STUDIES RELATING TO PUPPY GOLD NUTRIENTS AND FORMULATION

Am J Clin Nutr. 2004 Nov;80(5):1322-6. Related Articles, Links

Bone mass is recovered from lactation to postweaning in adolescent mothers with low calcium intakes.

Bezerra FF, Mendonca LM, Lobato EC, O'Brien KO, Donangelo CM.

Laboratorio de Bioquimica Nutricional e de Alimentos, Instituto de Quimica, Universidade Federal do Rio de Janeiro, Brazil.

BACKGROUND: Adolescent mothers may be at increased risk of irreversible bone loss during pregnancy and lactation, particularly when calcium intake is low. OBJECTIVE: Longitudinal changes in bone mass from lactation to postweaning were evaluated in 10 adolescent mothers aged 15-18 y who habitually consumed <500 mg Ca/d. DESIGN: Total-body bone mineral content (TBBMC), total-body bone mineral density (TBBMD), and lumbar spine bone mineral density (LSBMD) were measured at lactation (6-24 wk postpartum) and after weaning (12-30 mo postpartum). Serum hormones (intact parathyroid hormone, estradiol, and prolactin), serum calcium, and markers of bone turnover [urinary N-telopeptide cross-linking region of type I collagen (NTx) and plasma activity of bone alkaline phosphatase] were measured at lactation. RESULTS: TBBMC, total calcium content, TBBMD, and LSBMD increased from lactation to postweaning (P < 0.01). TBBMD and LSBMD were, respectively, 3.6% and 9.7% lower than predicted at lactation and 0.3% and 4.8% lower than predicted in the postweaning period. The increase in age-matched TBBMD adequacy was correlated with the time after resumption of menses (r = 0.86, P < 0.01). Calcium accretion from lactation to postweaning correlated negatively with estradiol (r = -0.86) and prolactin (r = -0.69) and positively with intact parathyroid hormone (r = 0.72) and NTx (r = 0.84) measured at lactation (P < 0.05). CONCLUSIONS: It appears that adolescent mothers with habitually low calcium intakes recover from lactation-associated bone loss after weaning. The rate of bone accretion, however, may not be sufficient to attain peak bone mass at maturity. Hormones regulating bone turnover during lactation may influence bone recovery in adolescent mothers.

Br J Nutr. 2005 May;93(5):593-9.

The influence of erythrocyte folate and serum vitamin B12 status on birth weight.

Relton CL, Pearce MS, Parker L.

Paediatric and Lifecourse Epidemiology Research Group, School of Clinical Medical Sciences (Child Health), Newcastle University, Sir James Spence Institute, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP, UK. c.l.relton@ncl.ac.uk

The extent to which maternal folate and vitamin B12 modulate infant birth weight is unclear. The present study investigated mothers in early gestation (mean 11.5 (sd 5.8) weeks) and neonates, at delivery. Erythrocyte (RBC) folate (mothers: n 683; neonates: n 614) and vitamin B12 (mothers: n 534; neonates: n 614) were measured. Data on smoking habits were available for 44 % of pregnancies (n 443). The relationship between vitamin levels and birth weight standardized for gender and gestational age was investigated, using linear regression and adjusting for possible confounding variables (maternal age, parity). Results are presented as standardized regression coefficients (b). Increasing maternal age was associated with elevated RBC folate (b 0.11 (95 % CI 0.08, 0.15), P<0.001; n 674) and smoking was associated with a decrease in maternal RBC folate (b -1.38 (95 % CI -1.92, -0.86), P=0.001; n 319). Neonatal RBC folate was predicted by maternal RBC folate (b 0.08 (95 % CI 0.04, 0.11), P=0.001; n 315) and maternal vitamin B12 (b 0.08 (95 % CI 0.01, 0.16), P=0.02; n 252). Smoking influenced maternal vitamin B12 status (b -0.88 (95 % CI -1.49, -0.27), P=0.005; n 231). Using univariate regression, smoking significantly influenced infant birth weight (b -2.15 (95 % CI -3.24, -1.04), P<0.001; n 437). However, the effect of smoking on birth weight was statistically non-significant when considered in a multivariate regression model, leaving maternal RBC folate as the only significant predictor of birth weight (b 0.25 (95 % CI 0.08, 0.42), P=0.005; n 145). These findings suggest that maternal folate status is an important determinant of infant birth weight. The combined effects of smoking and reduced RBC status on birth weight require further investigation.

J Nutr. 2004 Jan;134(1):86-92. Related Articles, Links

Supplementation of sows with L-carnitine during pregnancy and lactation improves growth of the piglets during the suckling period through increased milk production.

Ramanau A, Kluge H, Spilke J, Eder K.

Institute of Nutritional Sciences, Martin-Luther University, Halle-Wittenberg, D-06108 Halle/Saale, Germany.

