The data that supports the patents is very clear and of course is only a tiny fraction of the clinical data that will be published over the next couple years. I'll take that as a "no". An assumption that any canned food is better than any dry food is erroneous and there are risks associated with anything we do. I am not opposed to canned food - I feed my own cats a canned food for the majority of their caloric intake - but I don't think it appropriate to insinuate that all dry foods are bad and all canned foods are better. Such is simply not the case by any means. I disagree. A canned food is better for a cat than an *equal quality* dry food. The dry and canned foods in the study I cited were the same brand. Agreed, if that is what Joesephine Consumer actually bought. When buying dry foods the cost per day to feed the cats is about 25% of the cost of feeding canned foods. If Josephine Consumer elects to spend a few extra bucks buying a better quality food, the same dollars spent will buy a much better quality dry food than a canned food. Not so. The "best" dry food cannot be as digestible as an equal quality canned food. How could it be when only *dry* powered ingredients can be use in dry foods compared to fresh or whole meats and other ingredients used in canned foods. Not many consumers are as interested and concerned as consumers who typically read this NG. Most are looking for convenience and to some degree price, even in the premium sector. How many posts have we read even on this NG regarding the cost of any given food? If Josephine Consumer elects to spend only X dollars per month feeding her cat - then those dollars will buy a far better quality dry food than a canned food. No. Dry food is simply cheaper and more convenient than canned food. |
#57
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"Phil P." wrote in message ... "Steve Crane" wrote in message oups.com... Phil P. wrote: Steve, I'd say its enough to make people err on the side of caution since there was a direct association between dry food and IC, and also because there are no benefits of feeding dry food- unless its a dental diet, and still, the benefits are minimal and don't offset the risks. I might agree if while we are "erring" on the side of caution we were taking a look at the incidence rate of many other diseases and using the same caution. But alas that isn't the case. The carbophobics are so intent accepting the hypothesis that canned food is the cure for every disease known to cats. Point in fact it is not - and never will be. Steve, I didn't say canned food is a "cure for every disease known to cats". However, it may prevent a few. Canned food is the first-line treatment for interstitial cystitis, crystalluria, urolithiasis, IBD, and recently, diabetes. Now, if cats with these diseases are *switched* to canned food for management and to prevent recurrence, feeding canned food from the git-go may prevent these diseases from ever developing. The ONLY thing that has been proven in favor of canned foods is the issue of greater excretion of water through the urine rather than the feces. Increased dilution of the urine will reduce the chance of urolith formation. Urolith formation affects less than 2% of cats at some point in thier life. That 2% statistic comes from the Veterinary Medical Data Base at Purdue It only represents a portion of the cats seen at the 26 veterinary university hospitals in N.A. A very small % of owners bring their cats to vet school hospitals. Thus, its not representative of the owned feline population that develop FLUTD or urolithiasis. Actually the stat I was trying to quote does not come from Perdue but rather from the Elizabeth Lund study. Even so - the Perdue data is a cross section of the real world. Is it likely to reflect a higher incidence of disease - yes - but the trends remain valid. In my experience and our vets' general practices, I think the RL incidence of FLUTD is much higher than 2%. 2% still represents millions of cats! Any risk is unacceptable if its an unnecessary risk. But ONLY 2 million cats. (I know 2 million is a lot) It is annoying to find a focus on canned food as a resolution uroliths, and ignore renal disease, which according to the Perdue data has had a massive increase between 1990 and 2000. In a ten year stretch the incidence in cats over 15 went from less than 1% to 11%. While everyone is scurrying around worrying about canned foods to deal with a 2% problem, we run the great risk that they will elect to provide canned foods which contain much higher levels of phos than is typically found in dry foods. It's simply the nature of the beast. What are you talking about? Even most of *your* dry foods are higher in phosphorus on a caloric basis than most of *your* canned foods! In addition, when consuming dry food the total phosphorus intake is *multiplied* because dry food is less digestible and therefore, the cat must eat more food, and in doing so, ingests more phosphorus and magnesium. In fact, one of the FUS studies cited in the previous edition of SACN stated the urinary magnesium concentration was *three times higher* when cats consumed a dry food than when they ate a canned diet, even though the magnesium content in the dry matter of the diets was the *same*. Steve, many studies were done thoughout the years that looked into the possibility of dietary iodine being a causative factor in hyperthyroidism. None were ever found. If you know of one that me and our vets missed, let me know, Our patents were published in December this past year. The data that supports the patents is very clear and of course is only a tiny fraction of the clinical data that will be published over the next couple years. I'll take that as a "no". An assumption that any canned food is better than any dry food is erroneous and there are risks associated with anything we do. I am not opposed to canned food - I feed my own cats a canned food for the majority of their caloric intake - but I don't think it appropriate to insinuate that all dry foods are bad and all canned foods are better. Such is simply not the case by any means. I disagree. A canned food is better for a cat than an *equal quality* dry food. The dry and canned foods in the study I cited were the same brand. Agreed, if that is what Joesephine Consumer actually bought. When buying dry foods the cost per day to feed the cats is about 25% of the cost of feeding canned foods. If Josephine Consumer elects to spend a few extra bucks buying a better quality food, the same dollars spent will buy a much better quality dry food than a canned food. Not so. The "best" dry food cannot be as digestible as an equal quality canned food. How could it be when only *dry* powered ingredients can be use in dry foods compared to fresh or whole meats and other ingredients used in canned foods. Not many consumers are as interested and concerned as consumers who typically read this NG. Most are looking for convenience and to some degree price, even in the premium sector. How many posts have we read even on this NG regarding the cost of any given food? If Josephine Consumer elects to spend only X dollars per month feeding her cat - then those dollars will buy a far better quality dry food than a canned food. No. Dry food is simply cheaper and more convenient than canned food. Dr Mr Potatoe Head Just kidding man... Looka here! Why does dry Create Crystali? |
#58
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Justin L wrote:
On 12 Jul 2005 19:15:51 -0700, "PawsForThought" wrote: snip Steve, it's too bad you can't debate without resorting to exaggerations. Do you honestly believe that people think "canned food is the cure for every disease known to cats"? minor snip What, it's not???? aaarrrgghh!!!??!!! Nope, only in people |
#59
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Brad wrote:
Does anyone leave any room for the possibilities that the makers of dry food have corrected problems they may have had in the past after all there is a huge market out there and I am sure they want their share of it. I just hope people like PhilP keeps an open mind in changes to the dry food industry but it doesn't seem like most of the experts will leave any possibility open. I don't think it's possible for a manufacturer to correct the problems caused by a dry food diet, or the food wouldn't be dry anymore. As you can see in these studies, it's the dryness of the food, and the subsequent moisture volume, and water deficiency that can cause problems: nutrition.org -- Markwell et al. 128 (12): 2753S ---------------------------------------------------------------------------= ----- Abstract of this Article Reprint (PDF) Version of this Article Similar articles found in: Journal of Nutrition Online PubMed PubMed Citation Search Medline for articles by: Markwell, P. J. || Smith, B. H. E. Alert me when: new articles cite this article Download to Citation Manager The Journal of Nutrition Vol. 128 No. 12 December 1998, pp. 2753S-2757S The Effect of Diet on Lower Urinary Tract Diseases in Cats1 Peter J. Markwell2, C. Tony Buffington*, and Brigitte H. E. Smith Waltham Centre for Pet Nutrition, Waltham-on-the-Wolds, Melton Mowbray, Leicestershire, UK and * College of Veterinary Medicine, The Ohio State University, Columbus, OH "Because dietary ingredients and feeding patterns influence the volume, pH and solute concentration of urine, diet can contribute to the etiology, management or prevention of recurrence of some causes of lower urinary tract disease. Most research assessing the effect of diet has focused on the latter two aspects, primarily because of interest in struvite urolithiasis. Manipulation of urine pH through dietary means has proven an effective tool for the management and prevention of struvite urolithiasis; acidification of urine, however, may be a risk factor for calcium oxalate urolithiasis, which now appears to occur with approximately equal frequency in cats. Prediction of urine pH from dietary analysis would thus be a valuable tool, but considerable further research is required before this can be achieved with commercial canned foods. With the growing importance of urolith types other than struvite, alternatives to the measurement of urine pH are required to assess critically the likely beneficial (or detrimental) effects of manipulation of nutrient profile. Measurement of urinary saturation may permit the development and fine tuning of nutrient profiles aimed at controlling lower urinary tract diseases in cats that are associated with