Krmivá

[fosilia]

aj tak si budeš tvrdit svoje. ja viem svoje ty vieš svoje ok a mala by si si spravit strednu pomohlo by ti to

Dakujem za tvoje rady dovtedy budem radsej nadalej varit lebo z Canonu sa moj pes tazko naje.

http://f20.yahoofs.com/hkblog/js1G0_qLE ... GBynqfmBzp

[Fraga]

Fosilia ty si baba? ja myslela že chlap nejak sa mi to domotalo. Tak sorry ked som pisala ako chlapovi

inak písala som do RC ohladom tých ich granulí a BHA a BHT. Ja tiež krmim RC ne moc ale krmim a som zatial spokojna...

BHT nepoužívajú a k BHA mi odpísali toto :

Čo sa týka vašej otázky, na internete sa nachádza obrovské množstvo rôznych informácii aj dezinformácii z rôznych overených aj neoverených zdrojov. Royal Canin používa antioxydant BHA (Butyl-Hydroxy-Anisole) v svojich produktoch, aby ochránil tuky pred oxydáciou a znehodnotením. Ako iste viete, v tuku je rozpustných veľa vitamínov a pokiaľ chceme aby tvrdenie na obale o obsahu vitamínov (ale aj iných látok) platilo aj na konci expiračnej doby, je nevyhnutné tuky chrániť. Keďže podobne ako vy sa pýtajú aj iní ľudia v iných krajinách, v prílohe vám posielam odpoveď na túto otázku od Pascale Pibot z výskumného centra Royal Canin aj s citovaním použitých zdrojov. (čo je v prílohe je všetko v angl. takže mne by to musel niekto preloziť a preto to sem nedavam)

Čo sa týka samotného výberu a použitia BHA (BHT nepoužívame), Royal Canin presne vie čo robí. Naviac existuje veľa podporných argumentov pre jeho použitie:

1. Európska legislatíva pre Pet Food povoľuje použiť BHA v dávke < 150 ppm. Royal Canin ho používa v nižšej dávke.

2. BHA je povolené aj na použitie v potrave pre ľudí.

3. Nie je žiadny dôkaz karcinogenicity BHA u ľudí, psov a mačiek. Existujú o tom desiatky odborných výskumov a článkov, za všetky vám nižšie prikladám sumár 2 článkov.

4. U psov a mačiek ešte žiadna štúdia nepotvrdila nebezpečenstvo použitia BHA.

5. Naopak, mnohé články popisujú priaznivé účinky BHA u ľudí v boji proti rakovine (niektoré takisto prikladám nižšie v maili).

[fosilia]

Sorry som dazdovka.
Daj sem tu prilohu nech sa pobavim.
Tak za prve BHA v ludskej vyzive. Zabudla senora napisat ze sa jedna len o niektore suche plody zvlast sa to tyka korenin, kde asi tazko spapame kilo.
Za druhe ukaz mi testera, ktory bude BHA testovat na mackach a psov.
Prokurator by sa potesil.
Vsetky vysledky, ktore su dnes zname sa robili na laboratornych zvieratach. To asi senora z RC nevie. Ody na radost o norme EU, ktora len opisala normu AAFCO, pricom tu sa davky znizili na 30ppm. Ludia zvladnu 5ppm.
Kazdy antioxidant ma preto tento nazov pretoze urcite vies co je volny radikal. O konzervacii preto aby krmivo bolo dostatocne zakonzervovane je hlavne koli ekonomickej vyhode predlzenia trvanlivosti produktu a nema nic spolocne sp zdravou vyzivou.

Skoda ze si sa neopytala preco nepouzivaju v kuracej mucke ciste maso ked krmivo je take drahe a melu cele kurence. Potom treba pisat na obal kuraco-kostna mucka. A co podiel kuraco-kostnej mucky. Preco to nechcu nikde zverejnovat. Ze to zle vyzera nevadi, ludia takto veria ze krmivo obsahuje ciste kuracie maso.