Recent studies showed that piglets of sows fed diets supplemented with L-carnitine grow faster during the suckling period than piglets of control sows fed diets without L-carnitine. This study was undertaken to investigate the effect of L-carnitine supplementation in sows on milk production and milk constituents. An experiment was performed in which two groups of 20 gilts each were fed diets with or without supplemental L-carnitine during pregnancy (0 vs. 125 mg L-carnitine daily/sow) and lactation (0 vs. 250 mg L-carnitine daily/sow). The experiment was continued over two reproductive cycles. L-carnitine-treated sows had larger litters (P<0.01) and higher litter weights (P<0.05) than control sows. Piglets of L-carnitine-treated sows had lower birth weights (P<0.05) but grew faster during the suckling period (P<0.01) and were heavier (P<0.05) at weaning than piglets of control sows. L-carnitine-treated sows had higher milk yields on d 11 and 18 of lactation than control sows (P<0.05). Milk of L-carnitine-treated sows had higher concentrations of total and free carnitine than milk of control sows (P<0.001); concentrations of fat, protein and lactose and the amounts of gross energy in the milk did not differ between the two groups of sows. The amounts of protein (P<0.05) and lactose (P<0.05) were higher in L-carnitine-treated sows than in control sows; the amount of energy secreted with the milk tended to be higher in carnitine-treated sows than in control sows (P<0.10). The study suggests that piglets of carnitine-treated sows grow faster during the suckling period than those of control sows because they ingest more nutrients and energy with the milk.

Antiviral Res. 2003 Nov;60(3):193-9. Related Articles, Links

Antiviral activity of lactoferrin against canine herpesvirus.

Tanaka T, Nakatani S, Xuan X, Kumura H, Igarashi I, Shimazaki K.

Dairy Science Laboratory, Graduate School of Agriculture, Hokkaido University, Sapporo, Hokkaido 060-8589, Japan. tetsuya@anim.agr.hokudai.ac.jp

Lactoferrin (LF) is an iron-binding protein that is found in milk and other mammalian secretions. We found that bovine lactoferrin (bLF) inhibited both the in vitro infection and replication of canine herpesvirus (CHV) in Madin-Darby canine kidney (MDCK) cells. Incubation of CHV with bLF prevented subsequent infection of MDCK cells. Furthermore, proteins from CHV-infected MDCK cells were resolved by SDS-PAGE, and then bLF CHV-binding proteins were identified by far Western blotting. We demonstrated that the anti-CHV activity of bLF was due to its interaction with CHV as well as with MDCK cells. Both the apo- and holo-forms of bLF inhibited virus multiplication independently of their iron-withholding properties. We also demonstrated that human LF had anti-CHV activity. Our findings suggest that LF could be effective in dogs to provide protection against CHV infection

Adv Exp Med Biol. 1994;357:71-90. Related Articles, Links

The effects of lactoferrin on gram-negative bacteria.

Ellison RT 3rd.

Department of Medicine, University of Massachusetts School of Medicine, Worcester 01655, USA.

Lactoferrin is an iron-binding protein found in human mucosal secretions as well as the specific granules of polymorphonuclear leukocytes. A variety of functions have been ascribed to the protein, and it appears to contribute to antimicrobial host defense. In particular, it has been shown to have direct effects on pathogenic microorganisms including bacteriostasis and the induction of microbial iron uptake systems. Still its overall physiologic role remains to be defined. It has appeared logical that antimicrobial activity of the protein arises from sequestration of environmental iron thereby causing nutritional deprivation in susceptible organisms. This argument is buttressed by the finding that selected highly virulent pathogens have evolved techniques to subvert this effect and use the protein as an iron source. However, recent observations indicate that the protein has additional properties that contribute to host defense. Work by several groups has shown that the protein synergistically interacts with immunoglobins, complement, and neutrophil cationic proteins against Gram-negative bacteria. Further, both the whole protein and a cationic N-terminus peptide fragment directly damage the outer membrane of Gram-negative bacteria suggesting a mechanism for the supplemental effects. This review will summarize these diverse observations with a consideration of how the in vitro work relates to the physiological role of the protein.

Br J Nutr. 2003 Nov;90(5):979-86. Related Articles, Links

Infant intake of fatty acids from human milk over the first year of lactation.

Mitoulas LR, Gurrin LC, Doherty DA, Sherriff JL, Hartmann PE.