a range of different mineral types. The majority of cats with signs of lower urinary tract disease do not, however, have urolithiasis; indeed, no specific cause can be established in most of these cats. Recent observations suggest that recurrence rates of signs in cats classified as having idiopathic lower urinary tract disease may be more than halved if affected animals are maintained on high, rather than low moisture content diets. J. Nutr. 2753S-2757S, 1998 "Clinical disorders of the lower urinary tract of cats are not new phenomena. Kirk (1925), for example, described "retention of urine" as a very common condition in cats. He also noted that the most common cause of the problem was obstruction of the urethra by a sabulous material; less frequent causes were cystic or urethral calculi. Blount (1931) noted that seven different types of urinary calculi could occur in cats, and that "triple phosphates" (presumably magnesium ammonium phosphate) were present in the majority of calculi deposited in alkaline urine. Milks (1935) recorded only one urethral calculus from a cat in his own studies, but suggested that there was evidence indicating that they were fairly common in cats. This is in contrast to the observations of Krabbe (1949) who noted no examples of "real stone formers" in a series of over 1000 cats seen at the Royal Veterinary and Agricultural College in Copenhagen throughout the 1930s and 1940s. "Sedimentation" of the urine was reported, however, in ~1% of cases. These observations demonstrate that uroliths and urethral plugs have afflicted cats for many years. Although they are difficult to relate to more recent data, the observation by Krabbe of an ~1% incidence is strikingly similar to the estimates of 0.64 and 0.85% reported more recently in Europe and the U.S. (Lawler et al. 1985, Walker et al. 1977). The term feline urological syndrome (FUS)3 was coined in 1970 to describe "the feline disease syndrome characterized by dysuria, urethral obstruction, urolithiasis and hematuria " (Osbaldiston and Taussig 1970). Interestingly, despite use of the term urolithiasis in the definition of FUS, no occurrences of urolithiasis appeared among the cases reported (Osbaldiston and Taussig 1970). A study of 46 cats with "FUS" led to the conclusion that "FUS may not be a single disease entity, but rather a group of separate urological problems." Thus the term FUS describes the presence of signs of lower urinary tract disease without implying any specific cause. Subsequent epidemiologic studies identified many risk factors associated with FUS (Willeberg 1984). Proposed dietary influences, the results of many diet-related studies and the fact that struvite (the stone most commonly associated with FUS) is composed of magnesium, ammonium and phosphorus led toward the conclusion that most cases of FUS were diet induced and away from investigation of other potential causes. Noting the confusion that subsequently arose surrounding the term FUS, it has been proposed that it be used either as a synonym for lower urinary tract disorders in cats (Osborne et al. 1984) (Osbaldiston and Taussig's original meaning) or abandoned altogether (Markwell and Buffington 1994). It has been proposed that signs of lower urinary tract disease in the absence of a specific diagnosis be simply called idiopathic lower urinary tract disease; in cases in which a specific cause is identified, the appropriate descriptive term should be used (Markwell and Buffington 1994). View larger version (20K): [in this window] [in a new window] Fig 1. Effect of changing activity product on saturation and its effect on crystallization and crystal growth. Modified from Markwell and Buffington (1994) with permission. View this table: [in this window] [in a new window] Table 1. Results from regression of mean urine pH values on dietary base excess (BE) in cats fed canned foods1 Fig 2. Some solutes affecting crystallization in urine. Other factors affecting crystal formation include time, temperature, and the presence, absence and effectiveness of endogenous protein crystallization inhibitors. WHAT ARE THE MAIN CAUSES OF SIGNS OF LOWER URINARY TRACT DISEASE IN CATS IN THE 1990S? Two detailed investigations of specific causes of signs of lower urinary tract disease in cats have been reported. The first study described 143 cases of hematuria and dysuria, collected between 1982 and 1985 (Osborne et al. 1989, Kruger et al. 1991). Urethral plugs were present in 32 cases, urolithiasis without urinary tract infection (UTI) in 30 cases, UTI alone in two cases and UTI with uroliths in two cases. Seventy-seven cases were classified as idiopathic. Idiopathic disease was present in ~69% of the nonobstructed cats. In a more recent study, 132 cats with signs of lower urinary tract disease were evaluated by the Ohio State University urology service (Buffington et al. 1997). Twelve of these cats had urethral obstruction and a further 11 had concurrent systemic disease. Etiologies were not reported in the obstructed cats. Specific causes for the signs of lower urinary tract disease were identified in 29 of the remaining cats. Urolithiasis (eight struvite, seven calcium oxalate, one unknown) was present in 16 cats (14.7% of nonobstructed cats without concurrent