[ZEwa]

Sice pisem trochu odveci ale k teme krmiva: neboli tu spominane granule od americkeho vyrobcu ANF. Prosim ak ma niekto skusenosti, resp.aky nazor mate? Ja krmim morcacie s jacmenom pre psov s citlivym zazivanim a alergiami, zatal spokojnost - krasna srst, ziadne lupiny ci sucha koza, hafa v kondicii, aktivna.
Zlozenie:Turkey meal/28%/, barley, brewers rice, chicken fat, beet pulp, natural flavors, brewers yeast, salt, dried egg product, lecithin, fish meal, flaxseed, fish oil, Yucca Schidigera extract, cholin chloride, potassium chloride, methionine, ferrous sulfate, vitamin E supplement, zinc sulfate, manganese sulfate, biotin supplement, copper sulfate, vitamin A supplement, niacin, calcium pantothenate, riboflavin supplement, vitamin B12 supplement, ascorbic acid, pyridoxine hydrochloride, thiamine mononitrade, vitamin D3 supplement, calcium iodate, menadione sodium bisulfite complex, folic acid, sodium selenite.

Dakujem za pripadne odpovede k mojej otazke.
Totiz mam teraz druheho psa. 5meacne stena irskeho teriera, ktore bolo u chovatelky krmene Eucanuba junior pre stredne plemena tak by som chcela krmit obidve hafy jednou znackou a chcem prejst na ANF /samozrejme stenacie/ pa a dik

[Fraga]

Food Chem Toxicol 2000 Jul;38(7):599-605

Intake of butylated hydroxyanisole and butylated hydroxytoluene and stomach cancer risk: results from analyses in the Netherlands Cohort Study.

Botterweck AA, Verhagen H, Goldbohm RA, Kleinjans J, van den Brandt PA.

Department of Epidemiology, Maastricht University, The Netherlands.
AAM.Botterweck@Epid.unimaas.NL

Both carcinogenic and anticarcinogenic properties have been reported for the synthetic antioxidants butylated hydroxyanisole (BHA) and butylated

hydroxytoluene (BHT). The association between dietary intake of BHA and BHT and stomach cancer risk was investigated in the Netherlands Cohort Study (NLCS) that started in 1986 among 120,852 men and women aged 55 to 69 years. A semi-quantitative food frequency questionnaire was used to assess food consumption. Information on BHA or BHT content of cooking fats, oils, mayonnaise and other creamy salad dressings and dried soups was obtained by chemical analysis, a Dutch database of food additives (ALBA) and the Dutch Compendium of Foods and Diet Products. After 6.3 years of follow-up, complete data on BHA and BHT intake of 192 incident stomach cancer cases and 2035 subcohort members were available for case-cohort analysis. Mean intake of BHA or BHT among subcohort members was 105 and 351 microg/day, respectively. For consumption of mayonnaise and other creamy salad dressings with BHA or BHT no association with stomach cancer risk was observed. A statistically non-significant decrease in stomach cancer risk was observed with increasing BHA and BHT intake [rate ratio (RR) highest/lowest intake of BHA = 0.57 (95% confidence interval (CI): 0.25-1.30] and BHT = 0.74 (95% CI: 0.38-1.43). In this study, no significant association with stomach cancer risk was found for usual intake of low levels of BHA and BHT.



25: Exp Toxicol Pathol 1996 Feb;48(2-3):189-95

Epigenetic carcinogens: evaluation and risk assessment. Williams GM, Whysner J. American Health Foundation, Valhalla, NY 10595-1599, USA.
Regulatory policies in the U.S. have been developed based upon a single model of cancer causation, which assumes chemical-induced genetic alterations. Such a model predicts some degree of cancer risk even at extremely low exposure levels.