Biochemistry and Molecular Biology, School of Biomedical and Chemical Sciences, Faculty of Life and Physical Sciences, The University of Western Australia, 35 Stirling Highway, Crawley WA 6009, Australia. Leon.Mitoulas@uwa.edu.au

Despite the importance of human milk fatty acids for infant growth and development, there are few reports describing infant intakes of individual fatty acids. We have measured volume, fat content and fatty acid composition of milk from each breast at each feed over a 24 h period to determine the mean daily amounts of each fatty acid delivered to the infant from breast milk at 1, 2, 4, 6, 9 and 12 months of lactation in five women. Daily (24 h) milk production was 336.60 (SEM 26.21) and 414.49 (SEM 28.39) ml and milk fat content was 36.06 (SEM 1.37) and 34.97 (SEM 1.50) g/l for left and right breasts respectively over the course of the first year of lactation. Fatty acid composition varied over the course of the day (mean CV 14.3 (SD 7.7) %), but did not follow a circadian rhythm. The proportions (g/100 g total fatty acids) of fatty acids differed significantly between mothers (P<0.05) and over the first year of lactation (P<0.05). However, amounts (g) of most fatty acids delivered to the infant over 24 h did not differ during the first year of lactation and only the amounts of 18:3n-3, 22:5n-3 and 22:6n-3 delivered differed between mothers (P<0.05). Mean amounts of 18:2n-6, 18:3n-3, 20:4n-6 and 22:6n-3 delivered to the infant per 24 h over the first year of lactation were 2.380 (SD 0.980), 0.194 (SD 0.074), 0.093 (SD 0.031) and 0.049 (SD 0.021) g respectively. These results suggest that variation in proportions of fatty acids may not translate to variation in the amount delivered and that milk production and fat content need to be considered.

Am J Clin Nutr. 2004 Jan;79(1):139-47. Related Articles, Links

Dose response of bone mass to dietary arachidonic acid in piglets fed cow milk-based formula.

Blanaru JL, Kohut JR, Fitzpatrick-Wong SC, Weiler HA.

Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Canada.

BACKGROUND: The addition of arachidonic acid (AA) and docosahexaenoic acid (DHA) to infant formula was recently approved in North America. In piglets, dietary AA is linked to elevations in bone mass. OBJECTIVE: The objective was to investigate the effects of varied amounts of dietary AA on bone modeling and bone mass with the use of the piglet model for infant nutrition. DESIGN: Male piglets (n = 32) were randomly assigned to receive 1 of 4 formulas supplemented with AA (0.30%, 0.45%, 0.60%, or 0.75% of fat) plus DHA (0.1% of fat) from days 5 to 20 of life. Measurements included biomarkers of bone modeling, fatty acid status, and whole-body and femur bone mineral content; bone area was measured by dual-energy X-ray absorptiometry. Differences among groups were detected with two-factor analysis of variance. Regression analyses were used to determine factors responsible for bone mineral content after dietary AA was accounted for. RESULTS: Proportions of AA in plasma, liver, and adipose were modified by the dietary treatments, but bone modeling was not affected. Liver AA was positively related to plasma insulin-like growth factor 1 and calcitriol and urinary N-telopeptide. Whole-body bone mineral content was elevated in the piglets fed 0.60% and 0.75% AA and was best predicted by dietary AA and bone resorption. CONCLUSIONS: This study confirms that dietary AA alters bone mass and clarifies the best amount of AA to add to the diet of pigs born at term. Because the amount of dietary DHA was held constant, whether other amounts of DHA are related to bone mass requires investigation.

Plasma beta-casomorphin-7 immunoreactive peptide increases after milk intake in newborn but not in adult dogs

M Singh, CL Rosen, KJ Chang and GG Haddad

Department of Pediatrics (Pulmonary Division), Columbia University College of Physicians and Surgeons, New York, New York 10032.

To determine the relation between milk intake and plasma levels of beta- casomorphins as a function of age, we studied the levels of beta- casomorphin-7 immunoreactive material (BCMIR) in 2- and 4-wk-old beagle neonates and adult dogs following milk intake. We used three kinds of milk: 1) bovine casein-based milk formula; 2) canine bitch's milk, and 3) soy protein-based (noncasein) formula. Using a new extraction technique, BCMIR was isolated from plasma and assayed by radioimmunoassay at 0, 2, 4, and 6 h after feeding. We found that BCMIR increased significantly in both 2- and 4-wk-old puppies post bovine and canine milk feeding, but not after soy protein formula. Base-line values were about 80-120 fmol/ml and increased to 100-120% 2 h after bovine casein intake in the older puppies and by 4 h in the younger group. BCMIR levels were undetectable in adult dogs before or after bovine milk feeding. Beta-casomorphin-7 added to plasma was rapidly degraded whereas BCMIR was stable. Chromatographic profiles demonstrated that the BCMIR moiety is larger than beta-casomorphin-7. Our data suggest that the appearance of BCMIR in the plasma of neonatal dogs is a result of beta-casein degradation along a permeable gastrointestinal mucosa. We speculate that morphiceptin and beta- casomorphins can be cleaved from BCMIR and may have important physiologic effects

Am J Vet Res. 1999 Sep;60(9):1088-91. Related Articles, Links

Comparison of insulin-like growth factor-I concentration in mammary secretions and serum of small- and giant-breed dogs.