systemic disease), anatomic defects in 12 (this included one of the cats with urolithiasis), neoplasia in 2 (this included one cat with urolithiasis), and urinary tract infection in 1. Ten cats were considered to have behavioral abnormalities and 70 had idiopathic cystitis (64.2% of nonobstructed cats without concurrent systemic disease). These data stress the importance of idiopathic disease; it is interesting to note that the proportion of nonobstructed cases with idiopathic disease was similar in both studies, despite the 10-y gap between them. The more recent study does show, however, that urolithiasis remains an important cause of lower urinary tract disease in cats. It also suggests that two types of urolith predominate (struvite and calcium oxalate), an observation supported by extensive data on quantitative analysis of uroliths (Kirk et al. 1995, Osborne et al. 1995a and 1995b). DOES DIETARY MODIFICATION HAVE A ROLE IN THE MANAGEMENT OR PREVENTION OF ANY OF THE LOWER URINARY TRACT DISEASES SEEN IN CATS IN THE 1990S? Diet can contribute to the etiology, management or prevention of recurrence of some of these causes of lower urinary tract disease because dietary ingredients and feeding patterns influence the volume, pH and solute concentration of urine. Knowledge of these effects of diet and of the specific cause of signs in individual cases of lower urinary tract disease enables identification of those cases in which modification of the diet may truly be of value. Augmenting urine volume may be a reasonable prophylactic measure for a number of types of lower urinary tract disease. If the influence of diet on this parameter is set aside, dietary modifications may be appropriate only in the cases of lower urinary tract disease in which precipitation of minerals plays a significant part [based on the data cited above, urethral plugs were present in~22% and uroliths in ~13-22% of cases of lower urinary tract disease (Buffington et al. 1997, Kruger et al. 1991, Osborne et al. 1989)]. Furthermore, although dietary recommendations appropriate to the management of some mineral types are well developed, those for other types (particularly calcium oxalate) require extensive further research. DOES AUGMENTING URINE VOLUME HAVE A ROLE IN MANAGING OR PREVENTING ANY OF THE LOWER URINARY TRACT DISEASES SEEN IN CATS IN THE 1990S? Most research relating diet to lower urinary tract disease in cats has focused on mineral content, or more recently, on the effect of diet on urinary pH; much less research has been devoted to the effect of diet on urine volume or specific gravity. It can be predicted from theoretical considerations that increasing urine volume for a given solute load has a greater influence on the likelihood of struvite crystal formation than a reduction in urinary magnesium concentration (Markwell and Buffington 1994, Marshall and Robertson 1976). This concept has also been demonstrated experimentally in studies of struvite activity product in feline urine (Buffington et al. 1990). In addition, enhancing urine volume may increase the frequency of urination, which should hasten crystalloid and crystal transit time through the urinary tract, thus reducing the potential for crystal growth. Holme demonstrated that hematuria, induced in cats by feeding a high magnesium, low moisture-containing diet, could be abolished by feeding the same diet as a slurry containing 80% water (Holme 1977). Of particular importance, perhaps, are recent observations in cats classified as having idiopathic lower urinary tract disease. The proportion of cats showing recurrence of lower urinary tract disease was significantly less in a group fed a canned, commercial acidifying diet (11%) than in another group fed the dry formulation of the same product (39%) (Markwell et al. 1998). The mechanism for this effect was not determined in the study, but was considered likely to be the result of changes in the concentration or type of solutes in urine and/or changes in urine volume. Epidemiologic studies of signs of lower urinary tract disease conducted in the 1970s implicated dry cat foods as a risk factor (Reif et al. 1977, Walker et al. 1977, Willeberg 1984); more recently, consumption of dry foods has been implicated as a risk factor specifically for idiopathic lower urinary tract disease (Buffington et al. 1997). Multiple diet-related factors may be involved with this increased risk, but included within these is the tendency for cats to produce smaller volumes of more concentrated urine when fed dry foods (Burger et al. 1980, Gaskell 1985). Explanations originally offered for these observations were that cats might not repair a water deficit as well as dogs, and that cats fed dry foods take in less water. These interpretations clearly require further discussion. In studies of five cats and three dogs, Adolph (1947) found that both species incurred similar water deficits in 48=B0C environments when water was available. After heat exposure without available water, dogs replaced moderate, but not severe deficits more rapidly than did cats. Both species, however, drank proportionately more than humans when dehydration exceeded 5%. These results suggest that differences in response to dehydration between dogs and cats, if they exist