Many chemicals that produce tumors in experimental animals have been shown to act by epigenetic mechanisms that do not involve an attack by the chemical on DNA leading to subsequent genetic alteration. Such indirect mechanisms require prolonged exposures to high levels of chemicals for the production of tumors. For chemicals that are carcinogenic in this manner, the cancer mechanism would not be operative at exposures below a threshold at which the relevant cellular effect does not occur. Also, in contrast to DNA-reactive mechanisms, epigenetic
effects may be unique to the rodent species used for testing. Certain chemical tumorigens have been well studied and provide examples for the of mechanistic information in risk assessment. Butylated hydroxyanisole and saccharin are nongenotoxic food additives for which no risk to humans is predicted based upon low exposure levels and the likelihood that humans are either insensitive or much less sensitive to the tumorigenic effects found in rodent test species. For another non-genotoxic food additive d-limonene, the mechanism that underlies kidney tumor development in male rats is not expected to be operative in humans at all. The pharmaceutical phenobarbital represents a large group of non-genotoxic liver microsome enzyme inducers, which produce liver cancer in mice at levels that are near to therapeutic doses in humans.
Epidemiology studies have not shown phenobarbital-related tumors in humans, indicating that humans may be less sensitive to the effects of phenobarbital.

The mechanistic considerations involved in the risk assessment of these agents demonstrate that humans are not at risk from current exposure levels of many epigenetic carcinogens.

Advantages of BHA:

The following articles show that BHA is good for health!
Anticarcinogenic effect on humans
Food Chem Toxicol 1999 Sep-Oct;37(9-10):1027-38

Safety assessment of butylated hydroxyanisole and butylated hydroxytoluene as antioxidant food additives.

Williams GM, Iatropoulos MJ, Whysner J.

Department of Pathology, New York Medical College, American Health Foundation

Valhalla, 10595, USA.

Butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) are widely

used antioxidant food additives. They have been extensively studied for
potential toxicities. This review details experimental studies of genotoxicity
and carcinogenicity which bear on cancer hazard assessment of exposure to humans. We conclude that BHA and BHT pose no cancer hazard and, to the contrary, may be anticarcinogenic at current levels of food additive use.

Anticarcinogenic effect on animals

Food Chem Toxicol 1999 Sep-Oct;37(9-10):985-92

Phenolics: blocking agents for heterocyclic amine-induced carcinogenesis.

Hirose M, Takahashi S, Ogawa K, Futakuchi M, Shirai T.

First Department of Pathology, Nagoya City University, Medical School, Nagoya, Japan.

Chemopreventive effects of synthetic and naturally occurring antioxidants on heterocyclic amine (HCA)-induced rat carcinogenesis and mechanisms of inhibition were assessed. In a medium-term liver bioassay, combined treatment with 0.03% 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) and synthetic antioxidants such as 1-O-hexyl-2,3,5-trimethylhydroquinone (HTHQ), butylated hydroxyanisole

(BHA), butylated hydroxutoluene (BHT), tert-butylhydroquinone (TBHQ) or propyl
gallate, each at a dose of 0.25%, inhibited development of preneoplastic

glutathione S-transferase placental form (GST-P) positive foci as compared with

MeIQx alone, after initiation with diethylnitrosamine (DEN). Of these

antioxidants, HTHQ showed the greatest activity. 8-Hydroxydeoxyguanosine

(8-OHdG), a marker for DNA damage induced by active oxygen species, and

malonedialdehyde and 4-hydroxynonenal levels were not largely influenced by the

treatment with MeIQx or antioxidants, either alone or in combination. In the same medium-term liver bioassay, effects of some naturally occurring

antioxidants, such as green tea catechins (GTC), hesperidin, chlorogenic acid, quercetin, rutin, curcumin, daidzin, ferulic acid and genistein were also examined. Of these antioxidants, only GTC tended to inhibit GST-P positive foci development, while quercetin, rutin, curcumin, daidzin, ferulic acid and genistein all exerted significant enhancing effects. Examination of HTHQ influence in a medium term liver bioassay with HCA Glu-P-1, in which the experimental period was extended for up to 26 weeks, also demonstrated a significant decrease in the incidence of liver tumours to 40% in the group treated with 0.5% HTHQ and 0.03%
2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1) as compared with the Glu-P-1 alone value of 89%. Effects of HTHQ on colon carcinogenesis induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) were evaluated in a
two-stage colon carcinogenesis model using 1,2-dimethylhydrazine (DMH) as an initiator. At week 36, the multiplicity of colon tumours induced by 0.02% PhIP after DMH initiation (9.1+/-6.2/rat) was dose-dependently decreased by the combined treatment with 0.5% HTHQ (3.6+/-1.8, P < 0.001) and 0.125% HTHQ (6.2+/-3.2, not significant). Similarly, the incidence of mammary carcinomas in female F344 rats induced by oral administration of 0.02% PhIP (40%) for 52 weeks was significantly decreased by simultaneous treatment with 0.5% HTHQ (5%).