White ME, Hathaway MR, Dayton WR, Henderson T, Lepine AJ.

Department of Animal Science, College of Agricultural, Food, and Environmental Sciences, University of Minnesota, St. Paul 55108, USA.

OBJECTIVE: To determine insulin-like growth factor-I (IGF-I) concentrations in canine mammary secretions and serum during lactation and to compare them between small and giant breeds of dogs. ANIMALS: 7 gestating Beagles and 4 gestating Great Danes. PROCEDURE: Dogs were fed a common nutritionally complete and adequate gestation and lactation diet. Milk samples were collected at postpartum hour 12 and postpartum days 3, 7, 14, 21, and 28 after IV oxytocin administration. Two puppies/litter were identified at whelping for collection of blood samples corresponding to the days of milk sample collection plus days 35 and 42. Maternal blood samples were obtained on days 1, 7, and 42 from Beagles and days 1, 7, and 28 from Great Danes and were acid/ethanol extracted and analyzed by use of a radioimmunoassay. RESULTS: Maternal serum IGF-I concentration was greater in Great Danes at all sample collection times. Similarly, colostrum from Great Danes contained more IGF-I, compared with that of Beagles (70 ng/ml vs 40 ng/ml, respectively). These values decreased to approximately 10 ng/ml by day 3 in both breeds and remained between 10 and 20 ng/ml for the duration of lactation. Growth rate and serum IGF-I concentration were greater in Great Dane puppies at birth to day 42. CONCLUSIONS AND CLINICAL RELEVANCE: High IGF-I concentration in colostrum may be biologically important for newborn puppies. Body mass and serum IGF-I concentration are directly correlated in growing Beagle and Great Dane puppies. Serum IGF-I concentration may be an indicator of growth potential in dogs.

Cornell Vet. 1993 Apr;83(2):107-16. Related Articles, Links

Serum chemistry and lipid profiles in neonatal beagle puppies fed homemade milk replacer formulas.

Chandler ML, Miller E, Olson PN, Ralston SL.

Department of Clinical Sciences, College of Veterinary Medicine, Fort Collins 80523.

Milk replacer formulas based on cow's milk and egg yolks are frequently recommended for use in neonatal puppies. These formulas are lower in protein, kilocalories, calcium, and phosphorus than bitch's milk. In addition, the cholesterol content is greater than bitch's milk. The effect of feeding these formulas on serum chemistry profiles, lipid profiles, and alkaline phosphatase isoenzyme profiles of 5-week-old beagle puppies was studied. Three groups of beagle puppies were fed bitch's milk (control) (n = 18), a homemade milk-egg-oil formula (Formula 1) (n = 18), or a homemade milk-egg-oil formula supplemented with additional calcium and phosphorous (Formula 2) (n = 18). Concentrations of serum urea nitrogen, albumin, and total CO2 were lower (P < 0.05), and concentrations of serum phosphorus, globulins, sodium, chloride, and cholesterol were higher (P < 0.05) in formula-fed puppies than bitch-fed puppies. Serum potassium concentration was lower in the puppies fed Formula 1 than in the control puppies (P < 0.05), and serum potassium concentration in the puppies fed Formula 2 was not significantly different from that in puppies fed Formula 1 or the control puppies. Total triglyceride (TG) and high density lipoprotein2 cholesterol (HDL2) concentrations were similar in all three groups of puppies but the combined high density lipoprotein1 (HDL1) plus low density lipoprotein (LDL) cholesterol fraction was higher (P < 0.05) in the formula-fed puppies and accounted for the majority of the increase in cholesterol. There were no differences (P < 0.05) in total serum alkaline phosphatase (ALP) or bone-derived ALP (BALP) concentrations among the groups, however there was a higher (P < 0.05) serum concentration of liver-derived ALP (LALP) in the Formula 1-fed puppies. Feeding homemade egg and cow's milk-based puppy replacement formulas is not recommended for long term use.

Probl Vet Med. 1992 Sep;4(3):545-50. Related Articles, Links

Feeding to optimize canine reproductive efficiency.

Moser E.

The relationship between nutrition and reproduction is a topic of importance to veterinarians and breeders. Nutrient deficiencies, excesses, and imbalances all are capable of altering reproductive performance. Healthy adult dogs should be fed a diet high in digestibility, low in residue, and high in nutrient bioavailability. Rarely is nutritional intervention necessary during the first half of gestation. During the last half of gestation, switching to a growth/lactation diet and increasing intake by 1.2 to 1.4 x maintenance is indicated. Depending on breed and pup numbers, at peak lactation, feed intake may need to be increased by 2 to 4 x maintenance. The feeding goals of lactation are to minimize loss of bitch body condition score and optimize milk production and pup growth. After weaning, the female who is in poor body condition should remain on a diet rich in protein, fat, and trace nutrients until she is physically/nutritionally repleted.

