Dry Food Good For Teeth and Gum Health?

"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

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.

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.

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.

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!!!??!!!

"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.

"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?

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

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

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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)."

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Lauren=20
See my cats: http://community.webshots.com/album/56955940rWhxAe

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.