Alpha-tocopherol and chlorophyllin only reduced the multiplicity of carcinomas.

Analysis of the influence of HTHQ on metabolic activation of Glu-P-1 or PhIP after incubation with rat S9 mixture and NADPH by HPLC, revealed that each major metabolite was strongly reduced by the addition of HTHQ. Immunohistochemically detected PhIP-DNA adduct positive nuclei in the colon induced by continuous oral treatment with 0.02% PhIP for 2 weeks decreased by the combined treatment with 0.5 or 0.125% HTHQ. These results indicate that synthetic antioxidant HTHQ is a very strong chemopreventor of heterocyclic amine (HCA)-induced carcinogenesis
and that depressed metabolic activation rather than antioxidant activity is
responsible for the observed effect.

Cancer Lett 1999 Apr 1;137(2):123-30

Evaluation of butylated hydroxyanisole, myo-inositol, curcumin, esculetin, resveratrol and lycopene as inhibitors of benzo[a]pyrene plus 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced lung tumorigenesis in A/J mice.

Hecht SS, Kenney PM, Wang M, Trushin N, Agarwal S, Rao AV, Upadhyaya P.

University of Minnesota Cancer Center, Minneapolis 55455, USA.

hecht002@gold.tc.umn.edu

The potential activities of butylated hydroxyanisole (BHA), myo-inositol,

curcumin, esculetin, resveratrol and lycopene-enriched tomato oleoresin (LTO) as

chemopreventive agents against lung tumor induction in A/J mice by the tobacco

smoke carcinogens benzo[a]pyrene (BaP) and

4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were evaluated. Groups of

20 A/J mice were treated weekly by gavage with a mixture of BaP and NNK (3

micromol each) for 8 weeks, then sacrificed 26 weeks after the first carcinogen

treatment. Mice treated with BHA (20 or 40 micromol) by gavage 2 h before each

dose of BaP and NNK had significantly reduced lung tumor multiplicity. Treatment

with BHA (20 or 40 micromol) by gavage weekly or with dietary BHA (2000 ppm),

curcumin (2000 ppm) or resveratrol (500 ppm) from 1 week after carcinogen

treatment until termination had no effect on lung tumor multiplicity. Treatment

with dietary myo-inositol (30,000 ppm) or esculetin (2000 ppm) from 1 week after

carcinogen treatment until termination significantly reduced lung tumor

multiplicity, with the effect of myo-inositol being significantly greater than

that of esculetin. Treatment with dietary LTO (167, 1667 or 8333 ppm) from 1

week before carcinogen treatment until termination had no effect on lung tumor

multiplicity. The results of this study demonstrate that BHA is an effective

inhibitor of BaP plus NNK-induced lung tumorigenesis in A/J mice when

administered during the period of carcinogen treatment and that, among the

compounds tested, myo-inositol is most effective after carcinogen treatment.



Toxicol Appl Pharmacol 1995 Nov;135(1):45-57

Induction of phase I and phase II drug-metabolizing enzyme mRNA, protein, and activity by BHA, ethoxyquin, and oltipraz.

Buetler TM, Gallagher EP, Wang C, Stahl DL, Hayes JD, Eaton DL.

Department of Environmental Health, University of Washington, Seattle 98195,

USA.