at all, are relatively small and probably not clinically relevant as a risk factor for lower urinary tract disease. It is also doubtful that cats reduce water intake in some unusual way when fed dry foods. It has been shown that cats fed diets containing differing amounts of moisture drink quite different amounts of water (Burger et al. 1980). A large number of these differences may be accounted for by changes in the potential renal solute load (PRSL) of the diets fed. The PRSL of a diet is the amount of solute, i.e., minerals and nitrogen, that must be excreted in the urine (Kohn and DiBartola 1992, Ziegler and Fomon 1989). The PRSL has been estimated as the urea (mg nitrogen/28) plus the sum of the sodium, chloride, phosphorus and potassium content of the diet (mg N/28 + Na + Cl + K + P) (O'Connor and Potts 1969). Calculations of PRSL reveal that the majority of diet-induced changes in water intake (Burger et al. 1980, Jackson and Tovey 1977, Kane et al. 1981), or urine formation (Sauer et al. 1985) reported in several studies can be explained by the solute load of the diet. "Similar data were reported in another study involving cats fed a single diet to which increasing amounts of water were added (Gaskell 1985). When the water content of the food was 10 or 45%, total water intake, urine volume and specific gravity were not different among groups. When the water content of the food was increased to 75%, however, total water intake and urine volume increased, and urine specific gravity decreased. Because the diet was the same in all cases, water intake (from food) probably increased as a consequence of increased food intake to meet energy needs from the water-diluted diet. Thus the differences in urine volumes and specific gravities observed in some of the studies discussed may be more a reflection of differences in the PRSL and/or the energy content of dry and wet diets, rather than moisture content per se. In consequence, if a cat is changed from a dry to a wet diet as part of a management program for lower urinary tract disease, it is important to ensure that the intended increases in urine volume and decreases in specific gravity actually occur. DOES MANIPULATING URINE PH HAVE A ROLE IN MANAGING OR PREVENTING ANY OF THE LOWER URINARY TRACT DISEASES SEEN IN CATS IN THE 1990S? "Dietary manipulation has been a mainstay of the management and prevention of struvite urolithiasis in cats for some years, primarily because of the influence of dietary ingredients on urine pH. Urine pH is a much more important determinant of struvite formation than is the magnesium content of the diet (Buffington et al. 1985, Buffington 1988, Marshall and Robertson 1976, Taton et al. 1984). Changing pH has a proportionately much greater effect on changing struvite activity product (solute activity is the concentration of crystalloid that is free to react with other solutes in a solution, and is the ultimate determinant of crystal formation) than changing the concentration of one or more of the crystalloid components of struvite. Reduction of urinary pH through dietary manipulation is thus the most reliable means of creating urine that is undersaturated with struvite; under these circumstances, crystallization and crystal growth will not occur, and preformed material will dissolve (Fig. 1) (Buffington 1988, Markwell and Buffington 1994). Acidification of the urine may not be appropriate, however, in the management of other types of urolith. It has been suggested, for example, from epidemiologic data that acidifying diets, and in particular those that result in a urine pH 6.29, may increase the risk of calcium oxalate formation (Kirk et al. 1995, Osborne et al. 1995b). Given this background, the ability to predict the likely urinary pH resulting from consumption of a particular diet from its analysis would be of considerable value. "Major dietary contributors of acid include the oxidation of sulfur amino acids and the balance of metabolizable anions and cations (Brosnan and Brosnan 1982, Patience and Wolynetz 1990). Oxidation of organic cations yields hydrogen ions, whereas oxidation of organic anions consumes them (Lennon et al. 1966). The net concentration of these organic ions can be measured indirectly by analyzing inorganic cations and anions in the diet (Austic and Patience 1988). This approach to predicting the influence of diet on urine pH and acid base balance has been evaluated in a number of species, including humans (Lennon et al. 1966), pigs (Patience and Wolynetz 1990) and cats (Kienzle et al. 1991, Kienzle and Schuknecht 1993, Kienzle and Wilms-Eilers 1994). "The initial studies reported in cats evaluated whether the dietary "base excess" [calculated from the sum of "alkalogenic" components (calcium, magnesium, sodium and potassium) minus the sum of "acidifying" components (phosphorus, chloride, methionine and cysteine)] could be used to predict urinary pH (Kienzle et al. 1991, Kienzle and Schuknecht 1993). These studies suggested that there was a highly significant correlation between dietary base excess and mean urine pH. They involved, however, only six wet and four dry commercial diets. We have conducted studies to determine if the same principle could be applied across a much wider range of canned