Am J Clin Nutr 2002 Mar;75(3):570-80

A randomized controlled trial of long-chain polyunsaturated fatty acid supplementation of formula in term infants after weaning at 6 wk of age.

Birch EE, Hoffman DR, Castaneda YS, Fawcett SL, Birch DG, Uauy RD.

Retina Foundation of the Southwest, Dallas, TX 75231, USA. ebirch@retinafoundation.org

BACKGROUND: The critical period during which the dietary supply of long-chain polyunsaturated fatty acids (LCPs) may influence the maturation of cortical function in term infants is unknown. OBJECTIVE: The aim of the present study was to determine the relative importance for maturation of the visual cortex of the dietary supply of LCPs during the first 6 wk of life compared with that during weeks 7-52. DESIGN: A randomized controlled clinical trial of LCP supplementation in 65 healthy term infants who were weaned from breast-feeding at 6 wk of age was conducted to determine whether the dietary supply of LCPs after weaning influenced the maturation of visual acuity and stereoacuity. RESULTS: Despite a dietary supply of LCPs from breast milk during the first 6 wk of life, infants who were weaned to formula that did not provide LCPs had significantly poorer visual acuity at 17, 26, and 52 wk of age and significantly poorer stereoacuity at 17 wk of age than did infants who were weaned to LCP-supplemented formula. Better acuity and stereoacuity at 17 wk was correlated with higher concentrations of docosahexaenoic acid in plasma. Better acuity at 52 wk was correlated with higher concentrations of docosahexaenoic acid in plasma and red blood cells. No significant effects of diet on growth were found. CONCLUSION: The results suggest that the critical period during which the dietary supply of LCPs can influence the maturation of cortical function extends beyond 6 wk of age.

Am J Vet Res. 2001 Aug;62(8):1266-72.

Related Articles, Links

Changes in protein and nutrient composition of milk throughout lactation in dogs.

Adkins Y, Lepine AJ, Lonnerdal B.

Department of Nutrition, College of Agricultural and Environmental Sciences, University of California, Davis 95616, USA.

OBJECTIVE: To evaluate changes in protein and nutrient composition of milk throughout lactation in dogs. SAMPLE POPULATION: Milk samples collected from 10 lactating Beagles. PROCEDURE: Milk samples were collected on days 1, 3, 7, 14, 21, 28, 35, and 42 after parturition and analyzed to determine concentrations of nitrogen, nonprotein nitrogen, casein, whey proteins, amino acids, lipids, lactose, citrate, minerals, and trace elements. Optimum conditions for separating casein from whey proteins and distribution of milk proteins throughout lactation were assessed by use of polyacrylamide gel electrophoresis. RESULTS: Protein concentration was high in samples collected on day 1 (143 g/L), decreased through day 21 (68.4 g/L), and increased thereafter. Concentration of nonprotein nitrogen did not change throughout lactation (5.7 to 9.9% of total nitrogen content). Casein-to-whey ratio was approximately 70:30 and remained constant throughout lactation. Lactose concentration increased from 16.6 g/L on day 1 to 34.0 to 40.2 g/L on days 7 to 42. Lipid concentration ranged from 112.5 to 1372 g/L. Citrate concentration increased from day 1 (4.8 mM) to day 7 (6.6 mM), then gradually decreased until day 42 (3.9 mM). Iron, zinc, copper, and magnesium concentrations decreased during lactation, whereas calcium and phosphorus concentrations increased. Calcium-to-phosphorus ratio remained constant throughout lactation (approx 1.6:1). Energy content of milk ranged from 1,444 to 1,831 kcal/L. CONCLUSIONS AND CLINICAL RELEVANCE: Protein and nutrient composition of milk changes throughout lactation in dogs. These data can provide valuable information for use in establishing nutrient requirements of puppies during the suckling period.

Hypertension. 2004 Jun 7 [Epub ahead of print] Related Articles, Links

Perinatal L-Arginine and Antioxidant Supplements Reduce Adult Blood Pressure in Spontaneously Hypertensive Rats.

Racasan S, Braam B, Van Der Giezen DM, Goldschmeding R, Boer P, Koomans HA, Joles JA.

Departments of Nephrology and Hypertension and Pathology, University Medical Center, Utrecht, The Netherlands.