Various natural and synthetic compounds are known to protect against cancer by

elevating phase II detoxification enzymes. Generally classified as

monofunctional, these inducers are believed to trigger cellular signal(s) that

activate gene transcription through an antioxidant or electrophile response

element (ARE/EpRE) in responsive genes. In contrast, the phase I enzymes of drug

metabolism (cytochrome P450s) are not believed to be induced by monofunctional

inducers and P450 genes have not been found to contain functional ARE/EpREs. In

this study, rats were treated with the monofunctional inducers tert-butylated

hydroxyanisole, ethoxyquin, and oltipraz to study the inducibility of individual

glutathione S-transferase isozymes, NADP(H):quinone oxidoreductase,

gamma-glutamylcysteine synthetase, UDP-glucuronosyl transferase, and cytochrome

P450 enzymes. Hepatic mRNAs were analyzed on Northern blots using gene-specific

oligonucleotide probes for GST Ya1, Ya2, Yc1, Yc2, Yb1, Yb2, and Yf, for UGT

1*06, and for P450 1A1, 1A2, 2B1, 2C11, 3A2, and 4A1. NADP(H):quinone

oxidoreductase and gamma-glutamylcysteine synthetase mRNAs were detected using

cDNA probes. All the phase II detoxification enzymes analyzed, except GST Yf,

were induced by the three monofunctional inducers, suggesting that these genes

may be regulated by a mechanism involving an ARE/EpRE element in their promoter

region. Interestingly, it was found that ethoxyquin was a particularly good

inducer for both members of the P450 2B family, 2B1 and 2B2, and both ethoxyquin

and oltipraz were also capable of modestly inducing P450 1A2 and 3A2. Oltipraz

was found to slightly induce P450 2B2, but not 2B1, at the dose and time

analyzed. Induction of mRNA generally correlated well with induction of protein

levels determined by Western blot and/or enzyme activity measurements for

selected enzymes. The results of this study suggest that many phase II enzymes

may contain ARE/EpRE elements in addition to those confirmed to be regulated by

a mechanism involving ARE/EpRE elements. In addition, it was found that several

P450 enzymes were induced by monofunctional inducers, suggesting a possibility

that some phase I enzymes may also be regulated by a mechanism involving

ARE/EpRE elements.



Food Chem Toxicol 1996 Apr;34(4):327-35

Inhibitory effects of the dietary antioxidants butylated hydroxyanisole and

butylated hydroxytoluene on bronchioloalveolar cell proliferation during the

bleomycin-induced pulmonary fibrosing process in hamsters.

Ikezaki S, Nishikawa A, Enami T, Furukawa F, Imazawa T, Uneyama C, Fukushima S,

Takahashi M.

Division of Pathology, National Institute of Health Sciences, Tokyo, Japan.

The effects of dietary antioxidants on bleomycin (BLM)-induced pulmonary

fibrosis were investigated in Syrian golden hamsters. In addition, the influence

on cell proliferative activity in bronchioloalveolar hyperplastic lesions during

the lung fibrosing process was evaluated in terms of argyrophil nucleolar

organizer regions (AgNORs) and proliferating cell nuclear antigen (PCNA). Male

6-wk-old hamsters were divided into six groups. Groups 1-3 were intratracheally

instilled with BLM at a dose of 2.5 U/kg body weight on days 0 and 14, and then

given a diet supplemented with 1% butylated hydroxyanisole (BHA), or 1%

butylated hydroxytoluene (BHT), or basal diet alone for the following 41 days.

Groups 4-6 were given 1% BHA, 1% BHT or basal diet without BLM treatment for the

same time period as that in those of groups 1-3. The mortality rate of animals

in group 1 (BLM/BHA) (one in 20; 5%) was lower than in those of groups 2

(BLM/BHT) (three in 20; 15%) and 3 (BLM alone) (four in 20; 20%). BHA and BHT

treatments significantly inhibited lung weight gains by BLM (P < 0.05).

Histopathologically, both BHA and BHT reduced BLM-induced pulmonary

histopathological changes such as fibrosis, macrophage aggregation and

epithelial proliferation, with a tendency for correlation with accumulation of

type III collagen. In addition, antioxidant treatment significantly lowered the

mean numbers of AgNORs (P < 0.01) and PCNA-labelling indices (P < 0.05) in the

hyperplastic bronchioloalveolar lesions. The results thus indicate that these

antioxidants exert inhibitory effects on proliferation of hyperplastic lesions

associated with lung fibrosis.