commercial foods. In the course of these studies, 32 canned diets from a range of manufacturers were evaluated (Smith et al. 1995). These were fed to groups of four to eight healthy, adult cats for between 10 and 23 d. The cats were housed individually in purpose-built lodges, and urine pH was measured continuously using an automated system that has been described previously (Markwell and Smith 1993). Dietary analyses were used to calculate the base excess for each food using four different equations (Table 1). Individual mean urine pH values were then regressed on individual base excess intakes (calculated for each cat during each trial using its mean food intake) to investigate the suitability of a linear relationship. Although all four methods of calculating dietary base excess provided significant linear relationships, none of the resultant regression equations explained 28% of the variability seen in urine pH values (Table 1). "A second approach to evaluating the data was to establish whether various combinations of the individual components used to calculate dietary base excess could be used to predict urinary pH. When the individual intakes of each component were regressed against individual urine pH results, the best linear regression procedure suggested a more effective relationship to be the following: (units are g/100 g diet as fed). This relationship accounted for 35.5% of the variation seen in pH values. The signs of the coefficients were in agreement with expectations, i.e., increases in pH were positively correlated with the calcium, sodium and potassium content, and negatively correlated with the methionine and phosphorus content of the diet. These data indicate that dietary content may explain a significant proportion of the variation seen in the urine pH of meal-fed cats. More research is required, however, before dietary analysis can be used to yield an accurate prediction of the urine pH of cats fed commercial canned foods. DIET AND URINARY SATURATION "The primary goal of dietary manipulation to alter urinary pH and solute concentration is to achieve urine that is undersaturated with calculogenic crystalloids, although as described above, enhancement of urine volume may have the added benefit of increasing the frequency of urination, and hence reducing retention time. Undersaturation of urine is a prerequisite for urolith dissolution, and supersaturation with calculogenic crystalloids is an essential requirement for formation of a crystal nucleus, the initial step in development of a urine crystal (Fig. 1) (Buffington 1988, Markwell and Buffington 1994, Osborne et al. 1995a)." ---------------------------------------------------------------------------= ----- Lauren=20 See my cats: http://community.webshots.com/album/56955940rWhxAe |
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Phil P. wrote: "Steve Crane" wrote in message oups.com... Steve, I didn't say canned food is a "cure for every disease known to cats". However, it may prevent a few. Canned food is the first-line treatment for interstitial cystitis, crystalluria, urolithiasis, IBD, and recently, diabetes. Now, if cats with these diseases are *switched* to canned food for management and to prevent recurrence, feeding canned food from the git-go may prevent these diseases from ever developing. By that logic every cat should be fed k/d canned as soon as they are an adult. Renal failure is more common than many of those diseases combined. In my experience and our vets' general practices, I think the RL incidence of FLUTD is much higher than 2%. We always think so for a number of reasons. Cats that are not ill don't get into the vet clinic, so the population you are looking at is vastly different than the population as a whole. Secondly we've all experienced what happens when we buy a new car - suddenly we notice all kinds of people who were as smart as we were and bought the same model. I'll take that as a "no". As you please. Agreed, if that is what Joesephine Consumer actually bought. When buying dry foods the cost per day to feed the cats is about 25% of the cost of feeding canned foods. If Josephine Consumer elects to spend a few extra bucks buying a better quality food, the same dollars spent will buy a much better quality dry food than a canned food. Not so. The "best" dry food cannot be as digestible as an equal quality canned food. How could it be when only *dry* powered ingredients can be use in dry foods compared to fresh or whole meats and other ingredients used in canned foods. Phil, You know better than this. The cost of shipping water - which is +70% of the product makes that completely impossible. Digestibility values wouldn't even come close to altering the net cost difference between two foods. Further "dry powdered ingredients" are not the primary ingredients in dry foods, anymore than they are in canned foods. Chicken used in canned foods can be exactly the same chicken used in canned foods. The only difference is this extrusion process which removes the water, the type (dry powdered versus otherwise) of ingredient changes hardly at all. It is entirely possible to have a dry food that is mroe digestible than a canned food - happens all the time. |
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