Embryo cross-transplantation and cross-fostering between spontaneously hypertensive rats (SHR) and normotensive rats (WKY) suggest that perinatal environment modulates the genetically determined phenotype. In SHR the balance between NO and reactive oxygen species (ROS) is disturbed. We hypothesized that increasing NO and diminishing ROS in perinatal life would ameliorate hypertension in adult SHR. Pregnant SHR and WKY and their offspring received L-arginine plus antioxidants (vitamin C, vitamin E, and taurine) during the last 2 weeks of pregnancy and then until either 4 or 8 weeks after birth. Systolic blood pressure (SBP) and urinary excretion of protein, nitrates (NOx), and thiobarbituric acid reactive substances (TBARS) were measured. At 48 weeks of age rats were euthanized for glomerular counts. Perinatal supplements reduced SBP persistently in SHR and prevented the SBP increase observed in aging WKY. Initially NOx excretion was lower and TBARS excretion higher in SHR than WKY. There was a direct effect on NOx excretion in supplemented pregnant SHR and their offspring, but no increase was observed after stopping the supplements. TBARS excretion was only depressed up to 14 weeks by the supplements despite persistent differences in SBP. Consistent effects on nephron number were absent. Mild proteinuria, present in control SHR at 48 weeks, was prevented in all supplemented rats. Perinatal supplementation of NO substrate and antioxidants results in persistent reduction of SBP and renal protection in SHR, although effects on NOx and TBARS were only transient. This suggests a critical role for perinatal pro- and antioxidant balance in programming BP later in life.

 