Cancer Lett 1998 Jan 9;122(1-2):151-6

Postnatal effect of smokeless tobacco on phytic acid or the butylated

hydroxyanisole-modulated hepatic detoxication system and antioxidant defense mechanism in suckling neonates and lactating mice.

Singh A, Singh SP.

Human Genetics Laboratory, School of Life Sciences, Jawaharlal Nehru University,

New Delhi, India.

The present study evaluates the potential of smokeless tobacco to

translactationally modify the chemopreventive efficacy of phytic acid and

butylated hydroxyanisole (BHA) via modulation of the hepatic xenobiotic

detoxication system and antioxidant defense mechanism in the murine system.

Phytic acid (1000 mg/kg b.w./day) by gavage while BHA (1% w/w) in diet induced a

significant increase in the levels of glutathione-S-transferase (GST), acid

soluble sulfhydryl (-SH), cytochrome b5 (Cyt. b5) and cytochrome P-450 (Cyt.

P-450) in lactating dams and suckling pups. The hepatic levels of GST and -SH

were significantly depressed whereas microsomal Cyt. b5, Cyt. P-450 and MDA

levels were elevated in groups treated with smokeless tobacco (50 or 100 mg/kg

b.w./day). The data reveals the inhibitory potential of smokeless tobacco on

phytic acid-induced GST/GSH system efficiency besides the significant

augmentation by smokeless tobacco on phytic acid or BHA-induced microsomal phase

I enzymes. The direct or translactational modulation in the levels of xenobiotic

detoxication system enzymes suggests the potential of smokeless tobacco to

modify the chemopreventive efficacy of phytic acid or BHA.



J Pharm Pharmacol 1996 Sep;48(9):940-4

Protective effect of butylated hydroxyanisole on adriamycin-induced

cardiotoxicity.

Vora J, Khaw BA, Narula J, Boroujerdi M.

Department of Pharmaceutical Sciences, Northeastern University, Boston, MA

02115, USA.

Adriamycin has a wide spectrum of antitumour activity with dose-related

cardiotoxicity as a major side effect. This cardiotoxicity has been suggested to

result from the generation of oxygen free radicals. The objective of the present

study was to investigate the influence of the antioxidant, butylated

hydroxyanisole co-therapy on the cardiotoxicity of adriamycin, in-vivo. The

aqueous solubility of butylated hydroxyanisole was enhanced by inclusion complex

formation with hydroxypropyl-beta-cyclodextrin. The extent of drug-induced

myocardial damage in rats was assessed using intravenous 111In-labelled

antimyosin Fab and chronological changes in serum creatine kinase levels. There

was a dose-related increase in myocardial antimyosin uptake in rats, which

reached a plateau at an adriamycin dose of 10 mg kg-1. The antimyosin uptake at this dose (% dose g-1 = 0.1942 +/- 0.0150, n = was significantly reduced by co-administration of butylated hydroxyanisole with adriamycin (10 mg kg-1 of each) to 0.1462 +/- 0.0116 (n = 5, P < 0.05). Assessment of cardiotoxicity in the rats was also performed by measuring serial changes in serum creatine kinase levels. Increasing doses of adriamycin caused an increase in serum creatine kinase levels with peak values obtained between 2 and 8 h after dosing. These values decreased upon co-administration of butylated hydroxyanisole with adriamycin at 10 mg kg-1, each and 30 mg kg-1 each by 29 and 41%, respectively.

On the other hand, butylated hydroxyanisole did not inhibit the tumouricidal activity of adriamycin as investigated in-vitro using the NMU rat mammary

adenocarcinoma cell-line. The significant reduction in anthracycline

cardiotoxicity by butylated hydroxyanisole coadministration may result from its scavenging action on adriamycin-mediated free-radical formation or its enhancement of activity of enzymes involved in the metabolism of adriamycin.

dufam ze sa to skoplo cele

[dexter13]

@ZEwa

ANF je dobre krmivo ale sedi zlozenim aj stavbou granul skor malym psikom prip. strednym

[fosilia]

Fraga dakujem. fakt ma pobavilo ako v Holandsku zeny tlacili do seba majonezu... Cakal som nieco ine nie vytiahnute studie z PubMedu. A len tie co mu vyhovovali. preco neposlal tie druhe. Hmm chlebodarca nedovolil.

Toto napise pracovnik RC. Prepac ale toto je silne zavadzanie.

Prva studia zacina v roku 1974 a konci v roku 2003. Dalsie vacsinou nezverejnene v odbornej literature siahaju az do roku 2005. To za prve. Za druhe ak niekto o sebe tvrdi, ze je odbornik nemoze porovnavat hlodavca s clovekom.
Najskor si treba zistit co je to forestomachs a potom nieco porovnavat.

Dnes pise sa rok 2007 je jasne ze tato latka je zakerna v tom, ze sa sprava zvlastne. Posobi ako antioxidant a dokonca moze sa spravat ako vhodna prevencia pri tvorbe rakovinotvornych buniek ale z nicoho nic sa z nej stava zakerna latka, ktora likviduje napr.oblicky, zacne napomahat uz postihnutym bunkam a je koniec.

Preto si vsimni ze v odbornej literature sa BHA oznacuje ako problemova latka a u tvrdych odporcov ako karcinogenna latka. Bohuzial oba vyrazy su pravdive. Je jasne ze testy sa budu i nadalej vykonavat na hlodavcoch a nie na psoch ci mackach. Avsak kto to bude financovat, ked v minulosti FDA dalo suhlas s konzervovanim granulovanych krmiv s dopocucenim znizit davky na 30. V malych davkach sa vyhodnotilo ze je BHA bezpecny ale opat to je velmi riskatne tvrdenie.

My to nevyriesime tak pozrime sa na pohlad v podstate poslednych informacii o tomto syntetickom antioxidante pohladom od Judity E. Foulke , ktora jasne poukazuje na to co pisem. Nastastie nie je pracovnikom Walthamu teda majitela znacky RC. A vsimnite si ake dalsie znacky tato firma vyraba.

http://www.waltham.com/brands.htm

Mozu dnes zacat tvrdit ze budu konzervovat bez BHA. Asi tazko. Vysoke zaruky a sila penazi to nedovoli... Ano boli nuteni pri vyrobe americkeho krmiva RC natural blend zmenit konzervaciu ale to sa krmiv v EU netyka.

BHA and the related compound butylated hydroxytoluene (BHT)
have been used for years, mostly in foods that are high in fats and
oils. They slow the development of off-flavors, odors, and color
changes caused by oxidation. When the food additives amendment was
enacted, BHA and BHT were listed as common preservatives considered
generally recognized as safe (GRAS). GRAS regulations limit BHA and
BHT to 0.02 percent or 200 parts per million (ppm) of the fat or
oil content of the food product.
Lawrence Lin, Ph.D., of FDA's Center for Food Safety and
Applied Nutrition, explains, "The 0.02 percent allowed relates only
to the product's fat content. For example, if a product weighs 100
grams and one of those grams is fat, the quantity of BHA in the
product cannot exceed 0.02 percent of that one gram of fat."
BHA is also used as a preservative for dry foods, such as
cereals. But because such foods contain so little fat, the amount
of BHA allowed cannot be measured against the percentage of fat,
explains Lin. Therefore, as manufacturers petitioned FDA for
approvals for this use, the agency set limits for each type of
food. On cereals, for example, FDA limited BHA to 50 ppm of the
total product.
In 1978, under contract with FDA, the Life Sciences Research
Office of the Federation of American Societies for Experimental
Biology (xxxxx) examined the health aspects of BHA as part of FDA's
comprehensive review of GRAS safety assessments. xxxxx concluded
that although BHA was safe at permitted levels, additional studies
were needed.
Since that evaluation, other studies suggested that at very
high levels in the diets of laboratory animals, BHA could cause
tumors in the forestomach of rats, mice and hamsters, and liver
tumors in fish. Many experts examined the data and concluded the
tests did not establish that such problems could exist in humans,
mostly because humans do not have forestomachs. Other studies
showed that BHA was protective, inhibiting the effect of some
chemical carcinogens, depending on the conditions of the tests.
Studies on BHA were reviewed by scientists from the United
Kingdom, Canada, Japan, and the United States. Their findings were
published in 1983 in the Report of the Working Group on the
Toxicology and Metabolism of Antioxidants and reviewed in the 1990
Annual Review of Pharmacology and Toxicology. The 1983 report
stated that data from a Japanese study showed a high incidence of
cancerous tumors and papillomas (benign tumors of the skin or
mucous membranes) of the forestomach of treated rats and that the
effect was dose-related. The report also mentioned the possible
existence of a no-effect level, based on dose response, and noted
that the level which produced cancer in this study was many
thousands of times higher than the level to which humans are
exposed.
In November 1990, Glenn Scott, M.D., a physician then living
in New York who has since moved to Cincinnati, filed a petition
with FDA, asking the agency to prohibit the use of BHA in food.
Scott cited animal studies to support his request. Before acting on
Scott's petition, however, FDA asked xxxxx to reexamine the
scientific data on BHA. By March 1994, xxxxx is scheduled to
provide FDA with a report on the most current scientific
information bearing on the relationship of BHA ingestion to cancer
in animals.