ANIMAL NATURALS THE INSIDE TRUTH ON PET FOOD AND SUPPLEMENTS   The pet food industry has some dirty secrets that they hoped you’d never discover...but I’m blowing the whistle on them. And are they gonna be mad.   But you’re being ripped off and your animals are suffering for it, in my opinion. And it’s been going on for decades.   Strong words, I know, but after 20 years studying what’s actually used in commercial pet foods these days, I just couldn’t keep my mouth shut any longer.   That’s why I put together this special investigative report. Once you’ve “digested” all this information, I’m certain that you’ll be as disgusted and outraged as I am. First things first (or what’s not in the food): Judging from their advertisements and pretty photos, commercial pet foods contain choice cuts of beef, fresh grains, chicken breast, meat, eggs, rice…all the nutrition your dog could ever need. The same wholesome quality you eat, right? Wrong. Sounds great, I know, but look at it from a commercial point of view; those ingredients are costly, not to mention more desirable for human consumption. They’re just too expensive and good for lowly dogs.   I’ve gotten down and dirty and checked out the commercial manufacturers and I can tell you (as can industry watchdogs) that none of the big commercial producers use any of the above desirable ingredients in their feeds. The pictures they use of wholesome foods are flat out lies. Okay, so what is in the food? You might be sorry you asked. Remember your mental image and the photos they use of that wholesome healthy food, the beef, the chicken, those tasty whole grains…now, brace yourself for a reality check.   Those choice cuts of beef are really cow brains, tongues, esophagi and fetal tissue that may be dangerously high in hormones. Much of the meat is diseased and even cancerous. Because using that great looking meat means they’d have to actually pay for it, and as you’ll learn, pet food companies don’t buy anything human-grade.   Those “whole grains” have had the starch removed for cornstarch powder and often the oil has been extracted (by chemical processing) for corn oil, or are remnants from the milling process. Those grains that are truly whole have usually been deemed unfit for human consumption because of mold, contaminants, poor quality, or poor handling practices. Or worse, ultra-high pesticide concentrations.   The last few years alone, dozens of dogs died from aflatoxin poisoning-traced to rotting grains rejected for human use, but just perfect for dog foods. After all, it’s only dogs, so who cares?   Then, because the manufacturers know that the food is utterly devoid of any real nutrition it is “fortified” with vitamins and minerals. As sick as this fortification joke is, it’s made even worse by the fact that the nutrients added are also rejected for humans use and full of their own contaminants. Why? Because the ingredients they are using are not wholesome, and the harsh manufacturing practices that are required to produce those cute shapes destroy what little nutritional value the food ever had. It’s kind of like depleted uranium—it looks the same but lacks the original zap. Remember, everything in pet food is scrap material from the human food industry. It’s unfit, unsafe or condemned for human use. Hello!   So humans benefit all around at the expense of your pet. Pet food manufacturers get great prices on the “waste materials”. Hint—if pet food companies don’t buy it, it’s fed to pigs before slaughter. Human food processing companies save money twice, once when they sell the materials that to them are merely garbage, and a second time when they avoid having to pay to dispose of that same disgusting muck. Is that a great business or what? Hungry yet? It gets worse… If this sounds like some sort of conspiracy, that’s because it is, at least in my opinion. It’s not by chance that four of the five largest U.S. pet food companies are subsidiaries of the major multi-national food corporations: Heinz, Nestle, Mars, Colgate-Palmolive and Ralston-Purina (who disguises this by having two separate food companies, one for human and the other for animal feeds). Remember the Recent E-Coli Scare? It’s no wonder that dogs everywhere aren’t dropping like flies from e-coli infections. It’s testimony to the hardy evolutionary design of our best friends that they can survive given the incredibly high degree of bacterial contamination in the commercial foods we give them. Where humans drop like flies with food poisoning, dogs tough it out; but they suffer in their own way, too.   According to API, the Animal Protection Institute, the problem is extreme. Parts deemed unfit for human food, include animals classed as “4-D” (dead, diseased, dying or disabled). These animals (which do not meet human-food qualifications) are sent to pet food processors straight away.   4-D meat includes meat that is revolting beyond words: pus-laden, gangrenous “green liver” syndrome and worse. Suffice to say, if you’ve ever seen the meat that goes into today’s pet foods, you would not feed it anymore. And when you see the term “meat or poultry by-products” what does that mean? Quite simply, that’s what’s left of the carcass after human and mechanical de-boning and processing have been completed: bones, blood, pus, intestines, bowels, ligaments, subcutaneous fat, hooves, horns, beaks and any other parts that humans cannot or will not knowingly eat.   Maybe by-products should be renamed “bye-bye products”. But because of their low cost, they’re a staple of modern-day pet food. The fox is watching the doghouse! The Pet Food Institute (the trade association for pet food manufacturers) acknowledges the importance of by-products as a source of additional income for farmers and food processors.   The truth is that most of these remnant foods are not only indigestible, they also provide a questionable source of nutrition for our animals. At best. So it strikes me as more than a little ironic that an organization such as this calls itself the Pet Food Institute. Perhaps what it should really be called is the “human food waste product recycling club”. At least that would be a more accurate description of their focus and intent. Call a spade a spade. Remember the 70’s movie “Soylent Green”? In this cheesy movie, Charlton Heston screamed “Soylent Green is people!” Story line, they took people who died, ground them up, then fed them to other people in a product called Soylent Green. It was a well-guarded secret so nobody knew they were actually eating other people. Well modern day pet foods are the real life equivalent of “Soylent Green”.   Fact is, the Soylent Green process feeds your dogs every day. Though you surely won’t find dogs or cats listed as ingredients on any pet food labels, the San Francisco Chronicle reported that euthanized companion animals were found in pet foods. This was vehemently denied by manufacturers; however, the American Veterinary Medical Association confirmed the Chronicle’s story.   Think about it. Do you really believe the thousands of road kills, pets dying at veterinary clinics and animal shelters every day go to doggy heaven. I grew up with TV cartoons showing old racehorses going to the rendering glue factory. My research leads me to believe it’s the same for dogs today. So how is this effecting my pet? “From his experience as a veterinarian and federal meat inspector, P. F. McGargle, D.V.M., has concluded that feeding slaughterhouse wastes to animals increases their chance of getting cancer and other degenerative diseases. Those wastes, he reports, can include moldy, rancid or spoiled meats as well as tissues severely riddled with cancer. These meat scraps can also contain hormone levels comparable to those that have produced cancer in laboratory animals.   Dr. McGargle attributed these high levels to two causes: synthetic hormones routinely fed to livestock to stimulate rapid growth, and meat meal whose source is often glandular wastes and fetal tissues from pregnant cows. Both are naturally high in hormones. When livestock is slaughtered and the meat is processed, the hormones are still active. High hormone levels have the most severe effect on cats, which are extremely sensitive to them. The tissues or pellets that are used to fatten steers and caponize chickens, for example, are considered toxic to cats, even in very low levels. These hormones are not destroyed by the high temperature and pressure cooking that pet food manufacture requires. And what in the world is that terrible smell? Ever walk around the back of a restaurant that has a fryer? Did you notice that awful greasy rancid smell? You know, the one near that dumpster labeled industrial grease or oil disposal?   Ever feel like that freshly opened bag of dog food smelled exactly the same way? You should. It does smell the same. That’s because the fat added to most commercial dog foods is refined animal fat, recycled kitchen grease, and other oils too rancid or deemed inedible for human use.   These rancid fats are generally sprayed directly onto dried kibble or extruded pellets to make a product which even a dog won’t eat more palatable. While certain fats provide the luster and sheen to your dogs coat, the sparkle to his eyes and the extra calories working dogs require, the rancid fats that are discarded by restaurants or are rendered from slaughterhouse animals are not nearly so beneficial.   In fact, these rancid fats are being blamed for a host of new health related problems in dogs including; diarrhea, vomiting of bile, gas, bad breath and even severe digestive problems. In puppies and kittens, whose digestive tracts are not fully developed, these rancid fats can cause permanent damage leading to a lifetime of digestion and assimilation problems. Even in foods designed to be less allergenic, such as lamb and rice formulas, rancid fats can cause your pet to experience a reaction. Do you put your dog “out to pasture”? Of course you don’t. Dogs don’t graze. And you don’t feed your dog wheat or hay or corn either. Or do you? In the last decade, as the populace of this country has moved its diet more and more towards grains and away from animal proteins, the amount of grain products in animal foods has increased proportionally.   This has happened for two reasons; first, because we are consuming less meat, the amount of animals slaughtered has decreased and the byproducts of those slaughtered animals have undergone a like decline. Second, with an increase in human grain usage, grain unfit for human consumption, moldy grain and grain byproducts have all become progressively more available.   It should come as no surprise that corn and wheat are far from ideal for dogs or cats from a nutritional standpoint. Cats in particular suffer from diets that include a predominance of grain. That is because cats are obligate omnivores. That is, they require meat to fulfill certain physiological needs.   Another problem with feeding predominately grain based foods has to do with the grains themselves. Many of the grains that find there way into commercial pet foods have become wet, or moldy or contaminated by a fungus. In 1995 Nature’s Recipe was forced to pull nearly 20 million worth of dog food contained wheat contaminated by a fungus that produced vomitoxin and aflatoxin which is a kind of poison called a mycotoxin that is given off when mold grows.   Peanuts are particularly susceptible to aflatoxin problems as the fungi which produce it tend to grow especially well on peanut hulls. Of course it probably won’t amaze you at this point to discover that peanut hulls are another major constituent of certain commercial pet foods.   How could this terrible fungus occur in pet foods. Well…testing, which is not great even for human foods, is almost nonexistent for pet products. Was that you or the dog? Flatulence. It’s funny to blame it on your dog when you do it, but not nearly so funny when your dog does it all the time. Nevertheless, soy, which has been known to cause flatulence in dogs, has become an increasingly common ingredient in commercial foods. Another increasingly common reason for canine farting is intestinal blockages.   The culprit; among others, humectants – ingredients such as corn syrup and corn gluten meal which bind water molecules to prevent oxidation – also bind the water in such a way that the food actually sticks to the colon and may cause blockage and fermentation—methane gas. The blockage of the colon may well cause an increased risk of cancer of the colon or rectum. Pickled or preserved? Sodium nitrite, butylated hydroxytoluene, ethoxyquin, butylated hydroxyanisole, propyl gallate, tertiary butylhydroquinone and other equally evil sounding compounds are being added to commercial dog foods.   Why?   Because when you combine all of the aforementioned toxic decomposed, diseased, hormone laden and rancid ingredients into one product, the only thing that will keep them from becoming so utterly putrid is to lace them with powerful chemicals to keep them “stable”.   We might as well be storing them in formaldehyde. And if you think the names of these chemicals sound bad, take a look at the problems they cause; cancers of the stomach, intestines and blood, kidney damage, central nervous system disorders, depressed immune function, liver damage other forms of chronic and acute chemical toxicity.   Even foods labeled “preservative free” may have one or more of the above chemicals added. That’s because the government does not require the manufacturer to list on the ingredient label anything added to ingredients prior to incorporation into the finished food. Thus, when rancid fat is preserved with ethoxyquin prior to arrival at a pet food manufacturers facility, the manufacturer, provided it does not add additional ethoxyquin to the material, is not required to list ethoxyquin anywhere on the label. Just how prevalent are these preservatives in the food? A recent analysis determined that two-thirds of the pet foods produced in the US had synthetic preservatives added by the manufacturers. Of the remaining third, 90% included ingredients that were already stabilized by synthetic preservatives.   Today, there are more than 8,600 recognized food additives with absolutely zero toxicity information on 45% of them! Of those that have been analyzed only 5% have had a complete health hazard assessment. Many of these chemicals are known to be carcinogenic above a certain level but are still allowed to be added in concentrations below the known carcinogenic amount.   This is misleading because many of these compounds are not readily cleared from the body and can thus build up to very high levels over time.   Ethoxyquin, for example, was found in dogs’ livers months after it had been totally removed from their diet. Since when do dogs need to be fed insecticide as part of a healthy diet? The answer to this question should be obvious. NEVER! Here’s another alarming fact: 60% of all herbicides, 90% of all fungicides and 30% of all insecticides have been proven to cause cancer in and of themselves. Virtually all of these chemicals find there way into commercial pet food via the added grains and meats used.   Worse still, upwards of 80% of these chemicals, 49,000 in all, have virtually no toxicity data. In other words neither you, nor I, nor any scientist in any lab in the world has any idea what they will do to you pet today, tomorrow or ten years from now.   Another recent study found that these same chemicals lead to chromosomal mutations, double-strand DNA breaks and numerous mutations.   To your dog, this means a greater incidence of cancer and other diseases. To your breeding program, this means lower survivability, mutated puppies and genetic aberrations that will make the pups non-salable.   Just recently, I received the following notice from the FDA Center for Veterinary Medicine: August 14, 1997