[tigricka]

Ahoj fosilia, prosím, čo si myslíš o tomto krmive? ACANA Puppy Large Breed ? Teraz krmim eucanubou puppy and large a chcela by som zmeniť granule za niečo kvalitné, ale lacnejšie. Mám 5 mesačné šteniatko dobermanka. Ak nie sú lepšie, tak mi poraď prosím, čím by si krmil ty, alebo či je tá eucanuba dobrá a mám ostať pri nej. Za odpoveď ďakujem.

[Amaguk]

Amaguk - ako mam skusat surovu stravu, ked Hoshiko nechce surove maso ani za svet? Skusala som aj len trochu obvarene, ale ani to nechce.
... Dakujem

Amaguk, prosim, porad. Netrpezlivo cakam odpoved, ale asi si to prehliadla, bolo tu toho naraz viac.

Aj vcera som psici na skusku hodila masovu kost, ocuchala, odisla, ani nezakusla. Maso tiez do papulky nedala....


Inak, o tom Timberwolfe som pocula aj ja - od slovenskeho majitela netoveho obchodu, ze do dvoch mesiacov bude



Evka, ako sa ma Tesak?

ahoj, bola som par dni mimo BA. na tovju otazku som ti poslala SS, aby sme tu nerozoberali veci OT

[tigricka]

Ahoj Fosilia, nikde som nenašla ani zmienku o krmive Ontario Puppy Large Breed. Poznáš to? Je to nejaké kanadské, nič viac neviem. Čím doporučuješ krmiť dobermana? Dík

[fosilia]

Kanadske? Nenechaj sa klamat obchodnikmi a pozri sa na EAN na obale.
O tomto krmive sa popisalo hadam dost. Pre mne nie.

[Fraga]

Fosilia a čo hovoríš na českú Calibra? ujo mi povedal superpremiove krmivo je? nie je?

[fosilia]

Fraga
Adult large:
drůbeží maso a produkty drůbežího původu, rýže, kukuřice, drůbeží tuk.
a zrazu v anglickom prekalde je nieco ine:
chicken meal (>24 %), rice, corn, poultry fat
Zdroj: www.calibra.cz

[Fraga]

hih vidim že sa baviš no čo už hadam z toho neumrú ja mam jazvece kúpila som smolku. Skôr ako o zloženie (viem že to obsahuje ryžu, kukuricu a možno aj mäsko) išlo o tie škaredé BHT a BHA, resp. či tam niečo také zlé nie je...

[fosilia]

hih vidim že sa baviš no čo už hadam z toho neumrú ja mam jazvece kúpila som smolku. Skôr ako o zloženie (viem že to obsahuje ryžu, kukuricu a možno aj mäsko) išlo o tie škaredé BHT a BHA, resp. či tam niečo také zlé nie je...

Uz ten prvy text je jasny zmes hydiny pomlete vsetko s kostami a hura do textu chicken meal. Co ta stalo vreco tohoto superpremioveho krmiva?